DISEASES OF CIRCULATORY SYSTEM

1. Diagnostic approach:
2. Principles of circulatory failure :

Heart failure
Due to:
- Defect in heart filling
- Abnormality in myocardium
Or in conducting system
- Excessive work load

Peripheral failure
due to:
-Loss of fluid
-Dilatation of peripheral vessels.
-Pooling of blood in

- Combination of above

peripheral system

Consequences
1. Either complete or partial hamper in, - Exchanges of fluid, electrolytes, oxygen, & nutrients
& excretory substances.
2. The first critical system is nervous system to be affected.
Diagnostic approach
i)
ii)

History, inspection, palpation & percussion need especial experiences.

Auscultation by stethoscope or phonendoscope reveal about heart sounds, sometimes
position of heart also.
Tachycardia increased rate of heart beat
Bradycardia - Decreased rate of heart beat
Transient sound Normal, 1st, 2nd, 3rd, & 4th,
Murmur sound
Pericardial rub

- abnormal sound or adventitives

- Pericardial heart sound.

Rhythm Regularity of successive pulse.

Rhythmic deviation in rhythm.
iii)

Blood pressure in animal not easy,it has been tried in dog & house by
Dog tibia artery

House - Middle coceygeal artery.

Done man Brachial artery.
By sphygonometer

Pressure

Systolic
(Ventricular contraction)

Diastolic
(Ventricular relaxation.)

Hypertension increased Pressure

Hypo-tension - decreased Pressure

iv)

Angiography

Electro cardiogram is

not common in livestock done in human.

PERICARDITIS
Inflammation of pericardium is called ~. It may be acute or chronic and effusive, Fibrinous or
adhesive traumatic Pericarditis is widely prevalent in cattle but not in house.

Aetiology
1. TRP in cattle is most frequent.
2. Localization of blood borne diseases- in all sps.
3. Extension of inflammation from pleurisy & myocardium- in all sps.
Symptoms
Bacteria
i)

Pasteurellosis

ii)
iii)
iv)
v)
vi)
vii)

Sheptococcus sps
Salmonella spp
Leptospira- spp
Mycoplasmal spp
Mycobere ferium spp.
Glassers disease in pig.

Viral
i.
ii.

Infectious feline peritonitis

Canine distemper

Fungal
i)
Coccidioisomycosis
ii)
Actonomycosis
chronic uremia may set up pericardial lesion.

Others

Clinical findings
i)
ii)
iii)

Pain, reluctant to move & abducted elbows, arching of back & shallow abdominal
respiration
103 to 106o f temperature & increased pulse rate & weak pulse.
Fibrinous Pericarditis in horse is mainly fasted by marked muffling sounds, Tachycardia,
distension of jugular vein & ventral edema.

Diagnosis
1. 1.Clinical findings Abducted elbow , muffling sound
2. Ecg (electro-cardio gram graphic recording of the electrical potentials produced in
association with the heart beat)
3. X-ray reveals foreign body, displacement e.t.c.

Differential diagnosis
i)
Pleurisy confused by friction sound differentiate by synchronization of friction sounds
with respiratory cycle.
Absence of other pericardial infn symptoms.
ii)

Murmur sounds due to pericardial sounds are present throughout

Congenital defects the cardial cycle breaks

iii)
iv)

Muffling sounds due to pleurisy Careful examination reveals pulmonary emphysema

Hydro pericardium Aspiratory puncture may accompanying with edema.

i)

TRD Leukocytosis & shift to the left.

Treatment
Use of specific antibiotic for specific causative agent.
i)
ii)
iii)

Non specific treatment is use of broad-spectrum antibiotic & salt

Paracentesis & use of diuretics is use fuel.
Salt free diet & use of fribrinolytic drugs like oxalate

MYOCARDITIS:
Inflammation of heart muscle is kwon as Myocarditis

Aetiology
1. Non infective: due to Auto-immune condition and toxicity of heavy metals eq.
Arsenic,hg,lead, copper etc.
2. Infective agent
a) Virus - FMD virus in young one.i.e. Equine infections anaemia,Canine parvo virus,&
canine distemper.
b) Bacteria Clostridium chauvoei, steptococcous staphy bococess.
c) Funfus cryptocossus.
d) Parasiles eq. Cyst, trypanosoma, toxoplasma, strongyless etc.
Pathogenesis
Clinical findings
i)
ii)
iii)
iv)
v)
vi)

Ineffective cardiade output & passive verous congestion.

Mycocardial degeneration leads to acute cardial failure & death.

Increased Pulse rate & arrhythmia.

Dyspnoea & weakness.
Exhaustion & increased temperature in infective condn.
Chronic venous congestion & heart failure.
Syncope & death.
Acute death (i.e. without sign & symptom)

Diagnosis
Difficulty by Clinical symptoms.

D. Diagnosis
i)
ii)

Electro-cardiography.(ECG)
Difficult to differentiable from endocardium

Treatment
i)
ii)

Treatment of primary cause.

Symptomatic treatment but in large animal may not be useful.

ENDOCARDITIS
Inflammation of endocardium with interference in blood ejection or valvular stenosis is
Endocarditis which is characterized clinically by it is manifestation and murmur sound of heart.

Aetiology
Farm animal Bacteria (strep to, Corynebacterium, clostridium, Mycoplasma, erycepaothrix,
and Escherichia coli )
Virus also i.e. influenza
Horse: above cause as well as migrating strongylus larvae.

Pathogenesis
Due to implantation of bacteria on to the valves from the blood stream result bacteremia or
embolism of the valve capillaries leads to myocardial disease may cause inflammation of
endothelium, its damage or edema of valve. Congenital cardiac defect may also predispose valve
problem or stressful work of valve & endocarditis, vegetative and ulcerative type of lesions may
cause problems on blood ejection & flood. Fragments of vegetative lesions after detaching may
come into circulation & result embolic end arteritis military Pulmonary abscesses, abscesses on
myocardium, kidney & joints chronic lesions on value results adhesions of cusps. Shrinking
distortion and thickening of the valve cusps. At this stage inference of blood flood occurs &
congestive heart failure always results.

Involvement
Cattle: - Most frequently right arterio-ventricular value and left arterio-ventricular.
Horse Aortic semi lunar valves most frequent (value of aorta origin) and pulmonary
value origin of pulmonary artery which each value consists three flap (cusps), less
frequently left a tro- ventricular value.

Clinical findings
i)
Murmur sound on auscultation at the cardiac over and poor exercise tolerance.
ii)
Moderate fluctuating fever;
iii)
Secondary involvement of other organs result Peripheral lymphadenitis, embolic
pneumonia, nephritis, arthritis, tenosynovitis, or Myocarditis.
iv)
Loss of condition pale mucous membrane & increased heart rate.
v)
In cattle additional symptoms are Grunting respiration, moderate ruminal tympany,
scouring or constipation, blindness, facial paralysis, muscle weakness, recumbency,
jaundice & sudden death. Distension of jugular vein, general edema and a systolic &
diastolic murmur sound in many cases. Periodic ill thrill is common history.
vi)
In horse- jugular proment in terminal stages & hot edema.
vii)
In swine Agalactia, loss of wt, intolerance in exercise & dyspnoea at rest.

Diagnosis
i)
ii)

Difficult from clinical symptoms.

Phonocardiography: - Technique for recording heart sounds & murmurs. These are picked
up by microphone placed over the heart.

Differential diagnosis
Endocarditis & Pericarditis and other causes of cardiac failure are confusion. In cattle
confusion mostly occur in lympomatosis
i)

In endocarditis.
Acute
- lencocytosis & shift to the left Monocytes increased, increased
macrophages & severe anaemia in
Chronic: - Hyper-gamma-globulinemia in bacterial infn. Repeated examination of
urine gives proteinuria & bacteria in urine.

ii)

Echocardiography reveals about echoes from vegetative lesion & defect

abnormal value movement.

Treatment:i.
Not so hopeful.
ii.
Blood culture & drug sensitivity test. Use of specific or broad spectrum
antibiotics.
iii.
Streptococcus infn in cattle is difficult because its resistance so procaine benzyl
penicillin @ 20000 units/kg*daily*for 7-10 days or longer.
iv. Amino glycoside are combined form first five days if temperature not reduces,
infection is under control. Again 7 days or more treatment must be continued.
v. Treatment with macrolides (eq. Erythromycin) & ampicillin is effective but they
are expensive.
vi.
Chances of relapse is move, of signs of congestive heat failure prognosis is
unfavorable.
HYPERTOPHY AND DILATION OF HEART
Compensatory result
Hypertrophy and dilatation of heart can collectively be called cardiac enlargement. Physiological
hypertrophy of heart is the normal physiological enlargement of heart in race or athletic animals.
Enlargement o heart is due to Persistent increased work loads that are associated with
cardiovascular disease, the heart may respond

Cardiac hypertrophy is due to increased pressure load

By dilatation, hypertrophy or combination of both

Cardiac hyper tropy
Usual response of

Cardiac dilation
- Usual response

- Increased pressure load & in this there is

increased volume load & probably

Increment of individual fibre, size

results from fiber re-arrangement.

Increase in total mass.

- Compensatory mechanism
fos coronary circulation
In state of cardiac insufficiency

- By this increased volume of blood

can be ejected (by single contract)
or per unit contraction.
-Depends on laplace loud which

Increased tension request for producing

Increased inside chamber
Cardiac reserve the normal heart has the capacity to in release body weight
several folds in response to normal physiological demands created by
exercise and to a less extent by pregnancy, by lactation & by digestion.
Collectively this response comprise the cardiac reserve
.
Clinical findings
o Degree of enlargement is a good indication of degree of cardiac embarrassment but accurate
measurement is impracticable.
o Increased Pressure on heart, flow load;0.
o Presence of myocardial diseased increased of cardiac reserve.
Diagnosis
By careful auscultation & palpation of apex beat of heart.
D. Diagnosis

Displacement heat by space occmpying lesions.

Ventral collapse of lung & upw and displacement of heat
Radiography & eco-cariographic.

Treatment
Treatment of primary causes.

CONGESTIVE HEART FAILURE

Failure of the heart to maintain circulatory equilibrium at rest and congestion of venous circuit
accompanied by dilation of vessels, edema of the lungs of periphery, enlargement of the heart
with increased rate is known as ~. Pulmonary circulation implies left sided heart failure and
systemic venous circulation implies right sided heart failure.
Aetiology
1. Any factor or disorder which causes Myocarditis, endocarditis or Pericarditis which interfere
in blood flood.
2. Any disease which weakens the face of myocardial contraction(may be due to nutrition)
3. Any type of alveolar diseases e.g. Stenosis, congenital defect persistent defect arteries,
rupture of value or aortic valued effect

4. Myopathy or myocardial infarction.

5. Chronic pulmonary emphysema or disease eg. Fibrosis of lungs, emphysema.
6. Hypertension due to altitude (more time to exchange the gasses due to law concn of 02) or any
other causes.
7. Congenital pulmonary steno sis, vascular abnormality
ENDOCARDITIS
Pathogenesis
Persistent work load for a long time on the heart may be either due to a pressure load or a flood
load. Lesions of aortic or pulmonary value result in pressure load (if high pressure needed to
pump) and a flood load or volume load (more volume of the blood to be ejected) is generally due
to acquired or congenital heart defects.

When an increase load is placed upon ejection of the blood from the heart or the contractile
power or the myocardium is reduced, compensatory mechanism including heart rate, ventricular
filling, re distribution of blood flood, dilatation and hypertrophy came into play to maintain
increased circulatory equilibrium. This results reduction in cardiac reserve & poor exercise
tolerance.

When the compensatory mechanisms reach then physiologic limit & the heart is unable to cope
with the circulatory requirement at rest congestive heart failure develops.

The weakened heart cannot maintain adequate arterial pressure on kidney which consequences
retention of salt & water leading to blood volume. This large blood volume cannot be handled
by failing chamber. Consequently there will be stagnation or congestion of blood in that circuit.
Increased blood volume required increased stretching of myocardium to be ejected which is
impossible beyond the physiologic limit & results cardiac failure.

Clinical findings
A. Left sided cardiac failure :- (oxygenated blood obstruction)
- Dyspnoea ( respiration & depth) at rest, cough, presence of moist cracles, at the base of
the lungs, cyanosis, increased heart rate.
B. Right sided cardiac failure ( systemic failure)
o Edema, Anasarca(ventral surface of the body neck and jugular vein )

o Ascites, hydrothorax, hydro pericardium.

o Enlarged liver & palpable at right costal arch with thickened & rounded
edge.
o Oliguria, concentrated urine & presence of albumen.
o Lose Faeces, decreased weight of body with due to edema but rapid loss of
condition.
o Dilated superficial veins mainly the jugular.
Epistaxis in horses (may be)
Diagnosis
By clinical symptoms.
i)

ECG.(electro-cardiography)

D. Diagnosis
i)

Peritonitis :- On Paracentesis presence of bacteria & Leukocytosis

- Absence of cardiac involvement.
ii)
Ruptured bladder :- Oliguria
- BUN(Blood urea nitrogen) & peritoneal flood nitrogen
- Abdominal pain & strain to Micturation .
iii)
Hepatic fibrosis :
- Jaundice & photosensitization.
- Liver function test.
iv)
Edema: - May occur in mare & condition near to calving date.
- There is no jugular engorgement. & evidence of cardiac involvement.
- May be due to endo parasites or hypo-proteinuria. Dyspnoea May be due
to pulmonary edema
- Pulmonary emphysema
- Allergic or anaphylactic stage
- Fog fever of cattle
Line of Treatment
1.
2.
3.
4.
5.

Provide rest so that there is less demand of blood.

Perform specific causative agent treatment.
Use salt free diet in edematous condition
Use diuretics to treat edematous condition.
In severe condition vein section is suggested as an emergency treatment @ 4-8ml blood /kg
body wt at a time. It cannot be repeated before 7 days.
6. Use of digitalis: - As per needed.
Induce with little dose achieve desired therapeutic result without toxic symptoms & maintain
as per needed is digitalization.
7. Supportive therapy on needed: - 02 for anoxia Tranquillizes for pain,
Body cannot thrive the condition & animal dies. Usually it is unfavorable

Treatment
1. Since there is no specific treatment, symptomatic treatment should be followed. To reduce
the spasm or cramp and to sooth the nerves anti-spasmodic like chlorpromazine,
Phenobarbitone, etc. are used.
2. To correct neurological disorders methyldopa (lardopa) 500mg tab once daily followed by
tab/week can be given. Or trihexypnendyl hcl (pecitane-lederle) 2 mg (1 tab) B.I.D. orally.
3. Vit. B .complex + vitamin c. should be given.
Prevention
1. Since the disease is a sequlae of Distemper, it should treat with additional 10 days after the
apparent symptoms manifestation causes.

Simple Indigestion in Ruminants

(Mild dietary indigestion)

Simple indigestion is a minor disturbance in ruminant GI function that occurs most

commonly in cattle and rarely in sheep and goats. Simple indigestion is a diagnosis
of exclusion and is typically related to an abrupt change in the quality or quantity of
the diet.
Etiology
Almost any dietary factor that can alter the intraruminal environment can cause
simple indigestion. The disease is common in hand-fed dairy and beef cattle
because of variability in the quality and quantity of their feed. Dairy cattle may
suddenly eat excessive quantities of highly palatable feeds such as corn or grass
silage; beef cattle may eat excessive quantities of relatively indigestible, poorquality roughage during winter. During drought, cattle and sheep may be forced to
eat large quantities of poor-quality straw, bedding, or grain. Simple indigestion can
result from suddenly changing the feed, using spoiled or frozen feeds, introducing

urea to a ration, turning cattle onto a lush cereal grain pasture, or introducing
feedlot cattle to a high-level grain ration.
Simple indigestion is usually associated with a sudden change in the pH of the
ruminal contents, such as a decrease in ruminal pH due to excessive fermentation
or an increase in ruminal pH due to putrefaction of ingested feed. It can also result
from the accumulation of excessive quantities of relatively indigestible feed that
may physically impair rumen function. Multiple animals are usually simultaneously
affected because simple indigestion has a nutritional basis, although the severity of
the clinical signs can vary among animals.
Clinical Findings
The clinical signs depend on the type of animal affected and cause of the disorder.
Silage overfeeding causes anorexia and a moderate drop in milk production in dairy
cattle. The rumen is usually full, firm, and doughy; primary contractions are
decreased in rate or absent, but secondary contractions may be present although
usually decreased in strength. Temperature, pulse, and respiration are normal. The
feces are normal to firm in consistency but reduced in amount. Recovery usually is
spontaneous within 2448 hr.
Simple indigestion due to excessive feeding of grain results in anorexia and ruminal
hypomotility to atony (stasis). The rumen is not necessarily full and may contain
excessive fluid. The feces are usually soft to watery and foul smelling. The affected
animal is bright and alert and usually begins to eat within 24 hr. A more severe
digestive upset due to excessive feeding of grain is described as grain overload
(see Grain Overload in Ruminants).
Diagnosis
A diagnosis of simple indigestion is based on a history of an abrupt change in the
nature or amount of the diet, multiple animals being affected, and the exclusion of
other causes of forestomach dysfunction. The diagnosis is confirmed by collection
and examination of ruminal fluid, which may have an abnormal pH (<6 or >7),
decrease in the numbers and size of protozoa, or prolonged methylene blue
reduction time (a measure of bacterial activity).
The systemic reaction and painful responses to deep palpation of the xiphoid in
traumatic reticuloperitonitis are not seen. The history and the absence of ketonuria
help eliminate ketosis from consideration. The possibility of left displaced

abomasum usually can be eliminated by simultaneous percussion and auscultation.

Vagal indigestion, abomasal volvulus, and cecocolic volvulus become more readily
detectable as they progress. Grain overload is differentiated from simple indigestion
by its greater severity and the pronounced fall in the pH of the rumen contents to
<5.5.
Treatment
Treatment is aimed at correcting the suspected dietary factors. Spontaneous
recovery is usual when animals are fed a typical ruminant diet. Administration of
20 L of warm water or saline via a stomach tube, followed by vigorous kneading of
the rumen, may help restore rumen function in adult cattle. Magnesium hydroxide
PO may be useful when excessive amounts of grain have been ingested, but
magnesium hydroxide should only be administered to cattle with low ruminal pH
(<6), otherwise excessive forestomach and systemic alkalinization can result.
Purported rumenatorics (eg, nux vomica, ginger, tartar emetic,
parasympathomimetics) are not recommended as ancillary treatments. If too much
urea (see Nonprotein Nitrogen Poisoning) or protein has been ingested, vinegar
(acetic acid) may be administered PO to return rumen pH to the normal range. If the
number or activity of ruminal microbes is reduced, administration of 48 L of ruminal
fluid from a healthy cow will help. (see Ruminal Fluid Transfer.) Oral or intravenous
electrolyte solutions may be needed to correct electrolyte and acid-base
abnormalities, particularly in dehydrated cattle.

Grain Overload in Ruminants

(Lactic acidosis, Carbohydrate engorgement, Rumenitis)

Grain overload is an acute disease of ruminants that is characterized by rumen

hypomotility to atony, dehydration, acidemia, diarrhea, toxemia, incoordination,

collapse, and in severe cases, death.
Etiology and Pathogenesis
The disease is most common in cattle that accidentally gain access to large
quantities of readily digestible carbohydrates, particularly grain. Grain overload also
is common in feedlot cattle when they are introduced to heavy grain diets too
quickly. Wheat, barley, and corn are the most readily digestible grains; oats are less
digestible. Less common causes include engorgement with apples, grapes, bread,
batter's dough, sugar beets, potatoes, mangels, or sour wet brewer's grain that was
incompletely fermented in the brewery. The amount of feed required to produce
acute illness depends on the kind of grain, previous experience of the animal with
that grain, the nutritional status and condition of the animal, and the nature of the
ruminal microflora. Adult cattle accustomed to heavy grain diets may consume 30
45 lb (1520 kg) of grain and develop only moderate illness, while others may
become acutely ill and die after eating 20 lb (10 kg) of grain.
Ingestion of toxic amounts of highly fermentable carbohydrates is followed within 2
6 hr by a change in the microbial population in the rumen. The number of grampositive bacteria (Streptococcus bovis) increases markedly, which results in the
production of large quantities of lactic acid. The rumen pH falls to 5, which
destroys protozoa, cellulolytic organisms, and lactate-utilizing organisms, and
impairs rumen motility. The low pH allows the lactobacilli to utilize the carbohydrate
and to produce excessive quantities of lactic acid. The superimposition of lactic acid
and its salts, L-lactate and D-lactate, on the existing solutes in the rumen liquid
causes osmotic pressure to rise substantially, which results in the movement of
excessive quantities of fluid into the rumen, causing dehydration.
The low ruminal pH causes a chemical rumenitis, and the absorption of lactate,
particularly d-lactate, results in lactic acidosis and acidemia. In addition to metabolic
(strong ion) acidosis and dehydration, the pathophysiologic consequences are
hemoconcentration, cardiovascular collapse, renal failure, muscular weakness,
shock, and death. Animals that survive may develop mycotic rumenitis in several
days and hepatic abscesses several weeks or months later. They may have
evidence of ruminal epithelial damage at slaughter. The relationship between grain
overload and chronic laminitis in cattle is unclear.
Clinical Findings

Carbohydrate engorgement results in conditions ranging from simple indigestion

(see Simple Indigestion in Ruminants) to a rapidly fatal acidemia and strong ion
(metabolic) acidosis. The interval between overeating and onset of signs is shorter
with ground feed than with whole grain, and severity increases with the amount
eaten. A few hours after engorgement, the only detectable abnormality may be an
enlarged rumen and possibly some abdominal pain (manifest by belly kicking or
treading of the hindlimbs). In the mild form, the rumen movements are reduced but
not entirely absent, the cattle are anorectic but bright and alert, and diarrhea is
common. The animals usually begin eating again 34 days later without any
specific treatment.
Within 2448 hr of the onset of severe overload, some animals will be recumbent,
some will be staggering, and others will be standing quietly; all will be completely off
feed. Immediately after consuming large quantities of dry grain, cattle may engorge
themselves on water, but once ill they usually do not drink at all.
Body temperature is usually below normal, 98101F (36.538.5C); however, in
animals exposed to the sun in hot weather, it may be increased to 106F (41C).
Respirations tend to be shallow and rapid, up to 6090/min. The heart rate usually
is increased in accordance with severity of the acidemia; the prognosis is poor for
cattle with heart rates >120 bpm. Diarrhea is common and usually profuse and
malodorous. The feces are soft to liquid, yellow or tan, and have an obvious sweetsour odor. The feces frequently contain undigested kernels of the feed that has
induced the overload. In mild cases, dehydration equals 46% body wt, but losses
may reach 1012% in severe cases.
In severe grain overload, the primary contractions of the rumen are completely
absent, although the gurgling sounds of gas rising through the large quantity of fluid
are usually audible on auscultation. Ballottement and auscultation of the left flank
may elicit fluid-splashing sounds in the rumen. The contents of the rumen, as
palpated through the left paralumbar fossa, may feel firm and doughy in cattle that
were previously on a roughage diet and have consumed a large amount of grain. In
cattle that have become ill on smaller amounts of grain, the rumen will feel not
necessarily full, but rather resilient because of the excessive fluid. Severely affected
animals stagger and may bump into objects; their palpebral reflex is sluggish or
absent, and the pupillary light reflex is usually present but slower than normal.
Affected animals commonly lie quietly, often with the head turned into the flank, and
their response to any stimulus is much decreased so that they resemble cases of

parturient paresis.
Acute laminitis may be present and is most common in those animals that are not
severely affected; chronic laminitis may develop weeks or months later. Anuria is a
common finding in acute cases, and diuresis after fluid therapy is a good prognostic
sign.
Death may occur in 2472 hr, and rapid development of acute signs, particularly
recumbency, indicates a need for aggressive treatment. A reduction in heart rate,
rise in temperature, return of ruminal movement, and passage of large amounts of
soft feces are more favorable signs. However, some animals appear to improve
temporarily but become severely ill again 34 days later, probably because of
severe bacterial and fungal rumenitis; death from acute diffuse peritonitis usually
follows in 23 days. In pregnant cattle that survive the severe form of the disease,
abortion may occur 1014 days later.
Diagnosis
The diagnosis is usually obvious if the history is available and multiple animals are
affected. The diagnosis can be confirmed by the clinical findings, a low ruminal pH
(<5.5 in cattle unaccustomed to a high grain diet), and examining the microflora of
the rumen for the presence of live protozoa. When only one animal is involved and
there is no history of engorgement, the diagnosis is less obvious, but the clinical
signsa static rumen with gurgling fluid sounds, diarrhea, ataxia, and a normal
temperatureare characteristic. Rumen fluid analysis in these animals is required
to confirm the diagnosis of grain overload.
Although parturient paresis (see Parturient Paresis in Cows) may resemble rumen
overload, diarrhea and dehydration are not typical, the intensity of heart sounds is
reduced, and the response to calcium injection is usually dramatic. Peracute
coliform mastitis and acute diffuse peritonitis may also resemble overload, but
usually a careful examination will reveal the cause of the toxemia.
To avoid an increase in pH on exposure to air, the pH of rumen fluid obtained by
oro-ruminal stomach tube or ruminal paracentesis should be checked promptly.
Normally, the pH in cattle on roughage is 67; in those on a high grain diet, 5.56.0.
Values below 5.5 are strongly suggestive of grain overload, and a rumen pH <5.0
indicates severe acidemia and metabolic acidosis. Wide-range (211) pH indicator
paper is suitable for field use. Ruminal fluid should also be examined

microscopically if access to a laboratory is available; fluid from affected cattle will

have decreased numbers of protozoa (particularly large and medium sized
protozoa). A Gram's stain of ruminal fluid will reveal a change from predominantly
gram-negative bacteria (normal) to predominantly gram-positive bacteria in grain
overload, with a concomitant loss in bacterial diversity.
Increased blood d-lactate and l-lactate and inorganic phosphate concentrations,
mild hypocalcemia, and reduced urinary pH are also seen, but it is seldom
necessary to check such values to make a firm diagnosis. The diagnostic problem
is to properly assess which animals require vigorous therapy (or slaughter), which
require supportive therapy, which have only a mild indigestion that will correct itself
if water and grain intake are restricted and hay and exercise are provided, and
which need nothing beyond their routine care and ration. In an outbreak of overload
involving several animals, it is necessary to identify those animals that need the
most intensive therapy and those that will recover with minimal medical therapy.
If the cattle are found while still eating, it is possible that some of the group will fall
into each category, and close monitoring is necessary to minimize losses. Cattle
found while engorging or shortly thereafter should be allowed no more concentrate
or water, but plenty of good hay for up to 24 hr, and should be forced to walk
periodically. Cattle that appear normal at the end of the first day are probably in
good health, although if even one is ill, all should be monitored closely for 48 hr.
Most of those that have eaten enough concentrate to be affected seriously show
signs within 68 hr.
Treatment
For all cattle suspected of having eaten large quantities of concentrate, it is
believed that restricting water intake for the first 1824 hr is helpful, although this
has not been proven. If overload is serious, slaughter for salvage should be
considered; in feeders nearing the end of their feeding period, it may well be the
most economical choice. Mortality is high in severely affected animals unless
aggressive therapeutic measures are initiated early. In such animals, removal of
rumen contents and replacement with ingesta taken from healthy animals is
necessary. In animals that are still standing, rumenotomy is preferred to rumen
lavage, because animals may aspirate during the lavage procedure and only
rumenotomy ensures that all ingested grain has been removed. Rumen lavage may
be accomplished with a large stomach tube if sufficient water is available. A largebore tube (2.5 cm inside diameter, 3 m long) should be used, and enough water

added to distend the left paralumbar fossa; gravity flow is then allowed to empty out
what it will. Repeating this 1520 times achieves the same results (and requires
about as much time) as using rumenotomy to empty and wash out the rumen with a
siphon.
Emptying the rumen should be followed by rumen inoculation (see Drugs for
Specific Purposes in the Ruminant Digestive System) and, if not accomplished
before signs of severe illness are evident, by rigorous fluid therapy to correct the
metabolic acidosis and dehydration and to restore renal function. Initially, over a
period of 30 min, 5% sodium bicarbonate solution should be given IV (5 L/450
kg). During the next 612 hr, a balanced electrolyte solution, or a 1.3% solution of
sodium bicarbonate in saline, may be given IV, up to as much as 60 L/450 kg body
wt. Urination should resume during this period. Usually, it is unnecessary and even
undesirable to also administer antacids PO (or intraruminally), particularly if IV
sodium bicarbonate has been administered. Procaine penicillin G should be
administered IM to all affected animals for at least 5 days to minimize the
development of bacterial rumenitis and liver abscesses. Thiamine should also be
administered IM to facilitate metabolism of l-lactate via pyruvate and oxidative
phosphorylation; grain overload animals also have low concentrations of thiamine in
rumen fluid due to the increased production of thiaminase by ruminal bacteria.
There is no effective preventive treatment for mycotic rumenitis.
Emptying the rumen is unnecessary in less severe cases. In these cattle,
magnesium hydroxide (500 g/450 kg body wt) should be added to warm water,
pumped into the rumen, and mixed therein via kneading the flank. This may be all
that is necessary if the rumen pH is >5 and the animal is still standing and
reasonably alert several hours after the engorgement. A heart rate of 7085 bpm,
weak ruminal contractions, normal body temperature, and especially willingness to
eat are additional reassurances that this therapy will suffice. If any question
remains, additional fluids should be given. During the convalescent period, which
may last 24 days, good-quality hay and no grain should be given, and the grain
then reintroduced gradually. If good appetite returns within 3 days, the prognosis is
good. However, if treatment was not started early enough to prevent acidification of
the ruminal contents, and mycotic infection of the rumen wall ensues, relapse is
likely within 35 days, and the prognosis is grave.
Prevention
Accidental access to concentrates for which the cattle have developed an appetite,

in quantities to which they are unaccustomed, should be avoided. Feedlot cattle

should be introduced gradually to concentrate rations over a period of 23 wk,
beginning with a mixture of 50% concentrate in the milled feed containing
roughage.
Last full review/revision March 2012 by Peter D. Constable, BVSc (Hons), MS,
PhD, DACVIM

Subacute Ruminal Acidosis

(Chronic ruminal acidosis, Subclinical ruminal acidosis)

Ruminant animals are adapted to digest and metabolize

predominantly forage diets; however, growth rates and milk
production are increased substantially when they consume highgrain diets. One consequence of feeding excessive amounts of
rapidly fermentable carbohydrates in conjunction with inadequate
fiber to ruminants is subacute ruminal acidosis, which is
characterized by periods of low ruminal pH, depressed feed
intake, and subsequent health problems. Chronic disease
conditions secondary to subacute ruminal acidosis can negate the
production gains accomplished by high grain feeding. Dairy cattle,
feedlot cattle, and feedlot sheep are all at high risk for developing
this condition. Although dairy cattle are typically fed diets that are
higher in forage and fiber compared with feedlot animals, this
advantage is offset by their much higher dry-matter intakes.
Etiology
Ruminal pH fluctuates considerably during a 24hr period
(typically between 0.51.0 pH units) and is determined by the
dynamic balance between the intake of fermentable
carbohydrates, buffering capacity of the rumen, and rate of acid

absorption from the rumen. If ruminal pH drops below ~5.5 (the

normal physiologic nadir) for more than a few hours a day in an
animal, it is considered to have subacute ruminal acidosis. By
convention, ruminal acidosis is considered subacute when the low
ruminal pH is caused by excessive accumulation of volatile fatty
acids (VFA) without persistent lactic acid accumulation, and when
the low ruminal pH is restored to normal by the animal's own
physiologic responses.
The ability of the rumen to rapidly absorb organic acids
contributes greatly to the stability of ruminal pH. It is rarely difficult
for peripheral tissues to utilize VFA already absorbed from the
rumen; however, absorption of these VFA from the rumen can be
an important bottleneck.
Ruminal VFA are absorbed passively across the rumen wall. This
passive absorption is enhanced by finger-like papillae, which
project away from the rumen wall and provide massive surface
area for absorption. Ruminal papillae increase in length when
cattle are fed higher-grain diets; this presumably increases
ruminal surface area and absorptive capacity, which protects the
animal from acid accumulation in the rumen. If the absorptive
capacity of these cells is impaired (eg, chronic rumenitis with
fibrosis), it becomes much more difficult for the animal to maintain
a stable ruminal pH following a meal.
One mechanism by which affected animals resolve ruminal
acidosis and return ruminal pH to normal is by selecting long
forage particles, either by choosing to preferentially consume long
dry hay or by sorting a mixed ration in favor of longer forage
particles. Another mechanism is by reducing overall feed intake.
Depressed dry-matter intake becomes especially evident if
ruminal pH falls below ~5.5. Intake depression may be mediated
by pH receptors and/or osmolality receptors in the rumen.
Inflammation of the ruminal epithelium (rumenitis) could cause
pain and also contribute to intake depression during subacute
ruminal acidosis.

Absorption of VFA inherently increases as ruminal pH drops.

These acids are absorbed only in the protonated state. Because
they have a pKa of about 4.8, the proportion of these acids that
are protonated increases dramatically as ruminal pH decreases
below 5.5. Unfortunately, ruminal carbohydrate fermentation shifts
to lactate production at lower ruminal pH (mostly due
toStreptococcus bovis proliferating and shifting to lactate instead
of VFA production); this can offset gains from VFA absorption.
Ruminal lactate production is undesirable because lactate has a
much lower pKa than VFA (3.9 vs. 4.8). For example, lactate is 5.2
times less protonated than VFA at pH 5.0. As a result, lactate
stays in the rumen longer and contributes to the downward spiral
in ruminal pH.
Additional adaptive responses are invoked if lactate production
begins. Lactate-utilizing bacteria, such as Megasphaera
elsdenii and Selenomonas ruminantium, begin to proliferate.
These beneficial bacteria convert lactate to other VFA, which are
then easily protonated and absorbed. However, the turnover time
of lactate utilizers is much slower than that of lactate synthesizers.
Thus, this mechanism may not be invoked quickly enough to fully
stabilize ruminal pH. Periods of very high ruminal pH, as during
feed deprivation, may inhibit populations of lactate utilizers (which
are sensitive to higher ruminal pH) and leave them more
susceptible to severe ruminal acidosis.
Besides disrupting microbial balance, feed deprivation causes
cattle to overeat when feed is reintroduced. This creates a double
effect in lowering ruminal pH. Cycles of feed deprivation followed
by overconsumption greatly increase the risk for subacute ruminal
acidosis.
Low ruminal pH during subacute ruminal acidosis also reduces
the number of species of bacteria in the rumen, although the
metabolic activity of the bacteria that remain is very high.
Protozoal populations are particularly limited at lower ruminal pH;
the absence of ciliated protozoa in ruminal fluid is often observed
during bouts of subacute ruminal acidosis. When fewer species of

bacteria and protozoa are present, the ruminal microflora are less
stable and less able to maintain normal ruminal pH during periods
of sudden dietary change. Thus, periods of subacute ruminal
acidosis leave animals more susceptible to future episodes of
ruminal acidosis.
Pathogenesis
Low ruminal pH may lead to rumenitis, erosion, and ulceration of
the ruminal epithelium. Once the ruminal epithelium is inflamed,
bacteria may colonize the papillae and leak into the portal
circulation. These bacteria may cause liver abscesses, which may
eventually lead to peritonitis around the site of the abscess. If the
ruminal bacteria clear the liver (or if bacteria from liver infections
are released into circulation), they may colonize the lungs, heart
valves, kidneys, or joints. The resulting pneumonia, endocarditis,
pyelonephritis, and arthritis are often difficult to diagnose
antemortem. Postmortem evaluation of these conditions in
animals that are slaughtered, culled, or that died on the farm can
be very beneficial.
Caudal vena cava syndrome is caused by the release of septic
emboli from liver abscesses; this septic material then travels via
the caudal vena cava to the lungs. These bacteria proliferate in
lung tissue and may ultimately invade pulmonary vessels, causing
them to rupture. This is observed clinically as hemoptysis and
even peracute deaths due to massive pulmonary hemorrhage.
Subacute ruminal acidosis has also been associated with laminitis
and subsequent hoof overgrowth, sole abscesses, and sole
ulcers. The severity of laminitis depends on the duration and
frequency of metabolic insult. These foot problems generally do
not appear until weeks or months after the initiating event. The
mechanism by which subacute ruminal acidosis increases the risk
of laminitis has not been fully characterized.
Clinical Findings
The major clinical manifestation of subacute ruminal acidosis is
reduced or cyclic feed intake, or both. Other associated signs

include decreased efficiency of milk production, reduced fat test,

poor body condition score despite adequate energy intake,
unexplained diarrhea, and episodes of laminitis. High rates of
culling or unexplained deaths may be noted in the herd. Sporadic
nosebleeds due to caudal vena cava syndrome may also be
observed. The clinical signs are delayed and insidious. Actual
episodes of low ruminal pH are not identified; in fact, by the time
an animal is observed to be off-feed, its ruminal pH has probably
been restored to normal. Diarrhea may follow periods of low
ruminal pH; however, this finding is inconsistent and may be
related to other dietary factors as well.
Diagnosis
Subacute ruminal acidosis is diagnosed on a group rather than
individual basis. Measurement of pH in the ruminal fluid of a
representative portion of apparently healthy animals in a group
has been used to assist in making the diagnosis of subacute
ruminal acidosis in dairy herds. Animal selection should be from
highest-risk groups: cows between ~1530 days in milk in
component-fed herds, and cows between ~50150 days in milk in
herds fed total mixed rations. Ruminal fluid is collected by
rumenocentesis and its pH is determined on a pH meter. Twelve
or more animals are typically sampled at ~24 hr after a grain
feeding (in component-fed herds) or 610 hr after the first daily
feeding of a total mixed ration. If >25% of the animals tested have
a ruminal pH <5.5, then the group is considered to be at high risk
of subacute ruminal acidosis. This type of diagnostic tool should
be used in conjunction with other factors such as ration
evaluation, evaluation of management practices, and identification
of health problems on a herd basis.
Milk fat depression is a poor and insensitive indicator of subacute
ruminal acidosis in dairy herds. Cows and herds with severe
subacute ruminal acidosis may have normal milk fat tests. Thus, it
is vitally important not to exclude a diagnosis of subacute ruminal
acidosis in a dairy herd that has a normal milk-fat test.
Treatment

Because subacute ruminal acidosis is not detected at the time of

depressed ruminal pH, there is no specific treatment for it.
Secondary conditions may be treated as needed.
Prevention
The key to prevention is reducing the amount of readily
fermentable carbohydrate consumed at each meal. This requires
both good diet formulation (proper balance of fiber and nonfiber
carbohydrates) and excellent feed bunk management. Animals
consuming well-formulated diets remain at high risk for this
condition if they tend to eat large meals because of excessive
competition for bunk space or following periods of feed
deprivation.
Field recommendations for feeding component-fed concentrates
to dairy cattle during the first 3 wk of lactation are usually
excessive. Feeding excessive quantities of concentrate and
insufficient forage results in a fiber-deficient ration likely to cause
subacute ruminal acidosis. The same situation may be seen
during the last few days before parturition if the ration is fed in
separate components; as dry-matter intake drops before calving,
dry cows preferentially consume concentrates instead of forage
and develop acidosis.
Subacute ruminal acidosis may also be caused by errors in
delivery of the rations or by formulation of rations that contain
excessive amounts of rapidly fermentable carbohydrates or a
deficiency of fiber. Recommendations for the fiber content of dairy
rations are available in the National Research Council
report, Nutrient Requirements of Dairy Cattle (see Nutritional
Requirements of Dairy Cattle). Dry-matter content errors in total
mixed rations are commonly related to a lack of adjustment for
changes in moisture content of forages.
Including long-fiber particles in the diet reduces the risk of
subacute ruminal acidosis by encouraging saliva production
during chewing and by increasing rumination after feeding. The
provision of adequate long-fiber particles reduces the risk for

ruminal acidosis but cannot eliminate it. If a total mixed ration is

fed, it is important that the long-fiber particles not be easily sorted
away from the rest of the diet; this could delay their consumption
until later in the day or cause them to be refused completely.
Sorting can be prevented by providing long-fiber particles that are
<5 cm in length, by having adequate (50 to 55%) moisture in
the mixed ration, and by including ingredients such as liquid
molasses that help ration ingredients stick together.
Ruminant diets should also be formulated to provide adequate
buffering. This can be accomplished by feedstuff selection and/or
by the addition of dietary buffers such as sodium bicarbonate or
potassium carbonate. Dietary cation-anion difference (DCAD) is
used to quantify the buffering capacity of a diet; diets for animals
at high risk for ruminal acidosis should be formulated to provide a
DCAD of >250 mEq/kg of diet dry matter, using the formula (Na +
K) (CI + S) to calculate DCAD.
Supplementing the diet with direct-fed microbials that enhance
lactate utilization in the rumen may reduce the risk of subacute
ruminal acidosis. Yeasts, propionobacteria, lactobacilli, and
enterococci have been used for this purpose. Ionophore (eg,
monensin sodium) supplementation may also reduce the risk by
selectively inhibiting ruminal lactate producers and by reducing
meal size.
Last full review/revision March 2012 by Garrett R. Oetzel, DVM,
MS

Bloat in Ruminants
(Ruminal tympany)

Bloat is an overdistention of the rumenoreticulum with the gases of

fermentation, either in the form of a persistent foam mixed with the ruminal
contents, called primary or frothy bloat, or in the form of free gas separated
from the ingesta, called secondary or free-gas bloat. It is predominantly a
disorder of cattle but may also be seen in sheep. The susceptibility of
individual cattle to bloat varies and is genetically determined.
Death rates as high as 20% are recorded in cattle grazing bloat-prone pasture,
and in pastoral areas, the annual mortality rate from bloat in dairy cows may
approach 1%. There is also economic loss from depressed milk production in
nonfatal cases and from suboptimal use of bloat-prone pastures. Bloat can be
a significant cause of mortality in feedlot cattle.
Etiology and Pathogenesis
In primary ruminal tympany, or frothy bloat, the cause is entrapment of the
normal gases of fermentation in a stable foam. Coalescence of the small gas
bubbles is inhibited, and intraruminal pressure increases because eructation
cannot occur. Several factors, both animal and plant, influence the formation
of a stable foam. Soluble leaf proteins, saponins, and hemicelluloses are
believed to be the primary foaming agents and to form a monomolecular layer
around gas rumen bubbles that has its greatest stability at about pH 6.0.
Salivary mucin is antifoaming, but saliva production is reduced with
succulent forages. Bloat-producing pastures are more rapidly digested and
may release a greater amount of small chloroplast particles that trap gas
bubbles and prevent their coalescence. The immediate effect of feeding is
probably to supply nutrients for a burst of microbial fermentation. However,
the major factor that determines if bloat will occur is the nature of the ruminal
contents. Protein content and rates of digestion and ruminal passage reflect
the forage's potential for causing bloat. Over a 24-hr period, the bloat-causing
forage and unknown animal factors combine to maintain an increased
concentration of small feed particles and enhance the susceptibility to bloat.

Bloat is most common in animals grazing legume or legume-dominant

pastures, particularly alfalfa, ladino, and red and white clovers, but also is
seen with grazing of young green cereal crops, rape, kale, turnips, and
legume vegetable crops. Legume forages such as alfalfa and clover have a
higher percentage of protein and are digested more quickly. Other legumes,
such as sainfoin, crown vetch, milk vetch, fenugreek, and birdsfoot trefoil, are
high in protein but do not cause bloat, probably because they contain
condensed tannins, which precipitate protein and are digested more slowly
than alfalfa or clover. Leguminous bloat is most common when cattle are
placed on lush pastures, particularly those dominated by rapidly growing
leguminous plants in the vegetative and early bud stages, but can also be
seen when high-quality hay is fed.
Frothy bloat also is seen in feedlot cattle, and less commonly in dairy cattle,
on high-grain diets. The cause of the foam in feedlot bloat is uncertain but is
thought to be either the production of insoluble slime by certain species of
rumen bacteria in cattle fed high-carbohydrate diets or the entrapment of the
gases of fermentation by the fine particle size of ground feed. Fine particulate
matter, such as in finely ground grain, can markedly affect foam stability as
can a low roughage intake. Feedlot bloat is most common in cattle that have
been on a grain diet for 12 mo. This timing may be due to the increase in the
level of grain feeding or to the time it takes for the slime-producing rumen
bacteria to proliferate to large enough numbers.
In secondary ruminal tympany, or free-gas bloat, physical obstruction of
eructation is caused by esophageal obstruction due to a foreign body (eg,
potatoes, apples, turnips, kiwifruit), stenosis, or pressure from enlargement
outside the esophagus (as from lymphadenopathy or sporadic juvenile
thymic lymphoma). Interference with esophageal groove function in vagal
indigestion and diaphragmatic hernia may cause chronic ruminal tympany.
This also occurs in tetanus. Tumors and other lesions, such as those caused
by infection with Actinomyces bovis, of the esophageal groove or the
reticular wall are less common causes of obstructive bloat. There also may be
interference with the nerve pathways involved in the eructation reflex.
Lesions of the wall of the reticulum (which contains tension receptors and
receptors that discriminate between gas, foam, and liquid) may interrupt the

normal reflex that is essential for escape of gas from the rumen.
Ruminal tympany also can be secondary to the acute onset of ruminal atony
that occurs in anaphylaxis and in grain overload; this causes a reduction in
rumen pH and possibly an esophagitis and rumenitis that can interfere with
eructation. Ruminal tympany also develops with hypocalcemia. Chronic
ruminal tympany is relatively frequent in calves up to 6 mo old without
apparent cause; this form usually resolves spontaneously.
Unusual postures, particularly lateral recumbency, are commonly associated
with secondary tympany. Ruminants may die of bloat if they become
accidentally cast in dorsal recumbency or other restrictive positions in
handling facilities, crowded transportation vehicles, or irrigation ditches.
Clinical Findings
Bloat is a common cause of sudden death. Cattle not observed closely, such
as pastured and feedlot cattle and dry dairy cattle, usually are found dead. In
lactating dairy cattle, which are observed regularly, bloat commonly begins
within 1 hr after being turned onto a bloat-producing pasture. Bloat may
develop on the first day after being placed on the pasture but more commonly
develops on the second or third day.
In primary pasture bloat, the rumen becomes obviously distended suddenly,
and the left flank may be so distended that the contour of the paralumbar
fossa protrudes above the vertebral column; the entire abdomen is enlarged.
As the bloat progresses, the skin over the left flank becomes progressively
more taut and, in severe cases, cannot be tented. Dyspnea and grunting are
marked and are accompanied by mouth breathing, protrusion of the tongue,
extension of the head, and frequent urination. Occasionally, vomiting occurs.
Rumen motility does not decrease until bloat is severe. If the tympany
continues to worsen, the animal will collapse and die. Death may occur within
1 hr after grazing began but is more common 34 hr after onset of clinical
signs. In a group of affected cattle, there are usually several with clinical bloat
and some with mild to moderate abdominal distention.
In secondary bloat, the excess gas is usually free on top of the solid and fluid
ruminal contents, although frothy bloat may be seen in vagal indigestion

when there is increased ruminal activity. Secondary bloat is seen

sporadically. There is tympanic resonance over the dorsal abdomen left of the
midline. Free gas produces a higher pitched ping on percussion than frothy
bloat. The distension of the rumen can be detected on rectal examination. In
free-gas bloat, the passage of a stomach tube or trocarization releases large
quantities of gas and alleviates distention.
Lesions
Necropsy findings are characteristic. Congestion and hemorrhage of the
lymph nodes of the head and neck, epicardium, and upper respiratory tract
are marked. The lungs are compressed, and intrabronchial hemorrhage may
be present. The cervical esophagus is congested and hemorrhagic, but the
thoracic portion of the esophagus is pale and blanchedthe demarcation
known as the bloat line of the esophagus. The rumen is distended, but the
contents usually are much less frothy than before death. The liver is pale due
to expulsion of blood from the organ.
Diagnosis
Usually, the clinical diagnosis of frothy bloat is obvious. The causes of
secondary bloat must be ascertained by clinical examination to determine the
cause of the failure of eructation.
Treatment
In life-threatening cases, an emergency rumenotomy may be necessary; it is
accompanied by an explosive release of ruminal contents and, thus, marked
relief for the cow. Recovery is usually uneventful with only occasional minor
complications.
A trocar and cannula may be used for emergency relief, although the
standard-sized instrument is not large enough to allow the viscous, stable
foam in peracute cases to escape quickly enough. A larger bore instrument
(2.5 cm in diameter) is necessary, but an incision through the skin must be
made before it can be inserted through the muscle layers and into the rumen.
If the cannula fails to reduce the bloat and the animal's life is threatened, an
emergency rumenotomy should be performed. If the cannula provides some

relief, an antifoaming agent can be administered through the cannula, which

can remain in place until the animal has returned to normal, usually within
several hours.
Fig. 1

Cannulation of rumen, cow.

Illustration by Dr. Gheorghe
Constantinescu.

When the animal's life is not immediately threatened, passing a stomach tube
of the largest bore possible is recommended. A few attempts should be made
to clear the tube by blowing and moving it back and forth in an attempt to find
large pockets of rumen gas that can be released. In frothy bloat, it may be
impossible to reduce the pressure with the tube, and an antifoaming agent
should be administered while the tube is in place. If the bloat is not relieved
quickly by the antifoaming agent, the animal must be observed carefully for
the next hour to determine if the treatment has been successful or if an
alternative therapy is necessary.

A variety of antifoaming agents are effective, including vegetable oils (eg,

peanut, corn, soybean) and mineral oils (paraffins), at doses of 250500 mL.
Dioctyl sodium sulfosuccinate (docusate), a surfactant, is commonly
incorporated into one of the above oils and sold as a proprietary antibloat
remedy, which is effective if administered early. Poloxalene (2550 g, PO) is
effective in treating legume bloat but not feedlot bloat. Placement of a rumen
fistula provides short-term relief for cases of free-gas bloat associated with
external obstruction of the esophagus.
Control and Prevention
Prevention of pasture bloat can be difficult. Management practices that have
been used to reduce the risk of bloat include feeding hay, particularly
orchardgrass, before turning cattle on pasture, maintaining grass dominance
in the sward, or using strip grazing to restrict intake, with movement of
animals to a new strip in the afternoon, not the early morning. Hay must
constitute at least one-third of the diet to effectively reduce risk of bloat.
Feeding hay or strip grazing may be reliable when the pasture is only
moderately dangerous, but these methods are less reliable when the pasture
is in the pre-bloom stage and the bloat potential is high. Mature pastures are
less likely to cause bloat than immature or rapidly growing pastures.
The only satisfactory method available to prevent pasture bloating is
continual administration of an antifoaming agent during the risk period. This
is widely practiced in grassland countries such as Australia and New Zealand.
The most reliable method is drenching twice daily (eg, at milking times) with
an antifoaming agent. Spraying the agent onto the pasture is equally
effective, provided that the animals have access only to treated pasture. This
method is ideal for strip grazing but not when grazing is uncontrolled. The
antifoaming agent can be added to the feed or water or incorporated into feed
blocks, but success with this method depends on adequate individual intake.
The agent can be painted on the flanks of the animals, from which it is
licked during the day, but animals that do not lick will be unprotected.
Available antifoaming agents include oils and fats and synthetic nonionic
surfactants. Oils and fats are given at 60120 mL/head/day; doses up to 240
mL are indicated during dangerous periods. Poloxalene, a synthetic polymer,

is a highly effective nonionic surfactant that can be given at 1020 g/head/day

and up to 40 g/head/day in high-risk situations. It is safe and economical to
use and is administered daily through the susceptible period by adding to
water, feed grain mixtures, or molasses. A similar polymer (Alfasure) and a
water soluble mixture of alcohol ethoxylate and pluronic detergents (Blocare
4511) also are effective but lack approval by the FDA. Ionophores are effective
in preventing bloat, and a sustained-release capsule that is administered into
the rumen and releases 300 mg of monensin daily for a 100-day period
protects against pasture bloat and improves milk production on bloat-prone
pastures.
The ultimate aim in control is development of a pasture that permits high
production, while keeping incidence of bloat low. The use of pastures of
clover and grasses in equal amounts comes closest to achieving this goal.
Bloat potential varies between cultivars of alfalfa, and low-risk LIRD (low
initial rate of digestion) cultivars are available commercially. The addition of
legumes with high condensed tannins to the pasture seeding mix (10%
sainfoin) can reduce the risk of bloat where there is strip grazing, as can the
feeding of sainfoin pellets.
To prevent feedlot bloat, rations should contain 1015% cut or chopped
roughage mixed into the complete feed. Preferably, the roughage should be a
cereal, grain straw, grass hay, or equivalent. Grains should be rolled or
cracked, not finely ground. Pelleted rations made from finely ground grain
should be avoided. The addition of tallow (35% of the total ration) may be
successful occasionally, but it was not effective in controlled trials. The
nonionic surfactants, such as poloxalene, have been ineffective in preventing
feedlot bloat, but the ionophore lasalocid is effective in control.
Last full review/revision March 2012 by Clive C. Gay, DVM, MVSc, DVSc
(Hons), FACVSc, DACIM (Hons)

Traumatic Reticuloperitonitis
(Hardware disease, Traumatic gastritis)

Traumatic reticuloperitonitis develops as a consequence of perforation of the

reticulum. It is important as differential diagnosis of other diseases marked by stasis
of the GI tract because it causes similar signs. Traumatic reticuloperitonitis is most
common in mature dairy cattle, occasionally seen in beef cattle, and rarely reported
in other ruminants.
Cattle commonly ingest foreign objects because they do not discriminate against
metal materials in feed and do not completely masticate feed before swallowing.
The disease is common when green chop, silage, and hay are made from fields
that contain old rusting fences or baling wire, or when pastures are on areas or
sites where buildings have recently been constructed, burned, or torn down. The
grain ration may also be a source due to accidental addition of metal.
Etiology
Swallowed metallic objects, such as nails or pieces of wire, fall directly into the
reticulum or pass into the rumen and are subsequently carried over the
ruminoreticular fold into the cranioventral part of the reticulum by ruminal
contractions. The reticulo-omasal orifice is elevated above the floor, which tends to
retain heavy objects in the reticulum, and the honeycomb-like reticular mucosa
traps sharp objects. Contractions of the reticulum promote penetration of the wall by
the foreign object. Compression of the ruminoreticulum by the uterus in late
pregnancy and straining during parturition increase the likelihood of an initial
penetration of the reticulum and may also disrupt adhesions caused by an earlier
penetration.
Perforation of the wall of the reticulum allows leakage of ingesta and bacteria,
which contaminates the peritoneal cavity. The resulting peritonitis is generally
localized and frequently results in adhesions. Less commonly, a more severe
diffuse peritonitis develops. The object can penetrate the diaphragm and enter the
thoracic cavity (causing pleuritis and sometimes pulmonary abscessation) and the
pericardial sac (causing pericarditis, sometimes followed by myocarditis).
Occasionally, the liver or spleen may be pierced and become infected, resulting in

abscessation, or septicemia can develop.

Fig. 2

The relationship between the

reticulum, diaphragm, and
heart/pericardium in large ruminants.
Illustration by Dr. Gheorghe
Constantinescu.
Clinical Findings
The initial penetration of the reticulum is characterized by the sudden onset of
ruminoreticular atony and a sharp fall in milk production. Fecal output is decreased.
The rectal temperature is often mildly increased. The heart rate is normal or slightly
increased, and respiration is usually shallow and rapid. Initially, the cow exhibits an
arched back; an anxious expression; a reluctance to move; and an uneasy, careful
gait. Forced sudden movements as well as defecating, urinating, lying down, getting
up, and stepping over barriers may be accompanied by groaning. A grunt may be
elicited by applying pressure to the xiphoid or by firmly pinching the withers, which
causes extension of the thorax and lower abdomen. The grunt can be detected by
placing a stethoscope over the trachea and applying pressure or pinching the
withers at the end of an inspiration. Tremor of the triceps and abduction of the
elbow may be seen.
In chronic cases, feed intake and fecal output are reduced, and milk production
remains low. Signs of cranial abdominal pain become less apparent, and the rectal

temperature usually returns to normal as the acute inflammation subsides and

peritoneal contamination is walled off. Some cattle develop vagal indigestion
syndrome (see below) due to the adhesions that form after foreign body perforation,
particularly those on the ventromedial reticulum.
Cows with pleuritis or pericarditis due to foreign body perforation usually are
depressed, tachycardic (>90 bpm), and pyrexic (104F [40C]). Pleuritis is manifest
by fast, shallow respiration; muffled lung sounds; and possibly pleuritic friction rubs.
Thoracentesis may yield several liters of septic fluid. Traumatic pericarditis is most
commonly characterized by muffled heart sounds; however, early in the disease
process pericardial friction rubs or gas and fluid splashing sounds (washing
machine murmur) can be heard on auscultation. Jugular vein distention and
congestive heart failure with marked submandibular and brisket edema is a
frequent sequela of traumatic reticulopericarditis. Prognosis is grave with these
complications. Penetration through the pericardium into the myocardium usually
results in extensive hemorrhage into the pericardial sac or ventricular arrhythmias
and sudden death.
Diagnosis
This can be based on history (when available) and clinical findings if the cow is
examined when signs initially appear. Without an accurate history and when the
condition has been present for several days or longer, diagnosis is more difficult.
Other causes of peritonitis, particularly perforated abomasal ulcers, can be difficult
to distinguish from traumatic reticuloperitonitis. Differential diagnoses should include
conditions that can produce variable or nonspecific GI signs, eg, indigestion,
lymphosarcoma, or intestinal obstruction. Abomasal displacement or volvulus
should be ruled out by simultaneous auscultation and percussion. Pleuritis or
pericarditis of nontraumatic origin produces signs similar to those associated with
foreign body perforation.
Although not always necessary, laboratory tests may be helpful. In many cases,
there is a neutrophilia with a left shift. Serum haptoglobin, amyloid-A, and total
plasma protein concentrations may be markedly increased, and plasma fibrinogen
concentrations may be elevated. Affected cattle may have coagulation
abnormalities, as evidenced by prolonged prothrombin time, thrombin time, and
activated partial thromboplastin time. The acid-base status and serum electrolyte
levels are typically normal because abomasal and small-intestinal absorption can
remain normal. However, marked hypokalemic, hypochloremic metabolic alkalosis

can be seen, presumably because adynamic ileus from peritonitis can affect
abomasal and GI motility and resorption of abomasal secretions. The metabolic
alkalosis can be created or exacerbated by treatment with alkalinizing agents such
as magnesium hydroxide used as a laxative. Peritoneal fluid analysis can be helpful
in determining if peritonitis is present, particularly the concentration of D-dimer and
the neutrophil percentage in the peritoneal fluid. However, the peritonitis frequently
becomes walled off, and in these cases peritoneal fluid may be within the reference
range unless obtained from within the lesion. The presence of a magnet in the
reticulum can be determined by movement of a magnetic compass in the region of
the cranioventral abdomen; the presence of a magnet in the reticulum makes
traumatic reticuloperitonitis very unlikely unless the penetrating object is not
magnetic.
Ultrasonography of the ventral abdomen is the most accurate means of diagnosing
localized peritonitis near the reticulum and characterizing the reticular contraction
frequency. It rarely identifies the presence of a penetrating object. Ultrasonography
of the heart and thorax is very useful in the diagnosis of pleuritis and pericarditis as
a sequelae to traumatic reticuloperitonitis.
Lateral radiographs of the cranioventral abdomen can detect metallic material in the
reticulum but should only be taken after oral administration of a magnet. To
determine whether the reticulum is currently perforated, the foreign body must be
visible beyond the border of the reticulum, unattached to the magnet in the
reticulum, or positioned off the floor of the reticulum. A depression in the
cranioventral aspect of the reticulum or identification of an abscess (by gas
accumulation outside a viscus), soft-tissue masses, or a fluid line in the cranial
abdomen are also reliable radiographic findings of penetration. Portable
radiographic units cannot penetrate the reticular area of standing adult cattle, and
the cow may need to be transported to where there is equipment with sufficient
power. The cow should not be placed in dorsal recumbency in order to obtain
radiographs because such manipulation places stress on adhesions and may lead
to a localized peritonitis becoming a diffuse peritonitis due to gravitational spread of
infection.
Electronic metal detectors can identify metal in the reticulum but do not distinguish
between perforating and nonperforating foreign bodies.
Treatment

Treatment of the typical case seen early in its course may be surgical or medical.
Either approach improves the chances of recovery from 60% in untreated cases
to 8090%. Surgery involves rumenotomy with manual removal of the object(s)
from the reticulum; if an abscess is adhered to the reticulum, it should be aspirated
(to confirm that it is an abscess) and then drained into the reticulum. Antimicrobials
should be administered perioperatively. Medical treatment involves administration of
antimicrobials to control the peritonitis and a magnet to prevent recurrence.
Because of the mixed bacterial flora in the lesion, a broad-spectrum antimicrobial
agent such as oxytetracycline (16 mg/kg, IV, sid) should be used. Penicillin (22,000
IU/kg, IM, bid) is used widely and is effective in many cases despite its limited
spectrum. Affected cows should be confined for 12 wk; placing them on an inclined
plane (elevated in front) is believed by some to limit further penetration of the
foreign object, but supporting studies are lacking. Supportive therapy, such as oral
or occasionally IV fluids and SC calcium borogluconate, should be administered as
needed. Rumen inoculation is beneficial in some cases with prolonged ruminal
stasis and loss of normal flora.
More advanced cases, those with obvious secondary complications, or those that
do not respond to initial medical or surgical therapy should be evaluated from an
economic perspective; if the cow is of limited value, slaughter should be considered
if the carcass is likely to pass inspection.
Prevention
Preventive measures include avoiding the use of baling wire, passing feed over
magnets to remove metallic objects, keeping cattle away from sites of new
construction, and completely removing old buildings and fences. Additionally, bar
magnets may be administered PO, preferably after fasting for 1824 hr. Usually, the
magnet remains in the reticulum and holds any ferromagnetic objects on its surface.
There is good evidence that giving magnets to all herd replacement heifers and
bulls at 1 yr of age minimizes the incidence of traumatic reticuloperitonitis.

Vagal Indigestion Syndrome in Ruminants

(Chronic indigestion)

Vagal indigestion syndrome is characterized by the gradual development of

abdominal distention secondary to rumenoreticular distention. The distention was
originally thought to be the result of lesions affecting the ventral vagus nerve. Vagal
indigestion syndrome is seen most commonly in cattle but has been reported in
sheep.
Etiology and Pathogenesis
Diseases that result in injury, inflammation, or pressure on the vagus nerve can
result in clinical signs of vagal indigestion syndrome. However, vagal nerve damage
is not present in most cases of vagus indigestion, and the most common cause is
traumatic reticuloperitonitis (see Traumatic Reticuloperitonitis). Conditions resulting
in mechanical obstruction of the cardia or reticulo-omasal orifice (eg, papillomas or
ingested placenta) can also result in vagal indigestion if ruminoreticular distention is
present and the condition is subacute to chronic.
Historically, there were 4 types of vagal indigestion described based on the
purported site of the functional obstruction. Type I was failure of eructation or freegas bloat, type II was a failure of omasal transport, type III was secondary abomasal
impaction, and type IV was indigestion of late gestation. Type I and IV are rare.
Type I vagal indigestion, or failure of eructation, results in free-gas bloat and has
been attributed to inflammatory lesions in the vicinity of the vagus nerve, such as
localized peritonitis, adhesions (usually after an episode of traumatic
reticuloperitonitis), or chronic pneumonia with anterior mediastinitis. Other potential
causes for type I vagal indigestion include pharyngeal trauma, which affects a more
proximal part of the vagus nerve, and esophageal compression by abscesses or
neoplasia, such as lymphosarcoma. Vagal indigestion can develop in cattle after
abomasal volvulus without abomasal impaction. These cases would presumably fall
into the category of type I vagal indigestion with damage to the vagal nerve near the
reticulum and omasum.
Type II vagal indigestion, more correctly termed failure of omasal transport,
develops as a result of any condition that prevents ingesta from passing through the
omasal canal into the abomasum. Adhesions and abscesses (reticular or single liver

abscesses) are the most common cause of failure of omasal transport and are
usually located on the right or medial wall of the reticulum near the route of the
vagus nerve. Reticular abscesses and adhesions are almost invariably the result of
traumatic reticuloperitonitis. Mechanical obstruction of the omasal canal by ingested
material (eg, plastic bags, rope, placenta) or masses (eg, lymphosarcoma,
squamous cell carcinoma, granulomas, or papillomas) can also cause chronic
ruminoreticular distention due to failure of omasal transport.
Type III vagal indigestion is a secondary abomasal impaction. Primary abomasal
impaction develops due to feeding of dry, course roughage, such as straw, in a
chopped or ground form with restricted access to water and usually during
extremely cold temperatures (see Dietary Abomasal Impaction). Secondary
abomasal impaction is seen most commonly after an episode of traumatic
reticuloperitonitis or occasionally as a sequela to abomasal volvulus. Mechanical
fixation of the reticulum to the ventral abdominal floor in cows with reticuloperitonitis
interferes with the normal sieving action of the reticulum, with passage of large fiber
particles (>2 mm length) into the abomasum. The abomasum has difficulty in
emptying the larger particles of food because of the increased viscosity, and they
accumulate in the abomasum, resulting in abomasal impaction.
Type IV vagal indigestion, or partial forestomach obstruction, is poorly defined. It
typically develops in cattle during gestation and is more appropriately termed
indigestion of late gestation. The condition is thought to be related to the enlarging
uterus shifting the abomasum to a more cranial position, which inhibits normal
abomasal emptying.
Clinical Findings
The clinical signs vary to some extent with the location of the obstruction. In all
cases, there is a gradual development (over days to weeks) of abdominal distention
secondary to ruminoreticular distention. Distention of the dorsal and ventral sacs of
the rumen results in an L-shaped rumen on rectal examination. Left dorsal and left
and right ventral distention of the abdomen causes a papple (pear plus apple)
shape as viewed from behind.
Cattle with vagal indigestion syndrome have a diminished appetite, which typically
improves temporarily if distention is relieved. Milk production gradually decreases,
fecal output is reduced, and the rumen develops a splashy fluid consistency. The
feces are characteristically very scant and sticky and may contain longer than

normal particles. The strength of rumen contractions is decreased; however, rumen

motility is often increased (34 contractions/min). It is commonly possible to see
movements of the left abdominal wall that mirror the movements of the hyperactive
rumen. However, rumen contraction sounds are not audible because the contents
have become frothy due to the prolonged contractions and failure of the rumen to
empty.
Temperature and respiratory rate are usually normal; however, these can be
increased depending on the cause. Bradycardia is present in 2540% of cases and
is due to decreased feed intake rather than a direct stimulation of the vagus nerve.
Tachycardia develops as the disease progresses and cattle become dehydrated.
Over time, the animal develops a rough hair coat, loses condition, and becomes
weak (in some cases to the point of recumbency) with marked clinical signs of
dehydration.
On rectal palpation, the rumen is distended with gas or froth that occupies the entire
left abdomen, pushing the left kidney to the right of the midline. The ventral sac of
the rumen is enlarged and palpable to the right of the midline (the characteristic Lshaped rumen). It is important to recognize that diagnosis of vagal indigestion
syndrome requires the presence of a markedly increased ruminoreticular volume.
Palpation of the lower half of the right side of the abdomen below the costochondral
junction may detect an impacted abomasum that feels doughy. Hematologic findings
vary. The PCV can be increased because of dehydration or decreased because of
bone marrow depression (anemia of chronic disease). The WBC may be normal,
increased, or decreased. If an inflammatory condition such as peritonitis is present,
the neutrophil to lymphocyte ratio is typically reversed, and a neutrophilia may be
present. Lymphocytosis can be seen with vagal indigestion due to lymphosarcoma.
Leukopenia may be present with diffuse peritonitis. Increased serum globulin and
total protein can be seen with abscesses.
Metabolic status is normal, or metabolic alkalosis may be present. The serum
chloride concentration varies with the site of the obstruction. It is usually normal if
the lesion is proximal to the abomasum. A low serum chloride concentration is
consistent with reflux of chloride from the abomasum into the rumen (internal
vomiting) and obstruction at the level of the abomasum (type III). Metabolic alkalosis
is typically present if serum chloride is decreased. Rumen chloride concentration is
increased in type III vagal indigestion and provides a useful method for
differentiating type II from type III vagal indigestion. The serum potassium

concentration is usually low due to decreased potassium intake in the feed. Serum
calcium concentration is often moderately decreased because of ongoing milk
production, but it is rarely low enough to cause recumbency. Serum urea and
creatinine concentrations increase with dehydration due to prerenal azotemia.
Diagnosis
Diagnosis is based on the presence of subacute to chronic ruminoreticular and
abdominal distention. Because vagal indigestion is by definition a subacute to
chronic disease, this diagnosis should not be made in cattle that have not been sick
for at least several days, which rules out acute rumen tympany and acute frothy
bloat. Other causes of abdominal distention, such as ascites and uterine
enlargement, are included in the differential diagnosis and can almost invariably be
ruled out by rectal palpation due to the absence of ruminoreticular distention.
Occasional cases of longstanding obstruction of the cecum or small intestine can
cause severe ruminoreticular and abdominal distention; however, palpable cecal or
small-intestinal distention is also palpable rectally. In addition, the rumen is
distended but not L-shaped, and a characteristic ping is present in the case of
cecocolic volvulus.
Diagnosing the specific cause of vagal indigestion is more difficult but is important
because of differences in treatment and prognosis. Physical examination, rectal
examination, CBC, blood acid-base determination, and serum biochemical values
are often useful. Peritoneal fluid analysis can support the diagnosis of peritonitis if
total protein or nucleated cells are increased. Lateral radiographs of the reticulum
should be taken to identify an opaque linear foreign body (eg, wire) or reticular
abscess. Ultrasonography of the cranioventral abdomen can indicate the presence
of focal peritonitis and the reticular contraction rate. Definitive diagnosis often
requires exploratory surgery (left paralumbar fossa laparotomy and rumenotomy).
Treatment and Prognosis
If the value of the animal justifies treatment, surgery is almost always needed to
identify and potentially correct the underlying cause. Medical management alone is
usually ineffective. A left paralumbar fossa laparotomy and rumenotomy provides
the opportunity for definitive treatment in some cases. Emptying the rumen at the
time of surgery may help restore normal rumen motility. Stimulation of low-threshold
tension receptors in the reticulum occurs under normal circumstances and causes
reflex reticuloruminal contractions. However, severe distention causes stimulation of

high-threshold receptors that have the opposite effect and inhibit contractions.
Supportive or symptomatic therapy should be provided in all cases, which typically
involves correcting dehydration as well as calcium and electrolyte deficits,
commonly with oral fluids and electrolytes. Severely dehydrated animals and those
with longstanding disease require IV fluids. Fresh water and normal feed should be
available. Transfaunation at surgery or via oroesophageal intubation may help
reestablish normal rumen flora in cattle with chronic anorexia. Antimicrobials
(procaine penicillin or oxytetracycline) should be given if the underlying cause is
infectious or if a rumen fistula is created.
Treatment of type I vagal indigestion (failure of eructation) also typically involves
creating a rumen fistula to allow free gas to escape. If surgery is not economically
feasible and the underlying cause of vagal indigestion has been identified and
treated, a rumen trocar can be placed temporarily. Such trocars are commercially
available and must be secure and self-retaining to prevent potentially fatal leakage
of rumen contents into the peritoneal cavity. The trocar should not be removed for at
least 2 wk to allow firm adhesions to form between the rumen and body wall.
The prognosis for animals with type I vagal indigestion is usually favorable. After
creation of a rumen fistula, the signs of vagal indigestion resolve in nearly all cases.
However, animals with chronic respiratory disease or pharyngeal trauma may not
recover from the underlying condition. Leakage of ingesta from fistulas can cause
off-flavored milk. Peritonitis can develop from leakage around the fistula or following
rumenotomy; however, this should not happen with good surgical technique.
Type II vagal indigestion (failure of omasal transport) rarely responds to supportive
or symptomatic therapy without surgical intervention. Left paralumbar fossa
laparotomy and rumenotomy can be used to identify adhesions in the vicinity of the
reticulum, reticular or hepatic abscesses, or obstruction of the omasal canal.
Removal of foreign bodies, wires, and some masses at surgery and lancing of
perireticular abscesses into the reticulum affords a fair to good prognosis. A
diagnosis of lymphosarcoma at surgery warrants a grave prognosis. Reticular
abscesses identified at surgery should be cautiously drained into the reticulum, and
antibiotics given for 1014 days. Reportedly, 83% of cattle with reticular abscesses
respond favorably to treatment. Identification of adhesions in the vicinity of the
reticulum warrants a fair to good prognosis with surgery, antibiotic therapy, and
appropriate supportive treatment. Hepatic abscesses must be drained by a second

surgery. Large-bore cannulas placed through the body wall, through the adhesions,
and into the abscess will drain the purulent material. However, recurrence is more of
a problem with hepatic abscesses than with reticular abscesses.
Animals with type III vagal indigestion (secondary abomasal impaction) diagnosed
without surgery usually do not receive further treatment because of the poor
prognosis, particularly if there is a history of traumatic reticuloperitonitis or abomasal
volvulus. If the diagnosis is made at surgery or if the abomasal impaction is thought
to be dietary, dioctyl sodium sulfosuccinate can be infused directly into the
abomasum via the reticulo-omasal orifice after emptying the rumen. A nasogastric
tube can be passed into the abomasum via the reticulo-omasal orifice at surgery
and left in place for continued treatment (1 gal of mineral oil daily for 35 days). If
possible, impacted material should be removed manually through the reticuloomasal orifice. Other lesions, such as abscesses in the medial wall of the reticulum,
should be identified and drained. Abomasotomy and removal of abomasal contents,
using a right paracostal approach with the cow in left lateral recumbency, can be
performed as a last resort. However, recurrence of the impaction is common. Pyloric
obstruction in cattle is rare and is most often due to a foreign body obstructing the
lumen. Pyloromyotomy is almost never effective in resolving abomasal impactions.
Type III vagal indigestion has a poor prognosis regardless of the cause or the
treatment. However, cattle with mild to moderate primary abomasal impactions will
respond to therapy, although severely affected animals will not (see Dietary
Abomasal Impaction). Cattle with secondary impactions due to traumatic
reticuloperitonitis or as a sequela of abomasal volvulus seldom recover. Animals
with foreign bodies (eg, trichobezoars) obstructing the pylorus have a good
prognosis if the obstruction is removed.
Therapeutic induction of parturition has been recommended for treatment of cattle
with type IV vagal indigestion (indigestion of late gestation), and some cows have
improved with this treatment; however, because type IV vagal indigestion is a poorly
defined condition, the prognosis is always guarded. A more specific prognosis is
based on response to therapy and identification of a specific lesion at exploratory
celiotomy and rumenotomy.
Prevention
The most common cause of vagal indigestion syndrome is traumatic
reticuloperitonitis, which causes adhesions and abscesses that interfere with

reticular motility and the appropriate stratification of feed particles for passage
through the abomasum. Therefore, prevention of traumatic reticuloperitonitis is
important. Good management practices may prevent some cases of vagal
indigestion associated with chronic pneumonia. Early diagnosis of abomasal
volvulus, with same-day surgical correction, may prevent some cases.

Ruminal Drinking

Ruminal drinking is caused by failure of the reticular groove reflex and results in
ruminal acidosis in calves on a liquid diet. The disorder presents as primary chronic
disease (ruminal drinking syndrome) in veal calves, and in its acute form as a
complication secondary to different neonatal diseases, most commonly neonatal
diarrhea. It has also been described in artificially fed lambs.
The reticular groove is a muscular structure extending from the cardia to the
reticulo-omasal orifice. Its correct closure is a precondition for the direct passage of
ingested milk or milk replacer into the abomasum. When partial or total failure of the
reticular groove to close occurs, milk spills into the reticulorumen and is fermented
to short-chain fatty acids and/or lactic acid. The subsequent drop in the pH of the
ruminal contents to values that occasionally fall below 4 leads to variable degrees
of inflammation of the mucosa of the forestomachs and the abomasum. In chronic
cases, hyperkeratosis or parakeratosis of the ruminal mucosa can lead to
impairment of ruminal motility with chronic or recurrent tympany. Additionally,
atrophy of the intestinal villi and a decrease in brush border enzyme activity with
maldigestion and malabsorption have been observed.

Systemic consequences of acute ruminal drinking are mainly due to absorption of

organic acids from the digestive tract. In particular, the L- and D-isomers of lactic
acid may lead to metabolic acidosis with the accumulation of D-lactate because of
an absence of a specific enzyme for its metabolism in mammals. This accumulation
of d-lactate has recently been found to be responsible for clinical signs such as
depression, ataxia, and general weakness.
Primary dysfunction of the reticular groove occurs as a result of stressful situations
(prolonged transport, grouping, change in feeding techniques) especially in bucketfed veal calves. Clinical signs usually appear some weeks after the arrival of the
calves at the fattening units and are characterized by inappetence, depression,
poor growth, hair loss, recurrent tympany, ventral abdominal distention, and passing
of clay-like feces. Fluid-splashing sounds can be heard on succussion of the left
flank. Recovery of fermented ruminal contents via stomach tube is diagnostic. In
these advanced, chronic cases the prognosis is poor. If the disease is detected
early enough, feeding small volumes of milk from a nipple-bottle or bucket may be
successful. Additionally, the closure of the reticular groove can be triggered by
allowing the calf to suck a finger before the milk feed is offered.
Acute ruminal acidosis secondary to other disorders is most commonly seen in
calves with neonatal diarrhea but occurs also in other painful or weakening
diseases. In these cases the clinical picture is usually dominated by the underlying
disease. In cases of severe rumenitis, calves may exhibit teeth grinding, arching of
the back, and slight abdominal distention. Force-feeding of inappetent or primarily
anorectic calves can also cause ruminal acidosis or worsen the situation by
providing substrate for further fermentation.
The prognosis for secondary ruminal drinking depends mainly on the success of
treatment of the underlying disease. Calves with metabolic acidosis and
dehydration due to neonatal diarrhea will usually recover spontaneously from
ruminal drinking after adequate treatment, and the condition will in general remain
unrecognized. In calves that were force-fed or that do not respond to treatment as
expected, ruminal drinking should be considered, and an examination of the ruminal
fluid should be performed. Removal of the contents and lavage with warm water via
stomach tube may be beneficial, especially after prolonged force-feeding.
Prophylaxis of ruminal drinking consists of early treatment of diseased calves,
adequate feeding techniques, and minimizing stress in purchased calves.

Ruminal Parakeratosis

Ruminal parakeratosis is a disease of cattle and sheep characterized by hardening

and enlargement of the papillae of the rumen. It is most common in animals fed a
high-concentrate ration during the finishing period. It also is seen in cattle fed
rations of heat-treated alfalfa pellets, as well as in calves with prolonged ruminal
acidosis due to ruminal drinking. It does not appear to be related to the feeding of
antibiotics or protein concentrates. Incidence in a group may be as high as 40%.
The lesions are thought to be caused by the lowered pH and the increased
concentration of volatile fatty acids (VFA) in the ruminal fluid, and do not usually
develop in cattle fed unprocessed whole grain (on which animals gain weight as
readily). This may be related to the higher pH and higher concentration of acetic
acid compared with the longer chain VFA in the ruminal contents.
Many of the papillae are enlarged and hardened, and several may adhere together
to form bundles. The papillae of the anterior ventral sac are commonly affected. In
cattle, the roof of the dorsal sac may show multiple foci (each 23 cm 2) of
parakeratosis. In sheep, abnormal papillae may be visible and palpable through the
wall of the intact rumen. Affected papillae contain excessive layers of keratinized
epithelial cells, particles of food, and bacteria. The rumens of affected cattle are
difficult to clean in the preparation of tripe. The abnormal epithelium, by interfering
with absorption, may reduce efficiency of feed utilization and rate of gain, although
there is little evidence to support this theory.
Ruminal parakeratosis may be prevented by finishing animals on rations that
contain unground ingredients in the proportion of 1 part roughage to 3 parts
concentrate. The necessity and economics of prevention are not well defined.

Peritonitis
Peritonitis is an inflammatory process that involves the peritoneal
cavity and its serosal surface, the peritoneum. This may result from
trauma, surgery or vascular damage associated with an intestinal
obstruction and or accident or from gastrointestinal ulceration.

Peritonitis is a serious and complex process that is often

accompanied by various degrees of abdominal pain,
progressive signs of hypovolemia and septicemia and or
enterotoxemia

Peritonitis may be primary or secondary disease. As a

primary disease it results commonly by rupture of or spread
of infection from a site less commonly by perforation of the
abdominal wall from the exterior. Individual causes are as
follows:

Etiology
Cattle & Buffalo:

Traumatic Reticulo peritonitis

Perforation or leakage of abomasal ulcer

Rupture of abomasums after torsion

Ruminitis of cattle due to acute CHO indigestion

Hepatic abscess of black disease in cattle and horses

Rupture of vagina in young heifers during violate coitus

Deposition of semen in the peritoneal cavity

Injection of hypertonic solution i.e calcium preparation in

milk fever.

Intraperitoneal injection of non sterile solutions.

Spontaneous uterine rupture during parturation due to

dystokia.

Spontaneous rupture of rectum at calving.

Specific disease including tuberculosis and sporadic bovine

encephalomyelitis.

Horses

Rupture of dorsal sac of caecum or colon at foaling

Administration of non-steroidal anti-inflammatory drugs causing caecal

stasis and dilation and eventually perforation.

Rectal rupture or tar during rectal examination

After the attack of strangle due to Streptococcus equi or Corynebacterium

equi infection.

Gastric erosion and rupture related to ulceration caused by larva of

Gastrophillus or Habronema spp.

Leakage from a caecal perforation caused by a heavy infestation of

Anoplocephala perfoliata tapeworms.

Actinobacillus equuili infection

Sheep

Goat

Infestation with Oesophagostomum sps larvae

Serositis or arthritis caused by Mycoplasma sps.

Serositis-arthritis caused by Mycoplasma sps.

Pathogenesis
a) Toxemia

Microbial population

Tissue degradation/decomposition

Toxin elaboration

Toxin absorption via peritoneum

Toxemia

Death within 24 48 hours.

b) Shock and haemorrhages

Deposition of gut contents, infected uterine contents into peritoneal

cavity and haemorrhage resulting from the rupture

Hypovolemia

Peripheral circulatory failure, shock and haemorrhage.

c) Paralytic ileus

Transient hypermotility of the gut

Reflex sympathetic stimulation

Inhibition of gut motility

Paralysis of intestinal musculature

Paralytic ileus.

d)Abdominal pain

Irritation of the nerve endings

Persistent pain

Transmission through spinal cord

Rigidity of the abdominal wall

Arched back posture

Evidence of pain on palpation of abdominal wall.

e) Muscle weakness

Peritoneal infection

Increased adrenocortical activities

Increased production of glucocorticoides - aldosterone

Na ion retention and potassium ion loss

Muscle weakness

f) Adhesions

Adhesion causes partial and complete obstruction of the intestine or

stomach

Interfere with normal gut motility.

Vagus indigestion in cattle and intestinal obstruction in horses.

Symptoms
1.Peracute diffuse peritonitis

Severe weakness, depression and circulatory failure.

Animal is recumbent and often unable to rise, depressed almost to the

point of coma.

Subnormal temperature 99 -100 F.

High pulse rate(110-120/min).

Peracute cases with severe toxemia usually dies within 24 - 48 hours.

In mares, rupture of dorsal sac of the cecum during foaling causes

abdominal pain followed by shock and death occurs 4 -15 hours after the
rupture.

2.Acute and Subacute peritonitis

Toxemia with fever is always present i.e.106 F for 24 36 hrs but then
return to normal and in terminal stage it usually falls to subnormal.

Moderate increase in pulse and respiratory rate

Amount and composition of faeces is always abnormal. Faeces may be

completely absent for periods up to 3 days.

Faeces have thick sludge like consistency and be tenacious and difficult to
remove from the rubber, gloves and have foul smell.

In cows with acute peritonitis, ruminal contents are reduced or absent.

In horse, gut stasis is evidenced by an absence or reduction of gut sounds

on auscultation.

In cattle, abdominal pain is evidenced by disinclination to move and lie

down

Lying down with great care and grunting with pain. Arched back condition
and lowering of the head .

In horse, abdominal pain is evidenced by flank watcing, kicking at the

belly going down and rolling.

3. Chronic peritonitis

Indigestion and toxemia-due to adhesion

Takes a long course even for a month

Loss of appetite, slight rise of temperature and mild colic.

Abdominal distension and accumulation of fluid in the

peritoneal cavity.

In horse, weight loss is severe and there are usually

intermittent abdominal pain suggesting intestinal colic.

Diagnosis
1.By rectal palpation fibrous adhesions
2.By radiographical examination for evidence of obstruction (bowel dilation,
free abdominal air).
3.Blood examination

Differential Leucocytic Count is useful aid

Leukopenia,neutropenia and marked increase in immature neutrophils

(degenerative left shift) ( Acute diffuse peritonitis).

In less severe forms of acute peritonitis

Leucocytosis due to a neutrophilia with appearance of immature

neutrophils

In acute local peritonitis commonly seen in acute TRP in cattle, there

is normal total leucocyte count or a slight increase

In chronic peritonitis, the total and differential leucocyte count may be

normal or there may be leukocytosis with marked neutropenia and
occasionally increase total no of lymphocytes and monocytes.

4. By PM findings

Thick cheesy covering over most of the viscera.

Haemorrage into the subserosa, exudation and fibrin deposits in the

peritoneal cavity.

By cultural examination-abdominal paracentesis for the presence of

organisms.

5. By differential diagnosis
Traumatic Reticulo Peritonitis

Extension of the neck and arching of back

Cow may stand with abducted elbow and hind feet in the gutter to
alleviate the abdominal pain.

Triceps muscle often tremble

Decrease in rumen motility or complete atony.

Animal may grunt with pain as viscera are pressed forward.

Teatment
Streptopenicillin, ampicillin,tetracycline etc.

Siquil injection

Isotonic or electrolyte solution (N.S. Dextrose).

Stabilize the patient supportive therapy, correction of acidbase balance,

serum calcium to promote gastrointestinal motility.

Blood transfusions

High dose of vitamin B. complex

Surgery-peritoneal debridement, irrigation and drainage.

Intraperitoneal injection may give maximum concentration of

drug at the site of inflammation. There is some danger of
causing adhesions and subsequently intestinal obstruction.

DISEASES OF CIRCULATORY SYSTEM

3. Diagnostic approach:
4. Principles of circulatory failure :

Heart failure
Due to:
- Defect in heart filling
- Abnormality in myocardium
Or in conducting system
- Excessive work load

Peripheral failure
due to:
-Loss of fluid
-Dilatation of peripheral vessels.
-Pooling of blood in

- Combination of above

peripheral system

Consequences
3. Either complete or partial hamper in, - Exchanges of fluid, electrolytes, oxygen, & nutrients
& excretory substances.
4. The first critical system is nervous system to be affected.
Diagnostic approach
v)
vi)

History, inspection, palpation & percussion need especial experiences.

Auscultation by stethoscope or phonendoscope reveal about heart sounds, sometimes
position of heart also.
Tachycardia increased rate of heart beat
Bradycardia - Decreased rate of heart beat
Transient sound Normal, 1st, 2nd, 3rd, & 4th,
Murmur sound
Pericardial rub

- abnormal sound or adventitives

- Pericardial heart sound.

Rhythm Regularity of successive pulse.

Rhythmic deviation in rhythm.
vii)

Blood pressure in animal not easy,it has been tried in dog & house by
Dog tibia artery
House - Middle coceygeal artery.
Done man Brachial artery.
By sphygonometer

Pressure

Systolic
(Ventricular contraction)

Diastolic
(Ventricular relaxation.)

Hypertension increased Pressure

Hypo-tension - decreased Pressure

viii)

Angiography

Electro cardiogram is

not common in livestock done in human.

PERICARDITIS
Inflammation of pericardium is called ~. It may be acute or chronic and effusive, Fibrinous or
adhesive traumatic Pericarditis is widely prevalent in cattle but not in house.

Aetiology
4. TRP in cattle is most frequent.
5. Localization of blood borne diseases- in all sps.
6. Extension of inflammation from pleurisy & myocardium- in all sps.

Symptoms
Bacteria
viii)
ix)
x)
xi)
xii)
xiii)
xiv)

Pasteurellosis
Sheptococcus sps
Salmonella spp
Leptospira- spp
Mycoplasmal spp
Mycobere ferium spp.
Glassers disease in pig.

Viral
i.
ii.

Infectious feline peritonitis

Canine distemper

Fungal
i)
Coccidioisomycosis
ii)
Actonomycosis
chronic uremia may set up pericardial lesion.

Others

Clinical findings
iv)
v)
vi)

Pain, reluctant to move & abducted elbows, arching of back & shallow abdominal
respiration
103 to 106o f temperature & increased pulse rate & weak pulse.
Fibrinous Pericarditis in horse is mainly fasted by marked muffling sounds, Tachycardia,
distension of jugular vein & ventral edema.

Diagnosis
4. 1.Clinical findings Abducted elbow , muffling sound
5. Ecg (electro-cardio gram graphic recording of the electrical potentials produced in
association with the heart beat)
6. X-ray reveals foreign body, displacement e.t.c.

Differential diagnosis
iv)
Pleurisy confused by friction sound differentiate by synchronization of friction sounds
with respiratory cycle.
Absence of other pericardial infn symptoms.
v)

Murmur sounds due to pericardial sounds are present throughout

Congenital defects the cardial cycle breaks

vi)
iv)

Muffling sounds due to pleurisy Careful examination reveals pulmonary emphysema

Hydro pericardium Aspiratory puncture may accompanying with edema.

ii)

TRD Leukocytosis & shift to the left.

Treatment
Use of specific antibiotic for specific causative agent.
iv)
v)
vi)

Non specific treatment is use of broad-spectrum antibiotic & salt

Paracentesis & use of diuretics is use fuel.
Salt free diet & use of fribrinolytic drugs like oxalate

MYOCARDITIS:
Inflammation of heart muscle is kwon as Myocarditis

Aetiology
3. Non infective: due to Auto-immune condition and toxicity of heavy metals eq.
Arsenic,hg,lead, copper etc.
4. Infective agent
e) Virus - FMD virus in young one.i.e. Equine infections anaemia,Canine parvo virus,&
canine distemper.
f) Bacteria Clostridium chauvoei, steptococcous staphy bococess.
g) Funfus cryptocossus.
h) Parasiles eq. Cyst, trypanosoma, toxoplasma, strongyless etc.
Pathogenesis
Clinical findings

Ineffective cardiade output & passive verous congestion.

Mycocardial degeneration leads to acute cardial failure & death.

vii)
viii)
ix)
x)
xi)
xii)

Increased Pulse rate & arrhythmia.

Dyspnoea & weakness.
Exhaustion & increased temperature in infective condn.
Chronic venous congestion & heart failure.
Syncope & death.
Acute death (i.e. without sign & symptom)

Diagnosis
Difficulty by Clinical symptoms.

D. Diagnosis
iii)
iv)

Electro-cardiography.(ECG)
Difficult to differentiable from endocardium

Treatment
iii)
iv)

Treatment of primary cause.

Symptomatic treatment but in large animal may not be useful.

ENDOCARDITIS
Inflammation of endocardium with interference in blood ejection or valvular stenosis is
Endocarditis which is characterized clinically by it is manifestation and murmur sound of heart.

Aetiology
Farm animal Bacteria (strep to, Corynebacterium, clostridium, Mycoplasma, erycepaothrix,
and Escherichia coli )
Virus also i.e. influenza
Horse: above cause as well as migrating strongylus larvae.

Pathogenesis
Due to implantation of bacteria on to the valves from the blood stream result bacteremia or
embolism of the valve capillaries leads to myocardial disease may cause inflammation of

endothelium, its damage or edema of valve. Congenital cardiac defect may also predispose valve
problem or stressful work of valve & endocarditis, vegetative and ulcerative type of lesions may
cause problems on blood ejection & flood. Fragments of vegetative lesions after detaching may
come into circulation & result embolic end arteritis military Pulmonary abscesses, abscesses on
myocardium, kidney & joints chronic lesions on value results adhesions of cusps. Shrinking
distortion and thickening of the valve cusps. At this stage inference of blood flood occurs &
congestive heart failure always results.

Involvement
Cattle: - Most frequently right arterio-ventricular value and left arterio-ventricular.
Horse Aortic semi lunar valves most frequent (value of aorta origin) and pulmonary
value origin of pulmonary artery which each value consists three flap (cusps), less
frequently left a tro- ventricular value.

Clinical findings
viii) Murmur sound on auscultation at the cardiac over and poor exercise tolerance.
ix)
Moderate fluctuating fever;
x)
Secondary involvement of other organs result Peripheral lymphadenitis, embolic
pneumonia, nephritis, arthritis, tenosynovitis, or Myocarditis.
xi)
Loss of condition pale mucous membrane & increased heart rate.
xii)
In cattle additional symptoms are Grunting respiration, moderate ruminal tympany,
scouring or constipation, blindness, facial paralysis, muscle weakness, recumbency,
jaundice & sudden death. Distension of jugular vein, general edema and a systolic &
diastolic murmur sound in many cases. Periodic ill thrill is common history.
xiii) In horse- jugular proment in terminal stages & hot edema.
xiv) In swine Agalactia, loss of wt, intolerance in exercise & dyspnoea at rest.
Diagnosis
iii)
iv)

Difficult from clinical symptoms.

Phonocardiography: - Technique for recording heart sounds & murmurs. These are picked
up by microphone placed over the heart.

Differential diagnosis
Endocarditis & Pericarditis and other causes of cardiac failure are confusion. In cattle
confusion mostly occur in lympomatosis

iii)

In endocarditis.
Acute
- lencocytosis & shift to the left Monocytes increased, increased
macrophages & severe anaemia in
Chronic: - Hyper-gamma-globulinemia in bacterial infn. Repeated examination of
urine gives proteinuria & bacteria in urine.

iv)

Echocardiography reveals about echoes from vegetative lesion & defect

abnormal value movement.

Treatment:vii.
Not so hopeful.
viii.
Blood culture & drug sensitivity test. Use of specific or broad spectrum
antibiotics.
ix.
Streptococcus infn in cattle is difficult because its resistance so procaine benzyl
penicillin @ 20000 units/kg*daily*for 7-10 days or longer.
x.
Amino glycoside are combined form first five days if temperature not reduces,
infection is under control. Again 7 days or more treatment must be continued.
xi.
Treatment with macrolides (eq. Erythromycin) & ampicillin is effective but they
are expensive.
xii.
Chances of relapse is move, of signs of congestive heat failure prognosis is
unfavorable.
HYPERTOPHY AND DILATION OF HEART
Compensatory result
Hypertrophy and dilatation of heart can collectively be called cardiac enlargement. Physiological
hypertrophy of heart is the normal physiological enlargement of heart in race or athletic animals.
Enlargement o heart is due to Persistent increased work loads that are associated with
cardiovascular disease, the heart may respond

Cardiac hypertrophy is due to increased pressure load

By dilatation, hypertrophy or combination of both

Cardiac hyper tropy
Usual response of

Cardiac dilation
- Usual response

- Increased pressure load & in this there is

increased volume load & probably

Increment of individual fibre, size

results from fiber re-arrangement.

Increase in total mass.

- By this increased volume of blood

- Compensatory mechanism
fos coronary circulation or per unit contraction.
In state of cardiac insufficiencyDepends on laplace loud which
producing

can be ejected (by single contract)

Increased tension request for
Increased inside chamber

Cardiac reserve the normal heart has the capacity to in release body
weight several folds in response to normal physiological demands
created by exercise and to a less extent by pregnancy, by lactation
& by digestion. Collectively this response comprise the cardiac
reserve
.
Clinical findings
o Degree of enlargement is a good indication of degree of cardiac embarrassment but accurate
measurement is impracticable.
o Increased Pressure on heart, flow load;0.
o Presence of myocardial diseased increased of cardiac reserve.
Diagnosis
By careful auscultation & palpation of apex beat of heart.
D. Diagnosis

Displacement heat by space occmpying lesions.

Ventral collapse of lung & upw and displacement of heat
Radiography & eco-cariographic.

Treatment
Treatment of primary causes.

CONGESTIVE HEART FAILURE

Failure of the heart to maintain circulatory equilibrium at rest and congestion of venous circuit
accompanied by dilation of vessels, edema of the lungs of periphery, enlargement of the heart
with increased rate is known as ~. Pulmonary circulation implies left sided heart failure and
systemic venous circulation implies right sided heart failure.
Aetiology

8. Any factor or disorder which causes Myocarditis, endocarditis or Pericarditis which interfere
in blood flood.
9. Any disease which weakens the face of myocardial contraction(may be due to nutrition)
10. Any type of alveolar diseases e.g. Stenosis, congenital defect persistent defect arteries,
rupture of value or aortic valued effect
11. Myopathy or myocardial infarction.
12. Chronic pulmonary emphysema or disease eg. Fibrosis of lungs, emphysema.
13. Hypertension due to altitude (more time to exchange the gasses due to law concn of 02) or any
other causes.
14. Congenital pulmonary steno sis, vascular abnormality
ENDOCARDITIS
Pathogenesis
Persistent work load for a long time on the heart may be either due to a pressure load or a flood
load. Lesions of aortic or pulmonary value result in pressure load (if high pressure needed to
pump) and a flood load or volume load (more volume of the blood to be ejected) is generally due
to acquired or congenital heart defects.

When an increase load is placed upon ejection of the blood from the heart or the contractile
power or the myocardium is reduced, compensatory mechanism including heart rate, ventricular
filling, re distribution of blood flood, dilatation and hypertrophy came into play to maintain
increased circulatory equilibrium. This results reduction in cardiac reserve & poor exercise
tolerance.

When the compensatory mechanisms reach then physiologic limit & the heart is unable to cope
with the circulatory requirement at rest congestive heart failure develops.

The weakened heart cannot maintain adequate arterial pressure on kidney which consequences
retention of salt & water leading to blood volume. This large blood volume cannot be handled
by failing chamber. Consequently there will be stagnation or congestion of blood in that circuit.
Increased blood volume required increased stretching of myocardium to be ejected which is
impossible beyond the physiologic limit & results cardiac failure.

Clinical findings
C. Left sided cardiac failure :- (oxygenated blood obstruction)

- Dyspnoea ( respiration & depth) at rest, cough, presence of moist cracles, at the base of
the lungs, cyanosis, increased heart rate.
D. Right sided cardiac failure ( systemic failure)
o Edema, Anasarca(ventral surface of the body neck and jugular vein )
o Ascites, hydrothorax, hydro pericardium.
o Enlarged liver & palpable at right costal arch with thickened & rounded
edge.
o Oliguria, concentrated urine & presence of albumen.
o Lose Faeces, decreased weight of body with due to edema but rapid loss of
condition.
o Dilated superficial veins mainly the jugular.
Epistaxis in horses (may be)
Diagnosis
By clinical symptoms.
ii)

ECG.(electro-cardiography)

D. Diagnosis
v)

Peritonitis :- On Paracentesis presence of bacteria & Leukocytosis

- Absence of cardiac involvement.
vi)
Ruptured bladder :- Oliguria
- BUN(Blood urea nitrogen) & peritoneal flood nitrogen
- Abdominal pain & strain to Micturation .
vii)
Hepatic fibrosis :
- Jaundice & photosensitization.
- Liver function test.
viii) Edema: - May occur in mare & condition near to calving date.
- There is no jugular engorgement. & evidence of cardiac involvement.
- May be due to endo parasites or hypo-proteinuria. Dyspnoea May be due
to pulmonary edema
- Pulmonary emphysema
- Allergic or anaphylactic stage
- Fog fever of cattle
Line of Treatment
7. Provide rest so that there is less demand of blood.
8. Perform specific causative agent treatment.
9. Use salt free diet in edematous condition
10. Use diuretics to treat edematous condition.
11. In severe condition vein section is suggested as an emergency treatment @ 4-8ml blood /kg
body wt at a time. It cannot be repeated before 7 days.
12. Use of digitalis: - As per needed.

Induce with little dose achieve desired therapeutic result without toxic symptoms & maintain
as per needed is digitalization.
7. Supportive therapy on needed: - 02 for anoxia Tranquillizes for pain,
Body cannot thrive the condition & animal dies. Usually it is unfavorable
Treatment
4. Since there is no specific treatment, symptomatic treatment should be followed. To reduce
the spasm or cramp and to sooth the nerves anti-spasmodic like chlorpromazine,
Phenobarbitone, etc. are used.
5. To correct neurological disorders methyldopa (lardopa) 500mg tab once daily followed by
tab/week can be given. Or trihexypnendyl hcl (pecitane-lederle) 2 mg (1 tab) B.I.D. orally.
6. Vit. B .complex + vitamin c. should be given.
Prevention
2. Since the disease is a sequlae of Distemper, it should treat with additional 10 days after the
apparent symptoms manifestation causes.
URINARY INCONTINENCE

Urinary incontinence (UI) is any involuntary leakage of urine. It can be a common and
distressing problem, which may have a profound impact onquality of life. Urinary incontinence
almost always results from an underlying treatable medical condition but is under-reported to
medical practitioners. There is also a related condition for defecation known as fecal
incontinence.
Causes
The most common causes of urinary incontinence in women are stress
urinary incontinence and urge urinary incontinence. Women with both
problems have mixed urinary incontinence. Stress urinary incontinence is
caused by loss of support of the urethra which is usually a consequence of
damage to pelvic support structures as a result of birth. It is characterized by
leaking of small amounts of urine with activities which increase abdominal
pressure such as coughing, sneezing and lifting

Polyuria (excessive urine production) of which, in turn, the most frequent

causes are: uncontrolled diabetes mellitus, primary polydipsia (excessive

fluid drinking), central diabetes insipidus andnephrogenic diabetes insipidus.

[2]
Polyuria generally causes urinary urgency and frequency, but doesn't
necessarily lead to incontinence.

Caffeine or cola beverages also stimulate the bladder.

Enlarged prostate is the most common cause of incontinence in men after

the age of 40; sometimes prostate cancer may also be associated with
urinary incontinence. Moreover drugs or radiation used to treat prostate
cancer can also cause incontinence.[3]

Disorders

like multiple

sclerosis, spina

bifida, Parkinson's

disease, strokes and spinal cord injury can all interfere with nerve function of
the bladder.
Pathophysiology
Continence and micturition involve a balance between urethral closure
and detrusor muscle activity. Urethral pressure normally exceeds bladder
pressure, resulting in urine remaining in the bladder. The proximal urethra
and bladder are both within the pelvis. Intraabdominal pressure increases
(from coughing and sneezing) are transmitted to both urethra and bladder
equally, leaving the pressure differential unchanged, resulting in continence.
Normal voiding is the result of changes in both of these pressure factors:
urethral pressure falls and bladder pressure rises.

Diagnosis
Patients with incontinence should be referred to a medical practitioner
specializing in this field. Urologists specialize in the urinary tract, and some
urologists further specialize in the female urinary tract. A urogynecologist is
a gynecologist who has special training in urological problems in women.
Family physicians and internists see patients for all kinds of complaints, and
are well trained to diagnose and treat this common problem. These primary
care specialists can refer patients to urology specialists if needed.

A careful history taking is essential especially in the pattern of voiding and

urine leakage as it suggests the type of incontinence faced. Other important
points include straining and discomfort, use of drugs, recent surgery, and
illness.
The physical examination will focus on looking for signs of medical conditions
causing incontinence, such as tumors that block the urinary tract, stool
impaction, and poor reflexes or sensations, which may be evidence of a
nerve-related cause.
A test often performed is the measurement of bladder capacity and residual
urine for evidence of poorly functioning bladder muscles.
Other tests include:

Stress test the patient relaxes, then coughs vigorously as the doctor
watches for loss of urine.

Urinalysis urine is tested for evidence of infection, urinary stones, or other

contributing causes.

Blood tests blood is taken, sent to a laboratory, and examined for

substances related to causes of incontinence.

Ultrasound sound waves are used to visualize the kidneys, ureters, bladder,
and urethra.

Cystoscopy a thin tube with a tiny camera is inserted in the urethra and
used to see the inside of the urethra and bladder.

Urodynamics various techniques measure pressure in the bladder and the

flow of urine.
Patients are often asked to keep a diary for a day or more, up to a week, to
record the pattern of voiding, noting times and the amounts of urine
produced.
Types

Stress incontinence, also known as effort incontinence, is due essentially to

insufficient strength of the pelvic floor muscles.
Urge incontinence is involuntary loss of urine occurring for no apparent
reason while suddenly feeling the need or urge to urinate.
Overflow incontinence: Sometimes people find that they cannot stop their
bladders from constantly dribbling or continuing to dribble for some time
after they have passed urine. It is as if their bladders were constantly
overflowing, hence the general name overflow incontinence.
Mixed incontinence is not uncommon in the elderly female population and
can sometimes be complicated by urinary retention, which makes it a
treatment challenge requiring staged multimodal treatment.[4]
Structural incontinence: Rarely, structural problems can cause incontinence,
usually diagnosed in childhood (for example, an ectopic ureter). Fistulas
caused by obstetric and gynecologic trauma or injury can lead to
incontinence. These types of vaginal fistulas include, most commonly,
vesicovaginal fistula and, more rarely, ureterovaginal fistula. These may be
difficult to diagnose. The use of standard techniques along with a
vaginogram or radiologically viewing the vaginal vault with instillation of
contrast media.[5]
Functional incontinence occurs when a person recognizes the need to urinate
but cannot make it to the bathroom. The urine loss may be large. Causes of
functional incontinence include confusion, dementia, poor eyesight, poor
mobility, poor dexterity, unwillingness to toilet because of depression,
anxiety or anger, drunkenness, or being in a situation in which it is
impossible to reach a toilet.[6] People with functional incontinence may have
problems thinking, moving, or communicating that prevent them from
reaching a toilet. A person with Alzheimer's Disease, for example, may not
think well enough to plan a timely trip to a restroom. A person in a
wheelchair may be blocked from getting to a toilet in time. Conditions such
as these are often associated with age and account for some of the
incontinence of elderly women and men in nursing homes. [7] Disease or
biology is not necessarily the cause of functional incontinence. For example,

someone on a road trip may be between rest stops and on the highway; also,
there may be problems with the restrooms in the vicinity.
Nocturnal enuresis is episodic UI while asleep. It is normal in young children.
Transient incontinence is a temporary version of incontinence. It can be
triggered by medications, adrenal insufficiency, mental impairment,
restricted mobility, and stool impaction (severe constipation), which can
push against the urinary tract and obstruct outflow.
Giggle incontinence is an involuntary response to laughter. It usually affects
children.

Treatment

Attempt should be made to control primary cause

Measures should be taken to prevent infection

Bladder should be emptied if there is distension

Neurovitamin should be used to induce contraction power of urinary

bladder.

Stilbesterol or testosterone therapy may be required.

Exercises
One of the most common treatment recommendations includes exercising
the muscles of the pelvis. Kegel exercises may strengthen a portion of the
affected area. According to many industry specialists, the pelvic floor is
actually a group of muscles and connective tissues running side-to-side
and front to back along the bony ridges of the pelvis. To understand this is
better to visualize the pelvic floor as a 'hammock' or 'bowl'. For everything
to be working properly, this hammock should be broken out like every
other muscle in the body.

Medications
A
number
of
medications
exist
to
treat
incontinence
including: fesoterodine, tolterodine and oxybutynin. While
a
number
appear to have a small benefit, the risk of side effects are a concern. For
every ten or so patient treated only one will become able to control their
urine and all medication are of similar benefit.
Surgery
Surgery may be used to alleviate incontinence only after other treatments
have been tried. Many surgical options have high rates of success.
Urodynamic testing seems to confirm that surgical restoration of vault
prolapse can cure motor urge incontinence.

HAEMATURIA
Escape of red blood cells (RBC) through urine is known as haematuria (red urine).In severe
cases of hematuria blood may be voided as grossly visible clots more commonly it causes a deep
red to brown coloration of the urine. Less severe cases may show only cloudiness that settles to
form a red deposit on standing. The haematuria may be so slight that it is detectable only on
microscopic examination of a centrifuged sediment.
ETIOLOGY
Hematuria can result from;
Prerenal causes when vascular damage occurs, such as trauma to the kidney, septicaemia
and purpura hemorrhagica.
Renal causes include acute glomerulonephritis, renal infarction, embolism of the renal
artery, tubular damage as caused by toxic insult, and pyelonephritis.
Postrenal haematuria occurs particularly in urolithiasis and cystitis.
Enzootic haematuria of cattle when haemorrhage originates from tumors of the urinary
bladder.
Hematomas of the bladder wall (cystic hematoma) cause hematuria in neonatal foals.
Typically, lesions of the kidney, bladder, and proximal urethra cause hemorrhage
throughout or towards the end of urination, whereas lesions of the middle and distal
urethra are responsible for bleeding at the beginning of urination.
CLINICAL FINDINGS
If the bladder or urethra are involved in the process that causes haematuria, abnormalities may be
detectable on physical examination. Gross haematuria persisting for long periods may result in
severe blood loss anaemia and shows clinical signs similar to anaemia. Severe urinary tract
haemorrhage of undetermined origin in aged mares has been recorded.

DIAGNOSIS
Blood in urine gives positive results on biochemical tests for haemoglobin and myoglobin.
Because red blood cells can be lysed in dilute urine, red-colored urine should be examined
microscopically for the presence of erythrocytes. The presence of a heavy brown deposit is not
sufficient basis for a diagnosis of haematuria as this may also occur in hemoglobinuria.
Differentiation should be made between haematuria and haemoglobinuria .In haematuria intact
R.B.C. will be observed under microscope but in haemoglobinuria there will be no such intact
R.B.C.
On centrifugation, haemoglobinuria will show uniform red colour but in case of haematuria there
will be three distinct layers, R.B.C. at the bottom, a thin layer of W.B.C. and then a layer of
plasma at the top. Endoscopic examination reveals haemorrhage in one ureter but
ultrasonographic examination of the kidneys does not reveal any significant abnormalities.
Surgical removal of the affected kidney is not recommended, as the haemorrhage sometimes
reoccurs in the remaining kidney.
Diagnosis can further be done in following ways;

Full Clinical History and Comprehensive physical examination

o
To rule out or identify underlying causes of the problem, and to identify all
symptoms and pathologies present.

Full Urine Tests Urine Specific Gravity, Dipstix and Cytology

o
To identify whether the animal is concentrating their urine properly, and to
identify any possible infections or crystals which may indicate a UTI or bladder stones?

Laboratory Urine Tests Urine Culture and Sensitivity testing, Urethral Crystal Analysis
(stones)
o
To determine the specific bacterium causing the urinary tract infection and to
determine which antibiotics will be effective against that infection. Also, crystal analysis can
be used to identify the composition of the bladder stones, which is necessary to formulate
treatment and prevention plans.

Special Blood Tests - Coagulation Profiles if suspecting bleeding/clotting disorders

To ascertain if there is a bleeding disorder, and distinguish the type of bleeding
disorder, whether it be a clotting factor deficiency, a platelet deficiency, etc.
Imaging, X-RAYS, Ultrasound, Endoscopy, Contrast radiography
To located undiagnosed masses, tumours, etc which may be causing the bleeding

Biopsies (Kidneys, Urethra, bladder, etc). Methods include: Ultrasound guided,

Traumatic Urethral Catheterisation, Full surgical biopsies
o
To obtain samples of suspicious tissues to be tested by a pathologist. Allows
further identification of the underlying cause.
Hormone Tests (testosterone, oestrone sulphate, etc) if suspecting dogs may be showing
signs of being in season

LINE OF TREATMENT
Treatment is entirely dependent upon the underlying cause. Please see vet to have the bloody
urine diagnosed, so a correct treatment can be started. With this symptom, there isn't any
standard symptomatic therapy that vets are likely to implement whilst waiting on a definitive
diagnosis.

Correction of primary cause with institution of appropriate measures.

Use of haemostatics to control bleeding.
Use of systemic alkalisers.
Treatment with calcium and vitamin K may be necessary to induce blood clotting.

SUMMARY
Blood in the urine is a symptom which can be seen in most domestic animals. It can be caused by
a variety of different diseases or pathologies, and is diagnosed with tests ranging from blood and
urine tests to imaging. Symptomatic treatment involves the use of anti-nausea medication and
dietary modification. As always, seek veterinary consultation at all times.
PYELONEPHRITIS

Nephritis
Nephritis is inflammation of the nephrons in the kidneys.The most prevalent form of acute nephritis is
glomerulonephritis. This condition affects young more often than it affects adult.It is inflammation of the
glomeruli, or small round filters located in the kidney.
Types
Nephritis

Glomerulonephritis

pyelonephritis

Glomrulonephritis
It is inflammation of the glomeruli, or small round filters located in the kidney.

interstialnephritis

Interstialnephritis
Nephritis with increase of interstitial tissue and thickening of vessel walls and malpighian corpuscles; it may
be due to overuse of analgesics, mercury poisoning, gout, or any of various other conditions.it is a form of
nephritis affecting the interstitium of the kidney surrounding the tubules. This disease can be either acute,
meaning it occurs suddenly, or chronic, meaning it is ongoing and eventually ends in kidney failure.
Pyelonephritis
(from Greekpyelum, meaning "renal pelvis" nephros, meaning "kidney", and -itis, meaning "inflammation")
is an ascending urinary tract infection that has reached the pyelum or pelvis of the kidney. It is a form of
nephritis that is also referred to as pyelitis. Severe cases of pyelonephritis can lead to pyonephrosis (pus
accumulation around the kidney), urosepsis (a systemic inflammatory response of the body to infection),
kidney failure and even death. Pyoelonephritis is bacterial infection characterized by inflammation of renal
parenchyma and renal pelvis or ascending infection of lower urinary tract. It is highly fatal chronic purulent
inflammation of pelvis of the kidney. It occurs chiefly in cows but has been recorded in sheep, goat, horse,
buffalo, and dog. More than 75% cases are bilateral
Classification
Acute pyelonephritis
Acute pyelonephritis is an exudativepurulent localized inflammation of the renal pelvis (collecting system)
and kidney. The renal parenchyma presents in the interstitium abscesses (suppurativenecrosis), consisting
in purulent exudate (pus): neutrophils, fibrin, cell debris and central germ colonies (hematoxylinophils).
Tubules are damaged by exudate and may contain neutrophil casts. In the early stages, the glomerulus
and vessels are normal. Gross pathology often reveals pathognomonic radiations of bleeding and
suppuration through the renal pelvis to the renal cortex.
Chronic pyelonephritis
Chronic pyelonephritis implies recurrent kidney infections, and can result in scarring of the renal
parenchyma and impaired function, especially in the setting of obstruction. A perinephricabscess (infection
around the kidney) and/or pyonephrosis may develop in severe cases of pyelonephritis. ]
Xanthogranulomatous pyelonephritis
Xanthogranulomatous pyelonephritis is an unusual form of chronic pyelonephritis characterized by
granulomatousabscess formation, severe kidney destruction, and a clinical picture that may resemble renal
cell carcinoma and other inflammatory renal parenchymal diseases. Most patients present with recurrent
fevers and urosepsis, anemia, and a painful renal mass. Other common manifestations include kidney
stones and loss of function of the affected kidney. Bacterial cultures of renal tissue are almost always
positive.[13]Microscopically, there are granulomas and lipid-laden macrophages (hence the term xantho-,

which means yellow in ancient Greek). It is found in roughly 20% of specimens from surgically managed
cases of pyelonephritis.[2]

ETIOLOY

usually ascending microorganisms, most often bacteria

in females with uncomplicated pyelonephritis usually E. coli
causative microorganisms are usually E. coli, Klebsiella, Proteus, Serratia, Pseudomonas,
Enterococcus, and S. aureus
if S. aureus is found, suspect bacteremic spread from a distant focus (e.g. septic emboli in infective
endocarditis) and suspect (possible multiple intra-renal microabscesses or perinephric
abscess)Secondary to bacterial infection of the lower urinary tract.
Spread from embolic nephritis of haematological origin such as Septicemia in cattle caused by
Pseudomonas aeroginosa.
Specific pyelonephritis caused by Corneybacteriumrenale in cattle, Corneybacteriumsuis in pigs.
Urinary stasis or obstruction due to any cause like calculi, neoplasms, neurogenic bladder etc.
Vesicoureteral reflex

PATHOGENESIS
The development of pyelonephritis depends upon the common presence of infection in the urinary
tract and the stagnation of urine , permitting multiplication and progression of the infection. Urinary
stasis may occur as a result of bacterial infection and blocking of ureter by inflammatory swelling or
debris, by pressure from uterus in pregnant females, and by obstructive urolithiasis. The infection
ascends not always bialaterally and invades uereters the renal pelvis. Involvement of the papillae
occurs & lesions develop in the renal medulla although the lesions may extend to the cortex
.Toxemia & fever results if renal involvement is bialatteral& sufficiently uremic develops.
Pyelonephritis is always accompanied by pyuria and haematuria because of inflammatory lessions
of ureters and bladder.

CLINICAL FINDINGS
Loss of condition over a period of a week or month.
High rise tempertaure may fluclates.
Dull,depression &anorexia.

 Stiff gait; tenderness of lumber region.

Frequent micturition & straining during urination.
Decrease in millk production.
One or both kidney show enlarge.
Urine may be haematuria,proteinuria.

Laboratory examination
Urinalysis may show signs of urinary tract infection. Specifically, the presence of nitrite and white blood
cells on a urine test strip in patients with typical symptoms are sufficient for the diagnosis of pyelonephritis,
and are an indication for empirical treatment. Blood tests such as a complete blood count may show
neutrophilia. Microbiological culture of the urine, with or without blood cultures and antibiotic sensitivity
testing are useful for establishing a formal diagnosis, ]and are considered mandatory.
Differential diagnosis

Acute appendicitis

Acute cholecystitis

Acute diverticulitis

Pancreatitis

Basal pneumonia

Herpes zoster affecting somatic segments of T12 & L1

Line of treatment

Broad spectrum antibiotics such as penicillin

Diuretics can be used
Acidifier or alkalizer to alter ph
Urease inhibitor to convert urea to NH3 by bacteria
Drugs such as neomicine, vencamicine, gentamicine are contraindicated

Nephrosis
INTRODUCTION:
Nephrosis refers
to
a
non-inflammatory nephropathy. Also
refers
as nephrotic syndrome, nephrosis is any degenerative disease of the renal
tubules. It is an accumulation of symptoms and signs characterized by
proteinuria (>3.5gm/day), hypoproteinemia (mainly albumin), edema (fluid
retention) and hypercholesterloemia (>5.72mmol/L).Nephrosis can be
caused by any kidney diseases or it may be secondary to any other disorder.
The treatment and prognosis vary depending on the cause.
ETIOLOGY
Nephrotic syndrome is caused by various disorders that damage the kidneys, particularly the
basement membrane of the glomerulus.

Membranous glomerulopathy

Minimal change glomerulopathy

Diabetic glomerular disease

Membranous glomerulonephritis

Abnormalities in the function of Thymus derived T-cell lymphocytes.

Complement deficiencies

Amyloidiosis

Focal segmented glomeruloscleriosis

Pathophysiology
Proteinuria: This is the fundamental and highly important change of Pathophysiology in which
the kidneys (the glomeruli) become 'leaky' and protein, instead of remaining in the blood, leaks
out into the urine.
Hypoproteinemia: The main protein that leaks from the blood into the
urine is albumin. A low blood level of albumin is a main feature of Nephrotic

syndrome. Due to albuminemia, plasma oncotic pressure is diminished as a

result; there is shift in fluid from vascular to interstitial space.
Edema: Edema is due to the fluid retention due to kidney failure.
Hyperlipidemia (Hyper-cholestrolemia): There is increase in cholesterol,
Tri-glyceride, Low Density Lipo protein and Very low density lipo protein. It is
due to change in the balance of Lipo protein level in blood.

Pathogenesis:
.Following Morphologic Patterns are associated with Nephrosis.
1). Minimal-change disease (MCNS):
The name 'minimal change' comes from the fact that there is virtually no change detectable in the
glomeruli if a sample of kidney is looked at under the microscope. Although the glomeruli look
normal under the microscope, there seems to be some minor change in the glomeruli that allows
leakage of protein. The cause of minimal change disease is not clear. It probably has something
to do with a slight change in the immune system, or perhaps a reaction of parts of the immune
system to some unidentified factor. It usually responds well to treatment with steroid medication
and does not cause kidney failure in most cases.
2). Focal segmental glomerulosclerosis (FSGS):
This is a condition where small scars (sclerosis) develop on some glomeruli.
The cause is unknown in most cases. However, a reaction of the immune
system to something, or to various different things, is thought to be the
cause.
3). Membranous nephropathy:
This is sometimes called membranous nephritis or membranous
glomerulonephritis. It is a common cause of nephrotic syndrome in adults. In
this condition there is some thickening of the membrane in the glomeruli
(the 'filter' of the glomeruli) which makes the glomeruli 'leaky' to protein.
However, there are various conditions that can result in membranous
nephropathy developing. For example, an abnormal reaction of the immune
system to some infections or drugs can cause this disease.
Clinical Findings:

1).Edema: Swelling (edema) is the most common symptom. It may occur:

In the face and around the eyes (facial swelling)

In the arms and legs, especially in the feet and ankles
In the belly area (swollen abdomen)

2).Other symptoms include:

Foamy appearance of the urine
Weight gain (unintentional) from fluid retention
Poor appetite
High blood pressure
Urine may appear frothy.
Tiredness, lethargy and a poor appetite.
Diarrhoea and/or vomiting (especially in calfhood).
If the nephrotic syndrome persists for a long time then you may develop
wasting of your muscle. Some conditions of the kidney can cause high blood
pressure and/or kidney failure.
Clinical Pathology:
1. Urinary protein: In 24hrs total urinary protein > 0.1g/kg. May occur granular and red cell
casts.
2. Total Serum protein: 30g/L. Albumin levels are low (20g/L).
3. Serum cholesterol and triglycerides: Cholesterol 5.7mmol/L (220mg/dl).
4. ESR: 100mm/hr
5.Serum proteins electro- phoresis: Decreased Albumin level

Line of Treatment:
The goals of treatment are to relieve symptoms, prevent complications and
delay progressive kidney damage.
1).A low salt diet may help with swelling in the hands and legs. Water pills
(diuretics) may also help with this problem.
2).Corticosteroids and other drugs that suppress or quiet the immune system
may be used.e.g. Prednisolone

3). Medications to reduce cholesterol and triglycerides may be needed, most

commonly statins.
4). Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor
blockers (ARBs) are the medicines most often used in this case. ACE
inhibitors may also help decrease the amount of protein loss in the urine.
5). Vitamin D may need to be replaced if nephrotic syndrome is chronic and
unresponsive to therapy.
6). Blood thinners may be required to treat or prevent clot formation

Orchitis
Introduction
Inflammation and swelling of the testes, caused by infection (most often mumps) or chemical or
physical injury. The testicles' rich blood and lymphatic supply block most infections in the
absence of severe injury.
Etiology
Physical cause
Trauma
Infectious causes
Bacteria
o Streptococcus zooepidemic
o Brucella abortus
o Mycobacterium tuberculosis
o Actinomyces pyogens
o Nocardia farcinia
Virus
o Bovid herpis virusIII (IBR-IPV)
Types
Autoimmune orchitis
Rete testes or efferent ducts are starting sites
When disruption of blood-testes is so severe that spermatozoa are outside their normal
containment within the testes, epididymis ductus deferens and urethra, a foreign body
granulomatous reaction occurs
Non specific orchitis

Mild, multifocal, subacute interlobular inflammation

Cause unknownare
No gross lesion
Microscopically
Lymphocytes foci present between tubules and around vessels
Intertubular orchitis
Arises from infection ascending from urethra, urinary bladder, ductus deferens and epididymis
Inflammation in seminiferous tubules which can spoil over into interstitium
Necrotizing orchitis
Can begin as an intratubular disease or can arise hematogenously
Affected areas are so severely inflamed and necrosis is so extensive that the original structure are
formed a caseous mass
Grey brown initially soft and later firm, necrotic debris replaces an irregular but large portion of
testis. In few extremely severe cases a fistula develops through the scrotum
Granulomatous orchitis
Includes formation of multiple possible coalescing , inflammation nodules displacing and
replacing parenchyma
Pathophysiology
Inflammation of tunica vaginalis/epididymis can be secondary to intratubular, necrotizing and
granulomatous
Fibrinous exduate distends the cavity of tunica vaginalis
Foci of necrosis of parenchyma expand and coalesce so that much of the testis is involved
becoming either liquefied or caseous and gritty
Surrounding tunics and any surviving parenchyma become densely fibrinous
Eventually the testis become smaller and suspended in abundant fluid/semi fluid exudates

Symptoms

Blood in the semen

Discharge from penis

Fever

Groin pain

Pain with intercourse or ejaculation

Pain with urination (dysuria)

Scrotal swelling

Tender, swollen groin area on affected side

Tender, swollen, heavy feeling in the testicle

Testicle pain that is made worse by a bowel movement or straining

Signs and tests

A physical examination may show:

Enlarged or tender prostate gland

Tender and enlarged lymph nodes in the groin (inguinal) area on the affected side

Tender and enlarged testicle on the affected side

Tests may include:

Complete blood count (CBC)

Testicular ultrasound

Tests to screen for chlamydia and gonorrhea (urethral smear)

Urinalysis

Urine culture (clean catch) -- may need several samples, including initial stream,
midstream, and after prostate massage
Line of treatment
1. In the inflamed area cold water or ice pack is applied
2. Antibiotics
Cefalexin:
Dog/cat: 10-30 mg/kg bw Tid
Cattle/buffalo: 5-10mg/kg bw Tid
Ciprofloxacin:
Dog/cat: 5-15mg/kg Bw
Cattle/sheep:4-5mg/kg Bw
3. Analgesic and anti-inflammatory
0.2-0.3 mg/kg BW

Pharyngitis

Inflammation of pharynx characterized by couglig painful swallowing and loss

of appetite is called . it is common in dog, horse and pigs characteriged by
purulent bilateral nasal discharge. Inflammation of pharynx leads to
conatriction of lumen of pharynx known as "angina" or "cynache".

Etiology:1. Physical cause:i) It is most common in forma animals.

ii) Tranmatic inyury during balling or drenching or in tracheal intubation.
iii) Hot or cold initant substance ingestion.

iv) Foreigh bodies ludged in the pharynx.

2. Infectious causes:Cattle
i)
ii)
iii)

Oral necrobacillosis, actinobacillosis.

Infectious bovine rhinotracheitis (IBR).
Pharyngeal phlegmon or intermandibular cellulites generally due
to fusobacterium necrophorum.

Horse
i)
ii)
iii)

Streptocoecus equi, Bacillus anthracis,

Equine Herpes virus-1, parainfluenza viruse, adeno virus, rhino
virus, virus arteritis, inflnenza.
Hyperplasia of lymphold tissues in pharyngeal mucosa.

Pigs
i)
ii)

Bacillus anthracis Aujeszky is disease

Staphylococeal & stncptococeus infh,

Pathogenesis:i)

Due to inflammation the animal disincline to eat & difficult

inswallowing. Viral infection in case of horse there is severe swelling
of retropharyngeal lymphnode which makes obstruction during
swallowing.

Clinical symptoms:i)
ii)
iii)
iv)
v)
vi)
vii)

Animal refuse to eat, drink and difficult swallowing.

Palpapation at throat will provide paraoxymal cough.
Mucopurulent nasal discharge,
Sometimes it may come out blood spontaneously regurgitation of
fluid and food through nostrils.
Dull and depression, animal stands extends head there is drooling of
saliva & sometimes respiratory difficulty.
Toxaemia may be developed in oval necrobacillosis in fh and
strangles.
Empyema of gutlural pouches is possible in horse

viii)

ix)
x)

xi)

In pharyngeal phlegmon there is acute onset 106-107F fever in

cattle rapid heart beat, dy profound. Depression & sever
swelling of soft tissues at posterior to mandible. Death may oceus
after 36-48 hrs.
Palpation with the acid of mouth gag in cattle & endoscopic
examination through hostril in hone is performed to examine about
foreigh bodies.
Pharyngitis is a common disease of respiratag system in horse,
chronic pharyngitis cause exercise tolerance, frequent and
persistent conghing easly tirness, breakaye in the training and some
times discharge as exndnates from nostrils & mouth.
Aspiratarge phenumonia may develop & collapse of lungs.
INTUSSUSCEPTION

SYNONYMS:
Definition : This is form of acute intestinal obstruction caused b y the
telescoping of a section of a bowel into a portion immediately behind it.
Etiology: The mechanical causes of intussusceptions are irregular or
excessive peristaltic movement. Enteritis, intentional parasites, error in diet
and tumowrs of the bowel are possible exciting cause. Intussusception
occurs most frequently in cattle, not infrequent in sheep and less common in
swine & horses. The common site of all is the ileo-caecal junction with the
ileum invaginated into the colon.
PATHOGENESIS:
Type most commonly encountered are
a)
b)
c)
d)
e)
f)
g)

Jejunum into jejunum is referred as jujunal intussusceptions.

Jejunum into ileum is referred as jujunoileal intussusceptions.
Jleum into caecum is referred as ileocaecal intussusceptions.
Caecum into caecum referred as caecal- intussusceptions.
Caecum into colon is referred as caeco-colic intussusceptions.
Colon into colon is referred as colonic intussusceptions.
Colon into rectum is referred as colorectal intussusceptions.

A portion which has become narrower and longer, due to

constriction of circular fibres and relaxation of longitudinal fibres, is
invaginated into a part immediately behind. The mesentry also goes into and
venous congestion occurs leading tosrpasmodic contnactuse hence pain.

STRANGULATION IN HORSES:

Strangulation is pressure on any part of body that causes obstruction of

blood flow. It may occur on both respiratory as well as digestive
system .strangulation on the neck that can cause injury to the spinal
cord, brain stem or neck structure; complete airway obstruction; cardiac
arrest; or death. Strangulation may be purposeful or result from an
accident.

The act of suffocating (someone) by constricting the windpipe; no

evidence that the choking was done by the accused. It is constriction of
a body parts as to cut off the flow of blood or other fluid; strangulation of
intestine.

Cause of strangulation in equine:

The one most lethal causes behind colic are strangulation/torsion (a twist in the
gastrointestinal system of a horse) and intussusception (the intestine slides back
into itself, causing blockage). In both cases the blood supply may be partially or
more completely cut off, resulting in dead tissue, & the passage of blood can be
blocked. The horses with hindgut acidosis tend to have flaccid colons, which are
more susceptible to twist. Gas can also cause portion of the GI tract to rise & folds
in on itself.A horses naturals diet is made up of grass , leaves & bark, yet because
of the performance demands put on the todays horses, they are often fed
processed grains & sweet feed that are high in carbohydrates , is can be lead to
hindgut acidosis, resulting in a lower Ph. in the colon & cecum. Higher level of
acidity can modify the delicate microbial balance in the hindgut & may comprise
the mucosal lining of the colon.Colonic ulcer form which may allow endotoxin to
enter the bloodstream restricting blood flow to the colon & small intestine. Tissue
may eventually die, resulting infood blockage & induced colic.
In truth the exact sequence is unknown. But there is significant amount of research
that shows a connection between feeding horses grain rich in simple
carbohydrates &condition that can lead to colic.

Has limited access to quality hay

Travels & competes regularly

Exercised rigorously

Pathophysiology:

Complete obstruction of passage. Complete impairment of defecation. In verminous

aneurism, there is severe colic due to blood clots in blood vessel of mesentery
leading to less supply of blood to intestine with subsequent gangrenous changes
of intestine; this may lead to toxemia and death. There will be increased heart
rate and signs of dehydration. There will be acidosis and vascular shock.

This is characterized by a physical obstruction of the intestine, which can be due to

impacted food material, stricture formation, or foreign bodies.
The primary pathophysiological abnormality caused by this obstruction
is related to the trapping of fluid within the intestine oral to the
obstruction.

This is due to the large amount of fluid produced in the upper gastrointestinal tract dailyand the fact that this is primarily re-absorbed in
parts of the intestine downstream from the obstruction. The first
problem with this degree of fluid loss from circulation is one of
decreased plasma volume, leading to a reduced cardiac output,
and acid-base disturbances.

There also occur serious effects on the intestine itself, which

becomes distended due to the trapped fluid, and by gas production from
bacteria.

It is this distension, and subsequent activation of stretch receptors

within the intestinal wall, that leads to the associated pain. With
progressive distension of the intestinal wall, there is occlusion of blood
vessels, firstly veins, then arteries.

The difference in time to onset of occlusion is due to the relatively more

rigid walls of arteries compared with veins.

Impairment of blood supply leads firstly to hyperemia and congestion,

and ultimately to ischemic necrosis and cellular death.
The poor blood supply also has effects on the vascular endothelium,
leading to an increased permeability. This results initially in leakage of
plasma, and eventually blood into the intestinal lumen. In the opposite
fashion, gram-negative bacteria
and endotoxins
can
enter
the
bloodstream, leading to further systemic effects.

Symptoms:

Biting at his side, pawing

Laying down for longer than normal

Continuous shifting of the weight on the hind limbs

Decreased appetite or not eating at all.

Signs:
Sign of moderate pain:

Persistent movement (even in the stall)

Frequently pawing at the ground with a fore limb

Respectively lying down &then getting back upturning , rolling after lying
down

Grunting, kickingat thebelly frequently turning the head to the flank.

Sign for severe pain

Profuse sweating

Continuous rolling

Persistent movement

Getting up & down violently

General sign

Lethargic , Poor hair coat

Difficulty in bending, collecting or extending

Unwillingness to engage the hind end

Regular or intermittent diarrhea , Grain in manure

Treatment

Feed smaller but more frequent meals allow starches to digest before
reaching the horse hindgut,preventing hindgut acidosis.

Increase turnout, reduce feed concentrates & add more quality forage

Slow food intake by adding chaff (chopped hay) to meals to help reduce
your horses risk for strangulation.

Flunixine, megulimine (banamine) is a popular choice of drugs not only

relieves pain but also break fever.

Flushing

surgery

Treatment by providing supplement:

Oat oil

Oat flour

Yeast

Glutamine

Threonine

Diagnosis:
First observe the horse and Note the following:
General condition and behavior (calm, restless, alert, dull,apathetic);
Frequency of abdominal pain (none, intermittent or continuous);
Frequency of abdominal sounds (normal, increased, decreased or absent);
Abdominal size (normal, reduced, distended);
Nature of peripheral pulse (normal or weak);
packed cell volume;
Capillary refill time (the length of time it takes for gums toreturn to normal color
after pressure is applied);

 Other signs (sweating, wounds, etc.);

Water intake,
Presence of and consistency and regularity of feces.
Further examination of the colic patient includes a measure of pulse and
respiratory rates (normal resting pulse rate is 36 beats/minute and respiration rate
is 8-16 breaths/Minute). Rectal palpation and passing a stomach tube. The
stomach tube should always be passed to rule out the possibility of stomach
overload. Often the stomach tube acts as a treatment, since it can release fluids
or gas from the stomach.

Urticaria : (Nettle & hives)

It is an allergic condition (acute or chronic) characterized by

appearance of wheals on the skin surface. It may be primary resulting
directly form the effect of the pathogen or secondary as a part of
syndrome.
Etiology:A. Primary Urticaria:
Insect stings, contact with stinging plants.
Ingestion of unusual food with allergen usually a protein, recent
change of diet.
Drug administration eg. Penicillin or serum.
Death of warble fly larvae in tissue.
Milk allergy in jersey condition when cows dried off.
B. Secondary Urticaria:
Respiratory tract infection in horses including strangles and viral
infections.
Erysipelas in pigs.
Pathogenesis:
Urticarial lesion are characteristic of an allergic reaction. A
primary dilation of capillaries causes erythema of the skin and
exudation through damaged capillaries wall leads to local edema of
dermis, compression of capillaries and swelling.
Clinical findings:

1. Onset of acute appearance in large area of body.

2. Urticaria are of flat top, elevated and tense to touch ranging 0.5
to 5 cm in diameter.
3. Usually no itching existing in stinging cases,
4. Neither exudation nor weeping occurs.
5. Co-symptoms of allergy like diarrhea, slight rise of temperature
may be present. Lesions may persist for 3 to 4 days.
Diagnosis
By clinical symptoms.
Diff: diagnosis:
Angio-neurotic edema :- Involvement of s/c tissue with larger
size of wheals usually involving larger area than in Urticaria.
i) Urticaria involvement of skin only.
Treatment:I) Spontaneous recovery is common.
II) Use of antihistaminic-provides unique result.
III) Parenteral use of adrenaline can be done, single RX
IV) Use of mild purgative for constipated.
V) Topical application of soothing agents viz lotions of NaHco3,
while lotion
VI)
In large animal therapy parenteral.

Psoriasis
It is a chronic inflammatory skin disease with scabb formation. Itching
scaly patches forms in elbows, knees, legs and other parts of the
body. It is a common disease in human being and mostly affects
during childhood. The disease may be associated with arthritis termed
as psoriatic arthritis. There is no known cure and treatment although
palliative (lesson) lotion, ointments etc. can used/tried.

Erythema

Abnormal flushing of the skin caused by dilatation of the blood

capillaries is called ~. It may be produced by various conditions; it is
often a sign of inflammation and infection; vi3 various septicaemias,
salmonellosis, pasteurellosis, erysipelas and hog cholera. Early
erythema is produced in photosensitization.

In case of human beings erythema nodosum is a disease of sudden

onset, characterized by fever, joint pains and an eruption of painful
swellings on the legs. Some times toxins can also cause erythema in
man.

The lesion are cherry seen in white skin eg. In swine and in the
mucosa of oral, vaginal and conjunctiva.
Diagnosis:
Is done by clinical symptom and treatment is done to primary
causes.

Dermatomycoses:

A group of fungal diseases collectively come under dermatomycoses. Amont them :1. Epizootic lymphangitis in horse:
It is a cuppurative chronic contagious disease
characterized by lymphadenitis and ulcers of the skin. It is
caused by Histoplasma farciminosum.
2. Sporotrichosis: It is a contagious disease of horses
characheriged by development o fcutaneous nodules and vlcers
on the limbs and may also accomapined by lymphangitis. It is
caused by sporotricum sheneki.
3. Bursattee or swamp cancer :- It is a common lesion of the skin
and mucosae of horses and rare in cattle. It is caused by larave
of Habronema megastoma and chiefly fungus pythium sps.

4. Maduromycosis : It is also a disease of horses characterized by

cutaneous granuloma caused by variety of fangus eg.
Helminthosporium spiciferum. Brachyeladium spiciferum etc.
5. Ringworm :- The invasion of the keratinized epithelial cells and
hair fibers by dermatophytes is called ring worm.

Etiology: Horse : Trichophyton equinum

Tr.Mentagrophytes
Microsporum equinum
gypseum
Cattle :Tr. Verrucosum
Tr.Mentagrophytes
Tr.Megnini
Pig :
Tr.
Mentagrophytes; Tr. Verrucosum var
Ochraceum
Tr.
Verrucosum
Canis trichophytum caninum etc.
Sheep :Tr. mentagrophygtes
Tr.Gypseum
Tr.Quickeanum
Microsporum
Goat :Tr. Verrucosum
In all sps:Trichophyton
Microsporum In horse, pig, & small animals.
Transmission mode of fungus:

1. By contact with infected animals/man.

2. By fomites, grooming kits, beddings, harness, horse blankets,
sacs and other contact materials.
3. By stables or kennels.
4. Winter season is appropriate since increase R.H.
5. Young are more susceptible.
6. Carrier animals with spore of fungus.
Pathogenesis:

The pathogenic dermatophytes invade the stratum corneum and

hairs. They autolyse the hair fibers and hair is digested; broken-off
and alopecia results. Toxic substances liberated froom the pathogen
causes inflammatory reaction also called dermatophytic reaction;
producing hyperemia, capillary dilatation and edema of the epidermal
layers. Exudation from eroded epithelial layers, epithelial debris and
fungal mycellium-hyphae produce crusts:A characteristic and very specifit
lesion. The skin lesion
progresses in acentrifugal mmanner with small tiny appearance of the
periphery and central depression.
Secondary bacterial infections due also common. Demodex and
sarcoptes mites may associate the lesion and if associated give the
appearance of moth eaten stratum corneum called kerion. The
propagation of lesion depend on humidity, alkaline PH and aerovic
condition.

Clinical findings:I) In cattle grey or white crusted raised lesions are seen above the
skin. Lesions are circular having diameter upto 3cm. Lesions are
mostly seen in head, neck, perineum but generalized diffusion of
lesion isnot uncommon.
II) In case of horse, lesions are noted on head,(around eyes &
nostrils) neck, chest, shoulders, back. Folliculitis due to deep
infection may be see.
III) In case of sheep-goat crusted or scaly patches are noted on the
face, head, neck, back where as in swine lesions are located on
trunk with superticial nature.
IV) Alopecia, scale or cursts in dog. Vesicles or pustules in
secondary infected cases.
Diagnosis:
1. By clinical symptoms
2. Skin scrappings & culture
3. Examination by using woods lamp.
Treatment :1.

Local treatment :
Clip hair-remove crusts
Topical paint of tine. Iodine in large animals
White fields ointment application:

Salivglic acid = 1 part.

Benzoic acid = 2 part.
Vaseline acid = Q.s.

2.
i)
ii)

4% Ointment
himax/charmil ointment.
Systemic treatment:
10% sod. Iodide @ 1 gm/14 kg b.ut i/v
griseofulrin
@ 25 mg/1 b body out orally *3-4 weeks daily in day
@ 65 mg/15 kg *7 day orally in calf
@ 2.5 gm/24 hrs * 7-14 days orally in horse

iii) ketoconazole
@ 10-30 mg/kg daily orally.
Control:
i) Isolation
ii) Separate grooming
iii) Disinfection with 2.5 5% pnenotic disinfectable.
Disinfection with 0.25% sodium hypochlorite.
With 2% formaldefyde + 1 % caustic soda.
iv) Vit a supportive to young ons.
v) Vaccination.
a) Live vaccine eg. Russian LTF-130 has good result in europe +
scandinavia : tri faviforme
b) Live vaccine tri equinum in horse
c) Killed vaccine moderate result.

Photosensitization
(slough sickness/grass poisoning)

It is the disease caused by the sensitization of the superficial

layers of lightly pigmented skin to light of certain wave length.
Commonly observed in cattle & may happen in sheep-goat & horse.
Eitology:
Photodynamic agents are principal cause the agent ove in
sufficient concentration in skin. When light of certain wovelength talls
photodynamic agents get activation-photosensitigation occurs.
Type : (Etiological basis)
I) Primary photosensitization: Due to ingestion of preformed photodynamic agents. Or certain
plants eg. Brick wheat, trifolium, brassica.
Phenothiazine, phenothiazinesulfoxde, acriflavin, rose bengal
etc. are also cause ~.
II) Hepatogenous photosensitization:
Due to faulty excretion through liver (may in bile duct
obstruction,hepatic insufficiency)
Photodynamic agents go in peripheral circurlation rather than
exerction.
III) Phylloerythrin: - It is end product of chlorophyll. It should be
excreted but because of hepatic problem it may go to peripheral
circulation to induce photosensitization. Eg. Rye grass.
IV) Due to aberrant pigment :
Due to abnormal metabolism. Porphyrin, the pigment is not
metabolized effectively and accumulates in system. Acts as
photodynamic agent.
V) Others:
Chemicals
eg.
CTC,
corticosteroids,
pnenanthridium(trypanosoma treating medicine).
Congenital hepatic disfunction
Leptospirosis
Photosensitize action due to unknown etiology
Clinical signs :
i) Erythema & edema at hairless part.
ii) Mostly seen in ears, eyelids, muzzle, face, lateral aspect of teat
& at valva & peritoneum.
iii) Intense imitation & animal rubs the affected part.
iv) Dropping ears & shapeless, dyspnoea due to nasal obstruction,
dysphagia due to swelling of lips.

v) Exudation of skin, closure of eyelids, nostrils. Necrosis &

gangrene with sloughing of affected parts.
vi) Shock in severe, increase body tempt 106-107of
vii)
Nervous sign Ataxia, posterior paralysis, blindness.
Diagnosis:
1. History & clinical sign.
2. Liver function test
Treatment:
1)
2)
3)
4)
5)
6)
7)

change of diet & placing

laxative ration in decrease further absorption
breed soln eg. Enzootic area dark colored animals
anittistamine use.
Anitbitics use.
Astringents for topical.
Liver extract + 5% glucose saline
Hyperkeratosis:

A condition in which excessive keratinigation of epithelial cells.

Etiology:i) due to pressure in pressure points eg elbows
ii) poisoning of chlorinated naphthalene compound, arsenic etc.
iii) intierited congenital ichthyosis(fish scale disease) of cattle.
Pathogenesis:
Contineous adhesions of epithelial scale is caused by excessive
keratinization of epithelial cells & intrer cellular bridegs and
hypetrophy of straturm corneum. In poisoning there is deficiency of
vit a for cell division.
Clinical finding:
i) Thick, corrugated skin at hairless part.
ii) Dryness & scaliners.
iii) Tissure development
iv) Secondary infection
Clinical pathology:
Histological examination Thickened 5% corneum.
Diagnosis:

From parakeratosis

Treatment:
i) Treatment of primary cause
ii) Use of keratolytic ointment (salicylic acid oint)
Otitis

Inflam. Of external ear otitis exterma

Inflam. Of middle ear otitis media
Inflam. Of internal ear otitis interna
Aetiology:
i) Alkaline soas causes otitis externa
ii) Strepto, staph, psendomonas, proteus infn
iii) Fungal like otomycosids infn
iv) Parasites eg otodected cynotis in dog/cat
Psoroptes cynotis in cattle /buff.
Sarccsstes cynotis in goat
v) Otitis media & interna due to extendion of lesions through
tiematogenous route, exteranl ear infn & from naso-phargnx.
Clinical findings:

Shaking of head & irritation

Susceptoble age 100k-400ks in calf , lambs
Otorrhea, offensive odor of exudates.
Affected side downward, circling movement with
affected side.
Emaciation, anorexia, decrease prodn
Violent shaking may cause tiematoma
Slightly size of body tempr.
Diagnosis :
#

History & clinical symptoms.

Culture & examination of discharged material

# Auriscopic examination & radiography.

centre of

Line of treatment:
1 Treatment of primary cases
2 Analgesics & anaesthetics to decrease
3 Antibiotics munomycin, dc etc.
4 Steroids ge.
Chronic needs-surgical correction.

Diseases of Skin
And its associated Structures

Dermatology is the science, which deals with the study of the skin or
coat of the animal either from the normal physiological and anatomical
picture, or from the diseases, which affect the skin and its effects on the
animal health and production. The skin forms the largest single organ of the
body, performing not only a supportive anatomical role but also a wide
variety of important physiological functions essential to the well being of the
animal.

The skin is a heterogeneous organ, which serves as principal medium of

communication between the animal and to environment. The anatomical,
histological and physiological features of the skin vary between species &
breeds.
Anatomical and Histological Consideration
The skin is divided into two layers an outer layer which is called
epidermis and an inner layer known as dermis, and associated structures
which known as skin appendages including hairs, horns, claws, nails, hooves.
Sebaceous and sweet glands all develop from the epidermis in addition to
the smooth muscle fibers attached to hair follicles and distributed in the
dermis.

In general epidermis of mammals is composed of 5 layers as the following:

1.

Stratum germinativum or basal layer.

2.

Stratum spinosum or stratum Malpighii.

3.

Stratum granulosum.

4.

Stratum lucidum.

5.

Stratum corneum.

While the dermis composed of bundles of collagen, elastic and reticular

fibers within a homogenous ground of sulfuric and hyaluronic acids within the
matrix is population of Fibroblast, most cells and histocytes, blood vessels,
nerve endings are present.

Physiological Consideration
The main functions of the skin are:
Physical protection from trauma, temperature variations, invasion of
microorganisms and over exposure to sunlight.
The skin acts as biological barrier, which prevents the passage of harmful
agents into the body. Mechanical protection of the keratinized structures
against the environment.
Skin maintains the internal conditions of the individual so it acts as a barrier
for water and electrolytes and prevents their loss.
Synthesizing vitamin D by the action of ultra violet rays and transforming
steroids to vitamin D.
Aids in maintaining the normal Blood proteins by the action of peripheral
vascular dynamics.
Help in recognition of foreign protein as contact allergens and venom and
stimulate the antibody production. this is due to the presence of specific
immunoglobulin movement into and through the epidermis.

Skin lesions and their terminology

Nodules

Nodule is a circumscribed, solid elevation greater then l cm in diameter that

does not deform when palpated.
Nodule extends into the deeper layers of the skin, and it results from
cellular infiltrates into the dermis and subcutis.

Ulcers
An ulcer is a cutaneous defect resulting from a complete loss of the
epidermis and usually part of the underlying tissues.

Erosion
Erosion is a cutaneous defect resulting from partial loss of the epidermis
that does not penetrate beneath the basal laminar zone.

Papules
A papule is a solid, circumscribed, elevated lesion up to l cm in
diameter. Papules are essentially small nodules that do not extend
beneath the dermis.

Pustules
A pustule is a pas-fined, fluctuant, circumscribed, and elevated
accumulation of pus up to l cm in diameter.

Vesicles
A Vesicle is a fluid-filled, a cellular, circumscribed, elevated lesion
up to l cm in diameter. While, a bulla is a vesicle that is greater than l cm in
diameter.

Scaling
Scale is a visible accumulation of fragments of the horny layer of the
skin (Stratum corneum). It represents the final product of epidermal
keratinization.
Histologically, scale is recognized as hyperkeratosis, which may be
either parakeratosis or orthokeratosis. Grossly, it varies in appearance
(color), consistency, and adherence.

Crusts
Crusts are dried exudate that adheres to the skin surface and hair.
Crusts often cover erosions or ulcer; crusts are composed of
serum, cells, fibrin, and infectious agents. Dirt and medications.

Diseases of the skin and its associated structures

Importance of skin diseases
As well as being involved directly in a variety of disease process, the skin
and coat are influenced indirectly by the general health status of the
individual animal.
The incidence of skin diseases in domestic animals is high and it is
important to remember that some skin diseases are contagious, so that
prompt recognition is important and essential in order to prevent further
dissemination of the infection, and to assist control.
The risk to persons handling the animals affected with certain parasitic
disease of skin is an important public health responsibility for the veterinary
clinician as mange and ringworm.
Skin diseases cause restlessness at least to the animal and decrease body
weight gain and decreased its production.

Classification of skin diseases

(1) According of its origin

1- Primary skin diseases:
In this type of diseases initially at least the lesions are restricted to skin and
its associated structures, spread to other tissues may occurs later as
secondary complications. It is evidenced by the clinical examination, which
reveals that the lesions are restricted to skin without systemic reactions.
2- Secondary skin diseases:
In this type the lesions occur as the result of extension of the disease
process from another organ or tissues other than the skin, system reactions
are present with cutaneous lesions.

(2) According to the causative agent:

(A) Non-infectious skin diseases includes:
Diseases affect Epidermis
Pityriasis.
Parakeratosis.
Hyperkeratosis.
Pachydermia.
Impetigo.
Urticaria.
Dermatitis.
Eczema.
Photosensitization.
Diseases affect skin appendages
Alopecia.

Achromotrichia.
Seborrhea.
Acne.
Disease of subcutis:
Subcutaneous edema.
Angio neurotic edema.
Subcutaneous emphysema.
Lymphangitis.
Skin-Hemorrhages.
Gangrene.
Skin. Abscess.
(B) Infectious skin diseases includes:
(a) Viral diseases:
Cowpox - pseudo cow pox.
Contagious pustular dermatitis.
Swinepox - sheep, goat pox.
Bovine ulcerative mammilitis.
Warts = viral papillomatosis.
Epuine sarcoides.
Viral popular dermatitis.
Coital exanthema.
(b) Bacterial diseases:
Dermatophillosis = mud fever.
Impetigo.
Contagious acne.

Streptothrichosis.
Ulcerative Lymphangitis.
Glanders Farcy.
Subcutaneous abscesses.

(C) Mystic diseases:

Ring worm.
Epizootic Lymphangitis.
Sporothricosis.

(D) Parasitic diseases:

Lice infestation.
Ticks infestation.
Mange.
Psoropitc mange (Body mange, ear mange).
Sarcoptic mange (Red mange, Barn itch).
Demodectic mange (Follicular mange).
Chorioptic mange (Leg mange, tail mange).
Other diseases.
Parafilaria multipillosa.
Cutaneous neoplasms.
Granulomatous lesions.
Congenital skin lesions.
Diagnostic Methods In Dermatology:

The sequence of procedures in laying the foundations for an accurate

diagnosis is:
Case history,
Physical examination,
Skin scrapings.
Skin biopsy.
Initial diagnostic tests.
Differential diagnosis

(1) History:
A detailed history is obtained from the owner or person having most
contact with the animal. A good case history provides assistance in diagnosis
and treatment. The history must not be limited to cutaneous symptoms but
should include information on other systems.

General history taking:

(1) Age: Some skin diseases are associated with specific age group as for
example lymphadenitis.
(2) Sex: In females, skin disorders resulting from estrogenic imbalance
frequently develop. In males testicular tumors cause specific skin lesions
as hypotrichosis Hairlessness due to sertoli-cell tumor, which is one type of
Alopecia.
(3) Species and breed: Some species of animals and even certain breeds
develop skin lesions specifically.
(4) Environment: including climate and geographical conditions which effect
on the skin, such as distribution of trace elements in the soil may lead to
many of skin lesions. Also allergic skin disorder as in photosensitization may
be relate to environmental condition.

(5) Nutritional conditions: Some skin lesions are developed from

deficient nutrient in some vitamins, minerals and tract elements as facial
eczema due to vit. A and zinc deficiency and may due to excessive feeding
Alopecia in a yearling bullock suffering from advanced molybdenosis.

Principals of History taking In Relation to skin only:Has the patient previously suffered a disease? If so, what is the diagnosis?
Do of other animals of family have a similar skin disease?
Have the lesions been localized or generalized in many areas?
What has the duration of the lesions?
What is the usual behavior of the patient?
What type of the patient nutrient and source of water?
What is the patient history concerning external and internal parasite?

(2) Physical Examination:

A complete physical examination is carried out and the status of all
body system evaluated and nored. All parts of the skin are examined; the
coat being parted and skin palpated where necessary. Good lighting and use
of the magnifying lens are essential. The condition of the coat and the nature
and distribution of any lesions are noted and it is important to recognize the
different types of skin lesions and to describe them accurately.

(3) Differential diagnosis and selection of diagnostic tests:

Careful consideration of the history, together with the results of the
physical examination, will suggest a number of possible causes of condition.
The diagnostic procedures must be selected, which will confirm or eliminate
these possibilities. It is important to differentiate primary and secondary skin
disease.

* Diagnostic tests include:

Procedure

Pathogen pathology demonstrated

1- Woods lamp illumination.

2- Skin scrapings.
3- Hair plucking.
hair
4- Coat brushings.
5- Swab / crust samples.
6- Smear / wet preparation.
7- Biopsy:

Some of Microsporum species.

Ectoparasites, dermatophytes, helminthes.
Ectoparasites, dermatophytes,
morphology.
Ectoparasites, dermatophytes.
Fungi, bacteria, virus.
Bacteria, fungi, protozoa, cytology.
Bacteria, fungi, virus, histopathology,
histochemistry

8-Blood.
status, and

Cytology, Biochemistry, hormonal

serology.

Woods lamp illumination:The woods lamp illumination depends on a source of ultra-violet

radiation at wavelength, which excites a characteristic apple-green
fluorescence in about 50% of naturally occurring Microsporum canis
infection, and other Microsporum species also fluoresce. It is seen only in
infection of actively growing hair. The disadvantages of this method are, it
may give + ve result with other chemical agents as tetracycline, and failure
to demonstrate such fluorescence dose not rule out dermatophytes.

Skin Scrapings:
The skin scraping is one of the most valuable and commonly used tests
in veterinary dermatology, confirming the diagnosis of the ectoparasites and
dermatophytes. The hair, superficial scales, epidermis and contents of the
hair follicle mouths may be sampled by this technique.

Protocol of skin scrapings:

Select the area of scraping with great care to the predilection site for the
disease either ectoparasites or dermatophytes.
The hair should be firstly trimmed short.
Skin should be gently wiped with swab moistened with sterile water.
Scraping is done with scalp blade held firmly between the thumb and first
two fingers of one hand at angle of about 50% to the skin and drawn firmly
across the surface towards the operator. The surrounding skin is tensed with
fingers of other hand.
Scraping is continued until the first signs of bleeding appear. Moistening the
skin with water, mineral oil or glycerin for adherence of the scrapings to the
blade.
Microscopical examination of the scrapings.
Scrapings are suspended in a drop of oil on microscope slide, and covered
with cover slip, and examined under the x 10 objective. Microscope
condenser should be lowered to increase the contrast.
Scrapings are collected dry or moistened with water and suspended on slide
in 20% potassium hydroxide.
Suspension is warmed to accelerate clearing.
Cover slip is applied and the preparation is examined under the x 40
objectives.
Scrapings are collected in test tube or small beaker and add 4-10% sodium
or potassium hydroxide.
Heat gently, but not boil, until the hair is dissolved for about 5 minutes. If
the sample is boiled the parasite will be transparent and difficult to
diagnosis.
Maceration overnight without heat may be sufficient.
Allow the tube to stand for minutes and cooling.
Centrifuge the sample and examine the sediment.

Sample from the bottom by glass rode or dropper and transferred to slide
than cover with cover glass and examined microscopically under the low
power.
Scrapings can be collected dry in sealed paper envelope and then cultured
directly for isolation of dermatophytes on specific media.

Hair plucking:
Hairs from the chosen site are grasped firmly with forceps and plucked and it
may be inoculated directly onto specific media for mycological isolation and
identification. Or examined under the microscope with low power objective x
10 and the hairs are mounted between glass slides held together with tape.
Or under x 40 objective and hair held with mineral oil gives better resolution.

Coat brushing:
It is useful where the skin lesions are diffuse and infection of the hair or
superficial stratum corneum is suspected. Coat brushings enable the loose
hairs, scruff and crusts from large areas of the skin to be collected.
The animal is placed on sheet of clean paper.
The coat ruffled with coarse brush causing any loose material to be fall onto
the paper.
The collected materials are examined under the microscope under x 10
objectives in between glass slides.
Some debris is screened with woods lamp.
Sample may be put on slide and examined microscopically in mineral oil or in
20% potassium hydroxide.
If fungal or dermatophytes are suspected the brush cultures on specific
media.

Swab and Crust samples:

Cotton swabs are commonly used to sample pustular or exudative
lesions for smear preparation and isolation of bacteria and fungi e.g. Candida
from the skin.
The hair is first clipped from around the lesions.
Gentle cleaning with 70% Alcohol.
Pustules are opened with the tip of sterile needle.
The adjacent skin is gently squeezed.
The emerging pus collected on the tip of the swab and avoiding contact with
the skin.
The furuncular and scabby lesions are also sampled as pustules but scabs
are a potent source of microorganism as poxvirus and dermatophilosis.
Portion of scabs may be emuls

Smears and wet preparations:

Smears and wet preparations provide a rapid and relatively simple
means for the demonstration of m.o. and host cells in skin lesions. It is
particularly useful in demonstration of yeast and neoplastic cells.

Smears may be prepared in three ways:Direct impression smears are made by pressing the surface of moist skin
lesions, the base of freshly removed scab or the cut surface of a biopsy
specimen causing cells and exudate to adhere to it.
Smear also can be made from pus or exudate taken from the lesion and
spread thinly onto the slide.
Samples are collected on swab by scraping the affected skin. or by aspiration
using needle and syringe.
They are smeared onto the slide with swab or using bacteriological loop.

Smears may also made from emulsified scabs:

Slides should be cleaned with alcohol prior to use to promote adherence and
even distribution of the material.
The smears are air-dried, fixed by flooding with alcohol for one minute and
allowed to dry.
Staining smear with an appropriate technique depending on the features,
which are to be demonstrated. Most common stains are: Grams,
methyleneblue, Giemsa.
Wet preparations are unstained specimens prepares from exudate or scab
emulsions; as described by many researchers.
Drop of specimen is placed on the slide.
Normal saline is added to dilute the material or as mounting medium.
Cover slip is applied.
Examination under the microscope by phase-contrast illumination or with the
condenser lowered.

Biopsy samples:
These samples are usually obtained for histopathology:
Local anesthesia.
Hair is clipped with scissors.
Cleaning with 70% alcohol.
Incision of the skin or punch method is applied.
Specimen put in 10% formaline for at least 24 hours.

Blood samples:
Changes in the cellular or biochemical composition of the blood are useful in
confirming or ruling out differential diagnosis in dermatology.

Specialized tests as hormonal assays, and serological tests may be used to

identify specific conditions.
Collection of blood.

(A) Clotted blood or serum:

Cleaning the site of vein puncture.
Obtaining the blood in the containers as centrifuge tubes vials,
The container is left to clotted in sunlight in sleep manner to give large
surface area for oozing of serum.
Then centrifuge the sample for obtaining maximum amount of serum.
Transfer the serum into other tubes or vials and closed then preserved in
deep freezer.
Serum is collected for demonstration of biochemical composition such as
minerals including: Copper, Zinc, Manganese, Sulfur and other elements.
Iron and calcium.

(B) Whole Blood sample:

Blood samples are obtained by vein puncture using sterile needle and
adding anticoagulants as heparin and EDTA. Whole blood samples are
obtained for detection the cellular changes, which may be the cause, are as
result of diseased skin. This changes to be detected necessitate the
following:Erythrocytic count.
Total leucocytic count.
Differential leucocytic count.
Haematocrite value.
Special Pathology
The reaction of the skin to noxious stimuli varies with the severity and
depth of injury. In the corium or dermis the reaction is the same as that of

other tissues due to presence of blood vessels, nerve fibers, lymphatic

vessels and connective tissues. The epidermis due to purely cellular
composition reacts differently.
(A) Acute Reaction:
If the reaction is acute, the development of lesions begins with swelling
and edema of prickle cell layer and so called spongiosis. If the edema is
severe enough, cell rupture and fluid collects as foci which gradually emerge
through the stratum corneum and appear as vesicles. Should the foci rupture
before reaching surface, the result is weeping of the area.

(B) Sub-Acute Reaction:

The intercellular edema interferes with the normal functions of the
granular cells in the prickle layer and gives rise to abnormal formation of
cornified epithelium, and result in thickening of epidermis. All layer are
affected specially stratum corneum because of improper keratinization and
failure of exfoliation this is so called parakeratosis; it may be accompanied
by pronounced thickening of prickle cell layer with prolongation of
interpapillary processes and so called acanthosis, the disease state in this
case named pachydermia.

Acanthosis in association with the deposition of keratin pigment

described as Acanthosis nigricans, which is common in dog and human,
associated with thyroid dysfunction.

Skin diseases due to allergens:

When an allergen is applied on sensitized skin, local rise in histamine
levels leading to an accumulation of eosinophils. If the histamine level
increased about the detoxifying capacity of eosinophils, it will escape to
vascular system and blood level of histamine rise. This is transitory and be
overcome in about 1-2 hours after removal of allergen.
Examination of histamine level or eosinophils count may be of diagnostic
value.

The local skin reaction to the allergen is due to the vascularity effect of
histamine.
If the reaction is severe enough other organs may showing histamine
toxicity, this also may occurs when the allergens ingested which produce
reactions on other end organs and including skin.
Principles Of Treatment Of Diseases Of The Skin
Removal of hair coat and debris to enable topical applications to come into
contact with the causative agent is preferable.
Accurate diagnosis must be preceding the selection of drugs.
In bacterial diseases sensitivity tests on culture is advisable.
In allergic diseases and photosensitization may be impossible and the only
symptomatic treatment is the solution.
Removal of causative agents by specific treatment for each once.
Prevent secondary infection by using bacteriostatic drugs.
Prevent further damage from scratching by using local anesthetic ointments
or centrally acting sedatives.
When large area of skin is involved, prevent absorption of toxic subs. by
continuous irrigation or application of absorptive dressing.
n cases of fluid losses; it must be given as isotonic fluid by the parentral
administration.
Good ration specially protein and sulfur containing amino acids to help in
repair of skin.

Skin Diseases
(1) Pityriasis = Dandruff
It is non-infectious condition characterized by the presence of bran-like
scales on the skin surface.

Etiology:

Hypovitaminosis A and B especially riboflavin and nicotinic acid mainly in

pigs.
Nutritional deficiency acids as linolenic acid.
Poisoning by iodine which causing fatty acid deficiency.
Lice, flea and mange infestations.
May be with ringworm.

Pathogenesis:
The scales are keratinized epithelial cells and these are sometimes
softened and become greasy due to exudation of sebum or serum.
Avitaminosis A results in overproduction of keratinized epidermis. Excessive
desquamation due to parasitic infestation is another way of pathogenesis
and developing scales.

Diagnosis:
Primary Pityriasis depends upon the examination of skin scrapings.
Differentiation from hyper-and parakeratosis. Skin scrapings to eliminate
parasites and Fungi.

Treatment:
Correction of primary agents.
Using of balanced ration emollient ointment and alcoholic lotion.
Salicylic acid incorporated in ointment and lotions.

(2) Hyperkeatosis
It is the accumulation of excessive keratinized epithelial cells on the surface
of the skin Resulting in thickening of the skin with or without hair loss .

Etiology
Localized at pressure points as elbow when the animal lays habitually on
hard surface Mechanical.
Chronic poisoning with arsenic compounds.
Poisoning with highly chlorinated naphthalene compound used in industry as
in wool preservation.
Inherited as congenital ichthyosis = fish scale disease of cattle . ( Alopecia
with plates of horny layer allover the skin; this occurs in newly born animals
specially calves) .
Pathogenesis
Local compression leads to accumulation of keratinized epithelial cells.
Excessive keratinization of epithelial cells and intercellular bridges and
hypertrophy of stratum corneum.
In cases of poisoning with chlorinated naphthalene, it causes deficiency of
the granular layer of epidermis and causing atrophy of epithelial cells .
Clinical finding
The skin becomes thicker than normal and usually hairless and corrugated .
Skin becomes dry and fissures develop in grid like fashion .
Secondary infection through the fissures when the skin is wet .
Diagnosis
Differentiation from parakeratosis.

Skin scrapings to eliminate ectoparasites and fungal infection.

Histological examination of skin biopsy to detect the thickened stratum
corneum.
Treatment
Correction of the primary cause.
Us of balanced ration, emollient ointment and alcoholic lotion.
Salicylic acid incorporated in ointment and lotions.
Using of vitamin A as 6000 I.U

(3) Parakeratosis
It is a condition of the skin in which keratinization of epithelial cells is
incomplete .

Etiology
Non , specific chronic inflammation of cellular epithelium which leads to
faulty keratinization of horny cells.
Dietary deficiency of saturated fatty acids. Additional dietary zinc
deficiency along with copper alleviates the condition, which is effectively
prevented by supplements of soybean oil or some other suitable source of
linoleic acid.
Inherited dermatosis vegitans in pigs.
Pathogenesis
Edema of prickle cell layer, with dilatation of intercellular lymphatic vessels
and leucocytic infiltration lead to Imperfect keratinization at granular
epithelium. Layer of epidermis produces sticky and soft horn cells, which
retain their nuclei and they tend to stick from large masses and either still
fixed to underlying tissues or may fall off as forge scales.

Clinical Findings

Lesions may be diffuse and extensive but often confined at flexor aspects of
joints.
Reddening, thickening and gray coloration of skin.
Cracks and fissures also develop and removal of scales leave raw and red
surface.
Diagnosis
Histologically: imperfect keratinization is evident.
When the scales are removed it leaves raw and red area so differentiation
from hyperkeratosis will be easy.
Treatment
The deficiency in ration must be corrected buy addition of zinc continuously
using zinc sulphate or zinc oxide.
Removal of scales by using keratolytic ointment as that of salicylic acid
ointment or by warm soapy water.
Local application of astringents as white lotion paste.
(4) Urticaria (Nettle Rash)

Urticaria is an allergic condition characterized by the appearance of wheals

on the skin surface.

Etiology
It may be a primary lesion resulting from the direct effect of pathogen on
the skin , or may be secondary as part of a syndrome .

(A) Primary Urticaria due to:

Insect bites.
Ingestion of unusual food mainly protein and sudden changes of diet is a
predisposing factor.

Drug administration (e.g. penicillin).

Death of warble fly larvae in tissues.

(B) Secondary Urticaria due to:

Alimentary tract disturbances in horse.
Respiratory tract infection in horse.
Along the course of some disease.

Pathogenesis
Urticaria represents a type of immediate hypersensitivity on which the
binding of antibody with antigen results in release of Histamine.
Primary dilatation of capillaries causes erythema of skin .
Exudation from damaged capillaries leads to local edema of epidermis with
swelling and pallor due to compression of capillaries.
The lesions remain red at the edges and only the epidermis is involved.

Clinical Findings
Lesion develop rapidly, large in numbers, ranges from 0.5 - 5 cm diameter
with flat-topped steep-sided plaques, and tense to touch.
No exudation or weeping occurs; No itching except with insect bite.
Plaques mainly found at back, flank, neck and legs.
It may subside in 24 hours or last up to 5 days.

Clinical Pathology

There is an increase of histamine level and local increase of eosinophils

count.

Diagnosis
Urticaria must be differentiated from angioneurotic edema; In cases of
edema, the subcutaneous tissues are involved.

Treatment
Antihistaminic with parentral administration of adrenaline.
A mild purgative and corticosteroids may be used.
Local astringent as white lotion, calamine lotion or dilute solution of sodium
bicarbonate.
In large animals, parentral administration of calcium salts.
Changing the diet is helpful in cases of food allergy.
(5) Eczema: Eczematous Dermatoses:
It is an inflammatory reaction of the epidermal cell to exogenous or
endogenous substances to which cells are sensitized. This occurs when the
skin is in contact with allergens either applied on skin and so called
exogenous or arise from blood stream and known as endogenous allergen.

Etiology
(A) Predisposing Factors
Nutritional deficiency, trauma and chemicals.
Genetic causes.
Prolonged soiling, dampness and accumulation of debris.
Constant scratching due to external parasites.

(B) Exogenous Allergens:

Using of chemicals as antiseptics and disinfectants.
Some Ectoparasites as flea-saliva in dog and cat, which cause
hypersensitivity of skin.

(B) Endogenous Allergens:

These are substances, which are ingested and absorbed through the gut and
introduced to blood stream and affect on the skin indirectly ingestion
proteins.

Pathogenesis
Primary lesion is erythema, Spongiosis due to in intra and intercellular
edema forming vesicles which is characteristic for eczema, this leads to
rupture of vesicles and causes weeping of skin with formation of scabs. This
occurs in acute stage of eczema and may disappear rapidly Chronic form
may persist accompanied with parakeratosis and pachydermia.

Clinical findings
True eczema is rare in large animals.

In typical form
Erythema, papules and vesicles on the back of animal, weeping of the
surface mainly in longhaired dogs.
Itching, scratching and rubbing which aggravate the condition.

In chronic form
Alopecia in many areas of skin.

Scaling and hypertrophy of skin.

Pachydermia but no discontinuity of skin.

Diagnosis
The clinician must define the cause and exclude other disease but it is
difficult.

Treatment
Improve environmental condition of animal, change of bedding and diet, will
be useful.
Treatment of internal and external parasites.
Sedatives in early stags.
Antihistaminic.
Corticosteroids as anti-inflammatory.
Local application of astringent on weeping area, In addition to local
anesthetic agent.
(6) Alopecia

Alopecia is deficiency of hair or wool coat. It is a manifestation of many

disease as eczema, dermatitis, and mange.

Etiology
In most of species, hair loss occurs normally in the spring and autumn for the
coat to be changed. However, hair loss may be due to failure of follicle to
produce a fiber or it may due to damage hairs previously.

(A)Failure of follicle to produce hair fibers

Inherited hypotrichosis, symmetrical Alopecia. The skin in the affected area

becomes completely bald.
Congenital hypothyroidism goiter due to deficiency of iodine in dam.
Congenital, after viral infection of dam as in Bovine Viral Diarrhea in cattle
and sheep.
Infection of follicles or neurogenic due to damage of peripheral nerve.

Sertoli cell tumors in Male dog.

(B)Damage of produced fibers

It is mainly symptomatic Alopecia due to other diseases.
Dermatomycosis as ringworm, (dermatophytosis).
Poisoning of thallium or molybdenum.
Deficiency of copper and zinc and vit. A, vit. E.
Excessive palm - whale or soybean in milk replaces of calves usually result
in weakness of hair fibers.
Traumatic as in sweat itch of horses.
In case of symptomatic alopecia it is a temporary case or condition that will
be improved by removal of the original causes.

Pathogenesis
In many of metabolic alopecia there is weakness of fibers, which
degenerated rapidly.
In congenital Alopecia, there is failure in follicles to form fibers.
Damages of nerve ending and blood capillaries are impaired.

Chemical depilation may occur by cytotoxic agents cytoplasmic

degeneration in follicle of hair (chemotherapy).

Clinical findings
Stumps of breakage or new-formed fibers are seen.
Skin may be shiny and thinner than normal (this is true only when fibers fail
to grow).
There are manifestations of primary disease.
Scratching or rubbing.

Diagnosis
Clinical signs.

Treatment
Treatment of primary causes.
Improve the diet with balanced quantities.
Improvement of blood supply of skin.
In gonadal disorders, castration or administration of gonadal hormones might
be useful in reactivation.

(7) Dermatitis

The term dermatitis include those condition characterized by inflammation

of the deeper layer of the skin, including the lymphatic with secondary
involvement of epidermis.

Etiology
The causes and types of dermatitis in all animals classified into:

1- Bacterial dermatitis:
Due to invasion of bacteria as in udder impetigo in cattle.
Pyoderma due to Staph. aureus.
2- Mycotic dermatitis
Dermatophilus congolensis in sheep, cattle, and horses.
Ringworm
Strawberry foot Rot, (dermatophilus pedis).
3-Viral dermatitis
Poxvirus infection.
Contagious pustular dermatitis.
Lumpy skin disease in cattle.
Foot & Mouth disease, vesicular exanthema.
Vesicular stomatitis mucosal disease.
Blue tongue bovine malignant catarrh.
4- Parasitic dermatitis
Mange and other mites.
Myiasis of hypoderma and others.
5- Nutritional dermatitis
Deficiency of vit. B. complex, vitamin, A, zinc, nicotinic acid, riboflavin, biotin,
pantothenice acid.
6- Physical dermatitis

Sunburn and photosensitization.

7- Chemical dermatitis
Arsenical compound.
Potassium mercuric iodide.
8- Allergic dermatitis

Pathogenesis
Involvement of deeper layers including blood vessels, lymphatic and
epidermis.
Black necrosis at the site of inflammation.
Erythema with other factors causes an increase in the thickness of skin
accompanied by edema.
Pain or itching.

Clinical findings
Erythema and hotness of the affected part of the skin.
Vesicular lesion and edema of skin.
Scab formation, necrosis or gangrene may occur.
Phlegmon may be developed, distinctive suppurative lesions.
Tenderness.
Systemic reactions may occur ( such as toxemia, septicemia ).
Secondary bacterial infection may result in pus formation.

Treatment
Treatment of the primary cause.
Supportive treatment by local and systemic application.

Antihistaminic.
Astringents.
Anesthetic agents.
Antibiotic administration to prevent secondary complication.
Parentral fluid should be administered in case of shock.
High protein diet.

(8) Phtosensitization (Light Sensitization = Sunburn)

It is secondary damage following injury to superficial layer of relatively unpigmented skin by the energy released from interaction between light of
certain wavelength and photodynamic agents. Dermatitis develops when the
sensitized skin is exposed to strong light.

Etiology and types of photosensitization

If the photodynamic agents are present in sufficient concentration in the
skin, dermatitis occurs when skin is exposed to light.

(1) Primary photosentization

This type is due to ingestion of exogenous photodynamic agents usually in
lush green plants and the animals affected within 5 days from going onto
pasture and symptoms are disappeared when the animal is removed away
from pasture and this differs according to the susceptibility of animals. The
most active form occurs naturally in plants and causes photosensitization
are:

a- Miscellaneous substance as acridin dyes and rose Bengal.

b- Fagopyrin in seeds of dried plants of buck wheat.
c- Perloline from perennial rye grass.

(2) Photosensitization due to aberrant pigment synthesis:

May be due to production of abnormal metabolism, the only example is
inherited congenital porphyries in domestic animals due to excessive
production of prophyrins substance, Which is the photo dynamic agent.

(3) Hepatogenous photosensitization

This is due to accumulation of normal metabolic products as a result of
failure to excretion through the liver.
Normally a photosensitizing substance, which is known, as phylloerythrin is
normal end product of chlorophyll metabolism and excreted in the bile.
When the level of phylloerythrin is increased due to hepatitis or cholangio
hepatitis and other cause of obstruction of biliary passage and reach in level
in skin to the point, which make it sensitive to light.
This is the most common form on all animals especially that fed on green
pasture also occurs in other animals fed only on hay and other stored feed.
Fungus on perennial ryegrass.
Algae on drinking water.
Pasture and crop plants as millet grass, weeds.

Chemicals as
Caron tetrachloride.
Corticosteroides.
Infectious as leptospirosis.

Congenitally defective hepatic function.

Such as inherited Southdown lambs, which has an inherited defect in

excretion of bile.

Clinical signs
It may be accompanied with photosensitive dermatitis.
Skin lesions are characteristic and concentrated on dorsum side of back,
vulva, lateral aspect of teats face ear.
Lesions are markedly clear from the normal skin.
Erythema edema of the skin.
Intense irritation, lacerating face and may be rubbing it.
When the teats are affected, kicking at the belly and swimming into ponds to
cool areas of pain.
Dyspnoea due to nasal obstruction, Dysphagia due to swelling of lips and
closure of eyelids.
The skin lesions may be extensive and cause shock.
Nervous manifestation blindness, posterior paralysis.
Peculiar sensitivity to water may seen in sheep with facial eczema.

Diagnosis
Primary cause must be detected.
Differential diagnosis from mycotic dermatitis and clostridium novyi in sheep.
The uses of serum enzyme tests are recommended.

Treatment

A) General treatment includes

Immediate removal from direct sunlight.
Laxatives to eliminate toxic materials.
Prevent further ingestion of toxic substance.

B) Local treatment includes

Antihistaminic, corticosteroids.
Prophylactic dose of antibiotics.
Local application of ointments-Astringents.
(9) Seborrhea

It is an excessive excretion of sebum on the skin surface.

Etiology
True of primary seborrhea mainly occurs in human is rarely in animals.
Secondary seborrhea accompanied with dermatitis and skin irritation as in
eczema, mange and in
Cases of:
Greasy heel in horse.
Flexural seborrhea in cattle.
Exudative epidermitis in pigs.

Pathogenesis:
Increased blood supplies to the skin and increase hair growth will leads to
increase excretion of sebum.

Clinical findings
. Primary seborrhea
Greasiness of skin with oily substance of sebum.
Trophy of sebaceous gland may be observed on histology.

. Secondary seborrhea
a. Flexural seborrhea, lesions found on groins and medial aspect of thights,
fissure between the two halves of udder. Extensive out pouring of sebum,
malodorous with irritation is seen. Shedding of oily skin leaving raw area
under the lesion.

b. Greasy heel in horses

Usually in hind legs due to prolonged standing in unsanitary and muddy
barns.
Thickening at the part of lesion at the coronet and painful to touch causing
lameness.
Soreness and excoriation called scratches at the pastern and may extend to
coronary band.
When the thickening of skin and subcutaneous tissues is marked, it will
interfere with normal movement of the limbs.

Diagnosis
It must be defined whether the lesions are primary or secondary.
Flexural seborrhea may be mistaken with injury.
Greasy heal seborrhea may be mistaken with chorioptic mange.
Treatment
Treat original cause.

Antibiotics and antiparasitic.

Washing with warm water and soap and keep the skin at the affected part
clean and dry.
Application of an ointment locally made up of:
5part salicylic acid:
3 part boric acid
2 part phenol
2 part mineral oil
2 part petrol jelly
At 5- days interval will result good prognosis and treatment in greasy heel of
horse.

Moving the animal to dry and clean land.

(10) Achromotrichia

It is bands of depigmentation in black wool fleece due to transient deficiency

of copper in diet. In cattle deficiency. of copper and increase molybdenum in
diet will result in depigmentation of skin.

Causes
Copper deficiency and increased molybdenum in diet.
Damaged or destroyed pigment cells melanocytes by the pressure as
harness, Parafilaria infestation.
Congenital vitiligo in the offspring of mares.
Symptoms
Marked bands of depigmented coat mainly around the eyes.
In horse, perineum, prepuce, face, under the tail, are the main involved area.
The entire coats also change of its normal colour due to decrease
concentration of melanocyte cells.

(11) Acne

The term acne refers to all infections of hair follicles by the acne bacillus,
which is diphtheria organism, but it may also include all suppurative
organisms including staphylococci and more properly known as sycosis.
Etiology
Staphylococcal dermatitis in horse.
Canadian horse pox caused by corynebacterium pseudotuberculosis.
Demodectic mange.
Pathogenesis

When insspisated secretion and debris block sebaceous gland ducts or by

pressure, it will predispose the condition.
Hypertrophy of sebaceous glands and increased excretion also predispose to
the condition.

Clinical findings
Formation of nodules at the base of hair follicles and then pustules.
It may be ruptured and contaminate the surrounding skin and further lesions
appears.
Hair at the site of lesions is usually easy to shed.
The lesions are painful and rupture under pressure.

Clinical pathology
Swabs for bacteriological and parasitological examination are helpful

Diagnosis
Clinical signs has to be differentiated from impetigo.

Treatment
Clean the skin and wash with disinfectants.
Local application of antimicrobial ointment.
Systemic administration of antibiotic in generalized course.
Isolation of infected animals.

(12) Impetigo

It is a superficial eruption of thin walled, usually small vesicles surrounded

by a zone of erythema, the vesicles develop into pustules and rupture to
from scabs.
Etiology
In animals the main organism is staphylococcus organism and most causes
are : Udder impetigo in cows, infectious dermatitis or contagious Pyoderma
of baby pigs caused by unspecified strept and staphylococci .
Pathogenesis
Causative organism enters through abrasion, causing lesions followed by
rupture of vesicles and resulting in contamination of surrounding skin.

Clinical findings.
Vesicles are seen on hairless parts of the body and surrounded by erythema.
Rupture of the vesicles and causing scab formation.
Involvement of hair follicles and leads acne formation.

Treatment
Local treatment.
Bathing of animals with germicidal skin wash twice daily is usually adequate.

(8) Phtosensitization (Light Sensitization = Sunburn)

It is secondary damage following injury to superficial layer of relatively unpigmented skin by the energy released from interaction between light of
certain wavelength and photodynamic agents. Dermatitis develops when the
sensitized skin is exposed to strong light.

Etiology and types of photosensitization

If the photodynamic agents are present in sufficient concentration in the
skin, dermatitis occurs when skin is exposed to light.

(1) Primary photosentization

This type is due to ingestion of exogenous photodynamic agents usually in
lush green plants and the animals affected within 5 days from going onto
pasture and symptoms are disappeared when the animal is removed away
from pasture and this differs according to the susceptibility of animals. The
most active form occurs naturally in plants and causes photosensitization
are:

a- Miscellaneous substance as acridin dyes and rose Bengal.

b- Fagopyrin in seeds of dried plants of buck wheat.
c- Perloline from perennial rye grass.

(2) Photosensitization due to aberrant pigment synthesis:

May be due to production of abnormal metabolism, the only example is
inherited congenital porphyries in domestic animals due to excessive
production of prophyrins substance, Which is the photo dynamic agent.

(3) Hepatogenous photosensitization

This is due to accumulation of normal metabolic products as a result of
failure to excretion through the liver.
Normally a photosensitizing substance, which is known, as phylloerythrin is
normal end product of chlorophyll metabolism and excreted in the bile.
When the level of phylloerythrin is increased due to hepatitis or cholangio
hepatitis and other cause of obstruction of biliary passage and reach in level
in skin to the point, which make it sensitive to light.

This is the most common form on all animals especially that fed on green
pasture also occurs in other animals fed only on hay and other stored feed.
Fungus on perennial ryegrass.
Algae on drinking water.
Pasture and crop plants as millet grass, weeds.

Chemicals as
Caron tetrachloride.
Corticosteroides.
Infectious as leptospirosis.
Congenitally defective hepatic function.

Such as inherited Southdown lambs, which has an inherited defect in

excretion of bile.

Clinical signs
It may be accompanied with photosensitive dermatitis.
Skin lesions are characteristic and concentrated on dorsum side of back,
vulva, lateral aspect of teats face ear.
Lesions are markedly clear from the normal skin.
Erythema edema of the skin.
Intense irritation, lacerating face and may be rubbing it.
When the teats are affected, kicking at the belly and swimming into ponds to
cool areas of pain.
Dyspnoea due to nasal obstruction, Dysphagia due to swelling of lips and
closure of eyelids.
The skin lesions may be extensive and cause shock.

Nervous manifestation blindness, posterior paralysis.

Peculiar sensitivity to water may seen in sheep with facial eczema.

Diagnosis
Primary cause must be detected.
Differential diagnosis from mycotic dermatitis and clostridium novyi in sheep.
The uses of serum enzyme tests are recommended.

Treatment
A) General treatment includes
Immediate removal from direct sunlight.
Laxatives to eliminate toxic materials.
Prevent further ingestion of toxic substance.

B) Local treatment includes

Antihistaminic, corticosteroids.
Prophylactic dose of antibiotics.
Local application of ointments-Astringents.
(9) Seborrhea

It is an excessive excretion of sebum on the skin surface.

Etiology
True of primary seborrhea mainly occurs in human is rarely in animals.

Secondary seborrhea accompanied with dermatitis and skin irritation as in

eczema, mange and in
Cases of:
Greasy heel in horse.
Flexural seborrhea in cattle.
Exudative epidermitis in pigs.

Pathogenesis:
Increased blood supplies to the skin and increase hair growth will leads to
increase excretion of sebum.

Clinical findings
. Primary seborrhea
Greasiness of skin with oily substance of sebum.
Trophy of sebaceous gland may be observed on histology.

. Secondary seborrhea
a. Flexural seborrhea, lesions found on groins and medial aspect of thights,
fissure between the two halves of udder. Extensive out pouring of sebum,
malodorous with irritation is seen. Shedding of oily skin leaving raw area
under the lesion.

b. Greasy heel in horses

Usually in hind legs due to prolonged standing in unsanitary and muddy
barns.
Thickening at the part of lesion at the coronet and painful to touch causing
lameness.

Soreness and excoriation called scratches at the pastern and may extend to
coronary band.
When the thickening of skin and subcutaneous tissues is marked, it will
interfere with normal movement of the limbs.

Diagnosis
It must be defined whether the lesions are primary or secondary.
Flexural seborrhea may be mistaken with injury.
Greasy heal seborrhea may be mistaken with chorioptic mange.
Treatment
Treat original cause.
Antibiotics and antiparasitic.
Washing with warm water and soap and keep the skin at the affected part
clean and dry.
Application of an ointment locally made up of:
5part salicylic acid:
3 part boric acid
2 part phenol
2 part mineral oil
2 part petrol jelly
At 5- days interval will result good prognosis and treatment in greasy heel of
horse.

Moving the animal to dry and clean land.

(10) Achromotrichia

It is bands of depigmentation in black wool fleece due to transient deficiency

of copper in diet. In cattle deficiency. of copper and increase molybdenum in
diet will result in depigmentation of skin.

Causes
Copper deficiency and increased molybdenum in diet.
Damaged or destroyed pigment cells melanocytes by the pressure as
harness, Parafilaria infestation.
Congenital vitiligo in the offspring of mares.
Symptoms
Marked bands of depigmented coat mainly around the eyes.
In horse, perineum, prepuce, face, under the tail, are the main involved area.
The entire coats also change of its normal colour due to decrease
concentration of melanocyte cells.

(11) Acne

The term acne refers to all infections of hair follicles by the acne bacillus,
which is diphtheria organism, but it may also include all suppurative
organisms including staphylococci and more properly known as sycosis.
Etiology
Staphylococcal dermatitis in horse.
Canadian horse pox caused by corynebacterium pseudotuberculosis.
Demodectic mange.
Pathogenesis

When insspisated secretion and debris block sebaceous gland ducts or by

pressure, it will predispose the condition.
Hypertrophy of sebaceous glands and increased excretion also predispose to
the condition.

Clinical findings
Formation of nodules at the base of hair follicles and then pustules.
It may be ruptured and contaminate the surrounding skin and further lesions
appears.
Hair at the site of lesions is usually easy to shed.
The lesions are painful and rupture under pressure.

Clinical pathology
Swabs for bacteriological and parasitological examination are helpful

Diagnosis
Clinical signs has to be differentiated from impetigo.

Treatment
Clean the skin and wash with disinfectants.
Local application of antimicrobial ointment.
Systemic administration of antibiotic in generalized course.
Isolation of infected animals.

(12) Impetigo

It is a superficial eruption of thin walled, usually small vesicles surrounded

by a zone of erythema, the vesicles develop into pustules and rupture to
from scabs.
Etiology
In animals the main organism is staphylococcus organism and most causes
are : Udder impetigo in cows, infectious dermatitis or contagious Pyoderma
of baby pigs caused by unspecified strept and staphylococci .
Pathogenesis
Causative organism enters through abrasion, causing lesions followed by
rupture of vesicles and resulting in contamination of surrounding skin.

Clinical findings.
Vesicles are seen on hairless parts of the body and surrounded by erythema.
Rupture of the vesicles and causing scab formation.
Involvement of hair follicles and leads acne formation.

Treatment
Local treatment.
Bathing of animals with germicidal skin wash twice daily is usually adequate.
Diseases of the urinary system
Anatomy and physiology
The composition of blood is kept constant mainly through the selective
elimination of water and solutes by the kidneys rather than by these
materials in food. This control involves balancing the body's input of ions and
water with the amounts excreted. As Na+ and Cl- are the most abundant
somatically active solutes in plasma, control of plasma volume and tonicity
can be largely achieved by controlling the amounts of these ions and water
excreted.

Functions of the kidney

1- Excretory:
Excretion of water products and drugs in the urine.
2- Regulatory:
The kidney regulates the volume, osmotic pressure and reaction of the blood.
3-Endocrine:
The kidney produces the following hormones.
(a) Rennin- angiotensin system: It is produced by the juxtaglomerular
apparatus which is made of specialized cells on the smooth muscle cells
located on the afferent glomerular arteriole as it enters the glomerulus.
These cells secrete rennin which converts angiotensinogen in the blood to
angiotensin I. Angiotensin II is generated from angiotensin I by angiotensin
converting enzyme. Angiotensin II is both a vasoconstrictor and the most
important stimulus for release of aldosterone.
(b) Erythropoietin: is a glycoprotein produced mainly by the kidney and is
one of the major stimuli of erythropoiesis.
(c) Prostaglandin: The kidney produces prostaglandin E2, a powerful
vasodilator agent.
4-Metabolic:
(a) Vitamin D metabolism: Naturally occurring vitamin D requires
hydroxylation in the liver and again by the kidney to produce 1.25
dihydroxychole-calciferol. Loss of this metabolic activity in diseased kidney
results in renal osteodystrophy.
(b) Protein and polypeptide hormones: The kidney is the major site for
catabolism of insulin, parathyroid hormone and calcitonin. In renal failure,
the metabolic clearance of these hormones is reduced.

Gross structure of the kidney

The basic unit of kidney function is the nephron of which there are about
1,000,000 nephrons in each kidney. Urine formed in the tubular part of the

nephron collects in the renal pelvis and then flows through the ureter to the
bladder for subsequent elimination via the urethra (Figs 1 and 2).

Fig. 1: Diagrammatic represent the normal anatomical arrangement of

urinary system
The glomerulus (about 200 mm in diameter) is formed by invagination of a
tuft of 50 anatomizing capillaries into the dilated blind end of the nephron
(Bowman's capsule). The capillaries are supplied by an afferent arteriole &
drained by a slightly smaller efferent arteriole. The glomerular membrane
separates blood from the glomerular filtrate in Bowman's capsule that is
composed of three layers: 1- Endothelial layer of the capillary.

2- Basement membrane.
3- Layer of epithelial cells.

Fig. 2: Diagrammatic represent the normal histological structure of the

nephron.

The permeability of the glomerular membrane is 100-500 times that of the

usual capillary. The endothelial cells lining the glomerulus have thousands of
small holes (fenestrae). Outside the endothelial cells is a basement
membrane, composed of a meshwork proteoglycan fibrillae, which has also
large spaces through which fluid can filter. A layer of epithelial cells lines the

outer surface of the glomerulus. These cells consist mainly of finger like
projections that cover the basement membrane. These fingers form slits
called slit-pores through which the glomerular filtrate filters.
Functionally the glomerular membrane permits the passage of substances up
to 4 nm in diameter & does not allow the passage of those with diameter
greater than 8 nm.
The proximal convoluted tubules (PCT) is made of a single layer of cells
which show on their luminal edges brush border due to the presence of
numerous microvilli.
The structure of the loop of Henle differs according to its location in the
kidney.
Cortical nephrons have short loops of Henle with a thin descending limb & a
thick ascending limb. The cells lining the thick segment of the loop of Henle
form a larger lumen & lack of prominent brush borders. In contrast,
juxtamedullary nephrons have somewhat longer loops of Henle and thin
segments on both sides of the loop.
The distal convoluted tubule (DCT) has a similar structure to the thick
segment of the loop of Henle. DCT from large number of different nephrons
drain into a common collecting duct & then via a papillary duct into the renal
pelvis. The largest collecting ducts empty through the renal pelvis through
the tips of the renal papillae, which protrude into the renal calyces. A kidney
has about 250 large collecting ducts, each of which transmits the urine from
4000 nephrons. The epithelial lining of the collecting duct is composed of a
layer of cuboidal cells, which gradually become taller as the collecting tubule
merges into capillary duct. Nephrons are arranged into 10-15 groups called
maligning pyramids. The nephrons are all oriented so that the Bowman's
capsules with related proximal & distal tubules are situated in the outer
layers of the kidney cortex while the loops of Henle & Malpighian pyramids
form the medullary rays.

Fig 3: Diagrammatic representation of the blood supply to cortical and

juxtamedullary Nephrons.

Principles of renal insufficiency

Disease of the kidneys, and in some instances of the ureters, bladder and
urethra, reduce the efficiency of the kidney's functions, disturbances in
protein, acid- base solute and water homeostasis and in excretion of the
metabolic end-products will result.
It is noteworthy to mention that, diseases of the bladder and urethra are
more common and more important in farm animals than the diseases of the
kidneys; but some studies on renal insufficiency is necessary because many
disease condition such as pyelonephritis, embolic nephritis, amyloidosis and
nephrosis, all may eventually lead to renal insufficiency or renal failure.

Renal insufficiency

It is defined as a degree or relative loss of renal function, but the animal

can survive its state. Meanwhile, renal failure is defined as complete loss of
renal tissue function and the animal can't survive or can't continue its
existence.
Renal efficiency depends on the functional integrity of the individual
nephrons. Renal insufficiency can occur because of:
* Extra-renal causes - abnormalities in the rate of blood flow to the renal
tissues.
* Intrinsic factors from the kidneys such as:
(a) Abnormalities of the glomerular filtration rate.
(b) Abnormalities of tubular reabsorption.
The first one (extrarenal) is depending upon the vasomotor and in animals is
affected only by emergencies such as in hemorrhage, shock and dehydration
which may lead to renal ischemia causing tubular necrosis with eventual
development of renal insufficiency.
Glomerular filtration and tubular reabsorption can be affected independently
of other such as in hemoglobinuric nephrosis, the glomeruler filtration is
unaffected while the tubular reabsorption is depressed. However, because of
the common blood supply to the glomerulus and tubule, damage to any part
of the nephron is usually followed by damage of the remaining part.
The development of renal dysfunction is depends on the degree of loss of
renal function. If the degree of loss, and there fore the degree of dysfunction
is such that the animal is not able to continue its existence, it is said to be a
state of renal failure and the clinical syndrome of uremia is manifested.

Pathophysiology of the renal insufficiency

Damage to the glomerular epithelium destroys its selective permeability

and permits the passage of plasma proteins mainly albumin into the capsular
fluid. Complete cessation of the glomerular filtration may occur when there is
an extensive damage to the glomeruli, particularly if there is acute swelling
of the kidneys, but in many instances the anuria of the terminal stages of
acute renal disease is caused by back diffusion of all glomerular filtrate
through the damaged tubular epithelium.
When the renal damage is less severe, the compensatory mechanism on the
part of residual nephrons is to maintain the total glomerular filtration by
increasing the glomerular filtration rate. Decreased glomerular filtration is
also reflected by retention of the blood urea and other nitrogenous end
products of metabolism. Although blood level of urea is not significant in the
production of clinical signs, they are used as a measure of glomerular
filtration rate.
When the glomerular filtration is reduced, phosphate and sulphate retention
also occurs and may precipitate to renal metabolic acidosis. Phosphate
retention may cause secondary hypocalcaemia due to increased calcium
excretion in the urine. Variations of the potassium levels in serum also occur
and usually depend on potassium intake. Hyperkalemia is a serious
complication and may lead to myocardial asthenia and fatal heart failure.
Hyponatremia eventually occurs in all cases of renal failure and clinical
dehydration may occur due to loss of large quantities of fluids caused by
solute diuresis.

Renal failure
Renal failure may be acute or chronic depending on the progress rate of the
dysfunction and the degree of loss of renal function.

(1) Acute renal failure:

Pathology of acute renal failure:

Acute renal failure is characterized by a sudden decline in the glomerular
filtration rate and concurrent development of uremia.

Renal failure may result from complete loss of function of a large number
of nephrons, partial loss of function of most nephrons, or any combination of
them.
The predominant pathophysiologic mechanisms causing this decline in the
filtration rate are decreased glomerular hydrostatic pressure and/or
increased Bowmans capsule pressure.
Decreased glomerular hydrostatic pressure: is usually due to hemodynamic
changes including:
1-Constriction of different arterioles.
2-Fibrin occlusion of renal vasculature.
3-Changes in renal blood flow.
4-Any reflex mechanism secondary to tubular obstruction in individual
nephron.
Increased Bowmans capsule pressure:
Tubular collapse.
Changes in glomerular permeability.
Causes of these tubular and vascular changes or factors are probably
interdependent in acute renal failure.
The causes of acute renal failure can be dividing into: Hemodynamic changes.
Toxic tubular nephrosis.
Immunologic disorders.
Acute inflammation and / or obstruction.
Any condition that predisposes the patient to marked hypotension and / or
release of endogenous pressor agents has the potential to initiate
hemodynamicelly-mediated acute renal failure.
Systemic hypotension and / or arteriole constriction, along with tubular
obstruction, causes the decrease in renal perfusion.

Endotoxemia and complement-mediated ceagulopatties are involved in

hemodynamic factors.
Nephrotoxins tubular swelling and necrosis of proximal cortical tubular
cells.
Tubular epithelial diseases lysosomal dysfunction, mitochondrial
dysfunction, abnormal protein synthesis resulting in tubular obstruction or
epithelial swelling.
Immunologicelly mediated acute renal failure is usually a result interstitial
nephritis or glomerulonephritis.
Causes pf acute renal failure: -

In Horse

In Ruminants

Hemodynamic causes

Hemodynamic causes.

Toxic nephrosis

Toxic plants.

Immunologic causes.

Drugs, chemicals.

Endogenous.

Mycotoxins.

Septic.

(2) Chronic renal failure:

Pathophysiology of chronic renal failure

It is a result of slow and oftenly progressive loss of nephron function and /
or population. Failure occurs when enough nephrons are lost or their function
is sufficiently decreased to affect body condition and function.
- Chronic renal failure in large animals is usually the result of progressive
glomeruler disease, which may be Immunologically, mediated, or of tubular
interstitial diseases caused by obstructive, unreversed or progressive,
nephrotoxic septic, hemodynamic.

- With either acute or chronic renal failure, more than two-thirds of nephron
function must be lost for clinical signs of uremia to be noted.

Causes In Ruminants

Causes In Horse

Tubulointerstitial causes:
Any of toxic, whether vascular

Chronic obstruction

Septic causes
Chronic or intermittent
obstruction

Chronic pyelonephritis

Chronic pyelonephritis
Granulomatous infiltration
Neoplasia
Glomerular causes:
Renal hypoplasia

Amyloidosis

Amyloidosis

Glomerulonephritis

Glomerulosclerosis
Principal manifestations or clinical features of the urinary tract disease

The major manifestations of U.T. disease are:

Abnormalities of the urine composition.
Abnormalities of the daily urine flow.
Pain and dysuria.
Uremia (principal manifestation in renal failure).
Rupture of the U.B., renal pelvis and urethra.
Defect in nervous control of the urination.

Urachal leakage of urine.

(1) Abnormal constituents of urine

(a) Proteinurea:
It means the presence of protein in the urine. Normal urine in all animal
species contains little or small amount of protein from desquamation of
epithelial cells and other sources, but the amount is insufficient to produce a
positive reaction to the standard test. One exception is the urine of newborn
calves 40 hrs old after receiving colostrums and sheds urine of high protein
contents. Also, urine of equines has an increased protein level, and
consequently their urine appears turbid.
Proteinuria is usually associated the following disease conditions:
Hemoglobinuria, myoglobinuria, hematuria.
Glomerulonephritis, renal infarction, nephrosis, amyloidosis, congestive
heart failure.
Excessive excretion of protein in the urine leads to hypoproteinarmia and
manifested clinically as muscular weakness, general depression and reduced
work capability of the animal. The clinical significance of proteinuria as an
indication of renal diseases is much greater when the formed elements
including casts and cells are present in the urine of the diseased animal.
Chronic proteinuria or massive acute proteinuria may cause hypoproteinemia
as in case of oglomerulonephritis, acute tubular nephrosis in horses and in
amyloidosis in cattle.

(b) Casts and cells:

Casts are organized, tubular structures, which vary in appearance depending
on there composition. They occur only when the kidneys are involved in the
disease process. They present as an indication of inflammatory or
degenerative changes in the kidney where they formed by agglomeration of
desquamated cells and protein. R.B.Cs, W.B.Cs and epithelial cells may
originate at any part of the urinary tract.

(c) Hematuria:
It is the presence of intact blood cells in the urine. It may appear as gross
blood clots passed at the beginning, during, or at the end of urination or as
more uniformed discoloration of the urine throughout the urination without
clots. It large clots are present, obstruction of U.T. may occur, resulting in
stranguria and dysuria.
Haematuria may result from prerenal, renal or postrenal causes as following:
Prerenal causes of hematuria:
When vascular damage occurs such as:
Trauma to kidneys.
Septicemia.
Purpura hemorrhagica in horses.
Renal causes of hematuria:
Acute glomerulonephritis.
Pyelonephritis.
Tubular damage due to toxic insults such as sulphonamide toxicity.
Embolism or Renal A.
Renal infarction.
Post renal causes of hematuria:
Urolithiasis.
Urethritis, cystitis.
Enzootic hematuria in cattle tumor in U.B., which is usually accompanied
by blood losses.
Causes of Haematuria

Urethra

In Horse

In Ruminants

Calculi

Calculi

Urethritis

Urethritis

Bladder

Kidney

Habranemiasis

Trauma

Calculi

Calculi

Cystitis

Cystitis

Neoplasia

Papilloma

Bleeding diathesis

Bleeding diathesis

Amorphous debris

Polyps

Calculi

Pyelonephritis

Trauma

Trauma

Nephritis

Infarction

Vascular anomaly

MCF

Parasitic migration
Neoplasia
Gomerulopathy
Papillary necrosis

If the blood is equally distributed in the urine This could be kidney

damage.
Hematuria at the beginning of urination This could be urethral damage.
Hematuria at the end of urination This could be vesicle damage.
Hematuria after exercise, especially, in horse This could be cystic calculi.
Uniform discoloration of urine without clots, you got to make sure the
discoloration is hematuria and not Hburia, bilirubinuria or myoglobinuria.

(d) Crystalluria:

It is the presence of crystals in the urine the presence of crystals in urine of

herbivorous animals have no special significance unless they occur in large
numbers and one associated with irritation of U.T. It may occur with no
clinical signs or may indicate a severe problem in renal tissues or U.T.
infection.
Calcium carbonate and triple phosphate crystals are more common as urine.
It they are observed, the possibilities of urinary tract infection and / or a
potential for obstruction should be considered.
If they congregate into large masses, they may obstruct renal pelvis, ureters,
urethra or the urethral opening while smaller formations may obstruct the
individual nephrons.

(e) Pyuria:
It is the presence of purulent debris in the urine. Pyuria indicates an
inflammatory exudation at any point of the urinary tract, usually renal pelvis
and bladder. This purulent debris may appear in the form of grass clots or
shreds or only detectable by microscopic examination.
Pyuria is usually accompanied by the presence of bacteria in the urine. Also,
dysuria, stranguria and crystalluria are evident. A fever may or may not be
present in such cases, but urine scalding of the perineum is usually present.

(f) Hemoglobinuria:
It is defined as presence of hemoglobin in the urine. False hemoglobinuria
occurs with cases of hematuria when the R.B.Cs are destroyed and liberate
their contents of hemoglobin into urine. Meanwhile, true hemoglobinuria is
manifested by deep red discoloration of the urine caused by lysis of R.B.Cs
due to many diseases such as:
Bacillary hemoglobinuria.
Babesiasis.
Copper intoxication.
Water intoxication.

(g) Myoglobinuria:
It is the presence of myoglobin in the urine. Myoglobinuria is a good
evidence of severe muscular destruction such as in azoturia in horses. It may
be observed inenzootic muscular dystrophy but the amount of myoglobin in
such young animals is insufficient to cause the problem.
Because the molecule of myoglobin is much smaller than that of hemoglobin,
it is usually excreted in the urine in the diseased cases without staining of
blood serum.

(h) Glucosuria and Ketonuria:

Glucosuria is not common in large animals but occurs usually in pet animals
such as in diabetes mellitus. Glucosuria in large animals is usually associated
with the following disease conditions:
Enterotoxaemia is caused by clostridium peferinges type D.
Rabred cattle.
Administration of dextrose solution, treatment by using adrenocorticotrophic
hormones, cortisone.
Cases of nephrosis.
Meanwhile, ketonuria is more common in cattle and sheep as in cases of
starvation, pregnancy toxemia and acetonemia in cattle.
(i) Indicanuria:
It is the presence of Indican substance in the urine (potassium indoxyl
sulphonate). Presence of excessive amount of this substance in the urine
indicates an increased absorption of the detoxificated end products from
gastrointestinal tract. Such condition is usually associated the cases of
constipation and obstruction of the intestine.

(j) Creatinuria:
Excessive breakdown of muscular tissues leads to increase amount of
creatinine in the urine and considered a good indication for muscular
dystrophy.

(2) Abnormalities of the daily urine flow Polyuria:

It is the passage of abnormally large amounts of urine.

This may be normal response when excessive fluid and / or electrolytes are
presented to tubules of healthy kidney.
Evaluation of an animal with polyuria should begin with inquiry about any
history of drug or fluid administration or laboratory evidence of renal
disease.

Osmolality or specific gravity:

If the osmolality is close to isoenuric range (similar to plasma concentration
regardless of patients fluid volume status) primary renal disease should
be considered.

Determination of GFR would be indicated:

If the basic measurements of GFR (e.g. serum creatinine, and 12-or 14hr
creatinine clearance) are not abnormal water deprivation test may be
needed to determine the ability of tubules to concentrate urine.
An alternative to this test is to measure the fractional excretion of sodium
in the urine.
Sodium excretion is greater the 1 % is highly suggestive of primary tubular
disease.
This measurement is performed on collected urine and serum samples by
measuring the creatinine and sodium in both the serum and the urine.
Fractional excretion of sodium is than determined by the formula:
If the specific gravity or osmolality of the urine is less than that of the
plasma, - diabetes insipidue should be considered.
It may be the result of secretion of vasopressin or response of kidney
tubules and receptors to vasopresin.

Causes of polyuria in Horses and Ruminants:

Acute and chronic renal failure.
Hyperglycemia Diabetes mellitus.
Psychogenic water intoxication.
Fluid steroid administration.
Diuretic.
Salt deficiency or toxicity.
Diabetes insipidus.
Severe deficiency of Cl-K- or urea.

(b) Oliguria and Anuria:

Oliguria means reduction in the daily urine output.
Oliguria usually results from:
Terminal stages of nephritis.
Congestive heart failure.
Peripheral circulatory failure.
Renal ischemia.
Dehydration and hemorrhage.
Partial obstruction or stenosis of the urinary passages.
Hot weather and excessive salivation, and excessive sweating.
Meanwhile, anuria means complete absence of urine. Such case is usually
observed in many disease problems such as complete bilateral obstruction of
urinary passages, acute form of tubular necrosis.

(3) Dysuria and stranguria:

Dysuria is difficult or painful urination.

Stranguria is slow and painful urination.
It is difficult to differentiate between dysuria and stranguria in large animals
and they are usually caused by:
Urethral obstruction.
Inflammation of the urethra, bladder or both.
Neurologic conditions that prevent normal emptying of urine, from the
bladder.
The horse voids urine very actively and forcefully. Both male and female
adult horses normally may groan and strain on urination. In other species of
animals urination is passive, and straining or groaning associated with
urination normally could not be observed.
Clinical signs in horses:
Straining, urination of shorter duration than normal or frequent attempts at
urination that produce only small amounts of urine.
The urine may be discolored e.g. blood urine. (Normal horse urine is very
cloudy because it contains large quantities of calcium carbonate and
mucous).
Clinical signs in ruminants:
The clinical signs are similar to those in horses, except that urine dribbling is
more common in male goat and sheep with calculi.
Vocalization is more common in male gouts with calculi.
Urine scalding of the perineal region or rear legs may be noted in either
ruminants or horses.
Intermittent prolapse of the prepuce is marked in.
Dysuria or stranguria in large animals may be confused with tenesmus.
(4) Urachal leakage of urine:

The clinical signs of incomplete urachal closure in newborn animals are

visible dripping of urine from the ventral abdomen and / or swelling of
umbilical area. Improper closure may be the causes by inflammatory
diseases or incomplete closure.

Diagnosis is based on:

1.History.
2.Clinical findings (pain, fever, exudate).
3.Percutaneous palpation and / or ultrasonograplray.

Treatment:
Surgical removal of infected urachus and / or umbilical vessels.

(5) Uremia

This term is used to describe the clinical syndrome, which occurs in the
terminal stage of renal insufficiency. It may be also applied to the symptoms
mainly gastrointestinal and nervous which could result from various types of
advanced renal diseases.
Renal failure is manifested by the clinical state of uremia, which is
characterized by an increase in the blood levels of total protein and urea
nitrogen and by retention of other solutes, and urinary constituents in the
blood.
Uremia may be the result of a cute or chronic renal failure. It seems most
reasonable that several toxins are associated with the uremic process,
including azutaemia. However, the etiology of uremia is the same of acute
and chronic renal failure.
The predominant clinical signs of uremia seen in large animals are
depression, anorexia, seizures and encephalopathy, which may occur, in

severe episodes. Weight loss, oral erosions, gastro intestinal ulcers, melena
and accumulation of excessive dental tarter are also observed in the
diseased cases.

Abnormalities, which interact to produce signs of uremia:

(a) Auto intoxication:

a. 1. Electrolytes (excess or deficiency):
Increased sodium over hydration.
Reduced sodium dehydration.
Increased potassium

myocardial asthenia and fatal heart failure.

Reduced potassium

muscular weakness.

Polyuria, vomiting and diarrhoea leading to dehydration.

Oliguria and anuria leading to overhydration
Acid-base imbalance:
Renal metabolic acidosis is evidenced.
Hormones:
Reduced production of erythropoitin hormone usually results in nonregenerative anemia.
Accumulation of waste products of metabolism.

(b) Body compensation:

Polyuria results in compensatory polydipsia.
Hypocalcaemia results in compensatory release of parathormone.
Metabolic acidosis results in increased rate and depth of respiration
(hyperpnoea) aiming to eliminate the excess CO2.

Assessment of the urinary system and diagnosis of the urinary tract (UT)
diseases

(I) History:
It is very important to make a few remarks on the history, before or prior to
discussing physical examination findings, due to its importance in diagnosing
the UT diseases. In selected cases, the history may be more important than
the clinical examination findings in diagnosis of a UT disease, e.g. a
castrated male goat with pain and stranguria should be assumed to have
urinary calculi unless other cause can be proven.
As a general rule, diseases of the lower tract are often very noisy (easily
recognized by the owners), whereas diseases of the upper tract are of then
more subtle; an exception to this is subacute contagious bovine (CB)
pyelonephritis in cattle.

(II) Assessment of gross and microscopic structure:

Rectal palpation: Refer to the practical note vet. Clinic diagnosis.
Percutaneous biopsy of the kidney.
The causes of renal failure usually can be determined by history, urine
analysis, renal function tests, and physical examination for obstructive
causes, negating the need for a renal biopsy.
Radiography:
Enlargement of the renal pelvis found in pyelonephritis or hydronephrosis,
Urethral enlargement or aberrant locations, or defects in continuity of the
excretory urinary tract can be determined using I /V injection of 1 mL / kg.
B.wt. of Renografin.
Urinary tract endoscopy:
Direct visualization of most of the lower urinary tract is possible with rigid
and flexible endoscopes. Cystoscopic examination can be valuable in
determining suspected abnormalities such as site of hematuria, pyuria and
ureteral obstruction.

Ultrasonography:
Ultrasonography is useful for assessing location of individual structures of
the urinary system and lesions within those structures.

(III) Catheterization (Refer to practical note of clinical examination).

(IV) Urinalysis:
Urinalysis should be completed within 15-30 minutes of collection. If this is
not possible it should be refrigerated, as prolonged exposure to room temp
before analysis can result in growth of bacterial cells, dissolution of delicate
casts, cellular degeneration resulting in loss of cellular details, and change in
pH. Urinalysis includes examinations of all the physical, biochemical and
microbiological of findings of the urine.
Urine specific gravity.
Color smell.
Viscosity.
PH of urine in herbivorous animals is alkaline 7.9 to 0.05.
Biochemical findings.
Microbiological examination.
(V) Renal function tests:
The simplest and most important tests of urinary functions are the
determination of whether or not the urine is being voided.
Renal function tests evaluate the functional capability of the renal
tissues (kidneys). In general these tests assist to know: Blood flow to the kidneys.
Glomerular filtration.
Tubular function.

We can classify these tests into three groups depending on whether they are
based on the exam of blood or urine, or both.

(1) Tests conducted on urine:

Specific gravity: is the simplest test to measure the capacity of renal tubules
to conserve fluids and excrete solutes. In most species of animals, specific
gravity ranges from 1.028 to 1.095.
In chronic renal diseases, sp. gr. falls down to up to 1.010.
Osmololity of fluid is an alternative to sp. gr. and it gives a more accurate
assessment of tubules capacity to conserve fluid and excrete solutes.

(2) Tests conducted on blood:

These tests depend on either:
The accumulation of metabolites normally excreted by the kidneys (in cases
of insufficiency).
Excretion of endogenous substances by the kidney.
Creatinine and BUN are essential components of evaluation of renal function.
Creatinine and BUN do not rise significantly above the normal range until 6075% of nephrons are destroyed.
Glomerular filtrations rate has been estimated by: I /V injection of
sodium sulphanilate, then to follow the disappearance of this substance.
Renal Blood flow may be evaluated by measuring the half time
of disappearance of dye such as phenolsulphthalein (PSP) as given by I /V
injection.

(3) Tests conducted on urine and blood:

Water deprivation test. It can be used to assess the renal concentrating
ability in horse.
Fractional excretion of sodium.

General principles of treatment of urinary tract diseases

(Basic Idea of Treatment)

The initial treatment of acute renal failure (ARF) in all animals aimed to
remove the predisposing factors, removing the primary cause, and restoring
normal fluid balance by correction of dehydration, electrolytes and acid- base
abnormalities.
Serum concentration of sodium, chloride, potassium and bicarbonate should
be monitored daily and replaced or corrected as needed.
After correction of any volume and electrolyte deficits, an attempt should
be determine disorder of ARF as oliguric or plyuric, by using the following
one of the following:
1. Estimation total plasma proteins.
2. Estimation central venous pressure, and / or by measuring fluid input
compared to its output.

In oliguric animal:
I/V injection of Manitol 20% solution at a dose rate of 0.25-2 gm /kg B.w.
Furosemide (Lasix) at a dose rate of 1-2 mg / kg B.W. every 2 hours until
diuresis.
Dopamine at a dose rate of 1-5 Mg /Kg /min in 5% dextrose solution I/V
with Frusemide may be useful to improve urine output.

In Non- oliguric animal:

I/V injection of 0.9 NaCl or balanced electrolyte solution at a dose rate of 4080 ml / kg / day until there is a precipitous drop in serum creatinine.
Continuation with 10-20 ml / Kg / day.

Sedation could be obtained by using xylazin at a dose rate of 0.4-0.8 mg /

Kg. by I .V injection.
The most frequently used antimicrobial drugs that are recommended for UT
infection are:
Trimethoprim / sulfadiazine.
Nitrofurantain.
Ampicillin, Amoxicillin,
Penicillin Gentamycin.
Cephalosporins.
Antimicrobial therapy for infection of lower tract should be continued for 7-10
days, and it should be continued for 2-4 week for upper tract infection.
Bacterial culture should be made 7-10 day post treatment, and second
antimicrobial dose may be needed.

Use of Antiemetic (in dogs) in cases of uremia, such as:

Cimetidine (Tagamet):
10 mg /Kg. B.wt I / V injection on 2nd .day.
You can give it orally to the animal when vomiting stops.
Ranitidine.
2-4 mg /kg. B.wt twice / day.
Gastrointestinal coating agents:
Kaolin, Pectin 3 times / day orally.

Restriction of food for at least 24 hrs during therapy

Diseases of the kidney

1- renal ischemia

It means reduction or decline of the blood flow through the kidneys, which
is usually the result of circulatory failure. There is transient oliguria followed
by anuria and uremia if the failure is not connected.

Pathogenesis:
Sudden reduction in cardiac output due to any cause.
Lowering of blood pressure.
Accumulation of the metabalites that are normally excreted such as BUN and
creatinine, giving rise to prerenal Azotemia.
Reduction of the glomerular filtration, which increases the tubular resorption
and reduced urine flow (oliguria).
Up to a certain level, the degenerative changes are reversible by restoration
of renal blood flow; but if the ischemia is severe enough and of sufficient
duration, the renal damage is permanent.
The parenchymatous lesions vary from tubular necrosis to diffuse cortical in
which both tubules and glomeruli are affected.
Plugging of the tubules with casts of coagulated protein may exacerbate
uremia acute hemolytic anemia and acute muscular dystrophy with
myoglobinuria, but ischemia is also an important factor.
Clinical findings:
Renal ischemia does not appear as a distinct disease and the clinical signs of
the primary disease mask its signs.
The general clinical picture is one of acute renal failure.
Clinical pathology:
1. Urinalysis.
2. Monitoring BUN, creatinine level in serum.

Passage of large volume of low specific gravity urine after a period of oliguria
is usually a good indication of a return of normal glomeruler and tubular
function.
On urinalysis, proteinuria is an early indication of damage to the renal
parenchyma.

Treatment:
Correction of fluid, electrolytes and acid base balance.
Supportive treatment as suggested for ARF (if there is renal damage).

2- Pyelonephritis

Definition:
It is bacterial inflammation of kidney and renal pelvis. Pyelonephritis
develops most commonly from ascending infection through the lower urinary
tract. It is characterized clinically by pyuria, dysuria or stranguria,
suppurative nephritis, cystitis and ureteritis.

Etiology:
In most cases it results following bacterial infection of the lower urinary tract.
Spread from embolic nephritis of hematological origin (descending infection)
such as septicemia of cattle caused by Pseudomonas aeruginosa.
Specific pyelonephritis caused by corgnebacterium renal in cattle
and Eubacterium suis in pigs is also recorded.
Pathogenesis:
The development of pyelonephritis is depending up on:
Common presence of infection in U.T.
Stagnation of urine.

Reflux of urine from the bladder.

Urine stasis can occur as a result of:
Blocking of the ureters by inflammatory swelling or debris, by pressure from
the uterus in pregnant females, and by obstructive urolithiasis.
Infection ascends the ureters and invades renal pelvis causing pyelitis and
involves the papillae causing diptheriod destruction, and then it extends to
involve the medulla and cortex.
Signs of toxemia and fever, usually accompany expensive bilateral infection,
uremia may develop if the lesions are sufficiently extensive. Pyelonephritis is
always accompanied by hematuria because of the inflammatory lesions of
the ureters and bladder.
Clinical findings:
The first sign observed may be the passage of blood stained urine in some
cases.
In other cases, the first sign may be an attack of colic, manifested by
swishing of the tail, kicking at the abdomen and treading of the feet.
Straining to urinate; such attacks are caused by obstruction of the ureter or
renal calyx by pus or tissue debris.
The onset is gradual with fluctuating temperature (39.5 C).
Capricious appetite, loss of condition and fall in milk yield over a period of
weeks.
The most obvious sign is the presence of pus, blood, mucous and tissue
debris in the urine, particularly at last portion voided.
Urination is frequent, painful and may occur in a dribble rather than a
stream.
Rectal examination may be negative in the early stages, but later there is
usually detectable thickening and contraction of bladder wall and
enlargement of one or both ureters.
Left kidney may show enlargement, absence of lobulation and pain on
palpation.

In many cases (chronic) there are no distinct clinical signs referable to the
U.S. and may have, history of chronic weight loss and in such cases
urinalysis is important in diagnosis.
Clinical pathology:
Urine analysis for blood and protein.
Urine pH is greater than 8.5 (Alkaline).
Urine specific gravity is 1.008-1.212.
Microscopic examin pyuria, debris, blood cells.
Bacteriological culture
Hypoalbuminemia and Hypergammaglobulinemia.
Elevations of BUN 1.5 mg / dL and cr. 100 mg / dL. Which carry a grave
prognosis.
Treatment:
General principles for treatment of U.T. infections.
Acidification of urine by the administration of monobasic sodium phosphate
(100 gm daily for several days).
Antibiotic therapy; penicillin remains the antibiotic of choice in this cases.
15.000 IU / Kg B.Wt of procaine penicillin for at least 3 weeks.
Unilateral Nephroctomy may be carried out in valuable animals.
Improving appetite, milk yield and clearing of urine expect good prognosis.

3- Glomerulonephritis

This form of nephritis involves primarily the glomerulus then may extend
to involve the interstitial tissues (secondarily) and rarely the blood vessels.
Glomerulonephritis is an immunologic disease or disorder that results in
deposition of Ag-Ab complexes in the GBM or anti-GBM antibody to the
capillary walls, with consequent impairment of GF, GF and enhanced
permeability to plasma proteins.

Glomerulonephritis is an ucommon clinical renal disease in sheep and

occasionally as a clinical entity in cattle, but the cattle are usually not
examined until the disease process is advanced.

The three types are seen include:

Spontaneous proliferative glomerulonephritis.
Glomeoulonephritis of pregnancy toxemia in sheep.
Mesangiocapillary glomerulonephritis.
Clinical and lab. Findings:
Weight loss, chronic diarrhea and generalized edema.
Marked oliguria or even anuria in some cases.
Proteinuria, hypoalbuninemia and anemia.
Serum Cr. And BUN is elevated in advanced cases develop signs of
azotemia.
Treatment:
Is usually unrewarding.
Plasma transfusion.
Anabolic steroids.

4- Embolic nephritis

Embolic lesions in the kidney cause no clinical signs unless they are
extensive in which case toxemia followed by terminal uremia. Transitory
periods during which proteinuria and pyuria occur may be observed if urine
samples are examined at frequent intervals.

Causes:

Embolic suppurative nephritis or renal abscess may occur after any

septicemia and bacteremia when bacteria lodge in renal tissues the origin of
emboli may be: (A) Sporadic cases:
Valvular endocarditis in all species.
Suppurative lesions in uterus, udder, navel and peritoneal cavity of cattle.
(B) Associated with systemic infections such as: 1.Shigellosis in foals.
2.Erysipelas in pigs.
Septicaemic or bacteraemia strangles in horses.

Pathogenesis: Localization of single bacterial cell or bacteria in small clumps in renal tissues
development of embolic suppurative lesions.
Emboli block larger vessels than capillaries infarction, local ischemia in the
affected portion, and if this infarction is small there is no clinical signs.
Clinical signs only develop when emboli are multiple and destroy much of
renal parenchyma.
If the urine checked repeatedly, the sudden appearance of proteinuria, casts,
and microscopic hematuria without other signs of renal disease it suggests
infarction.
Clinical signs:
Embolic nephritis may pass without clinical signs due to insufficient renal
damage.
Enlargement of the kidney may be palpated by rectal examination.
Fatal uremia and toxemia may be occurring.
Large infarcts may cause bouts of transient abdominal pain.
Diagnosis:

Clinical signs.
Clinical pathology as that of pyelonephritis accompanied with cystitis or
urethritis.
P.M. lesions:
Enlargement of kidney with abscess formation.
Much fibrous tissue surrounding the lesions.
Treatment:
Sensitivity tests to chose proper antibiotics.
Antibiotics for about 7-10 days and may be injected with specific enzymes.
5-Interstitial Nephritis

It is a common disease of the dog, it may be acute diffuse or chronic

focal but is always non-suppurative. Focal interstitial nephritis white
spotted kidney. Acute type is usually caused by leptospirosis in dogs. Chronic
poisoning with caustic-treated roughages in cows leads to chronic form of the
disease.

Clinically is characterized by:

Polyuria with low specific gravity urine.
Vomiting polydepsia and depression.
Arched back in severe cases and temperature may be elevated.
Treatment:
Restoration of water and electrolyte balance is important.
Parentral administration of antibiotics.
6- Nephrosis

Nephrosis includes degenerative and inflammatory lesions of the renal

tubules uremia may develop acutely or as terminal stages after a chronic
illness manifested by polyuria, dehydration and loss of weight.

Etiology:
Most cases of nephrosis caused by toxins.

Toxins:
Mercuric compounds, selenium and organic copper compounds.
Oxalates in plants and fungi.
Thiabendazale anthelmintics.
Over dose w sulphonamides.
Haemodynamic factors:
Dehydration leading to concentration of toxins in the tubules.
Severe renal ischemia.
Heamoglobinurea causing hemoglobinuria nephrosis.
Pathogenesis:
In acute nephrosis there is obstruction to glomerular filterate flow through
the tubules obstructive oliguria and uremia.
In chronic cases there may be impairment of tubular reabsorption of solutes
and fluids.
Clinical signs:
In acute stage there is oliguria, protinuria and other symptoms of uremia as:
Anorexia, hypothermia, depression, weak pulse.
In cow there is continuous mild hypocalcemia.
Polyuria in chronic cases.

Diagnosis:
Clinical signs.
Clinical pathology.
Necropsy findings.
Treatment:
Correct the primary cause.
Water and electrolytes therapy.
Antibacterial agents.

7- Hydronephrosis
Cystic enlargement of the kidney due to obstruction of the ureter, caused
usually by urolithiasis and congenital anomalies in ureters it is seldom
detected clinically in farm animals.
8- Renal Amyloidosis
It is usually accompanied general amylosis in the body it occurs as a result
of long standing metabolic disorders of proteins and clinically manifested by
profuse-water diarrhea, signs of dehydration, hypoproteinurea.

Causes:
1.Suppurative lesions due to strept infection.
2.Pyogenic membranes, Abscess formation in liver-lung.
Pathogenesis:
Amyloid substances deposits in the glomeruli interfere the process of
glomerular filtration and permeability. This disturbance in permeability leads
to passage of protein causing proteinuria. Absorption of toxic amyloids
causes nephritic changes and edema in interstitial wall and renal
insufficiency.

Clinical signs:
Gradual loss of body weight.
Profuse watery diarrhea.
Urine with low specific gravity.
Depressed appetite, signs of dehydration.
Edema in intermaxillary space.
Diagnosis:
Clinical signs and Clinical pathology.

Differential diagnosis from:

1.Chronic enteritis.
2.Paratuberculosis.
3.Pyelonephritis.
4.Leukosis.
Diseases of the urinary bladder

1- Cystitis
Inflammation of the bladder is usually caused by bacterial infection and is
characterized clinically by frequent, painful urination and the presence of
blood, inflammatory cells and bacteria in the urine.

Etiology:
Cystitis occurs sporadically due to the introduction of microorganism into the
bladder, which is usually associated with trauma to the bladder, paralysis of
the bladder and stagnation of urine due to any cause.
The most common predisposing factors or the common association are:

1.Cystic calculus.
2.Dystocia or difficult parturition.
3.Late pregnancy.
4.Contaminated catheterization.
Cystitis can also occur because of ascending infection and accompanying
pyelonephritis caused by corynebacterium renal in cattle, Eubacterium suis
in pigs corynebacterium cystitidis, Escherichia coli, Streptococcus and
Pseudomonas.

Pathogenesis:
Bacteria frequently gain entrance to the bladder, but are usually removed by
the fluching action of voided urine before they invade the mucosa.
Stagnation of the urine with mucosal injury, facilitate invasion of the mucosa.
Irritation of stretch receptors in the bladder wall, as a result of this irritation
the animal is constantly stimulated to urinate and the U.B. remains empty.
Hence, signs relate to changes in urination behavior (dysuria, pollyuria,
stranguria and apparent incontinence).

Clinical findings:
Frequent and painful urination, accompanied by grunting.
Animal adopted the urination posture some minutes after the act of urination
has been completed.
The volume of passed urine each time is very small.
Moderate abdominal pain as manifested by treading with hind feets, kicking
at the belly, swishing with the tail.
A moderate febrile reaction.
Acute retention may develop if the urethra has been blocked by blood, or
pus.

Painful or palpation.
In chronic cases, the signs are less marked but frequent urination and small
volume of urine are the signs. The bladder wall may feel thickened in rectal
exam.

Diagnosis:

1.It is mainly rests on observation of clinical signs.

2.Clinical pathology findings:
Cellular findings in the urine, such as blood and pus.
Urine may have a strong ammonia small.
Urine may be turbid having much mucous.
Bacterial culture from the urine commonly shows microorganisms.
3.Necropsy findings:
Hyperemia, hemorrhage and edema of the mucosa.
Thickening of the wall in chronic cases.
Erosion of the papillary projections.
4.Differential Diagnosis:
(A) Pyelonephritis:
It is difficult to be differentiated, but the prognosis in case of cystitis is much
better.
Thickening of the bladder wall.
(B) Cystic urolithiasis:
It is usually detected by rectal palpation by ultrasongraphic and radiographic
examinations.
Urine flow is greatly restricted.

Distended bladder can be felt on rectal palpation.

Treatment:
The earlier treatment, is commended, the better the prognosis, and return to
normal production.
Antibiotic treatment for at least 10-14 days is highly recommended.
Water and salt should be always available.
Use of urine acidifiers such as ammonium chloride at a dose rate of 50-100
mg /kg twice a day.
Urinary antibiotic.

2- Paralysis of the bladder or Vesical paralysis

Vesical paralysis is uncommon in large animals caused mainly by the lesions
of lumbosacral part of the spinal cord. In the early stages of vesical paralysis
due to neurogenic injury, the bladder remains full with urine and dribbling of
urine occurs especially during movement; good flow of urine can obtained by
compression of the bladder through rectal examination.
However, regular catheterization is essential in conjunction with a
prophylactic dose of antibiotic to prevent the development of cystitis. Nerve
tonics, strychnine, belladonna and nux vomica are useful in such cases.

Obstruction of the urinary tract:

Calculi, blood, neoplasia, smegma, edema and / or cellulites may result in
obstruction of the urethra.
Calculi are most often CaCo3 stones that lodge in the pelvic urethra in the
stallions and geldings.
Blood clots resulting in obstruction of the urethra are rarely seen, but may be
found in association of renal trauma.

The most common neoplasia causing obstruction of the urethra is a

squamous cell carcinoma of the penis.
Many inflammatory and / or edematous diseases of the penis and urethra
may cause urinary obstruction.

3- Urolithiasis
Urinary calculi or uroliths include: Nephroliths, ureteral, cystic and urethral
calculi.

Nephroliths and ureteral calculi:

Ureteral calculi and renal stones may result in obstruction of one or both
ureters and renal pelvis.
The obstruction may be complete or incomplete and may be chronic or
intermittent.
Most commonly both kidneys and / or ureters are affected.
It is more common in young adult thoraughbred horses.
The stones are usually composed of CaCO3 or Ca. phosphate.
Because of the bilateral involvement and insidious nature of the disease,
most cases have progressed to chronic renal failure (CRF) before they are
noticed. Weight loss and / or poor performance are the most common
presenting complaint.
Cystic Calculi:
Cystic calculi occur sporadically in horses. They are usually singular and
either large and smooth or smaller and rough.
The most common clinical signs are hematuria after exercise, stranguria and
dysuria. Urinary in continence usually occurs in most cases.
Urolithiasis:
Urinary calculi or urolithiasis occur sporadically in ruminants. It becomes of
clinical importance when obstruction of the U.T. occurs.

Obstruction urolithiasis is almost exclusively a disease of males and

primarily affects steers, rams, bucks & whether, especially castrated
animals.
Three common clinical entities occur in urolithiasis syndrome which are:
Urethral obstruction.
Rupture of the urethra.
Rupture of the bladder.
As a result of these entites, obstructive urolithiasis are characterized
clinically by:
Complete retention of urine.
Unsuccessful efforts to urinate .
Distention of the U.B.
And eventually ruptured of the utethra or bladder .
Causes and Epidemiology :
Urolithiasis is a disease of all animal species, but of greater importance in
fattening steers and rams which fed high concentrate diet . Also, it occurs
among animals grazing an pasture that cantains high levels of oxalate, and
silica , The incidence of urolithiasis varies greatly with the season, and of
high value at winter season .

There are groups of factors that cantribute to urolithiasis :

Those factors which favor the development of a nidus about which
precipitation and concretion can occur .
Those factors which facilitate precipition of solutes on to the nidus and .
Those which favor concretion and cermenting precipitated salts to the
developing calculus .
(1) Nidus Formation :
A Nidus is usually a group of desquamated epithelial cells or necrotic tissues
that favor the deposition of crystals and other salutes around it.

Nidus or calculus may result from:

Local infection of the U.T.
Herd problem due to vitamin A deficiency.
Fattening problem e.g. Administration of massive doses of anabolic or growth
promoting such as estrogen preparation, (estradiol, stilbesterol) which lead
to massive desquamation of epithelium.
(2) Precipitation of solutes: The physical characteristics of urine, the amount of solutes of presented to
the kidneys for excretion and the balance between water and solutes in the
urine, all influence the ease of calculus formation.
Normally, urine is highly saturated solution containing large quantities of
solutes.
These salts are not precipitated, normally, because of the colloidal state
mechanism in the urine. This protective colloid prevents precipitation of
salutes and converts the urine into a gel.
This mechanism is so efficient up to certain point and its capacity to maintain
normal solution could be overcome by a number of factors. The degree of
super saturation of urine depends on the diet, PH of urine, a mount of water
intake and the presence of crystalloids inhibitors in the urine.
A- Diet: Plays an important role in solute precipitation in different ways:
Highly concentration diet rich in phosphate and oxalate increases the
incidence of metabolic defects that consequently increases the incidence of
urine solutes.
Hypervitaminosis D for example increases ca level in urine.
Cattle raised an grass pastures that contain high levels of silica (6%) have
high conc. of silicon dioxide in the reticulorumen fluid, which is converted
into salicylic acid, absorbed and then excreted in the urine until its values
increase above the supersaturation of urine, especially with reduced water
intake.

Salicylic acid may be polymerized to form large micelles, which may then
coalesce and precipitate in the urine protein to form a nidus, which continues
to grow in the presence of supersaturated urine.
B- pH of the urine:
PH of the urine has an effect on the solubility of some salts. Although
formation of siliceous calculi unaffected by changes in the urine PH, the
acidification of urine favors the dissolution of stones and reduces the
incidence of such calculi.
Mixed phosphate and carbonate calculi usually formed in alkaline urine than
in acid urine. So addition of ammonium chloride or phosphoric acid
decreases the incidence of calculi in fattening animals. This mainly due to
the effect of pH on urinary calcium citrate, which acts as buffer in urine
maintaining calcium in a soluble stake by formation of soluble calcium citrate
complex which is not dissociated.
Deposition of citrate contents favors the precipitate of solutes. Concentration
of urine favors the precipitate of solutes.
C- Water intake:
Obstructive urolithiasis occur a most frequently in winter season, and
reduced water intake is thought to result in increase concentration of
crystalloids in the urine.

(3) Factors favoring concretion and cementing:

Mucoprotein, especially mucopolysaccharide fraction may act as
commenting agent favor the formation and development of urinary calculi.
This may be the fact in the fattening steers that feed on:
High concentration diet with low roughage.
High phosphorus contents in the diet.
High level of mucoprotein in urine of fattening steers may result as rapid
turnover of supporting tissues in those animals making rapid gain in body
weight
High concentration diet rapid gain in body weight.

Rapid turnover of supporting tissues.

High level of mucoprotein in the urine.

Chemical composition of calculi:

It varies and depends mainly on the dietary intake of individual elements.
Calcium, ammonium, and magnesium carbonate are the common calculi in
cattle and sheep. Calcium carbonate and phosphate are more common in the
Horse. Silicon calculi are common in grazing cattle and sheep.
Calculi may be found as one stone, or more than one or as amorphous
sediment. They may be large and smooth or small and rough.

Clinical findings:
Calculi in the renal pelvis and ureters are not usually diagnosed clinically; but
rectal examination may help in diagnosis of urethral calculi especially if they
accompanied by hydronephrosis.
The animal is in state of restlessness, switches its tail, and may kick at the
abdomen and strains in attempts to urinate.
Frequent, painful urination with straining and grunting (in case of partial
obstruction).
Dribbing of Blood-Stained urine if complete anuria is not present.
Pulsation of the urethra at the ischial arch, which could be palpated rectally.
Swelling and hypersensitivity at the sigmoid flexure may be noted.
Rectal examination reveals distended bladder, which usually ruptures within
48 hours in complete obstruction.
In steers, calculi usually lodge at the proximal sigmoid flexure, while in rams,
bucks and withers, calculi are usually at the urethral process.
Pulse, respiration and temperature may be elevated in diseased sheep at
goats.
Finally, Azotemia develops.

Three common clinical entities occur in urolithiasis syndrome:

Urethral obstruction.
Rupture of the bladder.
Rupture of the urethra.
Urethral obstruction could be confused with many disease conditions and
must be differentiated from:
Bowel obstruction.
Tenesmus with enteritis, coccidiosis.
Acute indigestion.
Rupture of the urethra:
In the early stages, ruminant often go undetected resulting in necrosis with
eventually perforation of the urethra at the site of obstruction.

The most prominent clinical findings include:

Urine leaks through the defect and accumulates in the subcutaneous tissues
along the sheath and ventral abdominal wall resulting in ventral swelling or
what is called water belly.
Depressed appetite.
Rectal examination reveals either collapsed or partially distended bladder.
Rupture of the urethra must be differentiated from subcutaneous
abscessation, umbilical abscessation, umbilical hernia, haematoma of penis
and infected of the
Prepuce.

4- Rupture of the Bladder (Cystorrhexis)

This is the most serious sequel to urethral obstruction. When the bladder
ruptures, an initial relief occurs and clinical signs of that case may not
appear for 1-2 days later. By the next few days, uremia becomes severe,
progressive to severe depression; anorexia and dehydration could be
observed.
Ventral abdominal swelling may be detected by ballottement and urinary
bladder may not be palpated rectally. Rupture of the bladder is usually on the
dorsal aspect; it may consist of multiple holes or of single large tear.

Congenital defects of the urinary tract:

Previous or patent urachus = Urachal leakage.
Urethral Artesia: It is recorded in calves, and is manifested by failure to pass
urine and distension of the patent portion of the urethra.
Hypospadias: It means imperfect closure of the external male urethra in
newborn animals mainly in lambs. It is usually accompanied with
other neonate defects including atresia ani, and diaphragmatic hernia. The
cause is unidentified
Ectopic ureters: The ectopic ureter opens into the urogenital tract at a
place Other than such as cervix, urethra or vagina. The condition may be
unilateral with urinary incontinence from birth as major clinical sign.
Renal hypoplasia and dysphasia: Bilateral hypoplasia is recorded in piglets
and horses. Affected animal may be die at birth, few days or months after
that. In diseased animals, there were gradual onset of anorexia, weight loss
and lethargy.
Polycystic kidneys.
Rupture of the bladder.

Hydrothorax

INTRODUCTION
Hydrothorax is a typical pathological condition of the body
characterized by accumulation of water in the lungs, thoracic cavity or in
between the parietal & visceral pleural sac. It may also be a consequence of
unhygienic & in sterile laparotomy. It is generally seen in almost all lomestic
& wild animals & sometimes takes chronicity bringing about the fatal
consequences.
Hydrothorax is usually see as part of general oedema due to
congestive heart foul we (CHF) or hypoproteinaemia. Hydrothorax is also
associated with African horse sickness or bovine viral leucosis as the
secondary pathological condition. Chylous hydrothorax which is very rarely
seen may be due to ruptured thoracic duct. Hydrothorax is sometimes
accompanied by Pneumothorax. If any sort of infection is present,
hydrothorax may change into pyothorax due to the infection of pyogenic
bacteria which is characterized by muco- pwculent discharge from nostril.
Hydrothorax can generally be treated/ corrected by the aspiration of fluid but
it is not the reliable & permanent treatment.
ETIOLOGY
a)
b)
c)
d)
e)
f)
g)
h)
i)
j)

General heart failure:Congestive heart failure. (CHF)

Renal disorder
pericardial effusion
Hypoproteinaemia
Injury to Vagus nerve
Liver to disease
Pulmonary Neoplasia
Pleural Neoplasia
Diaphragmatic hernid etc

PATHOGENESIS:

Accumulation of fluid in the pleural sac causes compression

ateletasis of the ventral portions of the lungs & the degree of atelectasis

governs the severity of the resulting dyspnoea compression of the atria by

fluid may cause an increase in venous pressure in the great veins.

Presence of predisposing & exciting factors

Congestion, Inflammation of bronchial & alveolar

epithelium along with
Parietal & visceral pleura

Infiltration of neutrophils & secretion of straw colored exudates in the pleural

sac

The exudates becomes muco purulent /purulent if secondary infection

of different
Pyogenic bacteria / virus/ fungus

More & more fluid accumulation resulting into hydrothorax if untreated

timely.

Fig: - Mechanism of development of hydrothorax.

SYMPTOMS & CLINICAL FINDINGS

There is dyspned which usually develops gradually & an absence of breath

sounds accompanied by dullness or percussion over the lower parts of the
chest.

Ante mortem findings

Bulging of intercostals muscles in thin animals.
If fluid is sufficient, there is compression of the atria.
Engorgement of jugular veins.
Jugular pulse of increased amplitude.
Signs identical with other forms of pleural effusion.
Fluid usually accumulates in both th side.
Dyspnoea without fever.
oedema in other dependable parts of the body

CLINICAL PATHOLOGY & HISTOPATHOLOGY

Thoracic puncture will be followed by a flow of clear serous fluid. The
fluid is bacteriologic ally negative but may contain protein. Due to the
necThoracic prosis congestion & swelling of alveolar epithelium, typical
squalors epithelia are found to be distorted in appearance. Anisocytosis with
many food & water vacuoles are found.

DIAGNOSIS

Hydrothorax can be differentiated from the hem thorax by the absence of

pain, toxemia, and fever by the sterility lesions of the thorax including
tumors are not characterized by the accumulation of fluid. Radiographic
evidences are the only tool of laboratory diagnosis. Apparently, spot
diagnosis can be done with the help of typical signs & symptoms of the
disease.

TREATMENT

First of all primary conditions must be treated. If the dyspnoea is severe,

aspiration of fluid from the pleural sac causes a temporary improvement but
the fluid usually reaccumulates rapidly parenteral coagulants & blood
transfusion are rational treatments in severe hydrothorax surgical intervenes
followed if not corrected by aspiration of fluid. Correction of etiological
factors is done with appropriate measures for the elimination of the cause of
hydrothorax.

PREVENTION
Protection from the various predisposing factors & early treatment of
the animals with acute & chronic respiratory diseases are some of the few
measures of prevention. No clear evidence for the best treatment is available
hence for prevention liver & lung function & life expectancy should be
considered. Depending up on this assessment TIPS, single session
thoracovideoscopy with closure of diaphragmatic defects &/or pleurodesy
can be considered. High dose octreotide should be tried.
Epistaxis (symptom rather than a disease)

Bleeding from hose whatever the origin.Hapmoptysis-bleeding duving

coughing usually originating from lungs.

Susceptible animal
prone.Cattle-rane.

form

Epistaxis:

-Horse-

most

prone

Dogs-

Etiology: Horse Lesions of nasal cavity, naso-pharynx, nycotic infection of

guttural pouch(due touleration of artery)

Resions of lungs.
Pulmonary lesions.
Exercise induced haemorrhages.
Tranmatic injung , mechanical injung due to stomach tube while
passing.
Space occupying growth(e.g. granuloma, fumor etc.)
Nalsal maggot infn

Dogs

Nasal polyps.
Shake venom causing clotting defect.
Thrombongtopenia
Copper, phosphorus & mercurial poisoning.
Glanders.
Genetic,horedilong.

traumatic injung.
Cattle- Bracken fern
Moldy sweet clover
Symptoms: I)
II)

Either unilateral or bilateral nasal bleeding.

Bleeing may be small in quantity-just paint or it may be huge
ever from mouth.Massive bleeing from nostril- rhinorrhagio.

Diagnosis: I) By clinicla symptom.

D.Diagnosis :-

1) Mycotic uleration unilateral bleeing. Of guttual pouch

2) Race induced epistaxis- during race of the horse.
3) Traumatic/ machanical polyps,grassloma- by careful examination
& history by endoscope.
4) Phangeal lesion induced expstaxis- frequent swallowing & short
cough.
5) Thrombocy topenia- blood examination.
6) Epistaxis due to poisoning by history.
7) Haemoptysis bleeing from lungs should be
Haematemesis- bleeing from stomach d ifferenttialted

I) Color

Haemoptysis

Haematemetis

ii) pH

Alkaline

Acidic

iii) Farticle mixed

Spcitum

c food

iv) Symptoms

cough

vomiting

Treatment: -

I) Rest the animal

II) Isolate primary cause & treat accoudingly.
III) Treat if the consequence is of systemic disene e.g. glandes in
hope, poisoning etc.
IV) Use cold park at frontal & nasal bones.
V) Drop dilute epinephrine (1:5*104) into the nostril.
VI) Inject adrenochrople(nemostatic) in seven condition
VII)
Pllgged c epinephrine soaked cotton.
VIII)
Vit k, & ca therapy helps in blood clotting
IX) In save, blood hansfusion.
X) In none race induced hemorrhages use of
Coagulants
Estrogens
Fursemide
Are used but the reason is not known.
Expentional clenbutero
Atropine
B Laryngitis

Inflammation of langnx (vocal card) and bronchi is called ~ & ~.

It is characterized by cough, difficult or noisy inspiration. It is
difficult to differentiable the again of as passage which is
affected.

Antilogy: -

Cattle - infections bovine rhino tracheitis

calf diptheria (haemophilus somnus)

laryngeal abscess (due to congenital convitation of artesxoid
cartilage)

Sheep - Chronic infn of actinomyces pyogenes.

Horse- Equine herpes virus

Pig

Equine viral artiritrs

Equine viral influenza
Strangles (strep equs)
- Swine influenza

Symptoms :-

Coughing and inspiratory dysphoea.

In acute laryngitis: - soft tissues around larynx (swollen)
enlarged & pain ful.
Painful cough.
Increased Temperature & Toxaemia.
Cannot eat & drink.
Deep respiration; force ful & prolonged inspiration.
Death of animal due to asphyxia.

Diagnosis: In larygitis :- Coughting & inspirating dysphoea.

Large sound on anscultation.

Confirmative by largngoscopic examination.
Excessive quantity of mucus, may be c flecks of blood or pvs in
the pharynx.
Bronchitis Need especial endoscopic examination.Difficult in
differential diagnosis from pneunmoniya.
Treatment: 1) Rest the animal & provide concortable environment. viral inf n
will spontaneously corrected
2) Beacterial infn use broadspectus antibiotics, or soffar.
3) Diphtheritic calues are treated by sulfamethazine
4) Dexamethasone & antibiotics in largngeal abscen.
5) In chondritis broad spectur for 3 weeks or more.
6) In dyspnoea use tracheal tube for emergecy.

Verminous bronchitis

Brochitis due to parasitic in festation is called.

Symptoms:

Coughting dry & nasal discharge.

Gradual loss of body condition & prodn
Abaemia , hypo-proteinaemial & occasional edema.

Diagnosis:
i) on fie-1st stage larra & omm.
ii) On nasal discharge- larrae examination.
iii) Eosinophilia on blood DLC.
Treatment:
I)
a)
I)
II)

Filarial worm treatment:

larva by diethyl carbamazine @ 40 mg/kg-daily
adult: feribendazole, albenda,or levamisole invermeetin.
Lung warm by ivomec

BRONCHO-PNEUMONIA
The inflammation of the lung parenchyma usually accompanied with the
inflammation of the bronchioles is broncho-pneumonia. The term
pneumonitis literally means inflammation of the lungs. This term is used by
the pathologist .But, recent view indicates that in pneumonitis the walls of
the alveoli show prominent changes whereas in pneumonia the alveolar
lumen reveals most characteristics changes. It is manifested clinically by
rapid shallow breathing, cough, fever with adventitious vesicular sounds like
rales, ronchi etc. Bacterial pneumonia may produce the signs of toxemia. All
species of animals irrespective of ages suffer from pneumonia.
Aetiology
A. Predisposing factors
Exposure of animal in damp place and cold environment.

 Housing in an ill ventilated room.

Exertion due to extensive work.
Long transport by train or ship.
Severe hunger.
Chronic under nutrition.
Exposure to cold wave during winter month.
Sudden changes in weather.
Cardiac weakness.
Recumbence for a long period of time.
Other debilitating diseases.
Inhalation of dust, irritating vapors.
Pneumonia frequently develops in animals that have been heated and
then rapidly chilled.
B. Exciting factors
Bacterial agents
Cattle; Streptococcuc Spp., Staphylococcus Spp., Corynebacterium
pyogenes, Klebsiella pneumoniae, Mycoplasma mycoides (contagious
bovine pleuropneumonia), Pseudomonas Spp., (Mycobacterium
tuberculosis) , Sphaerophorus necrophorus.
Horse; Streptococcus equi, Staphylococcus aureus, Corynobacterium equi,
salmonella Spp., E. coli, pasteurella Spp., Pseudomonas Spp.
Sheep and Goat ; Streptococcus Spp., Staphylococcus Spp., Pasteurella
Spp , Corynoacterium pyogenes., E. coli., Mycoplasma Spp., Actinobacillus
lignieresi.
Pig; Streptococcus Spp., Haemophilus suis, Pasteurella multocida.,
Corynobacterium pyogenes ., Bodetella bronchiseptica., Mycoplasma Spp.,
Salmonella Spp., E. coli.

Dog; Bordetella bronchoseptica. , Klebsiella pneumoniae ., E. coli.,

Pseudomonas Spp.
Cat; Streptococcus
Mycoplasma Spp.

Spp., Staphylococcus Spp., Haemophilus Spp.,

Viral agents
Cattle; Viral pneumonia of calf, Para influenza - 3, Adenovirus, Rhinovirus.
Horse; Equine influenza, Equine infectious pleuropneumonia , Equine viral
Rhinopneumonitis , Adenovirus.
Sheep and goat; Sheep pox, Goat pox, Maedi (progressive interstitial
pneumonia), Jaagsiekte (pulmonary adenomatosis), Infleunza virus type A2,
Reovirus, Adenovirus.
Pig; Swine influenza, Virus pneumonia of pigs.
Dog and cat; Feline viral Rhinotracheitis, canine distemper, Canine parainfleunza, Canine adenovirus type-2, Infectious canine hepatitis virus,
Roevirus , Herpes virus.
Fungal agents; Aspergillus fimigatus (Aspergillosis ) , Histoplasma
capsulatum (Histoplasmosis), Blastomyces dermatitis (Blastomycosis) .
Coccidiodes immitis (Coccidiomycosis) Cryptococcus neoformans
(Cryptococcois).
Parasitic agents; Dictyocaulus viviparous in cattle; Dictyocaulus filarial in
goat and sheep; Dictyocaulus arnfield in horse, Metastrongylus apri in pig;
Protostrogylus rufescens in sheep and goat; Ascaris Spp., in calf and pig:
Muellerius capillaries in sheep; Toxoplasma gondii in sheep; Aleuristrongylus
abstrusus in cat; Angiostrongylus vasorum in dog; Pneumocystis carinii in
dog; Paragonimus westermani in dog and cat; Toxoplasma gondii in dog
and cat. Filaroides milksi and Filaroides hirthi in dog. Migration of larvae
of Toxocara canis, Toxocara cati ,Strongyloides stercoralis and
Ancyclostoma cannium.
Physical agents; Aspiration of fluids, drugs, chemicals etc. Inhalation of
dust, pollen, smoke, gas, chemical and medicinal vapour. Dipping of animals
for ectoparasitic treatment (dipping pneumonia).

Pathogenesis; the offending agents must have to break the pulmonary

defensive mechanism to set up inflammatory processes. Mode of
transmission is usually an extension of tracheo -bronchial disease, spread of
systematic diseases to the lungs and primary involvement of lungs.
The process by which pneumonia develops varies with the causative agents,
their virulence and the portal if their entry into lung parenchyma. The entries
of transmission are as follow;
Tracheo- bronchogeneous; This is the most common route. Some
infectious agents like Aspergillus fumigatus , Strepto and Staphylococcus , E.
coli ,C. pyogenes etc. invade the lungs through this route.
Clinical finding
This may remain in association with bronchial and pleural infection.
Moist, painful, productive cough; Cough is paroxysmal in nature.
Nasal discharge is serous at initial stage but with the progression of the
disease, it will turn to mucoid , mucopurulent to purulent.
Rapid shallow respiration (polypnoea) is the characteristic sign of early
pneumonia. Respiration is abdominal in type.
Dysponea and labored breathing occur in the later stages when much
of the lung tissues become non functional.
There is sharp rise of body temperature.
Anorexia, dullness, depression and an increased pulse rate.
Gradual loss of body condition.
Reluctance to move, Tendency to lie down.
Stand with abducted elbow with extension of head and neck.
There may be the signs of pain on palpation.
On percussion dull sound may be heard if there is consolidation.
Auscultation will reveal adventitious sounds. In the early congestive
stages of broncho- pneumonia and interstitial pneumonia, the vesicular
murmur is very prominent. In the latter stages, rales develop in
broncho -pneumonia but in uncomplicated interstitial pneumonia clear,

harsh, bronchial tones are audible. In consolidation, bronchial tones are

the only sounds audible over the affected lung but moist and crapulent
rales can be heard at the periphery of the affected part. Consolidation
also causes increased audibility of the heart sound. When there is
concomitant pleurisy it may produce pleuritic friction rub in the early
stages and muffling of sound in the late exudates stages.In chronic
case, there will be dry rales (ronchi) - sibilant or sonorous on character.
Neutrophilia is the feature of bacterial pneumonia.

CLINICAL PATHOLOGY
i.
ii.
iii.

iv.
v.
vi.
vii.
viii.

Cultural examination of nasal discharge and swab.

Aspiration of tracheal and bronchial exudates and their culture,
isolation of organism and in vitro antibacterial sensitivity test.
Blood examination for W.B.C. and R.B.C., E.S.R. and
haemoparasite. Neutrophilia in bacterial infection,
neutropaenia in viral infection and eosinophilia for parasitic
infection. Increased E.S.R. in chronic wasting disease.
Serological tests for viral infection.
For deep mycotic infection serologic tests like Agar gel immunediffusion test has been found to be satisfactory .Precipitation test
and the complement fixation test are also used.
Examination of faeces to recover parasitic ova.
Radiographic examination.
For other tests refer earlier page.

DIAGNOSIS
Respiratory distress may result from involvement of other systems.
Congestive heart failure, the terminal stage of anemia, hyperthermia and
acidosis may show respiratory problem. But, the above condition will not
show any adventitious sounds characteristic of pulmonary disease.

Pulmonary oedema; No fever and toxemic manifestation.

Emphysema; No fever and toxemic manifestation; expiratory disponea.
Pneumothorax; Collapse of lungs.
Pleurisy; Pleuritic frictional rub on auscultation.

Upper air way diseases; Signs like respiratory disorders; cough,

adventitious sounds may be observed. But the sounds are mostly marked in
inspiration. In pneumonia, sounds are audible in both inspiratory and
expiratory phage.

LINE OF TREATMENT
1) Insulation of affected and careful surveillance of the remainder
group.
2) Use of specific antibacterial agent is desirable.
3) 3) Penicillin 20-40 lakh i.u. for large animals and 4-8 lakh i.u. for
small animal for 5-7 days. Streptomycin sulphate 2.5-5 g. For
large animal and 0.5 to 1 g for small animal for 5-7 days through
intramuscular route. Besides ampicillin , amoxicillin or
tetracycline , cephalexin, alincomycin, cotrimaxazole may be
used.
4) Sulpha drugs may be used. Sulphamezathine (33.5%)solution or
sulphadimin (33.5%) solution _15-30 ml/50 kg body weight
through intravenous or subcutaneous route.This gives promising
through in pasteurellar pueumonia (H.S.)
5) Trimethoprim and sulphadiazine / silphamethazole preparation
may be used preferably in small animal.
6) In parasitic pneumonia, drugs like Diethylcarbamazine citrate,
tetramisole , levamisole , fenbendazole etc. may be used.
7) In fungal pneumonia, Grisovin or nystatin is used. In small
animal like dog and cat Amphotericin-B @ 0.5 mg/kg body
weight. The calculated dose may be added in 500 ml 5% solution
of Dextrose and be given slowly through intravenous route.
Ketoconazole @ 10 mg/kg three times per day orally has been
found to be efficious.
8) A course of antihistamins should be given.
9) A course of steroid is found to be helpful in some cases.
10)
Sedative expectorant e.g. Pot. Iodide; stimulant
expectorant e.g. Ammon carb; inhalant expectorant e.g. Tr.
Benzoin Co. may be used depending on condition and nature of
cough.

11)
Analeptics e.g. Leptazole, Nikethamide 3 to 5 mg/lb body
weight through subcutaneous or intramuscular route.
12)
Vitamin C and calcium therapy may be done to rejuvenate
the pulmonary parenchyma.

Pneumothorax
Entry of air into the pleural cavity
embarrassment and collapse of the lung.

leading

to

respiratory

Etiology:
1) Rupture of lung.
2) Puncture of chest wall.
Rupture of lungs due to:

Rib fracture by traumatic injury.

Rupture during contusing in weekend parenchyma condn e.g.
Emphysema.
During thoraco centesis.

Pathogenesis
Loss of negative pressure in pleural cavity collapse death due
to anoxia.
Symptoms: - I) Unilateral in farm animals & bilateral in house
II) Inspiratory dyspnoea & total terminate.
III) If unilateral, the affected side does not show respiratory
movement where on the other shows compensatory function
leading to more bulging.
IV) Absence of normal resionant murmur sound on a affected side,
& heart apex beat & hearth is displaced to unaffected side.
V) Introduction of infective agent leads to serious pleurisy.
Diagnosis :
i) By clinical findings.
Differential diagnosis :

i) Diaphragmatic hernia rare in farm anima.

Occurs in traumatic reticulitis & not manifested by respiratory
problems.
ii) Large herniation cause respiratory stress.
With liver, stomach- Peristaltic movement on & intestine
auscultation
iii) Radiographic examination Shows
displacement of heart & mediastinum.
Treatment :-

collapse

of

lung

i) Effort to create live pressure inside the pleural cavity by using

a needle with in to the pleural cavity
ii) Use of Heimlich chest drainage value.
iii) Rest the animal & check not allow to develop pleurisy.
iv) Traumatic cases by surgical correction.

Asthma :

~ a condition of painful expulsion of gases with effort of

course.
Etiology :

Farm animals bronchitis

Horse
- cause/or broken wind
Birds
- fungus Aspergillosis.
Man
- Summer asthma due to fungus, pollen allergy
In all
- May be nervous origin.

Symptoms : - Painful expulsion of gases.

In day, chronic bronchitis leads to asthma in which respiratory

distress in irregular interval.
Diagnosis : By symptoms.

Differential. Diagnosis

In horse by broken wind.

Treatment
i) amyl nitrate inhalation
ii) antispasmodic
iii) antihistaminic
Regular exercise & diet.

Broken wind-specific to horse(heaves)

Substituted by-long standing respiratory disease

~double effort-to expire the air ducts several pathological processes
in the lungs.

Causes : Chronic pathological condn of lungs due to str. equi

Hypersensitivity to reaction.
Allergic reaction due to extrinsic factors.
Chronic bronchitiss.
tumor, parasitic disease.
Pathogenesis :All causes over inflation of alveoli(called functional emphysema)destruction of alveoli; reduces surface area for gross exchange, &
pulmonary vascular bed loss of elasticity of lung.
Sign : I) Active contraction of chest & abdominal muscles
II) Double expiratory effort.

III) Hypertrophy of rectus abdomintus muscle & formation of

heaves line beneath the posterior aspect of the cage- a
feature of the condition
IV) Dry cough short & shallow.
V) Faster breathing, wheezing, nasal discharge & intolerance of
exercise.
Diagnosis : - I) Clinical symptoms.

Diff. Diagnosis :
i) Detailed clinical examn is recommended.
ii) Evaluation of corticosteroid & drugs response.
iii) Serological test
iv) Autopsy.(pm examination)
v) Long worm, tuberculosis & hydatid cyst.
Treatment I) Not so effective except the primary cause treatment.

Rhinitis
(Nasal catarrh,coryza.)

Defn:

Inflammation of the nasal mucous member manifested by

serous, mucous, sero-mulous or muco-purulent or purulent
discharge.
Classification :1. Acute
2. Chronic
Acute rhinitis :- ( serous or mucoid type)

A eitiology :- predisposing fefor Too cold or humid weather.

Ill ventilated shed or shed c fumes dust, smokes,

density.

stocking

 Chemical vapaur like NH3,CL2,S.

Shress of hard working, & malnutrition.
Sudden change in weather,& individual susceptibility of animal.
Exciting factor
i) Viruses
- eq. Para influenza canine distemper
infer. Bovine rhinorsacheitis.
ii) Bacteria
eq. Strepto,staphy, stranges, pastenvella etc.
iii) Fungus
Aspergillus fumigatus
Rhino sporidius
Mucor
iv) Parasites

- Schistosoma nasalis in cattle

Oestrus ovis in sheep

Syngamus level in cat
v) Allergic foutors- pollen grains

dust, somkes, fumes.

vi) Adeno carcinoma- causes unilateral rhinitrs.
vii) Other - infection of sinuses, traumatic injung etc.

Clinical symptoms :-

1. Either Uni.- or bilateral discharge. Discharge. Discharge may be

copius or scanty and serous, mucous or purulent, is the
characteristic.
2. Continuous or intermittent discharge may be greenish, toetid
nad musty odor.
3. Frequent sheezing and general malaise in allergic one.
4. Erosion of nasal mucosa, evythema or ulceration.
5. Due to limitation animal shakes and rubs the nauzzle & nose
may lead to bleeding.
6. Conjunctivitis & sub-maxillary lymph node may be enlarged.
7. May increase body tempr due to bacteriemia or viraemia.
8. Course of disease varies from 4 to 10 days.
Diagnosis
1. By clinicl symptoms.

Differential diagnosis:1. Bilateral discharge-may be originated from lungs, trouble, with

nasal irritation pharynx & bronchi.
2. Discharges only when head is lowered may be due to
empyema & intermittent para nasal sinuses.
3. Purulent, continuous
Unilateral discharge- Infn of guttural puch without nasal
limitation
4. Discharge from lacrymal infn of conjunctiva..
duet(careful examination)
5. Discharges with ingested- pharyngitis & esophageal obstruct
material.
6. Infectious cores of Rhinitis increased body temperature . i.e..
persistent Bovine malignant catarrh- Mortality high. Rinder
pest,
Inclusion body rhinitis in pig plaque adher to
hair,face,eye,lashes.
7. Parasitic by fie or nasal swab.

Treatment:1. Correct predisposing factors and isolate the specific cause of

rhinitis.
2. Wash the nasal arific by physiological soln.
3. In cases of infections by virus, bacteria use antibiotics.
I) pro. Penicillin @ 10-40 lakh i.u. 5-7 days l.animal.
@ 4-8 lakh i.u. 5-7 days s. animal.
II) streptopenicillin @ 20 lakh or 2.5
III) tetracycline or oxytetracycline @ 2-5 mg/kh I/mnI/
IV) suitamethagine, sulphadimidine 331/3% @
1 gr/7.5 kg for large animal.
1. Use antiseptic inhalant vapour of t.t. oil, in benzoin, in camphor,
creolin etc. it will help to expel the expectorant.
2. 1 % chlorbutol (anivalferial & antifimgal agent) sol n in liq.
Parathin is dropped- small animals.
3. Anihistaminic ing.- in sllegic.
4. In fungal :Thaibendazole @ 10 mg/kg body wt. Sith 10-20 ml. Water
bid c nasal tubes

@ 20 mg/kh b.oot. daily daily*6 weeks

Chronic rhinitis:-

Mucopurulent nasal discharge.

Aetiology

1
2
3
4
5
6
7

Sequelae of acute rhinitis.

Adeno carcarcinoma- malignatit tum.of esithelium.
Empyema in tecth & sinuses.
Chronic schistotoma nasalis infn in cattle.
Chronic tunges infn chronic funges infn
Infestation by pasture miles ex. Tyrophagus palmarum
Glanders in horse (actinobasellus malles)

Symptoms: 1. Muco-purulent nasal discharge.

2. May be congosted and ulcerated MM.
3. May ve extension of head or neck.
4. Difficult in respiration.
5. Enlargement of sub-maxillary lymphnode.
Treatment: -

1) Specific treatmentE.g. Granuloma by anthiomalin @ 20ml I/m tollowed by 15ml I/m

at 3 days internal 2 injections.
E.g. Rhinosporidiosis-hy surgical correction.
2) Systemic antibiotics & sulfa-dmags.
3) Multicstamins to restore vitality.
4) Acetylarsation soln to increased circulation at the sile of inth
small animal: 9.4% acetyl AR. 2ml I/m x on alternated .- animal
23.6% acefyl ar. 10ml I/m x on alternated
Pneumonia

Inflammation of lung parenchyma uscally accompained

inflammation of bronchioles & ofted by pleurisy. Characferiged by respiratry rate

by

cough
abnormal breath suounds son ansculation
toxaemia (in boterial pnenmonia)
Broncho pneumonia : - involement of bronchioles
Plenro

- pneumonia : - involement of pleurisy.

Classification : -

i) According to extension or involement :

a) Broncho pneumonia.
b) Plenro- pneumonia.
i) According to origin.
a) Primary pneumonia.
b) Secondary pneumodina.(miral complicated by buteria)
i) Accoding to etilogical:
a) Viral pneumonia
b) Boneferial
c) Fungal
d) Parasitic
e) Aspiratory
f) Inhalation
g) Allergic
h) Hypostatic done to accumulation of flurid
i) Chemical ogent
j) Physical ogent
1) According to lesions:
i) Lobar pneumonia whole love invoived
ii) Lovular pneumonia less localized & patchy
iii) Intersitital - inflammation of fibrons tissues than parenchyma
iv) Alveolar pneumonia- involvement of alveolar wall.
v) Embolic pneumonia - done to foreign material obstructed type of
lession.
vi) Granulomatous pneumonia overgrowth.

Etiology:

Pre-disposing factors: These factors dont produce/establish pneumonia but help in the
establishment of disease; these are similar on in other user respiratory
tract infection.

Aetiology of pneumonia: -

1. Bacterial agents :
Cattle: Strep to cocues spp

Staphylococues spp
Caryneboreferium pyogenes
Klebsiella pneumoniae
Mycoplasma mycoides (CBPP)
Pseudomonas spp
Mycobacterium tuberculosis
Spherophorus necrophorus.
Horse: - sheptococeus equi

staphylococeus qureus
corynebare terium eques
salmonella spp
pasteurella spp
pseudomonas spp
e.coli
Sheep/goat

Strep tocous spp

Staphylococcus spp
Pastenrella spp
Corynebase terium pyogenes
Mycoplasma spp
Actionbacillus

Pig - salmonella spp

Dog:

streptoccus spp
pasterrella multocida
c. pyogenes.
Bordetella bronchospetica
Haemophilus suis my coplasma spp, e.coli
- Bordetella spp
kelbdiell pneumonia
e.coli
psendomonas.

1. viral/causes: Cattle Parainfluenza-3.

Adenovirus
Reovirus
Viral pneumonia of calf
Horse: -

Equine intluenza
Quine infections plenro-pneumonia
Equine viral rhino pneumonia
Adenorvirus
Sheep/goat: -

Maedi ( progressive interstital/pneumonia)

Pulmonary adenomatosis(jaagseekte)
Influenza virus type A2
Reo virus
Adenovirus.
Sheep/goat pox
Pig -:

Swine fluenza
Virus pneumonia of pigs.
Dog/cat : -

Feline viral rhinotracheitis

Canine distemper
Canine para influenza
Infections canine hepatitis

 Reovirus,herpes virus, canine adenovirus type A2

1. Fungal cause :

1.

Aspergillus fumgigatus
Histoplasma capsulatum
Blastomyces dermatitidis
Cowidioides immitis
Cryptococess heoformans.
Parasitic
Sheep/Goat :- Dictyoculus filaria

Protostrongylus rufescens
Toxoplasma gondii
Cattle : - Dictyocaulus viviparus, ascaris spp.
Horse : - D. arnfeldc

Parascaris equorum
Pig :- Ascaris spp

Meta strongylus apri

Dog: - Toxpplasam gondii

Tpxpcare canis
Angiostrongylus vasorum
Anoylostoma caninum
5 Physical agent:
Aspiration of fluids,drangs, chemicals etc.
Inhalation of dust, pollen,vapour etc
Dipping pneumonia.
Systmic mycoses.
Pulmonary consolidation & fibrosis by toxins.
Pulmonary defense mechanism: BALT:Broncho associaned
Lymphoid tissue T cells.
Any stressors
The pulmonary detense mechanism
Weaning.
Transport
Fumes

*
*
*

Ill ventitation
Deprived feed
Change of weather

I) Aerodynamic filtration by nasal carities.

II) Shrezing
III) Local nasal antibody
IV) Laryngeal retlex
V) Cough reflex
VI) Muco-cilling transport mechanisms.
VII)
Alveolar machrophages
VIII)
Systemic & local antibody.

More than 10mm size 100%Partieles are removed by mucosal

surface of upper
More than 5 mm size 80%Respiratary tract

Particles 1-2 mm settle in alveolar spaces due to gravity

Paritcles less than 0-2 mm settle in alveolar spaces due to diffusion
of air
These partieles must be cleared by alveolar
Macrophages otherwise this predispose to pneumonia.

Susceptible animal

Is cattle

Because it has: -

I) Small physiogical gasesus exchange capacity

* 100 alveslar or bronchiolar o2 level law o2 tensic
*
pulmonary detense mechanism.

I) Greater resultant basal ventilalong activity :

* inspired as move contaminated c intectious, allergenic or
noxious substances
II) Lung has greater degree of compartmentalization
* Airway hypoxia peripheral to airway
* reduced phoyocytosis retension of infectious agent develop
pneumonia.
Portal of entry :Clinical symptoms: -

1. Rapid, shallow respiration cardinal sign. & early pneumonia

dyspnoea at
latter stages.
2. Cough, type varies c nature of lesion.
a) Broncho pneumonia accompained by moist, apinful cough
b) Interstitial pneumonia accompained by dry hacking cough
3. Cyanosis- when large areas of sung affected.
4. Nasal discharge may or may not.
5. Order of breath varies :i) Decay odor when large amount of pus in air passage
ii) Putrid eq. Pulmonary gangagrene. In horse.
6.
Bacterial broncho pneumonia Toxaemia, anorexia,
depression
tachycardia & reluctance to move & lie down are common
in early.
1. In chronic broncho-Pneumonia,there is chronic toxaemia, rough
hair coat & a gaunt appearance.
2. - Heart rates & moderate persistent fever.

3. In advanced pulmonary disease, - grunt on expiration & open

mouth breathing.
* copious bilated muco purulent nasal discharge.
* Chronic productive cough.
* On auscultation large breath sounds.
1.Bacterial pneumonia :-

It is associated
with pleural and bronchial infection. Cough is most, painful and
productive.
*

Nasal discharge is serous type in beginning as the disease

progresses it turns to muciod, muco-purulent or purulent.
* Polypnoea in tintial stage of pneumonia.
* Respiration is abdominal type.
* Dyspnoea due to non-functioning of lung tiesues in latter
stages of pneumonia.
*
Tempr.
* Anorexia, dullness, depression is observed
* Reluetance to move and animal lie down.
* On palpationj,sign of pai.
* In the early stage of broncho- pneumonia murmur sound is
prominent. At the periphery of the attected part, orepitating
sound is produced.
* Neutrophilia is the feature of bacteriall pneumonia.
2. Viral pneumonia
There will be dry and unproductive cough. Nasal
discharge will be serous in the beginning followed by mucopurulent. Nasal discharge becomes purulent because of
bacterial infection. Polypnoea & in tempr. These will be
dehydration and emaciation. Loss of appetite, Neutropenia and
lymptocytosis.
3. Parasitic pneumonia or verminous pneumonia :
There os cough & it becomes frefquent and dishessy.
Protrusion of tongue. Mucus and sometimes with worm
congh is out. Nasal discharge is sero-mucoid. Loss of body
condition but tempr is normal. Emaciation and anorexia
sometimes with diamhoea is niticed. There may be edema
of sub-maxillary region,exy lid. Animal become bey weak,
tall do & die.

4. Mycotic pneumonia :There will be most cough and mucoid

nasal discharge. Dyspnoea, emaciation & loss of strength respiration
os abdomianal thpe, stimulating diashreymatic hernia. There may be
hemorrhagic nasal discharge & the expectorated mass will be green or
yelow color. Anaemia & dehydration. Tempr may be due to II nd ary
becterial infn.
1. Aspiratory pneumonia :(fanlty drenching) gangrenous
pneumonia
Mostly it is total. There is always a history of faulty drenching.
Nasal discharge is thick & mucopurulen.

* Portal of entry:
Etioligical agents enter to lungs by :- different ways.

1) Traches bronchogenous route :- The most common way of

infection to aspergilles streptococeus, staphylococcus, Ecoli,
corynebacterium or inhaled porticles/fumes.
2) Hematogenous route :- systemic The entry is through
blood vascular system. Salmonella, pasteurella, and parasitic
lorvae can enter through this route.
3) Penetrating wounds of lungs :- If there will be wound in
pleura by bullet or by accident, boreria can enter throuhg the
lung and cause pneumonia.
4) Through lymphatic system : - First lymph gland is afected
and the bacteria will transfer to lungs through lymph ressels.
Evidence of aspiratory materials in the nasal discharge. Anorexia and
rapid loss of condition. Animal will feel pain onpalpation and
percussion. Protrusion of tongue and mouth breating. Abdominal type
of resp. prognosis in horse is bad or gnarded but in case of coprine &
bovine it is variable.

Diagnosis/ D.Diognosis :Difficult in diagnosis by tow important errors :

A) Whether animal is suffering from pneumonia or by other

infections diseces
B) Matire amd dise pneumonia/ spentic dype.
It ocessb because pneumotia isnot defected clincially become
the abnormal lung sounds are apparently not obvious & presence
of dyspnoea may be due to other diseases of body system.
1.
i) Congtestive heart failure
ii) Terminal stages of anaemia
iii) Poisoning by histortoxic agent
Bnormal
Eg. Hydrocyanic acid

Produce
But not
Respiratory

Embarissment
Sounds
iv) Ju[er thermia Hydrocyanic acid
v) Acidosis Hydrocyanic acid.
2.
i) Pulmonary edema & congestion
ii) Embolism of pulmonary artey Absence of fever & toxaemia.
iii) Emphysema.
3
Pneumothorax Collapse of lungs, absence of breath sounds
- Inspiratory dyspnea

4.
Shallow abdominal type of respiration
* Pleurrtic triction sounds effusion os minimal
* muttling sounds if effusion is maximal
5.
Diseases of upper - More trequent cough.
Respiratory trct
of inspiratory ( laryngitis/Trcheitis) Dyspnoea

Pleuritis

- Vanging degree

* Sounds on mid cerrical reasion to lungs

* But in pneumonia inspiratory as well as expiratory sounds.
5. Cultural examination & DLC for type of pneumonia.

6. Serodigical examination CFT, precipitation test & agou jel

immuno- diffusion test for viral for mycofie.
7. Examination of faeces & radiography in small animal.
Treatment.:-

1. Isolation of sick animal & careful surveillance of the remainder

group.
2. Choice of antibacterial agent on the basis of tentative diagnosis
& previous experience.
3. Long acting antiliniorobial seems feasible but blood level
doesnot reach high as short acting ones. So in seven cases short
acting must be chosen.
4. Treatment of pneumonia may fail due to :
i) Advaced condition of disease
ii) Development of plurisy & pulmonary abssecesses
iii) Dung resistant bactaria
iv) Inadequate dosage of drug
v) Presence of other lesions or disease.
1. Virral pneumonia complicated by mycoplasma may make
treatment failure due to intracellular location of mycoplom
2. Corticosterioid may be used in acute condition.
3. Bronchoditlors eq. Clenbuterol & NSAIDs are ise fi; om jprse &
cattle.
4. Sultas & potentiated sulphas are usefuel inaspiratory
pneumonia.
5. Griseofulun, Nystatin,Amphotericin-B, Keto conazole in fungal.
6. Animal is placed in warm, ventilated, lighted, lighted, dustfree
comfortable
shed with
fx plentry of fresh drinking water.
7. force feeding is indicated if the animal is anorexic.
8. If 91 is to be given, slow date must be mainained other wise
right ventricle failure & death ocucers, dn to heart failure.
9. If possible provision of oxygen- in hypoxia.
10.
No
use
of
respiratory sitmulants eg. Nikethinamide, lepatgolo, 5-10 % co2,
picrotoxion etc.
11.
Antihistaminic
may be useful.

Pulmonary emphysema:

Definition: Distension of the lung tissue caused by over-distension of alreolt

with rupture of alveolar walls with or without escape of with in to
the interstitial spaces. C linically it is characterized by dyspnoea,
hyperpnea, poor exercicw tolerance and forced expiration.

Aetiology:Cattle A cute interstitial pneumonia

*
*
*
*
In all

Parasitic pneumonia
Perforation of the loung by foreign body
Plant poisoning.
Pulmonary absless.
apecies :-

* Secondary to broncho pneumonia

* Acute chemicla injuys
* Foreign body pneumonia in pigs
* Chronic obstractive pulmonary disease(CDPD) in horse.
Pathogenesis:Inefficiency of eracuation of pulmonary airspace and failure of normal
gaseous exchange in the lungs.
Clinical findings :*
*
*
*
*

Not defectable in cattle clinically.

Plumonary emphysema is of diffused type.
Force ful expiration may produce grunt.
Pespiratory dyspnoea.
In severre condition sub-countaneous emphysema over the
withers.
Diagnosis :I) May be confused with acute pulmonary congestion and edema
cansed by anaphylaxis.
* But there is no forced expiration

II) Pneumonia There is fuer and localization

of
abnormal
respiratory sounds. But in emphysema the sound is wide
distributed.
III) Pneumothorax Absence of breath sounds. & forced inspiration.
IV) Lung worm infestation by FIE.
V) Polyoythemia (
in Hb concern)
leukocytosis & shift to the left in secondary bronchopneumonia,
and eosinophilia in allergic conditions.
Treatment : I) No specific treatment
II) Atropine, antihistaminic and corticosterfoids are being used with
controvertial efficing.
III) Not good.
Pleurisy : -

Inflammation of pleura, which produces pain during respiration and

climically manifested by shallow and rapid respiration, is called ~.
More common in human.
Type :A) According to pleural fhrid :I) dry
II) Moist
A) According to course of disease:
i) Acute
ii) Sub-acut Accompained by empyema & respiratory
embarrassment.
iii) Chronic- Fibrinous adhesions and minor interference with
respiratory movement.
A) According to etiology:i) Primary eq. Penetration usually traumatic
ii) Secondary eq. By best. Infn.
Etiology :i) It is always part of a primary disease of lungs.
ii) Primarily it is due to traumatic cases in all species.
iii) In cattle :- Infection due to p,multocida, p.hemolytica.
* Tuberculosis, CBPP, sporadic bovine encephalomyelitis
* Septic pleural effusion due to non specific disease.

Per foration of diaphraym in TRP & spread into pleural carity by

lumphatics.
Horse : - Rupture or extension to the plasma of a pre-existing
pulmonary abscess, granuloma or chronic pneumonic lesionc.

Steptococeus equi infn.

Pig : - Glasser is disease
-Pleuro
pneumonia

Sheep/Goat : - plerro pneumonia caused by

haemohilus sps. & haemophilus sps.

mycoplasma sps &

In All Sps :- P. Multocida & P. Hemolytica infn

Pathogenesis :
There

are

stages
1. Early acute, dry stage :- Contact of parietal & visceral surface of
pleura causes pain, respiration is shallow and rapid.
2. IInd stage of plenrisy : - Production of sero-fibrinous
inflammatory exudate which collects in pleural sac & collapse of
lung.
3. In third stage of pleurisy :- fluid is reabsorbed and adnesions.
Restricting movement of the lyungs & chest, but respiratory
interference is minimal.
Clinical symptoms :1) Early stage rapid, shallow respiration & animal feels pain
during respiration. Animal is anxiety.
2) Abdominal respiration.
3) Abducted bloods. Important sign. (TRP)
4) Disinclined to move.
5) Tempr & pulse rate.
6) Toxaemia, anorexia and depression.
7) In horse colicky symptoms & ventral edema.
8) Inspiratory dyspnoea.
9) If pleurisy is unlateral affected side chest movement is
restricted.

10)
In
chronic
pleurisy eq. Due to t.b. in cattle symptomless- wt loss in horse
dominant symptoms rather than respiratory embarrasement
In horse on ausculation friction or plentric triction sounds.

Diagnosis :- Diagnosed on the basis of friction rub or inflamm otory

exudate in the pleural sac. ~ Usually with pneumonia so diagnosis is
difficult.
Differential D :
a)
*
b)
*
*
c)
*
d)

Pneumonia Crackeles anad wheezes sounds less distinct

Coughting fluctuate sounds.
Emphysema Friction rub loud crackles sound.
Expiratory dyspnoea.
Typanic sound on percussion.
Hydro thorax & plemothorax- No tempr, Toxaema & pain.
Aspiratory examination for confirmation.
pulmonary congeston & edema - Vesicular murmur and ventral
conslidation.
e) pleurisy Dullness on percussion.(Typical symptom)
* Fresence of fever & toxatmia.
* Pleuritic friction sound.
* Lab analysis of pleural fluid reveals.
*
Lencocytes (4*104-10*104 N1) and protein conch upto 50g.
* pleuros copy can be done to inspect pleural carity.
INTRODUCTION
Inflammation of the epithelium of bronchi and bronchioles is bronchitis. It is
an inflammation, which extends in various depths of mucosae of bronchial
tubes. It is manifested with the production of mucoid and mucopurulent type
of nasal discharge with resultant productive husky cough classification.
1) According to the extension of infection
a) Tracheo-bronchitis
It is a disease where there is inflammation of tracheal and
bronchial epithelium. It has got no age barrier. It may affect dogs of any ages. It is
contagious (highly) in nature.
b) Broncho pneumonia
It is a disease where there is inflammation of the lung
parenchyma accompanied with the inflammation of the breathing, cough, fever with
adventitious vesicular sounds like rales, ronchi etc.

2) According to the duration and severity of disease.

a) Acute bronchitis
short duration and comparatively severe then chronic.
b) Chronic bronchitis

longer duration and less severe.

3) According to the etiological agent

a) Parasitic bronchitis
b) Viral bronchitis

E.g.
E.g.

Verminous Bronchitis

Infectious bronchitis

Infectious bronchitis is a disease of poultry, acute and highly contagious disease. It is

characterized by sneezing, coughing, respiratory rales etc.

ANATOMY OF BRONCHUS( for reference only)

Trachea is an elastic tube, 60cm long; extends from larynx to the level of the base of the
heart and is made up of cartilages. There are about 50to60 cartilages in the form of incomplete
rings with the open end placed dorsally. The rings are completed by connective tissue and
smooth m/s of tracheal muscles. The tracheal tube terminates by bifurcating into two bronchi at
the base of the heart, which enter into corresponding lung.

Bronchus

Right bronchus

Right lobar bronchi

Right-segmented bronchi

Left bronchus

Left lobar bronchi

Left segmented bronchi

Bronchioles

BRONCHILA TREE
ETILOGY
1) Acute trachea-Bronchitis:
a) Inhalation of irritant
dust, feed, industrial fumes, medicaments, smoke.
b) Infections

i) Bacterial

ii) Viral
bovine rhinotracheitis
iii) Parasites

Pasteurellosis
Ranikhet disease, infectious bronchitis of fowls, infectious
lungworms.

2) Chronic Bronchitis:
a) Mild, continuous irritants smoke and dust;
b) Chronic venous congestion as in heart disease
c) Chronic infection of upper respiratory tracts-chronic sinusitis.
d) Bronchiectasis
e) Most common cause in animals is lungworm infection, Tuberculosis and lung
abscesses.
3) Infectious Bronchitis:
a) RNA virus of corona viridae, very fragile virus.
Other causes of bronchitis are
Sudden change in environmental temperature.
Exposure to cold and damp weather
Over crowding of animals during long transportation.
Keeping the animals in poor ventilated house.
Drenching of animals in odd times of day.
Too much washing of animal with cold water.
Malnutrition and exertion on transportation.

 Drinking too cold water after exercise or race.

PATHOGENESIS
1. Acute/ chronic Bronchitis
Inhalation of irritant
(dust, dirt, industrial gases, toxic fumes)
Chemicals, smoke etc

Mucosae of the bronchi and bronchioles become

irritation of mucosae

Inflamed thickene and congested.

As a result, there is infiltration of inflammatory cell

bronchial epithelium
And predominantly neutrophils in the inflamed cell.

Due to inflammation, there is ed permeability of

obstruction of air passage

increase elasticity of
And swelling.

swelling causes partial

Bronchial epithelium.

Over production of mucus due to sed activity of

Inspiratory dysponea

The mucus secreting cells and glob let cells. (Secretion

Of mucus may be mucoid mucopuruient or purulent
Depending on the nature of inflammatory process)

In severe cases, the epithelium of the mucosae may be

of exudates.

coughing causes expulsion

Destroyed and covered by exudates. Exudates may be

Catarrhal, fibrinous or purulent.

2. Infectious Bronchitis: Although birds of ages are susceptible, birds of 1-4 weeks of age are severely
affected. The mortality is 20-90% with secondary infection with mycoplasma or septicaemial
E.col:. Incubation period varies from 18-36 hrs.

Inhalation or direct contact between birds to bird.

Infection goes to trachea and lungs and then vitamin develops

Then goes to various organ like kidney, oviduct where they damage
the tubules of kidney and ed
absorption of H2O and electrolyte.

Lead to dehydration and acidosis.

CLINCAL FINDINGS: Acute / chronic Bronchitis: -

Productive dry, harsh tyae of cough.

Cough is spasmodic in nature .
Cough is noticed predominantly in the morning hrs.
Animal may expectorate large volume of mucus with coughing.
There is elevation of body temperature.
Respiratory rate is increased.
Nasal discharge remains mucoid, muco purulent or purulent.
Respiration is predominantly abdominal in type.
There is extension of head and neck.
In severe attack there is dyspnoea and mouth breathing.
Auscaltation will reveal moist rales. Some cases may show dry rales and crepitate rales .
In chronic case, there is plenty of ronchi and crepitation all over the chest.
There will be the evidence of emphysema in later stage.

Infectious Bronchitis
Clinical sign may appear within 36-48 hrs of infection.
a) Sing in young chicken up to 6weeks of age: Distressed breathing breaks kept open and extends upward.
Tracheal rales, sneezing, hoarse coughing.
Wet eye, general malaise with depression and retracted growth.

Huddle together and mortality ranges from 25-60%.

b) Signs in growing chicks: Intensity and manifestation is less severe.
Distressed breathing and tracheal rales.
Respiratory noise, distinctly heard during night.
Increased drinking, Urolithiasis.
c) Sings in laying birds: fall in egg production up to 50%
belt egg.
Soft shell, asymmetry and corrugation on outline.
Loss of albumin viscosity, broken chalaza and egg floats freely.
Damage the full functional oviduct.
LESION: Acute Trachea-Bronchitis: Macroscopically: -The mucosae is thickened, reddened and covered by on exudates, which may
be catarrhal, fibrinous or purulent.
In aspiration of foreign objects, a gangrenous bronchitis is seen in which there is
extensive necrosis of the mucosae, which sloughs. The well of the bronchus may also be
destroyed.

Microscopically: a) There is congestion and infiltration by inflammatory cells in which neutrophils

predominate.
b) There may be increased secretion of mucus and in severe cases, the epithelium may be
destroyed.
c) In lumen contains mucus, leucocytes, dead epithelial cells, lungworm and their ova.
Chronic Bronchitis: Macroscopically: a) The bronchial mucosae is thickened and velvety feel.

b) Sometimes it (bronchial mucosae) may be congested pale and edematous.

c) Exudate is mucoid or mucopurulent.
d) In case of worm infection, it is mixed with worms and their eggs.
e) Bronchi may also be dilated.
Microscopically: a) There is infiltration by lymphoid cells.
b) Ciliated epithelium is lost and replaced by a cuboidal variety.
c) Mucus glands may show atrophy.
d) Lymphoid follicles may be formed in the walls of the bronchi.
Infectious Bronchitis: Catarrhal or cheesy exudates in trachea and bronchi.
Caseous plug in the trachea and bronchi at bifurcation.
Cystic dilation of oviduct.
Ova rupture with thin, watery albumin and yolk.
Enlarged kidney with deposition of ureate.
Ureter distended with ureate.
Stone in kidney in layers.

DIAGNOSIS: 1) Symptoms, P.M. and histopathological changes.

2) Isolation of virus in chick embryo.
3) Inoculation of tracheal exudates or suspension.
4) Serological test: a) Serum neutralization test
b) Agar gel precipitation test.
c) CFT, EAT, ELISA etc.
DIFFERENTIAL DIAGNOSIS
It should be differentiated from the following diseases:

1) Chronic pulmomary tuberculosis

Diurnal variation of temperature, sputum for acid-fast
organism, x-ray, tuberculin test and consolidation of lungs.
2) Bronchiectasis
this can be diagnosed by radiography- honeycomb appearance of lung
field may be seen. Bronchography This will confirm the diagnosis of dilation of bronchus.
3) Bronchogenic carcinoma
Raadiography, cytological examination of sputum, pleural
fluid, bronchial wash; Biopsy during bronchoscopy.
4) Pneumonia
High-rise of temperature, severe dysponea, moist rales, vesicular murmur,
toxaemia; radiography, haematology and isolation of causative factors are important to arrive at a
diagnosis.
5) Cardiac disease

Cardiac murmur, no rales or ronchi, cardiac arythmia; E.C.G.finding.

TREATMENT AND CONTROL

Attempt should be made to eliminate all predisposing factors.
Antiseptic inhalation to be given e.g. Tr. Benzoin co., oil Eucaliptus; Tr. Camphor etc.
To depress cough, anodyne expectorant should be given.
Ext. Belladona sicca

1gm

Pot. Iodide

4gm

Codein phosphate

0.5g

Pulv. Glycerrhiza

20g

Treacle

Q.S

Mft. Elect, sig. B.i.d. as electuary

Antibiotics like penicilline, streptomycin combination, ampicillin and oxytetracycline are
useful.
A courses of antihistamine preparations should be given E.g Avil, Histal etc (to inhibit
release of histamine)
For parastites, Fenbendazole, tetramisole, Levamisole or diethyl carbamazine citrate should
be given.
Rest, warmth and proper hygienic conditions are to be maintained.

Nebulizer may be given to remove the mucus plug from R.T.

Infectious Bronchitis
No medication is available that will alter or shorten the course of disease. Increasing the
tempr in the room and under the hover by 5-10c may lower mortality.
Immunization may be carried out the use of live vaccine, which produce relatively mild
respiratory sign. These vaccines are usually given in the drinking water. Such product should be
used according to the manufacture specific recommendations.
Vaccines: 1) Avian IB vaccine (Living) Baif
1st administration at 5-10days of age @ 2 drops in nostril
2nd administration at 6-8weeks of age @ 2 drops in nostril
3rd administration at 14-16 weeks of age in drinking water.
2) Avian IB vaccine (live) srini
1st administration at the age of 4-6weeks @ 1 drop in eye.
Other measures are: Management practices are strickly to be followed.
Strict isolation and repulation with one day chicks following the clearing and disinfection
of poultry house.
Air borne spread can be prevented by ventilating houses with filtered air under positive
pressure.
Birds of different age groups should be raised separately.
Vaccination programme.
Albuminuria
Introduction:
Albuminuria is a pathological condition wherein albumin is present in the urine. It is a type
of proteinuria. The occurrence of albuminuria indicates a disturbance of the barrier function
of endothelial cells, basement membrane or of a structural-renal disease (including diseased
podocytes). Its incidence is strongly associated with increased cardiovascular morbidity and
mortality. Blood pressure control and the blockade of the renin-angiotensin-aldosteron-system

(RAAS), respectively, is the central mechanism to reduce cardio-vascular-renal end points as

well as mortality.
Complications of albuminuria include the following:

Pulmonary edema due to fluid overload

Acute renal failure due to intravascular depletion
Increased risk of bacterial infection, including spontaneous bacterial peritonitis
Increased risk of arterial and venous thrombosis, including renal vein thrombosis
Increased risk of cardiovascular disease
Causes:
The kidneys normally do not filter large molecules into the urine, so albuminuria can be an
indicator of damage to the kidneys or excessive salt intake. It can also occur in patients with
long-standing diabetes, especially type 1diabetes.
Causes of albuminuria can be discriminated between by the amount of protein excreted.

The nephrotic syndrome usually results in the excretion of about 3.0 to 3.5 grams per 24
hours.

Nephritic syndrome results in far less albuminuria.

Microalbuminuria (between 30 and 300 mg/24h or mg/l of urine or g/mg of creatinine)

can be a forerunner of diabetic nephropathy.

Systemic diseases that result in an inability of the kidneys to normally reabsorb the
absorbs through the renal tubules
Obesity
Hypertension
Overproduction of albumins that are capable of passing through the normal glomerular
basement membrane (GBM) and that consequently enter the tubular fluid in amounts that
exceed the capacity of the normal proximal tubule to reabsorb them
A defective glomerular barrier that allows abnormal amounts of albumins of intermediate
molecular weight to enter the Bowman space.

Pathophysiology:
The filtration of albumin across the abnormal glomerular capillary wall (GCW) exposes
mesangial and tubular cells to these proteins. Albumin protein is normally reabsorbed from the
glomerular filtrate in the proximal convoluted tubule (PCT).

Heavy albuminuria may exceed the capacity of lysosomes in the PCT cells to metabolize
reabsorbed protein, and toxic enzymes may leak into the cells and the surrounding renal
interstitium as a consequence of lysosomal degranulation. Whether the nephrotoxic protein is
albumin, nonalbumin protein, or both remains unclear.
Other proteins, such as transferrin, complement components, and low-density lipoproteins
(LDLs), also appear to be directly toxic to tubular cells. In addition, lipoproteins appear to be
toxic to mesangial cells and may contribute to the development of glomerular sclerosis.
A consequence of protein-mediated cytotoxicity is the production of chemokines and cytokines
that initiate an inflammatory response and ultimately lead to sclerosis and fibrosis.

Symptoms:

Anorexia
Reduced milk production
Lethargic
Heavy whitish foam in urine.

Diagnosis:
By sign and symptoms

Heavy whitish foam in urine

By urine test:

The amount of protein being lost in the urine can be quantified by collecting the urine for
24 hours, measuring a sample of the pooled urine, and extrapolating to the volume
collected.

Also a urine dipstick test for proteinuria can give a rough estimate of albuminuria. This is
because Albumin is by far the dominant plasma protein, and bromophenol blue the agent
used in the dipstick is specific to albumin.By Roberts Test:

2ml of Roberts reagent is taken in a test tube and 2ml of urine is also layered carefully on
the reagent by allowing the urine to flow down the sides of the test tube, by holding

slantingly( if urine is cloudy, the urine should be centrifused), whitish ring appears at the
point of contact in positive case.
Differential diagnosis:

Congestive heart failure

Infection
Diabetes
Kidney diseases
Multiple myeloma
Sickle cell disease
Rheumatoid arthritis
Lupus
Some type of cancer
Use of certain medicines

Treatment:

There is some evidence that dietary interventions (to lower red meat intake) can be
helpful in lowering albuminuria levels.
Low sodium and proteins intake in diets.
Angiotensin converting enzyme inhibitors (ACEi).
Angiotensin receptor blockers (ARBs).
Restrict dietary potassium when serum level is high.
Salt substitutes may be rich in potassium.

Prevention:

By controlling diabetes
By taking low protein diets in food
Regular exercise