VETS6208: PRINCIPLES OF ANIMAL DISEASES B

MODULE: CARDIORESPIRATORY DISORDERS

Formulae

Learning outcomes

• Upper respiratory tract pathology

o Understand and recognise the normal anatomy, functions and histology of the respiratory system
o Understand the defence mechanisms in the respiratory system of the normal host, their importance and the
likely outcomes when these are breaches or fail; e.g., normal microflora; rhinitis; structural and circulatory
disturbances of the lungs; pneumonia and pneumonitis; pulmonary congestion and oedema; pulmonary
embolism; metastatic neoplasia; atelectasis and emphysema; pleurisy and pleuritis
o Understand the common aetiologies leading to significant pathology of the respiratory system; e.g. mucosal
disease, infectious rhinotracheitis, herpesvirus, canine distemper, calicivirus, herpesvirus, influeza,
Streptococcus equi, Burkholderia mallei, strangles, pyothorax
o Understand how to use the five basic pathological processes to determine likely differential diagnoses to
explain common presenting signs of respiratory system pathology and what investigations can help
determine the. Most likely diagnosis, e.g. radiography, ultrasonography, fibroscopy, haematology, serum
chemistry, urinalysis, cytology, histopathology
• Integrate the microscopic and gross appearance of disease (infectious and non-infectious) with the likely
aetiopathogenesis of that disease. Formulate differential diagnoses by detecting and applying their knowledge of
generic disease principles to major body systems (cardiovascular, respiratory, nervous, urinary, endocrine,
musculoskeletal), particularly the principles of inflammation, repair, circulatory disturbances and abnormalities of
growth (including neoplasia)
• Identify key disease (infectious and non-infectious) of the cardiovascular, respiratory, nervous, urinary, endocrine,
musculoskeletal systems from case material and be able to integrate the important features of the key agents of
disease (parasites, bacteria, viruses, fungi) as well as the clinical pathology of the host response and the effect on the
host
• Apply and integrate a thorough understanding of the host immune response and the agent of disease to common and
important diseases of domesticated animals and wildlife to formulate rational and reasonable prophylaxis,
management and control measures
• Integrate and synthesise the pathophysiology (reflected in the clinical pathology and pathology) and the common
agents of disease (parasites, viruses, bacteria and fungi) affecting multiple organ systems
• Use pharmacokinetic and pharmacodynamic principles to illustrate the role of therapeutic medecines to ameliorate
infection and/or organ dysfunction
• Demonstrate and advanced understanding of the principles of clinical pathology including haematology, biochemistry,
serological and molecular diagnostic investigations, urinalysis and body fluid analysis, and be able to detect, describe
and interpret the key findings in these data through analysis and interpretation of case-based scenarios
• Demonstrate an advanced understanding of key infectious agent of disease (veterinary parasitology and veterinary
microbiology) important in the aetiology of cardiovascular and respiratory, urinary tract, musculoskeletal and nervous
system disease in animals, their role in ecosystems and the use and impact of anti-infectives on animal, pathogen and
commensal populations
• Apply and integrate a thorough understanding of the relationship between normal behaviour and biological fitness;
abnormal behaviours and unmet needs an/or compromised welfare, and how these factors need to be considered in
the diagnostic and therapeutic approach
• Demonstrate effective practical skills at sample collection and dispatch of a range of biological specimens for the
diagnosis of disease of various animal species. tHis includes ante-mortem samples taken in the clinic and post-mortem
samples taken during necropsies (post-mortem investigations)
• Utilise the principles and concepts in pathobiology, epidemiology, pharmacology, animal behaviour and diagnostic
imaging to formulate investigative frameworks and to direct therapeutic or management interventions for endemic
and transboundary diseases including zoonoses
• Bacteraemia and septicaemia
o Recall the main bacterial pathogens involved in causing bacteraemia and septicaemia in animals and
demonstrate a practical knowledge of how these pathogens are differentiated and determined to be the
causative agent of bacteraemia and septicaemia including what samples you would collect and how you
would collect them to maximise the chance of diagnosis
o Outline the host defence mechanisms that normally protect against bacteraemia becoming persistent and
explain the host and environmental factos that predispose animals to developing severe systemic disease as
a result of bacteraemia
 o Discuss the pathogenesis of infections caused by the main bacterial pathogens involved in causing
bacteramia and septicaemia outlined in the lecture including factors such as where they are normally found,
the source and route of transmission, and virulence factors that enable them to cause disease
o Using the available patient information, and the results from the patients’ haematology and biochemistry to
interret and discuss the results for the patient explaining in particular your understanding of bacteraemia,
septicaemia and a basic understanding of endotoxaemia
• Pharmacology of the respiratory tract
o Propose some mechanisms that result in bronchoconstriction and propse what receptor agonists or
antagonists may be indicated for bronchodilation
o Discuss why cats and horses are more prone to airway disease than dogs
o Discuss the factors to be considered when selecting a bronchodilator for acute versus chronic
bronchoconstriction
o Recount the mechanism of action for glucocorticosteroids to control inflammation and allergic reactions, as
well as their side-effects
o Discuss the indications for antihistamine use in small animal medicine
o Discuss the factors that need to be considered when selecting an antibiotic or antifungal agent for treating
lower respiratory diseases
o Define the following terms: expectorant, mucolytic, decongestant, antitussive
• Respiratory pathogens (streptococcus)
o Host defences: use your knowledge
• Lungworm and heartworm
o Understand parasite features and biology, host specificity, life cycles, epidemiology, environmental
conditions, pathogenesis, diagnosis and control
o Revise faecal flotation, direct smear for identification of cestodes, nematodes and trematodes
o Apply and combine specific diagnostic techniques to understand their limitations and advantages
o Apply Baermann diagnostics test to detect L1 of lungworms
o Explain what other samples (apart from faeces) can be used to diagnose L1 of lungworms
o Apply and understand the principle of the Baermann diagnostic test so you can perform an alternative test
and a watch glass or plastic water bottle
o Use the results from diagnostic techniques in combination with clinical signs to support your diagnosis
o Explain if absence of L1 in faeces is sufficient when treating for lungworms; identify drugs registered for
lungworm treatment in cats
o Suggest and communicate management for selected cases
o Perform a heartworm test and examine the diagnostic sensitivity (DSn) of current tests relative to
heartworm life cycle and infection rates
• Heartworm
o Explain biology, diagnosis and control of lungworms and heartworm and explain significance in animals na
dpublic health
o Understand factors behind the degree of harm caused by lungworm and heartworm
o Understand the life cycle and duration of each developmental stage of the canine heartworm Dirofilaria
immitis
o Explain the reasons why under current conditions in Sydney it is recommended to keep a dog on heartworm
prevention; reflect on the present status in Australia
o Understand the limitation and dangers of macrocyclic lactones in dogs
o Apply and reasons why diagnostic testing is essential before treatment
o Review the life ycle and duration of each developmental stage of Dirofilaria immitis
o Discuss and reason why under current condition in Sydney most dogs are on heartworm prevention; reflect
on the present status in Australia
o Apply and reasons why diagnostic testing is essential before treatment
o What is the efficacy of ML prevention
o Explain macrolactone susceptibility gap versus macrolactone drug resistance
• Pathology of the cardiovascular system
o Understand and recognise the normal anatomy, functions and histology of the cardiovascular system
o Understand the pathogenesis of heart failure, including the body’s compensatory mechanisms
§ Left- and right-sided congestive heart failure
§ Myocardial hyperplasia and hypertrophy
§ Cardiac dilatation
§ Developmental defects
o Understand the major causes and likely sequelae of valvular disease (e.g. endocardiosis and endocarditis)
and how to differentiate them grossly and histologically
o Using your understanding of cardiac function, pathological changes, their sequelae and the presenting
pathology, be able to predict the pathophysiology and sequelae of a lesion at a certain cardiovascular site,
particularly related to restrictive cardiac disease, pericardial disease and thromboses
 o Understand the common aetiologies leading to significant pathology of the cardiovascular system; e.g.,
congenital cardiac defects, Dirofilaria immitis, parasitic arteritis, feline infectious peritonitis, traumatic
reticulo-pericarditis, haemangioma, haemangiosarcoma, aneurysms, inflammation of the vessels, portocaval
shunts
o Understand how to use the 5 basic pathological processes to determine likely differential diagnoses to
explain common presenting signs of cardiovascular pathology and what investigations may help determine
the most likely diagnosis; e.g. imaging, haematology, serum chemistry, cytology, histopathology
• Respiratory system embryology
o The general formation and development of the lower respiratory tract from the gut tube
o The general formation and development of the diaphragm and the components from which it arises
• Cardiovascular system
o Understand the development of the heart, from the formation of the single heart tube to the establishment
of the four chambers
o The structures that contribute to the definitive aorta
o The function and fate of the vitelline and umbilical arteries and veins
o The changes that occur in the circulatory pathway in association with birth and why tese changes occur
o Relate common congenital heart diseases associated with fault in heart development to the developmental
stage/structure that went wrong
• Lower respiratory pathogens
o Outline the unique features of the influenza viruses infection including their effects on host defences and
predictable sequelae
o Discuss the general features of avian influenza virus infections and the principles of disease transmission
and control
o Discuss the recent developments in cross species infection of influenza and their implications for future
outbreaks
• Cardiovascular pharmacology
o Draw the structural layout (including nerves, neurotransmitters, receptors) of the peripheral nervous system
and to discuss the relevance of this information for selecting appropriate therapies in veterinary practice
o Discuss the effects that the peripheral nervous system ahs on the cardiovascular system by discussing the
effect of
§ Muscarinic receptor antagonists
§ A1 adrenoreceptor agonists and antagonists
§ B1 adrenoreceptor adonists and antagonists
o Define the terms chonotrope, inotrope and inodilator and give on examples of a positive chronotrope, and
positive and negative inotropes in terms on the effect ton recetprs (e.g. positive inotrope = B1
adrenoreceptor agonist)
o Discuss how arrhythmias may occur within the myocardium and outline the general principesl by which each
antiarrhythmic class exerts its effect
o Outine the mechanism of action of furosemide and angiotensin II inhibitors
o Outline the side effects of an overdose of furosemide
o Outline the indications for diuretic classes other thant the loop diuretic (furosemide)
o Outline why diuretics and angiotensin II inhibitors are used to treate congestive heart failure in companion
animals
o Identify that a drug is an ACE – by its generic name
o List the possible side and adverse effects of angiotensin inhibitors and describe why these occur, and how
they can be minimised
• Cardiac microbiology
o Discuss the role of canine and feline parvoviruses in the pathogeneis of leukopaenia and in PCv, myocarditis
o Discuss how the unique features of retroviruses facilitate their global survival and continued transmission
o Apply your knowledge of FIV and FeLV, in the context of a clinical scenario (transmission clinical
presentation, pathogenesis, diagnosis, control)

Index

1. Disorders of the cardiorespiratory system

a. Anaemia of bacterial and parasitic aetiology
b. Bacteraemia
c. Coagulopathies
d. Haematopoeitic neoplasia
e. Upper and lower respiratory tract pathogens
f. Respiratory tract pathology
g. Lungworms and ascarids
h. Congenital abnormalities
 i. Cardiovascular pathology
j. Pathogens of the cardiovascular system
k. Ascites: pathogenesis and diagnosis
l. Heartworm
m. Pharmacology
n. Imaging
o. Cardiovascular disease: heart failure

Cardiac disturbances:
• Electrical disruption
• Mechanical disruption
o PDA (patent ductus arteriosus)
o VSD (ventricular septal defect)

Pathologies:
• Failure of AV valve
o Pushing blood back into atrium
o Stretching of atrium
o Minimal blood enters venous system again due to venous valves
• Drop in blood V
o

End-diastolic volume (EDV): volume of blood in ventricle at end of diastole

Respiratory tract pathology

Respiratory tract pathologies:

• Rhinitis
• Pneumonias
• Pneumonitis
• Pulmonary congestion
• Pulmonary oedema
• Pulmonary embolism
• Metastatic neoplasia
• Atelectasis
• Emphysema
• Pleurisy
• Pleuritis
• Mucosal disease
• Infectious rhinotracheitis
• Herpesvirus
• Canine distemper
• Calicivirus
• Herpesvirus
• Influenza
• Strangles
• Pyothorax
• Streptococcus equi
• Burkholderia mallei
• Diseases of nasal plane
o Insect bite hypersensitivity
§ Usually due to mosquitoes
§ Allergy to insect saliva (anticoagulants, etc.)
§ Microscopically
• Eosinophils
• Thickening of skin
• Congestion
o 2ary infection (bacterial, fungal)
§ Cryptococcosis – 2ary to nasal cavity infection
o SCC
• Disease of nasal cavity and sinus
o Rhinitis
 o Sinusitis
o Epistaxis
• Larynx and trachea pathologies
o Laryngitis
o Tracheitis
o Laryngea haemiplegia
o Guttural pouch (horses)

1. How does lung oedema inhibit normal defence mechanisms?

Answer: Oedema in the lungs causes fluid in the alveoli and airways which interferes with the function of alveolar
macrophages and the mucociliary escalator, inhibiting the effectiveness of mucus to trap particles and the to beat and
move things up the airways. Fluid also encourages bacterial growth, especially if it contains protein.

2. If pneumonia is interstitial as opposed to within the alveoli, would that give clues into aetiology, and possibly leading
towards more of a haematogenous spread?

Answer: Yes. The aerogenous route of infection normally results in infection and inflammation centred on the airways
with inflammatory cells and fluid in the alveoli (pneumonia) whereas haematogenous route often leads to infections
and inflammation centred within the alveolar walls (pneumonitis).

3. Could you please explain the pathogenesis of embolic pneumonia caused by bacteria - I am very confused.

Answer: if an abscess elsewhere in the body (e.g., in the liver) ruptures it can release a shower of numerous bacteria
into the circulation which can then lodge in many organs , including the lungs especially due to the large, capillary
network.

4. Can you please explain why you get froth in the airways in pulmonary oedema

Answer: the oedematous fluid normally includes varying amounts of protein and with inhalation and exhalation the
moving air mixes with the fluid and causes bubbles to form. The more protein in the fluid, the longer the bubbles last
and so the more bubbles. Air movement also moves the bubbles (froth) into the larger airways so it can reach into the
trachea.

Common causes of aetiologies:

Congenital Inflammation/ immunity Physical DoG

Herpesvirus Pulmonary Metastatic neoplasia
Canine distemper virus congestion SCC
Calicivirus Pulmonary oedema
Influenza virus Pulmonary embolism
Streptococcus equi (Strangles) Atelectasis
Burkholderia mallei Emphysema
Rhinitis Pleurisy
Pneumonia Epistaxis
Pneumonitis Laryngeal hemiplegia
Pleuritis
Infectious rhinotracheitis
Rhodococcus equi (rattles)
Pyothorax
Insect bite hypersensitivity
Cryptococcosis
Sinusitis
Laryngitis
Tracheitis

Normal nasopharyngeal microflora:

Nasal cavity aetiologies:
• Proliferation of normal resident microbial flora
o Due to immunocompromise

Nasal cavity pathologies:

• Rhinitis
o Discharge
§ Serous
§ Catarrhal
§ Mucopurulent
§ Fibrinous/pseudomembranous
o Causes
§ Inhalation of irritant gases
• SO2, smoke, O3, NH3, ruminal gas
§ Inhalation of dust/dust mites
§ Viral
• Rinderpest (morbillivirus)
o Ulceration to lip mucosa
o Similar appearance to FMD
o Proliferat in
• Inclusion body rhinitis (pgs)
o Cytomegalovirus (herpesvirus)
• Feline viral rhinotracheitis
o Feline herpesvirus 1
o Signs
§ Oculonasal discharge
§ Conjunctivitis
o Become carries, shed virus
o Can cause 2ary infections
• Calicivrus
o Ulcerative stomatitis
o Ulcerat
o Bacterial rhinitis
§ Strangles (Streptococcus equi equi)
• Suppurative rhinitis
§ Glanders (horses)
• Zoonotic – 50% lethal if untreated
• Infected by ingesting horse meat
§ Meliodosis/pseudoglanders
• Burkholderia pseudomallei
o Affects most animals incl repitles, amphibians, birds
• Infection by: ingestion, inhalation, wound entry
• Tx: IV fluid therapy
• Dissemination via blood
o Atrophic rhinitis (pigs)
§ Inflammation and atrophy of nasal turbinates
o Mycotic rhinitis
§ Causes:
• Aspergillus spp. (e.g. A. fumigatus, dogs)
o Ubiquitous in env – opportunistic invaders
o Forms
§ Localised nasal form
• In immunocompetent animals
• 2ary to trauma
• Mostly dolichocephalic dogs
• Most common in brachycephalic cats – altered nasal
airflow, mucociliary clearance
§ Disseminated form
o Can be caused by oil spills (e.g. penguins)
o Signs
§ Sneezing
 § Bilateral epistaxis
§ Nasal swelling
o Diagnosis
§ Biopsy: fungal plaques
§ Rhinoscopy
§ CT scan
§ Clear thoracic scans
§ Rule out crypto, FeLV, FIV
§ Sinus trephination
§ Neutrophilic + lymphocytic + plasmacytic infiltration
§ Neutrophil + cellular debris exudate
o Tx by nebulisation of mycotic agents
§ Enrofloxacin
§ Fluconazole
§ Enilconazol
§ Ciprofloxacin
§ itraconazole
• Penicillum spp.
• Cryptococcus neoformans
o Most common micotic in
o Parasitic rhinitis
§ Oestrus ovis (nasal bot in sheep)
§ Nasal granulomas (cattle)
• Repeated exposure to allergens
• Perfuse mucopurulent nasal
o Allergic rhinitis
§ Sporadric in dogs and cats
§ Eosinophils in mucosa
§ Type 1 hypersensitivity
o Plasmacytic-lymphocytic rhinitis

Fungal rhinitis: 2 forms

Characteristic Disseminated form Localised nasal form
Cat Dog Cat Dog
Areas affected Lung, skin, bone, GIT
Common species Aspergillus
fumigatus
Pathogenesis Production haemolytic & Destruction of
dermonecrotoxic endotoxin conchae and
turbinates
­radiolucency in
nasal passages
Frontal sinus
osteomyelitis
Diagnosis False -ves on fungal culture
common
Signs Epistaxis Profuse
Purulent nasal discharge mucopurulent
White/yellow/green mould nasal discharge
mass on turbinate Epistaxis
Facial pain
Ulceration of the
nares
2ary to
immunocompromising
condition
Signalment Mostly brachycephalic Mostly
(alterations to mucociliary dolicocephalic
clearance, nasal airflow) German
Himalayan, Persians shepherds
Visualisation White/yellow/green mould plaques on turbinates
Rhinoscopy
 Histopathology Dichotomous branching septate hyphae + infiltrates
of macrophages + lymphocytes + neutrophils

Clinical signs of upper respiratory tract disease:

• Sneezing
• Excessive mucous production
o Nasal discharge
o Blockage of airways
o Mouth breathing
• Excessive tear production
• Inspiratory noise
• Pyrexia
• Local lymphadenomegaly
• Epistaxis – erosion of epithelium + congestion of capillaries
• Oedema and congestion in the face

Epistaxis: bleeding from nose

Type of discharge Appearance Components Typical causes

Serous Clear fluid Clear frluid from
submucosal sero
Catarrhal
Mucopurulent Distemper
Fibrinous/
pseudomembranous
Granulomatous Fungi
Mycobacteria
Actinomyces
FBs

-> Colour of discharge affected by type of bacteri and pigments they produce
->cattle use sticks to scratch irritation in their nose, so stick nasal FB is common

Common bacteria:

Complications of rhinitis:
• Extend into respiratory tract

Sinusitis:
• Causes
o Extension of rhinitis
o Dental disease – maxillary sinus in dogs and horses continuous
o Dehorning – cutting too close, affecting horn sinus continuous with nasal sinus

Epistaxis:
• Causes
o Trauma
o Erosion of blood vessels – 2ary to inflammation/neoplasia
o Mycotic infection of guttural pouch
o Clotting defects due to toxicants
o Exercise-induced (EIPH; horses)
o Ethmoidal haematomas
§ Rare
§ Signs
• Unilateral seroanguinous nasal discharge
 • Head deformation
•

EIPH: exercise-induced pulmonary haemorrhage in horses

Ticks

Ticks:
• Most important group of arthropods
• Obligate haematophagous
• Hosts: mammals, birds, reptiles, amphibians

Morphology:
• 8 legs in adults and nymphs
• 6 legs in larvae
•

Common tick species:

• Paraylsis tick (ixodes holocyclus)
• Rhipicephalus sanguineus (brown dog tick)
• Haemaphysialis longicornis (bush tick)
• Rhipicephalus australis – vector of tick fever

Tick Identification Classification Life- Diseases Common

cycle caused hosts
Paralysis tick 3- Tick
(Ixodes host paralysis
holocyclus)

Rhipicephalus
sanguineus
(brown dog
tick)
 Haemaphysalis
longicornis
(bush tick)

Rhipicephalus
australis
(Australian
cattle tick)

Ixodes holocyclus: paralysis tick

• Morphology
o Hypostome – enters into skin and achors
o Chelicera – cuts skin to allow entry of hypostome
o Palps
• Life cycle (120-140d)
o Annual in temperate regions
o Year-round
o 3-host life cycle

Rhipicephalus australis var microplus: Australian cattle tick

• Life-cycle
o 1-host cycle
o Spend 3w on host at a time
• Transoverial transmission
• Tropical, subtropical

Diagnosis:
• Presence + identification of ticks - preservation
• Worry
• Babesiosis (tick fever)
• Anaplasmosis
o Blood smear
Tick parasitic disease:
• Release of toxins
• Vectors of
o Tick typhus
o Rickettsia australis
o
• Anaemia
• Tick worry (irritation)
• Toxicosis – paralysis
• Inhibit immune processes
• Tick fever – disease caused by blood parasite carried by cattle ticks
o Babesiosis
§ Babesiosis bovis (‘red water’) – most common (80%)
• Signs: severe pyrexia, affected respiration, depression, anorexia
• Parasitaemia > ann
• Diagnosis
• Tx and control
o Quarantine of property 18-24m
o Pasture spelling for 3-5m during summer
 o Tick-resistant cattle, e.g. Bos indicus
o Acaricides
o Vx (Tick Guard) – improves gut antigens
o Attenuated Babesia/anaplasma vx – in calves <9m
§ Babesia bigemina (‘red water’)
§
o Anaplasmosis
§ Anaplasma marginale (prokaryote)
§ Anaplasma cenrale
§ Anasplasma platys

Tick management:
• Quarantine
• Pasture spelling (3-5 m)
• Tick-resistant cattle
• Acaricides
• Vaccine
• Tick fever vx
• Tick removal
o Don’t squeeze as salivary glands in whole fo body in Rhipicephalus – causes injection of toxins into blood

Babesia:
• 2 main species
o Babesia bovis
o Bebesia bigemina (not called babesiosis)
• Apicomplexan
• Most important genus of blood parasites of cattle in Australia
• Rod-shaped merozites in RBCs
• Do not distort shape of RBC
• Reprduction in vertebrate host by merogony (asexual)

Acaricides:
• Dogs
o Nexguard
o Simparica
o Bravecto
o Lotilaner
• Cats
o Lotilaner

Theleria
Theleriosis:
• ruminants
• Theleriosis
• East Coast Fever (Africa)
o T.p. parva
o T.p. lawrenci
• Tropical theileriosis – T. annulata
• Equine theileriosis (T. equi)
• Theileria buffeli/sergenti
• Theileria orientals (NX, Australia)
• 35% cattle hers affe
• Different species with differing levels of pathogenicity
• Infection in wild animals mostly

->causes theleriosis
Theleria:
• Microschizont infect lymphocytes that travel to high BP areas
• >10% of lymphocytes infeby 10d
• Lifetime immunity from Tc-mediated response
• Spread by tick n
• Tick carrier rate >

Signs:
• Death from dystocia
• Pale mm
• Anaemia
•

Diagnosis:
• Fever
• Swelling of superficial LNs
• Death
• LN biopsy for macroschizont (>6d)
• Blood smear for microschizont and piroplasma (>12d)

Treatment:
• Tetracycline – if detected very early
• Residual of 3-500d
• No registered tx in Austrlalia
• Buparvaquone (BPQ)
•

Prevention:
• Tick control
• vx (sporozites + LA tetracycline)
o decreases incidence after vaccination
• Babesial and I&T vaccine in
• Schizont-based recombinant vaccines (CMI-CTL)
• Sporozite-based (SN Ab preventing entry)
• Mechanical transfer by IV inoculation of infecf
o Does not cause clinical signs
• Do not move animals from non-endemic to endemic areas

Life cycle:
• Piroplasma – infect erythrocyte

Theleria orientalis:
• Host response
o Priroplasma
• 6-7w before show clinical signs
Seasonality:
• According to tick seasonl

1. Aug: nymph attaches and feeds for 5d

Modes of transmission:
• Mechnical
• Transplacental
• Colostral transmission
o Ab ELISA (MBPM)

Bacteraemia and septicaemia

Common patients:
• Neonates (neonatal septicaemia)
o Omphalitis (inflammation of
Portals of entry to blood:
• Traumatic/invasive events that compromise mucosal barriers
o Iatrogenic
• Direct inoculation into blood stream
o Contaminated needles
o Contaminated urinary or IV catheter

Common locations:
• Heart
• Brain
• Joints

Host defence against bacteramia:

• Phagocytic cells in spleen and liver
o Remove pathogens from circulation with IgM + IgG + complement

Diagnosis:
• Blood sample
o Blood culture bottle, 10:1 blood:broth
o Collect before commencing antimicrobial therapy
o Multiple samples from multiple venipuncture

Common pathogens:

Gram- rods Gram+

Enterobacteriaceae

Non-enteric E. coli syndromes:

• Pyometra
• Mastitis
• Cystitis
• glomerulonephritis
• Omphalitis
• Septicaemia
• Endocarditis
• Osteo

Non-enteric E. coli virulence factors:

• Endotoxin

Pasteurella:
• Gram- short rods
• Distinguished by oxidase test (oxidase +)
• Species
o P. mutocida
• Facultatively anaerobic

• Normal fl

Diseases caused:
• Fowl cholera
o Purulentt form
o Don’t see

Actinobacillus:
• A. equili
o Ss equuli – mm o
o Haemalyticus – from oral and GIT microflora of mare

Actinobacilus diseases:
• Sleepy fowl disease
• Acute septicaemia (A. suis)
• Localised septicaemia (meningitis, arthritis, abortion, arthritis, pneumonia, skn

Staphylococcus

Diseases caused by staph:

• Dermatoses
• Arthritis
• Osteomyelitis
• Urolithiasis
• Cystitis
• Botryomycosis (post-castration in horses)
• Mastitis
• Septicaemia
• Endocarditis
• Pneumonia
Streptococcus
• Point of entry
o Tonsils
o Pharynx

Erysipelotrhix:
• Species
o E. rhusiopathae (pigs, other domestic animals)
o E. tonsillarum
• Found in GIT of many wildlife
• Virulenc factors
o Don’t have endotoxin
o Neuraminidase
o Capsule
• Diseases caused
o Septicaemia
o Generalised skin infection
o Arthritis
o Vegetative cardiopathy
o Turkey erysipelas
• Infect blood first, then eventually inva

Erysipelothrix arthritis:
• Pannus formation
•

Diamond skin disease:

• Disruption of blood supply causes ulceration of skin and crusting

Vasculitis: type III hypersensitivity

Listeria

• Hosts: ruminants, other species

• 4 syndromes caused
o Visceral form (septicaemia)
o
->foals only insured if they are sure they obtained passive transfer – blood test carried out.

Neonatal isoerythorlysis: haemolytic disease of the newborn

• Foal has different blood type to mother from the sire
o Small leakage of blood into the
• Anti-RBC antibodies from the mother by colostrum -> destruction of RBCs

GC test:
• <4g/L = failure of passive transfer
• 4-8g/L = partial failure of passive transfer
• >8g/L = successful passive transfer

FPT: failure of passive transfer

Toxic changes to blood:

• Dohle bodies

Endotoxaemia:
• Presence of endotoxin in the blood
• Most of effect due to host overreacting in response to LPS
o Endotoxic shocj

Endotoxin = LPS
• Core acidic monosaccharide region
o Connects o rgion to A region
• Hydrophobic lipid A region
o Buried in outer mb
o Mediate most of toxic effects

Preogression of endotoxaemia: 1ug is all

1. Physical barriers breached – amount of endoxoin absorbed dx
2. iNitiatl contact between LPS and blood
3. Enxodtoin entres the blood n
4. LPS-LBP forms complex
5. LS-LBP attache to CD-14 receptor (within 30min)
6. Stimulation of macrophage
7. and binds with high affinity, specificity to cell surface receptors, e.g. CD14 on intaf
8. Liberates arachidonic acid in mb to form thromboxanes & prostaglandins, leukotrienes and lipoxins
9. Secretion of TNF-a, IL-!, Il-6 (pro-inflammtory mediators
10. Maturation of neutrophils to release more
11. TNF and IL-1
12. 2nd wave of cytokine productin by monocytes
a. GM-CSF
b. IL-8
c. IL-6
13. Monocytes activate neutrophils
a. Increased sensivity to complenet products
b. Release of cell contents and toxic O2 metabolites into endothelium
14. Consumptive coagulopathy
15. Systemic arterial hypotension + thrombosis -> toxic shock
16. Vascular leakage
17. Widespread intravascular coagulation
18. Small blood clost causes poor perfusion to tissue
19. Multiple organ failure
a. CNS = sturpor

Alternative outcomes to septicaemia:

•

Common exaples of enteric dz:

• Bacteri
• Alteration of the integrity of the bowl
• Non-enteric dz
o Metritis
o Pleuropneumonia

->dropping neutrophil levels indicate poor prognosis

Petechial haemorrhages:
• Platelet/clotting factor disorders

SIRS: systemic inflammatory response. Disproprotionate response to pathogen invasion or tissue injury

• Causes
o Infectious
§ Gram- bacteria
§ Gram+ bacteria
§ Fungal infection
§ Viraemia
§ Protozol infection
o Non-infectious causes
§ Pancreatitis
§ Heatstroke
§ Snake envenomation
§ Tissue trauma (crush injury, major surgery, burns)
• Massive systemic inflammatory response incited by cytokines released by macrophages
Respiratory Tract Infections

Medications for treating respiratory tract disease:

• Bronchodilators
• Anti-infectives
• Antihistamines
• Antitusives
• Expectorants
• Mucolytics
• Decongestants
• Oxygen supplementation
• Diuretics
• Humidification
 Cartilage Ciliated epithelium Glands SM
Trachea
Bronchi
Bronchioles (less) Not usually, large
ones may have
goblet cells
Alveoli
Airway size controlled by:
• Bronchial tone <- ANS-innervated SM

No. neurons 1st NT 1st R 2nd NT 2nd R

Somatic efferent Ach Nic
system 1
Blood vessels of 2 Ach Nic NA a,b adrenergic R
SNS
Sweat glands of 2 Ach Nic Ach Mus
SNS
Adrenal medulla 1 Ach Nic
(SNS)
PSNS 2 Ach Nic Ach Mus
Receptors:
Type Hormones Categories Found in Action
received
Adrenergic A, NA a1 Bronchial SM Contraction ->
Vascular SM bronchoconstriction
Vasoconstriction
a2 Nerve endings ¯transmitter release
Reduction of
parasympathetic
bronchoconstriction
b1 Bronchial SM, glands, Mediate airway calibre
alveoli, mast cells, and tone (b2 > b1)
cardiac muscle, ­HR and contractility
kidneys (b2) ­renin secretion
Ø b2 Bronchial SM Relax smooth muscle
Liver (bronchodilation)
Skeletal muscle ­Gluconeogenesis
­Glycogenolysis
b3 Adipose tissue ­lipolysis
Cholinergic Ach Nicotinic NM, NN
Muscarinic M3 Bronchial SM Contraction ->
Submucosal mucous bronchoconstriction
glands Secretion
M1,2,4,5
Histaminergic Histamine H1-4 SM (H1) Bronchoconstriction
Non-noradrenergic Various Mediates Feline asthma (5-HT)
non-cholinergic bronchomotor tone Bronchodilation
(NANC) (vasoactive Intestinal
Peptide (VIP))

Respiratory diseases

Respiratory system:
• Most common route of entry for organisms, esp. viruses

Respiratory tract defence mechanisms:

• Turbinate bones – create turbulence in air flow which cause particles to hit cilia and get trapped in mucus
• Copious mucous secretion to trap particles
• Sneezing
• Nasopharynx
o Cilia
• Larynx
o Physical barrier
o Cough receptors (many)
• Lower respiratory tract
o Mucociliary escalator
• Sterility
o Bronchi
o Broniloles
o Alveoli

Distance travelled by particles: in respiratory tract

Risk factors predisposing to disea

Methods of evidence collection:

• Tracheal wash
o Lo
o Pass tube 2/3 of way, then slide the actual tube into thio
• Bronchoalveolar lavage
o Pass tube within the other tube
o Find bacteria present in mucus
Isolation of strongyle larvae:
• Coproparasitology
o Faecal analysis
o Faecal agar plate culture
• Baermann method
o Cheaper, easier
o Needs a lot of glass funnels
o Cut at 2/3 of way up a plastic bottle, invert the end, place a small balloon on the end
o Place 5g of faeces onto 4 layers of gauze in funnel
o Leave to sediment overnight
o Collect balloon and analyse
o 90% sensitivity

Lung and heart nematodes:

• Metastrongyloidea (lungworms; metastrongyles ; superfamily)
o Reside in
§ Lungs
§ Pulmonary artery
§ Meninges
§ IM connective tissues
o Morphology
§ Small buccal capsule
§ Reduced male bursa
o Arranged in families that coincide with typical host
o Infective stage = L1 (passes in faeces; except in pigs)
o 3 different types of life cycles
§ Direct (e.g. Dictyocaulidae)
• L3 ingested
• Exsheaths and penetrates wall of intestine
• Migrates via lymphatic system to the lungs
• Adults in lungs lay eggs/larvae
• Carried up the trachea, swallowed
• Exit in faeces as L1
• L1->L3 in environment
§ Indirect (pig metastrongyles, rum protostrongyles, dog/cat/rat angiostrongyles)
• L1 passed in faeces
• Ingestion by earthworm/penetrate foot of snail/slug
• L1->L3 in IH
• IH eaten by DH
• L3 migrate to lungs
§ Direct (carnivores; filaroididae)
• L1 ingested
• Migration to lungs with dvlpt
o Types
§ Dictyocaulidae > Dictyocaulus
• 8cm white worms
• Trachea, bronchi
• Short, stout spicules, sponge-like appearance
• Cosmopolitan Aus, NZ
• PPP=21d
• Effects
o Occlusion of major airways
o predispose to 2ary bacterial infections
o hypersensitivity
§ Metastrongylidae > metastrongylus
• Pig bronchi, trachea
• 1-6cm thin worms
• Trilobed lips
• Cosmopolitan Aus and NZ
• Effects
 o Occlude airways
o 2ary bacterial infections
• Indirect life cycle – eggs passed in faeces rather than L1
• PPP=3-6wks
§ Protostrongylidae
• Rum lungs, sinuses, brain, IM tissues
•

Family > genus Species Host Reside in Disease PPP Significance

Dictyocaulidae > D. filaria Sheep, Trachea, Husk 21d Major pathogen in
Dictyocaulus goat bronchi temperate climates
D. viviparous Cattle Trachea, Husk 21d
bronchi
D. arnfieldi Horse, Trachea, 21d
donkey bronchi
Metastrongylidae > M. apri Pigs Bronchi, 3-6w
metatstrongylus trachea

M. salmi Pigs Bronchi, 3-6w

trachea
M. pudendotectus Pigs Bronchi, 3-6w
trachea
Anaemia

Factors affecting PCV, TPP:

• If PCV normal + TPP high
o Dehydration + anaemia
• If PCV low but RBC normal
o RBCs small –
• If PCV high but TPP normal
o 1ary polycythaemia
• If PCV high
o 1ary polycythaemia
o Relative polycythaemia – due to dehydration

RBCs: circulating levels balance of

• Production
• Loss

Intravascular haemolysis:
• D
o Expose Fc end of Ab
o Expose to phagocytes

Measure of adequacy of erythron:

• Haematocrit/PCV
o Examination of plasma
o Examination of buffy coat
• [Hb] – colorimetry
• RCC
o Haemocytometer (inaccurate)
o Automated counters (accurate except avian blood)

Regenerative anaemia: takes 2-3d for response to occur

• ­reticulocyte count
o Except horses
o Any presence of reticulocyte indivia
• Polychromasia, anisocytosis/macrocytosis, nRBCs
• Alteration in red cell indices
->Coomb’s test to test for Ab on RBCs

Cats:
Non-regenerative Grey area Regenerative
Reticulocyte % 1%<
Absolute reticulocyte
count

Dogs:
Non-regenerative Grey area Regenerative
Reticulocyte %
Absolute reticulocyte
count

Classifications of anaemia:
• Regenerative/non-regenerative
• Haemolytic/haemorrhagic
o Intravascular/extravascular haemolysis
• Microcytic/normocytic/macrocytic
o MCV = PCV/total RBC count x1000
• Hypochromic/normochromic
o Hyperchromia impossible – artefact
§ Haemolysis causes hyperchromia as more Hb in plasma

Macroytosis Microcytosis
Reticylocytosis
Greyhounds
Genetic diseases (poodles,
malamutes, min schnauzers

Non-regenerative:
• Abnormal BM
• Either
o Reduced (hypoproliferative)
§ Slow onset
o Defective (hypercellular)
§ Les common
§ Variable time-course dpeendsin

Type Sitmulus Left shift Other WBC Comments

Inflammation ­tissue demand +/- Variable
Physiological Adrenalin - L+, E-, M-
Stress Corticosteroids - L-, E-, m Common
Regenerative Non-specific BM +/- Variable Mainly dog
anaemia stimulation Usually haemolytic
Myeloid leukaemia Neoplasia - Varialbe, myelophsis Rare
Stress leukogram:

Bone marrow examination

• Use
o Ileac crest
o Flat bones
• Reasons to use
o Follow up persistent peripheral blood changes

Components to haemostasis:
• Vessel wall
• Platelets
• Coagulation factors
• (Fibrin)

Circulatory disturbances:
• Fluid distribution imbalance
o Oedema
o Shock
• Disorders of haemostasis
o Thrombosis
o Bleeding disorders
• Hyperaemia & congestion
• Infarction & ischaemia

Disorders of haemostasis:
• Bleeding disorders – inappropriate deficient haemostasis
o Consumptive coagulopathy
o Congenital coagulopathy
o
• Thrombosis - Inappropriate excessive haemostasis

Haemostasis:
• 1ary haemostasis – endothelial defects
o Vessels + platelets
o To further stabilise, fibrin + clotting factors seals platelets on defect
• 2ary haemostasis
o Re-bleeding after initial stop in bleeding
o Stabilising of 1ary by fibrin + clotting factors to seal platelets on defect
Coagulation cascade:
• Common pathway
• D

1. 1ary haemostasis
a. Platelet adhesion
b. Shape change of platelet
c. Granule release (ADP, TXA2)
d. Recruitment
e. Aggregation (haemostatic plug)
2. 2ary haemostasis
a. Tissue factor
b. Phospholipid complex expression
c. Thrombin activation
d. Fibrin polymerisation

Thrombosis:
• Injury to endothelial cell
o Exposure of subendothelial collagen
o Causes
§ Trauma
§ Toxaemia
• Hypercoagulability of blood
o Efficiency of antithrombin III in dogs
§ Plasma protease that in

Bleeding disorders:
• Signs
o Melena
o Petechiation (skin, MM) -> vascular endothelium defects, platelet inadequacy, vW factor deficiencies
o Ecchymoses
o Haematuria
• Types
o Vascular endothelium defects
o Platelet number and function
 o vW factor deficiency

Ecchymoses: large red patches on skin and mm

Haematoma: circumscribed extravascular collection of blood, usually clotted

• Blood in body cavities often unclotted

Important factors for haemorrhage:

• Location of bleeding
o Haemorrhage into pericardium prevents contraction of the heart
§ Cardiac tamponade sign of
• Speed of blood loss
o Fast -> haemorrhagic shock, failure of tissue perfusion
o Slow -> body will eventually adapt
• Amount of blood loss
o Loss of materials to form new cells
o Loss of circulating PP -> catabolism

Causes of haemorrhage: often >1 involved

• Vessel-related
o Mechanical trauma
o Neoplasia (1ary, 2ary)
o Vasculitis
o Cell injury
§ Sepitcaemia
§ Plant poisoning (e.g. bracken fern In cattle)
§ Chemical poisoning
• Disorders of haemostasis
o Platelet inadequacy
§ Thrombocytopaenia
§ Platelet dysfunction (most common)
o Clotting disorder
§ Clotting factor deficiency
§ Inherited
• Factor I, II, VII, VIII, IX, X, XII, vWF deficiency
• Haemophilia
§ Acquired
• Hepatic diseases – production of both coagulation factors and anticoagulants
• VitK agonist – required cofactor for II, VII, IX, X
o Warfarin
o Excessive fibrinolysis

Most common haemostasis disorders:

• Thrombocytopaenia
• Vit K antagonism
• Heritable factor deficiency
• (Hepatic insufficiency)
• (Acute DIC)
• Thromocytopathy

DIC: disseminate insufficiency coagulopathy

Tests -> PC APTT OSPT Fib FDP

Thrombocytopaenia ¯ N N N N
VIt K antagonism N ­ ­ N N
Heritable factor N Variable N
deficiency
Hepatic N ­ ­ ¯ N
insufficiency
Acute DIC ¯ ­ ­ ¯ ­
Thrombocytopathy N N N N N
Vasculopathy N N N N N
Diagnosis of bleeding disorders:
• Evaluation of platelet mass
o Macroplatelets more active but show up a lower mass
o Prone to machine error
• Coagulation factors evaluation
o Activated clotting time – tests for deficiencies or inhibition of I, C clotting factors
§ Time required for fibrin clot to form
§ Needs to be 5% of normal levels to affect activity
o Citrate plasma clotting test – more sensitive (2-4)
§ Needs to be 30-40% of normal levels before prolonged times
o Activated partial thromboplastin time (APTT) – I,C – “
o One-step prothrombin time (OSPT) (E,C) – “
o Thrombin clotting time (TCT) ( C) – “
• Fibrinolysis evaluation
• Signs
o Form of bleeding
• Hx

Most common initial assessment:

Pathways of clotting cascade:

• Extrinsic
• Intrinsic
• Common pathway
Lungworms:
• Aelurostrongylus abstrusus (cat lungworm)
o 5-10mm
o Adults live in lung parenchyma
o 10-15% cats
o PPP = 5-6w
o Indirect life cycle
o IH = slugs (<6wks), PH = rodents
o Mild clinical signs
§ May develop chronic cough
§ Can
§ Breathing difficulties
§ pneumonia
o Diagnosis
§ Mostly incidental
§ PM
§ Radiography
• Diffuse intersitital pattern with focal peribronchal densities
• Alveolar pattern if severe
• Angiostrongylus vasorum (French heartworm)
o <25mm adults
o RA and pulmonary arteries of dogs, wild canids
o Mostly W Europe
o Adults in the heart
o Direct L1 life cycle
o Diagnosis
§ L1 in faeces by Baermann technique
• Rat lungworm (Angiostrongylus cantonensis)
o Blood vessels of rodent lung
o PH = dogs, mammals (brushtail possums), birds (tawny frogmouths)
o Potentially zoonotic
o Indirect life cycle – PH ingest molluscs
o Clinical effects
§ Travel through brain and SC -> tissue damage
 § Inflammatory response to worm in NS
§ Neuro-angiostrongyliasis
o Signs
§ Bilateral hind limb paresis
§ Ataxia
§ Hind limb muscle wasting
§ Eosinophilic meningoencephalitis
• Dog heartworm (dirofilarial immitis)
o Adults in pulmonary arteries
o Diagnosis
§ Demonstration of microfilariae in blood
• Wet mount
• Centrifuge blood and wet mount buffy coat
§ Ag test
o Signs
§ Cough due to fluid in lungs
§ Coughing + v+
o Life cycle
§ Mosquito carries L1
§ Dvlpt in malphigian tubules
§ L3->L4 (3d)
§ L4 in SQ tissue, mm of thorax & abd
§ L5 migrate
o PPP = 6-8m
o Adults live 5-7y dogs, 2-3y cats
o Influences on prevalence
§
o L1 = microfilariae
o Prevalence currently ¯
o Pathogenesis
§ Strips of endothelium slough
o Tx
§ Doxy
§ Macrocyclic lactones
• Dog lungworm (Filaroides osleri)
o Adults in nodules in bifurcation of the trachea
o Transmission: L1s via saliva to pups during regurgitation/grooming
o Mostly dingoes, feral dogs
o PPP = 6-7m
o Nodules 2m post-infection
o Diagnosis
§ Tracheal wash
• Cattle lungworms (Dictyocaulus
viviparous)
o 40-80mm
o Common in dairy calves 4-
12m in winter rainfall
areas in spring
o Husk/hog fever
o Causes
§ Hypersensitivity
to migrating L4
and L5 in lungs
o Life cycle
§ L1 in faeces
§ L1->L3 in env
§ Ingestion from
grass
§ Penetrates
intestine ->
mesenteric LNs
§ Moults -> L4 in
LNs
 § Carried to lungs in bloodlymph
o Tx
§ Macrolactones
§ Vx indoor calves >8wks w/ hx of lungworm
§ Ivermectins
§
• Sheep lungworm (Dictyocaulus filaria)
• Sheep lungworm (Meullerius capillaris)

Lungworm species DH Site Action IH, PH

Aelurostrongylus Cat Lungs Cough
abstrusus
Angiostrongylus Rat PH= dog, human,
cantonensis wildlife
Dictyocaulus filaria Sheep, goat
Dictyocalus Cattle
viviparous
Metastrongylus spp. Pigs
Protostrongylus Sheep, goats
rufescens
Muellerius capillaris Sheep, goats
Angiostrongylus Dog
vasorum

Parasites that cause coughing:

• Lungworm adults
• Roundworms during migration

Ascarid Host Transmission PPP (milk) PPP (soil)

Toxocara canis Dog TU, TM 19-21 25-28
Toxocara cati Cat TM 19-21 25-28
Toxocara vitulorum Cow

TU = transuterine, TM = transmammary
Vectors of D. immitis:
• Culex annulirostris (freshwater marsh mosquito)
o Active mid-spring to late-autumn
o SE Australia
o Feed on humans, mammals, birds
• Aedes notoscriptus (common domestic mosquito)
o Attack humans and animals
o Feed evening to early morning

Tests for parasite larvae/eggs:

• WC test – place in gauze, place on watch glass, place warm water, allow to percolate through
• Direct smear – from thermometer onto a slide

Laryngeal problems

Laryngeal pathologies:
• Diverticulum of ventral Eustachian tube
o Guttural pouch mycoses
§ Carotid arteries and recurrent nerve runs through it
§ Pressure of pouch on the a. weakens wall and causes
§ Inhalation of fungal spores
§ Sequelae
• Epistaxis
• Inhalation of blood into lungs
• Mycotc thromboemboli due to disrupted capillaries causing cloting -> cerebral infarcts
• Laryngeal hemiplegia if recurrent laryngeal n affected
• Horner’s syndrome
o Guttural pouch empyema
§ Strangles (S. equi ss equi)

Nasal cavity microflora

Nasal cavity
• normal resident microbial flora preventing adherence and colonisation by more virulent organisms
Lungs:
o Fluid from intersitital space
o Dual blood supply
o Bronchiolar a.
o Pulmonary a.

Changes in

Normal defences:
• Sneezing
• Coughing
• Mucociliiary clearance (bronchi, trachea, nasal cavity)
• Phagocytosis by alveolar macrophages
• Coiled nasal conchae to create turbulence to trap FBs in the mucous layer
• BALT (bronchiole-associated lymphoid tissue)
o Modified epithelial cells (M-cells) line it
o Internalise particles found on their surface
o Transferred to APC

Alveoli
Alveolar

Impairment to normal defence mechanisms:

• Stress
• Concurrent infections
• Poor husbandry (stress, poor diet)
• Immunodeficiency
• Starvation
• Dehydration
• Corticosteroid therapy
• Trauma – damage to mm
• Anaesthesia
• Pulmonary oedema

Bronchiole pathologies:
• Bronchitis
o Acute bronchitis
§ Catarrhal
o Chronic bronchitis
§ Thick, oedematous mucosa
• Pneumonia – inflammation of airways + exudate in airways
o Complex interaction
o Predisposing events
• Pneumonitis/interstitial pneumonia – inflammation of airways with little exudate
o Causes
§ Aerogenous injury to alveolar epithelium
• Toxic gases, viruses
§ Haematogenous injury to alveolar endotheliam
• Septicaemia
• Toxic injury
• Bronchopneumonia
o Causes
o Types
§ Suppurative
• Exudate dominated by neutrophils
•
§ Fibrinous = lobar – quickly affect all lobules
• Incomplete resolution
• Pulmonary fibrosis & adhesions
• Haematogenous spread of agents
• Bacterial rhinitis
o 2ary to nasal cavity dz
o Bacteria – in rum:
§ Pasteurella multocida
§ Manheimia haemolytica
§ Haemophilus somnus
§ Arcanobacter pyogenes
§ Arcanobacter bovis
§ Fusobacterium necrophorum
§ Mycoplasma mycoides
§ Mycoplasma bovis
§ Chlamydophila
• Circulatory disturbances
o Congestion/oedema
§ Signs
• d
o Hameorrhage
§ Causes
• Severe congestion
• Disorders of haemostasis
• Trauma
• DIC
o Infarction, embolism
• Anthracosis
• Neoplasia
o 1ary
o 2ary
 § epithelial
• Structural disturbances
o Atelectasis
o Emphysema
• Pulmonary infarct – uncommon as dual blood supply. Need already compromised
o Occlusion of arterial supply
o Influence on site of infarct
§ Anatomy of circulation
§ Aetiology
• Thromboemboli
• Septic emboli
• Dirofilarial immitis
• Tumour
• Anthracosis – heavy black carbon deposits
o Common in animals in city
• Pneumoconiosis
o Uncommon in non-human animals
o Mostly adenocarcinomas
o 2ary haemangiosarcoma
• Atelectatic – failure of alveoli to open/remain open
o Congenital
o Acquired
§ Obstruction of airway
o Non-reversible
• Emphysema
o Overdistension of alveoli with air
o Causes
§ Obstructed outflow of air
§ Violent respiratory effort (agonal gasps)
o Types
§ Alveolar
§ Interstitial
• Violent respiratory efforts
§ Bullous emphysema – large areas of trapp
• Pleurisy
o Always check pleura as well in pneumonia as common
o Independent/2ary to pneumonia
• Pleural neoplasia
o Mesothelioma
§ Rare, escept in koalas
§ Affects
• Thoracic mesothelium
• Pericardial mesothelium
• Peritoneal mesothelium
• Diaphragmatic hernia
•

Pneumonia:
• Aetiology
a. Normal flora proliferation due to stress, other disease, poor husbandry
b. Bacteria (Rhodacoccus equi)
c. Viruses (canine distemper)
d. Mycoplasma
e. Fungi (Cryptococcus, aspergillus)
f. Protozoa
g. Inhalation of food and oil
• Classification
a. Aetiology
b. Type of exudate
c. Morphological features (marked, acute, diffuse)
d. Distribution of lesions (
• Types of pneumonia
 a. Embolic
• Septic emboli
b. Granulomatous
• Nodular
• FBs
• Fungi (Cryptococcus,
c. Mycobacterial, e.g. bovine TB
•
• Sequelae
a. Death
b. Complete resolution
c. Incomplete resolution
• Stages
1. Congestion – hyperaemia, oedema, congestion
2. Consolidation/red hepatisation – collapse of lung (atelectasis)
a. Red hepatisation -
b. Hardening to consistency of liver
3. Resolution
a. Exudate coughed up/drained by lymphatics
b. Normal cells pr
->many areas of the lungs can have different stages of pneumonia from different causes

Organism Disease Hosts Nature Source Pathogenesis Tx/ control

caused
Herpesvirus All animals Enveloped
RNA virus
Calicivirus
Bordatella Atrophic
bronchiseptica rhinitis (pigs)

Cryptococcus Fungus

Calicivirus:
• Major species
o Feline caliciviruses (FCV): URT infections
o Rabbit haemorrhagic disease virus (RHDV)
o Vesicular exanthema swine virus (extinct)
• Non-enveloped ssRNA
• Icosahedral symmetry with cup-shaped depressions
• Resistant to inactivation by standard detergent disinfectants
• Resistant to heat
• Inactivated by pH<3
• Enter by R-mediated attachment + endocytosis
• Pathogenesis
o Shut down host protein synthesis
• Wide range of tissue tropisms
o Depends on virus and strain
• Sign
o Blistering of skin/mouth and appendange mm (FCV, VES)
o Pneumonia (FCV)
CARDIAC PATHOLOGIES

Heart anatomy:
• Heart wall – 3 layers
o Epicardium = visceral pericardium
o Myocardium
§ Myocytes
§ L 3x thicker than R

Cardiac adaptation:
• Ventricular dilatation
o Response to ­CO
o Cardiomyocyte stretch ­ contractile force -> ­SV
• Cardiomyocyte hypertrophy
• Hypertrophy without dilatation -> decreased capacity

Cellular regenerative capacity:

• Continual contraction of intact myocytes impairs regeneration

Cardiopathies:
• Myocardial infarct
o Healing
• Pulmonic stenosis ->. hyperaemia in liver, systemic circulation
• Tricuspid insufficiency -> “
• Aortic stenosis -> hyperaemia in lungs, pulmonary circulation
• Mitral insufficiency -> “
• Pulmonic stenosis
• Infundibular pulmonary stenosis
o Post-stenotic turbulence
o Murmur due to turbulence
o Dilation of pulmonary trunk
o ­resistence to pulmonary outflow
o RV wall dilatation
o Post-stenotic dilation in ascending aorta distal to valve
o ­resistance to outflow ->
• Interventricular septal defect – opening at dorsal part of IV septum
o Turbulent flow from L->R
o R ventricular dilatation
• Interatrial septal defects
o Caused by
§ Failure of foramen ovale to close
o ­L atrial P
o Blood shunt L->R
• Left AV valve defect
o L
• Left AV valve dysplasia
• R AV valvular fusion and stenosis
o Rare
o RA enlarged
• Tetralogy of Fallot – congenital
o 4 different lesions
§ IV septal defect
§ R ventricular hypertrophy
§ Arotic dextroposition
§ Pulmonary stenosis
o RV>lLV P
o Deoxygenated bllod passes into
• Myocarditis
o 1ary
o 2ary to spread of
§ Vegetative valvular endocarditis
§ TRP
§ Bacteraemia
§ Toxoplasmosis (dogs, cats)
§ Blackleg (Clostridium chauvoei)
§ Parvovirus
§ Types
• Lymphocytic -> parvo in puppies
• Eosinophilic
o Idiopathic
o 2ary to parasitic infections, e.g. sarcocystis (protozoa)
• Endocardium
o Endocarditis
§ Valvular
• Large, adhering, friable, yellow-grey masses on valves (vegetations)
• Enlarges atrium
• Bacteria travel to brain, kidney, liver
• Vegetation can eventually occlude valvular orifice
• Accumulation of fibrin + bacterial colonies + strong neutrophils
• Disrupted valvular endothelium
o Fibrin deposition initiated
o Adherence and proliferation of bacteria
• Sequelae
o Septic emboli lodging in lungs, brain, spleen, joints, kidney -> abscessation,
infarction
• Diagnosis
o US
o Blood culture
o Non-infectious
§ Uraemic ulcertative
• Cardiomyopathy
o 1ary
o 2ary – to other cardiac disorders
§ Heritable
§ Nutrition, e.g. white muscle dz
• Hypertrophic cardiomyopathy
o 1ary: idiopathic
§ Uncommon in dogs – M German Shepherd
§ Common in cats, esp middle-aged males
§ Hypertrophy of individual myofiber
§ Interstitial fibrosis
§ Myocyte degeneration
§ ->CHF
§ Aortic thromboembolism
o 2ary: adaptive response to ­
§ Common in cats
• Low tissue C of Taurine
• Thrombosis
o Saddle thrombus (thromboembolism of caudal abd aorta in cats)
§ Hind limb paresis -> paralysis
§ Depression
§ Aggression, pain
§ Lack of toileting
§ Lack of femoral pulse
§ Cold hind limbs
• Endocardiosis – degeneration
o Valvular endocardiosis
§ Degeneration of valvular collagen
§ Most common cause of CHF but not important enough to be lethal
§ ­fibroblastic proliferation
• Pericardium
o Pericarditis
§ Fibrinous
• Usually spread haematogenously
• Horses: streptococcal infections
• Cattle:
o Pasteurellosis
o Black leg
o Coliform septicaemia
§ Granulomatous: Bovine tuberculosis
§ Supparative: TRP
o Hydropericardium – excess serous fluid
o Haemopericardium – whole blood acutely collects in pericardial sac
§ Causes
• spontaneous atrial rupture in dogs
• Rupture of intrapericardial aorta in horses
• Complication of cardiac injections
§ Death from cardiac tamponade
o Pericardial adhesions
o Pericardial blood effusion
• CHF
o ¯peripheral perfusion = forward failure
o Accumulation of blood behind failing chamber = backward failure
o Renal hypoxia
o ­renin release
o ¯erythropoietin produced in renal tubules
o ¯erythropoeisis in BM -> anaemia
o Hypervolaemia + water retention
§ ­ workload on a failing heart
§ ­ cardiac decompensation
o 1st organ to be affected depends on side of heart
§ RH: liver
• Systemic congestion, esp
o Liver
o Spleen
• Abd distension
• Ascites
• Depressed
• Wide stance - ¯P on abd
§ LH: lungs -> ­P due to back-up of blood
• Acute
o Alveolar septal oedema
o Alveolar capillaries become engorged, dilated, tortuous
o Pink, bubbly fluid in airways
• Chronic
 o Thickening fibrosis of alveolar septae
o Alveolar macrophages deployed to engulf RBCs -> heart-failure
cells
§ Macrophages full of haemosiderin/partially-digested RBCs

Stenosis: narrowing of lumen

Causes of CHF:

LH RH
• Loss of myocardial contractility
o Myocarditis
o Myocardial necrosis
o Cardiomyopathy
• Valvular insufficiency
o

Endocarditis vs endocardiosis:

Endocarditis Endocardiosis
Signalment Any age Old dogs
Signs
Appearance Smooth appearance

Causes of thromboembolism:
• Injury to endothelial cell
• Disruption to blood flow
• Hypercoagulability of blood

Causes of endocarditis:

Cats Dogs Pigs Horses Cattle

Valvular Streptococcus Streptococcus Streptococcus Streptococcus Actinomyces
spp spp. spp. equi pyogenes
E. coli E. coli Erysieplothrix Actinobacillus
Staphylococcal Staphylococcal rhusiopathae equuli
spp. spp.

Cavalier King Charles genetic problems:

• Mitral valve insufficiency
• Valvular endocardiosis

RH CHF signs:
• Acute
o Liver
§ Centrilobular hepatocytic degeneration
§
PM changes to heart:
• Clotting
o Red clots in chambers
o Fatty clots that contain few erythrocytes
• Haemopericardiom/pallor/crystalline depostis in lining tissue
o Esp. if IC injection
• Blood in RV sticky and brown

Cardiac embryology

Congenital disorders:
• ~-.7% dogs, 0.2-1% cats
• Common in Arabian horses
• Signs
o Heart murmur
o Exercise intolerance
o Heart failure

1. Formation of single heart tube

a. Lateral folding – fusion of L and R heart tubes
b. Cranial folding – folds pericardium over
2. Vitelline vessels form at same time as intraembryonic network
a. Networks link
3. Bending of heart tube
4. Partitioning of heart (wk4)
a. Heart enlarges x5
b. Paired projection (endocardial cushions, conotruncal ridges)
i. Extension from opposing walls, meet and fuse
c. Single projection – extends from a single wall (interatrial septa, interventricular septum)
d. Septum primum (RH)– 1ary interarterial septum
i. Foramen primum – gap between free edge of fold and endocardial cushions
e. Septum secundum (LH)
i. Foramen ovale – gap between free edge of septum and opposing atrial wall
ii. Forms before foramen primum obliterated
iii. Opening covered by septum primum (acts as valve)
iv. If R>L P,
5. Holes form in
6. Fusion of septum with endocardial cushions
7. Birth
a. Foramen ovale closes
b. ­P LA -> P on foramen ovale -> push towards septum -> fusion
c. Fossa ovale forms – depression in heart

Congenital defects:
• Atrial septal defect
o Ostium secundum
§ No closure of foramen ovale at birth -> ostium secundum
§ ­P in LA -> blood flow from L to R atrium
§ Few clinical problems except systolic murmur
o Ostium primum
§ More common in cats
§ 1st septum didn’t grow all the way through
§ Commonly associated with other defects

Heart tube

Paired projection Single projection

Endocardial cushions Interatrial septum
 Conotruncal ridges Interventricular septum

Vitelline vessels: vascular network in wall of yolk sac. Forms simultaneously to intraembryonic network and links itself to
that network

Respiratory embryology

1. Laryngotracheal diverticulum from floor of foregut

a. 4th pharyngeal pouch
2. Elongation -> LT tube
a. Narrowing of communication between foregut and
3. Lung buds form
a. Bifurcation of distal end of laryngotracheal tube
b. Endoderm infiltrates and lines tubes -> bronchial tree
c. Splachnic mesoderm infiltrates to form CT framework
4. Lung buds expand laterally into medial walls of intraembryonic coelom (IEC)
5. Branching of distal end of tube

Developmental stages:
• Embryonic – formation laryngotracheal groove, lung buds
• Pseudoglandular (late embryonic) – tubular branching to terminal sac level
• Canalicular
• Terminal sac
• Alveolar

Lower respiratory microbial pathogens

Diagnosis:
• Sputum sample
• Auscultation

Infectious causes of infectious canine tracheobronchitis (ICT):

• Canine parainfluenza virus 5 (CPiV-5)
• Canine adenovirus 2 (CAV-2)
• Canine influenza (H3N2 (avian), H3N8 (equine))
• Canine herpesvirus-1 (CHV-1)
• Canine respiratory coronavirus (CRCoV)

Virus family Genus Example species

Orthomyxoviridae Influenzavirus A Influenza A virus – main one in
animals
Influenzavirus B
Influenzavirus C
Thogotovirus Thogoto virus
Isavirus Infectious salmon anaemia virus

Influenza viruses:
• Enveloped segmented RNA virus
o Genetic reassortment
• High mutative rate
• Transmission: aerosolization
• Very fragile in env
o Sensitive to heat (56C, 30min)
o Can survive in faecal samples for 6d
• Proteins produced – used to name virses
o Haemagglutinin (HA) – binds to respiratory epithelium
§ 16 different types
§ Intramb sugar
o Neuraminidase (NA) – allows virus to detach when exiting cell (by budding)
 § 9 types
§ Causes cell destruction
• Enters cl=
• Cross-protection doesn’t occur between subtypes
o If antigenic drift – can give partial immunity
o If antigenic shift – no immunity
• Nomenclature:
o Genus (A,B or C) | origin host | geographical origin | isolate no.
| Year 1st isolated | HN

Pandemic: worldwide outbreak of virus that affects any age group

Epidemic: widespread occurrence of an infectious disease in a commmunity
at a particular time
Endemic: disease regularly found in a community or area (herpesvirus, cold
sores, EBV)

Epidemiology:
• Faecal contamination provides opportunity for infection with multiple
strains
o Influenza
• Natural reservoirs: wild aquatic birds
o Anseriformes (ducks, geese, swans)
o Charadriiformes (gulls, shorebirds
• Bind differently
• Pigs considered ‘mixing bowl’ for viruses – allows creation of new viruses
• Haemagglutinin attaches to sialic acid on host cells
• Entry into cytoplasm + viral replication
• Release of virion by budding
o Cleaving attachment of vesicle
• Different strain have preference for type of sialic acid they bind to
o Human strain = a2-6
o Avian = a2-3
o Pig = a2-6 and a2-3

Pathogenesis:
• Damage to respiratory epithelium allows 2ary bacterial infection
• Doesn’t cause symptoms in wild birds
• Coughed/sneezed virions -> entry to respiratory tract

Clinical signs:
• Fever
• Coughing
• Malaise
• Pneumonia

Pandemics: only 10 in last 500 years. Due to major antigenic shifts

• H1N1 (swine flu, 1918)
• H1N1 “Spanish flu”
o Most severe pandemic ever recorded
o Most young adults killed
o Killed 50-100 million (3-5% of world’s population)
• H5N1 (Hong Kong, 1997)
• H5N1 (Thailand, 2003)
o Fed fresh chicken carcasses from local slaughterhouse
o Clinical signs
§ Severe pyrexia
§ Respiratory distress
§ Death
o In big cats in Asia Europe
• Avian influenza
o Types
§ Low pathogenicity (LPI)
 § High pathogenicity (HPI)
o Signs
§ Coughing/sneezing
§ Cyanotic combs/wattles
§ Petechial/ecchymotic haemorrhages
§ Watery d+
§ Dyspnoea
§ Anorexia
§ ¯egg production
§ Head, face oedema
§ NS signs
• Occur due to
o Close association of large numbers of pigs, domestic poultry, wild waterfowl and people
• Often emerge in S China

Seasonal influenza epidemic:

• Semi-annual/seasonal
o Winter in temperature areas (climate, social factors)
o All year round in tropics
o

Essential features for pandemic:

• Ability to replicate and cause disease in humans
• Efficient person to person transmission
• Antigenically novel to humans
• 2nd bacterial infection

Canine influenza:
• Diagnosis
o Deep pharyngeal swab – with visible organic material on swab
o Conjunctival swab – rub inside eyelid
o Serology – paired titres
o PCR
• ‘kennel cough’
• Pathogenesis
• Source of infection
• 2ary infections from CPiV5, CAV2, Bb
• Self-lin
• Signs
o Gagging, retching
o Nasal discharge
o Don’t have signs of systemic illness
• Co-infections worse than agents alone
• Periodic paroxysmal coughs
• Transmission: inhalation by aerosolization
• Factors that facilitate trasmisission
o Introduction of new animals
o Ventilation
o Density of animals

Equine influenza:
• Equine herpesvirus 1
• Signs
o Sporadic/epidemic abortions
• Can extend to pulom
• Transmission
o Reactivation of latent virus in stressed animals
• Pathogenesis
o Damage to protective mucosal barrier
o ¯mucocllary clearance
o Immunosuppression, esp. macrophages, lymphocytes
• Upper RT only – due to major effect ei
• Usually in foals, weanlings

Most common canine respriatory pathogens:

Canine Equine
• Bordetella EHV-1
bronchiseptica EHV-4
• Oral anaerobes
• Pasteurella
multocida
• Mycoplasma
canis/cynos
• Streptococcus
• Klebsiella
pneumoniae
• Canine
parainfluenza 5
(CPI5)
• Canine adenvirus
2 (CAV2)
• Canine
distemper (CDV)
• Canine influenza
• Canine
herpesvirus 1
• Canine
coronavirus
• Lungworm
(Angiostrongylus)
•

Bordetella bronchiseptica: ‘party starter’

• Signs
o Mild to moderate airway dz
o Allow significant pathogens to colonise, e.g. Klebsiella pneumoniae
• Non-productive/productive goose honk cough
o Swelling of vocal folds
• Incubation period = 5=10d
Newcastle disease:
• Ruffled feathers
• Signs – v variable. Depends on virulence, tissue tropism, etc.

Normal URT defences:

• Tracheal mucociliary escalator
• Pulmonary alveolar macrophages

Chronic cardiac congestion:

• Stenosis
• Heartworm
• Myxomatous mitral valve disease
• Myocardial wall dysfunction
• Chronic

Causes of cardiac arrhythmias:

• Iatrogenic
• Intrinsic damage to myocardium
o Hypoxia
o Ischaemia
• Extrinsic factors
o Electrolyte imbalance
o Endotoxins
o Free radicals
o +ve inotrope overdose
o Tricyclic antidepressant overdose
 o Metabolic dz, e.g. hyperthyroidism
o

EMERGENCY RESPONSE

Cardiac arrest:
1. Airways – ensure patent and open
2. Breathing
3. Cardiac massage
4. Drugs
a. Adrenaline – can give several boluses, but if do not respond
b. Isoprenaline, noradrenaline if adrenaline not available
5. Post-emergency tx
a. Dobutamine/dopamine IV to ¯cardiac arrhythmias

Treatment bronchodilation:
• Salbutamol (B2 IV) – if not possible
o Intrathoracic/IC
o IM
• Adrenaline if salbutamol not available

Drug Administration
Dobutamine IV CRI
Dopamine IV CRI

Drug class Action E.g.

Muscarinic receptor antagonist +ve chronotrope Atropine
B1 receptor agonist +ve inotrope A, NA
+ve chronotrope
B1 receptor antagonist -ve inotrope All -olol drugs, e.g. atenolol,
-ve chronotrope propanolol
Loop diuretic Inhibits reabsorption of water in Furosemide
renal tubules
Potassium sparing diuretic Inhibits aldosterone action on renal Spironolactone
tubules, limiting water reabsorption
Angiotensin-converting enzyme Inhibits secretion of aldosterone and All -pril drugs
inhibitor inhibits formation of angiotensin II
Angiotensin II receptor inhibitor Inhibits action of angiotensin II on
arteries and arterioles
A1 receptor agonist Artery and arteriole contraction
Stimulation of B1, B2r

B1 AR antagonists:
• ¯F of contraction
• Used for
o ¯BP
o Counteract ­cardiac sympathetic stimulation
§ Hyperthyroidism in cats
§ Ventricular arrhythmias
§ Adrenal medulla tumours secreting adrenaline
§ Toxins (e.g. theobromine)
o Class II antiarrthmiac agent
o Occasionally CNS excitability/stress – but ineffective for seizures
o Hypertrophic cardiomyopathy
§ ¯F of contraction -> ­ventricular filling
§ ­CO
§ ¯need for cardiomyopathy
• Not widely used
• End in ‘-olol’
• E.g.
o Non-selective: propranolol
o Selective: atenolol
Muscarinic receptor antagonist:
• +ve chronotrope
•
• E.g. atropine

B1 adrenoreceptor agonists:
• +ve ionotrope
• E.g.
o Pimobendan (tablet, chewable, IV)
o Amrinone
o Milrinone (IV)
o Methylxanthines
§ Theophylline
§ Aminophylline
§ Theobromine

Pimobendan:
• Indication
o Dilated cardiomyopathy
o Myxomatous mitral valvular dz – prior to appearance of clinical signs
§ Supports remodelling of ventricles
• Eliminated by biliary route via faeces – eliminate problem with compromised kidney function
• Administered 0.25mg/kg BID
• Wide therapeutic index
• Few side-effects
o V+
• Not proarrhythmic

Antiarrhythmic agents:
Class Action Indication Examples
I Mb stabilisers block Na+ ion Tx of ventricular arrhtyhmias Lignocaine
channels
II B adrenoreceptor blocker Tx of supraventricular
arrhythmias
III Block K+ channels Tx ventricular arrhythmia
+/- B blocker activity
IV Ca2+ channel blocker Tx supraventricular
arrhythmias
V Cardiac glycoside Atrial fibrillation Digoxin
Supraventricular Ars

Cardiac congestion drugs:

• Angiotensin antagonist - ¯V
o Angiotensin converting enzyme (ACE) antagonists - inhibits E that convert angiotensin I->II
o Angiotensin II receptor antagonist
• Diuretic -> ¯venous return

Tx myxomatous mitral valve dz: triple therapy. Inferior therapeutic effect by themselves. Can be given in combined
formulations to ­o compliance
• Diuretic
• Angiotensin II inhibitor
• +ve inotrope (Pimobendan)

Diuretics:
• Loop diuretics – on LH – blocks uptake of Na, Cl, K
o Most effective
• Thiazides
• Potassium-sparing (aldosterone receptor agonist)
• Osmotic, e.g. mannitol
• Carbonic anhydrase inhibitor
o E.g. dorzolamide for glaucoma

Furosemide:
• Most effective loop diuretic
• Mild venodilation action
• Polar – mostly renal excretion
• Tablets, injectables
• Side-effects
o Na+ loss – but usually made up for by RAAS
o K+ loss – poor ability to replenish, particularly in cats
o Resistance

Indications of diuretics:
• Pulmonary oedema/oedema due to cell mb damage
• Acute hypercalcaemia
• Certain cases of anuria (osmotic diuretic)
• Overzealous IV fluid administration

ACE-I inhibitors:
• Conversion to active metabolite
• Inhibit formation angiotensin II
o ¯Na+ and H2O
• E.g.
o Benazepril (Fortekor)
o Enalapril (Enalfor)
o Imidapril (Prilium)
• Side-effects
o Interferes with angiotensin II maintenance of efferent arteriole tone
§ ¯tone
§ ¯GFR
§ Azotaemia (relatively rare, mild changes)
o Systemic hypotension (rare)
o Hyperkalaemia (rare)

Tx for proteinuria:
• Angiotensin inhibitors, e.g. telmisartan (Semintra)

Sequelae of proteinuria:
• Cause further kidney damage
o Proteins, lipids toxic to tubular epithelial cells
§ Inflammation
§ Apoptosis
o Excessive lysosomal processing of proteins
§ Lysosomal rupture
§ Intracellular release of cytotoxic enzymes
o Tubular obstruction by proteinaceous casts
• Indicator of CKD (dogs, cats)

Causes of red cell agglutination:

• Large platelets causing them to be counted as RBCs
o Falsely ¯MCV
Internal vomiting: can be present in horse as unable to vomit externally

Viral cardiac pathogens

Viral cardiac pathogens:
• Parvoviruses
Parvovirus:
• If dogs infected in utero or before 2wo, myocyte damage
o Cardiac dysfunction manifests from 8wo
• Feline counterpart doesn’t cause cardiac dysfunction
• Leukopaenia due to destruction of BM cells
• Small non-enveloped DNA virus
• Environmentally resilient
• No DNA pol – borrows

Retroviruses:
Subfamily Genus Example species
Orthoretrovirinae Alpharetrovirus Avian leukosis virus
Betaretrovirus Mouse mammary tumour virus
Gammaretrovirus Feline leukaemia virus
Koala retrovirus
Deltaretrovirus Bovine leukaemia virus
Epsilonretrovirus Walleye dermal sarcoma virus (fish)
Lentivirus FIV
Bovine immunodeficiency virus (BIV)
Caprine arthritis-encephalitis virus
(CAEV)
Equine infectious anaemia (EIAV)
Sheep ovine lentivirus (Visna Maedi)
Lion lentivirus

• Components
o Reverse transcriptase (RT)
o Integrase (IN)
• Insert themselves into the host genome
o Some capable of vertical transmission

Provirus:

Diagnosis:
• Identification of provirus by PCR

Endogenous vs exogenous retroviruses:

Endogenous Exogenous
Viraemia Yes No
Transmission Horizontal No horizontal
Vertical possible but uncommon Vertical only
Disease? Yes (not always) No

FIV:
• Transmission
o Bites from infected cats
o Blood transfusion
o Intramammary
§ Large V in milk but ingestion not efficient mode of transmission
§ 22% transmission to kittens
• Risk factor
o Age – due to accumulated risk of infection
o Outdoor cat
o M>F
o Close contact with other cats
o Stress
o Poor health and hygiene
• Too low C of Ag in blood for detection
• 6wk seroconversion
• ¯Th cells
• Lives within T-cells
• Pathology
o ¯CD4+ cells
• Clinical signs
o Lymphoid depletion
o Severe immunodeficiency
o Neoplasia
o Weight loss
o Chronic, recurrent opportunistic infections
o Recurrent GIT dz
o Neurologicla dz
o ¯survival rate to 6yo to
o B cell, multicentre lymphosarcoma – often involves abd structures
• Diagnostic test
o Idexx
§ V. sp, v. se
§ Cross-reacts with vx
o Zoetis
o Bionote

FeLV vs FIV:

FeLV FIV
Can cause haematological disturbances (leukocytopaenia, anaemia)
Infect and are transported around body within leukocytes (lymphocytes)
Can cause haematopoetic neoplasia (leukaemia)

Treatment:
• Re-test, esp. if vx
• Segregate from other cats
• Test + vx in-contact cats

FIV vx:
• Protective rate ­

Pros and cons of lab vs field study:

FeLV:
• Transmission
o Chronic exposure to virus
• Presentations
o Abortive infections
§ No Ag in blood or PCR
§ Ab
o Progressive a
o Regressive infection – doesn’t sprea dot
§ No ag in body and PCR
• Signlament
o Young animals
• Diagnosis
o Idexx
IMAGING OF THE THORACIC CAVITY

Abnormalities in thoracic x-ray:

• Ability to see diaphragm as single mb -> air in abd cavity
o Air from surgery (<8wks after surgery)
• Ability to see mediastinal structures -> pneumomediastinum
o Rupture of trachea -> incorrect ET placement
• White lung – fluid in lungs
o Pneumonia
• Loss of visibility of lung vessels – fluid in lungs
• Loss of visibility of heart contour but lung vessels still present
o Pleural effusion
• Ability to see lung lobes
• Pleural masses
o Herniation of abd contents
• Focalised opacity in lung
o Abscess
o Granuloma
o Neoplasia

Normal thoracic radiograph:

• Lungs black except for fine vessels
• Pericardium + heart able to be seen
• Thick diaphragm due to liver underneath
• Cannot see contour of lungs or different lobes

Dz Appearance Description
Pneumothorax

Pleural effusion Visualisation of

interlobal ifssures
 Retraction of lung
from thoracic wall
Low-opaque space
between lung and
thoracic wall
Silhouetting
Aspiration Hepatinisation of
pneumonia lung

Lung mass Lump visible only

only on opposite
lateral view x-ray
as lung becomes
atelectic when
dog placed on that
side and mass
becomes
indistinguishable
from lung
 ->L lateral projection: L side of animal is down on table
->dog is always facing L in all lateral views
Causes of wet lung:
• Pulmonary contusion
• Aspiration pneumonia – localised in cranioventral lung tissue due to gravity
• Pneumonia
o Bronchopneumonia (cranioventral)
• Pulmonary oedema
o LHF

Signs of wet lung:

• Soft tissue opacity
• Border effacement
• Air bronchograms
Taking x-rays:
• Always take 3 x-rays (dorsoventral, L lateral, R lateral

Reading heart x-rays:

• Cannot distinguish chambers of heart
• Estimate location of chambers according to silhouette of heart
• Cardiac silhouette composed of
o Pericardium
o Great vessels
§ Ascending aorta
§ Aortic arch
§ Main pulmonary artery

Visualising heart: often used in conjunction. Start with x-ray and follow up with echocardiogram if likely disease
• X-ray – useful only to diagnose CHF
o Poor at identifying cardiac dz – poor visualisation of the heart
• US
• Echocardiogram – cardiac dz
o Not v. useful for heart failure

Herpesvirus
Herpesviridae:
• Enveloped dsDNA
• Icosahedral capsid
• Fragile – do not survive well outside of body
• Transmission
o Short distance droplet spread
o Direct contact with mm
• Latency – all herpesvirus establish latency
o In neural ganglia in episomal (circular DNA) form
o Exit from latency
§ Intermittent or continuous shedding
§ Clinical or subclinical dz
• Cell-mediated immunity
• Immune response can only limit reactivation from latently-infected cells
• Diagnosis
o Clinical signs
o PCR (URT swabs, oral lesions, URT horses, aborted foals)
o Eosinophilic inclusion bodies on histopathology
 o Cell culture
o Examination for cytopathic effects
• Vx – only ¯ incidence of dz
o Feline herpesvirus 1 (MLV/killed)
o Equine herpesvirus 1, 4
o Gallid herpesvirus 2 (marek’s dz) (MLV/recombinant)
o Gallid herpesvirus 1 (infectious laryngotracheitis)
o Pseudorabies virus vaccines
o Bovine herpesvirus 1 (MLV/genetically modified)

Classification:
Order: Herpesvirales
• Herpesviridae (mammals, birds, reptiles)
o a (alphaherpesvirinae) (subfamily)
§ Localised skin/mm lesions in respiratory/genital tract
§ Signs
• Vesicles to pustules to shallow ulcers covered by pseudomembrane/scab
• Abortion (EHV1, CHV1, pseudorabies virus)
§ Often don’t form viraemia
§
o b
o g
• Alloherpesviridae (fish, frogs)
• Malacoherpesviridae (oysters)

EBV: Epstein-Barr Virus

• Proliferation of infected B cells
• Immune response against infected B cells causes glandulr feer

Pathogenesis:
1. Attach to cell surface R by viral glycoproteins protruding from viral envelope
2. Icosahedral nucleocapsid penetrates cell
a. Fusion of viral envelope with cell surface mb
3. DNA-protein complex enters nucleus
a. Shuts off host protein synthesis
4. Viral replication in host cell nucleus
5. Buds through nuclear mb – aquires an envelope
6. Mature virions accumulate in vacuoles in cytoplasm
7. Transfer to cell surface
8. Exit from cell by
a. Lysis
b. Exocytosis
c. Syncitia (cell-to-cell fusion)
9. Axonal spread from infected mucosal sites
10. Reactivation of latency by
a. Cold weather
b. Concurrent dz
c. Stress
d. Nutritional deficiencies
e. Immunosuppressive therapy

Subfamily Properties Example Disease caused

Alphaherpesvirinae Bovine herpesvirus 1 Infectious Bovine Rinotracheitis virus (IBR)
Infectious Pustular vulvovaginitis virus
Balanoposthitis
Bovine herpesvirus 2 Mammilitis/pseudo-lumpy skin disease virus
Bovine herpesvirus 5 Bovine encephalitis virus
Canid herpesvirus 1 Generalised haemorrhagic disease of pups
<4wks
Genital dz (adult dogs)
Caprine herpesvirus Conjunctivitis
1 (exotic) Respiratory, digestive, genital tract dz
 Equid herpesvirus 1 Equine abortion virus
Equine herpesvirus myeloencephalopathy
(EHM)
Equid herpesvirus 4 Equine rhinopneumonitis virus
Equid herpesvirus 3 Equine coital exanthema virus
Equid herpesvirus
6,8,9
Felid herpesvirus 1 Upper respiratory tract infections
Keratitis
Skin lesions
Gallid herpesvirus 1 Avian infectious laryngotracheitis virus
Gallid herpesvirus 2 Marek’s disease virus (tumours/paralysis)
Suid herpesvirus 1 Pseudorabies/Aujeszky’s disease virus
Betaherpesvirinae Slow replicative cycle Murid herpesvirus 1
Slow onset of cell and 2
lysis
Individual viruses has
restricted host range
Latency in secretory
glands,
lymphoreticular
tissue, kidney
Betaherpesviruses of
lab animals
Elephantid Endotheliotropic elephant herpesvirus
herpesvirus
Suid herpesvirus 2 Porcine cytomegalovirus
Gammaherpesvirinae Narrow host range, Equid herpesvirus
infect lymphoid, 2,5, 7
epithelial, fibroblastic
cells.
Feline
gammaherpesvirus 1
Bovine herpesvirus 4
Alcelaphine Malignant catarral fever (cattle, deer)
herpesvirus 1
Ovine herpesvirus 2 Malignant catarrhal fever
Caprine herpesvirus Malignant catarrhal fever (goat)
2

EHV1: Equine abortion virus

• V. similar to EHV4 so cross-reactive in a lot of tests
• ELISA capable of differentiating
• Most significant cause of abortions
• Signs
o Abortions late in pregnancy (4-9m)
§ Sporadric
§ Abortion storms (in large groups)
o No clinical sign in the mare
o Signs of aborted foetus
§ Icterus
§ Pale foci of necrosis on liver
§ Meconium staining of skin
§ Mm petechiation
§ SQ/pleural/peritoneal effusion
§ Splenomegaly with prominent lymphoid follicles
o Neonates
§ Respiratory distress
§ Interstitial pneumonia
§ Death
o Adults
§ Equine herpesvirus myeloencephalopathy (EHM) form
 • Viral vasculitis in blood vessels of blood vessels
• Thrombus formation
• Hypoxia of neural tissue
• Ataxia to forelimb & hindlimb paralysis
• Nasal discharge
• Incoordination
• Hindquarter weakness
• Recumbency
• Lethargy
• Urine dribbling
• Diminished tail tone
• Prognosis
o EHM
§ Good if doesn’t go into recumbency
• Transmission
o Foals infected by mare
o Mares infected by weanlings with 1ary EHV-1 infection
o Recrudescence of latent infection due to stress
• Incubation period = 2-10d
• Respiratory shedding = 7-10d
• Isolation period = 21d
• Prevention
o Killed vx for EHV-1, EHV4
§ 5th, 7th, 9th month of gestation
§ During abortion storm
o Vx doesn’t cover EHM
o Only provides short-term reduction of infection risks
• Diagnosis
o Clinical presentation
o Histopathology of PM on foetus
§ Eosinophilic intranuclear inclusion bodies in foetal liver, spleen, lung, thymus
§ Fluorescent Ab-staining/immunohistochemistry
o PCR of aborted foetus (lung, thymus, spleen)
o Isolation and culture from foetal liver, spleen, lung, thymus
o Ab to EHV1 in mare not v useful as
§ not produced in latent infection
§ Infection precedes abortion by several weeks
• Management
o Limit movement of broodmares in and out of herd
o Minimise stress in pregnant and lactating mares
o Separate into groups according to foaling date
o Quarantine index case

<7m foetus 7-11m foetus Neonates Adults

No response Abortion or birth and death within 2-3d Interstitial pneumonia, generalised dz, Encephalomyeitis
death

EHV3: Equine coital exanthema

• STD
• Acute
• Signs
o Papules/vesicles/pustules/ulcers
§ Penis/prepuce of stallions
§ External genitalia/perineal skin of mares
§ (nares, lips, conjunctiva)
o Perivascular lymphocyte accumulation
o Periglandular “
o Possible 2ary bacterial infection
o Depigmented scars/erosions/ulcers after 2w
• Transmission
o Fomites
 o Sexual bodily fluids
• Latency – reactivation from sacral ganglia
• Affects mostly keratinised epithelium
• T-dependent
• Diagnosis
o Clinical signs
o Serology
o Histopath
o PCR
• Tx
o Topical analgesic ointments
o No sex for 3w

EHV4: Equine rhinopneumonitis virus

• URT dz
• >2mo, <2yo
• Acute dz
• Signs
o Fever
o Lethargy
o Serous to mucopurulent nasal discharge
o Congested conjunctiva
o Submandibular lymphadenomegaly
• Tx
o Live-attenuated, inactivated vx

Canid herpesvirus 1 (CHV1):

• Signs
o Stillbirth/abortions/mummification in utero
o Acute fatal illness in 1-3wo
o >3wo
§ Depression
§ Anorexia
§ dyspnoea
§ Yellow-green d+
§ Colic
§ Mucopurulent nasal discharge
§ Petechial haemorrhages
§ Necrosis/haemorrhage in kidney, liver, lung
§ Death within 1-3d
§ Placental necrosis
o Adults
§ Enlargement of submucosal lymphoid dollicles
§ Vaginal hyperaemia
§ Petechial/ecchymotic haemorrhages
§ Not 1ay cause of respiratory distress
§ meningoencephalitis
• A-herpesvirus
• Sensitive to lipid solvents
• Inactivated >40C/common disinfectants
• Specific to canines
• Transmission
o Perinatal – contact with infected birth canal
o Oronasal secretions
o Shed from nsala/genital secretions for m-y
• Latency
o Trigeminal ganglia
o Lumbosacral ganglia
o Tonsils
o Parotid sg
• Exit of latency by stress, immunosuppressive drugs
• Pathogenesis
o Replication in nasal mucosa/pharynx/tonsils
o Spread within macrophages within blood to liver, kidneys, lymph, lungs, CNS
• Tx
o Killed vx for short-term protection
o Raising body T >33C
o Antiviral tx to prevent further spread (vidarabine)

Feline herpesvirus-1: Feline viral rhinotracheitis virus

• Signs
o Respiratory (sneezing, rhinitis, tracheitis)
o Bilateral serous to serosanguinous ocular discharge +/- mucus
§ Dried brown ocular exudate typical
o Non-ulcerative inflammation of cornea
o Ulcerative keratitis
o Dendritic corneal ulcers
o Transient keratocojunctivitis sicca (dry eye)
§ Ductal occlusion with inflammation/debris
§ Inflammation of lacrimal glands
o Bilateral conjunctival oedema
o Chronic rhinosinusitis (snuffling) – if affects underlying bone/cartilage
o Oral
o Nasal
o Skin lesions
o Abortion due to systemic illness
o Eosinophilic granulomatous inflammation
• Transmission
o Fomites
o Nose-to-nose contact
o Respiratory/ocular fluids up to 1.3m
o Sneezing onto mm
• Inactivated by most disinfectants
• Latency in 80% - re-emergence with stress
o Trigeminal ganglia
o 4-11d after stressful event
• Exit latency due to stress
• Shedding can be asymptomatic
• Most susceptible at 8w when maternal ab wane
• Incubation period = 1-7d
• Ddx
o FCV (50%)
o Chlamydia felis (few %)
o Bordatella bronchiseptica
• Pathogenesis
o Replication in mucosa of nasal septum, turbinates, nasopharynx, tonsils, mandibular LN, upper trachea
o Cell lysis -> necrosis
o Neutrophilic infiltration
o Elimination by immune system
• Tx
o AB
o Fluids
o Anti-inflammatories
o Virostatic agents
§ Idoxuridine as an ophthalmic solution
§ Acyclovir topical ointment until 1w after resolution of ocular signs
§ Famciclovir
§ Interferons (e.g. IFN-a) – reduces clinical dz but not shedding – needs more research
• Prevention
o Vx
§ ¯severity of dz
§ ¯load of latent virus in trigeminal ganglia
• Diagnosis
 o Clinical signs
o fam
o PCR from swabs/scrapings - ¯specificity
§ FHV1 present only coincidentally
§ FHV1 present only due to reactivation by another dz
o Histopathology – eosinophilic intranuclear inclusion bodies
->Continue with yearly vx as don’t know how long cell-mediated immunity for FHV lasts

Gallid herpesvirus 1 (Avian Infectious Laryngotracheitis, ILT):

• 4-18mo most susceptible
• Incubation 6-12d
• Signs
o Coughing
o Sneezing
o Nasal and ocular discharge
o Dyspnoea
o Depression
o Necrosis of trachea
o Conjunctivitis
o ¯egg production
• Transmission
o Aerosol droplets
o For months
• Diagnosis
o Clinical signs
o Histo
o Immunohistochemistry
o PCR
o Viral culture
• Prevention
o AIAO
o LA vx – but can cause outbreak due to reversion of train to virulence

GHV2: Marek’s dz: lymphoproliferative, neuropathic dz

• Signs
o Lameness
o Droopy wing
o Weakness
o Dropping head
o Paralysis of extremities
o Lymphoma in viscera and nerves
• Signlament: chickens 2-5mo
• Prevention: vx in ovo at 18d or 1do

BHV1:
• 3 presentations
o Infectious bovine rhinotracehitis (IBR)
o Infectious pustular vulvovaginitis
o Balanoposthitis
• Signs
o Rhinotracheitis
o Fatal bronchopneumonia
o Conjunctivitis
o Meingoencephalitis (young calves)
• Tx
• Latency – in trigeminal ganglia
• Tx = vx
o ML vx
o Use intranasal vx for pregnant cars

BHV2: Bovine mammillitis:

• Pseudolumph kin disease
• Mammilitis
• Stomatitis
• Diagnosis
o Clinical signs
o Viral isolation
o ­ab titre

BHV5: Bovine encephalitis virus

• Non-suppurative meningoencephalitis
• Distinguish by restriction endonuclease from BHV1