Académique Documents
Professionnel Documents
Culture Documents
10/30/16
Genus staphylococci
Genus streptococci
A. Genus staphylococci
General Characteristic
Gram-positive cocci
Non-sporulating, non-motile
Grape-like clusters
Facultative anaerobe
Round colony in media
Some of them are normal flora of the skin and mucus membrane
It can produce catalase, (d/t from streptococcus)
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1. Staphylococcus aureus
Habitat
Transmission
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Virulence factors
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3. d-toxin
Very small peptide toxin produced by most strains of S.
aureus
It is also produced by S. epidermidis.
The role of d-toxin in disease is unknown
4. Leukocidin
Is hemolytic, but less than alpha hemolysin
5. Coagulase and clumping factor
Coagulase is an extracellular protein which binds to
prothrombin in the host to form a complex called
staphylothrombin
It is reasonable to speculate that the bacteria could
protect themselves from phagocytic and immune
9
defenses by causing localized clotting. 10/30/16
6. Staphylokinase
Lyses fibrin
Localized fibrinolysis might aid in bacterial spreading
7. Other extracellular enzymes
Proteases
Lipase
Deoxyribonuclease (DNase)
Fatty acid modifying enzyme (FAME).
The first three provide nutrients for the bacteria, and it is
unlikely that they have anything but a minor role in
pathogenesis
o The FAME enzyme important in abscesses
Modify anti-bacterial lipids and prolong bacterial survival
o
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Clinical Manifestation
It causes superficial skin lesions such as boils and
furunculosis
More serious infections such as:
Pneumonia
Mastitis(inflammation
Meningitis,
of the breast )
and
UTI,
and
Deep-seated infections, such as: Osteomyelitis and endocarditis
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4. Exotoxins
Systemic release of -toxin causes septic shock, while
enterotoxins and TSST-1 are superantigens that may cause
toxic shock.
Staphylococcal enterotoxins cause emesis (vomiting) when
ingested and the bacterium is a leading cause of food
poisoning
Exfoliatin toxin causes the scalded skin syndrome in
neonates, which results in widespread blistering and loss of
the epidermis
There are two antigenically distinct forms of the toxin, ETA and ET-B
The toxins have esterase and protease activity and
apparently target a protein which is involved in maintaining
the integrity of the epidermis
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Superantigens
S. aureus secretes two types of toxin with superantigen
activity, enterotoxins, of which there are six antigenic types
(named SE-A, B, C, D, E and G), and toxic shock syndrome
toxin (TSST-1)
Enterotoxins
TSST-1
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Clinical significance
S. aureus causes
disease by infecting
tissues
typically
creating
abscesses
and/or by producing
toxins.
The
localized
host
response
to
Staphylococcal
infection
is
inflammation,
characterized
by
swelling, accumulation
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of pus, and necrosis of
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3. Acute Endocarditis
Generally associated with intravenous drug
abuse
Caused
by injection of contaminated
preparations or by needles contaminated
with S. aureus.
S. aureus also colonizes the skin around the
injection site, and if the skin is not sterilized
before injection, the bacteria can be
introduced into soft tissues and the
bloodstream, even when a sterilized needle
is used.
4. Septicemia
Is a generalized infection with sepsis
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5. Pneumonia
6. Nosocomial infections
S. aureus is one of the most common
causes of hospital-acquired infections,
often of wounds (surgical, decubital) or
bacteremia associated with catheters
7.Toxinoses
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Staphylococcal gastroenteritis
Is caused by ingestion of food contaminated
with enterotoxin-producing S. aureus.
Often contaminated by a food-handler,
these foods tend to be protein-rich and
improperly refrigerated. Symptoms, such as
NVD
Scalded skin syndrome
Involves the appearance of superficial
bullae resulting from the action of an
exfoliative
toxin
that
attacks
the
intercellular adhesive of the stratum
granulosum, causing marked epithelial
desquamation.
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22The bullae may be infected or
may result
Diseases
Clinical symptoms
Pathogenicity factors
Gastroenteritis 2-6 hours after ingesting
Enterotoxins A-E
(food poisoning) toxin: nausea, abdominal
preformed in food
- toxin ingested pain, vomiting, followed
preformed in
by diarrhea
food
Infective
Fever, malaise,
Fibrin-platelet mesh,
endocarditis leukocytosis, heart murmur
cytolytic toxins
(may be absent initially)
Abscesses/furun Subcutaneous tenderness, Coagulase, probably
cles/carbuncles redness and swelling; hot
the cytolysins
Toxic Shock
Fever, hypotension,
TSST-1
Syndrome
scarlatiniform rash which
desquamates (particularly
on palms and soles,
multiorgan failure
Impetigo
Erythematous papules to Coagulase, exfoliatins
bullae
Pneumonia
Productive pneumonia with
?, all
rapid onset, high rate of
necrosis and high fatality;
nosocomial, ventilator,
postinfluenza, IV drug
abuse, CF, CGD, etc.
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Surgical
Fever with cellulitis and/or
Coagulase,
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Coagulase-Negative Staphylococci
2. Staphylococcus epidermidis
Of twelve coagulase-negative Staphylococcal species
3. Staphylococcus saprophyticus
The
Laboratory DX
Specimen- surface swabs of wound, pus,
blood sputum, CSF, Feaces
Gram stains- gram positive cocci in cluster
Culture-grow well aerobically and in CO2
enriched media at 37 oC
Colony appearance
S.aureus Golden colony
S. epidermids- White colony
S. saprophytics-white or yellow colony
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Biochemical Test
Catalase test
Staphylococici- positive
Streptococci -negative
Coagulase test
S. aureus positive, Salt tolerant; ferments
mannitol on mannitol salt agar
S. epidermidis- negative
S. saprophytics - negative
Prevention
Prevention of contact with S-aureus is almost
impossible
Treatment
Ampicillin- for penicillin sensitive staphylococci.
???? Cloxacillin, Floxacillin- for penicillin resistance
staphylococci????
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B. Streptococcus
Gram positive
Facultative anaerobic
Non spores, Non motile
Catalase negative
Chain like
Lancefield grouping
Species-specific CHO cell wall antigens
Groups designated A-H, K-V
Some are not grouped
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importance
1. S. pyogens ----------- Lance field group
A
2. S.agalactial ----------- Lance field group
B
3. Enterococci ----------- Lance field group
D
NB.Viridan
Streptococci
and
anaerobic
Streptococci are not grouped under Lance field
classification
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1. S. pyogen
Nonmotile
Non sporeforming
Chains
Catalase-negative
Facultative anaerobe
Gram-positive
Group A, beta hemolytic
Streptococcus
Have a capsule composed of
hyaluronic acid????
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Streptococcus
pyogenes.
Uper.
Gram
stain
of
Streptococcus pyogenes in a
clinical
specimen.
Lower.
Colonies
of
Streptococcus
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Pathogenesis
Virulance factor
M protein: fibronectin-binding protein (Protein F) and
lipoteichoic acid for adherence, inhibit phagocytosis.
Hyaluronic acid capsule: as an immunological cover
and to inhibit phagocytosis
Invasins: such as streptokinase, hyaluronidase, and
streptolysins O & S
Exotoxins: such as pyrogenic (erythrogenic) toxin
which causes the rash of scarlet fever and systemic
toxic shock syndrome.
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Clinical significance
Acute pharyngitis(inflammation of pharynx) or
pharyngotonsilitis
Impetigo
Erysipelas
Puerperal sepsis
Acute rheumatic fever
Acute glomerulonephritis
Streptococcal TSS
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Laboratory diagnosis
Detection of the bacteria from clinical specimen
Gram stain
Culture
Catalase test negative
Identification from non pyogen B-hemolytic is by
bacitracin test, S. pyogen is more sensitive
Serology
Group A antigen can be detected using particles coated
with antibodies (latex agglutination)
ASO
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Treatment
Penicillin is still uniformly effective in treatment of
Group A Streptococcal disease
No effective vaccine has been produced, but specific Mprotein vaccines are being tested.
Prevention
Rheumatic fever is prevented by rapid eradication of the
infecting organism
Prolonged prophylactic antibiotic therapy is indicated
after an episode of rheumatic fever
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2. Streptococcus agalactiae
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Laboratory diagnosis
Smear- non motile gram positive cocci in chains
Culture- grow in aerobic and anaerobic environment at
temp 35-37oC
Grow in ordinary media with shiny or dry colonies with
gray white or colorless appearance
Shows clear zone of hemolysis(beta hemolysis) on blood Agar
Catalase: Negative
Bile solubility test: Negative
cAMP test: Positive
Bacitracin: Negative/resistant
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Encapsulated, spherical
Anaerobic
Lancet-shaped cocci
Fastidious
Alpha hemolytic
Transmission
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Virulance
Capsule
Choline binding proteins
Hemolysins
IgA protease
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Clinical significance
Laboratory diagnosis
1. Catalase negative; 2 H202 2 H20 + 02
2.Optochin test (ethylhydrocupreine HCl), inhibits
Optochin
growth of pneumococci but not viridans positive
Optochin negative
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5. Animal Inoculation
Fatal infection within 16-48 hours to mice injected
pneumococci antigen intraperitoneally
For experimental purposes
Serologic Diagnosis
Detection
of pneumococcal antibodies
Radioimmunoassay
Detection of capsular polysaccharide
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Treatment
Multiple antibiotic resistant strains of S. pneumoniae emerged in the
early 1970s
Increases in penicillin resistance have been followed by resistance to
cephalosporins and multidrug resistance
Antibiotic susceptibility testing is important
Prevention
There are two types of pneumococcal vaccine:
pneumococcal polysaccharide vaccine (PPV) and
pneumococcal conjugate vaccine (PCV7)
PPV: immunizes against 23 serotypes of
S. pneumoniae and is
indicated for the protection of high-risk individuals older than two
years
PCV7: is effective in infants and toddlers (six weeks to five years of age)
1. Neisseria gonorrhoeae
N.gonorrhoeae
is
frequently
observed
inside
polymorphonuclear leukocytes of clinical samples
obtained from infected patients
Usually transmitted during sexual contact or, more rarely,
during the passage of a baby through an infected birth
canal
It does not survive long outside the human body because
it is highly sensitive to dehydration
Gonococci are unencapsulated
Structure
1.Pili
Enhance attachment and resistance to phagocytosis
Among the most important virulence factors
At least twenty gonococcal genes code for pilin
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Pathogenesis
It is associated with the acute onset of symptoms and
purulent mucosal drainage due to the organisms ability to
recruit polymorphonuclear leukocytes (PMNs)
Pili and OMP II facilitate adhesion of the gonococcus to
epithelial cells of the urethra, rectum, cervix, pharynx, or
conjunctiva and, therefore, make colonization possible
Pili also enable the bacterium to resist phagocytosis
Gonococci produce an IgA protease that cleaves IgA,
helping the pathogen to evade immunoglobulins
After gonococci attach to the nonciliated epithelial cells
of the fallopian tube, they are surrounded by the
microvilli, which draw them to the surface of the mucosal
cell
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Host Defenses
Not everyone exposed to N. gonorrhoeae acquires the disease
This may be due to variations in the size or virulence of the
inoculum, to nonspecific resistance, or to specific immunity
Nonspecific factors have been implicated in natural resistance
to gonococcal infection
In women, changes in the genital pH and hormones may
increase resistance to infection at certain times of the menstrual
cycle
The variability in the susceptibility of gonococcal strains to the
bactericidal and bacteriostatic properties of urine is thought to
be one of the reasons some men do not develop a gonococcal
infection when exposed
Most uninfected individuals have serum antibodies that react
with
58 gonococcal antigens????
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Antigenic Variation
It is among several microorganisms whose surface
structures are known to change antigenically from
generation to generation during growth of a single strain
The antigenic structures of major interest are pili, Opa
proteins and LOS, for which there is evidence of antigenic
variation both in vitro and in vivo.
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Epidemiology
The only natural host for N. gonorrhoeae is the human
Gonorrhea is transmitted almost exclusively by sexual
contact
The highest rates occur in women between the ages of 15
and 19 years and in men 20 and 24 years of age
Gonorrhea is usually contracted from a sex partner who
is either asymptomatic or has only minimal symptoms
It is estimated that the efficiency of transmission after one
exposure is about 35% from an infected woman to an
uninfected man and 50 to 60% from an infected man to
an uninfected woman
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Clinical Significance
The organisms may cause a localized infection with the
production of pus, or may lead to tissue invasion, chronic
inflammation, and fibrosis.
A higher proportion of females than males are generally
asymptomatic; these individuals act as the reservoir for
maintaining and transmitting gonococcal infections.
Genitourinary tract infection presents with a yellow,
purulent urethral discharge and painful urination.
A greenish-yellow cervical discharge is most common,
often accompanied by intermenstrual bleeding.
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Diagnosis
Specimens for the laboratory diagnosis of gonorrhea
should be collected before treating the patient
N. gonorrhoeae grows best under aerobic conditions, and
most strains require enhanced CO2
N. gonorrhoeae ferments glucose but not maltose, lactose,
or sucrose.
Thayer-Martin medium (chocolate agar supplemented
with several antibiotics that suppress the growth of
nonpathogenic neisseriae and other normal and abnormal
flora) is typically used to isolate gonococcus
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Control
There is no effective vaccine to prevent gonorrhea
Candidate vaccines consisting of pilus protein or Por are of little
benefit
The development of an effective vaccine has been hampered by
the lack of a suitable animal model and the fact that an effective
immune response has never been demonstrated
Condoms are effective in preventing the transmission of
gonorrhea
The evolution of antimicrobial resistance in N. gonorrhoeae may
ultimately affect its control
Strains with multiple chromosomal resistance to penicillin,
tetracycline, erythromycin and cefoxitin have been identified in
different geographical areas
Sporadic
high-level resistance to spectinomycin and
fluoroquinolones
have been reported
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2. Neisseria meningitidis
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Virulence Factors
Meningoccal endotoxin (LOS) is responsible for many toxic
effects
Capsule
protects bacteria from antibody mediated
phagocytosis
Pili allow to colonization of nasopharynx
Pathogenesis
The meningococcus is an exclusively human parasite
It can either exist as an apparently harmless member of the
normal flora or produce acute disease
Meningococci range from carrier state to bacteremia
Pili attach to microvilli as introduction to invasion
Polysaccharide capsules are antiphagocytic
Spread to blood and CNS produce systemic endotoxemia
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LPS and PG trigger cytokine release 10/30/16
Manifestations
Meningitis is most frequent infection
Meningococcemia and rash may progress to disseminated
intravascular coagulation /DIC/
Meningococcal encephalitis
Pneumonia
Endocardiatis
Urethritis
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Diagnosis
Laboratory diagnosis
diplococci
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Biochemical reactions
Species
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Prevention
Rifampin is now the primary chemoprophylactic agent,
but ciprofloxacin has also been effective
A, C,Y, and W-135 polysaccharide vaccines are useful in
high-risk populations
Protein
conjugate vaccines(PCV) may enhance
immunogenicity in children
Nonimmunogenic serogroup B polysaccharide remains a
problem
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III. Enterobacteriaceae
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Classification
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Grow
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Transmission
Ingestion of contaminated food or water
Main sources of E.coli include:
Undercooked meat
Unpasteurized milk, apple juice and orange juice
Swimming in or drinking water contaminated with sewage
Unwashed vegetables and fruits
Bacteria in the diarrhea of infected persons can be passed on if
their hands are not washed well
Epidemiology
E.coli have world wide distribution
Many countries around the world are constantly suffering
from E. coli contamination
Is most common cause of diarrhea in tourists
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Antigens of E.coli
O antigen
Somatic (on LPS)
171 antigens
H antigen( protein )
Flagella
56 antigens
K antigen
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Virulence Factors
Fimbriae (Pili)
Hemolysins
Flagella
Exotoxins(Thermolabile toxin (LT) & Thermostable toxin
(ST)
Endotoxin LPS
Capsules
K antigens
Drug resistance plasmids
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Pathogenesis
Heat-labile (LT) enterotoxins: an A-B toxin which increases intracellular
levels of cAMP.
Subunit A causes intense and prolonged hyper-secretion of chloride ions
and inhibits the reabsorption of sodium and chloride
The gut lumen is distended with fluid and hypermotility and secretory
diarrhea occur, lasting for several days
It stimulates the production of neutralizing antibodies, and cross-reacts
with cholera toxin
The pathogenesis of LT is initiated by binding of LT-B subunits to the
ganglioside receptor GM1 found in caveolae on the host cell surface
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Pathogenesis
In EIEC the plasmid encode a gene for a K surface
antigen which enables to:
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Pathogenesis
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Pathogenesis
Do not invade mucosal cells as readily as Shigella, but EHEC
Diagnosis of E. coli
Clinical
Laboratory
Serology, culture, mcroscopy
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Treatment
Antibiotic therapy must take into consideration the resistance pattern
of the pathogen
Aminopenicillins
Ureidopenicillins
Cephalosporins,
Floroquinolones, or
Cotrimoxazole
losses
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2. Shigella
Enteric rods
Gram-negative
Facultative anaerobes
Non-spore forming
Oxidase negative
Non motile
Possess O and some have K antigens
Do not produce gas from glucose
Do not produce H2S on TSI
Non-lactose fermenters
Four species
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Pathogenesis
Two-stage disease:
Early stage:
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Virulence Factors
1.Invasiveness
Attachment (adherence) and internalization with complex
genetic control
Large multi-gene virulence plasmid regulated by multiple
chromosomal genes
2. Exotoxin (Shiga toxin)
3. Intracellular survival & multiplication
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Complications
Severe anorexia
Hypoproteinaemia
Dilation of the large intestine
Seizures
Anaemia
Hemolytic uremic syndrome(HUS)
Disseminated intravascular coagulation (DIC)
Reiter syndrome
Persistent diarrhoea
Rectal prolapse
Weight loss and malnutrition
Arthritis, conjunctivitis & urethritis
Myocarditis
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Laboratory diagnosis
Direct microscopy
Culture
Slide agglutination test
Macroscopy
Bright
red stool
Adherent to container
Odorless
small quantity
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Treatment
Replace fluids: Oral or IV rehydration with fluids and
electrolytes
Treat with antibiotics: trimethoprim/sulfamethoxazole,
Ampicillin, Ciprofloxacin,
Prevention and Control:
Hand washing, especially after defecation
Improved sanitation and hygiene
improve
sanitation
reduce overcrowding, etc.
No effective vaccine
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3. Salmonella
Gram-negative
Oxidase negative
Non-sporulated
Facultatively anaerobic
Motile
Produce gas from glucose
Produce H2S on TSI media
Non lactose fermenter
Ubiquitous/very common human and animal pathogens
Salmonellosis in humans usually takes the form of a selflimiting food poisoning (gastroenteritis), but occasionally
manifests
as a serious systemic infection (enteric
fever)
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or flagellar antigen
O or somatic antigen and
Vi antigen
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Habitat
The principal habitat of the salmonellae is the intestinal
tract of humans and animals
Typhi and Paratyphi A are strictly human serovars that
may cause grave diseases often associated with invasion
of the bloodstream.
Salmonella classification has undergone numerous
revisions; currently, all strains are grouped in two species:
S. enterica and S. bongori
2500 different serotypes
S.typhi, S.choleraesuis, and perhaps S.paratyphi A and
S.paratyphi B are primarily infective for humans, and
infection with these organisms implies acquisition from a
human
source
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Patogenesis
Salmonella infections in humans vary with;
Strain
Infectious dose
Nature of the contaminated food and
Host status
An oral dose of at least 105 S.typhi cells are needed to cause typhoid
in 50% of human volunteers
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1. Gastroenteritis
Infectious dose:
Typically about 1,000,000 bacteria
But much lower if the stomach pH is raised and if the
vehicle for infection is chocolate (about 100 bacteria)
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Virulence factors
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Pathogenesis
Pathogenic salmonellae ingested in food survive passage
through the gastric acid barrier
Invade intestinal mucosa
Invasion of epithelial cells stimulates the release of
proinflammatory cytokines
Induces an inflammatory reaction
Causes diarrhoea and may lead to ulceration and
destruction of the mucosa
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Clinical Features of
Gastroenteritis
Symptoms usually begin
within 6 to 48 hours
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2. Typhoid salmonellosis
Asymptomatic Carriage
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Laboratory Diagnosis
Specimen:
Blood, stool, urine, serum for typhoid fever
Blood =80% positive in the first week
Stool=70-80% positive in the second and 3rd week
Urine =20% positive in the third and fourth week
Serum for widal test Positive after second week of illness
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Serology
Widal test
The patient serum is tasted for O and H antibodies against
following antigen suspension
Serum agglutinins rise sharply during the second and third
weeks
High or rising titer of O ( 1:160) suggests that active
infection is present
High titer of H ( 1:160) suggests past immunization or past
infection
High titer of antibody to the Vi antigen occurs in some carriers
Treatment
Chloramphenicol (CAF)
Norfloxaclin???? Cipro
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4. Vibrio cholerae
Vibrios are curved, Gram-negative rods commonly found
in saltwater
Cells may be link end to end, forming S shapes and spirals
They are rapidly motile by means of a single polar
flagellum
Pathogenic vibrios include:
1. V. cholerae serogroup O1 strains -epidemic cholera;
2. Non-O1 V. cholerae and related strains that cause sporadic
cases of cholera like and other illnesses; and
3. V.parahaemolyticus and other halophilic vibrios, which
cause gastroenteritis and extraintestinal infections
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Structure
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Epidemiology
Transmission is through feco oral
Incubation period is hours-2 days
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Pathogenesis
To produce disease, V. cholerae must reach the small
intestine in sufficient numbers to multiply and colonize
Large doses required to pass stomach acid barrier
Pili mediate epithelial adherence
CT-stimulated intestinal hyper secretion; causes diarrhea
Small intestine loses liters of fluid
K+ and bicarbonate losses cause hypokalemia and
acidosis
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Cholera Toxin
CT is an A-B type ADP-ribosylating toxin
B subunit receptor is a ganglioside on cell surface
Its molecule is an aggregate of multiple polypeptide
chains organized into two toxic subunits (A1, A2) and
five binding (B) units.
A1 enters cytoplasm and ADP ribosylates regulatory G
protein
Adenylate cyclase becomes locked in active state
The cAMP causes the active secretion of Na, Cl, K,
HCO3 and water out of the cell into the intestinal lumen
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Manifestations
Extreme watery diarrhea causes large fluid loss
Dehydration and electrolyte imbalance are the major
problems
Diagnosis
The initial suspicion of cholera depends on recognition of the
typical clinical features in an appropriate epidemiologic
setting.
Bacteriologic diagnosis is accomplished by isolation of V.
cholerae from the stool.
The organism grows on common clinical laboratory media
such as blood agar and MacConkey agar
But its isolation is enhanced by the use of a selective
medium
(thiosulfate-citrate-bile salt-sucrose10/30/16
agar).
125
Treatment
Oral or intravenous fluid and electrolyte replacement is
crucial
Antimicrobic therapy can reduce duration and severity
Tetracyclines
Trimethoprim and
Erythromycin
Prevention
Water sanitation and cooking shellfish prevent infection
Vaccines prepared from whole cells, LPS, and CT B
subunit have been disappointing, providing protection that
is not long-lasting
Other Vibrios ?????
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5. Helicobacter Pylori
Helicobacter pylori is a small, curved, gram-negative,
rod-shaped bacterium.
H. pylori causes more than 90% of duodenal ulcers and
up to 80% of gastric ulcers
Growth requires a microaerophilic atmosphere and is
slow (3 to 5 days)
Epidemiology
H.pylori infection is one of the most common bacterial
infections in the world
Humans are the only known reservoir
Transmission by feco-oral pathway
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Pathogenesis
Virulance factor
Urease: ammonia production neutralizes acid
Flagella: allows the organisms to swim to the less acid pH
locale beneath the gastric mucus
Surface proteins (Cag protein)
Neutrophil-activating protein (NAP)
H. pylori colonization is virtually always accompanied by a
cellular infiltrate ranging from minimal mononuclear
infiltration of the lamina propria to extensive inflammation
with neutrophils, lymphocytes, and microabscess formation
This inflammation may be due to toxic effects of the urease or
the VacA
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Clinical manifestation
Primary infection with H. pylori is either silent or causes
an illness with nausea and upper abdominal pain lasting
up to 2 weeks
Years later, the findings of gastritis and peptic ulcer
disease include nausea, anorexia, vomiting, epigastric
pain, and even less specific symptoms such as belching
Many patients are asymptomatic for decades, even up to
perforation of an ulcer
Perforation can lead to extensive bleeding and peritonitis
due to the leakage of gastric contents into the peritoneal
cavity
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Diagnosis
The most sensitive means of diagnosis is endoscopic
examination, with biopsy and culture of the gastric mucosa
Active infection can also be diagnosed with a 13C- or 14Clabeled urea breath test or with a fecal antigen detection assay
H. pylori specific IgG (serum or salivary antibody) is a useful
marker for epidemiologic studies of past or current infection,
but its sensitivity is suboptimal
Treatment
H. pylori is susceptible to a wide variety of antimicrobial
agents
Requires combination therapy with two or more antibiotics
A typical regimen includes amoxicillin plus clarithromycin
plus a proton pump inhibitor, such as omeprazole
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Rod-shaped
Neither Gram+ve nor Gram -ve
Non-motile and non-sporulated
Obligate aerobe
Facultative intracellular parasite
Slow generation time (15-20hrs)
Lack exotoxins or endotoxins
Classified
as acid-fast bacteria
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Classification
Family: Mycobacteriaceae
Order : Actinomycetales
Genus: Mycobacterium
Four species under this genus:
M. tuberculosis complex
The non-tuberculosis mycobacteria
M. leprae and
M.ulcerance
M.tuberculosis
M.bovis------consumption of unpasteurized milk
M. leprae
M.aviumTB like disease (HIV Pts)
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TB disease in lungs
M.TB. present
M.TB. present
No symptoms
Not infectious
Defined as a case of TB
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Virulance
M. tuberculosis do not produce any toxins
Its ability to survive and multiply within macrophage is
its main virulence factor
The organism is slow growing and tolerates the
intracellular environment
It is known to prevent the acidification of the phagosome
that is needed for effective killing of microbes by
lysosomal enzymes
Lipoarabinomannan is a heteropolysaccharide that
inhibits macrophage activation by IFN-gamma
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Pathogenesis
Mycobacterium tuberculosis is spread by small airborne
droplets generated by:
Coughing
Sneezing
Talking or
Tinging
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Microscopy
Culture
Molecular diagnosis
Skin test
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Interpretation
Read 48 to 72 hours later
An area of measured induration of 10 mm or more
constitutes a positive reaction
No induration indicates a negative reaction
A positive PPD test indicates that the individual has been
infected at some time with M. tuberculosis or with a
strongly cross-reacting mycobacterium of another species
A negative PPD
test in a healthy
individual
indicates that he
or she has not
been infected
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with M.
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Radiographic procedures
The initial suspicion of pulmonary TB is often based on
abnormal chest radiographic findings in a patient with
respiratory symptoms
Treatment
Rifampicin
Isoniazide
Bactericidal, first line
Pyrazinamide
Streptomycin
Ethambutol
Ethionamide
Thiacetazone
Bacteriostatic
Paraminosalicylic acid
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Second line
Aminosalicylic
acid
Ethionamide
Cycloserine
Fluoroquinolon
es
Kanamycin
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2. M.leprea
Typical acid-fast bacilli-singly, in parallel bundles, or in
globular masses
Are regularly found in scrapings from skin or mucous
membranes (particularly the nasal septum) in lepromatous
leprosy
The bacilli are often found within the endothelial cells of
blood vessels or in mononuclear cells
Pathogenicity
M. leprae is transmitted from human to human through
prolonged contact
Obligate intracellular parasite of macrophages
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Clinical significance
Leprosy is a chronic granulomatous condition of peripheral
nerves and mucocutaneous tissues, particularly the nasal
mucosa.
It occurs between two clinical extremes: tuberculoid and
lepromatous leprosy
In tuberculoid leprosy, the lesions occur as large maculae
(spots) in cooler body tissues such as skin (especially the nose,
outer ears, and testicles), and in superficial nerve endings
Neuritis leads to patches of anesthesia in the skin
The lesions are heavily infiltrated by lymphocytes and giant and
epithelioid cells, but caseation does not occur.
The patient mounts a strong cell-mediated immune response
and develops delayed hypersensitivity which can be shown by
skin test with lepromin, a tuberculin-like extract of lepromatous
tissue.
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Lepromatous
Leprosy
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Tuberculoid
Leprosy
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Laboratory identification
M. leprae is an acid-fast bacillus.
It has not been successfully maintained in artificial
culture, but can be grown in the footpads of mice, which
may also be a natural host although playing no role in
human disease.
Laboratory diagnosis of lepromatous leprosy, where
organisms are numerous, involves acid-fast stains of
specimens from nasal mucosa or other infected areas.
In tuberculoid leprosy, organisms are extremely rare, and
diagnosis depends on clinical findings and the histology
of biopsy material
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V. Spirochetes
are
spiral shaped
Many are difficult to see by routine microscopy
Many are thin and take stains poorly
Only darkfield microscopy, immunofluorescence, or special staining
techniques that effectively increase their diameter can demonstrate
these spirochetes.
Some are strict anaerobes, others require low concentrations of
oxygen and still others are aerobic
Some have not been isolated in culture
Spirochetes that are important human pathogens are confined to three
genera:
Treponema (T. pallidum causes syphilis)
Borrelia (B.burgdorferi causes Lyme disease, B. recurrentis causes
relapsing fever) and
Leptospira (L. interrogans causes leptospirosis)
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1.Treponema pallidum
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Epidemiology
is an exclusively human pathogen
Transmission is by contact with mucosal surfaces or blood
In most cases, infection is acquired from direct sexual
contact with an individual who has an active primary or
secondary syphilitic lesion
Less commonly, the disease may be spread by non genital
contact with a lesion (eg, of the lip), sharing of needles by
intravenous drug users, or transplacental transmission to
the fetus within approximately the first 3 years of the
maternal infection
Modern screening procedures have essentially eliminated
blood transfusion as a source of the disease
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Pathogenesis
The spirochete reaches the subepithelial tissues through in
apparent breaks in the skin /passage between the epithelial
cells, where it multiplies slowly with little initial tissue
reaction
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Manifestations
I. Primary stage
Spirochetes multiply locally at the site of entry, and some
spread to nearby lymph nodes and then reach the
bloodstream
In 210 weeks after infection, a papule develops at the
site of infection and breaks down to form an ulcer with a
clean, hard base ("hard chancre")
The inflammation is characterized by a predominance of
lymphocytes and plasma cells
This "primary lesion" always heals spontaneously, but 2
10 weeks later the "secondary" lesions appear
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Diagnosis
Specimens include tissue fluid expressed from early
surface lesions for demonstration of spirochetes; blood
serum for serologic tests
1. Darkfield Examination
A drop of tissue fluid or exudate is placed on a slide and
a cover slip pressed over it to make a thin layer.
The preparation is then examined under oil immersion
with dark field illumination for typical motile spirochetes
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2. Serologic Tests
These tests use either nontreponemal or treponemal antigens
Nontreponemal includes:
VDRL (Venereal Disease Research Laboratory) and
RPR (rapid plasma reagin)
Treatment
Doxycycline and amoxicillin are the first-line antimicrobics
for the treatment of early Lyme disease and arthritis
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VI. Rickettsiae
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Clinical Features
Typhus group
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Disease
Louse-borne
typhus
Murine typhus
Scrub typhus
Spotted fever
group
Rocky Mountain
R. conorii
Spotted fever
R. rickettis
Rickettsial pox
R. akaris
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Host
Vector
Man
Rat
Body
louse
Rat flea
Rodents
Mite
rodents,
dogs
Rodents,
dogs
Mice
Tick
Tick
Mite
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1. Rickettisia Prowazeckii
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2. Rickettsia Typhi
Clinical Features:
Laboratory Diagnosis
Tetracycline
Chloramphenicol
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VII. Chlamydia
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C. psittaci
C. trachomatis and
C. pneumoniae
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1. Chlamydia psittaci
The natural hosts of C. psittaci are birds
This species causes infections of the respiratory organs,
the intestinal tract, the genital tract and the conjunctiva of
parrots and other birds
Humans are infected by inhalation of dust (from bird
excreta containing the pathogens)
After an incubation period of one to three weeks,
psittacosis /ornithosis presents with fever, headache, and
a pneumonia that often takes an atypical clinical course
The infection may, however, also show no more than the
symptoms of a common cold, or even remain clinically
silent
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Diagnosis
Diagnosis is primarily serologic
The pathogen can be grown from sputum in special cell
cultures
Therapy: Tetracyclines (doxycycline)
2. Chlamydia trachomatis
It is a pathogen that infects only humans
There are 15 serotypes of C trachomatis
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