C22 pt 2 Flashcards
Yersiniosis
- gram
- how to tell apart species
- epidemiology, weather
- shedding, outbreaks
- Gram negative, Y. enterocolitica and Y. pseudotuberculosis
o Must culture to tell apart (cold enrichment used) - Epidemiology poorly understood, survives cold weather
o Shed by carriers or wildlife, outbreaks usually under stressful conditions
Yersiniosis
- pathogenesis
- Invade enterocytes or M cells over Peyer’s patches
- Recruit neutrophils (local suppurative inflammation)
- Dissemination via lymphatics and portal vein
- Chronic cases: giant cells wall off lesions (pseudotuberculosis)
Yersiniosis in calves and deer?
- lesions
- less common presentations
- May cause fulminant fibrinous or fibrinohemorrhagic enterocolitis with diarrhea, mesenteric lymphadenitis, peritonitis, septicemia
- Hepatitis, abortion, mastitis, pneumonia less common
Yersiniosis in lambs, calves, piglets
- signs
- lesions
- Sometimes causes gradual onset diarrhea and ill thrift
- Thickened mesenteric lymphatics and enlarged, edematous LNs
- Fluid GI contents
Lawsonia intracellularis
- type of bacteria
- how to isolate
- causes what lesions? anatomic location
> symptoms
- mostly in what animals?
- Microaerophilic, nonflagellated, Gram -, curved or S-shaped rod
- Obligate intracellular pathogen – must use cell culture to isolate
- Causes proliferation of crypts in distal SI and/or LI
o Loss of functional surface area causes diarrhea
o Ill thrift and wasting due to protein loss
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Mostly: piglets, foals - also can infect dogs, rabbits, hamsters, ferrets
Lawsonia intracellularis in piglets
* Porcine proliferative enteropathy (PPE)
- how important, geographic spread
- age
- severity
- mortality
- signs
- disease depends on…
- cells infected? adeonomatosis formation?
- lesions
> where
- shedding
- serosa appearance
- most common cause of what in pigs
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- PM
o Globally prevalent and important disease, mostly weaned pigs but anytime 3 weeks +
o Varying severity (subclinical to reduced growth to severe weight loss and diarrhea)
o Can have high mortality due to progressive cachexia, hemorrhage, or perforation
o Disease depends on interaction with other gut bacteria
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1. Actively taken up by enterocytes
2. Replicate in dividing cells, causing proliferation of poorly differentiated cells (mechanism not known)
3. Elongation and branching of crypts/glands, mucosal thickening and villus atrophy
> Result is adenomatosis = thickened plaques on mucosa
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o Lesions are most consistent in the ileum but can extend to the cecum and spiral colon
o Shedding persists for weeks after infection
o Cerebriform appearance of serosa is almost pathognomonic
o The most common cause of necrotic enteritis in pigs, necrosis can be superficial or full thickness and may progress to stricture
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- Irregular mucosal thickening with folds and ridges
- May have ulcerated foci
- Coagulative necrosis with diphtheritic membrane
Lawsonia intracellularis in piglets
* Proliferative hemorrhagic enteropathy (PHE)
- severity
- age, morbidity, mortality
- PM appearance, lesions
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- histo
o Severity ranges from acute exsanguination to gradual melena/hematochezia
o More common in young adults, sporadic and low morbidity but half of cases may die
o Pale carcasses with blood on perineum, cerebriform ileal serosa with bloody contents
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- Silver stain shows bacteria
- Curved rods in apical cytoplasm
- Minimal inflammation
Lawsonia intracellularis in foals
- what disease
- age
- signs
- gross lesions?
- origin?
- Equine proliferative enteritis (EPE)
o Mostly seen in weanling foals: fever, lethargy, weight loss, diarrhea, hypoproteinemia
o Gross lesions in ileum can be subtle to nonexistent
o Severe or chronic cases resemble PPE in pigs (thickening, fibrinonecrotic membrane)
o Possibly originated from a rodent reservoir?
Spirochetal colitis in piglets
* Swine dysentery - agent?
- bacteria type
- age, infectivity
- transmission, outbreaks
- pathogenesis?
- morbidity, mortality, immunity
<>
- signs
- lesions
- anatomic location
Swine dysentery: Brachyspira hyodysenteriae
o Gram -, anaerobic, oxygen-tolerant, beta-hemolytic spirochete
o Highly infectious disease of weaned pigs (mostly 8-14 weeks old)
o Feco-oral transmission with outbreaks after introduction of carriers
o Pathogenesis poorly understood (invades enterocytes and produces endotoxin)
o Up to 90% morbidity and 30% mortality, usually produces immunity after recovery
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- Fever, poor growth
- Watery malabsorptive diarrhea +/- blood, mucus, fibrin
- Cecum and spiral colon ONLY
- Erosion is limited to the epithelium because it does not invade deeper
- Often lots of mucus, fibrin, and hemorrhage, sometimes pseudomembranes
Spirochetal colitis
* Porcine intestinal spirochetosis - agent
- bacteria property
- comparison to swine dysentery
- anatomic location
- lesions? histo?
- Porcine intestinal spirochetosis: Brachyspira pilosicoli
o Weakly beta hemolytic, milder disease than swine dysentery, wider host range
o Transient watery to mucoid diarrhea without blood, poor weight gain
o Unlike swine dysentery, can colonize long term and does not elicit protective immunity
o Lesions limited to cecum and colon
<><> - Severe case – fibrin mixed with necrotic debris on surface
- False brush border (early infection)
Clostridial disease
- bacterial characteristics
- what’s needed for disease?
- species, mostly
- in circulation?
- Gram + rods, often commensals, some change needed to favour disease (diet, antibiotic treatment, reduced motility, other pathogens, etc)
- Disease mostly seen in herbivores and sometimes dogs
- Called enterotoxemia if produce toxins that are absorbed into circulation
Clostridial disease
* Braxy
- agent?
- toxin and disease process
- species, age
- lesions
<>
- other disease causing claustridua
> blackleg
> botox
> Tyzzer’s
- Gram + rods, often commensals, some change needed to favour disease (diet, antibiotic treatment, reduced motility, other pathogens, etc)
- Disease mostly seen in herbivores and sometimes dogs
- Called enterotoxemia if produce toxins that are absorbed into circulation
- Braxy: C. septicum or C. sordelli
o Sporadic, predisposing factors unknown
o Toxin production leads to rapid onset of clinical signs and death
<> - lambs > calves
<> - Thickened, red, edematous, often emphysematous abomasum
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Other possible clostridial diseases
o C. chauvoei in tongue (’blackleg’)
o C. botulinum (toxin ingestion and paralysis)
o C. piliforme (Tyzzer’s disease, the only Gram - clostridium) sometimes causes mild enteritis
Clostridium perfringens
- virulence due to?
> toxins, 4 types
> when are they produced
- Dx
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- Toxinotypes
- toxins
> which are present in which types?
- effects of toxins
- which in healthy animals?
- which not in NA?
- Virulence is primarily due to 4 major toxins used to define toxinotypes
o All are produced during active growth, if no toxins = nonpathogenic
o Culture alone is not enough for diagnosis (some toxinotypes are commensals) – must
demonstrate presence of toxin in gut contents
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TOXINOTYPES: - A, C, D, E
> type E common in healthy animals
> Type B not present in NA
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TOXINS
Alpha - Cell membrane damage and necrosis
> in every toxinotype
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Beta - Pore-forming, causes intestinal necrosis. Inactivated by trypsin.
> type B, C
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Epsilon - Pore-forming, increases vascular permeability. Activated by enzymes including trypsin.
> type B, D
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Iota - Interferes with actin causing cell death. Activated by enzymes.
> type E
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Type A: alpha
Type B: alpha, beta, epsilon
Type C: alpha, beta
Tye D: alpha, epsilon
Type E: alpha, iota
Clostridium perfringens A
- common? found where?
- causes what in wounds
- poultry dz
- canine dz
- calf dz
- Most common as a commensal and in the environment
- Cause of gas gangrene in wounds (like other Clostridia)
- Necrotic enteritis in poultry (implicated but not proven in other species)
- Cause of some cases of canine gastrointestinal hemorrhage syndrome
o Peracute cases: sudden death with profuse bloody diarrhea - Abomasitis and tympany in calves, especially ruminal drinkers
o Reddening and ulcers; also common in normal calves
Clostridium perfringens C
- geography
- what animals? why?
- colostrum impact
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- common? difference from other toxotypes?
- Dx, toxin?
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- signs, progression
- anatomic location
- Worldwide distribution, disease mostly in neonatal livestock and foals
o Recall beta toxin is sensitive to trypsin – neonates have less trypsin
o Colostrum also inhibits trypsin activity (to protect immunoglobulins)
<><><><> - Unlike other toxinotypes, uncommon in healthy animals
o Need to isolate beta toxin to confirm disease, but toxin is unstable so absence does not rule it out as a cause
<><><><> - Disease similar in all species, usually within first hours to days of life
o Acute necrohemorrhagic enteritis, can resemble venous infarction
o Occasionally affects feedlot calves and adult sheep (‘struck’) - Jejunum and ileum most affected
Clostridium perfringens D
- small ruminant dz?
- toxin? lesions?
- associated risk
- presentation in sheep, goats
- subacute and chronic form name
- Enterotoxemia (pulpy kidney disease) is an important problem in small ruminants
o Sometimes also affects cattle
<> - Most of the lesions are due to epsilon toxin
o Absorbed and reaches brain, lungs, kidneys; damages endothelium
<> - Often associated with history of high grain or concentrate feeding but reason unclear o Poorly digested starch reaching small intestine?
<> - Varying presentations depending on age and species of host…
o Usually no diarrhea or mucosal damage in sheep, necrotizing lesions in goats
o Subacute and chronic forms also called focal symmetrical encephalomalacia (FSE)
Clostridium perfringens D
- sheep, age affected and signs
- goats, signs
> vaccine, signs
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- lesions
- Lambs > 2 weeks old and kids: acute course
o Found dead or brief neurologic signs
o Endocardial hemorrhage, edematous lungs
<> - Adult sheep: usually subacute to chronic
o Neurologic signs (FSE), not usually diarrheic
<><><><> - Adult goats: subacute
o Hemorrhagic diarrhea, colic, convulsions
o Death in 2-4 days, brain lesions less common than sheep
<> - Vaccinated adult goats: chronic
o Watery diarrhea with blood and mucus, colic, anorexia
<><><><> - Good fat stores
- Straw coloured serosal fluid that clots when exposed to air
- Fibrinonecrotic enteritis in goats
Clostridium difficile
- species
- where it lives
- what it does
- gut distribution
<>
- toxins, what they do
<>
- carriers
- toxinotyping
- horse, pig, rabbit, dog, cat, ostrich
<><><><> - Lives in soil and gut, common cause of hospital or antibiotic-associated diarrhea
o Variable distribution in gut depending on age and species
<><> - 2 toxins produced, A (enterotoxin) and B (enterotoxin and cytotoxin)
o Disable cell signalling pathways, interfere with cytoskeleton, promote release of
inflammatory mediators
o Result: apoptosis and inflammation with fluid gut contents
<><> - Carrier state is uncommon, but toxinotyping needed to rule out nontoxigenic strains
Clostridium difficile in the horse
- age, lesion location
- signs, severity, mortality
- looks like?
- Ddx
- lesions
- Any age affected, lesions anywhere from the small intestine to the colon
o Foals <1 month old mostly SI, older horses mostly colon
<><> - Variable clinical signs and severity
o Diarrhea (consistent), fever, colic, injected mucous membranes, shock, DIC
o Mortality 0-42%, lesions almost identical to C. perfringens C (can occur together)
o Other differentials: salmonellosis, Potomac horse fever, NSAID toxicity
<><> - Multifocal hemorrhage/hyperemia
- Thickened by edema
- Pseudomembrane and watery contents
Paratuberculosis (Johne’s)
- bacteria?
- Dx
- species
- Mycobacterium avium subspecies paratuberculosis (MAP)
- Slowgrowing–PCRtoconfirm
- Epidemiology best characterized in cattle, likely similar in other species
- Also occurs in these species:
- pigs, rabbits, sheep, deer, horses, llama, (humans?), (Other species infected but no disease)
Paratuberculosis (Johne’s)
- infectious dose
- route of infection
- pathogenesis
- if infection is not cleared…. what hapens?
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4 stages of infection
- which is most important source of infection?
- Infectious dose is higher for adults than neonates
o Usually infection of calves via feco-oral or contaminated milk/colostrum
o Enters via M cells or enterocytes over Peyer’s patches, invades macrophages
o Prevents phagolysosome fusion to survive, triggers proinflammatory cell-mediated
response that may clear infection
o If infection is not cleared, eventually shifts to ineffective antibody-mediated response
at the start of clinical disease
<><><><> - 4 stages of infection
Most important source of infection!
1) Silent: Infected but not shedding
2) Subclinical: Infected and progressive shedding but no signs, lasts 2-5 years
3) Clinical: Infected, shedding, signs present, rare in cows <2 years old
4) Advanced clinical: Terminal stages of disease
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Subclinical stage is the most important source of infection
Paratuberculosis (Johne’s)
- lesions, anatomic location
- signs and lesions
- Lesions mostly seen in the ileum, colon, and draining lymph nodes
o Granulomatous enteritis and villus atrophy, protein loss = wasting
o Malabsorption and inflammatory secretion overload resorption = diarrhea
<><><><> - ‘Hosepipe’ diarrhea and wasting
- Keep eating and may have intermittent or progressive diarrhea for weeks before cachexia and wasting begin
- Mineral plaques in aorta
- Diffuse mucosal thickening into transverse rugae
- Lymphangitis (thickened lymphatics) characteristic, may eventually involve lymph nodes
Paratuberculosis (Johne’s)
- in sheep and goats
> susceptibility
> incubation
> progression
> disease presentation
> lesions? histo?
- More susceptible than cows (especially goats), shorter incubation period o Exposure to higher doses in early life leads to faster progression
- Disease mostly in adults, chronic wasting without diarrhea
o GI lesions sporadic and milder than cows, often few bacteria
<><> - skinny animals but lack of fecal soiling
- Acid-fast stain to show bacteria in cells – useful in all species
Rhodococcus equi in foals
- where is it found?
- most important as what type of pathogen?
- lesions? why?
- bacteria in what cells?
- signs
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- also infects what animals
- Opportunist, normal flora in soil and GI tract, most important as a respiratory pathogen
o 50% also have dose-related GI tract lesions
o Likely due to swallowing bacteria-laden exudates coughed up from lungs - Bacteria found inside macrophages
<><><><> - Pyogranulomatous typhlocolitis +/- lymphadenitis
- May form abscesses or cause peritonitis
- Crater-like ulcers that are worst over Peyer’s patches
- Mostly affects cecum and colon
- Causes chronic diarrhea, wasting
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Also infects pigs, cattle, goats, humans (immunocompromised)
Neorickettsiosis in horses
* Aka Potomac horse fever
- agent
- type of pathogen
- where it replicates
- geography
- life cycle / vector / route of infection
- Aka Potomac horse fever, caused by Neorickettsia risticii
o Obligate intracellular pathogen that replicates in phagosomes
o Originally described around the Potomac River but now widespread in North and
South America
<><><><> - Flukes are the vector for the bacterium
- Infected mayflies drown in horse water buckets etc
- Accidentally ingested by horses
<><><><> - snail eats egg
> cercariae leaves snail
> infects aquatic insect > metacercaria
> insect may be eaten by horse, which becomes accidental host
Neorickettsiosis in the horse
- incubation, when are clinical signs?
- signs?
- severity? mortality?
- Dx
- lesions
- lesion location
- Incubation period 9-14 days, diarrhea occurs 1-3 days after onset of fever
- Variable severity, up to 30% mortality if untreated, confirm with PCR
- Endotoxic lesions, leukopenia, depression, inappetence, colic, lameness
<><><><> - Liquid, red-brown, foul smelling colon contents
- May have clusters of small (few mm) ulcers
- R dorsal colon worst
- Laminitis
Campylobacter spp.
- pathogenesis
- signs in chickens, pigs
- signs in dogs, foals, lambs
o Attach to and invade enterocytes, pathology due to toxin production
o Chickens asymptomatic (C. jejuni), pigs asymptomatic or diarrheic (C. coli)
o Mild diarrhea in dogs, foals, weaned lambs
Enterococcus spp.
- type of bacteria, can behave like what other bacteria sometimes?
- which ones can affect all species?
o Gram + cocci, mostly commensal but sometimes behaves like EPEC
o E. durans and E. hirae can affect any species
Bacteroides fragilis
- type of bacteria
- some secrete what? consequence?
o Non-spore forming obligate anaerobe, usually commensal
o Some secrete a protease that damages enterocytes, but don’t adhere to mucosa
