C22 Gastrointestinal Pathology V Flashcards
Bacterial virulence
- Attachment
- Colonization/entry
- Evasion of defences
- Multiplication, spread, damage
- Transmission
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Microbiota important in resisting virulence
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Virulence genes often clustered in unstable pathogenicity islands
Escherichia coli
- subtypes, what they do
- Many important virulence factors involved in colonization, adhesion, metabolic dysfunction, enterocyte death, vessel damage, invasion, septicemia, …
<><><><> - Clinical disease varies based on subtype and toxin production
o Enterotoxigenic (ETEC): secretory SI diarrhea in neonates due to enterotoxins
o Enteropathogenic (EPEC): enteroadherent or attaching-effacing, causes villus atrophy,
relatively uncommon
o Shiga toxin producing (STEC) aka verotoxin producing (VTEC) aka enterohemorrhagic
(EHEC): edema disease in pigs, disease in humans; adult cattle are the reservoir
o Enteroinvasive (EIEC): taken up by enterocytes can lead to septicemic colibacillosis, usually does not cause enteric disease
Escherichia coli: ETEC
- what does it cause
- lesions
- major virulence factors and what they do
> why young more susceptible
- Major cause of undifferentiated neonatal diarrhea in pigs, calves, and lambs
o NO GROSS OR HISTOLOGIC LESIONS
o 2 major virulence factors…
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1. Adherence via pili resists peristaltic flushing o aka fimbriae, protein polymers
o Can express combinations of adhesins,
affecting the area of intestine targeted
o Adhesin receptors mostly decrease from
birth to weaning (often only susceptible for
a few days)
o Colostral antibodies bind adhesins and
prevent disease
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2. Two classes of protein toxins produced that alter secretion and absorption without
altering intestinal morphology - Heat labile toxin (LT)
o Chloride secretion is followed by water (osmosis)
o Irreversible effect on cells - Heat stable toxin (ST)
o Inhibits Na/Cl transport (and therefore water resorption)
o Also causes chloride secretion in crypts
Escherichia coli: ETEC in pigs
- age groups
- predisposing factor
- signs
- Very common in neonates <1 week
- Postweaning diarrhea in pigs >3 weeks
o Usually something has promoted colonization (diet change, food hypersensitivity, concurrent rotavirus, etc)
o Nonfatal diarrhea, ill thrift for ~1 week
Escherichia coli: ETEC in lambs and calves
- age
- R/Os
- Common in first 2-3 days of life (before receptors are lost)
- Often concurrent with other pathogens
- Rule out other causes of undifferentiated diarrhea (coronavirus, rotavirus, cryptosporidiosis)
Escherichia coli: EPEC
- species
- how does it cause disease?
- severity
- diarrhea
- Rabbit, dog, pig
- Direct mucosal damage due to attachment to and effacement of epithelium
o Attaches via fimbriae, then secretes proteins that reorganize cytoskeleton
o Forms a pedestal-like structure around the bacterium (with microvillus loss) - Colonized epithelium sloughs, causing villus atrophy
o Severity related to extent of colonization (worst in distal SI and colon)
o Malabsorptive diarrhea, damaged colon can’t compensate for fluid loss
Escherichia coli: EHEC/STEC
- produces what? what does it do?
- species? serotype?
- Subset of EPEC that produce shiga toxin
o Inhibits protein synthesis, can induce apoptosis - Mostly cause disease in humans but animals are important as carriers (especially cattle)
o O157:H7 serotype most famous
Escherichia coli: EHEC/STEC in cattle
- age
- disease
- lesions
- recovery
- Erosive fibrinohemorrhagic enteritis between 3 days-4 weeks old
- Spiral colon and rectum most affected, also have villus atrophy
- Usually bright and afebrile, recover in 7-10 days
- Some develop septicemia
Escherichia coli: EHEC/STEC in dogs
- signs
- lesions
- Dysentery, sometimes hemolytic uremic syndrome
- Cutaneous and renal glomerular vasculopathy, aka ‘Alabama rot’
Escherichia coli: EHEC/STEC in pigs
* Edema disease
- signs? lesions?
- age / life stage
- mortality
- signs in survivors
- what is implicated?
- common? prevention?
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- PM
- Dx
- Edema disease
o Sudden death or neurological signs, not diarrheic/no gut lesions (enterotoxemia)
o Usually occurs within a few weeks of weaning or other feeding/management change
o Sporadic or outbreaks in good pigs, near 100% mortality
o Those that do not die suddenly show ataxia, tremors, convulsions for up to 1 day
o Shiga toxin that damages blood vessels implicated (genetic susceptibility involved)
o Now uncommon, likely due to vaccination and move to soybean/corn rations
<><><><> - Often subtle lesions, look for edema in at least one location
- Eyelid, CNS, colon, stomach, LNs, meninges etc
- Culture and serotype to confirm
- Clear, gelatinous fluid in mesocolon (common)
Escherichia coli: EHEC/STEC
* Postweaning E. coli enteritis
- age / life stage
- relationship to edema disease?
- morbidity, mortality
- pathogenesis and GI lesions?
- signs
- Dx
- PM
o Usually soon after weaning or other change
o Seen in the same population as edema disease, but affects different pigs
o High morbidity, variable mortality (deaths due to endotoxemia)
o Pathogenesis poorly understood – no villus atrophy
o Enterotoxin causes yellow, fluid diarrhea, flaccid SI with variable congestion
o Confirm via culture and serotyping
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- Gastric venous infarcts due to endotoxin-mediated thrombosis
- Also causes lesions in other tissues
Escherichia coli: EIEC in cattle, pigs
- replicate where
- lesions
- signs
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- may be connected to what idsease in dogs?
> breeds?
> signs?
> recovery
- Invade and replicate in SI and LI enterocytes, similar to Salmonella and Shigella
o Erosion and ulceration leads to inflammation, malabsorption, and protein loss
o Villus atrophy looks similar to viral enteritis - Sporadic diarrhea in neonatal pigs and calves
<><><><> - May be involved in histiocytic ulcerative colitis in dogs?
o Likely genetic predisposition in young boxers and French bulldogs
o Bloody mucoid diarrhea, anemia, weight loss, cachexia
o If bacteria are removed, lesions resolve
Septicemic colibacillosis in cattle
- age, risk factors
- entry route, pathogenesis
- Dx
- lesions
- Common, mostly neonates predisposed to infection
o Failure of passive transfer, comorbidity - Enter via umbilicus, respiratory, gut (often without enteritis)
o Endotoxin from dying bacteria causes vascular damage and shock (sudden death)
o Or chronic septicemia (joint and ocular infection, meningitis)
<> - Diagnosed via culture of multiple filter organs (lung, liver, kidney, spleen)
<> - Lesions vary from minimal to nonspecific lesions of sepsis
- Rubbery lungs
- White spotted kidney (interstitial nephritis)
- hypopyon
- Also fibrinous serositis, arthritis, meningitis, GI ulcers…
Salmonellosis
- most important type, serotypes
- Clinicopathologic syndromes
- host adaptation > disease
- Disease usually involves….
- carriers
- reservoirs
- Salmonella enterica is most important, 6 subspecies and thousands of distinct serovars o 60% are S. enterica subspecies enterica, serotypes are capitalized but not italicized
<><><><> - Clinicopathologic syndromes vary, can be localized to gut or systemic, some cause abortion
<><> - Host-adapted serotypes tend to cause severe systemic disease in adults and young (worse)
o Ex. S. Dublin in cattle and S. Choleraesuis in pigs - Wide range types mostly affect young and cause enterocolitis +/- septicemia
o Ex. S. Typhimurium
<><><><> - Disease usually involves compromised immune response or disrupted flora
<><><><> - Survivors are usually carriers for a while after disease, and some serotypes have
asymptomatic carriers (prone to resurgence of clinical disease)
<><><><> - Reservoirs: calves, piglets, chickens
Salmonellosis
- pathogenesis
> stages
- tissue affected
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- survival, systemic disease
- toxins, what they do
- diarrhea type
- other signs
- presentation? fatality?
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- septicemia from transient bacteremia?
- Pathogenesis split into entry, colonization, and invasion – facultative intracellular pathogen
- Often motile and flagellated
- First need sufficient dose that overcomes host defences
<><><><> - ingestion eg. via contaminated food
- can affect SI and LI
- Attachment in 2 stages
- Weak, reversible
- Receptor mediated and irreversible (causes loss of microvilli)
> enters epithelial cells of gut
> Some serovars enter via M cells in Peyer’s patches
> systemic spread / infection > requires ability to survive and replicate in macrophages
<><><><> - LPS facilitates survival (blocks degradation) and contributes to systemic disease
- Secretory enterotoxins block Cl- channels, inflammation can form pseudomembranes
- Diarrhea is a combination of secretory, malabsorptive, and exudative (inflammatory)
- Thrombosis of mucosal venules is common and causes ischemia
- Duration and severity of septicemia varies, but usually rapidly fatal in young animals
- In transient bacteremia, resident macrophages in filter organs take up bacteria o These replicate and can lead to secondary bacteremia or septicemia
