GI Pathogens 1 Flashcards
What are the main characteristics of E.coli bacteria
- Enterobacteriacae family
- Gram (-)
- Facultative anaerobe
- Flagella = motile
- Location: common commensal and found in environment
List 6 mechanisms of enteric disease + examples
Mechanism of Enteric disease
* Toxin: salmonella/some E.coli
* Inflammation: E. coli/salmonela
* Structural injury: salmonella/E. coli
* Disrupt neurotransmitter
* Alter cell cycle: Lawsonia intracellularis
* Dysfunction of electrolyte/fluid pumps: ETEC
What is the general pathogenesis of E.coli
- Transmit: ingest fecal material
- Colonize intestinal mucosa
List 4 pathotypes of E. coli
MANY pathotypes
- Enterotoxigenic (ETEC)
- Enteropathogenic (EPEC)
- Enterohemorrhagic (EHEC)
- Shigatoxin producing (STEC)
What is the virulence mechanism of ETEC
o Virulence factors
Bind receptors on cell surface
Make enterotoxin – bind receptors
Cause release of ions from cell = osmotic diarrhea
What is the virulence mechanism of EPEC
o Virulence factors
Bind and inject effector proteins into cells
* Intimin receptor (Tir) from enterocyte binds intimin/Tir from the bacteria
Change enterocytes causing malabsorption
Cause inflammation
What is the virulence mechanism of EHEC
o Virulence factors
Inject effector proteins and also have shiga toxin
Shiga toxin penetrates epithelium and affects other tissues (kidneys/other organs)
What is the virulence mechanism of STEC
o Virulence factors
No protein injection but have shiga toxin (shiga toxin aka vera toxin)
Causes edema due to action of shiga toxin
What are the common disease caused by ETEC
o Diseases caused
Neonatal diarrhea (scours) in cow/pig
Postweaning diarrhea in pigs
Edema disease in dogs
What are the common disease caused by EPEC
o Diseases caused
Post weaning diarrhea in pigs
What are the common disease caused by STEC
o Diseases caused
Diarrhea/dysentery in 2-8 week old calves
Can cows get STEC
No
they dont have the propeer receptor for the shiga toxin
calves can be affected because they may have receptor available
What are the general characteristics of ETEC infection
- ETEC
o Rapid infection
o Death soon after development of diarrhea
o Can be complicated by shock due to LPS (Lipid A) release
o Aka. enteric colibacillosis
What are the specific virulence factors that allow for ETEC colonization
Bind receptors on cell surface
* Pig fimbrial adhesins: F4 (K88)
* Ruminant fimbrial adhesins: F5 (K99)
What are the specific virulence enterotoxins produced in ETEC infection? What are their functions?
- 2 classes of enterotoxin: heat stable (ST: STa/STb) + heat labile (LT)
o STa: reduce absorption of electrolytes and water from villus/increase secretion of C/l/H2O in crypt
o STb: increase prostaglandin E2 and induce duodenal and jejunal secretion of water/electrolytes
o LT: increase Cl/water/PGE2 secretion = loosen tight junction
How long would a self-resolving E. coli infection last? Why?
2-5 d
because enterocyte are recycled in 2-5d from crypt to villus
Provide 8 examples of Non-Enteric E. coli (ETEC) Septicemia
- Umbilical infection in neonate
- Urogenital tract infection: dog/cat
- Mastitis in cow/pig
- Lung infection in pig/dog
- Pyometra dog/cat
- Septicemia in cow/pig/cat/dog
- Omphalitis/air-sacculitis/salpingitis/peritonitis in poultry
is fecal isolation of E. coli useful in dx?
no
* Fecal isolation not meaningful – because it is a commensal
How to diagnose E. coli (3 ways)
- Must demonstrate toxins/fimbrial antigens
o PCR
o Monoclonal Ig based techniques - Culture E. coli in blood – identify septicemia
Why is E. coli challenging to diagnose
commonly found in the environment
Explain the relationship between cattle and E. coli + examples
Cattle
* E. coli most common cause of diarrhea in <10d calf
* ETEC = diarrhea in neonatal calf
* EPEC and EHEC = diarrhea in older calf (2-30d – 4mo)
What are the risk factors of E. coli infection in cattle? How to prevent?
- Risk factors:
o Failure of passive transfer
o Poor hygiene/overcrowding
o Inappropriate volume/milk composition - Control:
o Dam vaccines (give 3 weeks apart – 3-6 week before calving)
o Adequate colostrum intake
o Oral commercial Ig
o Vx/antigens should contain K99 antigen
Describe the structure of shiga toxin and how to contributes to function
Shiga toxin:
* A sub-unit – active part (bind/inactivate ribosomes)
* B sub-unit – mediate cell binding
* Retrograde transfer through golgi – toxin becomes associated with rough ER
o Sub-unit A = cleaved > form A1 = active
* Require Gb3 receptor on cell surface
o Ex. adult cattle don’t have = not affected
What diseases are attributed to shiga toxin e coli in dogs, cows, and pigs
- Clinically
o Diarrhea/dysentery in 2-8 week old calf
o Hemolytic uremic syndrome in dog
o Edema disease in pig
What is the importance of E. coli in horses? How do you control it?
- Most important cause of septicemia in neonatal foals
- Less important as a primary cause of diarrhea (vs. calf/pig)
- Control: oral Ig for neonatal foal – give within 12h of birth
What type of e. coli do birds typically get?
- Avian-pathogen E. coli
What are the risk factors for E. coli infection in birds? What disease can it cause?
- Cause
o Diarrhea
o Septicemia
o Meningitis
o Polyarthritis
o Localized infection - Risk factor: poor hygiene (healthy birds resistant)
What are 3 types of e. coli that can affect pigs? What are the related diseases they cause?
- Enteric colibacillosis (ETEC) common in neonatal pigs
- ETEC: post weaning diarrhea
- STEC: Edema disease in piglets 1-2 week post weaning
What are the clinical signs of enteric colibacillosis etec in neonatal pigs? How to control it?
o Diarrhea/dehydration/whole litter affected
o Control: vaccine for sow
What is the pathogenesis of STEC infection in pigs?
- STEC: Edema disease in piglets 1-2 week post weaning
o Shiga toxin/neuro disease/eyelid and forehead swelling/GI edema
o 3-6d after non-intimate adherence of bacteria via F18 pilli
o Stx2e absorbed into bloodstream - bind and damage vascular endothelial cells in target tissue = edema/hemorrhage
What are the risk factors for STEC infection in pigs?
o Risk factors
Management problems around weaning
Weaning leads to GI epithelial change = temporary period of malabsorption
High protein diet provide substrate for EDEC
What type of e. coli affects dogs mainly and what is a common disease outcome?
o Found in the feces of normal dog
o Cause hemolytic uremic syndrome in young dogs/breed associated
What is the pathogenesis of hemolytic uremic syndrome in dogs
o Syndrome of bloody diarrhea then acute thrombocytopenia/microangiopathic anemia/anuric renal failure
o Shiga toxin preferentially binds renal endothelium
o In 5% dogs that develop diarrhea
What is the significance of e. coli in humans
Human
* STEC common in food borne illness
* Cause hemolytic uremic syndrome
What is the primary risk factor that predisposes animals for e. coli infection?
- Major risk factor = failure of passive transfer of immunity
What are the general characteristics of salmonella bacteria? Where is it found?
- Enterobacteriaceae family
- Gram (-)
- Flagella = motile
- Not commensal
- Found in subclinical carriers or environment
- Most common cause of food borne hospitalization/death
How are salmonella bacterias named? Why?
o Lots of serotypes but they all are Salmonella enterica enterica = named by serotype (S. typhimurium)
What are 3 classifications of salmonella? Provide associated examples
- Host restricted serotype: systemic infection
o Poultry: S. gallinarum
o Sheep: S. abortusovis - Host- adapted serotype:
o Cattle: S. Dublin
o Swine: S. choleraesuis - Unrestricted/broad host range serotypes: self limiting gastroenteritis
o S. typhimurium
o S. enteritidis
What is the pathogenesis of enteric salmonellosis?
- Direct route of infection
- Bind fimbrae – stimulate enterocytes to uptake in vacuole
- Either
o Proliferate in vacuole
Cause burst of cell and release of salmonella
o Go to basal membrane of enterocyte
Stimulate macrophage phagocytosis
Can survive phagocytosis (inhibit phago-lysosome fusion)
Leukocyte trafficking through LN
Can cause systemic infection or carrier state
What are 5 mechanisms for lesion formation for enteric salmonellosis? What are the common lesions?
o Enterotoxin = disrupt Cl channels = secretory diarrhea
o T3SS effector protein
o Stimulation of enterocyte death
o Acute inflammation = diarrhea/damage vascular endothelium
o Endotoxin-induced damage to vascular endothelium
- Common lesions: vasculitis/thrombosis/ischemia/infarction
List 6 clinical forms of enteric salmonellosis
- Peracute septicemic
- Acute enteric
- Chronic enteric
- Abortion
- Subclinical carrier without shedding
- Subclinical carrier that sheds
What large animals are primarily affected by salmonella? What is the pattern of infection?
- Mainly affect cattle/horse/pig
- Pig/Horse: Either individual or outbreak
- Cattle: affect individual animals usually due to stress
- Can have endemic salmonellosis
How do you diagnose salmonella infection in large animals
- Diagnosis: fecal culture with heavy growth
o Fecal culture with light growth = carrier
o Identify serotype
o Isolate salmonella from blood or tissue = septicemia
o Rising titre = active infection
Describe the relationship between salmonellosis and small animals
- Rare – most subclinical (10% dog/cat = carriers)
- Salmonella higher in raw diet
Can the same diagnostic methods be used to indicate salmonellosis in large animal vs small animal
no
in small animals:
* Isolation of salmonella in feces is not diagnostic for salmonellosis
LA:
* Diagnosis: fecal culture with heavy growth
o Fecal culture with light growth = carrier
o Identify serotype
o Isolate salmonella from blood or tissue = septicemia
o Rising titre = active infection
Explain the relationship between poultry and salmonella
- Salmonella found in feces/cloacal secretions = contaminate egg shell
Explain the relationship between reptiles and salmonella
Reptile
* S. arizonae
* Can cause outbreak in humans
* Rarely clinical – commonly carrier
Explain the relationship between humans and salmonella
Human:
* Zoonotic
* Typhoid fever: S. enterica
o Only affect humans
o Fever/headache/anorexia/constipation/death
o Transmit: food/water
What is the major risk factor for salmonellosis
Salmonella Risk factor: Major factor = stress
Can animals be resistant to salmonella
- Carnivores are resistant
What is the prominent lesion type that salmonella causes
- Cause infarction
What are the general characteristics of lawsonia intracellularis
Characteristics
* Obligate intracellular gram (-)
* Curved shape
What is the pathogenesis of lawsonia intracellularis
- Ingestions (can have species-species transmission)
- Association with enterocytes: infect crypt
- Replicate in ileal epithelium
- Endocytic internalization
o Intestinal thickening – proliferation of stem cells in crypts
o Maximal thickening = functional loss - Vacuolar escape/cytoplasmic multiplication
- Spread through mitosis of enterocytes
- Release bacteria from enterocytes at villous apices
- Spread via ileum/distal jejunum/cecum/colon
- Restricted to intestine/LN
List 4 types of lawsonia intracellularis manifestations? What species are affected
pigs mainly
- Porcine intestinal adenomatosis (PIA)
- Proliferative hemorrhagic enteropathy (PHE)
- Necrotic enteritis
- Regional ileitis
o In horse/dog/cat as well as pigs
What is the impact of Porcine intestinal adenomatosis (PIA) infection
- Porcine intestinal adenomatosis (PIA) = proliferation of glandular epithelium
What is the impact of * Proliferative hemorrhagic enteropathy (PHE) infection
- Proliferative hemorrhagic enteropathy (PHE) = proliferation of intestinal epithelium/blood loss in intestinal lumen
What is the impact of Regional ileitis infection
- Regional ileitis: strong proliferation of tunica muscularis of ileum
What are the common clinical signs of lawsonia intracellularis infection? What animals does it affect
- 18-36kg pigs affected
- Sudden onset diarrhea – watery-pasty brown + faint blood
- +/- yellow fibronecrotic fast (formed in ileum) passed in feces
- Most recover spontaneously
- Lots develop chronic necrotic enteritis with progressive emaciation
- Hemorrhagic form: cutaneous pallor/weakness/black or hemorrhagic feces (tarry feces)
What are the histologic lesions associated with lawsonia intracellularis
- Microscopic
o Week 1: microcolonies in apical cytoplasm of crypt cells + short/irregular microvilli
o Week 2-6: enterocyte hyperplasia, adenomatous proliferation
What are the gross lesions associated with lawsonia intracellularis infection
- Gross
o Terminal ileum
o Acute: thick/turgid ileum + lumen blood clots
o Chronic: irregular/patchy subserosal edema/thick mucosa/pseudomembrane/deep fold
What non-porcine species is also affected by lawsonia intracellularis? What are the clinical and gross signs? Diagnosis? Treatment?
Horses
* Signs:hypoproteinemia/emaciation/thick GI mucosa/severe hyperplasia of crypt epithelium
* Dx: serology/PCR
* Tx: abx
How is lawsonia intracellularis diagnosed?
Diagnosis
* Not culture: can only grow inside eukaryotic cells in very specific environmental conditions
* PCR
* Serology
* Histo: H&E stain
* Clinical signs + PM
How is lawsonia intracellularis treated and prevented?
Treatment and Control
* Antimicrobial (via IV in pigs)
* Avirulent vaccine (via water)
