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VETM 423 Bacteriology > GI Pathogens 1 > Flashcards

GI Pathogens 1 Flashcards

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1
Q

What are the main characteristics of E.coli bacteria

A
  • Enterobacteriacae family
  • Gram (-)
  • Facultative anaerobe
  • Flagella = motile
  • Location: common commensal and found in environment
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2
Q

List 6 mechanisms of enteric disease + examples

A

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

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3
Q

What is the general pathogenesis of E.coli

A
  • Transmit: ingest fecal material
  • Colonize intestinal mucosa
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4
Q

List 4 pathotypes of E. coli

A

MANY pathotypes

  • Enterotoxigenic (ETEC)
  • Enteropathogenic (EPEC)
  • Enterohemorrhagic (EHEC)
  • Shigatoxin producing (STEC)
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5
Q

What is the virulence mechanism of ETEC

A

o Virulence factors
 Bind receptors on cell surface
 Make enterotoxin – bind receptors
 Cause release of ions from cell = osmotic diarrhea

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6
Q

What is the virulence mechanism of EPEC

A

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

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7
Q

What is the virulence mechanism of EHEC

A

o Virulence factors
 Inject effector proteins and also have shiga toxin
 Shiga toxin penetrates epithelium and affects other tissues (kidneys/other organs)

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8
Q

What is the virulence mechanism of STEC

A

o Virulence factors
 No protein injection but have shiga toxin (shiga toxin aka vera toxin)
 Causes edema due to action of shiga toxin

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9
Q

What are the common disease caused by ETEC

A

o Diseases caused
 Neonatal diarrhea (scours) in cow/pig
 Postweaning diarrhea in pigs
 Edema disease in dogs

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10
Q

What are the common disease caused by EPEC

A

o Diseases caused
 Post weaning diarrhea in pigs

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11
Q

What are the common disease caused by STEC

A

o Diseases caused
 Diarrhea/dysentery in 2-8 week old calves

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12
Q

Can cows get STEC

A

No

they dont have the propeer receptor for the shiga toxin

calves can be affected because they may have receptor available

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13
Q

What are the general characteristics of ETEC infection

A
  • 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
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14
Q

What are the specific virulence factors that allow for ETEC colonization

A

 Bind receptors on cell surface
* Pig fimbrial adhesins: F4 (K88)
* Ruminant fimbrial adhesins: F5 (K99)

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15
Q

What are the specific virulence enterotoxins produced in ETEC infection? What are their functions?

A
  • 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
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16
Q

How long would a self-resolving E. coli infection last? Why?

A

2-5 d
because enterocyte are recycled in 2-5d from crypt to villus

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17
Q

Provide 8 examples of Non-Enteric E. coli (ETEC) Septicemia

A
  • 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
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18
Q

is fecal isolation of E. coli useful in dx?

A

no
* Fecal isolation not meaningful – because it is a commensal

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19
Q

How to diagnose E. coli (3 ways)

A
  • Must demonstrate toxins/fimbrial antigens
    o PCR
    o Monoclonal Ig based techniques
  • Culture E. coli in blood – identify septicemia
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20
Q

Why is E. coli challenging to diagnose

A

commonly found in the environment

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21
Q

Explain the relationship between cattle and E. coli + examples

A

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)

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22
Q

What are the risk factors of E. coli infection in cattle? How to prevent?

A
  • 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
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23
Q

Describe the structure of shiga toxin and how to contributes to function

A

 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

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24
Q

What diseases are attributed to shiga toxin e coli in dogs, cows, and pigs

A
  • Clinically
    o Diarrhea/dysentery in 2-8 week old calf
    o Hemolytic uremic syndrome in dog
    o Edema disease in pig
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25
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
26
What type of e. coli do birds typically get?
* Avian-pathogen E. coli
27
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)
28
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
29
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
30
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
31
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
32
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
33
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
34
What is the significance of e. coli in humans
Human * STEC common in food borne illness * Cause hemolytic uremic syndrome
35
What is the primary risk factor that predisposes animals for e. coli infection?
* Major risk factor = failure of passive transfer of immunity
36
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
37
How are salmonella bacterias named? Why?
o Lots of serotypes but they all are Salmonella enterica enterica = named by serotype (S. typhimurium)
38
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
39
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
40
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
41
List 6 clinical forms of enteric salmonellosis
* Peracute septicemic * Acute enteric * Chronic enteric * Abortion * Subclinical carrier without shedding * Subclinical carrier that sheds
42
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
43
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
44
Describe the relationship between salmonellosis and small animals
* Rare – most subclinical (10% dog/cat = carriers) * Salmonella higher in raw diet
45
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
46
Explain the relationship between poultry and salmonella
* Salmonella found in feces/cloacal secretions = contaminate egg shell
47
Explain the relationship between reptiles and salmonella
Reptile * S. arizonae * Can cause outbreak in humans * Rarely clinical – commonly carrier
48
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
49
What is the major risk factor for salmonellosis
Salmonella Risk factor: Major factor = stress
50
Can animals be resistant to salmonella
* Carnivores are resistant
51
What is the prominent lesion type that salmonella causes
* Cause infarction
52
What are the general characteristics of lawsonia intracellularis
Characteristics * Obligate intracellular gram (-) * Curved shape
53
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
54
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
55
What is the impact of Porcine intestinal adenomatosis (PIA) infection
* Porcine intestinal adenomatosis (PIA) = proliferation of glandular epithelium
56
What is the impact of * Proliferative hemorrhagic enteropathy (PHE) infection
* Proliferative hemorrhagic enteropathy (PHE) = proliferation of intestinal epithelium/blood loss in intestinal lumen
57
What is the impact of Regional ileitis infection
* Regional ileitis: strong proliferation of tunica muscularis of ileum
58
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)
59
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
60
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
61
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
62
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
63
How is lawsonia intracellularis treated and prevented?
Treatment and Control * Antimicrobial (via IV in pigs) * Avirulent vaccine (via water)

VETM 423 Bacteriology (18 decks)

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