GI Pathogens 2 Flashcards

1
Q

What are the general Characteristics of clostridia

A
  • Gram (+)
  • Anaerobic
  • Make spores
  • Exotoxins
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2
Q

What are the 3 relevant types of clostridium

A

Clostridia (C. perfringens and difficile and piliforme)

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3
Q

What are the 4 toxins produced by C. perfringens

A

o Alpha: phospholipase (dermonecrotic/hemolytic/cytolytic)
o Beta: pore forming activity/hemorrhagic (dermonecrotic/hemolytic/cytolytic)
o E: alter cell membrane permeability causing edema
o L: cytoskeleton damage = necrosis
o Theta: hemolysin (perfringolysin) - (form pores/cytolytic/osmotic diarrrhea)

  • Toxins: alpha toxin, most with theta toxin (cholesterol dependent cytolysin = perfringolysin)
  • 5 toxinotypes: A, B, C, D, E – make 4 major toxins
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4
Q

List a histotoxic and enteric clostridia

A

C. perfringens

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5
Q

What type of toxin does type A C. perfringens have

A
  • Type A: alpha toxin (also theta toxin)
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6
Q

What type of toxin does type B C. perfringens have

A
  • Type B: toxin A, B, e
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7
Q

What type of toxin does type C C. perfringens have

A
  • Type C: toxin A, B
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8
Q

What type of toxin does type D C. perfringens have

A
  • Type D: a, e

mainly produces epsilon toxin - converted to active form in intestine

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9
Q

What type of toxin does type E C. perfringens have

A
  • Type E: A, l
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10
Q

What is the disease manifestation of type A C. perfringens in poultry, pigs, horses, and cows

A

o Poultry: necrotic enteritis
o Suckling and feeder pigs: necrotizing enterocolitis
o Equine> hemorrhagic mucosal necrosis
o Beef: abomasal ulcer/tympany
o Dairy: necrotic enteritis in calf
o Adult cattle: haemorrhagic bowel syndrome

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11
Q

What is the disease manifestation of type B C. perfringens

A

o Ovine hemorrhagic enterotoxemia
o Hemorrhagic enteritis

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12
Q

What is the disease manifestation of type C C. perfringens

A

o Neonatal hemorrhagic or necrotizing enterotoxemia

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13
Q

What is the disease manifestation of type D C. perfringens

A

o Ovine enterotoxemia

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14
Q

What is the disease manifestation of type E C. perfringens

A

o Bovine hemorrhagic enteritis

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15
Q

What C. perfringens toxin causes food poisoning

A

o CPE enterotoxin
 Zoonotic/cause food poisoning
 Pore forming (cytotoxic) and interfere with tight junctions (alter paracellular permeability)

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16
Q

What are the associated lesions with type A C. perfringens

A

o Lesions
 ‘red gut’ – large sections of small intestine or red/purple and full of blood
 Sudden death in dairy/feedlot cow (enterotoxemia)

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17
Q

What factors contribute to development of type D C. perfringens infection

A

o Associated with alteration in GI microbiota: diet change (high concentrate) – overeating disease
o Short course of disease > fatal

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18
Q

What is the general pathogenesis of type A C. perfringens infection

A

o Pathogenesis
 Overgrowth of C. perfringens
 Enzymes allow cleavage of mucin on epithelium
 Act on TNFa = cause sloughing of epithelium
 Activate host proteases to cut off basal epithelium
 Phospholipase affect membranes of epithelium and vasculature
 = necrosis/hemorrhage/sloughing epithelium

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19
Q

What are the lesions and main species affected by type D C. perfringens infection

A

o Lesions:
 Enterotoxemia
 Pulpy kidney
o Species: Calf/goat/horse/mostly lambs

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20
Q

What are the clinical manifestations of C. difficile in pigs and people

A

C. Difficile: Clostridioides difficile
* Human: antibiotic associated diarrhea
o Diarrhea/pseudomembranous colitis/fulminant colitis
* Pig: neonatal (1-7d) = mesocolonic edema (full of yellow fluid)

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21
Q

What is the main clinical consequence of C. difficile

A
  • Neutrophilic diarrhea
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22
Q

What are the toxins produced by C. difficile and what are their functions

A

 TcdA acts on the apical side = disrupt tight junction = allow TcdB to enter and act on basal side of enterocyte

o Toxins: A (TcdA enterotoxin) + B (TcdB cytotoxin)
 Inactivate regulation of actin cytoskeleton = open tight junctions = cell death
 Increase proinflammatory cytokines + activate enteric NS = PMN chemotaxis and fluid secretion

 Form volcano lesions in intestine (inflame cells leak into lumen)

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23
Q

How do you diagnose C. perfringens infection

A
  • C. perfringens: PE/gross/histo lesions
    o Anaerobic culture with double zone of hemolysis
    o Multiplex PCR or ELISA = identify toxin
24
Q

How do you diagnose C. difficile infection

A
  • C. difficile: anaerobic culture
    o Neutralization test/ELISA = identify toxin (best way for dx)
25
Q

How to prevent clostridia in cattle

A
  • 7 way cattle vaccine: C. chauveoi (blackleg) /septicum /sordelli (malignant edema)/novyi (black disease)/perfringens (3 types)
26
Q

What are the general characteristics of C. piliforme

A
  • Spore forming – can live 1 year in dirty bedding
  • Obligate anaerobic + obligate intracellular
  • Cause icterus: alter liver function
27
Q

How to stain C. piliforme

A
  • Gram (-) – but gram (+) under strictly anaerobic conditions
  • gram stain depends on the environment
  • Stain with silver stain or giemsa stain
28
Q

What is the disease that C. piliforme causes in horses? How do they get it? Prognosis? Prevention?

A
  • Tyzzers disease: foals
    o From ingestion of spores from environment
    o Unknown pathogenesis
    o Poor prognosis
    o No vaccine
    o Farm hygiene
29
Q

What is the disease that C. piliforme causes in dog/cat? How do they get it? Main lesions? Prognosis?

A
  • Tyzzers disease: dog/cat

o Due to ingesting rodent feces with spores

o Higher risk if stress/immunosuppressed

o Lesions: thickened intestine mucosa in distal ileum and proximal colon + foamy dark brown feces
o Poor prognosis = fatal

30
Q

What is the pathogenesis of tyzzers disease in dogs/cats

A

o Locally proliferate in enterocytes – spread to liver – colonize hepatocytes = multifocal periportal hepatic necrosis due to toxin
 Necrotic ileitis or colitis

31
Q

What is the main risk factor for clostridium infection

A

Risk factors: disruption to normal GI microbiota

32
Q

What is the morphologic characteristic of spirochetes

A
  • Thin/long/flexible bacteria
33
Q

How to stain spirochetes

A
  • Silver stain (gram (-) but less effective than silver stain)
34
Q

What are the 4 main genus’s of spirochete GI bacteria

A
  • Genus
    o Leptospira
    o Borrelia
    o Treponema
    o Brachyspira
35
Q

What are the 2 main types of brachyspira causing GI disease

A

Brachyspira (B. hyodysenteriae and pilosicoli)

36
Q

What animals does B. Hyodysenteriae infect

A
  • Pigs – 6-12 weeks
37
Q

What are the general characteristic s of B. Hyodysenteriae? What type of disease does it cause

A
  • Infectious colitis
  • Oxygen tolerant anaerobe
  • Obligate symbiotic
  • Environmentally resistant
38
Q

What are the clinical and gross signs of B. Hyodysenteriae

A

o Emaciation
o Lots of mucus-y feces
o Dehydration
o Edema of large intestine walls
o Low mortality but high production loss

39
Q

How to diagnose B. Hyodysenteriae

A
  • Diagnose: post mortem
    o Fluorescent stain
    o Anaerobic culture
    PCR
40
Q

What is a main virulence factor of B. pilosicoli

A

B. pilosicoli
* Virulence factors
o Beta hemolysins (can kill cells)

41
Q

What is the pathogenesis of B. pilosicoli

A

o Verry motile in mucin
o Chemotaxis
o Attach to apical membrane of enterocutes = loss of microvilli
o Serine protease secretion = damage tight junctinos = parracytoss
o chronic extracellular infection – in goblet cells and lamina propria
o colonic malabsorption = osmotic diarrhea

42
Q

What are the general characteristics of campylobacter spp.

A
  • gram (-)
  • microaerophilic
  • commensal in intestines and repro tract
43
Q

What are 3 relevant types of campylobacter spp

A

o C. fetus fetus and C. fetus venerealis = abortion
o C. jejuni = enteritis

44
Q

What are the main risk factors and clinical signs of C. jejuni? What else should be considered

A
  • Zoonotic
  • Risk: young/immunocompromised
  • Clinically: self limiting diarrhea (+/- mucoid/blood)
    o Fever
45
Q

How is diagnosis and treatment of C. jejuni complicated?

A
  • Diagnosis: difficult to confirm in animals without diarrhea
    o Can worsen the effects of other GI pathogens
  • Treat: resistance is more common (resistant to fluoroquinolones)
46
Q

What are the main types of helicobacter

A
  • Types:
    o H. felis, bizzozeronii, heilmanni
    o H. pylori
47
Q

What type of disease is helicobacter associated with

A
  • Associated with chronic gastritis in dogs
48
Q

What are the general characteristics of yersinia spp

A
  • Family: Enterobacteriaceae (also salmonella/e. coli)
  • Gram (-)
  • Facultative anaerobe
49
Q

What are the 3 main types of yersinia

A

o Y. pseudotuberculosis and enterocolitis

o Y. pestis
 Plague
 Human/cat/rodent

50
Q

What is the clinical manifestation of Y. pseudotuberculosis and enterocolitis and what species does it affect? How to prevent

A

 Enterocolitis/sporadic abortion – diarrhea
 Farm animal/wildlife/humans – deer (common)/sheep
 Vaccine available

51
Q

What is the clinical manifestation of Y. pestis and what species does it affect

A

 Plague
 Human/cat/rodent

52
Q

What 4 pathogens cause enteric disease in cattle

A

Johnes dz

Salmonella

Clostridia

Neonatal diarrhea - ETEC

53
Q

What 4 pathogens cause enteric disease in horse

A

Salmonella

Potomac horse fever

Clostridium associated enterocolitis

Lawsonia intracellularis

54
Q

What 2 disease complexes and the associated pathogens cause enteric disease in foals

A

Bacterial enterocolitis in neonaatal foals
- kleibsiella
- salmonella
- e. coli
- clostridia

haemorrrhagic diarrhea in foals
- C. perfringens
- Bacteroides fragilis
- rhodococcuss equi

55
Q

What 6 pathogens cause enteric disease in pigs

A

Salmonella

C. difficile/perfringens (type C)

ETEC

Brachyspira hyodysenteriae (dysentery) or pilosicoli (spirochetosis)

Lawsonia intracellularis

56
Q

What 6 pathogens cause enteric disease in cat/dogs

A

Salmonella

Campylobacter

Helicobacter

Shiegllosis

Tyzzer’s disease

C. perfringens