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block 4 > Digestive Tract Infections I > Flashcards

Digestive Tract Infections I Flashcards

1
Q

fusobacterium necrophorum general features

A
  • gram neg
  • obligate anaerobic bacilli or filaments(not branching filaments just physically bacilli that don’t split off from each other)
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2
Q

fusobacterium necrophorum found where

A
  • natural inhabitant of mucus membranes

- can survive in envionrment

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3
Q

fusobacterium -> what

A

oral infections and some laryngeal infections cows and sheep (mostly cows)

  • calf diphtheria
  • bullnose in swine
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4
Q

when susceptible to fusobacterium necrophorum

A

before oral mucus membranes totally intact so most common in calves

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5
Q

calf diphtheria see what

A

oral- foul smelling necrotic swelling in cheek

laryngeal see inflamed larynx, painful C+, difficulty swallowing, foul breath

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6
Q

bullnose in swine

A
  • necrotic rhinitis caused by fusobacterium necrophorum
  • involves soft tissue of nose and face (NOT BONE bone is atrophic rhinitis) -> swellings of face -> difficult to eat -> dec food intake
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7
Q

how develops bullnose in swine

A
  • injury to oral and nasal cavity -> this moving in -> infection bc fusobacterium necrophorum usually commensal
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8
Q

diagnosis fusobacterium necrophorum

A
  • culture anaerobically

- necrotic material from lesions

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9
Q

tx fusobacterium necrophorum

A

antibiotics

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10
Q

brachyspira spp. general chracteristics

A
  • gram neg
  • spirochetes
  • motile via periplasmic flagella
  • O2 tolerante anaerobes (Wnt grow in O2 but will survive)
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11
Q

brachyspira spp. id

A
  • v thin wnt see on gram stain
  • use silver stain
  • use wet mount
  • use fluorescent antisera
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12
Q

flagella and immune system

A
  • PAMP = hidden by membrane in intact bacteria to avoid activating immune system
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13
Q

brachyspira spp. found where

A
  • digestive tract

- survive 1 month in environment

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14
Q

brachyspira spp. transmission

A

fecal/ oral

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15
Q

Brachyspira hyodysenteria ->

A
  • swine dysentery signs = mucohemorrhagic d+, dehydration
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16
Q

carriers of brachyspira hyodysenteria

A

rodents

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17
Q

Brachyspira species of concern

A
  • brachyspira hyodysenteriae

- brachyspira pilosicoli

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18
Q

brachyspira pilosicoli -> what

A
  • mild persistent diarrhea

- dehydration over time

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19
Q

brachyspira pilosicoli effects who

A
  • pigs
  • dogs
  • birds
  • ZOONOTIC
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20
Q

diagnosis brachyspira spp.

A
  • stool specimines, rectal swabs, mucosal scrapings
  • anerobic conditions for growth
  • PCR
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21
Q

Brachyspira spp. tx

A
  • antibiotics

- rodent control = important bc Brachyspira hyoiddysenteria carried by rodents

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22
Q

Escherichia coli general features

A
  • gram neg
  • bacillus
  • facultative anaerobe
  • family = enterobacteriaesea
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23
Q

Escherichia coli found where

A
  • natural inhabitant of intestines, environment
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24
Q

Escherichia coli transmission GI

A
  • fecal/ oral
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25
Q

pathotypes of Escherichia coli that effect the gut

A
  • enterotoxigenic E. coli (ETEC)
  • shiga toxin-producing E coli (STEC and EHEC- enterohemorrhagic E.coli)
  • diff pathotypes formed bc diff virulence factors of E. coli
26
Q

ETEC (enterotoxigenic E. coli)

-> what?

A
  • secretory D+
  • dehydration
  • fluid imbalance
27
Q

ETEC effects who

A
  • young animals
  • neonatal pigs
  • weanling pigs
  • neonatal calves
  • neonatal lambs
  • each group above effected by diff strains*
28
Q

ETEC host specific?

A
  • very host specific even affect diff ages of diff hosts bc adhere to species- specific pili so = v host specific
  • pills are plasmid encoded so can move from strain to strain
29
Q

ETEC pathogenic mechanisms

A
  • ingested bacteria adhere through pili to intestinal epithelium
  • Adherent bacteria produce enterotoxins which alter cell signaling (encoded on mobile genetic elements)
30
Q

limitations of attachment to pili by ETEC

A
  • can only attach if only if receptor for pills = present (receptor maybe transiently expressed only at certain times in animals life, particularly young animals )
31
Q

enterotoxins produced by ETEC

A
  • heat labile toxin (LT) (some enterotoxin forms make heat liable toxins)
  • heat stable toxin (ST-STa, STb, EAST1) (all enterotoxin forms make heat stable toxins)
32
Q

effects of enterotoxins produced by ETEC

A

alter cell signaling -> secretion of electrolytes and fluids into intestinal lumen -> D+, dehydration, possible death

33
Q

diagnosis E. coli

A
  • complicated bc commensal flora

- look for virulence factors (ELISA, latex agglutination methods) or genes that encode them (PCR)

34
Q

Escherichia coli tx

A
  • fluid and electrolyte therapy

- antibiotics (not necissary but can reduce bacterial load)

35
Q

Escherichia coli prevention

A
  • hygeine
  • vac (contain pili and inactivated LT)
  • anti-F5 pilus antiserum
36
Q

mycobacterium avium general characteristics

A
  • gram pos
  • acid fast
  • obligate aerobe
  • bacillus
37
Q

mycobacterium avium found where

A
  • intestinal tract of infected animals

- can survive in environment

38
Q

mycobacterium avium spread

A
  • fecal/ oral = birds

- milk/ colostrum = mammals (rarely also across uterus)

39
Q

Mycobacterium avium species of intrest

A
  • mycobacterium avium spp. paratuberculosis

- mycobacterium avium spp. avium

40
Q

mycobacterium avium spp. paratuberculosis -> what

A
  • Johne’s dx
  • REPORTABLE
  • maybe zoonotic
41
Q

Johne’s dx cause, type dx, effects who

A
  • caused by mycobacterium avium
  • granulomatous dx
  • effects cows, sheep, goats
42
Q

Johne’s dx cattle

A
  • weight loss but eating well
  • dec milk production
  • severe dx only in 5% infected animals (see severe d+)
43
Q

Johne’s dx subclinical cows see what

A
  • look fine but won’t gain weight

- longer calving interval

44
Q

mycobacterium avium spp. paratuberculosis pattern of infection

A
  • young animals = suceptible to infection wnt see dx until 2-4 yrs old (bc long incubation)
45
Q

mycobacterium avium pattern of infection

A
  • young usually infected but won’t see disease until animal much older bc 1-2 yr incubation
46
Q

Johne’s dx sheep and goats see what

A
  • milder d+

- herd or flock unthriftiness = main sign

47
Q

granulomas in Johne’s dx

A
  • bacteria in macrophages in ileoecal region, dnt form perfectly walled off granulomas, more diffuse granulomatous inflam -> thickening of intestinal epithelium -> Mal absorptive d+
48
Q

Johne’s dx pathogenesis

A
  • bacteria ingested in colostrum/ milk/ fecally contaminated H2O -> bacteria cross m cells -> bacteria taken up by macrophages -> bacteria mult in macrophages -> bacterial cell wall components induce inflam (monocytes surround proliferating bacteria, granulomatous lesions formed) -> thickening of intestinal walls -> malabsorptive d+
49
Q

diagnosis of Johne’s dx

A
  • no good mechanism bc high risk of false neg (lots of specific but not sensitive tests, per, Elisa)
  • can do gram stain but again not very good
  • johnin test inoculation iv = largely out of favor
50
Q

tx Johne’s dx

A
  • clarithromycin and macrolide = effective but expensive

- diagnose and slaughter

51
Q

Johne’s dx vac

A
  • vac exists but not used in all states in us bc concern that animals can look pos on tb skin test
52
Q

mycobacterium avium spp. avium -> what

A
  • avian tuberculosis = a

chronic granulomatous dx

53
Q

avian tuberculosis effects who

A
  • primarily chickens also other birds
  • animals infected young dont see dx till old but many chickens slaughtered so int see dx in the at all
  • ZOONOTIC
54
Q

avian tuberculosis signs

A
  • infected by ingestion -> lesions in intestine and liver -> lesions spread to resp tract
  • D+
  • dec egg production
  • progressive emaciation
  • depression
55
Q

avian tuberculosis diagnosis

A
  • gross lesions on autopsy
  • culture
  • clinical signs
56
Q

avian tuberculosis tx

A
  • resistant to common anti-tb drugs so slaughter poultry, more valuable birds treated
57
Q

virulence factors of e. coli

A
  • enterotoxins
  • heat liable toxins
  • heat stable toxins
  • pilli
58
Q

fusobacterium necrophorum usually in what conditions

A

unsanitary conditions

59
Q

brachyspira hyzdysenteriae in swine industry

A
  • was mostly gone in swine industry now is re-emerging
60
Q

economic impact of Johne’s dx

A
  • economically important in dairy industry
61
Q

what induces inflam with mycobacterium avium

A

waxy cell wall

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