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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
pathotypes of Escherichia coli that effect the gut
- 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
ETEC (enterotoxigenic E. coli) | -> what?
- secretory D+ - dehydration - fluid imbalance
27
ETEC effects who
- young animals - neonatal pigs - weanling pigs - neonatal calves - neonatal lambs * each group above effected by diff strains*
28
ETEC host specific?
- 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
ETEC pathogenic mechanisms
- ingested bacteria adhere through pili to intestinal epithelium - Adherent bacteria produce enterotoxins which alter cell signaling (encoded on mobile genetic elements)
30
limitations of attachment to pili by ETEC
- 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
enterotoxins produced by ETEC
- 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
effects of enterotoxins produced by ETEC
alter cell signaling -> secretion of electrolytes and fluids into intestinal lumen -> D+, dehydration, possible death
33
diagnosis E. coli
- complicated bc commensal flora | - look for virulence factors (ELISA, latex agglutination methods) or genes that encode them (PCR)
34
Escherichia coli tx
- fluid and electrolyte therapy | - antibiotics (not necissary but can reduce bacterial load)
35
Escherichia coli prevention
- hygeine - vac (contain pili and inactivated LT) - anti-F5 pilus antiserum
36
mycobacterium avium general characteristics
- gram pos - acid fast - obligate aerobe - bacillus
37
mycobacterium avium found where
- intestinal tract of infected animals | - can survive in environment
38
mycobacterium avium spread
- fecal/ oral = birds | - milk/ colostrum = mammals (rarely also across uterus)
39
Mycobacterium avium species of intrest
- mycobacterium avium spp. paratuberculosis | - mycobacterium avium spp. avium
40
mycobacterium avium spp. paratuberculosis -> what
- Johne's dx - REPORTABLE - maybe zoonotic
41
Johne's dx cause, type dx, effects who
- caused by mycobacterium avium - granulomatous dx - effects cows, sheep, goats
42
Johne's dx cattle
- weight loss but eating well - dec milk production - severe dx only in 5% infected animals (see severe d+)
43
Johne's dx subclinical cows see what
- look fine but won't gain weight | - longer calving interval
44
mycobacterium avium spp. paratuberculosis pattern of infection
- young animals = suceptible to infection wnt see dx until 2-4 yrs old (bc long incubation)
45
mycobacterium avium pattern of infection
- young usually infected but won't see disease until animal much older bc 1-2 yr incubation
46
Johne's dx sheep and goats see what
- milder d+ | - herd or flock unthriftiness = main sign
47
granulomas in Johne's dx
- bacteria in macrophages in ileoecal region, dnt form perfectly walled off granulomas, more diffuse granulomatous inflam -> thickening of intestinal epithelium -> Mal absorptive d+
48
Johne's dx pathogenesis
- 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
diagnosis of Johne's dx
- 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
tx Johne's dx
- clarithromycin and macrolide = effective but expensive | - diagnose and slaughter
51
Johne's dx vac
- vac exists but not used in all states in us bc concern that animals can look pos on tb skin test
52
mycobacterium avium spp. avium -> what
- avian tuberculosis = a | chronic granulomatous dx
53
avian tuberculosis effects who
- 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
avian tuberculosis signs
- infected by ingestion -> lesions in intestine and liver -> lesions spread to resp tract - D+ - dec egg production - progressive emaciation - depression
55
avian tuberculosis diagnosis
- gross lesions on autopsy - culture - clinical signs
56
avian tuberculosis tx
- resistant to common anti-tb drugs so slaughter poultry, more valuable birds treated
57
virulence factors of e. coli
- enterotoxins - heat liable toxins - heat stable toxins - pilli
58
fusobacterium necrophorum usually in what conditions
unsanitary conditions
59
brachyspira hyzdysenteriae in swine industry
- was mostly gone in swine industry now is re-emerging
60
economic impact of Johne's dx
- economically important in dairy industry
61
what induces inflam with mycobacterium avium
waxy cell wall

block 4 (23 decks)

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