Digestive Tract Infections I Flashcards
fusobacterium necrophorum general features
- gram neg
- obligate anaerobic bacilli or filaments(not branching filaments just physically bacilli that don’t split off from each other)
fusobacterium necrophorum found where
- natural inhabitant of mucus membranes
- can survive in envionrment
fusobacterium -> what
oral infections and some laryngeal infections cows and sheep (mostly cows)
- calf diphtheria
- bullnose in swine
when susceptible to fusobacterium necrophorum
before oral mucus membranes totally intact so most common in calves
calf diphtheria see what
oral- foul smelling necrotic swelling in cheek
laryngeal see inflamed larynx, painful C+, difficulty swallowing, foul breath
bullnose in swine
- 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
how develops bullnose in swine
- injury to oral and nasal cavity -> this moving in -> infection bc fusobacterium necrophorum usually commensal
diagnosis fusobacterium necrophorum
- culture anaerobically
- necrotic material from lesions
tx fusobacterium necrophorum
antibiotics
brachyspira spp. general chracteristics
- gram neg
- spirochetes
- motile via periplasmic flagella
- O2 tolerante anaerobes (Wnt grow in O2 but will survive)
brachyspira spp. id
- v thin wnt see on gram stain
- use silver stain
- use wet mount
- use fluorescent antisera
flagella and immune system
- PAMP = hidden by membrane in intact bacteria to avoid activating immune system
brachyspira spp. found where
- digestive tract
- survive 1 month in environment
brachyspira spp. transmission
fecal/ oral
Brachyspira hyodysenteria ->
- swine dysentery signs = mucohemorrhagic d+, dehydration
carriers of brachyspira hyodysenteria
rodents
Brachyspira species of concern
- brachyspira hyodysenteriae
- brachyspira pilosicoli
brachyspira pilosicoli -> what
- mild persistent diarrhea
- dehydration over time
brachyspira pilosicoli effects who
- pigs
- dogs
- birds
- ZOONOTIC
diagnosis brachyspira spp.
- stool specimines, rectal swabs, mucosal scrapings
- anerobic conditions for growth
- PCR
Brachyspira spp. tx
- antibiotics
- rodent control = important bc Brachyspira hyoiddysenteria carried by rodents
Escherichia coli general features
- gram neg
- bacillus
- facultative anaerobe
- family = enterobacteriaesea
Escherichia coli found where
- natural inhabitant of intestines, environment
Escherichia coli transmission GI
- fecal/ oral
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
ETEC (enterotoxigenic E. coli)
-> what?
- secretory D+
- dehydration
- fluid imbalance
ETEC effects who
- young animals
- neonatal pigs
- weanling pigs
- neonatal calves
- neonatal lambs
- each group above effected by diff strains*
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
ETEC pathogenic mechanisms
- ingested bacteria adhere through pili to intestinal epithelium
- Adherent bacteria produce enterotoxins which alter cell signaling (encoded on mobile genetic elements)
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 )
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)
effects of enterotoxins produced by ETEC
alter cell signaling -> secretion of electrolytes and fluids into intestinal lumen -> D+, dehydration, possible death
diagnosis E. coli
- complicated bc commensal flora
- look for virulence factors (ELISA, latex agglutination methods) or genes that encode them (PCR)
Escherichia coli tx
- fluid and electrolyte therapy
- antibiotics (not necissary but can reduce bacterial load)
Escherichia coli prevention
- hygeine
- vac (contain pili and inactivated LT)
- anti-F5 pilus antiserum
mycobacterium avium general characteristics
- gram pos
- acid fast
- obligate aerobe
- bacillus
mycobacterium avium found where
- intestinal tract of infected animals
- can survive in environment
mycobacterium avium spread
- fecal/ oral = birds
- milk/ colostrum = mammals (rarely also across uterus)
Mycobacterium avium species of intrest
- mycobacterium avium spp. paratuberculosis
- mycobacterium avium spp. avium
mycobacterium avium spp. paratuberculosis -> what
- Johne’s dx
- REPORTABLE
- maybe zoonotic
Johne’s dx cause, type dx, effects who
- caused by mycobacterium avium
- granulomatous dx
- effects cows, sheep, goats
Johne’s dx cattle
- weight loss but eating well
- dec milk production
- severe dx only in 5% infected animals (see severe d+)
Johne’s dx subclinical cows see what
- look fine but won’t gain weight
- longer calving interval
mycobacterium avium spp. paratuberculosis pattern of infection
- young animals = suceptible to infection wnt see dx until 2-4 yrs old (bc long incubation)
mycobacterium avium pattern of infection
- young usually infected but won’t see disease until animal much older bc 1-2 yr incubation
Johne’s dx sheep and goats see what
- milder d+
- herd or flock unthriftiness = main sign
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+
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+
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
tx Johne’s dx
- clarithromycin and macrolide = effective but expensive
- diagnose and slaughter
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
mycobacterium avium spp. avium -> what
- avian tuberculosis = a
chronic granulomatous dx
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
avian tuberculosis signs
- infected by ingestion -> lesions in intestine and liver -> lesions spread to resp tract
- D+
- dec egg production
- progressive emaciation
- depression
avian tuberculosis diagnosis
- gross lesions on autopsy
- culture
- clinical signs
avian tuberculosis tx
- resistant to common anti-tb drugs so slaughter poultry, more valuable birds treated
virulence factors of e. coli
- enterotoxins
- heat liable toxins
- heat stable toxins
- pilli
fusobacterium necrophorum usually in what conditions
unsanitary conditions
brachyspira hyzdysenteriae in swine industry
- was mostly gone in swine industry now is re-emerging
economic impact of Johne’s dx
- economically important in dairy industry
what induces inflam with mycobacterium avium
waxy cell wall
