Digestive tract infections II Flashcards
salmonella enterica general features
- gram neg
- bacillus
- fac anaerobe
salmonela enteric found whre
- natural inhabitant of intestines
- weidley distributed in envonrment
salmonella enterica transmission
fecal oral
salmonella enterica serovars
- 2500 serovars
- some non host adaptive
- some highly host adaptive but found in other hosts
- some entirely host resticted
what dictates what is seen with salmonella enterica infection
- age
- host type
- serovar infecting
weanling animals salmonella enteirca host restricted/ host adapted serovars
- pneumonia
newborn animals salmonella enteirca host restricted/ host adapted serovars
septicemia, high fever, rapid death
older animals salmonella enteirca host restricted/ host adapted serovars
- systemic type dxs, arthritis, abortion ect
young animals non host adaptied serotypes salmonella enterica
- febrile d+
- watery d+
- usually mucus in it maybe blood
- anorexia
- +/- dehydration
- non-host adapted serotypes salmonella enterica primarily effected young animals*
salmonella enterica effects who
- primarily cows swine, also seen in other ruminants (sheep/ goats)
- dx in horses usually associated w/ predisposing factors
- chickens and turkeys outside us
- ZOONOTIC
chickens and turkeys salmonella enterica
- dx outside us from host restricted serovars THIS IS REPORTABLE
- chickens and turkeys carry non host restricted serovars which dont cause illness in them but can cause infection in ppl that consume them
how do humans get salmonella enterica
- foodbord transmisison
- most commonly poultry and eggs
pathogenesis salmonella enterica
- bacteria ingested in material contaminated with feceus
- salmonella enterica induces its own uptake into epithelial cells (ability to do this bc genes on pathogenicity island aka mobile genetic element)
- facultative intracell pathogen of macrophages (survives via alteration phagocytic vacuole, ability to do this bc genes on pathogenicity island aka mobile genetic element)
- bacterial factors induce infam response (some bacteria will be sacrificial bacteria)
inflam response caused by salmonella enterica and serovars responsible for it
- inflam -> environmental changes in intestines -> abundance of molecules favorable to growth of Salmonella enterica over normal microbiota
- inflam also -> d+
- inflam caused by non host adapted salmonella enterica host restricted and host adapted salmonella enterica come in bit more stealthily and enter macrophage but dont -> inflam instead spread systemically -> septicemia in younger animals (more severe dx)
diagnosis salmonella enterica
- stool culture (will shed several weeks after animal clears infection)
- grow culture on enriched media or differential media
tx salmonella enterica
- antimicrobials early on and for septicemia, once inflam strarts it will clear this as quickly as antimicrobials
salmonella enterica vac
- for cows and pigs attenuated = best
how serovars written
- written like species name but non italicized and capitalized with just Salmonella in front of them (no enterica)
- we dont need to know serovar names
non host adaptive serovars tend to be seen where
only in certain animals
neorckettsia species family
anaplasmatacea
neorickettsia species of intrest
- neorickettsia risticii
- neorickettsia helminthoeca
neorickettsia spp. features
- two membranes, no cell wall lack lipopolysacharides; have cholesterol from host
- stain gram neg but not truly gram neg
- obligate intra cell bacteria
- obligate aerobes
- multiply incide monocytes
neorickettsia spp. carrier how
- associated with trematodes
- snails = 1st int host
- different 2nd int hosts
neorickettsia risticii -> what / what are clinical signs
- Potomac horse fever in horse
- febrile d+
- leukopenia
neorickettsia risticcii lifecycle
- found in trematodes that start in snails -> insects -> horse ingests insects (caddisflies or mayflies)
- seen in warmer months bc this is when these insects = around to transmit this
Neorickettsia helminthoeca lifecycle
snails -> fish (generally fluke) -> dog (or raccoon but raccoons show o signs of dx if get infected)
neorickettsia helminthoeca -> what in wno
- salmon poising dx in dogs
- febrile d+ (HIGH FEVER), enlarged lns, weight loss, persistent d+
- raccoons no signs of dx
salmon poising dx seen where
seen in pacific north west and ca of US and Brazil
diagnosis Neoricketssia risticii
- serologically (paired tiers bc looking for rising antibody titers)
- PCR
diagnosis neorickettsia helminthoeca
- contains bacteria inside vacuoles (morale) inside macrophages in ln aspirates
- look for stool sample for fluke eggs and if these dogs have febrile d+ more severe dx signs and on west coast = supportive evidence for Salmond poisoning dx
neorickettsia helminthoeca treatment
tetracycline effective if given early
neorickettsia spp. vac
yes for Neorickettsia ristcii doesn’t work well bc of antigenic variation
campylobacter species general features
- gram neg
- curved bacillus
- microaerophilic (prefer low concentrations of oxygen to grow, don’t grow in ambient air)
campolyobacter spp. effects who
- puppies
- MOSTLY IMPORTANT AS ZOONOTIC PATHOGENS
- many animals carry but dont get sick
campylobacter spp inhabitant of where
- gi tract
campylobacter spp. transmission how
fecal/ oral (acquired by ingestion)
campylobacter spp. -> what in who
puppies get gastroenteritis (mild d+ to watery d+ w/ mucus and bld)
- ZOONOTIC
important species of campylobacter
- campylobacter jejuni
- campylobacter coli
campylobacter spp. diagnosis
- fecal samples
- incubated under reduced O2 conditions at 42 degrees C (like higher temp)
campylobacter spp. tx
- usually self limiting dx
- maybe fluids if needed
prevention campylobacter
- zoonotic source usually chicken -> ppl
- want to prevent introduction campylobacter into flock bc once colonized chicken = colonized for life
lawsonia intracellularis general chracteristics
- obligate intracellular
- gram neg
- curved bacillus
- microaerophilic
lawsonia intracellularis source of infection
- subclinically infected animals = source of infection
lawsonia intrecellularis transmssion
fecal/ oral
lawsonia intracellulars -> what in who
- porcine proliferative enteritis in pigs
- ileitis in pigs
- equine proliferative enteropathy in horses
lawsonia intracellularis chronic vs acute dx
- chronic dx = more common = in young pigs and horses; see anorexia, loose stools, progressive weight loss
- acute dx = in pigs 4months - 1yr of age; hemorrhagic anemia; rapid death; black tarry feces
lawsonia intracellularis diagnisos
- can’t grow on standard bacteriological media
- immunofluorescence tissue samples or pcr of stool
lawsonia intracellularis tx
- sensitive to most abs that can enter euk cells
lawsonia intracellularis vac
- live attenuated given in drinking water for pigs
- works off label for horses
salmonella enterica important cause of what
- febrile inflam d+ especially in ruminants and pigs; horses see dx after stress; severe dx with host-restricted serovars
- important food borne dx
lawsonia intracellularis proliferative enteropathy
see thickened intestinal mucosa -> malabsorpitve d+
- this is not intense inflam response -> thickening these are proliferative changes by intracell bacteria being inside crypt cells in cytosol and inducing proliferation -> thickening of intestinal mucosa -> malabsorpitve D+
