7. GI Pathogens 1 (Nicole) Flashcards
E coli stands for
Escherichia coli
- members of enterobacteriaceae family
-common commensals found in GI tract of normal animals and in environment
E coli are gram _______ & aerobic/anaerobic
negative, facultative anaerobes
are e coli mobile
yes - they have flagellae
enteric E.coli infections begin with
ingestions of fecal material - then E. coli colonizes intestinal mucosa (sits on microvilli)
- main kinds of E coli
Enterotoxigenic (ETEC), Enteropathogenic (EPEC), Enterohemorrhagic (EHEC), & shigatoxin producing (STEC)
ETEC - uses fimbrae to
attach and sit on villi and produce enterotoxins that bind to cell - cell gets damaged & sends out Cl- ions which causes watery diarrhea
EPEC - uses genes that allow binding of bacteria to villi -
this very close binding allows the e coli to inject effector proteins that damages the cells & causes malabsorption
EPEC has an actin bundle and ___________ formation
pedestal
shigatoxin delivery also requires
pedestal formation
does ETEC release LPS
yes! Large amounts released rapidly
WHAT IS THE most common cause of E coli diarrhea in farm animals
ETEC
ETEC most frequently encountered fimbrial adhesions in pigs
F4 (K88), F5, F6, F41
ETEC most frequently encountered fimbrial adhesions in ruminants
F5 (K99), F41, and F17
are enterotoxins virulence factors of ETEC
ya boi
2 major classes of enterotoxin produced by ETEC
heat stable (ST) comprised of STa and STb and heat labile (LT)
STa reduces the
absorption of electrolytes and water from the intestine at villus tips and elevates secretion of Cl- and H2O by crypt cells by opening channels in enterocytes
STb stimulates increase in
prostaglandin E2 levels, probably inducing the duodenal and jejunal secretion of water and electrolytes
LT stimulates elevated secretion of
Cl- and H2O and prostaglandin E2 increases, leading to intestinal secretion and loosing of tight junctions - leading to inflammation
what determines e coli pathotype?
virulence factors
main pathotypes of E coli
ETEC, EPEC, EHEC, STEC
can e coli septicaemia result from non-enteric infections
yes
is culture of E coli from feces very meaningful?
no - commonly present in healthy animals
-demonstration of toxins or fibril antigens more useful
EPEC - the intimin receptor (Air) translocates into the host cell and inserts itself into the
host-cell plasma membrane (process mediated by the T3SS). This receptor interacts with intimin on the bacterial surface, anchoring bacterium to the host cell
_____________ is the most common cause of diarrhea in calves less than 10 days old
e coli
ETEC diarrhea in calves hits at what time
< 3 days old
EPEC & EHEC diarrhea in calves hits at what age
2-30 days, can be up to 4 months
risk factors for E coli in calves
-failure of passive transfer
-poor hygiene/overcrowding
-inappropriate volume or composition of milk or milk replacer
is vaccine available for E coli in cattle?
yes! given to cow as 2 doses with 2nd dose 3-6 weeks before calving - one dose required for subsequent pregnancies
- commercially available antibodies can also be given
E coli vaccine and antibodies should contain ________ antigen
K99
E coli horses - causes __
diarrhea and septicemia in foals
what is the most important cause of septicaemia in neonatal foals
e coli !
- less important as a primary cause of diarrhea than in calves and pigs
how to treat e coli in foals
oral antibody for neonatal foals in available - administered within 12 hours of birth
E coli strains that cause disease in birds are often called
avian-pathogenic E coli (APEC)
APEC in birds causes
diarrhea, septicemia, meiningitis, polyarthritis, localized infections (swollen head syndrome)
APEC in birds associated with
poor hygiene - healthy birds usually resistant
- young and adult birds can be affected
E coli - pigs - which kind is most common in neonatal piglets
Enteric colibacillosis (ETEC) - causing diarrhea, dehydration, full litters affected
ETEC in pigs is there a vaccine
ya - available for pregnant sows
can ETEC cause disease in piglets after weaning
ya - post weaning diarrhea
what disease occurs in piglets 1-2 weeks after weaning
edema disease (secondary to enterotoxemia)
edema disease clinical signs
involvement of shiva togin
eyelid and forehead swelling
GI tract edema on necrospy (esp stomach and mesentery)
how do shiga toxins cause damage to cells
the toxin gets into the RER, and then is released into cytosol. it gets cleaved and then the subunit that got cleaved off interacts with ribosomes preventing protein synthesis = LETHAL!
Shiga toxin producing E. coli is implicated in which diseases in cows, dogs, and pigs
cows - diarrhea/dysentry
dogs - hemolytic uremic syndrome
pigs - edema disease
what are hallmarks of disease caused by STEC?
shiga toxins and development of attaching and effacing (AE) lesions
are STEC present in healthy and diarrheal dog’s feces?
ya
STEC - hemolytic uremic syndrome (HUS) occurs occasionally in young dogs of several breeds. There is a syndrome of _______________ followed by ___________, ______________, and ________________
bloody diarrhea, thrombocytopenia, microangiopathic anemia, anuric acute renal failure (kidneys show renal proximal tubular necrosis & hemorrhage)
HUS occurs in ______% of dogs that develop diarrhea - STEC
5
cause of HUS
O157:H7 EHEC and other STEC have been implicated as cause
Edema disease in pigs - colonization develops over __________ & is dependent on _______
3-6 days and is dependent on non-intimate adherence of the bacteria to epithelial cells in SI by F18 pili
colonization of STEC in edema disease is aided by management factors:
- at time of weaning intestinal epithelium goes through period of temporary malabsorption
- high protein diets contribute to presence of good substrate for rapid proliferation of EDEC in GI
edema disease pigs - what happens when shiga toxin type 2 (Stx2e) is absorbed into bloodstream?
absorbed toxin binds to and damages vascular endothelial cells in target tissues, resulting in edema and hemorrhage
are there EHEC (STEC) E coli outbreaks in humans?
ya - there was more info on this but that is human stuff so I didnt care but if u do - slide 26
what is the major risk factor for E coli infections
failure of passive transfer!!!!!!
salmonella is a member of what family & gram what
enterobacteriaceae
gram -ve
facultative anaerobe
are salmonella motile
yes - flagellae
is salmonella commensal
no - pathogen that can survive in asymptomatic carriers and in environment
- most common cause of hospitalization and death from food poisoning in humans
salmonella species
enterica or bongori - enterica more important
more than 2500 serotypes
salmonella - host restricted serotypes cause
systemic infection
salmonella - host adapted serotypes cause
systemic disease AND enteric infections
ex salmonella Dublin in cattle
salmonella - unrestricted or broad host range serotypes cause
mainly self limiting gastroenteritis
name 2 ways salmonella gets around body in enteric infection
- taken up by phagocytes and goes to mesenteric lymph nodes then liver (progresses into bacteremia) (DIRECT ROUTE)
- causes apoptosis of cell host and is then released into the bloodstream (INDIRECT ROUTE)
Direct route and indirect route of salmonella travel both start as reseeding but then go to
direct: reseeding –> amplification
indirect: reseeding –> persistence
salmonella in intestinal phase - what happens
adhesion, invasion, and multiplication
salmonella in systemic phase - what happens
cytokines are released from the cell and leukocytes go from blood vessel into tissues where they phagocytose the salmonella –> salmonella gets into blood stream
TYPICAL SALMONELLA LESIONS
vasculitis, thrombosis, ischemia, infarction
the lesions and clinical signs of salmonellosis are attributable to
-an enterotoxin that disrupts Cl- channels and produces a secretory diarrhea
- T3SS effector proteins
- the stimulation of enterocyte death
- acute inflammation that can locally cause diarrhea and damages vascular endothelium
- endotoxin-induced damage to vascular endothelium
name some clinical forms of salmonellosis
peracute septicemic, acute enteric, chronic enteric, abortion, subclinical carrier (no shedding), subclinical excretory (shedding)
salmonellosis can cause clinical disease in farm animals - mostly
cattle, horses, and pigs
- farms can be endemic
salmonella can occur in individuals or
in outbreak situations - adult cattle most typically affects stressed animals
how to diagnose salmonella (infection vs carrier status)
fecal culture with growth usually indicates infection
- fecal culture with light growth usually carrier status
- serotype identification can be performed
isolation of salmonella from blood or tissues indicates
septicaemia
- rising titer indicates active infection
do dogs and cats get clinical salmonellosis?
rarely ! most infections are subclinical - approximately 10% of dogs and cats are carriers
prevalence of salmonella is higher in dogs that eat
a raw diet ew
- however salmonella is isolated equally from the feces of healthy and diarrheic small animals
is isolation of salmonella from feces of a dog or cat sufficient to make a diagnosis of salmonellosis?
no!!!
salmonella pullorum, salmonella gallinarum, & salmonella enteritidis can infect the _______ in birds
oviduct and be transmitted through eggs
salmonella pullorum in eggs causes
pullorum disease or bacillary white diarrhea
- can cause septicaemia and death
- affects young chicks/turkeys up to 3 weeks of age
-
clinical signs of birds affected with salmonella pullorum/pullorum disease
anorexia, heat seeking, white fecal pasting around their cloacal vents, and often die
salmonella gallinarum causes
fowl typhoid
- looks like pullorum disease in young birds
- adults get acute septicaemia and die
what is paratyphoid in birds
non-host adapted salmonella infection in birds; salmonella enteritis or salmonella typhimurium
- usually subclinical infection
birds - salmonella in feces or vaginal secretions contaminate egg surface –> then what
may stay on surface or penetrate shell & salmonella grows inside shell
salmonella Arizonae most common serotype in
reptiles
salmonella infections in turtles, snakes, and lizards are sometimes the cause of
human infection
do reptiles demonstrate any symptoms of salmonella infection
rarely, but can be lifelong carriers
main risk factor for salmonella infection
STRESS
lawsonia intracellularis - obligate intracellular bacterium that is gram
negative
where does lawsonia intracellularis replicate
epithelial cells on the ileum
- can’t easily grow this bacteria
4 different forms of lawsonia intracellularis
- porcine intestinal adenomatosis
- proliferative hemorrhagic enteropathy
- necrotic enteritis
- regional ileitis
- porcine intestinal adenomatosis (PIA) is characterized by
proliferation of glandular epithelium
- proliferative hemorrhagic enteropathy (PHE) is shown as
proliferation of intestinal epithelium and blood loss in intestinal lumen
- necrotic enteritis (NE) is characterized by
necrosis of epithelium
- regional ileitis (RI) is characterized by
a strong proliferation of the tunica muscularis of the ileum - also observed in horses, dogs, and cats
after ingestion, L. intracellularis arrives in the ileum and will infect
the villous crypt cells
- the intestinal tissue will thicken by proliferation of stem cells in the crypt
final stage of infection by L intracellularis
maximally thickened intestinal wall with function loss of the mucosa
pigs infected with L. intracellularis will recover spontaneously OR
a significant number develop chronic necrotic enteritis with progressive emaciation. Haemorrhagic form –> cutaneous pallor, weakness, and passage of hemorrhagic or black tarry feces
pigs with lawsonia intracellularis feces description
watery to pasty, brownish, or faintly blood stained
- pigs may pass yellow fibronecrotic casts that have formed in the ileum
acute and chronic lesions l. intracellularis
acute: thickened and turgid ileum, and luminal blood clots, congested
chronic: irregular, patchy, subserosal edema. Ideal mucosa is thickened, with deep folds and patches of pseudomembrane
transmission of l. intracellularis
species to species transmission occurs: isolates are not species specific
how to diagnose l. intracellularis
dead animal: ileal mucosal PCR (GOLD STANDARD) or histology (H&E enterocyte proliferation)
alive: Fecal PCR with clinical signs or serological assay
how to treat l. intraceullaris
IV antimicrobials for acutely affected pigs
rest of herd: in feed or water to reduce severity of enteritis and prevent chronic form
is there a vaccine for lawsonia intracellularis
yes - live avirulent vaccine administered via the water is highly efficacious - should be administered to gilts and boars during acclimitization prior to introduction to a herd
l. intracellularis in horses clinical signs
hypoproteinemia, emaciation, thickening of mucosa (jejunum and ileum), severe hyperplasia of crypt epithelium
treatment the same & diagnosis the same as pigs (PCR, serology, dont culture)
