Lecture 6: GI 1 Flashcards
what are the three main pathotypes of Escherichia Coli?
Enterotoxigenic (ETEC)
Enteropathogenic (EPEC)
Enterohemorrhagic (EHEC)
Escherchia coli bacteria are gram ______, are ______ anerobes, and move via _______. They are common ______ meaning they are found in the GI tract of normal animals
negative
facultative
flagellae
commensals
how is Escherchia coli transmitted and what is the first step in it’s pathogenesis?
via feal oral route
it colonizes the intestinal mucosa
ETEC is a little different in the way it attaches to the enterocytes in the GI tract compared to EPEC and EHEC. Explain briefly how each type attaches to cells.
ETEC just barely touches the cell and does not intimately bind, then delivers enterotoxins into the cell
EPEC anchors itself to the host cell’s cytoskeleton via intimin/tir receptor and there is actin pedestal formation which provides the bacteria with support. It then uses a type 3 secretion system to inject host cell effector proteins.
EHEC also uses the actin pedastal formation similar to EPEC, but it injects shiga toxins into the host cells
neonatal animals that have diarrhea, especially cattle, are likely to have
ETEC (enterotoxigenic E coli)
an infection with enterotoxigenic E coli may progress so rapdily that….
death occurs before development of diarrhea and is referred to as enteric colibacillosis complicated by shock. this is due to large amounts of LPS by ETECT (lipid A portion most responsible for symptoms of shock)
ETECT produces enterotoxins. There are two major classes, heat stable (ST) and heat labile (STa & STb). Describe how they work
STa: reduce the absroption of elecrolytes and water from the intestine
STb: induces duodenal and jejunal secretion of water and electrolytes
how does EPEC (enteropathogenic E coli) successfully anchor itself to the host cell?
once EPEC forms an actin pedestal, the intimin receptor translocates into the host cell and inserts itself into the host cell plasma membrane, which is all mediated through the T3SS (inject it’s own receptor). This receptor interacts with intimin on the bacterial surface which anchors the bacterium to the host cell.
E coli septicemia can also result from non enteris infections such as:
- umbillical infection of neonates
- urogenital tract infections
- mastitis
- lung infections
how do you diagnose E coli?
- isolation of E coli from feces is not very meaningful because E coli is often found in healthy animals
- it’s better to find the toxins or fimbrial antigens via PCR or monoclonal antibody based techniques
- in cases of septicemia you can culture the blood
_______ is the most common cause of diarrhea in calves less than 10 days old
E coli
ETEC is usually less than 3 days old
EPEC and EHEC usually in slightly older calves, 2-30 days or up to 4 months sometimes
what are som risk factors for developing an E coli infection in cattle?
- failure of passive transfer
- poor hygiene or overcrowding
- inappropriate volume or composition of milk or milk replacer
the E coli vaccine given to cows is initially given to cows how? is there any other options besides the vaccine?
- as two doses, 3 weeks apart, with second dose 3-6 weeks before calving
- there are commercially available antibodies you can put in the milk
_____ is the most important cuase of septicemia in neonatal foals, but less imporant as a primary cause of diarrhea than in calves and pigs
E coli
what is the E coli that infects birds called? what clinical signs will you see in birds? birds that get this are usually associated with what?
APEC (avian pathogenic E coli)
C/S: diarrhea, septicemia, meningitis, polyarthritis, localized infections
- usually associated with poor hygiene (healthy birds are resistant)
Enteric colibacillosis is common in ____. What signs will you see? Which pathotypes cause this?
neonatal piglets
C/S: diarrhea, dehydration, whole liter often affected
ETEC and EHEC
post weaning diarrhea in pigs is caused by what E coli pathotype?
ETEC
What is edema disease and what E coli pathotype causes it? What are some clinical signs?
- a disease secondary to enterotoxemia that occurs inpiglets 1-2 weeks after weaning
- EHEC
C/S: neurologic disease, eyelid and forehead swelling, GI tract edema on necropsy
descibe in detail how Shiga toxins work!
A subunit is associated with a pentamer of B subunits which mediate binding to a specific receptor, Gb3, on the host epithelial or endothelial cells, which allows the toxin to be internalized by receptor mediated endocytosis. The toxin then moves to the golgi, then to the rough endoplasmic reticulum, then into the cytoplasm. Subunit A is cleaved and a resulting A1 unit interacts with ribosomes to inhibit protein synthesis which kills the cell.
in order for a shiga toxin to work, what must be present?
a Gb3 receptor!
shiga toxin producing E coli (STEC) causes 3 big diseases in animals. list them plz and thx
- diarrhea and dysentery in calves
- hemolytic uremic syndrome in dogs
- edema disease in pigs
true or false: STEC are present in the feces of healthy and diarrheal dogs
TRUE GURL GOOD JOB
STEC causes what disease in dogs? Describe the clinical signs?
hemolytic uremic syndrome (HUS)
usually affecting younger dogs, they will have bloody diarrhea followed by thrombocytopenia, microangiopathic anemia, and anuric acute renal failure. They kidneys will show renal proximal tubular necrosis and hemorrhage
STEC causes what disease in pigs? describe the pathogenesis and clinical signs?
edema in pigs
pathogenesis: colonization of the bacteria is dependent on non-intimate adherence of the bacteria to the epithelial cells in the small intestine by F18 pili. The Stx2e toxin is absroped into the bloodstream and damages vascular endothelial cells in target tissues resulting in edema and hemorrhage
why does STEC cause edema disease in piglets at the time of weaning?
at the tie of weaning, the intestinal epithelium undergoes changes that lead to a period of temporary malabsroption. High protein diets contribute to the prescence in the intestine of an abundance of rich subsrate for rapid proliferation of EDEC (edema E coli).
_____ is the most common type of E coli involved in food borne outbreaks. It usually causes ______, which is a common cause of kiney failure in young children.
EHEC (sometimes referred to as STEC)
hemolytic uremic syndrome
how does EHEC/STEC in humans cause kidney failure?
the shiga toxin damages blood vessels in kidney, causing thrombi formation in the kidney microvasculature leading to ichemia and necrosis
whatis the MAJOR risk factor for an E coli infection to develop?
failure of passive transfer of immunity from mom
salmonella differs from E coli in what way? in what ways are they similar?
they are both gram neg, facultative anaerobes, using flagellae, and both have the ability to use T3SS.
salmonella is NOT a commensal like E coli. It can survive in asymptomatic carriers and in the environment.
______ is the most common cause of hospitalization and death from food poisoning in humans
salmonella
name the genus, species, and subspecies of the GI salmonella bacteria.
genus: salmonella
species: enterica
subspecies: enterica
there are more than 2500 serotypes of these bacteria like typhimurium and enteritidis, etc
give 3 examples of host restricted serotypes of salmonella and the respective species they infect
typhi (humans), gallinarum (poultry), abortusovis (sheep)
what are two examples of host adapted serotypes of salmonella and the respective species
dublin (cattle), choleraesuis (swine)
what are two examples of un-restricted or broad host range serotypes of salmonella, usually self limiting gastroenteritis
typhimurium, enteritidis
what are salmonella pathogenicity islands?
culsters of genes on the chromosome that encode virulence factors such as secretory systems, adhesins, etc
what is the pathogenesis of a salmonella infection? LOTS OF DETAIL PLEASE
after the bacteria uses the T3SS complex to anchor to the cell and enter via endocytosis into a salmonella containing vacuole, one of two things happen:
- once in the vacuole, a second T3SS injects proteins that optimize conditions for bacterial replication and survival within the cell. More virulence factors then allow the replicating bacteria to escape the phagosome which causes an intracellular inflammatory response resulting in cell death. This releases the bacteria into the intestinal lumen, where they can go on to infect more enterocytes.
OR
- Secretory system proteins cause translocation of the vacuole to the basolateral side of the enterocyte, where the bacteria are released and taken up by phagocytes (especially dendritic cells) in the lamina propria. Salmonella can evade degradation in the phagocytes through virulence factors, and hitches a ride via leukocyte trafficking to the mesenteric lymph nodes. Salmonella that escape the lymph nodes cause a bacteremia that seeds the liver, this allows reseeding of the intestine via bacteria in the bile.
the lesions and clinical signs of salmonellosis are attributable to what 4 things?
- an enterotoxin that disrupts Cl- channels and produced a secretory diarrhea
- stimulation of enterocyte death
- acute inflammation that locally causes diarrhea and damages the vascular endothelium
- endotoxin induced damage to the vascular endothelium
what are the 4 big things that are typical of salmonellosis?
- vasculitis
- thrombosis
- ischemia
- infarction
what are the 6 clinical forms of salmonellosis?
- peracute septicemic
- acute enteric
- chronic enteric
- abortion
- subclinical carrier (no shedding)
- subclinical excretor (shedding)
salmonellosis primarily causes clinical disease in ______. It typically affects individual animals that are ______
farm animals like cattle, horses, and pigs
stressed
what are some ways to diagnose salmonellosis in a farm setting?
- fecal culture–>heavy growth usually indicates infection, light growth usually indicates carrier status
- serotype identification
- isolation from blood oor tissues indicates septicemia
- rising titres indicate active infection
true or false: dogs and cats often get clinical salmonellosis
false! they rarely get clinical salmonellosis
approx _____% of dogs and cats are salmonella carriers
10
prevalence of salmonella is higher in dogs and cats that…
are fed raw meat diets
if you culture feces from a dog and it comes back positive for salmonella, does this indicate a salmonella infection?
no
which serotypes of salmonella infect poultry and can be transmitted via eggs?
S. pullorum, S. gallinarum, S. enteritidis
the most common serotype of salmonella in reptiles is _______
S. arizonae
true or false: reptiles infected with salmonella usually do not have symptoms but can become lifelong carriers
true!
which salmonella serotype causes typhoid fever in humans? what are clinical signs of this disease? how is this bacteria spread?
S. enterica ser typhi
C/S: fever, headache, anorexia, constipation, death
spread via contaminated food or water
WHAT IS THE BIGGEST RISK FACTOR FOR SALMONELLA INFECTION???????
STRESS!!!!!
lawsonia intracellularis is an obligate intracellular gram ____ bacteria, and it replicates in the _______. Cultivation requires ____________and atmosphere of 82% N2, 9% CO2, 9% O2
negative
epithelial cells of the ileum
dividing eukaryotic cells
what are the four different forms of lawsonia intracellularis infection
- porcine intestinal adenomatosis
- proliferative hemorrhagic enteropathy
- necrotic enteritis
- regional ileitis
what are the first 3 basic steps of a lawsonia intracellularis infection?
- afer ingestion, the bacteria arrives in the ileum and infects the villous crypt cells
- the intestinal tissue thickens by proliferation of stem cells in the crypts
- final stage: maximally thickened intestinal wall with function loss of the mucosa membrane
what are the clinical signs of a lawsonia intracellularis infection?
sudden onset of diarrhea, feces are watery to pasty, brownish, faintly blood stained, pigs may pass yellow fibrinonecrotic casts that have formed in the ileum.
what is the prognosis of pigs infected with lawsonia intracellularis?
most will recover spontaneously, but many develop chronic necrotic enteritis with progressive emaciation
the hemorrhagic form of lawsonia intracellularis infection is characterized by:
pallor, wekaness, passage of hemorrhagic or black tarry feces
what are signs of lawsonia intracellularis in horses? how would you diagnose and/or treat the horse?
hypoproteinemia, emaciation, thickening of mucosa, severe hyperplasia of crypt epithelium
diagnosis: you cannot culture, you have to do serology or PCR
treatment: antimicrobials
what disease does this horse have?
infection with lawsonia intracellularis
what are some gross lesions woud see in an infection of lawsonia intracellularis in a pig, both in acute and chronic infections?
lesions will be in terminal ileum
acute: thickened and turgid, with a corrugated serosal surface and luminal blood clots, congested
chronic: irregular, patchy, subserosal edema, ileal mucosa is thickened with deep folds and patches of pseudomembrane
how do you diagnose and/or treat a pig with suspected lawsonia intracellularis infection?
diagnosis: histologic observation of characteristic proliferation and inflammation of mucosal crypts, a PCR test, bacterial culture to rule out salmonella and swin dyssentery. Since the bacteria is present in many swine herds, the presence of positive PCR or antibodies means nothing.
treatment: there is a live avirulent vaccine you can put in the water, but you can treat with antimicrobials either IV in super serious cases, or put them in feed and water to reduce severity and prevent the chronic form
