Transcript collibacillosis

Colibacillosis (E. coli diarrhea)
Eman Ahmed
12214
Perihan Mohamed
12231
What is Colibacillosis?
Colibacillosis: Infectious disease of man and •
animals with bacteria called Escherichia coli.
Infection can cause severe diarrhea or septicemia.
The bacteria can also produce toxins which can
affect other parts of the body also.
Colibacillosis is the most common infectious •
bacterial disease of poultry and is seen in cattle,
pigs, goats, and other mammals. It is a common
disease that is seen worldwide in places ranging
from Egypt, Bangladesh, and Malaysia to America.
Causative agent:
Colibacillosis is caused by infection with the •
bacteria Escherichia coli (E. coli). The bacteria
Escherichia coli occur commonly in the intestinal
tract of many animals.
Note: The main factor in these infections is •
inadequate passive immune transfer from the dam
to calf (inadequate ingestion or absorption or
inadequate antibodies in colostrum), exposure to
the pathogen before colostrum was ingested,
immediately after birth, inclement weather, use of
milk replacers as opposed to whole milk, and poor
hygiene.
Route of infection:
Transmission of pathogenic E. coli often occurs •
via fecal–oral transmission.
Clinical signs:
Colibacillosis usually is signaled by the
appearance of diarrhea:
Severe watery diarrhea caused by enteritis
Lack of appetite and water consumption
Rapid dehydration
Sunken eyes
Stunted growth, inactivity and
unresponsiveness
Acidosis (Hyperchloremic acidosis is caused by
the loss of too much sodium bicarbonate from
the body, which can happen with severe
diarrhea)
Morbidity and mortality are very variable
depending on which infection/infections the E.
coli strain causes in a particular flock of
animals.
Colibacillosis signs are nonspecific and vary
widely among different hosts.
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Pathogenesis:
Cow : •
Secondary Infection Omphalitis.
Arthritis.
Cystitis.
Mastitis.
Pyelonephritis.
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Pig : •
Gut Edema.
Young pigs cause enteric colibacillosis.
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Avian : •
Hjarre’s Disease : Colligranuloma.
Omphalitis
Peritonitis.
Salphingitis.
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E. coli infections in animals and humans •
cause disease by at least five different
general mechanisms:
The first mechanism→ Enterotoxic
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colibacillosis:
Def. :
Secretory small bowel (intestine) diarrhea,
stimulated by enterotoxins which are produced by
E.coli colonizing the mucosa of small intestine. This
condition is an important cause of diarrhea in
neonatal animals.
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Pathogenesis: The enterotoxins enter the •
intestinal mucosa and cause the secretion of
chloride, with sodium and water following
from the crypts. Water is drawn into the
intestine to normalize the resultant NaCl,
thus the diarrhea is termed secretory.
Affected animals are dehydrated, with a •
"tucked-up" abdomen. Subsequent to
dehydration, the eyes sunken. Animals that
die from ETEC infections are often
emaciated and have diarrheic feces pasted
around their perineum.
Microscopically:
Presence of bacteria lining the surface of •
the enterocytes. Presence of Neutrophils.
With some strains of E.coli, there may be
necrosis of some villi.
Macroscopically: •
At necropsy, the small intestine is dilated, •
flaccid, and filled with translucent, yellow fluid
and sometimes gas. Chyle is present in the
mesenteric lymphatic vessels similar to animals
without enteric disease, indicating that unlike
the mal absorptive diseases of SI, absorption
proceeds normally in cases of ETEC.
The second mechanism→ Enterocyte- 2) •
adherent E.coli strains:
These strains colonize the surface of the •
epithelial cells, do not produce recognized
enterotoxin, but are associated with villus
atrophy. They are not currently known to occur
in domestic animals.
The third mechanism→ Enterotoxemic
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colibacillosis:
Def.: {Edema disease in swine}
In this
condition a toxin produced by specific strains
of E.coli colonizing the small intestine is
absorbed and has its pathogenic effect on
tissues other than the gut.
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Pathogenesis: Pathogenic E. coli colonize •
and proliferate in the small intestine.
Enterotoxins produced by pathogen strains
induce the disease, causing damage to small
arteries and arterioles. Degenerative
angiopathy leads to increased vascular
permeability and accumulation of edema at
various sites, most notably colon, stomach,
small intestine, eyelids, and brain.
Macroscopically:
Edema disease is primarily a disease of the •
vasculature, and gross lesions consist of
subcutaneous edema and edema in the
submucosa of the stomach, particularly in the
glandular cardiac region. The edema fluid is
usually gelatinous. The edema may be
accompanied by hemorrhage. Fibrin strands
may be found in the peritoneal cavity, and
serous fluid may be found in both the pleural
and peritoneal cavities.
Microscopically:
A degenerative angiopathy affecting arteries •
and arterioles and necrosis of the smooth
muscle cells in the tunica media are present.
The fourth mechanism→ Septicemic
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colibacillosis:
It is a common manifestation of disease caused •
by this organism. The intestine is not
necessarily the portal of entry, and there may
not alimentary disease. The signs of E.coli
septicemia are referable mainly bacteremia,
endotoxemia, and the effect of bacterial
localization in a variety of tissue spaces
throughout the body.
The fifth mechanism→ Enteroinvasive
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colibacillosis:
Enteroinvasive E.coli strains have the capacity •
to invade the epithelium of the intestine and
cause acute exudative enteritis, often
endotoxemia, and perhaps terminal
septicaemia. Enteroinvasive colibacillosis is
apparently rare in domestic animals.
Pathogenesis: •
Enteroinvasive E.coli infecting humans and •
certain other species which have the capacity to
invade or to be internalized by surface
enterocytes of the small and large intestine, in
which they multiply.
Multiplication of the organism within epithelial •
cells results in local erosion and ulceration,
associated with acute inflammation in the
mucosa. Diarrhea is described as grey-yellow.
Macroscopic lesion: •
significant changes were confined to the small
intestine:
The mucous membrane is muddy and
thickened.
The intraluminal contents from the jejunum to
the colon were liquid and yellow.
There is mucosal erosive and ulcers.
Congestion of small intestine.
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Microscopic lesion: •
Blunting of villi (Villous atrophy).
Ulcerative enteritis.
Lengthening of crypt.
Congestion of the blood vessels.
Infiltration of neutrophils and other
inflammatory cells .
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