2. BACTERIAL DISEASES
• Bacterial diseases are a significant cause of morbidity,
mortality, and economic loss in hamsters.
• Infections causing diarrhoea and associated high mortality are
among the most significant and well-described diseases of the
Syrian hamster.
• Many of these bacterial enteritides cause diarrhea and have a
common presentation: diarrheal staining of the perineum or
wet tail.
3. PROLIFERATIVE ILEITIS
• Escherichia coli, Campylobacter spp., viruses, and chlamydia,
have been implicated.
• Proliferative ileitis is the most common bacterial enteritis of
Syrian hamsters.
• Synonyms -
o wet tail,
o regional enteritis,
o terminal ileitis,
o atypical transmissible ileal hyperplasia.
4.
5. CLINICAL SIGNS:
• Hamsters affected with proliferative ileitis have fetid, watery
diarrhoea
• Hunched posture, rough coat, and emaciation.
• Blood may be found around the anus if an intussusception
occurs causing intestinal blockage.
• Hypothermia, abdominal distension and terminal convulsions
have been reported.
• Syrian hamsters with chronic proliferative ileitis may have
palpable abdominal masses due to thickening of the ileum,
abscesses, and enlarged lymph nodes
6.
7. Marked thickening of the terminal jejunum and ileum (arrows).
Serosal hyperemia and enlargement and suppuration of mesenteric and
ileocecal lymph nodes
8. LESIONS:
• Marked increase in mucosal thickness due to hyperplasia of
the crypt and villous epithelium .
• loss of villous architecture,
• villi necrosis
• Inflammation of the laminapropria,
• crypt abscesses and micro abscesses of the intestinal wall.
• Mucosal edema and lymphoid hyperplasia.
• Concomitant increase in mitotic activity and cellular
immaturity in the crypt epithelium with proliferative ileitis.
10. WARTHIN STARRY SILVER STAIN
Reveals numerous organisms (arrows) which appear as a brown
haze in the apical cytoplasm of mucosal and crypt epithelial cells.
11. TREATMENT
• Antibiotic treatment of hamsters with proliferative ileitis has
had variable results and may result in chronic, inapparent
infections.
• Outbreaks may be controlled by the removal of affected
hamsters from the colony, and by using good sanitation and
management practices.
• The only method that ensures that proliferative ileitis has been
eradicated is elimination of the colony and replacement with
noninfected hamsters.
13. ANTIBIOTIC ASSOCIATED
ENTEROCOLITIS.
• Clostridium difficile is an anaerobic bacteria that produces a
powerful cytotoxin.
• C. difficile can be found in low numbers in the caeca of many
normal hamsters and may also be acquired from the
environment.
• Overgrowth of C. difficile can result from the use of several
antibiotics including penicillin, ampicillin, erythromycin,
lincomycin, and tetracycline (16).
• Use of antibiotics upsets the balance of the normal intestinal
flora; the resulting disease is antibiotic-associated
enterocolitis.
14. CLINICAL SIGNS
• Antibiotic-associated enterocolitis and clostridial
enterotoxemia include
o anorexia,
o rough haircoat,
o profuse watery diarrhoea and
o marked dehydration.
• Acutely affected hamsters die within 4 to 10 days.
• Death may also occur with no previous clinical signs.
• Hamsters with chronic clostridial enterotoxemia experience
weight loss and have soft, semi-formed feces
18. PREVENTION
• Antibiotic-associated colitis can be prevented by not using
antibiotics in the hamster.
• Most of the factors that predispose hamsters to clostridial
enterotoxemia are unknown; however, use of a high fat,
atherogenic diet has been identified as a risk factor for
developing this disease.
• Vancomycin, administered orally daily at 20 mg/kg body weight,
is effective in preventing and controlling clostridial disease once
it has been diagnosed in a group of hamsters.
• The major adverse effect of vancomycin treatment is
development of severe gaseous distension of the cecum and death
in some hamsters
19. TYZZER’S DISEASE
• Clostridium piliforme,
is an obligate
intracellular
flagellated, spore-
forming bacteria.
• Transmission is fecal-
oral through the
ingestion of spores
21. • Hepatomegaly and multifocal hepatic necrosis (arrows) as seen on the left.
• General loss of tone, and serosal edema, usually most pronounced in the
cecum.
22. Typical microscopic lesion in the liver:
• A focal area of necrosis bordered by neutrophils and lesser numbers of
monocytes (small arrows).
• Exterior to the border of inflammatory cells are dying hepatocytes (white
arrows) that appear more eosinophilic than normal hepatocytes.
23. • Focus of necrosis with a border of inflammation can be seen.
• C. piliforme organisms appear as black figures arranged in pick-up sticks
clumps in dying hepatocytes at the border of the lesion
27. SALMONELLOSIS
• Salmonella typhimurium and Salmonella enteriditis are the
most common isolates from diseased hamsters.
• Transmission is by the fecal-oral route and usually results from
ingestion of fecal-contaminated food, water, or bedding.
28. Clinical signs
• lethargy, rough haircoat, anorexia, weight loss, and increased
respiratory rate.
• Diarrhea is not a consistent clinical sign, and feces are usually
soft and light in color.
• Inapparent infections occur, and death may occur with no
previous clinical signs.
• The most frequent gross necropsy lesions are
o pulmonary hemorrhages,
o multiple small white foci on the liver, and
o hyperemic lymph nodes.
• Enteritis may be observed.
31. Campylobacter jejuni
• Diarrhea- proliferative ileitis,
• C. jejuni is a zoonotic agent causing abdominal cramping and
diarrhea in infected people.
Escherichia coli
• Enteropathogenic strains of Escherichia coli - acute enteritis
and proliferative ileitis,
• adult hamsters -enterocecocolitis
Yersiniosis
• chronically thin with intermittent diarrhea.
• Caseous nodules in the intestine, liver, spleen, lymph nodes
and lungs were observed at necropsy.
33. Clinical signs:
• Nasal and ocular discharge,
• anorexia,
• depression,
• dehydration,
• labored breathing and
• weight loss.
Gross lesions:
• Multifocal consolidation of the lungs,
• conjunctivitis,
• otitis interna
34. MASTITIS
• Streptococcus spp., Pasteurella spp., and E. coli have been
implicated in the development of mastitis in lactating
hamsters.
• Infection occurs 7 to 10 days after parturition.
• Litters from affected dams are runted and may be cannibalized.
• Infected mammary glands are firm, hemorrhagic, and contain
purulent exudate.
• Neutrophilic infiltration of the gland is found microscopically