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DISEASES OF
HAMPSTERS
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.
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.
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
Marked thickening of the terminal jejunum and ileum (arrows).
Serosal hyperemia and enlargement and suppuration of mesenteric and
ileocecal lymph nodes
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.
MICROABSCESSES OF THE INTESTINAL WALL (ARROWS)
WARTHIN STARRY SILVER STAIN
Reveals numerous organisms (arrows) which appear as a brown
haze in the apical cytoplasm of mucosal and crypt epithelial cells.
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.
CLOSTRIDIAL DISEASES
• Clostridium difficiale
• Clostridium piliforme
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.
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
HEMORRHAGIC ILEOCOLITIS. -MARKEDLY HEMORRHAGIC DISTAL SMALL
INTESTINE(ARROWS).
ALSO NOTE THE DISTENDED CECUM.
Acute clostridial enterotoxemia
hyperemia or redness of the smallintestine and hemorrhage and vascular congestion of
the vessels of the cecum
Marked mucosal hemorrhage, submucosal edema and
loss of mucosal architecture
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
TYZZER’S DISEASE
• Clostridium piliforme,
is an obligate
intracellular
flagellated, spore-
forming bacteria.
• Transmission is fecal-
oral through the
ingestion of spores
HAMSTERS THAT DIED WITH TYZZER’S
DISEASE.
• Hepatomegaly and multifocal hepatic necrosis (arrows) as seen on the left.
• General loss of tone, and serosal edema, usually most pronounced in the
cecum.
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.
• 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
Irregular and distorted mucosal epithelium, mucosal
inflammation, and submucosal edema
C. PILIFORME ORGANISMS MAY BE FOUND IN THE MUCOSAL
(ARROWS) OR CRYPT EPITHELIUM
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.
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.
Microscopic lesions
• septic, occluding thrombosis of pulmonary venules,
• multifocal interstitial pneumonia,
• multifocal hepatic necrosis
• thrombosis.
Large thrombus partially occluding an hepatic vein (arrows).
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.
Respiratory disease
Clinical signs:
• Nasal and ocular discharge,
• anorexia,
• depression,
• dehydration,
• labored breathing and
• weight loss.
Gross lesions:
• Multifocal consolidation of the lungs,
• conjunctivitis,
• otitis interna
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

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diseases of hampsters.pptx

  • 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.
  • 9. MICROABSCESSES OF THE INTESTINAL WALL (ARROWS)
  • 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.
  • 12. CLOSTRIDIAL DISEASES • Clostridium difficiale • Clostridium piliforme
  • 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
  • 15. HEMORRHAGIC ILEOCOLITIS. -MARKEDLY HEMORRHAGIC DISTAL SMALL INTESTINE(ARROWS). ALSO NOTE THE DISTENDED CECUM.
  • 16. Acute clostridial enterotoxemia hyperemia or redness of the smallintestine and hemorrhage and vascular congestion of the vessels of the cecum
  • 17. Marked mucosal hemorrhage, submucosal edema and loss of mucosal architecture
  • 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
  • 20. HAMSTERS THAT DIED WITH TYZZER’S DISEASE.
  • 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
  • 24. Irregular and distorted mucosal epithelium, mucosal inflammation, and submucosal edema
  • 25. C. PILIFORME ORGANISMS MAY BE FOUND IN THE MUCOSAL (ARROWS) OR CRYPT EPITHELIUM
  • 26.
  • 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.
  • 29. Microscopic lesions • septic, occluding thrombosis of pulmonary venules, • multifocal interstitial pneumonia, • multifocal hepatic necrosis • thrombosis.
  • 30. Large thrombus partially occluding an hepatic vein (arrows).
  • 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