I.Cheek Pouch Impaction
II. Cholangiofibrosis
III. Endoparasites
IV. Hamster Enteritis Complex
V. Salmonellosis
VI. Tyzzer's Disease
Hamsters have huge lateral pouches in the oral cavity which are used for food storage. These pouches occasionally become impacted with food and require manual evaluation.
Cholangiofibrosis (also called cholangiohepatitis and chronic hepatitis
and cirrhosis) is a recently described syndrome in hamsters with histopathological
similarities to primary biliary sclerosis in humans (thought to be of autoimmune
origin) and lymphocytic cholangiohepatitis in horses and cats. Affected
hamsters display no clinical signs or gross lesions but exhibit abnormal
hepatic serum chemical profiles, hepatic portal lymphoplasmacytic infiltrates
with bile duct hyperplasia (see photo), pericholangial fibrosis and centrilobular
pancreatitis. The etiology is unproven but a Helicobacter
species tentatively named H. cholecysticus has been isolated from
the gallbladders of affected hamsters. Treatment and control are
unknown at this time.
Cestodes
A. Etiology: Rodentolepis nana (dwarf tapeworm) and
Hymenolepis
diminuta infect hamsters with a moderate rate of incidence.
Rodentolepis
nana adults range from 25 to 40 mm long and less than 1 mm wide and
have an armed rostellum (see photo). Hymenolepis diminuta
adults
range from 20 to 60 mm in length and 3 to 4 mm wide with no hooks on the
scolex. 
B. Transmission: Rodentolepis nana and Hymenolepis diminuta can be transmitted indirectly with cockroaches, beetles, or fleas as intermediate hosts. Rodentolepis nana can also be transmitted by direct ingestion of hexacanth ova and autoinfection in which the entire life cycle occurs in the small intestine without ingestion of ova (direct life cycle is 14 to 16 days).
C. Clinical Signs: Usually there are no external signs of infection. Impactions have been reported with heavy infections resulting in intestinal obstruction.
D. Diagnosis: Diagnosis can be made by fecal flotation and
examination for hexacanth ova (see photo), direct examination of intestines
with a dissecting microscope, or histopathological examination of the small
intestine. 
E. Treatment: Niclosomide (Yomesan) at 10 mg/100 gm body weight given in a treatment at 7 day intervals is effective but not currently available in the U.S. Thiabendazole at 0.33% crushed and mixed in pulverized feed for 7 to 14 days have been effective. Praziquantel at 5.1 -11.4 mg/kg IM, SQ or PO (repeat in 10 days) can be used in both hamsters and gerbils.
F. Control: Cockroaches should be eliminated and infected animals killed or treated.
Public Health Significance: People become infected with R. nana from contact with the ova; since autoinfection can occur, a heavy parasite load may quickly develop.
Pinworms
A. Etiology: Syphacia mesocricetus is the hamster pinworm
(see photo). Syphacia obvelata and Syphacia muris are
also capable of infecting hamsters. Prevalence of a pinworm infection
is low, however the incidence of parasitism within individual colonies
may be high.
B. Transmission: Syphacia sp. deposit eggs in the perianal region. Transmission of infection occurs via ova ingestion. The eggs are very light and have been shown to aerosolize, resulting in widespread exposure.
C. Clinical signs: No signs are usually seen. Heavy parasite loads may lead to rectal prolapse or perianal irritation.
D. Gross Pathology: Pinworms are easily recognized as white hair-like nematodes in the cecum.
E. Diagnosis: Direct exam of cecal contents to identify adult
worms, and fecal flotation, and perianal tape test for ova (see photo)
are routinely used diagnostic methods. 
F. Treatment: If treatment is desired, two doses of piperazine (10 mg/ml water) for 7 days followed by 5 days without treatment is effective. Thiabendazole at 0.1% in the feed for 3 to 4 weeks is also effective. To prevent reinfection the environment should be thoroughly cleaned to remove ova. Although ivermectin has been successfully used to treat pinworm-infected mice and rats at a dose of 0.2 to 0.4 mg/kg, similar treatments of hamsters should be effective, but have not been reported.
G. Control: Rigid sanitary procedures, and use of filter hoods should be employed to prevent aerosol transmission. Regular ova examinations with treatment may control the parasitism.
Protozoa
Spironucleus muris (left photo), Giardia sp., Tritrichomonas
sp.,
and
Entamoeba
sp. (right photo) are protozoa which commonly inhabit
the small and large intestine without causing clinical signs. When
the luminal contents become more fluid, as in the case of bacterial enteritis,
these protozoa take advantage of the opportunity to replicate, and frequently
aggravate the inflamed intestinal tract.
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Another name for this frequently occurring syndrome is wet-tail. Enteritis occurs most frequently in 2 to 3 week-old hamsters and results primarily from colonization with pathogenic bacteria. Any enteric disease in hamsters will be complicated by proliferation of commensal flagellated enteric protozoa and amoeba.
A. Clostridial Enteritis
Enteric disease associated with variable morbidity and mortality may
result from overgrowth of Clostridium perfringens, C. difficile,
and perhaps C. spireforme. These anaerobic bacteria produce
toxins that cause edema and hemorrhage, and occasionally mucosal dysfunction
and necrosis. Clostridial enteritis manifests as 2 syndromes.
The first is acute diarrheal disease in hamsters with cecal bacteria dysbiosis
from dietary changes, antibiotic therapy, concurrent diseases or other
physiologic stressors that can disrupt the cecal microbiota. Antibiotics
implicated in clostridial enteritis include lincomycin, erythromycin, penicillin,
ampicillin, gentamycin, vancomycin and cephalosporins. The disease
is tentatively diagnosed at necropsy when serosal and mucosal hemorrhages
of the cecum and sometimes the lower intestine are observed (A.).
The second syndrome occurs in older (>6 mo) hamsters usually on experimental
studies that often do not involve changes in diet or oral medication.
Hamsters slowly lose weight and die without developing diarrhea.
Gross lesions include mild dehydration and thickening of the cecal wall
with thick to watery cecal contents. The cecal mucosa is hyperplastic with
variable lymphoplasmacytic inflammatory cell infiltrate (B.). Definitive
diagnosis for either syndrome can be made by identification of the
bacteria in anaerobic cultures or by detection of the iota-like toxins
(toxin A and B of C. difficile) in cecal filtrates. In one
study, treatment with vancomycin ameliorated clinical disease in the chronic
clostridial syndrome, but cessation of antibiotic therapy resulted in return
of the disease. Control measures are targeted at control of environmental
stressors, and cessation of oral medications.
. 
B. Colibacillosis
1. Etiology: E. coli recovered from hamsters with colibacillosis has virulence factors that allow for adherence to mucosal cells and production of enterotoxins or invasion. The incidence of disease is moderate.
2. Transmission: The disease is transmitted via direct contact, fecal-oral and fomite contamination.
3. Predisposing Factors: A high carbohydrate or vitamin imbalanced diet, exposure to infected animals, shipment stress, overcrowding, and lack of fresh water are stressful events that precipitate disease. Certain strains of hamsters may be more susceptible than others, i.e., long-haired fawn and teddy bear.
4. Clinical Signs: Generally the disease is acute in onset, with
2- to 4-week-old hamsters developing a profuse yellow watery diarrhea that
mats the area around the tail. Dehydration and death quickly ensues. 
5. Pathology: Lesions are most obvious in the small intestine
and cecum. Fluid and gas dilate the small intestine and cecum, and
occasional serosal edema is observed. The stomach is usually empty
and gas-filled. There is submucosal edema and effacement of enterocytes
colonized by bacteria in the small intestine or cecum. Often, there
is little to no inflammatory cell infiltrate in the lamina propria or submucosa. 
6. Diagnosis: Culture of the gut with recovery of pure culture
of E. coli is strong evidence for disease. Evaluation for
virulence factors, such as the production of toxins, or of proteins necessary
for adherence and/or invasion is required to differentiate the isolate
from the nonpathogenic E. coli that may be found in low numbers in healthy
hamster gut.
7. Treatment: Supportive treatment for dehydration with lactated Ringer's solution given SQ (5% to 15% of body weight) and Kaopectate (1-2 ml PO) for diarrhea may be effective. Antimicrobial therapy may actually worsen the bacterial population imbalance and lead to development of a fatal enteritis.
8. Control: Even though colibacillosis outbreaks are generally associated with stress every effort should be made to prevent cage to cage transmission of feces. Strict sanitation practices such as washing hands or changing gloves between cage or animal manipulations, and use of cage covers may reduce the spread of the disease. Examination of husbandry practices to identify and correct stressful conditions should help limit the duration of the disease. Dams may develop maternal antibody which may protect the next litter(s), but this immunity is short-lived.
C. Proliferative ileitis and typhlitis
1. Etiology: This disease is similar to proliferative bowel disease in swine and ferrets. Gram negative, curved bacilli are often associated with this disease in all three species and are referred to as Campylobacter-like organsims. In swine, increased understanding of biochemical and physical structures of the organisms have led to the classification of the bacillus as Lawsonia intracellularis. L. intracellularis is also believed to be the etiologic agent associated with proliferative ileitis in hamsters. The literature also identifies other possible causative or conrtributive agents such as lactose negative E. coli, Campylobacter coli, and chlamydial organisms.
2. Transmission: The disease is transmitted via direct fecal-oral contact and fomite contamination.
3. Clinical Signs: Acute disease is manifest by lethargy, anorexia,
irritability, ruffled hair, diarrhea, dehydration, and death. The
moist feces stain the base of the tail. The disease occurs primarily
in hamsters 3 to 10 weeks of age, has been noted in adult animals debilitated
by concurrent disease(s). 
4. Pathology: Lesions are most obvious in the ileum and cecum.
Fluid feces dilate the ileum and cecum, and edema and hemorrhage may be
observed on the serosa. The ileum may appear more rigid (tubular)
and thicker on cross-section. On histologic exam, affected intestinal segments
are affected with mild to moderate segmental hyperplasia of the mucosa.
The crypts are elongated and tortuous with marked proliferation of enterocytes
and occasionally goblet cells (A.). 
Proliferation of goblet cells is often marked. Lymphoid hyperplasia
and edema are often present. Migrating leukocytes are seen near the
base of the villi. The villous tips undergo coagulation necrosis
as the disease progresses. Additional bacterial involvement may cause
accumulation of purulent exudate in the crypts and formation of microabscesses
in the intestinal wall. Silver stains (B.) are needed
to reveal numerous curved bacilli (arrows) in the apical cytoplasm of the
enterocytes. 
5. Diagnosis: Diagnosis is made primarily by recognition of characteristic
gross and histologic lesions. Multiple attempts have been made to
grow the causative agent on an artificial medium, but standardized growth
requirements have not been optimized. Verification of the causative
agent can be accomplished by a polymerase chain reaction (PCR) assay using
fresh or frozen gut samples.
6. Treatment: Antimicrobial therapy provides inconsistent and variable results. Erythromycin at 20 mg/kg body weight PO or 200 mg/ml drinking water has been demonstrated to reduce mortality associated with the enteritis. Erythromycin is the preferred treatment for Syrian hamsters, in spite of the relative risk for altering the intestinal bacterial flora. Teddy bear hamsters are sensitive to erythromycin, and should be dosed at 10 mg/kg. Neomycin (10 mg/kg body weight), tetracycline hydrochloride (400 mg/L drinking water), and metronidazole (Flagyl, 0.1% in drinking water) have also been reported to be moderately successful therapies. Supportive treatment for dehydration with oral electrolyte solutions or Gatorade, lactated Ringer's solution given subQ (5% to 15% of body weight) and Kaopectate (1-2 ml PO) for diarrhea may be effective.
7. Control: The disease is difficult to limit in a group of infected animals. High sanitary standards, absence of stresses, and cage filter covers may reduce the severity of an outbreak. When antibiotic treatment is used, animals may succumb again to the disease when therapy ceases. Breeding animals should be separated to prevent production of additional susceptible weanlings until the disease has run it course, and no new cases develop.
A. Etiology: Salmonella enterica serovars Typhimurium and Enteritidis are Gram-negative, invasive enteric bacteria. Incidence of infection and disease is low.
B. Transmission: Food, water and bedding may be contaminated by infected feces from wild rodents.
C. Clinical Signs: The disease may only be manifest as acute death. Clinical signs are seen primarily in pregnant or recently delivered females and infant or weanling hamsters. Diarrhea is usually not present but pregnant females may abort and become cachexic.
D. Pathology: Fluid-filled small intestine and cecum may be observed in young hamsters. The lungs have a patchy hemorrhagic and partly grayish appearance. Small white foci are seen in the liver. The most significant lesion is septic, partially occluding thrombosis of pulmonary venules with underlying necrosis and erosion of the vessel walls. There are focal areas of interstitial pneumonia and lobular collapse. Thrombosis of liver venules and multifocal necrosis of the liver, lymph nodes and spleen are found.
E. Diagnosis: Recovery of Salmonella sp. from fecal or lesioned organ cultures is diagnostic. Use of enriched or selective media, and collection of feces and lymph node or liver homogenates from multiple animals enhances the opportunities to recover Salmonella, especially when the disease has become enzootic.
F. Control: Treatment is not recommended, and elimination of colony animals is recommended. Aggressive sanitation procedures should be aimed at preventing contamination of food, bedding or water by wild vermin. Also proper sanitation of cages and water equipment is required.
Public Health Significance: Humans ingesting S. typhimurium contaminated food or water experience a transient diarrhea.
Tyzzer's disease, caused by Clostridium piliforme, has been reported
to occasionally produce overt disease in hamsters. Infected hamsters
exhibit hunched posture and rough hair coats with or without diarrhea.
Sudden death is a feature of the disease. Gross pathologic lesions
include enterocolitis with edema, lymphadenitis and rarely multifocal liver
necrosis (white arrow). Diagnosis is made by demonstration of the
organism in gut epithelium or hepatocytes by use of silver (black arrow),
Giemsa, or PAS staining techniques. Antibodies to
Clostridium
piliforme have not been reliably detected by the ELISA, even when C.
piliforme recovered from hamster was used as the ELISA antigen.
There is no treatment that specifically eliminates the intracellular pathogen.
Short-term administration of metronidazole or tetracycline has curbed the
effusive nature of the diarrhea and decreased mortality, but does not decrease
the morbidity. Since the bacteria is a spore-former, control of disease
transmission is aimed at reducing spore contact. This is accomplished
by use of cage covers, by washing of hands or changing of gloves between
cage or animal manipulations, and disinfection of cage and room surfaces
with sporocidal disinfectants (such as 1% bleach solutions). Morbidity
and mortality diminishes as the infection becomes endemic. The most
financially efficient recourse to eliminating Tyzzer's disease in breeding
colonies of hamsters is to depopulate, disinfect and restock with uninfected
hamsters.
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