Parasites_AG Flashcards
Giardia muris
• Etiology: Flagellated protozoa inhabiting duodenum of mice, rats, and hamsters
• Clinical Signs: Often subclinical unless proliferate extensively or immunodeficient
• Epizootiology:
o Rats resistant to mice and hamster isolates
o C3H/He are more susceptible
o BALB/c and C57Bl/10
o Female mice more resistant
Giardia muris
• Pathology:
o Gross: Limited to small intestine, may contain yellow or white watery fluid
o Histopathology: organisms in lumen adhere to microvilli or reside in crevices, crypt/ villus ratio may be reduced, and elevated numbers of inflammatory cells
• Diagnosis: detection of trophozoites in the small intestine or wet mounts of fecal material (ellipsoidal cysts with four nuclei), serology, or PCR
• Treatment: 0.1% dimetridazole, proper sanitation/ disinfection
Spironucleosis: Spironucleus muris
• Etiology: flagellated protozoa, smaller than Giardia, often secondary pathogen
• Clinical Signs: subclinical unless young, stress, or immunocompromised
• Epizootiology:
o Transmitted between mice and hamsters
o Also affects rats
o Inbred strains may vary in their susceptibility
Spironucleosis: Spironucleus muris
• Pathology:
o Gross: water, red- brown, gaseous intestinal contents
o Histopathology: distension of crypts and intervillous spaces by pear-shaped trophozoites. Stain with periodic acid-Schiff staining
• Diagnosis: identify trophozoites in the intestinal tract (smaller then Giardia and Tritrichomonas, no sucking disk or undulating membrane) or PCR
• Treatment: 0.1% dimetridazole, proper sanitation/ disinfection
Tritrichomoniasis (Tritrichomonas muris, minuta, wenyoni)
- Etiology: nonpathogenic protozoa of mice, rats, and hamsters
- Pathology: affects cecum, colon, and small intestine
- Diagnosis: microscopy or PCR
Eimeria falciformes
- Etiology: coccidian affecting large intestine of mice, rare
- Usually nonpathogenic, unless young or immunocompromised
- C3H/He, CBA/H are susceptible, B10 are moderately susceptible, and BALB/c are resistant
- Diagnosis: oocysts in feces, histopathology
Entaemoeba muris
- Etiology: amoebae found in cecum and colon of mice, rats, and hamsters.
- Fecal – oral transmission.
- Clinical Signs: Nonpathogenic
Cryptosporidium muris
- Etiology: Coccidian found in gastric mucosa. Affects mice and rats.
- Infection occurs through ingestion of oocysts in contaminated feed and water. Sporozoites released in stomach and infect glandular gastric epithelium. Intracellular parasite.
- Clinical Signs: Uncommon and only pathogenic in immunodeficient mice
- Dx: oocysts in fecal sample, histopathology, IFA
Klosiella muris
• Etiology: renal coccidiosis in wild mice, but rare in laboratory mice
• Clinical signs: usually nonpathogenic
• Life cycle:
o infected by ingestion of sporulated sporocysts. Sporozoites released from the sporocysts enter the bloodstream and infect endothelial cells lining renal arterioles and glomerular capillaries, where schizogony occurs. Mature schizonts rupture into Bowman’s capsule to release merozoites into the lumen of renal tubules. Merozoites can enter epithelial cells lining convoluted tubules, where the sexual phase of the life cycle is completed. Sporocysts form in renal tubular epithelium and eventually rupture host cells and are excreted in the urine, but oocysts are not formed.
• Pathology: gray spots may be seen on kidneys (necrosis, granulomatous inflammation, hyperplasia)
• Diagnosis: detection of organisms in tissues
• Treatment: none
Encephalitozoon cuniculi
- Etiology: microscporidian infecting many species.
- Epizootiology: Direct life cycle. Obligate intracellular parasite. Doesn’t usually cause disease in mice but leads to interstitial nephritis in rabbits. Ingestion of spores excreted in urine propogates infection.
- Diagnosis: cytology of ascetic fluid smears, histopath of brain (Goodpasture stain or Giemsa), PCR, and ELISA serology. No treatment.
- ZOONOTIC!
Toxoplasma gondii
- Etiology: coccidian parasite.
- Epizootiology: Cats are primary host and are infected through eating infected intermediate hosts (any warm blooded animal, including rodents) or ingesting sporulated oocysts. Laboratory rodents infected after ingesting oocyst contaminated feed or bedding. Cysts can be formed in almost any organ, with affinity for central nervous system tissue.
- Clinical signs: nonpathogenic
- Diagnosis: ELISA serology, histopathology, and PCR.
- Treatment: Prevent contact with cats and autoclave feed/ bedding as oocytes are resistant to chemical disinfectants and drying.
- ZOONOTIC!
Hymenolpeis (Rodentolepis) nana: dwarf tapeworm
• Epizootiology: infects mice, rats, hamsters, and humans. Direct or indirect life cycle (H. nana only cestode that does not require intermediate host!). Arthropods are indirect hosts. Prepatent period: 20-30 days. Potentially zoonotic!
• Clinical Signs: weight loss and focal enteritis, clinical disease is rare
• Pathology: cysticerci in lamina propria of small intestine
• Diagnosis: fecal flotation for eggs, direct examination of intestines
o H. nana has rostellar hooks and eggs with polar filaments while H. diminuta does not.
o H. diminuta (rat tapeworm) requires intermediate arthropod host so rarely found in modern colonies
• Treatment: praziquantal for 5 days
Syphacia obvelata
- Etiology: affects mice, rats, gerbils, and hamsters.
- Clinical signs: typically subclinical
- Epizootiology: Direct life cycle (11-15 days prepatent period). Females deposit eggs on skin/ hair of perianal region and they embryonate within hours. Embryonated eggs ingested and larvae migrate to cecum. Females deposit eggs on perianal region as they leave the host. Reinfection via retro-migration is debated. Evidence of strain resistance.
- Pathology: gross lesions are not prevalent, just see adults in lumen
- Diagnosis: tape test to find banana shaped eggs. Prevalence higher in 4-5 week old mice. Direct observation of adults in intestines, ELISA, PCR.
- Treatment: piperazine, ivermectin, benzimidazole. Beware toxicity. Long lasting eggs- strict sanitation necessary.
Aspiculuris tetraptera
- Etiology: other pinworm of mice, other rodents susceptible but infection is rare.
- Clinical signs: subclinical, heaviest infection 5-6 weeks after exposure
- Epizootiology: Direct life cycle. Emrboyonated eggs ingested and larvae reside in crypts of colon. 23-25 day prepatent period, direct life cycle. Eggs excreted in mucous layer covering fecal pellets. Require 5-8 days at 24C to embronate (become infective) once laid.
- Diagnosis: fecal flotation for ellipsoidal eggs, direct exam of intestines for adult worms
- Treatment: same as S. obvelata. Immune expulsion and resistance to reinfection common.
Mycoptes musculinus:
most common, 8-14 day life cycle.
• Usually a mixed infection with M. musculi. May affect other parts of body.
• More ambulatory and tends to spread over the body more so than M. musculi.
• Hair shafts necessary for successful colonization
• Non burrowing. Feed on skin secretions (not blood)
• Pathology: strain dependent, but may be associated with pruritic dermatopathology in B6 and BALB/c mice. May see ulcerative dermatitis, erythema, lymphadenopathy, and mast cells within skin. IgE may be elevated.
• Clinical signs: generally unnoticed
