INTERNAL PARASITES OF RABBITS I. Nematodes A. Trichostrongylidae - General morphology: Filariform worms with poorly developed buccal capsules; males have cuticular bursa copulatrix which is supported by rays. 1. Obeliscoides cuniculi - rabbit stomach worm a) Prevalence: Rare or absent b) Morphology: No buccal capsule. Females have pointed tail and vulva is in caudal part of body. Eggs are oval and thin shelled. c) Location: Stomach d) Life cycles: Direct. Eggs passed feces --> Hatch in approximately 30 hr.; develop to infective stage in 6 days --> Ingested by rabbit --> Parasite develops to maturity in stomach. e) Clinical signs: Usually none. In severe infections failure to gain weight or weight loss could result. f) Pathology: Hemorrhagic gastritis g) Diagnosis: Identification of eggs in feces and adults in stomach. h) Treatment: Fenbendazole 50 ppm in feed for 5 days. 2.Nematodirus leporis a) Prevalence: Uncommon b) Morphology: Males have a bursa with rounded lobes and parallel, mediolateral and caudolateral rays. Eggs are large and oval. c) Location: Small intestine d) Life cycle: Direct. Similar to O. cuniculi, except adults are in small intestine. e) Clinical signs: None f) Pathology: Inapparent. g) Diagnosis: Identification of eggs in feces and adults in small intestine. h) Treatment: None listed...ivermectin? 3. Trichostrongylus calcaratus a) Prevalence: Rare or absent b) Morphology: Male has asymmetrical dorsal rays and two short nearly equal spicules. Vulva of female is 1 mm or slightly less from the tip of the tail. Nearly spherical. c) Location: Small intestine d) Life cycle: Eggs passed in feces --> Hatch and develop to infective stage in 6 days --> Infective larvae ingested by host. e) Clinical signs: Usually none. In severe infections failure to gain or weight loss could result. f) Pathology: Anemia g) Diagnosis: Identification of eggs in feces and adults in small intestine. h) Treatment: None listed...ivermectin? B. Oxyuridae - General characteristics: Esophagus has a posterior bulbar enlargement, and the intestine has no diverticula. Females have a finely pointed tail. 1. Passalurus ambiguus - rabbit pinworm a) Prevalence: common b) Location: Cecum and large intestine. c) Morphology: Males have a single curved spicule. Females have a vulva at the anterior end and a long tail (posterior to the anus) which has annular rings over the caudal segment. Eggs are oval and slightly flattened on one side. d) Life cycle: Direct. Females produce eggs that are embryonated when oviposited--> Host ingests egg. e) Clinical signs: None, even in heavy infections. f) Pathology: None g) Treatment: Piperazine for two days in food or water; fenbendazole 50 ppm in feed for 5 days. 2. Dermatoxys veligera a) Prevalence: Found occasionally in domestic rabbits; rare or absent in laboratory rabbits. b) Location: Cecum c) Morphology: Males have small spicules. Females have a vulva located in the cranial half of their body. Eggs are oval and slightly flattened on one side. d) Life cycle: probably direct. e) Clinical signs: None listed. f) Pathology: Typhlitis g) Diagnosis: Identification of eggs in feces and adults in cecum. h) Treatment: Piperazine, (also possibly ivermectin?) C. Trichuridae 1. Trichuris leporis - rabbit whipworm a) Prevalence: Uncommon in domestic rabbits. Incidence is unknown in laboratory rabbits, but is probably common. b) Location: Cecum and large intestine. c) Morphology: Anterior body is filiform; caudal portion contains reproductive and digestive structures. Eggs are characteristic of whipworms, and have bipolar plugs. d) Life cycle: Females lay eggs which are passed in the feces of the host. The entire life cycle has not been studied but is probably direct. e) Clinical signs: None listed in references, but probably none in light infection and failure to gain weight or weight loss in heavy infections. f) Pathology: Nothing listed in references. (Probably none except in heavy infections.) g) Diagnosis: Identification of characteristic eggs in feces and adults in cecum and large intestine. h) Treatment: None listed. II. Cestodes General: Rabbits can be definitive or intermediate hosts of tapeworms. A. Definitive host 1. Cittotaenia variabilis a) Prevalence: Rare or absent b) Location: Small intestine c) Morphology: Adults may reach length of 4.5 cm. The scolex is unarmed. d) Life cycle: Oribatid mites may be intermediate host. e) Clinical signs: none f) Pathology: None known g) Diagnosis: Diagnosed by finding eggs or proglottids in feces of host or finding worms in small intestine at necropsy. h) Treatment: None listed ...praziquantel? B. Intermediate host (In each case, the dog is the definitive host.) 1. Taenia pisiformis a) Prevalence: Found occasionally in domestic rabbits. b) Location: The cysticercus form of the parasite found in the liver of the rabbit and less commonly attached to the mesentery. c) Life Cycle: Embryonated egg ingested by host - -> Hatches in small intestine --> Embryo passes to liver and develops --> Reaches surface of liver and passes into peritoneal cavity d) Clinical signs: Usually none. In heavy infections, abdominal distention, lethargy and weight loss. e) Pathology: Attached cysticerci cause little damage. Fibrous tracts through liver parenchyma or small white foci on surface. f) Diagnosis: Identification of cysts in peritoneal cavity. g) Control: Feed and bedding should be protected from contamination by carnivores. 2. Taenia serialis a) Prevalence: Rare in domestic rabbits. b) Location: The coenurus form of the parasite is found in connective tissue of muscles and may reach 4-5 cm in diameter. c) Life cycle: Similar to T. pisiformis, except that larval stage usually develops in subcutaneous tissue rather than liver and peritoneal cavity. d) Clinical signs: Usually only subcutaneous swellings and usually in the flank area. e) Pathology: Subcutaneous cysts. Rarely cysts occur in brain, peritoneal cavity, liver, and other organs. f) Diagnosis: Tentative diagnosis is based upon palpation of characteristic, movable, subcutaneous cyst. Definitive diagnosis is made at necropsy. g) Treatment and control: Surgical removal of cysts. Prevention is same as for T. pisiformis. III. Trematodes A. Intermediate Host 1. Fasciola hepatica - Since it has been reported that rabbits serve as reservoirs for this infection, laboratory rabbits have been used to study this parasite, its disease process, and for testing anthelmintics. IV. Protozoa A. Sporozoa 1. Eimeria stiedae - (Synonyms: Monocystis stiedae Coccidium oviforme Coccidium cuniculi) a) Prevalence: Common b) Location: Bile duct epithelium c) Life cycle: Ingestion of sporulated oocysts --> Sporozoites excyst in duodenum --> Penetrate intestinal mucosa --> Travel to liver via portal circulation (lymphatic spread also possible) --> Invade epithelial cells of bile ducts --> Become schizonts and undergo schizogony --> Merozoites--> Merozoites invade contiguous epithelial cells--> Second generation merozoites undergo gametogony--> Microgametes and macrogametes--> Fertilization--> Oocysts --> Unsporulated oocysts break out of host cells, pass into lumen of bile ducts--> Pass out in feces. Prepatent period is 18 days. d) Clinical signs: Often none. In heavy infections, rabbits may become anorectic and debilitated due to interference with hepatic function and blockage of bile ducts. Diarrhea, especially terminally, or constipation may be noted. Hepatomegaly may cause an enlarged, pendulous abdomen. Icterus may be present in advanced stages. Death is usually rare, except in young rabbits with heavy infections. e) Pathology: Liver is frequently enlarged and contains yellowish-white lesions of varying size. These lesions are bile ducts which contain a yellow exudate. The gallbladder may also be enlarged and contains the same exudate. A fibrous capsule may surround some lesions and may make the liver difficult to cut. Ascites may also be present. Microscopically, destruction and regeneration of bile duct epithelium is observed. This results in marked papillomatous hyperplasia, bile duct reduplication and cystic enlargement of bile ducts. Lymphocytes, plasma cells and occasional epithelioid cells infiltrate the involved areas. Bile ducts are enlarged and may rupture, which initiates a severe granulomatous response. Fibrosis may be a prominent feature. The exudate is composed primarily of oocysts and sometimes includes inflammatory cells. Biliary outflow may be obstructed by the exudates. resulting in distended bile ducts. Ischemic necrosis may be present in contiguous liver parenchyma due to impression of blood vessels by the swollen bile ducts, but hepatic cells per se are not parasitized. f) Diagnosis: Identification of oocysts in feces using a direct smear, flotation, or concentration- flotation methods. The oocysts are ovoid or ellipsoidal. One pole is flattened and contains a micropyle. The wall is smooth and yellow-orange. Number of oocysts should be correlated with necropsy findings. In acute disease, oocysts may not be present in feces, and necropsy is required to establish the diagnosis. At necropsy exudate from dilated bile ducts and gallbladder can be examined for oocysts. g) Treatment and control: 0.02% sulfamerazine sodium in drinking water; sulfaquinoxaline sodium 0.05% in drinking water or 0.03% feed can be administered safely to rabbits for prolonged periods. Sulfamethoxine at a concentration sufficient to ensure a dose of 75mg/kg can be administered in feed for 7 consecutive days. It is thought that drug therapy controls the organism until natural immunity develops. The use of nitrofurans is controversial. Excellent husbandry can eliminate coccidiosis or keep it to a low level. Infected rabbits can be eliminated from the population. Barrier systems may be used. It is important to prevent fecal contamination of feed and water. A 10% ammonia solution is lethal to oocysts. Young rabbits should be separated from the dam as soon as possible, since suckling rabbits are especially susceptible to coccidiosis. Vermin must be controlled, and it should be explained to animal caretakers that they can mechanically transmit the disease. 2. Eimeria irresidua, E. magna, E. media, E. perforans and others a) Prevalence: Very common b) Location: Intestinal tract; different species prefer various areas. c) Life cycle: Transmission is by ingestion of sporulated oocysts. It is generally accepted that "night feces" which the rabbits eat, do not contain infectious oocysts. Sporulated oocysts are ingested --> Sporozoites are liberated in the intestinal tract and enter epithelial cells --> Multiply by schizogony involving 2 generations of 8 to 32 merozoites --> Gametogony and liberation of a large number of male mirogametes (comma-shaped) and female macrogametes --> Fertilization of macrogametes by microgametes --> Sporogony --> Oocysts develop --> Extruded into lumen --> passed out in feces --> Become infective after formation of 4 sporocysts, each containing 2 sporozoites. d) Clinical signs: Vary considerably. Rabbits may have no clinical signs. More severely affected rabbits (usually young) lose weight or fail to gain. Diarrhea, if present, can be intermittent to profuse and watery with mucus and blood; such animals have intense thirst. Deaths are due to dehydration and secondary bacterial infections. In cases of extremely heavy primary infections, rabbits may die before oocysts are passed in the feces. e) Pathology: The parasitized intestinal epithelial cells die, and this may cause ulceration and accumulation of a mixed mononuclear exudate. This may cause grossly observable multiple white lesions in the intestinal wall. f) Diagnosis: Fecal preparations (as for hepatic coccidiosis) and histological sectioning. g) Treatment and control: Same as for hepatic coccidiosis. B. Toxoplasmida 1. Toxoplasma gondii (Synonym: T. cuniculi) a) Prevalence: Uncommon in United States b) Location: Brain, lymph nodes, spleen, liver, kidneys, lungs, heart, and eyes. c) Life cycle: Transmitted to most animals by eating infected animals and also by the transplacental route. Transmission to herbivorous animals such as the rabbit, is probably by plant material contaminated with feces. d) Clinical signs: Acute disease -- Found most commonly in young rabbits. Sudden anorexia, fever, (greater than 104 F) and increased respiratory rate. Rabbits develop a serous or seropurulent ocular and nasal discharge, become lethargic, and central nervous signs of localized or generalized convulsions may occur a few days after initial signs are noticed. Paralysis may develop, especially in the hindquarters. Death usually occurs 2 to 8 days after the onset of signs. Chronic Disease -- Found most commonly in older rabbits. Anorexia and emaciation with anemia are common sequels. Central nervous signs, such as paralysis of the hindquarters may occur. Rabbits may die suddenly or recover. e) Pathology: Acute disease -- Extensive necrosis of the spleen, liver, lungs, and heart. Grossly, these organs are swollen with multiple necrotic foci. Histologically, RE elements and vascular connective tissue are most commonly affected. Marked cellular necrosis is present, with or without infiltration of inflammatory cells. T. gondii trophozoites are located both intra- and extracellularly. Chronic disease -- Grossly, edematous enlargement of various organs and scattered necrotic foci may be observed. Histologically, pronounced reticuloendothelial hyperplasia is seen, especially in lymph nodes, spleen, liver, and central nervous system. Toxoplasma organisms are more difficult to demonstrate than in the acute disease. Latent -- Cysts in CNS may or may not induce a tissue reaction. Gliosis and granulomatous encephalitis with nonsuppurative meningitis and perivascular cuffing may be observed (similar to lesions of encephalitozoonosis). f) Diagnosis: Usually done by a combination of histopathological examination of lesions, morphological identification of organisms, and serological methods. In acute toxoplasmosis, smears of peritoneal exudate, mesentery or omentum can be stained with Wright-Giemsa and examined for organisms. The organism can be isolated by injecting (IP) toxoplasmosis-free mice or hamsters with suspect material. (Pretreat mice and hamsters with cortisone acetate SQ) Serological tests -- Sabin-Feldman dye test, fluorescent antibody test, complement fixation, and carbon immunoassay. g) Treatment and control: Treatment is usually not practical, but sulfa drugs, pyrimethamine, tetracyclines, or pyrimethamine with triple sulfa may be used. Good husbandry is essential. Most disinfectants are ineffective, but heating and drying will inactivate the oocysts. If toxoplasmosis is present with a colony, only seronegative animals should be used for breeding. h) Public health significance: Rabbits may be a significant reservoir for the disease in man. 2. Sarcocystis cuniculi (Synonyms: Sarcocystis leporum) a) Prevalence: Rare b) Location: Cardiac and skeletal muscle c) Morphology: Cysts in muscle are up to 5 mm long and are limited by a wall containing radial spines called cytophaneres. The cysts may or may not be septate. It is theorized that the cysts form septa as they mature. Trophozoites are banana- shaped and slightly pointed at one end; they are motile. d) Life cycle: Exact life cycle is unknown, but is thought to be simple, without sexual stages. Trophozoites are motile when released from the cysts and reproduce by binary fission. Transmission is by ingestion of trophozoites in muscle tissue or those passed in feces. Horizontal transmission by fleas and by ingestion of infective excreta have been suggested but not proven. e) Clinical signs: Light to moderate infections are asymptomatic. Heavy infections may cause lameness. f) Pathology: Lesions are located in cardiac and skeletal muscle, especially in hindlegs, flanks, and loins. In heavy infections cysts may be seen grossly as white streaks running in the direction of muscle fibers. Microscopically, there may be no inflammatory response around the encysted organisms. Degeneration of the cyst wall and release of trophozoites can result in severe focal myocarditis and myositis characterized by mineralization and infiltration of lymphocytes, plasma cells, eosinophils, and macrophages. Scarring may be evident. The cysts produce a strong endotoxin, sarcocystin, which has been associated with the observed myositis, but its mechanism has not been established. g) Diagnosis: Gross pathological appearance. Smears of infected muscle can be stained with Giemsa or examined by phase microscopy for trophozoites. h) Treatment and control: No known treatment. Modern methods of raising rabbits has made the incidence virtually zero. i) Public health significance: Sarcocystis infections have been reported in humans, and it is thought that these cases probably represent transmission from animals. C. Microsporida 1. Encephalitozoon cuniculi (Synonym: Nosema cuniculi) a) Location: Brain and kidneys b) Morphology: Mature spore is oval and vacuolated. It has a polar filament which can be seen with EM. This organism was differentiated from Nosema on the basis that Nosema possesses diplokarya (two nuclei in contact with each other) throughout its developmental cycle. Only the proliferative forms of Encephalitozoon contain more than one nucleus, and these are never attached to each other. c) Life cycle: Sporoplasm is extruded from the spore at the end of the polar filament and enters host cells by an unknown mechanism. The organism forms a vacuole inside the mammalian cell, and proliferative forms multiply at the periphery of the vacuole. The vacuole becomes distended, and endoparasites may also play a role. Vertical transmission in the rabbit is strongly suspected but is not considered to be a common route. (It has been demonstrated in the mouse). e) Clinical signs: Usually asymptomatic, but occasionally convulsions, tremors, torticollis, paresis, and coma may be observed. f) Pathology: Kidney -- Grossly, either multiple white pinpoint areas or multiple, 2-4 mm indented gray areas on cortical surface. The kidney has a granular appearance in severe infections. Microscopically, one may see granulomatous nephritis or degrees of tubular degeneration with interstitial infiltration of lymphocytes and plasma cells with fibrosis. Scars often extend from the cortical surface to the medulla. Brain -- Lesions of granulomatous encephalitis are usually not grossly observable. Lesions may occur in all areas of the brain, most commonly with a perivascular and periventricular distribution. Focal granulomas are observed with a central area of necrosis, surrounded by lymphocytes, plasma cells, microglia, epithelioid cells, and sometimes giant cells. In other cases only dense accumulations of glial cells may be noted. Perivascular cuffing with lymphocytes and plasma cells is a prominent feature, especially in the areas of brain lesions. Lesions of the cerebellum and spinal cord are rare. Focal nonsuppurative hepatitis and myocarditis are rare but have been reported. g) Diagnosis: Usually by histopathology on basis of characteristic lesions and the organism (although the organism may not be found in the lesions). Smears of tissue suspensions and body fluids can be stained and examined directly. An intradermal skin test using antigen prepared by lysing E. cuniculi organisms is very sensitive. There is also an immunoperoxidase test and an enzyme immunoassay. The indirect fluorescent antibody technique is also very useful. One source (Pakes, 1984) rated several diagnostic tests and found IFA and CF to be very sensitive indicators. Tissues and body fluids from infected rabbits can be inoculated (IP) into mice (concomitant cortisone treatment of the mice facilitates the assay). Mice develop ascites in 2-3 weeks and smears of the fluid can be fixed with methanol, stained with Giemsa, and examined for the organism. h) Treatment and control: No known treatment. Since infections are usually inapparent, control and prevention is difficult. Cesarean derivation is probably not a viable approach since transplacental transmission appears to be possible. i) Public health significance: Since there have been rare human cases in which Encephalitozoon or Encephalitozoon-like organisms have been observed, the public health significance is not known. D. Flagellates and Amoebae 1. Chilomastix cuniculi a) Prevalence: Common b) Location: Cecum c) Morphology: Trophozoite is pyriform, has 3 anterior flagellae, anterior nucleus and a large cytostomal groove near the anterior end. d) Transmission: Ingestion of organisms passed in feces. e) Clinical signs: None f) Pathology: Nonpathogenic g) Diagnosis: Microscopic examination of fecal smear or cecal contents. h) Treatment: None listed. 2. Giardia duodenalis (Synonyms: Hexamita duodenalis; Lamblia cuniculi) a) Prevalence: Common b) Location: Cranial small intestine c) Morphology: Two anterior nuclei, 4 flagella. Cysts contain 2-4 nuclei. d) Transmission: Fecal-oral; cysts are passed in feces. e) Clinical signs: None f) Pathology: Nonpathogenic g) Diagnosis: Microscopic examination of fecal smear or cranial intestinal contents. h) Treatment: Metronidazole i) Public health significance: The rabbit organism does not appear to be transmissible to man. j) Notable feature: Rabbits are used to cultivate Giardia spp. 3. Monocercomonas cuniculi (Synonyms: Eutrichomastix cuniculi, Trichomastix cuniculi) a) Prevalence: Unknown; probably common b) Location: Cecum c) Morphology: Pyriform, with a posterior axostyle. There are 3 anterior and 1 posterior flagella. d) Clinical signs: None e) Pathology: Nonpathogenic f) Diagnosis: Microscopic examination of fecal smear or cecal contents. g) Prevention and control: Good management and sanitation practices 4. Retortamonas cuniculi (Synonym: Embadomonas cuniculi) a) Prevalence: Uncommon b) Location: Cecum c) Morphology: Trophozoites are usually ovoid and may have a tail-like process. They have an anterior nucleus, cytosome and flagellum. Cysts are oval. d) Transmission: Ingestion of organisms passed in feces. e) Clinical signs: None f) Pathology: Nonpathogenic g) Diagnosis: Microscopic examination of fecal smear or cecal contents. h) Prevention and control: Good management and sanitation practices. 5. Entamoeba cuniculi (Synonyms: Entamoeba coli, forma cuniculi, Entamoeba muris) a) Prevalence: b) Location: c) Morphology: d) Transmission: e) Clinical Signs: f) Pathology: g) Diagnosis: Microscopic examination of fecal smear or cecal contents. h) Prevention and control: Good management and sanitation practices. E. Organisms of Uncertain Classification 1. Pneumocystis carinii a) Prevalence: Unknown, because usually latent. b) Location: Lungs c) Morphology: Trophozoites are usually crescent-shaped but can be round, or oval. Cysts are spherical and usually contain 8 trophozoites. Ultrastructural studies have described a thick and thin-walled form. It is thought that the thick-walled form represents the true encysted stage, while the thin-walled form comprises the foamy material observed in pulmonary alveoli by light microscopy. d) Life cycle: The life cycle has not been fully elucidated. Direct contact seems to be necessary for transmission, and aerosol is the most probable route. Transplacental transmission has been documented in man and cannot be ruled out for rabbits. e) Clinical signs: None f) Pathology: Ranges from a few loci of mild pneumonitis confined to subpleural areas to extensive interstitial pneumonia characterized by alveolar infiltration with macrophages, lymphocytes and occasionally plasma cells. Free or cyst-bound organisms are commonly seen among PAS-positive foamy material in alveoli. There is occasional phagocytosis of cysts by macrophages. g) Diagnosis: Demonstration of organisms in smears or sections. (See ACLAM test, p. 281 for description of stains and advantages of each.) h) Treatment and control: Sulfadiazine in combination with antiprotozoal drugs such as pyrimethamine has been efficacious in rats, but have not been evaluated in rabbits. Cesarean derivation and barrier maintenance has been suggested, but the possibility of vertical transmission has not been ruled out. i) Public health significance: Has not been established. It has been postulated that naturally infected animals may act as a reservoir of disease in man. j) Notable feature: Rabbits injected with P. carinii may serve as a model for the disease in man. TABLE Comparison of Eimeria sp. infecting Rabbits(1) Mean size of oocysts (um) Shape Other distinguishing characteristics E stiedoe 37x20 ellipsoidal Smooth, light- (lindemann, 1865) yellow wall wide Kisskalt and thin micropyle no Hartmann, 1907 residual body in E irresidua oocyst suprocyst with terminal knob (stiedae body) REFERENCES 1. Weisbroth, S.H., Flatt, R.E., Kraus, A.K., The Biology of the Laboratory Rabbit, Academic Press, 1974. 2. Flynn, R.J., Parasites of Laboratory Animals. Iowa State University Press/Ames, 1973. 3. Soulsby, E.J.L., Helminths, Arthropods and Protozoa of Domesticated Animals (Manning), 1968. 4. Jubb, K.V.F., Kennedy, P.C., Palmer, N. Pathology of Domestic Animals, Vol. @, 1985. 5. Cox, J.C., Gallichio, H.A., Pye, D., Walden, N.B.: Application of immunofluorescence to the establishment of an Encephalitozoon cuniculi-free rabbit colony. Lab. Anim. Sci. (1977) 27, 204-209. 6. Cox, J.C., Horsburgh, R., Pye, D.: Simple diagnostic test for antibodies to Encephalitozoon cuniculi based on enzyme immunoassay. Lab. Anim. Sci. (1981) 15, 41-43. 7. Duwel, D., Brech, K: Control of Oxyuris in rabbits by fenbendazole. Lab. Anim. (1981) 15, 101-105. 8. Gannon, J.: The immunoperoxidase test diagnosis of Encephalitozoon cuniculi in rabbits Lab Anim. (1978) 12, 125-127. 9. Kellett, B.S., Bywater, J.E.C.: A modified India-ink immunoreaction for the detection of encephalitozoonosis. Lab Anim. (1978) 12, 59-60. 10. Pakes, S.P., Shadduck, J.A., Olsen, R.G.: A diagnostic skin test for encephalitozoonosis (nosematosis) in rabbits. Lab. Anim. Sci. (1972) 22, 870-877. 11. Waller, T., Bergguist, N.R.: Rapid simultaneous diagnosis of toxoplasmosis and encephalitozoonosis in rabbits. by carbon immunoassay. Lab. Anim. Sci. (1982) 32, 515-517. 12. Wosu, N.J., Shadduck, J.A., Pakes, S.P., Frenkel, J.K., Todd, K.S., Jr., Conroy, J.D.: Diagnosis of encephalitozoonosis in experimentally infected rabbits by intradermal and immunofluorescence tests. Lab. Anim. Sci. (1977) 27, 210-216. 13. Schiffer, S.P., Goodwin, B.T., Drug Formulary for Laboratory Animals - 1988. Proceedings of 1988 Penn Annual Conference. PICTORIAL APPENDIX --SELECTED ILLUSTRATIONS AND PHOTOGRAPHS-- PICTURE REFERENCES 1. Baker, H.J., Lindsey, J.R., Weisbroth, S.H., The Laboratory Rat, Vol. I, Academic Press, 1979. 2. The Laboratory Rabbit, Academic Press, 1974. Sizes of Mouse Helminths Syphacia muris male 1.2-1.3 mm female 2.8-4.0 mm Syphacia obvelata male 1.1-1.5 mm female 3.4-5.8 mm Aspicularis tetraptera male 2.0-2.6 mm female 2.6-4.7 mm Nippostrongylus braziliensis male 2.1-4.5 mm female 2.5-6.2 mm Capillaria hepatica 17-100 mm Hymenolepis nana length 20-40 mm width 0.5-1.0 mm Cysticercus fasciolaris strobilocercus - up to 12 cm Size of Rat Helminths Syphacia muris male 1.2-1.3 mm female 2.8-4.0 mm Syphacia obvelata male 1.1-1.5 mm female 3.4-5.8 mm Trichinella spiralis male 1.4-1. 6 mm female 3-4 mm Trichosomoides crassicauda male 1.3-3.5 mm female 9-10 mm Heterakis spumosa male 6-10 mm female 7-13 mm Capillaria hepatica 17-100 mm Moniliformis moniliformis male 6-8 cm female 10-32 cm Gongylonema neoplasticum not listed Hymenolepis nana length 20-40 mm width 0.5-1.0 mm Hymenolepis diminuta length 20-60 mm width 4 mm Cysticercus fasciolaris strobilocercus - up to 12 cm Size of Rabbit Helminths Passalurus ambiguus male 4.1 mm female 6.6 mm Trichostrongylus calcaratus male 4.7-6.6 mm female 5.8-7 mm Dermatoxys veligera male 8-11 mm female 16-17 mm Obeliscoides cuniculi male 10-14 mm female 15-18 mm Nematodirus leporis male 8-13 mm female 16-20 mm Trichuris leporis male 29-32 mm female 32 mm Cittotaenia variabilis length 4.5 cm width 1 cm Taenia pisiformis cysticercus - up to 18 mm in diameter Taenia serialis coenurus - up to 50 mm in diameter Fasciola hepatica length - up to 30 mm width - up to 13 mm