INTERNAL PARASITES OF RABBITS

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(There is a lot more information about paraites in animals than there

is about parasites in humans. Reading about parasites in general will

broaden your education about parasites as most act similarly.)

 

 

 

http://netvet.wustl.edu/species/rabbits/rabparas.txt

 

 

 

 

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: <missing>

 

b) Location: <missing>

 

c) Morphology: <missing>

 

d) Transmission: <missing>

 

e) Clinical Signs: <missing>

 

f) Pathology: <missing>

 

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.,

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 - u