Life cycle: There are five merogony stages. The first-generation meronts are in the glands of the lower small intestine, the second-to fifth-generation meronts are in the caecum and colon. The second-, third-and fourth-generation meronts are in the superficial epithelium, and the fifth-generation meronts and the gamonts are in the crypts. Gamonts and gametes appear about 7 days, and oocysts appear in the faces about 9 days after infection. Sporulation time is 4 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. flavescens is highly pathogenic for young rabbits, causing high morbidity and mortality and is a major problem on commercial rabbit farms.

Pathology: There is thickening of the intestinal wall of the caecum and colon with petechial haemorrhages and loss of epithelium in the caecum and colon.

Eimeria intestinalis

Predilection site: Small intestine (Fig. 9.2)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: There are three merogony stages. First-generation meronts are at the base of the villi in the lower ileum. There appear to be two types of second-generation meronts in the distal part of the villi, followed by third-generation meronts in the same location on the villi. Gamonts begin developing 8 days post infection, and are located above the host cell nucleus in the epithelial cells of the villi. The prepatent period is 9–10 days and the patent period 6–10 days. Sporulation time is 3 days.

Fig. 9.2 Predilection site of Eimeria intestinalis.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. intestinalis is highly pathogenic, causing diarrhoea and emaciation.

Pathology: There is oedema of the intestinal wall with destruction of the crypts in the ileum and lower jejunum. Greyish white foci may coalesce forming a sticky purulent layer in the small intestine.

Eimeria exigua

Predilection site: Small intestine (Fig. 9.3)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: Development takes place in the ileum and lower jejunum but details of the life cycle are unknown. The prepatent period is 7 days. The sporulation time is 1 day.

Geographical distribution: Unknown, probably worldwide

Pathogenesis and clinical signs: This species is not considered pathogenic or only slightly pathogenic. Infections are usually asymptomatic but heavy infections may cause slight depression of growth.

Eimeria perforans

Predilection site: Small intestine (Fig. 9.4)

Parasite class: Sporozoasida

Fig. 9.3 Predilection site of Eimeria exigua.

Fig. 9.4 Predilection site of Eimeria perforans.

Family: Eimeriidae

Life cycle: The endogenous stages are found in the epithelial cells of the villi and crypts of the small intestine, especially the middle section. There are two asexual generations, followed by gametogony. The prepatent period is 5 days and the patent period is 12–32 days. Sporulation time is 1.5–2 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. perforans is one of the less pathogenic intestinal coccidia of rabbits, but it may cause mild to moderate signs in a heavy infection. Symptoms are usually mild, but in heavy infections there may be anorexia, diarrhoea, weakness, weight loss and growth retardation.

Pathology: The duodenum may be enlarged and oedematous, and may appear a chalky white colour. The jejunum and ileum may contain white spots and streaks and petechiae have been observed in the caecum.

Eimeria irresidua

Predilection site: Small intestine (Fig. 9.5)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: There are four merogony stages. First-generation meronts are in the crypts, second-generation meronts are in the lamina propria, and third-and fourth-generation meronts and gamonts are in the villous epithelium in the jejunum, and to a lesser extent the ileum. The prepatent period is 9 days. Sporulation time is 4 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: Mildly pathogenic causing a depression in weight gain and in some cases diarrhoea. During this time, there is a reduction in food and water consumption as well as faecal excretion. Occasionally causes mortality depending on the level of infection.

Fig. 9.5 Predilection site of Eimeria irresidua.

Fig. 9.6 Gamonts of Eimeria irresidua.

Pathology: Catarrhal inflammation of the small intestine, particularly the jejunum, may be seen. On postmortem there may be enteritis, with gross thickening of the intestine. Large numbers of meronts and gamonts may be found in mucosal scrapings. His-topathological examination shows a congested and thickened mucosa with villous atrophy, villous fusion and crypt hyperplasia with numerous parasite stages present within the mucosa (Fig. 9.6).

Eimeria media

Predilection site: Small intestine (Fig. 9.7)

Parasite class: Sporozoasida

Fig. 9.7 Predilection site of Eimeria media.

Family: Eimeriidae

Life cycle: There are two merogony stages. The endogenous stages are found above or below the host cell nuclei of the epithelial cells and submucosa of the villi of the small intestine, mainly jejunum and ileum. The prepatent period is 5–6 days and the patent period is 15–18 days. Sporulation time is 2 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. media is slightly to moderately pathogenic, causing a depression in weight gain and in some cases diarrhoea. During this time, there is a reduction in food and water consumption as well as faecal excretion.

Pathology: The affected parts of the intestine, mainly the duodenum, are oedematous with greyish foci. In heavy infections, the lesions may extend into the large intestine.

Eimeria vejdovskyi

Predilection site: Small intestine (Fig. 9.8)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: Development takes place in the ileum and lower jejunum but details of the life cycle are unknown. The prepatent period is 10 days. The sporulation time is 2 days.

Geographical distribution: Unknown, probably worldwide

Fig. 9.8 Predilection site of Eimeria vejdovskyi.

Fig. 9.9 Predilection site of Eimeria coecicola.

Pathogenesis and clinical signs: This species is considered only slightly pathogenic. Infections are usually asymptomatic but heavy infections may cause slight depression of growth.

Pathology: Lesions occur only in the ileum and distal jejunum following heavy infection.

Eimeria coecicola

Predilection site: Large intestine (Fig. 9.9)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: The number of generations is unknown. The meronts are in the epithelial cells of the ileum and the gamonts in the epithelial cells of the vermiform process of the caecum. The gamonts are usually sited beneath the host cell nucleus. The prepatent period is 9–11 days, the patent period 7–9 days. Sporulation time is 4 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: This species is not considered pathogenic and infection is not associated with clinical signs.

Pathology: In heavy infections, lesions may be seen in the crypts of the vermiform appendix.

Eimeria magna

Predilection site: Small intestine (Fig. 9.10)

Parasite class: Sporozoasida

Family: Eimeriidae

Fig. 9.10 Predilection site of Eimeria magna.

Life cycle: There are two or three merogony stages. The meronts develop in the villar epithelial cells from the middle of the jejunum to the posterior end of the ileum. They lie either above or below the host cell nucleus. The prepatent period is 7 days and the patent period 12–21 days. Sporulation time is 2–3 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. magna is mildly to moderately pathogenic, causing a depression in weight gain and in some cases diarrhoea. During this time, there is a reduction in food and water consumption as well as faecal excretion. A large amount of mucus may be passed in the faeces. Mortality may occur depending on the level of infection.

Pathology: The intestinal mucosa is hyperaemic and inflamed. Epithelial sloughing may occur. Large numbers of meronts and gamonts may be found in mucosal scrapings. Histopathological examination shows a congested and thickened mucosa with villous atrophy, villous fusion and crypt hyperplasia.

Eimeria piriformis

Predilection site: Colon (Fig. 9.11)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: There are three generations of meronts found in the proximal and distal colon. The prepatent period is 9 days and the patent period is 5–10 days. Sporulation time is 4 days.

Fig. 9.11 Predilection site of Eimeria piriformis.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. piriformis is mildly to moderately pathogenic. Infection causes anorexia, diarrhoea, weakness, weight loss and growth retardation, and in heavy infections can result in death.

Pathology: Endogenous stages are found in the wall of the large intestine on histopathology.

Entamoeba cuniculi

Predilection site: Caecum

Parasite sub-phylum: Sarcodina

Family: Endamoebidae

Description: Trophozoites are 20–30 μm in diameter. The cysts are 10–33 μm in diameter and contain a single nucleus.

Hosts: Rabbit

Life cycle: Trophozoites divide by binary fission. Before encysting the amoebae round up, become smaller and lay down a cyst wall. Each cyst has one nucleus. Amoebae emerge from the cysts and grow into trophozoites

Geographical distribution: Worldwide

Pathogenesis: Non-pathogenic

Retortamonas cuniculi

Synonym: Embadomonas cuniculi

Predilection site: Caecum

Parasite sub-phylum: Mastigophora

Family: Retortamonadorididae

Description: Trophozoites are ovoid, 7–13 × 5–10 μm, with an anterior flagella and a posterior trailing flagella emerging from the cytosomal groove and occasionally have a tail-like process. Cysts are pyriform or ovoid, 5–7 × 3–4 μm.

Hosts: Rabbit

Life cycle: Reproduction is by binary fission. Infection occurs by ingestion of the cyst stage.

Geographical distribution: Worldwide

Pathogenesis: Non-pathogenic

Diagnosis: Diagnosis is based on the identification of the characteristic trophozoites.

PARASITES OF THE RESPIRATORY SYSTEM

Several protostrongylid nematodes are found in the lungs of wild rabbits. These are listed in the parasite checklist at the end of the chapter.

Echinococcus granulosus

See Chapter 3 (Sheep and goats).

PARASITES OF THE LIVER

Capillaria hepatica

Synonym: Callodium hepatica, Hepaticola hepatica

Predilection site: Liver

Parasite class: Nematoda

Superfamily: Trichuroidea

Hosts: Rat, mouse, squirrel, rabbit and farmed mus-telids; occasionally dog, cat and man

Taenia serialis

Synonym: Coenurus serialis

Predilection site: Small intestine (definitive host; intramuscular and subcutaneous connective tissue (intermediate host)

Parasite class: Cestoda

Family: Taeniidae

Final hosts: Dog, fox and other canids

Intermediate hosts: Rabbit, hare and rarely rodents and man.

Fig. 9.12 Predilection site of Eimeria stiedai.

Geographical distribution: Worldwide

For more information see Chapter 6 (Dogs and cats).

Eimeria stiedai

Predilection site: Liver, bile ducts (Fig. 9.12)

Parasite class: Sporozoasida

Family: Eimeriidae

Life cycle: The sporozoites emerge from the sporocysts in the small intestine and migrate to the liver via the lymph vessels. Merogony occurs above the host cell nucleus in the epithelial cells of the bile ducts. The number of asexual generations is uncertain, but there appear to be at least six. In due course, some merozoites form macrogametes and others form microgamonts. The latter produce large numbers of comma-shaped biflagellate microgametes. These fertilise the macrogametes which lay down an oocyst wall, break out of the host cell and pass into the intestine with the bile, and then out in the faeces. The prepatent period is 18 days and the patent period 21–30 days. The sporula-tion time is 2–3 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: This species, which occurs in the bile ducts, reaches the liver via the portal vein and then locates in the epithelium of the bile ducts where it results in a severe cholangitis. Grossly the liver is enlarged and studded with white nodules. Some of the symptoms seen are due to interference with liver function. Mild cases may be asymptomatic. In more severe infections the animals become inappetant and lose weight. There may be diarrhoea, jaundice, ascites and polyuria. The symptoms may become chronic, or death may occur in 21–30 days. Clinical signs of E. stiedai infection include wasting, diarrhoea, ascites and polyuria.

Fig. 9.13 Gamonts of Eimeria stiedai within hyperplastic bile duct epithelium.

Pathology: The liver may become markedly enlarged, and white circular nodules or elongated cords may be visible. These nodules are sharply initially circumscribed, but later coalesce. The bile ducts are grossly enlarged and are filled with developing parasites. There is pronounced hyperplasia of the bile duct epithelial cells, and the epithelium is thrown into folds. Each cell contains one or more parasites (Fig. 9.13).

Other helminths found in the liver of wild rabbits are listed in the parasite checklist at the end of the chapter.

PARASITES OF THE CIRCULATORY SYSTEM

Rickettsia conorii

Common name: Boutonneuse fever, Mediterranean spotted fever, Indian tick typhus, east African tick typhus

Predilection site: Blood

Order: Rickettsiales

Family: Rickettsiaceae

For a more detailed description see Chapter 6 (Dogs and cats).

Hepatozoon cuniculi

Predilection site: Spleen

Parasite class: Sporozoasida

Family: Hepatozoidae

Description: Merocysts may reach 4–6 mm in diameter.

Hosts: Rabbit

Life cycle: The life cycle is unknown. Meronts are found in the spleen and gamonts within leucocytes.

Geographical distribution: Reported in Italy

Pathogenesis: Not known

PARASITES OF THE NERVOUS SYSTEM

Encephalitozoon cuniculi

Synonym: Nosema cuniculi

Predilection site: Blood

Class: Microsporasida

Family: Nosematidae

Description: Microsporidia are obligate, intracellular, spore-forming protozoa. Trophozoites are 2–2.5 × 0. 8–1.2 μm in tissue sections or 4 × 2.5 μm in smears. Spores are about 2 μm long and contain a spirally coiled polar filament with four to five coils.

Hosts: Rabbit, dog, red fox (Vulpes vulpes), blue fox (Alopex lagopus), silver fox, cat, mouse, rat, man

Life cycle: The infective spore stages are highly resistant and can survive for many years. When spores are ingested, the polar tube is everted and when fully extended the sporoplasm passes through the tube and is innoculated into the cytoplasm of the host cell. There then follows a phase of multiplication by binary or multiple fission (merogony). This is followed by sporogony to form sporoblasts, which then mature into spores.

Geographical distribution: Worldwide

Pathogenesis: In rabbits, infection is very common causing granuloma formation in the kidneys, liver and brain. Infection in the brain causes convulsions, tremors, torticollis, ataxia, urinary incontinence, coma and death.

Clinical signs: Many infected rabbits are asymptomatic, although clinical signs such as head tilt, urinary incontinence, posterior paresis and anterior uveitis have been reported.

Diagnosis: Diagnosis in the live animal is difficult and is usually based on identifying the lesions on histopa-thology and observation of the organisms in Giemsa, Gram’s or Goodpasture-carbol fuchsin stains. A serum ELISA test is available.

Pathology: In the rabbit, microscopic lesions consist of focal granulomas and pseudocysts in the brain and kidneys, with occasional severe, focal interstitial nephritis.

Epidemiology: Transplacental infection occurs in rabbits and rodents, but is probably rare with most infections in these animals acquired by ingestion of spores. Evidence suggests that in many countries, infection in rabbits is common.

Treatment: Treatment with benzimidazoles (fenbenda-zole, oxfendazole and albendazole) has been reported in rabbits. Fenbendazole is given at 20 mg/kg and albendazole 15 mg/kg for 28 days. Corticosteroids may suppress granulomata formation, and should be used with caution.

Control: Control in rabbits depends on testing individuals, isolation and treatment. The primary source of infection is urinary excretion and ingestion of spores. Strict hygiene should therefore be followed with raised food dishes and use of water bottles rather than bowls. Rabbits should not be housed in tiered hutches where urine contamination of cages below is common.

Notes: There are reports of E. cuniculi acting as a zoonosis, particularly in immunocompromised individuals.

PARASITES OF THE REPRODUCTIVE/UROGENITAL SYSTEM

No parasites of veterinary significance reported.

PARASITES OF THE LOCOMOTORY SYSTEM

Toxoplasma gondii

Predilection site: Muscle, lung, liver, reproductive system, central nervous system

Order: Sporozoasida

Family: Sarcocystiidae

Intermediate hosts: Any mammal, including man, or birds.

Final host: Cat, other felids

For more details see Chapter 3 (Sheep and goats).

Sarcocystis cuniculi

Predilection site: Muscle

Order: Sporozoasida

Family: Sarcocystiidae

Description: In the rabbit, the sarcocysts are elongate, compartmented and up to 5 mm × 5 mm. The cyst wall has numerous fine projections up to 11 μm long, packed into a tight pile. Metrocytes are 4–5 μm in diameter.

Final host: Cat

Intermediate host: Rabbit

Life cycle: Infection in the rabbit is by ingestion of sporocysts in cat faeces. Complete details of the merogony phase of development are not known. Ultimately, merozoites penetrate muscle cells where they encyst, giving rise to broad banana-shaped bradyzoites contained within a sarcocyst, which is the infective stage for the carnivorous final host.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: Non-pathogenic.

Diagnosis: Diagnosis is made by microscopic identification of the characteristic cysts. They may be sometimes visible macroscopically.

Epidemiology: Little is known of the epidemiology, but it is clear that where cats are able to hunt or catch rabbits then transmission is likely. The longevity of the sporocysts shed in the faeces is not known.

Treatment and control: Not necessary

ECTOPARASITES

MITES

Psoroptes cuniculi

Synonym: Psoroptes ovis, Psoroptes cervinus, Psoroptes bovis, Psoroptes equi

Common name: Ear canker mite

Predilection site: Ears

Parasite class: Arachnida

Sub-class: Acari

Order: Acariformes

Sub-order: Sarcoptiformes (Astigmata)

Family: Psoroptidae

Description: Mites of the genus Psoroptes are nonburrowing mites, up to 0.75 mm in length and oval in shape (Fig. 3.43). All the legs project beyond the body margin. Its most important recognition features are the pointed mouthparts and the three-jointed pretarsi (pedicels) bearing funnel-shaped suckers (pulvilli).

Adult females have jointed pretarsi and pulvilli on the first, second and fourth pairs of legs and long, whiplike setae on the third pair. In contrast, the smaller adult males, which are recognisable by their copulatory suckers and paired posterior lobes, have pulvilli on the first three pairs of legs and setae on the fourth pair. The legs of adult females are approximately the same length, whereas in males the fourth pair is extremely short.

The Psoroptes mite described as P. cuniculi is found primarily in rabbits, where it is usually localised in the ears, causing ear mange (psoroptic otocariasis). P. cuniculi may also be found in the ears of sheep and horses, causing irritation and head shaking, and also in sheep associated with haematomas.

In adult Psoroptes cuniculi, the outer opisthosomal setae are, on average, slightly shorter than those seen in P. ovis. Nevertheless, the usefulness of this character is questionable, since there is considerable variation and overlap in the lengths of the setae between the two groups, and the mean length of the setae of mites is known to decrease with the age of a body lesion. It appears very likely that P. cuniculi is simply a host-adapted population of the species P. ovis.

Hosts: Rabbit, goat, sheep and horse

Life cycle: The eggs of Psoroptes cuniculi are relatively large (about 250 μm in length) and oval. The hexapod larva, which hatches from the egg, is about 330 μm long. The larva moults into a protonymph, the protonymph moults into a tritonymph and the tritonymph moults to become an adult. Egg, larval, protonymph and tritonymph stages and the adult pre-oviposition period each require a minimum of 2 days to be completed, giving a mean egg to adult time of about 10 days.

Geographical distribution: Worldwide

Pathogenesis: Psoroptes cuniculi localises in the ears, where the mites may occur at relatively low intensities, but occasionally proliferate causing severe mange in which the auditory canal may be completely blocked with greyish debris. If untreated, the infection may extend over the rest of the body with scabs, loss of hair and excoriation from scratching. The initial preclinical stages may last for several months, during which the infestation is difficult to spot and causes little obvious problems to the infested rabbit. Mites are nonburrowing and therefore are found only in exudate, not in tissue.

Clinical signs: In the initial stages of the infection, small skin scales appear deep in the ear canal. These yellow-grey scales can be relatively thick; they contain large numbers of parasites, mite eggs, skin cells and blood. If untreated the scales begin to crust and may eventually grow to a thickness of 10 mm and fill the ear in severe cases. Scratching behaviour and shaking of the head may occur, and scabs and loss of hair may be observed in the ears. Eventually the mites may spread out of the ear and over the rest of the body.

Diagnosis: A sample of scab should be taken from the infected area. When placed in a glass jar or beaker the highly mobile mites will leave the scab and start to migrate up the sides of the jar. Mites can then be collected and examined under a microscope for key features: oval outline, all legs projecting beyond the body margin, three-jointed pre-tarsus.

Pathology: At low population densities, little pathology may be evident. In a rapidly expanding population, however, there may be chronic erosive and proliferative eosinophilic dermatitis.

Epidemiology: When in its preclinical phase deep in the ear, transmission is uncommon. However once the infestation has spread transmission is more likely, primarily through physical contact but also may occur via the environment.

Treatment: Treatment is as for otodectic mange of cats and dogs. Insecticidal preparations such diazinon applied daily for 4 days, and repeated in 10 days have been found to be effective. Treatment with injected ivermectin is highly successful. The infected bedding should be burnt and the housing thoroughly disinfected. The crust will resolve itself, without the need to clean the ears, falling off approximately 10 days after the first treatment.

Control: All in-contact animals should be treated. The housing must be disinfected to prevent reinfection. Regular inspection of the animal, paying particular attention to the ears, should help to control the parasite and reduce the effects of subsequent infestations.

Cheyletiella parasitivorax

Common name: Rabbit fur mite

Predilection site: Most commonly found on the dorsum, above the tail and on the neck, but may occur all over the body.

Parasite class: Arachnida

Sub-class: Acari

Order: Acariformes

Sub-order: Trombidiformes (Prostigmata)

Family: Cheyletidae

Description: Adults are about 400 μm in length and ovoid (Fig. 9.14). They have blade-like chelicerae that are used for piercing their host, and short, strong, opposable palps with curved palpal claws. The palpal femur possesses a long, serrated dorsal seta. The body tends to be slightly elongated with a ‘waist’. The legs are short; tarsal claws are lacking and the empodium is a narrow pad with comb-like pulvilli at the ends of the legs. Adults are highly mobile and are able to move about rapidly.

Fig. 9.14 (a) Adult female Cheyletiella parasitovorax, dorsal view (reproduced from Baker et al., 1956). Genu of the first pair of legs of adult females of (b) Cheyletiella parasitovorax, (c) Cheyletiella blakei and (d) Cheyletiella yasguri.

Three very similar species of Cheyletiella are of veterinary importance and are common: Cheyletiella yasguri on dogs, C. blakei on cats and C. parasitivorax on rabbits. All three species are morphologically very similar. However, the solenidion, on the genu of the first pair of legs, is described as globose in C. parasitivorax, conical in C. blakei and heart-shaped in C. yasguri. Nevertheless, this feature can vary in individuals and between life cycle stages, making precise identification difficult. Identification to genus and knowledge of the host is usually sufficient for diagnosis, but it is important to be aware of the potential for crosstransmission of the various species of Cheyletiella from other in-contact hosts.

Host: Rabbit

Life cycle: All developmental stages occur on the host animal. Eggs are glued to hairs 2–3 mm above the skin. A prelarva and then a larva develop within the egg, with fully developed octopod nymphs eventually emerging from the egg. The mites then moult through two nymphal stages before the adult stage is reached. The life cycle is completed in approximately two weeks. The mites live in the hair and fur, only visiting the skin to feed on lymph and other tissue fluids. They feed on these fluids by piercing the epidermis with their stylet-like chelicerae. Adults can survive for at least 10 days off the host without feeding, or longer in cool environments.

Geographical distribution: Worldwide, particularly North America, Europe, Asia, Australia and New Zealand.

Pathogenesis: Cheyletiella is relatively common in rabbits, but the mite is not highly pathogenic at low densities and is often found in young animals in good physical condition. It is a characteristic of the dermatitis caused by Cheyletiella that many skin scales are shed into the fur, giving it a powdery or mealy appearance, and the presence of moving mites among this debris has given it the common name of ‘walking dandruff’. There is usually very little skin reaction or pruritus. In the rare severe case, involving much of the body surface, crusts are formed. Cheyletiella parasitivorax is capable of transmitting the myxomatosis virus among European rabbits.

Clinical signs: Infestation can result in eczema-like skin conditions and associated pruritus and hair loss. Severe cases may show serous exudate and extensive alopecia.

Diagnosis: In any case of excessive scurf or dandruff, Cheyletiella should be considered in the differential diagnosis. On parting the coat along the back, and especially over the sacrum, scurf will be seen, and if this is combed out on to dark paper the movement of mites will be detected among the debris. Skin scraping is not necessary as the mites are always on the skin surface or in the coat.

Pathology: The pathology of Cheyletiella infestation is poorly understood. In many cases there is very little skin reaction or pruritus. However, in severe cases rabbits may show alopecia with red, scaly skin and dermatitis with hyperkeratosis.

Epidemiology: Cheyletiella parasitivorax is a common fur mite of rabbits. It is highly contagious and can spread rapidly through rabbit colonies. Transmission is usually by direct contact with infested animals although the parasite can survive for over 10 days off the host, therefore bedding and housing can act as a source of infestation.

Treatment: Topical acaricides, such as pyrethrin and dichlorvos-containing sprays, are effective against Cheyletiella. Systemic treatment with ivermectin on three occasions, 7 days apart, is effective. Selamectin spot-on has also been used effectively. Fipronil should only be used with great caution because it has been associated with deaths in some cases.

Control: All in-contact animals should be treated, bedding replaced and housing disinfected.

Notes: Of all the mite infestations of domestic animals, this is one of the most readily transferable to humans. The mites can penetrate clothing and are easily transferred, even on short periods of contact. It is often found that when a positive diagnosis has been made on a pet, there is a history of persistent skin rash in the owner’s family. In contrast to the condition in its natural hosts, the infestation in humans causes severe irritation and intense pruritus. The early sign is an erythema, which may progress to a vesicular and pustular eruption. Cases in humans invariably clear up spontaneously when the animal source has been treated.

Listrophorus gibbus

Common name: Fur mite

Predilection site: Skin

Parasite class: Arachnida

Sub-class: Acari

Order: Acariformes

Sub-order: Sarcoptiformes (Astigmata)

Family: Listrophoridae

Description: L. gibbus is a small, brown non-burrowing mite, occasionally present at low to moderate densities on domestic rabbits.

Table 9.2 Occasional mite parasites of rabbits.

Host: Rabbit

Geographical distribution: Worldwide

Life cycle: It is an obligate parasite, completing all stages of the life cycle (egg, larva, nymph. adult) on the host.

Pathogenesis and clinical signs: L. gibbus may cooccur with C. parasitivorax. This mite is generally considered to be non-pathogenic and is found primarily on the back and abdomen.

Diagnosis: Hair plucks can be examined under a dissecting microscope or with hand lens for the characteristic brown mite or its eggs.

Treatment and control: As for C. parasitivorax

FLEAS

Spilopsyllus cuniculi

Common name: Rabbit flea, European rabbit flea

Predilection site: Ears

Parasite class: Insecta

Parasite order: Siphonaptera

Family: Pulicidae

Description: The rabbit flea, S. cuniculi, has both pronotal and genal ctenidia, the latter being composed of four to six oblique spines. Adults are dark brown, and females are, on average, 1 mm in length; males are slightly smaller. Eyes are present and the frons at the front of the head is rounded with the frontal tubercle conspicuous. There are two stout spines beneath the eye (Fig. 11.27).

Hosts: Rabbit, hare, dog, cat

Life cycle: The rabbit flea, S. cuniculi, occurs largely on the ears. It is more sedentary than most other species of flea and remains for long periods with its mouthparts embedded in the host. The life cycle of this species is believed to be mediated by host hormones imbibed with the host blood. The presence of progesterones inhibits or delays flea maturation. Following mating, the adult female rabbit ovulates and, about 10 days before parturition, the levels of oestrogens and corticosteroids in the blood increase. These hormones cause the fleas to attach tightly to their host and stimulate development of the eggs of the female flea. Reproductive hormones of the pregnant female host stimulate maturation of the ovaries and oocytes of feeding female fleas and testicular development in males. These fleas can only reproduce after feeding on a pregnant doe. This serves to synchronise the life cycles of the flea and its host and results in the emergence of adult fleas at the same time as a new litter of host animals are born. The adult fleas become ready to mate when the litter is born: an airborne kairomone emanating from the newborn rabbits and their urine boosts copulation. The hormones of the host also cause adult fleas to increase the rate of feeding and defecation by about five times. This provides an abundance of food in the burrow for the newly hatched larvae. Oviposi-tion occurs soon after adults have transferred on to the newborn young. The larvae feed on organic matter in the nest debris and mature 15–45 days later when they infest the host littermates before they disperse from the burrow. Populations of S. cuniculi may increase dramatically during the rabbit breeding season.

Adult female fleas on bucks or non-pregnant does are more mobile and will move to pregnant does if able. The rise in ear temperatures during rabbit mating will also stimulate movement of fleas from one rabbit to another.

Geographical distribution: Worldwide

Pathogenesis: When rabbits are not breeding, the distribution of S. cuniculi is related to skin temperature, with fleas usually congregating on the ears. Because they assemble here in large numbers, the intensity of bites may cause considerable irritation and tissue damage.

The rabbit flea may also be found on cats and dogs, which hunt or frequent rabbit habitats. On these hosts they are commonly found on the face and attached to the pinneal margin.

Spilopsyllus cuniculi is the main vector of myxomatosis and it also transmits the non-pathogenic Trypanosoma nabiasi.

Clinical signs: These fleas may cause a great deal of irritation and tissue damage at the congregation sites on the ears.

Diagnosis: The fleas may be seen on the skin of the host animal, particularly around the ears. They have a more sedentary habit than most fleas, and will remain on the ear even when it is handled.

Epidemiology: The fleas can survive for up to 9 months at low temperatures without feeding. The main method of transmission is from the mother to her young.

Table 9.3 Occasional flea parasites of rabbits.

Treatment: Imidacloprid may be used in rabbits to kill adult fleas on contact. Fipronil should only be used with extreme care in rabbits due to its potential toxicity.

Control: Not usually necessary. In case of repeated infestation the source should be identified and contact prevented; all in-contact animals should be treated; bedding should be replaced and housing disinfected.

Table 9.3 lists species of fleas which have also been found on rabbits. For more details see Chapter 11 (Facultative ectoparasites and arthropod vectors).

FLIES

Lucilia sericata

Synonym: Phaenicia sericata

Common name: Greenbottle, sheep blowfly

Predilection site: Skin wounds

Parasite class: Insecta

Family: Calliphoridae

Description, adults: Lucilia sericata blowflies measure up to 10 mm in length and are characterised by a metallic greenish to bronze sheen.

Description, larvae: Larvae are smooth, segmented, and measure 10–14 mm in length. They possess a pair of oral hooks at the anterior extremity, and at the posterior peritremes bearing spiracles.

Hosts: Mainly sheep, but a range of other domestic and wild animals may be affected including humans.

Life cycle: Female blowflies lays clusters of 225–250 yellowish cream eggs on wounds or soiled hair, attracted by the its odour. The eggs hatch into larvae in about 12 hours. The larvae then feed, grow rapidly and moult twice to become fully mature maggots in 3 days.

Geographical distribution: Worldwide

Pathogenesis: Blowfly strike of domestic rabbits and occasionally other domestic mammals and birds may be very common, particularly if dirty, debilitated by clinical disease or wounded. Strike is a very serious condition in rabbits and death may result within a few days.

Clinical signs: Infested animals show extensive skin ulceration, shock, weakness, depression, lethargy and anorexia.

Diagnosis: This is based on the clinical signs and recognition of maggots in the lesion.

Pathology: Struck animals have a rapid increase in body temperature and respiratory rate. The animals show extensive tissue damage, become anaemic and suffer severe toxaemia.

Epidemiology: Predominantly a summer problem in temperate areas, but may occur all year round in more tropical regions.

Treatment: Once the problem is diagnosed, affected rabbits should be separated and the area surrounding the lesion clipped. Where possible larvae should be removed. The rabbit may require sedation, intravenous fluid therapy and analgesia. Ivermectin may be used to kill any remaining feeding larvae. Unless caught in its early stages the prognosis must be guarded, since myiasis can be extremely damaging to rabbits relatively quickly.

Control: To prevent fly-strike, formulations of pour-on cyromazine are available specifically for rabbits. They offer prevention for up to 8–10 weeks. Longer term steps should be taken to prevent diarrhoea and faecal contamination of the hair, either through worm control or diet as required.

Note: Several other species of blowfly or fleshfly may also strike rabbits in various parts of the world. The treatment is as described above for L. sericata.

Cuterebra

See Rats.

GUINEA PIGS

PARASITES OF THE DIGESTIVE SYSTEM

SMALL INTESTINE

Hymenolepis diminuta

See Rats and mice.

Rodentolepis nana

See Rats and mice.

Eimeria caviae

Predilection site: Large intestine

Parasite class: Sporozoasida

Family: Eimeriidae

Description: Oocysts are ellipsoidal or ovoid, smooth, brown, 13–26 × 12–23 μm, without a micropyle, or polar granule but with a residuum.

Life cycle: Following ingestion of oocysts, sporozoites enter the intestinal epithelium to become first-generation meronts. Following a further three mero-gony generations gamonts appear in epithelial cells of the large intestine leading the excretion of oocysts in the faeces. The prepatent period is about 7 days and the patent period approximately 4–5 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: E. caviae is usually non-pathogenic but may occasionally cause diarrhoea and mortality. Clinical signs include unthriftiness, poor weight gain in young animals; droppings are slimy and contain blood.

Diagnosis: Diagnosis is based on identification of oocysts in the faeces in association with clinical and pathological findings.

Pathology: Lesions seen at postmortem occur in the mucosa of the colon and consist of small white, or pale yellow plaques and petechial haemorrhages. In severe infections the whole mucosa may be destroyed. There have also been reports of hepatomegaly with focal necrosis containing oocysts.

Epidemiology: Crowding and lack of good sanitation promote spread of coccidiosis. Breeding establishments and rescue centres are potential sources of infection. Older guinea pigs are generally immune from disease but may seed the environment with oocysts leading to infection in young animals that have no previous exposure.

Treatment: Information on treatment in the guinea pig is scanty, although by analogy with other host species, the use of sulphonamides, such as sulphamezathine, should be tried.

Control: Good sanitation and isolation are effective measures in preventing coccidiosis. If possible, guinea pigs should be housed on wire floor cages to reduce the incidence of infection. Standard disinfectants are ineffective against coccidial oocysts but ammonia-based products are effective.

Cryptosporidium wrairi

Predilection site: Small intestine

Parasite class: Sporozoasida

Family: Cryptosporidiidae

Description: Mature oocysts are ovoid, 4.8–5.6 × 4.0–5.0 μm (mean 5.40 × 4.6 μm), with a length:width ratio of 1.17. First-generation meronts are 3.4–4.4 μm when mature and contain eight merozoites; second-generation meronts contain four merozoites. Developing macrogametes are 4–7.0 μm in size.

Life cycle: Oocysts, each with four sporozoites, are liberated in the faeces. Following ingestion, the sporozoites invade the microvillous brush border of the enterocytes and the trophozoites rapidly differentiate in 3–4 days to form meronts with eight merozoites followed by a second merogony stage containing four merozoites. Gametogony follows after two generations of meronts usually around 13–15 days post infection. The prepatent period has not been reported.

Geographical distribution: Unknown

Pathogenesis and clinical signs: The infection has only been reported in small guinea pigs (weighing 200–300 g) and is not associated with diarrhoea or overt signs of disease. Clinical signs are usually inapparent.

Diagnosis: Oocysts may be demonstrated using Ziehl–Nielsen-stained faecal smears in which the sporo-zoites appear as bright red granules. Speciation of Cryptosporidium is difficult, if not impossible, using conventional techniques. A range of molecular and immunological techniques has been developed, that include the use of immunofluorescence (IF) or enzyme-linked immunosorbent assays (ELISA). More recently, DNA-based techniques have been used for the molecular characterisations of Cryptosporidium species.

Pathology: There may be chronic enteritis depending on the severity of infection. Lesions are usually focal when only limited areas of the intestine are affected. The organisms are more numerous in the posterior ileum and are distributed over the entire surface of the intestinal villi but are more numerous towards the tips and absent in the crypts.

Epidemiology: The primary route of infection is mainly direct animal-to-animal transmission by the faecal–oral route.

Treatment and control: Not required

Giardia intestinalis

See Chapter 6 (Dogs and cats).

LARGE INTESTINE

Paraspidodera uncinata

Predilection site: Large intestine

Parasite class: Nematoda

Superfamily: Ascaridoidea

Description, gross: Male worms are 16–17 mm and females 18–21 mm.

Description, microscopic: The egg is ellipsoidal, 43 × 31 μm

Host: Guinea pig

Life cycle: The life cycle is direct. Eggs passed in the faeces are infective after 3–5 days. When ingested they migrate to the caecum and colon and mature in about 45 days.

Geographical distribution: Worldwide

Pathogenesis and clinical signs: Generally considered non-pathogenic, although heavy infections may cause weight loss, debility and diarrhoea.

Diagnosis: Diagnosis is based on identification of eggs in the faeces or adult worms in the large intestine.

Epidemiology: This caecal worm occurs naturally in the caecum and colon of the wild guinea pig in South America and in laboratory guinea pigs around the world. Infection is usually associated with guinea pigs housed in outdoor runs.

Treatment and control: Piperazine at 3 g/l in the drinking water for 7 days is effective. Ivermectin at 200–500 μg given subcutaneously is also likely to be effective. Control is based on good hygiene and management.

A number of protozoa are found in the caecum of the guinea pig. All are considered non-pathogenic. Entamoeba caviae and Tritrichomonas caviae are common in the caeca of laboratory guinea pigs.

Entamoeba caviae

Predilection site: Caecum

Parasite class: Sarcodina

Family: Endamoebidae

Description: Trophozoites are 10–20 μm in diameter. The nucleus, when stained has a central or eccentric endostome with a ring of relatively coarse peripheral granules. The cysts, which are rare, are 11–17 μm in size and contain eight nuclei when mature.

Tritrichomonas caviae

Predilection site: Caecum

Parasite class: Zoomastigophorasida

Family: Trichomonadidae

Fig. 9.15 Tritrichomonas caviae.

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