rabbit diseases by Abohemeed Aly

Rabbit Diseases http://veterinarydiseases.blogspot.com DR_ABOHEMEED@YAHOO.COM

BACTERIAL DISEASES I. Pasteurellosis II. Bordetellosis III. Colibacillosis IV. Tyzzer's Disease V. Staphylococcus Infections VI. Venereal Spirochetosis (Rabbit Syphilis, Vent Disease, Cuniculosis) VII. Proliferative Ileotyphlitis VIII. Salmonellosis IX. Tularemia X.lestriosis

Pasteurellosis A. Etiology: Pasteurella multocida is a small, Gram-negative, non spore-forming bipolar rod. B. Transmission: Transmission occurs by direct contact, aerosol, venereal, and hematogenous routes. Incidence of infection and disease is high (probably > 90%). Many rabbits are asymptomatic carriers. The incidence of bacterial carriage is no different in antibiotictreated rabbits.

C. Disease Forms: Upper respiratory disease ("snuffles"), pneumonia, otitis media, pyometra, orchitis, subcutaneous abscesses, conjunctivitis and septicemia are manifestations of P. multocida infection.

SnufflesThis is the most common manifestation of pasteurellosis. Clinical signs characteristically include serous to mucopurulent nasal exudate with sneezing and coughing. Exudate may be seen on the medial aspect of the forepaws. Signs may subside temporarily only to recur throughout life.

Lesions include reddened mucosa in acute infections, thickened mucosa in chronic infections, and exudate in nasal cavity and paranasal sinuses. Antibiotic therapy (Table) usually causes abatement of clinical signs. The prognosis for disease improvement or remission is good, however there is a good chance of recurrence.

Nasal secretions

Nasal discharge is so chronic that the fur is actually missing.

mucopurulent nasal discharge

Difficulties in Respiration

Enzootic Pneumonia Affected rabbits frequently die acutely with no signs (especially young rabbits); anorexia and depression may be observed. Acute pneumonia lesions include red-grey foci of consolidation of the cranioventral lung lobes with or without hemorrhage. Chronic pneumonia is characterized by generalized consolidation, encapsulated abscesses, fibrinopurulent or mucopurulent pleuritis and pyothorax. If the pneumonia is recognized early, aggressive antibiotic therapy may be of some value. The prognosis for all cases of pneumonia is poor.

Pulmonary Edema

Pneumonea

Pneumonia

Contaminated Lungs by Pasteurella

Enzootic Pneumonia

3. Otitis Media Usually there are no clinical signs. Torticollis will occur if the function of the internal ear is compromised, either by direct bacterial invasion or by the damaging effects of the bacterial toxins. Nervous signs and incoordination are observed if the bacteria extends to the meninges. Creamy, white exudate in middle ear is found either uni- or bilaterally. When treated with antibiotics at the first indication of a head tilt, rabbits with otitis media may improve or stabilize.

In rabbits with severe torticollis, corticosteroid therapy may be indicated. Bulla osteotomies and lavage of the tympanic bullae has proven to be a fruitless approach to treatment. The torticollis may progress in spite of antibiotic therapy, so the prognosis is guarded.

torticollis

4. Genital Infections Venereal or hematogenous transmission may occur. Affected rabbits may have a vaginal discharge which may be serous to mucopurulent and/or a history of infertility. The uterus can be palpably enlarged with pyometra. Acute infection of the uterus is characterized by slightly dilated horns filled with grey exudate.

In chronic infections the uterine horns are greatly dilated with purulent exudate, and are fragile. In affected bucks, one or both testicles may be enlarged, tender, firm and may contain abscesses. The health of affected rabbits can be salvaged by surgical removal of diseased tissues coupled with antibiotic therapy. The prognosis for recovery after surgery is good.

Healthy uterus

The healthy pink uterine horns are easily seen (white arrow).

Uterine infection

UTERINE INFECTION

6. Conjunctivitis Signs include epiphora with blephorospasm, eyelids closed by excessive mucopurulent exudate and facial staining. Reddened conjuctiva with serous to mucopurulent adherent exudate are found. Often there is inflammation and eventual stenosis of the nasolacrimal duct, resulting in chronic epiphora and hair loss. The use of antibiotic ophthalmic ointments will improve most cases. Occasionally, the nasolacrimal duct may need to be flushed to remove inspissated purulent material.

Lacrimation

D. Predisposing Factors: Onset of clinical disease is often associated with some underlying stressor, such as a marked change in environmental temperature or humidity, poor ventilation, poor sanitation, and overcrowding. Physiologic conditions that also predispose to disease is age (very young or very old), pregnancy, nutritional state, and genetics. Some rabbit stocks are genetically hardier, and can carry Pasteurella throughout life without developing clinical disease.

Diagnosis This problem is so prevalent, and the symptoms so characteristic, that Pasteurella is part of the tentative diagnosis anytime a rabbit shows the above symptoms. During the physical exam a fever might be present along with an increase in the sounds heard in the lungs with the stethoscope. Cultures can be performed to confirm that Pasteurella Multocida is indeed present. Rabbits with a negative culture result could still be harboring Pasteurella. Blood samples are commonly used along with x-rays. X-rays might show changes in the chest or infection in the middle ear.

D i a g n o s i s

This is what these lungs could look like on an autopsy. All the white spots correspond to the white spots on the radiograph above.

Diagnosis Lung

F. Treatment: Most Pasteurella isolates are sensitive to penicillin. Only sulfaquinoxaline and tetracycline have known withdrawal times and can be used for rabbits raised for slaughter. Short term use of certain oral antibiotics, such as ampicillin or amoxicillin, or prolonged systemic antibiotic therapy with any drug may upset the cecal bacterial flora. If anorexia or diarrhea occurs during therapy, stop treatment immediately. Dietary supplementation with high fiber foods, alfalfa or high fiber pelleted diets, or with yogurt containing live Lactobacillus cultures may reduce intestinal upsets.

Antibiotics Commonly Dispensed for Rabbits Enrofloxicin Procaine penicillin Sulfaquinoxaline Tetracycline

2.5 to 5 mg/kg b.i.d. for 5 to 7 days (oral and injectable) 40 to 60,000 IU/kg body weight IM s.i.d. for 3 to 10 days 0.256 gm/50 gm feed for 30 days or 226 gm/ton of feed 300 mg/liter of water for 7 days, or 5 mg/kg q.i.d. for 7 days

5. Abscesses Contaminated wounds and septicemia are common routes for abscess development in a variety of locations, but especially in the subcutis. The presence of subcutaneous swellings which are filled with creamy exudate and may have draining fistulous tracts is typical of Pasteurella abscesses. Treatments include sedation of the rabbit prior to lancing and flushing superficial abscesses t.i.d. with Betadine or chlorhexidine. Systemic antibiotic therapy should be provided for 1 week. If the infections persist, surgical resection may be required.

Abscesses are treated surgically. Rabbits have a very thick and tenacious discharge when they form an abscess, and require more care than the abscesses of most other animals. Surgical removal can be difficult, especially in the chronic cases, because the abscessed area can become extensive in nature. Multiple surgeries might be needed, and wound care at home is necessary.

This is a severe abscess on the back of a rabbit that has been anesthetized and is undergoing surgery to correct its problem. The wound has just been opened by the scalpel blade at the top left of the screen (arrow).

Abscesses

The wound is filled with pus (the correct word is purulent) that must be completely removed. Any infection that is not removed will cause the abscess to return. It is very thick and does not lend itself to easy removal.

Abscesses

The underlying tissue that has been exposed to this infection has to be removed also. It is diseased and will be a source of further infection if it is not completely removed.

Abscesses

This is the final appearance of the wound after all the purulent material and diseased tissue has been removed after 30 minutes of surgery. The rubber tube (arrows) running from top to bottom is called a penrose drain tube. Its function is to allow further drainage of the infection. The tube will be removed in 5 days, the sutures will be removed in 10 days.

Abscesses

Some pasteurella abscesses are chronic in nature, and contain more dead tissue than purulent material. The following pictures show a case of a rabbit referred to us that had been treated with routine drainage and antibiotics for several weeks. The purulent material on the inside was diminished, but the tissue that remained was either dead or dying and had to be surgically removed.

This is the face of the rabbit that is laying on its left side. Its mouth is towards the right, the white arrow points to its right eye. The abscess is the large circular area below and to the left of the eye.

Abscesses

The diseased tissue (black arrow) is gently dissected away from the healthy tissue. The healthy jaw muscle (white arrow) is apparent .

A large incision had to be made to remove all of this diseased tissue. It extends from the base of the ear all the way under the chin. These sutures will be removed in 10-14 days.

Abscesses

G. Control The best control for pasteurellosis is good husbandry techniques and culling of rabbits with clinical disease. Since most all rabbits carry Pasteurella multocida in the nasal cavity, management measures are aimed at controlling the clinical disease expression. The rabbitry must have good ventilation, low ammonia levels, and low humidity to decrease incidence of this disease.

In a breeding colony situation, all infected rabbits with clinical disease should be culled for many reasons. (In spite of antibiotic therapy, the chance of disease recurrence is high. Rabbits with clinical signs shed large numbers of organisms into the environment. The best way to improve the genetic hardiness is to remove breeders with clinical disease prior to introduction into the rabbitry.

If possible, weanling rabbits should be raised separately from the breeding colony. Clean automatic waterers and cages in which diseased rabbits were housed and then spray with 1% bleach solution to kill residual bacteria. (Bleach will eventually damage galvanized caging, so alternative disinfectants can be used.) All new arrivals should be quarantined

II. Bordetellosis Etiology: Bordetella bronchiseptica is a small gramnegative, alpha-hemolytic, nonfermenting rod. Incidence of infection is high with a low incidence of disease. B. Transmission: Routes of transmission include aerosol and direct contact. Many rabbits are asymptomatic carriers, and may harbor both Bordetella and Pasteurella.

D. Gross Pathology: The characteristic lesion is erythematous nasal mucosa with adherent exudate. E. Diagnosis: Definitive diagnosis is made by culture of the organism. Smear and gram stain of nasal exudate may be helpful. C. Clinical Signs: Signs are similar to snuffles and include upper respiratory infection with serous to mucopurulent nasal exudate and sneezing. Pneumonia uncommonly develops.

F. Treatment: Enrofloxian (2.5 to 5.0 mg/kg bid for 5 to 7 days), Oxytetracycline (0.1 mg/ml drinking water) Tylosin (2 to 4 mg/kg IM b.i.d., then s.i.d. for 3 to 5 days) are effective in reducing clinical signs. As with pasteurellosis, antibiotic therapy may have to be repeated when rhinitis recurs, which may happen. Antibiotic therapy does not eliminate the carrier state.

Bordetellosis

G. Control: Isolation and treatment of sick animals, decreasing stressful conditions, and preparation of and vaccination with an autogenous bacterin are all adequate control measures. The bacterin may not eliminate the carrier state, but may help prevent expression of clinical disease.

BACTERIAL DIARRHEAL DISEASES The initial approach to treating diarrhea in a rabbit is similar to that used for companion animals. Obtaining a thorough history is imperative. Questions to ask include recent changes in the rabbits' environment, husbandry, diet, including supplemental foods, antibiotics or home remedies. Even the addition of a new pet, especially a carnivore, can serve as a sufficient stressor.

A diagnostic workup should include a complete physical exam including abdominal palpation, fecal flotation for coccidia, and fecal cultures. Ancillary tests may include blood work, and abdominal radiographs (plain and contrast studies) if warranted. Supportive therapy should be directed at correcting and maintaining hydration (via parenteral and oral fluid therapy) and stimulating the appetite in an attempt to restore normal gut flora using live yogurt cultures and fiber-containing treats. Antibiotics should be judiciously used as they may further upset the gut flora.

III. Colibacillosis Etiology: Escherichia coli is a gram-negative, lactose-fermenting, indole positive rod. Rabbits are known to be affected by nontoxin producing, enteropathogenic E. coli (EPEC). EPEC adhere to the intestinal mucosa through a 2-step process. First, a bacterial pilus first allows attachment of the bacterial cell to the enterocyte.

A secretory diarrhea is induced by an unknown mechanism. Receptors for EPEC attachment to the epithelial cells are not present in newborn rabbits. They first appear at 21 days and reach normal adult levels by 35 days. The stress of weaning and loss of passively acquired maternal antibody contribute to susceptibility at this time.

B. Clinical Signs: Rabbits have diarrhea, fever, anorexia, and may consume more water than usual. C. Pathology: Fecal-stained perineal fur and fluid-filled intestinal contents with serosal vascular injection are seen.

Colibacillosis

Edema and pyogranulomatous cellularity of the lamina propria without mucosal ulceration are prominent histopathologic findings. Edema or hemorrhage can be seen in the submucosa. Small bacterial rods (arrow) adhered to and effacing enterocyte margins are common in the ileum and cecum.

D. Treatment: Fluid therapy and supportive care are indicated. The salicylates in Pepto bismol may be protective. Chlorpromazine (1 to 10 mg/kg IM) may help decrease fluid loss from the the secretory diarrhea.

IV. Tyzzer's Disease Etiology: Clostridium piliforme, an obligate intracellular bacterium, is a Gram-negative, pleomorphic, filamentous organism that can produce spores. B. Transmission: Spore ingestion (fecal-oral). Spores can remain viable at moderate to freezing temperatures for extended periods of time (> 1 year). The disease is perpetuated in breeding colonies by the infection of bunnies born into the colony. The incidence of disease is moderate.

C. Clinical Signs: Usually rabbits are affected shortly after weaning when passive immunity, if present, has waned. Acute, profuse watery to mucoid diarrhea, dehydration and death within 12 to 48 hours after onset of diarrhea are typical. The mortality rate is high. Exposure of naive adult rabbits may cause little to no clinical disease.

D. Pathology: Lesions in weanling rabbits include edema and hemorrhage of mucosa, submucosa, and musculature of intestinal tract (A.). It is unusual to see an enlarged liver with multifocal tan to yellow foci of necrosis or hemorrhage of the myocardium as is described in the literature. Extensive mucosal necrosis with a granulomatous cellular mucosal infiltrate may occur in the ileum, cecum, and proximal colon. Visualization of the bacterium is enhanced with use of silver stains.

Argyrophilic intracellular bacteria in clusters or "pick-up-sticks" or haystack clumps are present in viable enterocytes in areas of granulomatous enteritis (B.), and if heaptic necrosis is observed, in hepatocytes adjacent to an area of necrosis.

Tyzzer’s A

E. Diagnosis: Histopathological examination of liver or cecum stained with silver will be diagnostic if intracellular bacterial rods are observed. PCR of feces, intestinal tissue or liver can be used to document the presence of the bacterium. An ELISA is useful to detect antibody in recovered or asymptomatically infected rabbits. F. Treatment: No therapy has been uniformly successful. Supportive therapy may help when the enteric disease is mild and the rabbit is still eating.

G. Control: Prevent overcrowding and use good sanitation techniques. Stresses such as weaning and high environmental temperature may precipitate an outbreak. To minimize the stress of weaning, let the bunnies stay in the original cage and remove the doe. Work to prevent temperature fluctuations and keep the rabbits well-ventilated in high temperatures with fans. The spores are resistant to many disinfectants. A 1% bleach solution will inactivate spores that remain after the fecal material has been washed off soiled cages. Temperatures of water used to clean cages may also inactivate spores if the cages and supplies are allowed to contact 82oC water for no less than 15 minutes.

V. Staphylococcus Infections Etiology: Staphylococcus aureus is a Gram-positive, hemolytic, coagulase-positive coccus. B. Transmission: Aerosol and direct contact (organism present in oral cavity of non-clinical carriers) are primary routes of infection. Incidence of infection is moderate, but the incidence of disease is low.

C. Clinical Signs: There is a wide range of clinical disease forms. S. aureus may cause suppurative infection in any organ or any site. Subcutaneous abscesses, mastitis with abscess formation, dermatitis, upper respiratory infection with mucopurulent nasal discharge, and septicemia with depression, anorexia, fever, and death have been reported. Of these disease syndromes, abscess formation and mastitis are most commonly reported.

Abscesses Abscesses may occur subcutaneously or in the viscera. At necropsy thick-walled abscesses filled with purulent exudate are found. Diffuse congestion and petechiation of viscera may be seen in septicemic animals. Clinicopathologic lesions are similar to those of pasteurellosis. Presumptive diagnosis may be made by making a smear and gram stain of the exudate. Culture and antibiotic sensitivities are needed for a definitive diagnosis and choice of treatment.

If the organism is sensitive to penicillin, 40,000 IU/kg procaine penicillin, IM s.i.d., for 3 to 5 days may be effective. Subcutaneous abscesses should be lanced and flushed with germicidal solution along with administration of systemic antibiotics. Surgical extirpation may be necessary to resolve chronic abscesses. To decrease the incidence of abscesses, the cages must be kept clean, fighting animals separated, and clinically ill rabbits isolated.

2. Mastitis Mastitis or blue breast disease is commonly found in herds with intensified production. Infection of gland occurs through trauma to the teat, ascending infection through the teat canal, or secondary to septicemia. Mastitis occurs just after kindling. The mammary glands are swollen, usually not discolored, and may develop abscesses. Frequently there is loss of function of the affected gland and rarely the doe may die.

Bunnies may die because of infected milk or not grow as well because of decreased function of the gland. Therapy includes hot packing the affected gland, systemic antibiotic therapy, and transfer of bunnies to a healthy lactating doe. To prevent mastitis, keep nest boxes clean and dry. Limit feed to the doe just prior to kindling to prevent excessive milk production and stagnation. Cull all affected does.

Mastitis

VII. Salmonellosis Etiology: Salmonella enterica serovars are Gram-negative aerobic, nonlactose fermenting, H2S producing rods. B. Transmission: Salmonellae are transmitted by ingestion through direct contact with contaminated feces, food or fomites. Incidence of infection is rare. C. Clinical Signs: Acute disease is characterized by anorexia, fever, dehydration, diarrhea (hemorrhagic), death, and abortions.

D. Pathology: Lesions are consistent with those of septicemia and include congestion and hemorrhage of the viscera associated with septicemia, ulcerative colitis, and focal necrosis of liver. E. Diagnosis: Definitive diagnosis is made by isolation of the bacteria through culture of blood, spleen, mesenteric lymph nodes and feces on selective media (brilliant green, selenite, citrate, or tetrathionate). F. Treatment: Since antibiotic therapy does not eliminate bacterial carriage, it is advisable to eliminate the colony and restock.

G. Control: Good management practices will prevent infection. Disinfection, replacement with clean stock and prevention of wild bird or rodent contamination of bedding, water, or food should prevent future or continued problems. Public Health Significance: Man can contract Salmonella from infected rabbits.

Rabbit Syphilis, Vent disease Treponematosis Etiology: Treponema paraluis-cuniculi Treponematosis is also known as rabbit syphilis, vent disease, or venereal spirochetosis. The disease is contracted venereally or by young rabbits in contact with an infected dam. The disease is characterized by dry, crusty exudate overlying ulcers in the skin and mucous membranes. Lesions commonly occur on the vulva (shown here), prepuce, and anus.

Rabbit Syphilis, Vent disease Diagnosis is confirmed by Darkfield examination of scrapings from the lesions for the presence of the spirochete Treponema paraluis-cuniculi Treatment Treponematosis can be treated successfully with three injections of Benzathine penicillin with procaine penicillin G, 84,000 IU/kg given IM at 7-day intervals. All animals from an infected colony must be treated to eradicate the disease There are NO public health hazards associated with the disease.

Rabbit Syphilis, Vent diseaseâ&#x20AC;?

PARASITIC DISEASES I-Coccidiosis II. Encephalitozoonosis III. Passalurus ambiguus IV. Baylisascaris procyonis V. Cestodes VI. Mites VII. Fleas and Lice VIII. Cuterebra Infestation

I. Coccidiosis

Hepatic coccidia

A. Hepatic Coccidia 1. Etiology: Eimeria stiedae 2. Transmission: Ingestion of sporulated oocysts (unsporulated in freshly voided feces) is the mode of transmission. The incidence of infection is moderate to high. 3. Pathogenesis: Eimeria stiedae exists in the duodenum, travels to the liver via the bloodstream or lymphatics, and invades epithelial cells of bile ducts to begin schizogeny. 4. Clinical Signs: Signs predominate in young rabbits and may include anorexia,

Hepatic coccidia

debilitation, and pendulous abdomen with hepatomegaly noted on abdominal palpation. Mortality is low except in young rabbits.

5. Pathology: An enlarged liver with multifocal, flat, yellow-white lesions containing yellow exudate and occasionally a distended gallbladder that contains bile may be seen at necropsy (A.). The pathognomonic microscopic lesion is marked periportal fibrosis surrounding enlarged bile ducts lined with hyperplastic bile duct epithelium that harbors inflammatory cell infiltrates, and E. stiedae macrogametes, microgametocytes and oocysts.

Hepatic coccidia

Coccidiosis. Enlarged liver with multi-focal grayish-white coalescing lesions and yellowish liquid pus caused by E. Liver Coccidiosis

7. Diagnosis:

Hepatic coccidia Diag.

An antemortem diagnosis can be made by examination of feces by direct smear, flotation or concentration/flotation methods. It can be difficult to identify E. steidae oocysts in fecal specimens since they may not be readily shed in the bile. On necropsy, the recognition of the flat liver lesions and identification of oocysts in the bile provide diagnostic information. The histological appearance of liver with identification of intraepithelial coccidial organisms will allow diagnosis from tissue biopsies.

Hepatic coccidia treat.

8. Treatment: Drugs approved as coccidiostats for rabbits used for meat include sulfamerazine (0.02% in water), sulfaquinoxaline (0.05% in water or 0.03% in feed), sulfamethoxine (75 mg/kg BW in feed), and lasalocid (68-113 gms per ton of feed). Hepatic coccidia are difficult to eliminate with anticoccidial therapy, and lasalocid has been the most successful of the listed drugs in treating hepatic coccidiosis.

Hepatic coccidia control

9. Control: Rabbits should be housed on wire-meshed floors. Bottoms of cages are to be brushed daily to remove adherent feces, and cleaned and disinfected regularly (1% chlorox). Weanlings should be raised separate from adults. Feeding fresh greens or hay will prevent use of forage that may be contaminated with droppings from wild rabbits.

Intestinal Coccidia

B. Intestinal Coccidia 1. Etiology: Eimeria magna, Eimeria irresidua, Eimeria perforans, and Eimeria media are frequently observed pathogenic species. All species infect the intestinal tract and replicate in the absorptive epithelium of the mucosa. 2. Transmission: Transmission occurs by ingestion of sporulated oocysts. Incidence of infection is high.

3. Clinical Signs:

Intestinal Coccidia

Signs vary and are most severe in young rabbits. Poor weight gain, diarrhea ranging from mucoid to watery to hemorrhagic, polydipsia and sometimes acute death are seen. Older rabbits may shed coccidial oocysts without expression of clinical disease. 4. Gross Pathology: Fluid intestinal contents are often observed in heavily parasitized rabbits. One may see multiple white patches or ulcers on mucosal surface of the small or large intestine.

Intestinal coccidioses

Intestinal Coccidia

5. Diagnosis: Antemortem diagnosis can be made by examination of feces by direct smear, flotation or concentration/flotation methods. A postmortem diagnosis can be made on examination of mucosal scrapings and by observation of coccidial organisms on histological sections of intestine

Oocysts

Treatment

D. Treatment: As mentioned in the above section, drugs approved as coccidiostats for rabbits used for meat include sulfamerazine (0.02% in water), sulfaquinoxaline (0.05% in water or 0.03% in feed), sulfamethoxine (75 mg/kg BW in feed), and lasalocid (68-113 gms per ton of feed) have been provided in schedules of 3-weeks-on / 3weeks-off periods.

Control

E. Control: Rabbits should be housed on wire-meshed floors. Bottoms of cages are to be brushed daily to remove adherent feces, and cleaned and disinfected regularly (1% chlorox). Weanlings should be raised separately from adults. Feeding fresh greens or hay will prevent use of forage that may be contaminated with droppings from wild rabbits.

Pinwor m

III. Passalurus ambiguus Pinworm

The rabbit pinworm does not cause clinical disease in infected rabbits. The rabbit pinworm has a direct life cycle and adult pinworms reside in the cecum and large intestine. The males are 4.1 mm long, 300 Âľm in diameter with a single curved spicule. The females 6.6 mm long with long tail posterior to vulva. The eggs are flattened on one side.

Pinworm

Treatment Piperazine adipate (0.5 gm/kg to 0.75 gm/kg s.i.d. for 2 days in food or water) is effective. Ivermectin at 0.2 mg/kg is most likely effective. Control of infection is aimed at preventing ingestion of contaminated feces.

V. Cestodes Rabbir play as intermediate host for Tape worm which infected dog & cat Infection in rabbits is of greater importance because the larval stages of the parasite develop in different organs and the musculature and often cause decreased food utilization and wasting of the host. The carcass or portion of the carcass may also be unfit for human consumption in severe cases which further contributes to the economic loss.

Tape worm larvae in rabbits Cysticercus pisiformis

is the cystic stage of Taenia pisiformis which occurs in dogs and rarely in cats The mature larvae are found in the peritoneal cavity and frequently in the mesentery of rabbits The cysts are the size of a pea, hence the name C. pisiformis. They are filled with clear fluid in early stages. There is formation of pus in older lesions

Rabbit Cysticercus

Tapeworm larvae in rabbits. Cysticercus pisiformis in the mesentery of rabbit.

Cysticercus pisiformis in rabbit

Cysticercus fasciolaris is the cystic stage of Taenia taeniaeformis, known as the cat tapeworm. This parasite can be recognized by the lack of a neck and the bellshaped posterior segments. The intermediate host are the rabbit, rat, mouse and other rodents. Cysticercus fasciolaris is 2.5 cm long and develops in the liver

Cysticercus fasciolaris

Coenurus serialis is the intermediate stage of Taenia serialis, a tapeworm of the dog and fox. Coenurus serialis is almost fatal to hares, rabbits and other related rodents. It is passed into the connective tissue of the lumbar muscles, hind leg muscles and rarely into the jaw muscles. Coenurus serialis may also occur accidentally in the brain and muscle tissue of humans. The mature cyst in rabbits is ovoid or round, approximately 5 cm in diameter and has scolices the size of a rice grain. It may have as many as forty scolices. Sometimes these Coenuri behave like hydatids by budding off new cysts internally or externally. These internal cysts are frequently fertile. The external cysts are attached by stalks and are often sterile. They resemble a bunch of grapes

Coenurus serialis

Encephalitozoonosis def. :

is an infection caused by the protozoal parasite, Encephalitozoon cuniculi. Protozoa are one-cell organisms that infect various cells or tissues of the body and behave as tiny parasites. Infection with E. cuniculi generally affects some combination of the kidneys, brain, heart, and lungs.

Encephalitozoonosis is transmitted by ingestion of the parasite, through contact with contaminated urine, or passed through the placenta from the mother to her unborn pups. There is no breed or sex predilection.

â&#x20AC;˘ Sings : 1. Stunted growth 2. Kidney failure 3. Neurologic abnormalities such as aggressiveness, convulsions, blindness or paralysis 4. Sudden death

â&#x20AC;˘Treatment usually consists of supportive therapy. No specific treatment has been designed to date that successfully kills this protozoal organism.

Encephalitozoonosis (nosematosis) chronic interstitial nephritis

Encephalitozoonosis (nosematosis) ln brain

Mites

VI. Mites Ear Mite

A. Psoroptes cuniculi - ear mite

1. Etiology: This nonburrowing, obligate mite has a high incidence of occurrence in meat, laboratory and pet rabbits. The life cycle is completed in around 21 days.

2. Clinical Signs: Scratching at ears with hind feet and the presence of crusty exudate in the pinnas with an underlying moist dermatitis are characteristic. The parasites do not cause otitis media since they do not penetrate the tympanic membrane.

Ear Mite

3. Diagnosis: Mites can be observed with an otoscope or on a mineral oil preparation of the crusty exudate. The mites are oval-shaped with well-developed legs, pointed pedicles, and bell-shaped suckers on the end of pedicles.

Ear Mite

4. Treatment: Crusts are gently removed from the canal. Mineral oil with or without acaricide in the ear canal will kill the mites. Ivermectin at doses of 0.2 to 0.4 mg/kg SC will eliminate most infections with a single treatment. Antibiotic cream can be used if the ear is infected. 5. Control: Infected animals should be isolated. During treatment, the cage should be disinfected

B. Cheyletiella parasitovorax - fur mite

Fur Mite

1. Etiology: C. parasitovorax is a small, noninvasive mite, with a low to moderate incidence of infection. 2. Clinical Signs: Partial alopecia of dorsal trunk or scapular region with a fine, grey scale on erythematous skin results from infestation. (The mite is often called "walking dandruff.") There is some pruritis. 3. Diagnosis: Examination of the pelt will reveal small white mites with piercing chelicerae and large curved palpal hooks, and the eggs are attached to hair shafts.

Fur Mite

4. Treatment:

Fur Mite

Rabbits can be dusted or sprayed with pyrethrin preparations or silica gel acaricides, with repeat treatments at 10 day intervals. Ivermectin at 0.2 to 0.4 mg/kg SC should also be effective. 5. Control: Infested rabbits should be isolated during treatments. Cleaning and spraying the rabbit's environment with insecticidal preparations aids in decontamination of the fomites. Public Health Significance: This parasite can cause a transient pruritic rash in hypersensitized people, especially children.

C. Listrophorus gibbus - fur mite

Fur Mite

1. Etiology: L. gibbus is a small, nonburrowing mite present at low to moderate incidence in domestic rabbits. It is an obligate parasite, completing all stages of the life cycle on the host. 2. Clinical Signs: This mite is currently considered non-pathogenic and is found primarily on the back and abdomen. 3. Diagnosis: The hair shafts can be examined under a dissecting microscope or with hand lens for the characteristic brown mite or its nits.

Fur Mite

Control: Isolate infected animals. Topical acaricides and ivermectin as described for cheyletiella are thought to be effective in treatment.

VII. Fleas and Lice

Fleas and Lice

Rabbits are commonly infested with Ctenocephalides sp., especially C. felis. The infestation may be asymptomatic, but may induce mild pruritis and alopecia. Rabbits can be dusted and sprayed with pyrethrin products. Do not use the flea product Frontline in rabbits since rabbit deaths have been associated with its use. The environment should be treated to control this parasitism. Haemodipsus ventricosis (Blood Sucking Louse).

The anapleurid louse is rarely found on domestic rabbits. Weakness, anemia, ruffled fur and pruritis (secondary dermatitis) are common signs of infection. Fleas and Lice

The pelt can be examined with a dissecting microscope or a hand lens. Nits, as well as the adult anopleurid louse (head narrower than body), may be found on the hair. Rabbits should be treated with pyrethrin products, silica gel acaricides or ivermectin (0.2 to 0.4 mg/kg SubQ) at 10 day intervals for 2 treatments. This louse spends its entire life cycle on the rabbit with little horizontal transmission. Isolation is an effective means of control while treating the infected rabbit.

VIII. Cuterebra Infestation

Cuterebrid flies

Cuterebrid flies known as rabbit warble flies. Cuterebriasis occurs mostly in wild rabbits, but may occur in domestic rabbits housed outdoors. Incidence peaks in the summer and late fall. Single or multiple large subcutaneous swellings containing encysted larvae with a fistula in the center are the characteristic lesions (left photo). When the larval fly is ready to pupate, it leaves the swelling and drops to the ground (right photo). Secondary bacterial infections may complicate the disease.

Cuterebrid flies

These lesions are treated by removing the larva (without crushing it) and flushing the wound, or by surgical resection of the wound. Prevention of infestation includes moving the cage indoors, or by surrounding the hutch with screen to prevent fly exposure

Cuterebrid flies

Myiasis •Outside housed rabbits •Fly eggs laid in open wound •Underlying causes •Depression, skin eroded/necrotic •Check skin folds, perineum, entry into body cavities •Tx – Clipping, cleaning larvae removal (surgery)

Viral diseases

VIRALDISEASES I. Myxoma Virus II. Rabbit (Shope) Fibroma Virus III. Rabbit (Shope) Papilloma Virus IV. Rabbit Oral Papilloma Virus V. Viral Hemorrhagic Disease (Viral Hemorrhagic Fever, Viral Necrotizing Hepatitis)

I. Myxoma Virus Myxoma V

A. Etiology: Myxomatosis is caused by any one of several strains of myxoma virus, a member of the leporipoxvirus group. Virulence of the different strains ranges from a mortality incidence of 99% in European rabbits to less than 30%. Incidence is high in endemic areas in the Pacific coastal states. B. Transmission: The principal mode of transmission is via arthropod vectors (mosquitoes, fleas, flies, gnats). Transmission may also occur by contact with infected material from ocular discharges or oozing skin lesions of infected rabbits, contaminated spines of thistles, and the claws of predatory birds. Virus-infected skin nodules on wild rabbits, Syvilagus sp., are reservoirs of the agent.

C. Symptoms: In domestic rabbits, the clinical disease picture is largely predicated by the strain of virus involved as well as genetic resistance of the breed of rabbit. Myxoma V

California Strain of Virus: In the peracute form, rabbits die within a week of exposure showing slight edema of the eyelids and depression immediately prior to death. With the acute form in which rabbits survive for 1 to 2 weeks, symptoms are edema of the eyelids resulting in a droopy appearance of the eye; inflammation and edema around the anal, genital, oral, and nasal orifices; skin hemorrhages; and convulsions. A nodular lesion develops at the site of inoculation with both forms, but it is not a clearly defined tumor.

Myxoma V

Standard Laboratory Strain of Virus: This strain induces a mean survival time of 11 days. Around 3 to 4 days post inoculation, a primary tumor becomes evident, and generalized tumors are seen on the 6th or 7th day. At this time, a mucopurulent nasal discharge and pronounced edema of the eyes and base of the ears are seen. By day 10, hard lumps cover much of the body.

D. Pathology:

Myxoma V

The most prominent gross lesions are skin tumors and pronounced cutaneous and subcutaneous edema. Skin hemorrhages and subserosal petechial and ecchymotic hemorrhages in the stomach and intestines may be observed. Various degrees of congestion will occur in the visceral organs depending on the severity of the disease. Skin tumors {Epidermal cells overlying the tumor may appear normal in early stages of the tumor proliferation, or they may show hyperplasia or degeneration in later stages. Intracytoplasmic inclusions (arrows) are observed most commonly in cells of the prickle-cell layer of the epidermis, and in the stellate myxomatous cells}.

F. Diagnosis: A diagnosis can be made from the clinical and pathological picture, virus isolation, and PCR amplification of viral sequences from tissue specimens. Serological tests including fluorescent antibody techniques, plaque-neutralization, and ELISA have been developed but are not commercially available. Myxoma V

G. Control: Control is achieved through vector control and adequate screening of the rabbitry, by quarantine of new animals, and isolation of all sick animals. A common practice, once a death from myxomatosis is diagnosed, is to cull all rabbits whose body temperature exceeds 40oC in an attempt to remove animals incubating the virus before shedding occurs. A vaccine was developed but has not been used as the vaccine caused clinical myxomatosis in some vaccinated rabbits.

Rabbit Fibroma V

II. Rabbit (Shope) Fibroma Virus A. Etiology: Fibroma virus is a member of the leporipoxvirus group and is closely related to myxoma virus. The virus has widespread incidence in both domestic and wild rabbit populations. (USA) B. Transmission: The natural transmission cycle is not known although arthropod vector transmission is likely.

Rabbit Fibroma V

C. Clinical Signs: Tumors occur on the legs or feet, on the muzzle, and around the eyes. The tumors are subcutaneous and not attached to underlying tissue. Metastases from the original tumor do not occur. The infected adult rabbit remains clinically normal otherwise. Tumors will typically regress after a period of months. Spontaneous and experimental infections of neonatal domestic rabbits, however, has produced cutaneous and visceral tumors.

Rabbit Fibroma V

E. Diagnosis: Clinical signs and lesion morphology are primary diagnostic tools. F. Control: This is not considered to be an important problem in domestic rabbits. In outdoor rabbitries, vector control is advised.

III. Rabbit (Shope) Papilloma Virus

Rabbit Papilloma

A. Etiology: A member of the papovavirus group. This disease is seen most frequently in cottontail rabbits of the Midwest with outbreaks in domestic rabbits. Incidence of disease is low. B. Transmission: Arthropod vector transmission of the natural disease has been demonstrated. The mosquito is thought to be the main vector in transmission from feral to domestic rabbits. C. Clinical Signs: Horny warts are found on the eyelids and ears. The growths are well keratinized, and the upper surface is irregular and split. The growths are easily scratched or knocked off. These sites later heal without complication.

IV. Rabbit Oral Papilloma Virus

Oral Papilloma

A. Etiology: A member of the papovavirus group, this virus is the only member of the papovavirus group having the domestic rabbit as its natural host. There is moderate incidence of disease. B. Transmission: Spread is by direct contact of oral secretions containing sloughed epithelial cells from the oral warts. Infection occurs in the abraded epithelium of the tongue. C. Clinical Signs: This is a benign disease characterized by numerous whitish growths on the underside of the tongue, oral cavity epithelium or gingiva. These later become pedunculated and ultimately ulcerate. The growths regress when the rabbit becomes immune.

V. Viral Hemorrhagic Disease (Viral Hemorrhagic Fever, Viral Necrotizing Hepatitis) VHD

The disease was first reported in China in 1984, and has since been reported in Europe, parts of Asia, Mexico and the United States. A. Etiology: A calicivirus has been recovered from infected rabbits. Apparently strains of virus with varying degrees of virulence have been recovered from rabbits from different parts of the world. B. Transmission: The agent can be spread by direct contact, biting arthropods and fomites, including handling of infected rabbit meat and by-products.

Rabbit Hemorrhagic Disease Rabbit, liver. All liver lobes are swollen, pale and have a reticular pattern

Rabbit Hemorrhagic Disease Rabbit, liver. There is a large area of pallor (necrosis) with a prominent reticular pattern

Rabbit Hemorrhagic Disease Rabbit, liver. This chronically affected liver contains pale areas of postnecrotic scarring

Rabbit Hemorrhagic Disease Rabbit, kidney. There are petechiae throughout the cortex and the medulla is severely congested

Rabbit Hemorrhagic Disease Rabbit, lungs. The trachea is filled with foam, and the lungs are mottled and noncollapsed (severe pulmonary edema

Rabbit Hemorrhagic Disease Rabbit, heart. There are multiple epicardial hemorrhages

Inherited diseases

INHERITEDDISEASES I. Malocclusion II. Buphthalmia III. Splay Leg IV. Hydrocephalus

Malocclusion

I. Malocclusion

There are both hereditary and environmental causes of malocclusion. Hereditary mandibular prognathism is apparent by 3 weeks of life and is due to an autosomal recessive trait with incomplete penetrance. Malocclusion of premolars and molars has been reported in older rabbits. As a rabbit's incisor teeth grow 10 CM per year, it is necessary to clip them (but not too close) every 6 to 8 weeks.

Dog nail clippers, bone or wire cutters and a rotary tool with disc attachment may be used to trim teeth. Care should be taken to prevent shattering the incisors. .

Malocclusion

Buphthalmia

II. Buphthalmia

ยง It is a congenital glaucoma caused by an autosomal recessive defect with incomplete penetrance. ยง There is abnormal production and removal of aqueous from the anterior chamber. ยง Clinical signs may occur as early as 2 to 3 weeks of age, but are more common at 3 to 4 months of age. ยง Signs include slight cloudiness progressing to increasing cloudiness of the cornea, a prominent eyeball, conjunctivitis, keratitis, ulceration, and rupture of the cornea. ยง The condition may be unilateral or bilateral.

Buphthalmia

Splay Leg

III. Splay Leg

Is a familial or polygenic condition with varying clinical manifestations. Affected rabbits cannot adduct affected limbs. The condition may affect one or more limbs. Starvation due to inability to reach food or water dishes may occur. Autosomal recessive with incomplete penetrance. and some homozygous recessives will even be phenotypically normal.

Splay Leg

Splay Leg (R=normal)

Hydrocephalus

IV. Hydrocephalus Ă&#x2DC;The mode of inheritance of this trait is questionable but has been reported to be autosomal recessive associated with dwarfing and brachygnathism. Ă&#x2DC;Vitamin A deficiency in pregnant does may cause hydrocephalic young to be born. Ă&#x2DC;Vitamin A toxicity of gravid does has also been suspected of causing skeletal abnormalities (limb deformities, large fontanels) and hydrocephalus in stillborn term offspring as has been reported in toxicities in humans.

Miscellaneous

MISCELLANEOUS DISEASES I. Hairballs (Trichobezoar) II. Traumatic Vertebral Fracture (Paralysis of the Hindquarters, Broken Back) III. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis IV. Enterotoxemia V. Heat Prostration VI. Sore Hocks (Ulcerative Pododermatitis) VII. Dermatophytosis VIII. Pregnancy Toxemia

e l l a n e o u s

I. Hairballs (Gastric Tricho-bezoar) Hair ball

A. Etiology: Hairballs can form in the stomach as the rabbit grooms itself or a cagemate. Insufficient fiber in the diet can also lead to increased hair consumption. Incidence of hairball formation is high although abnormal digestive function pribably rarely occurs unless the hair ball is extensive. B. Clinical Signs: Generally, hairballs are not a problem and are found incidentally at necropsy. Occasionally, they will cause a partial or complete obstruction; these hairballs may be palpable, and the rabbit will stop eating and lose weight. The rabbit may be bright, alert and afebrile with a history of anorexia and lack of feces excretion of several days duration.

Destination of stomach due to hair ball Hair ball

Hair ball

C. Diagnosis: Palpation and contrast radiography. Diagnosis

D. Treatment: Treatments are centered on correcting dehydration and re-establishing normal gut function. Rehydrate rabbit and administer enteral protectants.

Administration of metaclopromide (0.3 mg/kg SQ every 8 hours) will help stimulate peristalsis, and often will stimulate the rabbit's appetite. Force feeding of pulverized food in water or yogurt may help stimulate the appetite. E. Prevention: Diets high in plant fiber has dramtically reduced the incidence of the clinical syndrome.

Hair ball

Palpation

treatment

Gastrotomy

opened stomach with the hair mat.

Hair ball

II. Traumatic Vertebral Fracture (Paralysis of the Hindquarters, Broken Back) Broken back

A. Etiology: This condition has a sudden onset and coincides with struggling or inadequate support of the hindquarters when handling. Frequently, the incident is not observed (or recognized), and the rabbit is found paralyzed in the cage. The occurrence is frequent. B. Clinical Signs: Posterior paralysis or paresis, loss of skin sensation, and loss of motor control of anal sphinctor and urinary bladder are typical signs.

Broken back

C. Pathology: Broken back

The most common site of fracture is the L7 lumbar vertebral body or its caudal articular processes. D. Diagnosis: The diagnosis is made with clinical signs, neurological examination and/or radiography. E. Treatment: If bladder and anal sphinctor control remain intact, and there is still hind limb pain perception, complete recovery may occur within 2 to 4 weeks with cage rest. Surgical correction and fixation of the fracture is not recommended because of the fragility of the bones.

Clinical sign

Clinical signs

The clinical signs of dislocation or fracture range from hindlimb weakness to complete motor paralysis of the hind quarters, loss of skin sensation, and, possibly, loss of anal sphincter and bladder control.

III. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis Mucoid Enteropathy (ME)

A. Etiology: The cause(s) of the ME disease complex is not well defined and the disease is uncommon.. However, multiple factors including diet, intestinal flora and the shift from neonatal to adolescent digestive physiology are thought to contribute to development of the disease. Diets low in fiber (<10%) result in a higher incidence of ME. Escherichia coli, Clostridia sp. (C. welchii type A, C. perfringens) have been associated with ME.

Coccidiosis has also been incriminated in potentiating or triggering ME. (ME)

Search for viral agents has been unsuccessful. Reproduction of the disease by causing cecal impaction with subsequent bacterial toxin production, has been successful. B. Clinical Signs: There is acute onset of disease in 7 to 10 week old rabbits characterized by anorexia, polydipsia, a subnormal body temperature (37o-39oC), a rough hair coat, mucoid to liquid, tan diarrhea with perineal staining, and abdominal distention with gas and fluidfilled intestines.

Affected rabbits may grind their teeth. Death usually occurs in 2 to 4 days. Rabbits usually survive the protracted course of 7 to 14 days (ME)

C. Pathology: Grossly distended fluid and gas-filled stomach, watery duodenal and jejunal contents, pasty contents in ileum, dry matter and gas in cecum (often impacted), and gelatinous mucus in colon are frequently observed. The characteristic lesion is goblet cell hyperplasia with no inflammatory response in the small and large intestines; occasionally see goblet cell hyperplasia of gallbladder, pancreatic and bile duct epithelia, and tracheal epithelial cells may be noted.

(M E)

D. Diagnosis: histopathology.

Clinical signs, gross lesions, and (ME)

E. Treatment: Supportive therapy, providing alfalfa for fiber and cholestyramine to absorb toxins has been recommended. F. Control: Provision of high fiber feeds (18 - 20 % fiber) drastically reduces the incidence of mucoid enteropathy. Rabbits received after shipping should not be fed the first day. A small amount of a high fiber diet may be fed the next day, with a gradual increase to a full ration by day 5.

Enterotoxemia

IV. Enterotoxemia A. Etiology: Clostridial species, principally C. difficile and C. spiroforme, proliferate and produce toxins to induce this disease. ยง Clostridial exotoxins induce secretory and vascular effects. A history of antibiotic therapy with BS antibiotics including oral ampicillin, clindamycin or lincomycin, may be associated with this disease. ยง Clostridial enteritis may occur in rabbits that have not been treated with any antibiotics. Diets high in carbohydreates enhance the overgrowth of Clostridium species. Change in gut flora and other stressors leading to anorexia may predispose to disease.

PATHOGENESIS

B. Clinical Signs:

Enterotoxemia

Sudden death with no previous signs of illness or watery diarrhea 2 to 3 days prior to death are the usual signs. Affects all ages, primarily recently weaned rabbits. C. Pathology: Prominent gross lesions observed include in a large, fluid-filled edematous cecum with serosal congestion and hemorrhage and watery mucoid feces in the colon (A.). Microscopically, severe lesions include a necrotic erosive or ulcerative typhlitis with swelling and loss of enterocytes and pseudomembrane formation (B.). The mucosa and submucosa are infiltrated with heterophils and there is submucosal edema and hemorrhage. Large Gram-positive bacilli with spores can often be observed on the mucosal surface.

Enterotoxemia

Enterotoxemi a

D. Diagnosis: Diagnosis is achieved by the history of antibiotic treatment or environmental/dietary stressors, and isolation or PCR amplification of Clostridium species from cecal contents. An antigen capture ELISA is available for cytotoxins A and B of C. difficile. C. spiroforme may be seen as a spiral bacillus on a direct smear. E. Treatment: Due to the acute course of the disease, there is usually no treatment. Supportive fluid therapy, kaopectate, and yogurt may be helpful. F. Control: Do not use lincomycin or clindamycin in rabbits. Eliminate extreme dietary changes and minimize environmental stressors.

V. Heat Prostration

Heat Prostration

Rabbits are very sensitive to heat. Tachypnea, cyanosis, prostration, and blood-tinged fluid on nose and mouth may be observed with heat prostration. Temperatures above 35 oC can be dangerous. The rabbit should be immersed in cool water, or covered with alcohol or water soaked cloths. The rectal temperature should be monitored to ensure reduction of body heat and to prevent induction of hypothermia. Housing in shaded areas provided with fans or water sprays in hot weather will keep rabbits cool. Limit feeding of rabbit food will prevent obesity, which may be an additional predisposing factor to overheating.

Heat Prostration

Initial stage.

Extreme exhaustion.

VI. Sore Hocks (Ulcerative Pododermatitis)

Sore hocks

Sore hocks occur because of pressure necrosis of the skin from bearing a heavy body weight on a hard or wire surface. There is genetic predisposition in breeds such as the Rex which have poorly furred footpads and rounded metacarpal bones . Common findings are circumscribed ulcers over the metatarsus and metacarpus, covered by a scab. There may be purulent exudate under the scab.

Severely affected rabbits may be anorexic, debilitated, and die. Sore hocks

Use soft dry bedding, a resting board in wire cages, and topical zinc and iodine ointments or an antibiotic ointment if secondarily infected. Use systemic antibiotics if abscesses are present or if the rabbit is debilitated. Cull affected animals and do not use for breeding stock. Decrease environmental humidity. Caution: Fecal pellets need to be brushed off the resting board daily to prevent ingestion of infective parasite ova/oocysts.

Sore hocks

Foot sores

Pododermatitis

Predisposing factors for pododermatitis include a rough cage floor such as woven wire, a heavy, mature animal and, according to some, overgrown toenails. Pododermatitis

A smooth, impervious resting board should be provided for the rabbit. If the animal is overweight, it should be placed on a restricted diet

Pododermatitis

Dermatop hytosis

VII. Dermatophytosis A. Etiology: Trichophyton mentagrophytes is an opportunistic, ubiquitous fungal soil organism. B. Incidence: There is high incidence of the carrier state, with low incidence of disease. C. Clinical Signs: A crusty, pruritic, patchy alopecia on the head which spreads to the paws and other parts of the body is typical (see photo). Secondary bacterial infections are common. D. Diagnosis: Based on clinical signs, scraping and identification of spores on hair shaft or mycelia within hair shaft, and culture on Sabaraud or DTM agars.

Dermatophytosis

E. Treatment: Topical treatment with a fungicide (Tresiderm, Iodine, Conofite cream) or griseofulvin (25 mg/kg in aqueous suspension or 0.375 gm powdered form/lb food for 14 days) has been successful. Topical 10% chlorox solution is also effective. Griseofulvin therapy should be used with caution in breeding herds, as the incidence of teratogenesis is associated with treatment.

Dermatophytosis

F. Control: Disinfect cage and nest boxes with 10% bleach solution. There is a possibility of transmission of infection to people handling the rabbits, so gloves should be worn when treating the rabbits. Ventilation should be improved to decrease the relative humidity, and all filters, water pads, curtains/blinds or other materials used to control the air temperature should be replaced weekly to prevent collection of fungus spores.

VIII. Pregnancy Toxemia

Pregnanc y Toxemia

A. Etiology: The pathogenesis of pregnancy toxemia is not well known, but may be similar to ketosis in sheep. Predisposing factors include breed, age, sex, obesity, and number of previous litters. There is a high incidence in some rabbitries. B. Clinical Signs: Signs range from a mild, nearly asymptomatic condition to a severe, rapidly fatal disease. The most common signs are depression, dyspnea, acetic odor to the breath, decreased urine production, abortion, CNS signs, and sudden death just prior to or just after kindling.

Pregnancy Toxemia

C. Pathology:

Gross lesions are general obesity, areas of necrosis in the mesenteric fat, and pale yellow liver, heart, and kidneys. Fatty changes are seen microscopically in the liver, heart, and kidneys. D. Control: Weight gain in breeding and non-pregnant does should be monitored, and controlled by limiting the amount of feed they are allowed to consume.

Urolithiasis Etiology Diet, infection (rare) Unusual calcium metabolism Urinary fraction excretion rate Mammals = 2%, rabbits = 45-60% Dietary levels â&#x20AC;&#x201C; urine levels

Clinical signs Anorexia, weight loss, depression, pain urine staining, anuria, dysuria Diagnosis Palpation, radiographs, urinalysis

Treatment Dietary modification, bladder flushing, cystotomy

Moist dermatitis resulted from drooling. The gross lesions consist of inflammation, alopecia, ulceration, and necrosis of the affected skin. Chronic wetness associated with dental problems, leaking watering systems, or continual contact with urine as result of poor husbandry practices predispose to the condition The underlying conditions causing chronic wetness must be identified and corrected. Then the animal can be treated by clipping nearby hair and applying mild antiseptic scrubs and antibiotic ointments

Moist dermatitis

Overgrown teeth

Overgrown Teeth Overgrown teeth

ØRabbit teeth grow continuously throughout their lives. ØNormal chewing action wears them down just to the point that they don't overgrow. ØThis is one of the reasons it is important to feed your rabbit a high fiber diet. ØA rabbit that has a malocclusion does not have this normal wearing action and can suffer overgrown teeth. ØThis problem can be serious enough to inhibit the ability to eat. ØMost rabbits do fine if their teeth are trimmed periodically.

Overgrown teeth

On select cases we will remove the problem teeth.

Treatment This patient has overgrown lower incisors. They are definitely inhibiting its ability to chew. They need periodic trimming every 2-4 weeks to prevent recurrence.

Overgrown teeth

Overgrown

They are trimmed with a special scissors that will not crack them. If needed, they are also filed to remove any sharp edges. This technique should not be tried by inexperienced people because teeth are brittle in nature, and in this case are weaker than normal due to the abnormality. They can easily fracture because of these two factors. In addition, rabbits can fracture their back if not properly restrained.

Overgrown trim

Overgrown teeth

â&#x2DC;ťEven though the upper incisors are not as long as the lower, they also need trimming because they are growing into the lower jaw. â&#x2DC;ťEven though the upper incisors are not as long as the lower, they also need trimming because they are growing into the lower jaw.

Overgrown teeth

â&#x2DC;ťOur friend feels much better, and can now get back to normal rabbit activity. â&#x2DC;ťHe needs to return in 2-4 weeks to have his teeth checked.

Ove rgro wn teet h

Overgrown teeth

â&#x2DC;ťThis rabbit has an upper right incisor (arrow) that has been chronically infected. â&#x2DC;ťWe decided to remove the incisors because trimming the teeth was not solving the problem.

Overgrown teeth

Removal infected incisor

☻As you saw from the x-ray pictures the roots of these incisors are very deep and they curve significantly. ☻Great care must be taken during their removal so they don't crack at the root. ☻In this picture we are gently breaking down the attachment of the tooth to the gums.

Removal

After Removal

This is the appearance immediately after surgery.

◆In some rabbits the problem is much more serious than overgrown and unsightly incisors. ◆These rabbits have severe problems with their molar teeth, preventing them from eating properly. If untreated they can die. ◆A large part of their problem is a diet that is too low in fiber. ◆This causes improper wearing down of the molars, and even can lead to elongation of the roots of the incisors. ◆Rabbits with this problem are not eating well, losing weight, and are slobbering. ◆Looking into a rabbits mouth is not the easiest thing in the world to do.

These roots are normal. The arrow on the left points to the incisors, the one below points to the molars. Can you see the difference in the molars from the abnormal rabbit above.

Overgrown molar teeth

Ove rgro wn mol ar teet h

Now that Mike is finally anesthetized we can gain access to his molar teeth. The white arrow points to one of them deep in his oral cavity.

These are the teeth immediately after removal. Removed teeth

The roots are on the bottom.

A close up of one of them shows the infection around the root (on the right). Removed infected tooth

Prevention of overgrowth

Prevention ☻One of the most important things you can do to keep your rabbit's teeth healthy is to feed a high fiber diet. This consists of mostly timothy hay or timothy hay pellets. ☻Regular exams by one of our doctors will also catch this problem before teeth get infected or your rabbit becomes ill.

Rabbit neuter

Rabbit Neuter (castration) ☻Male rabbits are neutered (castrated) for a variety of reasons. ☻It helps minimize fighting behavior, makes it impossible to impregnate females, and prevents testicular cancer. ☻Here is the more traditional ways rabbits have been neutered. ☻Also, how we do it with the laser.

Rabbit Neuter

The reason the male rabbit in the following slide has one testicle substantially larger than the other is due to cancer. Removal of this testicle is needed for treatment. If this buck had been neutered at a young age this problem would not have occurred.

Rabbit Neuter

☻The followings are the normal testicles of a rabbit about to undergo a neuter. ☻The hair has been clipped on the abdomen and the surgical site has been cleaned. ☻The arrow points towards the head.

Rabbit Neuter

☻Using laser for neuters. ☻It has significant advantages over the scalpel blade. ☻In this picture just starting the laser incision.

Rabbit Neuter

â&#x2DC;ťWith the laser there is no bleeding and much less postoperative pain and swelling. â&#x2DC;ťYou can see the testicle appearing on the left where the scrotum has been incised by the laser.

Rabbit Neuter

☻After the testicle is gently pulled out of the scrotum it is ligated with 2 sutures before it is cut off. Rabbit Neuter

☻You can see the first suture at the bottom (arrow). ☻Again, bleeding.

note

the

lack

Rabbit Neuter

â&#x2DC;ťInstead of sutures we seal the scrotum with a special adhesive. â&#x2DC;ťThis minimizes surgical time, there is no post-operative discomfort or itchiness from sutures, and you do not need to return for suture removal.

Rabbit Neuter

NE OP LAS TIC S

Neoplastics

NEOPLASTIC DISEASES I. Uterine Adenocarcinoma II. Lymphosarcoma III. Miscellaneous Neoplastic Diseases

Neoplastics

The incidence of spontaneously occurring tumors in rabbits is generally low. Only recently has the pet rabbit population survived long enough to permit data collection on tumor incidence. As with other species, tumor incidence is influenced by such factors as age, breed predilection for certain tumors, breed resistance, and sex.

I. Uterine Adenocarcinoma

Uterine Neoplastic

☻ The most common tumor of rabbits is the uterine adenocarcinoma. ☻Females have a history of reproductive disturbance prior to detection of the tumor. ☻Fertility is diminished, litter size is reduced, stillbirths are more numerous, and desertion of the litter by the doe is common. ☻Other symptoms are dystocia, fetal retention in utero, abdominal pregnancy, and fetal resorption.

☻The period of altered reproductive function precedes tumor detection by 6 to 10 months. Uterine Neoplastic

☻The duration in time between clinical detection and death (usually postmetastasis) is 12 to 24 months. ☻Uterine nodules can be palated or observed on radiographs or laparatomy. ☻The incidence of neoplasia is most common in New Zealand rabbits but has been observed in other rabbit breeds.

Palpation

Uterine Neoplastic

Uterine adeno-carcinoma

Uterine Neoplastic

Is the most common neoplasm of rabbits. Firm, ovoid, hemorrhagic nodules form along the mesometrial junction. They can be seen on either side of the cervix in this image. They are usually 1-5 cm in diameter and regularly spaced. The time course of the disease may be five to twenty months. Late in the disease, metastasis occurs, and death results.

Uterine Neoplastic

Nutritional deficiencies

Vitamin E

Vitamin E deficiency Causes: The recommended level of vitamin E is 40 mg of alpha tocopherol per kg of feed. Deficiencies occur if there is an insufficient amount of the vitamin in the feed or an increased requirement for the vitamin. Increased requirements are associated with liver disease, such as coccidiosis, or if the animals are on a diet high in unsaturated fatty acids.

Vitamin E

Signs The signs of vitamin E deficiency are muscular stiffness, weak knees, reduced feed consumption, loss of weight, neonatal mortality, and infertility. There will be creatinuria and increased serum creatine phosphokinase.

Vitamin E

Vitamin E deficiency The gross lesions of vitamin E deficiency are muscle atrophy and extreme paleness of the muscle. The paravertebral muscles, diaphragm, masseter, and voluntary mucles of the rear leg are commonly affected. Histologically, hyaline degeneration of muscle fibers can be seen, with loss of striations, clumping of sarcoplasm, atrophy of muscle fibers,

Vitamin E

Treatment

Treatment consists of administering di-alpha tocopherol intramuscularly, as shown, or orally, 15 mg/kg of body weight for 7 days.

Vitamin E

VITAMIN A DEFICIENCY

Signs of Vitamin A Deficiency Signs of Vit A deficiency

The clinical manifestations of Vitamin A deficiency include: droopy ears as seen on this image. This is due to weakening of cartilage. Other signs are retarded growth and eye lesions. Eye lesions start as cloudy corneas and advance to full blown keratitis and blindness.

Droopy ears

Pup with hydrocephalus Hydrocephalus

Vitamin A deficiency fertility in both sexes.

impairs

Fetuses may be aborted or reabsorbed, or born with hydrocephalus, as shown in the lower pup on this image.

Hydrocephalus

Neurologic deficiency

Rabbit with neurologic deficiency Bone deformities and neurologic disturbances are seen in advanced states of Vitamin A deficiency.

Neurologic deficiency

II. Lymphosarcoma Lymphosarcoma

☺ The second most common rabbit neoplasm is the lymphosarcoma. ☺Susceptibility to the disease is believed due to an autosomal recessive gene expressed in the homozygous state. ☺It is considered a tumor of juvenile and young adult rabbits. ☺A tetrad of necropsy lesions considered pathognomonic for lymphosarcoma in the domestic rabbit are:

L y m p h o s a r c o m a

1) enlarged kidneys, light tan in color with irregular lumpy surface, and thickened cortex but normal medulla; 2) hepatomegaly with a diffuse pattern of small pale foci; 3) splenomegaly; and 4) lymphadenopathy, in which all of the lymph nodes in the body may be involved in the neoplastic process. Histologically, the normal architecture of the nodes is obliterated by masses of infiltrating neoplastic lymphoblasts.

Kidney Lymphosarcoma

III. Miscellaneous Neoplastic Diseases Miscellaneous Neoplastics

Other commonly reported tumors of the rabbit are Embryonal nephromas, Bile duct adenomas, Mammary gland papillomas, Mammary adenocarcinomas, and Squamous cell carcinoma.

ZOONOTIC DISEASES

Zoonotic

ZOONOTIC DISEASES I.Dermatophytosis II. Encephalitozoonosis III. Salmonellosis IV. Tularemia V. listeriosis

Dermatophytosis

I. Dermatophytosis

A. Etiology: Trichophyton mentagrophytes is an opportunistic, ubiquitous fungal soil organism. B. Incidence: There is high incidence of the carrier state, with low incidence of disease. C. Clinical Signs: A crusty, pruritic, patchy alopecia on the head which spreads to the paws and other parts of the body is typical (see photo). Secondary bacterial infections are common. D. Diagnosis: Diagnosis is based on clinical signs, scraping and identification of spores on hair shaft or mycelia within hair shaft, and culture on Sabaraud or DTM agars.

Dermatophytosis

Treatment

E. Treatment: 첫Topical treatment with a fungicide (Tresiderm, Iodine, Conofite cream) or 첫griseofulvin (25 mg/kg in aqueous suspension or 0.375 gm powdered form/lb food for 14 days) has been successful. 첫Topical 10% chlorox solution is also effective. 첫Griseofulvin therapy should be used with caution in breeding herds, as the incidence of teratogenesis is associated with treatment.

Control

F. Control: 첫Disinfect cage and nest boxes with 10% bleach solution. 첫There is a possibility of transmission of infection to people handling the rabbits, so gloves should be worn when treating the rabbits. 첫Ventilation should be improved to decrease the relative humidity, and all filters, water pads, curtains/blinds or other materials used to control the air temperature should be replaced weekly to prevent collection of fungus spores.

III. Salmonellosis

Salmonellosis

A. Etiology: Salmonella enterica serovars are G -ve aerobic, nonlactose fermenting, H2S producing rods. B. Transmission: Ingestion through direct contact with contaminated feces, food. Incidence of infection is rare. C. Clinical Signs: Acute disease is characterized by anorexia, fever, dehydration, diarrhea (hemorrhagic), death, and abortions. Rabbits that recover from acute disease are asymptomatic shedders. D. Pathology: Lesions are consistent with those of septicemia and include congestion and hemorrhage of the viscera associated with septicemia, ulcerative colitis, and focal necrosis of liver.

E. Diagnosis:

Salmonellosis

Definitive diagnosis is made by isolation of the bacteria through culture of blood, spleen, mesenteric lymph nodes and feces on selective media (brilliant green, selenite, citrate, or tetrathionate). F. Treatment: Since antibiotic therapy does not eliminate bacterial carriage, it is advisable to eliminate the colony and restock. G. Control: Good management practices will prevent infection. Disinfection, replacement with clean stock and prevention of wild bird or rodent contamination of bedding, water, or food should prevent future or continued problems.

IV. Tularemia

Tularamia

A. Etiology: Francisella tularensis is a G-ve, pleomorphic rod. B. Transmission: Blood sucking arthropods (squirrel flea, deerfly, mosquitoes, lice) as mechanical or biological vectors. Direct contact, ingestion, or aerosol (rare). The incidence of infection in domestic rabbits is rare. C. Clinical Signs: Depression, anorexia, ataxia, and death are the nonspecific signs associated with this disease. D. Gross Pathology: Widespread visceral congestion, splenomegaly, consolidated and congested lungs, and multiple pinpoint white foci on the liver and spleen are characteristic lesions.

Tularami a

Hepatic necrosis

V. listeriosis Etiology Listeriosis usually results from infection by Listeria monocytogenes, a Gram positive rod in the family Listeriaceae Transmission The reservoirs of infection are the soil &Infected animals can shed L. monocytogenes in the feces, milk and uterine discharges.It is also found in aborted fetuses and occasionally in the nasal discharges and urine of symptomatic animals

Clinical Signs meningitis, meningoencephalitis or, less frequently, septicemia. The clinical signs of a central nervous system (CNS) infection may include confusion, seizures, cranial nerve deficits, ataxia, tremors or myoclonus. Brain abscesses are also seen. Other conditions that have been reported are endocarditis, septic arthritis, osteomyelitis and rare cases of pneumonia The gross lesions were characteristic of, but not diagnostic for, a number of disease entities of rabbits. In this rabbit, lesions included necrosis of the liver, uterus, and adrenal gland Grossly, the liver had diffusely scattered miliary white foci which, on cut surface, extended into the parenchyma. The uterus was darkened with multiple serosal ecchymotic hemorrhages, and contained placentomes and fetuses in various stages of decomposition