Diseases of Hedgehogs

Dilated cardiomyopathy (see Cardiomyopathies) is a common postmortem finding, with an incidence of 38% in captive African hedgehogs. The etiology is not known; however, genetic and nutritional causes have been suggested. Affected hedgehogs are typically ≥ 3 yr old, although it may be seen in animals as young as 1 yr of age. Males are slightly overrepresented. Signs include dyspnea, decreased activity, weight loss, an auscultable murmur, ascites, and acute death. Radiographs typically demonstrate varying degrees of cardiac enlargement, pulmonary edema, pleural effusion, hepatic congestion, and abdominal fluid. Common gross necropsy findings associated with cardiovascular disease in hedgehogs include cardiomegaly, hepatomegaly, pulmonary edema and/or congestion, hydrothorax, ascites, and pulmonary or renal infarcts. Normal echocardiographic measurements have been published for the African pygmy hedgehog. These reference intervals, along with subjective evaluation of wall motion and chamber size, can be used to confirm the diagnosis of dilated cardiomyopathy. Hematologic and biochemical testing are useful to screen for concurrent problems and to monitor the effects of therapeutic agents. Therapy with furosemide, enalapril, and digoxin may be helpful. Alternatively, furosemide, pimobendan, and supplementation with oral carnitine have been used. The longterm prognosis for hedgehogs with congestive heart failure is poor.

Saddle thrombus and pulmonary thromboemboli have been seen. Myocardial mineralization and splenic extramedullary hematopoiesis may exist in pet hedgehogs with concurrent diseases; the clinical significance of these lesions is unknown. Congenital erythropoietic porphyria was reported in a 6-mo-old male inbred pet African hedgehog.

GI obstructions are most often caused by ingestion of rubber, hair, or carpet fibers. Signs include acute anorexia, lethargy, and collapse. Vomiting may be present but often is not. Diagnosis of obstruction is complicated by the fact that gaseous dilation of the GI tract can be a nonspecific finding in ill hedgehogs. A fatal intestinal mesenteric torsion has also been reported. Alimentary inflammation, including esophagitis, gastritis, enteritis, colitis, and gastric ulceration with perforation, has also been seen. Most of these hedgehogs had nonspecific signs such as decreased appetite and weight loss; vomiting and diarrhea were not seen. A case of gastroesophageal intussusception and megaesophagus has been reported in a hedgehog. This animal’s clinical signs included dyspnea, vocalization, and salivation; vomiting ensued before death.

Enteritis may be caused by Salmonella or other bacteria. Salmonellosis in hedgehogs may be clinically silent or may cause diarrhea, weight loss, decreased appetite, dehydration, lethargy, and death. Diagnosis should be confirmed with fecal culture, using Salmonella-enriching medium. Although treatment is indicated in hedgehogs with clinical signs of disease, owners should be advised of the zoonotic potential and the risks of creating antibiotic resistance. Alimentary candidiasis (Candida albicans) and cryptosporidiosis are other reported infectious diseases. Although numerous species of nematodes, cestodes, and protozoa have been identified in wild hedgehogs, their significance in pets appears to be minimal.

Diarrhea also can be associated with some commercial diets or inappropriate foods such as milk. GI neoplasia, particularly lymphosarcoma, is relatively common. Other considerations for GI signs include dietary change, toxins, hepatic disease, and malnutrition. Hedgehog digestion does not rely on bacterial fermentation, and there is no evidence of antibiotic sensitivity as is seen in herbivorous mammals. Hematochezia should be clearly differentiated from urinary or vaginal bloody discharge.

Hepatic lipidosis is relatively common and may be a sequela of cardiomyopathy, neoplasia, starvation, obesity, toxicosis, pregnancy, or infectious disease. Signs may include lethargy, inappetence, icterus, diarrhea, and signs of hepatic encephalopathy. Diagnosis is supported by testing for hepatic enzymes, plasma bilirubin, and bile acids. Radiography and ultrasound-guided liver aspirates may also be performed. Treatment for hepatic lipidosis is similar to that in other species. Other important causes of liver failure include primary and metastatic hepatic neoplasia. Hepatic necrosis caused by human herpes simplex virus 1 was reported in a hedgehog that received dexamethasone.

Acariasis caused by Caparinia spp (psoroptic mite) is very common. Infestation with Notoedres spp (sarcoptic mite) has also been reported in hedgehogs. Signs include lethargy, decreased appetite, hyperkeratosis, seborrhea, quill loss, loose quills, and white or brownish crusts (mite droppings) at the base of the quills and around the eyes. Hedgehogs may scratch or rub themselves, but many individuals do not have obvious pruritus. Some animals have subclinical infestations. Diagnosis is confirmed by identifying mites and eggs (nits) via skin scraping. Treatment consists of ivermectin or a combination of ivermectin and amitraz. All bedding must be removed, and cage furnishings disinfected or discarded. During treatment, the cage is lined with paper that must be changed daily. All hedgehogs in the home should be treated concurrently.

Pet hedgehogs may be infested with fleas; however, cat and dog fleas generally do not infest African pygmy hedgehogs. This is likely because of the hedgehog’s low body temperature. Treatment consists of topical or systemic flea control agents. Shampoo and powder products that are safe for kittens appear to be safe for hedgehogs. Tropical rat mites, Ornithonyssus bacoti, may also cause flaky skin and loss of spines; fipronil spray is an effective treatment.

Dermatophytosis is a common clinical disease in African pygmy hedgehogs; however, infection without significant clinical signs is also possible. Dermatophytes (Trichophyton erinacei, T mentagrophytes, Microsporum spp, and Arthroderma benhamiae) cause crusting dermatitis, especially around the face and pinnae. Quill loss may also be noted. Although some animals may scratch with the hindlimbs or rub against stationary objects, many individuals do not display signs of pruritus. Some infections are secondary to other dermatopathies, such as acariasis or trauma. Diagnosis is confirmed by culturing spines in dermatophyte test medium. Treatment consists of topical antifungal agents, with systemic griseofulvin or ketoconazole if needed. Lime-sulfur dips may also be used. Other hedgehogs in the home may be subclinically infected, and treatment of all animals is recommended.

Contact dermatitis may result from unsanitary bedding. Cellulitis has been linked to secondary myositis and sepsis; the primary cause in most of these cases was trauma. Staphylococcus simulans was reported to cause dermatitis characterized by a broad, well-circumscribed area of hyperkeratosis and alopecia on the back of a hedgehog. Allergic dermatitis has been anecdotally described; restricted antigen diets, antihistamines, and glucocorticoids may be helpful. Pruritus may be observed with development of new spines, as occurs in young hedgehogs. Pemphigus foliaceus has been reported; loss of spines, flaking skin, moist erythema, and epidermal collarettes were seen. Dexamethasone injections were reported to be an effective treatment.

Skin neoplasia is common. Squamous cell carcinoma, lymphosarcoma, and sebaceous gland carcinoma have been described. Papillomas of suspected viral etiology have been reported; recurrence in other sites after excision is common. Cutaneous and subcutaneous nodules may also be caused by abscesses, mycobacteriosis, and Cuterebra larvae.

Myositis secondary to cellulitis has been reported. Osteoarthritis has also been seen. Bone cysts should be considered as a differential for mandibular masses, along with neoplasia and trauma. Fractures can occur when a limb becomes entrapped in a wire cage or exercise wheel. Splinting can be performed for distal limb fractures. Surgical correction may also be performed, but any fixation device must be able to withstand the hedgehog's strong rolling-up mechanism. Lameness may be caused by ingrown toenails, arthritis, nutritional deficiencies, pododermatitis, constriction of a foot or digit by fibrous material, neurologic disease, or neoplasia.

Neoplasia in hedgehogs is very common in both sexes. A variety of tumor types affecting every body system has been reported. According to one survey, the body systems in which most tumors were found were the integumentary, hemolymphatic, alimentary, and endocrine systems. The most common tumors are mammary gland tumors, lymphosarcoma, and oral squamous cell carcinoma. The median age at time of diagnosis is 3.5 yr, although tumors may be seen in animals as young as 2 yr old. In one survey, > 80% of the tumors were malignant. Proliferative uterine tumors or polyps are common and are associated with vaginal bleeding, hematuria, and weight loss. Ovariohysterectomy allows prolonged survival of hedgehogs with uterine tumors. Some sarcomas have been associated with retroviral infection.

Signs depend on the location and severity of disease and may include palpable masses, weight loss, anorexia, lethargy, diarrhea, dyspnea, and ascites. Diagnosis is based on cytology or histopathology. Diagnostic imaging and blood testing may help determine the extent of the disease and establish a prognosis. Treatment generally includes surgical excision and supportive care, although other treatment modalities may be helpful. Not every mass in pet hedgehogs is neoplastic; for example, abscesses, bone cysts, papillomas, and uterine polyps are seen.

Neurologic signs (particularly ataxia) may be caused by torpor, hepatic encephalopathy, postpartum eclampsia, malnutrition, trauma, intervertebral disc disease, toxins, infarcts, infectious causes (eg, parasitic migration, rabies), otitis media, demyelination, polioencephalomalacia, or neoplasia.

Hedgehogs kept in cold (or sometimes excessively high) temperatures may enter a state of torpor or dormancy. In this state, the hedgehog has a greatly diminished response to stimulation, decreased heart and respiratory rates, and possibly increased susceptibility to infection. Dormancy can last for several weeks, during which the hedgehog may have periods of activity with ataxia.

Hypocalcemia may result from postpartum eclampsia, malnutrition, or for unknown reasons, and usually responds to calcium supplementation.

Intervertebral disc disease has been reported. Both cervical and lumbar lesions have been identified; multiple discs were affected in each of these hedgehogs. Radiographic findings included spondylosis, disc-space narrowing, and disc mineralization. Necropsy findings included degeneration of the nucleus pulposus and annulus fibrosus, dorsal extrusion of disc material, and mineralization of the nucleus pulposus. One case had evidence of fibrocartilaginous embolism. Temporary improvement with corticosteroids has been described in two cases of intervertebral disc disease.

Vestibular signs may be caused by otitis media/internal or central neurologic disease.

Demyelinating paralysis (wobbly hedgehog syndrome) occurs in as many as 10% of pet hedgehogs. Onset can occur at any age but is more common in animals <2 yr old. An early sign is the inability to close the hood. This progresses to mild, intermittent ataxia. The signs gradually increase in severity and include falling, tremors, exophthalmos, scoliosis, seizures, muscle atrophy, self-mutilation, and severe weight loss. The paralysis usually ascends from hindlimbs to forelimbs and usually leads to complete paralysis within 9–15 mo after the onset of signs. Death occurs within 18–25 mo. Appetite is usually normal until the terminal stages, when most hedgehogs become dysphagic. The diagnosis is confirmed at necropsy. Histopathologic lesions include vacuolization of white matter (cerebrum, cerebellum, brainstem, and spinal cord), axonal swelling, degeneration of spinal cord ventral tracts, and axonal and myelin degeneration in brain white matter. Peripheral nerves may also be involved. Inflammation of the CNS is not associated with wobbly hedgehog syndrome. The etiology is unknown, but a hereditary basis is suspected. Numerous treatments have been attempted without success. Euthanasia is warranted when the quality of life is compromised. A single case of pneumonia virus of mice in an African hedgehog with suspected wobbly hedgehog syndrome, resulting in nonsuppurative encephalitis with vacuolization of the white matter, has been reported.

Obesity is common. Healthy hedgehogs should be able to roll up completely, without any fat deposits protruding. Treatment includes reducing high-fat foods, rationing the main diet, and increasing exercise. Weight reduction should be gradual to prevent hepatic lipidosis, and owners should monitor their pet’s weight. Nutritional excess or deficiency may occur with unbalanced diets; for example, calcium deficiency may result from a diet consisting mainly of invertebrates. Moist diets may predispose hedgehogs to periodontal disease. Other nutritional diseases are uncommon.

Hedgehogs are prone to corneal ulcers and other ocular injuries. Diagnosis and treatment are as for other species, although administration of topical medication can be difficult. Blind hedgehogs navigate their captive environments with minimal detriment to their quality of life.

According to one report, ocular proptosis is relatively common and carries a poor prognosis for viability of the eye. Hedgehogs have a shallow orbit that may predispose them to proptosis, especially if excessive fat accumulation or orbital inflammation is present. Concurrent neurologic disease may result in ocular trauma.

Oral neoplasia, particularly squamous cell carcinoma, is common in hedgehogs. Dental disease, including calculus, gingivitis, and periodontitis, is also common. Periodontal disease is often associated with a bacterial component. The addition of abrasive items to the diet (eg, hard kibble, charcoal, or bone) and antibiotics are recommended for prevention and treatment of periodontal disease, respectively. Dental prophylaxis, periprocedural antibiotics, and tooth extraction may be necessary to treat severe dental disease. If advanced periodontal disease requires extraction of all the teeth, hedgehogs can be maintained on soft food. Tooth fractures and dental abscesses are also seen. Actinomyces infection has been reported; anaerobic culture and treatment should be considered for dental abscesses in hedgehogs.

Excessive tooth wear occurs in older hedgehogs, and hedgehogs with this condition should be fed a soft diet. Hedgehog teeth do not grow continuously and should not be trimmed. Hedgehogs are susceptible to wedging of hard items (eg, peanuts) against the palate. Stomatitis may develop in males that bite their mates; treatment is with soft food and antibiotics.

Pinnal dermatitis is common; skin crusts, accumulated secretions, and a ragged pinnal margin may be seen. Dermatophytes and acariasis are important causes; other possibilities include nutritional deficiencies, dry skin, seborrhea with hyperkeratosis, and extension of ear canal disease. Ear mites (Notoedres cati) are occasionally seen; signs, diagnosis, and treatment are as for cats (see Otodectic Mange). Bacterial or yeast otitis externa is also seen; these infections are often secondary to acariasis or another cause of chronic inflammation. Signs include purulent discharge, odor, and sensitivity of the face and ear. Otic cytology, skin scrapings, cleansing, and topical antimicrobial/anti-inflammatory therapy are used as for other species. Otitis media/interna can also be seen.

Posthitis may be caused by substrate entrapment in the prepuce. Hemorrhagic vulvar discharge is often caused by uterine neoplasia or endometrial polyps. Pyometra and metritis have been reported. Dystocia also is seen and treated as in other small mammals. Premature births occasionally occur; the prognosis for young without a suckling reflex is poor. Agalactia may be suspected if neonates lose condition within 72 hr after birth. Diagnosis may be confirmed by attempting to express the mammary glands; however, this usually requires anesthesia and may cause the dam to abandon or cannibalize her young. Causes of agalactia include malnutrition, stress, lack of oxytocin, inadequate mammary development in young females, and mastitis. Supportive care for weak neonates includes warming to normal body temperature over 1–3 hr, fluid support, and caloric support once normothermia has been achieved.

Predisposing factors for upper and lower respiratory tract infection are suboptimal environmental temperature; aromatic, dusty, or unsanitary bedding; concurrent disease causing immunocompromise; and aspiration of material from an oral infection. Signs include nasal discharge, increased respiratory noise, dyspnea, lethargy, inappetence, and sudden death. Radiographs, hematologic testing, and culture of tracheal or lung lobe aspirates are useful in diagnosis. Treatment includes antibiotics, nebulization, supportive care, and correction of underlying problems. Differential diagnoses for dyspnea are pulmonary neoplasia and cardiac disease.

A case of fatal corynebacterial bronchopneumonia has been reported in a pet African hedgehog. Pasteurella spp and Bordetella bronchiseptica can cause respiratory infections in European hedgehogs and are possibly important in Atelerix as well. Lungworms can also cause pneumonia, but this is unlikely in indoor pets. The existence of cytomegalovirus in African hedgehogs has been questioned; in any case, it is highly unlikely in domestically raised pets.

Cystitis and urolithiasis cause changes in urine color, stranguria, pollakiuria, inappetence, and lethargy. Urinalysis with culture and radiographs should be obtained. Renal disease is also common (50% prevalence in a necropsy survey) and in many cases may be secondary to systemic disease. Genetic or dietary factors may contribute to the high prevalence. Nephritis, tubular necrosis, nephrocalcinosis, glomerulosclerosis, renal infarcts, polycystic kidneys, neoplasia, and various glomerulonephropathies have been identified. Signs associated with renal disease tend to be nonspecific, although polyuria and/or polydipsia may be noted. Diagnosis should be based on urinalysis and serum chemistry panels. Treatment consists of correcting the underlying cause, fluid therapy, and supportive care.

Several strains of Salmonella are found in pet hedgehogs, including S Tilene, S Typhimurium, and S Enteritidis. Many cases of transmission to people have been documented, particularly in young children. It should be assumed that all pet hedgehogs can carry and transmit Salmonella. Because infected animals may shed intermittently, a negative culture cannot exclude the carrier state. Treatment aimed at eliminating the carrier state is unlikely to be successful and may lead to antibiotic resistance.

Human dermatophytosis from pet hedgehogs is also well documented. African pygmy hedgehogs can be subclinical carriers of Trichophyton mentagrophytes var erinacei, Microsporum spp, and Arthroderma benhamiae. In addition, some people are extremely sensitive to contact with African hedgehog spines and develop transient, markedly pruritic urticaria after handling a hedgehog.

Wild African hedgehogs are susceptible to foot-and-mouth disease. To prevent introduction of this disease to the USA, importation of African hedgehogs was banned by the USDA in 1991.

Rabies has not been reported in wild or captive African hedgehogs, but the salivation that occurs during anting is occasionally mistaken as a sign of rabies. A single report of rabies in a wild European hedgehog exists.

Human herpes simplex virus 1 was recovered from the liver of a pet African hedgehog that died acutely after glucocorticoid treatment for intervertebral disc disease. Monkeypox virus DNA was recovered from an African hedgehog housed with many other exotic species at a pet distributor facility in Illinois. Candida infection of the footpads and intestine of the African pygmy hedgehog has been reported. Acute intestinal cryptosporidiosis has been reported. A single case of Chagas’ disease (Trypanosoma cruzi) was reported in a captive African hedgehog housed outdoors in Texas.

African pygmy hedgehogs are considered susceptible to a variety of infectious agents, based on susceptibility observed in other hedgehog species. Possible bacterial zoonoses include Yersinia pseudotuberculosis, Y pestis, Mycobacterium marinum, M avium intracellulare, Coxiella burnetii (Q fever), and Leptospira spp. Possible viral zoonoses include Crimean-Congo hemorrhagic fever, arboviral tickborne encephalitides, and paramyxoviruses of the Morbillivirus group. Chlamydia psittaci and Toxoplasma gondii have been isolated from wild European hedgehogs.