Hedgehogs can develop a variety of illnesses, including cardiovascular disease, gastric ulceration, acariasis, neoplasia, dental problems, and pneumonia. Clinical signs are usually nonspecific, such as lethargy, weakness, and anorexia, which emphasizes the importance of diagnostic testing, despite the need for chemical restraint.
Cardiomyopathy is a common postmortem finding in captive African hedgehogs. The etiology of the disease is not known; however, genetic and nutritional causes have been suggested. Affected hedgehogs are typically ≥3 years, although cardiomyopathy may occur in animals as young as 1 year. Clinical signs include dyspnea, decreased activity, weight loss, an auscultable murmur, ascites, and acute death. Radiographic analysis can 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.
Suspected cardiac disease indicates a need for full-body imaging and a full cardiovascular examination, including ECG and an echocardiogram. Normal echocardiographic measurements have been published for African pygmy hedgehogs. Hematologic and biochemical testing are useful to screen for concurrent problems and to monitor the effects of therapeutic agents. Therapy with cardiovascular drugs commonly used in veterinary medicine to treat congestive heart failure (eg, diuretics, ACE inhibitors, pimobendan) may be helpful initially, but the longterm prognosis for hedgehogs with congestive heart failure is poor.
GI obstructions are often caused by ingestion of rubber, hair, or carpet fibers. Clinical signs include acute anorexia, lethargy, and collapse. Vomiting may occur. Marked gaseous dilation of the GI tract can be a nonspecific finding in ill hedgehogs, complicating diagnosis. Alimentary inflammation, including esophagitis, gastritis, enteritis, colitis, and gastric ulceration with perforation, has been reported. Most of the affected hedgehogs had nonspecific signs such as decreased appetite and weight loss; vomiting and diarrhea were not observed.
Enteritis may be caused by Salmonella or other bacteria. Salmonellosis in hedgehogs may be asymptomatic, may cause diarrhea, weight loss, decreased appetite, dehydration, lethargy, and death. Diagnosis should be confirmed with fecal culture testing, 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 antimicrobial resistance. Alimentary candidiasis (Candida albicans) and cryptosporidiosis are other reported infectious diseases. Many species of nematodes, cestodes, and protozoa have been identified in wild hedgehogs; however, they seem to be far less prevalent in pet hedgehogs.
Some commercial diets cause diarrhea, as do foods inappropriate for hedgehogs (ie, milk). GI neoplasia, particularly lymphosarcoma, is relatively common. Other considerations for GI signs include diet change, toxins, hepatic disease, and malnutrition. Hedgehog digestion does not rely on bacterial fermentation, and there is no evidence of antimicrobial sensitivity as occurs in small rodents and rabbits. Hematochezia must be differentiated from urinary or vaginal bloody discharge.
Hepatic lipidosis is somewhat common and may be a sequela of numerous disease processes. Clinical signs include lethargy, inappetence, icterus, diarrhea, and signs of hepatic encephalopathy. Obese animals may have subclinical hepatic lipidosis. Diagnosis is supported by testing for hepatic enzyme activities, plasma bilirubin and bile acid concentrations. Radiography and ultrasound-guided liver aspiration may also be performed. Treatment for hepatic lipidosis is similar to that in other species.
Acariasis caused by Caparinia tripilis (psoroptic mite) is very common. Both male and female C tripilis mites have three long setae on the third pair of legs. The mnemonic “three-on-three” may help with recollection. Infestation with Notoedres spp (sarcoptic mite) has also been reported in hedgehogs.
Clinical signs of acariasis include:
Hedgehogs may scratch or rub themselves, but many do not display evidence of pruritus. Some hedgehogs can harbor subclinical infestations. Diagnosis is confirmed by identifying mites and eggs (nits) via superficial skin scraping or tape impression. Treatment consists of administration of selamectin (20–30 mg/kg topically every 21–28 days) or ivermectin (0.3–0.4 mg/kg, PO or SC, every 10–14 days for 3–5 treatments). In some cases, ivermectin alone may not effectively treat mite infestations. Bedding must be removed, and any items in the cage must be disinfected or discarded. During treatment, the cage should be lined with paper that is changed daily. All hedgehogs in the home should be treated concurrently.
Dermatophytosis is a common clinical disease in African pygmy hedgehogs; however, infection without notable 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 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 administration of topical antifungals (eg, enilconazole, clotrimazole) in spray or shampoo formulations and/or oral agents (eg, terbinafine, itraconazole). Lime-sulfur dips may also be used. Other hedgehogs in the home may be subclinically infected, and treatment of all animals is recommended.
Skin neoplasia is common. Squamous cell carcinomas, epitheliotropic T-cell lymphomas, papillomas, and sebaceous gland carcinomas have been reported.
Pinnal dermatitis is a common condition in hedgehogs; skin crusts, accumulated secretions, and a ragged pinnal margin may be observed. Dermatophytes and acariasis are important differential diagnoses for this condition; other possibilities include nutritional deficiencies, dry skin from inappropriate husbandry, or nonspecific seborrhea. Ear mites (Notoedres cati) are occasionally present; signs, diagnosis, and treatment are as for cats. Bacterial or yeast otitis externa infections are often secondary to acariasis or another cause of chronic inflammation. Clinical 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 also occurs in hedgehogs.
Fractures can occur when a limb is trapped in a cage wire or exercise wheel. Distal limb fractures can be splinted. Surgical correction may also be performed, but any fixation device must be able to withstand the hedgehog's strong rolling-up mechanism. Causes of lameness include ingrown toenails, arthritis, nutritional deficiencies, pododermatitis, constriction of a foot or digit by fibrous material, neurologic disease, or neoplasia.
Neoplasia is extremely common in African pygmy hedgehogs. A wide variety of tumor types affecting virtually every body system has been reported. Major body systems affected are the integumentary, reproductive, hemolymphatic, and alimentary systems. Commonly reported tumors include mammary gland tumors, lymphosarcomas, and oral squamous cell carcinomas. Proliferative uterine tumors or polyps are common and are associated with vaginal bleeding, hematuria, and weight loss; ovariohysterectomy can allow for prolonged survival. Although neoplasia is most commonly diagnosed in hedgehogs >3 years old, tumors are observed in patients as young as 2 years old. In one survey, > 80% of the tumors were malignant, and it is not rare for hedgehogs to have more than one type of neoplasia concurrently. Some sarcomas have been associated with retroviral infection.
Oral squamous cell carcinomas are extremely common in African pygmy hedgehogs and often present as gingival swellings. These tumors are locally invasive, and affected animals may have facial asymmetry, loose or missing teeth, and gingivitis. Eosinophilic leukemia has been reported in hedgehogs with nonspecific clinical signs. A peripheral eosinophilia is not always present. Postmortem findings can include gross splenic pathology and infiltration of neoplastic eosinophils in multiple organs (including bone marrow) with neoplastic eosinophils. The prognosis for eosinophilic leukemia appears poor: in most reports, the disease course was rapid and patients died soon after diagnosis.
Clinical signs of neoplastic disease depend on the location and severity of disease and may include palpable masses, marked lethargy, neurologic signs, weight loss, anorexia, diarrhea, dyspnea, and ascites. Diagnosis is based on cytologic or histopathologic evaluation.
Diagnostic imaging to evaluate for signs of local invasion or metastasis, as well as a CBC and serum chemistry panel, can be helpful when attempting to determine prognosis. For many neoplasia types, surgical excision and supportive care are treatments attempted, although other treatment modalities can be used. Although malignant neoplastic disease is very common in hedgehogs, other causes of masses have been reported in this species, including abscesses, bone cysts, papillomas, and uterine polyps.
Hedgehogs with severe, systemic disease without CNS involvement also commonly present with apparent neurologic abnormalities, confounding diagnosis.
Neurologic signs (particularly ataxia) may be caused by:
Demyelinating paralysis or “wobbly hedgehog syndrome” (WHS) has been reported since the mid-1990s in captive African pygmy hedgehogs. The onset of WHS commonly occurs in animals <2 years old but can occur at any age. In contrast, intervertebral disc disease typically occurs in older animals.
One of the earliest indications of WHS is the inability to roll into a ball (“close the hood”). Mild, intermittent ataxia follows. Clinical signs gradually increase in severity and may include falling to one side, tremors, unilateral exophthalmos, scoliosis, seizures, muscle atrophy, self-mutilation, and marked weight loss. The paralysis usually ascends from hindlimbs to forelimbs and can lead to complete paralysis 9–15 months after the onset of clinical signs. Death usually occurs 18–25 months after the onset of clinical signs. Appetite is usually normal until the terminal stages, at which point most hedgehogs become dysphagic.
Diagnosis of demyelinating paralysis is confirmed via necropsy examination. WHS has been described as a "spongy myelinopathy," with bilateral, symmetrical status spongiosis of multiple CNS sites, including the cerebellum, medulla oblongata, and spinal cord. Peripheral nerves may also be involved. Inflammation of the CNS is not associated with WHS. The etiology of WHS remains unknown, but a hereditary basis is suspected. Numerous treatments have been attempted without success. Although supportive care and hand feeding can be performed, euthanasia is warranted when the quality of life is compromised.
Cold temperatures (< 68°F [20°C]) or sometimes, very high temperatures, may cause torpor in hedgehogs. 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. If a hedgehog housed at inappropriate temperatures is presented nonresponsive, torpor should be considered. Prognosis is good. A quiet, warm environment should be provided and fluid therapy administered, and the patient should be monitored for greater alertness over the next several hours.
Hypocalcemia may result from postpartum eclampsia, malnutrition, or for unknown reasons and usually responds to calcium supplementation.
Intervertebral disc disease (IVDD) has been reported in hedgehogs. Clinical signs associated with IVDD include progressive hind limb ataxia, urinary stasis, loss of proprioception, and lameness. These clinical signs are similar to those of WHS. In IVDD, cervical and lumbar lesions have been identified; multiple discs may be affected. Radiographic findings include spondylosis, disc-space narrowing, and disc mineralization. Necropsy findings in hedgehogs with IVDD may include degeneration of the nucleus pulposus and annulus fibrosus, dorsal extrusion of disc material, and mineralization of the nucleus pulposus. Evidence of fibrocartilaginous embolism was noted in one patient. Temporary improvement with corticosteroids has been described in two cases of IVDD.
As in other species, head tilt or circling may be caused by otitis media/interna or primary neurologic disease.
Obesity is very common in pet hedgehogs. Obese hedgehogs are often unable to completely roll up into a ball because of large subcutaneous fat deposits. These deposits are commonly located in the axillary and rump areas. Reducing high-fat foods, avoiding free-choice feeding, and increasing exercise can help manage obesity. Hiding food in the substrate or distributing it around the enclosure increases exercise through foraging activity. Weight reduction should be gradual to prevent clinical signs associated with hepatic lipidosis, a common finding in African pygmy hedgehogs. Nutritional excess or deficiency may occur with unbalanced diets; for example, calcium deficiency may result from a diet consisting mainly of invertebrates.
Hedgehogs are susceptible to corneal ulcers and other ocular injuries. Diagnosis and treatment are similar to those for other species, although administration of topical medication can be difficult. Blindness does not seem to appreciably reduce the quality of life of pet hedgehogs or impair their ability to move around their cages.
Ocular proptosis is relatively common; prognosis for viability of the affected eye(s) is poor. Hedgehogs' shallow orbits may predispose them to proptosis, especially with excessive fat accumulation or orbital inflammation. 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. Treatment is with antimicrobials. The addition of abrasive items to the diet (eg, hard kibble) is recommended for prevention. Dental prophylaxis, periprocedural antimicrobials, and tooth extraction may be necessary to treat severe dental disease. In cases of advanced periodontal disease requiring extraction of all teeth, hedgehogs can be maintained on a diet of soft food.
Tooth fractures and dental abscesses also occur. 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 softer diet. Hedgehog teeth do not grow continuously and should not be trimmed. Hedgehogs are prone 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 antimicrobials.
Hemorrhagic vulvar discharge or hematuria is common in female hedgehogs and is often caused by uterine neoplasia or endometrial polyps, although differential diagnoses such as cystitis or lower urinary tract infections should be considered.
Pyometra and metritis have also been reported in hedgehogs. Dystocia is 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 hours 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 its young.
Predisposing factors for upper and lower respiratory tract infection in hedgehogs are suboptimal environmental temperature; aromatic, dusty, or unsanitary bedding; concurrent disease causing immunocompromise; and aspiration of material from an oral infection. Clinical signs include nasal discharge, increased respiratory noise, dyspnea, lethargy, inappetence, and sudden death. CT scan, radiographs, hematologic testing, and culture of respiratory secretions are useful for diagnosis. Treatment includes antimicrobials, nebulization, supportive care, and correction of underlying problems. Differential diagnoses for dyspnea are pulmonary neoplasia and cardiac disease.
Cystitis and urolithiasisin hedgehogs cause changes in urine color, stranguria, pollakiuria, inappetence, and lethargy. Urinalysis with culture should be obtained and diagnostic imaging performed. Kidney disease is also common and in many cases may be secondary to systemic disease. Genetic or dietary factors may contribute to the high prevalence of kidney disease. Nephritis, tubular nephrosis, glomerulosclerosis, infarcts, polycystic kidneys, neoplasia, and glomerulonephropathy have been reported. Clinical signs associated with kidney disease tend to be nonspecific, although polyuria and/or polydipsia may occur. Diagnosis should be based on urinalysis and serum chemistry panels. Treatment consists of correcting the underlying cause, if possible, administration of fluid therapy, and supportive care.
Several strains of Salmonella occur commonly in hedgehogs, particularly S Enterica serovar Tilene, S Typhimurium, and S Enteritidis; in many cases, hedgehogs are asymptomatic carriers. Numerous cases of transmission to humans have been documented, particularly in young children, even without direct contact with the affected animals. Hedgehogs have soft, messy feces and a tendency to walk through their droppings, facilitating the spread of Salmonella. Anyone handling hedgehogs should assume that the hedgehog carries and transmits Salmonella and should take appropriate measures, including washing hands immediately after handling, not allowing hedgehogs or fomites to contact food or food preparation areas, and keeping cages clean.
Because infected animals may shed salmonellae intermittently, a negative culture does not exclude a carrier. Treatment aimed at eliminating the carrier state is unlikely to be successful and may lead to antimicrobial resistance.
Dermatophytosis in humans, transmitted from pet hedgehogs, is also well documented. African pygmy hedgehogs can be subclinical carriers of Trichophyton mentagrophytes erinacei, Microsporum spp, and Arthrodermabenhamiae. In addition, some humans are extremely sensitive to contact with African hedgehog spines and develop transient, markedly pruritic urticaria within minutes of handling hedgehogs.
Wild African hedgehogs are susceptible to foot-and-mouth disease. Importation of African hedgehogs into the US, therefore, was banned by the USDA in 1991 to prevent introduction of this disease.
Rabies has not been reported in wild or captive African hedgehogs, although the salivation that occurs during self-anointing behavior may be mistaken as a sign of rabies.