Feline calicivirus-associated dermatitis

Numerous viral infections of the cat can involve the skin, including infections by poxviruses which are considered the most frequent. Skin lesions are also reported to occur sporadically during infection by retroviruses, papillomaviruses, coronaviruses and herpesviruses, and, more recently, by caliciviruses.

Feline calicivirus (FCV), belonging to the family of Caliciviridae, is a common cause of infection  of the upper respiratory tract of the cat. As occurs in other RNA viruses, the genome of FCV mutates easily, leading to a highly variable degree of pathogenicity between one strain and another. This correlates with the different clinical forms of calicivirus infection, which range from asymptomatic to fatal, with different tissue tropism. The most common form of calicivirus infection is the acute form, which is characterized mainly by fever, rhinitis, conjunctivitis and oral ulcers, which usually involve the tongue but can also be found on the palate, gums, lips and nasal philtrum. Chronic infection can lead to the development of chronic, progressive gingivitis and/or stomatitis associated with clinical symptoms such as halitosis, dysphagia, sialorrhoea, anorexia and weight loss.

Published reports of dermatological lesions induced by calicivirus are fairly rare; these lesions initially appear as vesicles and papules and then evolve into crusts, erosions and ulcerations.They are confined mainly to the head and neck, with a subsequent tendency to spread. The signs are often associated with erosions of the oral mucosa (particularly of the dorsum of the tongue and the palate) and the foot pads (Fig. 1). There is almost always concomitant involvement of the upper respiratory tract with symptoms of rhinotracheitis and conjunctivitis.

A virulent systemic form of FCV (known as haemorrhagic-like fever or virulent systemic FCV) has recently been described. This infection can be asymptomatic, cause mild or severe symptoms or be fatal, with the mortality rate in adult subjects ranging from 33 to 60%. While the first two forms of calicivirus infection (acute and chronic) are typically due to vaccine-sensitive strains of the virus, the virulent systemic form is caused by vaccine-resistant strains and generally develops within catteries or colonies of cats; it tends to have a sudden onset and spread rapidly. The clinical signs observed in these cases include lethargy, anorexia, mild or severe fever, runny nose and eyes, conjunctivitis (Fig. 2), ulcers of the oral cavity, dyspnoea, lameness, jaundice, pleural effusion (these latter signs are associated with a poor prognosis), diarrhoea, vomiting, petechiae, ecchymoses, disseminated intravascular coagulation and sudden death.

Many symptomatic subjects infected by virulent systemic FCV develop oedema of the muzzle and limbs, and ulcerative-crusting lesions distributed particularly on the ears, muzzle, nostrils, periocular regions, distal parts of the limbs and foot pads.

Very recently a nosocomial infection due to virulent systemic FCV was reported to have occurred in a veterinary clinic in France. The infection broke out in March and lasted for about 1 month. The clinical signs, the course of the infection, the clinicopathological manifestations and the lesions were typical of the systemic form of calicivirus infection. Some cats had cutaneous oedema, which was widespread or localised to the limbs, while others also developed ulcerative dermatitis, erosive skin lesions, alopecia and crusts and ulcers on the posterior limbs and foot pads.

In these cases, the diagnosis is strongly supported by the history and clinical findings and can be confirmed by histological and immunohistochemical studies carried out on skin samples. The histological changes in these lesions include hydropic degeneration and epidermal necrosis due to the cytopathic effect of the virus. The immunohistochemical studies can identify viral antigens in the cytoplasm of the epithelial cells. In cases with mild or moderate systemic signs, the differential diagnosis includes herpesvirus-related dermatitis and autoimmune diseases, as well as, in some cases, indirectly induced skin lesions (vasculopathies, immune complex deposition, and secondary opportunistic infections).

An atypical form of calicivirosis has been described in two cats, which, following routine ovariohysterectomy developed anorexia, depression and pustular dermatitis at the site of the surgical wound in the absence of respiratory or conjunctival symptoms. One cat subsequently developed necrotising dermatitis of the surgical wound as well as lingual ulcers, dyspnoea, and a lung infection, and was euthanized. The other cat responded positively to stepped treatment with prednisolone, initially administered at a dose of 2 mg/Kg/die for 2 days. In both cases, histological studies of the skin lesions showed pan-epidermal pustular dermatitis with necrosis of the epidermis; the epithelial cells within the pustules were immunohistochemically positive for FCV.

FCV antigen has also been found in skin biopsies taken from the chin of a cat with acne and in various samples taken from rhinopharyngeal polyps. However, since FCV is a ubiquitous virus, its direct involvement in the aetiology of these diseases has not yet been demonstrated.

The treatment of calicivirus infection is symptomatic and should be adapted to the severity of the symptoms. The use of glucocorticoids for the virulent systemic forms is controversial; some authors have reported a reduction in mortality in cats treated with prednisolone (1 mg/kg every 12 hours). Furthermore, it is recommended that the animals’ environment and cages are cleaned with a solution of sodium hypochlorite, since FCV, not having an envelope, is resistant to lipid solvents.

Suggested readings

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