Felipedia

© P. A. Pesavento, N. J. MacLachlan, L. Dillard-Telm, C. K. Grant and K. F. Hurley Pathologic, Immunohistochemical, and Electron Microscopic Findings in Naturally Occurring Virulent Systemic Feline Calicivirus Infection in Cats Vet Pathol 41:257-263 (2004) http://www.vetpathology.org/cgi/content/full/41/3/257

Caliciviruses are non-enveloped, positive-sense, and single-strandedRNA viruses and include RVHDV, European brown hare syndromevirus (EBHV), and vesicular exanthema of swine viruses. Felinecalicivirus (FCV) is a common pathogen of cats. Multiple strainsof FCV exist and infection can cause a variety of manifestations,including fever, rhinitis, pneumonia, and oral ulcers.^1,4,10Although morbidity is high, mortality is usually low exceptin kittens as a consequence of pneumonia. In 1998 an outbreakof severe disease in cats caused by an unusually virulent strainof FCV was described and reproduced in SPF cats.⁷ At least sixdifferent outbreaks of similar disease characterized by highmortality have since been recognized in the United States, butthe lesions have not previously been described in detail.⁵.

Caliciviruses appear to have a predilection for the epithelium of the oral cavity and the deep tissues of the lungs. Some caliciviruses are non-pathogenic. Some induce little more than salivation and ulceration of the tongue, hard palate, or nostrils; others produce pulmonary oedema and interstitial pneumonia. Clinically, it is often impossible to differentiate FHV from FCV infection. Two strains may produce a transient “limping syndrome” without signs of oral ulceration or pneumonia. These strains produce a transient fever, alternating leg lameness, and pain on palpation of affected joints. Signs occur most often in 8- to 12-wk-old kittens and usually resolve without treatment. The syndrome may occur in kittens vaccinated against FCV because no vaccine protects against both of the strains that produce the “limping syndrome.”

Calicivirus has also been found in cats with lymphocytic-plasmacytic stomatitis (LPS). The superficial lesions heal rapidly, and the infected cat regains appetite 2-3 days after onset. The clinical course usually is 7-10 days. An acute febrile response, inappetence, and depression are common signs. Serous rhinitis and conjunctivitis also can occur.

A rare, but potentially lethal variant of the calicivirus is one that causes an often fatal disease in cats. In contrast to the relatively mild symptoms that characterizeinfection of cats with the usual field strains of FCV, infectionwith virulent systemic FCV (VS-FCV) is devastating, with mortalityrates ranging between 33% and 60%.⁵ Adult cats that were previouslyvaccinated against calicivirus infection were prominently affectedin these outbreaks, and adult cats were at higher risk for severedisease and death as compared with kittens. In addition to ulcerationand nasal or ocular discharge, signs characteristic of VS-FCVinfection include profound fever, anorexia, marked subcutaneousedema (especially of the limbs and face), icterus, alopecia,crusting, and ulceration of the nose, lips, pinnae, and feet.

Fig. 1. Paw; cat No. 4. The epithelial lining of the footpads of P2 and P5 have sloughed. There is peripheral ulceration at the pad-haired skin junction of P4. HE.
Fig. 2. Skin; cat No. 2. Extensive necrosis of the follicular epithelium. Arrowhead indicates remnant viable epithelium. HE. Bar = 70 µm.
Fig. 3. Pawpad, haired skin junction; cat No. 1. Extensive infiltration of neutrophils with accompanying karyorrhexis and karyolysis of epithelial cells at the junction between haired skin (left) and footpad (right). Asterisks indicate dermal-epidermal junction, which is obscured by necrosis of the epithelium. HE. Bar = 140 µm.
Fig. 4. Lung; cat No. 4. Interstitial pneumonia with marked type II pneumocyte hyperplasia. HE. Bar = 92 µm. Inset: Fibrin deposits within alveolar capillaries. Bar = 45µm.
Fig. 5. Liver; cat No. 4. There is individualization of hepatocytes, scattered hepatocyte necrosis, and fibrin deposits (inset, arrowheads). HE. Bar = 72 µm. Inset bar = 40 µm.

Fig. 10. Cat No. 1. Purified VS-FCV. Particles are 33.5 nm in diameter and have the scalloped borders and surface indentations typical of Caliciviridae. Direct electron micrograph. Bar = 64 nm.
Fig. 11. Skin; cat No. 1. A membrane-bound fragment contains paracrystalline arrays of virions. Transmission electron micrograph. Bar = 332 nm.
Fig. 12. Skin; cat No. 3. Paracrystalline arrays of virus particles within the nucleus of an epithelial cell are associated with protofilaments. Asterisk indicates cytoplasmic cytokeratin bundles. Transmission electron micrograph. Bar = 456 nm.

Clinical signs and lesions of VS-FCV infection are likely toresult from a combination of epithelial (cytolytic) and endothelialinjury.

Very little is known about the pathogenesis of virulent strainsof FCV. Caliciviridae exhibit a remarkable genetic diversity.^3,8VS-FCV strains of FCV are genetically distinct, which likely explains the very striking and characteristic lesions that these viruses induce in susceptible cats.