4.3  Cats
Rimmelzwaan et al. (2006) assessed the virulence of a H5N1 virus in cats by infecting them by intratracheal inoculation or through feeding on virus-infected chicks. Within 2 days, most animals developed fever, conjunctivitis, lethargy, and labored breathing. Virus was detected in the throat, nasal, and rectum, regardless of the original site of infection. The virus spread systemically and was detected in the respiratory and digestive tracts, liver, kidney, heart, brain, and lymph nodes. Cellular damage in infected tissues correlated with the detection of viral proteins. Histopathological examination of the lungs revealed multiple or coalescing foci of inflammation and necrosis in the bronchioles. The alveolar and bronchiolar lumina were infiltrated with alveolar macrophages, neutrophils, and erythrocytes, mixed with fibrin, edema fluid, and cellular debris. More importantly, some alveoli were covered by hyaline membranes, which are also seen human lungs upon autopsy. Hyaline membrane formation has not been observed in mice or other animal models. The epithelium of bronchiolar and alveolar walls, which were moderately thickened, also had evidence of both necrosis and hyperplasia. There was also edema and moderate accumulation of mononuclear cells around pulmonary artery branches. Although there has been some work in defining the cat influenza model for evaluating pathogenesis of H5N1 infections, few if any studies have been published which describe the suitability of the cat for doing vaccine (Karaca et al., 2005, Vahlenkamp et al., 2008) and antiviral efficacy studies.