Domestic cats are susceptible to infection with low pathogenic avian influenza viruses from shorebirds

Abstract

Domestic cats are susceptible to infection with highly pathogenic avian influenza virus H5N1, resulting in pneumonia and in some cases, systemic spread with lesions in multiple organ systems. Recent transmission of the 2009 pandemic H1N1 influenza virus from humans to cats also resulted in severe pneumonia in cats. Data regarding the susceptibility of cats to other influenza viruses is minimal, especially regarding susceptibility to low pathogenic avian influenza viruses from wild birds, the reservoir host. In this study, the authors infected 5-month-old cats using 2 different North American shorebird avian influenza viruses (H1N9 and H6N4 subtypes), 3 cats per virus, with the goal of expanding the understanding of avian influenza virus infections in this species. These viruses replicated in inoculated cats based on virus isolation from the pharynx in 2 cats, virus isolation from the lung of 1 cat, and antigen presence in the lung via immunohistochemistry in 2 cats. There was also seroconversion and lesions of patchy bronchointerstitial pneumonia in all of the cats. Infection in the cats did not result in clinical disease and led to variable pharyngeal viral shedding with only 1 of the viruses; virus was localized in the alveolar epithelium via immunohistochemistry. These findings demonstrate the capacity of wild bird influenza viruses to infect cats, and further investigation is warranted into the pathogenesis of these viruses in cats from both a veterinary medical and public health perspective.

Figure 1.

Lung; cat; inoculated with avian influenza virus RT/625 (H6N4), day 7 post innoculatin (pi). The bronchiolar lumen is filled by macrophages with peribronchiolar lymphocytes and plasma cells. Bronchiolar epithelial regeneration is evident with hypertrophied, irregular bronchiolar epithelium. HE. Figure 2. Lung; cat; inoculated with avian influenza virus RT/625 (H6N4), day 7 post inoculation (pi). Note thick perivascular cuffs of lymphocytes. HE. Figure 3. Lung; cat; inoculated with avian influenza virus RT/645 (H1N9), day 7 post inoculation (pi). Marked type II pneumocyte hyperplasia with numerous macrophages in alveolar lumens. HE. Figure 4. Lung; cat; inoculated with avian influenza virus RT/645 (H1N9), day 7 post inoculation (pi). Macrophages fill alveolar lumens. HE. Figure 5. Tracheobronchial lymph node; cat; inoculated with avian influenza virus RT/625 (H6N4), day 7 post inoculation (pi). Immunohistochemistry for influenza A viral antigen labels the cytoplasm of macrophages. Streptavidin-biotin immunoperoxidase method with hematoxylin counterstain. Figure 6. Lung; cat; inoculated with avian influenza virus RT/645 (H1N9), day 7 post inoculation (pi). Nuclear immunoreactivity for influenza A viral antigen (red) with cytoplasmic immunoreactivity for cytokeratin AE1/AE3 (brown) in pneumocytes. Streptavidin-biotin immunoperoxidase method (cytokeratin AE1/AE3) and alkaline phosphatase method (nucleoprotein of influenza A) with hematoxylin counterstain. Inset: Higher magnification of a pneumocyte showing both nuclear immunoreactivity for influenza A viral antigen (red) and cytoplasmic immunoreactivity for cytokeratin (brown).