Highly pathogenic avian influenza virus (H5N1) infection in red foxes fed infected bird carcasses

Abstract

Eating infected wild birds may put wild carnivores at high risk for infection with highly pathogenic avian influenza (HPAI) virus (H5N1). To determine whether red foxes (Vulpes vulpes) are susceptible to infection with HPAI virus (H5N1), we infected 3 foxes intratracheally. They excreted virus pharyngeally for 3-7 days at peak titers of 103.5-105.2 median tissue culture infective dose (TCID50) per mL and had severe pneumonia, myocarditis, and encephalitis. To determine whether foxes can become infected by the presumed natural route, we fed infected bird carcasses to 3 other red foxes. These foxes excreted virus pharyngeally for 3-5 days at peak titers of 104.2-104.5 TCID50/mL, but only mild or no pneumonia developed. This study demonstrates that red foxes fed bird carcasses infected with HPAI virus (H5N1) can excrete virus while remaining free of severe disease, thereby potentially playing a role in virus dispersal.

Figure 1

Infectious virus titers obtained from pharyngeal, nasal, and rectal swabs of foxes infected intratracheally with highly pathogenic avian influenza (HPAI) virus (H5N1) (left, black symbols) or fed chicks infected with HPAI virus (H5N1) (right, gray symbols) at various time points after infection. No virus was isolated from any swabs of the negative-control foxes. TCID₅₀, median tissue culture infectious dose.

Figure 2

Lesions and associated expression of influenza virus antigen in respiratory and extrarespiratory organs of foxes infected intratracheally with HPAI virus (H5N1), at 7 days postinoculation. A) Lungs of control fox sham-inoculated with phosphate-buffered saline. B) Lungs of intratracheally inoculated fox presenting extensive consolidated lesions (darkened areas), characterized by C) diffuse alveolar damage and regeneration (type II pneumocyte hyperplasia) and D) expression of influenza virus antigen in the nucleus and, to a lesser extent, cytoplasm of mononuclear and epithelial cells. E) Focus of inflammation and cardiomyocytic necrosis in the heart, associated with F) expression of influenza virus antigen in the nucleus of cardiomyocytes. G) Focus of gliosis and neuronal necrosis in the cerebrum, associated with H) expression of influenza virus antigen in the nucleus and, to a lesser extent, cytoplasm of glial cells and neurons. Panels C–H, original magnification ×40.