Haematological and histological findings in birds experimentally infected with highly pathogenic H5N2 avian influenza virus

Abstract

Experimental infection of specific-pathogen-free (SPF) Leghorn chickens with a highly pathogenic H5N2 avian influenza virus produced cellular hyperplasia in the bone marrow at 36 hours post infection (hpi) and haematological evidence of monocytosis, thrombocytopenia and heterophilia was also detected. An early, significant and progressive haematological change was thrombocytopenia starting at 24 hpi without an increase of prothrombin time. The findings suggest that highly pathogenic avian influenza virus interferes only with the primary haemostatic mechanisms by consumption of thrombocytes, while the secondary haemostatic mechanisms remain intact.

Up to new tricks – A review of cross-species transmission of influenza A viruses

“…While ‘fowl plague’, the disease caused by highly pathogenic avian influenza (HPAI) viruses in poultry, has been recognized since the late 18th century, the close relationship between the infectious agents causing ‘fowl plague’ and mammalian influenza was not demonstrated until 1955 (Webster et al , 1992; Alexander and Brown, 2000). HPAI viruses are restricted to H5 and H7 subtypes and clinical signs associated with infection in birds vary according to the species, age, virus strain, and environmental factors involved (Webster et al , 1992; Alexander and Brown, 2000; Swayne and Suarez, 2000; Mutinelli et al , 2003; Jones and Swayne, 2004; Ramirez et al , 2005; Isoda et al , 2006). Typically, HPAI viruses are not maintained in the wild waterfowl population, but are thought to appear by introduction of H5 and H7 low-pathogenicity avian influenza viruses (LPAI) in land-based poultry and subsequent mutation to HPAI in these birds (Rohm et al , 1995; Subbarao et al , 2006).…”

“…Typically, HPAI viruses are not maintained in the wild waterfowl population, but are thought to appear by introduction of H5 and H7 low-pathogenicity avian influenza viruses (LPAI) in land-based poultry and subsequent mutation to HPAI in these birds (Rohm et al , 1995; Subbarao et al , 2006). Clinical signs associated with HPAI infection may include cessation of egg laying, high fever, subcutaneous and internal hemorrhages, necrosis of the comb and wattles, edema of the head and neck, and cyanosis of the unfeathered skin (Alexander and Brown, 2000; Swayne and Suarez, 2000; Ramirez et al , 2005; Isoda et al , 2006). In contrast to LPAI viruses, which cause only mild respiratory disease and minimal to no mortality, HPAI viruses spread systemically and infection often rapidly results in death (Swayne and Suarez, 2000).…”