Pathobiology and innate immune responses of gallinaceous poultry to clade 2.3.4.4A H5Nx highly pathogenic avian influenza virus infection

Kateri Bertran,Dong-Hun Lee,Charles L Balzli,David E Swayne,David L Suarez,Miria F Criado,Mary J Pantin-Jackwood,Erica Spackman

doi:10.1186/s13567-019-0704-5

Abstract

In the 2014–2015 Eurasian lineage clade 2.3.4.4A H5 highly pathogenic avian influenza (HPAI) outbreak in the U.S., backyard flocks with minor gallinaceous poultry and large commercial poultry (chickens and turkeys) operations were affected. The pathogenesis of the first H5N8 and reassortant H5N2 clade 2.3.4.4A HPAI U.S. isolates was investigated in six gallinaceous species: chickens, Japanese quail, Bobwhite quail, Pearl guinea fowl, Chukar partridges, and Ring-necked pheasants. Both viruses caused 80–100% mortality in all species, except for H5N2 virus that caused 60% mortality in chickens. The surviving challenged birds remained uninfected based on lack of clinical disease and lack of seroconversion. Among the infected birds, chickens and Japanese quail in early clinical stages (asymptomatic and listless) lacked histopathologic findings. In contrast, birds of all species in later clinical stages (moribund and dead) had histopathologic lesions and systemic virus replication consistent with HPAI virus infection in gallinaceous poultry. These birds had widespread multifocal areas of necrosis, sometimes with heterophilic or lymphoplasmacytic inflammatory infiltrate, and viral antigen in parenchymal cells of most tissues. In general, lesions and antigen distribution were similar regardless of virus and species. However, endotheliotropism was the most striking difference among species, with only Pearl guinea fowl showing widespread replication of both viruses in endothelial cells of most tissues. The expression of IFN-γ and IL-10 in Japanese quail, and IL-6 in chickens, were up-regulated in later clinical stages compared to asymptomatic birds.

Highlights

The H5 A/goose/Guangdong/1/1996 (Gs/GD) lineage of highly pathogenic avian influenza (HPAI) virus has spread across multiple continents, affecting wild birds, poultry, and humans [1]
An H5N8 HPAI virus with all 8 gene segments of Eurasian origin and the reassortant H5N2 HPAI virus were detected in a captive-reared gyrfalcon (Falco rusticolus) and a wild Northern pintail duck (Anas acuta), respectively, in Washington state, U.S Over the 7 months, the U.S poultry industry experienced an unprecedented outbreak caused by these H5 HPAI viruses, with more than 7.5 million turkeys and 42.1 million chickens having died
Mortality, and gross lesions Previously, we determined that intrachoanal inoculation of 6 log10 mean egg infectious dose (EID50) of either H5N2 or H5N8 virus caused 80–100% mortality in the six gallinaceous species [39, 40], with the exception of H5N2 virus that caused 60% mortality in chickens [39] (Table 1)

Summary

Introduction

The H5 A/goose/Guangdong/1/1996 (Gs/GD) lineage of highly pathogenic avian influenza (HPAI) virus has spread across multiple continents, affecting wild birds, poultry, and humans [1]. America was a reassortant H5N2 with five Eurasian avian influenza (AI) virus gene segments (including the H5 clade 2.3.4.4 hemagglutinin) and three North American wild bird lineage low pathogenic AI (LPAI) virus gene segments [3, 4] detected in November 2014 in British Columbia, Canada. Virus was detected in 21 backyard flocks that included: (i) minor gallinaceous poultry species (quail, guinea fowl, pheasants, partridges, and grouse) on the same premise; (ii) different breeds of chickens and turkeys; and (iii) domestic ducks and geese [5, 7]. The game bird poultry industry and backyard flocks in both developed and developing countries are known to suffer from HPAI epidemics [19]

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