Avian Nephritis Viral Infections
Avian nephritis viral (ANV) infections are contagious infections of chickens characterized by renal damage and visceral urate deposits, growth retardation, and limited mortality. They are seen mainly in chickens <7 days old, but interstitial nephritis can be observed in chicks up to 4 weeks old. ANV infections have been reported worldwide. Subclinical infections are common and have been detected by serologic surveys in some SPF flocks and in turkeys. ANV was also associated with increased mortality in 4-week-old ducklings and with late dead duck and goose embryos.
The causal viruses are avian nephritis viruses (ANVs, which are astroviruses), some of which were previously termed enterovirus-like viruses (ELVs), although a second astrovirus of chickens, chicken astrovirus (CAstV), and some strains of infectious bronchitis virus (IBV), also cause kidney disease, urate deposits, and growth problems. The descriptions below relate to ANV only. Strains of ANV vary in virulence and in antigenicity. Transmission occurs by direct or indirect contact. Vertical transmission can also occur but appears less common. Infection can be transmitted by oral administration of virus to day-old birds. Virus is consistently isolated from the kidneys or feces during the first 10 days after infection.
Clinical signs of avian nephritis viral infections vary from none to mortality resulting from kidney disease or severe growth retardation. Diarrhea and growth retardation are common in broilers. Outbreaks with mortality of 0%–10% can occur in chicks newly hatched to as old as 7 days; cardinal necropsy findings are renal damage and visceral urate deposits (baby chick nephropathy).
Nephritis is a common necropsy finding for birds with an avian nephritis viral infection. Gross and microscopic lesions are often seen in the kidneys. Swelling, paleness, or yellowish discoloration with excessive urate deposition is frequent. Histologic lesions consist of a degeneration of the epithelial cells with infiltration of granulocytes, interstitial lymphocyte infiltration, and moderate fibrosis. In the latter stages, lymphoid follicles develop.
Some ANVs induce only intestinal lesions varying from decreased length of the microvillus border to total desquamation of the intestinal epithelium.
Nephropathogenic strains of infectious bronchitis virus and CAstV also cause interstitial nephritis. Therefore, when nephritis is diagnosed, it is necessary to identify the causative agent, but this can be complicated by coinfections of ANV and CAstV, which are common.
Although ANV and related viruses may be isolated by inoculation of suspected material (kidney or rectal contents) in the yolk sac of SPF chick embryos and in chick kidney cells, many ANVs are difficult to isolate. The best way to detect ANV is by reverse transcriptase (RT)-PCR or real-time, quantitative RT-PCR of kidney or gut content samples. These tests are designed to detect multiple strains and allow quick differentiation from other viruses.
Serologic diagnosis can be made using direct or indirect immunofluorescence, seroneutralization, or ELISA tests, but these may detect only a limited number of strains of ANV because of its high antigenic diversity, and they are not widely available.