Occurrences of avian encephalomyelitis virus in naturally infected chicks in Saudi Arabia's Eastern Province

Abstract

Background: A neurological infectious viral disease, avian encephalomyelitis was initially discovered in 2-week-old commercial chicks in 1930 and classified as a neurotropic viral disease.

Aim: A neurological outbreak caused by avian encephalomyelitis virus (AEV) in young chicks was first reported in Al-Ahsa in the Kingdom of Saudi Arabia (KSA) in 2010. The aim of this article is to examine the AEV in KSA, Al-Ahsa Province.

Methods: Gizzard, proventriculus, cerebrum, cerebellum, and medulla oblongata tissue samples were collected from infected chicks for histopathology test and molecular identification.

Results: Infected chicks showed neurological signs particularly incoordination, mild head and neck tremors, stretching of legs, and lameness. The average morbidity and mortality rates were 35% and 10%, respectively. At necropsy, no obvious identifiable macroscopic lesions were found in the infected chicks. Nonsuppurative encephalomyelitis was found histopathologically in the central nervous system, mainly in the cerebral molecular layer. Microscopic lesions in the proventriculus showed masses of heavy numbers of small lymphocytes within the muscular layer. RT-PCR followed by sequence analysis revealed that The KSA strain (KJ939252) is intimately related to chicken European strains from Poland (KC912695) and the United Kingdom (AJ225173) with identity 99.6% than Chinese strains (AY225319, AY517471, and AY275539) with identity ranged between 94.6% and 95%. The phylogenetic tree analysis showed that the KSA strain is grouped in a similar clade with chicken European strains.

Conclusion: The pattern of disease findings was typical of vertically transmitted AEV. The spread of AEV in Saudi Arabia is most likely due to the trade of birds and bird products with European countries.

Keywords: Avian encephalomyelitis; Broiler chicks; Molecular identifications; Saudi Arabia.

Fig. 1.. a- Cerebral molecular layer showing perivascular cuffing (arrow) and microgliosis. H&E ×400. b- Proventriculus showing heavy infiltration of lymphocytes within the muscular layer (arrow). H&E ×400.

Fig. 2.. Agarose gel electrophoresis of RT-PCR from naturally diseased young chicks with AEV. Lane M, molecular weight PCR marker; Lane 1, brain; Lane 2, proventriculus; Lane 3, AEV vaccine kept as positive control; Lane 4, nuclease-free water kept as negative control.

Fig. 3.. Nucleotide sequence alignment of about 495 bp within the VP2 gene of AEV using the ClustalW program. *The KSA strain.

Fig. 4.. Phylogenetic tree of the nucleotide sequences of the VP2 gene of KSA isolate (marked with a solid triangle) and the available references strains from GenBank using maximum likelihood method with bootstrap values for n = 100 replicates.