Multiple Introductions of Influenza A(H5N8) Virus into Poultry, Egypt, 2017

After high mortality rates among commercial poultry were reported in Egypt in 2017, we genetically characterized 4 distinct influenza A(H5N8) viruses isolated from poultry. Full-genome analysis indicated separate introductions of H5N8 clade 2.3.4.4 reassortants from Europe and Asia into Egypt, which poses a serious threat for poultry and humans.

and is now endemic among poultry in Egypt (2). Also in Egypt, the number of H5N1 infections in humans is the highest in the world, and low pathogenicity influenza A(H9N2) virus is widespread among poultry and has infected humans (2). Despite extensive vaccination, H5N1 and H9N2 viruses are co-circulating and frequently reported (2). In 2014, highly pathogenic avian influenza A(H5N8) virus clade 2.3.4.4 was isolated, mostly from wild birds, in several Eurasian countries and was transmitted to North America. However, in 2016 and 2017, an unprecedented epidemic was reported in Asia, Africa, and Europe (3). In Egypt, during November 30-December 8, 2016, a total of 3 H5N8 viruses were isolated from common coot (Fulica atra) (4) and green-winged teal (Anas carolinensis) (5). To provide data on the spread of the virus in poultry, we genetically characterized 4 distinct H5N8 viruses isolated from commercial poultry in Egypt in 2017.
No epidemiologic links between farms were observed.
HA of the 4 H5N8 viruses in this study clustered in 1 distinct branch (Figure), and NA clustered in 2 phylogroups (online Technical Appendix 1 Figure 2). The PB2, nucleoprotein, M, and NS genes of viruses from Ck12 and Ck21 (from chickens in the same governorate, February and May 2017) clustered together, and the same genes from viruses from Dk18 and Ck15 (from ducks and chickens in 2 governorates) clustered in 2 distinct phylogenetic groups. However, viruses from Ck12 and Ck15 have similar but not identical PA gene segments (online Technical Appendix 1 Figure 3).
These data suggest 4 different introductions of H5N8 virus into poultry in Egypt, independent of viruses isolated from captive birds (4,5). Multiple separate introductions of H5N8 virus into Europe also occurred (10). Further studies are needed to identify the source(s) of introduction. The separate introductions of different reassortants of H5N8 clade 2.3.4.4 virus from Europe and Asia into Egypt indicate a serious threat for poultry and human health.
In most locations except for Russia, tick-borne encephalitis is mainly caused by the European virus subtype. In 2015, fatal infections caused by European and Siberian tick-borne encephalitis virus subtypes in the same Ixodes ricinus tick focus in Finland raised concern over further spread of the Siberian subtype among widespread tick species.
T he causative agent of tick-borne encephalitis (TBE), tick-borne encephalitis virus (TBEV), is endemic throughout Europe and Asia; ≈10,000 cases are reported annually (1). TBEV is an enveloped, positive-sense RNA virus in the family Flaviviridae, genus Flavivirus (2). The westernmost range of the Siberian subtype (TBEV-Sib) extends to Finland and the Baltics, where the European subtype (TBEV-Eur) also circulates. TBEV-Eur is the only subtype found in the rest of Europe (3).
In TBEV-infected patients, neurologic signs appear as the virus passes to the central nervous system; infection is manifested as meningitis, encephalitis, or meningoencephalitis. During 2010-2016, a total of 20 cases of TBE were reported from Kotka archipelago, Finland, a previous TBEV-Sib focus (4). We report 2 fatal TBEV infections acquired 1 month apart in patients on Kuutsalo Island, Kotka archipelago, in 2015.
Patient 1 was a previously healthy 36-year-old woman who had visited Kuutsalo 10 days before fever onset. A week later, she experienced sudden-onset headache, left arm numbness, and impaired vision. Head computed tomography results were unremarkable. Two days later, she experienced disorientation and right hemiparesis and was taken to a tertiary care center. Cerebrospinal fluid (CSF) test results showed pleocytosis. Magnetic resonance images indicated pathologically increased signal in cortical sulcus regions (Figure, panel A). Despite receipt of acyclovir, doxycycline, and ceftriaxone, her condition deteriorated rapidly. Head computed tomography showed cerebellar herniation; the patient had dilated pupils and no pain reaction. CSF and serum were positive for TBEV IgM but negative for TBEV RNA; hemagglutination inhibition results showed a low titer (20) of TBEV-specific antibodies in serum. The patient died 2 weeks after fever onset.
TBEV was isolated from the cerebellum in SK-N-SH neuroblastoma cells, and the whole genome for TBEV-Sib was obtained. A pool of TBEV-Sib-positive Ixodes ricinus ticks collected from the neighboring island in 2011 (4) was subjected to viral whole-genome sequencing. This virus and the virus from patient 1 had 3 nt differences resulting in 2 aa mutations, R868K (NS1) and V1452A (NS2B), and clustered together in the Baltic clade of TBEV-Sib (online Technical Appendix Figure 2). Patient 2 was a 66-year-old man with hypertension, diabetes, and chronic lymphatic leukemia. He had frequently