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ABSTRACT:Although the Mallard (Anas platyrhynchos) is considered an important maintenance host for low pathogenic avian influenza (LPAI) viruses, viral cell tropism and pathology in naturally infected birds are largely unknown. In August 2006, we collected 19 free-living hatch-year Mallards that were positive for LPAI virus by real-time reverse-transcriptase polymerase chain reaction (RRT-PCR) in combined oropharyngeal and cloacal swabs. We investigated virus infection and associated lesions in the digestive and respiratory tracts by RRT-PCR, virus culture, immunohistochemistry (IHC), and histology. By RRT-PCR, 15 birds were positive in cloacal bursa, colon/cloaca, or both, and three were positive in lungs. Virus was isolated from eight birds and typed as H2N3 (three birds), H3N3 (two birds), H3N8 (one bird), H4N6 (one bird), and H?N3 (one bird). By IHC, birds were positive in the cloacal bursa (eight birds), colon (three), cecum (two), or ileum (one). Cell types infected were superficial epithelial cells of the bursa and epithelial cells of the intestinal villi and, less commonly, mucosal glands. By histology, there was no evidence of lesions associated with LPAI virus infection. These results show that epithelia of the cloacal bursa and of the lower intestine are important sites of natural LPAI virus infection in freeliving hatch-year Mallards. The lack of lesions associated with this infection suggests that there is a strong selection by LPAI virus to cause minimal virulence in this maintenance host species.

Highly pathogenic avian influenza (HPAI) is essentially a poultry disease. Wild birds have traditionally not been involved in its spread, but the epidemiology of HPAI has changed in recent years. After its emergence in southeastern Asia in 1996, H5 HPAI virus of the Goose/Guangdong lineage has evolved into several sub-lineages, some of which have spread over thousands of kilometers via long-distance migration of wild waterbirds. In order to determine whether the virus is adapting to wild waterbirds, we experimentally inoculated the HPAI H5N8 virus clade 2.3.4.4 group A from 2014 into four key waterbird species—Eurasian wigeon (Anas penelope), common teal (Anas crecca), mallard (Anas platyrhynchos), and common pochard (Aythya ferina)—and compared virus excretion and disease severity with historical data of the HPAI H5N1 virus infection from 2005 in the same four species. Our results showed that excretion was highest in Eurasian wigeons for the 2014 virus, whereas excretion was highest in common pochards and mallards for the 2005 virus. The 2014 virus infection was subclinical in all four waterbird species, while the 2005 virus caused clinical disease and pathological changes in over 50% of the common pochards. In chickens, the 2014 virus infection caused systemic disease and high mortality, similar to the 2005 virus. In conclusion, the evidence was strongest for Eurasian wigeons as long-distance vectors for HPAI H5N8 virus from 2014. The implications of the switch in species-specific virus excretion and decreased disease severity may be that the HPAI H5 virus more easily spreads in the wild-waterbird population.

Abstract. More than 10,000 Caspian seals (Phoca caspica) were reported dead in the Caspian Sea during spring and summer 2000. We performed necropsies and extensive laboratory analyses on 18 seals, as well as examination of the pattern of strandings and variation in weather in recent years, to identify the cause of mortality and potential contributory factors. The monthly stranding rate in 2000 was up to 2.8 times the historic mean. It was preceded by an unusually mild winter, as observed before in mass mortality events of pinnipeds. The primary diagnosis in 11 of 13 seals was canine distemper, characterized by broncho-interstitial pneumonia, lymphocytic necrosis and depletion in lymphoid organs, and the presence of typical intracytoplasmic inclusion bodies in multiple epithelia. Canine distemper virus infection was confirmed by phylogenetic analysis of reverse transcriptase-polymerase chain reaction products. Organochlorine and zinc concentrations in tissues of seals with canine distemper were comparable to those of Caspian seals in previous years. Concurrent bacterial infections that may have contributed to the mortality of the seals included Bordetella bronchiseptica (4/8 seals), Streptococcus phocae (3/8), Salmonella dublin (1/8), and S. choleraesuis (1/8). A newly identified bacterium, Corynebacterium caspium, was associated with balanoposthitis in one seal. Several infectious and parasitic organisms, including poxvirus, Atopobacter phocae, Eimeria-and Sarcocystis-like organisms, and Halarachne sp. were identified in Caspian seals for the first time.

A previously unidentified morbiUivirus was isolated from two harbour porpoises , (Phocoena phocoena)

Foxes experimentally fed infected bird carcasses excrete virus for > 5 days without exhibiting severe disease and may thus disperse the virus.

In December 2000, an infectious disease spread through a captive breeding group of African wild dogs (Lycaon pictus) in Tanzania, killing 49 of 52 animals within 2 months. The causative agent was identified as Canine distemper virus (CDV) by means of histologic examination, virus isolation, reverse transcriptase-polymerase chain reaction analysis, and nucleotide sequencing. This report emphasizes the importance of adequate protection against infectious diseases for the successful outcome of captive breeding programs of endangered species.

Measles remains endemic in many East