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Historically, highly pathogenic avian influenza viruses (HPAIV) rarely resulted in infection or clinical disease in wild birds. However, since 2002, disease and mortality from natural HPAIV H5N1 infection have been observed in wild birds including gulls. We performed an experimental HPAIV H5N1 infection of black-headed gulls (Chroicocephalus ridibundus) to determine their susceptibility to infection and disease from this virus, pattern of viral shedding, clinical signs, pathological changes and viral tissue distribution. We inoculated sixteen black-headed gulls with 1 × 10(4) median tissue culture infectious dose HPAIV H5N1 (A/turkey/Turkey/1/2005) intratracheally and intraesophageally. Birds were monitored daily until 12 days post inoculation (dpi). Oropharyngeal and cloacal swabs were collected daily to detect viral shedding. Necropsies from birds were performed at 2, 4, 5, 6, 7, and 12 dpi. Sampling from selected tissues was done for histopathology, immunohistochemical detection of viral antigen, PCR, and viral isolation. Our study shows that all inoculated birds were productively infected, developed systemic disease, and had a high morbidity and mortality rate. Virus was detected mainly in the respiratory tract on the first days after inoculation, and then concentrated more in pancreas and central nervous system from 4 dpi onwards. Birds shed infectious virus until 7 dpi from the pharynx and 6 dpi from the cloaca. We conclude that black-headed gulls are highly susceptible to disease with a high mortality rate and are thus more likely to act as sentinel species for the presence of the virus than as long-distance carriers of the virus to new geographical areas.

Objectives: Alcohol-use disorders in adolescents are associated with gray matter (GM) abnormalities suggesting neurotoxicity by alcohol. However, recently similar GM abnormalities were found in non-drinking children with a family history (FH) of alcohol dependence (AD). The question thus rises whether these abnormalities represent a transient delay in brain maturation or a persistent risk factor for developing neuropsychiatric disorders, rather than a (neurotoxic) consequence of AD. This study investigated whether a FH of AD in non-drinking adults is associated with abnormal GM-volumes similar to those observed in drinking and non-drinking adolescents with a FH of AD., Methods: GM-images were analyzed using Voxel-Based Morphometry in non-alcoholics with (FH+; N = 36) and without (FH-; N = 107) familial AD. Additionally we controlled for possible confounders: diagnosis of depression/anxiety, childhood trauma and familial depression/anxiety., Results: Smaller GM-volumes were shown in the right parahippocampal gyrus in FH+ compared with FH-. Results were unaffected by confounders., Conclusions: We demonstrated an effect of familial AD in non-alcoholic adults on GM volume in the parahippocampal gyrus, similar to drinking and non-drinking FH+ adolescents. These findings suggest that GM abnormalities in the parahippocampal gyrus represent a persistent biological susceptibility for AD or related psychopathology and not neurotoxicity of alcohol or delayed brain maturation.