Avian Influenza A(H7N2) Virus in Human Exposed to Sick Cats, New York, USA, 2016.

An outbreak of influenza A(H7N2) virus in cats in a shelter in New York, NY, USA, resulted in zoonotic transmission. Virus isolated from the infected human was closely related to virus isolated from a cat; both were related to low pathogenicity avian influenza A(H7N2) viruses detected in the United States during the early 2000s.

Beak necrosis in Hungarian partridges (Perdix perdix) associated with beak-bits and avian poxvirus infection.

Proliferative growth, consistent with poxvirus infection, encapsulated plastic beak-bits and covered the dorsal portion of the upper beak and nares of adult male and female captive-raised Hungarian partridges. Three representative birds were submitted to the Wisconsin Veterinary Diagnostic Laboratory for necropsy. Lesions in the necropsied birds extended through the nares, where the plastic bit ends are designed to rest. The lesions also variably extended caudally into the oropharynx and cranially within the beak epithelium, and included palate deformity and beak necrosis. Poxvirus was diagnosed in all of the birds examined based on histopathology, electron microscopy, and polymerase chain reaction amplification and sequencing. This report is the first to describe avian pox lesions associated with the application of beak-bits and the resulting beak and oral pathology.

Encephalitis in aborted bovine fetuses associated with Bovine herpesvirus 1 infection.

Brain tissue from 12 aborted bovine fetuses submitted to the Wisconsin Veterinary Diagnostic Laboratory revealed histologic lesions that consisted of glial nodules and variable degrees of mononuclear inflammation, microhemorrhage, neuronal necrosis, and cerebral cortical cavitation. A diagnosis of Bovine herpesvirus 1 (BHV-1) abortion had been made in all of these cases through multiple testing modalities. Brain tissue from 8 of the 12 fetuses was immunohistochemically stained with a monoclonal antibody specific to BHV-1, and, in 5 fetuses, there was positive intralesional staining of neurons, glial cells, and endothelial cells. This preliminary data suggested that herpesviral infection of brain tissue led to the described neurologic lesions. BHV-1 was then amplified from brain tissue in all 12 of the fetuses and was confirmed by partial sequencing of the thymidine kinase and glycoprotein C genes. To the authors' knowledge, neurologic lesions have not previously been described in BHV-1-infected fetuses, nor has BHV-1 previously been identified in bovine fetal brain tissue. The neurologic histopathology attributed to BHV-1 infection in these cases overlaps with the neurologic lesions produced by Neospora caninum, a common etiologic agent of bovine abortion. Therefore, when bovine fetal neurologic lesions are found, both etiologies should be considered and then distinguished by using additional diagnostic tools.

First Detection of Avian Lineage H7N2 in Felis catus.

In December 2016, influenza A (H7N2) was first detected among cats in the New York City shelter system with subsequent widespread transmission. The sequence of the first clinical isolate, A/feline/New York/16-040082-1/2016(H7N2), and its genetic similarity to the live bird market lineage of H7N2 low-pathogenicity avian influenza are described.

Prolonged intermittent virus shedding during an outbreak of canine influenza A H3N2 virus infection in dogs in three Chicago area shelters: 16 cases (March to May 2015).

OBJECTIVE To estimate an appropriate isolation period for dogs infected with canine influenza A H3N2 virus on the basis of the duration of virus shedding. DESIGN Retrospective case series. ANIMALS 16 dogs, from 3 Chicago area shelters, naturally infected with canine influenza A H3N2 virus. PROCEDURES Medical records of 16 affected dogs were reviewed. Nasal swab specimens from each dog had been tested periodically for a minimum of 15 days following an initial positive real-time reverse transcriptase PCR (rRT-PCR) assay result for influenza A virus shedding. Amplicons were purified, quantified, and sequenced by the Sanger DNA sequencing technique. Virus isolation and sequence results of canine influenza A H3N2 virus from nasal swab specimens were obtained in conjunction with signalment, description of clinical signs, type of treatment, and outcome. RESULTS Viruses from each dog were identified as canine influenza A H3N2 virus on the basis of DNA sequencing. The interval between first and last positive rRT-PCR assay results ranged from 13 to 24 days, whereas the time interval from first reported clinical signs to last positive assay results ranged from 15 to 26 days. Isolation of canine influenza A H3N2 virus was successful in the late shedding period from nasal swab specimens of 4 dogs at 15 and 20 days after the first positive rRT-PCR assay result and 18 to 20 days after the first clinical signs. Clinical signs resolved for all dogs that remained in the shelters during the testing period. CONCLUSIONS AND CLINICAL RELEVANCE Dogs infected with H3N2 virus should be isolated for a period of ≥ 21 days following onset of illness. Even when resolution of clinical signs occurs sooner than 21 days, shedding of H3N2 virus may persist.

Immunity to blood-stage murine malarial parasites is MHC class II dependent.

To determine whether MHC class II antigen presentation is essential for the induction of protective immunity against blood-stage malarial parasites, we used gene-targeted knockout (KO) mice to follow the time-course of nonlethal Plasmodium yoelii and Plasmodium chabaudi infections in two models of MHC class II deficiency. Infection of MHC class II KO (A(-/-)) mice with either parasite species resulted in an unremitting hyperparasitemia, whereas MHC-intact control mice resolved their parasitemia. In contrast, invariant chain KO (Ii(-/-)) mice, which present antigen via recycled but not nascent MHC class II molecules, eventually cured their infections when infected with P. yoelii. P. chabaudi parasitemia declined to subpatent levels in most Ii(-/-) mice but then recrudesced. Immunity to blood-stage malaria may be achieved by cell-mediated and antibody-mediated mechanisms of immunity, as such, the findings in A(-/-) mice indicate an essential role for MHC class II presentation of malarial antigens. Moreover, they suggest that protective immune responses to malarial antigens capable of eliminating blood-stage parasites are T cell dependent and can be induced with antigens processed in early and late endosomes.

Plasmodium chabaudi adami: interferon-gamma but not IL-2 is essential for the expression of cell-mediated immunity against blood-stage parasites in mice.

Cell-mediated immunity (CMI) may be important in immunity against blood-stage malaria. Accordingly, we examined the role of type 1 cytokines in the resolution of Plasmodium chabaudi adami malaria in mice genetically modified to have type 1 cytokine gene defects. Parasitemia was prolonged in double knockout (IL-2(-/-), IFNgamma(-/-)) mice compared to control mice. Despite deficiencies in gammadelta T cell and B cell subsets, these mice produced anti-malarial antibodies and eventually cured their infections, possibly by antibody-mediated immunity. However, because acute P. c. adami parasitemia may also be suppressed by CMI, the requirements for IL-2 and IFNgamma were evaluated in mice lacking B cells and functional IL-2 or IFNgamma genes. Acute malaria in J(H)(-/-), IL-2(-/-) mice was prolonged, but eventually cured. In contrast, J(H)(-/-), IFNgamma(-/-) mice developed unremitting parasitemia. These data strongly suggest that IFNgamma, but not IL-2, plays an essential role in the expression of CMI against P. c. adami infections. This finding may prove useful in developing malarial vaccines aimed at inducing CMI.