Serosurvey of Coyotes (Canis latrans), Foxes (Vulpes vulpes, Urocyon cinereoargenteus), and Raccoons (Procyon lotor) for Exposure to Influenza a Viruses in the USA

Species can alleviate competition by reducing diet overlap. Nonnative coyotes (Canis latrans (Say, 1823)) and historically native gray foxes (Urocyon cinereoargenteus (Schreber, 1775)) have expanded their ranges and may compete with native red foxes (Vulpes vulpes (Linnaeus, 1758)). To examine potential competition among canids in Maine, we compared δ13C and δ15N from muscle and hair samples to assess relative resource use, and we compared frequency of occurrence of prey items from stomach contents to assess diets. For these species, red foxes consumed anthropogenically-based foods the most in fall-early winter, gray foxes consumed anthropogenically-based foods the most in summer, and coyotes consumed anthropogenically-based foods the least in all seasons. Coyotes held the highest relative trophic position in fall-early winter, red foxes held the highest relative trophic position in summer, and gray foxes held the lowest relative trophic position. Based on stomach contents, gray foxes had the broadest diet and consumed the most plants, and coyotes had the narrowest diet. Red foxes were the only species to show isotopic niche overlap with both potential competitors across seasons. Thus they may be most susceptible to competitive exclusion among these canids, with implications for community dynamics as ranges shift due to human activity.

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Influenza Virus Infections in Cats

Viruses ◽

10.3390/v13081435 ◽

2021 ◽

Vol 13 (8) ◽

pp. 1435

Author(s):

Tadeusz Frymus ◽

Sándor Belák ◽

Herman Egberink ◽

Regina Hofmann-Lehmann ◽

Fulvio Marsilio ◽

...

Keyword(s):

Influenza A ◽

Current Data ◽

Morbidity Rate ◽

Virus Infections ◽

Influenza A Viruses ◽

Highly Pathogenic ◽

The Usa ◽

Cat Diseases ◽

And Control ◽

Mild Fever

In the past, cats were considered resistant to influenza. Today, we know that they are susceptible to some influenza A viruses (IAVs) originating in other species. Usually, the outcome is only subclinical infection or a mild fever. However, outbreaks of feline disease caused by canine H3N2 IAV with fever, tachypnoea, sneezing, coughing, dyspnoea and lethargy are occasionally noted in shelters. In one such outbreak, the morbidity rate was 100% and the mortality rate was 40%. Recently, avian H7N2 IAV infection occurred in cats in some shelters in the USA, inducing mostly mild respiratory disease. Furthermore, cats are susceptible to experimental infection with the human H3N2 IAV that caused the pandemic in 1968. Several studies indicated that cats worldwide could be infected by H1N1 IAV during the subsequent human pandemic in 2009. In one shelter, severe cases with fatalities were noted. Finally, the highly pathogenic avian H5N1 IAV can induce a severe, fatal disease in cats, and can spread via cat-to-cat contact. In this review, the Advisory Board on Cat Diseases (ABCD), a scientifically independent board of experts in feline medicine from 11 European countries, summarises current data regarding the aetiology, epidemiology, pathogenesis, clinical picture, diagnostics, and control of feline IAV infections, as well as the zoonotic risks.

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TGF-β-induced IL-6 prevents development of acute lung injury in influenza A virus-infected F508del CFTR-heterozygous mice

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00078.2015 ◽

2015 ◽

Vol 308 (11) ◽

pp. L1136-L1144 ◽

Cited By ~ 15

Author(s):

Parker S. Woods ◽

Mia F. Tazi ◽

Nicholas M. Chesarino ◽

Amal O. Amer ◽

Ian C. Davis

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Influenza A Virus ◽

Influenza A ◽

Lavage Fluid ◽

Health Concern ◽

Transmembrane Conductance Regulator ◽

Influenza A Viruses ◽

Lung Dysfunction ◽

The Usa

As the eighth leading cause of annual mortality in the USA, influenza A viruses are a major public health concern. In 20% of patients, severe influenza progresses to acute lung injury (ALI). However, pathophysiological mechanisms underlying ALI development are poorly defined. We reported that, unlike wild-type (WT) C57BL/6 controls, influenza A virus-infected mice that are heterozygous for the F508del mutation in the cystic fibrosis transmembrane conductance regulator (HETs) did not develop ALI. This effect was associated with higher IL-6 and alveolar macrophages (AMs) at 6 days postinfection (d.p.i.) in HET bronchoalveolar lavage fluid (BALF). In the present study, we found that HET AMs were an important source of IL-6 at 6 d.p.i. Infection also induced TGF-β production by HET but not WT mice at 2 d.p.i. TGF-β neutralization at 2 d.p.i. (TGF-N) significantly reduced BALF IL-6 in HETs at 6 d.p.i. Neither TGF-N nor IL-6 neutralization at 4 d.p.i. (IL-6-N) altered postinfection weight loss or viral replication in either mouse strain. However, both treatments increased influenza A virus-induced hypoxemia, pulmonary edema, and lung dysfunction in HETs to WT levels at 6 d.p.i. TGF-N and IL-6-N did not affect BALF AM and neutrophil numbers but attenuated the CXCL-1/keratinocyte chemokine response in both strains and reduced IFN-γ production in WT mice. Finally, bone marrow transfer experiments showed that HET stromal and myeloid cells are both required for protection from ALI in HETs. These findings indicate that TGF-β-dependent production of IL-6 by AMs later in infection prevents ALI development in influenza A virus-infected HET mice.

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