Influenza A virus (H5N1) infection in cats causes systemic disease with potential no

[Anne]

• Am J Pathol. 2006 Jan;168(1):6-8.

[SIZE=+1]Influenza A virus (H5N1) infection in cats causes systemic disease with potential novel routes of virus spread within and between hosts.[/SIZE]

Rimmelzwaan GF, van Riel D, Baars M, Bestebroer TM, van Amerongen G, Fouchier RA, Osterhaus AD, Kuiken T.

Department of Virology, Erasmus MC, P.O. Box 1738, 3000 DR Rotterdam, The Netherlands.

The ongoing outbreak of avian influenza A virus (subtype H5N1) infection in Asia is of great concern because of the high human case fatality rate and the threat of a new influenza pandemic. Case reports in humans and felids suggest that this virus may have a different tissue tropism from other influenza viruses, which are normally restricted to the respiratory tract in mammals.
To study its pathogenesis in a mammalian host, domestic cats were inoculated with H5N1 virus intratracheally (n = 3), by feeding on virus-infected chicks (n = 3), or by horizontal transmission (n = 2) and examined by virological and pathological assays. In all cats, virus replicated not only in the respiratory tract but also in multiple extra-respiratory tissues.
Virus antigen expression in these tissues was associated with severe necrosis and inflammation 7 days after inoculation. In cats fed on virus-infected chicks only, virus-associated ganglioneuritis also occurred in the submucosal and myenteric plexi of the small intestine, suggesting direct infection from the intestinal lumen. All cats excreted virus not only via the respiratory tract but also via the digestive tract. This study in cats demonstrates that H5N1 virus infection causes systemic disease and spreads by potentially novel routes within and between mammalian hosts.

 

[Vibrant62]

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential no

This is an important study. I would hope that autopsy becomes possible in H5N1 victims, and where it is, that researchers examine for simialar GI signs to determine if gastronintestinal routes of infection are also occuring in humans. If this should prove to be the case, the range of syptomatic presentations monitored for possible H5N1 infection needs to be extended as a matter of urgency. This is especially true in areas known to have human confirmed cases as part of cluster developmental monitoring.

 

[Anne]

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential

http://www.cdc.gov/ncidod/EID/vol11no07/pdfs/04-1313.pdf
here, you have one case with documentation

 

[Niko]

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential

Here is the pdf Anne provided - loads quicker


View attachment 04-1313.pdf

 

[kent nickell]

Re: Influenza A virus (H5N1) infection in cats causes systemic disease with potential no

Hum Pathol. 2006 Apr ;37:381-90 [Pubmed] [Scholar] [Select] [Drop] [Hide] [Show]
The comparative pathology of severe acute respiratory syndrome and avian influenza A subtype H5N1-a review.
Wai-Fu Ng, Ka-Fai To, William W L Lam, Tak-Keung Ng, Kam-Cheong Lee
The pathology of 2 zoonotic human viral infections that recently emerged, severe acute respiratory syndrome (SARS) due to coronavirus (SARS-CoV) and avian influenza A subtype H5N1, is reviewed and compared based on the literature and the cases examined by the authors. Pneumocytes are the primary target of infection resulting in diffuse alveolar damage. Systemic cytokine activation results in hemophagocytic syndrome, lymphoid depletion, and skeletal muscle fiber necrosis. Severe acute respiratory syndrome induces a more fibrocellular intra-alveolar organization with a "bronchiolitis obliterans organizing pneumonia"-like pattern and presence of multinucleated histiocytes and pneumocytes. H5N1 causes a more fulminant and necrotizing diffuse alveolar damage with patchy and interstitial paucicellular fibrosis. Severe acute respiratory syndrome associated coronavirus persists in the lung up to the second month, whereas H5N1 persists in the lung up to the third week. Severe acute respiratory syndrome associated coronavirus disseminates to blood, urine, feces, gastrointestinal tract, and liver. There is recent report of possible cerebral involvement by H5N1 and its isolation in the blood, gastrointestinal tract, and cerebrospinal fluid. More pathologic studies are urgently needed.

http://lib.bioinfo.pl/pmid:16564911

These authors are from the Department of Pathology, Princess Margaret Hospital, Kowloon West Cluster Hospitals, Hong Kong Special Administrative Region, China and Department of Anatomical and Cellular Pathology, the Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong Special Administrative Region, China

I couldn't find the whole article on line but here are some excepts from the actual paper:


Some of the limited pathologic reports they were able to review were

F/13 1997/Hong Kong duration of disease 30days (organizing diffuse alveolar damage, reactive hemophagocytic syndrome, lymphoid depletion, hepatic centrilobular necrosis, acute renal tubular necrosis, microglial nodules with demyelination in cerebral white matter)

F/25 1997/Hong Kong duration of disease 30days similar to above except for normal brain

M/33 2003/Hong Kong duration of disease 10days similar to above except for normal brain

F/26 2004/Thailand duration of disease 10days similar to above, brain not specified

M/6 2004/Thailand duration of disease 17days diffuse alveolar damage, interstitial lymphoplasmacytic infiltrate, bronchiolitis, histiocytosis in lymphoid system but no hemophagocytosis, reactive hepatitis, small foci of necrosis in brain

3 additional cases from 2004/Thailand with age, sex and duration of disease not specified lung and spleen examined only, diffuse alveolar damage with hyaline membrane, atypical lymphocytes in spleen


Reverse transcriptase-polymerase chain reaction was done on the lung of case 4 and 5 dying at days 10 and 17, respectively, and both were positive. Viral culture or RT-PCR was done in other organs including the brain, kidney, liver, bone marrow, heart, intestine, lymph node, and spleen. These were all negative edxcept for one case. For case 5, RT-PCR of small and large intestine and the spleen was positive for H5N1. The relevant investigators have also demonstrated positive-stranded viral RNA indicating viral replication only in the lung and intestine. Another clinical article had reported a broader occurrence of H5N1 in other organs. A 4-year-old boy in Vietnam presented with diarrhea followed by encephalopathy and death. H5N1 influenza virus was isolated form the cerebrospinal fluid, rectal swab, throat, and serum specimens. This was actually the first report of isolation of H5N1 from extrapulmonary sites. Unfortunately, postmortem was not done and the pathology of the gastrointestinal tract and brain was unknown.

Both SARS and H5N1 share similar pathology and pathogenesis. Pneumocytes are the primary target of the infection. The systemic cytokine activation results in reactive hemophagocytic syndrome in the lymphoreticular system and possibly also mediates other organ damage. The acute tubular necrosis of the kidney is likely to be the consequence of systemic hypoxia and shock rather than direct invasion of the viruses.

The development of acute respiratory distress syndrome in SARS is generally in the second week of the illness (first peak on day 11), whereas that for H5N1 is at the end of the first week (median time, day 6)

As the virus H5N1 may undergo adaptational mutation to the new human host environment, wider pathologic targets in the human body may become possible. Biopsy and postmortem study of new human H5N1 cases are urgently needed for further elaboration. In ducks, H5N1 is a systemic disease affecting multiple organs including the central nervous system. So far, evidence of cerebral involvement is noted in 2 autopsied cases (cases 1 and 5) and 1 clinical case. All these 3 cases were children aged 4 tro 13 years and may indicate a predisposition in children.

In conclusion, both SARS and H5N1 share similar pathology and pathogenesis,. H5N1 appears more fulminating and carries a mortality about 5-fold that of SARS. The management of both SARS and H5N1 would involve earliest eradication of the virus by appropriate antiviral regime and possible immunomodulation to downgrade or control the diffuse alveolar damage. The optimal ways to achieve these targets still await further exploration.