Influenza virus and proteolytic bacteria co-infection in respiratory tract from individuals presenting respiratory manifestations

Abstract

SUMMARYA role for proteolytic bacteria in the exacerbation of influenza virus has been shown in natural hosts such as pigs and humans. Four hundred seven samples were collected from the respiratory tract of individuals presenting clinical manifestations, during influenza season (2003)(2004)(2005) in São Paulo City. The aim of this study was to evaluate the incidence of determined bacteria coinfecting virus in human respiratory tract. Tests, such as bacteriological, immunofluorescence (IF), RT/PCR and hemagglutination (HA) were used for bacterial and viral investigation. Thirty seven (9.09%) positive for influenza virus were screened by IF. The RT/PCR confirmed the presence of influenza virus in these samples. Bacterial and agar casein tests demonstrated that 18 (48.64%) individuals were infected with proteolytic bacteria such as Staphylococcus spp., Streptococcus spp. and Pseudomonas spp. Among these samples, 13 (35.13%) were co-infected with influenza A virus. Influenza type B, co-infecting bacteria were found in five (13.51%) samples. In vitro the S. aureus protease increased the influenza HA titer after contact for 30 min at 25 ºC. Results revealed the occurrence of co-infection with proteolytic bacteria and influenza in the evaluated individuals. This finding corroborates that virus versus bacteria synergism could be able to potentiate respiratory infection, increasing damage to hosts.

Identification of swine influenza A virus and Stenotrophomonas maltophilia co-infection in Chinese pigs

“…Swine influenza viruses can cause disease in humans [1]. Several cases of co-infection of influenza A virus and S. maltophilia in humans have also been reported [11,25]. S. maltophilia is a multidrug resistant bacterium and possesses a high degree of resistance towards most commonly used broad-spectrum antibiotics, which is also confirmed in this study [26,27].…”

Effects of Bacterial Microflora of the Lower Digestive Tract of Free-Range Waterfowl on Influenza Virus Activation

“…Previous studies of influenza virus and coinfecting proteolytic bacteria in the respiratory tract demonstrated Aerococcus viridans, Staphylococcus aureus, and Stenotrophomonas maltophilia to activate influenza virus in vivo (16,23,30,31). We also observed these three organisms in the avian lower digestive tract.…”

“…Although viral infection in host cells of the small intestine, colon, and cecum has been demonstrated (13,14,27,33), the proteases responsible for viral activation remain unknown (11). Thus, the fundamental question arises-could microbes present in the lower digestive tract provide proteases capable of cleaving hemagglutinin much like those found in the avian, swine, and human respiratory tracts (3,4,16,17,19,23,25,30,31)? Several studies have been carried out describing indigenous avian intestinal microflora; however, these studies focused primarily on diseases affecting commercial poultry and the potential of free-ranging birds to transport and disseminate pathogenic microorganisms to humans (5,12,32).…”

Proteolytic bacteria in the lower digestive tract of poultry may affect avian influenza virus pathogenicity

“…Numerous works have investigated the potential role of microbial proteases in HA cleavage (Tashiro et al, 1987a,b;Akaike et al, 1989;Scheiblauer et al, 1992;Akaike et al, 1994;Byrum and Slemons, 1995;Callan et al, 1997;Mancini et al, 2005Mancini et al, , 2008McCull-ers, 2006). However, these studies have been limited to normal microflora of avian and mammalian respiratory tracts.…”

“…A similar protease was identified from Clara cells in rat and mouse bronchial epithelium (Kido et al, 1992). Several studies have investigated the interaction of influenza A virus with bacteria-associated development of pneumonia after combined viral-bacterial infection (McCullers, 2006;Mancini et al, 2008). Some strains of Staphylococcus aureus, Streptomyces griseus, and Aerococcus viridans secrete proteases that directly cleave the HA of several, but not all, type A influenza viruses (Klenk et al, 1977;Tashiro et al, 1987a,b;Scheiblauer et al, 1992).…”