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Op vrijdag 19 juni 2009 16:56 schreef Pietverdriet het volgende:[..]
Bij de spaanse griep gingen miljoenen mensen dood, meer als in de eerste wereldoorlog gesneuveld zijn, dat klopt, maar ik heb nog geen echte aanwijzing gezien of gehoord dat deze griep zo dodelijk is.
Er gaan per jaar een 800 mensen dood als gevolg van het niet voldoende luchten van huizen, daar hoor je ook vrijwel nooit wat over. Integendeel, huizen worden zo gebouwt dat het erg lastig is goed te luchten.
Vergelijkingen met het aantal doden t.o.v de spaanse griep gaan mank >>
Influenza A virus (IAV) causes respiratory tract infections leading to recurring epidemics with high rates of morbidity and mortality. In the past century IAV induced several world-wide pandemics, the most aggressive occurring in 1918 with a death toll of 20–50 million cases.
However, infection with IAV alone is rarely fatal. Instead, death associated with IAV is usually mediated by superinfection with bacteria, mainly Streptococcus pneumoniae. The reasons for this increased susceptibility to bacterial superinfection have not been fully elucidated. We previously demonstrated that triggering of TLR7 causes immune incompetence in mice by induction of lymphopenia. IAV is recognized by TLR7 and infections can lead to lymphopenia. Since lymphocytes are critical to protect from S. pneumoniae it has long been speculated that IAV-induced lymphopenia might mediate increased susceptibility to superinfection. Here we show that sub-lethal pre-infections of mice with IAV-PR8/A/34 strongly increased their mortality in non-lethal SP infections, surprisingly despite the absence of detectable lymphopenia. In contrast to SP-infection alone co-infected animals were unable to control the exponential growth of SP. However, lymphopenia forced by TLR7-triggering or antibody-mediated neutropenia did not increase SP-susceptibility or compromise the ability to control SP growth. Thus, the immune-incompetence caused by transient lympho- or leukopenia is not sufficient to inhibit potent antibacterial responses of the host and mechanisms distinct from leukodepletion must account for increased bacterial superinfection during viral defence.
Characterization of an IAV/S. pneumoniae co-infection model
To establish a model system for IAV/S. pneumoniae synergism in the mouse we established two sublethal infections with either the mouse-adapted viral strain PR8/A/34 or the pneumococcal strain TIGR4. 0.04 MLD50 of IAV caused a mild disease with a transient mean loss of max. 10% body weight up to day 7 of the infection, which was resolved by day 12 post infection (Fig. 1A). Likewise, a sublethal course of S. pneumoniae was established after infection with 1×105 CFU that was not detectable by weight changes of infected animals (Fig. 1A). A productive infection was verified from nasopharyngeal lavages at day 7 p.i. in all infected animals (Fig. 1B). Survival-curves showed that both infections were sublethal to 80% (IAV) or 88% (S. pneumoniae) of all animals although single individuals could still succumb to the infection as seen elsewhere [10].
The combined sublethal infections with IAV followed by S. pneumoniae 7 days later were highly synergistic leading to 63% mortality within 2 days after the bacterial superinfection (Fig. 1C). The lung homogenates of animals succumbing to the co-infection showed high CFU in their tissues similar to the levels observed in the rare cases of lethal courses from single infections (Fig. 1D).
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2654096Meerdere studies wijzen uit dat het aantal doden voornamelijk kwam door hygiënische omstandigheden. Dezelfde griep nu zou een totaal andere impact hebben.
Bacteria main cause of 1918 deathshttp://www.abc.net.au/science/articles/2009/02/06/2484125.htmStrep infections and not influenza may have killed most people during the 1918 influenza pandemic, which suggests predictions about a new pandemic could be exaggerated, say US researchers.
The findings suggest that amassing antibiotics to fight bacterial infections may be as important as stockpiling antiviral drugs to battle flu, they say.
Professor Keith Klugman of Emory University, Atlanta and colleagues report their findings in the journal Emerging Infectious Diseases.
The team looked at information available about the 1918 flu pandemic, which killed between 50 million and 100 million people globally in the space of about 18 months.
Some research has shown that on average it took a week to 11 days for people to die - which fits in more with the known pattern of a bacterial infection than a viral infection, write Klugman and colleagues.
"We observed a similar 10-day median time to death among soldiers dying of influenza in 1918."
People with influenza often get what is known as a "superinfection" with a bacterial agent. In 1918 it appears to have been Streptococcus pneumoniae.
"Neither antimicrobial drugs nor serum therapy was available for treatment in 1918," Klugman's team write.
Today there are vaccines that protect against different strains of S. pneumonia, which cause infections from pneumonia to meningitis.
http://www.mrwonkish.nl Eurocrisis, Documentaires, Economie