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Tuomanen EI.: Pathogenesis of pneumococcal inflammation: otitis media Vaccine. 19 Suppl 1:S38-40, 2000 Pneumococci cause damage to the ear in otitis media with an association with bacterial meningitis. The pathogenesis of injury involves host response to cell wall constituents and the pore-forming toxin, pneumolysin. Release of cell wall constituents, particularly during antibiotic-induced bacterial lysis, leads to an influx of leukocytes and subsequent tissue injury. The signal transduction cascade for this response is becoming defined and includes CD14, Toll-like receptor 2, NFkB, and cytokine production. The second source of injury is the cytotoxicity of the pore forming toxin, pneumolysin. Decreasing the sequelae of otitis can be achieved by an increased understanding of the site-specific mechanisms of pneumococcal-induced inflammation.

Cunningham MW.: Pathogenesis of group A streptococcal infections. Clinical Microbiology Reviews. 13):470-511, 2000 Group A streptococci are model extracellular gram-positive pathogens responsible for pharyngitis, impetigo, rheumatic fever, and acute glomerulonephritis. A resurgence of invasive streptococcal diseases and rheumatic fever has appeared in outbreaks over the past 10 years, with a predominant M1 serotype as well as others identified with the outbreaks. Emm (M protein) gene sequencing has changed serotyping, and new virulence genes and new virulence regulatory networks have been defined. The emm gene superfamily has expanded to include antiphagocytic molecules and immunoglobulin-binding proteins with common structural features. At least nine superantigens have been characterized, all of which may contribute to toxic streptococcal syndrome. An emerging theme is the dichotomy between skin and throat strains in their epidemiology and genetic makeup. Eleven adhesions have been reported, and surface plasmin-binding proteins have been defined. The strong resistance of the group A streptococcus to phagocytosis is related to factor H and fibrinogen binding by M protein and to disarming complement component C5a by the C5a peptidase. Molecular mimicry appears to play a role in autoimmune mechanisms involved in rheumatic fever, while nephritis strain-associated proteins may lead to immune-mediated acute glomerulonephritis. Vaccine strategies have focused on recombinant M protein and C5a peptidase vaccines, and mucosal vaccine delivery systems are under investigation.

Prevention of HIV exposure is the best line of defense to prevent occupational transmission of HIV as there is no vaccine available to develop specific immunity and the postexposure prophylaxis is toxic. Following appropriate workplace practices in the laboratory focus on preventing needlesticks or other sharps injuries and exposure of mucous membranes and abraded skin to HIV-infected blood or body fluids.

The FDA has approved vaccines to prevent HPV infections in young women: Gardasil, Merck & Co, quadrivalent vaccine, FDA approved June 2006 Cervarix, GlaxoSmithKline Biologicals, bivalent vaccine, FDA approved October 2009Vaccination is recommended for young women and immunization before the onset of sexual activity. If the vaccine is received after a HPV infection, it protects the individual from other HPV types that they have not been infected with, assuming these types are included in the vaccine. Gardasil and Cervarix are both recombinant vaccines administered in a set of three doses. Once vaccinated, regular cervical screening is required to detect infections and abnormal cytology from HPV types not contained in vaccines.

The 2009 H1N1 influenza virus was first detected in the United States on April 15, 2009.The virus was a unique combination of influenza virus genes never previously identified in either animals or people; they were most closely related to swine-lineage H1N1 viruses (hence the designation of "swine influenza"). However, epidemiological investigations of initial human cases did not identify exposures to pigs and it became apparent that this new virus was circulating among humans and not among U.S. pig herds.By April 21, 2009, the Centers for Disease Control and Prevention (CDC) began working on development of a new vaccine effective against this new strain. On April 24, 2009, the CDC uploaded complete gene sequences of the 2009 H1N1 virus to a publicly accessible international influenza database. At the same time vaccine development was occurring, work was also being done at CDC to help laboratories more quickly identify the 2009 H1N1 virus in patient samples. A real time PCR assay developed by the CDC was cleared for use by the Food and Drug Administration (FDA) under an Emergency Use Authorization (EUA) on April 28, 2009.The development of an effective, rapidly performed molecular assay was critical, because a CDC evaluation of non-molecular rapid influenza assays indicated that while these tests were capable of detecting the novel H1N1 strain when present in high concentrations, the overall sensitivity was low. Positive results with these assays were useful, but negative results did not rule out infection with influenza.

Judicious use of antimicrobials, especially in outpatient settings, can help control the emergence of CA-MRSA and limit the acquisition of additional resistance by existing strains. Regardless of origin, minimizing antibiotic selective pressure that favors the development of resistant strains is essential to controlling the emergence of these strains in both hospital and community settings.The development of vaccines to prevent S. aureus infection in both healthcare and community settings holds great promise. Recently (2007) a vaccine based on an immunotherapeutic licensed to Merck has shown promising results in a clinical trial against hospital acquired S. aureus infections, while Nabi Biopharmaceuticals, Ft. Lauderdale, FL, are developing the "next generation" of StaphVax, which will contain antigen against S. aureus detoxified Panton Valentine Leucocidin and the cytolytic alpha-toxin.

Preventive measures are actions that you can take to protect yourself from bloodborne pathogens. They include:Obtaining the hepatitis B vaccine Following standard precautions

There are approximately 800,000 to 1.4 million individuals with chronic hepatitis B in the United States. Worldwide it is estimated that there are 350 million people infected with HBV, which contributes to an estimated 620,000 deaths worldwide each year.*The annual number of occupational infections has decreased 95% since hepatitis B vaccine became available in 1982, from more than 10,000 in 1983 to less than 400 in 2001.*** Reference: Hepatitis B information for health professionals. CDC website. Available at: http://www.cdc.gov/hepatitis/HBV/HBVfaq.htm#overview. Accessed October 28, 2011.**Reference: Exposure to blood: What healthcare personnel need to know. CDC website. Available at: http://www.cdc.gov/ncidod/dhqp/pdf/bbp/Exp_to_Blood.pdf. Accessed October 28, 2011.

You can avoid exposure to Hepatitis B by taking the appropriate precautions which include: Hepatitis B vaccine Standard precautions Proper work practices Personal protective equipment

The Hepatitis B Vaccine is one of the most important ways to prevent infection. About 90% of people who receive it get immunity.The present recombinant vaccine is made by genetically altered bakers yeast and contains no blood components. It is very safe.Side effects are minimal. Symptoms such as temporary soreness at the injection site, mild fever, or joint pain may occur but are rare.The procedure consists of three shots in the upper arm given over a six month period.The OSHA standard requires that employers provide the vaccine free of charge to you if your occupation puts you at risk. You may decline the vaccine; but you will be asked to sign a Declination Statement.

Susceptibility to an influenza virus strain is dependent on the immune status of the human host, since our bodies become immune only to the strains that we have been exposed to previously (either naturally or by vaccination). The lack of previous exposure to this subtype resulted in the rapid spread and increased number of infections, especially in the younger population. Respiratory infections occurred, even among those individuals who had received the seasonal flu vaccine because that vaccine was not formulated to protect against the influenza A 2009 H1N1 subtype.