Updates
By Carol A. Kemper, MD, FACP, Clinical Associate Professor of Medicine, Stanford University, Division of Infectious Diseases; Santa Clara Valley Medical Center, Section Editor, Updates Section Editor, HIV, is Associate Editor for Infectious Disease Alert
Nosocomial Transmission of Invasive Group A Strep
ProMED-mail post, March 5, 2005; www.promedmail.org
On Marh 5, 2005, the Arizona Republic newspaper reported spread of invasive Group A streptococcal infection to a health care worker at the Flagstaff Medical Center, resulting in severe infection requiring hospitalization. The case patient was hospitalized in early February with necrotizing fasciitis and streptococcal toxic shock syndrome (STSS). Within 6 days, a health care worker, who apparently had contact with the case patient, developed pneumonia, bacteremia, and STSS. Further details were not provided, and the mechanism of transmission (contact vs air) was not known.
Transmission of invasive Group A streptococcal infections has been described in the nosocomial setting, nursing homes, rehab facilities, and even within households. Generally, the risk of transmission is believed to be low, especially in young, healthy individuals.
In an attempt to identify the risk of secondary transmission of these infections, the Ontario Group A Streptoccocal Study Group examined 323 cases of invasive streptococcal infections from 1992 to 1993, for an estimated annual incidence of ~1.5/100,000. Necrotizing fasciitis occurred in 6%. Risk factors for invasive disease included older age and chronic underlying disease, such as diabetes, malignancy, HIV-infection, varicella infection, and alcohol abuse. Of the 323 cases, 45 (14%) occurred in the nosocomial setting and 13 (4%) occurred in nursing homes, often in smaller clusters. Two cases occurred in household contacts, for an estimated risk of 3.2/1000, ~ 200 x the risk of the general population. This data suggest that patients hospitalized with invasive streptococcal infection (eg, fasciitis, bacteremia, and STSS) should be isolated. The value of screening and treatment of household contacts has not been examined, although the spread of invasive disease-causing isolates may be difficult to demonstrate.
Durability of HBV Vaccination
McMahon BJ, et al. Ann Intern Med. 2005;142:333-341.
The durability of hepatitis b vaccination has not been well delineated. While some experts recommend that health care workers receive a single booster vaccination at 8 to 10 years, there are no formal recommendations for this in the health care setting. Furthermore, the durability of vaccination in all these little kids now receiving vaccine is not known, and there are no guidelines for reassessment of titers or repeated vaccination later in life. Although one can measure persistence of anti-HBs antibody, the loss of detectable antibody (> 10 IU/L) over time does not necessarily imply loss of protection, as cellular immunity may provide a sufficiently protective role.
Longitudinal studies suggest that even when anti-HBs wane over time in heavily vaccinated populations, breakthrough infections are uncommon. McMahon and colleagues examined 1578 Alaskan natives who received 3 doses of HBV vaccine at the age of 6 months or older in 1981-1982. Slightly more than half (53%) were available for re-assessment 15 years later, during which mean plasma levels of anti-HBs decreased from an initial level of 872 IU/L to 27 IU/L. Higher levels of initial anti-HBs, male age, and age greater than 4 at the time of vaccination were associated with higher antibody levels 15 years later.
During the 15 years of followup, 16 documented and 8 possible breakthrough HBV infections occurred (1.26 per 1000 person-years), all of which were asymptomatic. Breakthrough infections were significantly more frequent in vaccine non-responders than responders. Interestingly, 2 persons were infected with wild type HBV and 4 were infected with wild type HBV and HbsAg variants.
Children who received HBV vaccine when they were less than 4 years had the fastest decline in antibody levels—meaning that just as they’ll be reaching their late teens and 20s, and becoming sexually active and potentially at risk for transmission of HBV—their titers will have waned. This leaves open the question of whether and when children vaccinated at a young age may require booster vaccination.
Did Shakespeare Have Syphilis?
Ross JJ. Clin Infect Dis. 2005;40: 399-404.
Syphilis was widespread in England by the 16th century, especially in London. Shakespeare moved to London about this time, leaving behind his pregnant wife in Stratford, and by the early 1590s, had gained enormous wealth and popularity. But, he spent his later years in social isolation, and died bloated, bald, and chronically ill.
Dr. Ross, who has obviously spent considerable time analyzing Shakespeare’s plays and sonnets, theorizes that Shakespeare’s evident knowledge of bawdy sex, frequent references to venereal disease, and his familiarity with symptoms of STDs suggest the bard may have had first hand knowledge of STDs such as gonorrhea and syphilis. As just one example, Dr. Ross points to a total of 55 lines in "Measure for Measure" alluding to STDs. His writings are full of references to "cankers," "hoar leprosy", "limekilns in the palms" (possibly a reference to secondary syphilis), and "incurable bone-ache" (possibly syphilitic periostitis).
The sonnets also display frequent references to "burning love," which when viewed in a different light, may refer to the dysuria of gonorrhea rather than unrequited amour. The poet seeking a remedy for the "new fire" acquired from his mistresses "eye" and "love’s fire heats water," again possible references to dysuria and gonorrhea.
Although many conditions could be interpreted similarly, Dr. Ross maintains they are more than likely references to symptoms of STDs, especially when interpreted in light of his bawdy humor and later misogyny. Dr. Ross pushes his argument further, postulating that Shakespeare’s later years were plagued by tremors, agitation, an inconstant temper, social isolation, and alopecia—all of which could have been the result of mercury poisoning—a common Elizabethan treatment for syphilis.
Mortality in HCV/HIV Co-Infection
El-Sarag HB, et al. Clin Gastroenterol Hepatol. 2005;3:175-183.
In order to examine the impact on mortality of HCV infection among HIV-infected patients, El-Sarag and colleagues from the Houston Veterans Affairs Medical Center and Baylor College performed a retrospective cohort study of HIV-infected patients between 1991-2000. A second separate analysis was performed for a similar group of patients identified after September 1996, following the introduction of highly active antiretroviral therapy, which became readily available about that time (the HAART era).
A total of 18,081 HIV-infected patients were identified for the initial analysis, of whom 5320 had HCV/HIV co-infection. A total of 1642 patients were excluded because of pre-existing liver disease. Patients were censored as of September 1996, to ensure no possible effect of HAART. In Cox multiple regression analysis, the HCV/HIV co-infection group had an adjusted mortality about half that of those HIV-infected patients without HCV (hazard risk ratio 0.55, P < .0001), after controlling for sex, age, year of diagnosis, and severity of HIV disease. For patients identified during the HAART era, the adjusted hazard ratio mortality for co-infection to HIV mono-infected pts. was .83 (P = .003).
These data suggest—somewhat provocatively—that patients with HCV co-infection had lower levels of mortality than patients with HIV-infection alone, which flies against popular belief. Earlier studies suggest that HCV co-infection increases mortality in HIV disease, or at a minimum has little effect. El Sarag et al suspect that some of the variation between this and earlier study results may be attributable to the VA population, which is older, had ready access to health care, are more likely to be drug abusers, and less likely to be men who have sex with men, which may influence the timing and detection of infections of these two. Possible additional sources of variation between this and earlier studies may be due to differences in proportions of those with HCV-related liver disease, severity of HIV disease (CD4 count data was not available), and other comorbidities.
Interestingly, most of the difference between the hazard ratios for the 2 analyses could be accounted for by the improved survival in the HIV-monoinfected group as the result of HAART. Interestingly, there was little change in the mortality of co-infected patients before and after the introduction of HAART—a significant finding of its own, and confirming other reports that patients with HCV infection have a blunted immune response to the introduction of HAART.
On Marh 5, 2005, the Arizona Republic newspaper reported spread of invasive Group A streptococcal infection to a health care worker at the Flagstaff Medical Center, resulting in severe infection requiring hospitalization.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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