Updates
July 1, 2000 4 minutes read
Updates
By Carol A. Kemper, MD, FACP
Did PEP Prevent HIV Infection in this Girl?
Source: Katzenstein TL, et al. Ann Intern Med 2000;133:31-34.
This report documents the re-markable story of an unfortunate 13-year-old girl who failed to develop evidence of HIV infection following receipt of HIV-contaminated blood and extended postexposure prophylaxis (PEP). The blood donor presented with acute HIV infection and a high viral load 25 days following a bloody head butting incident in a gay bar in Copenhagen, Denmark. It was subsequently learned that he had donated blood one week earlier.
Packed cells from the donation had already been administered two days earlier to a 13-year-old girl undergoing corrective orthopedic surgery. Immediate testing of the donor’s fresh frozen plasma still available in storage demonstrated a positive HIV RNA with about 11,000 copies/mL but a negative p24 antigen. The girl’s viral load was barely detectable at 3 copies/mL—possibly a false-positive test result, although entirely feasible given the circumstances. Within 48 hours of the transfusion, she was started on PEP with zidovudine, lamivudine, and indinavir. Within days, ritonavir and then nelfinavir were substituted for indinavir because of intolerance. "PEP" was continued for nine months, during which time there was no further evidence of HIV infection by antibody assay, PCR, or culture. She was found to be homozygous for the CCR5 gene (indicating that she was not refractory to HIV infection). Laboratory studies remained negative for six months after discontinuation of PEP therapy.
Infusion of HIV-infected blood is believed to be uniformly associated with the development of infection in the recipient. It therefore seems likely that infection would have occurred in the absence of PEP, although the initial pretreatment HIV test results in the recipient were inconclusive. Whether a more commonly used PEP regimen, administered for one to four weeks, would have been sufficient or whether the extended PEP administered in this high-risk situation was necessary to successfully thwart infection remains uncertain.
45-Year Outcome of HCV Infection
Source: Seeff LB, et al. Ann Intern Med 2000;132:105-111.
Reports suggest that up to 20% of patients with hepatitis C virus (HCV) infection may progress to chronic liver disease. Using archived serum samples collected between 1948 and 1954, Seeff and colleagues at the Veterans Affairs Medical Center in Washington, DC, were able to assess the natural history of HCV infection on 8568 military personnel originally recruited for a study of group A streptococcal infection. Antibodies to HCV were detected in 17 (0.2%) of the banked sera using ELISA and recombinant immunoblot assay.
More than 45 years later, liver disease had been diagnosed in two of 17 HCV-positive persons (11.8%) vs. 205 of those who were HCV-negative (2.4%). Seven (41%) of the HCV-positive persons had died compared with 2226 (26%) of those who were HCV negative (relative risk, 1.5; CI, 0.8-2.6). Of those who were HCV-positive, one (5.9%) had died due to liver disease (42 years after the original phlebotomy); five had died from unrelated causes and one for unknown reasons a median of 37 years later. In comparison, 119 HCV-negative persons (1.4%) had died of liver disease. Although retrospective studies are often fraught with problems, this extended natural history study suggests that the risk of progression to chronic liver disease in apparently healthy individuals infected with HCV may be less than suggested by other reports.
Avoid Antibiotics in Children with E. coli 0157:H7
Source: Wong CS, et al. N Engl J Med 2000;342:1930-1936.
Earlier reports suggested that the administration of antibiotics to cultures of Escherichia coli 0157:H7 increased the risk of Shiga toxin release. In order to assess the possibility that hemolytic-uremic syndrome (HUS) may be increased because of the administration of antibiotics, Wong and colleagues conducted a prospective cohort study of 71 children younger than 10 years of age with diarrhea due to E. coli 0157:H7. Among the 71 subjects, nine received antimicrobial therapy and 10 developed HUS. Surprisingly, the administration of antibiotics was significantly associated with the risk of HUS (relative risk = 14.3; CI = 2.9-70.7). HUS developed in five of nine patients (56%) receiving antibiotics compared with four of 62 (8%) who did not receive antibiotics (P < 0.001).
Other factors associated with an increased risk of HUS included how quickly a stool culture was obtained during the initial illness and a higher initial white blood cell count—both of which are probably reflective of the severity of illness at presentation. While 35% of patients with white blood cell (WBC) counts ranging from 14.3-24.6 cells/mm3 developed HUS, only 6% of those with WBC counts of 8800-11,000 cells/mm3 and none with lower WBC counts did. The sex of the child, the presence of fever, vomiting, or bloody diarrhea, or the type of antibiotic administered were not predictive of HUS. Each of the E. coli strains recovered in children with HUS were sensitive to the agent received. This report strongly suggests that antibiotics should not be administered to children suspected of having gastroenteritis due to E. coli 0157:H7 until the results of cultures are available.
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