Epidemiology of a mumps outbreak in a highly vaccinated island population and use of a third dose of measles-mumps-rubella vaccine for outbreak control--Guam 2009 to 2010.

BACKGROUND: Despite high 2-dose measles-mumps-rubella (MMR) vaccine coverage, a large mumps outbreak occurred on the US Territory of Guam during 2009 to 2010, primarily in school-aged children. METHODS: We implemented active surveillance in April 2010 during the outbreak peak and characterized the outbreak epidemiology. We administered third doses of MMR vaccine to eligible students aged 9-14 years in 7 schools with the highest attack rates (ARs) between May 18, 2010, and May 21, 2010. Baseline surveys, follow-up surveys and case-reports were used to determine mumps ARs. Adverse events postvaccination were monitored. RESULTS: Between December 1, 2009, and December 31, 2010, 505 mumps cases were reported. Self-reported Pohnpeians and Chuukese had the highest relative risks (54.7 and 19.7, respectively) and highest crowding indices (mean: 3.1 and 3.0 persons/bedroom, respectively). Among 287 (57%) school-aged case-patients, 270 (93%) had ≥2 MMR doses. A third MMR dose was administered to 1068 (33%) eligible students. Three-dose vaccinated students had an AR of 0.9/1000 compared with 2.4/1000 among students vaccinated with ≤2 doses >1 incubation period postintervention, but the difference was not significant (P = 0.67). No serious adverse events were reported. CONCLUSIONS: This mumps outbreak occurred in a highly vaccinated population. The highest ARs occurred in ethnic minority populations with the highest household crowding indices. After the third dose MMR intervention in highly affected schools, 3-dose recipients had an AR 60% lower than students with ≤2 doses, but the difference was not statistically significant and the intervention occurred after the outbreak peaked. This outbreak may have persisted due to crowding at home and high student contact rates.

ORF36 protein kinase of Kaposi's sarcoma herpesvirus activates the c-Jun N-terminal kinase signaling pathway.

alpha-, beta-, and gamma-Herpesviruses encode putative viral protein kinases. The herpes simplex virus UL13, varicella-zoster virus ORF47, and Epstein-Barr virus BGLF4 genes all show protein kinase domains in their protein sequences. Mutational analysis of these herpesviruses demonstrated that the viral kinase is important for optimal virus growth. Previous studies have shown that ORF36 of Kaposi's sarcoma herpesvirus (KSHV) has protein kinase activity and is autophosphorylated on serine. The gene for ORF36 is expressed during lytic growth of the virus and has been classified as a late gene. Inspection of the ORF36 sequence indicated potential motifs that could be involved in activation of cellular transcription factors. To analyze the function of ORF36, the cDNA for this viral gene was tagged with the FLAG epitope and inserted into an expression vector for mammalian cells. Transfection experiments in 293T and SLK cells demonstrated that expression of ORF36 resulted in phosphorylation of the c-Jun N-terminal kinase. Autophosphorylation of ORF36 is important for JNK activation because a mutation in the predicted catalytic domain of ORF36 blocked its ability to phosphorylate JNK. Western blot analysis, using phosphospecific antibodies, revealed that mitogen-activated kinases MKK4 and MKK7 were phosphorylated by ORF36 but not by the kinase-negative mutant. Binding experiments in transfected cells also demonstrated that both the wild type and kinase-negative mutant of ORF36 form a complex with JNK, MKK4, and MKK7. In addition, using a tetracycline-inducible Rta BCBL-1 cell line (TREx BCBL1-Rta), JNK was phosphorylated during lytic replication, and inhibition of JNK activation blocked late viral gene expression but not early viral gene expression. In summary, these studies demonstrate that KSHV ORF36 activates the JNK pathway; thus this cell signaling pathway may function in the KSHV life cycle by regulating viral and/or cellular transcription.

Male mammary fistula complicating senescent gynecomastia.

Mammary fistulas occurring in males are extremely rare, the first being described in 1974 by Tedeschi et al. (1). Our detailed review of the world literature has revealed a total of just 20 cases of mammary fistulas in males; a total which includes three cases of mammary fistulas in infants and three cases associated with human immunodeficiency virus (HIV) infection. Mammary fistulas develop between the lactiferous ducts and areolar skin. Altered duct anatomy and microarchitecture may predispose a patient to mammary fistulas. This discussion focuses on mammary fistulas in males where smoking is a likely etiologic factor, and therefore examines a clinical rarity with just 14 reported cases in the literature. The treatment of mammary fistulas in males is the same as for females once the diagnosis has been made.