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Purpose Global data on age-specific prevalence of human papillomavirus (HPV) infection in males, especially for oncogenic HPV types 16 and 18, are essential for future efforts to prevent HPV-related diseases, including expanded access to HPV prophylactic vaccines for boys and young men. Methods A systematic review of peer-reviewed publications was conducted to summarize worldwide data on genital HPV-DNA prevalence in men. Studies using polymerase chain reaction or hybrid capture detection assays were included. Results Approximately 6,600 abstracts were identified. Of them, 64 reported age-specific HPV prevalence and were included in the review. Of these, 38 were from populations at high risk of HPV infections, such as sexually transmitted infection clinic attendees, human immunodeficiency virus-positive males, and male partners of women with HPV infection or abnormal cytology. The largest proportions of studies were from Europe (38%) and North America (25%), with smaller proportions from Central and South America (19%), Asia (11%), and Africa (5%). Across all regions, data on HPV prevalence were generally limited to men >18 years of age. HPV prevalence was high among sexually active men in all regions but with considerable variation, from 1% to 84% among low-risk men and from 2% to 93% among high-risk men. Peak HPV prevalence spanned a wide range of ages and was generally not concentrated in the younger age groups. Age-specific prevalence curves were relatively flat or declined only slightly following peak prevalence. Conclusions Genital HPV infection in men varies widely, both between and within high- and low-risk groups and by geographic region. Compared with that in women, HPV prevalence in men seems to peak at slightly older ages and remains constant or decreases slightly with increasing age, suggesting persistent HPV infection or a higher rate of reinfection.

Global data on age-specific prevalence of human papillomavirus (HPV) infection overall, and for high-risk HPV types 16 and 18, are essential for the future implementation of HPV prophylactic vaccines for cervical cancer prevention.A systematic review of peer-reviewed publications was conducted to summarize worldwide data on genital HPV-DNA prevalence in women. Studies with clear descriptions of polymerase chain reaction or hybrid capture detection assays were included.A total of 346,160 women were included in 375 studies. Of 134 studies with age-stratified HPV prevalence data (116 low sexual risk populations, 18 high sexual risk populations), over 50% were from Europe and the Middle East (38%) and North America (19%), with smaller proportions from Asia and Australia (21%), Central and South America (11%), and Africa (10%). Across all geographical regions, data on HPV prevalence were generally limited to women over 18 years of age. Consistently across studies, HPV infection prevalence decreased with increasing age from a peak prevalence in younger women (or =25 years of age). In middle-aged women (35-50 years), maximum HPV prevalence differed across geographical regions: Africa (approximately 20%), Asia/Australia (approximately 15%), Central and South America (approximately 20%), North America (approximately 20%), Southern Europe/Middle East (approximately 15%), and Northern Europe (approximately 15%). Inconsistent trends in HPV prevalence by age were noted in older women, with a decrease or plateau of HPV prevalence in older ages in most studies, whereas others showed an increase of HPV prevalence in older ages. Similar trends of HPV 16 and/or 18 prevalence by age were noted among 12 populations with available data.Genital HPV infection in women is predominantly acquired in adolescence, and peak prevalence in middle-aged women appears to differ across geographical regions. Worldwide variations in HPV prevalence across age appear to largely reflect differences in sexual behavior across geographical regions. Further studies of HPV prevalence in adolescents are needed for all geographic regions.

Very little is known about how environmental changes such as increasing temperature affect disease dynamics in the ocean, especially at large spatial scales. We asked whether the frequency of warm temperature anomalies is positively related to the frequency of coral disease across 1,500 km of Australia's Great Barrier Reef. We used a new high-resolution satellite dataset of ocean temperature and 6 y of coral disease and coral cover data from annual surveys of 48 reefs to answer this question. We found a highly significant relationship between the frequencies of warm temperature anomalies and of white syndrome, an emergent disease, or potentially, a group of diseases, of Pacific reef-building corals. The effect of temperature was highly dependent on coral cover because white syndrome outbreaks followed warm years, but only on high (>50%) cover reefs, suggesting an important role of host density as a threshold for outbreaks. Our results indicate that the frequency of temperature anomalies, which is predicted to increase in most tropical oceans, can increase the susceptibility of corals to disease, leading to outbreaks where corals are abundant.

Listeria monocytogenes is a facultatively anaerobic short gram-positive rod-shaped bacterium that infects a wide range of animals, including ruminants, monogastric animals, birds, fish, rodents, and humans. Infection with this obligate intracellular pathogen causes 3 distinct clinical entities, septicemia, encephalitis, and abortion, which rarely occur simultaneously in the same animal. The septicemic form affects the viscera with or without meningoencephalitis and is common in monogastric animals, whereas encephalitis and abortion occur principally in adult ruminants. Chinchillas are considered one of the species more susceptible to visceral listeriosis, especially when reared in confinement. Listeriosis in chinchillas has been described in many areas of the United States during a period (1949-1955) when chinchilla pelts were prized commodities in the fur industry. More recently, chinchillas have become a widely used animal model for studies of noise-induced hearing loss. An outbreak of disseminated visceral listeriosis occurred in a breeding colony of 130 chinchillas located in northern Idaho. The chinchillas in this operation were raised for pelts. Polygamous breeding was practiced; 1 male had access to 8 females. The feed, open sacks of commercially formulated chinchilla pellets and a bale of hay, was stored on a wood pallet. To promote maintenance of their hair coats, a dust bath pan was provided for the animals. During December 1995, there was an unusually large influx of mice into the chinchilla building, and on several occasions the owners noted mouse droppings in the feed. By January 1996, the colony experienced a 23% mortality (30 of 130) in breeding animals of various ages. Approximately 4 days prior to death, the animals were anorectic and hunched, and some had torticollis. Many animals were found dead without premonitory clinical signs. Four chinchillas (2 dead males, 1 dead female, 1 moribund female) were submitted to the Washington Animal Disease Diagnostic Laboratory for necropsy. All 4 chinchillas were emaciated and lacked subcutaneous and retroperitoneal fat. Consistent gross lesions in the 3 dead chinchillas included multifocal 0.1-0.3-cm-diameter whitetan foci affecting the capsular surfaces and parenchyma of the liver, mesenteric lymph nodes, and the serosa of the small and large intestines, particularly the cecum and colon. Individual differences in postmortem lesions are listed in Table 1. Animal A, a dead female, had a 2-cm rectal prolapse and colonic intussusception in addition to the visceral foci. The intussusception consisted of a 3-cm segment of dark red prox