Hepatitis A virus (HAV) is spread by faecal-oral contact or ingestion of contaminated food or water. Lifelong immunity is conferred by infection or vaccination, so anti-HAV seroprevalence studies can be used to indicate which populations are susceptible to infection. Seroprevalence rates are highly correlated with socioeconomic status and access to clean water and sanitation. Increasing household income, education, water quality and quantity, sanitation, and hygiene leads to decreases in HAV prevalence. Japan, Australia, New Zealand, Canada, the United States, and most European nations have low anti-HAV rates. Although anti-HAV rates remain high in most Latin American, Asian, and Middle Eastern nations, average seroprevalence rates are declining. Surveys from Africa generally indicate no significant decline in anti-HAV rates. Because the severity of illness increases with age, populations with a high proportion of susceptible adults should consider targeted vaccination programmes.

A maximum likelihood procedure is given for estimating household and community transmission parameters from observed influenza infection data. The estimator for the household transmission probability is an improvement over the classical secondary attack rate calculations because it factors out community-acquired infections from true secondary infections. The mathematical model used does not require the specification of infection onset times and, therefore, can be used with serologic data which detect asymptomatic infections. Infection data were derived by serology and virus isolation from the Tecumseh Respiratory Illness Study and the Seattle Flu Study for the years 1975-1979. Included were seasons of influenza B and influenza A subtypes H1N1 and H3N2. The transmission characteristics of influenza B and influenza A(H3N2) and A(H1N1) outbreaks during this period are compared. Influenza A(H1N1), A(H3N2) and influenza B are found to be in descending order both in terms of ease of spread in the household and intensity of the epidemic in the community. Children are found to be the main introducers of influenza into households. the degree of estimation error from the misclassification of infected and susceptible individuals is illustrated with a stochastic simulation model. This model simulates the expected number of detected infections at different levels of sensitivity and specificity for the serologic tests used. Other sources of estimation error, such as deviation from the model assumption of uniform community exposure and the possible presence of superspreaders, are also discussed.

A compartmental model is presented for the spread of HIV in a homosexual population divided into subgroups by degree of sexual activity. The model includes constant recruitment rates for the susceptibles in the subgroups. It incorporates the long infectious period of HIV-infected individuals and allows one to vary infectiousness over the infectious period. A new pattern of mixing, termed preferred mixing, is defined, in which a fraction of a group's contacts can be reserved for within-group contacts, the remainder being subject to proportional mixing. The fraction reserved may differ among groups. In addition, the classic definition of reproductive number is generalized to show that for heterogeneous populations in general the endemic threshold is BDc,, where cr is the mean number of contacts per infective. The most important finding is that the pattern of contacts between the different groups has a major effect on the spread of HIV, an effect inadequately recognized or studied heretofore.

The occurrence of influenza was followed in Tecumseh, Michigan during the five year period 1976-1981 by identifying onset of acute respiratory illness and by virus isolation and serology. Type B outbreaks were observed in 1976-1977 and 1979-1980, type A (H3N2) in 1977-1978 and 1980-1981, and type A (H1N1) viruses in 1977-1978, 1978-1979, and 1980-1981. Evidence of low level circulation of viruses in the year preceding an outbreak was not obtained. Age-specific isolation rates from specimens collected by the community physicians differed from age-specific isolation rates from specimens collected from the surveillance, suggesting the operation of a selection mechanism in the former. Symptoms associated with virus isolation were strongly influenced by age. Within age groups, several variables, especially median duration, indicated type A (H3N2) had produced the most severe illnesses, type A (H1N1) the mildest, with type B intermediate. Age-specific infection rates determined by serology for the 1976-1977 and 1977-1978 influenza seasons confirmed the consistently high rates for type A (H3N2) in children with some fall-off with increasing age. Type A (H1N1) rates peaked in children aged 5-19 years and type B in children aged 5-14 years. This may be related in part to insensitivity of the hemagglutination inhibition test in those under age 5 years. Infection with type A (H1N1) was detected at low frequency in adults. Pathogenicity was calculated based on the serologic data. It was estimated for all ages combined that, at a minimum, type A (H3N2) infection produced febrile illness in 25% of cases and type B infection produced respiratory illness in 34% of cases.

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The combination of two factors gives early HIV infection an especially strong influence on transmission dynamics: (a) increased transmission probabilities and (b) increased transmission potential of partners infected during this period. Most attention has been focused on the first factor because it fits the way we usually think about risk factors affecting individuals. The second factor acts not on individuals, but across chains of transmission. It is missed by models with constant partnership formation rates over an individual's life or with random mixing. It cannot be assessed from available data collected from individuals. Its assessment requires data from both individuals in a partnership. We demonstrate that this second effect can be so strong that early infection can dominate transmission dynamics even when transmission probabilities are only modestly increased. This second effect is not directly parameterized in our models but arises from two realistic types of temporal variation in partnership formation: (a) Partnership formation rates vary by age with preferential partnership formation in one's own age group, and (b) individuals of any age can experience transient periods of high-risk partnership formation. In a model with only the age-related effect, early infection is observed to dominate transmission dynamics when 20% of transmissible virus is allocated to the first 6 weeks of infection, 7% to middle infection, and 73% to late infection. This domination occurs both early in the course of an epidemic and later when endemic infection levels have been reached. When the second effect is added, early infection is seen to dominate transmission in a model allocating 10% of transmissible virus to the first 6 months, 40% to middle infection, and 50% to late infection. In this model, transmission probabilities during early infection are only 4.17 times those of middle infection and half those of late-stage infection.

To better understand the etiology of recurrent urinary tract infection (UTI), the authors followed a cohort of 285 female college students with first UTI for 6 months or until second UTI. A first UTI due to Escherichia coli was followed by a second UTI three times more often than was a non-E. coli first UTI (24 vs. 8%; p = 0.02). In a logistic regression analysis limited to the 224 women from the University of Michigan Health Service and the University of Texas at Austin Health Service from September 1992 to December 1994, with a first UTI due to E. coli, vaginal intercourse increased the risk of a second UTI with both a different (odds ratio (OR) = 1.60, 95% confidence interval (CI): 1.19, 2.15) and the same (OR = 1.37, 95% CI: 0.91, 2.07) uropathogen, as did using a diaphragm, cervical cap, and/or spermicide (same uropathogen: OR = 1.53, 95% CI: 0.95, 2.47; different uropathogen: OR = 1.77, 95% CI: 1.22, 2.58). Condom use decreased the risk of a second UTI caused by a different uropathogen (OR = 0.68, 95% CI: 0.48, 0.99) but had no effect on a second UTI caused by the same E. coli (OR = 0.99; 95% CI: 0.66, 1.50). Type or duration of treatment was not associated with a second UTI. Although the risk of second UTI is strongly influenced by sexual behavior, women with a first UTI caused by E. coli are more likely than are those with a non-E. coli first UTI to have a second UTI within 6 months.

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