Contributions of environmental and genetic factors to IgG subclass responses against Plasmodium falciparum antigens RESA and MSP2 were investigated among adults in a highly endemic area of Papua New Guinea. Heritabilities were estimated using variance component analysis. Familial aggregation of several responses was found, including IgG1, IgG2 and IgG3 responses against RESA, IgG1 and IgG3 responses against the 3D7 form of MSP2 and IgG1, IgG2 responses against the FC27 form of MSP2. Allowance for sharing of houses explained some of the non-genetic variance but not the familial aggregation. The variance of IgG3 responses against RESA and IgG1, IgG2 against MSP2 (FC27) was partly explained by sharing of HLA class II genotypes, although heritability was low. Segregation analyses indicated that any genetic regulation was more complex than governed by a single major gene. Such host genetic variation in responses to specific malaria antigens has implications for immuno-epidemiology and vaccine development.

The prevalence and incidence of Trypanosoma evansi infections in village buffaloes in Central Java were estimated using parasitological tests, two antigen-detection ELISAs (2G6 Ag-ELISA and Tr7 Ag-ELISA), an antibody-detection ELISA (IgG ELISA) and a card agglutination test (CATT). Of 2387 village buffaloes tested in five districts, 4% (95% confidence interval [CI]: 3%, 5%) were positive with the microhaematocrit test (MHCT), 58% (95% CI: 56%, 60%) were positive with the 2G6 Ag-ELISA and 70% (95% CI: 68%, 72%) were positive with the Tr7 Ag-ELISA. An increasing prevalence with age was found and the proportion of positive buffaloes was highest in the over 84 months-old age-group (68%) with the 2G6 Ag-ELISA and in the 37–60 months-old age-group (78%) with the Tr7 Ag-ELISA. Parasitaemic buffaloes were found in more than half of the villages visited. Corrected village-specific prevalence values obtained with the two Ag-ELISAs ranged from 0% to over 100%, and prevalence differed significantly (P[les ]0·0001) between villages in four of the five districts. Overall, 10% of buffaloes tested in markets were found to be parasitaemic and 39, 56 and 47% were found positive with the 2G6 Ag-ELISA, IgG ELISA and CATT, respectively. Incidence rates varied according to the test used and ranged from 0·22 (95% CI: 0·09, 0·44) to 0·44 (95% CI: 0·24, 0·76), per animal-year at risk, in two villages. The results highlight the importance of using validated diagnostic tests to obtain accurate estimates of prevalence and incidence. These parameters are needed, for example in mathematical models, for the development and evaluation of different control strategies for T. evansi infections in buffaloes.

The objective of this study was to investigate the dynamics of PRRSV infection and to quantify transmission within a breeding herd, and its impact on herd performance. For this purpose a longitudinal study was performed in a closed breeding herd of 115 sows. Statistical methods and Monte Carlo simulations based on stochastic SIR models were used to analyse the observational data. Moreover, a case-control study was performed to determine whether seroconversion of sows during gestation was associated with aberrant litters. The transmission parameter R was estimated to be 3·0 (95% confidence interval 1·5–6·0) for the model version based on the most plausible assumptions that the infectious period lasts 56 days and no lifelong immunity exists after infection. Based on simulations using a breeding herd of equal size the average time-to-extinction was estimated to be 6 years; using a herd of twice the size, it was 80 years. Furthermore, in contrast to the epidemic phase of the disease, the endemic phase was not detrimental to herd performance.