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Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of West Indian Medical Journal is the property of West Indian Medical Journal (WIMJ) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Limited specimen collection and testing for influenza occurred in the English and Dutch-speaking Caribbean countries prior to the 2009/2010 influenza pandemic. Caribbean Epidemiology Centre (CAREC) member countries rapidly mobilized to collect specimens during the pandemic and a vast majority of confirmed cases during the pandemic period were influenza A(H1N1)pdm09., Objectives: To describe the aetiology and distribution of acute respiratory illness (ARI) among laboratory confirmed cases during the first year after the 2009/2010 influenza pandemic in the English- and Dutch-speaking Caribbean., Results: In total, 774 specimens were tested and 394 (52.7%) cases had positive laboratory confirmation. Respiratory syncytial virus (RSV) (28.4%) and influenza A(H3N2) (23.1%) were most frequently detected. RSV activity peaked in July 2011 while influenza A(H3N2) peaked in October 2010. Influenza was responsible for illness in greater numbers in persons 15-64 years while RSV was seen in primarily in children<5 years and adults>65 years. Other agents confirmed include rhinovirus (12.9%), influenza B (10.9%) and influenza A(H1N1)pdm09 (9.4%)., Conclusions: RSV and influenza A(H3N2) were the most common viruses identified during the first year after the influenza A(H1N1)pdm09 pandemic. Influenza was detected every month with peak activity corresponding to that typically seen in North America (October to March). In order to determine the seasonality of influenza and RSV, laboratory data from subsequent years and increased specimen submission is needed., (© 2013 John Wiley & Sons Ltd.)

Objective: Human papillomavirus (HPV) genotypes and their relative prevalences were determined in a cohort of 310 sexually active women in Trinidad, West Indies., Methods: Cervical samples were collected with Ayre's spatulas and endocervical brushes. Samples were used for the conventional Papanicolaou test and for determining HPV genotypes by amplification of a section of the viral L1 gene, followed by DNA sequencing and probe hybridization., Results: HPV infections were identified in 126 of 310 (40.6%) women. Of them, 83 (65.8%) were infected with high-risk HPV, 16 (12.7%) with low-risk HPV, and 27 (21.4%) with HPV types of unknown risk. HPV 52 (12.7%) was the most frequently occurring high-risk type, followed by HPV 66 (10.3%), HPV 16 (9.5%), and HPV 18 (8.6%). High-risk types HPV 16 and HPV 66 were each found in 3 (20.0%) and HPV 18 was found in 1 (6.6%) of the 15 women with abnormal cytology., Conclusions: Cervical HPV prevalence and heterogeneity of HPV genotypes are high in this Trinidad cohort. The relative importance of HPV genotypes in the development of cervical lesions needs further investigation in Trinidad in order to better understand the epidemiology of HPV infections as well as to determine the role of HPV testing in the screening, prevention, and control of cervical cancer. This pilot study provided important information on the prevalence of HPV genotypes, which will be used in future nationwide studies.

Objective: To describe mortality trends and potential years of life lost (PYLL) due to leading causes of death in 21 Caribbean countries during 1985, 1990, 1995 and 2000., Methods: Mortality data for 1985, 1990, 1995 and 2000 were analyzed to identify regional mortality trends using crude, age-specific and age-adjusted death rates and potential years of life lost. The variables used were age, gender and underlying cause of death., Results: During 1985-2000, there was an overall 5% decrease in age-adjusted mortality rates and male mortality exceeded female mortality. Heart disease was the leading cause of death, with cancers, cerebrovascular diseases, diabetes mellitus and hypertensive disease also among the top five causes in most years. Prostate cancer and cancer of the uterus and breast were the leading causes of death due to cancers. HIV disease (AIDS) featured in the ten leading causes of death for the first time in 1995 and was the 5th leading cause in 2000., Conclusion: During the period 1985-2000, countries experienced an increase in mortality due to non-communicable diseases, AIDS and assaults (homicides); the latter two causes were most common among the 15-44 year age group. In 2000, AIDS, heart disease and assault (homicide) were the largest contributors to PYLL.

Objectives: To determine whether, because of the extensive recent spread of HIV infection in South Asia, South Asians (those people who classify themselves as Indian, Pakistani, Bangladeshi or Sri Lankan in origin) resident in the UK were at increased risk of HIV infection and to review current surveillance systems for detecting any such increase., Design: Analysis of: ethnic grouping and probable country of infection recorded on voluntary confidential reports of AIDS cases and newly diagnosed HIV infections; blood donation testing data; reports of imported gonorrhoea infections; country of birth data from the unlinked anonymous (UA) survey of Sexually Transmitted Disease (STD) clinic attenders; district of residence data from the UA survey of pregnant women; ethnic grouping of prevalent diagnosed HIV infections., Results: Few reported AIDS cases or HIV infections were found in people of South Asian ethnic origin and few reported HIV or gonorrhoea infections were associated with exposure in South Asia. Data derived from the UA programme suggested as yet no increase in HIV prevalence in either STD clinic attenders born in South Asia or in pregnant women resident in districts containing substantial numbers of ethnic South Asians., Conclusions: There was no evidence that South Asians resident in the UK are currently at greater risk of HIV infection than people of white ethnicity or, therefore, that south Asian heterosexuals are a group deserving priority in HIV prevention. However, as rapid spread of HIV infection is being recorded in the Indian subcontinent, continuous monitoring is necessary. This will be facilitated by improved collection of ethnic group information in all surveillance activities.

Objective: To devise and validate a method for adjusting HIV seroprevalences in pregnant women to estimate population prevalences among all women in their child-bearing years., Design: Birth and termination rates from women with known HIV infection in the United Kingdom were calculated according to the likely route of HIV infection and whether HIV infection was diagnosed., Methods: Birth and termination rates were weighted and combined to produce summary statistics. Comparisons were then made with population birth and termination rates to derive summary relative inclusion ratios (RIRs), the relative probabilities of including HIV-infected and uninfected women in seroprevalence surveys of pregnant women., Results: The derived RIRs for women having live births were close to unity: 1.03 [95% confidence intervals (CI) 0.90-1.17] for London and 0.80 (Cl, 0.71-0.89) for elsewhere in England and Wales. This indicates that currently observed overall seroprevalences among pregnant women having live births in London would be similar to those among all women of the same age, while elsewhere it would be slightly underestimated. Sensitivity analysis indicated that RIRs could, however, vary three-fold (0.47-1.56) according to the proportion of diagnosed maternal infections and the mix of maternal HIV-exposure categories. The method was validated by using it to predict the ratio of unlinked seroprevalences between women having terminations and live births in London. It predicted a ratio of 1.74: 1, which is close to the observed ratio of 2.07 : 1., Conclusions: Application of HIV seroprevalences from pregnant women to whole populations may need adjustment for fertility rates among HIV-infected women. A general method for this has been derived and validated. Gathering fertility data for HIV-infected women is a useful adjunct to serosurveillance.

HIV prevalence estimates for pregnant women from unlinked anonymous surveys are becoming increasingly available and can be used to determine the prevalence of HIV in women in the same population. The ratio of prevalence in pregnant women to that in all women is influenced by HIV-related risk behaviours that are different for pregnant and nonpregnant women and also by differences in fertility level among infected and uninfected women. This ratio is affected by biases that are likely to be culturally and socially specific. A model is proposed for the qualification and quantification of these biases and hence the estimation of general female population prevalence from serosurveillance data on pregnant women.