International Journal of TROPICAL DISEASE & Health

Gender, Risk, and Mortality in Sub‑Saharan Africa: A Comparative Analysis of Maternal and Male Deaths with Evidence from The Gambia

Ibrahim Sahr Momoh, Jainaba Jallow, Patrick Lebbie — Thu, 08 Oct 2026 00:00:00 +0000

Background: Sub-Saharan Africa carries a disproportionate burden of preventable maternal deaths while also experiencing substantial male mortality across communicable diseases, injuries, violence, non-communicable diseases, and other life-course risks. These burdens are both shaped by sex and gender, but their causal pathways and service-delivery requirements are not interchangeable.

Objective: To compare the causal structures, implementation barriers, and strength of evidence informing maternal- and male-mortality policy in sub-Saharan Africa, with a focused interpretation of evidence from The Gambia.

Methods: A structured narrative review was updated through July 2026 using PubMed/MEDLINE-indexed literature, publisher records, and authoritative WHO and United Nations sources. Priority was given to systematic reviews, meta-analyses, population-based studies, cohort studies, implementation evaluations, and recent regional burden analyses published from 2015 onward. Evidence was synthesised across burden, access, quality, continuity of care, intervention effectiveness, and mortality endpoints.

Results: Maternal mortality policy has a comparatively coherent intervention pathway linking antenatal care, skilled attendance, emergency obstetric care, referral, transport, respectful care, and postpartum follow-up, but losses between these components remain common. Male mortality is more heterogeneous and requires life-course and multisectoral responses. The strongest male-specific intervention evidence remains concentrated in HIV, where men often enter care later and have poorer cascade outcomes. HIV self-testing, differentiated delivery, and integration can improve testing, linkage, retention, and viral suppression, although mortality benefits are not consistently demonstrated. Evidence from The Gambia shows continuing maternal mortality, substantial male involvement in reported road fatalities, marked sex differences in the HIV treatment cascade, and unmet mental-health and sexual-health needs among some groups of men.

Conclusions: A gender-responsive mortality agenda should combine shared health-system infrastructure with differentiated pathways. Maternal survival requires reliable emergency and reproductive care, while male survival requires earlier and more acceptable access to prevention, diagnosis, treatment, and multisectoral risk reduction. Evaluation should privilege mortality, effective coverage, quality, equity, and cost rather than service contacts alone.

Toxoplasma gondii Infection: From Environmental Transmission and Host–parasite Interactions to Clinical Disease, Diagnosis, and Translational Opportunities

Zainab W. Kermasha — Sat, 10 Oct 2026 00:00:00 +0000

Toxoplasma gondii is an obligate intracellular apicomplexan that links environmental contamination, food-animal production, wildlife ecology, maternal-fetal health, and opportunistic disease. The outcome of infection is determined by interactions among parasite developmental stage and genotype, host immune competence, tissue context, route and magnitude of exposure, and the parasite’s ability to reprogramme host-cell biology. This review integrates environmental transmission with molecular pathogenesis, immunity, persistence, clinical disease, diagnosis, and translational opportunities. Felids shed environmentally resistant oocysts that contaminate soil, water, and food, whereas tissue cysts maintain foodborne transmission. After invasion, tachyzoites form a non-fusogenic parasitophorous vacuole and inject rhoptry and dense-granule effectors that modulate host transcription, interferon-mediated restriction, cell death, migration, and nutrient acquisition. While IL-12/IFN-γ-driven cellular responses define protective immunity, differences between murine and human cell-autonomous immunity limit direct extrapolation from experimental models. Maintenance of chronic infection is biologically active rather than inert and involves persistence and reactivation through the BFD1-BFD2 differentiation circuit (Waldman et al., 2020; Licon et al., 2023), tissue-cyst architecture (Blader et al., 2015; Sullivan & Jeffers, 2012; Weiss & Kim, 2013; Eberhard et al., 2025), metabolic remodelling (Wang et al., 2026), and ongoing immune surveillance (Matta et al., 2021; Eberhard et al., 2025). Clinically, disease ranges from asymptomatic infection to congenital disease, ocular toxoplasmosis, encephalitis, and disseminated disease in immunocompromised hosts. Serology remains the main diagnostic tool, but determining when infection occurred is difficult because IgM may persist and assays vary. Molecular assays provide direct evidence of parasite DNA, but their performance is highly dependent on specimen type, parasite load, extraction procedure, and target. Current therapies effectively suppress replicating tachyzoites but do not reliably clear tissue cysts, which remains a major translational bottleneck in chronic-stage biology. Standardised diagnostics, human-relevant experimental systems, stage-specific therapeutics, multistage vaccines, integrated parasite-host omics, and One Health surveillance linking human cases with livestock, felids, wildlife, food, water, and environmental contamination will be required for future advances.

Nanoplastics and Cardiovascular Health: A Review of Environmental Exposure, Biological Mechanisms and GeoHealth Implications

B. Vasudevan, K. Katturajan — Tue, 13 Oct 2026 00:00:00 +0000

Background: Plastic production and waste have expanded rapidly, and small plastic particles are now documented across environmental compartments and in several human tissues. Nanoplastics are of particular concern because their small size, large specific surface area and dynamic biomolecular corona may alter transport, cellular uptake and toxicity.

Objective: This narrative review synthesises evidence on environmental exposure to micro- and nanoplastics, cardiovascular mechanisms, emerging human observations and the GeoHealth dimensions of risk, and it explicitly separates evidence of exposure from evidence of causation.

Methods: The review was organised around four domains: (i) environmental sources and pathways; (ii) internal distribution and analytical measurement; (iii) vascular, inflammatory and thrombotic mechanisms; and (iv) population-level inequities and governance. A curated bibliography of 69 sources was screened for relevance, with emphasis on human tissue studies, mechanistic experiments, atmospheric transport, cardiovascular epidemiology and analytical methods. Evidence was graded by study type and by its position along an exposure-to-outcome chain.

Results: Exposure may occur through inhalation, ingestion and dermal contact, with atmospheric transport, road–tyre wear, drinking water, food systems and waste streams producing geographically heterogeneous mixtures. Experimental evidence supports oxidative stress, endothelial barrier disruption, inflammation, cellular senescence, inflammasome activation and altered coagulation as plausible pathways. Human studies have reported plastic particles in blood, lung, placenta, vascular tissue, heart tissue and atheroma. One observational clinical study associated particles in carotid atheroma with higher subsequent cardiovascular event rates. Measurements nevertheless remain method-dependent, and observational evidence does not yet establish causality.

Conclusion: Nanoplastics should be treated as an emerging environmental cardiovascular hazard within a One Health and GeoHealth framework. Progress requires harmonised detection, exposure reconstruction, longitudinal cohorts, mixture-aware toxicology, spatially resolved monitoring and prevention policies that address the full plastic life cycle.

Seroprevalence of Herpes Simplex Type 2 among People Living with HIV in Ile-Ife, Nigeria

M. M. Oripelaye, F. O. Olanrewaju, A. A. Ajani, O. T. Fabusuyi — Sat, 10 Oct 2026 00:00:00 +0000

Background: Sexually transmitted infections (STIs) are diseases of public health importance that affect the reproductive health of the general population. Genital herpes contributes to the burden of STIs, affecting 520 million people globally. Infection with herpes simplex virus type 2 (HSV-2) is lifelong and poses a risk of reactivation among immunosuppressed individuals. Recurrent genital herpes can be debilitating and can severely impair the quality of life of people living with HIV (PLHIV). This study aimed to determine the serological prevalence of HSV-2 among PLHIV and assess its relationship with disease severity.

Materials and Methods: This cross-sectional study evaluated 92 PLHIV aged 18–70 years who were recruited using simple random sampling at the Virology Research Clinic of the Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife, Nigeria. The sample size was determined using the Kish formula. Data were collected using a pro forma and analysed using IBM SPSS version 25.0, and the presence of HSV-2 antibodies was confirmed using ELISA.

Results: The mean age of PLHIV was 37.95 ± 10.41 years. The seroprevalence of HSV-2 among PLHIV was 41.3%. The prevalence of HSV-2 among PLHIV with early and advanced HIV disease was 39.4% and 46.2%, respectively, with no statistically significant difference between the two groups (X² = 0.352, P = 0.640). The associations with CD4⁺ count (X² = 2.182, P = 0.366), age (X² = 0.065, P = 0.968), and gender (X² = 1.160, P = 0.281) were not significant. The logistic regression model accounted for 10.4% to 14.0% of the variance in HSV-2 positivity. The full logistic regression model, which included age, gender, education level, and marital status, was statistically significant (X²(4) = 9.981, P = 0.041).

Conclusion: The findings reveal a high burden of HSV-2 seropositivity among PLHIV, underscoring the need to prevent HSV-2 reactivation by delaying HIV disease progression.