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Background Varicella causes a major health burden in many low- to middle-income countries located in tropical regions. Because of the lack of surveillance data, however, the epidemiology of varicella in these regions remains uncharacterized. In this study, based on an extensive dataset of weekly varicella incidence in children ≤10 during 2011–2014 in 25 municipalities, we aimed to delineate the seasonality of varicella across the diverse tropical climates of Colombia. Methods We used generalized additive models to estimate varicella seasonality, and we used clustering and matrix correlation methods to assess its correlation with climate. Furthermore, we developed a mathematical model to examine whether including the effect of climate on varicella transmission could reproduce the observed spatiotemporal patterns. Results Varicella seasonality was markedly bimodal, with latitudinal changes in the peaks' timing and amplitude. This spatial gradient strongly correlated with specific humidity (Mantel statistic = 0.412, P =.001) but not temperature (Mantel statistic = 0.077, P =.225). The mathematical model reproduced the observed patterns not only in Colombia but also México, and it predicted a latitudinal gradient in Central America. Conclusions These results demonstrate large variability in varicella seasonality across Colombia and suggest that spatiotemporal humidity fluctuations can explain the calendar of varicella epidemics in Colombia, México, and potentially in Central America. [ABSTRACT FROM AUTHOR]

Despite the availability of effective vaccines, the persistence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) suggests that cocirculation with other pathogens and resulting multiepidemics (of, for example, COVID-19 and influenza) may become increasingly frequent. To better forecast and control the risk of such multiepidemics, it is essential to elucidate the potential interactions of SARS-CoV-2 with other pathogens; these interactions, however, remain poorly defined. Here, we aimed to review the current body of evidence about SARS-CoV-2 interactions. Our review is structured in four parts. To study pathogen interactions in a systematic and comprehensive way, we first developed a general framework to capture their major components: sign (either negative for antagonistic interactions or positive for synergistic interactions), strength (i.e., magnitude of the interaction), symmetry (describing whether the interaction depends on the order of infection of interacting pathogens), duration (describing whether the interaction is short-lived or long-lived), and mechanism (e.g., whether interaction modifies susceptibility to infection, transmissibility of infection, or severity of disease). Second, we reviewed the experimental evidence from animal models about SARS-CoV-2 interactions. Of the 14 studies identified, 11 focused on the outcomes of coinfection with nonattenuated influenza A viruses (IAVs), and 3 with other pathogens. The 11 studies on IAV used different designs and animal models (ferrets, hamsters, and mice) but generally demonstrated that coinfection increased disease severity compared with either monoinfection. By contrast, the effect of coinfection on the viral load of either virus was variable and inconsistent across studies. Third, we reviewed the epidemiological evidence about SARS-CoV-2 interactions in human populations. Although numerous studies were identified, only a few were specifically designed to infer interaction, and many were prone to multiple biases, including confounding. Nevertheless, their results suggested that influenza and pneumococcal conjugate vaccinations were associated with a reduced risk of SARS-CoV-2 infection. Finally, fourth, we formulated simple transmission models of SARS-CoV-2 cocirculation with an epidemic viral pathogen or an endemic bacterial pathogen, showing how they can naturally incorporate the proposed framework. More generally, we argue that such models, when designed with an integrative and multidisciplinary perspective, will be invaluable tools to resolve the substantial uncertainties that remain about SARS-CoV-2 interactions. [ABSTRACT FROM AUTHOR]

There is growing experimental evidence that many respiratory viruses—including influenza and SARS-CoV-2—can interact, such that their epidemiological dynamics may not be independent. To assess these interactions, standard statistical tests of independence suggest that the prevalence ratio—defined as the ratio of co-infection prevalence to the product of single-infection prevalences—should equal unity for non-interacting pathogens. As a result, earlier epidemiological studies aimed to estimate the prevalence ratio from co-detection prevalence data, under the assumption that deviations from unity implied interaction. To examine the validity of this assumption, we designed a simulation study that built on a broadly applicable epidemiological model of co-circulation of two emerging or seasonal respiratory viruses. By focusing on the pair influenza–SARS-CoV-2, we first demonstrate that the prevalence ratio systematically underestimates the strength of interaction, and can even misclassify antagonistic or synergistic interactions that persist after clearance of infection. In a global sensitivity analysis, we further identify properties of viral infection—such as a high reproduction number or a short infectious period—that blur the interaction inferred from the prevalence ratio. Altogether, our results suggest that ecological or epidemiological studies based on co-detection prevalence data provide a poor guide to assess interactions among respiratory viruses. [ABSTRACT FROM AUTHOR]

Vibrio cholerae, the bacterium responsible for the disease cholera, is a naturally-occurring bacterium, commonly found in many natural tropical water bodies. In the context of the U.N. Sustainable Development Goals (SDG) targets on health (Goal 3), water quality (Goal 6), life under water (Goal 14), and clean water and sanitation (Goal 6), which aim to "ensure availability and sustainable management of water and sanitation for all", we investigated the environmental reservoirs of V. cholerae in Vembanad Lake, the largest lake in Kerala (India), where cholera is endemic. The response of environmental reservoirs of V. cholerae to variability in essential climate variables may play a pivotal role in determining the quality of natural water resources, and whether they might be safe for human consumption or not. The hydrodynamics of Vembanad Lake, and the man-made barrier that divides the lake, resulted in spatial and temporal variability in salinity (1–32 psu) and temperature (23 to 36 °C). The higher ends of this salinity and temperature ranges fall outside the preferred growth conditions for V. cholerae reported in the literature. The bacteria were associated with filtered water as well as with phyto- and zooplankton in the lake. Their association with benthic organisms and sediments was poor to nil. The prevalence of high laminarinase and chitinase enzyme expression (more than 50 µgmL−1 min−1) among V. cholerae could underlie their high association with phyto- and zooplankton. Furthermore, the diversity in the phytoplankton community in the lake, with dominance of genera such as Skeletonema sp., Microcystis sp., Aulacoseira sp., and Anabaena sp., which changed with location and season, and associated changes in the zooplankton community, could also have affected the dynamics of the bacteria in the lake. The probability of presence or absence of V. cholerae could be expressed as a function of chlorophyll concentration in the water, which suggests that risk maps for the entire lake can be generated using satellite-derived chlorophyll data. In situ observations and satellite-based extrapolations suggest that the risks from environmental V. cholerae in the lake can be quite high (with probability in the range of 0.5 to 1) everywhere in the lake, but higher values are encountered more frequently in the southern part of the lake. Remote sensing has an important role to play in meeting SDG goals related to health, water quality and life under water, as demonstrated in this example related to cholera. [ABSTRACT FROM AUTHOR]

Background: Varicella causes a major health burden in many low- to middle-income countries located in tropical regions. Because of the lack of surveillance data, however, the epidemiology of varicella in these regions remains uncharacterized. In this study, based on an extensive dataset of weekly varicella incidence in children ≤10 during 2011-2014 in 25 municipalities, we aimed to delineate the seasonality of varicella across the diverse tropical climates of Colombia., Methods: We used generalized additive models to estimate varicella seasonality, and we used clustering and matrix correlation methods to assess its correlation with climate. Furthermore, we developed a mathematical model to examine whether including the effect of climate on varicella transmission could reproduce the observed spatiotemporal patterns., Results: Varicella seasonality was markedly bimodal, with latitudinal changes in the peaks' timing and amplitude. This spatial gradient strongly correlated with specific humidity (Mantel statistic = 0.412, P = .001) but not temperature (Mantel statistic = 0.077, P = .225). The mathematical model reproduced the observed patterns not only in Colombia but also México, and it predicted a latitudinal gradient in Central America., Conclusions: These results demonstrate large variability in varicella seasonality across Colombia and suggest that spatiotemporal humidity fluctuations can explain the calendar of varicella epidemics in Colombia, México, and potentially in Central America., Competing Interests: Potential conflicts of interest. TK received research grants from the Gemeinsamer Bundesausschuss ([G-BA] Federal Joint Committee, Germany) and the Bundesministerium für Gesundheit ([BMG] Federal Ministry of Health, Germany), outside the submitted work. He has also received personal compensation from Eli Lilly and Company, Teva Pharmaceuticals, TotalEnergies SE, the BMJ, and Frontiers. Conflicts that the editors consider relevant to the content of the manuscript have been disclosed., (© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America.)