Age of first infection across a range of parasite taxa in a wild mammalian population.

Exploring the relationship between incidence and the average age of infection during seasonal epidemics

Newborn mammals have an immature immune system that cannot sufficiently protect them against infectious diseases. However, variation in the effectiveness of maternal immunity against different parasites may couple with temporal trends in parasite exposure to influence disparities in the timing of infection risk. Determining the relationship between age and infection risk is critical in identifying the portion of a host population that contributes to parasite dynamics, as well as the parasites that regulate host recruitment. However, there are no data directly identifying timing of first infection among parasites in wildlife. Here, we took advantage of a longitudinal dataset, tracking infection status by viruses, bacteria, protists and gastro-intestinal worms in a herd of African buffalo (<i>Syncerus caffer</i>) to ask: how does age of first infection differ among parasite taxa? We found distinct differences in the age of first infection among parasites that aligned with the mode of transmission and parasite taxonomy. Specifically, we found that tick-borne and environmentally transmitted protists were acquired earlier than directly transmitted bacteria and viruses. These results emphasize the importance of understanding infection risk in juveniles, especially in host species where juveniles are purported to sustain parasite persistence and/or where mortality rates of juveniles influence population dynamics.

Detecting exposure to new or emerging pathogens is a critical challenge to protecting human, domestic animal, and wildlife health. Yet, current techniques to detect infections typically target known pathogens of humans or economically important animals. In the face of the current surge in infectious disease emergence, non-specific disease surveillance tools are urgently needed. Tracking common host immune responses indicative of recent infection may have potential as a non-specific diagnostic approach for disease surveillance. The challenge to immunologists is to identify the most promising markers, which ideally should be highly conserved across pathogens and host species, become upregulated rapidly and consistently in response to pathogen invasion, and remain elevated beyond clearance of infection. This study combined an infection experiment and a longitudinal observational study to evaluate the utility of non-specific markers of inflammation [NSMI; two acute phase proteins (haptoglobin and serum amyloid A), two pro-inflammatory cytokines (IFNγ and TNF-α)] as indicators of pathogen exposure in a wild mammalian species, African buffalo (Syncerus caffer). Specifically, in the experimental study, we asked (1) How quickly do buffalo mount NSMI responses upon challenge with an endemic pathogen, foot-and-mouth disease virus; (2) for how long do NSMI remain elevated after viral clearance and; (3) how pronounced is the difference between peak NSMI concentration and baseline NSMI concentration? In the longitudinal study, we asked (4) Are elevated NSMI associated with recent exposure to a suite of bacterial and viral respiratory pathogens in a wild population? Among the four NSMI that we tested, haptoglobin showed the strongest potential as a surveillance marker in African buffalo: concentrations quickly and consistently reached high levels in response to experimental infection, remaining elevated for almost a month. Moreover, elevated haptoglobin was indicative of recent exposure to two respiratory pathogens assessed in the longitudinal study. We hope this work motivates studies investigating suites of NSMI as indicators for pathogen exposure in a broader range of both pathogen and host species, potentially transforming how we track disease burden in natural populations.

Brazil is a middle-income country undergoing the epidemiological transition. Effects of changes in daily life habits and access to clean water, sanitation and urban services on a growing urban population have contributed to a double burden of both infectious and noncommunicable chronic diseases. Studies have indicated that parasite infections may modulate the human immune system and influence the development of allergic conditions such as asthma. However, there is no consensus in the published literature on the effects of parasitic infections on allergy, perhaps as a consequence of factors determining the epidemiology of these infections that vary between populations such as age of first infection, duration and chronicity of infections, parasite burden and species, and host genetic susceptibility. In this review, we discuss the observations from Brazil concerning the relationship between parasite infections and allergy.

Human Immunodeficiency Virus Pre-Exposure Prophylaxis: Is it the Answer?

BackgroundEpidemiological analyses indicate that the age distribution of natural cases of transmissible spongiform encephalopathies (TSEs) reflect age-related risk of infection, however, the underlying mechanisms remain poorly understood. Using a comparative approach, we tested the hypothesis that, there is a significant correlation between risk of infection for scrapie, bovine spongiform encephalopathy (BSE) and variant CJD (vCJD), and the development of lymphoid tissue in the gut.MethodsUsing anatomical data and estimates of risk of infection in mathematical models (which included results from previously published studies) for sheep, cattle and humans, we calculated the Spearman's rank correlation coefficient, rs, between available measures of Peyer's patch (PP) development and the estimated risk of infection for an individual of the corresponding age.ResultsThere was a significant correlation between the measures of PP development and the estimated risk of TSE infection; the two age-related distributions peaked in the same age groups. This result was obtained for each of the three host species: for sheep, surface area of ileal PP tissue vs risk of infection, rs = 0.913 (n = 19, P < 0.001), and lymphoid follicle density vs risk of infection, rs = 0.933 (n = 19, P < 0.001); for cattle, weight of PP tissue vs risk of infection, rs = 0.693 (n = 94, P < 0.001); and for humans, number of PPs vs risk of infection, rs = 0.384 (n = 46, P = 0.008). In addition, when changes in exposure associated with BSE-contaminated meat were accounted for, the two age-related patterns for humans remained concordant: rs = 0.360 (n = 46, P = 0.014).ConclusionOur findings suggest that, for sheep, cattle and humans alike there is an association between PP development (or a correlate of PP development) and susceptibility to natural TSE infection. This association may explain changes in susceptibility with host age, and differences in the age-susceptibility relationship between host species.

Immunity is one of the most variable phenotypic traits in animals; however, some individuals may show less fluctuation in immune traits, resulting in stable patterns of immune variation over time. It is currently unknown whether immune variation has consequences for infectious disease risk. In this study, we identified moderately stable immune traits in wild African buffalo and asked whether the stability of these traits affected bovine tuberculosis (TB) infection risk. We found that adaptive immune traits such as the level of interferon-γ (IFN-γ) released after white blood cell stimulation, the number of circulating lymphocytes and the level of antibodies against bovine adenovirus-3 were moderately repeatable (i.e. stable) over time, whereas parameters related to innate immunity either had low repeatability (circulating eosinophil numbers) or were not repeatable (e.g. neutrophil numbers, plasma bacteria killing capacity). Intriguingly, individuals with more repeatable IFN-γ and lymphocyte levels were at a significantly higher risk of acquiring TB infection. In stark contrast, average IFN-γ and lymphocyte levels were poor predictors of TB risk, indicating that immune variability rather than absolute response level better captured variation in disease susceptibility. This work highlights the important and under-appreciated role of immune variability as a predictor of infection risk.

The effects of demographic change on disease transmission and vaccine impact in a household structured population

Mathematical models for the dynamics of directly transmitted viral and bacterial infections are guides to the understanding of observed patterns in the age specific incidence of some common childhood diseases of humans, before and after the advent of vaccination programs. For those infections that show recurrent epidemic behavior, the interepidemic period can be related to parameters characterizing the infection (such as latent and infectious periods and the average age of first infection); this relation agrees with the data of a variety of childhood diseases. Criteria for the eradication of a disease are given, in terms of the proportion of the population to be vaccinated and the age-specific vaccination schedule. These criteria are compared with a detailed analysis of the vaccination programs against measles and whooping cough in Britain, and estimates are made of the levels of protection that would be needed to eradicate these diseases.

Aerosol generating procedures, dysphagia assessment and COVID-19: A rapid review.

Fine-grain mobility data empirically quantify the propensity for human mixing to be indoors across the US and improve understanding of the relationship between the physical environment and infection risk in light of global change.

Fine-grain mobility data empirically quantify the propensity for human mixing to be indoors across the US and improve understanding of the relationship between the physical environment and infection risk in light of global change.

BackgroundIdentifying patterns and drivers of infection risk among host communities is crucial to elucidate disease dynamics and predict infectious disease risk in wildlife populations. Blood parasites of the genera Plasmodium and Haemoproteus are a diverse group of vector-borne protozoan parasites that affect bird populations globally. Despite their widespread distribution and exceptional diversity, factors underlying haemosporidian infection risk in wild bird communities remain poorly understood. While some studies have examined variation in avian haemosporidian risk, researchers have primarily focused on host ecological traits without considering host phylogenetic relationships. In this study, we employ a phylogenetically informed approach to examine the association between host ecological traits and haemosporidian infection risk in endemic bird communities in the Western Ghats Sky Islands.MethodsWe used parasite sequence data based on partial mitochondrial cytochrome b gene, that was amplified from genomic DNA extracted from 1177 birds (28 species) across the Western Ghats to assess infection of birds with haemosporidian parasites. We employed a Bayesian phylogenetic mixed effect modelling approach to test whether haemosporidian infection risk was affected by seven species-specific and four individual-level ecological predictors. We also examined the effect of host phylogenetic relationships on the observed patterns of variation in haemosporidian infection risk by estimating phylogenetic signal.ResultsOur study shows that host ecological traits and host phylogeny differentially influence infection risk by Plasmodium (generalist parasite) and Haemoproteus (specialist parasite). For Plasmodium, we found that sociality, sexual dimorphism and foraging strata were important ecological predictors. For Haemoproteus, patterns of infection risk among host species were associated with sociality, species elevation and individual body condition. Interestingly, variance in infection risk explained by host phylogeny was higher for Haemoproteus parasites compared to Plasmodium.ConclusionsOur study highlights that while host ecological traits promoting parasite exposure and host susceptibility are important determinants of infection risk, host phylogeny also contributes substantially to predicting patterns of haemosporidian infection risk in multi-host communities. Importantly, infection risk is driven by joint contributions of host ecology and host phylogeny and studying these effects together could increase our ability to better understand the drivers of infection risk and predict future disease threats.Graphical abstract

A smorgasbord of firsts: Taxonomy, morphology, and ecology of parasites in wildlife - Invited papers from the 4th International Congress on Parasites of Wildlife 2021/2022, Kruger National Park, South Africa.

BackgroundBovine tuberculosis (BTB) is a zoonotic disease of global importance endemic in African buffalo (Syncerus caffer) in sub-Saharan Africa. Zoonotic tuberculosis is a disease of global importance, accounting for over 12,000 deaths annually. Cattle affected with BTB have been proposed as a model for the study of human tuberculosis, more closely resembling the localization and progression of lesions in controlled studies than murine models. If disease in African buffalo progresses similarly to experimentally infected cattle, they may serve as a model, both for human tuberculosis and cattle BTB, in a natural environment.Methodology/Principal findingsWe utilized a herd of African buffalo that were captured, fitted with radio collars, and tested for BTB twice annually during a 4-year-cohort study. At the end of the project, BTB positive buffalo were culled, and necropsies performed. Here we describe the pathologic progression of BTB over time in African buffalo, utilizing gross and histological methods. We found that BTB in buffalo follows a pattern of infection like that seen in experimental studies of cattle. BTB localizes to the lymph nodes of the respiratory tract first, beginning with the retropharyngeal and tracheobronchial lymph nodes, gradually increasing in lymph nodes affected over time. At 36 months, rate of spread to additional lymph nodes sharply increases. The lung lesions follow a similar pattern, progressing slowly, then accelerating their progression at 36 months post infection. Lastly, a genetic marker that correlated to risk of M. bovis infection in previous studies was marginally associated with BTB progression. Buffalo with at least one risk allele at this locus tended to progress faster, with more lung necrosis.Conclusions/SignificanceThe progression of disease in the African buffalo mirrors the progression found in experimental cattle models, offering insight into BTB and the interaction with its host in the context of naturally varying environments, host, and pathogen populations.