Studies in humans and laboratory animals link stable gut microbiome “enterotypes” with long-term diet and host health. Understanding how this paradigm manifests in wild herbivores could provide a mechanistic explanation of the relationships between microbiome dynamics, changes in dietary resources, and outcomes for host health. We identify two putative enterotypes in the African buffalo gut microbiome. The enterotype prevalent under resource-abundant dietary regimes, regardless of environmental conditions, has high richness, low between- and within-host beta diversity, and enrichment of genusRuminococcaceae-UCG-005. The second enterotype, prevalent under restricted dietary conditions, has reduced richness, elevated beta diversity, and enrichment of genusSolibacillus. Population-level gamma diversity is maintained during resource restriction by increased beta diversity between individuals, suggesting a mechanism for population-level microbiome resilience. We identify three pathogens associated with microbiome variation depending on host diet, indicating that nutritional background may impact microbiome-pathogen dynamics. Overall, this study reveals diet-driven enterotype plasticity, illustrates ecological processes that maintain microbiome diversity, and identifies potential associations between diet, enterotype, and disease.

Coinfecting parasites and pathogens remain a leading challenge for global public health due to their consequences for individual-level infection risk and disease progression. However, a clear understanding of the population-level consequences of coinfection is lacking. Here, we constructed a model that includes three individual-level effects of coinfection: mortality, fecundity, and transmission. We used the model to investigate how these individual-level consequences of coinfection scale up to produce population-level infection patterns. To parameterize this model, we conducted a 4-y cohort study in African buffalo to estimate the individual-level effects of coinfection with two bacterial pathogens, bovine tuberculosis (bTB) and brucellosis, across a range of demographic and environmental contexts. At the individual level, our empirical results identified bTB as a risk factor for acquiring brucellosis, but we found no association between brucellosis and the risk of acquiring bTB. Both infections were associated with reductions in survival and neither infection was associated with reductions in fecundity. The model reproduced coinfection patterns in the data and predicted opposite impacts of coinfection at individual and population scales: Whereas bTB facilitated brucellosis infection at the individual level, our model predicted the presence of brucellosis to have a strong negative impact on bTB at the population level. In modeled populations where brucellosis was present, the endemic prevalence and basic reproduction number ($R_0$) of bTB were lower than in populations without brucellosis. Therefore, these results provide a data-driven example of competition between coinfecting pathogens that occurs when one pathogen facilitates secondary infections at the individual level. Significance Infection with multiple parasite species is common and the majority of coinfections involve at least one long-lasting infection. Our data-driven model of chronic coinfection dynamics shows that accurate prediction at the population level requires quantifying both the individual-level transmission and mortality consequences of coinfection. The infections characterized in this study compete at the population level. When one pathogen facilitates both the transmission and progression of the second pathogen, the prevalence of the first pathogen is reduced. This mechanism of competition is unique compared with previously described mechanisms and occurs without cross-immunity, resource competition within the host, or convalescence. We recommend assessing the generality of this mechanism, which could have important consequences for other chronic, immunosuppressive pathogens such as HIV or TB.

Rift Valley fever (RVF) is an emerging zoonotic mosquito‐borne infectious disease that has been identified as a risk for spread to other continents and can cause mass livestock mortality. In equatorial Africa, outbreaks of RVF are associated with high rainfall, when vector populations are at their highest. It is, however, unclear how RVF virus persists during the inter‐epidemic periods and between seasons. Understanding inter‐epidemic persistence as well as the role of vectors and hosts is paramount to creating effective management programmes for RVF control. We created a mathematical model for the spread of RVF and used the model to explore different scenarios of persistence including vertical transmission and alternate wildlife hosts, with a case study on buffalo in Kruger National Park, South Africa. Our results suggest that RVF persistence is a delicate balance between numerous species of susceptible hosts, mosquito species, vertical transmission and environmental stochasticity. Further investigations should not focus on a single species, but should instead consider a myriad of susceptible host species when seeking to understand disease dynamics.

Persistence of acute viruses: How do highly contagious viruses that cause acute infections hang on to cause recurrent problems in a population? It should be expected that such infections would fade out as herd immunity develops, but foot and mouth disease virus (FMDV) can reemerge. Jolles et al . explored how FMDV remains endemic in African buffalo and serves as a reservoir for disease in domestic livestock (see the Perspective by Hampson and Haydon). The authors found that the virus persists in the population in carrier animals. Inconspicuous, rare, and sporadic transmission rescues the virus from fade-out, assisted by antigenic shift and the seasonal birth of susceptible calves. —CA