Unhealthy herds and the predator-spreader: Understanding when predation increases disease incidence and prevalence.

Disease ecologists now recognize the limitation behind examining host-parasite interactions in isolation: community members-especially predators-dramatically affect host-parasite dynamics. Although the initial paradigm was that predation should reduce disease in prey populations ("healthy herds hypothesis"), researchers have realized that predators sometimes increase disease in their prey. These "predator-spreaders" are now recognized as critical to disease dynamics, but empirical research on the topic remains fragmented. In a narrow sense, a "predator-spreader" would be defined as a predator that mechanically spreads parasites via feeding. However, predators affect their prey and, subsequently, disease transmission in many other ways such as altering prey population structure, behavior, and physiology. We review the existing evidence for these mechanisms and provide heuristics that incorporate features of the host, predator, parasite, and environment to understand whether or not a predator is likely to be a predator-spreader. We also provide guidance for targeted study of each mechanism and quantifying the effects of predators on parasitism in a way that yields more general insights into the factors that promote predator spreading. We aim to offer a better understanding of this important and underappreciated interaction and a path toward being able to predict how changes in predation will influence parasite dynamics.

Season and prey identity mediate the effect of predators on parasites in rodents: a test of the healthy herds hypothesis.

The healthy herds hypothesis (HHH) suggests that predators decrease parasitism in their prey. Repeated tests of this hypothesis across a range of taxa and ecosystems have revealed significant variation in the effect of predators on parasites in prey. Differences in the response to predators (1) between prey taxa, (2) between seasons, and (3) before and after catastrophic disturbance are common in natural systems, but typically ignored in empirical tests of the HHH. We used a predator exclusion experiment to measure the effect of these heterogeneities on the tri-trophic interaction among predators, parasites and prey. We experimentally excluded mammalian predators from the habitats of hispid cotton rats (Sigmodon hispidus) and cotton mice (Peromyscus gossypinus) and measured the effect of exclusion on gastrointestinal parasites in these rodents. Our experiment spanned multiple seasons and before and after a prescribed burn. We found that the exclusion of the same predators had opposite effects on the parasites of small mammal prey species. Additionally, we found that the effect of mammal exclusion on parasitism differed before versus after fire disturbance. Finally, we saw that the effect of predator exclusion was highly dependent on prey capture season. Significant effects of exclusion emerged primarily in the fall and winter months. The presence of so many different effects in one relatively simple system suggests that predator effects on parasites in prey are highly context dependent.

Epidemic time series similarity is related to geographic distance and age structure.

Objective: More similar locations may have similar infectious disease dynamics. There is clear overlap in putative causes for epidemic similarity, such as geographic distance, age structure, and population size. We compare the effects of these potential drivers on epidemic similarity compared to a baseline assumption that differences in the basic reproductive number (R 0) will translate to differences in epidemic trajectories. Methods: Using COVID-19 case counts from United States counties, we explore the importance of geographic distance, population size differences, and age structure dissimilarity on resulting epidemic similarity. Results: We find clear effects of geographic space, age structure, population size, and R 0 on epidemic similarity, but notably the effect of age structure was stronger than the baseline assumption that differences in R 0 would be most related to epidemic similarity. Conclusions: Together, this highlights the role of spatial and demographic processes on SARS-CoV2 epidemics in the United States.

Infectious disease: Dog diets may drive transmission cycles in human Guinea worm disease.

Domestic dogs have an important role in the ecology of transmission of the Guinea worm, a debilitating human parasite. A new study documents how fish content in dogs' diets can predict Guinea worm infection status, suggesting additional avenues for control.

Investigating Flubendazole as an Anthelmintic Treatment for Guinea Worm (Dracunculus medinensis): Clinical Trials in Laboratory-Reared Ferrets and Domestic Dogs in Chad.

Dracunculus medinensis (Guinea worm [GW]), a zoonotic nematode targeted for eradication, has been managed using interventions aimed at humans; however, increases in domestic dog GW infections highlight the need for novel approaches. We conducted two clinical trials evaluating the efficacy of subcutaneously injected flubendazole (FBZ) as a treatment of GW infection. The first trial was conducted administering FBZ to experimentally infected ferrets; the second trial involved administering FBZ or a placebo to domestic dogs in the Republic of Tchad (Chad). We found contrasting results between the two trials. When adult gravid female GW were recovered from ferrets treated with FBZ, larvae presented in poor condition, with low to no motility, and an inability to infect copepods. Histopathology results indicated a disruption to morulae development within uteri of worms from treated animals. Results from the trial in Chadian dogs failed to indicate significant treatment of or prevention against GW infection. However, the difference in treatment intervals (1 month for ferrets and 6 months for dogs) or the timing of treatment (ferrets were treated later in the GW life-cycle than dogs) could explain different responses to the subcutaneous FBZ injections. Both trials provided valuable data guiding the use of FBZ in future trials (such as decreasing treatment intervals or increasing the dose of FBZ in dogs to increase exposure), and highlighted important lessons learned during the implementation of a field-based, double-blinded randomized control trial in Chadian dogs.

Estimating R 0 from early exponential growth: parallels between 1918 influenza and 2020 SARS-CoV-2 pandemics.

The large spatial scale, geographical overlap, and similarities in transmission mode between the 1918 H1N1 influenza and 2020 SARS-CoV-2 pandemics together provide a novel opportunity to investigate relationships between transmission of two different diseases in the same location. To this end, we use initial exponential growth rates in a Bayesian hierarchical framework to estimate the basic reproductive number, R 0, of both disease outbreaks in a common set of 43 cities in the United States. By leveraging multiple epidemic time series across a large spatial area, we are able to better characterize the variation in R 0 across the United States. Additionally, we provide one of the first city-level comparisons of R 0 between these two pandemics and explore how demography and outbreak timing are related to R 0. Despite similarities in transmission modes and a common set of locations, R 0 estimates for COVID-19 were uncorrelated with estimates of pandemic influenza R 0 in the same cities. Also, the relationships between R 0 and key population or epidemic traits differed between diseases. For example, epidemics that started later tended to be less severe for COVID-19, while influenza epidemics exhibited an opposite pattern. Our results suggest that despite similarities between diseases, epidemics starting in the same location may differ markedly in their initial progression.

Do predators keep prey healthy or make them sicker? A meta-analysis.

Ecological theory suggests that predators can either keep prey populations healthy by reducing parasite burdens or alternatively, increase parasitism in prey. To quantify the overall magnitude and direction of the effect of predation on parasitism in prey observed in practice, we conducted a meta-analysis of 47 empirical studies. We also examined how study attributes, including parasite type and life cycle, habitat type, study design, and whether predators were able to directly consume prey contributed to variation in the predator-prey-parasite interaction. We found that the overall effect of predation on parasitism differed between parasites and parasitoids and that whether consumptive effects were present, and whether a predator was a non-host spreader of parasites, were the most important traits predicting the parasite response. Our results suggest that the mechanistic basis of predator-prey interactions strongly influences the effects of predators on parasites and that these effects, although context dependent, are predictable.

Identifying correlates of Guinea worm (Dracunculus medinensis) infection in domestic dog populations.

Few human infectious diseases have been driven as close to eradication as dracunculiasis, caused by the Guinea worm parasite (Dracunculus medinensis). The number of human cases of Guinea worm decreased from an estimated 3.5 million in 1986 to mere hundreds by the 2010s. In Chad, domestic dogs were diagnosed with Guinea worm for the first time in 2012, and the numbers of infected dogs have increased annually. The presence of the parasite in a non-human host now challenges efforts to eradicate D. medinensis, making it critical to understand the factors that correlate with infection in dogs. In this study, we evaluated anthropogenic and environmental factors most predictive of detection of D. medinensis infection in domestic dog populations in Chad. Using boosted regression tree models to identify covariates of importance for predicting D. medinensis infection at the village and spatial hotspot levels, while controlling for surveillance intensity, we found that the presence of infection in a village was predicted by a combination of demographic (e.g. fishing village identity, dog population size), geographic (e.g. local variation in elevation), and climatic (e.g. precipitation and temperature) factors, which differed between northern and southern villages. In contrast, the presence of a village in a spatial infection hotspot, was primarily predicted by geography and climate. Our findings suggest that factors intrinsic to individual villages are highly predictive of the detection of Guinea worm parasite presence, whereas village membership in a spatial infection hotspot is largely determined by location and climate. This study provides new insight into the landscape-scale epidemiology of a debilitating parasite and can be used to more effectively target ongoing research and possibly eradication and control efforts.