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Dromedary, or one-humped, camels Camelus dromedarius are an almost exclusively domesticated species that are common in arid areas as both beasts of burden and production animals for meat and milk.Currently, there are approximately 30 million dromedary camels, with highest numbers in Africa and the Middle East. The hardiness of camels in arid regions has made humans more dependent on them, especially as a stable protein source. Camels also carry and may transmit disease-causing agents to humans and other animals. The ability for camels to act as a point source or vector for disease is a concern due to increasing human demands for meat, lack of biosafety and biosecurity protocols in many regions, and a growth in the interface with wildlife as camel herds become sympatric with non-domestic species. We conducted a literature review of camel-borne zoonotic diseases and found that the majority of publications (65%) focused on Middle East respiratory syndrome (MERS), brucellosis, Echinococcus granulosus, and Rift Valley fever. The high fatality from MERS outbreaks during 2012-2016 elicited an immediate response from the research community as demonstrated by a surge of MERS-related publications. However, we contend that other camel-borne diseases such as Yersinia pestis, Coxiella burnetii, and Crimean-Congo hemorrhagic fever are just as important to include in surveillance efforts. Camel populations, particularly in sub-Saharan Africa, are increasing exponentially in response to prolonged droughts, and thus, the risk of zoonoses increases as well. In this review, we provide an overview of the major zoonotic diseases present in dromedary camels, their risk to humans, and recommendations to minimize spillover events.

Oocyst shedding in domestic and wild felids is a critical yet understudied topic in Toxoplasma gondii ecology and epidemiology that shapes human and animal disease burden. We synthesized published literature dating from the discovery of felids as the definitive hosts of T. gondii in the 1960s through March 2021 to examine shedding prevalence, oocyst genotypes, and risk factors for shedding. Oocyst shedding prevalence in many geographic regions exceeded the commonly accepted 1% reported for domestic cats; crude prevalence from cross‐sectional field studies of domestic cat shedding ranged from 0% in Australia to 18.8% in Africa, with greater variation in reports of oocyst shedding in free‐ranging, wild felids. Shedding in wild felid species has primarily been described in captive animals, with attempted detection of oocyst shedding reported in at least 31 species. Differences in lifestyle and diet play an important role in explaining shedding variation between free‐ranging unowned domestic cats, owned domestic cats and wild felids. Additional risk factors for shedding include the route of infection, diet, age and immune status of the host. It is widely reported that cats only shed oocysts after initial infection with T. gondii, but experimental studies have shown that repeat oocyst shedding can occur. Factors associated with repeat shedding are common amongst free‐ranging felids (domestic and wild), which are more likely to eat infected prey, be exposed to diverse T. gondii genotypes, and have coinfections with other parasites. Repeat shedding events could play a significant yet currently ignored role in shaping environmental oocyst loading with implications for human and animal exposure. Oocyst presence in the environment is closely linked to climate variables such as temperature and precipitation, so in quantifying risk of exposure, it is important to consider the burden of T. gondii oocysts that can accumulate over time in diverse environmental matrices and sites, as well as the spatial heterogeneity of free‐ranging cat populations. Key directions for future research include investigating oocyst shedding in under‐sampled regions, genotyping of oocysts detected in faeces and longitudinal studies of oocyst shedding in free‐ranging felids.

No abstract

Toxoplasma gondii is a ubiquitous zoonotic parasite that can infect warm-blooded vertebrates, including humans. Felids, the definitive hosts, drive T. gondii infections by shedding the environmentally resistant stage of the parasite (oocysts) in their feces. Few studies characterize the role of climate and anthropogenic factors in oocyst shedding among free-ranging felids, which are responsible for the majority of environmental contamination. We determined how climate and anthropogenic factors influence oocyst shedding in free-ranging domestic cats and wild felids using generalized linear mixed models. T. gondii oocyst shedding data from 47 studies were systematically reviewed and compiled for domestic cats and six wild felid species, encompassing 256 positives out of 9,635 total fecal samples. Shedding prevalence in domestic cats and wild felids was positively associated with human population density at the sampling location. Larger mean diurnal temperature range was associated with more shedding among domestic cats and warmer temperature in the driest quarter was associated with lower oocyst shedding in wild felids. Increasing human population density and temperature fluctuation can exacerbate environmental contamination with the protozoan parasite T. gondii. Management of free-ranging domestic cats could lower the burden of environmental oocysts due to their large population sizes and affinity with human settlements.