Infectious disease is an important driver of extinctions and population declines. With a few exceptions, such as the fungal disease chytridiomycosis in frogs, disease is probably underestimated as a cause of both local and global extinction because it often co-occurs with other more overt drivers of extinction, and its signs can be easily overlooked. Here, we discuss issues around attributing extinction to infectious disease and overview key underlying factors. We then examine the extent to which anthropogenic influences, such as climate change, habitat destruction and exotic species introductions, are likely to lead to increased extinction risk in association with infectious disease. Finally, we discuss strategies to mitigate the threat of extinction due to infectious disease.

For infections to be maintained in a population, pathogens must compete to colonize hosts and transmit between them. We use an experimental approach to investigate within-and-between host dynamics using the pathogen Pseudomonas aeruginosa and the animal host Caenorhabditis elegans. Within-host interactions can involve the production of goods that are beneficial to all pathogens in the local environment but susceptible to exploitation by non-producers. We exposed the nematode host to ‘producer’ and two ‘non-producer’ bacterial strains (specifically for siderophore production and quorum sensing), in single infections and coinfections, to investigate within-host colonization. Subsequently, we introduced infected nematodes to pathogen-naive populations to allow natural transmission between hosts. We find that producer pathogens are consistently better at colonizing hosts and transmitting between them than non-producers during coinfection and single infection. Non-producers were poor at colonizing hosts and between-host transmission, even when coinfecting with producers. Understanding pathogen dynamics across these multiple levels will ultimately help us predict and control the spread of infections, as well as contribute to explanations for the persistence of cooperative genotypes in natural populations.

Ecological and genetic factors have influenced the composition of the human microbiome during our evolutionary history. We analysed the oral microbiota of the Agta, a hunter–gatherer population where some members have adopted an agricultural diet. We show that age is the strongest factor modulating the microbiome, probably through immunosenescence since we identified an increase in the number of species classified as pathogens with age. We also characterised biological and cultural processes generating sexual dimorphism in the oral microbiome. A small subset of oral bacteria is influenced by the host genome, linking host collagen genes to bacterial biofilm formation. Our data also suggest that shifting from a fish/meat diet to a rice-rich diet transforms their microbiome, mirroring the Neolithic transition. All of these factors have implications in the epidemiology of oral diseases. Thus, the human oral microbiome is multifactorial and shaped by various ecological and social factors that modify the oral environment.

Triatoma virus (TrV) is a small, non-enveloped virus that has a+ssRNA genome and is currently classified under the Cripavirus genus of the Dicistroviridae family. TrV infects haematophagous triatomine insects (Hemiptera: Reduviidae), which are vectors of American trypanosomosis (Chagas disease). TrV can be transmitted through the horizontal faecal–oral route, and causes either deleterious sublethal effects or even the death of laboratory insect colonies. Various species of triatomines from different regions of Latin America are currently being reared in research laboratories, with little or no awareness of the presence of TrV; therefore, any biological conclusion drawn from experiments on insects infected with this virus is inherently affected by the side effects of its infection. In this study, we developed a mathematical model to estimate the sample size required for detecting a TrV infection. We applied this model to screen the infection in the faeces of triatomines belonging to insectaries from 13 Latin American countries, carrying out the identification of TrV by using RT-PCR. TrV was detected in samples coming from Argentina, which is where the virus was first isolated from Triatoma infestans (Hemiptera: Reduviidae) several years ago. Interestingly, several colonies from Brazil were also found infected with the virus. This positive result widens the TrV's host range to a total of 14 triatomine species. Our findings suggest that many triatomine species distributed over a large region of South America may be naturally infected with TrV.

Oropsylla hirsuta is the primary flea of the black-tailed prairie dog and is a vector of the plague bacterium, Yersinia pestis. We examined the population genetic structure of O. hirsuta fleas collected from 11 prairie dog colonies, 7 of which had experienced a plague-associated die-off in 1994. In a sample of 332 O. hirsuta collected from 226 host individuals, we detected 24 unique haplotype sequences in a 480 nucleotide segment of the cytochrome oxidase II gene. We found significant overall population structure but we did not detect a signal of isolation by distance, suggesting that O. hirsuta may be able to disperse relatively quickly at the scale of this study. All 7 colonies that were recently decimated by plague showed signs of recent population expansion, whereas 3 of the 4 plague-negative colonies showed haplotype patterns consistent with stable populations. These results suggest that O. hirsuta populations are affected by plague-induced prairie dog die-offs and that flea dispersal among prairie dog colonies may not be dependent exclusively on dispersal of prairie dogs. Re-colonization following plague events from plague-free refugia may allow for rapid flea population expansion following plague epizootics.

The success of a pathogen depends not only on its transmission to new hosts, but also on its ability to colonize and persist within its current host. Studies of within-host dynamics have focused on only a few diseases of humans, whereas little is known about the factors that influence pathogen populations as they develop inside non-human hosts. Here, we investigate pathogen dynamics occurring within bumble bees (Bombus impatiens) infected by the gut trypanosome Crithidia bombi. Infection by C. bombi showed several features characteristic of vertebrate diseases, including a rapid initial increase in infection intensity, marked oscillations in parasitaemia, and the stimulation of a systemic immune response in infected bees. Within-host dynamics generated substantial variation in the infectiousness and flower-visiting behaviour of bumble bees. Changes in bee foraging that arise from infection may influence the probability of C. bombi transmission between bees at flowers.

The skin site at which ticks attach to their hosts to feed is the critical interface between the tick and its host, and tick-borne pathogens. This site is highly modified by the pharmacologically active molecules secreted in tick saliva. For pathogens, it is an ecologically privileged niche that many exploit. Such exploitation is referred to as saliva-activated transmission (SAT) – the indirect promotion of tick-borne pathogen transmission via the actions of bioactive tick saliva molecules on the vertebrate host. Here we review evidence for SAT and consider what are the most likely candidates for SAT factors among the tick pharmacopoeia of anti-haemostatic, anti-inflammatory and immunomodulatory molecules identified to date. SAT factors appear to differ for different pathogens and tick vector species, and possibly even depend on the vertebrate host species. Most likely we are searching for a suite of molecules that act together to overcome the redundancy in host response mechanisms. Whatever they turn out to be, the quest to identify the tick molecules that mediate SAT is an exciting one, and offers new insights to controlling ticks and tick-borne diseases.

Defensive behaviour is one of the principal ways vertebrate hosts regulate the blood-feeding success of vector insects. Intrinsic variation in the intensity and efficiency of this biting avoidance behaviour depends on host: (1) species, (2) size, (3) age, (4) health and (5) individuality. In this paper we summarize data on the relative importance of each of these host-associated factors in regulating mosquito feeding and transmission of mosquito-borne diseases.