Pathogen Avoidance Research Articles

Examining pathogen avoidance in predator-prey and scavenging systems

That predators ‘cull the sick and the weak’ is an adage in ecological texts, but the mechanisms by which disease is curtailed within ecosystems has puzzled ecologists for many years. Advances in our understanding of host-pathogen interactions have revealed defense mechanisms implemented by hosts that minimize infectious diseases in wild populations. Defense mechanisms for hosts include adaptations that ameliorate fitness loss or preemptively limit pathogen exposure, and these mechanisms underlie fundamental questions about how scavenging or predation influence pathogen transmission. A key lens for our understanding of predator-prey and scavenging dynamics include behaviorally-mediated trade-offs weighed by consumers between nutritional gains and pathogen exposure risks. Consequently, the degree to which pathogens and associated diseases perpetuate through food webs can be partly attributed to behavioral responses of predators and scavengers, particularly their selection or avoidance of diseased prey and infected carcasses. Even so, examinations of avoidance or preference by predators and scavengers to diseased carrion are underrepresented. Here we identify areas for future research focused on behavioral immunity that could illuminate where, when, and how pathogen transmission reverberates through ecological communities. While directly attributing behavioral responses to pathogen exposure may be challenging, particularly for organisms with low susceptibility to spillover, identifying these responses though experimentation or observation help describe complex systems regarding infectious disease.

Genetic Variation in Trophic Avoidance Behaviour Shows Fruit Flies are Generally Attracted to Bacterial Substrates.

Pathogen avoidance behaviours are often assumed to be an adaptive host defence. However, there is limited experimental data on heritable, intrapopulation phenotypic variation for avoidance, a strong prerequisite for adaptive responses to selection. We investigated trophic pathogen avoidance in 122 inbred Drosophila melanogaster lines, and in a derived outbred population. Using the FlyPAD system, we tracked the feeding choice that flies made between substrates that were either clean or contained a bacterial pathogen. We uncovered significant, but weakly heritable variation in the preference index amongst fly lines. However, instead of avoidance, most lines demonstrated a preference for substrates containing several bacterial pathogens, showing avoidance only for extremely high bacterial concentrations. Bacterial preference was not associated with susceptibility to infection and was retained in flies with disrupted immune signalling. Phenotype-genotype association analysis indicated several novel genes (CG2321, CG2006, and ptp99A) associated with increased preference for the bacterial substrate, while the amino-acid transporter sobremesa was associated with greater aversion. Given the known fitness benefits of consuming high-protein diets, our results suggest that bacterial attraction may instead reflect a dietary preference for protein over carbohydrate. More work quantifying intrapopulation variation in avoidance behaviours is needed to fully assess its importance in host-pathogen evolutionary ecology.

Toll-like receptor signaling in neurons modulates C. elegans feeding behavior in a hunger state-dependent manner

Animals face the risk of encountering pathogenic microbes while foraging for resources. Assessing the risk of nutrition vs. infection can result in the behavioral regulation of immune processes. Behavioral immunity in the nematode roundworm Caenorhabditis elegans (C. elegans) is regulated, in part, by the innate immune molecule TOL-1: a homolog of vertebrate Toll-like Receptor (TLR) proteins that influences C. elegans pathogen avoidance behaviors by promoting the development of CO2-detecting chemosensory neurons. While TOL-1′s role in pathogen avoidance is well established, its role in an opposing behavior – foraging – has not been examined. In addition to pathogenic bacteria, preferred food for C. elegans, such as Escherichia coli (E. coli), create significant and aversive environmental CO2 levels which may limit feeding behaviors in a tol-1 dependent manner. We have found that in addition to conferring antibacterial immunity, TOL-1 signals in neurons through the p38 MAPK PMK-1 to promote turning behavior and limit foraging when food is abundant and that the anorectic TOL-1/PMK-1 pathway is attenuated during starvation to promote foraging These data highlight the dynamic role of a conserved innate immune cascade in neurons during both high and low hunger states and identify mechanisms underlying the neuro-immune control of feeding strategies.

Compressed sensing based approach identifies modular neural circuitry driving learned pathogen avoidance.

An animal's survival hinges on its ability to integrate past information to modify future behavior. The nematode C. elegans adapts its behavior based on prior experiences with pathogen exposure, transitioning from attraction to avoidance of the pathogen. A systematic screen for the neural circuits that integrate the information of previous pathogen exposure to modify behavior has not been feasible because of the lack of tools for neuron type specific perturbations. We overcame this challenge using methods based on compressed sensing to efficiently determine the roles of individual neuron types in learned avoidance behavior. Our screen revealed that distinct sets of neurons drive exit from lawns of pathogenic bacteria and prevent lawn re-entry. Using calcium imaging of freely behaving animals and optogenetic perturbations, we determined the neural dynamics that regulate one key behavioral transition after infection: stalled re-entry into bacterial lawns. We find that key neuron types govern pathogen lawn specific stalling but allow the animal to enter nonpathogenic E. coli lawns. Our study shows that learned pathogen avoidance requires coordinated transitions in discrete neural circuits and reveals the modular structure of this complex adaptive behavioral response to infection.

The impact of disgust learning on memory processes for neutral stimuli: a classical conditioning approach

ABSTRACT Disgust is a basic emotion that promotes pathogen avoidance and can contaminate nearby neutral stimuli. This study investigates how neutral stimuli, which have acquired disgust value through classical conditioning, are processed in episodic memory. The Category Conditioning paradigm was utilised to assign emotional significance to neutral stimuli, followed by a recognition test conducted immediately or 24 h after conditioning (Experiment 1). The results revealed that neutral stimuli that acquired disgust value were recognised with greater accuracy and higher liberal bias compared to other neutral stimuli in the recognition test conducted after 24 h, but not immediately. Present study also indicates that the memory enhancement observed with disgust did not manifest in the context of fear (Experiment 2). Additionally, the results varied when neutral stimuli associated with disgust were presented with disgusting stimuli in recognition test (Experiment 3). Thus, the present study demonstrates that the memory advantage of disgust extends to associated stimuli when they are presented in a list without disgusting stimuli.

Pseudomonas aeruginosa modulates both Caenorhabditis elegans attraction and pathogenesis by regulating nitrogen assimilation

Detecting chemical signals is important for identifying food sources and avoiding harmful agents. Like many animals, C. elegans use olfaction to chemotax towards their main food source, bacteria. However, little is known about the bacterial compounds governing C. elegans attraction to bacteria and the physiological importance of these compounds to bacteria. Here, we address these questions by investigating the function of a small RNA, P11, in the pathogen, Pseudomonas aeruginosa, that was previously shown to mediate learned pathogen avoidance. We discovered that this RNA also affects the attraction of untrained C. elegans to P. aeruginosa and does so by controlling production of ammonia, a volatile odorant produced during nitrogen assimilation. We describe the complex regulation of P. aeruginosa nitrogen assimilation, which is mediated by a partner-switching mechanism involving environmental nitrates, sensor proteins, and P11. In addition to mediating C. elegans attraction, we demonstrate that nitrogen assimilation mutants perturb bacterial fitness and pathogenesis during C. elegans infection by P. aeruginosa. These studies define ammonia as a major mediator of trans-kingdom signaling, implicate nitrogen assimilation as important for both bacteria and host organisms, and highlight how a bacterial metabolic pathway can either benefit or harm a host in different contexts.

Optimizing Clubroot Management and the Role of Canola Cultivar Mixtures.

The sustainable cultivation of canola is under threat from clubroot disease (Plasmodiophora brassicae). The pathogen's resting spores can survive in the soil for extended periods, complicating disease management. Therefore, effective clubroot control requires a combination of tactics that provide multiple layers of protection. Management strategies have focused on pathogen avoidance and reducing disease levels in infested fields. The sanitation of machinery and field equipment remains the most effective method for preventing the pathogen's introduction into non-infested fields. For disease reduction, crop rotation, liming, chemical control, and host resistance are commonly employed, with the use of clubroot-resistant cultivars being the most effective to date. However, resistance breakdown has been observed within four years of the introduction of new cultivars, jeopardizing the long-term effectiveness of this approach. A promising yet underexplored strategy is the use of cultivar mixtures. This approach leverages mechanisms such as the dilution effect, the barrier effect, induced resistance, disruptive selection, and the compensatory effect to control the disease. Cultivar mixtures have the potential to reduce the impact of clubroot on canola production while preserving pathogen population structure, thereby minimizing the likelihood of resistance breakdown. Given its potential, further research into cultivar mixtures as a management strategy for clubroot disease is warranted.

Cognitive markers of the uncanny valley effect

In his essay “The Uncanny Valley", Masahiro Mori notes the following: People will experience negative feelings towards a humanoid object if some of its features reveal its mechanical nature. When the nature of the object and its features are consistent, there is no such abrupt negative response. This transition to negative affect has been called the "uncanny valley" effect. One of the most popular explanations for this effect is the evolutionary hypothesis. Its main concept is the «pathogen avoidance system», an evolutionary mechanism responsible for the induction of aversion in response to the sight of a sick member of the species. Like the authors, we hypothesise that the same system is involved in the formation of the uncanny valley effect. In our study, subjects were asked to perform a task in which they had to match images of faces in three categories (healthy, infected, "uncanny") with one of two categories (alive/not alive). The result was that healthy faces were categorised with less accuracy and speed than uncanny faces. Our results provide partial support for the evolutionary hypothesis. In a subsequent experiment, we decided to clarify the influence of the atypicality of the faces presented on our earlier results by comparing the recognition success of three groups of faces: unusual/uncanny/typical. It was shown that unusual faces were recognised significantly more accurately than uncanny or typical faces.

Frontal alpha asymmetries and behavioral immune system: moderating role of behavioral inhibition system

Background and purpose: Behavioral immune system is a cluster of psychological mechanisms enabling detection and avoidance of pathogens in one’s immediate environment. Its presumed activation has been implicated in myriads of psychological phenomena, stemming from pathogen related disgust to more complex behaviors, such as mate choice and xenophobic cognitions. However, little is known about its biological underpinnings. The aim of this preliminary study was twofold: 1) to explore the role of another neuropsychological system governing avoidant motivations, the behavioral inhibition system, in pathogen-induced disgust and 2) to determine if frontal hemispheric asymmetries (a neural correlate of avoidant motivations) might serve as indicators of behavioral immune system activation. Materials and methods: 62 participants completed the Behavioral inhibition scale. Based on their z-scores, two extreme groups were formed: high (n=9) and low behavioral inhibition (n=9) group. After the baseline EEG recordings, participants were exposed to a set of neutral stimuli, followed by a set of pathogen disgust inducing stimuli. The frontal asymmetry (FAA) indexes (lnR-LnL) were calculated within both low (8-10 Hz) and high (11-13 Hz) alpha frequency bands on analogue pairs of frontal electrodes. Results: There were no baseline FAA differences between groups. However, compared to low behavioral inhibition group, high behavioral inhibition group showed larger shifts in FAA on frontopolar locations while watching the pathogen related disgust-inducing stimuli, as compared to neutral photographs. Conclusions: This pattern of FAA shifts suggests that high behavioral inhibition individuals attend to pathogen threat related cues more readily, i.e., have a more reactive behavioral immune system. With this preliminary study we are proposing a new line of research in order to determine if there is evidence of a calibrated response in terms of interplay between one’s immune status and pathogen treat related neural reactivity.

Regulator of Lipid Metabolism NHR-49 Mediates Pathogen Avoidance through Precise Control of Neuronal Activity.

Precise control of neuronal activity is crucial for the proper functioning of neurons. How lipid homeostasis contributes to neuronal activity and how much of it is regulated by cells autonomously is unclear. In this study, we discovered that absence of the lipid regulator nhr-49, a functional ortholog of the peroxisome proliferator-activated receptor (PPAR) in Caenorhabditis elegans, resulted in defective pathogen avoidance behavior against Pseudomonas aeruginosa (PA14). Functional NHR-49 was required in the neurons, and more specifically, in a set of oxygen-sensing body cavity neurons, URX, AQR, and PQR. We found that lowering the neuronal activity of the body cavity neurons improved avoidance in nhr-49 mutants. Calcium imaging in URX neurons showed that nhr-49 mutants displayed longer-lasting calcium transients in response to an O2 upshift, suggesting that excess neuronal activity leads to avoidance defects. Cell-specific rescue of NHR-49 in the body cavity neurons was sufficient to improve pathogen avoidance, as well as URX neuron calcium kinetics. Supplementation with oleic acid also improved avoidance behavior and URX calcium kinetics, suggesting that the defective calcium response in the neuron is due to lipid dysfunction. These findings highlight the role of cell-autonomous lipid regulation in neuronal physiology and immune behavior.

Pseudomonas fluorescens 15 small RNA Pfs1 mediates transgenerational epigenetic inheritance of pathogen avoidance in C. elegans through the Ephrin receptor VAB-1.

C. elegans are exposed to a variety of pathogenic and non-pathogenic bacteria species in their natural environment. Correspondingly, C. elegans has evolved an ability to discern between nutritive and infectious bacterial food sources. Here we show that C. elegans can learn to avoid the pathogenic bacteria Pseudomonas fluorescens 15 (PF15), and that this learned avoidance behavior is passed on to progeny for four generations, as we previously demonstrated for Pseudomonas aeruginosa (PA14) and Pseudomonas vranovensis, using similar mechanisms, including the involvement of both the TGF-β ligand DAF-7 and Cer1 retrotransposon-encoded virus-like particles. PF15 small RNAs are both necessary and sufficient to induce this transgenerational avoidance behavior. Unlike PA14 or P. vranovensis, PF15 does not use P11, Pv1, or a small RNA with maco-1 homology for this avoidance; instead, an unrelated PF15 small RNA, Pfs1, that targets the C. elegans vab-1 Ephrin receptor gene is necessary and sufficient for learned avoidance, suggesting the evolution of yet another bacterial sRNA/C. elegans gene target pair involved in transgenerational inheritance of pathogen avoidance. As VAB-2 Ephrin receptor ligand and MACO-1 knockdown also induce PF15 avoidance, we have begun to understand the genetic pathway involved in small RNA targeted pathogenic avoidance. Moreover, these data show that axon guidance pathway genes (VAB-1 and VAB-2) have previously unknown adult roles in regulating neuronal function. C. elegans may have evolved multiple bacterial specificity-encoded small RNA-dependent mechanisms to avoid different pathogenic bacteria species, thereby providing progeny with a survival advantage in a dynamic environment.

Neuronal basis and diverse mechanisms of pathogen avoidance in Caenorhabditis elegans.

Pathogen avoidance behaviour has been observed across animal taxa as a vital host-microbe interaction mechanism. The nematode Caenorhabditis elegans has evolved multiple diverse mechanisms for pathogen avoidance under natural selection pressure. We summarise the current knowledge of the stimuli that trigger pathogen avoidance, including alterations in aerotaxis, intestinal bloating, and metabolites. We then survey the neural circuits involved in pathogen avoidance, transgenerational epigenetic inheritance of pathogen avoidance, signalling crosstalk between pathogen avoidance and innate immunity, and C. elegans avoidance of non-Pseudomonas bacteria. In this review, we highlight the latest advances in understanding host-microbe interactions and the gut-brain axis.

Antagonism between neuropeptides and monoamines in a distributed circuit for pathogen avoidance

Pathogenic infection elicits behaviors that promote recovery and survival of the host. After exposure to the pathogenic bacterium Pseudomonas aeruginosa PA14, the nematode Caenorhabditis elegans modifies its sensory preferences to avoid the pathogen. Here, we identify antagonistic neuromodulators that shape this acquired avoidance behavior. Using an unbiased cell-directed neuropeptide screen, we show that AVK neurons upregulate and release RF/RYamide FLP-1 neuropeptides during infection to drive pathogen avoidance. Manipulations that increase or decrease AVK activity accelerate or delay pathogen avoidance, respectively, implicating AVK in the dynamics of avoidance behavior. FLP-1 neuropeptides drive pathogen avoidance through the G protein-coupled receptor DMSR-7, as well as other receptors. DMSR-7 in turn acts in multiple neurons, including tyraminergic/octopaminergic neurons that receive convergent avoidance signals from the cytokine DAF-7/transforming growth factor β. Neuromodulators shape pathogen avoidance through multiple mechanisms and targets, in agreement with the distributed neuromodulatory connectome of C.elegans.

Pathogen Avoidance and Outgroup Avoidance During the First Wave of the COVID‐19 Pandemic

AbstractBehavioral immune system (BIS) theory explains that humans possess an adaptive psychological mechanism that helps them stay away from potential sources of pathogens. The theory claims that potential sources of pathogens also include outgroups, such as racial and ethnic minorities, because outgroup members potentially carry infectious diseases to which ingroup members have not developed immunity. In order to examine this controversial claim, the current study investigated how outgroup avoidance was associated with other types of pathogen avoidance during the COVID‐19 pandemic. During the first wave of the COVID‐19 pandemic, participants from the United States (N = 386) responded to questions pertaining to pathogen threat, pathogen avoidance, and outgroup avoidance. The data were statistically analyzed to identify significant associations between those variables. The results indicated that outgroup avoidance was positively associated with avoidance of personal pathogen cues (i.e., social distancing) but no other types of pathogen cues (i.e., wearing a mask and washing hands). This result aligns with the recent theoretical argument that the outgroup avoidance activated by the BIS (e.g., xenophobia) is a byproduct of avoiding infected ingroup rather than outgroup individuals.

Neuronal NPR-15 modulates molecular and behavioral immune responses via the amphid sensory neuron-intestinal axis in C. elegans

The survival of hosts during infections relies on their ability to mount effective molecular and behavioral immune responses. Despite extensive research on these defense strategies in various species, including the model organism Caenorhabditis elegans, the neural mechanisms underlying their interaction remain poorly understood. Previous studies have highlighted the role of neural G-protein-coupled receptors (GPCRs) in regulating both immunity and pathogen avoidance, which is particularly dependent on aerotaxis. To address this knowledge gap, we conducted a screen of mutants in neuropeptide receptor family genes. We found that loss-of-function mutations in npr-15 activated immunity while suppressing pathogen avoidance behavior. Through further analysis, NPR-15 was found to regulate immunity by modulating the activity of key transcription factors, namely GATA/ELT-2 and TFEB/HLH-30. Surprisingly, the lack of pathogen avoidance of npr-15 mutant animals was not influenced by oxygen levels. Moreover, our studies revealed that the amphid sensory neuron ASJ is involved in mediating the immune and behavioral responses orchestrated by NPR-15. Additionally, NPR-15 was found to regulate avoidance behavior via the TRPM (transient receptor potential melastatin) gene, GON-2, which may sense the intestinal distension caused by bacterial colonization to elicit pathogen avoidance. Our study contributes to a broader understanding of host defense strategies and mechanisms underlining the interaction between molecular and behavioral immune responses.

Neuronal NPR-15 modulates molecular and behavioral immune responses via the amphid sensory neuron-intestinal axis in C. elegans.

The survival of hosts during infections relies on their ability to mount effective molecular and behavioral immune responses. Despite extensive research on these defense strategies in various species, including the model organism Caenorhabditis elegans, the neural mechanisms underlying their interaction remain poorly understood. Previous studies have highlighted the role of neural G-protein-coupled receptors (GPCRs) in regulating both immunity and pathogen avoidance, which is particularly dependent on aerotaxis. To address this knowledge gap, we conducted a screen of mutants in neuropeptide receptor family genes. We found that loss-of-function mutations in npr-15 activated immunity while suppressing pathogen avoidance behavior. Through further analysis, NPR-15 was found to regulate immunity by modulating the activity of key transcription factors, namely GATA/ELT-2 and TFEB/HLH-30. Surprisingly, the lack of pathogen avoidance of npr-15 mutant animals was not influenced by oxygen levels. Moreover, our studies revealed that the amphid sensory neuron ASJ is involved in mediating the immune and behavioral responses orchestrated by NPR-15. Additionally, NPR-15 was found to regulate avoidance behavior via the TRPM (transient receptor potential melastatin) gene, GON-2, which may sense the intestinal distension caused by bacterial colonization to elicit pathogen avoidance. Our study contributes to a broader understanding of host defense strategies and mechanisms underlining the interaction between molecular and behavioral immune responses.

(056) The Association Between Disgust Sensitivity, Sexual Desire, Relationship Satisfaction in Finland

Abstract Introduction Disgust is a basic emotion directed towards certain objects to avoid harm (Angyal, 1941), mainly pathogens. Research, however, has proposed a heterogeneity of disgust beyond pathogen avoidance to generate the functional model, which proposed the functionally distinct domains of disgust: moral, pathogen, and sexual. This model proposes that sexual disgust is an avoidance of sexual contact with unfit partners that may yield unfit offspring (Tybur & de Vries, 2013), this may be due to other anxiety related disorders (Davey, 2011 and Troop et al., 2002) Objective This study focuses on the association between disgust sensitivity with sexual desire, and relationships satisfaction. Hypothesis: elevated levels of disgust sensitivity are negatively associated with sexual desire and relationship satisfaction. Methods Invitation letters were sent out to the registered Finnish population in the Finnish Central Population Registry to participate in a(n) (online) survey, 9,319 individuals responded to the invitation and completed the survey and agreed to participate in the research. The tools used in this study were Perceived Relationship Quality Component (PRQC), Sexual Desire Inventory (SDI), and the Three-Disgust Domain Scale (TDDS). Results The results indicate that the sexual desire and sexual disgust sensitivity, are negatively correlated, the relationship satisfaction correlations are positive except the men pathogen disgust which is a negative correlation between pathogen disgust sensitivity and relationship satisfaction. The correlation between the study variables indicated that among men and women sexual disgust is negatively correlated with sexual desire, and the correlation of relationship satisfaction and sexual disgust was positively correlated. Conclusions The results show the negative association of sexual disgust with sexual desire, but there is a positive relationship between sexual disgust and relationship satisfaction. Disclosure No.

Ambrosia beetles adjust dispersal preferences to their degree of exhaustion

Abstract Delayed dispersal of sexually mature offspring is a fundamental component of cooperative breeding in fungus farming ambrosia beetles. These beetles dwell in logs of recently deceased trees, where female offspring postpone reproduction and invest in alloparental care before dispersing to found a new nest. The wood quality affects investment of adult offspring in alloparental care and hence the breeder's reproductive success. This raises the question of whether dispersing breeders choose habitats strategically to optimise breeding prospects and modulate their offspring's helping propensity. To answer this question, here we tested experimentally whether during dispersal, Xyleborinus saxesenii Ratzeburg (Coleoptera: Scolytinae) uses olfactory cues emitted by mutualistic or pathogenic fungi as an information source on prospective habitat quality. As the mutualistic relationship between the fungi and beetles is obligate, fungus scent should provide a reliable source of information on habitat quality, indicating prior successful colonisation by conspecifics. We found no evidence for direct pathogen avoidance. However, the beetles clearly responded to scent of their mutualistic fungi, dependent on dispersal state. At the onset of dispersal, females avoided the scent of fungus mutualists, whereas they were attracted to them after being exhausted by an experimentally prolonged dispersal time. The observed change of preference during dispersal suggests that beetles freshly emerging from their home gallery may choose pristine habitat by avoiding mutualist scent. This might help to avoid competition with conspecifics and potential pathogen and parasite cross contamination. Exhausted beetles, however, may accept these risks and choose successfully colonised habitat to avoid starvation. State‐dependent adjustment of habitat preferences may be exhibited also in other economically impactful bark and ambrosia beetles, which prompts further study of the olfactory cues used by these beetles during dispersal.

Pathogens or promiscuity? Testing two accounts of the relation between disgust sensitivity and binding moral values.

A recurrent observation in the field of moral psychology is that disgust sensitivity is associated with greater moralization of the binding (and particularly sanctity) moral domains. It is generally assumed that these effects are the result of disgust's role as an emotion that motivates pathogen avoidance (i.e., the pathogen avoidance account), yet alternative disgust-based accounts of moralization, namely those grounded in sexual avoidance (i.e., the promiscuity avoidance account), might also explain these observations. Across two studies (total N = 2,718), involving 10 diverse samples (from Australia, the United States, and Brazil), we found that after controlling for the shared variance of pathogen and sexual disgust, only measures of sexual disgust exhibited a positive (and strong) association with the binding moral foundations. These results argue against the pathogen avoidance account of disgust-binding effects and instead support the promiscuity avoidance account. Above all, this work highlights the utility of delineating the dimensionality of disgust to better characterize the different disgust-based motives underlying moral cognition. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Neurobiology of Pathogen Avoidance and Mate Choice: Current and Future Directions.

Animals are under constant threat of parasitic infection. This has influenced the evolution of social behaviour and has strong implications for sexual selection and mate choice. Animals assess the infection status of conspecifics based on various sensory cues, with odours/chemical signals and the olfactory system playing a particularly important role. The detection of chemical cues and subsequent processing of the infection threat that they pose facilitates the expression of disgust, fear, anxiety, and adaptive avoidance behaviours. In this selective review, drawing primarily from rodent studies, the neurobiological mechanisms underlying the detection and assessment of infection status and their relations to mate choice are briefly considered. Firstly, we offer a brief overview of the aspects of mate choice that are relevant to pathogen avoidance. Then, we specifically focus on the olfactory detection of and responses to conspecific cues of parasitic infection, followed by a brief overview of the neurobiological systems underlying the elicitation of disgust and the expression of avoidance of the pathogen threat. Throughout, we focus on current findings and provide suggestions for future directions and research.