Luteal phase immunosuppression and meat eating.

Immunosuppression during pregnancy makes the mother vulnerable to pathogens. Because meat is the principal source of ingestible pathogens, pregnancy raises the costs of meat eating. Natural selection has crafted a mechanism involving changes in nausea susceptibility and olfactory perception that reduces meat consumption during pregnancy. Evidence is presented showing that the luteal phase is marked by both immunosuppression and changes in nausea susceptibility and olfaction; meat consumption may be reduced during this period, suggesting a mechanism similar to pregnancy sickness. Constraints on compensatory increases in meat consumption outside of the luteal phase explain why women eat less meat than men. Meat is the principal target of acquired aversions. Women possess more aversions than men, suggesting that prophylactic mechanisms sometimes result in longstanding dietary changes. Reproductive immunosuppression explains many aspects of dietary behavior and sheds light on factors that may have contributed to gender-based divisions of labor during hominid evolution.     

Food Aversions and Cravings during Pregnancy on Yasawa Island,Fiji

Women often experience novel food aversions and cravings during pregnancy. These appetite changes have been hypothesized to work alongside cultural strategies as adaptive responses to the challenges posed by pregnancy (e.g., maternal immune suppression). Here, we report a study that assessed whether data from an indigenous population in Fiji are consistent with the predictions of this hypothesis. We found that aversions focus predominantly on foods expected to exacerbate the challenges of pregnancy. Cravings focus on foods that provide calories and micronutrients while posing few threats to mothers and fetuses. We also found that women who experience aversions to specific foods are more likely to crave foods that meet nutritional needs similar to those provided by the aversive foods. These findings are in line with the predictions of the hypothesis. This adds further weight to the argument that appetite changes may function in parallel with cultural mechanisms to solve pregnancy challenges.     

Innate food aversions and culturally transmitted food taboos in pregnant women in rural southwest India: Separate systems to protect the fetus?

Pregnancy increases women's nutritional requirements, yet causes aversions to nutritious foods. Most societies further restrict pregnant women's diet with food taboos. Pregnancy food aversions are theorized to protect mothers and fetuses from teratogens and pathogens or increase dietary diversity in response to resource scarcity. Tests of these hypotheses have had mixed results, perhaps because many studies are in Westernized populations with reliable access to food and low exposure to pathogens. If pregnancy food aversions are adaptations, however, then they likely evolved in environments with uncertain access to food and high exposure to pathogens. Pregnancy food taboos, on the other hand, have been theorized to limit resource consumption, mark social identity, or also protect mothers and fetuses from dangerous foods. There have been few tests of evolutionary theories of culturally transmitted food taboos.We investigated these and other theories of psychophysiological food aversions and culturally transmitted food taboos among two non-Western populations of pregnant women in Mysore, India, that vary in food insecurity and exposure to infectious disease. The first was a mixed caste rural farming population (N = 72), and the second was the Jenu Kurubas, a resettled population of former hunter-gatherers (N = 30). Women rated their aversions to photos of 31 foods and completed structured interviews that assessed aversions and socially learned avoidances of foods, pathogen exposure, food insecurity, sources of culturally acquired dietary advice, and basic sociodemographic information. Aversions to spicy foods were associated with early trimester and nausea and vomiting, supporting a protective role against plant teratogens. Variation in exposure to pathogens did not explain variation in meat aversions or avoidances, however, raising some doubts about the importance of pathogen avoidance. Aversions to staple foods were common, but were not associated with resource stress, providing mixed support for the role of dietary diversification. Avoided foods outnumbered aversive foods, were believed to be abortifacients or otherwise harmful to the fetus, influenced diet throughout pregnancy, and were largely distinct from aversive foods. These results suggest that aversions target foods with cues of toxicity early in pregnancy, and taboos target suspected abortifacients throughout pregnancy.     

Embryo quality: the missing link between pregnancy sickness and pregnancy outcome

Pregnancy sickness is widespread yet its etiology is poorly understood. It is almost certainly endocrine in origin and most likely a product of placental hormones, with human chorionic gonadotropin being the strongest candidate. It has long been known that greater levels of nausea and vomiting during pregnancy are associated with a lower incidence of spontaneous abortion, yet the causal mechanisms remain unclear. One current popular explanation is that nausea and vomiting during pregnancy is fetoprotective, inducing aversions to foods, especially meat, dairy and seafoods, which may carry toxins, pathogens or mutagens. However, most spontaneous abortions arise from genetic or epigenetic defects that are present at or near conception. Moreover, measurements of human chorionic gonadotropin (hCG) at the time of implantation, particularly its hyperglycosylated isoform, accurately predict subsequent spontaneous abortion. Thus the developmental fate of most embryos is fixed before the onset of the symptoms of pregnancy sickness. An alternative explanation for the link between pregnancy sickness and spontaneous abortion is the embryo quality hypothesis: high quality embryos are both more likely to produce the biochemical antecedents of pregnancy sickness and avoid spontaneous abortion. Recent work has shown that the link between pregnancy sickness and spontaneous abortion grows stronger with maternal age, dramatically so in mothers 35 or older. This reflects the parallel rise in the incidence of autosomal aneuploidies with maternal age. The link between pregnancy sickness and spontaneous abortion exists not because nausea and vomiting during pregnancy is fetoprotective, but because nausea and vomiting is an index of a high quality embryo. Pregnancy sickness is not adaptive per se, but the result of an antagonistic pleiotropy over thyroid function, where embryos use hCG to modulate maternal thyroid hormone production during gestation. Embryos benefit from the thyroid hormone production that is key to neurodevelopment, but produce maternal nausea and vomiting as a by-product. Pregnancy sickness, however, may still serve to protect embryo quality but by a different mechanism that posited under the MEPH. Embryo quality is protected by calibrating the dietary intake of a micronutrient – iodine – critical to neuromotor development. For most humans over most of our evolutionary history, iodine has been in short supply, and iodine deficiency is still the most common source of cognitive impairment across the globe. Thus it is of interest that the food aversions most commonly associated with pregnancy sickness, to meat, dairy and seafoods, are also the chief dietary sources of iodine. There is a further intriguing property about iodine: both too little and too much during early pregnancy are damaging to embryo brain development. Given that pregnancy sickness is closely linked to iodine intake and thyroid function (hypothyroidism is associated with lower levels of nausea and vomiting, hyperthyroidism with more), an obvious interpretation emerges. The previously described link between diet and pregnancy sickness – pregnancy sickness is less likely when plants and particularly corn/maize are the sole food staples – arises not because plant food staples are safe, as previously suggested, but because these foods are iodine poor and may, in addition, be goitrogenic. Pregnancy sickness, which reduces the dietary intake of iodine, is clearly maladaptive under conditions of iodine deficiency and hypothyroidism. Conversely, higher levels of pregnancy sickness induced by hyperthyroidism may protect embryos from the inimical effects of excessive dietary iodine during early gestation by reducing the intake of iodine rich foods.     

Morning sickness: adaptive cause or nonadaptive consequence of embryo viability?

"Morning sickness" is the common term for nausea and vomiting in early human pregnancy (NVP). Recent interest in why NVP occurs-that is, in the evolutionary costs and benefits of NVP-has spurred the development of two alternative hypotheses. The "prophylaxis," or "maternal and embryonic protection," hypothesis suggests that NVP serves a beneficial function by expelling foods that may contain harmful toxins and microorganisms and triggering aversions to such foods throughout pregnancy. The alternative "by-product" hypothesis suggests that NVP is a nonfunctional by-product of conflict--over resource allocation--between the pregnant woman and the embryo. The critical predictions of the prophylaxis hypothesis have been developed and tested, whereas the by-product hypothesis has not been subjected to similar scrutiny. To address this gap, we developed a graphical model and used it to derive predictions from the by-product hypothesis under two different assumptions, namely, that NVP is either (i) a by-product of current conflict between a pregnant woman and an embryo or (ii) a by-product of honest signals of viability produced by the embryo. Neither version of the by-product hypothesis is fully consistent with available data. By contrast, the timing of NVP, its variation among societies, and associated patterns of food cravings and aversions are consistent with the prophylaxis hypothesis.     

EXPLORATION OF THE SENSORY CHARACTERISTICS OF CRAVED AND AVERSIVE FOODS

This research examined the sensory characteristics of craved and aversive foods, as determined by 70 healthy adults. Cravings and aversions were identified by 66% and 53% of subjects. Typically, cravings were intermittent, and the items were sweet tasting and pleasant smelling. In contrast, aversions were chronic, and the items were described as either bitter or bad (e.g., soapy, mealy, dusty) tasting, and exhibiting an unpleasant smell. Chemesthetic attributes were frequently associated with cravings and aversions, particularly texture and thermal sensations with the former whereas texture and irritating sensations were associated with the latter. The findings suggest that sensory characteristics of foods may provide salient cues for the formation of cravings and aversions.     

A Review of Zoonotic Infection Risks Associated with the Wild Meat Trade in Malaysia

The overhunting of wildlife for food and commercial gain presents a major threat to biodiversity in tropical forests and poses health risks to humans from contact with wild animals. Using a recent survey of wildlife offered at wild meat markets in Malaysia as a basis, we review the literature to determine the potential zoonotic infection risks from hunting, butchering and consuming the species offered. We also determine which taxa potentially host the highest number of pathogens and discuss the significant disease risks from traded wildlife, considering how cultural practices influence zoonotic transmission. We identify 51 zoonotic pathogens (16 viruses, 19 bacteria and 16 parasites) potentially hosted by wildlife and describe the human health risks. The Suidae and the Cervidae families potentially host the highest number of pathogens. We conclude that there are substantial gaps in our knowledge of zoonotic pathogens and recommend performing microbial food safety risk assessments to assess the hazards of wild meat consumption. Overall, there may be considerable zoonotic risks to people involved in the hunting, butchering or consumption of wild meat in Southeast Asia, and these should be considered in public health strategies.     

The timing and specificity of prenatal immune risk factors for autism modeled in the mouse and relevance to schizophrenia

Autism is a highly heritable condition, but there is strong epidemiological evidence that environmental factors, especially prenatal exposure to immune challenge, contribute to it. This evidence is largely indirect, and experimental testing is necessary to directly examine causal mechanisms. Mouse models reveal that prenatal immune perturbation disrupts postnatal brain maturation with alterations in gene and protein expression, neurotransmitter function, brain structure and behavioral indices reminiscent of, but not specific to, autism. This likely reflects a neurodevelopmental spectrum in which autism and schizophrenia share numerous genetic and environmental risk factors for difficulties in social interaction, communication, emotion processing and executive function. Recent epidemiological studies find that early rather than late pregnancy infection confers the greater risk of schizophrenia. The autism literature is more limited, but exposures in the 2nd half of pregnancy may be important. Mouse models of prenatal immune challenge help dissect these observations and show some common consequences of early and late gestational exposures, as well as distinct ramifications potentially relevant to schizophrenia and autism. Although nonspecificity of immune-stimulated mouse models could be considered a disadvantage, we propose a broadened perspective, exploiting the possibility that advances made investigating a target condition can contribute towards the understanding of related conditions.     

The landscape of human proteins interacting with viruses and other pathogens

Infectious diseases result in millions of deaths each year. Mechanisms of infection have been studied in detail for many pathogens. However, many questions are relatively unexplored. What are the properties of human proteins that interact with pathogens? Do pathogens interact with certain functional classes of human proteins? Which infection mechanisms and pathways are commonly triggered by multiple pathogens? In this paper, to our knowledge, we provide the first study of the landscape of human proteins interacting with pathogens. We integrate human–pathogen protein–protein interactions (PPIs) for 190 pathogen strains from seven public databases. Nearly all of the 10,477 human-pathogen PPIs are for viral systems (98.3%), with the majority belonging to the human–HIV system (77.9%). We find that both viral and bacterial pathogens tend to interact with hubs (proteins with many interacting partners) and bottlenecks (proteins that are central to many paths in the network) in the human PPI network. We construct separate sets of human proteins interacting with bacterial pathogens, viral pathogens, and those interacting with multiple bacteria and with multiple viruses. Gene Ontology functions enriched in these sets reveal a number of processes, such as cell cycle regulation, nuclear transport, and immune response that participate in interactions with different pathogens. Our results provide the first global view of strategies used by pathogens to subvert human cellular processes and infect human cells. Supplementary data accompanying this paper is available at http://staff.vbi.vt.edu/dyermd/publications/dyer2008a.html.     

Similarities in Food Cravings and Mood States Between Obese Women and Women Who Smoke Tobacco

The present study assessed food cravings in a cohort of 229 women who differed in smoking history (i.e., never smoker, former smoker, and current smoker) and body weight (i.e., normal weight, overweight, and obese). Each subject completed the Food Craving Inventory (FCI), which measures cravings for sweets, high fats, carbohydrates/starches, and fast‐food fats, and the Profile of Mood States (POMS), which measures psychological distress. Smoking and obesity were independently associated with specific food cravings and mood states. Current smokers craved high fats more frequently than former and never smokers. They also craved starches more frequently and felt more depressed and angry than never smokers, but not former smokers. Whereas cravings for starchy foods and some mood states may be characteristic of women who are likely to smoke, more frequent cravings for fat among smokers is related to smoking per se. Similarly, obese women craved high fats more frequently than nonobese women and depression symptoms were intensified with increasing body weights. We hypothesize that the overlapping neuroendocrine alterations associated with obesity and smoking and the remarkable similarities in food cravings and mood states between women who smoke and women who are obese suggest that common biological mechanisms modulate cravings for fat in these women.     

Neuroendocrine aspects of placenta and pregnancy

Placenta plays a central role in the regulation of physiological mechanisms of pregnancy, and in particular is the organ of communication between mother and fetus. This action is also related to its ability to produce hormones, growth factors and cytokines during the progression of pregnancy, and in response to stimuli such as stress and inflammation/infection. In the last years the understanding of the physiological and pathological functions of human placenta revealed the hypersecretion of hormones in presence of gestational diseases and raised the question whether this mechanism is cause of disorders of pregnancy, or part of an adaptive response of placenta to resolve adverse conditions. However, there are evidences indicating that changes of placental hormone secretion may have clinical usefulness, since they are measurable in biological fluids, and may be used as predictive markers or prognostic tools. Of particular interest is the role of corticotropin releasing hormone, urocortins and activins in the maintaining physiological pregnancy and in the pathogenesis of diseases (preterm birth and preeclampsia).     

Toxoplasma gondii: from animals to humans

Toxoplasmosis is one of the more common parasitic zoonoses world-wide. Its causative agent, Toxoplasma gondii, is a facultatively heteroxenous, polyxenous protozoon that has developed several potential routes of transmission within and between different host species. If first contracted during pregnancy, T. gondii may be transmitted vertically by tachyzoites that are passed to the foetus via the placenta. Horizontal transmission of T. gondii may involve three life-cycle stages, i.e. ingesting infectious oocysts from the environment or ingesting tissue cysts or tachyzoites which are contained in meat or primary offal (viscera) of many different animals. Transmission may also occur via tachyzoites contained in blood products, tissue transplants, or unpasteurised milk. However, it is not known which of these routes is more important epidemiologically. In the past, the consumption of raw or undercooked meat, in particular of pigs and sheep, has been regarded as a major route of transmission to humans. However, recent studies showed that the prevalence of T. gondii in meat-producing animals decreased considerably over the past 20 years in areas with intensive farm management. For example, in several countries of the European Union prevalences of T. gondii in fattening pigs are now <1%. Considering these data it is unlikely that pork is still a major source of infection for humans in these countries. However, it is likely that the major routes of transmission are different in human populations with differences in culture and eating habits. In the Americas, recent outbreaks of acute toxoplasmosis in humans have been associated with oocyst contamination of the environment. Therefore, future epidemiological studies on T. gondii infections should consider the role of oocysts as potential sources of infection for humans, and methods to monitor these are currently being developed. This review presents recent epidemiological data on T. gondii, hypotheses on the major routes of transmission to humans in different populations, and preventive measures that may reduce the risk of contracting a primary infection during pregnancy.     

Strain Interactions as a Mechanism for Dominant Strain Alternation and Incidence Oscillation in Infectious Diseases: Seasonal Influenza as a Case Study

Background

Many human infectious diseases are caused by pathogens that have multiple strains and show oscillation in infection incidence and alternation of dominant strains which together are referred to as epidemic cycling. Understanding the underlying mechanisms of epidemic cycling is essential for forecasting outbreaks of epidemics and therefore important for public health planning. Current theoretical effort is mainly focused on the factors that are extrinsic to the pathogens themselves (“extrinsic factors”) such as environmental variation and seasonal change in human behaviours and susceptibility. Nevertheless, co-circulation of different strains of a pathogen was usually observed and thus strains interact with one another within concurrent infection and during sequential infection. The existence of these intrinsic factors is common and may be involved in the generation of epidemic cycling of multi-strain pathogens.

Methods and Findings

To explore the mechanisms that are intrinsic to the pathogens themselves (“intrinsic factors”) for epidemic cycling, we consider a multi-strain SIRS model including cross-immunity and infectivity enhancement and use seasonal influenza as an example to parameterize the model. The Kullback-Leibler information distance was calculated to measure the match between the model outputs and the typical features of seasonal flu (an outbreak duration of 11 weeks and an annual attack rate of 15%). Results show that interactions among strains can generate seasonal influenza with these characteristic features, provided that: the infectivity of a single strain within concurrent infection is enhanced 2−7 times that within a single infection; cross-immunity as a result of past infection is 0.5–0.8 and lasts 2–9 years; while other parameters are within their widely accepted ranges (such as a 2–3 day infectious period and the basic reproductive number of 1.8–3.0). Moreover, the observed alternation of the dominant strain among epidemics emerges naturally from the best fit model. Alternative modelling that also includes seasonal forcing in transmissibility shows that both external mechanisms (i.e. seasonal forcing) and the intrinsic mechanisms (i.e., strain interactions) are equally able to generate the observed time-series in seasonal flu.

Conclusions

The intrinsic mechanism of strain interactions alone can generate the observed patterns of seasonal flu epidemics, but according to Kullback-Leibler information distance the importance of extrinsic mechanisms cannot be excluded. The intrinsic mechanism illustrated here to explain seasonal flu may also apply to other infectious diseases caused by polymorphic pathogens.     

Hijacking mitochondria: bacterial toxins that modulate mitochondrial function

Bacterial infection has enormous global social and economic impacts stemming from effects on human health and agriculture. Although there are still many unanswered questions, decades of research has uncovered many of the pathogenic mechanisms at play. It is now clear that bacterial pathogens produce a plethora of proteins known as "toxins" and "effectors" that target a variety of physiological host processes during the course of infection. One of the targets of host targeted bacterial toxins and effectors are the mitochondria. The mitochondrial organelles are major players in many biological functions, including energy conversion to ATP and cell death pathways, which inherently makes them targets for bacterial proteins. We present a summary of the toxins targeted to mitochondria and for those that have been studied in finer detail, we also summarize what we know about the mechanisms of targeting and finally their action at the organelle.     

Dimorphic foraging behaviors and the evolution of hominid hunting.

In contemporary foraging societies men typically hunt more than women. This observation has played an important role in many reconstructions of hominid evolution. The gender difference in human hunting, likely a product of both ecological and cultural factors, is mirrored by a similar sex difference among nonhuman primates. Existing explanations of such primate behavioral dimorphism are augmented by the recognition of an additional factor that may contribute to differences between males and females in the value of meat. Episodic female immunosuppression is a normal part of reproduction. Because meat is a source of pathogens, females can be expected to exhibit less constant attraction to meat. Sexual dimorphism in the attraction to meat may then contribute to dimorphic foraging specializations, a divergence that is likely augmented by the differential value of insectivory across the sexes. With the rise of cultural transmission of foraging knowledge, dimorphic foraging behaviors would have been reinforced, creating a more comprehensive gender-based division of labor.     

A crucial role for exopolysaccharide modification in bacterial biofilm formation, immune evasion, and virulence

Biofilms play an important role in many chronic bacterial infections. Production of an extracellular mixture of sugar polymers called exopolysaccharide is characteristic and critical for biofilm formation. However, there is limited information about the mechanisms involved in the biosynthesis and modification of exopolysaccharide components and how these processes influence bacterial pathogenesis. Staphylococcus epidermidis is an important human pathogen that frequently causes persistent infections by biofilm formation on indwelling medical devices. It produces a poly-N-acetylglucosamine molecule that emerges as an exopolysaccharide component of many bacterial pathogens. Using a novel method based on size exclusion chromatography-mass spectrometry, we demonstrate that the surface-attached protein IcaB is responsible for deacetylation of the poly-N-acetylglucosamine molecule. Most likely due to the loss of its cationic character, non-deacetylated poly-acetylglucosamine in an isogenic icaB mutant strain was devoid of the ability to attach to the bacterial cell surface. Importantly, deacetylation of the polymer was essential for key virulence mechanisms of S. epidermidis, namely biofilm formation, colonization, and resistance to neutrophil phagocytosis and human antibacterial peptides. Furthermore, persistence of the icaB mutant strain was significantly impaired in a murine model of device-related infection. This is the first study to describe a mechanism of exopolysaccharide modification that is indispensable for the development of biofilm-associated human disease. Notably, this general virulence mechanism is likely similar for other pathogenic bacteria and constitutes an excellent target for therapeutic maneuvers aimed at combating biofilm-associated infection.     

Attaching and effacing pathogen-induced tight junction disruption in vivo

Diarrhoea is a hallmark of infections by the human attaching and effacing (A/E) pathogens, enterohaemorrhagic Escherichia coli (EHEC) and enteropathogenic E. coli (EPEC). Although the mechanisms underlying diarrhoea induced by these pathogens remain unknown, cell culture results have suggested that these pathogens may target tight junctions. Tight junctions in the colon function as physical intercellular barriers that separate and prevent mixing of the luminal contents with adlumenal regions of the epithelium. Consequently, it is thought that the disruption of intestinal epithelial tight junctions by A/E pathogens could result in a loss of barrier function in the alimentary tract; however, this remains unexamined. Here we demonstrate for the first time that A/E pathogen infection results in the morphological alteration of tight junctions during natural disease. Tight junction alteration, characterized by relocalization of the transmembrane tight junction proteins claudin 1, 3 and 5, is a functional disruption; molecular tracers, which do not normally penetrate uninfected epithelia, pass across pathogen-infected epithelia. Functional junction disruption occurs with a concomitant increase in colon luminal water content. The effects on tissue are dependent upon the bacterial type III effector EspF (E. coli secreted protein F), because bacteria lacking EspF, while able to colonize, are defective for junction disruption and result in decreased proportions of water in the colon compared with wild-type infection. These results suggest that the diarrhoea induced by A/E pathogens occurs as part of functional tight junction disruption.     

The role of P2 receptors in controlling infections by intracellular pathogens

A growing number of studies have demonstrated the importance of ATP_e-signalling via P2 receptors as an important component of the inflammatory response to infection. More recent studies have shown that ATP_e can also have a direct effect on infection by intracellular pathogens, by modulating membrane trafficking in cells that contain vacuoles that harbour intracellular pathogens, such as mycobacteria and chlamydiae. A conserved mechanism appears to be involved in controlling infection by both of these pathogens, as a role for phospholipase D in inducing fusion between lysosomes and the vacuoles has been demonstrated. Other P2-dependent mechanisms are most likely operative in the cases of pathogens, such as Leishmania, which survive in an acidic phagolysosomal-like compartment. ATP_e may function as a “danger signal” that alerts the immune system to the presence of intracellular pathogens that damage the host cell, while different intracellular pathogens have evolved enzymes or other mechanisms to inhibit ATP_e-mediated signalling, which should, thus, be viewed as virulence factors for these pathogens.     

Monocytes/macrophages in HIV infection and tuberculosis.

Mycobacterium tuberculosis (MTB) and human immunodeficiency virus type 1 (HIV-1) are virulent intracellular pathogens that enter and replicate within macrophages, which represent their reservoire. Public health problems are greatly compounded when the two diseases co-exist, and this is the reason why Acquired Immunodeficiency Syndrome (AIDS) and tuberculosis (TB) have been termed "the cursed duet", given the synergistic effect they exert one each other. With the depression of immunity caused by HIV-1 infection, latent MTB infection is much more likely to progress to clinically significant disease. On the other hand, TB results in activation of T cells and macrophages that may harbor latent HIV. Here some data are reviewed that can contribute to clarify the mechanisms involved in the concurrent infection, given that MTB infection has been shown to be able to: a) enhance HIV-1 replication in macrophages, b) augment CC-CKR5 (CCR5) expression on macrophage membrane, and, c) induce apoptosis in a portion of infected macrophages.     

The evolution of resistance against good and bad infections

Opportunities for genetic exchange are abundant between bacteria and foreign genetic elements (FGEs) such as conjugative plasmids, transposable elements and bacteriophages. The genetic novelty that may arise from these forms of genetic exchange is potentially beneficial to bacterial hosts, but there are also potential costs, which may be considerable in the case of phage infection. Some bacterial resistance mechanisms target both beneficial and deleterious forms of genetic exchange. Using a general epidemiological model, we explored under which conditions such resistance mechanisms may evolve. We considered a population of hosts that may be infected by FGEs that either confer a benefit or are deleterious to host fitness, and we analysed the epidemiological and evolutionary outcomes of resistance evolving under different cost/benefit scenarios. We show that the degree of co‐infection between these two types of infection is particularly important in determining the evolutionarily stable level of host resistance. We explore these results using the example of CRISPR‐Cas, a form of bacterial immunity that targets a variety of FGEs, and we show the potential role of bacteriophage infection in selecting for resistance mechanisms that in turn limit the acquisition of plasmid‐borne antibiotic resistance. Finally, beyond microbes, we discuss how endosymbiotic associations may have shaped the evolution of host immune responses to pathogens.