How parasite interaction strategies alter virulence evolution in multi‐parasite communities

The majority of organisms host multiple parasite species, each of which can interact with hosts and competitors through a diverse range of direct and indirect mechanisms. These within‐host interactions can directly alter the mortality rate of coinfected hosts and alter the evolution of virulence (parasite‐induced host mortality). Yet we still know little about how within‐host interactions affect the evolution of parasite virulence in multi‐parasite communities. Here, we modeled the virulence evolution of two coinfecting parasites in a host population in which parasites interacted through cross immunity, immune suppression, immunopathology, or spite. We show (1) that these within‐host interactions have different effects on virulence evolution when all parasites interact with each other in the same way versus when coinfecting parasites have unique interaction strategies, (2) that these interactions cause the evolution of lower virulence in some hosts, and higher virulence in other hosts, depending on the hosts infection status, and (3) that for cross immunity and spite, whether parasites increase or decrease the evolutionarily stable virulence in coinfected hosts depended on interaction strength. These results improve our understanding of virulence evolution in complex parasite communities, and show that virulence evolution must be understood at the community scale.     

Host genetic architecture in single and multiple infections

Hosts are often target to multiple simultaneous infections by genetically diverse parasite strains. The interaction among these strains and the interaction of each strain with the host was shown to have profound effects on the evolution of parasite traits. Host factors like genetic architecture of resistance have so far been largely neglected. To see whether genetic architecture differs between different kinds of infections we used joint scaling analysis to compare the genetic components of resistance in the red flour beetle Tribolium castaneum exposed to single and multiple strains of the microsporidian Nosema whitei. Our results indicate that additive, dominance and epistatic components were more important in single infections whereas maternal components play a decisive role in multiple infections. In detail, parameter estimates of additive, dominance and epistatic components correlated positively between single and multiple infections, whereas maternal components correlated negatively. These findings may suggest that specificity of host–parasite interactions are mediated by genetic and especially epistatic components whereas maternal effects constitute a more general form of resistance.     

Within-host parasite dynamics,emerging trade-off,and evolution of virulence with immune system

Abstract.— Virulence is an evolutionary paradox because parasites never benefit from their host's death. The adaptive explanation of virulence is classically based upon the existence of physiological constraints that create a trade-off between parasites' epidemiological traits (virulence, transmissibility, and clearance). Here we develop an epidemiological model where infections are dynamic processes and we demonstrate how these dynamics generate a trade-off between emerging epidemiological parameters. We then study how host's immune strength modifies this trade-off and hence influences virulence evolution. We found that in acute infections, where parasites are engaged in a race with immune cells, immunity restrains more the duration of the infection than its intensity. As a consequence parasites evolve to provoke more virulent but shorter infections in strongly immunized hosts.     

Coevolution of virulence and immunosuppression in multiple infections

Many components of host–parasite interactions have been shown to affect the way virulence (i.e. parasite‐induced harm to the host) evolves. However, coevolution of multiple parasite traits is often neglected. We explore how an immunosuppressive adaptation of parasites affects and coevolves with virulence in multiple infections. Applying the adaptive dynamics framework to epidemiological models with coinfection, we show that immunosuppression is a double‐edged sword for the evolution of virulence. On one hand, it amplifies the adaptive benefit of virulence by increasing the abundance of coinfections through epidemiological feedbacks. On the other hand, immunosuppression hinders host recovery, prolonging the duration of infection and elevating the cost of killing the host (as more opportunities for transmission will be forgone if the host dies). The balance between the cost and benefit of immunosuppression varies across different background mortality rates of hosts. In addition, we find that immunosuppression evolution is influenced considerably by the precise trade‐off shape determining the effect of immunosuppression on host recovery and susceptibility to further infection. These results demonstrate that the evolution of virulence is shaped by immunosuppression while highlighting that the evolution of immune evasion mechanisms deserves further research attention.     

Host mortality, predation and the evolution of parasite virulence

One of the most accepted views in the theoretical literature on virulence evolution is that a parasite's virulence will evolve to higher levels when its host's background mortality rate increases. Surprisingly, however, although many sources of background mortality involve predation, there has not yet been any theoretical research that explicitly considers how the dynamics of this important ecological interaction affects virulence evolution. Here, we consider how predation affects virulence evolution by explicitly introducing a predator into a classical susceptible–infected–susceptible epidemiological model. We find that, contrary to previous predictions, different sources of host mortality affect virulence evolution in different ways. Moreover, the way in which virulence evolution is affected depends on how tightly coupled the predator's dynamics are to the host population, and this can result in somewhat counterintuitive results. For example, indirect ecological effects can cause elevated host mortality to result in the evolution of lower parasite virulence, even if this elevated mortality arises from factors unrelated to predation.     

Simple and noninvasive method for assessment of digestive efficiency: Validation of fecal steatocrit in greenfinch coccidiosis model

相似文献   

Analysis of antibiotic resistance and virulence patterns in Klebsiella pneumoniae isolated from human urinary tract infections in India

In this study, 504 urine samples collected from patients suffering from urinary tract infection (UTIs) were screened for the presence of Klebsiella pneumoniae. The overall occurrence of Klebsiella spp. and K. pneumoniae was found to be 23·2% (117/504) and 16·8% (85/504) respectively. Antibiotic susceptibility testing of 85 K. pneumoniae isolates was carried out by disc diffusion which revealed alarming levels of antibiotic resistance (ABR). Antimicrobial resistance was prominently observed against cefpodoxime (76·47%) followed by ampicillin (70·59%), ceftriaxone (52·94%), cefoxitin (50·59%), amoxyclav (48·24%), ofloxacin (45·88%), cefotaxime (44·71%), cefepime (43·53%) and doxycycline hydrochloride (40%). A small percentage of strains also exhibited resistance to other antimicrobials in the range of 7–35%. Around 77·6% of the isolates were found to be resistant to three or more antibiotic classes and 66·7% of the isolates had multiple antibiotic resistance index values >0·2. Screening of virulence genes in 85 K. pneumoniae isolates revealed that uge gene was the most predominant (11/85, 12·9%), followed by rmpA (9/85, 10·5%), kfu (4/85, 4·7%) and aerobactin genes (2/85, 2·35%). Further, the overall percentage of biofilm producers were found to be 17·65% (15/85). This study warrants hospitals and health care centres to reduce misuse of antibiotics and manage UTI with appropriate treatment after performing antibiotic susceptibility testing.     

Evolution of host resistance and trade‐offs between virulence and transmission potential in an obligately killing parasite

Standard epidemiological theory predicts that parasites, which continuously release propagules during infection, face a trade‐off between virulence and transmission. However, little is known how host resistance and parasite virulence change during coevolution with obligate killers. To address this question we have set up a coevolution experiment evolving Nosema whitei on eight distinct lines of Tribolium castaneum. After 11 generations we conducted a time‐shift experiment infecting both the coevolved and the replicate control host lines with the original parasite source, and coevolved parasites from generation 8 and 11. We found higher survival in the coevolved host lines than in the matching control lines. In the parasite populations, virulence measured as host mortality decreased during coevolution, while sporeload stayed constant. Both patterns are compatible with adaptive evolution by selection for resistance in the host and by trade‐offs between virulence and transmission potential in the parasite.     

Intraspecific competition and the evolution of virulence in a parasitic trematode

Intrahost competition between parasite genotypes has been predicted to be an important force shaping parasite ecology and evolution and has been extensively cited as a mechanism for the evolution of increased parasite virulence. However, empirical evidence demonstrating the existence and nature of intraspecific competition is lacking for many parasites. Here, we compared within-host competitiveness between genetic strains of Schistosoma mansoni with high (HIGH-V) or low (LOW-V) virulence to their intermediate snail host, Biomphalaria glabrata. Groups of snails were exposed to either one or the other of two parasite strains, or a mixed infection of both strains, and the resulting progeny were identified using a molecular marker. In two separate experiments investigating simultaneous and sequential infections, we demonstrated that the lifetime reproductive success of parasite strain HIGH-V was reduced in the presence of a faster replicating parasite genotype, LOW-V, regardless of whether it was in a majority or minority in the initial inoculum of the simultaneous exposure or of its relative position in the sequential exposure experiment. Thus, we demonstrate competition between parasite genotypes and asymmetry in competitive success between parasite strains. Moreover, since the less virulent strain investigated here had a competitive advantage, we suggest that a high frequency of multiple infections could favor the evolution of less, rather than more, virulent parasites in this system.     

Regulation of virulence and antibiotic resistance by two-component regulatory systems in Pseudomonas aeruginosa

The Gram-negative opportunistic pathogen Pseudomonas aeruginosa ubiquitously inhabits soil and water habitats and also causes serious, often antibiotic resistant, infections in immunocompromised patients (e.g. cystic fibrosis). This versatility is mediated in part by a large repertoire of two-component regulatory systems that appear instrumental in the regulation of both virulence processes and resistance to antimicrobials. Major two-component regulatory system proteins demonstrated to regulate these diverse processes include PhoP–PhoQ, GacA–GacS, RetS, LadS, and AlgR, among others. Here, we summarize the current body of knowledge of these and other two-component systems that provides insight into the complex regulation of virulence and resistance in P. aeruginosa .     

Biofilm of Candida albicans: formation,regulation and resistance

Candida albicans is the most common human fungal pathogen, causing infections that range from mucous membranes to systemic infections. The present article provides an overview of C. albicans, with the production of biofilms produced by this fungus, as well as reporting the classes of antifungals used to fight such infections, together with the resistance mechanisms to these drugs. Candida albicans is highly adaptable, enabling the transition from commensal to pathogen due to a repertoire of virulence factors. Specifically, the ability to change morphology and form biofilms is central to the pathogenesis of C. albicans. Indeed, most infections by this pathogen are associated with the formation of biofilms on surfaces of hosts or medical devices, causing high morbidity and mortality. Significantly, biofilms formed by C. albicans are inherently tolerant to antimicrobial therapy, so the susceptibility of C. albicans biofilms to current therapeutic agents remains low. Therefore, it is difficult to predict which molecules will emerge as new clinical antifungals. The biofilm formation of C. albicans has been causing impacts on susceptibility to antifungals, leading to resistance, which demonstrates the importance of research aimed at the prevention and control of these clinical microbial communities.     

The role of capsular antigens in serum resistance and in vivo virulence of Escherichia coli

Abstract To identify critical microbial determinant(s) in serum resistance and in vivo virulence, 5 strains of Escherichia coli with different combinations of K and O types were examined along with their unencapsulated mutants. All 3 E. coli strains possessing the K1 capsule were considerably more resistant to normal human serum in vitro and more virulent in newborn rats than their isogenic mutants lacking the K1 capsule. In contrast, two K5 encapsulated strains and their unencapsulated mutants were essentially the same for their degree of serum resistance and in vivo virulence. These findings suggest that for the demonstration of serum resistance and in vivo virulence, a capsule is required for E. coli strains encapsulated with K1, whereas certain E. coli strains encapsulated with K5 may not need a capsule.     

Shigella in Brazilian children with acute diarrhoea: prevalence,antimicrobial resistance and virulence genes

Diarrhoeal disease is still considered a major cause of morbidity and mortality among children. Among diarrhoeagenic agents, Shigella should be highlighted due to its prevalence and the severity of the associated disease. Here, we assessed Shigella prevalence, drug susceptibility and virulence factors. Faeces from 157 children with diarrhoea who sought treatment at the Children''s Hospital João Paulo II, a reference children´s hospital in Belo Horizonte, state of Minas Gerais, Brazil, were cultured and drug susceptibility of the Shigella isolates was determined by the disk diffusion technique. Shigella virulence markers were identified by polymerase chain reaction. The bacterium was recovered from 10.8% of the children (88.2% Shigella sonnei). The ipaH, iuc, sen and ial genes were detected in strains isolated from all shigellosis patients; set1A was only detected in Shigella flexneri. Additionally, patients were infected by Shigella strains of different ial, sat, sen and set1A genotypes. Compared to previous studies, we observed a marked shift in the distribution of species from S. flexneri to S. sonnei and high rates of trimethoprim/sulfamethoxazole resistance.     

Antimicrobial resistance and virulence genes profiles of Arcobacter butzleri strains isolated from back yard chickens and retail poultry meat in Chile

This research aims to investigate the presence and pathogenic potential of Arcobacter in poultry meat samples purchased in the retail market of Valdivia (South of Chile) as well as in faecal samples from backyard chickens from rural areas around this city. The isolates obtained were identified by molecular methods. Furthermore, putative virulence genes were assessed by PCR and the antimicrobial resistance was tested by phenotypic methods. Arcobacter was present in 41·6% of the samples, with the highest value in retail poultry meat (55·7%) followed by backyard production (28·0%). Arcobacter butzleri was the most prevalent species (75·6%) followed by Arcobacter skirrowii (14·8%) and Arcobacter cryaerophilus (9·6%). An 8·5% of A. butzleri strains from meat were resistant to both ciprofloxacin and tetracycline and 6·1% were resistant to erythromycin, while none was resistant to gentamycin, unlike strains from domestic chickens, which showed no resistance. Furthermore, A. butzleri strains from chicken meat presented a higher prevalence of virulence genes than strains from domestic chickens. In fact, in this last group, some genes (hecA, hecB and irgA) were completely absent. Therefore, this study provides insight on the epidemiology of Arcobacter in Chilean poultry and suggests that under traditional breeding conditions strains are, apparently, less pathogenic and drug resistant.     

Host life span and the evolution of resistance characteristics

There is a wide variety of resistance mechanisms that hosts may evolve in response to their parasites. These can be functionally classified as avoidance (lower probability of becoming infected), recovery (faster rate of clearance), tolerance (reduced death rate when infected), or acquired immunity. It is commonly thought that longer lived organisms should invest more in costly resistance. We show that due to epidemiological feedbacks the situation is often more complex. Using evolutionary theory we examine how the optimal investment in costly resistance varies with life span in a broad range of scenarios. In the absence of acquired immunity, longer lived populations do generally invest more in resistance. If hosts have acquired immunity, the optimal resistance may either increase or decrease with increasing life span. In addition, there may be evolutionary bistability with high and low investments in avoidance or tolerance. The optimal investment in the duration of acquired immunity always increases with life span, and due to bistability, shorter lived hosts may commonly not evolve any immunity. In contrast, the optimal investment in the probability of acquiring immunity initially increases and then decreases with life span. Our results have important implications for the evolution of invertebrate and vertebrate immunity, and for the evolution of acquired immunity itself.     

Streptogramin resistance patterns and virulence determinants in vancomycin-susceptible enterococci isolated from multi-component deli salads

Aims: This study examined vancomycin-susceptible Enterococcus (VSE) from deli salads for streptogramin resistance and presence of cpd, agg and gelE genes. Methods and Results: Fifteen VSE from retail salads were isolated for identification and antimicrobial susceptibility testing by MicroScan, Etest and agar diffusion. Clinical vancomycin-resistant Enterococcus (n = 32) and animal VSE (n = 17) were included for comparative purposes. Multiplex PCR was used to detect the following genes: agg, gelE, cpd, vatD, vatE and sodA. Results showed fewer streptogramin-susceptible Enterococcus faecium isolated from salad (1/6, 17%) and animals (6/10, 60%) than from clinical (26/29, 90%) sources. A low level of erythromycin susceptibility was detected among salad (2/6, 33%) and animal (3/10, 30%) Ent. faecium isolates. Food and animal VSE demonstrated similarities in antimicrobial resistance profiles. All Enterococcus faecalis carried one or more of the selected genes cpd (40%), gelE (33%) and agg (27%). The vatD or vatE genes were not detected in any of the isolates. Conclusions: Experiments demonstrated that streptogramin resistance and virulence genes agg, cpd and gelE are present in enterococci isolated from deli salads. Significance and Impact of the Study: This study provides useful information regarding streptogramin resistance and virulence determinants in enterococci from foods associated with multi-component ingredients.