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PubMed2005

Conflict between parasites with different transmission strategies infecting an amphipod host.

Competition between parasites within a host can influence the evolution of parasite virulence and host resistance, but few studies examine the effects of unrelated parasites with conflicting transmission strategies infecting the same host. Vertically transmitted (VT) parasites, transmitted from mother to offspring, are in conflict with virulent, horizontally transmitted (HT) parasites, because healthy hosts are necessary to maximize VT parasite fitness. Resolution of the conflict between these parasites should lead to the evolution of one of two strategies: avoidance, or sabotage of HT parasite virulence by the VT parasite. We investigated two co-infecting parasites in the amphipod host, Gammarus roeseli: VT microsporidia have little effect on host fitness, but acanthocephala modify host behaviour, increasing the probability that the amphipod is predated by the acanthocephalan's definitive host. We found evidence for sabotage: the behavioural manipulation induced by the Acanthocephala Polymorphus minutus was weaker in hosts also infected by the microsporidia Dictyocoela sp. (roeselum) compared to hosts infected by P. minutus alone. Such conflicts may explain a significant portion of the variation generally observed in behavioural measures, and since VT parasites are ubiquitous in invertebrates, often passing undetected, conflict via transmission may be of great importance in the study of host-parasite relationships.

Acanthocephala↗
PubMed1991

Intervening sequences (IVSs) in the 23S ribosomal RNA genes of pathogenic Yersinia enterocolitica strains. The IVSs in Y. enterocolitica and Salmonella typhimurium have a common origin.

The 23S ribosomal RNA (rRNA) was shown to be in two fragments in pathogenic Yersinia enterocolitica. The cleavage site in the structural gene of the 23S rRNA was occupied by an intervening sequence (IVS) of about 100 nucleotides, analogous to IVSs found in salmonellae (Burgin et al., 1990). Nucleotide sequences of IVSs of several Y. enterocolitica strains revealed that the IVSs of the highly virulent Y. enterocolitica serotypes strains, and the IVS of Salmonella typhimurium were about 90% similar. On the other hand, the IVSs of the highly and the poorly virulent Y. enterocolitica serotypes were only about 60% similar. These results give the impression that at some point during the IVS evolution, the highly virulent Y. enterocolitica and S. typhimurium both received their IVSs at about the same time from the same source, and that the poorly virulent serotypes received their IVSs earlier. We also found that strain LB5010, derived by extended mutagenization of S. typhimurium LT2, had lost the IVSs originally present in LT2, and that this loss had created a new 'hairpin loop' which substituted for the original 'hairpin loop'.

Base Sequence↗
PubMed2003

Shared control of epidemiological traits in a coevolutionary model of host-parasite interactions.

Most models concerning the evolution of a parasite's virulence and its host's resistance assume that each component of the relationship (transmission, virulence, recovery, etc.) is controlled by either the host or the parasite but not by both. We present a model that describes the coevolution of host and parasite, assuming that the rate of transmission or the virulence depends on both genotypes. The evolution of these traits is constrained by trade-offs that account for costs of defense and attack strategies, in line with previous studies on the separate evolution of the host and the parasite. Considering shared control by the host and the parasite in determining the traits of the relationship leads to several novel predictions. First, the host should evolve maximal investment in defense against parasites with an intermediate replication rate. Second, the evolution of the parasite strongly depends on the way the host's defense is described. Third, the coevolutionary process may lead to decreasing the parasite's virulence as a response to a rise in the host's background mortality, contrary to classical predictions.

Adaptation, Physiological↗
PubMed2001

Evolutionary genomics of pathogenic bacteria.

Complete genome sequences are now available for multiple strains of several bacterial pathogens and comparative analysis of these sequences is providing important insights into the evolution of bacterial virulence. Recently, DNA microarray analysis of many strains of several pathogenic species has contributed to our understanding of bacterial diversity, evolution and pathogenesis. Comparative genomics has shown that pathogens such as Escherichia coli, Helicobacter pylori and Staphylococcus aureus contain extensive variation in gene content whereas Mycobacterium tuberculosis nucleotide divergence is very limited. Overall, these approaches are proving to be a powerful means of exploring bacterial diversity, and are providing an important framework for the analysis of the evolution of pathogenesis and the development of novel antimicrobial agents.

Bacteria↗
PubMed2004

Bacteriocins, spite and virulence.

There has been much interest in using social evolution theory to predict the damage to a host from parasite infection, termed parasite virulence. Most of this work has focused on how high kinship between the parasites infecting a host can select for more prudent exploitation of the host, leading to a negative relationship between virulence and parasite kinship. However, it has also been shown that if parasites can cooperate to overcome the host, then high parasite kinship within hosts can select for greater cooperation and higher growth rates, hence leading to a positive relationship between virulence and parasite kinship. We examine the impact of a spiteful behaviour, chemical (bacteriocin) warfare between microbes, on the evolution of virulence, and find a new relationship: virulence is maximized when the frequency of kin among parasites' social partners is low or high, and is minimized at intermediate values. This emphasizes how biological details can fundamentally alter the qualitative nature of theoretical predictions made by models of parasite virulence.

Bacteria↗
PubMed2000

Bacterial virulence gene regulation: an evolutionary perspective.

Coevolution between bacteria and their plant or animal hosts determines characteristics of the interaction, the bacterial virulence genes involved, and the regulatory systems controlling expression of virulence genes. The long-standing association between Salmonellae and their animal hosts has resulted in the acquisition by Salmonella subspecies of a variety of virulence genes and the evolution of complex regulatory networks. The particular repertoire of virulence genes acquired by different Salmonella enterica subspecies and the regulatory systems that control them dictate subspecies-specific infection characteristics. Although the association between Vibrio cholerae and humans appears to be more recent, to reflect a simpler pathogenic strategy, and to involve fewer virulence genes than that of Salmonellae, complex virulence-regulatory networks have nonetheless evolved. In contrast, there is no evidence for acquisition of virulence genes by horizontal gene transfer in bordetellae, and their virulence regulon is less complex in overall structure than those of salmonellae and Vibrio cholerae. In Bordetellae, subspecies-specific differences in pathogenic strategy appear to result from differential gene expression within and across Bordetella subspecies.

Biological Evolution↗
PubMed2006

Comparison of the transmissibility of Trypanosoma congolense strains, isolated in a trypanosomiasis endemic area of eastern Zambia, by Glossina morsitans morsitans.

Transmission experiments were conducted to compare the transmissibility of genetically different Trypanosoma congolense (Savannah subgroup) strains isolated from cattle in a trypanosomiasis endemic area of eastern Zambia. A total of 17 strains were compared. Three strains were extremely virulent with a short pre-patent period, high parasitaemia and a short median survival time (between 5 and 9 days) in mice. The remainder of the strains belonged to the moderate (6 strains) or low (8 strains) virulence categories with median survival times between 10 and 30 days and >30 days, respectively. Batches of 40 teneral Glossina morsitans morsitans (Diptera: Glossinidae) were offered a single bloodmeal on mice infected with one of those strains. Flies were dissected to determine their infection status 21 days later. The proportion of flies with procyclic and metacyclic infections differed significantly between trypanosome strains and were significantly higher in flies infected with extremely virulent strains (P=0.033 and P=0.016 for the differences in the procyclic infection rate of strains with moderate and low virulence, respectively and P=0.005 and P=0.019 for the differences in the metacyclic infection rate of strains with moderate and low virulence, respectively). On the other hand, moderately virulent strains had, in general, higher procyclic and metacyclic infection rates compared to low virulent strains. But the differences were not significant (P>0.05). The outcome of those experiments shows clear differences in transmissibility of trypanosome strains associated with their virulence. This observation confirms the theory for the evolution and maintenance of virulence in a parasite population and may explain the persistence of virulent trypanosome strains in a susceptible host population.

Animals↗
PubMed2004

Comparative analysis of Marek's disease virus (MDV) glycoprotein-, lytic antigen pp38- and transformation antigen Meq-encoding genes: association of meq mutations with MDVs of high virulence.

Marek's disease (MD) is a highly contagious lymphoproliferative and demyelinating disorder of chickens. MD is caused by Marek's disease virus (MDV), a cell-associated, acute-transforming alphaherpesvirus. For three decades, losses to the poultry industry due to MD have been greatly limited through the use of live vaccines. MDV vaccine strains are comprised of antigenically related, apathogenic MDVs originally isolated from chickens (MDV-2), turkeys (herpesvirus of turkeys, HVT) or attenuated-oncogenic strains of MDV-1 (CVI-988). Since the inception of high-density poultry production and MD vaccination, there have been two discernible increases in the virulence of MDV field strains. Our objectives were to determine if common mutations in the major glycoprotein genes, a major lytic antigen phosphoprotein 38 (pp38) or a major latency/transformation antigen Meq (Marek's EcoRI-Q-encoded protein) were associated with enhanced MDV virulence. To address this, we cloned and sequenced the major surface glycoprotein genes (gB, gC, gD, gE, gH, gI, and gL) of five MDV strains that were representative of the virulent (v), very virulent (vv) and very virulent plus (vv+) pathotypes of MDV. We found no consistent mutations in these genes that correlated strictly with virulence level. The glycoprotein genes most similar among MDV-1, MDV-2 and HVT (gB and gC, approximately 81 and 75%, respectively) were among the most conserved across pathotype. We found mutations mapping to the putative signal cleavage site in the gL genes in four out of eleven vv+MDVs, but this mutation was also identified in one vvMDV (643P) indicating that it did not correlate with enhanced virulence. In further analysis of an additional 12 MDV strains, we found no gross polymorphism in any of the glycoprotein genes. Likewise, by PCR and RFLP analysis, we found no polymorphism at the locus encoding the pp38 gene, an early lytic-phase gene associated with MDV replication. In contrast, we found distinct mutations in the latency and transformation-associated Marek's EcoRI-Q-encoded protein, Meq. In examination of the DNA and deduced amino acid sequence of meq genes from 26 MDV strains (9 m/vMDV, 5 vvMDV and 12 vv+MDVs), we found distinct polymorphism and point mutations that appeared to correlate with virulence. Although a complex trait like MDV virulence is likely to be multigenic, these data describe the first sets of mutations that appear to correlate with MDV virulence. Our conclusion is that since Meq is expressed primarily in the latent/transforming phase of MDV infection, and is not encoded by MDV-2 or HVT vaccine viruses, the evolution of MDV virulence may be due to selection on MDV-host cell interactions during latency and may not be mediated by the immune selection against virus lytic antigens such as the surface glycoproteins.

Amino Acid Sequence↗
PubMed2019

Large-scale genome analysis of bovine commensal Escherichia coli reveals that bovine-adapted E. coli lineages are serving as evolutionary sources of the emergence of human intestinal pathogenic strains.

How pathogens evolve their virulence to humans in nature is a scientific issue of great medical and biological importance. Shiga toxin (Stx)-producing Escherichia coli (STEC) and enteropathogenic E. coli (EPEC) are the major foodborne pathogens that can cause hemolytic uremic syndrome and infantile diarrhea, respectively. The locus of enterocyte effacement (LEE)-encoded type 3 secretion system (T3SS) is the major virulence determinant of EPEC and is also possessed by major STEC lineages. Cattle are thought to be the primary reservoir of STEC and EPEC. However, genome sequences of bovine commensal E. coli are limited, and the emerging process of STEC and EPEC is largely unknown. Here, we performed a large-scale genomic comparison of bovine commensal E. coli with human commensal and clinical strains, including EPEC and STEC, at a global level. The analyses identified two distinct lineages, in which bovine and human commensal strains are enriched, respectively, and revealed that STEC and EPEC strains have emerged in multiple sublineages of the bovine-associated lineage. In addition to the bovine-associated lineage-specific genes, including fimbriae, capsule, and nutrition utilization genes, specific virulence gene communities have been accumulated in stx- and LEE-positive strains, respectively, with notable overlaps of community members. Functional associations of these genes probably confer benefits to these E. coli strains in inhabiting and/or adapting to the bovine intestinal environment and drive their evolution to highly virulent human pathogens under the bovine-adapted genetic background. Our data highlight the importance of large-scale genome sequencing of animal strains in the studies of zoonotic pathogens.

Animals↗
PubMed2006

Natural selection for rash-forming genotypes of the varicella-zoster vaccine virus detected within immunized human hosts.

The Oka vaccine strain is a live attenuated virus that is routinely administered to children in the United States and Europe to prevent chickenpox. It is effective and safe but occasionally produces a rash. The vaccine virus has accumulated mutations during its attenuation, but the rashes are not explained by their reversion, unlike complications reported for other viral vaccines. Indeed, most of the novel mutations distinguishing the Oka vaccine from the more virulent parental virus have not actually become fixed. Because the parental alleles are still present, the vaccine is polymorphic at >30 loci and therefore contains a mixture of related viruses. The inoculation of >40 million patients has consequently created a highly replicated evolutionary experiment that we have used to assess the competitive ability of these different viral genotypes in a human host. Using virus recovered from rash vesicles, we show that two vaccine mutations, causing amino acid substitutions in the major transactivating protein IE62, are outcompeted by the ancestral alleles. Standard interpretations of varicella disease severity concentrate on the undeniably important effects of host genotype and immune status, yet our results allow us to demonstrate that the viral genotype is associated with virulence and to identify the key sites. We propose that these loci have pleiotropic effects on the immunogenic properties of the virus, rash formation, and its epidemiological spread, which mould the evolution of its virulence. These findings are of practical importance for reducing the incidence of vaccine-associated rash and promoting public acceptance of the vaccine.

Chickenpox Vaccine↗
PubMed1990

Virulence of lizard malaria: the evolutionary ecology of an ancient parasite-host association.

The negative consequences of parasitic infection (virulence) were examined for two lizard malaria parasite-host associations: Plasmodium agamae and P. giganteum, parasites of the rainbow lizard, Agama agama, in Sierra Leone, West Africa; and P. mexicanum in the western fence lizard, Sceloporus occidentalis, in northern California. These malaria species vary greatly in their reproductive characteristics: P. agamae produces only 8 merozoites per schizont, P. giganteum yields over 100, and P. mexicanum an intermediate number. All three parasites appear to have had an ancient association with their host. In fence lizards, infection with malaria is associated with increased numbers of immature erythrocytes, decreased haemoglobin levels, decreased maximal oxygen consumption, and decreased running stamina. Not affected were numbers of erythrocytes, resting metabolic rate, and sprint running speed which is supported by anaerobic means in lizards. Infected male fence lizards had smaller testes, stored less fat in preparation for winter dormancy, were more often socially submissive and, unexpectedly, were more extravagantly coloured on the ventral surface (a sexually dimorphic trait) than non-infected males. Females also stored less fat and produced smaller clutches of eggs, a directly observed reduction in fitness. Infected fence lizards do not develop behavioural fevers. P. mexicanum appears to have broad thermal buffering abilities and thermal tolerance; the parasite's population growth was unaffected by experimental alterations in the lizard's body temperature. The data are less complete for A. agama, but infected lizards suffered similar haematological and physiological effects. Infected animals may be socially submissive because they appear to gather less insect prey, possibly a result of being forced into inferior territories. Infection does not reduce clutch size in rainbow lizards, but may lengthen the time between clutches. These results are compared with predictions emerging from several models of the evolution of parasite virulence. The lack of behavioural fevers in fence lizards may represent a physiological constraint by the lizards in evolving a thermal tolerance large enough to allow elimination of the parasite via fever. Such constraints may be important in determining the outcome of parasite-host coevolution. Some theory predicts low virulence in old parasite-host systems and higher virulence in parasites with greater reproductive output. However, in conflict with this argument, all three malarial species exhibited similar high costs to their hosts.

Animals↗
PubMed2005

Evolutionary history of the genus Listeria and its virulence genes.

The genus Listeria contains the two pathogenic species Listeria monocytogenes and Listeria ivanovii and the four apparently apathogenic species Listeria innocua, Listeria seeligeri, Listeria welshimeri, and Listeria grayi. Pathogenicity of the former two species is enabled by an approximately 9 kb virulence gene cluster which is also present in a modified form in L. seeligeri. For all Listeria species, the sequence of the virulence gene cluster locus and its flanking regions was either determined in this study or assembled from public databases. Furthermore, some virulence-associated internalin loci were compared among the six species. Phylogenetic analyses were performed on a data set containing the sequences of prs, ldh, vclA, and vclB (all directly flanking the virulence gene cluster), as well as the iap gene and the 16S and 23S-rRNA coding genes which are located at different sites in the listerial chromosomes. L. grayi represents the deepest branch within the genus. The remaining five species form two groupings which have a high bootstrap support and which are consistently found by using different treeing methods. One lineage represents L. monocytogenes and L. innocua, while the other contains L. welshimeri, L. ivanovii and L. seeligeri, with L. welshimeri forming the deepest branch. Based on this perception, we tried to reconstruct the evolution of the virulence gene cluster. Since no traces of lateral gene transfer events could be detected the most parsimonious scenario is that the virulence gene cluster was present in the common ancestor of L. monocytogenes, L. innocua, L. ivanovii, L. seeligeri and L. welshimeri and that the pathogenic capability has been lost in two separate events represented by L. innocua and L. welshimeri. This hypothesis is also supported by the location of the putative deletion breakpoints of the virulence gene cluster within L. innocua and L. welshimeri.

Bacterial Proteins↗
PubMed1998

Phylogenetic relationships among highly virulent Newcastle disease virus isolates obtained from exotic birds and poultry from 1989 to 1996.

Newcastle disease virus [NDV (avian paramyxovirus type 1 [APMV1])] isolates were recovered from imported exotic birds confiscated following importation into the United States, from waterbirds in the United States, and from poultry. The exotic birds probably originated from Central and South America, Asia, and Africa. The NDV isolates were initially characterized as highly virulent because of a short mean death time in embryonated chicken eggs. The isolates were typed as neurotropic or viscerotropic velogenic by intracloacal inoculation of adult chickens. Intracerebral pathogenicity index values for the virulent NDV isolates ranged from 1.54 to 1.90, compared to a possible maximum value of 2.0. These isolates had a dibasic amino acid motif in the fusion protein cleavage site sequence required for host systemic replication. Sequence differences were detected surrounding the fusion protein cleavage site and the matrix protein nuclear localization signal, indicating evolution of highly virulent NDV. Phylogenetically, these isolates were categorized with other highly virulent NDV strains that caused outbreaks in southern California poultry during 1972 and in cormorants in the north central United States and southern Canada during 1990 and 1992. These isolates are related to NDV that may have the APMV1 strain chicken/Australia/AV/32 or a related virus as a possible progenitor. Recent virulent NDV isolates and those recovered during disease outbreaks since the 1970s are phylogenetically distinct from current vaccine viruses and standard challenge strains.

Animals↗
PubMed2003

The in vitro evolution of BCG vaccines.

The bacillus Calmette-Géurin (BCG) family of vaccines currently implemented to prevent tuberculosis (TB) consist of clonal bacterial strains independently shaped by nearly a half-century of evolution. Derived from virulent Mycobacterium bovis, daughter strains of BCG were additionally passaged under the same laboratory conditions that resulted in its original attenuation. Genomic loss of the RD1 region has been demonstrated to coincide with attenuation from virulence, while deletions occurring after the loss of RD1 are speculated to be responsible for BCG's over-attenuation. To provide a more complete description of their total genomic variation, the genomic content of BCG strains are investigated by Affymetrix GeneChip. Because clinical isolates of M. tuberculosis have previously been characterized via GeneChip interrogation, analysis permits the comparison of in vivo versus in vitro evolution of M. tuberculosis complex subspecies. The contrast between the two modes of evolution are discussed in its relevance towards TB pathogenicity.

BCG Vaccine↗
PubMedDate not supplied

Epidemiology of group A streptococcal infections--their changing frequency and severity.

The frequency and severity of streptococcal infections and their sequelae have declined dramatically in the past century, yet the prevalence of streptococcal infections is still high. The reasons for this decline must be intimately related to host resistance, virulence of the agent, and environmental factors, especially crowding. Close examination of these fundamental influences does not reveal any evidence that humans have become less resistant to streptococcal infections, but they react less violently. There is some evidence that the agent may have lost a degree of its virulence. The decline in morbidity and mortality due to streptococcal infections began long before antibiotics, especially penicillin, were available. However, penicillin has proved to be an important factor in prevention of streptococcal infections, especially in rheumatic fever prophylaxis. There are certain indications that repeated streptococcal infections due to similar M types, occurring in young children over the past several decades, have resulted in some degree of immunity as well as the possible evolution of less virulent, but not less infectious, strains of group A streptococci. Also, a decrease in crowding would be expected to result in fewer streptococcal infections. Although there are more people in the world than at any other time in the history of man, urban population density in the western world, at least, is less than in the late 1800s and early 1900s.

Adolescent↗
PubMed1992

Co-ordinate expression of virulence genes by ToxR in Vibrio cholerae.

Evolution of complex regulatory pathways that control virulence factor expression in pathogenic bacteria indicates the importance to these organisms of being able to distinguish time and place. In the human intestinal pathogen Vibrio cholerae, control over many virulence genes identified to date is the responsibility of the ToxR protein. ToxR, in conjunction with a second regulatory protein called ToxS, directly activates the genes encoding the cholera toxin; other ToxR regulated genes are not activated directly by ToxR. For some of these genes, ToxR manifests its control through another activator called ToxT. Expression of toxT, which encodes a member of the AraC family of bacterial transcriptional activators, is ToxR dependent and is modulated by in vitro growth conditions that modulate expression of the ToxR virulence regulon. Thus, as in other regulatory circuits, co-ordinate expression of several genes in V. cholerae results from the activity of a cascading system of regulatory factors.

Bacterial Proteins↗
PubMed2004

Lessons learned from the genome analysis of ralstonia solanacearum.

Ralstonia solanacearum is a devastating plant pathogen with a global distribution and an unusually wide host range. This bacterium can also be free-living as a saprophyte in water or in the soil in the absence of host plants. The availability of the complete genome sequence from strain GMI1000 provided the basis for an integrative analysis of the molecular traits determining the adaptation of the bacterium to various environmental niches and pathogenicity toward plants. This review summarizes current knowledge and speculates on some key bacterial functions, including metabolic versatility, resistance to metals, complex and extensive systems for motility and attachment to external surfaces, and multiple protein secretion systems. Genome sequence analysis provides clues about the evolution of essential virulence genes such as those encoding the Type III secretion system and related pathogenicity effectors. It also provided insights into possible mechanisms contributing to the rapid adaptation of the bacterium to its environment in general and to its interaction with plants in particular.

Amino Acid Sequence↗
PubMed1980

Persistence of the virulence of Aeromonas salmonicida strains kept in river sediments.

The persistence of pathogenicity in two strains of Aeromonas salmonicida maintained in river sediments was studied at different times. Cultures were kept about nine months, and the virulence was compared to its initial value exhibited by the same strain, subcultivated in rainbow trout fingerlings. Trials involved intramuscular injection of comparable doses of bacteria to batches of 30 fish held at 15 degrees C, and recording of subsequent mortalities. No difference was found during the first six months, after which a decrease of pathogenicity resulted in its disappearance before the ninth month. Progressive decrease in incubation temperatures was also exerted to simulate an artificial wintering, but did not alter the evolution of the virulence. The possible role of mud as a source of contamination for fish is discussed.

Aeromonas↗