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Rapid evolution and ecological host-parasite dynamics.

Traditionally, the termination of parasite epidemics has been attributed to ecological causes: namely, the depletion of susceptible hosts as a result of mortality or acquired immunity. Here, we suggest that epidemics can also end because of rapid host evolution. Focusing on a particular host-parasite system, Daphnia dentifera and its parasite Metschnikowia bicuspidata, we show that Daphnia from lakes with recent epidemics were more resistant to infection and had less variance in susceptibility than Daphnia from lakes without recent epidemics. However, our studies revealed little evidence for genetic variation in infectivity or virulence in Metschnikowia. Incorporating the observed genetic variation in host susceptibility into an epidemiological model parameterized for this system reveals that rapid evolution can explain the termination of epidemics on time scales matching what occurs in lake populations. Thus, not only does our study provide rare evidence for parasite-mediated selection in natural populations, it also suggests that rapid evolution has important effects on short-term host-parasite dynamics.

Animals↗

Demonstration of OspC type diversity in invasive human lyme disease isolates and identification of previously uncharacterized epitopes that define the specificity of the OspC murine antibody response.

Outer surface protein C (OspC) of the Lyme disease spirochetes is an important virulence factor that has potential utility for vaccine development. Of the 21 OspC types that have been identified, it has been postulated that types A, B, I, and K are specifically associated with invasive infections. Through an analysis of isolates collected from patients in Maryland we found that OspC types C, D, and N are also associated with invasive infections. This observation suggests that there is greater diversity in the group of OspC types associated with invasive infection than has been previously suggested. Detailed knowledge of the antigenic structure of OspC is essential for vaccine development. To determine if the antibody response to OspC is type specific, recombinant proteins of several different OspC types were immunoblotted and screened with sera from mice infected with isolates having known OspC types. These analyses revealed a high degree of specificity in the antibody response and suggested that the immunodominant epitopes of OspC reside in the variable domains of the protein. To localize these epitopes, OspC fragments were generated and screened with serum collected from infected mice. These analyses led to identification of previously uncharacterized epitopes that define the type specificity of the OspC antibody response. These analyses provide important insight into the antigenic structure of OspC and also provide a basis for understanding the variable nature of the antibody response to this important virulence factor of the Lyme disease spirochetes.

Animals↗

Surface carbohydrate composition of a tapeworm in its consecutive intermediate hosts: individual variation and fitness consequences.

Carbohydrates on parasite surfaces have been shown to play an important role in host-parasite coevolution, mediating host non-self recognition and parasite camouflage. Parasites that switch hosts can change their surface molecules to remain undetected by the diverse immune systems of their different hosts. However, the question of individual variation in surface sugar composition and its relation to infectivity, virulence, immune evasion and growth of a parasite in its different hosts is as yet largely unexplored. We studied such fitness consequences of variation in surface sugars in a sympatric host-parasite system consisting of the cestode Schistocephalus solidus and its intermediate hosts, a copepod and the three-spined stickleback. Using lectins to analyse the sugar composition, we show that the tapeworm changes its surface according to the invertebrate or vertebrate host. Importantly, sugar composition seems to be genetically variable, as shown by differences among tapeworm sibships. These differences are related to variation in parasite fitness in its second intermediate host, i.e. infectivity and growth. Surface sugar composition may thus be a proximate correlate of the evolutionarily relevant variability in infectivity and virulence of parasites in different hosts.

Animals↗

On the origin and evolution of the human immunodeficiency virus (HIV).

The human AIDS viruses--HIV-1 and HIV-2--impose major burdens on the health and economic status of many developing countries. Surveys of other animal species have revealed that related viruses--the SIVs are widespread in a large number of African simian primates where they do not appear to cause disease. Phylogenetic analyses indicate that these SIVs are the reservoirs for the human viruses, with SIVsm from the sooty mangabey monkey the most likely source of HIV-2, and SIVcpz from the common chimpanzee the progenitor population for HIV-1. Although it is clear that AIDS has a zoonotic origin, it is less certain when HIV-1 and HIV-2 first entered human populations and whether cross-species viral transmission is common among primates. Within infected individuals the process of HIV evolution takes the form of an arms race, with the virus continually fixing mutations by natural selection which allow it to escape from host immune responses. The arms race is less intense in SIV-infected monkeys, where a weaker immune response generates less selective pressure on the virus. Such a difference in virus-host interaction, along with a broadening of co-receptor usage such that HIV strains are able to infect cells with both CCR5 and CXCR4 chemokine receptors, may explain the increased virulence of HIV in humans compared to SIV in other primates.

Animals↗

The role of pyocyanin in Pseudomonas aeruginosa infection.

Pyocyanin (PCN) is a blue redox-active secondary metabolite that is produced by Pseudomonas aeruginosa. PCN is readily recovered in large quantities in sputum from patients with cystic fibrosis who are infected by P. aeruginosa. Despite in vitro studies demonstrating that PCN interferes with multiple cellular functions, its importance during clinical infection is uncertain. This is partially caused by the difficulty in defining the contribution of PCN among the numerous virulence factors produced by P. aeruginosa during infection. In addition, few cellular pathways that are affected by PCN are known. This review briefly highlights recent advances that might clarify the role of PCN in P. aeruginosa pathogenesis.

Animals↗

Evolution of black yeasts: possible adaptation to the human host.

Ascomycetous black yeasts show adaptations to a wide array of environmental conditions. Dothideaceous black yeasts are mostly found on plant leaves, while among herpotrichiellaceous species there are numerous opportunists on humans. Factors which are of ecological significance include the presence of melanin and carotene, formation of thick cell walls and meristematic growth, presence of yeast-like phases, presence of additional forms of conidiogenesis, thermo- and osmotolerance, adhesion, hydrophobicity, production of extracellular polysaccharides, siderophores and acidic or alkaline secondary metabolites. The potential pathogenicity of a species is partly determined by its natural ecological niche. Dothideaceous black yeasts are osmotolerant rather than pathogenic. Herpotrichiellaceous black yeasts probably have low competitive ability and are found in rather special niches as secondary saprophytes, e.g., on bacterial mats, on other fungi or in poor environments. Some species possibly utilize animal vectors for dispersal.

Adaptation, Physiological↗

Consumption coagulopathy associated with shock in acute African swine fever.

We studied the evolution of shock using a comprehensive array of haematological tests in pigs infected with the highly virulent strain Malawi '83 (Lilongwe 20/1). A sudden onset of illness was observed between day 5 and 7 after inoculation with development of flush, episodes of epistaxis and melaena. Prior to these clinical signs, initiation of a consumption coagulopathy was demonstrated with loss of antithrombin III and plasminogen activity. Our findings indicate that during infection with this highly virulent strain the development of a consumption coagulopathy precedes and possibly contributes to shock, which results in haemorrhage and death.

Acute Disease↗

A fitness advantage from the pLVPK plasmid fuels the global spread of a carbapenem-resistant hypervirulent Klebsiella pneumoniae high-risk clone: ST11-KL64.

BACKGROUND: The global emergence of carbapenem-resistant hypervirulent Klebsiella pneumoniae (CR-hvKP), particularly the ST11-KL64 subclone acquiring pLVPK-like virulence plasmids, represents a critical public health threat. This study investigates the epidemiological dominance and molecular mechanisms underlying ST11-KL64's fitness advantage over KL47 variants. METHODS: We performed comparative genomic analysis on 43,722 K. pneumoniae genomes (2011-2022) from 112 countries, focusing on ST11-CRKP strains. Capsular typing (KL64 vs. KL47), virulence gene profiling (aerobactin, RmpADC), and plasmid stability analysis were conducted using Kleborate, RAST, and PlasmidFinder. Plasmid-chromosome interactions were characterized through hybrid assembly approaches. RESULTS: ST11-KL64 demonstrated rapid expansion post-2016, surpassing KL47 as China's dominant CRKP subtype (40.5% vs. 28.9%), with regional predominance in Zhejiang (62.3%) and Sichuan (58.7%) provinces. Notably, 94.8% of KL64 strains maintained intact pLVPK plasmids with high aerobactin carriage (60.5%), while KL47 exhibited frequent plasmid fusion (58.8% with IncFIB[pNDM-Mar]) or chromosomal integration (41.4%), resulting in lower virulence potential (27.3% aerobactin+). Genomic analysis revealed KL64's superior plasmid stability (71.2% gene retention vs. KL47's 43.6%) and clinical correlation with severe outcomes (OR = 2.34, 95%CI 1.67-3.28). CONCLUSION: The ST11-KL64 subclone's epidemiological success stems from stable pLVPK plasmid maintenance, enabling simultaneous carbapenem resistance and hypervirulence. These findings highlight the urgent need for genomic surveillance targeting plasmid-mediated virulence in CRKP outbreaks, particularly in critical care settings where horizontal gene transfer may accelerate strain evolution.

Klebsiella pneumonia↗

Bacterial genomics and adaptation to life on plants: implications for the evolution of pathogenicity and symbiosis.

Many bacteria form intimate associations with plants. Despite the agricultural and biotechnological significance of these bacteria, no whole genome sequences have yet been described. Plant-associated bacteria form a phylogenetically diverse group, with representative species from many major taxons. Sequence information from genomes of closely related bacteria, in combination with technological developments in the field of functional genomics, provides new opportunities for determining the origin and evolution of traits that contribute to bacterial fitness and interactions with plant hosts.

Adaptation, Biological↗

Lateral gene transfer and the nature of bacterial innovation.

Unlike eukaryotes, which evolve principally through the modification of existing genetic information, bacteria have obtained a significant proportion of their genetic diversity through the acquisition of sequences from distantly related organisms. Horizontal gene transfer produces extremely dynamic genomes in which substantial amounts of DNA are introduced into and deleted from the chromosome. These lateral transfers have effectively changed the ecological and pathogenic character of bacterial species.

Bacteria↗

Mechanisms of chronic enteroviral persistence in tissue.

Although the association remains controversial, enteroviruses have been implicated in the aetiology of several chronic diseases in humans. Investigations in vitro lead to better understanding of virus-cell interactions, and improve our knowledge of the molecular factors that are involved in the establishment and maintenance of these infections. Recent findings suggest that the most important factor in the establishment of a persistent infection is receptor usage. Studies of the mechanisms that are at work in these in-vitro models of viral infection have shown that there is frequently a co-evolution of mutant cells with higher resistance to viral infection and of virus variants with increased virulence (i.e. variants with the ability to utilize other cell-surface molecules as receptors).

Animals↗

Genome of staphylococcal phage K: a new lineage of Myoviridae infecting gram-positive bacteria with a low G+C content.

Phage K is a polyvalent phage of the Myoviridae family which is active against a wide range of staphylococci. Phage genome sequencing revealed a linear DNA genome of 127,395 bp, which carries 118 putative open reading frames. The genome is organized in a modular form, encoding modules for lysis, structural proteins, DNA replication, and transcription. Interestingly, the structural module shows high homology to the structural module from Listeria phage A511, suggesting intergenus horizontal transfer. In addition, phage K exhibits the potential to encode proteins necessary for its own replisome, including DNA ligase, primase, helicase, polymerase, RNase H, and DNA binding proteins. Phage K has a complete absence of GATC sites, making it insensitive to restriction enzymes which cleave this sequence. Three introns (lys-I1, pol-I2, and pol-I3) encoding putative endonucleases were located in the genome. Two of these (pol-I2 and pol-I3) were found to interrupt the DNA polymerase gene, while the other (lys-I1) interrupts the lysin gene. Two of the introns encode putative proteins with homology to HNH endonucleases, whereas the other encodes a 270-amino-acid protein which contains two zinc fingers (CX(2)CX(22)CX(2)C and CX(2)CX(23)CX(2)C). The availability of the genome of this highly virulent phage, which is active against infective staphylococci, should provide new insights into the biology and evolution of large broad-spectrum polyvalent phages.

Amino Acid Sequence↗

Serial passage of the opportunistic pathogen Aspergillus flavus through an insect host yields decreased saprobic capacity.

To study the early stages of the effect of host restriction on pathogen evolution, we subjected the opportunistic fungus Aspergillus flavus to a serial propagation scheme, whereby insect-virulent conidia were selected for repeated passage through an insect host (Galleria mellonella larvae) for 5 generations. Of the 35 lineages promulgated through this scheme, there were no consistent changes in virulence, which was measured by percent mortality of the larvae. There were, however, increases in the number of conidia on the insect cadavers (9 of 35 lineages) and decreases in the number of days between death and the appearance of fungal growth on the cadavers (4 of 35 lineages). Notably, most of the lineages (28 of 35 lineages) demonstrated a statistically significant decrease in the diameter of the colonies subcultured onto artificial media, indicating a decreased ability to grow saprobically. Conversely, most of the A. flavus cultures successively grown on agar media (9 of 10 lineages) exhibited no change in colony diameter after 15 rounds of subculturing. Propagation of the opportunist A. flavus through the insect host G. mellonella resulted in a diminished capacity to grow on an alternate substrate, while maintaining or increasing its ability to use the host as a nutrient supply.

Animals↗

[The role of integrons in dissemination of antibiotic resistance].

Bacteria can transfer genetic information to get protection against most antibiotics. The acquisition of resistance genes involves genetic mobile elements such as plasmids and transposons. Another genetic structures, named integrons, have been described and contain one or more gene cassettes located at a specific site. Integrons contain an intI gene encoding a site-specific recombinase belonging to the integrase family and a recombination site attI. A gene cassette includes an open reading frame and, at the 3'-end, a recombination site attC. Integration or excision of cassettes occurs by a site-specific recombination mechanism catalyzed by the integrase. However, insertion can rarely occur, at non-specific sites leading to a stable situation for the cassette. Cassettes are transcribed from a common promoter located in the 5'-conserved segment and expression of distal genes is reduced by the presence of upstream cassettes. Most gene cassettes encode antibiotic resistant determinants but antiseptic resistant genes have also been described. Integrons seem to have a major role in the spread of multidrug resistance in Gram-negative bacteria but integrons in Gram-positive bacteria have been recently described. Moreover, the finding of super-integrons with gene cassettes coding for other determinants (biochemical functions, virulence factors) in different Gram negative bacteria suggests that integrons are probably implied in bacterial genome evolution.

Anti-Bacterial Agents↗

Comparison of Vibrio cholerae pathogenicity islands in sixth and seventh pandemic strains.

Epidemic Vibrio cholerae strains possess a large cluster of essential virulence genes on the chromosome called the Vibrio pathogenicity island (VPI). The VPI contains the tcp gene cluster encoding the type IV pilus toxin-coregulated pilus colonization factor which can act as the cholera toxin bacteriophage (CTXPhi) receptor. The VPI also contains genes that regulate virulence factor expression. We have fully sequenced and compared the VPI of the seventh-pandemic (El Tor biotype) strain N16961 and the sixth-pandemic (classical biotype) strain 395 and found that the N16961 VPI is 41,272 bp and encodes 29 predicted proteins, whereas the 395 VPI is 41,290 bp. In addition to various nucleotide and amino acid polymorphisms, there were several proteins whose predicted size differed greatly between the strains as a result of frameshift mutations. We hypothesize that these VPI sequence differences provide preliminary evidence to help explain the differences in virulence factor expression between epidemic strains (i.e., the biotypes) of V. cholerae.

Cholera↗