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PubMed2006

Update on pathogen reduction technology for therapeutic plasma: an overview.

Human plasma for therapeutic use, besides having optimal viral safety, must contain optimal levels of all coagulation factors and protease inhibitors to be clinically effective. Several new technologies for pathogen reduction of plasma (PRT) exist and are entering the stage of clinical testing. The main objective of this overview is to provide an update on the current states of three promising photoactive technologies that target pathogen nucleic acid for pathogen inactivation, applicable to single unit fresh-frozen plasma (FFP) and to highlight the experiences gained with classical pathogen reduction of pooled plasma using solvent-detergent (SD) treatment. It should be emphasized that none of the currently applied methods inactivate all types of pathogens and all have some effect on plasma quality when compared to fresh-frozen plasma. Pooled SD-plasma is the best documented clinical product, followed by methylene blue light treated (MBLT)-plasma. Recently, Psoralen light treated (PLT)-plasma has been introduced (CE-marked product in Europe) while Riboflavin light treated (RLT)-plasma is still under development. In principal, PRT for plasma not only differs in terms of the spectrum and log of pathogen reduction potential, but also in respect to the physicochemical/biological characteristics, and profiles of the adverse reactions, particularly in vulnerable patient groups. Therefore, an additional practical step such as oil extraction followed by chromatography to remove the solvent/detergent, and filtration or the use of some special absorbing matrix is required to reduce the residual photosensitive chemicals, their metabolites and photo adducts. This is required to improve the safety margin of the final product. Moreover, while it may be convenient to think that a combined pathogen reduction technology could improve the spectrum of known pathogens to be inactivated, one needs, in practice, to balance between the degree of pathogen reduction and the loss of some plasma protein activity. From the quality point of view, SD-plasma is a pooled standardized pharmaceutical product with extensive in-process control. However, both differences in production processes and the plasma source can influence final product quality. On the other hand, single unit plasma derived from nucleic acid PRT cannot be monitored by pharmaceutical process control and demonstrates the wide range of concentrations normally observed for plasma proteins. Pooling has the disadvantage that one single plasma unit can contaminate a whole pool, but this can be offset by several advantages that pooling and the SD process offer. Among these are reduction of a possible pathogen load by dilution and by neutralizing antibodies in the plasma pool, dilution and possible neutralization of antibodies and allergens which essentially eliminates transfusion-related acute lung injury (TRALI) and reduces allergic reactions significantly, removal of residual blood cells, cell fragments and bacteria, and removal of the largest von Willebrand-factor (vWF) molecules. On the other hand, some streamlining is required for technologies using single units of plasma, such as the use of plasma from male non-transfused donors to reduce TRALI and to avoid the O blood group in order to meet current specifications for FFP [Seghatchian J. What is happening? Are the current acceptance criteria for therapeutic plasma adequate? Transfus Apheresis Sci 2004; 31:67-79], and to exploit the potential benefit to inactivate residual lymphocytes and prevent transfusion-associated graft versus host disease. The cost effectiveness of pathogen inactivation is very low (> 2 million US dollar/life year saved), if however, non-infectious complications such as TRALI are taken into account; the cost for SDP is reduced to < 50,000 British pound/life year saved for those 48 years. Finally, from the therapeutic standpoint, two important questions still remain to be answered. First, whether the various pathogen reduced plasma products are clinically interchangeable and second, whether the conventional quality requirements of FFP are still adequate for the newer plasma products. These questions can only be answered by a head to head comparison, followed by large-scale clinical trials.

Blood Component Removal↗

PubMed2000

Effects of total pathogen burden on coronary artery disease risk and C-reactive protein levels.

Infection and inflammation have been suggested to play roles in coronary artery disease (CAD). We hypothesized that: (1) CAD risk is associated with the aggregate number of pathogens (pathogen burden), and (2) increased pathogen burden is associated with elevated levels of C-reactive protein (CRP), a marker of inflammation. We evaluated 233 patients for CAD. Blood samples from each patient were tested for immunoglobulin-G (IgG) antibodies to cytomegalovirus (CMV), Chlamydia pneumoniae, hepatitis A virus (HAV), herpes simplex virus type 1 (HSV-1) and HSV type 2 (HSV-2), and for the CRP levels. Of the 233 study subjects, 68% had evidence of CAD by coronary angiography. Although the prevalence of seropositivity for each pathogen tended to be higher in the patients with CAD than those without, only the association between CAD and seropositivity to HAV was significant in multivariate analysis. Over 75% of study subjects had been exposed to > or =3 of the 5 pathogens tested, and analysis determined that increasing pathogen burden was significantly associated with increasing CAD risk, even after adjustment for traditional CAD risk factors. The prevalence of CAD was 48%, 69%, and 85% in individuals with antibodies to < or =2 pathogens, to 3 or 4 pathogens, and to 5 pathogens, respectively. A similar association between increasing pathogen burden and CRP levels was also found. The pathogen burden remained a significant predictor of CRP levels after multivariate analysis. Our data suggest that infection does play a role in the genesis of atherosclerosis. However, the risk posed by infection is related to the pathogen burden that may contribute to CAD through inflammatory responses.

Adult↗

PubMed2001

Antibody-based resistance to plant pathogens.

Plant diseases are a major threat to the world food supply, as up to 15% of production is lost to pathogens. In the past, disease control and the generation of resistant plant lines protected against viral, bacterial or fungal pathogens, was achieved using conventional breeding based on crossings, mutant screenings and backcrossing. Many approaches in this field have failed or the resistance obtained has been rapidly broken by the pathogens. Recent advances in molecular biotechnology have made it possible to obtain and to modify genes that are useful for generating disease resistant crops. Several strategies, including expression of pathogen-derived sequences or anti-pathogenic agents, have been developed to engineer improved pathogen resistance in transgenic plants. Antibody-based resistance is a novel strategy for generating transgenic plants resistant to pathogens. Decades ago it was shown that polyclonal and monoclonal antibodies can neutralize viruses, bacteria and selected fungi. This approach has been improved recently by the development of recombinant antibodies (rAbs). Crop resistance can be engineered by the expression of pathogen-specific antibodies, antibody fragments or antibody fusion proteins. The advantages of this approach are that rAbs can be engineered against almost any target molecule, and it has been demonstrated that expression of functional pathogen-specific rAbs in plants confers effective pathogen protection. The efficacy of antibody-based resistance was first shown for plant viruses and its application to other plant pathogens is becoming more established. However, successful use of antibodies to generate plant pathogen resistance relies on appropriate target selection, careful antibody design, efficient antibody expression, stability and targeting to appropriate cellular compartments.

Antibodies, Viral↗

PubMed2001

Evolution of pathogen virulence: the role of variation in host phenotype.

Selection on pathogens tends to favour the evolution of growth and reproductive rates and a concomitant level of virulence (damage done to the host) that maximizes pathogen fitness. Yet, because hosts often pose varying selective environments to pathogens, one level of virulence may not be appropriate for all host types. Indeed, if a level of virulence confers high fitness to the pathogen in one host phenotype but low fitness in another host phenotype, alternative virulence strategies may be maintained in the pathogen population. Such strategies can occur either as polymorphism, where different strains of pathogen evolve specialized virulence strategies in different host phenotypes or as polyphenism, where pathogens facultatively express alternative virulence strategies depending on host phenotype. Polymorphism potentially leads to specialist pathogens capable of infecting a limited range of host phenotypes, whereas polyphenism potentially leads to generalist pathogens capable of infecting a wider range of hosts. Evaluating how variation among hosts affects virulence evolution can provide insight into pathogen diversity and is critical in determining how host pathogen interactions affect the phenotypic evolution of both hosts and pathogens.

Biological Evolution↗

PubMedDate not supplied

The pathogenicity of Entamoeba histolytica is related to the capacity of evading innate immunity.

The host and parasite factors that influence susceptibility to Entamoeba histolytica infection and disease are not well understood. Entamoeba histolytica pathogenicity has been considered by focusing principally on parasite rather than host factors. Thus, research has concentrated on explaining the molecular differences between pathogenic E. histolytica and non-pathogenic E. dispar. However, the amoeba molecules considered most important for host tissue destruction (amoebapore, galactose/N-acetyl galactosamine inhibitable lectin, and cysteine proteinases) are present in both pathogenic E. histolytica and non-pathogenic E. dispar. In addition, the genetic differences in pathogenicity among E. histolytica isolates are unlikely to completely explain the different outcomes of infection. Considering that the principal difference between pathogenic and non-pathogenic amoebas lies in their surface coats, we propose that pathogenicity of the amoebas is related to the composition and properties of the surface coat components (or pathogen-associated molecular patterns, PAMPs), and the ability of innate immune response to recognize these components and eliminate the parasite. According to this hypothesis, a key feature that may distinguish pathogenic (E. histolytica) from non-pathogenic (E. dispar) strains is whether or not they can overcome innate immune defences. A corollary of this hypothesis is that in susceptible individuals the PAMPs are either not recognized or they are recognized by a set of Toll-like receptors (TLRs) that leads to an inflammatory response. In both cases, the result is tissue damage. On the contrary, in resistant individuals the innate/inflammatory response, induced through the activation of a different set of TLRs, eliminates the parasite.

Animals↗

PubMed2004

Pathogenicity islands in bacterial pathogenesis.

In this review, we focus on a group of mobile genetic elements designated pathogenicity islands (PAI). These elements play a pivotal role in the virulence of bacterial pathogens of humans and are also essential for virulence in pathogens of animals and plants. Characteristic molecular features of PAI of important human pathogens and their role in pathogenesis are described. The availability of a large number of genome sequences of pathogenic bacteria and their benign relatives currently offers a unique opportunity for the identification of novel pathogen-specific genomic islands. However, this knowledge has to be complemented by improved model systems for the analysis of virulence functions of bacterial pathogens. PAI apparently have been acquired during the speciation of pathogens from their nonpathogenic or environmental ancestors. The acquisition of PAI not only is an ancient evolutionary event that led to the appearance of bacterial pathogens on a timescale of millions of years but also may represent a mechanism that contributes to the appearance of new pathogens within a human life span. The acquisition of knowledge about PAI, their structure, their mobility, and the pathogenicity factors they encode not only is helpful in gaining a better understanding of bacterial evolution and interactions of pathogens with eukaryotic host cells but also may have important practical implications such as providing delivery systems for vaccination, tools for cell biology, and tools for the development of new strategies for therapy of bacterial infections.

Bacteria↗

PubMed2000

Pathogenicity islands and the evolution of microbes.

Virulence factors of pathogenic bacteria (adhesins, toxins, invasins, protein secretion systems, iron uptake systems, and others) may be encoded by particular regions of the prokaryotic genome termed pathogenicity islands. Pathogenicity islands were first described in human pathogens of the species Escherichia coli, but have recently been found in the genomes of various pathogens of humans, animals, and plants. Pathogenicity islands comprise large genomic regions [10-200 kilobases (kb) in size] that are present on the genomes of pathogenic strains but absent from the genomes of nonpathogenic members of the same or related species. The finding that the G+C content of pathogenicity islands often differs from that of the rest of the genome, the presence of direct repeats at their ends, the association of pathogenicity islands with transfer RNA genes, the presence of integrase determinants and other mobility loci, and their genetic instability argue for the generation of pathogenicity islands by horizontal gene transfer, a process that is well known to contribute to microbial evolution. In this article we review these and other aspects of pathogenicity islands and discuss the concept that they represent a subclass of genomic islands. Genomic islands are present in the majority of genomes of pathogenic as well as nonpathogenic bacteria and may encode accessory functions which have been previously spread among bacterial populations.

Bacteria↗

PubMed2006

A model for predicting feed intake of growing animals during exposure to pathogens.

A general model is proposed for predicting the effects of subclinical pathogen challenges of different doses and virulence on the relative feed intake (RFI) of animals. The RFI is defined as the feed intake (FI, kg/d) of the animal challenged by a pathogen divided by its FI in the same state had it not been challenged. Actual FI can be predicted from the RFI and the animal's state. The RFI was assumed to be affected only when animals were naïve to a particular pathogen (i.e., had not previously experienced it) and when the challenge dose was above a predetermined threshold. The model is for the period from recognition of a pathogen through acquisition and subsequent expression of immunity. The way in which RFI changes with time is described by 5 main parameters and is based on data for RFI during different pathogen challenges of a range of hosts. Lag time (L, d) is the delay from a pathogen challenge until any effects on RFI are seen. Reduction time (R, d) describes the time it takes for the lowest value of RFI (lambda) to be achieved. The duration time (D, d) describes the time that lambda is maintained for, and rho (RFI/d) describes the rate of recovery of RFI until RFI = 1. There is no compensatory intake, and RFI is always < or = 1. The effects of host resistance on the values of the model parameters are proposed. Attempts were made to parameterize the model; when data were scarce, initial parameter values were derived on conceptual grounds. Predictions of the effects of pathogen dose, virulence, and host resistance are described and discussed. When comparing the responses in RFI for different genotypes, it is crucial to define the pathogen challenge (in terms of dose and virulence) and the degree of resistance of different hosts. Possible interactions between dose, virulence, and resistance were explored. Feed intake of healthy and challenged animals, at a time, may be different once the challenged animal has recovered (RFI = 1). The issue of reductions in FI during pathogen challenges is important for nutritionist and animal breeders. The large variation that has been observed for reductions in FI during pathogen challenges may be a viable point of selection. The points highlighted will aid selection strategies by quantifying the effects of pathogen dose and virulence, and time, on the FI of challenged animals. The proposed model may be integrated with other models of growth to predict animal performance during exposure to pathogens.

Animal Diseases↗

PubMedDate not supplied

[Plasticity of bacterial genomes: pathogenicity islands and the locus of enterocyte effacement (LEE)].

Many bacterial virulence attributes, like toxins, adhesins, invasins, iron uptake systems, are encoded within specific regions of the bacterial genome. These in size varying regions are termed pathogenicity islands (PAIs) since they confer pathogenic properties to the respective micro-organism. Per definition PAIs are exclusively found in pathogenic strains and are often inserted near transfer-RNA genes. Nevertheless, non-pathogenic bacteria also possess foreign DNA elements that confer advantageous features, leading to improved fitness. These additional DNA elements as well as PAIs are termed genomic islands and were acquired during bacterial evolution. Significant G+C content deviation in pathogenicity islands with respect to the rest of the genome, the presence of direct repeat sequences at the flanking regions, the presence of integrase gene determinants as other mobility features,the particular insertion site (tRNA gene) as well as the observed genetic instability suggests that pathogenicity islands were acquired by horizontal gene transfer. PAIs are the fascinating proof of the plasticity of bacterial genomes. PAIs were originally described in human pathogenic Escherichia (E.) coli strains. In the meantime PAIs have been found in various pathogenic bacteria of humans, animals and even plants. The Locus of Enterocyte Effacement (LEE) is one particular widely distributed PAI of E coli. In addition, it also confers pathogenicity to the related species Citrobacter (C.) rodentium and Escherichia (E.) alvei. The LEE is an important virulence feature of several animal pathogens. It is an obligate PAI of all animal and human enteropathogenic E. coli (EPEC), and most enterohaemorrhegic E. coli (EHEC) also harbor the LEE. The LEE encodes a type III secretion system, an adhesion (intimin) that mediates the intimate contact between the bacterium and the epithelial cell, as well as various proteins which are secreted via the type III secretion system. The LEE encoded virulence features are responsible for the formation of so called attaching and effacing (AE) lesions in the intestinal epithelium. Due to its wide distribution in animal pathogens, LEE encoded antigens are suitable vaccine antigens. Acquisition and structure of the LEE pathogenicity island is the crucial point of numerous investigations. However, the evolution of the LEE, its origin and further spread in E. coli, are far from being resolved.

Bacteria↗

PubMed2006

Association and host selectivity in multi-host pathogens.

The distribution of multi-host pathogens over their host range conditions their population dynamics and structure. Also, host co-infection by different pathogens may have important consequences for the evolution of hosts and pathogens, and host-pathogen co-evolution. Hence it is of interest to know if the distribution of pathogens over their host range is random, or if there are associations between hosts and pathogens, or between pathogens sharing a host. To analyse these issues we propose indices for the observed patterns of host infection by pathogens, and for the observed patterns of co-infection, and tests to analyse if these patterns conform to randomness or reflect associations. Applying these tests to the prevalence of five plant viruses on 21 wild plant species evidenced host-virus associations: most hosts and viruses were selective for viruses and hosts, respectively. Interestingly, the more host-selective viruses were the more prevalent ones, suggesting that host specialisation is a successful strategy for multi-host pathogens. Analyses also showed that viruses tended to associate positively in co-infected hosts. The developed indices and tests provide the tools to analyse how strong and common are these associations among different groups of pathogens, which will help to understand and model the population biology of multi-host pathogens.

Ecosystem↗

PubMed2003

Impact of pathogen burden in patients with coronary artery disease in relation to systemic inflammation and variation in genes encoding cytokines.

The number of infectious pathogens to which an individual has been exposed (pathogen burden) has been linked to the development and the prognosis of coronary artery disease (CAD). The interaction among infection, genetic host susceptibility, and CAD remains unclear. This study was aimed at evaluating the modulation of the association between CAD and pathogen burden, by serum levels of inflammatory markers and polymorphisms of the interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha genes. Immmunoglobulin (Ig) G or IgA antibodies to 8 pathogens were determined in 991 patients with CAD and 333 control subjects. Serum levels of high-sensitivity C-reactive protein, fibrinogen, IL-6, and TNF-alpha were also measured. All subjects were genotyped for the IL-6/G-174C, the TNF/C-851T, and the TNF/G-308A polymorphisms. Analysis of single pathogens demonstrated a positive relation to the presence of CAD for some (Chlamydia pneumoniae, cytomegalovirus, Helicobacter pylori, and herpes virus simplex type 1), but not all pathogens. A strong association between increasing pathogen burden and CAD was confirmed, even after adjustment for risk factors. The prevalence of a high pathogen burden (>/=4 pathogens) was 50% in patients and 21% in controls (p <0.0001). A high pathogen burden was associated with decreased high-density lipoprotein cholesterol levels (p <0.001). The association between CAD and pathogen burden was modulated by the IL6/G-174C polymorphism, the odds ratio being higher in heterozygotes than in both types of homozygotes (p <0.05). This interaction appeared to be mediated by variations in serum IL-6 levels. No such interaction was detected with any of the 2 TNF-alpha polymorphisms.

Aged↗

PubMed2002

Emerging foodborne pathogens.

The broad spectrum of foodborne infections has changed dramatically over time, as well-established pathogens have been controlled or eliminated, and new ones have emerged. The burden of foodborne disease remains substantial: one in four Americans is estimated to have a significant foodborne illness each year. The majority of these illnesses are not accounted for by known pathogens, so more must remain to be discovered. Among the known foodborne pathogens, those more recently identified predominate, suggesting that as more and more is learned about pathogens, they come under control. In addition to the emergence or recognition of new pathogens, other trends include global pandemics of some foodborne pathogens, the emergence of antimicrobial resistance, the identification of pathogens that are highly opportunistic, affecting only the most high-risk subpopulations, and the increasing identification of large and dispersed outbreaks. New pathogens can emerge because of changing ecology or changing technology that connects a potential pathogen with the food chain. They also can emerge de novo by transfer of mobile virulence factors, often through bacteriophage. Though this is rarely observed, it can be reconstructed. Better understanding of the ecology and dynamics of phage transmission among bacteria will help us to understand the appearance of new pathogens in the future. One may look for emerging foodborne pathogens among the silent zoonoses, and among the severe infections affecting the immunocompromised humans. We should expect the unexpected. In the past, separating human sewage and animal manure from human food and water supplies was critical to improving public health. Now, our health depends increasingly on the safety of the feed and water supplies for the animals themselves. The successes of the 20th century and the new challenges we face mean that public health vigilance, careful investigation of new problems, responsible attention to food safety from farm to table, and partnerships to bring about new foodborne disease control measures will be needed for the foreseeable future.

Animals↗

PubMed2003

Determination of eight selected periodontal pathogens in the subgingival plaque of maxillary first molars in Japanese school children aged 8-11 years.

To prevent the onset or progression of periodontitis, we must understand when periodontal pathogens are first harbored and how they develop the biofilm that causes periodontal disease. The purpose of this study was to determine the relationship between clinical status and selected periodontal pathogens in subgingival plaque in school children. This study was conducted with 95 school children, 8-11 years old. The presence and distribution of eight selected periodontal pathogens sampled from the maxillary right first molar were determined by an indirect immunofluorescent technique and compared with clinical parameters. Of the 95 sites sampled, only one site had all eight pathogens and five sites did not have any of the eight pathogens. The mean number of positive pathogens per site was 3.5 +/- 1.8 and mean percentage of positive pathogens was 3.82 +/- 4.22%. The number and total percentage of positive pathogens were strongly correlated with the Plaque Index (PI). In addition, the number of positive pathogens was correlated to the presence of subgingival calculus. The most frequently found pathogens were Campylobacter rectus (84.2%) and Eikenella corrodens (83.2%), and the least, Actinobacillus actinomycetemcomitans serotype c (7.4%). Of the eight pathogens, the frequency and distribution of Porphyromonas gingivalis were significantly correlated with PI and the presence of calculus. In addition, seven sites with both P. gingivalis and Bacteroides forsythus showed a correlation with gingival inflammation. In conclusion, the presence of P. gingivalis or P. gingivalis and B. forsythus may be a risk marker to be sought in screening for the onset of periodontal disease.

Aggregatibacter actinomycetemcomitans↗

PubMed2005

Species coexistence and pathogens with frequency-dependent transmission.

Pathogens that infect multiple hosts are commonly transmitted by vectors, and their transmission rate is often thought to depend on the proportion of hosts or vectors infected (i.e., frequency dependence). A model of a two-host, one-pathogen system with frequency-dependent transmission is used to investigate how sharing a pathogen with an alternative host influences pathogen-mediated extinction. The results show that if there is frequency-dependent transmission, a host can be rescued from pathogen-mediated extinction by the presence of a second host with which it shares a pathogen. The study provides an important conceptual counterexample to the idea that shared pathogens necessarily result in apparent competition by showing that shared pathogens can mediate apparent mutualism. We distinguish two types of dilution effect (pathogen reduction with increasing host diversity), each resulting from different underlying pathogen transmission processes and host density effects. These results have important consequences for understanding the role of pathogens in species interactions and in maintaining host species diversity.

Animal Diseases↗

PubMed2005

An agent-based and spatially explicit model of pathogen dissemination in the intensive care unit.

OBJECTIVE: To develop and disseminate a spatially explicit model of contact transmission of pathogens in the intensive care unit. DESIGN: A model simulating the spread of a pathogen transmitted by direct contact (such as methicillin-resistant Staphylococcus aureus or vancomycin-resistant Enterococcus) was constructed. The modulation of pathogen dissemination attending changes in clinically relevant pathogen- and institution-specific factors was then systematically examined. SETTING AND PATIENTS: The model was configured as a hypothetical 24-bed intensive care unit. The model can be parameterized with different pathogen transmissibilities, durations of caregiver and/or patient contamination, and caregiver allocation and flow patterns. INTERVENTIONS: Pathogen- and institution-specific factors examined included pathogen transmissibility, duration of caregiver contamination, regional cohorting of contaminated or infected patients, delayed detection and isolation of newly contaminated patients, reduction of the number of caregiver visits, and alteration of caregiver allocation among patients. MEASUREMENTS AND MAIN RESULTS: The model predicts the probability that a given fraction of the population will become contaminated or infected with the pathogen of interest under specified spatial, initial prevalence, and dynamic conditions. Per-encounter pathogen acquisition risk and the duration of caregiver pathogen carriage most strongly affect dissemination. Regional cohorting and rapid detection and isolation of contaminated patients each markedly diminish the likelihood of dissemination even absent other interventions. Strategies reducing "crossover" between caregiver domains diminish the likelihood of more widespread dissemination. CONCLUSIONS: Spatially explicit discrete element models, such as the model presented, may prove useful for analyzing the transmission of pathogens within the intensive care unit.

Caregivers↗

PubMed2006

Pathogens, density dependence and the coexistence of tropical trees.

There is increasing interest in the role played by density-dependent mortality from natural enemies, particularly plant pathogens, in promoting the coexistence and diversity of tropical trees. Here, we review four issues in the analysis of pathogen-induced density dependence that have been overlooked or inadequately addressed. First, the methodology for detecting density dependence must be robust to potential biases. Observational studies, in particular, require a careful analysis to avoid biases generated by measurement error, and existing studies could be criticized on these grounds. Experimental studies manipulating plant density and pathogen incidence will often be preferable, or should be run in parallel. Second, the form of density dependence is not well understood and, in particular, there are no data indicating whether pathogens cause compensating or overcompensating density responses. Owing to this, we argue that the potential for pathogen-induced density dependence to generate diversity-enhancing outcomes, such as the Janzen-Connell effect, remains uncertain, as coexistence is far more probable if density dependence is overcompensating. Third, there have been few studies examining the relative importance of intra- or interspecific density dependence resulting from pathogens (or, more widely, natural enemies). This is essentially equivalent to asking to what extent pathogens are host-specific. If pathogens are generalists, then mortality rates will respond to overall plant density, irrespective of plant species identity. This will weaken the intraspecific density dependence and reduce the diversity-promoting effects of pathogens. Finally, we highlight the need for studies that integrate observations and experiments on pathogens and density dependence into the whole life cycle of trees, because as yet it is not possible to be certain of the degree to which pathogens contribute to observed dynamics.

Biodiversity↗

PubMed1998

Extracellular enzyme activities potentially involved in the pathogenicity of Mycobacterium tuberculosis.

To evaluate the potential contribution of extracellular enzymes to the pathogenicity of mycobacteria, the presence of selected enzyme activities was investigated in the culture filtrates of the obligate human pathogen Mycobacterium tuberculosis, M. bovis BCG, the opportunistic pathogens M. kansasii and M. fortuitum, and the non-pathogenic species M. phlei and M. smegmatis. For M. tuberculosis and M. bovis, 22 enzyme activities were detected in the culture filtrates and/or cell surfaces, of which eight were absent from the culture fluids of non-pathogens: alanine dehydrogenase, glutamine synthetase, nicotinamidase, isonicotinamidase, superoxide dismutase, catalase, peroxidase and alcohol dehydrogenase. These activities, which correspond to secreted enzymes, formed a significant part (up to 92%) of the total enzyme activities of the bacteria and were absent from the culture fluids and the cell surfaces of the non-pathogenic species M. smegmatis and M. phlei. The extracellular location of superoxide dismutase and glutamine synthetase seemed to be restricted to the obligate pathogens examined. The difference in the enzyme profiles was not attributable to the growth rates of the two groups of bacteria. The presence of the eight enzyme activities in the outermost compartments of obligate pathogens and their absence in those of non-pathogens provides further evidence that these enzymes may be involved in the pathogenicity of mycobacteria. In addition, the eight enzyme activities were demonstrated in the cell extract of M. smegmatis. Stepwise erosion of the cell surface of M. smegmatis to expose internal capsular constituents showed that the various enzyme activities, with the possible exception of superoxide dismutase, were located more deeply in the cell envelope of this bacterium. This suggests that the molecular architecture of the mycobacterial envelopes may play an important role in the pathogenicity of these organisms.

Bacterial Capsules↗

PubMed1994

Virulence of vector-borne pathogens. A stochastic automata model of perpetuation.

To determine how virulence may be perpetuated in populations of vector-borne pathogens, we simulated their fitness in a stochastic simulation based on cellular automata. Thereby, directly transmissible pathogens that differed in virulence were permitted to compete for hosts with similarly virulent pathogens that could infect hosts remotely because they were vector-borne. Fitness was defined as the proportion of the host population infected with each pathogen at equilibrium. Virulent, directly transmitted pathogens prevailed solely when their infectivity was transient. When duration of infectivity exceeded that of host survival, the less virulent pathogen invariably prevailed. Although remotely transmitted virulent pathogens persisted somewhat longer than did virulent pathogens that were transmitted directly, they never perpetuated themselves. We conclude that populations of vector-borne pathogens may retain pathogenicity somewhat longer than do those that are directly transmitted, but that both kinds of pathogens tend to become nonvirulent.

Animals↗