Individual Host Susceptibility Research Articles

Correlates of disease severity in bluetongue as a model of acute arbovirus infection.

Most viral diseases display a variable clinical outcome due to differences in virus strain virulence and/or individual host susceptibility to infection. Understanding the biological mechanisms differentiating a viral infection displaying severe clinical manifestations from its milder forms can provide the intellectual framework toward therapies and early prognostic markers. This is especially true in arbovirus infections, where most clinical cases are present as mild febrile illness. Here, we used a naturally occurring vector-borne viral disease of ruminants, bluetongue, as an experimental system to uncover the fundamental mechanisms of virus-host interactions resulting in distinct clinical outcomes. As with most viral diseases, clinical symptoms in bluetongue can vary dramatically. We reproduced experimentally distinct clinical forms of bluetongue infection in sheep using three bluetongue virus (BTV) strains (BTV-1IT2006, BTV-1IT2013 and BTV-8FRA2017). Infected animals displayed clinical signs varying from clinically unapparent, to mild and severe disease. We collected and integrated clinical, haematological, virological, and histopathological data resulting in the analyses of 332 individual parameters from each infected and uninfected control animal. We subsequently used machine learning to select the key viral and host processes associated with disease pathogenesis. We identified and experimentally validated five different fundamental processes affecting the severity of bluetongue: (i) virus load and replication in target organs, (ii) modulation of the host type-I IFN response, (iii) pro-inflammatory responses, (iv) vascular damage, and (v) immunosuppression. Overall, we showed that an agnostic machine learning approach can be used to prioritise the different pathogenetic mechanisms affecting the disease outcome of an arbovirus infection.

Inflammatory cell responses in biliary mucosa during Opisthorchis viverrini infection: Insights into susceptibility differences among hosts.

Individual host susceptibility is believed to be a risk factor in the interaction between the host and the parasite. Since studying time series in humans is limited, animal models are replaced. This study aims to explore and compare the pattern of inflammatory cell types along the biliary tract and their association with proliferative lesions in the early development of cholangiocarcinoma from susceptible and nonsusceptible animal models. Thirty male Syrian golden hamsters and 30 BALB/c mice, serving as the susceptible and nonsusceptible animal models, were used in this comparative study. The animals were infected with 50 Opisthorchis viverrini metacercariae via gastric intubation. At days 1, 2, 7, 14, 28, and 56 postinfection (p.i.), five animals were randomly selected from each group and humanely sacrificed. The hepatobiliary tissues were collected and processed for histopathological study. Histochemical and immunohistochemical staining were applied to differentiate the inflammatory cell types. Kruskal-Wallis and Mann-Whitney tests were applied to assess all semi-quantitative and quantitative variables. The correlation between each variable was also analyzed using Spearman rank at a p-value < 0.05. The results demonstrated that mice had different patterns of infiltrating cell types when compared to hamsters. This suggested that the cellular response to the infection in mice occurred earlier than that in hamsters. The response in mice reached its peak at D7 to D14 and then rapidly declined at D28. In contrast, although the inflammatory response in hamsters started slowly, the response reached the peak at D28 and maintained a high level until D56. Significant differences in the number of inflammatory cells between mice and hamsters were seen at D1 (p = 0.047), D7 (p = 0.049), D28 (p = 0.040), and D56 (p < 0.040). The inflammatory responses to O. viverrini infection in the nonsusceptible animal model occurred and declined earlier while the response in the susceptible animal model occurred later in a gradual manner. Both rodents are suitable animal models for the studies of opisthorchiasis susceptibility.

PRESENCE OF SNP OF INTERLEUKIN17F IN PATIENTS WITH PERIODONTITIS IN A BULGARIAN POPULATION

Introduction: It`s well known that the periodontitis is а complex disease initiated by bacteria, but modified by environmental factors and the host response. As any other chronic disease, the periodontal disease is influenced by the individual predisposition of the patient to develop the specific symptoms. The increasing number of studies in the area of the genetic factors and mechanisms of the patient to develop the specific condition is leading to the need for certain polymоrphism’s to be studied in details for the Bulgarian population. Aim: The recent study aims to identify the presence of SNP of IL-17F in the Bulgarian population. Materials and methods: In the study, 40 patients with periodontitis stage II, III and IV and 10 healthy control subjects were taking part. The age of the subjects varied between 23 and 75 with an average value of 46 years. Clinical and radiographic methods to establish the basic periodontal parameters were used. Laboratory methods were performed by means of Real-Time PCR for determination of SNP of Interleukin 17F (IL-17F) (-7488C/T rs_763780). The statistic data was processed with PCA – IBM SPSS Statistics Version 21. From all of the patients, informed consent was taken. Results: The recent study collected information about the dominating genotype when studying SNP of IL-17 F for patients with periodontitis. The presence of two genotypes was established – genotype TT (92%) and genotype CT (8%). We have established specific tendencies about the distribution of major parameter for diagnosis of periodontitis such as BoP and BL/Age in both groups. The individual host susceptibility can be used as a diagnostic parameter leading to the development of screening methods in order suspectable individuals to be found. Conclusion: The study has contributed to clarifying the genetic characteristic of the tested subject. The results confirmed the data from different studies that aim to research the genetic polymorphism of IL-17F in relation to periodontitis.

The change of susceptibility following infection can induce failure to predict outbreak potential by R₀.

Time-varying individual host susceptibility to a disease due to waning and boosting of immunity is known to induce rich long-term behavior of the disease transmission dynamics. Simultaneously, the impact of the time-varying heterogeneity of host susceptibility on the short-term behavior of epidemics is not well-studied despite the availability of a large amount of epidemiological data on short-term epidemics. This paper proposes a parsimonious mathematical model describing the short-term transmission dynamics by taking into account waning and enhancing susceptibility following the infection. In addition to the common classification in the standard SIR model, i.e., "no epidemic" as R₀≤1 or normal epidemic as R₀>1, the proposed model also shows the "delayed epidemic" class when an epidemic takes off after the negative slope of the epidemic curve at the initial phase of the epidemic. The condition for each of the three classes is derived based on the obtained explicit solution for the proposed model.

What happened to Koch's postulates in diarrhoea?

In 1890, Robert Koch has formulated postulates describing what criteria a parasite has to fulfil to qualify as an aetiological agent for an infectious disease. Since then Koch's postulates have experienced reformulations by nearly every generation of microbiologists reflecting new discoveries changing the understanding of infectious diseases pathogenesis. The latest addition to this discussion is the role of the host commensal microbiota in turning infections into disease. After an overview of the historical developments of the postulates, data on diarrhoea aetiology from Bangladesh with respect to Koch's postulates were analysed. In countries with a low environmental hygiene standard, some recognized bacterial enteropathogens appear as a necessary, but not sufficient condition for diarrhoea. The possibility emerges that the loss of a physiological commensal gut microbiota equilibrium ('dysbiosis') is an important co-factor for some bacterial pathogens to induce diarrhoea. Koch's hypothesis '1 pathogen + 1 host = 1 disease' is therefore better formulated as 'X (pathogen/s) + Y (local milieu) + Z (individual host susceptibility) = disease'.

Listeria monocytogenes dose response revisited--incorporating adjustments for variability in strain virulence and host susceptibility.

Evaluations of Listeria monocytogenes dose-response relationships are crucially important for risk assessment and risk management, but are complicated by considerable variability across population subgroups and L. monocytogenes strains. Despite difficulties associated with the collection of adequate data from outbreak investigations or sporadic cases, the limitations of currently available animal models, and the inability to conduct human volunteer studies, some of the available data now allow refinements of the well-established exponential L. monocytogenes dose response to more adequately represent extremely susceptible population subgroups and highly virulent L. monocytogenes strains. Here, a model incorporating adjustments for variability in L. monocytogenes strain virulence and host susceptibility was derived for 11 population subgroups with similar underlying comorbidities using data from multiple sources, including human surveillance and food survey data. In light of the unique inherent properties of L. monocytogenes dose response, a lognormal-Poisson dose-response model was chosen, and proved able to reconcile dose-response relationships developed based on surveillance data with outbreak data. This model was compared to a classical beta-Poisson dose-response model, which was insufficiently flexible for modeling the specific case of L. monocytogenes dose-response relationships, especially in outbreak situations. Overall, the modeling results suggest that most listeriosis cases are linked to the ingestion of food contaminated with medium to high concentrations of L. monocytogenes. While additional data are needed to refine the derived model and to better characterize and quantify the variability in L. monocytogenes strain virulence and individual host susceptibility, the framework derived here represents a promising approach to more adequately characterize the risk of listeriosis in highly susceptible population subgroups.

Examining the “evolution of increased competitive ability” hypothesis in response to parasites and pathogens in the invasive paper wasp Polistes dominula

Successful invaders often become established in new ranges by outcompeting native species. The "evolution of increased competitive ability" hypothesis predicts that invasive species are subjected to less predation and parasitization than sympatric native species, and thus can allocate resources from defence and immunity to growth and fecundity, thereby achieving higher fitness. In this study, we examined whether American invasive Polistes dominula paper wasps have reduced immunocompetence. To explore this scenario, we tested their susceptibility towards parasites and pathogens at both the individual (immune defence) and colony levels, i.e. hygienic behaviour (removal of diseased individuals by nestmates). First, we examined the response to the specific coevolved parasite Xenos vesparum (lost after invasion) in terms of individual host susceptibility and hygienic behaviour. Second, we explored the response against general pathogens by quantifying the bacterial clearance in individual wasps after a challenge with Escherichia coli and hygienic behaviour after a challenge with the fungus Beauveria bassiana. Our results show that American invasive P. dominula have a higher response against X. vesparum at the colony level, but at the individual level their susceptibility is not significantly different from conspecifics of the native range. On the other hand, invasive P. dominula display lower response after a challenge with general pathogens at both the individual and colony levels. While supporting the hypothesis of a reduction of immunocompetence towards general pathogens in invasive species, these findings also suggest that the response against coevolved parasites might follow different evolutionary pathways which are not always easily predictable.

Towards common denominators in primary biliary cirrhosis: The role of IL-12

There have been significant advances in our understanding of the immunobiology of primary biliary cirrhosis (PBC) and, in particular, a rigorous dissection of not only the serologic abnormalities, including antimitochondrial autoantibodies (AMA), but also the definition of autoreactive CD4+ and CD8+ T cells [1]. Further, there is increasing evidence for the interplay of genetic and environmental factors in individual host susceptibility. One paradox has been the selected destruction of small bile ducts in PBC despite the presence of mitochondrial antigens in virtually all nucleated cells.

Linking Environmental Particulate Matter with Genetic Alterations

In their article, Tarantini et al. (2009) focused on the basic question of mutual relationships between environmental and genetic factors. From a more general point of view, this also involves the question concerning the relative role of “intrinsic toxicity” of xenobiotics and individual susceptibility or host response. In particular, data from epidemiologic and in vitro studies must cope with pathologic evidence for pathologists, as well as cause-and effect-relationships for pathophysiologists. In between are inferences and extrapolations on the basis of plausibility. Tarantini et al. (2009) showed, for the first time in humans, that reactive oxygen species (ROS)—which are considered one of the main cellular stressors generated by PM exposure—may produce genomic hypomethylation and increased expression and activity of inducible nitric oxide synthase (iNOS) not only in vitro, but in humans exposed to particulate matter (PM). Although this finding is expected, it is a step forward, based on DNA adduct generation produced by polycyclic aromatic hydrocarbons (PAHs) and other PM components, namely transition metals. Alterations of DNA methylation of the promoter is a common finding in environmental-related chronic or cancerous diseases. Alterations in DNA methylation and iNOS methylation, as observed by Tarantini et al. (2009) in association with exposure to PM < 10 μm in aerodynamic diameter, may represent an initial step in reproducing decreases in global DNA methylation content that are eventually observed in cardiovascular diseases and cancer. However, pathologists and pathophysiologists are required to interpret more correctly what this means. Subjects with inherited multi tumoral syndromes have a germline mutation, usually a point mutation present in all cells of the body, which determines the occurrence of multiple tumors in the same individual. The occurrence of DNA adducts or mutations in some cells or tissues due to exposure to PAHs or diesel exhaust does not necessarily induce clinically evident outcomes in the future, because each individual is endowed with a wide variety of natural defenses and repair mechanisms that usually overcome every type of DNA damage. Therefore, the first inference to avoid is that DNA adduct formation or alterations in the promoter methylation of a gene causes cancer in the absence of inherited or acquired predisposition (i.e., a point germline mutation of a tumor suppressor gene or an acquired sporadic mutation). In addition, even in patients with inherited multitumoral syndromes (i.e., in subjects with germline mutations of suppressor genes), tumor occurrence (type and severity) is also greatly influenced by epigenetic factors, environmental stimuli, or even long-distance catastrophes. We previously demonstrated an increased incidence of papillary thyroid carcinoma in three members of the same familial adenomatous polyposis (FAP) family (i.e., a kindred having a 1061 APC gene mutation). This mutation is responsible for FAP, in part as a side effect (long-term–long-distance) after the Chernobyl disaster, thus suggesting a wider than expected impact of environmental disasters in predisposed subjects (Cetta et al. 1997, 2000). Analogously, chronic exposure to toxic or carcinogenic environmental substances does not elicit the same results in all individuals. The final clinical outcome (cancer, asthma, pulmonary fibrosis, atherosclerosis, or coronary diseases) seems to be less dependent on the toxic potency of the pollutant or of the exposure dose and more on the individual susceptibility of the host (Cetta 2009a, 2009b). This approach should facilitate a better understanding of the < 5% incidence of mesotheliomas in subjects with the same chronic exposure to asbestos, or the absence of health effects in husbands with chronic occupational exposure to asbestos but the occurrence of mesotheliomas in wives with minor indirect exposure from their husbands (Cetta F, unpublished data). However, acute and chronic inflammation is the first pathological step. The final clinical outcome (e.g. cancer) does not depend on the first DNA adduct formed or a genetic mutation produced by xenobiotics. A long, automaintaining process will start, such as in liver cirrhosis, leading to cancer or chronic alterations as the final result of the interactions between host and the pathogenic agent. This process is greatly influenced by individual susceptibility or resistance. In PM-related diseases, a major role—in addition to the intrinsic toxicity of the xenobiotic—is played by individual host susceptibility and reactivity, similar to what occurs in auto immune or autoinflammatory diseases.

The effect of air pollution on asthma and allergy

Air pollution exposure is associated with increased asthma and allergy morbidity and is a suspected contributor to the increasing prevalence of allergic conditions. Observational studies continue to strengthen the association between air pollution and allergic respiratory disease, whereas recent mechanistic studies have defined the prominent role of oxidative stress in the proallergic immunologic effects of particulate and gaseous pollutants. The identification of common genetic polymorphisms in key cytoprotective responses to oxidative stress has highlighted the importance of individual host susceptibility to pollutant-induced inflammation. Future therapy to reduce the adverse effects of air pollution on allergic respiratory disease will likely depend on targeting susceptible populations for treatment that reduces oxidative stress, potentially through enhancement of phase 2 enzymes or other antioxidant defenses.

Influence of polymorphism of glutathione S-transferase T1 on Chinese infertile patients with varicocele

To investigate the influence of glutathione S-transferase T1 (GSTT1) gene polymorphism on Chinese infertile patients with varicocele, 63 infertile patients with varicocele and 54 healthy fertile controls were recruited in this case-control study. Our results show that oxidative damage may be the cause of infertility in patients with varicocele, and GSTT1 null genotype predisposes to over oxidative damage to spermatocytes of infertile patients with varicocele.

TEMPORAL AND SPATIAL CHARACTERIZATION OF AN INFESTATION OF PARATACHARDINA LOBATA LOBATA (HEMIPTERA: KERRIIDAE), A NEW INVASIVE PEST IN FLORIDA

The lobate lac scale, Paratachardina lobata lobata (Chamberlin) was first found in south Florida in 1999. Reported hosts are present in the germplasm collection located at the USDA/ARS Subtropical Horticulture Research Station in Miami, and the scale was first found there in the summer of 2002. A study was initiated to determine the spatio-temporal dynamics of a lobate lac scale infestation at SHRS from Jul 2003 to Jul 2005. Numbers and percentages of viable adults, and reproductive success as indicated by ratio of nymphs to viable adults (<2 cm diam and 30 cm long branch sample) were recorded. There were 55 plants evaluated over the ∼80 hectares study site. Infestation increased from 42% of sampled plants at the start of the study to 75% at the end, and most of the plants had low or moderate levels of infestation (between 0 and 100 adults per 30 cm branch) over the course of the study. Percentage of non-viable adults dropped from ∼27% at the start of the study to ∼7% by the end of the study, and ratio of nymphs to viable adults dropped from ∼9% to ∼2%. Spatial analysis showed that initial infestations were along the eastern edge of the sampled area, with populations declining over the first half of the study but then increasing during the second half. Over the course of the study, heavy infestations (≥100 scales per 30 cm branch) were found on only seven host plants. Among plants located in areas of high infestation probabilities, individual host susceptibility appeared to be the primary factor regulating infestation level.

Attaching-effacing Lesions Associated with Escherichia coli O157:H7 and Other Bacteria in Experimentally Infected Conventional Neonatal Goats

Four conventionally reared goats aged 6 days were inoculated orally with approximately 10(10) colony-forming units (cfu) of a non-verotoxigenic strain of Escherichia coli O157:H7. All remained clinically normal. Tissues were sampled under terminal anaesthesia at 24 (two animals), 48 and 72 h post-inoculation (hpi). E. coli O157:H7 was cultured from the ileum, caecum, colon and rectum of all animals, but the number of bacteria recovered at these sites varied between animals. Attaching-effacing (AE) lesions associated with O157 organisms, as confirmed by immunolabelling, were observed in the ileum of one of the two animals examined at 24 hpi, and in the ileum, caecum and proximal colon of an animal examined at 72 hpi. E. coli O157 organisms were detected at > or =10(5) cfu/g of tissue at these sites. In addition, AE lesions associated with unidentified bacteria were observed at various sites in the large bowel of the same animals. Lesions containing both E. coli O157 and unidentified bacteria (non-O157) were not observed. Non-O157 AE lesions were also observed in the large bowel of one of two uninoculated control animals. This indicated that three (one control and two inoculated) animals were colonized with an unidentified AE organism before the commencement of the experiment. The O157-associated AE lesions were observed only in animals colonized by non-O157 AE organisms and this raises questions about individual host susceptibility to AE lesions and whether non-O157 AE organisms influence colonization by E. coli O157.

Characterization of a North American orf virus isolated from a goat with persistent, proliferative dermatitis

The characterization of an orf virus (OV) isolated from skin lesions of a goat kid with severe, persistent, proliferative dermatitis, and designated orf virus-San Angelo 2000 (OV-SA00) strain, is described. The identity of OV-SA00 was confirmed by a combination of methods, including electron microscopy, amplification of specific fragments of viral DNA by polymerase chain reaction, restriction enzyme analysis of viral DNA and gene sequencing. Restriction endonuclease analyses of viral DNA and the protein profile studied by Western blot revealed differences between OV-SA00 strain and the profiles of other OV strains that have been published. The restriction enzyme profile of OV-SA00 was also different from the orf virus vaccine (OV-V) strain used to vaccinate this kid. Comparison of the nucleotide and deduced amino acid sequences indicated that OV-SA00 is closely related to OV-V strain, the Scottish OV strains orf11 and MRI Scab, and the human OV-CE/Shoe strain and more distant to bovine papular stomatitis virus (BPSV) reference strain and the pseudocowpox virus (PCPV)-MNV/Till strain. These results indicate that OV-SA00 is a strain of OV rather than a different parapoxvirus. Further studies are necessary to determine if the severity of orf-induced lesions in this goat kid was the result of individual host susceptibility factors.

Past attacks influence host selection by the solitary bark beetle Dendroctonus micans

Summary1. A spatio‐temporal study of host selection and local spread of a solitary bark beetle attacking live spruce Dendroctonus micans (Kugelann) was carried out using a combination of standard statistical methods, geostatistical analyses, and modelling. The study was based on data from three plots (150–300 trees, 0.3–1 ha) from 1978 to 1993. All trees were mapped and successful and abortive bark‐beetle attacks on each tree were counted annually. Because the attacked trees usually survived, temporal attack patterns as well as spatial patterns could be analysed.2. The distribution of successful insect attacks on the trees was slightly aggregative, indicating some degree of choice rather than totally random establishment.3. The level of yearly individual attacks per tree was very stable, suggesting that D. micans usually leave the host in which they develop.4. The attacked trees were distributed randomly in the plots; at the study's spatial scale, the insects dispersed freely throughout the plot (no spatial dependence).5. On the other hand, time dependence was strong; some trees were attacked repeatedly while others were left untouched.6. Among a choice of scenarios (random attack, fixed variability in individual host susceptibility, induced host susceptibility following random attack), the best fit was obtained with the model involving induced individual host susceptibility. This type of relation to the host tree contrasts strongly with patterns generally described in host–plant relationships (including gregarious, tree‐killing bark beetles), where local herbivore damage results in induced resistance.7. These results suggest that the first attacks in a new stand are made at random, that all or most of the beetles emerging from a tree disperse and resample the stand, and that they settle preferentially on trees that were colonised successfully by previous generations.

Risk factors for false-positive serological reactions for bovine brucellosis in Saône-et-Loire (France)

Since 1990, unusually high rates of false-positive serological reactions (FPSR) in bovine brucellosis screening have been observed in some countries of the European Union. The aim of this survey was to describe this phenomenon in a highly affected French Department, and to evaluate the links between some individual or herd factors and the occurrence of these FPSR. Before 1990, low backgrounds of FPSR were recorded (individual prevalence rate: less than 0.5 per 10 000). The phenomenon burst during the 1990–91 screening campaign, reached a peak in 1992–93 (50.5 per 10 000), and then decreased until the last studied campaign, 1995–96 (9.1 per 10 000). The phenomenon was transient and sporadic within a herd. At the herd-screening level, four assumed risk factors were isolated: (i) the probability of a herd-screening to be positive was closely and positively linked with the herd screening size; (ii) during a given screening campaign, the prevalence of FPSR decreased from December to November; (iii) the presence of at least one goat on the premises increased the risk for the 1992–93 and 1993–94 screening campaigns; and (iv) a previous FPSR in a given herd appeared to be a weak but significant risk factor. At the individual-animal level, herd size, sex and breed did not seem to be linked with FPSR appearance, while young animals were significantly more affected than older ones. However, global variations in herd or individual prevalences remained unexplained. The lack of link between FPSR and brucellosis is strengthened. The hypothesis of a widely spread causal agent with a low individual host susceptibility and/or a low probability of detecting FPSR animals can be supported by these results.

New Environmental Agents Associated With Lupus-Like Disorders

An increasing number of environmental agents are being investigated as possible risk factors in the etiology of certain connective tissue disorders. Exposure to a variety of therapeutic agents, foods and dietary supplements, occupational and other toxic exposures, and infectious agents has been associated with the onset of lupus-like disorders. The mechanisms by which these agents might induce lupus remain unknown but may involve alteration of cellular components or activation of the immune system. Individual host susceptibility factors, including pre-existing organ dysfunction and particular metabolic enzyme or immunogenetic phenotypes, may also be important risk factors for development of environmentally-associated lupus-like disorders. Awareness of the many environmental agents implicated with lupus and related disorders, and dissection of their pathogenetic mechanisms through appropriate case-controlled investigations, may identify additional toxic agents and may lead to a better understanding of the idiopathic lupus syndromes.

Noninfectious environmental agents associated with myopathies.

Increasing attention is being focused on environmental agents as possible factors in the etiology of certain connective tissue disorders. As our awareness in this area increases, the number and diversity of these agents is expanding yearly and now includes, in addition to infectious agents, a variety of foods and dietary supplements, drugs, occupational and other toxic exposures, biologics, and medical devices. Some of these agents have been associated with the development of muscle disease through mechanisms that involve alterations in the vascular supply to muscle, depletion of electrolytes, direct toxic effects on mitochondria or other metabolic processes, or activation of the immune system. Individual host susceptibility factors, including preexisting organ dysfunction and particular metabolizer or immunogenetic phenotypes, also appear to be important for development of the clinical syndromes identified as environmentally associated myopathies. Although data in this area are limited, they suggest that when susceptible individuals are exposed to selected agents, physiologic alterations occur that lead to myopathy. Physician awareness of chemicals implicated with myopathy and dissection of their pathogenetic mechanisms through human and animal studies may aid in the identification of additional toxic agents, minimize new cases in the future, and lead to a better understanding of the idiopathic myopathies.

Microbiology of recreational and therapeutic whirlpools

AbstractOver half of the reported outbreaks of whirlpool‐associated dermatitis and folliculitis have been caused by Pseudomonas aeruginosa, serotype 011. Illness caused by Staphylococcus aureus, Legionella pneumophila, Mycobacterium, Streptococci, and Acanthamoeba have been infrequently reported. The presence of microorganisms in water is not the only factor involved in infection transmission. Other factors in disease may be individual host susceptibility, immersion time, bather load, gender, and use of clothing. A bather's risk for P. aeruginosa dermatitis or folliculitis appears to depend on immersion in water colonized by P. aeruginosa, skin hydration with altered skin flora, and toxic reactions to extracellular enzymes or exotoxins produced by P. aeruginosa. Outbreaks of illness appear to be directly related to inadequate operational and maintenance procedures. Chemical and physical parameters should be routinely monitored. Microbiologic sampling of whirlpool water is not advised except in outbreak investigations.

Drosophila parasitoid–host interactions: vibrotaxis and ovipositor searching from the host's perspective

Two strains of Drosophila differing in host movement were simultaneously offered to a female parasitoid of either Leptopilina heterotoma or Asobara tabida. The number of encounters with the moving and nonmoving host strains was independent of larval movement forL. heterotoma whereas a highly significant effect of movement was found for A. tabida. This increased encounter rate of A. tabida with moving larvae resulted from the interaction of this parasitoid's searching strategy (vibrotaxis) and the polymorphic behaviour of the hosts. We conclude that differences in searching mode of two parasitoids of Drosophila larvae, A. tabida and L. heterotoma, can influence individual host susceptibility.