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PubMed2006

[Free-living amoebae as vehicles of pathogenic bacteria].

The free-living amoebae are ubiquitous organisms. They are found in humid soil and all water reservoirs, i.e. fresh, sea, freezing and hot water. They mainly feed on bacteria. Pathogenic properties of amoebae and the mechanisms underlying pathological changes induced during human infection have not yet been fully elucidated. They are the causative agents of primary amoebic meningo-encephalitis (PAM), granulomatous amebic encephalitis (GAE), a chronic progressive disease of the central nervous system, amebic keratitis (AK), a chronic eye infection; amebic pneumitis (AP), a chronic lung infection, and skin infection. Only a few isolates are strongly and permanently pathogenic to humans. Some isolates lose their pathogenic properties after one passage. It has been assumed that such "temporary", unstable pathogenic properties of the amoebae may be caused by internal factors carried by them. It is generally known that the free-living amoebae may be naturally infected with pathogenic bacteria, which have the ability to survive for a long time and to proliferate in the amoebae cells. The role of the amoeba in the process of maintaining, propagating and transmitting human pathogens has not been well recognized. It has been suggested that some infections can be acquired by inhaling aerosols containing amoebae cells filled with bacteria. The presence of bacteria inside the free-living amoebae possess a great challenge to organisations responsible for testing and inspecting the quality and cleanliness of surface waters, swimming pools and drinking water intakes.

Acanthamoeba↗

PubMedDate not supplied

[Pathogenic mutation or polymorphism? (How to find criteria)].

The classification of amino-acid substitutions into pathogenic mutations and harmless polymorphisms should be revised. In the recent years it was shown that some amino-acid substitutions considered as pathogenic mutations were polymorphisms. Similarly, some 'harmless' polymorphisms have been shown to be pathogenic mutations. Functional analysis considered as a good method to estimate the pathogenic nature of mutations is also limited. The selection of DNA samples for the control group is also difficult. Due to the molecular mechanism mediated by recently discovered exonic splicing enhancers and silencers (ESE and ESS) it is hard to predict a pathogenic effect of some mutations. In addition, the phenotype variability observed between unrelated patients harboring the same mutation may reflect the effects of modifying genes as well as the lack of association between mutation and "its" phenotype. The aim of this study is to describe the problem of the pathogenic effect of mutations.

Alternative Splicing↗

PubMed2006

Duplex PCR-hybridization based detection of pathogenic Leptospira in environmental water samples obtained from endemic areas in northeast region of Thailand.

Leptospirosis, a major health problem worldwide, is known to be endemic in the northeastern part of Thailand with the risk of infection by exposure to pathogenic Leptospira in contaminated aquatic environment. A method based on PCR-hybridization detection of pathogenic Leptospira in water was established. The method included filtration of water sample through membrane filters of two pore sizes, DNA extraction from filters using a guanidine thiocyanate extraction method, a duplex-PCR assay with two primer pairs, and hybridization with a synthetic LipL32 DNA probe. The duplex-PCR allowed detection of two products of 279 bp for LipL32 gene and 430 bp for 16S rRNA gene. In water samples artificially seeded with serovar bratislava, at least 10(3) cells could be analyzed by PCR-agarose gel electrophoresis and 1-10 cells by PCR-Southern blot hybridization. The protocol was applied to the detection of pathogenic Leptospira in environmental waters collected from endemic areas in the northeast region of Thailand. Of 100 water samples analyzed, 23 samples were positive for pathogenic Leptospira with PCR performed with Southern blot hybridization only, but none was detected by PCR-agarose gel-electrophoresis. However, PCR performed with the chemiluminescent LipL32 probe using the Fluorescein ULS labeling facilitated the detection of low numbers of pathogenic Leptospira in water. This method should prove useful for monitoring of pathogenic Leptospira pollution in environmental waters, and has the potential to become a valuable tool to the surveillance of leptospirosis in endemic areas, thus leading to enhanced public health protection.

Animals↗

PubMed2006

Development of a duplex-polymerase chain reaction for rapid detection of pathogenic Leptospira.

A duplex-polymerase chain reaction (PCR) for the rapid detection of pathogenic leptospires was developed by using two sets of newly designed primers which amplified in the same reaction two different DNA fragments simultaneously: 279-bp of LipL32 and 430-bp of 16S rRNA. For DNA extraction from bacterial cultures, the silica-based spin column method was found to be more suitable and was selected for the extraction of DNAs from all 92 bacterial strains including 56 strains of pathogenic Leptospira, 15 strains of non-pathogenic Leptospira and 21 other strains of bacteria. The PCR products were analyzed by agarose gel-electrophoresis with confirmation by Southern and dot hybridization using synthetic DNA probe prepared from LipL32 gene of a pathogenic reference strain, L. interrogans serovar pyrogenes. The duplex-PCR allowed detection of two products of 279 bp and 430 bp in all pathogenic Leptospira. Non-pathogenic Leptospira generated a single product of 430 bp. Other bacterial strains failed to reveal any amplification products. As little as 1 pg of pure DNA corresponding to 100 cells could be detected by agarose gel-electrophoresis, and 1-10 fg of pure DNA by hybridization.

DNA Probes↗

PubMedDate not supplied

In vitro biological differences between the pathogenic and the apathogenic Marek's disease herpesvirus.

When three pathogenic and four apathogenic isolants of Marek's disease herpesvirus (MDHV) were compared, the pathogenic isolants differed from the apathogenic isolants in their in vitro growth and sensitivity to plaque inhibition by dextran sulfate. Plaques by the pathogenic MDHV isolants were distinctively different in their morphology from those by the apathogenic isolants, the plaque difference being most pronounced in chick embryo fibroblase (CEF) and duck embryo fibroblast (DEF) cell cultures. The pathogenic isolants formed plaques similarly in both CEF and DEF cultures, whereas the apathogenic isolants did so readily in CEF cultures, but very poorly in DEF cultures. The pathogenic isolants replicated better in DEF than in CEF cultures, whereas the apathogenic isolants replicated better in CEF than in DEF cultures. The sensitivitty to plaque inhibition by dextran sulfate was greater for the apathogenic isolants than for the pathogenic isolants of MDHV.

Animals↗

PubMed1990

A herpes simplex type 1 ICPO deletion mutant demonstrates diminished pathogenicity during acute ocular infection in different host animals.

We compared a previously characterized herpes simplex type 1 alpha 0 deletion mutant, dlx3.1, which produced no functional ICP0, with its wild-type parental strain, KOS, during acute ocular infection of different host animals. Acute pathogenicity of the viral strains in NZ rabbits, Balb/c and A/J mice was evaluated by keratitis scores, ocular and trigeminal ganglionic viral titers, and host survival. We found that dlx3.1 was significantly less pathogenic than KOS. Host differences proved very important in the evaluation of acute pathogenicity. A species-dependent enhancement of ocular pathogenicity was demonstrated for dlx3.1 following a larger viral inoculum and host immunosuppression. We conclude that alpha 0 gene function appears to play an important role during acute ocular pathogenicity of HSV-1 in animal models. Furthermore, in vivo pathogenicity studies contribute important information in the evaluation of essential viral gene function.

Acute Disease↗

PubMed1987

A longitudinal study of asymptomatic carriers of pathogenic zymodemes of Entamoeba histolytica.

The value of treating subjects who pass Entamoeba histolytica cysts in their faeces is currently in question. In the endemic Durban area iso-enzyme electrophoresis of E. histolytica isolates indicated that 1% of the asymptomatic population are infected with pathogenic zymodemes. The outcome of these potentially invasive infections was established by means of a longitudinal survey. All subjects had strongly positive serological responses--10% of them developed amoebic colitis while the rest remained asymptomatic and spontaneous cure occurred within 1 year. Infections with pathogenic zymodemes occurred in family units and closely related individuals. Since they were cyst passers, good evidence was obtained for the existence of a carrier state for pathogenic E. histolytica. The value of sero-epidemiological surveys in determining the prevalence of pathogenic E. histolytica in a community was highlighted. Treatment of asymptomatic carriers with pathogenic zymodemes of E. histolytica is as essential as treatment of patients with invasive amoebiasis, and in both cases all contacts of affected individuals must also be treated if they are found to harbour pathogenic zymodemes of E. histolytica in order to ensure control of disease transmission.

Adolescent↗

PubMed1988

[Pathogen spectrum in suppurative meningitis with special reference to a patient sample].

In a five years period (1982 till 1986) the spectrum of pathogenic bacteria and fungi in acute meningitis was analysed. The appearance, spreading and suspected spectrum of pathogens have to be followed by special aspects considering effective therapeutic proceedings. 361 out of 392 positive cerebrospinal fluids (92.1%) were derived from only 3 (neurosurgical, neurological and pediatric department) out of 14 possible departments. Whereas in the pediatric department the classical pathogens of acute meningitis predominated, the patients in the neurosurgical department mainly showed nosocomial infections. There has to be considered the accidental infection, especially in the severely ill patients of the neurosurgical intensive care unit, which favours highly resistant pathogens. Furthermore, to initiate an infection, the pathogenicity of nosocomial microorganisms is not required to be high. The correlation of clinical signs and the proof of pathogens showed that often so called contaminants could be of higher value to be the infectious agent as assumed. Nevertheless, there seemed to be a regression of acute meningitis due to better diagnostic and therapeutic proceedings.

Adolescent↗

PubMed1982

An alternative role for specific antibody in neutrophil bactericidal activity against highly pathogenic group B streptococci.

An investigation was undertaken into the role of antibody and complement in neutrophil phagocytosis and killing of group B streptococci of low and high pathogenicity. Phagocytosis of both types of organism appears to be a nonspecific event requiring only nonspecific antibody or complement. However, neutrophil bactericidal activity is mediated by the pathogenicity of the infecting organism. Neutrophils alone can kill some streptococci of low pathogenicity, but their killing ability is considerably increased in the presence of specific antibody or complement. An active role for the alternative pathway of complement in the killing process was demonstrated for organisms of low pathogenicity. Neutrophils did not kill the highly pathogenic organisms in the absence of antibody and complement, and required specific antibody, but not complement, to kill these bacteria. The alternative complement pathway is not involved in killing of highly pathogenic organisms. Addition of specific antibody to neutrophils containing ingested bacteria stimulated the neutrophils to kill the intracellular bacteria, suggesting an alternative role for specific antibody in the killing process other than as an opsonin. It is suggested that activation of Fc receptors on the neutrophil surface initiates the bactericidal action of the neutrophils.

Animals↗

PubMed1994

Acquisition of pathogenicity of a Newcastle disease virus isolated from a Japanese quail by intracerebral passage in chickens.

Newcastle disease virus (NDV) was isolated from a Japanese quail (Cotornix cotornix japonica). The effect of intracerebral and intranasal passages of the NDV in chickens on the pathogenicity was studied. Pathogenicity of the viruses of different passage levels was compared with that of the original isolate by the mean death time with the minimum lethal dose in chicken embryos, intracerebral pathogenicity index in day-old chicks, intravenous pathogenicity index with 6-week-old chickens and the mortality rates of chickens and quails inoculated intravenously or intranasally. The original isolate from the quail did not kill chickens but only embryos and some one-day-old chicks, exhibiting a mesogenic character. Pathogenicity of the virus of the 10th intranasal passage was not different from that of the original isolate. The viruses passaged intracerebrally, on the other hand, killed chickens of all ages by either route of inoculation, showing a velogenic property. Virus recovery from the blood and the brain was positive only in the chickens infected with brain-passaged viruses by any route of inoculation. Virus titers in the tissues of chickens infected with the brain-passaged viruses were higher than those with the original isolate and the virus of the 10th intranasal passage. These results indicate that the enhanced pathogenicity of the mesogenic NDV isolate from the quail for chickens was induced by acquiring the properties of neurotropism and pantropism through intracerebral passage in chickens.

Animals↗

PubMedDate not supplied

Association between pathogenicity of infectious bursal disease virus and viral antigen distribution detected by immunohistochemistry.

Highly pathogenic infectious bursal disease virus (IBDV) strains (Ehime/91, DV86) and a moderately pathogenic strain (J1) were compared in order to clarify the association between the pathogenicity of IBDV and viral antigen distribution. Virus target cells in the bursa, thymus, spleen, and bone marrow were examined by transmission electron microscopy. Although all strains caused similar bursal atrophy, the highly pathogenic strains brought about a greater decrease in the thymic weight index and more severe lesions in the cecal tonsil, thymus, spleen, and bone marrow. Immunohistochemical detection of IBDV antigen in tissues from chickens infected with Ehime/91 and DV86 strains showed a higher frequency of antigen-positive cells in the spleen and bone marrow. Transmission electron microscopy indicated the presence of viral particles in the cytoplasm of epithelial reticular cells in the thymus and monocytes in the bone marrow. The results show that pathogenicity of field strains of IBDV correlates with lesion production in non-bursal lymphopoietic organs. The results also suggest that pathogenicity of IBDV may be associated with virus antigen distribution in non-bursal lymphopoietic organs.

Animals↗

PubMed1995

Immunoglobulin gene usage in the human anti-pathogen response.

The human antibody response to foreign pathogens is generated to a relatively small number of target surface proteins and carbohydrates that nonetheless have an extensive array of epitopes. The study of human monoclonal antibodies to different pathogens shows that there are a diversity of mechanisms used to generate a sufficient repertoire of antibodies to combat the invading pathogens. Although many different immunoglobulin gene elements are used to construct the anti-pathogen response, some elements are used more often than would be expected if all elements were used randomly. For example, the immune response to Haemophilus influenzae polysaccharide appears to be quite narrow, being restricted primarily to a specific heavy-chain gene, 3-15, and a lambda light-chain family II member, 4A. In contrast, for the immune response to cytomegalovirus proteins, a wider group of gene elements is needed. It is also surprising that despite an investigator bias for IgG- rather than IgM-secreting immortal B cells (because of their high affinity and neutralizing abilities), 26% of light chains and 13% of heavy chains showed a very low level of somatic mutation, equivalent to an IgM molecule that has not undergone affinity maturation. Although some highly mutated IgG molecules are present in the anti-pathogen response, most of the monoclonal antibodies specific for viruses or bacteria have a level of somatic hypermutation similar to that of the adult IgM repertoire. A number of studies have shown that there are similarities in the antibody responses to pathogens and to self (autoantibodies).(ABSTRACT TRUNCATED AT 250 WORDS)

Antibody Formation↗

PubMed1996

Mucosal immune responses to intestinal bacterial pathogens.

Current advances in the study of gut mucosal immunology and molecular biology have enhanced our ability to understand the pathogenesis of enteric bacterial infections as well as the role of the immune system in mediating both tissue injury and protection. In this article, we review the immunopathogenesis and the protective immune response to three enteric pathogens, Vibrio cholerae, Shigella, and Salmonella. Each of these pathogens has a distinctive mechanism by which it causes disease, ie, epithelial attachment, epithelial invasion, and epithelial invasion with systemic dissemination. Pathogenicity and immune response can be conceptualized in terms of the interaction of these enteric pathogens with the gut epithelial compartment, immune inductive sites (Peyer's patch of the small intestine and lymphoid follicles of the colon), and a common immune effector compartment in the laimina propria where protective antibody is secreted. V cholerae, the representative noninvasive pathogen, has fimbrial adhesins that mediate attachment and colonization of the luminal surface of epithelial cells where organisms secrete cholera toxin (CT), a potent enterotoxin that induces a voluminous diarrhea via adenylate cyclase-dependent chloride secretion. Protective immunity is based on secretory (s) immunoglobulin A directed against whole-cell components that prevent attachment to gut epithelial cells and is enhanced by CT, an immunogen with potent adjuvant activity. Shigella, an enteric pathogen that locally invades gut epithelium, subverts the usual mechanism of immune sampling by initially invading via M cells overlying inductive sites. Subsequent macrophage invasion induces apoptosis and the release of interleukin-1, a proinflammatory cytokine. This seems to be a critical initiating event in immune-mediated tissue injury. Protective immunity is serotype specific. Infection caused by Salmonella is characterized by mucosal invasion and systemic spread mediated by the organisms ability to survive within macrophages. Both antibody and cell-mediated immunity are important for protection against Salmonella.

Antibodies, Bacterial↗

PubMedDate not supplied

Comparative pathology of chickens experimentally inoculated with avian influenza viruses of low and high pathogenicity.

Pathologic changes and distribution of viral antigen as determined by immunohistochemistry were compared among 4-wk-old specific-pathogen-free chickens inoculated intratracheally with avian influenza virus (AIV) isolates of either low or high pathogenicity. Viruses of low pathogenicity, previously characterized as mildly pathogenic (MP), included A/chicken/Pennsylvania/21525/83 (H5N2) (MP-Penn) and A/chicken/Alabama/7395/75 (H4N8) (MP-Alab). Viruses of high pathogenicity included A/chicken/Pennsylvania/1370/83 (H5N2), A/chicken/Victoria/A185/85 (H7N7), and A/turkey/Ontario/7732/66 (H5N9). Extremely variable clinical signs ranging from mild respiratory distress to high mortality were present among chickens inoculated with these viruses. Chickens inoculated with highly pathogenic (HP) virus had histologic lesions of necrosis and inflammation in cloacal bursa, thymus, spleen, heart, pancreas, kidney, brain, trachea, lung, and skeletal muscle, whereas chickens inoculated with MP virus had histologic lesions most frequently in lung and trachea or lacked histologic lesions. Immunospecific staining for avian influenza viral proteins was most common in cells within heart, lung, kidney, brain, and pancreas of chicken inoculated with HP viruses, but immunospecific staining was present only and infrequently in trachea and lung of chickens inoculated with MP-Penn AIV. MP-Alab did not produce lesions nor have viral antigen in inoculated chickens but did produce serologic evidence of infection. The pattern of organ involvement and viral antigen distribution in chickens intratracheally inoculated with HP AIV isolates indicates a common capability to spread beyond the respiratory tract and confirms the pantrophic replicative, pathobiologic, and lethal nature of the viruses. However, variability in severity and lesion distribution exists between different HP AIVs. By contrast, MP viruses had the ability to replicate in respiratory or enteric tracts or both and produce lesions within the respiratory tract. These MP viruses exhibited a restricted ability to replicate or produce lesions or both in nonrespiratory or nonenteric tissues; such effects were associated with only sporadic deaths.

Animals↗

PubMed1997

Emerging pathogens for pneumonia in Singapore.

The death rate from pneumonia in Singapore has increased steadily over the past decade. The emerging respiratory pathogens may have contributed to this increased mortality. New challenges have arisen from changes in the characteristics of the host and the susceptibilities of the various pathogens to antibiotics. There has been a 60-fold increase in the incidence of penicillin resistance in Streptococcus pneumoniae, the major pathogen for community-acquired pneumonia (CAP). Gram-negative bacilli are the major pathogens in severe CAP with Klebsiella pneumonia being the most frequently isolated organism. There has been a small increase in the number of cases of Legionnaire's disease and a marked increase in the incidence of melioidosis. While the overall incidence of tuberculosis has been unchanged, the number of non-residents with tuberculosis has doubled in the past 5 years. The rising prevalence of human immunodeficiency Virus infection is reflected in an increasing number of apparently healthy young men who present with CAP caused by Pneumocystis carinii. There is increasing resistance to antibiotics among gram-negative bacilli and Staphylococcus aureus, the dominant pathogens in hospital-acquired pneumonia. New strategies are urgently needed to prevent the emergence of pathogens in the hospital environment which may be resistant to all known antibiotics.

AIDS-Related Opportunistic Infections↗

PubMed1998

Fate of transforming DNA in pathogenic fungi.

Genetic engineering is an important tool in helping us to define the molecular basis of pathogenicity and is also useful in helping us to identify new therapeutic targets in pathogenic fungi. Molecular genetic manipulation of micro-organisms requires the development of plasmid-mediated transformation systems that include: (i) infusion of exogenous DNA into recipient cells, (ii) expression of genes present on the incoming DNA, and (iii) stable maintenance and replication of the inserted DNA leading to expression of the desired phenotypic trait. Transformation systems have been developed for only a handful of fungi that are pathogenic to humans including several species of Candida, Cryptococcus neoformans, Histoplasma capsulatum, Blastomyces derrmatitidis, Aspergillus fumigatus, Wangiella dermatitidis (Exophiala dermatitidis) and Coccidioides immitis. Except for Candida species and A. fumigatus, where passage of exogenous DNA into recipient cells has been achieved readily using methods developed for transformation of Saccharomyces cerevisiae and Aspergillus nidulans, respectively, development of transformation systems in other pathogenic fungi has been delayed considerably and has only been possible recently with the introduction of electroporation and biolistic methods. Conventional spheroplasting methods or cell wall permeabilization methods using lithium acetate have not been successful for transformation of C. neoformans and work with only low efficiency in H. capsulatum. The fate of incoming DNA varies greatly in these pathogenic species regardless of their phylogenetic relationships. Understanding the fate of incoming DNA is critical for the construction of transforming vectors and the molecular manipulation of the organisms. In this symposium, recent advances in molecular genetic systems including transformation systems, the fate of incoming DNA and strategies for targeted integration are discussed in relation to four pathogenic fungi.

DNA, Fungal↗

PubMed2026

Tree Killer, Qu'est-ce Que C'est? Insights From Forest Pathogen Genomes.

Forests are central to planetary health but are increasingly challenged by emerging diseases driven by climate change, global trade, and anthropogenic disturbance. Despite the apparent resilience of long-lived, genetically diverse tree hosts, forest ecosystems have repeatedly experienced landscape-level pathogen-driven transformations. Advances in genomics, transcriptomics, and functional biology have transformed our understanding of how fungal and oomycete pathogens interact with their hosts across a continuum of lifestyles, from saprotrophy and necrotrophy to biotrophy. Here, we synthesize insights from comparative and population genomics and functional studies across diverse forest pathosystems to examine the traits that characterize successful tree pathogens. We highlight how lifestyle plasticity, adaptations to woody tissues, vector-mediated transmission, and biotrophic stealth enable pathogens to colonize perennial hosts and persist over long temporal scales. We further examine how genome plasticity, hybridization, and horizontal gene transfer generate adaptive potential that often outpaces host evolutionary responses under current environmental change. Finally, we discuss emerging genomic tools, including biosurveillance, machine learning-based classification, and genome editing, that are beginning to link genotype to phenotype and inform assessments of disease risk. By integrating genomic, ecological, and evolutionary perspectives, this review outlines general principles governing forest pathogen success and identifies priorities for future research aimed at improving understanding, early detection, and management of forest diseases in a changing world.

Trees↗

PubMed2025

Immune-mediated indirect interaction between gut microbiota and bacterial pathogens.

BACKGROUND: In many animals, survival during infection depends on the ability to coordinate interactions between the host immune system and gut microbiota. These tripartite interactions, in turn, potentially shape pathogen virulence evolution. A key regulator of the immune system and, hence, bipartite interactions in insects is the immune deficiency (Imd) pathway, which modulates gut microbiota and pathogens by synthesizing antimicrobial peptides (AMPs) through the NF-κB transcription factor Relish. However, whether Imd-dependent AMPs mediate indirect interactions between gut microbiota and pathogens in a tripartite context remains unclear. Using RNAi-mediated knockdown of Tenebrio molitor Relish (TmRelish), we hypothesized that Imd-dependent AMPs influence indirect interaction between Providencia burhodogranariea_B (P. b_B) infection and the gut microbiota. RESULTS: TmRelish knockdown altered bipartite interactions by disrupting gut microbiota load and composition, increasing pathogen load, and ultimately leading to higher host mortality during infection. However, we did not find support for our tripartite hypothesis that Imd-dependent AMPs mediate indirect interactions between the gut microbiota and P. b_B infection, suggesting the involvement of alternative regulatory pathways or Imd-independent mechanisms. Nevertheless, our investigations of tripartite interactions showed a positive effect of P. b_B infection on gut microbiota load, which in turn stimulated the expression of a subset of AMPs. However, this upregulation of AMPs did not result in reduced P. b_B load. Notably, the gut microbiota did not affect pathogen load but promoted host survival during P. b_B infection, indicating a role in increasing host tolerance rather than resistance. CONCLUSIONS: These findings suggest that while Imd-dependent AMPs may not mediate tripartite interactions in our system, microbiota-host interactions, such as microbiota-mediated immune priming and changes in microbiota load, can shape infection outcomes. These effects on infection outcomes almost certainly exert important selective pressures on the evolution of bacterial virulence.

Animals↗