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PubMed1977

Feline Panleukopenia. I. Pathogenesis in germfree and specific pathogen-free cats.

Germfree and specific pathogen-free cats were inoculated panleukopenia vivus. Total leucocyte counts decreased significantly in both germfree and specific pathogen-free cats. Clinical illness was not seen in any germfree cat. Specific pathogen-free cats had anorexia and slight diarrhea 5-6 days after inoculation. None of the cats died. Both germfree and specific pathogen-free cats had thymic involution. No other gross lesions were seen. Tissues for histological virus isolation and immunofluorescence studies were taken daily from days 2 through 6 after inoculation. Virus-infected cells and lesions of panleukopenia were seen in the small intestine of both germfree and specific pathogen-free cats. The incidence of virus-infected cells and lesions was greater in specific pathogen-free cats than in germfree cats.

Animals↗

PubMed2005

Interference between mild and pathogenic strains of infectious bursal disease virus in chickens.

Infectious bursal disease virus is a contagious, immunosuppressive disease of young chickens that is controlled by vaccination. Cross-protection occurs between different strains of the virus as a result of shared neutralizing epitopes. However, interactions between two antigenically similar strains (a mild and a pathogenic) coinfecting the same host have not been investigated. Groups of specific-pathogen-free chickens were inoculated with a mild strain followed by a pathogenic strain at 0, 16, 24, or 48 hr postinoculation (PI) with a mild strain. Virus persistence and the predominant strain of the virus were determined by reverse transcriptase-polymerase chain reaction and restriction fragment length polymorphism analysis, respectively, in bursas at 2, 4, 8, 14, and 21 days PI with the pathogenic strain. Severity of infection was assessed by the bursa/body weight ratios and histopathologic lesion scores. The mild virus interfered with replication of the pathogenic virus. The greatest interference was observed when the pathogenic strain was inoculated 24 hr PI with the mild strain. The interference phenomenon observed might be due to competition for host receptor sites or production of cytokine(s). This interference phenomenon could have practical implications for vaccine usage and protection.

Animals↗

PubMed2026

Systematic review on genomic insights into antimicrobial resistance in ESKAPE pathogens.

BACKGROUND: Antimicrobial resistance (AMR) is a major global public health threat. ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp.) pose a major threat owing to resistance to last-line antibiotics. Genomic surveillance is crucial to understanding global and regional antimicrobial resistance genes (ARGs) in AMR transmission. AIM: This systematic review synthesised global genomic evidence to identify global and region-specific ARGs distribution among ESKAPE pathogens. METHODS: Following PRISMA guidelines, studies published January 2019 to December 2024 were identified from PubMed, Google Scholar, and Web of Science. Eligible studies reported genomic characteristics and resistance patterns of one or more ESKAPE pathogens from any source. RESULTS: Seventy-seven studies were included, with most originating from Asia, followed by Europe and Africa. Clinical isolates predominated K. pneumoniae was the most frequently investigated pathogen, followed by S. aureus, P. aeruginosa, and A. baumannii. The most reported resistance genes were blaCTX-M, blaNDM, and blaSHV. Distinct regional patterns of antimicrobial resistance gene (ARG) distribution were observed, with tetracycline and quinolone resistance genes prevailing in Africa and South America, and blaOXA variants dominating in Asia and Europe. Region-specific ARG patterns were identified through descriptive synthesis and comparative analysis of study-reported frequencies. CONCLUSION: This review provides a synthesised global map of ARG distribution in ESKAPE pathogens, highlighting surveillance gaps in underrepresented regions and non-clinical settings. Addressing these gaps will support targeted genomic surveillance and stewardship programmes. WHAT THIS STUDY ADDS: This study contributes to the body of knowledge by mapping global and regional antimicrobial resistance gene patterns in ESKAPE pathogens, identifying key surveillance gaps and informing targeted AMR monitoring and stewardship strategies.

ESKAPE pathogens↗

PubMed2001

A simple transport system for radiation treatment of specific pathogen-free mice in lifetime studies.

To prevent the introduction of pathogens, specific pathogen-free (SPF) facilities generally have a "once out, never back" policy with respect to animals and materials. In a lifetime study of the long-term effects of ionizing radiation exposure in mice, large numbers of SPF mice needed to be transported from clean-animal barrier labs to a multiuser conventional building for radiation treatment and then back into the animal facility. The conventional building is known to harbor wild mice as well as insects, spiders, and mites, and this situation might potentiate the transfer of wild mouse pathogens to laboratory animals. Introduction of pathogens into the mouse population would jeopardize the entire study, but the radiation treatments were an essential component of the study. These considerations prompted development of a system for transporting individual animals out of and back into the facility without exposure to pathogens. The system consists of reusable transport/treatment vessels and transport protocols designed to minimize the potential for pathogen exposure.

Animals↗

PubMedDate not supplied

Assessing pathogenicity potential of waterfowl-origin type A influenza viruses in chickens.

Intravenous pathogenicity index (IVPI) tests on 29 wild duck-origin type A influenza viruses, two turkey-origin type A influenza viruses, and one chicken-origin type A influenza virus resulted in indices ranging from 0.0 to 0.49. Most of the wild duck-origin viruses and the two turkey-origin viruses had indices of 0.0, indicating they are not pathogenic. Six of the duck-origin viruses had indices ranging from 0.25 to 0.49, and the IVPI for A/chicken/Alabama/75 (H4N8) was 0.49, indicating they had low pathogenic potential. An IVPI of 1.25 up to the maximum score of 3.0 is necessary for a type A influenza virus to be classified as highly pathogenic. Gross lesions observed in chickens dying following intravenous viral challenge included kidney swelling with more prominent lobular patterns, but visceral urate deposits were not present. The usefulness of the IVPI test in evaluating the pathogenicity potential of nonpathogenic and low-pathogenic strains of avian influenza virus may be limited.

Animals↗

PubMedDate not supplied

Differentiation of pathogenic and nonpathogenic Escherichia coli isolated from poultry.

Twenty-one isolates of Escherichia coli recovered from chickens and turkeys were evaluated for pathogenicity in 1-week-old chicks. Fifteen produced coli-septicemia (pathogenic) and six were innocuous (nonpathogenic). Both pathogenic and nonpathogenic E. coli were tested for their ability to selectively absorb Congo red (CR) dye incorporated into agar medium. Eight of 15 pathogenic E. coli (somatic antigen types O1, O78, O11, O88, and OX9) absorbed the dye and produced red colonies (CR+) between 48 to 72 hours of incubation. All serotypes of E. coli with homologous somatic antigen O78 were CR+, while those of O2 antigen were CR- (white colonies). Five of six nonpathogenic E. coli also were CR+. In contrast to pathogenic E. coli, however, nonpathogenic isolates absorbed CR early, between 18 to 24 hours of incubation. Although CR dye binding did not correlate well with pathogenicity, it may be an identifiable property of some serotypes of E. coli.

Animals↗

PubMedDate not supplied

In vitro and in vivo characterization of avian reoviruses. I. Pathogenicity and antigenic relatedness of several avian reovirus isolates.

Pathogenicity, pathogenesis, and antigenic relatedness of four avian reovirus isolates obtained from commercially reared broilers were investigated. Chickens of various ages were inoculated both orally and intratracheally with reovirus. Based on disease signs, mortality, weight depression, tissue lesions, invasiveness, and viral persistence in chickens inoculated at 1 day of age, the isolates were classified as being of low, intermediate, or high pathogenicity. The low-pathogenicity isolate (2177) did not cause mortality, weight depression, or clinical disease. The isolate of intermediate pathogenicity (2035) produced low mortality rates (8%), some weight reduction by 7 weeks postinoculation, and microscopic lesions in the intestine and gastrocnemius tendons. The pathogenic isolates, 2408 and 1733, caused severe clinical disease characterized by stunting, feathering abnormalities, mortality as high as 84%, and microscopic lesions in the liver, intestine, pancreas, and/or gastrocnemius tendon. Highly pathogenic isolates also persisted longer in tissues of infected birds and elicited a more prompt and prolonged antibody response. Birds inoculated at 1 day or 1 week of age were more susceptible to reovirus-induced disease than birds inoculated at 2 weeks, suggesting an age-associated resistance. All isolates produced mortality with equal frequency in embryos. The isolates characterized were found to be antigenically similar based on cross-neutralization and cross-protection studies.

Age Factors↗

PubMed2006

Periodontal infections and coronary heart disease: role of periodontal bacteria and importance of total pathogen burden in the Coronary Event and Periodontal Disease (CORODONT) study.

BACKGROUND: Chronic inflammation from any source is associated with increased cardiovascular risk. Periodontitis is a possible trigger of chronic inflammation. We investigated the possible association between periodontitis and coronary heart disease (CHD), focusing on microbiological aspects. METHODS: A total of 789 subjects (263 patients with angiographically confirmed, stable CHD and 526 population-based, age- and sex-matched controls without a history of CHD) were included in the Coronary Event and Periodontal Disease (CORODONT) study. Subgingival biofilm samples were analyzed for periodontal pathogens Actinobacillus actinomycetemcomitans, Tannerella forsythensis, Porphyromonas gingivalis, Prevotella intermedia, and Treponema denticola using DNA-DNA hybridization. The need for periodontal treatment in each subject was assessed using the Community Periodontal Index of Treatment Needs (CPITN). The main outcome measures included total periodontal pathogen burden, number of the various periodontal pathogens in the subgingival biofilm, and periodontal treatment needs (according to the CPITN). RESULTS: In multivariable analyses, we found a statistically significant association between the periodontal pathogen burden (log10 of the sum of all pathogens) (odds ratio [OR], 1.92; 95% confidence interval [CI], 1.34-2.74; P<.001) or the number of A actinomycetemcomitans in periodontal pockets (log10) (OR, 2.70; 95% CI, 1.79-4.07; P<.001) and the presence of CHD. In addition, a statistically significant association between an increase in mean CPITN score by 1 and the presence of CHD (OR, 1.67; 95% CI, 1.08-2.58; P = .02) was observed. CONCLUSIONS: Our findings suggest an association between periodontitis and presence of CHD. Periodontal pathogen burden, and particularly infection with A actinomycetemcomitans, may be of special importance.

Adult↗

PubMed2006

Mass spectrometry-based proteomics for the detection of plant pathogens.

Plant diseases caused by fungi, oomycetes, viruses, and bacteria are devastating both to the economy and to the food supply of a nation. Therefore, the development of new, rapid methods to identify these pathogens is a highly important area of research that is of international concern. MS-based proteomics has become a powerful and increasingly popular approach to not only identify these pathogens, but also to better understand their biology. However, there is a distinction between identifying a pathogen protein and identifying a pathogen based upon the detection of one of its proteins and this must be considered before the general application of MS for plant pathogen detection is made. There has been a recent push in the proteomics community to make data from large-scale proteomics experiments publicly available in the form of a centralized repository. Such a resource could enable the use of MS as a universal plant pathogen detection technology.

Bacterial Proteins↗

PubMed1994

The evolution of virulence in parasites and pathogens: reconciliation between two competing hypotheses.

According to conventional wisdom, parasites and pathogens should evolve reduced virulence to their hosts, because more virulent parasites and pathogens are more likely to drive their hosts, and themselves, to extinction. But this view has been criticized for its reliance on group selection. According to an alternative perspective, selection will favor whatever level of virulence maximizes the rate of increase of the parasite or pathogen. This optimum virulence depends on the functional relationship between a parasite or pathogen's transmissibility and its effect on host mortality, with selection often favoring an intermediate degree of virulence. The thesis of this paper is that models in which intermediate levels of virulence are favored lead quite naturally to the further conclusion that parasites and pathogens should-up to a point-become less virulent over time, once the feedbacks between ecological and evolutionary processes are incorporated into the analysis. As a consequence of successive adaptations by the parasite or pathogen, the density of susceptible hosts is reduced, thereby altering the balance between selective forces so as to favor reduced virulence. However, the evolutionarily stable strategy that is achieved is bounded away from complete avirulence. We conclude that models in which intermediate virulence is favored do not necessarily contradict the conventional wisdom in the long run; in fact, these models provide a simple mechanistic explanation for the evolution of reduced virulence.

Animals↗

PubMed2000

Number of triplets in 16S rRNA gene related with pathogenicity of Bacillus spp. and Clostridium spp.

The relation between the number of some trinucleotides in the sequence of 16S rRNA gene and pathogenicity of bacterial species from the genera of Bacillus and Clostridium was revealed. The species of genus Bacillus, which are pathogenic for humans, mammals and insects, have an increased number of AAA and TAT triplets in 16S rRNA gene. Theoretically, these species, B. anthracis and B. cereus for example, may be detected in the specimen by the higher ratio of AAA plus TAT triplets to the number of GGG triplet. Species of genus Clostridium, which are pathogenic for humans and mammals, have a maximum ratio of AAA and TAT triplet numbers. This ratio was higher than 2.6 for pathogenic species and lower than 2.2 for saprophytic ones. These theoretical data may open a new way for detecting pathogenic bacteria through the determination of triplet numbers in the sequences of 16S rRNA or rRNA. However, the mechanism of evolutionary relation between the number of AAA and TAT triplets in the sequence of 16S rRNA gene and the pathogenicity of bacterial species is not known.

Bacillus↗

PubMed1996

Enteric pathogens associated with gastrointestinal dysfunction in children with HIV infection.

Infants and young children with HIV infection commonly suffer from gastrointestinal manifestations of their disease. Many HIV infected children have evidence of persistent diarrhoea, malabsorption, malnutrition or growth failure. The aetiology and pathogenesis of gastrointestinal dysfunction in HIV infected children have not been well defined. We performed immunocytochemical analyses on intestinal tissue from 19 HIV-infected children with gastrointestinal dysfunction or growth failure. None of these 19 children had microbial pathogens identified in faecal samples using standard microbiological methods. Intestinal tissues were obtained from the children by biopsy and were examined for antigens from Pneumocystis carinii, cytomegalovirus (CMV) and herpes simplex virus (HSV) using the avidin-biotin-complex immunohistochemical technique and monoclonal or monospecific antibodies. We detected at least one of these pathogens in samples from eight (42%) of 19 HIV infected children. P. carinii was the most prevalent pathogen, found in five of the eight HIV infected children. All of the children with intestinal pneumocystis infection were receiving prophylaxis directed at the prevention of pulmonary disease with this organism and none of them were undergoing active pulmonary infection. We also identified CMV antigens in intestinal tissues from four children and HSV antigens in intestinal tissues from one child. Two children were infected with more than one pathogen. On the other hand, none of these pathogens were found in the tissues obtained from 10 HIV-uninfected patients who had intestinal tissues obtained for chronic non-infectious diarrheal and inflammatory diseases (P < 0.01, Fisher's exact test). Our findings indicate that some children with HIV infection and gastrointestinal dysfunction may be infected with opportunistic pathogens despite negative analyses employing standard microbiological methods. Our study also indicates that HIV infected children can undergo intestinal infection with P. carinii despite the administration of standard immunoprophylactic regimens directed at the prevention of infection with this organism.

AIDS-Related Opportunistic Infections↗

PubMed2002

Sequence-specific identification of 18 pathogenic microorganisms using microarray technology.

We have developed a Multi-Pathogen Identification (MPID) microarray for high confidence identification of eighteen pathogenic prokaryotes, eukaryotes and viruses. Analysis of amplified products from pathogen genomic DNA using microarray hybridization allows for highly specific and sensitive detection, and allows the discrimination between true amplification products and false positive amplification products that might be derived from primers annealing to non-target sequences. Species-specific primer sets were used to amplify multiple diagnostic regions unique to each individual pathogen. Amplified products were washed over the surface of the microarray, and labelled with phycoerythrin-streptavidin for fluorescence detection. A series of overlapping 20-mer oligonucleotide probes hybridize to the entire diagnostic region, while parallel hybridizations on the same surface allow simultaneous screening for all organisms. Comparison to probes that differ by a single mismatch at the central position reduced the contribution of non-specific hybridization. Samples containing individual pathogens were analyzed in separate experiments and the corresponding species-specific diagnostic regions were identified by fluorescence among their highly redundant probe sets. On average, 91% of the 53 660 pathogen probes on the MPID microarray performed as predicted. The limit of detection was found to be as little as 10 fg of B. anthracis DNA in samples that were amplified with six diagnostic primer-pairs. In contrast, PCR products were not observed at this concentration when identical samples were prepared and visualized by agarose gel electrophoresis.

Animals↗

PubMed1996

Human pathogeneic fungi and their close nonpathogenic relatives.

In order to understand the relationships between human pathogenic fungi and their close, nonpathogenic relatives, we compared small-subunit ribosomal DNA sequences among four closely related pathogens, Histoplasma capsulatum, Blastomyces dermatitidis, Trichophyton rubrum, and Coccidioides immitis, and seven nonpathogenic fungi expected on morphological grounds to be their nearest relatives. We sequenced small-subunit RNA genes from these fungi and used both genetic distance and parsimony algorithms to evaluate their evolutionary relationships to the pathogens. We show that the pathogens are not a monophyletic group, but rather are interspersed among nonpathogenic fungi; thus it is likely that pathogenicity has arisen multiple times within this group. The saprobic fungi Chrysosporium parvum and Uncinocarpus reesii are the closest known relatives of the highly pathogenic Blastomyces dermatitidis and Coccidioides immitis, respectively, and thus may be considered primary candidates for model systems for researchers studying these fungi. The branching order suggests that the conidium (asexual spore) types aleurioconidia and arthroconidia do not define monophyletic groups and may be less distinct than their names suggest. Fungi with a complete life cycle are shown to have closest relatives that lack a known sexual cycle. Such analyses offer a means by which the sexual and asexual fungi could be integrated into a single classification system.

Base Sequence↗

PubMed1996

The Dynamics of Insect-Pathogen Interactions in Seasonal Environments

Models of insect-pathogen interactions in highly seasonal environments are developed. The models apply to insects such as many temperate forest pests that have a single generation per year and which are susceptible to viral disease only during their larval period. The disease kills the hosts after a fixed time period when infectious pathogen particles are released into the environment. Depending on the time taken to kill the host, one to many cycles of pathogen replication may occur during the portion of the year when susceptible hosts are present. A baseline model with linear disease transmission is always unstable although a stable equilibrium can be achieved if there is sufficient density dependence in the transmission process. Persistent, long-period cycles are virtually never observed. The release of pathogen particles prior to host death contributes towards stability although it does not result in limit cycles. Long-period cycles were found in two other extensions of the baseline model, one in which some hosts carry a sublethal infection which is transmitted to their offspring; and a second which includes a reservoir where pathogen particles are relatively long lived although unable to cause new infections. The relationship between this work and previous host-pathogen and host-parasitoid models is discussed.

Journal Article↗

PubMed2000

Characterization of the pathogenicity of members of the newly established H9N2 influenza virus lineages in Asia.

The reported transmission of avian H9N2 influenza viruses to humans and the isolation of these viruses from Hong Kong poultry markets lend urgency to studies of their ecology and pathogenicity. We found that H9N2 viruses from North America differ from those of Asia. The North American viruses, which infect primarily domestic turkeys, replicated poorly in inoculated chickens. Phylogenetic analysis of the hemagglutinin and nucleoprotein genes indicated that the Asian H9N2 influenza viruses could be divided into three sublineages. Initial biological characterization of at least one virus from each lineage was done in animals. Early isolates of one lineage (A/Chicken/Beijing/1/94, H9N2) caused as high as 80% mortality rates in inoculated chickens, whereas all other strains were nonpathogenic. Sequence analysis showed that some isolates, including the pathogenic isolate, had one additional basic amino acid (A-R/K-S-S-R-) at the hemagglutinin cleavage site. Later isolates of the same lineage (A/Chicken/Hong Kong/G9/97, H9N2) that contains the PB1 and PB2 genes similar to Hong Kong/97 H5N1 viruses replicated in chickens, ducks, mice, and pigs but were pathogenic only in mice. A/Quail/Hong Kong/G1/97 (H9N2), from a second lineage that possesses the replicative complex similar to Hong Kong/97 H5N1 virus, replicated in chickens and ducks without producing disease signs, was pathogenic in mice, and spread to the brain without adaptation. Examples of the third Asian H9N2 sublineage (A/Chicken/Korea/323/96, Duck/Hong Kong/Y439/97) replicated in chickens, ducks, and mice without producing disease signs. The available evidence supports the notion of differences in pathogenicity of H9N2 viruses in the different lineages and suggests that viruses possessing genome segments similar to 1997 H5N1-like viruses are potentially pathogenic in mammals.

Animals↗

PubMed2007

Biological robustness in complex host-pathogen systems.

Infectious diseases are still the number one killer of human beings. Even in developed countries, infectious diseases continue to be a major health threat. This article explores a conceptual framework for understanding infectious diseases in the context of the complex dynamics between microbe and host, and explores theoretical strategies for anti-infectives. The central pillar of this conceptual framework is that biological robustness is a fundamental property of systems that is closely interlinked with the evolution of symbiotic host-pathogen systems. There are specific architectural features of such robust yet evolvable systems and interpretable trade-offs between robustness, fragility, resource demands, and performance. This concept applies equally to both microbes and host. Pathogens have evolved to exploit the host using various strategies as well as effective escape mechanisms. Modular pathogenicity islands (PAI) derived from horizontal gene transfer, highly variable surface molecules, and a range of other countermeasures enhance the robustness of a pathogen against attacks from the host immune system. The host has likewise evolved complex defensive mechanisms to protect itself against pathogenic threats, but the host immune system includes several trade-offs that can be exploited by pathogens and induces undesirable inflammatory reactions. Due to the complexity of the dynamics emerging from the interactions of multiple microbes and a host, effective counter-measures require an in-depth understanding of system dynamics as well as detailed molecular mechanisms of the processes that are involved.

Adaptation, Biological↗

PubMed1994

Molecular communication between host plant and the fungal tomato pathogen Cladosporium fulvum.

Host genotype specificity in interactions between biotrophic fungal pathogens and plants in most cases complies with the gene-for-gene model. Success or failure of infection is determined by absence or presence of complementary genes, avirulence and resistance genes, in the pathogen and the host plant, respectively. Resistance, expressed by the induction of a hypersensitive response followed by other defence responses in the host, is envisaged to be based on recognition of the pathogen, mediated through direct interaction between products of avirulence genes of the pathogen (the so-called race-specific elicitors) and receptors in the host plant, the putative products of resistance genes. The interaction between the biotrophic fungus Cladosporium fulvum and its only host tomato is a model system to study fungus-plant gene-for-gene relationships. Here we report on isolation, characterization and biological function of putative pathogenicity factors ECP1 and ECP2 and the race-specific elicitors AVR4 and AVR9 of C. fulvum and cloning and regulation of their encoding genes. Disruption of ecp1 and ecp2 genes has no clear effect on pathogenicity of C. fulvum. Disruption of the avr9 gene, which codes for the race-specific 28 amino acid AVR9 elicitor, in wild type avirulent races, leads to virulence on tomato genotypes carrying the complementary resistance gene Cf9. The avirulence gene avr4 encodes a 105 amino acid race-specific elicitor. A single basepair change in the avirulence gene avr4 leads to virulence on tomato genotypes carrying the Cf4 resistance gene.

Cladosporium↗