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At least 433 records · Page 24Linked to original sources

Pathogenicity of hookworms. The significance of population regression for the pathogenicity of hookworms.

A method is described to estimate the reduction of the hookworm population in the host during the infection period (population regression). A formula is proposed to estimate the average worm population during the infection period, on the assumption that a decreasing hookworm population causes a decrease in daily blood loss. Daily blood loss per worm was calculated for Ancylostoma caninum: 43 microliters; for A. ceylanicum: 14 microliters for A. braziliense: 5 microliters. Accordingly hookworms cause blood loss one half to two thirds smaller than formerly assumed.

Ancylostoma↗

Prophylactic effect of tea on pathogenic micro-organism infection to human and animals. (1). Growth inhibitive and bacteriocidal effect of tea on food poisoning and other pathogenic enterobacterium in vitro.

0.5% tea powder of Oolong tea, green tea and black tea, respectively added to Tryptic soy agar (TSA) plates prepared non aseptically could inhibit the growth of colonies of St. aureus and airborne bacteria, but only very few fungi colonies. 0.5% tea powder of oolong tea, green tea and black tea, respectively added to Tryptic soy agar (TSA) plates prepared non aseptically could also inhibit the colonial growth of V. cholerae, V. parahaemorrhagiae, Sal. dysenteriae, Sal. typhi, Sal. paratyphi A and B. The suspension (10(-3) approximately 10(-4)) of E. coli could inhibit the colonial growth. 3% suspension of oolong tea, green tea, and black tea, respectively could kill V. cholerae and V. parahaemorrhagiae in 30 minutes. 3% suspension of oolong tea and green tea, respectively could kill Sal. Typhi B.

Animals↗

[Microscopic and ultramicroscopic lesions from experimental mycoplasma infection in respiratory tract of chickens. Possible difference between pathogenic and non pathogenic strains (author's transl)].

For three weeks after experimental infection of trachea and scroll bone with Mycoplasma gallisepticum no lesions were detected in scroll bone, but only an abundant mucous secretion. Mycoplasmas were present and adhered to cilia of epithelial cells. In trachea an almost complete destruction of cilia was observed allowing swollen epithelial cells to appear with mycoplasmas adhering to villi. Strain W31 serotype C caused no lesions but cells and cilia were covered with a thick layer of mucous.

Animals↗

[Genetic study of plasmid pVM82 which contributes to the pathogenicity of the pseudotuberculosis pathogen].

The large pVM82 plasmid isolated from epidemic strains of Yersinia pseudotuberculosis includes the 25MD segment, which encodes a series of properties affecting the virulence of the bacterium. Insertion mutants of pVM82 containing transposition-defective Tn2507 with a kanamycin-resistance marker in different Hind III fragments of the 25MD segment were obtained. By recombination between two homologous pVM82 containing genetic markers in different parts, deletion derivatives of pVM82 plasmid and insertions of the plasmid segment, carrying kanamycin-resistance marker, into a chromosome were obtained. Results were obtained suggesting the presence in the plasmid 25MD segment of a transposon-like structure capable of migrating from pVM82 plasmid onto a chromosome and from a chromosome and pVM82 onto pRP1.2 plasmid of a broad host range.

Chromosomes, Bacterial↗

[Current concepts on the pathogenicity of phytopathogenic bacteria].

What are the molecular determinants that make a bacterium a plant pathogen? In the last 10-20 years, important progress has been made in answering this question. In the early 20th century soon after the discovery of infectious diseases, the first studies of pathogenicity were undertaken. These early studies relied mostly on biochemistry and led to the discovery of several major pathogenicity determinants, such as toxins and hydrolytic enzymes which govern the production of major disease symptoms. From these pioneering studies, a simplistic view of pathogenicity arose. It was thought that only a few functions were sufficient to transform a bacterium into a pathogen. This view rapidly changed when modern techniques of molecular genetics were applied to analyse pathogenicity. Modern analyses of pathogenicity determinants took advantage of the relatively simple organization of the haploid genome of pathogenic bacteria. By creating non-pathogenic mutants, a large number of genes governing bacterium-host interactions were identified. These genes are required either for host colonization or for the production of symptoms. Even though the role of motility and chemotaxis in these processes is still unclear, it is clear that a strong attachment of Agrobacterium to plant cells is a prerequisite for efficient plant transformation and disease. Other important pathogenicity factors identified with a molecular genetic approach include hydrolytic enzymes such as pectinases and cellulases which not only provide nutrients to the bacteria but also facilitate pathogen invasion into host tissues. The precise role of exopolysaccharide in pathogenicity is still under discussion, however it is has been established that it is crucial for the induction of wilt symptoms caused by Ralstonia solanacearum. Trafficking of effector proteins from the invading bacterium into the host cell emerged recently as a new central concept. In plant pathogenic bacteria, protein translocation takes place through the so-called 'type II secretion machinery' encoded by hrp genes in the bacterium. These genes are present in representatives of all the major groups of Gram negative plant pathogenic bacteria except Agrobacterium. Most of these genes have counterparts in pathogens of mammals (including those of human) and they also play a central role in pathogenicity. Additionally, recent evidence suggests that a 'type IV secretion machinery' injects bacterial proteins into host cells. This machinery, originally found to be involved in the transfer of t-DNA from Agrobacterium into plant cells, was recently shown to translocate pathogenicity proteins in pathogens of mammals such as Helicobacter pylori and Brucella. Discovery of the trafficking of proteins from the pathogen into host cells revolutionized our conception of pathogenicity. First, it rather unexpectedly established the conservation of basic pathogenicity strategies in plant and animal pathogens. Second, this discovery changes our ideas about the overall strategy (or mechanism) of pathogenicity, although we still think the end result is exploitation of host cell nutritive components. Rather than killing the host cell from outside, we envision a more subtle approach in which pathogens inject effector proteins into the host cell to effect a change in host cell biology advantageous to the pathogen. Identification of the effector proteins, of their function and of the corresponding molecular targets in the host is a new challenge which will contribute to the conception of new strategies to control diseases.

Bacteria↗

Pathogen safety of manufacturing processes for biological products: special emphasis on KOGENATE Bayer.

Manufacturers of human therapeutic proteins derived from biological sources continuously strive to improve the pathogen safety profiles of these products. Efforts to improve pathogen safety margins for these biological products are directed towards several areas within the manufacturing processes including: (a) sourcing and screening of raw materials (b) determining the potential for manufacturing processes to reduce pathogen titres, and (c) incorporating methods designed specifically to remove or inactivate contaminating pathogens. Methods that could potentially reduce pathogen titres are a major focus for many manufacturers. In general, these methods are grouped into two categories, pathogen clearance and pathogen inactivation. Assessments are performed on small-scale, laboratory simulations of the manufacturing process of interest that are spiked with a known amount of a selected pathogen. These studies provide estimates of the potential for a process step to remove or inactivate a particular pathogen. There are several pathogen clearance/inactivation methods that are inherent in manufacturing processes, however, some methods are intentionally incorporated into manufacturing for the sole purpose of reducing putative pathogen titres. Not only are well-known pathogens such as viruses targeted, but also suspected pathogens such as those associated with the transmissible spongiform encephalopathies (TSEs). The production processes for the isolation of several biological products, including recombinant KOGENATE Bayer (Kogenate FS), have been evaluated for the ability to reduce pathogen titres and/or have been designed to incorporate methods for reducing potential pathogen safety risks. Several processing steps with the potential to reduce pathogen titres have been identified.

Biological Products↗

[Specified pathogen-free poultry flocks: the current situation].

Before the implementation of strategies to establish specified pathogen-free commercial poultry flocks, the ultimate goals need to be identified: 1) consumer protection by minimizing the risk for zoonotic diseases and food-borne pathogens, and/or 2) animal health protection against primary and secondary pathogens. The success for the establishment of specific pathogen-free poultry flocks depends on the biological characteristics, the epidemiological distribution and the transmission route of each pathogen. For zoonotic pathogens such as Salmonella Typhimurium, Salmonella Enteritidis, Campylobacter jejuni or the high pathogenic avian influenza virus, eradication has to be ultimate goal. Despite tremendous control efforts in field, only partial control of these pathogens has been achieved so far. In the future it will be necessary to continue these eradication efforts by combining optimized hygiene programs at all production levels with intensive monitoring and immunoprophylaxis. For primary pathogens affecting the health condition of poultry without known zoonotic potential, such as Salmonella Gallinarum, avian Mycoplasma or leucosis virus, specified pathogen free flocks have been established on the parent and grandparent level. In order to achieve a status free of these pathogens, rigid hygiene control, especially on the hatchery level and monitoring programs combined with elimination of pathogen- and antibody-positive birds were implemented. Nevertheless, the economically most important diseases of modern poultry production are of multifactorial origin. Ubiquitous secondary pathogens in combination with insufficient management or immunosuppressive agents induce great economic losses for the poultry producers. These secondary pathogens can not be eliminated due to their ubiquitous distribution. In the future only a reduction of these factorial diseases will be possible combining hygiene management and optimization of poultry husbandry. For the establishment of specified pathogen free poultry flocks in the field, risk analysis is necessary and the structure of poultry production has to be considered before and eradication program can be carried out successfully.

Animal Husbandry↗

Foodborne pathogens in milk and the dairy farm environment: food safety and public health implications.

Milk and products derived from milk of dairy cows can harbor a variety of microorganisms and can be important sources of foodborne pathogens. The presence of foodborne pathogens in milk is due to direct contact with contaminated sources in the dairy farm environment and to excretion from the udder of an infected animal. Most milk is pasteurized, so why should the dairy industry be concerned about the microbial quality of bulk tank milk? There are several valid reasons, including (1) outbreaks of disease in humans have been traced to the consumption of unpasteurized milk and have also been traced back to pasteurized milk, (2) unpasteurized milk is consumed directly by dairy producers, farm employees, and their families, neighbors, and raw milk advocates, (3) unpasteurized milk is consumed directly by a large segment of the population via consumption of several types of cheeses manufactured from unpasteurized milk, (4) entry of foodborne pathogens via contaminated raw milk into dairy food processing plants can lead to persistence of these pathogens in biofilms, and subsequent contamination of processed milk products and exposure of consumers to pathogenic bacteria, (5) pasteurization may not destroy all foodborne pathogens in milk, and (6) inadequate or faulty pasteurization will not destroy all foodborne pathogens. Furthermore, pathogens such as Listeria monocytogenes can survive and thrive in post-pasteurization processing environments, thus leading to recontamination of dairy products. These pathways pose a risk to the consumer from direct exposure to foodborne pathogens present in unpasteurized dairy products as well as dairy products that become re-contaminated after pasteurization. The purpose of this communication is to review literature published on the prevalence of bacterial foodborne pathogens in milk and in the dairy environment, and to discuss public health and food safety issues associated with foodborne pathogens found in the dairy environment. Information presented supports the model in which the presence of pathogens depends on ingestion of contaminated feed followed by amplification in bovine hosts and fecal dissemination in the farm environment. The final outcome of this cycle is a constantly maintained reservoir of foodborne pathogens that can reach humans by direct contact, ingestion of raw contaminated milk or cheese, or contamination during the processing of milk products. Isolation of bacterial pathogens with similar biotypes from dairy farms and from outbreaks of human disease substantiates this hypothesis.

Animals↗

Prevalence of pathogens in diabetic foot infection in South Indian type 2 diabetic patients.

AIM: To determine the prevalence of pathogens in diabetic foot infections, in relation to parameters like Wagner's grading, duration of diabetes and healing time. MATERIAL AND METHODS: A group of 654 (M:F, 433:221) type 2 diabetic patients with foot ulcers were studied. Specimens like pus, wound exudate and tissue were processed for smear for Gram's staining, aerobic and anaerobic culture, and biochemical identifications. RESULTS: In 654 diabetic patients, 728 pathogens were isolated. Aerobic pathogens were isolated in 437 (66.8%) patients and anaerobic pathogens were isolated in 217 (33.2%). As Wagner's grading increased, the prevalence of anaerobic pathogens also increased. Neuropathy was common in diabetic patients infected with both aerobic and anaerobic pathogens. Ulcers infected with anaerobic pathogens showed a longer healing time than ulcers infected with aerobic pathogens. There was no significant difference in peripheral vascular disease (PVD) in patients selected for the study. Among aerobic pathogens, Enterobacteriaceae family (48%), Staphylococcus species (spp) (18.2%), Streptococcus spp (16.8%) and Pseudomonas spp (17%) were seen frequently. Among anaerobes Peptostreptococcus spp and Clostridium spp formed 69.4%. Gram-negative anaerobes like Bacteroides spp and Fusobacterium spp were present in 30.6%. Healing time was longer when strict aerobic pathogen Pseudomonas spp and strict anaerobic pathogens were present (136.1 +/- 28.6 and 136.4 +/- 34.7 days, respectively). CONCLUSIONS: Diabetic foot infection is polymicrobial in nature. The healing time of wound infected with anaerobic pathogens was higher than those infected with aerobic pathogens. Anaerobic pathogens increased with the Wagner's grading. Presence of neuropathy increased the risk of foot infection.

Bacteria, Aerobic↗

Pathogen inactivation techniques.

The desire to rid the blood supply of pathogens of all types has led to the development of many technologies aimed at the same goal--eradication of the pathogen(s) without harming the blood cells or generating toxic chemical agents. This is a very ambitious goal, and one that has yet to be achieved. One approach is to shun the 'one size fits all' concept and to target pathogen-reduction agents at the Individual component types. This permits the development of technologies that might be compatible with, for example, plasma products but that would be cytocidal and thus incompatible with platelet concentrates or red blood cell units. The technologies to be discussed include solvent detergent and methylene blue treatments--designed to inactivate plasma components and derivatives; psoralens (S-59--amotosalen) designed to pathogen-reduce units of platelets; and two products aimed at red blood cells, S-303 (a Frale--frangible anchor-linker effector compound) and Inactine (a binary ethyleneimine). A final pathogen-reduction material that might actually allow one material to inactivate all three blood components--riboflavin (vitamin B2)--is also under development. The sites of action of the amotosalen (S-59), the S-303 Frale, Inactine, and riboflavin are all localized in the nucleic acid part of the pathogen. Solvent detergent materials act by dissolving the plasma envelope, thus compromising the integrity of the pathogen membrane and rendering it non-infectious. By disrupting the pathogen's ability to replicate or survive, its infectivity is removed. The degree to which bacteria and viruses are affected by a particular pathogen-reducing technology relates to its Gram-positive or Gram-negative status, to the sporulation characteristics for bacteria, and the presence of lipid or protein envelopes for viruses. Concerns related to photoproducts and other breakdown products of these technologies remain, and the toxicology of pathogen-reduction treatments is a major ongoing area of investigation. Clearly, regulatory agencies have a major role to play in the evaluation of these new technologies. This chapter will cover the several types of pathogen-reduction systems, mechanisms of action, the inactivation efficacy for specific types of pathogens, toxicology of the various systems and the published research and clinical trial data supporting their potential usefulness. Due to the nature of the field, pathogen reduction is a work in progress and this review should be considered as a snapshot in time rather than a clear picture of what the future will bring.

Anti-Infective Agents↗

Diagnosis of atypical pathogens in patients hospitalized with community-acquired respiratory infection.

The object of our study was to determine the proportion of atypical respiratory pathogens among patients hospitalized with a community-acquired respiratory infection. From September 1997 to May 1999, 159 patients (57% male, median age 55, range 1-88 y) admitted to 3 regional hospitals for a community acquired respiratory infection, were enrolled in the study. Microbiological diagnosis for the atypical pathogens Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella pneumophila was performed with PCR on a throat swab, sputum and/or broncho alveolar lavage (BAL). In addition, Legionella species other than L. pneumophila (L. non-pneumophila species) were detected by PCR. Two serum samples were collected and processed for M. pneumoniae and C. pneumoniae serology. In total, 27 patients (17%) were diagnosed with an atypical pathogen. Infection with M. pneumoniae was detected in 19 patients (12%) (PCR positive n = 7), with C. pneumoniae in 5 patients (3%) (PCR positive n = 0) and with L. pneumophila in 4 patients (2.5%) (PCR positive n = 4). In 54 (34%) patients routine microbiological investigations revealed aetiological agents other than the 3 atypical pathogens, the most frequently diagnosed pathogens being Streptococcus pneumoniae (n = 18), Haemophilus influenzae (n = 17), Gram-negative rods (n = 13), Moraxella catarrhalis (n = 6) and Staphylococcus aureus (n = 6). More than 1 pathogen was found in 13 patients. Atypical pathogens were found more often in the young age group (0-18 y), in contrast to bacterial pathogens that were found more often in the older age groups (> or = 65 y). Atypical pathogens were found less often in patients with a clinical presentation of atypical pneumonia. Legionella species other than L. pneumophila were found by PCR in 13 patients (8%), and in 6 patients in combination with another pathogen. An atypical pathogen (M. pneumoniae, C. pneumoniae or L. pneumophila) was found in 17% of the patients hospitalized with a community acquired respiratory infection, predominantly in the young age group. The role of Legionella non-pneumophila species as pathogen in community acquired respiratory infection needs to be determined. The clinical presentation does not predict the type of pathogen found.

Adolescent↗

Magnaporthe grisea genes for pathogenicity and virulence identified through a series of backcrosses.

We have identified genes for pathogenicity toward rice (Oryza sativa) and genes for virulence toward specific rice cultivars in the plant pathogenic fungus Magnaporthe grisea. A genetic cross was conducted between the weeping lovegrass (Eragrostis curvula) pathogen 4091-5-8, a highly fertile, hermaphroditic laboratory strain, and the rice pathogen O-135, a poorly fertile, female-sterile field isolate that infects weeping lovegrass as well as rice. A six-generation backcrossing scheme was then undertaken with the rice pathogen as the recurrent parent. One goal of these crosses was to generate rice pathogenic progeny with the high fertility characteristic of strain 4091-5-8, which would permit rigorous genetic analysis of rice pathogens. Therefore, progeny strains to be used as parents for backcross generations were chosen only on the basis of fertility. The ratios of pathogenic to nonpathogenic (and virulent to avirulent) progeny through the backcross generations suggested that the starting parent strains differ in two types of genes that control the ability to infect rice. First, they differ by polygenic factors that determine the extent of lesion development achieved by those progeny that infect rice. These genes do not appear to play a role in infection of weeping lovegrass because both parents and all progeny infect weeping lovegrass. Second, the parents differ by simple Mendelian determinants, "avirulence genes," that govern virulence toward specific rice cultivars in all-or-none fashion. Several crosses confirm the segregation of three unlinked avirulence genes, Avr 1-CO39, Avr 1-M201 and Avr1-YAMO, alleles of which determine avirulence on rice cultivars CO39, M201, and Yashiro-mochi, respectively. Interestingly, avirulence alleles of Avr1-CO39, Avr1-M201 and Avr1-YAMO were inherited from the parent strain 4091-5-8, which is a nonpathogen of rice. Middle repetitive DNA sequences ("MGR sequences"), present in approximately 40-50 copies in the genome of the rice pathogen parent, and in very low copy number in the genome of the nonpathogen of rice, were used as physical markers to monitor restoration of the rice pathogen genetic background during introgression of fertility. The introgression of highest levels of fertility into the most successful rice pathogen progeny was incomplete by the sixth generation, perhaps a consequence of genetic linkage between genes for fertility and genes for rice pathogenicity. One chromosomal DNA segment with MGR sequence homology appeared to be linked to the gene Avr1-CO39. Finally, many of the crosses described in this paper exhibited a characteristic common to many crosses involving M. grisea rice pathogen field isolates.(ABSTRACT TRUNCATED AT 400 WORDS)

Ascomycota↗

Diseases of humans and their domestic mammals: pathogen characteristics, host range and the risk of emergence.

Pathogens that can be transmitted between different host species are of fundamental interest and importance from public health, conservation and economic perspectives, yet systematic quantification of these pathogens is lacking. Here, pathogen characteristics, host range and risk factors determining disease emergence were analysed by constructing a database of disease-causing pathogens of humans and domestic mammals. The database consisted of 1415 pathogens causing disease in humans, 616 in livestock and 374 in domestic carnivores. Multihost pathogens were very prevalent among human pathogens (61.6%) and even more so among domestic mammal pathogens (livestock 77.3%, carnivores 90.0%). Pathogens able to infect human, domestic and wildlife hosts contained a similar proportion of disease-causing pathogens for all three host groups. One hundred and ninety-six pathogens were associated with emerging diseases, 175 in humans, 29 in livestock and 12 in domestic carnivores. Across all these groups, helminths and fungi were relatively unlikely to emerge whereas viruses, particularly RNA viruses, were highly likely to emerge. The ability of a pathogen to infect multiple hosts, particularly hosts in other taxonomic orders or wildlife, were also risk factors for emergence in human and livestock pathogens. There is clearly a need to understand the dynamics of infectious diseases in complex multihost communities in order to mitigate disease threats to public health, livestock economies and wildlife.

Animal Diseases↗

Local adaptation in the Linum marginale-Melampsora lini host-pathogen interaction.

The potential for local adaptation between pathogens and their hosts has generated strong theoretical and empirical interest with evidence both for and against local adaptation reported for a range of systems. We use the Linum marginale-Melampsora lini plant-pathogen system and a hierarchical spatial structure to investigate patterns of local adaptation within a metapopulation characterised by epidemic dynamics and frequent extinction of pathogen populations. Based on large sample sizes and comprehensive cross-inoculation trials, our analyses demonstrate strong local adaptation by Melampsora to its host populations, with this effect being greatest at regional scales, as predicted from the broader spatial scales at which M. lini disperses relative to L. marginale. However, there was no consistent trend for more distant pathogen populations to perform more poorly. Our results further show how the coevolutionary interaction between hosts and pathogens can be influenced by local structure such that resistant hosts select for generally virulent pathogens, while susceptible hosts select for more avirulent pathogens. Empirically, local adaptation has generally been tested in two contrasting ways: (1) pathogen performance on sympatric versus allopatric hosts; and (2) sympatric versus allopatric pathogens on a given host population. In situations where no host population is more resistant or susceptible than others when averaged across pathogen populations (and likewise, no pathogen population is more virulent or avirulent than others), results from these tests should generally be congruent. We argue that this is unlikely to be the case in the metapopulation situations that predominate in natural host-pathogen interactions, thus requiring tests that control simultaneously for variation in plant and pathogen populations.

Adaptation, Physiological↗

Imperfect vaccines and the evolution of pathogens causing acute infections in vertebrates.

A study by Gandon et al. (2001) considered the potential ways pathogens may evolve in response to vaccination with imperfect vaccines. In this paper, by focusing on acute infections of vertebrate hosts, we examine whether imperfect vaccines that do not completely block a pathogen's replication (antigrowth) or transmission (antitransmission) may lead to evolution of more or less virulent pathogen strains. To address this question, we use models of the within-host dynamics of the pathogen and the host's immune responses. One advantage of the use of this within-host approach is that vaccination can be easily incorporated in the models and the trade-offs between pathogen transmissibility, host recovery, and virulence that drive evolution of pathogens in these models can be easily estimated. We find that the use of either antigrowth or antitransmission vaccines leads to the evolution of pathogens with an increased within-host growth rate; infection of unvaccinated hosts with such evolved pathogens results in high host mortality and low pathogen transmission. Vaccination of only a fraction of hosts with antigrowth vaccines may prevent pathogens from evolving high virulence due to pathogen adaptation to unvaccinated hosts and thus protection of vaccinated hosts from pathogen-induced disease. In contrast, antitransmission vaccines may be beneficial only if they are effective enough to cause pathogen extinction. Our results suggest that particular mechanisms of action of vaccines and their efficacy are crucial in predicting longterm evolutionary consequences of the use of imperfect vaccines.

Animal Diseases↗