Chlamydia-induced ReA: immune imbalances and persistent pathogens

2011 ◽  
Vol 8 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Eric Gracey ◽  
Robert D. Inman
Keyword(s):  
Persistent Pathogens

scholarly journals Thymic Atrophy during Infection as a Host Response to Avoid Tolerance to Persistent Pathogens

2014 ◽  
Vol 4 (4) ◽  
pp. 384-393
Author(s):  
Leonardo Santos ◽  
Eugênia Terra-Granado ◽  
Luciana Conde ◽  
Ana Nardy ◽  
Alexandre Morrot
Keyword(s):  
Host Response ◽  
Thymic Atrophy ◽  
Persistent Pathogens

scholarly journals Persistent socioeconomic and racial and ethnic disparities in pathogen burden in the United States, 1999–2014

2019 ◽  
Vol 147 ◽  
Author(s):  
R. C. Stebbins ◽  
G. A. Noppert ◽  
A. E. Aiello ◽  
E. Cordoba ◽  
J. B. Ward ◽  
...  
Keyword(s):  
High School ◽  
Mexican American ◽  
Ethnic Disparities ◽  
The United States ◽  
Herpes Simplex Virus 1 ◽  
Simplex Virus ◽  
Persistent Pathogens ◽  
Pathogen Burden ◽  
Racial Ethnic ◽  
Over Time

Abstract The disproportionate burden of prevalent, persistent pathogens among disadvantaged groups may contribute to socioeconomic and racial/ethnic disparities in long-term health. We assessed if the social patterning of pathogen burden changed over 16 years in a U.S.-representative sample. Data came from 17 660 National Health and Nutrition Examination Survey participants. Pathogen burden was quantified by summing the number of positive serologies for cytomegalovirus, herpes simplex virus-1, HSV-2, human papillomavirus and Toxoplasma gondii and dividing by the number of pathogens tested, giving a percent-seropositive for each participant. We examined sex- and age-adjusted mean pathogen burdens from 1999–2014, stratified by race/ethnicity and SES (poverty-to-income ratio (PIR); educational attainment). Those with a PIR < 1.3 had a mean pathogen burden 1.4–1.8 times those with a PIR > 3.5, with no change over time. Educational disparities were even greater and showed some evidence of increasing over time, with the mean pathogen burden among those with less than a high school education approximately twice that of those who completed more than high school. Non-Hispanic Black, Mexican American and other Hispanic participants had a mean pathogen burden 1.3–1.9 times non-Hispanic Whites. We demonstrate that socioeconomic and racial/ethnic disparities in pathogen burden have persisted across 16 years, with little evidence that the gap is closing.

Diagnosis of mixed-forms of persistent infections in children with gastroduodenal pathology

2013 ◽  
Vol 4 (3) ◽  
pp. 56-60
Author(s):  
Faina Nikolayevna Ryabchuk ◽  
Valentina Aleksandrovna Aleksandrova
Keyword(s):  
Antiviral Therapy ◽  
Eradication Therapy ◽  
Morphological Structure ◽  
Stomach Mucosa ◽  
Persistent Infections ◽  
Persistent Viruses ◽  
Epstein Barr ◽  
Persistent Pathogens

In recent years more and more frequently when mucosa of the stomach at the same time with Нelicobacter Рylori (HP) in the mucosa of the stomach and duodenum found various persistent pathogens (viruses Gripp, Herpes , HV 1 and 2 tipe, virus Epstein-Barr and Citomegalovirus). The work is devoted to a thorough diagnosis of persistent viruses in children with gastroduodenitis, which was used in the treatment of adequate antiviral therapy, contributing to the disappearance of autoantibodies from the blood, increase the effectiveness of eradication therapy and a significant improvement of the morphological structure of the stomach mucosa in children.

Modeling Inactivation of Highly Persistent Pathogens in Household-Scale Semi-Continuous Anaerobic Digesters

2016 ◽  
Vol 33 (11) ◽  
pp. 851-860 ◽  
Author(s):  
Nathan D. Manser ◽  
Jeffrey A. Cunningham ◽  
Sarina J. Ergas ◽  
James R. Mihelcic
Keyword(s):  
Anaerobic Digesters ◽  
Persistent Pathogens

scholarly journals Accelerated phenology of blacklegged ticks under climate warming

2015 ◽  
Vol 370 (1665) ◽  
pp. 20130556 ◽  
Author(s):  
Taal Levi ◽  
Felicia Keesing ◽  
Kelly Oggenfuss ◽  
Richard S. Ostfeld
Keyword(s):  
Climate Warming ◽  
Small Mammal ◽  
Transmission Cycle ◽  
Persistent Pathogens ◽  
The Relationship ◽  
Tick Phenology

The phenology of tick emergence has important implications for the transmission of tick-borne pathogens. A long lag between the emergence of tick nymphs in spring and larvae in summer should increase transmission of persistent pathogens by allowing infected nymphs to inoculate the population of naive hosts that can subsequently transmit the pathogen to larvae to complete the transmission cycle. In contrast, greater synchrony between nymphs and larvae should facilitate transmission of pathogens that do not produce long-lasting infections in hosts. Here, we use 19 years of data on blacklegged ticks attached to small-mammal hosts to quantify the relationship between climate warming and tick phenology. Warmer years through May and August were associated with a nearly three-week advance in the phenology of nymphal and larval ticks relative to colder years, with little evidence of increased synchrony. Warmer Octobers were associated with fewer larvae feeding concurrently with nymphs during the following spring. Projected warming by the 2050s is expected to advance the timing of average nymph and larva activity by 8–11 and 10–14 days, respectively. If these trends continue, climate warming should maintain or increase transmission of persistent pathogens, while it might inhibit pathogens that do not produce long-lasting infections.

scholarly journals TCR affinity controls the dynamics but not the functional specification of the Th1 response to mycobacteria

2020 ◽  
Author(s):  
Nayan D Bhattacharyya ◽  
Claudio Counoupas ◽  
Lina Daniel ◽  
Guoliang Zhang ◽  
Stuart J Cook ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Division ◽  
T Cell ◽  
Immune Surveillance ◽  
Mycobacterial Infection ◽  
T Cell Response ◽  
Functional Specification ◽  
Tcr Affinity ◽  
Persistent Pathogens

AbstractThe quality of T cell responses depends on the lymphocytes’ ability to undergo clonal expansion, acquire effector functions and traffic to the site of infection. Although TCR signal strength is thought to dominantly shape the T cell response, by using TCR transgenic CD4+ T cells with different pMHC binding affinity, we reveal that TCR affinity does not control Th1 effector function acquisition nor the functional output of individual effectors following mycobacterial infection. Rather, TCR affinity calibrates the rate of cell division to synchronize the distinct processes of T cell proliferation, differentiation and trafficking. By timing cell division-dependent IL-12R expression, TCR affinity controls when T cells become receptive to Th1-imprinting IL-12 signals, determining the emergence and magnitude of the Th1 effector pool. These findings reveal a distinct yet cooperative role for IL-12 and TCR signalling in Th1 differentiation and suggests that the temporal activation of clones with different TCR affinity is a major strategy to coordinate immune surveillance against persistent pathogens.

scholarly journals Bordetella parapertussis Survives inside Human Macrophages in Lipid Raft-Enriched Phagosomes

2014 ◽  
Vol 82 (12) ◽  
pp. 5175-5184 ◽  
Author(s):  
Juan Gorgojo ◽  
Eric T. Harvill ◽  
Maria Eugenia Rodríguez
Keyword(s):  
Lipid Rafts ◽  
Lipid Raft ◽  
Whooping Cough ◽  
Dependent Manner ◽  
Bacterial Killing ◽  
Content Type ◽  
Bordetella Parapertussis ◽  
Human Macrophages ◽  
O Antigen ◽  
Persistent Pathogens

ABSTRACTBordetella parapertussisis a human pathogen that causes whooping cough. The increasing incidence ofB. parapertussishas been attributed to the lack of cross protection induced by pertussis vaccines. It was previously shown thatB. parapertussisis able to avoid bacterial killing by polymorphonuclear leukocytes (PMN) if specific opsonic antibodies are not present at the site of interaction. Here, we evaluated the outcome ofB. parapertussisinnate interaction with human macrophages, a less aggressive type of cell and a known reservoir of many persistent pathogens. The results showed that in the absence of opsonins, O antigen allowsB. parapertussisto inhibit phagolysosomal fusion and to remain alive inside macrophages. The O antigen targetsB. parapertussisto lipid rafts that are retained in the membrane of phagosomes that do not undergo lysosomal maturation. Forty-eight hours after infection, wild-typeB. parapertussisbacteria but not the O antigen-deficient mutants were found colocalizing with lipid rafts and alive in nonacidic compartments. Taken together, our data suggest that in the absence of opsonic antibodies,B. parapertussissurvives inside macrophages by preventing phagolysosomal maturation in a lipid raft- and O antigen-dependent manner. Two days after infection, about 15% of macrophages were found loaded with live bacteria inside flotillin-enriched phagosomes that had access to nutrients provided by the host cell recycling pathway, suggesting the development of an intracellular infection. IgG opsonization drastically changed this interaction, inducing efficient bacterial killing. These results highlight the need forB. parapertussisopsonic antibodies to induce bacterial clearance and prevent the eventual establishment of cellular reservoirs of this pathogen.

scholarly journals A Longitudinal Study of the Association Between Persistent Pathogens and Incident Depression Among Older U.S. Latinos

2018 ◽  
Vol 74 (5) ◽  
pp. 634-641 ◽  
Author(s):  
Amanda M Simanek ◽  
Cheng Zheng ◽  
Robert Yolken ◽  
Mary Haan ◽  
Allison E Aiello
Keyword(s):  
Odds Ratio ◽  
Inflammatory Markers ◽  
Total Sample ◽  
C Reactive Protein ◽  
Varicella Zoster ◽  
Reactive Protein ◽  
Severity Of Depression ◽  
Simplex Virus ◽  
Persistent Pathogens

Abstract Depression is estimated to affect more than 6.5 million Americans 65 years of age and older and compared with non-Latino whites older U.S. Latinos have a greater incidence and severity of depression, warranting further investigation of novel risk factors for depression onset among this population. We used data on 771/1,789 individuals ≥60 years of age from the Sacramento Area Latino Study on Aging (1998–2008) who were tested for cytomegalovirus (CMV), herpes simplex virus, varicella zoster, Helicobacter pylori, Toxoplasma gondii, and C-reactive protein (CRP) and interleukin-6 (IL-6) level. Among those without elevated depressive symptoms at baseline, we examined the association between each pathogen, inflammatory markers and incident depression over up to nearly 10 years of follow-up using discrete-time logistic regression. We found that only CMV seropositivity was statistically significantly associated with increased odds of incident depression (odds ratio [OR]: 1.38, 95% confidence interval [CI]: 1.00–1.90) in the total sample as well as among women only (OR: 1.70, 95% CI: 1.01–2.86). These associations were not mediated by CRP or IL-6 levels. Our findings suggest that CMV seropositivity may serve as an important risk factor for the onset of depression among older U.S. Latinos, but act outside of inflammatory pathways.

scholarly journals When environmentally persistent pathogens transform good habitat into ecological traps

2016 ◽  
Vol 3 (3) ◽  
pp. 160051 ◽  
Author(s):  
Clinton B. Leach ◽  
Colleen T. Webb ◽  
Paul C. Cross
Keyword(s):  
Habitat Quality ◽  
Transmission Rate ◽  
Pathogen Transmission ◽  
Ecological Trap ◽  
Patch Occupancy ◽  
Environmental Persistence ◽  
High Quality ◽  
Patch Occupancy Model ◽  
Wildlife Populations ◽  
Persistent Pathogens

Habitat quality plays an important role in the dynamics and stability of wildlife metapopulations. However, the benefits of high-quality habitat may be modulated by the presence of an environmentally persistent pathogen. In some cases, the presence of environmental pathogen reservoirs on high-quality habitat may lead to the creation of ecological traps, wherein host individuals preferentially colonize high-quality habitat, but are then exposed to increased infection risk and disease-induced mortality. We explored this possibility through the development of a stochastic patch occupancy model, where we varied the pathogen’s virulence, transmission rate and environmental persistence as well as the distribution of habitat quality in the host metapopulation. This model suggests that for pathogens with intermediate levels of spread, high-quality habitat can serve as an ecological trap, and can be detrimental to host persistence relative to low-quality habitat. This inversion of the relative roles of high- and low-quality habitat highlights the importance of considering the interaction between spatial structure and pathogen transmission when managing wildlife populations exposed to an environmentally persistent pathogen.

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