Immunomodulatory Effect of “Dr. M.S. Reddy’s Multiple Mixed Strain Probiotic Therapy” to Cure or Prevent Hospital Acquired (Nosocomial) Infections due to Clostridium difficile (C. diff), other Pathogenic Bacteria, and Autoimmune Diseases

2018 ◽  
Vol 11 (1) ◽  
pp. 3937-3949
Author(s):  
Malireddy S Reddy
Keyword(s):  
Immune System ◽  
Gastrointestinal Tract ◽  
Pathogenic Bacteria ◽  
Molecular Level ◽  
Host Immune System ◽  
Hospital Acquired Infections ◽  
The World ◽  
Probiotic Strains ◽  
The Individual ◽  
Hospital Acquired

The worldwide popularity of Dr. M.S. Reddy’s Multiple Mixed Strain Probiotic Therapy to treat or prevent the hospital acquired infections (nosocomial infections) arose a great interest in the medical community around the world (Reddy and Reddy, 2016; 2017). The following questions were raised on this subject: Does Multiple Mixed Strain Probiotics directly inhibit the pathogenic bacteria (C. diff) in the gastrointestinal tract or indirectly through modulation of the host immune system or both? To be more specific, what is the exact and/or hypothetical mechanism at molecular level behind the breakthrough discovery of Dr. M.S. Reddy’s Multiple Mixed Strain Probiotic Therapy?  To answer these questions, the specific immunomodulation regulatory functions of the individual Probiotic strains (on host) have beenresearched, investigated andoutlined in this article.  A detailed explanation(s) and hypotheses have been proposed outlining the possible cumulativedirect bacteriological and indirect immunomodulatory effects (at the molecular level) of the Multiple Mixed Strain Probiotics used in Dr. M.S. Reddy’s Multiple Mixed Strain Probiotic Therapy to successfully treat C. diff infection.  A detailed scientific and research attempts were made to correlate the Probiotic induced immune activities in relation to the reduction of the symptoms associated with the hospital acquired Clostridium difficile infection during and after the Multiple Mixed Strain Probioitc Therapy.  Results of the clinical trials, microbiological tests on feces, and the clinical blood tests significantly revealed that the reasons for the success of Dr. Reddy’s Multiple Mixed Strain Probiotic Therapy are multifold. Presumably, it is predominantly due to the immunomodulatory effect they have exerted on the host immune system along with the direct inhibition of C. diff bacteria by multiple Probiotics, due to the production of bacteriocins, lactic acid and nutritional competency.In addition, the size of the individual cells of the Probiotic strains in the Multiple Mixed Strain Probiotics and their significant effect on immunomodulation has been thoroughly discussed. Results clearly proved that if Probiotics are absent in the GI tract during C. diff infection, the chances of patient survival is zero.  This is because of the excess immune stimulation and incurable damage to the epithelial cell barrier of the gastrointestinal tract caused by C. diff bacteria.  The results also revealed, without any doubt, as of to-datethe latest discovery of Dr. M.S. Reddy’s Multiple Mixed Strain Probiotic Therapy is the best way to cure the deadly hospital acquired infections affecting millions of people around the world, with high degree of mortality.  This has been attested by several practicng medical professionals and scientists around the world (Reddy and Reddy, 2017).

scholarly journals Are mobile phones of health care workers portals of pathogenic organisms causing hospital acquired infections in intensive care units? A mini systematic review

2020 ◽  
Vol 47 (3) ◽  
pp. 207-214
Author(s):  
M. Mukhtar-Yola ◽  
B. Andrew
Keyword(s):  
Health Care ◽  
Intensive Care ◽  
Intensive Care Units ◽  
Mobile Phones ◽  
Health Care Workers ◽  
Pathogenic Bacteria ◽  
Cross Sectional ◽  
Hospital Acquired Infections ◽  
Care Workers ◽  
Hospital Acquired

Background: Health care workers at the bedside of critically ill babies freely carry their mobile phones in between procedures and handling  patients. Concerns are rising as this may contribute to nosocomial infections with pathogenic bacteria. Aim: To determine if mobile phones of health care workers in Intensive care units carry potentially pathogenic bacteria leading to hospital acquired infections. Design: Systematic review.Data sources: Electronic databases (Medline via ovid, CINAHL, Web of science) and hand Searching of references and citations were done to identify studies. Screening and inclusion criteria were used to identify studies with a cross-sectional or cohort design. The search was limited to journal articles published between 2008-2015 and to English language. Quality assessment was done using the National Institute of Health tool for observational studies. Data was extracted on to excel sheets and analysed using SPSS version 22.Results: Six studies with a cohort (1) or cross-sectional design (5) involving 1, 131 health care workers were reviewed. The overall quality of the studies was fair, and a narrative synthesis was done. The colonization rate of the mobile phones ranged between 46.3 % and a 100% with 13-50% carrying potentially pathogenic multidrug resistant microorganisms. Methicillin resistant staphylococcus aureus, Vancomycine resistant enterococci, acinobacter and coagulase negative staphylococci were reported across all studies and were recognized as leading causes of morbidity and mortalityin the ICU. Conclusion: Mobile phones Of HCW are portals of potentially pathogenic microorganisms, which could result in morbidity and mortality.Although no causal relationship could be established, strong associations have been reported. Guidelines by hospital infection control committees are needed on restriction, care and routine cleaning of mobile phones as well as further research. Key words: Health care worker, Intensive care unit, Hospital Acquired Infections, mobile phones

scholarly journals Extreme Dysbiosis of the Microbiome in Critical Illness

mSphere ◽  
2016 ◽  
Vol 1 (4) ◽  
Author(s):  
Daniel McDonald ◽  
Gail Ackermann ◽  
Ludmila Khailova ◽  
Christine Baird ◽  
Daren Heyland ◽  
...  
Keyword(s):  
Critical Illness ◽  
Organ Failure ◽  
Patient Outcomes ◽  
Pathogenic Bacteria ◽  
Hospital Acquired Infections ◽  
Icu Admission ◽  
Health Promoting ◽  
Hospital Acquired ◽  
Improve Patient ◽  
Normal Health

ABSTRACT Critical illness may be associated with the loss of normal, “health promoting” bacteria, allowing overgrowth of disease-promoting pathogenic bacteria (dysbiosis), which, in turn, makes patients susceptible to hospital-acquired infections, sepsis, and organ failure. This has significant world health implications, because sepsis is becoming a leading cause of death worldwide, and hospital-acquired infections contribute to significant illness and increased costs. Thus, a trial that monitors the ICU patient microbiome to confirm and characterize this hypothesis is urgently needed. Our study analyzed the microbiomes of 115 critically ill subjects and demonstrated rapid dysbiosis from unexpected environmental sources after ICU admission. These data may provide the first steps toward defining targeted therapies that correct potentially “illness-promoting” dysbiosis with probiotics or with targeted, multimicrobe synthetic “stool pills” that restore a healthy microbiome in the ICU setting to improve patient outcomes. Critical illness is hypothesized to associate with loss of “health-promoting” commensal microbes and overgrowth of pathogenic bacteria (dysbiosis). This dysbiosis is believed to increase susceptibility to nosocomial infections, sepsis, and organ failure. A trial with prospective monitoring of the intensive care unit (ICU) patient microbiome using culture-independent techniques to confirm and characterize this dysbiosis is thus urgently needed. Characterizing ICU patient microbiome changes may provide first steps toward the development of diagnostic and therapeutic interventions using microbiome signatures. To characterize the ICU patient microbiome, we collected fecal, oral, and skin samples from 115 mixed ICU patients across four centers in the United States and Canada. Samples were collected at two time points: within 48 h of ICU admission, and at ICU discharge or on ICU day 10. Sample collection and processing were performed according to Earth Microbiome Project protocols. We applied SourceTracker to assess the source composition of ICU patient samples by using Qiita, including samples from the American Gut Project (AGP), mammalian corpse decomposition samples, childhood (Global Gut study), and house surfaces. Our results demonstrate that critical illness leads to significant and rapid dysbiosis. Many taxons significantly depleted from ICU patients versus AGP healthy controls are key “health-promoting” organisms, and overgrowth of known pathogens was frequent. Source compositions of ICU patient samples are largely uncharacteristic of the expected community type. Between time points and within a patient, the source composition changed dramatically. Our initial results show great promise for microbiome signatures as diagnostic markers and guides to therapeutic interventions in the ICU to repopulate the normal, “health-promoting” microbiome and thereby improve patient outcomes. IMPORTANCE Critical illness may be associated with the loss of normal, “health promoting” bacteria, allowing overgrowth of disease-promoting pathogenic bacteria (dysbiosis), which, in turn, makes patients susceptible to hospital-acquired infections, sepsis, and organ failure. This has significant world health implications, because sepsis is becoming a leading cause of death worldwide, and hospital-acquired infections contribute to significant illness and increased costs. Thus, a trial that monitors the ICU patient microbiome to confirm and characterize this hypothesis is urgently needed. Our study analyzed the microbiomes of 115 critically ill subjects and demonstrated rapid dysbiosis from unexpected environmental sources after ICU admission. These data may provide the first steps toward defining targeted therapies that correct potentially “illness-promoting” dysbiosis with probiotics or with targeted, multimicrobe synthetic “stool pills” that restore a healthy microbiome in the ICU setting to improve patient outcomes. Podcast: A podcast concerning this article is available.

scholarly journals Genome Diversity of Epstein-Barr Virus from Multiple Tumor Types and Normal Infection

2015 ◽  
Vol 89 (10) ◽  
pp. 5222-5237 ◽  
Author(s):  
Anne L. Palser ◽  
Nicholas E. Grayson ◽  
Robert E. White ◽  
Craig Corton ◽  
Samantha Correia ◽  
...  
Keyword(s):  
Immune System ◽  
T Cell ◽  
Geographic Variation ◽  
Epstein Barr Virus ◽  
Sequence Variation ◽  
Host Immune System ◽  
Barr Virus ◽  
The World ◽  
Epstein Barr

ABSTRACTEpstein-Barr virus (EBV) infects most of the world's population and is causally associated with several human cancers, but little is known about how EBV genetic variation might influence infection or EBV-associated disease. There are currently no published wild-type EBV genome sequences from a healthy individual and very few genomes from EBV-associated diseases. We have sequenced 71 geographically distinct EBV strains from cell lines, multiple types of primary tumor, and blood samples and the first EBV genome from the saliva of a healthy carrier. We show that the established genome map of EBV accurately represents all strains sequenced, but novel deletions are present in a few isolates. We have increased the number of type 2 EBV genomes sequenced from one to 12 and establish that the type 1/type 2 classification is a major feature of EBV genome variation, defined almost exclusively by variation of EBNA2 and EBNA3 genes, but geographic variation is also present. Single nucleotide polymorphism (SNP) density varies substantially across all known open reading frames and is highest in latency-associated genes. Some T-cell epitope sequences in EBNA3 genes show extensive variation across strains, and we identify codons under positive selection, both important considerations for the development of vaccines and T-cell therapy. We also provide new evidence for recombination between strains, which provides a further mechanism for the generation of diversity. Our results provide the first global view of EBV sequence variation and demonstrate an effective method for sequencing large numbers of genomes to further understand the genetics of EBV infection.IMPORTANCEMost people in the world are infected by Epstein-Barr virus (EBV), and it causes several human diseases, which occur at very different rates in different parts of the world and are linked to host immune system variation. Natural variation in EBV DNA sequence may be important for normal infection and for causing disease. Here we used rapid, cost-effective sequencing to determine 71 new EBV sequences from different sample types and locations worldwide. We showed geographic variation in EBV genomes and identified the most variable parts of the genome. We identified protein sequences that seem to have been selected by the host immune system and detected variability in known immune epitopes. This gives the first overview of EBV genome variation, important for designing vaccines and immune therapy for EBV, and provides techniques to investigate relationships between viral sequence variation and EBV-associated diseases.

scholarly journals Bacteriocin Production: a Probiotic Trait?

2011 ◽  
Vol 78 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Alleson Dobson ◽  
Paul D. Cotter ◽  
R. Paul Ross ◽  
Colin Hill
Keyword(s):  
Immune System ◽  
Microbial Communities ◽  
Bacteriocin Production ◽  
Host Immune System ◽  
Diverse Group ◽  
Probiotic Strains ◽  
Important Trait ◽  
The Impact ◽  
Selection Of

ABSTRACTBacteriocins are an abundant and diverse group of ribosomally synthesized antimicrobial peptides produced by bacteria and archaea. Traditionally, bacteriocin production has been considered an important trait in the selection of probiotic strains, but until recently, few studies have definitively demonstrated the impact of bacteriocin production on the ability of a strain to compete within complex microbial communities and/or positively influence the health of the host. Although research in this area is still in its infancy, there is intriguing evidence to suggest that bacteriocins may function in a number of ways within the gastrointestinal tract. Bacteriocins may facilitate the introduction of a producer into an established niche, directly inhibit the invasion of competing strains or pathogens, or modulate the composition of the microbiota and influence the host immune system. Here we review the role of bacteriocin production in complex microbial communities and their potential to enhance human health.

scholarly journals OmpA-Mediated Biofilm Formation Is Essential for the Commensal Bacterium Sodalis glossinidius To Colonize the Tsetse Fly Gut

2012 ◽  
Vol 78 (21) ◽  
pp. 7760-7768 ◽  
Author(s):  
Michele A. Maltz ◽  
Brian L. Weiss ◽  
Michelle O'Neill ◽  
Yineng Wu ◽  
Serap Aksoy
Keyword(s):  
Immune System ◽  
Pathogenic Bacteria ◽  
Tsetse Fly ◽  
Symbiotic Bacteria ◽  
Tsetse Flies ◽  
Host Immune System ◽  
Content Type ◽  
African Trypanosomes ◽  
Sodalis Glossinidius

ABSTRACTMany bacteria successfully colonize animals by forming protective biofilms. Molecular processes that underlie the formation and function of biofilms in pathogenic bacteria are well characterized. In contrast, the relationship between biofilms and host colonization by symbiotic bacteria is less well understood. Tsetse flies (Glossinaspp.) house 3 maternally transmitted symbionts, one of which is a commensal (Sodalis glossinidius) found in several host tissues, including the gut. We determined thatSodalisforms biofilms in the tsetse gut and that this process is influenced by theSodalisouter membrane protein A (OmpA). MutantSodalisstrains that do not produce OmpA (SodalisΔOmpA mutants) fail to form biofilmsin vitroand are unable to colonize the tsetse gut unless endogenous symbiotic bacteria are present. Our data indicate that in the absence of biofilms,SodalisΔOmpA mutant cells are exposed to and eliminated by tsetse's innate immune system, suggesting that biofilms helpSodalisevade the host immune system. Tsetse is the sole vector of pathogenic African trypanosomes, which also reside in the fly gut. Acquiring a better understanding of the dynamics that promoteSodaliscolonization of the tsetse gut may enhance the development of novel disease control strategies.

scholarly journals Analysis of the intestinal microbiota in COVID-19 patients and its correlation with the inflammatory factor IL-18 and SARS-CoV-2-specific IgA

2020 ◽  
Author(s):  
Wanyin Tao ◽  
Shu Zhu ◽  
Guorong Zhang ◽  
Xiaofang Wang ◽  
Meng Guo ◽  
...  
Keyword(s):  
Immune System ◽  
Gastrointestinal Tract ◽  
Gut Microbiota ◽  
Disease Severity ◽  
Specific Cell ◽  
Host Immune System ◽  
Inflammatory Factor ◽  
Cytokine Storm

The current global COVID-19 pandemic is caused by beta coronavirus Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2), which already infected over 10 million and caused 500 thousand deaths by June 2020. Overproduction of cytokines triggered by COVID-19 infection, known as "cytokine storm", is a highly risk factor associated with disease severity. However, how COVID-19 infection induce cytokine storm is still largely unknown. Accumulating in vitro and in vivo evidence suggests that gut is also susceptible to COVID19 infection: Human intestinal organoids, an in vitro model which mimic the specific cell type and spatial structure of the intestine, were susceptible to SARS-CoV2 infection; A significant fraction of patients reported gut symptoms; Viral RNA may persist for more than 30 days and infectious virus could be isolated in fecal samples. The gastrointestinal tract is the primary site of interaction between the host immune system with symbiotic and pathogenic microorganisms. The bacteria resident in our gastrointestinal tract, known as gut microbiota, is important to maintain the homeostasis of our immune system. While imbalance of gut microbiota, or dysbiosis, is associated with multiple inflammation diseases5. It's possible that SARS-CoV-2 infection may lead to alternation of gut microbiota thus worsen the host symptom. IL-18 is a proinflammatory cytokine produced multiple enteric cells, including intestinal epithelial cells (IECs), immune cells as well as enteric nervous system, and was shown to increase in the serum of COVID-19 patients. Immunoglobin A (IgA) is mainly produced in the mucosal surfaces, in humans 40-60mg kg-1 day-1 than all other immunoglobulin isotypes combined, and at least 80% of all plasma cells are located in the intestinal lamina propria. Recent study showed that SARS-CoV-2 specific IgA in the serum is positively correlate with the disease severity in COVID-19 patients11. Here we investigated the alterations of microbiota in COVID-19 patients, and its correlation with inflammatory factor IL-18 and SARS-CoV2 specific IgA.

scholarly journals Helminths in the gastrointestinal tract as modulators of immunity and pathology

2017 ◽  
Vol 312 (6) ◽  
pp. G537-G549 ◽  
Author(s):  
Fumi Varyani ◽  
John O. Fleming ◽  
Rick M. Maizels
Keyword(s):  
Immune System ◽  
Gastrointestinal Tract ◽  
Intestinal Tract ◽  
Intestinal Inflammation ◽  
Host Immune System ◽  
Helminth Parasites ◽  
Middle Income ◽  
Middle Income Countries ◽  
Inflammatory Bowel ◽  
Developed World

Helminth parasites are highly prevalent in many low- and middle-income countries, in which inflammatory bowel disease and other immunopathologies are less frequent than in the developed world. Many of the most common helminths establish themselves in the gastrointestinal tract and can exert counter-inflammatory influences on the host immune system. For these reasons, interest has arisen as to how parasites may ameliorate intestinal inflammation and whether these organisms, or products they release, could offer future therapies for immune disorders. In this review, we discuss interactions between helminth parasites and the mucosal immune system, as well as the progress being made toward identifying mechanisms and molecular mediators through which it may be possible to attenuate pathology in the intestinal tract.

scholarly journals Detection of carbapenemase genes in Klebsiella pneumoniae isolates

2016 ◽  
Vol 144 (5-6) ◽  
pp. 307-311
Author(s):  
Mira Mihajlovic-Ukropina ◽  
Anika Trudic ◽  
Zora Jelesic ◽  
Deana Medic ◽  
Biljana Milosavljevic ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Dipicolinic Acid ◽  
Clinical Samples ◽  
Hospital Acquired Infections ◽  
The World ◽  
Genes Encoding ◽  
Vitek 2 ◽  
Synergy Test ◽  
Hospital Acquired ◽  
Public Health Institute

Introduction. Klebsiella pneumoniae is one of the leading causes of serious hospital-acquired infections worldwide among Enterobacteriaceae species. It is the most common producer of carbapenemases in many parts of the world. Objective. The aim of the study was to determine which enzymes were responsible for resistance to carbapenems in Klebsiella pneumoniae strains isolated at the Centre of Microbiology of Public Health Institute of Vojvodina. Methods. A total of 29 Klebsiella pneumoniae non-duplicated strains resistant to at least one carbapenem isolated from clinical samples of hospitalized patients between November 1st 2013 and April 30th 2014 were studied. The species identification and susceptibility were done using VITEK 2 (bioM?rieux, Marcy-l??toile, France) system. Phenotypic conformation of carbapenemase production was done by double-disc synergy test. PCR technique was performed for detection of genes encoding production of carbapenemases (blsKPC, blaVIM, bla NDM, blaOXA-48). Results. Isolates of Klebsiella pneumoniae resistant to at least one carbapenem showed positive on double- disc synergy test between meropenem and dipicolinic acid. All strains positive in phenotypic test contained blaNDM gene. In isolates resistant only to ertapenem, neither production of carbapenemases nor presence of genes encoding these enzymes were detected. Among these isolates, nine produced extended-spectrum ?-lactamase. Conclusion. The presence of NDM metallo-?-lactamase was determined in all Klebsiella pneumoniae isolates resistant to at least one carbapenem.

scholarly journals Adaptation to Adversity: the Intermingling of Stress Tolerance and Pathogenesis in Enterococci

2019 ◽  
Vol 83 (3) ◽  
Author(s):  
Anthony O. Gaca ◽  
José A. Lemos
Keyword(s):  
Gastrointestinal Tract ◽  
Immune Responses ◽  
Stress Tolerance ◽  
Molecular Mechanisms ◽  
Multidrug Resistant ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Hospital Acquired Infections ◽  
Hospital Acquired

SUMMARY Enterococcus is a diverse and rugged genus colonizing the gastrointestinal tract of humans and numerous hosts across the animal kingdom. Enterococci are also a leading cause of multidrug-resistant hospital-acquired infections. In each of these settings, enterococci must contend with changing biophysical landscapes and innate immune responses in order to successfully colonize and transit between hosts. Therefore, it appears that the intrinsic durability that evolved to make enterococci optimally competitive in the host gastrointestinal tract also ideally positioned them to persist in hospitals, despite disinfection protocols, and acquire new antibiotic resistances from other microbes. Here, we discuss the molecular mechanisms and regulation employed by enterococci to tolerate diverse stressors and highlight the role of stress tolerance in the biology of this medically relevant genus.

scholarly journals Bacterial autolysins trim cell surface peptidoglycan to prevent detection by the Drosophila innate immune system

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Magda Luciana Atilano ◽  
Pedro Matos Pereira ◽  
Filipa Vaz ◽  
Maria João Catalão ◽  
Patricia Reed ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Pathogenic Bacteria ◽  
Bacterial Virulence ◽  
Innate Immune ◽  
Molecular Signature ◽  
Host Immune System ◽  
Bacterial Proteins ◽  
Successful Infection ◽  
Bacterial Surfaces

Bacteria have to avoid recognition by the host immune system in order to establish a successful infection. Peptidoglycan, the principal constituent of virtually all bacterial surfaces, is a specific molecular signature recognized by dedicated host receptors, present in animals and plants, which trigger an immune response. Here we report that autolysins from Gram-positive pathogenic bacteria, enzymes capable of hydrolyzing peptidoglycan, have a major role in concealing this inflammatory molecule from Drosophila peptidoglycan recognition proteins (PGRPs). We show that autolysins trim the outermost peptidoglycan fragments and that in their absence bacterial virulence is impaired, as PGRPs can directly recognize leftover peptidoglycan extending beyond the external layers of bacterial proteins and polysaccharides. The activity of autolysins is not restricted to the producer cells but can also alter the surface of neighboring bacteria, facilitating the survival of the entire population in the infected host.

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