Serum Antibody Response to Toxins A and B of Clostridium difficile

Viscidi, Raphael P.; Laughon, Barbara E.; Yolken, R.; Bo-Linn, P.; Moench, Thomas R.; Ryder, Robert W.; Bartlett, John G.

doi:10.1093/infdis/148.1.93

Cited by 191 publications

(109 citation statements)

References 12 publications

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“…In this study, 176 patients (67%) were older than age 65 years; this high proportion of older patients may reflect that there are larger numbers of elderly hospitalized patients or that older individuals are more susceptible to C difficile infections. Elderly individuals have decreased humoral immunity to C difficile (38), which may increase their susceptibility to C difficile infections. Furthermore, the National Corporation of Swedish Pharmacies has reported research findings that the increased consumption of antibiotics among the elderly is not always clearly correlated with the higher prevalence of CDAD infections (26).…”

Section: Discussionmentioning

confidence: 99%

N‐CDAD in Canada: Results of the Canadian Nosocomial Infection Surveillance Program 1997 N‐CDAD Prevalence Surveillance Project

Hyland

Ofner-Agostini²,

Miller

et al. 2001

Canadian Journal of Infectious Diseases and Medical Microbiolog

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BACKGROUND:A 1996 preproject survey among Canadian Hospital Epidemiology Committee (CHEC) sites revealed variations in the prevention, detection, management and surveillance ofClostridium difficile-associated diarrhea (CDAD). Facilities wanted to establish national rates of nosocomially acquired CDAD (N-CDAD) to understand the impact of control or prevention measures, and the burden of N-CDAD on health care resources. The CHEC, in collaboration with the Laboratory Centre for Disease Control (Health Canada) and under the Canadian Nosocomial Infection Surveillance Program, undertook a prevalence surveillance project among selected hospitals throughout Canada.OBJECTIVE:To establish national prevalence rates of N-CDAD.METHODS:For six weeks in 1997, selected CHEC sites tested all diarrheal stools from inpatients for eitherC difficiletoxin orC difficilebacteria with evidence of toxin production. Questionnaires were completed for patients with positive stool assays who met the case definitions.RESULTS:Nineteen health care facilities in eight provinces participated in the project. The overall prevalence of N-CDAD was 13.0% (95% CI 9.5% to 16.5%). The mean number of N-CDAD cases were 66.3 cases/100,000 patient days (95% CI

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Section: Discussionmentioning

confidence: 99%

N‐CDAD in Canada: Results of the Canadian Nosocomial Infection Surveillance Program 1997 N‐CDAD Prevalence Surveillance Project

Hyland

Ofner-Agostini²,

Miller

et al. 2001

Canadian Journal of Infectious Diseases and Medical Microbiolog

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“…This initial immune challenge is thought to occur in infancy, as approximately 50 70% of healthy adults have detectable serum IgG and IgA antibodies to C. difficile toxins [Kelly et al 1992;SanchezHurtado et al 2008;Viscidi et al 1983;Warny et al 1994].…”

Section: Protective Role Of Regulatory Cytokinesmentioning

confidence: 99%

The host immune response to Clostridium difficile infection

Solomon

2013

Therapeutic Advances in Infection

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Clostridium difficile infection (CDI) is the most common infectious cause of healthcare-acquired diarrhoea. Outcomes of C. difficile colonization are varied, from asymptomatic carriage to fulminant colitis and death, due in part to the interplay between the pathogenic virulence factors of the bacterium and the counteractive immune responses of the host.Secreted toxins A and B are the major virulence factors of C. difficile and induce a profound inflammatory response by intoxicating intestinal epithelial cells causing proinflammatory cytokine release. Host cell necrosis, vascular permeability and neutrophil infiltration lead to an elevated white cell count, profuse diarrhoea and in severe cases, dehydration, hypoalbuminaemia and toxic megacolon. Other bacterial virulence factors, including surface layer proteins and flagella proteins, are detected by host cell surface signal molecules that trigger downstream cell-mediated immune pathways.Human studies have identified a role for serum and faecal immunoglobulin levels in protection from disease, but the recent development of a mouse model of CDI has enabled studies into the precise molecular interactions that trigger the immune response during infection. Key effector molecules have been identified that can drive towards a protective anti-inflammatory response or a damaging proinflammatory response.The limitations of current antimicrobial therapies for CDI have led to the development of both active and passive immunotherapies, none of which have, as yet been formally approved for CDI. However, recent advances in our understanding of the molecular basis of host immune protection against CDI may provide an exciting opportunity for novel therapeutic developments in the future.

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“…A number of studies also support the activation of humoral immune responses to C. difficile toxin proteins during CDI (reviewed in [66] ). Most healthy adults have detectable serum antibody titers to TcdA and TcdB (as well as nontoxin antigens) that may originate from transient environmental exposure to C. difficile from infancy [67] . The antitoxin antibody responses (e.g., IgG) in relation to the clinical course of CDI, as well as disease recurrence, have been reported in a number of studies [62,6871] .…”

Section: The Host Immune Response To C Difficile Infectionmentioning

confidence: 99%

Gastrointestinal dysbiosis and the use of fecal microbial transplantation inClostridium difficileinfection

Schenck

Beck

MacDonald

2015

WJGP

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The impact of antibiotics on the human gut microbiota is a significant concern. Antibiotic-associated diarrhea has been on the rise for the past few decades with the increasing usage of antibiotics. Clostridium difficile infections (CDI) have become one of the most prominent types of infectious diarrheal disease, with dramatically increased incidence in both the hospital and community setting worldwide. Studies show that variability in the innate host response may in part impact upon CDI severity in patients. That being said, CDI is a disease that shows the most prominent links to alterations to the gut microbiota, in both cause and treatment. With recurrence rates still relatively high, it is important to explore alternative therapies to CDI. Fecal microbiota transplantation (FMT) and other types of bacteriotherapy have become exciting avenues of treatment for CDI. Recent clinical trials have generated excitement for the use of FMT as a therapeutic option for CDI; however, the exact components of the human gut microbiota needed for protection against CDI have remained elusive. Additional investigations on the effects of antibiotics on the human gut microbiota and subsequent CDI will help reduce the socioeconomic burden of CDI and potentially lead to new therapeutic modalities.

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Serum Antibody Response to Toxins A and B of Clostridium difficile

Cited by 191 publications

References 12 publications

N‐CDAD in Canada: Results of the Canadian Nosocomial Infection Surveillance Program 1997 N‐CDAD Prevalence Surveillance Project

N‐CDAD in Canada: Results of the Canadian Nosocomial Infection Surveillance Program 1997 N‐CDAD Prevalence Surveillance Project

The host immune response to Clostridium difficile infection

Gastrointestinal dysbiosis and the use of fecal microbial transplantation inClostridium difficileinfection

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