Natural Clostridioides difficile Toxin Immunization in Colonized Infants.


Journal

Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213

Informations de publication

Date de publication:
06 05 2020
Historique:
received: 26 04 2019
accepted: 26 06 2019
pubmed: 30 6 2019
medline: 7 1 2021
entrez: 30 6 2019
Statut: ppublish

Résumé

Clostridioides (Clostridium) difficile colonization is common among infants. Serological sequelae of infant C. difficile colonization are poorly understood. In this prospective cohort study of healthy infants, stools serially collected between ages 1-2 and 9-12 months were tested for non-toxigenic and toxigenic C. difficile (TCD). Cultured isolates underwent whole-genome sequencing. Serum collected at 9-12 months underwent measurement of IgA, IgG, and IgM against TCD toxins A and B and neutralizing antibody (NAb) titers against toxin B. For comparison, antitoxin IgG and NAb were measured in cord blood from 50 mothers unrelated to study infants. Among 32 infants, 16 (50%) were colonized with TCD; 12 were first colonized >1 month before serology measurements. A variety of sequence types were identified, and there was evidence of putative in-home (enrolled siblings) and outpatient clinic transmission. Infants first colonized with TCD >1 month prior had significantly greater serum antitoxin IgA and IgG against toxins A (P = .02 for both) and B (P = .009 and .008, respectively) compared with non-TCD-colonized infants, and greater IgG compared with unrelated cord blood (P = .005). Five of 12 (42%) colonized infants had detectable NAb titers compared with zero non-TCD-colonized infants (P = .02). Breastfeeding was not associated with differences in serological measurements. TCD colonization is associated with a humoral immune response against toxins A and B, with evidence of toxin B neutralization in vitro. The extent and duration of protection against CDI later in life afforded by natural C. difficile immunization events require further investigation.

Sections du résumé

BACKGROUND
Clostridioides (Clostridium) difficile colonization is common among infants. Serological sequelae of infant C. difficile colonization are poorly understood.
METHODS
In this prospective cohort study of healthy infants, stools serially collected between ages 1-2 and 9-12 months were tested for non-toxigenic and toxigenic C. difficile (TCD). Cultured isolates underwent whole-genome sequencing. Serum collected at 9-12 months underwent measurement of IgA, IgG, and IgM against TCD toxins A and B and neutralizing antibody (NAb) titers against toxin B. For comparison, antitoxin IgG and NAb were measured in cord blood from 50 mothers unrelated to study infants.
RESULTS
Among 32 infants, 16 (50%) were colonized with TCD; 12 were first colonized >1 month before serology measurements. A variety of sequence types were identified, and there was evidence of putative in-home (enrolled siblings) and outpatient clinic transmission. Infants first colonized with TCD >1 month prior had significantly greater serum antitoxin IgA and IgG against toxins A (P = .02 for both) and B (P = .009 and .008, respectively) compared with non-TCD-colonized infants, and greater IgG compared with unrelated cord blood (P = .005). Five of 12 (42%) colonized infants had detectable NAb titers compared with zero non-TCD-colonized infants (P = .02). Breastfeeding was not associated with differences in serological measurements.
CONCLUSIONS
TCD colonization is associated with a humoral immune response against toxins A and B, with evidence of toxin B neutralization in vitro. The extent and duration of protection against CDI later in life afforded by natural C. difficile immunization events require further investigation.

Identifiants

pubmed: 31253983
pii: 5525163
doi: 10.1093/cid/ciz582
pmc: PMC7201415
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2095-2102

Subventions

Organisme : NIDDK NIH HHS
ID : P30 DK056338
Pays : United States
Organisme : NIAID NIH HHS
ID : K23 AI123525
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001422
Pays : United States
Organisme : NIAID NIH HHS
ID : K24 AI104831
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI132711
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI109776
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI116596
Pays : United States

Informations de copyright

© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America. All rights reserved. For permissions, e-mail: journals.permissions@oup.com.

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Auteurs

Larry K Kociolek (LK)

Department of Pediatrics, Northwestern University Feinberg School of Medicine.
Division of Infectious Diseases, Ann & Robert H. Lurie Children's Hospital of Chicago.

Robyn O Espinosa (RO)

Division of Infectious Diseases, Ann & Robert H. Lurie Children's Hospital of Chicago.

Dale N Gerding (DN)

Department of Medicine, Loyola University Chicago Stritch School of Medicine, Hines.
Department of Medicine, Edward Hines Jr Veterans Administration Hospital, Research Service, Hines.

Alan R Hauser (AR)

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago.
Department of Microbiology-Immunology, Northwestern University Feinberg School of Medicine, Chicago.

Egon A Ozer (EA)

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago.

Maria Budz (M)

Special Infectious Diseases Laboratory, Ann & Robert H. Lurie Children's Hospital of Chicago, Illinois.

Aakash Balaji (A)

Department of Pediatrics, Northwestern University Feinberg School of Medicine.

Xinhua Chen (X)

Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Robert R Tanz (RR)

Department of Pediatrics, Northwestern University Feinberg School of Medicine.
Division of Academic General Pediatrics and Primary Care, Ann & Robert H. Lurie Children's Hospital of Chicago, Illinois.

Nazli Yalcinkaya (N)

Department of Pathology and Immunology, Baylor College of Medicine and Texas Children's Hospital, Houston.

Margaret E Conner (ME)

Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas.

Tor Savidge (T)

Department of Pathology and Immunology, Baylor College of Medicine and Texas Children's Hospital, Houston.

Ciaran P Kelly (CP)

Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

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Classifications MeSH