Pneumococcal colonization rates are low in recipients of solid organ transplants, but most of the colonizing serotypes are not included in pneumococcal vaccines, according to study results published in BMC Infectious Diseases.
One of the major causes of death worldwide is Streptococcus pneumoniae. Invasive pneumococcal disease is an important cause of disease in the elderly; children (age <1 year); and in people with certain medical conditions, such as a history of organ transplantation. Invasive and non-invasive infection with S pneumoniae can be a significant reason for morbidity and mortality in solid organ transplant recipients, with a 12.8-fold greater incidence of invasive pneumococcal disease compared with the general population. Further, specific incidences vary according to the organ transplanted. The polysaccharide capsule is one of the most important virulence factors of S pneumoniae with approximately 90 different pneumococcal serotypes identified and 20 types causing most invasive pneumococcal disease. Knowing which serotypes are the most invasive has allowed for the development of current vaccines; however, although recommendations for solid organ transplant recipients emphasize vaccinating all candidates before transplantation, this is not practiced.
These recommendations are based on healthy individuals and not a well-defined cohort of solid organ transplant recipients. Colonization of the nasopharynx is an initial step in the evolution of invasive pneumococcal disease with transmission from human carriers. However, the prevalence of colonization and of the colonizing/infecting serotypes has not been studied in the population of people who receive solid organ transplantation; this information would further the understanding of the dynamics of serotypes in this population and whether those serotypes are included in currently available vaccines. Therefore, this prospective, observational, cohort study described the rate, characteristics, and clinical effect of S pneumoniae nasopharyngeal carriage in solid organ transplant recipients.
A total of 500 patients from a solid organ transplant recipient cohort at the University Hospital Virgen de Rocio in Seville, Spain were included in the study. Each patient provided 2 different pharyngeal swab samples during 2 different seasons: winter and spring/summer. To isolate the strains, optochin and bile solubility tests and antimicrobial susceptibility tests were performed for each isolate. Using sequential multiplex polymerase chain reaction, capsular typing was performed. To determine factors that were potentially associated with pneumococcal nasopharyngeal carriage and disease, a multivariate logistic regression analysis was performed.
Results showed that pneumococcal colonization in the solid organ transplant recipients was low and most of the colonizing serotypes in this population were not included in the pneumococcal vaccine. Of the included patients, 26 (5.6%) were colonized in the winter period and 15 (3.2%) in the spring/summer period. Compared with non-colonized patients, the colonized solid organ transplant recipients were more frequently men (P <.05) and cohabitated regularly with children (P <.001). Between both study periods, the most prevalent pneumococcal serotype was 35B and 45% of total isolates were included in the pneumococcal vaccine PPV23. The antimicrobial susceptibility tests showed that trimethoprim-sulfamethoxazole and macrolides were the less active antibiotics. Of the patients, 3 had non-bacteremic pneumococcal pneumonia and 2 of these patients died.
Overall, the study authors concluded that, “The incidence of non-bacterermic pneumococcal pneumonia was low, although two out of the three patients died, suggesting the need of pneumococcal vaccination for the [solid organ transplant recipients].”
Roca-Oporto C, Cebrero-Cangueiro T, Gil-Marques ML, et al. Prevalence and clinical impact of Streptococcus pneumoniae nasopharyngeal carriage in solid organ transplant recipients [published online August 6, 2019]. BMC Infectious Diseases. doi:10.1186/s12879-019-4321-8
This article originally appeared on Infectious Disease Advisor