HLA molecules and nasal carriage of Staphylococcus aureus isolated from dialysis and kidney transplant patients at a hospital in Southern Brazil
1 Ingá/UNINGÁ-Maringá Nursing College, Universidade Estadual de Maringá (UEM), Maringá, Brazil
2 Health Sciences Center, UEM, Maringá, Brazil
3 Department of Nursing, UEM, Maringá, Brazil
4 Department of Statistics, UEM, Maringá, Brazil
5 Department of Basic Health Sciences, UEM, Maringá, Brazil
6 Universidade Estadual de Maringá (UEM), Av. Colombo, 5790, Zona 07, Maringá, Paraná, Brazil 87020-900
BMC Research Notes 2012, 5:90 doi:10.1186/1756-0500-5-90Published: 9 February 2012
Healthy individuals can host Staphylococcus aureus in the nasopharynx, body surface and vagina. Most invasive infections by this bacterium are endogenous, caused by strains spread from the nasopharynx of carriers. S. aureus is a pathogen involved in the etiology of hospital- and community-acquired infections. Transplant and dialysis patients are at risk of colonization or infection by multi-resistant S. aureus. Infection is directly linked to individual immunity, and the major histocompatibility complex (MHC) plays a crucial role in determining susceptibility to diseases. Different MHC specificities have been shown to be more frequent in individuals suffering from certain diseases. This study aimed to investigate the association between HLA class I (HLA-A and -B) and class II (HLA-DRB1) molecules and nasal carriage of S. aureus in dialysis and kidney transplant patients at a hospital in Southern Brazil.
The sample consisted of 70 dialysis and 46 kidney transplant patients, totaling 116 patients. All subjects were typed for HLA molecules using LABType® SSO (One Lambda). Nasal swab samples of S. aureus were isolated from the nasal cavity (both nostrils) of patients undergoing dialysis or kidney transplantation.
In renal dialysis patients, HLA-A*02 was the most frequent allele in both carriers (25.5%) and non-carriers (21.2%) of S. aureus. Allele A*68 was not observed in the carrier group, but the allele was observed six times in the non-carrier group (p = 0.0097). Regarding HLA-B and HLA-DRB1, no allele was shown to be involved in protection against or susceptibility to carriage of S. aureus. In kidney transplant patients, allele A*03 was more frequent in the non-carrier (20.83%) than in the carrier (5.88%) group (p = 0.0486). HLA-B*15 was present in carriers (5.88%) and non-carriers (25%) (p = 0.0179). Regarding class II alleles, DRB1*03 appeared to be related to susceptibility to carriage of S. aureus (p = 0.0319).
Our findings suggest that HLA-DRB1*03 may be involved in susceptibility to nasal carriage of S. aureus in transplant patients. In addition, HLA-A*68 (dialysis patients) and HLA-A*03 and HLA-B*15 (transplant patients) appear to be associated with increased resistance to S. aureus nasal carriage.