Valerie S. James

Association between secretor status and respiratory viral illness.

OBJECTIVE--To determine whether non-secretion of blood group antigens is associated with respiratory virus diseases. DESIGN--Study of secretor status in patients with respiratory virus diseases determined by an enzyme linked immunosorbent assay (ELISA) developed to identify Lewis (Le) blood group antigen phenotypes (Le(a) non-secretor; Le(b) secretor). SUBJECTS--Patients aged 1 month to 90 years in hospital with respiratory virus diseases (584 nasal specimens). MAIN OUTCOME MEASURES--Criteria for validation of ELISA (congruence between results on ELISA testing of 1155 saliva samples from a previous study and previously established results on haemagglutination inhibition (HAI) testing, proportions of Le(a), Le(b), and Le- phenotypes in 872 samples of nasal washings from a previous study compared with the normal population). Secretor status of patients determined by ELISA and viruses isolated. RESULTS--Agreement between HAI and ELISA for 1155 saliva samples was 97%. Lewis antigens were detected by ELISA in 854 (97.9%) of nasal washings (Le(a) 233 (26.7%), Le(b) 621 (71.2%), and Le- 18 (2.1%)) in proportions predicted for a northern European population. Secretors were significantly overrepresented among patients from whom influenza viruses A and B (55/64, 86%; p less than 0.025), rhinoviruses (63/72, 88%; p less than 0.01), respiratory syncytial virus (97/109, 89%; p less than 0.0005), and echoviruses (44/44, p less than 0.0005) had been isolated compared with the distribution of secretors in the local population. CONCLUSION--Secretion of blood group antigens is associated with respiratory virus diseases.

Secretor status, smoking and carriage of Neisseria meningitidis.

A survey of ABO blood groups, secretor status and smoking habits among 389 students and staff of a school in which there was an outbreak of meningococcal disease found no difference in the distribution of the ABO blood groups but a significantly higher proportion of non-secretors (37.6%) in the population examined compared with that reported for previous surveys of the neighbouring population in Glasgow (26.2%) (P less than 0.0005). There was also a significantly higher proportion of non-secretors among carriers of meningococci (47%) compared with non-carriers (32%). Increased carriage of meningococci among non-secretors might contribute to the increased susceptibility of individuals with this genetic characteristic to meningococcal disease observed in previous studies. Although passive exposure to cigarette smoke has been associated with meningococcal disease, there was no association between passive smoking and carriage. There was, however, a significant association between active smoking and carriage.

Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome

Toxigenic strains of Staphylococcus aureus have been suggested to play a role in sudden infant death syndrome (SIDS). In this study we examined two factors that might enhance binding of toxigenic staphylococci to epithelial cells of infants in the age range in which cot deaths are prevalent: expression of the Lewis(a) antigen and infection with respiratory syncytial virus (RSV). By flow cytometry we demonstrated that binding of three toxigenic strains of S. aureus to cells from nonsecretors was significantly greater than to cells of secretors. Pre-treatment of epithelial cells with monoclonal anti-Lewis(a) or anti-type-1 precursor significantly reduced bacterial binding (P < 0.01); however, attachment of the bacteria correlated only with the amount of Lewis(a) antigen detected on the cells (P < 0.01). HEp-2 cells infected with RSV bound significantly more bacteria than uninfected cells. These findings are discussed in context of factors previously associated with SIDS (mothers smoking, bottle feeding and the prone sleeping position) and a hypothesis proposed to explain some cases of SIDS.

The role of bacterial toxins in Sudden Infant Death Syndrome (SIDS)

There is increasing evidence for the involvement of bacterial toxins in some cases of sudden infant death syndrome (SIDS), particularly the pyrogenic toxins of Staphylococcus aureus. This had led to the hypothesis that some SIDS deaths are due to induction of inflammatory mediators by infectious agents or their products during a period in which the infant is unable to control these normally protective responses. The genetic, developmental and environmental risk factors identified for SIDS are assessed in relation to frequency or density of mucosal colonisation by toxigenic bacteria and their effects on induction and control of inflammatory responses to the toxins.

Blood Group and Susceptibility to Disease Caused by Escherichia coli O157

Patients (n=186) infected during the Escherichia coli O157 outbreak in Scotland in 1996 were assessed for blood group markers (ABO, Lewis, and P) associated with other gastrointestinal infections. Binding of bacteria to epithelial cells was assessed by flow cytometry. Buffy coats from blood donors were examined for inflammatory responses to culture filtrates of the outbreak strain. Individuals of blood group O comprised 63.4% of patients, compared with 53.4% (P <.05) and 53.9% (P <.01) of neighboring populations in Airdrie and Glasgow, respectively; group O also comprised 64.3% of patients with hemolytic uremic syndrome (HUS) and 87.5% of patients who died (P <.05). No or weak agglutination by anti-P antiserum was observed for 40.7% of control persons (n=122), 61.5% of all patients (P =.0027), and 83.3% of patients with HUS (P =.013). The susceptibility of group O to E. coli was not associated with increased binding of bacteria to epithelial cells or with higher production of tumor necrosis factor (TNF)-alpha or interleukin-6. Leukocytes of P-negative blood donors produced higher levels of TNF-alpha than those of P-positive donors.

The Stonehouse study: secretor status and carriage of Neisseria species.

The genetically determined inability to secrete the water-soluble glycoprotein form of the ABO blood group antigens into saliva and other body fluids is a recognized risk factor for meningococcal disease. During a community-wide investigation of a prolonged outbreak of disease due to a B15:P1.16 sulphonamide-resistant strain of Neisseria meningitidis in Stonehouse, Gloucestershire (the Stonehouse survey), the ABO blood group and secretor status of almost 5000 residents was determined. The proportion of non-secretors in the Stonehouse population was significantly higher than the proportion of non-secretors among blood donors in the South West Region and in England generally. Seven of 13 Stonehouse residents with meningococcal disease who were tested were found to be non-secretors, a high proportion. The outbreak in Stonehouse cannot be explained solely in terms of the increased proportion of non-secretors. There was no clear correlation between the proportions of non-secretors in different areas within the town and the incidence of cases of meningococcal disease. Carriers of meningococci, whether outbreak or other strains, were not more likely to be non-secretors. The reasons why non-secretors are more susceptible to meningococcal disease remain to be determined, but they do not appear to be related to carriage of meningococci.

Increased prevalence of non-secretors in patients with Graves' disease: evidence for an infective aetiology?

pedal cyclists, 98 (19%) had mild concussion, 13 (3%) had severe head injuries, and 58 (11%) had cuts and grazes. The Oxford ring road encloses 227 km of road and only 23 km of cycle lane, of which 8 km are part of the road and 15 km are separate. The number of injuries per kilometre was 0 9 on the road, 0-4 on the road cycle lane, and 0-3 on the separate cycle track. Another vehicle caused or was involved in 1012 (55%) of the accidents.

Mannan binding lectin and the sudden infant death syndrome

Mannan binding lectin (MBL) may be important for innate immunity and some cases of sudden infant death syndrome (SIDS) may be preceded by bacterial infection. Therefore, relative MBL deficiency might be associated with susceptibility to SIDS. We measured MBL concentrations in 46 SIDS infants and 26 controls. The proportion of subjects with low MBL values was similar in the two groups. However, the mean for the SIDS group (3 micrograms/ml) was higher than that of the controls (2.2 micrograms/ml; P < 0.05). We interpret this difference as due to acute phase responses and suggest these findings are consistent with the view that some cot deaths are preceded by bacterial infections.

Making sense of the risk factors for sudden infant death syndrome (SIDS): infection and inflammation

Evidence from epidemiological and laboratory studies on sudden infant death syndrome (SIDS) has led to the following hypothesis. Some cases of SIDS are due to induction of in ̄ammatory mediators by infectious agents or their products during a period in which the infant is unable to control these normally protective responses. The genetic, developmental and environmental risk factors identi®ed for SIDS are assessed in relation to this hypothesis. # 2001 Lippincott Williams & Wilkins

Non-Secretion of ABO Blood Group Antigens and Susceptibility to Infectious Diseases

“Much more attention should be given to the combined effects of blood group and secretor state on susceptibility to bacterial infections.”(1).