Doris A.C. MacKenzie

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.

Factors influencing oral carriage of yeasts among individuals with diabetes mellitus

A total of 439 individuals with diabetes mellitus were examined for carriage of yeasts by the oral rinse and palatal swab techniques. Eighteen genetic or environment variables were assessed for their contribution to carriage of yeasts. The factor contributing to palatal and oral carriage of yeasts among individuals with insulin dependent diabetes mellitus (IDDM) was age (P < 0.01). The factor contributing to palatal carriage of yeasts among individuals with non-insulin dependent diabetes mellitus (NIDDM) was poor glycaemic control (glycosuria P < 0.01); carriage in the oral cavity as a whole was influenced additionally by non-secretion of ABH blood group antigens (P < 0.05). Introduction of a denture altered the above risk factors. For individuals with IDDM, oral carriage was associated with the presence of retinopathy (P < 0.05); palatal carriage was influenced by poor glycaemic control (HbA1P < 0.01, plasma glucose levels P < 0.05) and age (P < 0.05). For those with NIDDM, palatal carriage was associated with continuous presence of the denture in the mouth (P < 0.01); oral carriage was associated with plasma glucose levels (P < 0.05).

CHRONIC ATROPHIC ORAL CANDIDIASIS AMONG PATIENTS WITH DIABETES MELLITUS : ROLE OF SECRETOR STATUS

Non-diabetic individuals who are non-secretors of blood group antigens are prone to superficial infections by Candida albicans. In this study, 216 patients with diabetes mellitus who were denture wearers were examined for the presence or absence of denture stomatitis. There was an overall trend for non-secretors to be prone to denture stomatitis compared with secretors. Stepwise linear discriminant analysis was used to dissect the contribution of secretor status and other variables to the development of the disease. Secretor status was found to be a contributory factor among patients with non-insulin dependent diabetes but not among those with insulin-dependent diabetes. The possible reasons for this are discussed.

Identification of oral yeast species isolated from individuals with diabetes mellitus

Summary. In our epidemiological study of 439 patients with diabetes mellitus, the proportion of Candida albicans isolated by the oral rinse technique was 67%. A comparison of the conventional germ tube test with the API 20C Auxanogram kit revealed that 23.6% (129/546) of germ tubepositive species were not identified as C. albicans by the kit. The API 20C Auxanogram therefore underestimated the prevalence of C. albicans. Additionally, a significant number of yeasts (138/1050, 13.1%) isolated from these patients could not be reliably identified by the kit.

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

Adhesins Of Staphylococcus Aureus that Bind Lewisa Antigen

Sudden Infant Death Syndrome (SIDS) is defined as “the sudden death of any infant or young child which is unexpected by history, and in which a thorough postmortem examination fails to demonstrate an adequate cause of death” [Beckwith, 1969]. Since 1990, there has been a steady reduction in the numbers of SIDS in Britain [Court, 1995; Scottish Cot Death Trust, personal communication]; however, SIDS is still the major cause of post perinatal mortality during the first year of life. Petechiae in the lungs and thymus, liquid heart blood and empty bladder are common findings at autopsy [Berry, 1992]. While there is little evidence that could explain why the infant died, there are common findings that suggest immune or inflammatory reactions have been elicited before death(Table 1).

Assessment of Lewis blood group antigens and secretor status in autopsy specimens

The ability of enzyme linked immunosorbent assays (ELISA) to detect Lewis and H antigens in secretions obtained from 280 autopsies was assessed. The ELISA results were compared with those for matched blood specimens examined by agglutination of erythrocytes by monoclonal anti-Lewis(a) and anti-Lewis(b) antibodies. There was good agreement between the results for the two tests and the ELISAs could be used to determine secretor status of the subject. While determination of ABO group with monoclonal anti-A and anti-B was possible even with lysed blood, the results for Lewis typing by erythrocyte agglutination were poor if the sample was lysed or partially lysed. Detection of the antigens by ELISA was as efficient among elderly subjects as among younger ones and both H and Lewis antigens could be detected on erythrocytes and in secretions up to 127 h after death.