Management of hypercholesterolaemia in postmenopausal women

of time from geographic exposure to the organism to clinical infection is 26 years. " Serological prevalence surveys of endemic areas of melioidosis, including northern Queensland, have shown that a significant proportion of the human population is infected, most commonly with subclinical or latent infection. " However, it is not known how long the organism remains in the body or how many of those persons with latent infection will develop clinical disease with time. For these reasons, we asked all adults in an isolated Aboriginal community in northeastern coastal Queensland to take part in a study that began in 1979 and ended in 1986. Two hundred and fifty of the approximately 330 adults who were resident in the community entered the study. They were screened for the presence of circulating antibodies to Ps. pseudomallei by the indirect haemagglutination test,' and 25 (10070) persons were found to be seropositive (titres, equal to or greater than one in 40) in the test. On the basis of the results of detailed medical examinations and chest x-ray films, the disease status of the 25 persons with positive results of melioidosis serology was determined, and all persons were classified as having the subclinical form of melioidosis. These patients were asked to return to the clinic each year for a reassessment of their medical status and for an estimation of their melioidosis antibody levels. However, only six patients could be followed every year from 1979 to 1986; of these, four patients remained seropositive for significant levels of melioidosis antibodies after the seven-year follow-up. Twenty of the original 25 patients with subclinical melioidosis were reassessed in the final year of the study. Two patients had died but not of melioidosis and a further three patients were lost to follow-up. The distribution of specific antibody titres in serum samples from the 20 patients by the time after the diagnosis of melioidosis was made is given in the Table. By 1986, seven (35%) patients had become seronegative (titres, equal to or less than one in 20) for melioidosis; the sera of three (15%) patients gave borderline reactions (titre, one in 20); and the remaining 10 (50%) patients still were seropositive. In 1982 when all 20 patients also were tested, only four (20%) patients were seronegative and one (5%) patient gave a borderline positive result. During the programme, it was found that antibody levels in three of the patients had fallen to below titres of one in 40. However, in the following year, when these three patients were tested, they were found to be seropositive (range of titres, one in 40 to one in 320). This suggests either that technical aberrations in the test or that reactivation or reinfection with Ps. pseudomallei had occurred. In general, it was found that, over the seven-year observation period, patients whose sera gave titres of greater than one in 320 were likely to remain seropositive, while patients whose sera gave titres of equal to or less than one in 160 were more likely to become seronegative. In 1985, the sera from 108 adults from the community who had been tested in 1979 and who had been found to be seronegative for the presence of melioidosis antibody were retested by the indirect haemagglutination test. Two persons were found to be seropositive. There was no clinical, radiological or haematological evidence that, at any time during the study, any patient was suffering from clinical melioidosis. On one occasion, serum samples from two patients gave titres of one in 40 for immunoglobulin (Ig)M antibody to Ps. pseudomallei by the indirect fluorescent antibody test, a feature that usually is associated with active infection.s Others also have noted that elevated specific IgM antibody levels, as detected by this test, may be encountered occasionally in healthy persons. " Sixty-five per cent of persons with subclinical melioidosis still had detectable antibody levels (titres, equal to or greater than one in 20) seven years after the initial diagnosis, and the persistence of elevated titres in the indirect haemagglutination test is thought to indicate latent infection. ' However, because active infection with Ps. pseudomal/ei did not develop in any of the patients with melioidosis antibodies, it would appear that the rate of the conversion of the disease state from latent to active infection in patients who initially have been diagnosed as having subclinical melioidosis is so low that the exercise of the follow-up of asymptomatic patients with positive results of serological testing is not worth while. John E. Thompson, FRACP Cairns Base Hospital, The Esplanade. Cairns. QLD 4870 Leslie R. Ashdown, PhD Pathology Laboratory Commonwealth Department of Community Services and Health 11-15 Clifton Street. Townsville, QLD 4810 1. Sanford JP. Melioidosis: forgotten but not gone. Trans Am Clin Climat A. «oc 1977; 8: 201-205. 2. Mays EE, Ricketts RA. Melioidosis: recrudescence associated with bronchogenic carcinoma twenty-six years following initial geographic exposure. Chest 1975; 68: 261-262. 3. Ashdown LR, Guard RW. The prevalence of human melioidosis in Northern Queensland. Am J Trop Med Hyg 1984; 33: 474-478. 4. Ashdown LR. Indirect haemagglutination test for melioidosis. Med J Ausl 1987; 147: 364-365. 5. Ashdown LR. Relationship and significance of specific immunoglobulin M antibody response in clinical and subclinical melioidosis. J Clin Microbiol 1981; 14: 361-364. 6. Khupulaup K, Petchclai B. Application of indirect hemagglutination test and indirect fluorescent antibody test for IgM antibody for diagnosis of melioidosis in Thailand. Am J Trop Med Hyg 1986; 35: 366-369.