ABSTRACT
AIMS: To assess the role of migration from high-incidence countries, HIV/AIDS infection, and prevalence of multi-drug resistant organisms as contributors to tuberculosis (TB) incidence in New Zealand (NZ) relative to ongoing local transmission and reactivation of disease. METHODS: TB notification data and laboratory data for the period 1995 to 2004 and population data from the 1996 and 2001 Census were used to calculate incidence rates of TB by age and ethnicity, country of birth (distinguishing high and low -incidence countries), and interval between migration and onset of disease. Published reports of multi-drug-resistant TB for the period 1995 to 2004 were reviewed. Anonymous HIV surveillance data held by AIDS Epidemiology Group were matched with coded and anonymised TB surveillance data to measure the extent of HIV/AIDS coinfection in notified TB cases. RESULTS: Migration of people from high-TB incidence countries is the main source of TB in NZ. Of those who develop TB, a quarter does so within a year of migration, and a quarter of this group (mainly refugees) probably enter the country with pre-existing disease. Rates of local TB transmission and reactivation of old disease are declining steadily for NZ-born populations, except for NZ-born Maori and Pacific people under 40. HIV/AIDS and multi-drug-resistant organisms are not significant contributors to TB incidence in NZ and there is no indication that their role is increasing. CONCLUSION: TB incidence is not decreasing in NZ mainly due to migration of TB infected people from high-incidence countries and subsequent development of active disease in some of them in NZ. This finding emphasises the importance of regional and global TB control initiatives. Refugees and migrants are not acting as an important source of TB for most NZ-born populations. Those caring for them should have a high level of clinical suspicion for TB.
Subject(s)
Disease Outbreaks/prevention & control , Emigration and Immigration/statistics & numerical data , Tuberculosis/epidemiology , Acquired Immunodeficiency Syndrome/epidemiology , Acquired Immunodeficiency Syndrome/ethnology , Adult , Africa/ethnology , Age Distribution , Aged , Asia/ethnology , Australia/ethnology , Child , Comorbidity , Drug Resistance, Multiple/ethnology , Europe/ethnology , HIV Infections/epidemiology , HIV Infections/ethnology , Humans , Incidence , Middle Aged , New Zealand/epidemiology , North America/ethnology , Pacific Islands/ethnology , Population Surveillance , Tuberculosis/ethnologyABSTRACT
PURPOSE: P-glycoprotein 170 encoded by the multidrug resistance 1 (MDR1) gene exports various antiepileptic drugs out of the CNS, which leads to multidrug resistance. This study was performed to elucidate the relationship between single nucleotide polymorphisms (SNPs) in the MDR1 gene and drug resistance in Koreans with epilepsy. SUBJECTS AND METHODS: Three SNPs at nucleotide position 1236 in exon 12, 2677 in exon 21 and 3435 in exon 26 of the MDR1 gene were genotyped in 207 Korean epileptics. Subjects were classified according to whether they had drug-resistant (RS group; N=99) or drug-responsive epilepsy (RP group; N=108). The frequencies of genotype and haplotype were compared between the RS and RP groups. RESULTS: The frequencies of genotype and haplotype in the RS group were not statistically different from those in the RP group. CONCLUSIONS: In Korean epileptics, there was no significant relationship between three known SNPs in MDR1 and drug resistance. And there was no association of MDR1 haplotype based on above three sites with pharmacoresistance.
