Fiji leaf gall is an important disease of sugarcane in Australia and other Asia-Pacific countries. The causative agent is the reovirus Fiji disease virus (FDV). Previous reports indicate that there is variation in pathology between virus isolates. To investigate the amount of genetic variation found in FDV, 25 field isolates from Australia, Papua New Guinea and Malaysia were analysed by partial sequencing of genome segments S3 and S9. There was up to 15% divergence in the nucleotide sequence among the 25 isolates. A similar amount of divergence and pattern of relationships was found for each of the two genomic segments for most of the field isolates, although reassortment of genome segments seems likely for at least one of the Papua New Guinean isolates. The finding of a high level of variation in FDV isolated in different regions has implications for quarantine and disease management.
Insecticide-treated mosquito nets were first put to practical use in the Western Pacific Region. Less than a decade after conducting workshops and other promotional activities, millions of people were protected by 1989. This occurred before the availability of commercially produced pretreated nets and before global funding for mass net distribution. This paper describes the sequence of steps leading to regional control success. The beginning stages in 1979 recognized that treating torn mosquito nets was a viable control option. Basic net treatment procedures were established by 1983 and workshops were held the next 2 years in China, Cambodia, Laos, Malaysia, Papua New Guinea, Philippines, Solomon Islands, Vanuatu, and Vietnam. Malaria staff became convinced of net benefits and were motivated to impart their knowledge to others. Village inhabitants soaked the nets in washbasins containing permethrin or deltamethrin solution, then dried them horizontally on mats. By the 1990s, the population protected by nets had appreciably increased, and regional malaria cases confirmed by microscopy were markedly reduced. This coincided with commercial interest to mass-produce pretreated mosquito nets for worldwide use.
Nearly every 2 minutes, somewhere in the world, a woman dies because of complications of pregnancy and childbirth. Every such death is an overwhelming catastrophe for everyone confronted with it. Most deaths occur in developing countries, especially in Africa and southern Asia, but a significant number also occur in the developed world.
Buruli ulcer (BU) is the third most common mycobacterial disease in immunocompetent hosts. BU is caused by Mycobacterium ulcerans, which produces skin ulcers and necrosis at the site of infection. The principal virulence factor of M. ulcerans is a polyketide-derived macrolide named mycolactone, which has cytotoxic and immunosuppressive activities. We determined the severity of inflammation, histopathology and bacillary loads in the subcutaneous footpad tissue of BALB/c mice infected with 11 different M. ulcerans isolates from diverse geographical areas. Strains from Africa (Benin, Ghana, Ivory Coast) induced the highest inflammation, necrosis and bacillary loads, whereas the strains collected from Australia, Asia (Japan, Malaysia, New Guinea), Europe (France) and America (Mexico) induced mild inflammation. Subsequently, animals were infected with the strain that exhibited the highest (Benin) or lowest (Mexico) level of virulence in order to analyse the local immune response generated. The Mexican strain, which does not produce mycolactone, induced a predominantly T helper type 1 (Th1) cytokine profile with constant high expression of the anti-microbial peptides beta defensins 3 and 4, in co-existence with low expression of the anti-inflammatory cytokines interleukin (IL)-10, IL-4 and transforming growth factor (TGF)-beta. The highly virulent strain from Benin which produces mycolactone A/B induced the opposite pattern. Thus, different local immune responses were found depending on the infecting M. ulcerans strain.