Trachoma is the most common cause of infectious blindness worldwide.1 In 1996, WHO established the Alliance for the Global Elimination of Blinding Trachoma by the year 2020 (GET 2020), and recommended endemic countries to implement the SAFE strategy (surgery to correct distorted upper eyelids of patients with advanced disease; antibiotic treatment for the infection; facial cleanliness to reduce transmission; and environmental change to increase access to clean water and improve sanitation). Trachoma has recently been identified as a candidate for integrated control with other so-called neglected diseases.
A major component of the SAFE strategy is mass administration of the macrolide antibiotic azithromycin, which has been donated by Pfizer to national trachoma control programmes that are implementing the comprehensive strategy. This has provided the incentive to monitor the distribution of bacterial load in the community before and after treatment, and recent studies have measured the rate of reinfection after mass treatment in various epidemiological settings. These studies have shown the heterogeneous response of communities to mass treatment, with the prevalence of infection in some communities showing a sustained reduction, whereas in other communities prevalence rapidly returns to pretreatment levels. Furthermore, the likely effect of a reduction in the incidence of infection on the occurrence of scarring and blindness in later years of life remains unclear. Understanding the relation between the distribution of infection and disease in the population, the role of heterogeneity in the environment and in behaviour, and the response of trachoma-endemic communities to mass treatment remains a major challenge.
We review trachoma immunobiology and mechanisms of disease pathogenesis, and show how these mechanisms lead to observed distributions of bacterial infection and disease in the population. We begin with a brief overview of trachoma immunology and then provide a simple conceptual model of pathogenesis in infected individuals. We then review data on the population distribution of infection, bacterial load, and clinical disease in trachoma-endemic communities. Inclusion of the simple conceptual model of pathogenesis in a mathematical model of transmission reproduces the observed population distributions of infection, bacterial load, active disease, and blindness by age in a series of illustrative fits. Although the general fit of this model to a set of available data is good, the discrepancies underscore the importance of heterogeneity in the immune response of individuals to repeated infection. The Review ends with a discussion of the implications for the effect of control programmes on blindness caused by trachoma.
PCR and POC Assay
IgG anti-pgp3 speci?c antibody response was determined by direct ELISA. Microtitre plates were coated overnight at 4 8C with 100 ml of pgp3 at the concentration of 6 mg/ml in carbonate buffer pH 9.6, then blocked with skimmed milk 5% (w/v) in carbonate buffer pH 9.6. In subsequent stages, the wells received 100 ml of reagents diluted in skimmed milk containing 5% (w/v) Tween 20/ PBS pH 7.4. All sera diluted 1:100 were assayed in duplicate. Each plate assayed included replicate dilutions of two reference sera with known activity. The plates were incubated at 37 8C for 60 min, then washed ...