22 research outputs found

    Following in the footsteps of smallpox: can we achieve the global eradication of measles?

    No full text
    BACKGROUND: Although an effective measles vaccine has been available for almost 40 years, in 2000 there were about 30 million measles infections worldwide and 777,000 measles-related deaths. The history of smallpox suggests that achieving measles eradication depends on several factors; the biological characteristics of the organism; vaccine technology; surveillance and laboratory identification; effective delivery of vaccination programmes and international commitment to eradication. DISCUSSION: Like smallpox, measles virus has several biological characteristics that favour eradication. Humans are the only reservoir for the virus, which causes a visible illness and infection leading to life-long immunity. As the measles virus has only one genetic serotype which is relatively stable over time, the same basic vaccine can be used world-wide. Vaccination provides protection against measles infection for at least 15 years, although efficacy may be reduced due to host factors such as nutritional status. Measles vaccination may also confer other non-specific health benefits leading to reduced mortality. Accurate laboratory identification of measles cases enables enhanced surveillance to support elimination programmes. The "catch-up, keep-up, follow-up" vaccination programme implemented in the Americas has shown that measles elimination is possible using existing technologies. On 17th October 2003 the "Cape Town Measles Declaration" by the World Health Organisation and the United Nations Childrens Fund called on governments to intensify efforts to reduce measles mortality by supporting universal vaccination coverage and the development of more effective vaccination. SUMMARY: Although more difficult than for smallpox, recent experience in the Americas suggests that measles eradication is technically feasible. Growing international support to deliver these programmes means that measles, like smallpox, may very well become a curiosity of history

    Host erythrocyte polymorphisms and exposure to Plasmodium falciparum in Papua New Guinea.

    No full text
    Contains fulltext : 69991.pdf (Publisher’s version ) (Open Access)BACKGROUND: The protection afforded by human erythrocyte polymorphisms against the malaria parasite, Plasmodium falciparum, has been proposed to be due to reduced ability of the parasite to invade or develop in erythrocytes. If this were the case, variable levels of parasitaemia and rates of seroconversion to infected-erythrocyte variant surface antigens (VSA) should be seen in different host genotypes. METHODS: To test this hypothesis, P. falciparum parasitaemia and anti-VSA antibody levels were measured in a cohort of 555 asymptomatic children from an area of intense malaria transmission in Papua New Guinea. Linear mixed models were used to investigate the effect of alpha+-thalassaemia, complement receptor-1 and south-east Asian ovalocytosis, as well as glucose-6-phosphate dehydrogenase deficiency and ABO blood group on parasitaemia and age-specific seroconversion to VSA. RESULTS: No host polymorphism showed a significant association with both parasite prevalence/density and age-specific seroconversion to VSA. CONCLUSION: Host erythrocyte polymorphisms commonly found in Papua New Guinea do not effect exposure to blood stage P. falciparum infection. This contrasts with data for sickle cell trait and highlights that the above-mentioned polymorphisms may confer protection against malaria via distinct mechanisms

    Conquering malaria: enhancing the impact of effective interventions towards elimination in the diverse and changing epidemiology.

    No full text
    Malaria remains a major global disease burden causing just under a million deaths each year, mainly of children and pregnant women in sub-Saharan Africa. It consumes up to 40% of public health expenditure of these poor countries, causing in Africa US$ 12 billion in lost GDP every year. This should not be acceptable since malaria is preventable, and there is clear evidence that optimal use of current tools can reduce much of the suffering and deaths. Three major factors allowing this to happen include: (i) inadequate funding to implement a massive initial surge, to achieve universal coverage, (ii) weak country capacities for rapid scale up of such interventions and little or no use of evidence-guided methods, and (iii) insufficient coordination of efforts between national programmes, donors and technical agencies in strategic planning for sustaining gains and in building capacity. We discuss the importance of the surge and the kind of approaches that would accelerate the pace toward elimination and eventual eradication

    Reduced risk of Plasmodium vivax malaria in Papua New Guinean children with Southeast Asian ovalocytosis in two cohorts and a case-control study

    No full text
    BACKGROUND: The erythrocyte polymorphism, Southeast Asian ovalocytosis (SAO) (which results from a 27-base pair deletion in the erythrocyte band 3 gene, SLC4A1Delta27) protects against cerebral malaria caused by Plasmodium falciparum; however, it is unknown whether this polymorphism also protects against P. vivax infection and disease. METHODS AND FINDINGS: The association between SAO and P. vivax infection was examined through genotyping of 1,975 children enrolled in three independent epidemiological studies conducted in the Madang area of Papua New Guinea. SAO was associated with a statistically significant 46% reduction in the incidence of clinical P. vivax episodes (adjusted incidence rate ratio [IRR] = 0.54, 95% CI 0.40-0.72, p>0.0001) in a cohort of infants aged 3-21 months and a significant 52% reduction in P. vivax (blood-stage) reinfection diagnosed by PCR (95% CI 22-71, p = 0.003) and 55% by light microscopy (95% CI 13-77, p = 0.014), respectively, in a cohort of children aged 5-14 years. SAO was also associated with a reduction in risk of P. vivax parasitaemia in children 3-21 months (1,111/microl versus 636/microl, p = 0.011) and prevalence of P. vivax infections in children 15-21 months (odds ratio [OR] = 0.39, 95% CI 0.23-0.67, p = 0.001). In a case-control study of children aged 0.5-10 years, no child with SAO was found among 27 cases with severe P. vivax or mixed P. falciparum/P. vivax malaria (OR = 0, 95% CI 0-1.56, p = 0.11). SAO was associated with protection against severe P. falciparum malaria (OR = 0.38, 95% CI 0.15-0.87, p = 0.014) but no effect was seen on either the risk of acquiring blood-stage infections or uncomplicated episodes with P. falciparum. Although Duffy antigen receptor expression and function were not affected on SAO erythrocytes compared to non-SAO children, high level (<90% binding inhibition) P. vivax Duffy binding protein-specific binding inhibitory antibodies were observed significantly more often in sera from SAO than non-SAO children (SAO, 22.2%; non-SAO, 6.7%; p = 0.008). CONCLUSIONS: In three independent studies, we observed strong associations between SAO and protection against P. vivax malaria by a mechanism that is independent of the Duffy antigen. P. vivax malaria may have contributed to shaping the unique host genetic adaptations to malaria in Asian and Oceanic populations. Please see later in the article for the Editors' Summar

    Malaria Species And Southeast Asian Ovalocytosis Defined By A 27-BP Deletion In The Erythrocyte Band 3 Gene

    No full text
    To evaluate the resistance of SAO against species specific malaria infection, relationships between parasite species and the 27-bp deletion in the band 3 gene were studied in malaria endemic Sumba Island, eastern Indonesia. Thick blood films were prepared from patients with malaria symptoms (n=129) and healthy controls (n=231). Species of Plasmodium was identified by microscopic observation. The 27-bp deletion was screened by the PCR method. Among 231 healthy controls, 29 (12.6%) had the 27-bp deletion, whereas 14 (10.9%) among 129 patients confirmed with malaria infection harbored the 27-bp deletion. No significant difference was observed in the prevalence of the 27-bp deletion between controls and patients (p>0.8). There was no significant difference in the frequency of the 27-bp deletion between P. vivax and P. falciparum infected subjects at 5% level by Fisher’s exact test. The present result showing no correlation between the presence of the 27-bp deletion and infected parasite species is consistent with the post-invasion resistance hypothesis that may involve not a single malaria species

    Correspondence: Strengthening capacity, collaboration and quality of clinical research in Africa: EDCTP Networks of Excellence

    No full text
    Developing countries bear 90% of the global disease burden, but only access about 10% of globally available health research funding. Weak south–south networking hampers effective use of limited resources,production of critical mass of quality scientists, career opportunities and incentives to retain the few available scientists. The south must urgently act strategically to accelerate generation of talented scientists, createenabling environment and incentives to retain scientists and attract back those in diaspora. The creation of strong networks of excellence for clinical research among southern academic and research institutions is a novelstrategic approach championed by European and Developing Countries Clinical Trials Partnership to achieve the aforementioned goals and mitigate the high disease burden. It will promote strong collaboration, resource sharing and cross-mentorship allowing each partner to grow with complementary capacities that support each other rather than compete negatively. It will enable the south and Africa in particular to participate actively and own the means for solving its own health problems and raise the professional quality and capacity of southern institutions to forge better and equal partnership with northern institutions

    Haptoglobin levels are associated with haptoglobin genotype and a+-thalassaemia in a malaria-endemic area

    No full text
    Haptoglobin (Hp) is an acute phase protein that removes free hemoglobin (Hb) released during hemolysis. Hp has also been shown to be toxic for malaria parasites. a+-Thalassemia is a hemoglobinopathy that results in subclinical hemolytic anemia. a+-Thassemia homozygosity confers protection against severe malarial disease by an as yet unidentified mechanism. Hp levels were measured in a serial cross-sectional survey of children in Madang Province, Papua New Guinea (PNG). Hp levels were related to age, Hp genotype, Hb levels, parasitemia, splenomegaly, and ot+-thalassemia genotype. Surprisingly, children who were homozygous for a+-thalassemia had significantly higher levels of Hp than did heterozygotes, after controlling for relevant confounders. We suggest that this is the result of either reduced mean cell Hb associated with a+-thalassemia homozygosity or an elevated IL-6-dependent acute phase response
    corecore