Kamini N. Mendis
University of Colombo
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Clinical and Experimental Immunology | 1999
J. Wattavidanage; Richard Carter; K. L. R. L. Perera; A. Munasingha; S. Bandara; D. Mcguinness; A. R. Wickramasinghe; H. K. Alles; Kamini N. Mendis; S. Premawansa
We have investigated the association between alleles of the genes for tumour necrosis factor‐alpha (TNF‐α) and TNF‐β and severity of disease during malarial (Plasmodium falciparum) and other infections in the Sri Lankan population. Patients were categorized as having either (i) uncomplicated malaria, (ii) severe and complicated malaria, or (iii) severe and complicated infection in which a diagnosis of malaria had been excluded. For all the patients, as well as for a group of matched healthy controls, TNF‐α and TNF‐β allelic types were identified using the polymerase chain reaction (PCR) and allele‐specific oligonucleotide probes and restriction enzyme digestion. The odds in favour of carrying the TNFα*2 allele, mainly of the heterozygous genotype (TNFα*1,*2), were two to three times greater among individuals with severe disease, of either malarial or other infectious origin, relative to healthy controls or to those with uncomplicated malarial infections. No significant risk was associated with either of the alleles of TNF‐β.
Annals of Tropical Medicine and Parasitology | 2005
S.L. Pathirana; H.K. Alles; S. Bandara; M. Phone-Kyaw; M.K. Perera; A.R. Wickremasinghe; Kamini N. Mendis; S.M. Handunnetti
Abstract Although the ABO blood group of the human host has been reported to influence malarial infection, there have been few clinical observations on this effect. A hospital-based, comparative study was therefore performed to investigate the relationship between blood-group type and severe disease inPlasmodium falciparum malaria. Overall, 243 cases of malaria (163 uncomplicated and 80 severe) and 65 patients with severe, non-malarial infections were studied. In terms of ABO-blood-group composition, the patients with severe malaria were significantly different from the patients with the uncomplicated disease (P<0.001) and also from a population control described previously (P<0.0001). The patients with uncomplicated malaria or severe but non-malarial disease were, however, similar to the population control. The cases of severe malaria were significantly less likely to be of blood group O (P=0.0003), and significantly more likely to be of group AB (P<0.0001), than the patients with nonsevere malaria. It appears that individuals who are of blood-group O are relatively resistant to the severe disease caused by P. falciparum infection.
Transactions of The Royal Society of Tropical Medicine and Hygiene | 1996
Shiroma Handunnetti; D.M. Gunewardena; P.P.S.I. Pathirana; K. Ekanayake; Sudath Weerasinghe; Kamini N. Mendis
This paper reports on the features of recrudescent infections of chloroquine-resistant Plasmodium falciparum (CQRPf) malaria from a study in vivo of patients from a malaria endemic (n = 527) and non-endemic (n = 129) region of Sri Lanka where the incidence of RI resistance was 30% and 55%, respectively. In both groups of patients, the recrudescent infections which emerged after treatment of the primary infection with chloroquine (CQ) and primaquine had significantly lower peripheral parasitaemia (0.036% and 0.108% in endemic and non-endemic patients, respectively) compared to their primary infections (mean parasitaemia 0.13% and 0.49%; P = 0.021 and 0.002, respectively). The recrudescences of CQ resistant infections also gave rise to clinical disease of markedly reduced severity (average clinical scores of 10.1 and 8.2) compared to their primary infections (average clinical scores of 12.4 and 12.3; P = 0.003 and 0.001, respectively, in endemic and non-endemic patients). CQ resistant recrudescent infections therefore had a lower probability of being diagnosed and treated. In endemic patients, a higher proportion of CQRPf infections (57%) had gametocytaemia compared to the chloroquine sensitive ones (29%) (P = 0.014, chi 2 = 5.96) and were significantly more infective to mosquitoes (P = 0.047). these findings imply that, in areas where CQ resistance is prevalent, the continued use of the drug may confer a survival and propagation advantage on resistant parasites and favour the rapid expansion of their reservoir. In support of this, we also present epidemiological evidence showing that, in endemic areas, the proportion of P. falciparum patients carrying gametocytes has increased significantly since the emergence of chloroquine resistance. These findings are relevant to the management of drug resistance and malaria control in countries where P.falciparum is only partially resistant to CQ.
Clinical and Experimental Immunology | 2008
Nadira D. Karunaweera; Richard Carter; G. E. Grau; Dominic P. Kwiatkowski; G. Del Giudice; Kamini N. Mendis
Plasmodium vivax malaria infections in non‐immune individuals manifest as periodic clinical episodes of fever with chills and rigors known as paroxysms. We have demonstrated that in non‐immune patients the period of paroxysm is associated with the transient presence of plasma factors which kill gametocytes, the intra‐erythrocytic sexual stages of the malaria parasite which transmit the infection from humans to mosquito, rendering them non‐infectious to mosquitoes. Gametocytc killing in paroxysm plasma is mediated by tumour necrosis factor (TNF) acting in conjunction with other essential serum factor(s). Plasma TNF levels were elevated during a paroxysm. In semi‐immune individuals from a P. vivax‐endemic area clinical symptoms of malaria are mild and the parasite killing factors are not induced during paroxysm. Serum TNF levels were correspondingly lower in endemic patients during a paroxysm. Human peripheral blood mononuclear cells (PBMC) can be stimulated in vitro by extracts of P. vivax blood stage parasites to produce TNF and associated parasite killing factor(s), thus simulating in vitro the events that occur during a paroxysm, this being the release of parasite exo‐antigens by rupturing schizonts and the subsequent induction of PBMC to produce TNF and other parasite‐killing factors. We were able to show that convalescent serum from P. vivax semi‐immune individuals block the induction of TNF and parasite‐killing factors by malaria antigens in vitro, presumably through antibodies that neutralize parasite exo‐antigens. Thus, individuals living in malaria‐endemic areas appear to acquire clinical immunity to malaria by avoiding their induction during infection; we have shown that one such mechanism is the neutralization of parasite exo‐antigens that induce the production of parasite killing factors.
Parasitology Today | 1998
H.K. Alles; Kamini N. Mendis; Richard Carter
Malaria mortality in human populations varies greatly under different circumstances. The intense malaria transmission conditions found in many parts of tropical Africa, the much lower malaria inoculation rates currently sustained in areas of southern Asia, and the epidemic outbreaks of malaria occasionally seen on both continents, present highly contrasting patterns of malaria-related mortality. Here Harsha Alles, Kamini Mendis and Richard Carter examine malaria-related mortality under different circumstances and discuss implications for the management of malaria in these settings. They emphasize the power of rapid case treatment to save lives at risk under virtually all circumstances of malaria transmission.
Transactions of The Royal Society of Tropical Medicine and Hygiene | 1997
H.M. Kodisinghe; K.L.R.L. Perera; S. Premawansa; T. de S. Naotunne; A.R. Wickramasinghe; Kamini N. Mendis
Blood from 1053 persons who presented for treatment at outpatient clinics of government health institutions in Sri Lanka, and 250 who took part in a blood survey for malaria, was examined by thick blood film microscopy under routine field conditions, and by the ParaSight-F dipstick method. All the samples were also examined microscopically under laboratory conditions when 4 times the number of microscope fields were examined. Compared with this reference standard, the sensitivity and specificity of the ParaSight-F test were 90.2% and 99.1%, and those of microscopy in the field were 92.4% and 98.4% respectively, there being no statistically significant difference between the 2 methods. The ParaSight-F test reading correlated significantly and positively with the intensity of clinical disease of patients but not with their peripheral parasitaemia, indicating that it may be a more accurate measure of the true parasite load than microscopy, which detects only parasites which are in the peripheral blood and not those which are sequestered in deep organs. The ParaSight-F test, however, failed to detect Plasmodium falciparum infections with only gametocytes in the blood (19.6% of the infected blood samples in this study). The time taken for a patient to revert to negativity by the ParaSight-F test was also significantly longer, up to 14 d. This would make the test unsuitable for checking the response to antimalarial treatment within 14 d. In an endemic area it would therefore fail to detect drug resistant populations of parasites.
Molecular and Biochemical Parasitology | 1994
Shirley Longacre; Kamini N. Mendis; Peter H. David
Recombinant proteins derived from the Plasmodium vivax merozoite surface protein 1 have been produced in the baculovirus expression system. These proteins correspond approximately to the Plasmodium vivax analogs of the 42-kDa or 19-kDa C-terminal processing products previously described for Plasmodium falciparum. Each was produced in two versions, either as a membrane-bound entity located on the cell surface and probably carrying a glycosylphosphatidylinositol addition, or as a secreted entity lacking a membrane anchor. Many native conformational epitopes appear to be accurately reproduced in these molecules. Both the 42-kDa and 19-kDa analogs can be N-glycosylated in the baculovirus system and the N-glycosylation appears to be necessary for efficient secretion of both the 42-kDa and 19-kDa recombinant proteins.
Parasite Immunology | 1992
Asoka C. Gamage-Mendis; Jagath Rajakaruna; Richard Carter; Kamini N. Mendis
Summary Serum effects on gametocyte infectivity, that is, transmission blocking/enhancing immunity, were measured in the sera of 196 acute Plasmodium vivax patients who were residents of a malaria region in Kataragama, southern Sri Lanka. Direct mosquito feedings were also performed on 170 of these patients. Sera of about 48% of patients suppressed gametocyte infectivity significantly (by more than 75%) and of a smaller proportion (12%) had pronounced infectivity enhancing effects. Transmission immunity did not increase with age of patients, rather, immunity tended to be higher in younger patients. Data suggest that immunity levels are boosted by reinfections only if they occur within a period of 4 months from the previous infection, i.e., that immune memory for boosting does not last beyond 4 months. Enhancing effects in the sera of patients correlated with the absence of gametocytes at the time of investigation suggesting that enhancement occurs early during the course of a blood infection, and blocking later, when serum antibodies reach higher levels. The blocking and enhancing effects of a serum appears to depend not only on the antibody concentration in serum, but also on the intrinsic infectivity of the parasite isolate against which it is tested: thus, infectivity enhancing effects were potentiated by low intrinsic infectivities of the parasite isolate. The direct infectivity of patients to mosquitoes correlated with transmission immunity indicating that transmission immunity is an influential factor determining infectivity of malaria patients.
Parasite Immunology | 1994
Sunil Premawansa; Asoka C. Gamage-Mendis; Lakshman Perera; Steven Begarnie; Kamini N. Mendis; Richard Carter
Sera from acute primary Plasmodium falciparum patients in Sri Lanka were tested for the presence of antibodies against gamete antigens and for their functional effects of transmission blocking activity. Comparisons were made with corresponding data from a previous study from sera of patients from Papua New Guinea where malaria is more highly endemic. Although the prevalence of anti‐gamate antibodies in the two groups were broadly similar, the prevalence of infectivity suppressive effects in the Sri Lankan sera (56%) was less than in Papua New Guinea sera (75%), suggesting that the generation of functionally effective transmission blocking antibodies requires prolonged exposure to multiple inoculations of malaria. In Papua New Guinea sera there was a good correlation between transmission blocking effects and antibody responses to Pfs 230, a known target of transmission blocking antibodies. Among the Sri Lankan sera no strong correlation was found between transmission blocking effects and the presence of antibodies to gamete surface antigens Pfs 230 nor Pfs 48/45 as detected by immunoprecipitation of radio‐iodinated gamate proteins; a strong correlation was however, found between the intensity of response to gamete surface antigens by IFA and transmission blocking effects of these sera. It is possible therefore, that the antigens identified by IFA include non‐protein moieties and that these may be the targets of transmission blocking antibodies in sera from acute primary infections of P. falciparum.
Transactions of The Royal Society of Tropical Medicine and Hygiene | 1993
Asoka C. Gamage-Mendis; Jagath Rajakaruna; Sudath Weerasinghe; Chandana Mendis; Richard Carter; Kamini N. Mendis
The assessment of malarial infectivity, for example in the evaluation of transmission blocking immunity, is generally based on counting oocysts in mosquitoes fed on infected blood. Ultimate transmission of the disease may, however, depend on the sporozoite load in the mosquito and its relationship to the size of the inoculum introduced to man. We conducted a laboratory study on Anopheles tessellatus infected with 108 different natural isolates of Plasmodium vivax from patients and 24 of P. falciparum to determine the relationship between oocyst numbers, sporozoite loads, and the effect of these on mosquito mortality. It was found that the P. vivax parasite density was positively correlated with the proportion of mosquitoes infected by a given feed at both the midgut and gland stages of parasite development (correlation coefficient [r] = 0.77, P < 0.001 and r = 0.6, P < 0.05 respectively). A significant positive linear correlation was observed between the number of oocysts and sporozoites in P. vivax (r = 0.5; P < 0.05); the proportions of mosquitoes infected with oocysts and sporozoites were also similarly related, although in general about 15% of mosquitoes infected with oocysts failed to develop salivary gland infections with sporozoites. The number of mosquitoes infected with P. falciparum parasites was too low for statistical analysis. Infection with either species of parasite did not appear to affect mosquito survival, nor was parasite density in the mosquito correlated with mosquito mortality.