Currently, the laboratory diagnosis of toxocariasis, caused by Toxocara canis or T. cati, mainly relies on serological tests. Unfortunately, however, the specificities of most of the commercial tests that are available for the serodiagnosis of this disease are not very high and this may cause problems, especially in tropical countries where co-infections with other helminths are common. In an effort to develop a serological assay with improved specificity for the detection of Toxocara infection, an IgG(4)-ELISA based on a recombinant version (rTES-30USM) of the 30-kDa Toxocara excretory-secretory antigen (TES-30) has recently been developed. To produce the antigen, the TES-30 gene was cloned via assembly PCR, subcloned into a His-tagged prokaryotic expression vector, and purified by affinity chromatography using Ni(2+)-nitrilotriacetic-acid (Ni-NTA) resin. The performance of the ELISA based on the recombinant antigen was then compared with that of commercial kit, based on an IgG-ELISA, for the serodiagnosis of toxocariasis (Toxocara IgG-ELISA; Cypress Diagnostics, Langdorp, Belgium). Both assays were used to test 338 serum samples, including 26 samples from probable cases of toxocariasis. Assuming that all the probable cases were true cases, the assay based on rTES-30USM demonstrated a sensitivity of 92.3% (24/26) and a specificity of 89.6% (103/115) whereas the commercial kit exhibited a sensitivity of 100% (26/26) but a specificity of only 55.7% (64/115). The high sensitivity and specificity exhibited by the new IgG(4)-ELISA should make the assay a good choice for use in tropical countries and any other area where potentially cross-reactive helminthic infections are common.
Holoendemic malaria transmission in two small isolated forest communities and a coastal village was studied by (1) all night human bait collections of Anopheles species from inside and outside houses and (2) buffalo-biting and CDC light-trapping catches during March and November 1984. During the same period thick and thin blood films were collected from the human population, and spleen rates were determined in children from two to nine years of age. Using both the immunoradiometric assay (IRMA) and the dissection technique, more sporozoite-positive infections were detected in An. balabacensis and An. flavirostris in November than in March. IRMA confirmed the presence of Plasmodium falciparum sporozoites. An average of 76.2% of the An. balabacensis population lived long enough to have reached a point where infectivity with P. falciparum was possible in November. Although fewer than five adult females bit humans per night at any time, a resident could theoretically have received more than 160 infective bites in one year. A high frequency of feeding on humans, coupled with increased anopheline life expectancy, contributed to high estimates of falciparum malaria vectorial capacity (number of infections distributed per case per day); for An. balabacensis (1.44-7.44 in March and 9.97-19.7 in November) and for An. flavirostris (0.19-5.14 in March and 6.27-15.8 in November). These high values may explain the increased malaria parasite rates obtained from at least two forest communities. Correlation between actual and calculated rates of gametocytaemia was poorest in Kapitangan due to inadequate sampling of the human population. In Banggi island, malaria is stable and holoendemic, and the population enjoys a high degree of immunity.
One hundred and nine (9·8%) out of 1103 malaria patients examined in Sabah were deficient in glucose-6-phosphate dehydrogenase (G6PD). Sixty-nine of these G6PD-deficient patients were randomly allocated to one of three treatment regimes with (a) chloroquine, (b) chloroquine and primaquine or (c) sulfadoxine-pyrimethamine (Fansidar). No haemolysis was observed in group (a); except for a single mild case, no haemolysis was seen in group (c). However, in the primaquine group (23 patients), haemolysis occurred in seven of the 16 patients who had complete G6PD deficiency. Of these seven, five required blood transfusion and the other two developed acute renal failure, one requiring peritoneal dialysis. In the Fansidar group (c), four of the 22 patients took more than 15 days to clear the parasitaemia. Chloroquine resistance to falciparum infection was common in the patients given this anti-malarial.
Study site: Queen Elizabeth Hospital, Kola Kinabalu, Sabah, Malaysia
A trial of suppression of malaria by administration of combined sulphadoxine-pyrimethamine tablets every 28 days was undertaken in West Malaysia during 1972. One thousand subjects were followed over a 10-month period, including control groups on placebo and on weekly chloroquine. Subjects were examined monthly for parasitaemia, drug reactions, leucopenia, teratogenicity and haemolysis among the subjects deficient in glucose-6-phosphate dehydrogenase. Rates of new infections in the placebo group were 8.0% with Plasmodium falciparum and 6.2% with P. vivax; in the group receiving weekly chloroquine, 5.1% P. falciparum and 0.3% P. vivax; and in the group receiving monthly sulphadoxine-pyrimethamine, 0.3% P. Falciparum and 1.0% P. vivax. The effective rate of cure of new infections with P. falciparum by a single suppressive dose of combined sulphadoxine-pyrimethamine given the following month was 88.7%. No serious side effects were observed.