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T~~sacno~s OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE, VOL. 76, No. 6, 1982

Correspondence

To the Editor

Congenital malaria due to Plasmodium vivax: a case report from Sri Lanka

Congenital malaria occurs very rarely in infants born from mothers in endemic areas, although the parasitaemia of the placenta can be very high on the maternal side. In babies of non-immune mothers congenital malaria is less uncommon, but still rare. The case described by DE SILVA et al. (1982) was interesting because the infecting species was Piasmo- dium tivax. The authors treated the infant with chloroquine and primaquine. I wonder why: con- genital malaria can be compared to “transfusion”- malaria, so no exoerythrocytic forms will be present in the liver of the infant.

I have two questions of the authors: (i) what were the arguments for giving primaquine? (ii) why did they not give a high dose of chloroquine (450 mg in an infant of approximately 3 kg)?

In 1980 we saw a case of congenital malaria in The Netherlands also caused by P. vivux. The infant (body-weight 3.4 kg) was treated with chloroquine base, 110 mg in three days. We did not give primaquine. No relapse has occurred.

J. C. F. M. WETSTEYN Instituut voor Tropische Hygiene, Mauritskade 57, Amsterdam-O, The Netherknuis.

Reference De Silva, D. H. G., Mendis, K. N., Premaratne, U. N.,

lavatilleke. S. M. D. & Sovza. P. E. (1982). Congenital &aria dui to Pkwnodium~&x: a &se re&rt f&m Sri lmka. Transactions of the Royal Socie~ of Tropical Medicine and Hygiene, 76, 33-35.

Accepted for publication 24th July, 1982.

Congenital malaria due to Plasmodium vivax: a case report from Sri Lanka

We agree with the argument put forward by Dr. Wetsteyn in the preceding letter about the wssible absence of exoery&rocytic-forms in congenital malar- ia. But at the time of diagnosis, we could not entirely eliminate the possibilitv that infection had been vector-borne. It was only on serological follow-up of both the mother and child, together with the history of the child who had not been to an endemic area, that this possibility was eliminated.

We aDolo&e for not havine &en orecise details of the tre&meGt regime, whic& Gas & follows: (NB. 1-O mg of chloroquine phosphate is equivalent to O-6 mg of base): First day-loading dose of 150 mg

chloroquine phosphate (= 90 mg base) and six hours later 150 mg chloroquine phosphate (= 90 mg base) followed by two daily doses of 75 mg chloroquine phosphate (= 45 mg base).

We also wish to point out that the weight men- tioned (approximately 3 kg) was the birth weight and not the weight at the age of eight weeks.

D. G. H. DE SILVA Institute of Child Health, Nufild Building, Francis Road, Biwningham B16 8ET, England

Static electricity and sandflies In breeding and maintaining a colony of Phleboto-

mus papa&, we encountered a situation whereby the flies were affected by static electricity. We use plastic boxes as rearing and feeding chambers for the sandflies. Under dry environmental conditions, we noticed that the sandflies adhered to the walls, but could be released by eartbing the containers.

A high mortality rate was recorded in groups of sand&es exnosed to these conditions. This mav have been caused by the strain of the leg muscles &d the resulting loss of energy.

We now feed sandilies and carry out experiments using earthed chambers. No such problem occurs during maintenance, since the rearing chambers stand on wet filter paper and are therefore earthed.

This information could be of interest to sandfly breeders.

Y. SCHLEIN L. SCHNUR A. WARBURC A. E. GUNDERS*

Dept. of Parasitology, *Dept. of Medical Ecology, Hadassah Medical School, JerusaLzm, Israel

Concentration of microiilariae in mosquitoes during feeding

MCGRREW et al. (1982), in their interesting paper, record the marked concentratine effect that inaestion by Culex quinquefasciatus, Aedei aegypti or A&$&es gambiae had upon the density of microtiariae of Wuc~eria batzrofti in the blood of infected persons. The mosquitoes ingested from 8.6 to 12 times more mff than would be expected from their density in the blood and the size of the blood meals ingested. For the latter they use figures from the literaGe, and for An. gambiae from Prof. G. Davidson. These figures

TRANSACTIONS OF THE ROYAL Soc~rr~ OF TROPICAL MEDICINE AND HYGIENE, VOL. 76, No. 6, 1982. GXRESPONDENCE 851

have been obtained by weighing mosquitoes before and after feeding but, as I showed (REID, 1953), weighing may produce a large underestimate of the blood volume ingested, because the mosquitoes ex- crete considerable amounts of urine (&funs&r annu- lifera) or blood (An. barbirostris) during feeding. WHARTON (1962, p. 83) confirmed this, using a cat infected with Srugia pahangi. He counted the number of mff voided or retained by An. barbirostris and found that the latter number was less than one third of the number voided through the anus. Even so the number of mff retained “was equal to the number in 5.8cl.l of peripheral blood”. BOORMAN (1960), in an elegant experiment using radioactive cerium (which does not pass through the mosquito gut wall) to label the blood, was able to measure the true amount of mouse blood ingested by Ae. aegypti. He found it to be 4-O to 4.5 ul, compared to the usually accepted figure of about 2.5 pl. But if the urine passed at feeding, which was about l-5 ul, was added to 2.5 yl this gave close agreement with the cerium-derived figure.

of fluid after a blood rnd and the amount of h@l taken~ during feeding. Ann& of Tropical Medicine nndP&&tot-

So it seems that concentration of mff by the mosquito may be due to this excretion of fluids-when feeding. The striking differences between mosquito snecies, some of which void what appears to be whole blood, whilst others pass clear urine,-seems to warrant further investigation. Prof. G. Davidson (personal communication) finds that An. (Cellia) gumbiue (Pyre- tqpkur~s series) excretes only urine, but An. (C.) stephensi (Neocelliu series) passes blood. I have seen a specimen of An (C.) philippimmsis (also Neocellia series) passing numerous small droplets of blood.

With species that void fresh blood one wonders why they should continue to feed when apparently replete. For, when at rest feeding on the host, the engorged mosquito is probably at risk from the host and other hazards, so that completion of feeding in the shortest possible time should contribute to survival. Is it, in fact, whole blood that the mos- quitoes pass, or has something been extracted? The excretion or passing of fluids while feeding is well known among insects, especially sucking ones, e.g., a&ids feeding on lime trees (Tilia sm.) excrete honeydew, because the lime sap is rich m-sugars and low in protein which the aphids require. Many butterflies in the tropics congregate on moist earth, often on river banks where animals come to drink and have urinated. The butterflies suck up the soil moisture while maintaining a rythmic ejection of spurts of water drops from the anus. Presumably they are obtaining and concentrating salts.

Returning-to mosquitoes, what is the composition of fluids voided during: feeding and what is the reason for this behaviour? Does ea:h species consistently pass blood, urine or other fluids from the gut lumen? If so, is the nature of what is passed related to the taxonomic classification? These and other questions seem to need some inquiry.

‘43 The Orchard, Dorking, Surrey, RHS 4JT, England

J. A. REID

References Boorman, J. P. T. (1960). Observations on the fe@ng

habits of the mosquito A&s (StegtiyGiz) izegyptiI The loss

o&y, 54, 8-14. McGreevy, P. B., Kolstrup, N., Tao, J., McGreevy, M. M.

& Marshall, T. F. de C. (1982). Ingestion and develop- ment of Wuchereria bancrofii in Culex quinquefascia~, Anopheles gambiae and Aedes aegypi after feeding on humans with varying densities of microfilariae in Tanza- nia. Transactions of the Royal Sociev of Tropical Medicine and Hygiene, 76, 288-296.

Reid, J. A. (1953). Transmission of filariasis. Transactions of the Royal So&y of Tropical Medicine and Hygiene, 47, 84.

Wharton, R. H. (1962). The biology of Mansonia mos- quitoes in relation to the transmission of lilariasis in Malaya. BuUetins jivm the Institute for Medico1 Research, Federation of Malaya, 11, 114 pp.

Accepted for publication 22nd J&J, 1982.

Comments on Symposium on tumours in the tropics Dr. Paula COOK-MOZAFFARI’S paper (1982) on the

above subject was of great interest. We were, however, surprised that there was no mention of the effect of riboflavin deficiency on the squamous epithelium of the oesophagus and its relation to carcinoma of the oesophagus and cardio-oesophageal junction.

The vulnerability of the oesophagus and the aetiology of primary oesophageal cancer has attracted considerable attention during the last decade or more, as the global incidence has been found to vary widely (LANCET, 1967,1968,1969; BRITISH MEDICAL JOUR- NAL, 1968); for example its incidence in Kazakhstan is about 200 times higher than in Canada, and great variations in incidence also occur in various parts of Africa (KRAMCHANINOV, 1968; VAN RENSBURG, 1981). In America, oesophageal cancer is on the increase among the urban black races (ROGERS et al., 1982). DOLL (1969) thought that the marked differ- ences between the high and low incidence areas were associated with some unknown locally operative environmental or dietary factor-perhaps nitrosa- mines, other known or unknown natural or synthetic dietarv carcinogens, of which deficiency of riboflavin, or presence of its -antagonists may be one.

Our findinas in baboons (FOY et al.. 1972) and those of VA; RENSBURG (1981) in man, seem to underline the need to consider riboflavin deficiency as playing some role in the aetiology of wsophageal dysplasias and cancers, or to increase the susceptib- ility of the nutritionally deranged buccal and oesophageal squamous epithelium to the effects of carcinogens, acting either as initiators or promoters (FARBER, 1982). -

WYNDER & KLEIN (1965) found that the earliest microscopical changes in riboflavin deprived mice were in the squamous epithelial lined surfaces of the oesophagus and fore-stomach, the thickness of which was greatly reduced-and in our baboons associated with oesophageal ulceration and epithelial dysplasia. Wynder & Klein suggested that riboflavin deprivation made the mouse more susceptible to tumour produc-