Entamoeba histolytica and airline personnel

700 Alternative hypothesis for the evolution of chloroquine resistant Plasmodium falciparum in Africa Different mechanisms suggestedas responsible for the evolution and spread of chloroquine resistance of Plasmodium falciparum (CRPF) have recently been briefly reviewed (BjBrkman & Phillips-Howard, 1990: Transactions, 84, 323-324). However, none of them can fully explain the fast propagation of CRPF observed on the African continent. The introduction of CRPF into an area appears to be dependent on importation and the dissemination thereafter appears to be possible even in areas without undue use of chloroquine. One hypothesis has therefore been the general biological advantage of resistant over sensitive parasites irrespective of host fact’orssuch as chemotherapy or immunity. This is supported by someobservations with P. chabaudi in the animal model (ROSARIO et al., 1978: Lancet, i, 185-187). However, an immediate counter argument is why this genetic superior had not evolved before, so that CRPF strains already outnumber sensitive strains. Another hypothesis may be that chloroquine resistance represents one or many ‘neutral’ genes, and that resistant and sensitive strains have biologically equal viability. In an endemic area the two factors affecting parasite growth and population would then be chemotherapy and protective host immunity. Epidemioidgically &is is reflected by drug pressure and ‘herd immunitv’. The general nronaeation of CRPF can therefore”be expl&ed parEly byvselection due to the more or lesswide-spread use of chloroquine followed by spread and dilution in areasof non-use of chloroquine. Low immunity as a major contributor to the spread of CRPF cannot explain the fast propagation of CRPF in Africa. where the high ‘herd immunity’ in most Africa; countries wou’id rather contradict its involvement. The rapid development of CRPF seenin an outbreak in Somalia (Warsameet al., 1990: Journal of Tropical Medicine and Hygiene, 93, 284-289) reflects the combined effects of low ‘herd immunity’ due to migration, high transmission, and high drug pressure. An additional hypothesis may however also be suggested,namely that chloroquine-resistant parasites are antigenically different from sensitive ones. Resistant parasites may then represent a new phenotype in Africa to which semi-immune hosts in endemic areas are initially more susceptible. This would explain how, in many areas of Africa with high transmission at high immunity, CRPF very quickly becomes established up to a maximal level and it would also partly explain the temporary increase of parasite density and clinical manifestations which have been anecdotally reported. CRPF may later even possibly decrease, once the use of chloroquine declines in favour of other drugs, thus increasing the opportunities for sensitive narasites to which ‘herd immunitv’_I may by then haqe decreased. The relatively slower initial spread of CRPF in the 1960s and 1970s in south-east Asia, compared to Africa in the 198Os,may thus be explained by less selection force due to a generally lower degree of such ‘herd immunity’. Epidemiological studies on the early development and spread of CRPF into an area are necessary to elucidate these hypotheses. Such studies have been

started in Liberia and Somalia. The results do partly support the hypothesis of the relative selection of CRPF by existing ‘herd immunity’ (Bjarkman & Warsame, unpublished observations). Anders Bjiirkman Department of Infectious Diseases Roslagstulls Hospital, Bos 5651, S-114 89 Stockholm, Sweden

7 January

1991

The Becton Dickinson QBCIP analyser We wish to comment on the report by Moody et al. of their experiencewith the Becton Dickinson QBC II@ centrifugal haematological analyser for haemoparasites (1990: Transactions, 84, 782). We used the QBC in Thailand in 1988-1989. Our experience with it in a malaria hvnerendemic field setting Khantaburi, Thailand) was-identical to that of Moo&, Hunt-Cooke and Chiodini in London. However. we also evaluated the suitability of this system for use by ‘paratechnicians’ with no prior experience in fluorescence microscopy. These middle school level laboratory assistants were able to learn how to operate this instrument accurately after one week of training and supervision. Such an individual then performed the detection procedure at the samelevel of sensitivity (98.6%) as an experienced university-trained technician scanning a thick smear. We concluded that the QBC offers an advantage in ease of procedure and reduced microscopy time (particularly with low parasitaemia samples) in a laboratory which screens a large number of blood specimensfor malaria daily (Pornsilapatip et L&, 1990: Southeast Asian Journal of Tropical Medzczne and Public Health, 21, 534-540). Jaturaporn Pomsilapatip Henry Wilde Queen Saovabha Memorial Institute and Faculty of Medicine Chulalongkorn University 1871 Rama IV Road Bangkok 10330 Thailand 23 January 1991

Entamoeba histolytica and airline personnel We read with great interest the paper by Dr Weber

et al. on Entamoeba histolytica infection in flight personnel (1990: Transactions, 84, 803-805). We are

however hesitant about some of their conclusions. The cohort of subjects chosen represented a very particular group and conclusions derived from it cannot be extrapolated to the routine work of a travellers’ clinic, where patient structure, disease pattern and laboratory facilities would be quite different. Firstly, the facilities to determine zymodemes are seldom available, not only in developing countries but in industrialized ones as well. Secondly! the authors studied an extremely peculiar population, i.e., air flight personnel, with a high frequency of international travel and-as the paper reported-a high prevalence of homosexuality. The human immunodeficiency virus status of the subjects was not mentioned, and should infection be present undoubtedly their approach would change. Treatment of asymptomatic cyst passersin endemic

701 areas has been reviewed elsewhere (Nanda et al., 1984: Lancet, ii, 301-303), but the situation as far as travellers is concerned may be very different, with a risk of amoebae becoming pathogenic under certain circumstances with potential public health consequences. The cost-effectiveness relationship of drug treatment compared with the risks should complications arise and the cost of zymodeme analysis must be borne in mind, especially if a flight to London for every patient is needed, as was the case in the paper bv Weber et al. Moreover, cvsts are detected more frequently than trophozoites in symptomatic homosexuals (Peters et al.. 1986: Yournal of Clinical Microbiology, ‘24, 684-685). ” Z The topic of treating cyst-passers travelling to non-endemic areas remains a matter for discussion and further research.

A. Garcia-Forcada J. Gasc6n M. Corachln Tropical Medicine Unit Hospital Clinic i Provincial Villorroel 170 08036 Barcelona Spain

Entamoeba histolytica

reply

8 February 1991

and airline personnel: a

We wish to reply to the letter by Dr Garcia-Forcada and colleagues regarding our paper (1990: Transactions; 84, 803-805). Our subjects became infected with amoebae by the usual route, i.e., faecal-oral, consequently the results regarding their infections are similar to those found anywhere in the world, in any circumstances. Zymodeme profiles identify the exact ‘finger-print’ of the amoebae isolated and, as we reported, this agrees with data obtained by microscopy and serology. These latter techniques, are, without exception, readily available to all traveller’s clinics, and the value of serology is enhanced by our results. Zymodeme analysis is becoming increasingly available and at present is undertaken in laboratories on all continents and sub-continents from Europe to Australia. A lack of comprehension of our paper is indicated by the suggestion that infected subjects should have to fly

anywhere to receive a definitive diagnosis of an amoebic infection. Strains of Entamoeba histolytica never change their status in the host, whether pathogenic or nonpathogenic, as we showed quite clearly in our paper; the subjects are reviewed and followed up regularly. Also several published reports (including those by Goldmeier et al., 1986: Lancet, i, 641-644 and Allason-Jones et al., 1988: British Medical Journal, 297.6546561 demonstrated irrefutablv that. contrarv to the suggestion by Dr Garcia-Forcada’ and colleagues, amoebae do not become ‘pathogenic under certain circumstances’, many subjects having been followed up for almost a decade. These reports also deal with the question of concomitant HIV infections, which in fact- have no influence whatever on nonnathogenic E. histolvtica infections. One of us has now shown by rectal biopsy that terminal AIDS cases infected with non-pathogenic E. histolytica have suffered no parasite invasion at all. ‘Symptomatic homosexuals’, the unfortunate term used by Dr Garcia-Forcada et al., if infected with E. histolytica, are, as our paper reported, almost always infected with non-pathogenic strains. Such infections are characterized by the presence of cysts and not trophozoites (as stated in the penultimate sentence of the letter by Dr Garcia-Forcada et al.). The nub of our paper was that infection with non-pathogenic E. histolytica, diagnosed primarily by clinical observation, albeit supported by clinical laboratory investigations, does not need treating.

G. Weber W. Mohr K. Fleischer P. G. Sargeaunt Tropenmedizin Dienst, Deutsche Lufthansa, 6000 Frankfurt 25; Institut fiir Tropenmedizin, Oderfelderstrasse 6, Hamburg; Missioniirtzliche Klinik Wiirzburg, D-8700 Wiirzburg 1I. Federal Republic of Germany; Department of Medical Parasitology, London School of Hygiene and Troaical Medicine, Keipel Street, London, WCIE 7HT, UK

21 March 1991