CORRESPONDENCE

Many factors may influence the situation (REID, 1976). The snake may be diseased (COOPER, 1973), reducing the venom yield. In most bites, vipers inject less than 10% of the total venom available in the glands (ALLON and KOCHVA,

1974). We.

are, etc. J. E. COOPER

Clinical Research Centre, Middlesex HA1 3 UJ H. A.

REID

School of Tropical Medicine, Liverpool L3 5 QA 20th October 1975

265

than would a virus with a survival time measured in hours. Faecal transfer may be rapid enough for the amoebic cyst, but too slow for the virus. The introduction of hygiene would eliminate the virus before it could have much impact on the prevalence of the amoebae. In the absence of the virus in a community, E. histolytica would remain commensal, no matter how many people were harbouring it. The source of such a virus could only be from the disintegration of invasive amoebae from an active case. Only those hosts with an established commensal infection with E. histolytica would be susceptible. A number of viruses have been found in amoebae of various species, but their significance remains uncertain. Some seem to be strain-specific, and detectable only by their lytic action on other strains. Others have been detected on ultramicroscopy only. The field is wide open, but, in the absence of a naturally susceptible experimental host for the amoebae, proof of transformation may be difficult to establish. I am, etc.

References Allon, N. & Kochva, E. (1974). The quantity of venom injected into prey of different size by Viperapalaestinae in a single bite. Journal of Experimental Zoology, 188, 71-75. Cooper, J. E. (1973). Veterinary aspects of recently captured snakes. British Journal of Herpetology, 5, 368-374. Ionides, C. J. P. (1966). A Hunter’s Story. New York, Holt, Rinehart & Wilson. Lane, Margaret (1963). Life with Ionides. London, Hamish Hamilton. Reid, H. A. (1972). Snakebite, Part I: Clinical features. Tropical Doctor, 2 (4), 155-158. Reid, H. A. (1976). In preparation. Wykes A. (1960). Snake Man. London, Hamish Hamilton.

Formerly Director, Amoebiasis Research Unit, Durban, South Africa now State Health Laboratory, Private Bag X9020, Pietermaritzburg 3200, South Africa 4th December, 1975

The epidemiology of amoebiasis-an hypothesis Sm-Though the distribution of Entamoeba histolytica is alleged to be cosmopolitan, diseaseconsequent on invasion of the tissues by this parasite is restricted to relatively few areas. The endemic areas are much smaller, and though these are mainly in the tropics, there are others such as the informative situation in Saskatchewan. On the other hand, there are places without disease in which the reported prevalence of the parasite is much higher than that reported from areas where amoebic colitis and amoebic liver abscess are common. There is now general acceptance of Swellengrebel’s concept that the normal cycle of E. histolytica, which produces cysts, is commensal and confined to the lumen of the gut, and that invasion of the tissues is as abnormal for the amoeba as it is for the host. These invasive amoebae do not produce cysts, and thus have no hope of continued posterity in a new host. The behaviour of invasive amoebae is so different from that of the commensals that it is difficult to believe that they are the same entity. May not such changed behaviour be due to transformation of the amoebae by some viruslike agent? There are many analogies! The prophage of Corynebacterium diptheriae changes an avirulent organism into a dangerous form. Is not malignancy an example of a genetic change of behaviour in erstwhile mutualist cells? May not host-invasion be a manifestation of an alteration in the genetic structure of the amoebae? Let us assume that the transforming agent is a virus. It may not be-as there are non-living agents which can transform bacteria and even mammalian cells. If such a hyper-parasitic virus has a shorter external survival time than does the cyst of E. histolytica, then the epidemiological jig-saw would form a reasonable picture. If the cyst of E. histolytica could survive the external environment for, say, a week, it would reach more hosts

Route of entry of Onchocerca volvulus microfilariae into the eye SIR-I read with interest Dr. Duke’s letter (1976) reporting a case history which suggested that microfilariae of Onchocerca volvulus invaded the eyes from adult nodules in or near the orbit(s). He indicated that the most likely route of entry was along the sheaths of ciliary vessels and nerves, and asked if other readers could throw further light on the subject. In a letter to the American Journal of Ophthalmology (1973) I drew attention to an association between the peculiar distribution of localised posterior segment lesions of onchocerciasis and the anatomical sites of perforation by ciliary arteries, i.e. : (a) Lesions are commonly found to the outer side of the macula. This corresponds with the site at which the lateral long posterior ciliary artery, accompanied by a nerve, perforates the sclera and enters the choroid. (b) The classical Ridley fundus (1940) is a pear-shaped lesion involving the macula and the area immediately around the optic disc. This corresponds to the part of the sclera, close to the optic nerve and in the submacular area, where the short posterior ciliary arteries penetrate. (c) Peripheral fundal lesions are sometimes seen behind the insertion of the four rectus muscles, i.e. the sites at which the anterior ciliary arteries penetrate the sclera. These fundal lesions are described and illustrated by Ridley (1940) and Budden (1962). I concluded that the peculiar distribution of localised choroido-retinal lesions in onchocerciasis would be nicely explained by penetration of microfilariae along the sheaths of perforating arteries and nerves. Moreover, the migration of microfilariae, or their toxins, from these sites of penetration could lead to the more widespread lesions found in some patients. Furthermore, the frequent

R. ELSDON-DEW

The epidemiology of amoebiasis--an hypothesis.

CORRESPONDENCE Many factors may influence the situation (REID, 1976). The snake may be diseased (COOPER, 1973), reducing the venom yield. In most bit...
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