aspects of bilharziaAfrica

Somein southernR. J. PITCHFORD

When Bilharz discovered the parasite responsible for thedisease known as bilharzia, or schistosomiasis, in Egypt in1851, he named it Distomum haematobium. A few years later, in1858, Weinland and Cobbold independently discovered thatonly one of the suckers of D. haematobium contained an oralcavity; Weinland changed the generic name of the worm toSchistosoma and a little later Cobbold changed it to Bilharzia.Schistosoma is upheld by the International Laws of Nomencla­ture because the name was given first, but both bilharzia andschistosomiasis are used to denote the various diseases causedby the numerous species of the genus in man and animals.

In southern Africa, John Harleyl reported finding the eggsof Bilharzia capensis in the urine of patients from near Uiten­hage in the eastern Cape in 1864. He thought his fmdings relat­ing to the miracidia were sufficiently different from those ofBilharz to justify naming a new species. Cobbold,2 however,realized that the two species were identical and both are nowclassified as Schistosoma haematobium. There have been a fewartempts to resurrect the name capensis for the southern strainof the bladder parasite but there seems to be no valid justifica­tion for this move. Perhaps if it had been known that the diffe­rent strains required different snail host-species, the Capename might have survived for the southern strain, with muchchaos and confusion about a century later.

Becker3 was the first to incriminate Physopsis africana in1916 as the intermediate host of S. haematobium in southernAfrica. He injected cercariae from. wild snails caught in thevicinity of Nylstroom into a guinea-pig from which he laterrecovered three male schistosomes.4

At the time S. haematobium was the only schistosome withterminal spined eggs known in southern Africa and, in retro­spect, the worms might equally well have been S. mauheei, themales of which were until recently, impossible to differentiatefrom S. haematobium. S. mauheei was not reported until 1929as a parasite of sheep from near Humansdorp in the easternCape;5 today it is recognized as widespread and common insouthern Africa; it is interesting to note that Harley depictedthe eggs of S. mauheei and S. haematobium from man in 1864.

By 1900 S. haematobium was known to be endemic in seve­ral places in the eastern Cape as well as in Natal and nearRustenburg in west-eentral Transvaal. 2

In 1938 Annie Porter6 of the South African Institute forMedical Research defmed the geographic distribution of bil­harzia and the snail hosts in southern Africa. She noted thatthe snail-host distribution was wider than that of the disease,which in turn was much wider than that thought to existtoday.

Schistosome species and distribution insouthern Africa

The distribution of Schistosoma species in their defmitive hosts

White River, TvlR. J. PITCHFORD, M.R.C.S. (ENG.), L.R.C.P. (LOND.), D.T.M. & H., R.C.P.

(LaND.), R.C.S. (ENG.) (Retired Director of the MRC Bilharzia FieldUnit, Nelspruit, Tvl)

and of the intermediate hosts in the RSA, Botswana, SWAINamibia and Swaziland have been published from time totime by various authorities. 7

-9 The publications are perio­

dically reviewed and new or revised findings reported.

s. haematobium (Bilharz, 1852)For all practical purposes this parasite is definitive host spe­

cific to man in southern Africa. One female was reported froman African buffalo (Syncerus caffer) from the Kruger NationalPark and the eggs and a female were found in a vlei rat (Oto­mys angoniensis) from the vicinity of Komatipoort. lO

The parasite is found from Uitenhage in the south-easternCape, where it is probably somewhat rare today, eastwardsand north through the Ciskeian and Transkeian coastal beltsinto the coastal regions and midlands of Natal. It does notextend into the mountainous areas of the Drakensberg andcases reported from here are probably importations. Furthernorth the disease sweeps through the low- and middle-lyingareas of Swaziland and the Lowveld of the eastern Transvaaland the area north of the Zoutpansberg. It extends into centraland western Transvaal and eastern Botswana and furthernorth; the disease is endemic in parts of eastern Caprivi andKavango in north-east SWAlNamibia. S. haematobium is notfound south of the Magaliesberg and Witwatersrand nor inLesotho, the Orange Free State and Cape Province, excludingthe south-eastern coastal belt.

S. mansoni Sambon, 1907Like S. haematobium, S. mansoni is primarily a parasite of

man in southern Africa but it has been found in .three rodentspecies, a baboon and a waterbuck in the eastern TransvaalLowveld. These are all thought to be chance infections andincapable of maintenance without the outside assistance ofman. The parasite has a more restricted distribution than S.haematobium being confined in Transvaal to the area north ofthe Zoutpansberg and the eastern Lowveld with a few foci incentral Transvaal, the low-lying areas of Swaziland and thecoastal regions of Natal as far south as about Durban. Focioccur in eastern Caprivi and Kavango in north-east SWAINamibia and in Botswana around the Okavango swamps.

S. mattheei Veglia and Le Roux, 1929This parasite was probably originally a parasite of game in

southern Africa and would appear to be rather indiscriminatein its choice of defmitive hosts having been incriminated asparasitizing at least 13 species of game including numerousantelope species, zebra, warthog, bushpig and giraffe, at leastfour rodent species, as well as domestic stock (cattle, sheepand goats) in addition to baboons, vervet monkeys and man.Man, however, does not appear to be a particularly good host;the infection rates are never as high as those of S. haematobiumand S. mansoni or of S. mauheei in cattle and sheep; egg excre­tion is somewhat erratic; no authentic case of pure S. mauheeiin man has ever been found and all attempts to recover S.mauheei from man after passage through snails and rodents

80 BYLAE TOT SAMT 11 OKTOBER 1986

have resulted in the production of hybrid mauheel/haemaro­bium, which presumably would be capable of parasitizing alldefinitive hosts of the parents. A possible explanation is thats. mauheei males in man do not develop beyond the liver stageand the females are transported from the liver to the bladderor the gut by S. haematobium or S. mansoni males.

S. mauheei follows much the same distribution as S. haema­tobium but may extend beyond this especially in some areas inthe eastern Cape.

s. leiperi Le Roux, 1955 and S. margrebowieiLe Roux, 1933

Two other schistosomes, S. leiperi and S. margrebowiei arefound in northern Botswana and eastern Caprivi, which formtheir southern boundaries. Both parasitize numerous species ofthe family Bovidae (including cattle) and Equidae but not man,with the single exception of a patient from Mali with S. mar­grebowiei eggs found on rectal snip. IQ

S. edwardiense Thurston, 1964 and S. hippo­potami Thurston, 1963

S. edwardiense and S. hippopotami are both found in Hippo­poramus amphibius in the Kruger National Park. They appearto have different geographic distributions in the Park and tobe host specifIc to the hippopotamus - S. edwardiense has notbeen bred in the laboratory beyond the cercariae stage, andhas not been found in any other animal in nature; viable eggsof S. hippoporami have only been found in sections of thesuprarenals from where it would seem to be difficult to com­plete the lifecycle. ll It is possible that it may be a recognizedschistosome in an abnormal host.

Bulinus (Physopsis) sp. the common snail host of S. haemaro­bium, S. mauheei and S. leiperi extends well beyond thedistribution of the parasites, being found for instance in iso­lated foci in the Orange Free State. The snail hosts of S. man­soni Biomphalan·a sp. also extend beyond the distribution ofthe parasite; they thrive in north central SWA/Namibia(depending on availability of water), foci occur in Natal southof Durban and along the coastal belt of Transkei and farnorth-eastern Cape near Taung.

Schistosome transmission in southern Africa

In southern Africa human bilharzia is primarily an infection ofthe black and Indian populations living in rural areas, gene­rally under primitive hygiene and water conditions. Someagricultural practices and changes of living conditions of thehuman populations have played a large part in increasing andmaintaining infection rates at unacceptably high levels withinthe endemic area. Irrigation schemes, as found in southernAfrica, provide an abundance of ideal snail habitats which arenot subjected to floods or droughts; they provide an abun­dance of extremely popular swimming facilities for childrenand thus fulfil a vital role in the lives of rural children living inhot climates; they also provide abundant water which does nothave to be piped for household use. Generally, the farm la­bourers and their families are housed above and close to thecanals without sanitary facilities except the nearby openmiddens from where during rain faeces easily wash into thecanals and dams.

Rural black people empty their bowels between two andthree times a day and S. mansoni eggs may remain alive infaeces and water, without hatching, for several days; reducedcontact with potentially dangerous S. mansoni-infected wateris therefore nearly impossible because of the wide distribution

SUPPLEMENT TO SAMJ 11 OCTOBER 1986

potential of the eggs in flowing water before hatching. Thesituation is a little different with S. haematobium; urine dries ifvoided on dry land and the eggs it may contain will die. Themajority of the eggs are excreted for 2 - 3 hours aroundmidday and hatch rapidly after reaching water. Today themajority of children are in school until about 14hOO and emptytheir bladders at school or on the way home, but they stillswim at weekends and during the holidays and empty theirbladders while swimming.

An accusing fmger has been pointed at irrigation schemes,but bilharzia prevalence rates may be just as high in areaswhere there is no irrigation and numerous irrigation schemesexist in southern Africa which are not endemic to schistosomes.

Temperature plays an important role in supporting a healthyschistosome population and in confming the geographic distri­bution. Snail hosts of all parasites are incapable of survival inareas where freezing temperatures prevail for any length oftime; excessively high temperatures, if sustained for a longtime, appear to affect S. mansoni infections adversely. Deve­lopment of the larval stages in the snails to cercariae is prolong­ed with low autumn and winter temperatures and cercariaeshedding of the two human parasites ceases during winter insouthern Africa. This results in more or less simultaneousemergence of cercariae in late September and early October,after which transmission continues throughout the summer,declining in about April/May. S. mauheei transmission conti­nues throughout the year with some decrease during winter.Sporadic (as opposed to armual) transmission may take placein some fringe areas where temperatures are not always highenough for long enough for schistosome development withinthe snail to be completed every year.

Changes in river water temperatures brought about by bigdams might be sufficient to turn a previously non-endemicarea into an endemic one depending on the use to which thewater is put below the dam. Transference of water from onearea to another by syphon, canal or other means might alsoaffect the status quo at the receiving end by altering tempera­tures or by chemical changes in previously unsuitable snailhabitats.

Prevalence, pathology, morbidity anddiagnosis

There are probably between 3 and 4 million people infectedwith one or more species of schistosome in South Africa(excluding Swaziland, Botswana and SWA/Namibia). Preva­lence ranges from under 10% in some areas to about 80% inlarge areas of the eastern Transvaal Lowveld and Natal coastalareas. Infection rates of S. haemarobium are highest in theyounger age groups up to about 18 years of age after which therates fall quite rapidly; infection rates of S. mansoni are veryoften higher than those of S. haemarobium and do not fall asrapidly.

Infection rates of S. mauheei are generally low in man butfocal areas have been found with rates up to 40% on repeatedexamination of urine and faeces; although this parasite hybri­dizes with S. haematobium in man, no evidence has been foundof hybrid parasites in stock in nature. Infection rates in stockand game are generally high and well in excess of 60%; epide­mics in stock resulting in severe morbidity and high mortalityrates have been rare, about one every 10 - 12 years. Sheepseem to be the most severely affected.

In man severe disease has been amibuted to and associatedwith heavy worm loads but in southern Africa bilharzia as acause of death is very rare and many lesions are reversible withtime. Some workers have shown that there is no detectabledisability in respect of physical activity, growth rate and intel­ligence while others maintain that there is mental retardation

81

in children of schoolgoing age as a result of bilharzia infec­tions. Whatever the case, severe disease appears to be increas­ing in some areas of high endemicity. Whether this is theresult of increased human population or increased worm loads,or both or neither, is not known.

Methods of diagnosis of bilharzia are varied and numerousbut the fInding of viable ova in excreta or biopsy material isthe only reliable one, bearing in mind that: (I) S. haematobiumeggs are excreted only berween certain hours; (il) in manyareas S. mansoni co-exists with S. haematobium; (iil) onlyviable eggs are evidence of active infections; (iv) having beenlaid, eggs remain viable in tissues for about 3 weeks, even aftersuccessful treatment; (v) egg laying begins some 5 weeks afterexposure to S. mansoni and about 3 months after exposure toS. haematobium; and (VI) tests for cure should not start before3 weeks after the end of treatment and should include tests forS. mansoni and S. haemarobium.

The numerous serological tests available for 'rapid, cleanand painless diagnosis' do not differentiate berween the para­site species, they do not revert to negative even after successfultreatment, and they may show false-positives with other hel­minth infections or after exposure to animal schistosomes, e.g.S. leiperi or S. margrebowiei. These tests are, however, usefulin assisting diagnosis.

Numerous drugs are available; most of them are only par­tially ·effective against S. mansoni and none is suitable for masstreatment (because of expense) in areas where both parasitesare endemic.

Possible control measures

There is no single measure which can be employed over wideareas; each potential transmission site requires individual atten­tion depending on the prevalence rate, population density,water supply, living conditions, recreational facilities, andmany other facrors. Because of the amount of movement fromone area to another among black people it is essential thatlarge tracts of land are placed under control with the full co­operation of all individuals, local authorities and governmentdepartments within the area. Unfortunately, these may not beunder the control of a single governing body.

Theoretically, control measures can be installed over wideareas at enormous expense irrespective of the control methodchosen - molluscicides, medical treatment, environmentalmeasures or whatever. Molluscicides and medical treatmentare probably the most expensive in that they require repeated

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annual expenditure. Environmental control pays due regard tothe habits of the defInitive hosts such as swimming, recreation,laundering, washing, defaecating and urinating·in relation tothe schistosomes and involves no recurrent annual expendi­ture; it is initially expensive, depending on circumstances, andis already taking place in many areas - not specifIcally as ananti-bilharzia measure, but this is immaterial. There is littledoubt that if facilities such as swimming baths, communalpiped water, latrines, fI1ters, washing slabs, fencing, etc. areinstalled they are appreciated and used by the population atrisk. The difficulty is maintenance and abuse of the facilitiesprovided. The greatest proportion of the endemic areas lieswithin the independent black states and homelands and a tre­mendous effort would be required to overcome these difficul­ties. The white farmers within the endemic areas would havemuch the same problem with their labourers and their fami­lies, for the same reasons; stock on the other hand would farewell and the probable disappearance of S. marrheei from thefarm of Mc Matthee near Humansdorp since 1928, when hetook the advice of Le Roux following the epidemic whichcaused severe stock losses on the farm, is a good example.There are others.

REFERENCES

1. Harley J. On rhe endemic haematuria of rhe Cape of Good Hope. Med/ClurTram 1864; 47: 55-72.

2. Brock GS. On rhe bilharzia haematobia.J Path Bacr 1983; 2: 52-74.3. Becket JG. A pteliminary note on an intermediate host of Bilharzia haema­

. tobium in Transvaal, togerher wirh a description of rhe cercariae wirh whichrhe mollusc is infected. MedJ S Afr 1916; 11: 156-157.

4. Becker JG. A further note on bilharziasis in rhe Transvaal. Med J S Afr1916; 12: 42.

5. Veglia F, Le Row< PLo On rhe morphology of rhe schistosome (Schistosomamanheei sp. nov.) from sheep in rhe Cape Province (15rh Annual Report ofrhe Director of Veterinary Services, Union of Sourh Mrica, 1929). Ptetoria:Government Printer, 1930: 335-346.

6. Porter A. Larval trematoda found in certain Sourh African molluscs. Publica­tions of rhe Sourh African Institute fot Medical Research. 1938, vo!. 8, pp.

. 1-492.7. Gear JHS, Pitcbfotd RJ, Van Eeden JA. An Adas of Bilharzia in South

Africa. Johannesburg: State Healrh, SAIMR, SAMRc, 1980.8. Rudo BM. Report on the Botswana National Bilharziasis Suroey, October

1976 - October 1978. 1979: 1-40.9. Chaine JP. Schistosomiasis Preva.lena and Control in the Kingdom of Swazi­

land. Ministry of Healrh, Swaziland: US Public Healrh Assoc., InternationalDivision, Academy for Educational Development and Bilharzia ControlUnit, 1984.

10. Pitchford RJ. A check list of definitive hosts exhibiting· evidence of rhegenus Schislauma Weinland, 1858 acquited naturally in Mrica and rheMiddle East.J Helminthol1977; 51: 229-251.

I!. McCully RM, Van Niekerk JW, Kruger SP. Observations on rhe parhologyof bilharziasis and orher parasitic infections of Hippopotamus amphibius Lin­naeus 1758 ftom rhe Kruger National Park. OnderStepOOTt J Vet Res 1967;34: 563-618.

BYLAE TOT SAMT 11 OKTOBER 1986