The epidemiology of sleeping sickness in East Africa

316 TRANSACTIONS OF THE ROYAL SOCIETY OF TROPICAL MEDICINE AND HYGIENE. Vol. 56. No. 4. July, 1962.

T H E E P I D E M I O L O G Y OF S L E E P I N G SICKNESS IN EAST AFRICA V. EPIDEMICS ON THE ALBERT NILE ~ BY K. R. S. MORRIS, D.sc.t

Leverhulme Research Fellow, at Department of Pathology, Makerere College, Kampala, Uganda

The West Nile District, in the north-western corner of Uganda, resembles so closely the savannah woodland country of West Africa in its climate and vegetation, that the area falls naturally into the "Soudano-Guin&n" climate and vegetation zone of AUBRI'VILLE (1949), a fact which has exerted a marked influence on its predisposition to sleeping sickness. T h e district is bounded on its eastern side by the Albert Nile, to the north by the Sudan, and by the Congo in the west and south. These last three boundaries are roughly marked by a great arc of hills, from which numerous small rivers flow eastwards to the Nile. T h e population, shown as 336,000 at the last census in 1948, occupies the hilly country to the north, west and south, with a concentration, at over 200 persons per sq. mile, round the capital, Arua. The north of Koboko and Aringa counties bordering the Sudan is unpopulated, as is also a wide strip of country, much of it low lying, between the occupied hills and the Nile. A thin population, engaged mainly i n fishing and trading, is settled along the Nile banks, from Lake Albert to just within West Madi and again to the south-east of Moyo. An annual rainfall, varying from over 50 in. in the northern and western hilly parts to 35 in. on the south-eastern Nile flats, falls mainly between April and October, producing a marked 5 months' dry season. There are two important results; annual grass fires keep the vegetation to a sub-climax, and the rivers and streams run strongly in the rains, but dry up completely or to a series of interrupted pools towards the end of the dry season. The vegetation is generally of the dry savannah-woodland type, characterized by such tree species of the West African Guinea Zone as Butyrospermum parkii (valued for its butter nuts), Daniellia oliverii (used for canoes), Ficus guaphylocarpa, Diospyros rnespiliformis, Entada sudanica and species of Terminalia and Cornbretum. The more open woodland and grassland on the lower ground along the Nile are marked by the presence of species such as Balanites aegyptiaca, Tamarindus indica, Zizyphus abyssinica, Borassus aethiopum and of Acacia, which indicate the drier and hotter climate of the tension-belt between the Guinea and Sudan vegetation zones. The rivers and streams hold, for the greater part of their lengths, an evergreen riparian vegetation, dense but usually only a few yards in width, which forms the habitat of Glossina palpalis. Much of this riverine vegetation has been cleared in anti-tsetse operations at various times, so some of the rivers are now qmte open, others show different stages of regrowth. On the Nile plains the rivers spread out into areas of marshland, their courses become ill defined and riparian woody vegetation is lost. Thus, G. palpalis is absent from practically the whole strip of low lying country along the Nile and is only present intermittently on the banks of this river from near Lake Albert to a little north of Wadelai. T h e hilly country in the south-west of the District with altitudes of 4,500 to 5,900 feet, is also unsuitable for occupation by this tsetse. Glossina morsitans West. occurs fairly widely in the almost unpopulated parts along the Nile and G. pallidipes Aust. has been found near Rhino Camp. Game animals, from duiker to elephant, are found in the uninhabited country along the Nile and adjoining the Sudan border, but are almost completely absent from the populated country lying roughly westward of the main road Pakwach-Arua-Moyo, where the population densities range from 37 to 214 persons per sq. mile. * The previous paper in this series, Transactions, 1960, 54, 585, was Part IV (not "V" as printed). t T h e data on which this study is founded were obtained through the courtesy of the Uganda Administrative and Medical Departments, whose help, both with records and in the field, is gratefully acknowledged. I am also indebted to the Tsetse Control Department for their unfailing co-operation in giving details of tsetse distribution and control operations. The work was started under the East African Trypanosomiasis Research Organisation.

K. R. s. MORRIS THE INTRODUCTION OF SLEEPING SICKNESS AROUND

317 1900

The zone of dry savannah woodland in West Africa travers6s that quarter of the Continent lying roughly between the 10th and 13th parallels N., from Senegal to the Northern Cameroons just south of Lake Chad. This country has seen the heaviest and most extensive outbreaks of sleeping sickness, caused by Trypanosomagambiense, which have occurred in West Africa. From the Chad Province of former French Equatoria the same vegetation zone continues eastward, with a slight southerly trend, through Ubangi-Shari to Equatoria of the Southern Sudan, and then extends southwards to just within the West Nile and Acholi Districts of north-western Uganda. This formation is well shown in KEaY'S (1959) Vegetation map of Africa. Thus an ecological link extends from West to East Africa along this zone, sandwiched between the Sahara and the Congo forests. It is, moreover, a terrain suitable for human settlement and trade. It was almost inevitable that sleeping sickness should reach East Africa from West along this link. The evidence shows that it did so towards the end of the last century. The disease was well established on the Upper Ubangi River by 1886 (MARTIN, LESOEUV and ROUBAUD, 1909). In 1891, during his campaign against the slavers, General Ponthier noted cases among the Arabs defeated by him on the Bomokandi river, a tributary of the Ubangi and only 200 miles from the Albert Nile (DUKE and VAN HOOV, 1928). Ponthier's forces then moved on to contact Emin Pasha's men on the Albert Nile near Wadelai (BouLGEa, 1898). DUKE and VAN Hoov (op. cit) consider that sleeping sickness spread in an endemic wave across the basin of the Ubangi from the north-west to the south and east, thus causing its introduction into the north-east corner of the Congo. In 1902 BRUMPT (1906) found sleeping sickness along the whole length of the Welle river, another tributary of the Ubangi "depuis les sources jusqu'~ la embouchure du Congo," and DUTTON and TODD'S map (1906) marks its presence on the Upper Welle and on the neighbouring Aruwimi river in 1905. Another map by TODD (1906) shows this disease in the same year, 1905, to have reached Mahagi on the western shore of Lake Albert, and Loka in the Sudan, 80 miles north-west of Nimule and close to Yei, the scene of a fierce outbreak 5 years later. At the same time, 1905, Dr. Densham, investigating closely into the origins of sleeping sickness on the Albert Nile near Wadelai, obtained first-hand evidence that the disease had been in existence there for some time, judging by the presence of advanced cases, which had probably been infected for 4 or 5 years, and through finding villages already wiped out by an epidemic. He also noted that a large proportion of the patients he saw were coming from the Congo, and he was told by the natives that sleeping sickness had been known for some time previously on the Welle river, and its upper reaches the Kibali, in the Lugwarri districts of the Congo, adjoining the present West Nile District of Uganda. A number of Dr. Densham's patients came from Lugwarri and the natives averred that the sickness had reached the Nile from there (HODGES, 1908). A hundred miles to the north, in the Sudan, there is a clear picture of the introduction of T. gambiensefrom adjacent parts of the Congo well before 1910 (MORRIS, 1961). This sequence of events took place just at the time of a big increase in the amount and freedom of movement of the people in this area, consequent on European occupation in 1886 and the suppression of the Arab slavers, who had kept the country in a state of terrified repression. An increase in local traffic is notoriously effective in promoting the spread of Gambian trypanosomiasis. The evidence, then, is very convincing that the entry of trypanosomiasis from West Africa into the Nile basin took place along a route following the

318

E P I D E M I O L O G Y OF S L E E P I N G SICKNESS I N EAST AFRICA

Ubangi and Welle Rivers, and that this occurred in the decade before the beginning of th~s century. THE NILE EPIDEMIC OF 1 9 0 5 - 1 9 1 2

Once the infection was on the Nile, the spread up and down it was a certainty. Emin Pasha noted the ease and frequency of traffic by water between the Alurs on the Albert Nile and the Banyoro on the Victoria Nile (ScHwEINFURTHet al., 1888). For the same reason the first District Headquarters for Acholi was at Wadelai, on the east bank of the Nile opposite Emin Pasha's old fort. Thus, when investigations were started in 1904 by the Uganda Medical Department, sleeping sickness was found to be already established, not a recent introduction, in the Madi country adjoining the Albert Nile between Wadelai and Nimule (HODGES, 1907); over a dozen scattered cases were found along the lower 15 miles of the Victoria Nile before its outflow into Lake Albert (GREIG, 1905); and a severe though localized epidemic, with at least 200 deaths, was discovered in the north-west corner of the Bunyoro District between Lake Albert and the Victoria Nile (ADAMS, 1907). At Wadelai an epidemic developed of such severity as to cause the District Headquarters here to be abandoned in 1906 (DREw, 1911), and moved to a new site at Koba, in the angle between the Albert and Victoria Niles, 6 miles from their junction with Lake Albert. By 1910 a violent epidemic, with 1,000 deaths reported in that year, had developed around Koba, spreading with fatal rapidity among the very primitive natives there, whose whole life, based almost entirely on fishing and hunting and with practically no cultivation, kept them constantly at the waterside in intimate contact with G. palpalis (Father Medeghini, St. Joseph's Mission, Arua, pers. commun.). The Government station was moved to its present location at Gulu in 1912, and the whole population from a wide strip along the eastern banks of the Nile was moved in 1911, the Alur tribesmen across the river to the West bank, the Acholi to the Oytino river close to Gulu (MORRIS, 1959). Meanwhile the Wadelai epidemic had spread rapidly northwards (PEZZI D'ORNELLA, 1947), to give rise, in 1914, to a fierce epidemic on the Ayu River, a small tributary of the Nile marking the present boundary with the Sudan. This was the Kajo Kaji epidemic of the Sudan, and was dealt with by evacuation of the Ayu valley population by the Sudan authorities (STIGAND, 1923), but not before the disease had spread across the Nile to Opari, on its eastern bank just north of Nimule (BLOSS, 1960). THE DEVELOPMENT OF THE MADI EPIDEMIC 1 9 2 0 - 1 9 3 0

The evacuation of the many villages along the Albert Nile (see map in KING, 1912) musthave greatly reduced the incidence of trypanosomiasis without effecting its eradication, in contrast to the effect of similar and -almost simultaneous measures along the Lake Victoria shores and islands and along both banks of the Victoria Nile, which virtually stamped out the earlier epidemics of Lake Victoria and Bunyoro. Thus the Medical Department's Annual Reports for the years up to 1914 remark upon the decrease of sleeping sickness everywhere in Uganda except for the Albert Nile Valley, where it was "stationary," or "still smouldering among the villages." This state of affairs would be due to the evacuations being unilateral, confined to the eastern, Acholi bank of the Nile only. On the west bank the present West Nile District had a chequered infancy.. It started in 1876 as the Lado Enclave of the Sudan under Emin Pasha; in 1893 it was leased to King Leopold of the Belgians until, on his death in 1909, it was returned to the Sudan, but was hardly touched during either of these regimes;

K. R. S. MORRIS

319

finally it came to Uganda as the Nile Province in 1914. Under such circumstances neither co-ordinated action against trypanosomiasis, nor reliable information as to its status was to be expected, a plight which continued from 1914 to 1920, since the special investigations which were planned by the Uganda Government for this area were made impossible by World War I. By 1920 it was realized by the Medical Department that "large numbers of cases were occurring and have occurred on the Nile from Lake Albert to Nimule," and in 1921 Hale Carpenter was able to visit this area, and found sleeping sickness well established among the Madi tribes living on both sides of the Nile next to the Sudan border (CARPENTER, 1921). This was undoubtedly an extension of the 1914 outbreaks of Kajo Kaji and Opari. These epidemics were being controlled in the Sudan, but in Madi it was obviously on the increase. Carpenter's surveys showed 157 cases in 21,236 people examined in 1921, an incidence of 0.7 per cent., whereas in 1922 it had risen to 1 per cent., 250 cases being diagnosed in 24,300 examinations. The total for that year was 290 cases, and 200 deaths were reported. Extensive clearings of the G. palpalis infested bush were made at the watering places and road crossings, especially in East Madi where the incidence was slightly higher, and four of the most severely infected southern and eastern counties were evacuated, the people being moved to the less heavily infected north. The evacuated parts were declared a "prohibited area" and gland inspection posts were instituted at steamer landing stages on the Nile to prevent the transference of infection out of the district. During the next 2 years these measures were continued and increased, particularly the precautions aimed against the spread of infection to other districts. It reflects great credit to the work of the Medical and Administrative departments that the disease from this quite serious outbreak, which straddled the Nile, did not get carried up river to other districts by the steady stream of labourers travelling by steamer or canoe to Butiaba on Lake Albert, and beyond this port by foot (see MORRIS, 1960C). The effect of these measures locally appeared to be most satisfactory. In 1924 only 36 cases were found in 11,250 people examined (0.32 per cent.). The reduction was particularly marked in the centres of heaviest infection (CARPENTER, 1924). The reduction, however, must have been local and did not last long. The evacuated people were continually moving back to their old homes and thus the epidemic was renewed and prolonged; 124 cases were found in 1925 and for 5 years the epidemic continued at an incidence of over 100 cases a year, as can be seen from the following records from West and East Madi :-1925 1926 1927

124 cases 239 cases 159 cases by J u n e

1928 1929 1930

176 c a s e s 93 c a s e s by J u n e 32 cases

By 1930 an initial lack of co-operation of the Madi had been largely overcome and their confidence won, as a result of successful treatments. Three inspections were being made a year and a 99 per cent. turn-out of the people was estimated. The figures from now on were considered by Carpenter to be reliable. A recorded incidence of 7-24 cases a year for the next 10 years showed that this epidemic had really come to an end, and during the decade 1950-60, 0-3 cases a year appear in the annual returns. THE FIRST WEST NILE EPIDEMIC, 1927 TO 1934

Before the Madi epidemic had been got under control a serious new outbreak had started in the West Nile District. West Madi adjoins the northern counties of West Nile without any natural barrier, there is continual traffic between them, and conditions in the latter C*

320

E P I D E M I O L O G Y O F S L E E P I N G S I C K N E S S I N EAST AFRICA

territory, which is intersected by innumerable G. palpalis-infested streams, were recognized as being ideal for the development of epidemic trypanosomiasis. So, as soon as the Madi outbreak was detected, it was realized that there was a danger of a westward spread and a watch was kept on the adjacent West Nile counties of Aringa and Terego. Two events weakened the effectiveness of this watch. In 1922 Hale Carpenter, alarmed by the situation in Madi, had made a number of examinations with gland punctures in Aringa county, and several of the people examined had subsequently died. Attendances for examinations in this area became almost nil for several years after this. Secondly, the immediate removal of inhabitants from an area, without any compensation, as soon as many deaths from sleeping sickness were reported, was causing the natives within and beyond Madi to do everything to avoid a similar fate; deaths were not reported, sickness was concealed and inspections were avoided. Nevertheless, it is certain that the concern of the officials and Chiefs over the Madi epidemic would not have allowed the presence of cases in any numbers in the West Nile counties to go undetected for long. The first indication of the westward spread of infection outside Madi was the report of five deaths from trypanosomiasis in the West Nile District in 1925. An immediate examination of 6,501 people in Aringa county showed the presence of five more infections of T. gambiense, one of which was proved microscopically only on the third examination. Later Dr. Luow found one very advanced case in an Aringa village right on the main route from Madi. No further cases were found in 1926, despite search, but in 1927 a focus of the disease was discovered in Jonam County on the Albert Nile itself, in Mutir and Rogem villages, opposite Wadelai. Seven cases were found positive among 2,725 people examined, and there were others unconfirmed microscopically. It was considered that this was a longstanding endemic, which is highly probable, trypanosomiasis having been epidemic here and having caused the evacuation of Wadelai in 1906. The area is remote, without roads and difficult of access and the population is small, so an endemic could easily have persisted undetected for 20 years. At the end of 1927 a severe famine occurred in West Nile and Madi, bringing about a great increase of movement among the people, from village to village in search of food, and widely into the bush for hunting, and particularly along the rivers for fishing. For the past few years there had also been an increased movement of people out of Madi into the sleeping sickness-free West Nile District to avoid the restrictions and compulsory population shifts of the Madi control operations, and in response to new areas being made accessible for settlement by the building of roads. The famine movement caused a recrudescence of the epidemic in Madi and, with the migrations, evidently brought sufficient numbers of infected people into West Nile and stirred up the small focus already there, to start a serious outbreak in the north of this district. Early in 1928 a limited outbreak was found on the Dacha River, in Aringa, on the main paths coming from both Madi and Jonam. It was soon discovered that a serious epidemic was starting up. The disease spread rapidly into the heavily populated country on the upper reaches of the Koich River, immediately north of the Dacha, and by the end of the year nearly 700 cases had been found. In Jonam 53 new eases were reported, besides 18 deaths. Throughout 1929 the epidemic continued to spread along the Koich river and its many fly-infested tributaries into Koboko County and later across the Dacha and Orei rivers into Terego. BARRETT(1934) considered that the peak of the epidemic occurred in the first half of 1929, with 120 new cases a month being found in August. There followed a rapid decline in the rate at which infections were being incurred, until at the end of the

K. R. S. MORRIS

321

year 25 new cases a month were occurring, roughly one-third of the peak rate. Thereafter the rate appeared to become stabilized at this lower level without further reduction. Hale Carpenter gives 1,856 as the n u m b e r of cases treated in the West Nile in 1929, though the Medical Annual Report gives the figure at 1,459, the difference probably representing the n u m b e r diagnosed clinically and not hy microscope. In the same year the Jonam endemic also flared up into epidemic form, with an apparent tenfold increase, from 53 cases in 1928 to 539 in 1929. This recorded increase would be explained in part, however, by additional vigilance and efficiency in the search for patients. F r o m 1929, when the epidemic had drawn attention to the West Nile District, a sufficiently complete series of annual records of sleeping sickness has been obtained--from the files of the Medical Department and the District Commissioner's office--to make it possible to follow the course of the epidemic and subsequent endemic in some detail for the next 30 years. T h e r e are naturally some discrepancies, for example, that in the annual total of cases for 1929 just quoted. T h e District Commissioner's figures give the number of cases found positive during the annual inspections, which have been continued in the northern epidemic area since 1929 and throughout the district except for the south western highlands, since 1937. T h e Medical Department's figures usually, though not always, quote the n u m b e r of cases treated, which may include patients with only clinical symptoms and relapses. T h e District Commissioner's figures are in a more complete series. For this reason, and because of their consistency, these data have been used as far as possible in the compilation of Table I and Figure, which show the course of the disease since 1928. Separate figures for Aringa County are available from the start of this series and for all the counties in the district from 1937. It is instructive, as will be shown in the discussion, to present the data TABLE I.

Incidence of sleeping sickness in the West Nile District, Uganda; Aringa County contained the main, but not the only, primary epidemic loci. I

Date

Aringa County

Other Counties

1928 1929 1930 1931 1932 1933 1934 1935 1936 1937 1938 1939 1940 1941 1942 1943 1944

411 973 459 326 319 404 561 503 770 247 166 108 80 62 63 38 39

310 486 137 292 84 91 54 63 240 431 490 369 293 242 183 214 109

District Total 721 1459 596 518 403 495 615 566 1010 678 656 477 373 304 246 252 148

Date 1945 1946 1947 1948 1949 1950 1951 1952 1953 1954 1955 1956 1957 1958 1959 1960 1961 (Jam-April only)

Aringa County

Other Counties

District Total

22 13 4 3 3

85 90 20 6 14

1

8 1 1

107 103 24 9 17 9 3 6 12 20

2 5 10 18 7 2 14 7 23 9 8

2 2 1

8

2 5

4 19

1

8

7

30 10

1

0

8

Data are for only those cases diagnosed microscopically. Total numbers treated, which include clinicals, are usually higher; e.g. in the peak years 1929 and 1936 the numbers treated were 1856 and 1867 respectively.

322

E P I D E M I O L O G Y OF S L E E P I N G SICKNESs I N EAST AFRICA

2.000 ARINGA COUNTy . . . . . . . . .

I,QOC)800" 6C0" 400- ~' ~~ ~ ' ~l ~ , ~ -200 ~-

IOO 80 6o

.

~

REMAINING COUNTIES.................

~

, ~" " ~ '" " -~- - ~

!~

.

" ~'"..

X

i ...J

DISTRICT TOTAL

-.-\.y~_______~_. '.,

"x

~. "~'

"~

_~4o 20

~ 2. " I .... 1930

I . . . . . . 1935 1940

V L ....: '

'

I

'

1945

'

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I

'

1950

'

V '

~

I

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1955

,

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1960

FIGURE. Epidemics of Gambian sleeping sickness in the West Nile District of Uganda, showing the shift of the epidemic, after 1929 and 1936 peaks, from the northerly Aringa County to the rest of the district, and its return to the Aringa foci after 1950. The annual returns of cases found positive are plotted on logarithmic scale. The incidence for 1961 is for 4 months, January to April only. in three groups, the totals of cases for Aringa County alone, for the rest of the counties together, and for the District as a whole. Control measures, started in 1928, consisted of surveys and the treatment of cases at 3-month intervals in the infected areas; the clearing of fly-belt at water-holes and road crossings; the establishment of a "Sleeping Sickness Village" for the segregation of patients under treatment in Aringa; and restriction of the movement of people in and out of infected areas by a system of permits and passes. These measures were enforced by the passing of the Sleeping Sickness Ordinance of 1928 and the registration of the population in danger zones. It is possible that the imposition of these compulsory restrictions on a primitive and as yet loosely administered native people at first hastened, rather than checked, the spread of the epidemic. The cleared and policed roads and paths were rapidly forsaken for uncleared bush tracks where everyone could pass freely. The result was greatly increased contact with G. palpalis and a wider and more rapid dispersal of infections. It was 2 years before control showed its full effects. The decrease of the incidence of new infections noticed by Barrett at the end of 1929 continued, with a 60 per cent. fall in the number of cases in the Aringa epidemic in 1930, when only 459 cases were recorded from this area against nearly 1,000 in the previous year. Jonam showed a similar decline to 49 cases. But the disease had spread to a new focus around the district headquarters of Arua, where a sharp epidemic developed among a crowded population living on the banks of three small rivers infested with G. palpalis. There were 88 cases in 1930 and 91 in 1931. By the end of 1931 most of the rivers and streams around Arua had been cleared, producing a most satisfactory drop in the number of cases, only 29

K. R. S. MORRIS

323

being recorded in 1932. In the Aringa and Jonam areas also the incidence continued to fall in 1931 and 1932, in the latter year Aringa showing only 319 new cases and Jonam 24, the total for the District being 403. There can be no doubt that the very big fall in the numbers of cases was due in the main to the control operations which had been applied so promptly and so thoroughly by the Administrative and Medical Departments, but the fact that the fall was so abrupt immediately after the peak of the epidemic in August 1929, with the rate of finding new cases falling by two-thirds by the end of the year, led Barrett to the opinion that the initial decline was greatly accelerated by the subsidence of the famine, soon after the start of the rains in 1929, which was more effective than any artificial restrictions in stopping the wide-spread movement around the countryside and in restoring settled communities, which are more available and amenable to inspection and control than is a scattered population. The decline from the 1929 peak figures continued for the next 5 years in the southern loci of Arua and Jonam, where control was well established, but lasted for only 3 years, i.e., until 1932, in the main epidemic area of Aringa. THE SECOND WEST NILE

EPIDEMIC

IN

1936

An abrupt reversal of the fall in sleeping sickness in Aringa took place in 1933, and was explained in part by the Medical and Administrative teams being enabled to concentrate on this area in that year, with the southern foci under a large measure of control. An increased effort was made to trace patients to their homes, and this resulted in the discovery of many new cases which had escaped routine inspections. Also the areas round infected localities were closely searched, which often resulted in new loci being found. In other words it was apparent that the area of the 1929 epidemic had by no means been fully covered, either in survey or by control. A further source of failure in control lay in various weaknesses in the measures against tsetse which were now beginning to show up. In the first place the propensity of G. palpalis to move freely up and down rivers close to the water's edge was observed in the Koich River clearings, also the ability of this species to utilize long grass, apparently as permanent cover. These habits caused this fly to traverse very long clearings, even 3 to 4 miles in length (GIBBINS, 1941). In the clearings themselves the cut bush regenerated with much greater rapidity than had at first been realized, so that slashing two to three times a year was necessary to keep it down. Finally the most serious failure of all lay in the fact that the people tended to forsake their water-holes and washing places in cleared parts of the rivers, seeking in preference the shade and privacy of uncleared fly-belt at the ends of the clearings, thus defeating their whole aim. The rise in the number of cases from the Aringa area, which had started in 1933, continued in 1934, when 561 cases were recorded, double the figure for 1932. In 1935 a new outbreak occurred in Terego County and the following year, 1936, saw the disease at epidemic level once more in this northern infected area. Events have been well described by BROWN (1938). The main outbreak was still on the rivers Koich, Dacha, Orei and Anau, where an area of 500 square miles on their upper reaches showed infection rates of 6 per cent. and over, rising to 7.8 per cent. in some foci, with a zone of lower infection, from 2.4 to 5 per cent, located around its southern and eastern fringes. A total of 950 cases from this outbreak are recorded in the District Commissioner's returns and 60 cases from other areas, giving a total of 1,010 for the whole district. Again there is a discrepancy between this figure and

324

EPIDEMIOLOGY OF SLEEPING SICKNESS IN EAST AFRICA

that given in the Medical Department's Annual Report, which records 1,867 West Nile cases in 1936, As mentioned above, this epidemic peak coincided with an increase in the efficiency and extent of control operations, which were now concentrated upon this northern epidemic area. To work in this area alone a special Medical Officer and a District Officer were appointed. It was estimated that nearly 100 per cent. of the people were examined on inspections, which were repeated every 3 months in the heavily infected parts. Clearings were greatly increased in length, finally a considerable length of the Koich river being completely cleared of fly-belt. In this way a rapid reduction in the incidence of the disease was brought about during 1937 and the following years within the original outbreak area. But it was soon found that infections were once more spreading into surrounding parts of the District, that is to say, in the places where control measures were receiving less attention or had ceased altogether. In 1937 Terego, Omugo and Offude were badly infected and in 1938 new outbreaks as far south as Vurra were discovered. The District records show that by that date cases were coming in from almost all over the District. By 1939, with sleeping sickness apparently endemic throughout the West Nile except for the western and southern highlands, biannual inspection of the whole population was instituted, with quarterly inspections in the most heavily infected parts, as well as additional clearings. Although the war soon made it impossible to maintain the inspections and clearings to such an extent, yet the disease was now definitely under control, and its incidence continued to fall in all parts of the District until, by 1947, 11 years after the peak of the second epidemic, it had reached the low endemic status of around 10 cases a year, which has prevailed almost without interruption up to the present date. A feature of this second outbreak, which is of the greatest interest epidemiologically, is the striking shift in the concentration of infections, first from north to south in 1937, into the central belt of the District from the Aringa epidemic centre when control had been established there, then back again to this original northern focus in 1950, when the outbreak as a whole had been reduced and only a low endemic remained. Indeed, during the past 10 years the cases have all come from villages in one small part of the original epidemic area, the same locality which had seen the discovery of the first outbreak early in 1928. The spread of the epidemic at its heigl~t and its subsequent contraction to its primary loci are shown in Map 1, and can be well demonstrated by considering the incidence for Aringa County, which contains practically all the original loci, separately from that for the rest of the District. This is shown in the Figure and Table I, which illustrate clearly how the majority of the infections spread to localities outside Aringa in 1937, after the epidemic had reached its peak, but were localized again within that County once the endemic had reached its lowest point in 1951. It is rewarding to consider in even greater detail the events of the past 10 years in this hard endemic core, the key to the West Nile sleeping sickness problem. THE UNSTABLE ENDEMIC

PERIOD

1947-1961

The period of apparent low endemicity, which prevails until today, has been the subject of detailed studies made on four visits; in 1956, 1958 and twice in 1961. From 1950 to 1954 all but four of the trypanosomiasis cases occurred along one river, the Orei, which divides the counties of Aringa and Terego (Map 2). A small outbreak developed in 195354, with 29 eases in this one focus. In 1955 there were fewer infections, but they came

K, R. S. MORRIS

325

MnP 1. Showing the course of the epidemic. from a wider area, suggesting an outward spread. By 1957 the spread had, in fact, materialized, giving rise to a new outbreak on the Dacha River, 10 miles north-west of the Orei, close to where it crosses the main road, with 12 cases concentrated within a small area of about 3 sq. miles. This new focus produced seven cases in the following year, one came from the Orei river, and since this was the District total for 1958, it seemed as if the spread had ceased. However, the 1959 incidence of 30 cases, the highest annual figures since the big epidemics had been finally cheCked 12 years before, made it evident that the present outbreak was by no means yet under control. The Dacha focus showed an increased number of cases, and three neighbouring river systems were now possibly involved. Although the incidence fell to 10 cases in 1960, the distribution of these infections and of the eight found by the end of April in 1961, strengthened the suspicion that a dangerous outward spread was still in progress. The trend can be followed in Table II and Map 2. The study of these outbreaks is illuminating. At the end of 1953 the female relative of a leprosy patient from a camp close to Arua was sent to Dr. G. Nelson, the District Medical Officer, as a suspected trypanosomiasis case. There were no obvious palpable glands, but one small cervical gland was detected, gland juice was aspirated and found to contain trypanosomes (NELSON, 1954). The patient came from Uluba in Aringa County, one of the long-standing endemic centres, so the nurse at Aringa dispensary was told to do a house to house search for cases in the patient's home area. No suspects were found, so the nurse was then instructed to collect 100 thick-film blood slides from the patient's relatives and neighbours. Out of 124 slides taken six were positive with T. gambiense. A further thorough search in 1953 and 1954 revealed a total of 31 cases, 29 of which came from villages along the

326 TABLE II.

EPIDEMIOLOGY

OF

SLEEPING

SICKNESS

IN

EAST

AFRICA

Sleeping sickness cases found in surveys, or among patients coming to dispensaries or to hospital in the West Nile District, Uganda, 1951-61. 1951

1952

1953

1954

1955

1956

1957

1958

1959

1960

1961

(Jan.April only) Orei R~er Uluba Udupi Ladonga Lugbari

2 1 --

5 --

10 1

17 1

DachajureiBujors Wolo Nyoko Lomunga Langi

1 2

2 2

1

1

--

1 -1 --

1 ---

1 1

1

11 1

14 3

14 2 3

3 1 1

1 3 1

--

--

--

__

m

1

Oru River Omugo.

1

Atu River Aupi

1

1

--

4

--

--

1

--

--

3

Limaka River Yata Other localities Arua Ayivu

1

1

--

--

12

20

1

1

m

Not placed 6

1

1 --

3

1

2

1

Envetre River Olivu Ombakoro

Total

-1 -1

8

4

19

8

2

30

10

8

The figures are for cases diagnosed microscopically. Total numbers treated, which include those with clinical symptoms only, are greater. Orei river, which had an old clearing, thickly regrown and reinfested with G. palpalis. T h e s e cases had been missed in the routine biannual inspections. During this search Dr. Nelson discovered f r o m the Chief's death register that two people with "sleeping sickness" had died during the previous 6 months. T h e s e also had been missed b y the Sleeping Sickness I n spectors. I t was noticeable that the majority of patients showed a complete lack of symptoms, a marked characteristic in the earlier West Nile epidemics (BaowN, op. cir.). T h e outbreak was dealt with b y the segregation and treatment of patients, re-examination of the population on both sides of the Orei River by blood puncture and for clinical symptoms, and b y making an 8-mile-long clearing. a 3-monthly examination of this population, including blood slides f r o m all p u t into operation.

an immediate slides, gland Furthermore suspects, was

K. R. S. MORRIS

1953-54 1955-56 1957 1958 1959 1960 1961

Orei R. epidemic small o u t w a r d spread Dacha R. epidemic, Orei spread continues,

expansion of Dacha focus epidemic continues, marked o n t w a r d spread spread continues, new foci Atu & Envetre Rs. .

.

.

.

. . . . . .

Missions and' Churches Markets K n o w n movement of patient, on visits ,t

MAP 2.

,~

,s

1,

t,

327

31 cases II ,, 19 ,, 8 ,, 28 ,, 9 ,, 8 ,,

• © • [] A /k • i M 4- - - - ~

)~

T h e d i s t r i b u t i o n of sleeping sickness in the p r e s e n t e n d e m o - e p i d e m i c area of t h e W e s t Nile D i s t r i c t of U g a n d a .

During 1955 only three cases were found in the Orei River infected area, but four cases came from well outside the area. One of these patients, Akile, was a Headman living in Wolo, 10 m~es to the north, who had been in charge of the 1954 Orei River clearings. He was diagnosed only because he had been brought into Arua Hospital as a mental case at the end of May and this had led to trypanosomes being found in his glands, He must have been infected for over a year, and had therefore been missed by the inspections on three occasions. Meanwhile he had been a potential source of infection to G. palpalis on the Dacha River and its branch the Jurei, which lay less than a mile from his home. In 1956 only four cases were found, all within the original Orei River focus. These, together with those diagnosed in 1955, could be late developing cases, infected before the clearing of this river in 1954. In 1957 only one case came from the original Orei focus, but infections, evidently associated with this river, appeared at more widely spaced localities, from Lugbari in the south to Ladonga, some 12 miles to the north. At Wolo, on the Dacha River, a group of 12 cases

328

EPIDEMIOLOGY OF SLEEPING SICKNESS I N EAST AFRICA

appeared in a very small area close to the Headman, Akile's home. Six of these occurred in the same house, which was found to be less than 400 yards from a part of the Dacha River holding low evergreen riparian habitat of G. palpalis with a water-hole, used by this and many surrounding houses, set in the fly-belt. Tsetse of this species were seen at once on my visit in May, 1958. Although the Jurei river, which provides water for the homes of three other patients in this group, was deceptively open with only tall trees and long grass at this spot, G. palpalis was found on adjoining parts of this river by Mr. Woodcock of the Uganda Tsetse Control Department during surveys in 1958 and 1959. The lower incidence of only eight cases in 1958 was deceptive. All but one arose in the infected area at Wolo, showing that this focus was still active, an indication which was confirmed by the finding of 19 new infections here in 1959, many of which arose in houses on the Dacha and Jurei rivers, and on a third, hitherto uninfected branch, the Bujo, in places beyond the limits of the original narrow focus. Control of G. palpalis on these rivers, by spraying with Dieldrin, had been started by the Tsetse Control Department in November 1958, first down stream, south of the road, around the initial focus, but by June 1959 the whole of the upper reaches had been dealt with, causing virtual disappearance of the vector along 85 miles of river and tributary. At the same time the efficiency of the sleeping sickness inspections was greatly increased by their being taken over by the Medical Department, surveys being now done under direct supervision of a Medical Officer (Dr. C. L. Nelson), with a concentration of attention on the endemic area. The excellence of this new organization was such that, in the two surveys done in 1959, a 99 per cent. sample of the population was examined. The picture that resulted from this more intensive field work showed that the increase in numbers and in area observed in 1959 in the Dacha focus was also occurring elsewhere. Two other rivers were now involved. The Envetre, 5 miles west of the Orei, had shown three cases in its neighbourhood in 1957, and now had three more infected houses all drawing water from G. palpalis infested sources; the'Atu, a further 3 miles west, where a case had occurred in 1954 and one in 1955, showed two more in 1959. There was no doubt that the outward spread observed in 1955 and 1957 was still taking place. Disquieting confirmation came from the distribution of 10 cases found in 1960 and the eight which had already appeared in the first four months of 1961. A new village, Olivu, on the west bank of the Envetre, was now infected, another case arose in Aupi on the Atu River; other patients, although infected at Wolo (see under "movement" below), were living at considerable distances, with the risk of involving even more river systems in the present outbreak. One patient was diagnosed at Ayivu, on the Anau River nesrly half-way to Arua. The rapid extension of the epidemic between 1955 and 1961 is well shown by Table II and Map 2 considered together. A separate line of evidence on the seriousness of the situation today comes from examination of the sex ratio in the cases for the past 11 years (including January-April 1961), as set out in Table III. In Gambian trypanosomiasis during its narrowly focal endemic stage, when the majority o f infections are being acquired at tsetse-infested village water-holes, it is the women and ~:hildren who are the most exposed during their prolonged daily visit to the river, drawing water, bathing, washing clothes and pots, and, of course, gossiping. The change from endemic to epidemic status involves, besides a big increase in local water-hole infections, t h e setting up of new loci further afield, on the same or on neighbouring rivers. These are ~nore apt to affect the male population, who travel more extensively, both socially to meetings

329

K. R. S, MORRIS

TABLe III.

Male and female incidence of trypanosomiasis West Nile, 1951-61. 1952

1956

1957

1958

1959

1960

1961

6

1

13

1

16

6

4

3

14

3

6

7

14

4

4

12

20

4

19

8

30

10

8

1953

1954

1

9

?

3

Total

4

1951

1955

a n d markets, or in their day to day occupations of farming, hunting, gathering timber, and so on. The change over from a preponderance of infections among females to an excess among males in the years 1953, 1957, and 1959, marking the beginning of the three recent epidemics, is strikingly apparent in this Table. The persistence of an excess of male infections in 1960 and equality in 1961 can have only one interpretation, that the spread of the 1959 epidemic is still taking place. Two other points of importance emerged during these studies. Eight of the 31 patients in the 1953-54 outbreak were found to have died by 1958, and, by May of 1961, two of the patients treated in January of that year and four of the 30 diagnosed in 1959 had also died. It is possible that all of these did not die from relapsed trypanosomiasis, but it is quite certain that such a high proportion would not be due to chance, i.e., that they would not all have died from other causes. Some at least will have been relapsed cases, and during that stage they can become infective to the tsetse. Secondly, a great deal of movement goes on among these people, not only day to day movements, on visits to markets, etc., but the permanent shift of an entire household or of some of its members. Thus by 1958, four of the 36 infected households on the Orei river were found to have moved to other villages since the diagnoses had been made in 1953-56. Had such a move been made before, instead of after, diagnosis and treatment, the cases would have been recorded as from the new villages instead of from the Orei river, and the infected persons would have constituted a danger to these localities if their new houses were at all close to fly-beh of G. palpalis. During the 1961 visit several instances of individuals or households carrying infections into new localities were traced. The boy diagnosed in 1959 at Yata on the Limaka River had been living in Wolo a year previously. An infected boy, from a house in Wolo producing three cases in 1959, moved to Ladonga Mission School in 1960. The woman diagnosed at Langi (extreme east, Map 2) in 1961 often visited a daughter living in Wolo (next to an infected house), staying 3-4 days on each visit. Two Ombokoro families, infected in 1957 and 1959, had moved to Aupi in the next river valley, by 1960. The headman Akili who undoubtedly carried the infection from Uluba to Wolo in 1954-55 has already been mentioned. These movements are shown on Map 2, also the positions of churches and markets, attractions which induce a great deal of regular movement within a range as great as 12-15 miles. The above list is by no means complete--the information was gathered incidentally during the work--but it illustrates the reality of the danger inherent in these movements. The facts which emerge from these studies are: the remarkable viability of endemic Gambian trypanosomiasis, which enables it to persist for long periods, even at the deceptively low levels of three or four cases a year (see Table I); the explosive qualities latent in an endemic; the rapidity and facility with which infections can be spread on the change from endemic to epidemic status; finally the existence of well-defined endemic loci which

330

EPIDEMIOLOGY OF SLEEPING SICKNESS I N EAST AFRICA

evidently can retain their character for years. The lesson that is brought home is the danger, and the cost in recurrent annual expenditure, which arise from incomplete or inadequate vector control in these endemic foci. The Dacha and Orei valleys have probably harboured sleeping sickness for over 30 years; it was here that the disease made its first appearance in the West Nile district in 1928, and although both rivers, together with most of the neighbouring ones, had been extensively cleared of G. palpalis habitat by 1938, these clearings were not permanent and were not maintained once the epidemic had been reduced. Well before 1953 the fly-belt vegetation had regrown sufficiently to hold this tsetse on practically all these Aringa and Terego rivers, and with an increasing native population living along their lengths and visiting and crossing them daily, and with infections still present in the neighbourhood, an outbreak sooner or later was almost inevitable, Although the first outbreak, on the Orei fiver in the parishes of Uluba and Udupi, was small compared with the earlier epidemics, by the time it was discovered in 1953 and control measures started in 1954, it had attained sufficient magnitude to start an outward spread, facilitated by the large amount of movement that goes on among these people. The second outbreak, on the Dacha river 3 years later, showed how effective these movements are in lighting up further potential foci, and emphasizes the real danger latent in the situation here today. Control of the Dacha outbreak by spraying can be effective only as long as there is no further chance of re-invasion by tsetse and the re-introduction of trypanosomiasis, but both these dangers exist. Neither can it be said that control is established in the Orei focus, despite the first excellent clearing; cases are now coming from houses beyond its limits. The feature which must give rise to most concern, however, is the indication, not from isolated cases but from the occurrence of several consecutive infections, that new loci are already established at Aupe and Olivu, possibly also near Omugo, where entirely new river systems are involved, infested throughout their lengths with G. palpalis and running through heavily populated country. All the ingredients are present for further outbreaks, and the abnormally dry season of 1960-61, by intensifying the contact of the people with tsetse along these rivers, can only aggravate a threat already grave. EPIDEMIOLOGY

There is a wealth of material relevant to the epidemiology of Gambian trypanosomiasis in this West Nile history. Its significance can, perhaps, be most clearly brought out if it is discussed under three main headings; 1) the importance of human travel and movement; :2) the suitability of the terrain; and 3) the focal nature of the endemo-epidemics. These ~=onsiderations lead logically to the question of control. 1) It was shown in West Africa (MORRIS, 1951) that, since the human vector of T. gambiense has such vastly supericr powers of movement compared with the insect vector, it is the movements of people, not of tsetse, which have been responsible for many of the biggest outbreaks of sleeping sickness. The effect is especially liable to follow a marked increase in the amount of movement, such as results from trade, pacifications or invasions. TODD (1906) shows how the European penetration and development of the Congo after 1884, and especially the replacement by steamer traffic of the old canoe and caravan routes, led to a greatly accelerated spread of sleeping sickness up that river and its tributaries. The present West Nile studies reveal an important extension of this trend. Trypanosoma gambiense reached the eastern side of Africa from the west, entering the Albert Nile valley by way of the Upper Ubangui and its tributaries the Bomakandi and Welle Rivers, just after the

x. R.

s. M O R m S

331

final pacification of this region by the Belgians in 1890-92 had brought big increases in trade and traffic to an area previously held in terror and turmoil by the Arab slavers. The epidemics which arose on the Albert Nile were, for a time, local and it is of great significance that at that time 1905-12 the troubled history of the area west of the Nile, and the lack of administration and control, meant that little intercourse by land took place between a series of constantly warring tribes and villages. Even in 1911 the natives scarcely dared venture an hour's journey from their homes (KxNg, 1912) and in 1909 BoY,s (1928), hunting in the then Lado Enclave, found " . . . most of their time was spent in fighting with the people of the neighbouring villages, and some of them were killed every day." The opportunities for the spread of infections were practically nil, except along the Nile itself, and this was checked by the evacuation of the infected riverside populations. Even when the Lado Enclave came under Uganda's rule in 1914, the chances of progress and development were hindered by the war. Thus the quiescent period from 1912 to the start of the Madi epidemic in 1921 could be explained by the lack of information rather than of trypanosomiasis, because of the war-time diversions of attention and personnel. During this period the remote and inaccessible populations in Jonam County to the south, and in Kajo Kaji just over the Sudan border to the north, could easily have held unrecognized endemics; but Jonam has a population living on the Nile water-way, that of Kajo Kaji is on a big labour route. The post-war increase in river and road traffic, carrying thousands of labourers annually up and down this part of the Nile, was quite sufficient to have introduced infections into the well-populated Madi country, and thus to have given rise to the epidemic that started there in 1921. Considering the fact that there are no physical barriers between the contiguous West Madi and West Nile Districts, and that the former was soon showing a recorded 200-300 cases a year, which will be a minimum estimate, it is a tribute to the effectiveness of the measures applied to contain it that this epidemic did not spread into the West Nile earlier than 1928. By that time, however, resentment at control regulations and the opening up of new country in Aringa by road building was causing an increasing migration of people from Madi into the West Nile. Then came the famine of 1927-28, with the abnormal amount of local movement among the natives which it produced. By the end of 1928 the first big West Nile epidemic had started. There is no doubt that all this extra movement had triggered it off. There are the direct observations of Barratt on the spot to this effect, besides the analogy with similar happenings elsewhere. Finally, it is worth examining two more examples the spread of the 1936 epidemic almost throughout the district during the ensuing few years, and the extension of the recent 1953-59 epidemics from one river to another. Each event gives a striking exhibition of the way in which infection is spread by local traffic, the second instance, the happenings on the Orei and Dacha Rivers, being especially valuable in that their processes could be studied in such detail at the time they were taking place. In neither case, however, was there a detectable increase in movement to account for the start of the epidemic. Indeed the people's travels were being severely restricted in 1936; and in 1953-57, although traffic was still in the post-war upward trend, there is no evidence of any abnormal upward jump. The causation of these two events in fact comes more appropriately under the thi'rd heading for discussion. 2) Suitability of the terrain. The heaviest sleeping sickness outbreaks in West Africa occurred in the Guinea and Sudan vegetation zones of that region, and these zones stretch

332

E P I D E M I O L O G Y OF S L E E P I N G SICKNESS I N EAST AFRICA

unbroken across the centre of the Continent into north-western Uganda, forming a possible route whereby the disease could, and in fact did reach East Africa. During the two decades before and after the turn of this century records show an almost continuous series of epidemics along this corridor, from the basin of the Niger to the headwaters of the Nile. It is illuminating to examine the conditions in the epidemic area of the West Nile District which are typical of this Guinea-Sudan zone, and which proved so suitable for the development of epidemic Gambian trypanosomiasis. The population was, for Africa, high, averaging nearly 80 persons per sq. mile over approximately 500 sq. miles of country, being the most heavily populated part of the District after the region around Arua itself. A population of this density has a direct effect in providing an ample medium for the rapid multiplication of infections, and the indirect effects of destroying the vegetation and thus limiting the habitat of G. palpalis, and of so reducing the tsetse's wild hosts, in the form of game and reptiles, that the fly turns to man and domestic stock almost exclusively for food. G. palpalis was in fact not numerous. There are frequent references to the small numbers in which it was encountered and the narrowness of its range along the streams, it being unusual to meet with flies except at the water's edge or within the 2-5 yard-wide riparian fly-belt unless they were definitely following people or cattle away from the water. But its distribution was almost ubiquitous; the roads and paths in the terrain of the Koich, Dacha and Orei rivers crossed streams infested by this tsetse literally every 2-3 miles, and an estimate of the amount of G. palpalis fly-beh in this area at the time of the epidemic gave nearly 100 linear miles of riverine habitat in 100 sq. miles of country. Wherever the innumerable streams held permanent water, even if this was reduced to occasional pools in the dry season, G. palpalis was to be found. And, in a country with a 5-month dry season, the complete dependence of the people on these permanent and semi-permanent streams for water, grazing and good farm land brought them into repeated contact with this tsetse every day. Their houses, moreover, were rarely more than a mile from fly-belt, usually within 3-400 yards, often with the houses of a village grouped along both sides of a tsetse-infested river. It could be said that nearly 100 per cent. of the population were bitten by G. palpalis almost daily. Even those who escaped the every-day contacts at the waterside, through being unable to leave their huts, were in danger of being bitten at home by flies introduced by people and cattle returning from the river. In brief it was a pattern of man-fly contact in which a fairly heavy human population was in very close contact and, most important, repeated daily contact with the tsetse vector living in a restricted habitat, again with emphasis on restriction of the individual fly's range, though not of the distribution of its communities. It is a pattern already familiar in outbreak areas in Uganda and Kenya (MORRIS, 1959, 1960b), and strikingly similar to that found in the severe T. gambiense epidemics in the north of the Gold Coast and in the French Territories of the Upper Volta in West Africa. As in those territories, the anomaly existed of conditions adverse to the tsetse being favourable to the development of epidemic trypanosomiasis (MORRIS, 1949). Since the inhabitants and the tsetse were coming into daily contact at the same rivers, streams and water-holes, with minimum opportunity for dispersal of the fly, it can be seen that once T. gambiense was introduced there were optimum conditions for its rapid spread through both human and tsetse communities and almost no chance of its disappearance, short of outside interference or the automatic elimination of the human host by the parasite itself. This latter event, in fact, is known to have occurred in the big West African epidemics before the time that European intervention brought them under control. It was the study of these past, as well as of the existing outbreaks that led to an appreciation

K. R. S. MORRIS

333

of the focal nature of endemo-epidemic trypanosomiasis (MORRIS, 1951, 1960a, b, 1962), which is so well exhibited in the West Nile picture. 3) The focal nature of Gambian sleeping sickness arises from the dynamic qualities of the disease viewed in its endemo-epidemic form, i n which can be seen the attributes of growth and spread, or of decline, possessed by plant and animal communities. Thus, in a well developed and unchecked epidemic, a pattern of zonation is typically present, in which areas of heavy infection, the primary epidemic foci are surrounded by zones of much lightc, infection, often with linear extensions along trade and labour routes. Studies of the primary epidemic loci in West Africa showed them to contain a full complex of factors favouring th transmission of T. gambiense, i.e., there was an adequate population in close and regular contact with the tsetse vector which was living in a restricted, as opposed to an extensive, habitat. In the secondary areas of lighter infection the full complex of factors did not exist and, although the transmission of trypanosomiasis was taking place locally, it was considered that this would continue only as long as there was a constant renewal of infections from the adjacent primary loci and would cease if this source of supply was cut off. In other words, the secondary areas were mere extensions of the primary foci and could not start or maintain epidemic sleeping sickness on their own merits. To analogize with MACDONALD'S (1955) malaria theory, the disease here was existing below its "critical level." If this were true, complete control of the disease in the primary foci would result in its eventual disappearance from the secondary areas also, without their having to be subject to any interference by control. The soundness of this concept, with its logical development of the method of "focal attack" upon an epidemic, was proved when it was applied with success to the planning of control operations in the Gold Coast (MORRIS, 1950, 1951). One of the most valuable lessons arising from the West Nile studies is the striking illustration it provides of this focal concept of trypanosomiasis. Precise data are available for a sufficiently long period to demonstrate a complete cycle, the first expansion of an epidemic from its primary loci into the much more extensive secondary zones, followed by its disappearance from these zones as the general incidence fell, and contraction once more to the original small loci. From these, indeed, it now appears as if a new cycle is starting up. There are the primary loci on the Dacha, Orei and Koich rivers, where the disease first took hold on its introduction from Madi in 1928, and where, at the height of the epidemic, 120 new eases were developing a month and infection rates of 6 per cent. and over were widely prevalent. It was found in West Africa that at these rates an epidemic becomes very dangerous from the points of view of depopulation and'spread (MORRIS, 1952). The same studies showed that such high rates of infection occurred when the villages lay within a mile of the nearest habitat of the vector tsetse. In the Aringa epidemic probably more than half the inhabitants lived within that critical distance from G. palpalis fly-belt. Quite certainly the 1929 and 1936 epidemics in West Nile would have resulted in severe depopulation but for the admirable work of the Uganda Medical and Administrative Officers. As it was, the rapid rates at which the epidemics developed meant that by 1936 infections were so numerous that they were already spreading into other parts of the district before the situation in the primary loci was got under a satisfactory degree of control, a process which can be seen, repeated on a smaller scale, in the same foci today. By 1937 and 1938 the wide dispersal of the disease throughout the district, and its great reduction in the original outbreak area, created the impression that the epidemic itself was moving south (Fig. and Table I). In fact the southerly shift represented the lighting up of a series of secondary epidemic extensions

334

E P I D E M I O L O G Y OF S L E E P I N G SICKNESS I N EAST AFRICA

which, according to the focal concept, would not be self-maintaining, even at low endemic levels, once the supply of infections from the primary foci of the epidemic was cut off. This is exactly what happened. The disease disappeared very rapidly, and after 1947 completely, in every part of the district outside the northern Aringa-Terego epidemic area. It is true that in these secondary outbreaks there was interference, by control operations, but these ceased altogether during the war years, soon after 1940, so that within a few years, with clearings regrown and full of G. palpalis and the people no longer being examined on annual inspections, conditions in these secondary areas were exactly as they were before 1938. Yet no cases have arisen here since 1947. Those which occurred during the ensuing period of low endemicity all came from the area of the original primary foci, giving once more the illusion of a shift of the endemo-epidemic, this time from the south to north. In fact, as the records show (Table I, Fig.) infections had never completely disappeared from Aringa county. Another characteristic of the primary focus now emerges; the factors which make it such a dangerous reservoir and starting point for further epidemics are equally operative in rendering it difficult to bring under control, In the absence of successful control the same areas remain as foci of low, but very stubborn, endemics which retain all their dynamic potentialities for growth, as is now being shown so dramatically on the Orei and Dacha rivers. One of the most interesting and significant features in this whole story is the fact that these same rivers should signal the first West Nile outbreak in 1928, and the most recent and potentially dangerous recrudescence of the disease 30 years later. CONTROL

The strength of this epidemiological complex is at the same time its weakness. If these endemic loci, the essential reservoirs of T. gambiense during long periods of low endemicity, can be determined, these are the points to attack. Moreover, because of their limited extent it is possible for them to be subjected to control measures of sufficient intensity for the trypanosome to be eliminated completely. This is the principle of "focal attack," and elimination of the parasite from all primary loci throughout the infected area is the prerequisite for success. That this strategy can be effective, even with an epidemic at its height, may be deduced from the West Nile events, where the substantial reduction of the amount of infection in the primary loci in the Aringa-Terego area was followed by the complete disappearance of the disease throughout the rest of the district. Had trypanosomiasis been eradicated from those primary loci, which might well have happened but for the interruption of the excellent~work of Dr. Forbes Brown and others by World War II, the problem in West Nile District would have been solved once and for all more than a decade ago. In the Gold Coast the method was developed at a time when the Volta River epidemic was at its height (MORRIS, 1946). In the north-western epidemic area the primary foci lay in a number of river valleys, tributaries of the main Black Volta River. Tsetse eradication throughout each of these rivers was followed by the fullest possible development, giving stability to the reclamation and considerable economic gain to the people. The Volta itself and the country to the east and south, though heavily infested with the vector tsetse, were left untouched by fly control. By 1952, with 99 per cent. control of trypanosomiasis in these primary foci, substantial reductions were occurring spontaneously in the surrounding secondary zones. But on the north-eastern side, where this plan of control had not been applied, the disease remained strongly endemic, and in 1957-59 an epidemic with 900 cases developed, originating in foci which had been infected since 1933. The north-western

K. R. S. MORRIS

335

area, however, still remained comparatively free, with the exception of one small outbreak of 29 cases, and this was traced to the introduction of infection from one of the eastern loci (SCOTT, 1960). With trypanosomiasis at a low endemic level control is a very much simpler matter. In the first place the primary loci are much more easily detected, secondly the transmission of infections may be taking place at only one or two of several potential endemic loci. This may happen for quite a short time, as has been seen in the recent Aringa incidents. The single Orei River focus of 1950-54 had increased to two with the Dacha outbreak of 1957, and by 1959 at least four rivers were involved. Each of these had been a serious primary focus in the 1936 epidemic. In 1950 three were potential foci only. It is obvious that this is the stage at which to attack the problem. Unfortunately at this stage it appears unimportant to medical and administrative authorities. If this attitude can be overcome, by recalling the dynamic nature of trypanosomiasis, eradication can be effected with an absolute minimum of effort and disturbance to the country. But action must be taken at once, while the disease is still in its narrow endemic loci. Eradication failed on the Orei River because measures were not taken until the 1953-54 epidemic had actually developed, by which time infections had already spread. Since then the trypanosome has always been one jump ahead of control. In the Lake Edward endemic area of Uganda's Toro District, however, an outstanding success has been achieved. The partial control of the 1942 and 1946 epidemics in this area had left a residue of very low incidence, and from 1953 to 1955 all infections were being contracted on a single stream (MORRIS, 1960b). The elimination of G. palpalis on that one stream in 1955, by the Uganda Tsetse Control Department's spraying with DDT, has eradicated 7". gambiense from the whole area. From that year up to the end of 1961 not a single case has been recorded from this long-standing endemic area or from the District as a whole. This is not only a remarkable achievement, it is an irrefutable argument for the efficacy of focal attack, emphasizing the dividends which resuk if this be applied when the endemic is low--eradication at the cost of spraying a single stream. That the disease would ever have disappeared from this area spontaneously is extremely doubtful, the low endemic had been shifting from one stream to another for the previous 10 years. In Kenya's Nyanza Province, Gambian trypanosomiasis has been known for almost 60 years, and despite repeated attempts at control which often brought it to a very low incidence, it is still present today. The loci from which it has disappeared are on rivers where clearing or spraying has eradicated the vector, G. palpalis. The stubborn endemics in West Nile District tell the same story. The solution of the West Nile problem is now beyond the easy, one or two stream stage, but eradication without the expense of a major campaign is still possible, far more so at present than if a full-scale epidemic is allowed to develop. The recent trends leave no doubt that this can happen, with only piecemeal attempts at control. They also show that it could happen soon; the single focus in 1954, two in 1957, four, possibly five, by 1959. The general strategy of eradicating the trypanosome from the present loci still holds good, but the tactics as to how this can be best effected must now be suited to the larger area, with several separate river systems involved, and the obvious need for urgency. Although vector control is the ideal solution it would, if accomplished by clearing, be far too slow, if by spraying it would be very costly and lack permanence. The most practicable answer to this problem is mass chemoprophylaxis with pentamadine. This is a proved method in many parts of West and Central Africa for gaining rapid control under difficult conditions (ISCTR, 1958) and dramatic examples of its successful use for eradicating

336

EPIDEMIOLOGY OF SLEEPING SICKNESS I N EAST AFRICA

T. gambiense come from the Sudan, hardly 60 miles north of the West Nile outbreak (MORRIS, 1961). The population that would need protection in the affected parts of Aringa and Terego Counties could easily be dealt with by a single team of 10-12 technicians under a Medical Officer. Such a team can examine (blood as well as glands), and inject with the first dose of pentamadine, 400-500 people a day. This rate can be doubled when the second and third injections are given, 6 and 12 months later, when examination for trypanosomiasis is no" longer necessary. The present would appear a most opportune time for carrying out the operation. Earlier inefficiencies in survey, which let through so many cases (e.g., Akile who carried infection to Wollo), have now been overcome. There is improved treatment and a follow-up of patients is organized to deal with relapses. The greater efficiency in detecting and treating cases is not only a benefit to the communities' health, it gains their confidence and, with this, their co-operation. This now stands so high that the remarkable figure of 99 per cent. attendance at inspections is being obtained. Herein is fulfilled the first of the two conditions essential for success in a mass prophylaxis campaign, which breaks down if the population cannot be induced, or compelled, to attend. The second condition is that the re-introduction of infections should not take place, with G. palpalis still along the rivers. Re-introduction could occur from the Congo, Sudan or other parts of Uganda. The Congo, the source of the original entry of sleeping sickness can, in its present chaotic state, be dealt with only by an international body, or by strict regulation of immigrants. The Sudan has already put its house in order. The last of their seven epidemic areas will be free of T. gambiense within the next 2 years. The agent used for eradication in their two most recent and violent outbreaks has been pentamadine prophylaxis. There remains the possible sources of introduction from other parts of Uganda and Kenya, the main one being in Lango, 150 miles south-east. If trypanosomiasis can be eradicated from the West Nile, and this is perfectly feasible at the moment, it can be eradicated from the other areas also. The result, if the neighbouring Orientale Province of the Congo could be dealt with at the same time, would be to rid a large, ecologically homogeneous area of Central Africa of a menace which has been with it for 60 years. At its worst it depopulated great tracts of fertile land. At its present low incidence it still ties up man-power and attention which are out of all proportion to its immediate importance to health, but which cannot be relaxed lest renewed outbreaks occur.

SUMMARY

There is a close similarity between the ecological conditions (including human) of the country adjoining the Albert Nile in Uganda and those of the hinterland of West Africa where the huge and devastating outbreaks of Gambian sleeping sickness occurred during the past 100 years. B o t h areas lie in the Sudano-Guinea climate and vegetation zone, and are linked by a corridor of this type of country extending across Central Africa. Sleeping sickness spread along this corridor from west to east, reaching the Albert Nile in Uganda just before 1900. By 1904-5 epidemics had developed on the Nile, first at Wadelai, which had to be abandoned for this reason in 1906, then at Koba, abandoned in 1912, and finally 60 miles down-stream at Kajo Kaji and Nimule in the Sudan in 1914. Evacuation of the populations along the Nile checked the epidemic without eliminating the disease, which re-appeared in epidemic form in Madi in 1921. This was brought under control by 1930, by clearing the

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riverine habitat of the vector, Glossina palpalis, thrice yearly inspection of the population, restriction of the people's movements, and evacuation of the most heavily infected southern parts. No problem exists in Madi today. In 1927 an epidemic started in the adjoining West Nile District, with foci on the Dacha, Orei and Koich rivers in the north. The peak was reached by August, 1929, when 120 new cases per month were being found. A smaller epidemic occurred on the Nile itself in Jonam county in the south. Control measures similar to those in Madi, backed by the sleeping sickness ordinance of 1928, reduced the 1929 peak of 1,856 cases to 403 in 1932. In the following year this decline was reversed, and a second epidemic, with 1,867 cases treated in the year, had developed by 1936. Again the serious foci lay on the same rivers in Aringa and Terego counties in the north. An increase in the efficiency of control measures, and especially of the clearings against G. palpalis which now reached many miles in length, brought immediate reduction of the disease in 1937. By this time, however, infections had spread so rapidly south that by 1938 cases were coming in from all parts of the district. Extension of control activities brought this wide-spread epidemic to an end by 1947, after which a low endemic, averaging 10 cases a year, persisted until 1953. In 1953-54 a small outbreak with 29 cases occurred in a single focus on the Orei river, and was brought under control by treatment and an 8-mile clearing of re-grown G. palpalis habitat along the river. Although incidence in 1955-56 was low it showed a spread, which, in 1957, led to a second outbreak on the Dacha river, 10 miles to the north, with 19 cases in 1957-58. A third epidemic occurred in 1959, with 30 cases in that year, mostly from the Dacha focus, but with a much wider distribution, and with two, possibly three, other river systems now involved. The distribution of the 10 cases found in 1960 and the eight which had already occurred by April, 1961, confirms the original suspicion that a dangerous outward spread is still in progress. These studies lead to interesting epidemiological conclusions which are discussed under three main heads: 1) Human travel and movement, especially marked increases which result from pacifications, invasions or developments, have been responsible for many of the biggest outbreaks of Gambian sleeping sickness, and can promote a very rapid spread once an outbreak develops. 2) The vegetation, climate and human habits in the dry savannah-woodland zone create all the factors of close and sustained man-fly contact which lead to the development of severe epidemic trypanosomiasis. The most serious epidemics have, indeed, developed within this zone. 3) The focal nature of Gambian trypanosomiasis is shown, in a well-developed epidemic, by a pattern of zonation in which areas of high infection, the primary loci, are typically surrounded by zones of much lighter infection. These secondary zones are dependent for the maintenance of infection on its constant renewal from the primary loci. If this supply is cut off, infection in the secondary zones will eventually and spontaneously disappear. This focal concept leads to the method of "focal attack," in which action is concentrated on eliminating the disease completely from all primary foci, leaving the secondary zones untouched, to clear up spontaneously when the renewal of infection from the primary loci ceases. This method, which was developed in the Gold Coast before 1952, has been outstandingly successful in eradicating T. gambiense from the Lake Edward endemo-epidemic area in Western Uganda by D D T spraying of a single river against G. palpalis.

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EPIDEMIOLOGY OF SLEEPING SICKNESSIN EASTAFRICA

T h e present West Nile problem, with at least four rivers now involved, could be m o r e effectively attacked by mass chemoprophylaxis than by tsetse control. Experience elsewhere, including Sudan epidemics only 60 miles to the north, show that pentamadine prophylaxis could unquestionably eradicate trypanosomiasis f r o m this District. T h e other infected areas in U g a n d a and K e n y a could be similarly tackled. T h e r e would then remain only the Congo as a potential source of re-infestation. I f their Orientale Province could be dealt with on international lines, a very big area of Central Africa would be freed f r o m a costly and embarrassing menace. REFERENCES ADAMS, E. B. (1907).

Rep. Sleep. Sickn. Comm. roy. So¢., 8, 100. Climats, for~ts et ddsertification de l'Afrique tropicale. Paris: BARRETT, R. E. (1934). E. Afr. reed. ft., 11, 20. BLOSS, J. F. E. (1960). Proc. R. Soc. Med., 53, 421. BOULGER, D. C. (1898). The Congo States, London: BORES, J. (1928). The Company of Adventurers, London: BROWN, A. F. F. (1938). J. trop. Med. Hyg., 41, 200, 222, 234, 247, 265, 281,296. BRUMPT, E. (1906). La Nature, 28 Avril, 1906, p. 340 (Bull. Sleep. Sickn. Bur., 1,493). CARPENTER, C. D. H. (1921). Appendix to Uganda Med. Dept. Annual Report, 1921. (1924). 1bid., 1924. DREw, C. M. (1911). Bull. Sleep. Sickn., Bur., 3, 85. DUKE, H. L. & VAN HOOF, L. (1928). Final Rept. League of Nations S. S. Commission, 346, Geneva 1928. DUTTON, J. E. & TODD, J. L. (1906). Mem. Lpool Sch. trop. Med., 28, p. 25. GIBBINS, E. G. (1941). Ann. trop. Med. Parasit., 35, 195. GREIG, E. D. W. (1905). Rep. Sleep. Sickn. Comm. roy. Soc., 6, 273. HODCES, A. D. P. (1907). Ibid., 8, 86. (1908). Ibid., 9, 4. I S C T R (1958). 7th Meeting ISCTR pp. 101 et seq., Brussels 1958. KEAY, R. W. J. (1959). Vegetation Map of Africa, Oxford University Press. KING, H. H. (1912). Bull. ent. Res., 3, 89. MACDONALD, G. (1955). Indianff. Malar., 9, 261. MARTIN, G., LEBOEUF, A. & ROUBAUD, E. (1909). Bull. Soc. Path. exot., 2, 108. MORRIS, K. R. S. (1946). Bull. ent. Res., 37, 201. (1949). Trans. R. Soc. trop. Med. Hyg., 43, 165. (1950). I S C T R Paper No. 9, Antwerp 1950. (1951). Bull. ent. Res., 42, 427. - (1952). Ibid., 43, 375. (1959). Trans. R. Soc. trop. Med. Hyg., 53, 384. - (1960a). 1bid., 54, 71. - (1960b). 1bid., 54, 212. - (1960e). 1bid., 54, 585. - (1961). J. trop. Med. Hyg., 64, 217. (1962). Nature, London, 193, 1022. NELSON, G. S. (1954). West Nile Dist. Med. Dept. Annual Report, 1954, Arua. PEZZl D'OaNELLA, BARON, G. B. DE (1947). Sudan Notes, 28, 174. SCHWEINFORTH, G., RATZEL, F., FELKIN, R. W. ~; HARTLAND, G. (1888). Emin Pasha in Central Africa, London. SCOTT, D. (1960). W. Aft. med. ft., 10, 122. STIGAND, C. H. (1923). Equitoria, London. TODD, J. L. (1906). Lancet, 2, 6.

AUBREVEILLE, A. (1949).

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Uganda Medical Department's Annual Reports were the source of much material, especially those for 1910, 1911, 1914 and 1920 onwards. The Annual Reports of the District Commissioner, West Nile, supplied a valuable uninterrupted series of data from 1922 onwards.