A paper to an AMA conference in 1962
Tropical diseases in Northern Australia, individually and collectively, have been discussed by a number of authorities in much greater detail and far more ably than I can presume to attempt today, but I thought that in this year of my retirement, without too strict a definition of tropical disease, it might be of interest to you for me to sketch the background to my own 40 odd years of service in this field.
BUBONIC PLAGUE
One of my earliest childhood memories in the awe and dread inspired in me by sight of a ship quarantined for Plague outside Rockhampton, and by the conversation which this spectacle provoked amongst my elders. I was to meet Plague again when, as an R.M.O. at Brisbane Hospital in 1921, I had charge of Wattlebrae during the 1921-22 outbreak.
The story of Plague in Queensland is the story of ship-borne infection between ports from Brisbane to Cairns from 1900 to 1909, followed by an interval of twelve years and recrudescence and ultimate disappearance in the spring and summer of 1921-22.
In the first phase there was, over a period of 10 years, a total of 499 cases with 219 deaths. Of these, 152 cases and 69 deaths occurred in ports between Gladstone and Cairns.
In 1921-22, 57 cases were reported in Brisbane, 44 of these were bacteriologically positive and 27 died – a mortality of 61%.
I vividly remember the clinical picture presented by these unfortunates, the mounting fever and delirium, the anxious expression and the fateful third day when the temperature usually remitted briefly. If this remission was marked by a corresponding fall in the rate of pulse, prognosis was good. If, on the other hand, pulse rate increased, death within 24 hours could be confidently forecast.
In Townsville, 33 cases were reported between September 22nd and January 2nd. Of these 5 were Chinese found dead or moribund, diagnosis being confirmed at autopsy. Of the remaining 28, 15 died. Mortality from Plague in Townsville was 60%. In Cairns there were 18 cases between October 4th and December 9th – nine were fatal, a mortality of 50%.
FILARIASIS
Joseph Bancroft in 1874 demonstrated microfilariae in the blood of a patient suffering from chyluria and found adult filariae in an abscess in 1876 and in a hydrocele in the following year.
In 1902 microfilariae were demonstrated in the blood of 15% of surgical cases in the wards of the Brisbane General Hospital. In 1908 10.8% and in 1909-10 11.5% of unselected admissions to the Brisbane General Hospital were found infected.
In 1924 Sweet reported an incidence of 2.6% in Queensland generally and 5% in Brisbane.
In my time at the Brisbane General Hospital in the early 1920s some clinical condition of filarial origin was constantly to be found in the wards or in the Out-patient’s Department. The symptoms most commonly met were soft varicose groin gland, filarial orchitis, hydrocele, lymphangitis, abscesses of the skin of the extremities and abdomen, chyluria and chylocoele. Elephantiasis was relatively uncommon.
In 1938 Derrick found no cases in Brisbane. During the whole period 1937-1956, 37 cases were reported from the Brisbane General Hospital.
In the north the incidence of Filariasis has not been as high as that recorded in Brisbane. In 1892 O’Brien, commenting upon the sporadic occurrence of Filariasis in Queensland, warned that systematic search would probably show up many unsuspected cases in the north. Such a survey was undertaken by Brienl in 1911 when 3.1% of cases in the Townsville General Hospital were found infected. In 1922-23 Cilento and Richards found an incidence of 3.7% in North Queensland. A solitary acute case was reported from Mackay in 1956 and a survey of the coast from Rockhampton to Cairns in the following year demonstrated no cases.
The parasite Filaria lancrofti was undoubtedly introduced to the Queensland coast by indentured agricultural labourers from Melanesia. The disease reached its highest Australian incidence in centres where there was the heaviest concentration of indentured labour. The condition ultimately disappeared with the termination of the indenture system, repatriation of imported sources of infection and the application of routine measures of mosquito control.
Filariasis of indigenous origin has not been encountered in tropical Australia outside Queensland. I have seen cases of “Elephantiasis” in natives in the Northern Territory and Western Australia but these have all originated from granuloma venereum, and I think a case described by Goldsmith from Darwin in 1899 belongs in this category.
BERI BERI
P.M. Wood (Palmerston N.T.) reported serious outbreaks of paralysis and dropsy amongst young Chinese males in 1879-80. In a later outbreak in 1889 he saw 40 cases with 12 deaths and estimated that there had been 50 other deaths and many other cases amongst Chinese he had not seen.
He identified the condition as Beri Beri and reported its appearance amongst natives in the Palmerston Goal following a decision to transfer natives from the European to the Chinese ration.
Wood worried in a place and at a time when little was certainly known of Beri Beri, and his account is remarkable not only for its clinical perception but for the accurate observation and interpretation of the dietary factors involved in causation and cure.
Apart from the outbreaks reported by Wood, cases have been observed from time to time in the Asian crews of pearling luggers based on Thursday Island, Darwin and Broome. An outbreak principally affecting drovers and station hands was reported from Camooweal early this century. It was investigated by the Queensland Department of Public Health but, when the patients were found to be predominantly residents of the Northern Territory, details were not recorded.
SCURVY
Early British settlements along Australia’s northern coast appear to have relied for stores too heavily upon sea-borne supplies from Sydney, and Scurvy proved a major problem. Delays in arrival of store ships meant deprivation, for no alternative source of fresh meat or vegetables was available. In the small garrison of Raffles Bay there were, in October 1827, 42 cases of Scurvy and night blindness. These settlements were made in a country which, at that time, supported a healthy native population, practising no horticulture nor any animal husbandry, and to us today this incidence of Scurvy may seem difficult to explain.
Due allowance must be made for unawareness of the precise cause of Scurvy for cautious reliance upon known and accepted forms of diet and for suspicion of unfamiliar local flora and fauna engendered by cases of illness and poisoning reported in the more venturesome who tried them.
More difficult to excuse was an outbreak at the Finke River Mission, Central Australia, in 1928-29. This Mission, established some 50 years earlier, about 85 miles west of Alice Springs, had, at that time, a normal population of about 230. Stores were brought by camel team from the rail head at Rumbalara, some 200 miles away.
Water for household and garden purposes was drawn from shallow wells which became brackish during the dry season.
In the years after 1925 the Mission experienced a severe drought, the total rain fall for a period of 32 months being less than 9” and 1” falling during the twelve months ending February, 1929. Wells turned saline in October 1928, and no water was available for gardening from that time.
Supplies of beef ceased in January 1929, the cattle herd having been reduced from 3,000 to 200. The camels were too weak to load the stores at Rumbalara. No source of Vitamin C was available on the Mission from October, 1928. From this time onward the diet consisted of tea, sugar, and a paste prepared by mixing flour in boiling water in the proportion of 1 lb. for every 5 persons. At midday the issue was varied by the addition of barley or rice to the flour soup. This regimen continued until August, except that in April boiled peas and polished rice were added to the diet to prevent Beri Beri.
At this time Central Australia was administered from Canberra as a separate Territory, and had no medical service. In August 1929, as Chief Medical Officer North Australia, I was directed by the Minister to visit Hermansburg. I identified the condition as Scurvy and found there had been 110 cases with 37 deaths. There was no hospital, most of the sick had been left in huts and wurlies to the care of their fellows, by whom they were commonly abandoned to their fate. The worst cases were then moved to small, unventilated huts near the Superintendent’s quarters, were they lay in their agony in numbers far too great for the capacity of their quarters, their sufferings increased by the hardness of the floor on which they lay, and by pollution of the stagnant air with the acrid smoke of fires maintained within the huts to provide some measure of warmth. With identification of the disease as Scurvy and the inclusion of fresh fruit and swedes in the diet, the outbreak rapidly terminated.
ANCYLOSTOMIASIS
The existence of hookworm disease in Queensland was recognised towards the end of last century. Hogg at Goodna in 1889 demonstrated hookworm at autopay in cases of marked geophagia. In 1892 he referred to the closure of an Orphanage at Mackay because of a very intractable anaemia in the children. He suggested ancylostomiasis as the underlying cause, but had no confirmation.
At the International Colonial Medical Congress in 1892 J. Sydney Hunt of Hughenden quoted Ahearne of Townsville as stating that the chief obstacle to the acclimatisation of the white man in North Queensland was the anaemia caused by the tropical climate.
In the same year, Lockhart Gibson and Jeffries Turner in Brisbane, reporting cases of hookworm from Cairns, claimed that the influence of hookworm in producing anaemia in North Queensland was being overlooked and urged search for the ova as a diagnostic method.
By 1898 O’Brien was able to say that hookworm was a well recognised clinical entity in the white population along the entire Pacific slope of Queensland, diagnosis apparently usually resting upon anaemia and geophagy. He had no information on the incidence amongst aborigines, but recognised that earth eating was a widely prevalent habit amongst them.
The importance of hookworm in Queensland and in North Australia was not clearly understood until systematic surveys were undertaken by the Rockefeller Foundation in 1919. It was found that the overall incidence in the white population of the east coast of Queensland was 18% and in the aboriginal population 81%. In a survey I conducted in Cairns and environs in 1926, the overall incidence in the non-aboriginal population was 12.5%.
In the Northern Territory, Baldwin and Cooling in 1922 found the incidence amongst natives to be 75% at Bathurst Island Mission and 50% in Darwin. The incidence fell as the survey moved eastward – 38% at Goulburn Island Mission and nil at Elcho Island..
In Western Australia they found an incidence of 91% at Beagle Bay, 40% at Broome and 2% in Derby. It seems incontrovertible that the aborigines were originally free from hookworm and that the parasite was introduced by immigrant labour. This view is supported by the following observations:
- Focal distribution – Charlton reported an incidence of 81% in natives on Mornington Island Mission whilst natives living on the mainland opposite were unaffected. Those free at Mornington Island were recent arrivals. At Mitchell River Mission the incidence was 20% compared to 5% in natives on the peninsular generally.
- Observed extension – After the initial survey of 1922 in Western Australia and the Northern Territory, hookworm had been seen to extend to areas free at that time, e.g. missions.
- Parasite distribution – In the early survey of Queensland the prevailing parasite was then N. americanus, suggesting introduction from Melanesia. By contrast, the parasite in the Northern Territory and Western Australia was A. duodenale, indicating importation from Asia. This is consistent with the introduction of South Sea island plantation labourers to Queensland and by Asian pearlers and miners to the Northern Territory.
The influence of missions in raising the incidence and contributing to the dispersion of disease is as evident and important in hookworm as it was in leprosy.
LEPROSY
Chinese immigration to Australia began after 1850. The earlier cases of Leprosy in Australia were reported in 1866 in Chinese migrants in Vitoria. In 1889 J.M. Creed stated that there was no known Leprosy in Australia in 1865 except in immigrants from Asia. In Queensland, practically all early cases were coloured aliens, Chinese migrants or Melanesian plantation workers. In 1892 Joseph Bancroft considered in retrospect that several cases of Leprosy had come under his notice since 1866. These included several Melanesians suffering from what, for want of a better name, he called Islanders Toe Disease. He suggested that unless infected aliens were segregated, the disease would spread to native community.
Leprosy in aborigines in Queensland was first reported from Croydon in 1896 and Port Douglas in 1897 and 20 aliens were isolated from the Cape York Peninsula during the next 12 years. Concentration upon Government settlements and missions led to multiple infections.
In the Northern Territory, Leprosy was first reported in 1890 amongst railway construction workers and miners in the Burrundie-Pine Creek area. Amongst natives those first affected were tribes on the Mary and Alligator Rivers in contact with these Chinese camps, Maintenance of an effective inter-tribal quarantine by their eastern neighbours confined Leprosy to its original area for several years. In 1912 Brienl found it still confined there, but in 1925 I felt that missions at Goulburn Island and Oenpelli were breaking down inter-tribal barriers and Leprosy must be expected to move eastward.
A hospital for Leprosy was established on Channel Island in 1932 and cases were actively sought throughout the Territory and promptly isolated. New cases averaged about 16 per year and the known total continued at about 62, active search revealing no increased incidence.
In 1942 Japanese bombardment led to the dispersion of patients from Channel Island to their tribal country and by 1951, when active control was reimposed, cases already numbered 250. Today the total in isolation or under surveillance is over 600.
In Western Australia Leprosy was first reported in a Chinese in the Kimberleys in 1908. Shortly afterwards 4 cases were reported in aborigines.
Beagle Bay Mission, north of Broome, had been established 20 years before Leprosy was introduced there by a native from Derby in 1921. In the next 20 years 54 cases were removed from the mission. No Leprosy had been reported outside the Fitzroy Basin in 1924 and in 1933 a case was reported from Munja, on the East Kimberley coast, and within 7 years, 46 new cases were traced to this source. In 1940 the Forrest River-Drysdale area was still practically free. Within the next decade 27 cases were reported and the disease seemed to be spreading eastward.
In Northern Australia there was no Leprosy in the aboriginal population before white settlement. Infection was introduced in the late 19th Century by infected Asian and Pacific Island labour From these, infection spread first to natives who formed a link with the white population whom they served as concubines, domestic servants, nurses, taken into the home and living close to the family.
In North Queensland the disease was sporadic but did not obtain formidable proportions because of earlier native de-population and the State’s policy of segregation. The greatest single factor in the dissemination of Leprosy in the Northern Territory and Western Australia has been the concentration of natives from uninfected areas on missions in contact with open cases and the subsequent return of these to their own country.
MALARIA
There is no evidence that Malaria was endemic in Northern Australia before white settlement. Early explorers by land and sea and the earlier settlers did not observe or suffer from it. In 1824, however, Fort Dundas on Melville Island, suffered heavily from an outbreak of “fever” probably introduced from the Dutch East Indies.
That Malaria was prevalent in Queensland in 1862 is suggested by references to fever and ague in the McKinlay expedition. In 1866 Bourketown was suddenly scourged by Malaria introduced by a visiting vessel from Java, and of a previously healthy population of 76, 50 died.
In Cairns Malaria was very common in 1900, but it disappeared from the town proper by 1908 when, according to O’Brien, infection – almost exclusively benign tertian – existed right along the north Pacific Coast. In 1918 a survey by Brienl disclosed a carrier rate of 13.5% in the white population, the distribution of P.vivax and P.falciparum being equal. There was a small epidemic in 1922, but in 1927 Heydon could find none. During 1942 there were 700 cases of benign tertian following the introduction of infection by troops from New Guinea.
In 1910 there was an epidemic of sub-tertian malaria on Kidston and Einasleigh goldfields introduced by miners from New Guinea. In a population of 400 there were 120 cases with 24 deaths.
Many areas in the peninsular were infected in 1921-22 and most Europeans and natives were attacked during the wet season.
At the Intercolonial Medical Congress of 1889 P.M. Wood of Palmerston reported that Malaria was very prevalent in the Northern Territory in 1879-80 and in 1889. In 1909, of total admissions to the Darwin Hospital, 34% were attributed to fever. A very severed outbreak of sub-tertian malaria with a number of deaths occurred on the Umbrawarra Tin Field at this time following the immigration of miners from New Guinea. Brienl later reported the presence of Malaria on every mine field and cattle station visited by him in an extensive survey. In 1911 sub-tertian malaria spread to Melville Island, where there were 30 deaths amongst the natives.
Cases of sub-tertian malaria appeared in the Roper Valley during the dry season of 1929. The epidemic spread westward and by 1933 when it closed there had been 354 cases with 12 deaths. The Ord and Fitzroy River basins in the Kimberley division of Western Australia became involved in 1934. The number of cases is not known but 200 aboriginal and 15 white deaths were reported.
Mosquito control in the rural areas of the Territory not being practicable, an attempt was made in the later stages of the 1929-33 epidemic to control sub-tertian malaria by supplementing quinine with 3 days plasmochin therapy and by search for carriers who also were given plasmochin. Whether or not these measures were responsible for the complete disappearance of Falciparun Malaria from the Northern Territory, they must have materially reduced the opportunities for transmission.
After World War II Benign Tertian Malaria, apparently introduced by the Air Force to Gove, was found to be endemic at Yirrkala and in Eastern Arnhemland. P. vivas has on several occasions since been reintroduced to that area by servicemen and others from New Guinea.
During the years 1955-57, 188 cases were reported and the N.T.M.S. undertook an intensive campaign to eradicate infection by the routine treatment of carriers and cases with Primaquin. Since that time cases have been considerably fewer and have been limited almost exclusively to persons infected overseas so the risk of re-infection by their agency remains obvious.
It seems certain that:
- With the possible exception of the leptospirosis and aborvirus infections, tropical diseases are not indigenous to our north tropics.
- Certain infections introduced from time to time by immigration from endemic areas found the local areas suitable for their endemicity. They have since been largely brought under control by medical effort and social change.
- Not infrequently in the process the best intentioned, through obstinacy or ignorance, have been responsible for the worst disasters.
- Responsibility for the security of the north rests heavily upon the general practitioner. He must be alert to the early case, to initiate prophylaxis and apply appropriate treatment. For the control of such diseases as ancylostomiasis, malaria and filarial and Leprosy, he must secure the patient’s co-operation in the conscientious discharge of his prophylactic obligations and faithful compliance with the maintenance treatment.
Finally, it has been my privilege to know personal and at times to work with some of those who without benefit of modern research facilities, without contemporary honour or commensurate reward, have elucidated for us the variety of problems which confused and frustrate the profession in the north of the turn of the Century. Working with elementary equipment, inadequate sources of reference, and without ready access to others studying in the same field, they made this country safe for a healthy and prosperous white population. I am glad to take this opportunity as a colleague more concerned with the administrative side of public health, to pay a tribute of admiration and gratitude for their work which is apt to be too little regarded by a generation of Australians spared by it the hazards which always threatened the pioneers.