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5.4 Tuberculosis among the Aboriginal populations - source material .1 Early contact and diffusion (Stage II)

5.4.3 Clinical Features

disease' was widely prevalent with many Aborigines dying and consequently recommended to the government that the 'best medical talent procurable' be appointed to investigate the disease and if possible determine how it could be mitigated (Curr &

LeSouef 1879).

The number of deaths from tuberculosis was lowest at Lake Tyers settlement (9% of total) (Table 5.4). Only one death from tuberculosis, and very little sickness was reported between 1876-85 (Bulmer 1880-81) on this settlement. After 1885 there were a further 7 deaths reported from tuberculosis. The other settlements were not so fortunate.

At Lake Wellington, Hagenauer (1880-81) reported to the Board in 1880 that the state of health among the Aborigines seemed to be good 'although one could never rely on it'. His fears were realised because tuberculosis was to remain the principal cause of death on that settlement despite the care provided by two medical practitioners from the nearby town of Sale. The situation at the remaining stations in Victoria and South Australia was similar with tuberculosis consistently being a major contributor to mortality.

The body was quite emaciated prior to his dissolution and was in reality a living skeleton. On opening the cavity of the thorax the lungs presented chronic adhesions to the ribs, pericardium and sternum were for the greater part solid and hepatised, particularly the upper lobe of the left lung, which contained two or three large patches of a white caseous consistency. Both lungs were thickly interspersed with small hard white lumps of a tuberculated nature, although none of them had assumed a puriform state. The pericardium was much enlarged and contained about six ounces of fluid.

The liver was of extraordinary size, was hard and adhered to the diaphragm.

On separating this connection a large ulcer was discovered on its upper surface of a dirty gangrenous appearance; it contained a large quantity of blood in a fluid state, was thickly covered with white hard small lumps similar to those found in the lungs, which pervaded its internal structure also.

The whole peritoneal lining of the intestines exhibited the same tuberculated appearance but much larger in size and containing a thick yellowish purulent matter. The spleen was of natural size but hard and solid and on cutting into exhibited the same tuberculous formation with the aforesaid viscera. The peritoneal sack contained about four pints of water. The kidneys appeared healthy.

(Walsh, M., in Robinson n.d.; Plomley 1987: 933)

Table 5.5 Summary of autopsy reports 1837-1838 from Wybalenna Aboriginal settlement, Flinders Island, involving tuberculosis (Robinson n.d; Plomley 1987: 927-937)

Date Sex Age Symptoms Diagnosis*

20- 8-37 Female Adult Adhesion of lungs to surrounding membrane and ribs; extensive diffusion of tubercles externally and internally of both lungs; liver enlarged with small caseous foci; possible meningeal involvement

Miliary tuberculosis

30-12-37 Male Adult Adhesion of lungs to surrounding membrane; both lungs indurated; diffusion of tubercles on external and internal surface of lungs; extensive dissemination of tubercles to liver and intestines.

Miliary tuberculosis

12-5-38 Male Adult Extensive adhesion of lungs to surrounding membrane and ribs; both lungs indurated and dispersed with small tubercles; large purulent abscess on right lung; small intestines thickly coated with tubercles extending into peritoneum.

Miliary tuberculosis with possible cavitation of right lung.

2-6-38 Female Adult Right lung extensively adhered to pleura; cavity of thorax containing effusion of colourless serum

Pulmonary tuberculosis 21-6-38 Female 2 Adhesions of lungs; both lungs hepatised and

interspersed externally and internally with small tubercles; left lung with three caseous cavitations;

liver and spleen indurated and interspersed with tubercles; abscessing of pancreas.

Miliary tuberculosis;

cavitating tuberculosis 2-7-38 Female 7 Adhesion of lungs to surrounding tissue; 2 to 3

small suppurated lesions on lungs; liver enlarged with extensive miliary involvement; spleen and pancreas indurated, abscessed and covered with small tubercles; intestines inflamed and interspersed with tubercles

Miliary tuberculosis

6-8-38 Male Adult Extensive hepatisation of lungs with a number of caseated cysts.

Cavitating tuberculosis 3-9-98 Male 3 Extensive lung adhesion to surrounding tissue;

both lungs hepatised and dispersed with tubercles;

left lung abscessed; spleen thickly dotted with tubercles; liver enlarged.

Miliary tuberculosis

29-10-38 Female 60 Adhesion of lungs to ribs, sternum, and surrounding soft tissue; both lungs extensively hepatised with tubercles externally and internally;

large purulent cysts on both lungs; liver and spleen extensively disseminated with tubercles; cause of death given as phthisis.

Miliary tuberculosis, cavitating tuberculosis of lungs.

9-11-38 Female Adult Chronic adhesion of lungs to surrounding bone and soft tissue; right lung tuberculous; left lung severely necrotised and purulent; cause of death given as phthisis.

Pulmonary tuberculosis.

17-12-38 Female Adult Adhesion of lungs to surrounding tissue; both lungs indurated and covered externally and internally with small tubercles; internal tubercles larger; adhesion of liver, external tubercles; spleen enlarged and tuberculated externally and internally; extensive dissemination of tubercles along intestinal canal; cause of death given as phthisis.

Miliary tuberculosis

*Diagnoses taken from Plomley 1987: 927-937

In all cases but one the disease began as primary pulmonary tuberculosis, exhibiting adhesions and well-developed external and internal granuloma of the lungs.

The exception was a seven year old female, whose lungs were described as 'healthy except [for] a few adhesions of the left of a chronic nature with two or three small specks on its posterior surface in an incipient state of suppuration' (Walsh 1838). Systemic dissemination of the disease by haematogenous and/or lymphatic distribution to the abdominal organs followed the primary infection in ten of the twelve cases. One of the cases where this may not have happened was that of an 'aged' female who was suffering concurrently from pneumonia and the another, a female, whose abdominal viscera were described as 'natural' although the kidneys were large, but appeared healthy (Walsh 1838).

The organs infected were those favoured by miliary localisation, namely the liver and spleen. Renal involvement, was, however, uncommon. Abnormal kidneys were noted in only one case, that of a female whose kidneys were described as being 'quite flabby' (Walsh 1838). Miliary dissemination of tubercle bacilli involved the intestines in four cases and the pancreas in three.

Among the Ngarrindjeri in South Australia Taplin described the symptoms and the course of the disease:

It also very often manifests itself in the form of tabes mesenterica about the third or fourth year or even later. I have even known of a very bad case occurring in a man of 25. This constitutional tendency often appears in the form of induration and ulceration of the glands of the neck. Where it comes out [like] this it is generally cured and the person becomes healthy afterwards.

But its most usual and most fatal form is that of tubercular consumption. Any

accident to the chest seems to lead to the deposition of tubercle (Taplin 1876a).