Sixteen patients with imported schistosomiasis in Western Australia, a non-endemic area, are recorded. Ten with Schistosoma mansoni had lived there for over 20 years, three for over 31 years and two for more than 32 years. No record of a life span of 31 years for S. mansoni can be found in the literature. The principal symptomatology in three patients with S. mansoni was hypersplenism. Four patients with S. mansoni were asymptomatic. Ten had eosinophil counts greater than 0.3 X 10(9)/1 and one who showed no peripheral eosinophilia had numerous eosinophil myelocytes in his bone marrow. A diagnosis of schistosomiasis was initially suspected in five cases by respective discovery of eosinophil myelocytes in the bone marrow, radiological evidence of calcification of the bladder wall and beading of both ureters, cytoscopic findings of sandy patches in the bladder, discovery of ova in the wall of a fallopian tube at ectopic gestation and the presence of ova and an adult worm in a uterine leiomyoma. The risk of infection of the Ord River Dam is greater for S. japonicum than for the African species. An epidemiological feature of this series is that refugees from Poland contracted schistosomiasis (S. mansoni) in refugee camps in East Africa and then migrated to Western Australia between 1950 and 1953.

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Topical AC should be considered the local anaesthetic of first choice for suturing appropriate children's lacerations.

Primary pulmonary hypertension in a male patient began at the age of 6, and he died at 25, after a course of I9 years. No previous report of such a long course has been found.A congenital rather than a thrombotic cause is supported by the onset in a boy, the absence of breathlessness on exertion until his last few years, and the medial hypertrophy of the arterioles, without evidence of organic obstruction.Long intervals, up to 12 years, occurred without symptoms, and there was lack of constancy of the degree of effort required to produce syncope. It is suggested that these features resulted from a large reflex factor, in view of the absence of any great rise of pulmonary artery pressure on catheterization.Primary pulmonary hypertension is not so uncommon as was previously thought, or it is increasing in frequency. Wood (I956) recorded an incidence of O-I7 per cent among his patients with cardiovascular disease, and Fleming (I960) reported 8 patients in one year in Sydney. This case may be of interest because of its long duration, the onset of symptoms in a boy aged 6, the long intervals without symptoms, and inconstancy between the degrees of exertion and attacks of syncope. Case ReportThe patient, a European in Kenya, was 24 when first seen in June 1955. There was no family history of cardiac or other disease. He had one brother who was well. His symptoms began at 6 years when he used to faint for some seconds on exerting himself at games. Attacks persisted for 6 months, after which he was free from them for 12 years. They then recurred about once in two months but not consistently, for sometimes he could carry out physical exertion without attacks. His episodes again diminished in frequency, though occasional attacks continued until 2I, when they became more frequent and then gradually got worse and he had to discontinue playing games. He was more liable to attacks when exerting himself on a full stomach or walking fast uphill without 'getting previously warmed up'. He never passed urine or bit his tongue during attacks, though he sometimes bruised or cut his head and once fell and broke a tooth. His unconsciousness lasted up to a minute.He sometimes had minor attacks of tightness, but not pain, in the lower part of his chest, warning signs that he would faint if he continued his exertion. He also experienced slight breathlessness and sweating before attacks and was stated to go a grey colour. If he sat down when these symptoms developed they gradually passed away in three or four minutes. He had no breathlessness on exertion until his last few years, and no swelling of his feet or cough. He was observed to have bradycardia during attacks, and a trained nurse found his pulse rate I30 immediately after one. Apart from his syncope his general health was good. He did not smoke.On examination in I955, aged 24, he looked healthy. No cyanosis, clubbing, or dyspnoea at rest. Slight venous congestion of cervical veins with prominent a waves, but no oedema or enlargement of his liver. Pulse was 8o, regular, and of somew...