We have had recently an ANDYSEZ on radon by Ruth Lyons. I thought I would bring up a similar worrying story - which has a personal twist.

Living over the back fence from me when I was a boy was the Whitten family. The father, Wes, was, and still is, an internationally distinguished scientist. He obviously also was an unusually perceptive man. He predicted when I was a young teenager (if you can imagine such a thing!) that I would be either a veterinary surgeon or a biochemist. I was technician in a university biochemistry department for some years and I am still married to a vet!

In 1982, the Canberra Times and other NSW media reported in alarmist terms a disease amongst cavers. Some of the headlines were: DISEASE SCARE HITS WEE JASPER CAVES and BAT CAVES INFECTS 8 (the type is merely 60 mm (2½ inch) tall). These and similar lead to tortuous logic by the local Council whose press release is headed by: INFECTED BAT CAVES NOT WEE JASPER.

Although Church Cave, where the disease had been contracted, is less than 500 metres from the centre of Wee Jasper Village the Council's release went on to say "the council had received a lot of adverse publicity especially from the Australian Broadcasting Commission, which continually referred to the infested caves as Wee Jasper Caves, the real Wee Jasper Caves were several miles away and had been developed as a tourist attraction by the council" (then and now known as Carey's Caves).

The disease, histoplasmosis, was perceived to be "caused by bats" and thus the local Council's solution was to blow up Church Cave which was, and is still an important maternity site for the Eastern or Large Bent-wing Bat, Miniopterus schreibersii. Being a diligent young greenie I leapt to the defence of the bats and an interview was published in the Canberra Times on 2 November 1972.

The Council erected a sign at the cave entrance warning of its dangers - very few people have visited it since - except me! An account of the illness contracted by a party of six (not eight) was published in the Medical Journal of Australia in 1976 (Isbister et al. 1976).

Hunt et al. (1984) tried very hard to isolate Histoplasma capsulatum from the cave environment by a variety of methods including exposing small mammals in cages in the cave. They were ultimately successful but one of their number became infected in the process. In view of the fact "....that infection occurred despite the wearing of respirators, there is an obvious need for a more effective form of protection". Interestingly, Hunt et al. talk about eight, not six, infectees mentioned in the media.

Last summer another article appeared in the Canberra Times on Wee Jasper Caves. This quoted a local person as saying " ... some were too dangerous to explore because of bat guano. About 12 years ago, two boys died from lung disease after they spent some time in Church Cave". Again I leapt to the defence of the truth in the Times. This letter was sent to Wes Whitten in Canada by three separate people in Canberra. Subsequently Wes Whitten brought to my attention to a paper that he had published in the Journal of Occupational Health in 1992 (Whitten 1992). This is well worth reading for many reasons.

Whilst I was in Queensland at Rockhampton, Undara and Chillagoe last year for the ACKMA Conference I heard lots of anecdotal accounts of histoplasmosis amongst cave users. Earlier this year I had a letter from one of our members who had recently had a histoplasmosis "lump" removed from her breast and wanted to know if I had any information on the disease.

The disease is not "notifiable" in any Australian state and thus we will never be able to know just what its incidence is in this country. It is clear that it occurs and is a problem from time to time. What then is histoplasmosis? The following is abridged from Stevenson and Hughes (1988) who report less than 25 cases in Australia from 1948 until 1986 - 16 associated with Church Cave.

There are four main forms of the disease:

Acute Pulmonary Histoplasmosis - This is the most common manifestation and presents as a non-specific respiratory illness, commonly with cough, pyrexia and malaise, possibly weakness and pleuritic chest pains. Although recovery without therapy is usual, rarely there is a slowly progressive fibrosis ... which may lead to compression of major blood vessels.

Acute Disseminated Histoplasmosis - Infants, young children and immuno-deficient adults (possibly those with AIDS) are more prone to develop this condition which closely mimics miliary tuberculosis. The course of the illness is rapid and fatal if not treated.

Chronic Disseminated Histoplasmosis - Adult males are more commonly affected, whether in previous good health or possibly immuno-compromised. A range of clinical features may present, including patchy pneumonia, fever, mucosal ulceration.... endocarditis, hepatitis, meningitis and anaemia. The illness runs a progressive, sub-acute course over weeks or even years, usually ends fatally, unless treated. [This seems to be somewhat of an overstatement given that many hundreds of thousands, if not millions, of Americans have this form and never become aware of it!]

Chronic Pulmonary Histoplasmosis - This form is commoner in males over 40 years. The onset is gradual with cough, loss of weight, low grade pyrexia, increasing dysponea, possible night sweats and haemoptysis, simulating pulmonary tuberculosis.... Remissions and possibly spontaneous cure occur, however, in the majority of patients. Infections progress insidiously.....Death usually occurs over months or years.

These are rather sobering and alarming descriptions but would appear to be relevant to histoplasmosis outside Australia as I know of only one death attributable to the disease in this country. This death, from South Australia, was attributed to the unfortunate victim's next-door neighbour jack-hammering up the concrete floor of a chook-pen (Elery Hamilton-Smith, pers. comm.)

Isolation of Histoplasma capsulatum organism is difficult as Hunt et al. (1984) and Carol (1988) demonstrate. Stevenson and Hughes (1988) state that "a definitive diagnosis rests on isolation of Histoplasma in culture or observing typical yeasts in stained smears or histological sections". They go on to say that "Skin testing has little value in diagnosis and its use may affect the results of subsequent serological tests...." [emphasis mine].

The disease is only contracted by inhalation of the fungus; there is no person-to-person transmission and it is found in a wide range of domestic animals. There are specific treatments available.

In general it seems that histoplasmosis is far more likely to be contracted from keeping domestic birds or from disturbing accumulations of guano under starling and similar roosts. The disease seems to be most catchable in caves, and similar environments, with high nitrogen soils (e.g. enriched by bird or bat guano) where there is alternation between wet and dry conditions and a temperature of 20 to 30 degrees Celsius (Harden and Hunt 1985). Wet conditions will favour the growth of fungi whilst dry will encourage the development of spores and uplift as dust which can be inhaled.

It would appear that both the caving community and the medical profession need to know more about this disease. Whitten (1992) and Stevenson and Hughes (1988) are especially relevant to both parties.