Protozoa are not often mentioned in the NZMJ. Given that the three common indigenous ones, Giardia lamblia, Toxoplasma gondii and Trichomonas vaginalis generally cause distressing rather than life-threatening disease, that is no surprise. There are, however, over 200 000 named species of protozoa worldwide and a substantial minority are parasites of both vertebrates and invertebrates. There are over 50 species that humans may harbour, for better or for worse. So, as always with microorganisms, ‘there are a lot of them about’.

Amoebae lie within the phylum Rhizopoda within the kingdom Protozoa.1 There are six species that associate commonly with humans. Entamoeba histolytica is the cause of classical amoebiasis. E. dispar is the resuscitated species name for the morphologically indistinguishable organisms long considered and now securely known to be close, non-pathogenic relatives of E. histolytica. The remainder are also non-pathogenic: E .coli, the most common commensal human amoeba, Endolimax nana, Iodamoeba butschlii and E. gingivalis, though this last may contribute to gingivitis. Dientamoeba fragilis, though sounding like an amoeba, is in fact a flagellate without flagella and does not fit here taxonomically. All these parasitic organisms are anaerobic and lack mitochondria.

As well as these human parasites there are three other genera of amoebae that may cause disease in humans. All are very rare and the report by Cursons et al is an horrific local example of one of these diseases.2 Naegleria, Acanthamoeba and Balamuthia are aerobic, mitochondria-containing, free-living, opportunistic human pathogens that live in aquatic habitats and browse on bacteria.3 Indeed it is their ubiquitous nature and that of other free-living genera of amoebae that makes them the common introduction to the microscopic world of micro-organisms for school children in science classes. The free-living Amoeba proteus is the species most of us will have seen. As a side issue, all these and many other free-living amoebae ingest Legionella spp. Legionella spp. have adapted to replicate inside amoebae, providing, in a teleological sense, a safe niche from the vicissitudes of a purely aquatic lifestyle. These Legionella spp. are most likely transmitted to us within non-pathogenic amoebae:4 another example of the infinite subtleties of microbe–host interactions.

These three genera of opportunistic amoebae have a predilection for invading the tissues of the human central nervous system. Naegleria fowleri, as described in this paper,2 lives optimally in fresh water at 40–45 °C and is the cause of primary amoebic meningoencephalitis. Its association with disease related to the warm waters of the geothermal areas of the central North Island has been documented in the NZMJ, principally by Dr Ray Cursons and his colleagues in the laboratory, and by Dr David Pullon clinically, for over 30 years. As a child at boarding school for five years in Cambridge in the 1950s, so often spending exeat weekend days leaping in and out of Waikato hot pools, neither I, nor any one else, knew the risks we ran. French epidemiologists estimate that given 10 N. fowleri amoebae per litre of water and a likely inhalation or ingestion of 10 ml of water during swimming, the risk of human infection for a swimmer is 8.5 x 10-8!5 The risks are indeed minute. Following the recognition of the syndrome in the Waikato area in the 1960s and 1970s, it disappeared, presumably as a result of widespread publicity at the time, general public health advice and specific advice on pool care. The last of these involves the exclusion of soil from the water sources and the pools, filtration, appropriate chemical control and optimal water flow rates as Cursons et al describe.2

Clinical points of relevance regarding primary amoebic meningoencephalitis include the very short incubation period, which is generally of two to five days, although apparent incubation periods of 14 days have been suggested. Death, which is almost invariable, occurs rapidly within six days and without focal neurological abnormality. All seven reported survivors received high doses of systemic amphotericin with or without intrathecal amphotericin, though many other agents were added in clinical desperation.3,6

Acanthamoeba are also opportunistic free-living amoebae, replicating optimally at temperatures of 25–30 °C and capable of causing disease in both humans and animals. The central-nervous-system disease they produce is rare (<200 reports) and is characteristically a protracted and insidious one called granulomatous amoebic encephalitis. It is seen only in debilitated and immunosuppressed patients, eg, those with chronic liver disease, diabetes mellitus, AIDS, steroid treatment and chemotherapy, and after organ transplantation.3 It has not been reported in New Zealand and it is almost invariably fatal. In contrast, acanthamoeba keratitis is not rare, is seen in New Zealand and has been associated with several different Acanthamoeba species. It is limited to people who wear soft contact lenses and patients present with ocular discomfort and pain, photophobia and blurred vision. There is obviously an initial broad microbial differential diagnosis. The first case of acanthamoeba keratitis definitely confirmed in Auckland was in 1991, and since 1995 there have been eight proven cases in Auckland. The organism is also isolated a couple of times each year from contact lens solution or contact lens cases, unassociated with disease, in materials sent to and evaluated in the Mycology Division of the Department of Clinical Microbiology at Auckland Hospital (personal communication, K Rogers, Auckland, 2003). So, the organism is about and ever threatening. Successful treatment of acanthamoeba keratitis depends on early diagnosis, surgical debridement and frequently administered topical treatments with agents such as propamidines, diamidines, azole antifungals or polyhexamethyl biguanide.7

Balamuthia mandrillaris (first isolated from a pregnant mandrill baboon with meningoencephalitis in San Diego Zoo in 1990, in case you have forgotten) has never been isolated from the environment and unlike these other amoebae can be cultured only on mammalian cell lines. Disease due to this opportunistic pathogen is even more rare than those already described and there have been only about 70 cases reported, none from New Zealand. The illness is again a granulomatous amoebic encephalitis but this organism infects both immunocompromised and immunocompetent hosts.3 No one has survived this disease.

Reappearance of Naegleria fowleri disease in the central North Island in 2000 is another reminder that the price of avoiding environmental microbial risks like this is, as that of liberty, eternal vigilance. We live now in a world extraordinarily and unbelievably intolerant of risk. It seems almost miraculous that so much time has passed since the last episode. The paper is a timely reminder: it brings together the sophisticated modern molecular science by which the organism was precisely identified and, in contrast, the longstanding advice, simple but oh so critical, ‘Keep your head above water at all times in any geothermal pool.’

Author information: Rod Ellis-Pegler, Infectious Disease Physician, Auckland Hospital, Auckland

Correspondence: Dr Rod Ellis-Pegler, Department of Infectious Disease, Auckland Hospital, Private Bag 92024, Auckland. Fax: (09) 307 4940; email: RodEP@adhb.govt.nz