Plasmodium vivax malaria acquired in far north Queensland

Dianne L Brookes, Scott A Ritchie, Julie R Fielding and Mark R Loewenthal
Med J Aust 1997; 166 (2): 82.
Published online: 20 January 1997

In February 1996, vivax malaria was diagnosed in a man from a remote community in far north Queensland who had not visited a malarious area for the past 19 years. Microscopy and DNA studies of blood from other residents of the community did not identify a source of infection. It was suspected the infection was transmitted by mosquitoes from a neighbour who had been infected in Papua New Guinea, but whose blood was not available for DNA tests.

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Introduction - Clinical record - Investigations - Discussion - Acknowledgements - References - Authors' details



We report a case of Plasmodium vivax malaria that we conclude was acquired in far north Queensland in early 1996. There has been only one other report of malaria acquired in mainland Australia 1 since the country was declared malaria-free by the World Health Organization in 1981.


Clinical record

A 31-year-old white male presented to a Cairns general practitioner in early February 1996 with a two-day history of fever, headaches, generalised aches and pains, lethargy and loss of appetite. Two days later he was hospitalised with vomiting and dehydration; he was given intravenous fluids and discharged within 24 hours. He remained unwell and consulted his general practitioner again the following day.

A full blood count showed: lymphocytopenia (lymphocytes, 0.71 x 10 9 /L; normal, 1.5-4.0 x 10 9 /L); neutropenia (neutrophils, 1.95 x 10 9 /L; normal, 2.0-7.5 x 10 9 /L); and thrombocytopenia (platelets, 33 x 10 9 /L; normal, 150-450 x 10 9 /L). Haemoglobin concentration was in the normal range. On review of the routine blood film, schizonts of P. vivax were noticed, and malaria was diagnosed six days after onset of symptoms. The patient was treated with standard doses of chloroquine and primaquine, 2 and has remained well since.

The patient had never received a blood transfusion nor used intravenous drugs. He had travelled to Papua New Guinea (PNG) 19 years before presentation, and for most of 1995 had worked as a tradesperson in a remote Aboriginal community in far north Queensland. Over the 1995 Christmas-New Year period he spent seven days in Cairns, followed by 12 days south of Cairns, at Mission Beach. For the next 24 days before onset of symptoms, he worked at the community in far north Queensland.



Because the average incubation period for P. vivax malaria is 15 days (range, 12-17 days), 3 we investigated the possibility that the patient acquired malaria via a mosquito bite while at the community. It lies about 15¡ south of the Equator, 40 km from the coast of the Gulf of Carpenteria and about 450 km northwest from the closest international airport, at Cairns. The climate early in the year is monsoonal -- hot and humid with intermittent, heavy rainfall. Most of the population of about 1200 is Aboriginal.

Investigations of source: After diagnosis of the index case, blood films were collected from 20 residents of the community who were considered possible sources of infection. These comprised:

  • A person who had been diagnosed with P. vivax malaria in June 1995 (this had been acquired in PNG, and the person had remained well after appropriate treatment);

  • All 13 people who presented to the community health centre with an undiagnosed fever within three weeks of the diagnosis of the index case; and

  • Six people who had recently travelled from PNG. Further blood samples for DNA amplification by polymerase chain reaction were collected from five of these six people (blood was not available from one woman who had visited PNG in December 1995).

Malaria parasites were seen in the blood films of only one of these 20 people. This person was Melanesian, had arrived in Australia from PNG in November 1995 and had taken no malaria-prophylactic drugs. No parasites were found in thin peripheral blood films, but three early ring trophozoites were seen in thick films. Although definitive species identification could not be made on morphological grounds, DNA amplification detected only P. falciparum (A Baddeley, Centre for Public Health Sciences, Brisbane, and A Saul, Queensland Institute of Medical Research, Brisbane, personal communication). The person was treated accordingly. 2 No evidence of malaria was found by DNA amplification in the other four people tested.

The woman whose blood was not available for DNA amplification was also Melanesian, from PNG; she had lived in Australia for about four years and was related to the person with P. falciparum parasitaemia (who was staying with her). Although her house was about 2 km away from the home of the index patient, the latter often spent the evening socialising nearby. Both homes are about 50 m from a creek that runs along the periphery of the community.

Investigations of vector: Two days after diagnosis of the index case, surface waters at the community (such as puddles, wheel ruts, ditches, swamps and drains) were surveyed for mosquito larvae with a standard 350-mL dipper. Adult mosquitoes were collected in Centers for Disease Control (CDC) light traps, baited with carbon dioxide and 1-octen-3-ol. Traps were placed beside the creek, in the central built-up part of the community and near the homes of the index patient and of the person with P. falciparum parasitaemia and his relative. Larvae were stored in 70% ethanol and adult mosquitoes at -70oC before identification. 4

Results are shown in the Box. Most Anopheles larvae were collected from small puddles and wheel ruts near the creek. Most adult Anopheles mosquitoes were also collected near the creek, with fewer at the two houses, and very few from the central part of the community.

A larvicide, ( S )-methoprene, was used to treat surface waters where Anopheles larvae were breeding, and a residual insecticide, deltamethrin, was used for the thickly vegetated zone along the creek (along the periphery of the community). Further CDC light traps were set a week after initial mosquito collections, in the same locations along the creek as previously. Many Anopheles mosquitoes (12%, An. farauti s.l.) were still present (see Box).



We believe that this case represents local mosquitoborne transmission of P. vivax malaria at the community in far north Queensland, because:
  • The index patient had not been to a malarious area for 19 years. Although very long incubation periods and late hypnozoite relapses of P. vivax malaria (caused by reactivation of the dormant hepatic stage of the parasite) have been reported from temperate zones, 4,5 P. vivax malaria acquired in tropical regions, such as the Western Pacific region (including PNG), typically has a short incubation period (12-17 days), and relapses quickly (average, six weeks later). The usual duration of untreated P. vivax malaria is 1.5-5 years.3 Therefore, we conclude that this episode is not a late hypnozoite relapse of P. vivax malaria acquired in PNG.

  • The index patient was at the community during the usual incubation period for P. vivax malaria.

  • A competent malaria vector was present. There is strong evidence that An. farauti s.l. is the most important potential malaria vector in Australia, 6 and we showed that breeding An. farauti s.l. were present at the community. Further, although the index patient's home was screened, he often slept outside on the verandah because of the oppressive climate, and therefore was accessible to An. farauti s.l. mosquitoes during their peak biting hours (sunset to midnight). 7

  • There was a possible source of infection at the community. Although we did not identify another individual with P. vivax malaria, we believe that the woman whose blood was not available for DNA studies was infected. She had recently travelled to PNG, where P. vivax malaria is endemic, and our concerns are strengthened by the finding of low-level P. falciparum parasitaemia in her asymptomatic relative, who had recently come from the same region.
    Although she reported taking chloroquine and doxycycline prophylaxis during her visit, chloroquine-resistant malaria is well described in PNG. In addition, this prophylaxis will not prevent hypnozoite relapses. 3 Malaria symptoms may be less obvious in those who have chronic malaria, and may be further reduced by self-medication, which is common among PNG nationals (unpublished observations). Therefore, although we have not been able to prove that there was a source of infection (i.e., an untreated imported case) at the community, we believe that she was a possible source.

  • There was no evidence of modes of transmission other than via mosquitoes (e.g., via contaminated blood).

When an isolated case of malaria cannot be epidemiologically linked with another case of malaria, it is defined as "cryptic". 8 However, for the above reasons, we believe that this was a case of "introduced" malaria (malaria transmitted by mosquitoes from an imported case in an area where malaria does not usually occur). 8 Two episodes of locally acquired malaria in mainland Australia in 15 years attest to the rarity of local transmission, 6 despite frequent importations, particularly into the malaria-receptive north of Australia. 9 Nevertheless, sensitive and timely surveillance must be maintained to ensure that locally acquired cases are promptly recognised and investigated. Intensive mosquito-control measures may be needed, and other cases should be sought and treated promptly. Treatment should include primaquine as a gametocidal agent for P. falciparum . 10



We commend Heather Moseley for detecting malaria parasites in the index patient's blood film when malaria was not expected. We wish to thank Dr Bill Glavin and the health staff at the community for assistance with the investigation.



  1. Walker J. The role of a diagnostic reference laboratory in malaria surveillance. Comm Dis Intell 1996; 20: 302-304.
  2. Antibiotic Guidelines Subcommittee, Victorian Drug Usage Advisory Committee. Antibiotic guidelines. 8th ed. Melbourne: Victorian Medical Postgraduate Foundation, 1994: 103-107.
  3. Gilles HM. The malaria parasites. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 12-34.
  4. Lee DJ, Woodhill AR. The Anopheline mosquitoes of the Australasian region. Sydney: Australian Medical Publishing Company, 1944. Department of Zoology, University of Sydney, monograph no. 2.
  5. Bradley D, Newbold CI, Warrell DA. Malaria. In: Weatherall DJ, Ledingham JGG, Warrell DA. Oxford textbook of medicine. 3rd ed. Oxford: Oxford University Press, 1995: 835-862.
  6. Bryan JH, Foley DH, Sutherst RW. Malaria transmission and climate change in Australia. Med J Aust 1996; 164: 345-347.
  7. Service MW. The Anopheles vector. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 96-123.
  8. Zucker JR. Changing patterns of autochthonous malaria transmission in the United States: a review of recent outbreaks. Emerg Infect Dis 1996; 2: 37-43.
  9. Longbottom H. Epidemiology of malaria in Australia 1991-1995. Comm Dis Intell 1996; 20: 84-87.
  10. Warrell DA. Treatment and prevention of malaria. In: Gilles HM, Warrell DA. Bruce-Chwatt's essential malariology. 3rd ed. London: Edward Arnold, 1993: 164-195.

Received 5 Aug, accepted 26 Nov 1996  

Authors' details

Tropical Public Health Unit, Cairns, QLD.
Dianne L Brookes, RN, Public Health Nurse; Scott A Ritchie, PhD, Medical Entomologist; Andrew F van den Hurk, BAppSc, Vector Control Officer.
Cairns Base Hospital, Cairns, QLD.
Julie R Fielding, BAppSc, Supervising Scientist (Haematology); Mark R Loewenthal, DTM&H, FRACP, Infectious Diseases Physician.
No reprints will be available. Correspondence: D L Brookes, RN, Tropical Public Health Unit, PO Box 1103, Cairns, QLD 4870.
E-mail: troppub AT

  • Dianne L Brookes
  • Scott A Ritchie
  • Julie R Fielding
  • Mark R Loewenthal



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