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B J Currie

Publications and source records attributed to B J Currie.

121 records · Page 7Linked to original sources

An epidemiological study of snake bite envenomation in Papua New Guinea.

We report a study of 347 patients with snake bite envenomation in Papua New Guinea. The male: female ratio of the victims was 1.6:1 and their mean age was 24.5 years; 26% were children less than 15 years old. In all cases in which the bite site was known (334) the snake had bitten the extremities of the victim, with 71.3% of these bites being on the ankle or below. The patients came from three regions: urban Papua, rural Papua and (mostly rural) New Guinea. Snake bites occurred more frequently during the daytime in all regions, but this pattern was less obvious in New Guinea (P = 0.004), reflecting the predominance of the death adder (Acanthophis antarcticus) in New Guinea and of the taipan (Oxyuranus scutellatus canni) in Papua. Bites were commoner in the rainy season (November to April) in all groups, but this was less noticeable in rural Papua and New Guinea (P = 0.004). This may relate to seasonal activities of the rural population. The female:male ratio for patients from rural areas was higher for those 30 years of age and over than for those under 30 (P = 0.034), probably reflecting the increased gardening workload of older women. The incidence of envenomation and mortality rates after snake bite in Papua appear to have changed little over 25 years. However, increased relative numbers of taipans seem to be occurring in central Papua possibly related to the cane toad (Bufo marinus) and deforestation. We calculate the annual incidence of envenomation and the mortality rate per 100,000 to be 81.8 and 4.3, respectively, for rural central Papua, 21.8 and 2.1 for urban central Papua, and 3.0 and less than 1.0 for the Madang region of New Guinea. The importance of a standard management protocol and of improved first aid are emphasised.

Adolescent↗

Focal neurological signs in cerebral malaria accounted for by preceding neurological damage.

In 1987 at Port Moresby General Hospital, Papua New Guinea, two out of 103 adults with a final diagnosis of cerebral malaria had focal neurological signs noted on admission. In both cases the focal signs could be explained by documented prior neurological disease with residual focal damage. Focal neurological signs in patients presenting with malaria should prompt careful investigation to exclude other active neurological disease. Where no additional diagnosis is evident a history of past neurological damage may become apparent to explain the focal nature of the malaria presentation.

Adult↗

Diethylcarbamazine prophylaxis for human loiasis. Results of a double-blind study.

To determine whether infection with Loa loa could be prevented in temporary residents of endemic areas, we conducted a randomized, double-blind, placebo-controlled trial of diethylcarbamazine as a chemoprophylactic agent. Diethylcarbamazine (300 mg) or placebo was taken orally once a week by Peace Corps volunteers serving in Gabon, Cameroon, and the Central African Republic. The participants were assessed clinically and with serologic and parasitologic testing before and yearly during their two years of service. One hundred one persons satisfactorily completed the study. In Gabon (where exposure to the parasite was heaviest), 6 of 20 volunteers (30 percent) in the placebo group had clinical disease, as compared with none of 16 (0 percent) in the diethylcarbamazine-treated group (P less than 0.02). Of those taking placebo, 10 of 20 (50 percent) became seropositive for antifilarial IgG antibody, as compared with 2 of 16 (12 percent) in the drug-treated group (P less than 0.02). Exposure to the parasite appeared to be much lower among the 65 Peace Corps volunteers in Cameroon and the Central African Republic. No volunteer in either group in these countries had overt loiasis; 2 of 40 (5 percent) in the placebo groups in Cameroon and the Central African Republic seroconverted, as compared with none of 25 (0 percent) of those receiving diethylcarbamazine. Occasional nausea was the only symptom significantly associated with the prophylactic drug regimen. We conclude that diethylcarbamazine given orally once weekly can be an effective, acceptable chemoprophylactic agent to prevent loiasis in temporary residents of regions of Africa where Loa loa is endemic.

Adult↗

Method for preserving erythrocytic delta-aminolevulinic acid dehydratase activity that facilitates population studies on lead intoxication.

A method preserving the activity of the erythrocytic enzyme delta-aminolevulinic acid dehydratase (EC 4.2.1.24) was developed using a vehicle of 50% aqueous glycerol containing dithiothreitol (80 microM). Whole heparinized blood (0.5 ml) was added to 0.75 ml of this mixture in a cryovial tube (capacity 1.3 ml), mixed well and stored in a freezer at -20 degrees C for 21 days. Statistical comparison of the enzyme activity when freshly assayed and after storage indicated excellent agreement for quantitation of the non-activated enzyme (intraclass correlation coefficient = 0.99) and the activated enzyme (intraclass correlation coefficient = 0.98). This storage method will facilitate future population studies on lead intoxication, particularly those in remote locations.

Erythrocytes↗

Melioidosis: acute and chronic disease, relapse and re-activation.

In melioidosis-endemic regions the importance of re-activation of Burkholderia pseudomallei from latent foci remains unclear. This topic was assessed in a 10-year prospective study (1989-99) of melioidosis in the tropical north of the Northern Territory of Australia, together with other aspects of the nature of melioidosis. Incubation period from defined inoculating events was previously ascertained as 1-21 (mean 9) days. Of 252 total cases 244 (97%) were considered to be from recent acquisition of B. pseudomallei infection and 8 (3%) were considered to be re-activation from a latent focus. Acute illness occurred in 222 (88%) cases; 30 (12%) cases had chronic illness (symptomatic for > 2 months). Of the 207 patients surviving the initial illness, 27 (13%) had a confirmed relapse (mean time from initial diagnosis of 8 months), with 5 relapsing twice. Of these 32 relapses, 15 (3 fatal) were associated with poor adherence to the eradication therapy antibiotics and 10 (none fatal) were failures of eradication with doxycycline monotherapy. Following initial intensive therapy with ceftazidime or meropenem for at least 14 days, eradication therapy with trimethoprim-sulphamethoxazole monotherapy for at least 3 months had been more successful.

Acute Disease↗

Studies in vitro on the relative efficacy of current acaricides for Sarcoptes scabiei var. hominis.

Resistance of Sarcoptes scabiei to various topical therapies has been described, but clinical assessment of treatment failure is problematic and in-vitro assays are generally not available. We describe a simple in-vitro analysis used to evaluate the relative efficacy of a range of topical, oral, and herbal treatments available in Australia for the treatment of scabies. S. scabiei var. hominis mites were collected from skin scrapings obtained from 7 crusted scabies patients over a period of 2 years (1997 and 1998). Larvae, nymphal instars, and adult mites were tested within 3 h of collection and continuously exposed to selected commercially available treatment products until death, with the elapsed time recorded. Neem was the only product to show little acaricidal activity. Survival curves indicated that, of the other agents, 5% permethrin (Lyclear) had the slowest killing time, with 35% of mites still alive after 3 h, and 4% still alive after 18-22 h of constant exposure. In contrast, no mites were alive after 3 h exposure to 25% benzyl benzoate (Ascabiol), 1% lindane (Quellada), 5% tea tree oil and 100-8000 ng/g of ivermectin (Equimec). Despite the slower killing time with 5% permethrin, there was no evidence of any mite tolerance in vivo or treatment failure in any patients or contact cases.

Animals↗

Cryptococcus neoformans var. gattii infection in northern Australia: existence of an environmental source other than known host eucalypts.

The 2 known host trees of Cryptococcus neoformans var. gattii, Eucalyptus camaldulensis and E. tereticornis, do not occur naturally in the 'Top End' of the Northern Territory (NT) of Australia. Nine clinical isolates of C. neoformans var. gattii from the NT were analysed by random amplification of polymorphic deoxyribonucleic acid (RAPD) and polymerase chain reaction 'fingerprinting'. Two isolates were assigned to RAPD profile VGI, previously established as the common RAPD profile. The remaining 7 were assigned to profile VGII; 6 of these isolates were recovered from individuals living in the 'Top End'. The results strongly support the existence of an alternative environmental niche for C. neoformans var. gattii, as all isolates from Eucalyptus spp. in Australia to date have been of RAPD profile VGI.

Cryptococcosis↗

Ivermectin for Sarcoptes scabiei hyperinfestation.

OBJECTIVES: Crusted (Norwegian) scabies is an unusual variant of scabies caused by hyperinfestation with Sarcoptes scabiei. It has high morbidity, and secondary bacterial skin sepsis may result in life-threatening bacteremia. An open label study of oral ivermectin was carried out in patients with crusted scabies refractory to topical therapy. METHODS: Patients with refractory crusted scabies were prescribed oral ivermectin, one to three doses of 200 mg/kg at 14-day intervals, combined with topical scabicide and keratolytic therapy. RESULTS: Of the 20 patients who received ivermectin, 8 had a complete initial clinical response, a partial response was achieved in 9, and minimal improvement occurred in 3. Three doses of ivermectin were curative for 8 of 10 cases, but recurrence of scabies from presumed reinfestation occurred in at least half of these. CONCLUSION: The authors conclude that ivermectin is effective for crusted scabies; however, multiple doses may be required to achieve a cure, and recurrence 6 or more weeks after completing treatment is common.

Administration, Oral↗

Prospective study of jellyfish stings from tropical Australia, including the major box jellyfish Chironex fleckeri.

OBJECTIVE: To determine the immediate and delayed effects of jellyfish stings, and correlate these with microscopic identification of jellyfish nematocysts. DESIGN: Prospective study of patients presenting with jellyfish stings. PARTICIPANTS AND SETTING: 40 people presenting with jellyfish stings to the emergency department of a teaching hospital in tropical Australia between 1 August 1999 and 31 July 2000. MAIN OUTCOME MEASURES: Clinical diagnosis (sting by Chironex fleckeri, "Darwin carybdeid" or other jellyfish, or "Irukandji" syndrome); clinical severity; delayed hypersensitivity; and sticky-tape sampling and microscopic identification of nematocysts. RESULTS: Patients were aged 2-50 years, with eight aged under 15 years; 23 were male. Presentations were consistent with C. fleckeri sting in 28 cases, Darwin carybdeid sting in five, and Irukandji syndrome in four. Sticky-tape sampling was done in 39 patients and was positive for C. fleckeri nematocysts in 23 and for non-C. fleckeri nematocysts in six, with nematocysts not detected in 10 (including all four with Irukandji syndrome). All microscopically confirmed C. fleckeri stings had typical clinical presentations. None of the stings were life-threatening, and no antivenom was given. Delayed hypersensitivity reactions were seen in 11 of the 19 patients (58%) followed up after stings positive for C. fleckeri nematocysts. CONCLUSIONS: Although most jellyfish stings presenting to Royal Darwin Hospital I were caused by C. fleckeri, severe envenomation was rare. There was a strong association between clinical features and sticky-tape identification of nematocysts. Delayed hypersensitivity was common after C. fleckeri stings.

Adolescent↗

The neuropathology of melioidosis: two cases and a review of the literature.

Melioidosis is an infectious disease caused by Burkholderia pseudomallei and is hyperendemic in the Top End of the Northern Territory of Australia, as well as being widespread throughout tropical south east Asia. The infection is primarily acquired via the inoculation of compromised surface tissues by contaminated soils and water and it can cause an acute, rapidly fatal illness. Although pneumonia is the commonest manifestation, neurological presentations have been described, most notably encephalomyelitis. This paper presents the neuropathology of 2 fatal cases of neurological melioidosis and reviews the relevant literature.

Brain↗