Efficacy of five annual single doses of diethylcarbamazine for treatment of lymphatic filariasis in Fiji.

Annual single-dose treatments with diethylcarbamazine citrate (DEC) at a dose of 6 mg/kg have been reported effective in reducing microfilariae (mf) rate and density and applicable to large-scale filariasis control campaigns. However, the efficacy of such treatments has not been studied quantitatively in relation to different pretreatment levels of endemicity. This study of 32 villages in Fiji revealed that five treatments repeated annually steadily reduced village mf rate, and that the degree of reduction was not influenced by pretreatment levels of mf density or rate. This indicates that an annual dosage scheme is applicable to high-endemicity areas. The results also suggest that such treatment affected juvenile forms of Wuchereria bancrofti and may prevent them from reproducing.

Control of lymphatic filariasis by annual single-dose diethylcarbamazine treatments.

It has long been stressed that diethylcarbamazine citrate must be given at a total dosage of 72 mg per kilogram of body weight in 12 divided doses of 6 mg kg(-1) to obtain maximum effect against Wuchereria bancrofti. However, recent studies revealed that only a single dose at 6 mg kg(-1) could reduce microfilaria (Mf) counts by 90%, and that the effect would persist for 12-18 months. The annual repeat of the single-dose mass treatment was shown to be effective in reducing Mf prevalence and density in large-scale, long-term field trials. The scheme is simple and economic, and could be sustainable in many endemic areas, where health manpower and resources are often not sufficient. Annual single-dose mass treatments can be an effective weapon against human lymphatic filariasis, as discussed here by Eisaku Kimura and Jona Mataika.

Dengue type 1 epidemic with haemorrhagic manifestations in Fiji, 1989-90.

A dengue type 1 epidemic occurred in Fiji between July 1989 and July 1990. Virus isolation in C6/36 cell cultures and Toxorhynchites mosquitos yielded 36 strains. Of the 3686 cases recorded by the Ministry of Health, 60% involved indigenous Fijians and 37%, Indians. A house-to-house survey revealed that a large majority of patients had classical dengue symptoms and 8% reported haemorrhagic manifestations. Among the children and adults hospitalized for dengue, 43% had haemorrhagic manifestations, including epistaxis, gingival bleeding, haematemesis, melaena and haematuria. A total of 15 patients with haemorrhagic manifestations and/or shock died, 10 of whom were aged 0-15 years; the diagnoses were confirmed in four cases by virus isolation or serology.

PIP: Researchers reviewed the medical records of all cases of dengue and dengue-like illness in Fiji since 1971. During March-April 1990, in Fiji, interviews were conducted with 426 occupants of 81 randomly selected houses in Suva and its surrounding areas to examine the relationship between the incidence of true dengue and dengue-like illnesses and the reported incidence. 60% of the persons interviewed were Fijians and 31% were Indians. Health workers collected blood samples from acute cases. 36 strains of dengue 1 virus was isolated. A fever lasting more than 3 days accompanied by at least one of the following symptoms denoted dengue or dengue-like illness: headache, joint pains, muscle pains, rash, epigastric discomfort, and bleeding. There was an outbreak of clinical dengue 1 during 1989-1990 involving 3686 cases. The 1975 outbreak involved 1600-2400 cases of dengue hemorrhagic fever. The 1989-1990 incidence was higher among Fijians than Indians (60% vs. 37%). The dengue epidemic peaked in November 1989 (about 900 cases). The rate of dengue hemorrhagic fever was 8% (15 cases). Hemorrhage manifestations included nosebleeds (8 persons), gingival bleeding (2), vomiting of blood (2), blood in the urine (3), and passage of dark stools stained with blood (3). The case fatality rate was 8%. Hemorrhages of the stomach and lungs occurred in most fatal cases. 10 of the 15 fatal cases were aged 10-15 years. 182 (43%) of the respondents in the household survey had reported dengue-like illness in the last 6 months. Children were more likely to have had dengue than adults (51% of 0-9 year olds and 61% of 10-19 year olds vs. 32-33% for all other age groups). Among hospitalized dengue cases, 43% experienced hemorrhages.

Red cell enzyme and serum protein gene markers in Fijians.

A total of 332 persons from three localities in the Fiji Islands have been tested for genetic variation in 24 red cell enzyme systems and 4 serum protein systems. Polymorphic variation was present at 7 red cell enzyme loci and 1 serum protein locus. The remaining systems were invariant except for a single individual with a slow variant at the GOT1 locus and another individual with a D variant at the TF locus. The series from Nandi differed significantly from the Lau Islands for gene frequencies in GPT, ACP and ESD, Koro Island differed from the other localities at the PGD locus and from Nandi for ESD. Genetic distance analysis reveals that Lau Islands cluster with Western Samoa, Koro Island with New Caledonia (Vanuatu), with Nandi being separate.

An epidemic of Ross River virus infection in Fiji, 1979.

An explosive epidemic of polyarthritis caused by Ross River virus occurred in the Fijian islands from April to June 1979. Serological results suggest there was a low level of Alphavirus activity throughout Fiji before April 1979, but that following the epidemic up to 90% of the residents of some communities had antibody to Ross River virus. The clinical and laboratory findings in patients from the Fijian outbreak were similar to those seen in Australian cases.

Influenza virus A (H1N1) in Fiji.

In April and May 1978 the newly emerged H1N1 subtype of influenza A virus caused an influenza epidemic among children and young adults in Fiji. The virus apparently failed to spread to New Zealand at that time despite the fact that each week more than 1000 people travel by air from Fiji to New Zealand.

Mosquito-borne infections in Fiji. V. The 1971-73 dengue epidemic.

A dengue epidemic due to type 2 virus involving some 3,400 cases began in Fiji early in 1971, had a peak during May, June and July, and cases have continued to occur with a low incidence during 1972 and 1973. Many of the notified cases showed classical dengue fever symptoms and there were no confirmed cases of haemorrhagic fever. A serological survey indicated that there had been at least 20,000 subclinical infections. It is probable that the virus was introduced to Fiji either through the port of Lautoka or Nadi international airport in February 1971. The normal travel patterns of residents must have spread the virus to all the more accessible localities but, with the exception of Rotuma, it caused infections only in areas where Aedes aegypti was available as a vector. There was no evidence that pre-existing dengue type 1 serum antibody gave any protection during this epidemic.

Mosquito-borne infections in Fiji. I. Filariasis in northern Fiji: epidemiological evidence regarding factors influencing the prevalence of microfilaraemia of Wuchereria bancrofti infections.

A survey of microfilaraemia among the population of Vanua Levu, Taveuni and Koro islands in northern Fiji was conducted in 1968 and 1969 as a prelude to a campaign of mass treatment with diethylcarbamazine.The prevalences of microfilaraemia were found in the more moist conditions of Taveuni and Koro and on the windward southern side of Vanua Levu to be higher than on the drier northern side of Vanua Levu. On both sides of Vanua Levu prevalences were lower inland than near the coast.Under apparently similar environmental conditions those of Fijian ethnic origin exhibited a higher prevalence of microfilaraemia than that shown by Indians. This ethnic difference and a difference between the prevalences in male and female Fijians are considered to be due more to higher rates of recovery from microfilaraemia in Indians and Fijian women than to diminished exposure to mosquitoes. Mathematical models have been used as an aid to the interpretation of the data, and, where appropriate, comparison has been made with the prevalence of antibodies to dengue, an arbovirus having the same vectors.Household infections were analysed by computer techniques. Infections in large households were not proportionately higher than in small households, indicating that transmission was not intrafamilial. The clustering of infections within households, though present, was not marked. Among the occupants of outlying settlements the prevalence of microfilaraemia was relatively low indicating a lower risk of infection due to isolation.

Mosquito-borne infections in Fiji. II. Arthropod-borne virus infections.

Surveys of arbovirus activity in Fiji were conducted over a 10-year period from December 1959 to December 1969. No arboviruses were isolated from over 200,000 mosquitoes, 9000 ticks, or 575 serum samples. Eight thousand human and 1117 bird, bat and animal sera were tested for haemagglutination-inhibiting arbovirus antibody using a variety of group A, group B and Bunyamwera group antigens. Only a small number of low-titre reactions were found among the non-human sera, but 14% of all human sera were found to contain Group B antibody. The antibody prevalence increased with increasing age, from less than 1% for persons born since 1950, to 70% for persons born before 1900. The age differences in prevalence could be used to estimate the time and size of previous epidemics. Differences were found in antibody prevalence between the sexes, between ethnic groups and between persons from different regions. These differences could be explained in terms of climate, location and custom.Historical and serological evidence both suggest that all the antibody detected was due to past exposure to dengue virus. The very high proportion of the population with no dengue antibody makes Fiji a high-risk area for a further dengue epidemic. Dengue virus is known to be active in the Pacific and South-East Asia.

Mosquito-borne infections in Fiji. 3. Filariasis in northern Fiji: epidemiological evidence regarding the mechanisms of pathogenesis.

During a filariasis survey conducted in northern Fiji in 1968-9 examinations were made for microfilaraemia, enlarged lymph nodes and elephantiasis. Analysis of the microfilarial densities at different ages and the number of anatomical sites showing lymph gland enlargement or elephantiasis have been used to provide evidence on the clustering of infections and pathogenesis.Although there is no evidence of clustering of risk of infection, there is evidence favouring the clustering of adult filariae in individuals. Nevertheless the number of sites of lymph node enlargement do not correspond with this finding and statistical evidence suggests that lymph-node enlargement is not necessarily associated with the near presence in the body of adult filariae, whether dead or alive.Males of Indian ethnic origin showed a higher prevalence of elephantiasis than males of Fijian ethnic origin, but women of either ethnic race showed prevalences lower than those of men.The onset of elephantiasis at a site does not directly reflect the number of infections sustained in the local area, but it appears that filariasis first induces for a limited period a proneness to elephantiasis. During this period a random and discrete event may induce the onset of elephantiasis. The nature of the event is unknown, but it probably is not trauma.