Diseases of the Region in Time and Space

Arthropod-Borne Diseases

Malaria. Malaria has been a major cause of morbidity and mortality at least in the historical period throughout Melanesia, except Fiji, New Caledonia, and certain coral atolls. Although the anopheline mosquito vector is present in Micronesia, the Plasmodium parasite has not been introduced. Malaria is also absent from Polynesia (Norman-Taylor et al. 1964; Gurd 1967; Willis 1970; Henderson et al. 1971). The disease was endemic in the aboriginal lands of northern Australia before its eradication in 1962. Because of the continued presence of Anopheles in Australia, reintroduction from New Guinea or southeast Asia remains a threat (Moodie 1973).

In New Guinea, malaria is hyperendemic in the hot, wet lowlands. As the indigenous people were "pacified" by colonial administrations and forced to live in larger village units, the resultant proximity of large groups of people and numerous small pools of mosquito-breeding water facilitated the spread of malaria (Vines 1970). It did not reach the highlands, however, until the 1930s, as a result of European road building, airstrip construction, pond and ditch digging, along with increased migration of contract workers between coastal plantations and highland homes (Riley 1983). In some remote mountain valleys, the unstable parasite pool has become nearly self-sustaining in the 1970s. Plasmodium cannot, however, complete its life cycle in Anopheles at altitudes above 2,000 meters, where temperatures are below 16°C, even though its vector can survive higher up (Nelson 1971; Sharp 1982).

Although the Polynesian outlier atolls in Papua New Guinea and the Solomon Islands were initially free from malaria, it was introduced within a decade of first European contact in the nineteenth century to Ontong Java and Sikiana (Bayliss-Smith 1975). Malaria control efforts in the 1950s-70s have had varying degrees of success (Moodie 1973; Bayliss-Smith 1975; Taufa 1978). The Institute for Medical Research in Papua New Guinea has initiated clinical trials of a malaria vaccine.

In areas of endemic malaria, the disease has its greatest effect on children from 6 months to 5 years of age. Before 6 months they are protected by maternal antibodies, and after 5 years they have generally acquired some immunity of their own from repeated infections (Burnet and White 1972). However, increased incidence of malaria in Melanesia is not necessarily associated with increased infant mortality (Van de Kaa 1967). Low-protein diets for children under 3 years of age in some New Guinea communities may increase resistance to or decrease severity of the symptoms of malaria (Lepowsky 1985).

Malaria may have indirect effects on child health as well. Decreased maternal immunity to malaria during pregnancy poses problems for fetal oxygenation and growth - and consequent infant health -in that the unchecked plasmodia clog the placenta, disrupt red blood cells, and induce high fever. Thus, birth weights in the Solomon Islands increased a few months after initiation of a malaria control program (Taufa 1978).

Malaria has been a scourge of settlers, colonists, missionaries, laborers, soldiers, and tourists in Melanesia, just as it has been of the indigenous people. Symptoms are worse for those adults who have not acquired some immunity in childhood or are malnourished. Nineteenth-century Samoan missionaries for the London Mission Society died of malaria at various stations in Vanuatu (Howe 1984). In World War II, it caused considerable mortality among the Australian, American, and presumably Japanese forces, as well as among Melanesians from regions other than the coastal lowlands (Burnet and White 1972). Tourists, anthropologists, and Peace Corps volunteers in Melanesia today regularly take their weekly antimalarial doses, which are generally available over the counter in local pharmacies.

Filariasis. Filariasis was indigenous throughout the tropical Pacific. Different strains of Wuchereria bancrofti are transmitted by different mosquito vectors in different regions. Culex in Micronesia and Anopheles in some of the Papua New Guinea islands as well as the Solomon Islands and Vanuatu carry nocturnally periodic strains, whereas daybiting Aedes transmit nonperiodic strains in Polynesia, Tuvalu, Kiribati, Fiji, and New Caledonia (Norman-Taylor et al. 1964; Iyengar 1965; Gurd 1967; Vines 1970; Henderson et al. 1971; Chowning 1989). In the first half of the twentieth century, filariasis was highly prevalent in Polynesia except New Zealand (Iyengar 1965; Henderson et al. 1971; Montgomerie 1988). In the Cook Islands in 1946, 75 percent of the school children were infected (Beaglehole 1957), as was nearly half the Tahitian population in 1949 (McArthur 1967). However, in the same time period, the disease was much less common in Papua New Guinea, the Carolines, Marshalls, Marianas, and Kiribati (Kraemer 1908; Hetzel 1959; Maddocks 1973), and the progression to elephantiasis was rare. In Fiji, adult male plantation workers generally have the highest rates of infection, although equally high rates are found in women who work near mosquito-breeding areas in pandanus and coconut groves. Filariasis is more common on the less developed islands, where screens on windows are often absent and mosquito-breeding puddles are plentiful near houses; yet it does not exist on the very small islands in this archipelago. Major mosquito eradication campaigns in the middle of this century were fairly successful in Micronesia (Henderson et al. 1971), Marquesas, Tahiti, Samoa, Tonga (Iyengar 1965), and Torres Straits islands.

Dengue. Dengue epidemics have occurred for at least a century in Oceania in places where the Aedes mosquito has been present, generally on lush wet islands where unscreened rain catchment is close to houses. The 1885-6 epidemics in Fiji and New Caledonia spread eastward into Tahiti, causing miscarriages and excessive mortality in children in southern French Polynesia (McArthur 1967). Wallis and Futuna experienced an epidemic in 1907, as did Torres Straits islands in the early twentieth century, the northern Cook Islands in 1930-1 (McArthur 1967), Kiribati in the 1950s, and Fiji in 1943-4 and 1953 (Wilkinson et al. 1973). Epidemics occurred infrequently in aboriginal lands in tropical northern Australia, probably arriving from nearby southeast Asia (Moodie 1973).

Dengue hemorrhagic fever, which is frequently fatal in children, appears to be a post—World War II phenomenon along major transport routes in southeast Asia and the Pacific islands. It has appeared in Tahiti and elsewhere when at least one other strain of the virus co-occurred with the type 2 strain (Chastel and Fourquet 1972; Hammon 1973). In 1971-2, major outbreaks of dengue of varying severity occurred in coastal Papua New Guinea, Vanuatu, New Caledonia, Fiji, Nauru, Kiribati, Tuvalu, Western Samoa, Tonga, Niue, and Tahiti (Pichon 1973; Wilkinson et al. 1973; Zigas and Doherty 1973). The symptoms were relatively mild in most areas, with a type 2 strain as the sole causative agent. In Rabaul, the clinical features of the type 2 infection were more severe, but hemorrhage and shock were not seen (Zigas and Doherty 1973). Over half the population of Tahiti was affected, some of whom developed hemorrhagic fever. Severe hemorrhagic symptoms and high mortality characterized the Niue outbreak that struck one-third of the population (Pichon 1973).

Although dengue had ceased to exist in Micronesia by 1948 (Hetzel 1959), it was reintroduced into Palau in the late 1980s by Indonesian drift voyagers who landed on the southwestern outer islands. Since then, cases have appeared in neighboring Yap and in Guam. Aedes was thought to have been eradicated in Palau, but seems to have been reintroduced from southeast Asia. Signs in an eastern Micronesian airport in 1988 warned visitors of the danger of dengue spreading from Palau.

Respiratory Diseases

Respiratory infections, which are extremely common in hot humid climates, still constitute a major cause of mortality everywhere in the Pacific region. Upper respiratory infections routinely spread throughout villages or whole island populations soon after the arrival of a ship. Transfer is rapid in the generally crowded conditions where handwashing is far less frequent than personal touching, coughs and sneezes are rarely covered, and flies are plentiful.

Influenza. Influenza epidemics followed quickly upon first contact with Europeans and continued almost annually thereafter. The disease was first reported in Tahiti in 1772, Fiji in 1791-2, Samoa in 1830, the Cook Islands in 1837 (McArthur 1967), Pohnpei before 1841, Yap in 1843, the Marshall Islands in 1859, Pingelap in 1871 (Hezel 1983), Papua New Guinea in 1889 (Allen 1989), and remote Australia before 1890 (Moorehead 1966). The first epidemic in Fiji indirectly brought on a famine because of the depletion of food resources by the excessive number of funerary feasts prompted by the heavy mortality (McArthur 1967).

Adult mortality was high in the early influenza epidemics in each location. Later, given the wide-based population pyramid, the very young began to account for the greater share of mortality, although lessened immune responsiveness at both ends of the age spectrum has made influenza a special threat to the elderly as well. Certain of the subsequent epidemics were particularly severe in the mortality they generated. Among them were those that struck New Zealand in 1838 (Owens 1972), Fiji in 1839, Tahiti in 1843, Samoa in 1837 (McArthur 1967), Pohnpei in the 1840s, Kosrae in 1856-7, Palau in 1872 (Hezel 1983), Vanuatu in 1863 (Howe 1984), Wallis and Futuna in 1870 from Fiji, Polynesian outliers in Melanesia around 1900 (Bayliss-Smith 1975), Caroline Islands in 1877, 1927, and 1937 (Marshall 1975; Nason 1975), Kiribati in 1915,1935, and 1956, Papua New Guinea in 1957 and 1965 from eastern Australia (Warburton 1973), and Kiribati and Tuvalu in the 1960s (Henderson et al. 1971).

The influenza pandemic of 1918-19 swept across most of the Pacific, but spared Papua New Guinea, the Marquesas, and Australia, and some remote islands in every group. Although the highest mortality rate in the world for that epidemic was in Western Samoa (25 percent), neighboring American Samoa escaped altogether by quarantining all ships in its harbor. A single ship from Auckland carried the disease to Fiji, Tonga, and Western Samoa. However, the New Zealand-dependent Cook Islands major port was infected from Tahiti, where mortality was similar to that in Western Samoa. The highest mortality throughout the region was among 15- to 40-year olds and was generally caused by secondary bacterial pneumonia (McArthur 1967; Burnet and White 1972).

Diphtheria and Pertussis. Epidemics of diphtheria and pertussis (whooping cough) have been reported in various parts of the region since colonial times. The first diphtheria outbreaks in Australia occurred at a time when the disease had intensified in England and Europe. The disease appeared in southeast Australia and Tasmania in 1858-9 and in small scattered settlements in the far west in 1864 (Burnet and White 1972). Vanuatu experienced an epidemic in the 1860s (Howe 1984). It has since been rare in isolated aboriginal Australian communities (Moodie 1973) and in Papua New Guinea, although epidemics did occur in the 1950s and 1960s in the highlands of the latter. After the construction of their jet airport in 1965, Easter Islanders experienced a diphtheria epidemic.

Pertussis has caused high mortality in the nineteenth and twentieth centuries among infants and children in the highlands and islands of Papua New Guinea (Vines 1970; Paine 1973; Lindenbaum 1979), Vanuatu (Howe 1984), Australian aborigines (Moore-head, 1966; Moodie 1973), Kiribati, Fiji, Tonga, Western Samoa, Tahiti, Leeward and Cook Islands (McArthur 1967), and New Zealand Maori (Prior 1968).

Pneumonia. Secondary pneumonia usually causes the respiratory infection fatalities in this region. Pneumonia epidemics have occurred following influenza epidemics since first European contact (Mad-docks 1973). Mortality has been highest among the very young, the very old, and those in remote areas (Allen 1989). Pneumonia was rife in the goldfield labor camps in the mountains, perhaps because of the chilly nights with close contact among the workers around smokey fires and the scanty food rations which had to be carried in on workers' backs (Vines

1970; Riley 1973; Schlomowitz 1988). Because pneumonia is a particular problem for everyone in the highlands, a vaccine for the common pneumococci has been tested there recently (Riley 1973). In Papua New Guinea, pneumonia is endemic in rural areas and prevalent among young men who have recently migrated to towns (Hocking 1974). In highland Papua New Guinea domiciliary smoke has also been implicated in the chronic obstructive pulmonary disease (COPD), which is so common there (Vines 1970), although its high prevalence on the coast as well suggests repeated acute infections as a more likely cause (Woolcock, Colman, and Blackburn 1973).

Streptococcal Infections. Sequelae of repeated untreated streptococcal throat infections have also been a problem in many areas of Oceania. Rheumatic carditis is prevalent in Fiji (Gurd 1967), in French Polynesia, where it occurs frequently in children under 5 years of age (Houssiaux, Porter, and Fournie

1972), and among Australian aborigines (Moodie

1973) and New Zealand Maori (Prior 1968). Poststreptococcal glomerulonephritis is one of the most common causes of death among adult Australian part-aborigines in south Australia (Moodie 1973).

Tuberculosis. Tuberculosis, or "wasting sickness" as it was called, was introduced into Fiji in 1791 by a British ship (McArthur 1967). Reports of "consumption" among the Maori living near missionaries and sawyers from England began to increase in the 1820s (Owens 1972). Tuberculosis became common in much of Polynesia and some of Melanesia and aboriginal Australian lands by the mid-1800s, and was a major health problem for Australian aborigines by the turn of the century (Kuykendall 1966; Moorehead 1966; McArthur 1967; Moodie 1973; Bayliss-Smith 1975; Howe 1984). Interisland migration as well as ships from outside spread it widely throughout the Pacific during the nineteenth century. Although present in even remote areas of the New Guinea islands by the early 1900s (Chowning 1989), it reached the highlands only decades later. Travelers from the eastern highlands avoided overnight stays in the nearby lowland valleys because they feared tuberculosis; this custom also protected them from night-biting anophelines (Riley 1983). Tuberculosis was first introduced into certain populous areas of the highlands in 1970, and has occurred only sporadically since (Pust 1983).

The disease remains an important health problem in the modern Pacific, where crowded households and extensive sharing of personal articles facilitate spread, and intercurrent infections decrease resistance. The 1960s campaigns with screening, immunization, and chemotherapy have been at least somewhat successful in most island groups (Henderson et al. 1971).

Scrofula, characterized by tumors, wasting, neck swellings, and spinal curvature, was widespread in Polynesia in the early nineteenth century. A number of authors have equated it with tubercular adrenitis. Said to have been brought to Tahiti by British and Spanish explorers in the eighteenth century, scrofula was carried by Tahitian teachers to the Cook Islands in the 1830s, where it spread throughout the group in a time of famine, causing many deaths over the next 15 to 20 years (McArthur 1967).

Other Infectious Diseases

Leprosy. Leprosy was introduced into the region by Asian workers and immigrants in the nineteenth century, then spread with interisland migration. Although called the "Chinese disease" in Hawaii, the actual circumstances of introduction to those islands are unknown. It was present in the 1830s, and numerous cases were reported in 1863, a few years before the Molokai leper colony was established to isolate the afflicted. Hundreds were sent to Molokai over the years, yet many remained in their own communities. Hawaiian islanders did not fear the disease and therefore resisted this internment (Kuy-kendall 1966). Leprosy appears to have entered New Zealand in the 1850s, perhaps with Asian travelers, but was rare until the 1900s (Montgomerie 1988). Australian aborigines in the northeast acquired the disease from infected Chinese and Mela-nesian laborers in the nineteenth century (Moodie 1973). It was present in New Guinea in 1875 (Mad-docks 1973) and was brought into the northern Cook Islands in 1885 by a native son who had spent several years in Samoa with a leprosy sufferer from Hawaii (McArthur 1967). The disease spread to Easter Island (where it is still greatly feared) from Tahiti, and although widespread in Polynesia in 1900, it still had not reached the Caroline Islands (Kraemer 1908).

After World War II, leprosy also become widespread in Micronesia west of the Marshall Islands (Hetzel 1959), but was brought under control - even in a spot of high incidence — by 1970 (Sloan et al. 1972). In the 1970s, it was still sufficiently prevalent in Polynesia (including outliers), Fiji, and Kiribati, that immigrants to New Zealand from these islands reintroduced the disease every year (Gurd 1967; Leprosy Review 1973). Shared sleeping mats have been suspect in areas of increasing incidence. Leprosy is present throughout Melanesia as well (Gurd 1967; Willis 1970; Leprosy Review 1973; WHO Weekly 1973). In Papua New Guinea, the highest incidence is in the highlands, although it is also prevalent along the New Guinea coast (Vines 1970; Russell 1973). There are endemic foci among the northern Australian aborigines, but it is rare in other aboriginal communities (Moodie 1973). Many cases in rural areas remain undetected, so rates all over the region may actually be much higher. Outpatient treatment has largely replaced the leprosy hospitals built earlier this century (Henderson et al. 1971).

Measles. Measles, although present in much of the Pacific Rim in 1800, did not reach eastern Australia until 1828 and Hawaii until 1848. In the 1850s, it spread throughout Australia, to New Zealand, and into the islands (McArthur 1967; Cliff and Hagget 1985). In 1875, a London Mission Society ship carried measles along the Papuan coast of New Guinea. In the same year, a ship carrying Fijian royalty home from a visit with the governor of Sydney transported the virus to Norfolk Island, the Solomon Islands, and Vanuatu as well. The effect on Fiji was particularly devastating, as over a thousand representatives from most of the individual islands had gathered to greet the ill prince and to celebrate for 2 weeks Fiji as a new Crown Colony before dispersing home. The sudden loss of so many adults in Fiji, Tahiti, and Vanuatu contributed to the heavy mortality, as few remained able to provide food or care (Cliff and Haggett 1985).

Similar epidemics struck Kiribati in 1890 (Lambert 1975), and Tonga and Western Samoa in 1893 (McArthur 1967). Quarantine kept Fiji from all but local port outbreaks until 1903, when measles again swept through the group. The 1911 outbreak was mild on most islands, but severe in those few remote islands that had escaped earlier. Every epidemic thereafter came at shorter intervals, caused fewer deaths, and affected ever younger children only (Cliff and Haggett 1985). The same pattern-sporadic epidemics that become more frequent and less severe - has occurred everywhere in the region with regular outside contact or large populations. Small remote islands still have rare epidemics with variable mortality (McArthur 1967; Van de Kaa 1967; Brown and Gajdusek 1970; Vines 1970; Willis 1970; Henderson et al. 1971; Moodie 1973; Linden-baum 1979; Cliff and Haggett 1985).

Rubella. Rubella epidemics have been recently documented for Guam, remote Micronesian atolls, Western New Guinea, and Papua New Guinea and have been associated with excessive hearing impairment from in utero exposure (Brown and Gajdusek 1970; Stewart 1971; Allen 1989).

Mumps. Mumps was already present in the Cook Islands when it reached Samoa on a ship from California in 1851 (McArthur 1967). The disease subsequently spread over much of the region, although it did not appear in the New Guinea highlands until the 1940s (Lindenbaum 1979).

Scarlet Fever. Scarlet fever caused deaths among foreigners in French Polynesia and the Cook Islands in 1846-7, but remained mild among the islanders (McArthur 1967). Symptoms are similarly mild among Australian aborigines in recent times (Moodie 1973).

Chickenpox. In the twentieth century, chickenpox became more common and is now widespread in the region. High prevalence was reported from numerous island groups, New Guinea, and Australia in the 1930s (Moodie 1973; Allen 1989). In fact, it has been suggested that some of the smallpox reported for Australia and Papua was actually chickenpox (Mad-docks 1973; Moodie 1973).

Smallpox. Smallpox epidemics in the Pacific region resulted primarily from contact with outsiders. The first reported epidemic was in the Spanish colony of Guam in 1688 (Carano and Sanchez 1964). A century later, within a year of the founding of Port Jackson (now Sydney) in 1788, smallpox erupted among the aborigines camped nearby. The immune settlers were relatively unaffected, but large numbers of aborigines died (Moorehead 1966).

Trade ships and whalers brought the disease to many islands: Gambier in 1834, Tahiti in 1841, Pohnpei in the 1840s and in 1854, Hawaii in 1853-4, the Maori, Palau, and Polynesian outliers in Melanesia in midcentury, Papua in 1865, and the New Guinea coast in 1870-90. In many of these cases, sick passengers or crew were put ashore and died on the island, passing the disease to any who helped them. Islanders visiting the port spread the virus to their home communities nearby (McArthur 1967; Kuykendall 1968; Owens 1972; Maddocks 1973; Bayliss-Smith 1975; Nason 1975; Allen 1983, 1989; Hezel 1983).

The labor trade also introduced smallpox from

Asia and South America. In the 1860s, Polynesians returning to their homes after years of involuntary servitude in the mines of Peru contracted smallpox on board the ships (McArthur 1967). The first shipload of plantation workers from India introduced smallpox and cholera to Fiji in 1879. The need to train vaccinators locally led to the construction of the Suva Medical School in 1885 (Lander 1989). Cantonese laborers reintroduced the disease as they slipped undetected into Hawaii in 1881 (Kuykendall 1967). Before 1900, Javanese laborers for the plantations along the New Guinea coast introduced smallpox as they arrived. It spread into the nearby coastal mountains, up the Sepik River and across the channel to New Britain to remote areas not yet contacted by Europeans (Allen 1989; Chowning 1989).

Yaws. Yaws was present in the Pacific region prior to outside contact. Before the eradication campaigns of the mid-twentieth century, yaws was found among Australian aborigines, and in all of Melanesia, western Polynesia, Micronesia, French Polynesia, and Hawaii. Conversely, it was not present in New Zealand, Gambier, Easter, or Pitcairn Islands (Hetzel 1959; Pirie 1971-2; Moodie 1973). It occurred less commonly in particularly dry, cool, or high-altitude areas or in islands settled late.

Yaws was usually acquired by children from regular playmates. After recovery from the debilitating skin lesions, solid immunity to treponeme-caused yaws and to syphilis as well is attained. Incidence of yaws decreased as people washed with soap and covered their bodies with clothes (Pirie 1971-2). After World War II, the disease was virtually eradicated by penicillin injections, although antibodies remained in those who had been infected (Norman-Taylor et al. 1964; Fischman and Mundt 1971; Henderson et al. 1971; Davenport 1975). Some pockets of infection remained after the campaigns in the Marshall Islands (Hetzel 1959) and tropical northern Australia (Moodie 1973).

Hepatitis. Hepatitis B has been highly prevalent in the 1980s in Micronesia and in American Samoa, where public health posters announce "Hep is not hip." The Australia antigen for identifying the virus was isolated in 1967 from the blood of an anemic Australian aborigine who had received numerous transfusions. In the Solomon Islands, the antigen was commonly present in those with no clinical symptoms or predisposing history (Burnet and White 1972).

Hepatitis A is endemic in much of island Oceania and tropical Australia, subclinically infecting most of the indigenous population under age five (Moodie 1973), as might be expected in view of the warm climate and casual hygiene among children.

Poliomyelitis. Poliomyelitis, being epidemiological^ similar to infectious hepatitis in unvaccinated populations, was endemic in tropical Australia and the Solomon Islands before World War II, but provided only rare instances of paralysis (Cross 1971; Moodie 1973). Before the massive vaccination campaigns of the 1960s, most Guamanian under 3 years of age were already immune (Burnet and White 1972). Western and American Samoa experienced an epidemic in 1935 with highest mortality and morbidity among young adults rather than children. New Guinea and Guam had also been "virgin soil" for earlier polio epidemics (Burnet and White 1972). After World War II and before vaccination, epidemics occurred across the South Pacific (Peterson et al. 1966; Cross 1971). Vaccination and quarantine finally limited the spread (Peterson et al. 1966).

Acquired Immunodeficiency Syndrome (AIDS). AIDS has surfaced in various indigenous Pacific population in 1988—9. It is now present among urban-dwelling Australian aborigines, as well as among the people of Papua New Guinea, French Polynesia, Tonga, Marshall Islands, Guam (Karel and Robey 1988), Fiji CPacific Island Monthly 1988), Northern Marianas, American Samoa (but not Western Samoa), and Hawaii (information received at the Hawaii exhibit, Fifth International Conference on AIDS, Montreal). On the other hand, extensive screening in the Solomon Islands and Papua New Guinea found no individuals with the virus (HIV) in 1985-6.

Venereal Diseases

Syphilis and gonorrhea were brought into the Pacific by early explorers and whalers. Because syphilis might have been mistaken for yaws, tropical ulcer, scrofula, leprosy, or gonorrhea, confusion exists about the circumstances of introduction even though early ships' logs did comment on the presence of venereal diseases. In tropical Australia and the wet islands of the southwestern Pacific, where yaws was highly prevalent and promiscuity was not customary, syphilis has been a relative newcomer; in cooler New Zealand and drier or more recently settled islands of Micronesia and eastern Polynesia where yaws was less common and Europeans and island women often mixed more freely, syphilis was re corded soon after regular contact. British and French explorers in 1767-9 gave each other credit for the syphilis in Tahiti reported by Captain James Cook in 1769 and spread elsewhere in French Polynesia by explorers over the next few decades. Cook's surgeon wrote that the ship's crew introduced syphilis accidentally to Tonga in 1777 and knowingly to Hawaii in 1779, although other observers stated that the disease was present earlier in Hawaii (Moorehead 1966; McArthur 1967; Pirie 1971-2; Smith 1975; Stannard 1989). Venereal syphilis was found among the Maori before 1840 and became more prevalent but with milder symptoms by 1855 (Pirie 1971-2; Owens 1972). Pohnpei, Kosrae, the Marshall Islands, and Kiribati were also infected by whalers and traders in the 1840s and 1850s, but a century later the disease there had become almost nonexistent (Hezel 1983). Syphilis was unknown in northern Australia before 1939, but since then has spread among the aborigines around the country (Moodie 1973). Papua New Guinea highlands, where yaws had never existed, experienced an epidemic of syphilis in 1969, after the new highway opened up access. It was first reported in 1960 and has remained largely confined to the highlands (Linden-baum 1979; Lombange 1984).

Gonorrhea, often referred to in the region as "venereal disease," was first noted in 1769 in Polynesia and 1791 in Palau. Whalers, traders, and beachcombers passed gonorrhea back and forth with islanders in the 1830s through 1850s in the Caroline and Marshall islands, French Polynesia, and Hawaii, which were popular ports of call with more relaxed sexual attitudes than in most of western Polynesia or Melanesia (Pirie 1971-2; Hezel 1983). Venereal disease did reach one frequently visited Polynesian outlier by the 1850s, but has never been present on its more remote neighbors (Willis 1970; Bayliss-Smith 1975). The first reports of venereal disease on Papua New Guinea coasts were in 1902-8, but it has since become prevalent throughout the country (Pirie 1971-2; Lombange 1984). Thus with rare exceptions, the disease has become ubiquitous in Oceania, as it has in Australia in the same time period (Moorehead 1966; Moodie 1973).

Food- and Waterborne Diseases Enteric infections flourish in conditions commonly found throughout this region (Marshall and Marshall 1980; Allen 1983; Burton 1983; Reid 1983). They are often fatal in the very young or in those who for any reason quickly become dehydrated in the hot climate. Gastroenteritis is ubiquitous, al though less common in nomadic or low-density populations (Willis 1970; Reid 1983).

Cholera. Discrete epidemics of cholera have occasionally occurred. It was reported in Kiribati in 1841, among the Maori in 1838 and after 1840 (Owens 1972), and carried into Fiji by new South Asian plantation laborers (Lander 1989). Cholera has not been documented for either Papua New Guinea or Australia, even though the easily spread El Tor strain was present in neighboring western New Guinea and Sulawesi in 1962 (Moodie 1973; Riley 1983). Still a threat in modern times, cholera broke out in Kiribati in the late 1970s. An infected crewmember on a Japanese fishing vessel debarked in Truk, causing a major epidemic in 1982-3 which, until recently, devastated the tourist trade.

Diarrhea, Dysentery, and Clostridial Diseases. Epidemics of the "bloody flux," or bacillary dysentery, have plagued Pacific islanders at least since 1792, when a British explorer brought it to Tahiti. Unlike measles, these epidemics did not become more frequent and less severe with repetition in a given population. Severe epidemics of bacillary dysentery were often associated with concurrent civil wars, famines, typhoons, droughts, measles, incarceration on labor vessels, employment on the goldfields in Papua New Guinea, or ship visitations (McArthur 1967; Prior 1968; Bayliss-Smith 1975; Allen 1983; Burton 1983; Howe 1984; Schlomowitz 1988). Two notable epidemics of bacillary dysentery occurred in Papua New Guinea during World War II: one introduced by Japanese in the course of building an airstrip on the north coast using indigenous labor, and one introduced by members of an American military team in the central highlands. Australian soldiers also brought dysentery that they had earlier picked up in North Africa (Allen 1983; Burton 1983). The Marshall Islands have had epidemics of dysentery in recent years soon after imported chicken has been off-loaded and sold in local stores. It is endemic in most groups of aborigines (Moodie 1973). Typhoid fever and amebic dysentery have appeared throughout the islands and Australia as well (Hetzel 1959; Gurd 1967; McArthur 1967; Burnet and White 1972; Moodie 1973).

The third leading cause of death in the Papua New Guinea highlands is enteritis necroticans, known locally as pigbel. Peak incidence of this syndrome of bloody diarrhea, stomach pain, nausea, and vomiting occurs at 4 years of age. Those over 40 years old generally have developed immunity to the causative agent, Clostridium perfringens beta toxin. Feasts with literally heaps of pork occasionally punctuate the usual highland low-protein, largely sweet potato diet. Clostridia enter the slaughtered pork as it sits in the dirt and is handled regularly for about 4 days before the feast. It is ingested with the meat, colonizes the gut, and produces a toxin that should be inactivated by intestinal trypsin. However, protein deprivation or the presence of trypsin inhibitor from sweet potato (or from the ubiquitous Ascaris) prevents the enzyme from doing so. A vaccine for the toxin became available in the 1980s (Lindenbaum 1979; Murrell 1983).

Another clostridial disease, tetanus, occurs widely in the Pacific islands and Australia, even in areas without domestic animals (Gurd 1967; Moodie 1973; Lindenbaum 1979). The disease is not found on Easter Island, however, even though horses, cattle, goats, sheep, Clostridium tetani, and bare feet are common. Immunization as part of prenatal care in Papua New Guinea has reduced mortality from neonatal tetanus, which was once very high in rural areas where umbilical cords were cut with contaminated objects (Townsend 1985).

Helminth-Transmitted Diseases Intestinal-dwelling nematodes have been very common in the Pacific region wherever the soil is moist enough to keep their eggs alive. Generally prevalence of Ascaris and Trichuris is lower on dry atolls (e.g., Marshall and northern Cook islands) or in lowland rainforests (as on the New Guinea coast). However, the southern Cook and Caroline islands rainforests have had very high rates, whereas Ascaris is rare in Vanuatu (Hetzel 1959; Norman-Taylor et al. 1964; Vines 1967, 1970). Ascaris is widely distributed in aboriginal lands in Australia, but is more common in the cooler drier south (Moodie 1973). Enterobius is ubiquitous (Vines 1967).'Hookworms have had a low prevalence in Kiribati and isolated Pitcairn and Easter islands but are plentiful on wet lowlands. Necator has been far the more common parasite, although Ankylostoma has replaced it in Vanuatu. They have been highly prevalent in aboriginal lands in Australia, except in the Central Desert. They spread out from the tropical north with cattleherders. Eradication campaigns in many islands and among the Australian aborigines have had no enduring effect (Hetzel 1959; Norman-Taylor et al. 1964; Vines 1967, 1970; Willis 1970; Moodie 1973).


Other health problems have arisen as well from the close association between humans and various ani mals in this region. The disabling or even fatal dog tapeworm is common among Australian aborigines who keep dogs closeby in their camps (Moodie 1973). Cysticercosis, from pig tapeworm, was first introduced into the densely populated pig-raising highlands of Western New Guinea via a gift of infected pigs from nearby Bali in 1971. Within 4 years it had spread to the border with Papua New Guinea, and within 10 years had become a major cause of morbidity and mortality in that region, which has been a hotbed of rebellion against the alienation of Papuan lands by Indonesian settlers (Hyndman 1988).

Since 1948, epidemics of eosinophilic meningitis generally attributed to ingestion of rat lungworm, Angiostrongylus, have been reported in small areas dotted across the Pacific: New Caledonia, Pohnpei, Cook Islands, Tahiti, and Hawaii. In some of these cases, shellfish eaten raw were the intermediaries (Rosen et al. 1967).

Toxoplasmosis is endemic in much of Oceania and Australia, where cats appear to play a critical role in transmission (Wallace, Marshall, and Marshall 1972; Moodie 1973). Contact through breaks in the skin with water or mud contaminated with the urine of rats, pigs, or cattle has been responsible for leptospiro-sis among Australian aborigines working in sugarcane fields, as swineherds, or as stockmen in tropical northeastern Australia. This infection causes intermittent fever and meningitis (Burnet and White 1972). Bubonic plague persisted for 10 years in seaport rats in southeastern Australia before eradication efforts succeeded (Burnet and White 1972). Scrub typhus mites flourished in grassy clearings away from human villages in Papua New Guinea and northeastern Australia, causing minimal problems for indigenes but becoming the second leading cause of death — after malaria - among the foreign soldiers cutting through the Bush there in World War II (Burnet and White 1972).

Diet-Related Diseases

Anemia. Anemia is widespread among women in Oceania, especially at sea level. The proportion of women having hemoglobin levels below 12 grams-percent is higher than in any other region of the world (Wood and Gans 1981; Royston 1982). Anemia is especially common among children in Vanuatu and among New Zealand Maori (Norman-Taylor et al. 1964; Prior 1968). It has been documented occasionally for Micronesia, less in the western Carolines than in the Marianas or Marshalls (Hetzel 1959). Diet and malabsorption problems are respon sible for the high prevalence of iron-deficiency anemia among Australian aborigines (Moodie 1973).

Protein-calorie deficiency does occur, mostly in poor remote areas of the New Guinea mainland. Diet on the smaller islands, while simple, is usually sufficient (Vines 1970).

Goiter and cretinism have been problems in patches in inland Melanesia, where highland people have had to trade with coastal people for their sea salt. In 1955, colonial patrols worsened the situation in the Papua New Guinea highlands by trading in noniodized salt, which the highlanders preferred to their traditional supply. A campaign in the 1960s to reverse the deficiency with injections of iodized poppyseed oil was successful (Henderson et al. 1971; Lindenbaum 1979).

Diabetes and Obesity. Chronic diseases have increasingly become primary causes of morbidity and mortality in industrialized societies since the 1950s as immunization and chemoprophylaxis have reduced infectious diseases, as sedentary wage employment has become available, and as imported foods constitute an ever-growing share of people's diets. These diseases are distributed unevenly, occurring far less regularly in remote rural areas.

Non-insulin-dependent diabetes mellitus (NIDDM) is unusually prevalent among certain Pacific societies: Australian aborigines (Moodie 1973), New Zealand Maori (Prior 1968), Cook Islanders (Prior 1968), American Samoans (Baker and Crews 1986; Hanna and Baker 1986), Marshall Islanders and I-Kiribati (King et al. 1984), Nauruans (Patel 1984; Taylor and Thoma 1985), Torres Straits islanders (Patel 1984), Fijian women (King et al. 1984), and residents of Papua New Guinea's most acculturated urban but not rural or highland areas (Savige 1982; Patel 1984). The disease is more common among the wealthy (34 percent prevalence in affluent Nauru), the more acculturated, the urban, and perhaps the female. Its meteoric rise in the mortality statistics has paralleled increases in dietary refined carbohydrates and calories and decreases in exercise and dietary fiber.

Obesity even beyond the cultural ideal has also accompanied these changes in all of these areas as well as in the Marquesas and Solomons (Fried-laender and Rhoads 1982; Darlu, Couilliot, and Drupt 1984). Yet similar dietary changes and decreased activity level have not led to obesity or NIDDM on Easter Island. The familial tendency apparent within these populations and the extremely high rates among certain related island groups suggest a partial genetic basis. According to J. M.

Hanna and P. T. Baker (1986), the metabolic ability to gain weight rapidly and hold it may have given a selective advantage for long interisland voyaging with limited space to transport food. Crowding and psychosocial stress in acculturated urban areas may also play a role in the etiology. Compliance with treatment regimes (diet, exercise, daily insulin) in the absence of frank clinical symptoms has been low, especially among men who avoid seeking help unless their problem is evident and severe.

Surveys of blood pressure after World War II indicated that for most Pacific people, adult blood pressures averaged lower than for equivalent age groups in industrialized societies and did not rise with age (Norman-Taylor et al. 1964; Vines 1970; Shaper 1972; Moodie 1973; Gee 1983; Patrick et al. 1983; Ward 1983). However, in recent years hypertension and age-related increases have become much more common in areas where modern wage-earners are concentrated, obesity is obvious, and imported salt intake is high (Prior 1968; Henderson et al. 1971; Moodie 1973; Gee 1983; Patrick et al. 1983; Ward 1983; Taylor and Thoma 1985; Hanna and Baker 1986; Prior 1986). Coronary artery disease is also becoming more common in these same situations (Hanna and Baker 1986).

Chronic Degenerative Neurological Diseases Certain chronic degenerative neurological diseases that have close parallels in the industrialized world have been highly prevalent in very restricted locations in Oceania. Kuru, a subacute spongiform cerebellar encephalopathy caused by an unconventional slow virus, has been present in the Fore area of the eastern highlands of Papua New Guinea since 1920. In the 1950s, it was the most common cause of death in adult women and in children 5 to 16 years old in that area. The unusual age distribution was due to the local practice - extant from 1910 to 1955 - of cannibalism. The dead were consumed by female kin and young children of either sex. The virus entered via cuts in the skin as the flesh and brain were prepared. Two to 20 years later, symptoms appeared: ataxia, tremoring, pain, slurred speech, loss of smooth and voluntary muscle control, and pathological laughter. Death followed within nine months. The number of cases declined progressively after cannibalism was discontinued (Burnet and White 1972; Gajdusek 1977; Lindenbaum 1979).

Since before World War II, the indigenous Cha-morro of the Marianas Islands have had an extremely high incidence of a syndrome with varying combinations of Alzheimer-like dementia, amyotro phic lateral sclerosis, and Parkinsonism. Occasional cases with similar symptoms have also been found among Caroline Islanders, Filipinos, and Caucasians resident in the Marianas. The syndrome has also appeared in Chamorros 30 years after leaving Guam. Until recently, the Chamorro ate great quantities of the false sago plant seeds, which contain a toxin that causes degeneration of the same motor neurons that disappear in amyotrophic lateral sclerosis and Parkinsonism. On the other hand, a genetic susceptibility to the effects of such a toxin in this population has not been ruled out (Mathai 1970; Lewin 1987).

High incidence of an autosomal recessive congenital blindness (tapetoretinal degeneration with cataracts) on a single Carolinian atoll has been attributed to the fact that the island was almost isolated in the 2 centuries following the 1780 typhoon that killed all but nine of the men on the island (Brody et al. 1970).

Ciguatera, a frequently fatal fish poisoning caused by a curare-like toxin present in certain fish throughout the region, has been of grave concern in the Pacific islands where fish is the major protein food. The source of the toxin appears to be algae that grow on submerged World War II equipment or nuclear testing apparatus and are consumed by the fish. It has been reported in French Polynesia, Guam, Marshall Islands, and Hawaii, all of which provide appropriate surfaces for the algal growth (Banner et al. 1963; Henderson et al. 1971; Bagnis 1972).

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