1961–1975 cholera pandemic
|1961–1975 Cholera Pandemic|
|Bacteria strain||Vibrio cholerae biotype eltor|
|Location||Asia, Africa, Europe, the Americas (Mostly Worldwide except Oceania)|
|First outbreak||Makassar, South Sulawesi|
The 1961–1975 cholera pandemic (also known as the seventh cholera pandemic) was the seventh major outbreak of cholera and occurred principally from the years 1961 to 1975; the strain involved persists to the present. This pandemic, based on the strain called El Tor, started in Indonesia in 1961 and spread to Bangladesh by 1963. Then it went to India in 1964, followed by the Soviet Union by 1966. In July 1970, there was an outbreak in Odessa and in 1972 there were reports of outbreaks in Baku, but the Soviet Union suppressed this information. It reached Italy in 1973 from North Africa. Japan and the South Pacific saw a few outbreaks by the late 1970s. In 1971, the number of cases reported worldwide was 155,000. In 1991, it reached 570,000. The spread of the disease was helped by modern transportation and mass migrations. Mortality rates, however, dropped markedly as governments began modern curative and preventive measures. The usual mortality rate of 50% dropped to 10% by the 1980s and less than 3% by the 1990s.
In 1991, the strain made a comeback in Latin America. It began in Peru, where it killed roughly 10,000 people. Research has traced the origin of the strain to the seventh cholera pandemic. It was suspected the strain came to Latin America through Asia from contaminated water, but samples from Latin America and samples from Africa were found to be identical.
This rapid transmission of the pathogen around the globe in the 20th century can be attributed to the major hub, the Bay of Bengal, the main place from which the disease spread.
This pandemic can be categorized into two periods. During Period 1 (1961–1969), 24 Asian countries reported 419,968 cholera cases. In Period 2 (1970–1975), 73 countries from Asia, Africa, Europe and the Americas reported 706,261 cases. Cholera is caused by eating food or drinking water that is contaminated with the bacteria V. cholerae. It affects both children and adults, causing severe watery diarrhoea with dehydration.
Cholera is an acute diarrhoeal infection caused by the ingestion of food or water contaminated with the bacterium Vibrio cholerae. Most commonly the contamination of food or water occurs via faecal matter, and the infection is spread through the faecal-oral route. Cholera has also been found to be caused by eating raw shellfish. Symptoms of the disease appear between 12 hours and 5 days of infection, however, only 10% of infected people show severe symptoms of watery diarrhoea, vomiting and leg cramps. Cholera is diagnosed through a stool test or rectal swab and treatment takes the form of an oral rehydration solution (ORS). The ORS utilises equimolar concentrations of sodium and glucose to maximise sodium uptake in the small intestine, and carefully replaces fluid losses. In severe cases, the rapid loss of bodily fluids leads to dehydration and patients are at risk of shock. This requires administration of intravenous fluids and antibiotics. The transmission of cholera is closely linked to inadequate access to clean water and sanitation facilities and hence, at risk areas are slums and poor communities. The spread of cholera from 1961 to 1975 identify factors that played a role in the cholera pandemic. Terrorism, floods, improper sewage disposal and a lack of environmental hygiene were the main causes of the spread.
The history of the 7th pandemic can be traced to the beginning of 1961. The evolution of the classical cholera strain from the first 6 pandemics has been revealed through genetic analysis. The first observation of the new lineage comes from a laboratory in El Tor, Egypt, in 1897 and by this time, the ‘El Tor’ strain differed from its relatives by 30%. It originated in South-Asia then transitioned to its non-pathogenic form in the Middle East in 1900. It was sometime between 1903 and 1908 that the El Tor strain picked up DNA that triggered its ability to cause disease in humans. Hence, it had evolved into the El Tor pandemic strain. Makassar, South Sulawesi was the source of a 1960 outbreak of the El Tor strain, where it gained new genes that likely increased transmissibility. Cholera then spread overseas in 1961, indicating a pandemic strain. Many studies point to Indonesia as the source of the 7th cholera pandemic, however research has indicated that outbreaks in China between 1960 and 1990 were associated with the same sub-lineages. These strains spread globally from the Bay of Bengal on multiple occasions. This classifies China as both a sink and source during the pandemic spread of cholera throughout the 1960s and 1970s. This information that the pandemic spread of cholera may have been augmented by Chinese cases, in addition to China being named as an origin for bordering countries, contrasts with the view that the pandemic began in Indonesia, as many sources relay.
Spread and mortality
The El Tor cholera outbreak was first reported in Java, a seaside community near Kendal which was visited by travellers from Makassar in May 1961. Shortly after, Semarang and Djakarta became infected in June.
The disease was carried into Kuching, Sarawak when boats from Celebes participated in a regatta in Kuching and the first cholera cases appeared on 1 July. This outbreak lasted 2 weeks, infecting 582 persons with 79 deaths (17% mortality). By August, the outbreak had reached Kalimantan and Macau (13 patients and 6 deaths). The first case in Hong Kong appeared on 15 August in a community near Kwangtung, a fishing area. The second case was from a boat-dwelling population on the way from Kwangtung to Hong Kong. Hong Kong had 72 cases with 15 deaths (20.8% mortality).
By February 1, 1962, 4,107 people were infected with cholera, with 897 deaths (21.8% mortality). By September, despite a massive vaccination campaign, cholera had rapidly moved through the Philippines, where the number of infected people reached 15,000 by March 1962, with 2,005 deaths. In the Philippines alone, mortality reached 1,682 in 1962. It was then reintroduced into British Borneo supposedly by an asymptomatic traveller from Jolo Island. Outbreaks subsequently occurred in Cambodia, Thailand, Singapore and India.
In 1963, WHO declared that cholera remained the number-one killer in diseases subject to international quarantine, having been reported in Taiwan, Pakistan, Afghanistan, Iran, Southern Russia, Iraq, Korea, Burma, Cambodia, South Vietnam, Malaysia, Singapore, Nepal, Thailand, Uzbekistan and Hong Kong.
The mid-60s saw cholera infiltrate Southeast Asia, with outbreaks in Chittagong, Bangladesh, Cambodia, Thailand and Malaysia, and India in 1964. The El Tor strain then moved further westward, invading South Asia in 1965, including Pakistan, Nepal, Afghanistan, Iran and part of Uzbekistan SSR. Iran had been free from cholera since 1939 and had reported 2,704 cases by mid-October. When these outbreaks occurred in Iran, the Pasteur Institute of Iran produced 9.5 million cholera vaccines to protect the population of the eastern regions of Iran. In 1966 Iraq then reported its first case.
The cholera strain reached the Middle East and Africa in 1970 and spread rapidly. It is thought that a traveller returning from Asia or the Middle East introduced the disease into Africa. The Arabian Peninsula, Syria and Jordan became infected, followed by Guinea in August 1970. Cholera was first thought to have spread along waterways along the coast and into the interior along the rivers, November 1970 saw the modernised rapid transport of infected individuals. This allowed cholera to extend 1,000 km, when it appeared in Mopti, Mali. Subsequently, large gatherings of people facilitated the outward radiation of cholera and from 1970 to 1971, Sierra Leone, Liberia, Côte d'Ivoire, Ghana, Togo, Benin, Nigeria and southern Cameroon, experienced outbreaks. The west-African outbreak of cholera during 1970–1971 infected more than 400,000 persons. Africa carried a high cholera fatality rate of 16% by 1962. 25 countries were infected by the end of 1971 and between 1972 and 1991, cholera spread throughout much of the remainder of Africa.
An international campaign began in 1970, including the research laboratory in Dacca, the Southeast Asia Treaty Organisation (SEATO), the United Kingdom, Australia and various American agencies. Human volunteers took part in an NIH-sponsored series of tests to develop an effective cholera vaccine. At this time, new outbreaks of cholera were occurring in Egypt, South Korea and the Soviet Union.
The 1964 invention of the ORS was endorsed by WHO in the 1980s. It is estimated to have saved the lives of 40 million individuals infected with cholera. As a result of the achievements of ORS, the past 30 years have seen a cholera response centred around treating individuals who are affected in the short term, and attempting to provide safe water and improved hygiene in the long term.
Furthermore, the cholera pandemic beginning in 1962 is identified through the ‘El Tor’ biotype, which has fostered considerable research into this specific strain of cholera. This pandemic has conveyed the increased resistance of El Tor to the environment. This has heightened the risk of unknowing transmission from asymptomatic carriage in humans, as opposed to the classical biotype that caused the first six cholera pandemics.
The previous opinion of health workers who are against the administration of the cholera vaccine voiced that resources should be directed at rehydration and the provision of safe water and improved sanitation. This is because sanitised environments, appropriately cooking food before consumption, using sterilised water and following general personal hygiene, decrease the spread of cholera. As of yet, cholera control activities have been focused on emergency responses to outbreaks, with limited attention to the underlying causes that can prevent future recurrence. However, the development of new and improved cholera vaccines has allowed this approach to be revised. Further, recent research has advanced our understanding of cholera, its transmission and the immune response. Subsequently, a result of these advances has been the development of experimental cholera vaccines derived from non-living and attenuated live strains. The FDA recently approved a single dose live oral cholera vaccine called Vaxchora for adults aged 18–64 who are travelling to an area of active cholera transmission. Furthermore, a Haiti study shows lasting protection from a two-dose cholera vaccine. During the 2010–2017 cholera outbreak in Haiti, those who received the two doses of the vaccine were 76% less likely to become sick. This protection lasted 4 years.
Further, the clinical severity of this biotype causing pandemic cholera in 1962, has led to modern research into targeted administration of antimicrobials in the initial phase of an outbreak. This was tested in the 1970s with tetracycline and found not useful due to resistance against this antibiotic. However, questions have been raised alluding to newer drugs and whether the administration of these will be more useful than previous attempts.
The ongoing 7th pandemic has affirmed that the severity of cholera is still prevalent in society, an issue recognised by the Global Task Force on Cholera Control (GTFCC). They convened a high-level meeting with officials from cholera-affected countries, donors and technical partners to announce their strategy “The Global Roadmap to 2030”, an initiative to end cholera as a threat to public health by 2030. The three components of the strategy are: “early detection and quick response to contain the outbreaks; a multi-sectorial approach to prevent cholera recurrence, and, coordination of technical support and advocacy, resource mobilisation and partnership at the global level.
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