Third Pandemic is the designation of a major bubonic plague pandemic that began in Yunnan province in China in 1855. This episode of bubonic plague spread to all inhabited continents, and ultimately more than 12 million people in India and China alone, with 10 million people killed in India alone. According to the World Health Organization, the pandemic was considered active until 1959, when worldwide casualties dropped to 200 per year.
The name refers to this pandemic being the third major bubonic plague outbreak known to western sources. The first was the Plague of Justinian, which ravaged the Byzantine Empire and surrounding areas from 541 to 542. The second was the Black Death, which killed at least one third of Europe's population in a series of expanding waves of infection from 1346 to 1353.
Casualty patterns indicate that waves of this late-19th-century/early-20th-century pandemic may have been from two different sources. The first was primarily bubonic and was carried around the world through ocean-going trade, through transporting infected persons, rats, and cargoes harboring fleas. The second, more virulent strain, was primarily pneumonic in character with a strong person-to-person contagion. This strain was largely confined to Asia, in particular Manchuria and Mongolia.
The bubonic plague was endemic in populations of infected ground rodents in central Asia, and was a known cause of death among migrant and established human populations in that region for centuries; however, an influx of new people due to political conflicts and global trade led to the distribution of this disease throughout the world.
The initial outbreak occurred in Yunnan Province in south-western China in the 1850s. The disease was stable within the province, but was spread due to the Panthay Rebellion. The rebellion displaced local tribes, and also changed animal harvesting practices, leading to greater contact with infected animals. In addition, the rebellion meant that refugees from the conflict moved south, into regions of China with larger populations. The plague went with them, producing an increasing number of casualties. In the city of Canton, beginning in March 1894, the disease killed 60,000 people in a few weeks. Daily water-traffic with the nearby city of Hong Kong rapidly spread the plague. Within two months, after 100,000 deaths, the death rates dropped below epidemic rates, although the disease continued to be endemic in Hong Kong until 1929.
Plague came to British India in 1896, most likely from Hong Kong where the epidemic had been festering since 1894. Over the next thirty years, the country would lose 12.5 million people to the disease. Almost all cases were bubonic, with only a very small percentage changing to pneumonic plague. (Orent, p. 185) The disease was initially seen in port cities, beginning with Bombay (now Mumbai), but later emerged in Pune, Kolkata, and Karachi (now in Pakistan). By 1899, the outbreak spread to smaller communities and rural areas in many regions of India. Overall, the impact of plague epidemics was greatest in western and northern India—in the provinces then designated as Bombay, Punjab, and the United Provinces—while eastern and southern India were not as badly affected.
The colonial government's measures to control the disease included quarantine, isolation camps, travel restrictions and the exclusion of India's traditional medical practices. Restrictions on the populations of the coastal cities were established by Special Plague Committees with overreaching powers, and enforced by the British military. Indians found these measures culturally intrusive and, in general, repressive and tyrannical. Government strategies of plague control underwent significant changes during 1898–1899. By that time, it was apparent that the use of force in enforcing plague regulations was proving counter-productive and, now that the plague had spread to rural areas, enforcement in larger geographic areas would be impossible. At this time, British health officials began to press for widespread vaccination using Waldemar Haffkine’s plague vaccine, although the government stressed that inoculation was not compulsory. British authorities also authorized the inclusion of practitioners of indigenous systems of medicine into plague prevention programs.
Repressive government actions to control the plague lead the Pune nationalists to criticise the government publicly. On 22 June 1897, the Chapekar brothers, young Pune Hindus, shot and killed Walter Charles Rand, an Indian Civil Services officer acting as Pune Special Plague Committee chairman, and his military escort, Lieutenant Ayerst. The action of the Chapekars was seen as terrorism. The government also found the nationalist press guilty of incitement. Independence activist Bal Gangadhar Tilak was charged with sedition for his writings as editor of the Kesari newspaper. He was sentenced to eighteen months rigorous imprisonment.
Public reaction to the health measures enacted by the British Indian state ultimately revealed the political constraints of medical intervention in the country. These experiences were formative in the development of India's modern public health services.
The network of global shipping ensured the widespread distribution of the disease over the next few decades. Recorded outbreaks include:
Each of these areas, as well as Great Britain, France, and other areas of Europe, continued to experience plague outbreaks and casualties until the 1950s. The last significant outbreak of plague associated with the pandemic occurred in Peru and Argentina in 1945.
Researchers working in Asia during the "Third Pandemic" identified plague vectors and the plague bacillus. In 1894, in Hong Kong, Swiss-born French bacteriologist Alexandre Yersin isolated the responsible bacterium (Yersinia pestis) and determined the common mode of transmission. Japanese physician and researcher Kitasato Shibasaburō initially misidentified the bacterium. In 1898, French researcher Paul-Louis Simond demonstrated the role of fleas as a vector.
The disease is caused by a bacterium usually transmitted by the bite of fleas from an infected host, often a black rat. The bacteria are transferred from the blood of infected rats to the rat flea (Xenopsylla cheopsis). The bacillus multiplies in the stomach of the flea, blocking it. When the flea next bites a mammal, the consumed blood is regurgitated along with the bacillus into the bloodstream of the bitten animal. Any serious outbreak of plague in humans is preceded by an outbreak in the rodent population. During the outbreak, infected fleas that have lost their normal rodent hosts seek other sources of blood. The bacterium that causes this disease, Yersinia pestis, was named after Yersin. His discoveries led in time to modern treatment methods, including insecticides, the use of antibiotics and eventually plague vaccines.
The British colonial government in India pressed medical researcher Waldemar Haffkine to develop a plague vaccine. After three months of persistent work with a limited staff, a form for human trials was ready. On January 10, 1897 Haffkine tested it on himself. After the initial test was reported to the authorities, volunteers at the Byculla jail were used in a control test, all inoculated prisoners survived the epidemics, while seven inmates of the control group died. By the turn of the century, the number of inoculees in India alone reached four million. Haffkine was appointed the Director of the Plague Laboratory (now called Haffkine Institute) in Bombay.