[8] The measles virus may have emerged from rinderpest as a zoonotic disease around 600 BC, a period that coincides with the rise of large human settlements.

[3] The delayed appearance of these signs of illness account for the steady spread of the disease once a historical outbreak began: an animal infected by rinderpest undergoes an incubation period of 3–15 days.

Later, it was used successfully in several countries, although it was sometimes seen as too costly or drastic, and depended on a strong central authority to be effective (which was notably lacking in the Dutch Republic).

Their experiments confirmed the concepts of those who saw infectious diseases as caused by specific agents, and were the first to recognize maternally derived immunity.

[citation needed] Due to a very severe outbreak at the end of the 1760s, some of the best-known names in Dutch medicine became involved in the struggle against the disease.

[8] In this climate of discouragement and scepticism, Geert Reinders, a farmer in the province of Groningen and a self-taught man, decided to continue the experiments.

In certain areas, such as Aberdeenshire and Norfolk, farmers had banded together to provide mutual assurance by creating a resource pool against the risk of rinderpest.

Because the initial slaughter regime was not backed by compensation, it was the presence of a voluntary mutual assurance scheme that drove down the infection rates by guaranteeing payment for compliance with the government instruction.

[22] Spinage[27] establishes a critical commentary on the theory that in 1888, rinderpest was introduced into Abyssinia (modern Ethiopia) by the invading Italian army, which supposedly brought with them infected cattle from India.

"There is therefore no evidence in contemporary accounts that the rinderpest panzootic was imported from India with infected oxen to provision the Italian landing at Massawa."

Sunseri[21] concentrates on the detailed progress of the epizootic in German Tanzania, endeavouring to show that the disease was known to be present but was not officially recognised as being rinderpest.

He emphasises in particular the failure by the German government to rely on or accept a post mortem in 1892 professionally medically conducted on an affected animal that had been duly diagnosed as having rinderpest.

The governor, Julius von Soden, personally lost his own herd, and this may have led him to secure the post-mortem so as to challenge the official diagnostic silence.

Sunseri's thesis basically explains the German government's failure to recognise the true nature of the disease as permitting ineffective policies.

The local German government was short of cash, without a vet until the late 1890s and surrounded by innumerable serious cattle diseases apart from rinderpest.

The 1885 protectorate status of Tanzania (ruled by the German East Africa Company) had been interrupted by coastal rebellion: when formal German rule began and the military went inland in 1891 to pacify areas, they encountered massive cattle deaths ostensibly due to viral spread from wildlife (one assumes at waterholes).

The herded cattle were normally in transit and the long incubation period and delayed symptoms meant that spreading had taken place before illness was realised.

The 1896 drought resulted in fewer watering places being available, and a greater density of usage including both groups of cattle-owners and the wild animals.

Three river drinking places, mainly used by the Tswana group, recorded over 12,000 head of cattle regularly each; the government was reluctant to embark on wholesale destruction.

The connection between rinderpest and starvation was recognised by the British government as cause for urgent intervention by delivery of food relief.

Fencing, and quarantining coupled with killing of infected cattle, was a policy barely controllable in the expanses of the colony, though it had some success in England.

The policy was scorned and pilloried in the press: plenty of reports came out to the effect that the disease was spread by the quarantine guards and by the vets, all of whom were less than careful about disinfecting themselves.

Though cattle numbers revived subsequently, the consequent human toll was mass starvation in the absence of herding, hunting and farming.

This formed ideal habitat for tsetse fly, which carries sleeping sickness, and is unsuitable for livestock;[30] "hence the European view of an empty unspoiled Africa teeming with game".

[32] In 1868, there was a serious outbreak of rinderpest in India, which was investigated by Colonel James Hallen of the Indian Cattle Plague Commission leading to the publication of his survey in 1871.

In India, some farmers were reported as not hostile to tigers because of the consideration that their attacks on diseased or weaker animals reduced the risk of rinderpest.

[38] In 1917–18, William Hutchins Boynton (1881–1959), the chief veterinary pathologist with the Philippine Bureau of Agriculture, developed an early vaccine for rinderpest, based on treated animal organ extracts.

[44] Worldwide, the Global Rinderpest Eradication Programme was initiated in 1994, supported by the Food and Agriculture Organization, the OIE, and the International Atomic Energy Agency.

The resolution also called on the world community to follow up by ensuring that samples of rinderpest viruses and vaccines be kept under safe laboratory conditions and that rigorous standards for disease surveillance and reporting be applied.

[51] In 2015, FAO launched a campaign calling for the destruction or sequestering of the remaining stocks of rinderpest virus in laboratories in 24 countries, citing risks of inadvertent or malicious release.