Rinderpest

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Rinderpest

Also known as

Cattle plague, steppe murrain, contagious bovine typhus, rinderpest virus (RPV)

Description

Rinderpest was an acute infectious, highly contagious and often fatal viral disease of cattle and many other species of even-toed ungulates, including buffaloes, large antelope, deer, yaks, giraffes, wildebeests, and warthogs. It was the most important livestock disease from the 5th century on, but has now been eliminated after diligent control efforts around the world. This disease could be 100% fatal in some herds, and rapidly spread.

It was the most lethal plague known in cattle. All wild and domesticated species of the order Artiodactyla (cloven-hoofed mammals) were variably susceptible to rinderpest, although dissemination of the virus largely depended on continual transmission among domesticated cattle, buffalo, and yaks. The virus also infected goats and sheep.

The term Rinderpest is a German word meaning cattle plague. It is thought to have originated in Central Eurasia, and later spread to Europe and Asia, with cattle movement along trade and migration routes. The disease was also reported in the Americas and Australia in lower prevalence.

A cattle plague (which may have been rinderpest) is thought to be one of the 10 plagues of Egypt described in the Hebrew Bible. By around 3,000 BC, a cattle plague had reached Egypt, and rinderpest later spread through the remainder of Africa, following European colonization. In the 4th century, the Roman writer Severus Sanctus Endelechius described rinderpest in his book, On the Deaths of Cattle.

Cattle plagues recurred throughout history, often accompanying wars. They hit Europe especially hard in the 18th century, with three long panzootics (a disease affecting many species of animals, over a broad region), which varied in intensity and duration from region to region, taking place in the periods of 1709–1720, 1742–1760, and 1768–1786.

Rinderpest resulted in extensive famines in Africa and hindered agricultural development in Asia. Efforts to understand the pathogeny of the disease and provide adequate treatment and prevention were the driving force for scientific breakthroughs in the 18th and 19th centuries.

Serious outbreaks of the disease prompted founding of the first veterinary college (École Nationale Vétérinaire), in Lyon, France, in 1762. A major outbreak affected the entire British Isles for three years after 1865.

The disease entered Africa with imported domestic stock in the 1890s and ravaged herds of native ungulates. Around the turn of the century, a plague struck southern Africa. The outbreak in the 1890s killed an estimated 80 to 90% of all cattle in eastern and southern Africa, as well as in the Horn of Africa. A vaccine was developed that helped curb that epizootic, but the loss of animals caused famine which depopulated sub-Saharan Africa.

Common in Africa, the Indian subcontinent, and the Middle East, rinderpest was a major threat to livestock production.

The vast repercussions of the disease led to many eradication efforts. After several decades of success in eradicating rinderpest from Europe, the disease recurred unexpectedly in Belgium in 1920, and renewed efforts to eradicate it resulted in the creation of the World Organization for Animal Health (OIE) in 1924. The goal was to control infectious animal diseases at an international level and this led to establishment of several Veterinary Medicine schools across Europe and Asia.

After creation of the Food and Agriculture Organization (FAO) of the United Nations in 1946, the OIE and FAO signed a cooperation agreement in 1952. Thereafter, the two organizations (FAO and OIE) were major participants in several worldwide campaigns to combat rinderpest.

In 1969, an outbreak originated in Afghanistan, travelling westwards and promoting a mass vaccination plan, which by 197, had eliminated rinderpest in all areas of Asia except for Lebanon and India; both of those countries experienced further occurrences of the disease in the 1980s.

During the 1980s, an outbreak of rinderpest from Sudan spread throughout Africa, killing millions of cattle, as well as wildlife. In response, the Pan-African Rinderpest Campaign was initiated in 1987, using vaccination and surveillance to combat the disease. By the 1990s, nearly all of Africa, with the exception of parts of Sudan and Somalia, was declared free of rinderpest.

In 1994, the Global Rinderpest Eradication Program (GREP) by the Food and Agriculture Organization (FAO) of the United Nations led to effective rinderpest-control programs in affected areas of the world. Targeted date for eradication was 2011. In 2010 a preliminary report by GREP suggested that the disease had been successfully eradicated. Follow-up surveillance during the next year confirmed these findings.

In 2011 the World Organization for Animal Health declared eradication of the disease complete, making rinderpest the second viral disease eradicated from the world (smallpox was the first to be eradicated). The last reported rinderpest outbreak occurred in Kenya in 2001.

In June 2011, the United Nations FAO confirmed the disease was eradicated, making rinderpest the second disease in history to be fully wiped out (outside laboratory stocks), following smallpox. In June 2019 the UK destroyed its stocks of rinderpest virus, held at the Pirbright Institute in Surrey, which were most of the world’s retained samples.

This followed compilation of a digital record of the virus’s genetic code, thus eliminating the need to store samples as a protective resource in case the virus re-emerges. Researchers at that Institute expressed hope that other samples in laboratories around the world will also be destroyed, totally eradicating the virus from the Earth.

Signs

  • Fever
  • Loss of appetite
  • Discharges from eyes and nose
  • Drooling
  • Mouth ulcers
  • Labored breathing
  • Diarrhea
  • Dehydration
  • Abdominal pain
  • Skin eruptions

Cause

Rinderpest was caused by a paramyxovirus (genus Morbillivirus) closely related to the viruses that cause measles in humans and viral distemper in dogs. The measles virus possibly emerged from rinderpest as a zoonotic disease, maybe as early as 600 BC, a period that coincides with the rise of large human settlements. Measles had definitely emerged as a human disease by the 7th century. Scientists think measles virus evolved from the then-widespread rinderpest virus.

Rinderpest in livestock was transmitted by direct or indirect contact. After an incubation period of 3 to 15 days, fever, depression and loss of appetite were the first signs in an infected animal (sometimes with diarrhea that was watery and bloody), followed within a few more days by discharges from eyes and nose, salivation, mouth ulcers and necrotic lesions on the gums and tongue, and a disagreeable, fetid odor.

The hard and soft palates were often affected. The eye and nasal discharges became thick with pus, and the muzzle appeared dry and cracked. As the virus invaded internal organs, the animal exhibited labored breathing, dehydration, diarrhea, often with abdominal pain (and sometimes constipation and straining to pass feces). In many cases skin eruption developed on the back and flanks.

Lateral recumbency (flat on the ground), coma, and death occurred about 6 to 12 days after the first signs appeared. Actual cause of death was dehydration. Convalescence was prolonged in animals that survived, and could be complicated by concurrent infections due to immunosuppression. Morbidity (number of animals in the herd affected) was often 100% and mortality was up to 90% in epidemic areas, but in endemic areas (where the disease was common) morbidity was low and clinical signs were often mild.

Death rates during outbreaks were usually extremely high, approaching 100% in naïve populations with no prior exposure or immunity. Rinderpest was mainly transmitted by direct contact and by drinking contaminated water, and could also be transmitted by air.

Rinderpest virus is shed in nasal and eye secretions and can be transmitted during the incubation period (1–2 days before onset of fever). Transmission required direct or close indirect contact between susceptible animals and sick animals shedding the virus.

The role of fomites (inanimate objects) in transmission was negligible, because the virus was fragile, being inactivated within 12 hours of exposure to atmospheric heat and sunlight.

There was no carrier state, and recovered animals acquired lifelong immunity. In endemic areas, young cattle could become infected after maternal immunity disappeared and before vaccine-induced immunity began.

Prevention

Cell-cultured vaccines were effective in preventing rinderpest. Eradication of the disease in a particular area or region depended on control of the disease in wild animals and elimination of infected domestic animals. Immunization by vaccine combined with quarantine was an effective method of control.

Active immunity to rinderpest was lifelong, whereas maternal immunity lasted 6–11 months. Control in endemic areas was by immunization of all cattle and domestic buffalo more than 1 year old with an attenuated cell culture vaccine.

In these areas, outbreaks were controlled by quarantine and “ring vaccination” (vaccinating all animals in the surrounding areas to create a buffer zone around the outbreak) and sometimes by slaughtering all animals in the area. In epidemics, the disease was best eliminated by imposing quarantine and by slaughtering affected and exposed animals.

Control of animal movements was crucial for control rinderpest; many outbreaks were due to introduction of infected cattle to uninfected herds.

About the Author

EquiMed Staff

EquiMed staff writers team up to provide articles that require periodic updates based on evolving methods of equine healthcare. Compendia articles, core healthcare topics and more are written and updated as a group effort. Our review process includes an important veterinarian review, helping to assure the content is consistent with the latest understanding from a medical professional.

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