Rinderpest has been considered eradicated worldwide since 2011. It is a viral disease of cloven-hoofed animals and mainly affects cattle and buffalo. The typical course of the disease is an acute febrile illness with a very high mortality rate, depending on the virus strain. Small ruminants such as sheep and goats are also susceptible to the virus, but show only mild symptoms. However, they can transmit the virus to cattle.

Rinderpest was declared eradicated worldwide in 2011. The last outbreak occurred in Kenya in 2001.

Cattle and buffalo, various wild ruminant species (giraffes, yaks, antelopes, wildebeest, etc.), sheep and goats, pigs

Direct contact with body fluids from infected animals or over very short distances via aerosols, but also indirectly via contaminated water

Maximum 21 days

Fever, ocular and nasal discharge, erosions of all mucous membranes from oral cavity to anus, diarrhea, dehydration. Death after 10 to 12 days. Cattle, water buffalo, and yaks are most severely affected. In these species, mortality can reach 80 to 90%.

There is no therapy

A vaccine developed in 1960 was instrumental in eradicating rinderpest

Rinderpest has been considered eradicated worldwide since 2011

Rinderpest virus (RPV) is a morbillivirus (family of paramyxoviruses) with a single-stranded RNA genome with negative polarity. Morbilliviruses include important animal and human pathogenic viruses such as peste des petits ruminants virus (PPRV), canine distemper virus (CDV) and measles virus (MV).

Rinderpest probably originated in Asia and until the middle of the 20th century large parts of Asia, including Russia, China and Korea, were affected. From there, the rinderpest virus spread to Europe in the 18th and 19th centuries. Thanks to import controls, slaughtering and strict quarantine regulations, the disease was temporarily eradicated in Europe. In the 20th century, however, it was reintroduced to Europe through the import of infected animals. The last significant outbreak of rinderpest in Europe took place in Belgium in 1920, caused by an infected cow that was shipped from India to Brazil and came into contact with domestic cattle at the harbour. The same transport of infected cattle also led to the first outbreak of rinderpest in South America. Rinderpest was also introduced to Africa at the end of the 19th century, with devastating consequences for the livestock and wild animals there. The last outbreak of rinderpest worldwide occurred in Kenya in 2001.

High viral loads are found in the nasal and ocular secretions of infected animals. These can already be found during the incubation period, i.e. one to two days before the onset of fever. Transmission requires direct contact or close proximity between a susceptible and a sick animal. The role of contaminated surfaces as a source of infection is negligible, as the virus is very unstable and is completely inactivated by light and heat after just 12 hours. Animals that survive an infection with rinderpest develop lifelong immunity. In addition, there is no "carrier state", i.e. infected animals are virus-free after complete recovery and are not a source of new infections. There is only one serotype, which facilitated the development of an efficient vaccine.

Walter Plowright developed a live attenuated vaccine against rinderpest in 1960, which was produced in cell culture on bovine kidney cells by serially passaging an original virulent isolate. This vaccine was the first to produce no disease symptoms in the vaccinated animals and was therefore completely safe for all cattle, regardless of age, breed or sex. The vaccine also provided lifelong protection. This vaccine, or the thermostable variant (developed in the 1980s), contributed significantly to the eradication of rinderpest. In endemic areas, cattle and buffalo were vaccinated and additional measures, such as culling, were implemented to prevent the spread of rinderpest.

Symptoms

The classic course of rinderpest infection can be divided into 5 phases. After a short incubation period of 3 to 5 days, there is the prodromal phase, which is characterised by high fever. This is followed by the mucosal phase, in which lesions appear in the oral mucosa and purulent nasal and ocular secretions occur. The affected animals show a reduced general condition and suffer from loss of appetite. Post-mortem examinations show that necrotic lesions of the digestive system occur. Next comes the diarrhoeic phase, which is accompanied by severe, bloody diarrhoea. In this phase, the animals are severely exhausted, weak, dehydrated and die. In non-fatal cases, the fifth phase follows, in which the animals recover. This process can take several weeks. During this convalescence phase, pregnant animals may abort. In some cases, skin lesions or blindness occur due to severe eye infections. The latter was observed in an outbreak in kudus in Kenya, where severe inflammation of the conjunctiva and cornea was observed. With low virulent strains of rinderpest virus, the incubation period can be up to 15 days. The clinical disease can also be much less severe or absent altogether. Due to the suppression of the immune system caused by infection with morbilliviruses, secondary bacterial or parasitic infections often occur, which often have a strong influence on the course of the disease.

Surveillance and exclusion diagnostics in the post-extinction period are primarily based on molecular biological methods such as RT-PCR. Suitable sample materials include spleen, tonsils, lymph nodes, blood, ocular and nasal secretions from symptomatic animals.

Due to strict transport restrictions of RPV-suspicious or -positive materials, RPV clarification is performed exclusively in laboratories designated by the FAO/WOAH.