Rinderpest virus is a morbillivirus (paramyxovirus family), 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 by the mid-20th century had affected large parts of Asia with Russia, China and Korea. From there, the rinderpest virus spread to Europe in the 18th and 19th centuries. Through import controls, slaughter and strict quarantine regulations, the disease was temporarily eradicated in Europe. However, in the 20th century, a re-entry into Europe occurred through an importation of infected animals. The last significant outbreak of rinderpest in Europe occurred 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 port. The same transport of infected cattle also led to the first outbreak of rinderpest in South America. Rinderpest was also introduced into Africa in the late 19th century, with devastating consequences for livestock and wildlife there. The last outbreak of rinderpest worldwide occurred in Kenya in 2001.
Walter Plowright developed a live attenuated rinderpest vaccine in 1960, produced in cell culture on cattle kidney cells, by serial passages of an original virulent isolate. This vaccine was the first to produce no disease symptoms in vaccinated animals, making it completely safe for all cattle, regardless of age, breed, or sex. The vaccine protection also lasted a lifetime. This vaccine, or the thermostable variant (developed in the 1980s), was instrumental in eradicating rinderpest. In endemic areas, cattle and buffalo were vaccinated and additional measures such as culling were implemented to prevent the spread of rinderpest.
High viral loads are found in the nasal and ocular secretions of infected animals. These are found during the incubation period, one to two days before the onset of fever. Transmission requires direct contact or close proximity between a susceptible and a diseased animal. The role of contaminated surfaces as a source of infection is negligible because the virus is very unstable and is completely inactivated by light and heat after only 12 hours. Animals that survive infection with rinderpest develop lifelong immunity. In addition, there is no "carrier state," meaning that diseased animals are virus-free after complete recovery and are not a source of new infections. There is also only one serotype, which facilitated the development of an effective vaccine.
The classical course of rinderpest infection can be divided into 5 phases. After a short incubation period of 3 to 5 days, the prodromal phase occurs, which is characterized by high fever. This is followed by the mucosal phase, in which lesions of the oral mucosa occur and there is purulent nasal and ocular secretions. Affected animals show a decreased general condition and suffer from loss of appetite. Post-mortem examinations show that necrotic lesions of the digestive system occur. Next comes the diarrheic phase, which is accompanied by severe, bloody diarrhea. In this phase the animals are severely exhausted, weak, dehydrated, and die. In nonfatal cases, the fifth phase follows, during which the animals recover. This process may take several weeks. During this convalescent phase, abortions may occur in pregnant animals. 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 conjunctival and corneal inflammation was observed. In weakly virulent strains of rinderpest virus, the incubation period can be as short as 15 days. Also, clinical disease may be much weaker or absent. Due to the suppression of the immune system by infection with morbilliviruses, secondary bacterial or parasitic infections often occur, which often strongly influence the course of the disease.