Lumpy Skin Disease: Introduction, History, Geographic distribution Epidemiology, Causative Agent, Susceptible Hosts, Transmission, Treatment, Control, and prevention
The manifestation of skin nodules is a defining feature of the vector-borne pox illness Lumpy skin disease, which affects domestic cattle and Asian water buffalo. Infectious over much of Africa and the Middle East, the disease has recently migrated to the Balkans, the Caucasus, and the southern Russian Federation. It is also endemic to those regions. LSD outbreaks result in significant economic losses for the afflicted nations, but poor, small-scale, and backyard farmers are the hardest hurt. This is true even if all industry participants in the cattle business experience financial losses. The illness has a significant negative influence on milk production, animal body health, and cattle productivity. Abortion, infertility, and harm to hide are all consequences. Direct losses are increased by full or partial stamping-out charges. Restrictions on livestock commerce and transportation cause indirect costs.
Transmission can also happen by direct contact, contaminated feed or water consumption, spontaneous mating, or artificial insemination in addition to vectors. The best method for controlling the disease’s spread is widespread vaccination. There are effective LSD vaccines, and the sooner they are utilized, the less severe an outbreak’s expected economic effects will be.
Lumpy skin disease (LSD) is an extinct viral illness that causes significant economic losses as a result of chronic debility, decreased milk production, stunted growth, infertility, abortion, and occasionally death of affected animals. Additionally, hides may sustain serious and long-lasting harm, lowering their market value. Breeds with fine skin, such as Holstein Friesian (HF) and Jersey breeds, are more prone to LSD infection. The illness also impedes the export of cattle and cattle products from LSD-endemic nations. Initially, LSD was only seen in sub-Saharan African nations, though there have been unverified reports of the disease in Oman and Kuwaiti cattle. LSD outbreaks have been reported throughout the Middle East since 2000, and the disease may eventually become endemic, if only in some areas of the region. LSD incursion was first noted in Turkey and Iraq in 2013, indicating that there is a chance that the disease will continue to expand to the European Union, the Caucasus, and Asia. It is currently commonly accepted that blood-feeding insects like mosquitoes and stable flies mechanically spread LSD. This is corroborated by prior findings that linked most outbreaks to regions with a lot of biting flies, namely those along water courses and during the rainy season.
In 1929, Zambia published the first description of the LSD clinical condition. At first, either poisoning or an allergy to insect bites was assumed to be the cause. Between 1943 and 1945, there are also more occurrences in the Republic of South Africa, Botswana (Bechuanaland), and Zimbabwe (Southern Rhodesia). About 8 million cattle were infected by a panzootic illness in South Africa until 1949, which resulted in significant economic losses.
LSD was initially discovered and identified in East Africa (Kenya) in 1957, Sudan in 1972, and West Africa in 1974. Between 1981 and 1986, outbreaks of epizootic LSD were documented in Tanzania, Kenya, Zimbabwe, Somalia, and Cameroon, with fatality rates of 20% in infected cattle. Between 1929 and 1986, the illness was confined to a few nations in sub-Saharan Africa.
Kuwait was one of the Asian nations that reported using LSD in 1986. Later, other nations including the United Arab Emirates, the Arab Republic of Yemen, and the Democratic People’s Republic of Yemen verified or suspected several LSD instances. Similar to this, it is believed that the capripox outbreak in Israel in 1989 was brought about by infected Stomoxys calcitrans being transported on the wind from Ismailiya in Egypt. 1992 saw the discovery of LSD virus infection in cattle in Saudi Arabia. Additionally, LSD infection was recorded in Egypt in 2006 as a result of the importation of infected cattle from the African Horn countries, and despite a comprehensive immunization campaign, the disease spreads unexpectedly quickly throughout the entire nation. The LSD virus may have already been circulating in other Middle Eastern nations, according to Israel’s officials, who theorized after the drug was once more reported in Israel that year. Since 1990, there have been reports of LSD epidemics in the Middle East. The World Organization for Animal Health (OIE) reports that LSD has been discovered in Kuwait (1991), Lebanon (1993), Yemen (1995), United Arab Emirates (2000), Bahrain (2003), Israel (2006), and Oman (2010).
LSD epidemics typically develop in waves that are spaced out over several years. It is unknown whether the virus has a particular reservoir, how it survives between outbreaks, or where it does so. Although outbreaks are often seasonal, they can happen at any time since no season is entirely free of vectors in many affected countries. Large-scale LSD outbreaks are typically caused by the presence of an increasing number of naive (i.e., non-immune) animals, an abundance of active blood-feeding vectors, and unrestrained animal movement. The main instance is frequently connected to the introduction of new animals into a herd or close to one. Mortality rates are typically around 10%, and morbidity ranges from 2 to 45 percent. The host’s susceptibility is influenced by immunological function, age, and breed. In general, European cow breeds with strong milk production are more vulnerable than native African and Asian animals. Typically, cows with high milk production suffer the most. Experimentally and in the field, it is common to find viraemic, asymptomatic cattle among the infected animals. Therefore, it is crucial to take into account the potential presence of infected animals in an affected herd even if they are not exhibiting any outward clinical symptoms, as these animals are capable of propagating the virus via blood-feeding vectors. A significant danger of spread arises from the transportation of unvaccinated or immune-deficient animals from affected areas.
Except for Algeria, Morocco, Tunisia, and Libya, endemic and widespread lumpy skin condition affects all of Africa. LSD has spread across the Middle East since 2013 (Israel, the Palestinian Autonomous Territories, Jordan, Lebanon, Kuwait, Saudi Arabia, Iraq, Iran, Oman, Yemen, United Arab Emirates, and Bahrain). LSD also reached Turkey in 2013, where it is presently endemic. Azerbaijan (2014), Armenia (2015), Kazakhstan (2015), the southern Russian Federation (Dagestan, Chechnya, Krasnodar Kray, and Kalmykia), and Georgia all saw outbreaks after that (2016). The northern regions of Cyprus, Greece (2015), Bulgaria, the Former Yugoslav Republic of Macedonia, Serbia, Montenegro, Albania, and Kosovo have all seen an increase in LSD since 2014. (2016). LSD is now more likely to enter Central Asia, Western Europe, and Central-Eastern Europe.
The lumpy skin disease virus (LSDV), a member of the genus Capripoxvirus (CaPV) under the family Poxviridae, is the reason behind lumpy skin disease. The sheep pox virus (SPPV) and goat pox virus (GTPV), are closely related but phylogenetically distinct, and the lumpy skin disease virus shares the same genus. LSD, SPP, and GTP viruses have serological cross-reactions, thus there is only one serological type of LSDV. The huge, double-stranded DNA virus has very little genetic diversity and is highly stable. Therefore, unlike other TADs like foot-and-mouth disease, the farm-to-farm spread of LSDV cannot be tracked by sequencing the virus isolates (FMD).
Asian water buffalo (Bubalus bubalis) and cattle are both naturally infected by lumpy skin disease, however, the morbidity rate in the latter is substantially lower (1.6% vs. 30.8%). (El-Nahas et al., 2011). In sheep and goats, some LSDV strains can reproduce. Despite the prevalence of mixed herds of cattle, sheep, and goats, there is no epidemiological proof to date that small ruminants serve as a reservoir for LSDV. Following experimental infection in giraffes and impalas (Aepyceros melampus), clinical indications of LSD have been seen (Giraffa camelopardalis). Additionally, reports of the condition in springboks and Arabian oryx (Oryx leucoryx) have been made (Antidorcas marsupialis). It is unknown whether wild ruminants are susceptible to LSD or whether they may play a part in its epidemiology. Human beings are not affected by lumpy skin condition.
The first case of LSD is frequently linked to the transfer of cattle, whether authorized or unauthorized, between areas, or even nations. In reality, the virus might be able to cross large distances by cow migrations. Short-distance leaps are caused by a large number of local blood-feeding insect vectors eating on cattle and switching hosts often between feeds, which is equivalent to how far insects can fly (typically about 50 km). Although there is no proof that the virus replicates in vectors, it cannot be completely ruled out. According to ecosystems and geographic locations, the main vector may change. The ability to transfer the LSDV has been shown by the common stable fly (Stomoxys calcitrans), the Aedes aegypti mosquito, and various Rhipicephalus and Amblyomma spp. African tick species. The possibility of viral transmission from contaminated carcasses to ignorant live animals through insects has not been thoroughly investigated. Direct contact is thought to be ineffectual as an infection source, but it could happen. Animals with the virus may only experience viraemia for a few days, but in extreme situations, it may continue for up to two weeks. Animals with the contagious LSDV virus excrete it in their saliva, nasal discharges, and ocular discharges when they have lesions on their skin, mucous membranes in their mouths, and nasal cavities, and this can contaminate communal feeding and drinking areas. Up to 18 days after infection, infectious LSDV has been discovered in saliva and nasal discharge.
The virus remains in vectors, the environment, or both, according to field experience, as it takes naive cattle about a week or two to get infected when they are transferred to LSDV-infected holdings after they have been eradicated. Natural mating or artificial insemination may expose females to the virus since it lingers in the semen of infected bulls. It is known that infected pregnant cows give birth to calves with skin lesions. Suckling calves may contract the virus from skin sores in the teats or from milk that has been contaminated with it.
Clinical symptoms of lumpy skin disease and autopsy results
The incubation period lasts between four and seven days in experimentally infected animals, although it can last up to five weeks in spontaneously infected ones. Clinical indicators comprise:
1. Lachrymation and nasal discharge are typically the first symptoms seen.
2. The prefemoral and subscapular lymph nodes expand and become easily palpable.
3. A high fever (greater than 40.50C) may last for around a week.
4. Sharp decline in milk production.
5. The emergence of highly distinctive, nodular cutaneous lesions measuring 10 to 50 mm in diameter
6. Lesions can range in number from a few in moderate cases to several lesions in animals with severe infection.
7. Skin on the head, neck, perineum, genitalia, udder, and limbs are preferred places.
8. Deep nodules affect all skin layers, subcutaneous tissue, and occasionally even underlying muscles.
9. Necrotic plaques in the oral and nasal mucous membranes result in purulent or mucopurulent nasal discharge and excessive salivation, both of which contain high levels of virus.
10. Usually, the lesion’s centre ulcerates, and then a scab develops on top.
11. Nodules on the skin could last for several months.
12. The cornea of one or both eyes can occasionally develop painful ulcerative lesions that, in the worst circumstances, can result in blindness.
13. Skin lesions around joints and on the legs can cause lameness and deep subcutaneous infections that are worsened by secondary bacterial infections.
14. Common side effects include mastitis and pneumonia brought on by the virus itself or subsequent bacterial infections.
15. Subclinical Infections are frequent in the field. When an animal is transported to a butcher with several skin lesions, subcutaneous lesions are evident when the animal is skinned. Pox lesions can be seen on nearly every internal organ’s surface and across the whole digestive and respiratory tracts in a postmortem examination.
There is currently no known antiviral treatment specifically for LSD infection. Animals that are sick should be taken out of the herd and given supportive care, including antibiotics, anti-inflammatory medications, and vitamin injections. These treatments typically increase the likelihood of secondary bacterial infections, inflammation, and fever, which increases the animal’s appetite. Since mortality from LSD infection is often less than 3%, animals will frequently recover. If a subsequent bacterial infection occurs, full healing could take up to 6 months.
Control and Prevention
The disease is most likely spread by biting flies and a few species of ticks, and these vectors are difficult to quarantine and regulate movement against. Control in endemic areas must therefore be limited to immunoprophylaxis. LSD vaccination has been done in two different ways. The vaccine virus is now grown in cell culture, but the Neethling strain of LSD was attenuated in South Africa by 20 passes on the chorio-allantoic membranes of hens’ eggs.
In Kenya, cattle receive strong protection against LSD via vaccination made from sheep or goat pox viruses. Because the vaccine could otherwise serve as a source of infection for the susceptible sheep and goat populations, this vaccine has the drawback that it can only be used in nations where sheep pox or goat pox is endemic. To establish an appropriate defense against LSD, susceptible adult cattle should receive a vaccination every year. At the site of inoculation, about 50% of cattle experience swelling that is 10–20 mm in diameter; in dairy cows, this swelling may be accompanied by a brief decrease in milk production. Within a few weeks, the swelling goes away. To avoid interference from the maternal antibody, calves under 6 months old whose moms were either naturally infected or inoculated shouldn’t receive the vaccine. To stop epidemics, calves from sensitive cows should be immunized because they are more susceptible.