In 1909, a pathologist named Peyton Rose began working at the Rockefeller Institute in New York City. One day, a woman brought in a chicken of plmutrock striped with a large tumor. The tumor turned out to be a spinal cell sarcoma. Rose transplanted her to other birds and spent four generations. But she only ingested clean blood hens from the same small line of blood. The chickens of the same breed from the market, mites, pigeons and guinea pigeons were insensitive. A few months later, the tumor became much easier to transmit. Then Raus ran the tumor extract through a filter too thin for chicken cells and bacteria. The filtration was caused by other birds to sarcoma. In 1911, he published the results in the Journal of Experimental Medicine. It was the first clear demonstration that a malignant tumor could cause infection. The agent later called the sarcoma virus Raus. At first, the discovery did not give rise to much interest. A solid tumor was not considered a suitable model for mammalian cancer. Viruses were then associated with acute diseases, which are rapidly emerging in most of the infected. With the outbreak of World War I, Raus abandoned bird tumors, engaged in blood transfusion and helped build the first blood banks in the United States. He won the Nobel Prize in 1966, 55 years later. For 2011, it was the longest "incubation period" in 110 years of history for a physiology or medicine award. The Raus virus brought two more Nobel Prizes: in 1975, for opening a reverse transcript, and in 1989, for discovering the cellular origin of retrovirus oncogenes by example of src gene. The discovery of Raus had a predecessor. In 1908, Danes Ellerman and Bang described erythropylecosis in chickens, which was also transmitted by leachate. It was the first bird leukemia virus. But the malign nature of leukemia was not recognized at that time, and no such resonation as the work of Raus was discovered.
After the Civil War in the United States, Texas cattle went north. The journeys to the cattle towns of the Midwest were hundreds of miles away. The Longhorns themselves remained healthy. And the local livestock who shared their pastures with them soon became sick. The mortality rate among the northern livestock was up to 90 per cent. In 1866, the pastoralists Kansas and Missouri protested against the passage of Texas herds. The following year, the lawmakers of these states closed down parts of the districts for Texas cattle. In August 1868, cattlecars with cattle suffering from Texas fever arrived in New Jersey's livestockyards. More than half of the animals died on their way. The mystery was solved by scientists from the U.S. Department of Agriculture's Livestock Office, including Teobald Smith and Frederick Kilborn. In 1893, their bulletin on the nature, causes and prevention of Texas fever was published. It was the mite that carried it. In the report, the authors recalled that veterinarians who had not seen disease doubted early observations and some called them "roman in pathology". Texas fever is also called babiasiasia. It's called Babesia bovis and B. Bigemina, carry the Ripicephalus annulatus and R mites. microplus. The claw-babesia system was one of the first vector-borne diseases described in detail. The idea came out of this: to destroy the transmitter, and the disease would cease to spread. On July 1, 1906, the Bureau launched a mites elimination campaign involving 15 states. By that time, losses had been estimated at over $130 million per year. The territories were kept quarantined, cattle were driven through the baths at times, and peeled areas were protected from re-suspension. By 1943, the mites had been eliminated in most parts of the country. In Florida, it took another 17 years, including because the mites used white-tailed reindeer as backup owners. In the south of Texas, a permanent quarantine zone remained along the border with Mexico. For her protection, the Ministry has horse inspectors, "tic-riders." They catch stray cattle, examine them on mites and process them.
In 1999, the Western Nile virus was first detected in the western hemisphere. The first signs were dead ravens in New York City and the surrounding area, and the death of exhibition birds at the zoo. At the same time, encephalitis was registered in humans and first diagnosed as St. Louis'encephalitis. A real agent of human and animal disease was discovered when the virus was isolated from dead birds. In the autumn of 1999, veterinarian doctors in Long Island noticed an unusual group of neurological diseases in horses. The lab confirmed 20 cases: 19 horses and one pony. The first animal became ill on August 26, the last on October 23. The disease began acutely with an attack on the hind limbs, marked by a muscle tremor, and a part of animals'inability to rise. Four animals fell or were put to sleep, and 16 recovered completely. 20 out of 69 horses with no symptoms standing next to the sick found antibodies for the virus. In 2000, 23 cases were confirmed in the state of New York. Only 32% of sick horses had fever. They were compared to horses by the clinic with similar neurological signs, where no virus was found, and statistically significant differences were not detected. The authors'conclusion: No diagnosis of the West Nile virus in horses is available on one clinical basis. And the horses weren't an early signal: where they were sick, the virus was already found in wild birds, mosquitoes, or both.
The Varroy destructor mite was originally parasited on the eastern bee of Apis cerana. When the western honeybee Apis mellifera was brought to Asia, the tick moved to the new host. The owner has changed several haplotypes of the mite, but almost all over the world only one line of the Korean gaplotype has been scattered. One of the main differences between the owners is the breeding on which mites are reproduced. In Apis cerana, the mites reproduce almost exclusively on trubel fruit, which appears only in specific seasons. Apis mellifera has been available to him, and he's got a few months of bees per year. This allows the number of mites to grow exponentially. The infection in the eastern bee is low, and families survive without human help. Infected families of the Western Bee without processing acaricides are killed in 6 months to 2 years.
In 1546, Jerome Fractoria described the outbreak of disease in cattle under Verona. The story of the foot-and-mouth can be traced back to this description. Nearly 400 years later, in 1897, Friedrich Löffler and Paul Froch showed that the foot-and-mouth agent was called by a filtering agent. It's the first time they've shown that animal disease can cause a filtering agent. This is the beginning of an era of virology. The stork strikes the pairs – cattle, pigs, sheep, goats, and many wild hooves. Mortality is usually below 5%. Young people can be hard hit by myocardia, and death is high. Because of the huge losses in productivity and trade, foot-and-mouth is considered to be one of the most important diseases of agricultural animals.
In English villages, it has long been said that the milky ones who have suffered from cow smallpox do not suffer from natural diseases. In 1796, Edward Jenner decided to check it out. On May 14, he took the material from bubbles on Sarah Nelms'hand and inoculated eight-year-old James Fipps. In July, Jenner injected the boy with natural smallpox material; the disease did not develop. The Royal Society rejected Jenner's article, and in 1798 he published a brochure at his own expense. In it, he considered the cow to be a smallpox of horses that had passed on to cows – a theory that had been denied even in his lifetime. Jenner's disease itself called Latin variolae vaccinae, from vacca – "cow". Hence the name of the method is vaccination. This experience has begun a journey that has resulted in the complete elimination of natural smallpox.
In 1920, the rinderpest suddenly appeared in Belgium – a disease that killed all animals in some flocks. She was brought in by a zeba, and the cattle were taken from India to Brazil, and on their way to the port of Antwerp. The virus is rapidly transmitted between the pairs, especially cattle and buffalo. An outbreak in central Europe has shown that it is useless to fight animal diseases alone. On 25 January 1924, 28 States signed an agreement on the establishment of the International epizootic Bureau (IOB) with headquarters in Paris. Today, it is the World Organisation for Animal Health – WOAH. It wasn't the first time that we won. In the 1960s, mass vaccinations, the restriction of the movement of livestock and the destruction of sick animals drastically reduced the number of cases. But in the 1980s, when vaccination programmes stopped, the disease again devastated Africa. The Global Eradication Programme was coordinated by FAO with WOAH and IAEA. The latest rinderpest was detected in Kenya in 2001 and the world officially declared free of disease at the 79th General Session of WOAH in May 2011. This is the first animal disease eliminated worldwide, and the second infection after natural smallpox. But the point is early: samples of the virus and vaccines are still stored in laboratories. WOAH and FAO ensure that they are destroyed or kept under safe custody.
Африканскую чуму свиней долго считали чисто африканской проблемой. В природе её вирус носят бородавочники и кистеухие свиньи: они заражаются надолго, но не болеют. Вирус живёт и в клещах рода Ornithodoros, и такой природный резервуар уничтожить невозможно. У диких кабанов и домашних свиней тот же вирус вызывает тяжёлую болезнь с высокой смертностью.
За пределы Африки вирус выбирался и раньше. В 1957 году его завезли в Португалию, в 1960-м – повторно, и на Пиренейском полуострове болезнь продержалась до 1990-х годов. Острова тоже не спасали: в 1998 году АЧС впервые появилась на Мадагаскаре, а в конце 2007-го – на Маврикии.
Новая глава началась в апреле 2007 года у черноморского порта Поти в Грузии. Самым вероятным источником специалисты считают пищевые отходы с судов, в которых была мясная продукция из заражённой свинины. Дальше вирус пошёл быстро: к 9 июля 2007 года он был уже в 56 из 61 района Грузии, погибших и уничтоженных свиней насчитали больше 80 тысяч. В конце августа болезнь подтвердили в Армении.
Генетический анализ показал, что вирус из Грузии относится к генотипу II. Ближайшие родственники – вирусы из Мозамбика, Мадагаскара и Замбии, за тысячи километров от Кавказа. Ни насекомые, ни перелётные птицы для такого путешествия не понадобились: вирус проделал этот путь вместе с людьми – в свинине на борту судна.
Почему от АЧС так трудно избавиться, если она уже пришла? Авторы исследования называли несколько причин: дикие резервуары вируса, нехватку лабораторий для быстрой и точной диагностики и недостаток средств у ветеринарных служб. Там, где болезнь замечают поздно, она успевает уйти далеко.
Поэтому ветеринары так настойчиво говорят о пищевых отходах и продуктах из свинины: для этого вируса расстояние не преграда, если его везёт человек.
Overview of open sources. The information is reproduced with an indication of the source and a reference to the source; FACTOR is not an official source of information on epizootic conditions (official data - Rosselkhoznadzor, veterinary services of the constituent entities of the Russian Federation, WRIWH, WOAH). Quarantine and restrictions are established only by the acts of authorized bodies. The translation of foreign materials is machine-made, and the original is correct when it's broken. Report inaccuracy: vet@faktor.ru.
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