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Malignant Catarrhal Hot
Malignant catarrhal fever (Latin - Coryza gangraenosa; English - Malignantcatarrhal fever of ruminats; ZKG) is a sporadic non-contagious, mainly acute disease of cattle, buffalo, deer, as well as wild artiodactyl animals, characterized by febrile mucous fever of constant type membranes of the respiratory tract and gastrointestinal tract, damage to the eyes and central nervous system (see color. insert).
Historical background, distribution, hazard and damage. For the first time, an illness called “cattle typhoid” was described in 1832 by Anker. In Russia, malignant catarrhal fever (ZKG) was established by I. I. Ravich (1873), and V. Ya. Obolensky (1881) indicated its infectivity. The viral nature of ZKG was determined by Metam (1923), and Pearcey (1953) isolated the pathogen.
The disease is recorded on all continents. Due to the rare occurrence, economic damage is generally small. The most significant losses are livestock and reindeer husbandry in Scotland, Australia and New Zealand.
The causative agent of the disease. The causative agent is a DNA-containing, finally unclassified virus from the Herpesviridae family: the lymphotropic gammaherpesvirus, also called alcelaphine herpesvirus 1 (AHV-1), which persists in the body of wildebeest, causes gastrointestinal infections in cattle in Africa, and sheep herpes virus type 2 (ovid herpesvirus 2, OGT-2), causing disease in cattle and deer in Europe, America, etc.
Electron microscopy finds virions with a diameter of 140 ... 280 nm with an outer shell and a central capsid, as well as virions with a diameter of 100 nm, consisting of a mesh capsid. ZKG virus is reproduced for a short time on chicken embryos, culture of thyroid cells, lungs and adrenal glands of calves, causing CPD, which is characterized by the formation of cellular syncytia and intranuclear Taurus inclusion Cowdry. In sick animals, the virus is found in the blood, brain, parenchymal organs and lymph nodes.
The virus is unstable. The calf’s heparinized blood remains at room temperature for 24 hours, and at 4 ° C for 10 ... 12 days. It is sensitive to ether and chloroform. Under natural conditions, it is active for up to 35 days.
Epizootology. In vivo, malignant catarrhal fever often affects cattle and domesticated buffalo of all breeds, lines and ages. Cases of disease and virus isolation from sheep, goats, pigs and wild ungulates are described. African buffaloes and camels are considered immune. It is experimentally possible to reproduce the disease on calves, sheep, rabbits, guinea pigs and white mice.
Cattle and buffaloes usually fall ill between the ages of 1 to 4 years. In older animals (aged 8 ... 10 years), the disease is more severe than in young animals. Calves rarely get sick. Bulls and working oxen are more prone to disease than cows.
The source of the pathogen is sick animals and virus carriers, from the body of which the virus is secreted with nasal and conjunctival secretions, but not with saliva and urine. The duration of the virus, the methods of infection and ways of virus isolation have not been fully studied. With direct contact of sick animals with healthy, as well as transmissible, the disease is not transmitted.
It is believed that the reservoir of the pathogen are sheep, goats and wild artiodactyl animals of the deer family. This is justified by the fact that in most cases cattle become ill after close and prolonged contact with sheep. At the same time, there are known cases of diseases of cows and calves kept separately from sheep, which indicates the existence of other sources and reservoirs of the pathogen.
The virus is able to pass through the placenta and infect the fetus. Newborns can transmit the pathogen to other animals, which leads to the further spread of the disease.
In our country, ZKG is found in all zones, but more often in the central and northern regions of the country. In 60 ... 80% of cases, the disease manifests itself sporadically, less often in the form of small epizootic outbreaks lasting 40 ... 50 days. During this period, 1 ... 2 sick individuals are allocated daily. The animals are most seriously ill at the beginning of the outbreak, when the mortality rate reaches 90 ... 100%. In decaying foci, ZKG flows more easily. It is believed that such a difference depends on the physiological state of the animals: the least resistant individuals are the first to fall ill.
In individual farms, settlements and even courtyards, the disease can manifest itself stationary for 5 ... 11 years in a row.
The disease is recorded more often in the fall, sometimes in winter and spring, and very rarely in the summer. Predisposing factors are a sharp drop in temperature and increase in air humidity, hypothermia, poor ventilation, insufficient feeding of animals, giving them spoiled feed, and the joint content of cattle and small cattle.
Pathogenesis. The pathogenesis of the disease has not been studied in detail. It is suggested that pathogenetic mechanisms are associated with autoimmune processes. Soon after infection, the virus enters the bloodstream, accumulates during the incubation period in white blood cells, spleen and lymph nodes, and then penetrates the brain, various tissues and organs. The causative agent is initially phagocytosed by large granulocytes (stem cells), but is not lysed in them. It causes cell dysfunction, which, in turn, induces the polyclonal multiplication of T-lymphocytes and the autoimmune effect of cytolytic cells.
In response to the action of the virus, perivascular tissue infiltration of predominantly lymphocytic type is manifested. At the beginning of the disease, disseminated non-purulent encephalitis is noted, leading to diffuse cortical inhibition, which is manifested by clinical signs of severe brain damage already on the first day of the disease. In the next 2 ... 3 days, the mucous membranes of the eyes, respiratory and digestive organs are involved in the process. Inflamed epithelial tissue is necrotic, erosion and ulcers are formed.
Dead tissue serves as a good breeding ground for gut microbes and streptococci that secrete toxins, cause croupous diphtheria, and cause septicemia. Deep morphological damage and functional disorders ultimately lead to the death of the animal.
The course and clinical manifestation. The incubation period with ZKG ranges from 2 weeks to 10 months. Distinguish between super-acute, acute and subacute course, as well as four successive forms of the disease: with the defeat of most major organs; intestinal mucosa (intestinal form); mucous membranes of the mouth, nose and conjunctiva; atypical, or abortive, with skin lesions mainly in the head.
The disease begins with an increase in body temperature to 40 ... 42 ° C, which is kept at a constant level with slight fluctuations. Already in the prodromal period, signs of damage to the central nervous system are noted. Animals become shy, alert, they note violentness or, conversely, oppression , indifference, loss of balance, general weakness, muscle tremors, and later - clonic epileptiform seizures, coma.
In a super-acute course, in addition to the indicated signs, loss of appetite, thirst, atony of the scar, decreased milk yield, shortness of breath and rapid heartbeat are observed. The pulse is hard at first, later small and soft. The nose mirror is dry and hot. The feces are liquid, bloody, often fetid. At this stage, the disease can end in 3 ... 4 days with the death of the animal.
In an acute course, following the symptoms described above, on the first or second day, inflammation of the mucous membranes of the oral and nasal cavities appears. With eye damage, profuse lacrimation, photophobia, redness and swelling of the conjunctiva, adhesion of the eyelids are noted. Diffuse parenchymal keratitis is characterized by a change in the color of the cornea: it becomes dull, smoky, then milky white. Often small vesicles and ulcers form in the cornea. Developing iridocyclitis and keratitis can lead to perforation of the cornea and prolapse of the iris with the lens capsule. As a result, the patient
the animal goes blind on one or both eyes. In the event of a recovery, changes in the cornea are reversed, but vision remains weakened or not restored at all; less often the cornea is not affected.
Outflows from the nose are first serous-mucous, then purulent with an admixture of blood, fibrin and scraps of the epithelium. The prominent secret dries around the wings of the nose in the form of brown crusts. The mucous membrane of the nose is inflamed, covered with dirty gray overlays, when removed, bleeding ulcers are exposed.
Discharge from the nostrils has a putrid odor. As a result of swelling of the mucous membranes, narrowing of the lumen and obstruction of the nasal passages, breathing becomes rapid, tense and wheezing. When involved in the process of the mucous membrane of the larynx, choking phenomena are possible. When the respiratory tract is affected, bronchitis develops; first appears catarrhal, later croupous pneumonia, accompanied by a painful cough.
Inflammation of the mucous membranes of the accessory cavities of the head is accompanied by an increase in local temperature, the appearance of a dull sound during percussion of these cavities. With the transition of inflammation to the bone basis of the horns, the connection with the underlying tissues is broken and the horn covers disappear.
The mucous membrane of the mouth is dry, hot, reddened. Diphtheria overlays are visible on the gums, lips and tongue, after their removal bleeding erosion with uneven edges is exposed.
Difficulty swallowing, excessive salivation, colic, constipation or profuse diarrhea indicate damage to the mucous membranes of the gastrointestinal tract. Fecal fluid, with a fetid odor, contains an admixture of blood, fibrinous flakes and torn epithelium of the intestinal mucosa. The intestinal or intestinal form ends after 4 ... 9 days with the death of the animal.
Damage to the genitals is characterized by the appearance on the vaginal mucosa of croupous films and ulcers, and in pregnant animals - by abortion. The inflammatory process can spread to the mucous membrane of the bladder and to the kidneys. The result is cystitis and nephritis. In sick animals, urination is difficult and painful, urine is acidic; protein, blood, urinary cylinders, and renal epithelium are found in it.
Lymph nodes available for palpation are enlarged. Often on the skin of the whole body or head, neck, back, abdomen, udder, nasal mirror, a papular-vesicular rash appears with the formation of brown scabs, after their rejection bald areas of the skin are visible. In parallel with generalized damage to the lymph nodes, leukopenia and mononucleosis develop with the appearance of large immature shaped elements. The acute course lasts 4 ... 10 days and in 90 ... 100% of cases ends in death.
The subacute course is characterized by the same symptoms as the acute. However, they develop more slowly and are less pronounced. The disease is delayed, and the animals die by the 14 ... 21st day.
An atypical, abortive, or benign form of the disease is accompanied by a slight and short-term fever, mild inflammation of the mucous membranes of the nose, eyes, and mouth, but a clearly visible skin lesion in the form of exanthema. Animals tend to recover, but some may have fatal relapses.
Pathological signs. Posthumous changes depend on the form and course of the disease. In a super-acute course, they are characterized only by swelling of the liver or lymph nodes, degeneration of the heart muscle, or are generally invisible. The corpse of an animal is usually exhausted, quickly decomposes, rigor mortis is well expressed. The hair is ruffled, matte. The skin in the area of the tail and hind limbs is stained with feces, a liquid with putrid odor flows from the nasal and oral cavities. The blood is dark, thick. In the subcutaneous tissue, point and banded hemorrhages. Lymph nodes are enlarged, partially hemorrhagic, inflamed.
When examining the head on the mucous membrane of the lips and oral cavity, areas of redness and necrosis are found, in the nasal cavity and adnexal cavities - fibrinous deposits and purulent exudate. The mucous membranes of the larynx and trachea are covered with diphtheria films. The meninges are diffusely hyperemic with foci of hemorrhage and swollen (lymphocytic leptomeningitis and non-purulent encephalitis).
In the front lobes of the lungs, focal bronchopneumonia, in the back - acute interstitial edema. The heart muscle is flabby, on the endocardium banded hemorrhages. The liver and kidneys are hyperemic, degeneratively altered, and multiple point and spot hemorrhages are found under their capsule. The spleen is either not enlarged, or slightly swollen, its pulp is not softened, cherry red. On the mucous membranes of the abomasum, intestines, and urogenital apparatus, ulcerative hemorrhagic lesions.
Diagnostics and differential diagnostics. The disease is diagnosed on the basis of epizootological data, clinical signs and paratoanatomical changes. The fundamental possibility of using RSK, PCR, and histological studies as laboratory diagnostic methods has been proved. The specificity of Taurus inclusions, despite their frequent detection, is disputed.
In differential diagnosis, it is necessary to exclude cattle plague, foot and mouth disease, rabies, leptospirosis, listeriosis, viral diarrhea, infectious rhinotracheitis and poisoning. The use of laboratory methods (bacteriological, virological, serological, etc.) for differential diagnosis is mandatory.
Immunity, specific prevention. Immunity is not studied. Antibodies are detected in the blood of the convalescents, but the disease of the ZKG does not create long-term immunity and colostral antibodies do not protect the calves from experimental infection. A few weeks or months after recovery, the animals can become sick again, and in a more severe form. To create a vaccine against ZKG has not yet succeeded.
Prevention In order to prevent the occurrence of ZKG, it is necessary to strictly comply with the veterinary and sanitary rules for keeping animals, thoroughly carry out mechanical cleaning and preventive disinfection of the premises, separately keep large and small cattle in the room and graze.
Treatment. Conduct mainly symptomatic treatment aimed at preventing complications and increasing the body's resistance. Given the form of the disease, cardiac, sedative, anti-inflammatory, antimicrobial, diuretic, normalizing osmotic-dynamic balance, general restorative drugs are used,
biogenic stimulants, immunomodulators, antibiotics, nitrofuran series drugs and sulfonamides.
From the first days of the disease, animals are provided with the necessary conditions for feeding and keeping: they are placed in a darkened room, soft and succulent feeds are included in the diet, acidified water is drunk. Cold compresses are applied to the head. If necessary, a tracheotomy and craniotomy are performed.
Control measures. When a diagnosis is made, the farm, farm, yard is declared dysfunctional according to the WKS and restrictions are imposed. Prohibition of the entry and exit of livestock for breeding and production purposes, the joint grazing and watering of cattle and small cattle, the export and use of raw milk from sick and suspicious animals. The entire herd of dysfunctional herds is subject to daily clinical examination with a measurement of body temperature. Sick and disease-suspicious animals are immediately isolated and treated.
The current disinfection of premises, equipment, vehicles and other items is carried out after each case of the allocation of a sick animal, and then periodically until the outbreak is eliminated. It is treated with a hot solution of sodium hydroxide, sulfur-carbolic mixture, bleach or a clarified solution of bleach, formaldehyde solution, a suspension of freshly slaked lime (calcium hydroxide). Manure, feed residues and litter are disinfected in a biothermal way, and slurry with bleach. At the entrance to the premises, disinfectant rugs are installed.
Slaughter of sick and disease-suspicious animals for meat is permitted in the absence of high temperature and exhaustion. The carcasses are sent for digestion, and the heads and affected organs are sent for disposal. The skins are disinfected with a solution of sodium carbonate in a saturated solution of sodium chloride at an exposure of 24 hours. Milk is used for human consumption and animal feed only after disinfection by boiling it in place.
The farm, settlement is declared safe for malignant catarrhal fever 2 months after the last case of the isolation of a sick animal and the final disinfection.
Control questions and tasks. 1. In which farms and areas are most often registered WKG? 2. Назовите особенности эпизоотического процесса при ЗКГ и важнейшие клинические признаки болезни. 3. В чем заключается разница в клинико-эпизоотологическом проявлении злокачественной катаральной горячки и контагиозной плевропневмонии крупного рогатого скота? 4. Какие методы используют для диагностики болезни? 5. Обоснуйте применение рекомендованных для лечения симптоматических средств и антимикробных препаратов. 6. Перечислите мероприятия по профилактике и ликвидации ЗКГ
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ЗЛОКАЧЕСТВЕННАЯ КАТАРАЛЬНАЯ ГОРЯЧКА
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