The first signs of smallpox or smallpox. What is cowpox, symptoms of the disease and treatment methods

In a disinfected dry room, the floor is covered with a 10-centimeter layer of fresh straw, peat or sawdust. It is recommended to change the litter every day, removing cow dung. Do not allow your horned wards to trample on their own excrement, much less lie down in it, touching their udders.

Important! After suffering from smallpox, cows retain tissue-humoral post-infectious immunity for life.

For the health of cows and bulls, it is important that the barn has an appropriate microclimate:

• temperature regime - +5–15 °C;
• humidity - 60–70%;
• air exchange - for each centner of live weight 17 cubic meters. m/h (to achieve these indicators, regular ventilation of the barn is required);
• air circulation speed - 0.5 m/s;
• concentration of carbon dioxide - 0.25%, ammonia - 20 mg / cubic meter. m.

Many breeders specially sow areas with vetch, alfalfa or clover for their horned charges, and in order for the cattle to receive everything essential vitamins and minerals, feed it with corn silage, animal feed, brewer's grains, bran, grain feed mixtures and premixes.

Important! The virus that causes smallpox can survive in the bodies of blood-sucking insects for 100 days.

If the virus is localized on the mucous membranes of the oral cavity, provide the cattle with liquid or semi-liquid food during the illness. During illness, it is advisable to switch the animal to succulent food. It is especially useful to give infected individuals garlic greens and elderberry branches.

It is important for smallpox cows to milk every day. Be prepared for the process to be painful for both you and the animal. In extreme cases, veterinarians resort to a milk catheter.
During the period of illness, the import and export of new livestock is prohibited. Disinfection barriers must be installed on the farm territory. All restrictive measures last for 3 weeks from the moment of the last recovery.

Antibiotics, ointments and other drugs

The smallpox virus is specific, so the effectiveness of the fight against it can be demonstrated using the following list of medications:

1. An alcohol solution of iodine or chloramine (at a concentration of 3%), as well as Burov's liquid, is used as an antiseptic to cauterize new ulcers. The number of applications depends on the intensity of the smallpox rash.
2. Synthomycin, streptomycin, boric or zinc ointments are recommended for local processing inflamed skin lesions. Their action is aimed at accelerating skin regeneration. Apply at least 3 times a day.
3. Antibiotic therapy is prescribed by a veterinarian in cases where the animal has weak immunity and suffers from vitamin deficiency, as well as with the development serious complications(drugs and dosages depend on the specifics of the disease).
4. To wash pockmarks (this procedure is required before each milking), experienced livestock breeders use infusions of sorrel or elderberry leaves. More effective means They consider lotions from the same decoctions.

Is it possible to drink milk

To maintain good health, a person, like any other living creature, should eat exclusively high-quality foods. If they are received from sources of viral infection, then they are no longer classified as such.

Milk from smallpox cows does not differ in the best way in its chemical composition and contains a viral infection. According to experts, it can be destroyed by boiling for five minutes or pasteurizing for half an hour at a temperature of 85 °C.

Considering the stability of the smallpox pathogen and its mutational transformations, experts do not recommend drinking the milk of a sick cow. It is better to use it for household needs. It is important to take into account the methods of treating the animal. When it comes to antibiotic therapy, the cow product contains residual drug substances.
According to the doctor medical sciences, Head of the Laboratory of Biosafety and Nutrimicrobiome Analysis at the Research Institute of Nutrition of the Russian Academy of Medical Sciences Svetlana Sheveleva, instant reactions to such milk occur only in the case allergic reactions for penicillin, streptomycin, chloramphenicol.

Did you know? In memory of Dr. Edward Jenner, who first discovered methods of combating smallpox, and his vaccinations, at the suggestion of Louis Pasteur, vaccination materials began to be called “vaccines” from the Latin word “vacca”, which means “cow”.

However, if we drink milk every day with a residual amount of antibiotics exceeding acceptable standards, the body gets used to these substances, as a result of which its resistant functions are destroyed.

Prevention and vaccine against bovine pox

Most often, cowpox is observed in the autumn and winter seasons. To avoid viral infection, veterinarians recommend:

1. In August, begin preventive disinfection of the udder. This is done with the help of any antiseptic ointments that are used to treat cow's teats before each milking.
2. Strictly observe sanitary and hygienic rules - thoroughly wash the udder before milking warm water, then wipe with a clean towel. After milking, be sure to wipe the udder and teats, lubricating them with disinfectant cream. The clothes you wear when milking a cow must be clean and cannot be taken home.
3. Periodically disinfect areas where pastures and livestock are kept.
4. When importing new livestock, as well as feed and equipment, initially find out about the epizootic situation of the place from which you plan to arrive. Such animals must be kept in quarantine conditions for a month with regular inspection.
5. If we are talking about farm production, all personnel must undergo mandatory vaccination. After vaccination, the employee should not have contact with animals for two weeks.
6. If there is a threat of infection, vaccinate the entire livestock for preventive purposes.
7. Regularly, every 5 days, disinfect the premises with chloramine, including equipment and utensils.

Wash the udder with warm water before milking helped

There are hundreds of different pathogenic viruses and the diseases they cause in the world. But cowpox is a legend of its own, since it was its causative agent that was used to create the world's first vaccine. Today this disease is not so common, but it is still worth remembering for all owners of these animals.

What it is?

Causes of the disease

There are many rash-causing viruses that can infect many various types animals. Although the cowpox virus infects cattle, there have been many cases of transmission to other pets, since cows are not a natural reservoir for this pathogen. In particular, the virus has repeatedly described the infection of domestic cats and even cheetahs, and (very often) people who worked with cows.

In addition, the disease can occur in dogs, elephants and horses. Surprisingly, many scientists suggest that the natural host of the cowpox virus is... small mouse-like rodents!

Veterinarians are confident that smallpox epidemics in isolated cow herds (in isolated villages) are possible solely due to the actions of carriers. These may include: (Clethrionomys glareolus), the common vole (Microtus agrestis) and the house mouse (Apodemus sylvaticus).

When examining more than 1.5 thousand rodents, researchers determined that at least 27% of them were natural carriers of the virus. Typically, such “pedunculated reservoirs” do not show any signs of infection. Cases of cowpox (and regular ones) are reported in many European countries, including Austria, Belgium, France, Germany, the Netherlands, Great Britain, Scandinavia and throughout the former Soviet Union.

One can only guess what is happening in some countries of the Asian region and Africa. However, regular essays by naturalists and ethnographers indicate that cowpox is encountered more than regularly in these parts.

Spread of the disease

The spread of infection among cows and other domestic animals is believed to be quite low, but there is variation depending on geographical location one area or another. There is no breed, age or gender predisposition, but the risk of infection increases markedly during seasons when rodents begin to enter agricultural buildings en masse (for example, autumn).

Most often, cowpox occurs where animals are kept on free range, that is, in one way or another in contact with the external environment. In the conditions of modern automated complexes, where livestock are not allowed to walk and where deratization is regularly carried out, outbreaks of the disease are not recorded at all (with very rare exceptions).

Clinical signs of infection

As a rule, the virus enters the body through nutrition, by eating contaminated food or drinking contaminated water. In addition, cases of the disease have been recorded after bites from rats and mice. How does cowpox manifest? Its symptoms are quite characteristic. A viral infection becomes apparent after a few days when small, wrinkled nodules (papules) appear on the skin of the udder. This may be accompanied by a secondary bacterial infection, even leading to the formation of abscesses, so cowpox is not as harmless a disease as some owners think.

In addition, viremia (virus in the blood) develops. It spreads very quickly throughout all organs and tissues of the body, which often leads to severe consequences. Cases of formation of ulcerative lesions in gastrointestinal tract. In more mild situations, rhinitis, pneumonia and diarrhea develop. Fortunately, this does not always happen. As a rule, the maximum that threatens a cow is a short-term increase in body temperature, mild digestive upset and a short-term refusal to feed.

Further development of the infection

About ten days after the virus enters the body, more numerous, diffuse skin lesions develop in the form of papules and pustules. This is cow pox on the udder. Their shape can vary from oval to almost perfectly round; the diameter of the lesions rarely exceeds a centimeter. Most often, although this phenomenon is described in veterinary literature, in practice severe itching the animal does not experience.

After a few days, the pustules begin to become covered with crusts, which subsequently dry out and finally fall off the skin. These lesions can be observed on any part of the body, but are best seen on the udder. Cases of the development of papules and pustules on the skin of the nasal planum of cows have been described (although this is unusual).

When can a disease be deadly?

After about six to eight weeks, the infection “spontaneously” goes away. Important! If for some reason the animal was at this time receiving glucocorticoids (steroids), which have the extremely significant disadvantage of suppressing the immune system, or if it has any significant problems with the immune system (for example, leukemia), general septic damage to all body systems. So if you see pox on a cow's udder, treatment should under no circumstances involve the use of corticosteroids!

In such cases, severe purulent pneumonia usually ending in the death of the animal. If signs of respiratory tract damage appear, it is recommended to slaughter the cow for meat. So if your cow has smallpox on the udder (photos of pustules are on the pages of this material), you should not take the disease lightly.

Diagnostics

To confirm/refute the diagnosis, the veterinarian will take pieces of skin and samples of the contents of the papules. They are used to test for the presence of certain antibodies or the vaccinia virus itself. Infection can be confirmed using the following methods:

• Positive antibody titer in blood tests. This test is carried out using Important! Initially, antibodies are detected no earlier than 7-10 days after the pathogen enters the body (when the first clinical signs appear). If tests are done before this, the results will be false negative.
• Growing the virus in cell culture, as well as carrying out polymerase chain reaction (PCR). Detection of the genetic material of the pathogen with its subsequent identification. The test sample is taken from crusts that appear on the skin of the udder, since they contain a lot of viral bodies. These types of tests are considered the gold standard for diagnosis, but they require a well-equipped clinic and an experienced veterinarian. However, cowpox (the treatment of which we will discuss later) is usually so complex diagnostic techniques does not require.
• Skin biopsies also show characteristic changes in infected cells and, if necessary, the virus can be detected from these indirect signs(Although this method is less reliable, it is much simpler).

Information on the treatment of sick animals

So how to treat cowpox? In most cases, the lesions will heal without intervention within a few weeks of the onset of infection, and in mild cases no treatment is often required at all. Of course, this does not mean that the disease can be treated carelessly. If there are many rashes on the skin of the udder, and the cow’s immunity is already weakened by some kind of infection, the consequences can be very unfavorable, including the development of sepsis with massive bacterial damage.

If signs of deterioration are visible, the sick animal will definitely need treatment. There is no specific therapy, as with many other viral pathologies. Treatment is symptomatic and supportive. Thus, cowpox, the treatment (photos of the consequences of the pathological process are in the article) which we are discussing, does not have any specific features in comparison with other viral diseases.

What should I use to treat affected areas of the udder?

The udder skin is treated using zinc ointment. It allows the lesions to dry out and accelerates the regeneration process. Moisturizing ointments should not be used, as they may well contribute to maceration (softening) of the skin and simplify pathogenic microflora the task of penetration into its thickness. Because of this, smallpox in cows on the udder (treatment, photos - all this is in our material) can become fatal due to a fairly high probability of sepsis.

If the cow is not eating well, appetite stimulants and, if necessary, mild laxatives (such as Glauber's salt). When the temperature rises, the administration of intravenous buffer formulations and glucose solutions is indicated, which help relieve intoxication and help lower the temperature. It is vital to avoid prescribing glucocorticoids because clinical signs may become much worse.

Let us emphasize once again that in severe cases, when it comes to damage to the lower respiratory tract and lungs, it is recommended to slaughter for meat. In this regard, smallpox in cows on the udder (treatment, photos - you will find all this in our article) is a rather dangerous disease.

As a rule, antibiotics are not prescribed for this disease, since such drugs have no effect on viruses in principle. But at the slightest risk of developing secondary bacterial infections appointment antimicrobials quite justified. However, this decision should be made solely by the veterinarian. Here's how to treat cowpox.

Spread of infection and risks to people

Transmission from animal to animal is extremely rare, but in general it is possible, since you can easily infect a cow simply by rubbing the contents of the papules of her sick “companion” into her udder. For humans, cowpox infection is quite rare, but such cases do occur. In particular, it was on the basis of observations of milkmaids that the world's first vaccine was developed, so cowpox (a photo of which is in the article) can be recognized as a zoonotic disease.

If possible, work with sick cows by people with weakened immune systems should be limited. In addition, contact of sick animals with children is undesirable. Again, many pediatricians believe that it can be useful for young people to get sick from smallpox: despite its elimination in the world and the absence of infection in our country, the epidemiological situation in countries Central Asia complex, and there is a possibility of infection.

Disinfection measures

Cowpox (Cowpox) is a contagious disease characterized by intoxication of the body, fever and nodular-pustular rash on the skin and mucous membranes. The distribution is widespread. IN last years True (genuine) cowpox is relatively rare. More often, it is caused by the vaccinia virus, transmitted to cows mainly from milkmaids after vaccination (or their children) with smallpox detritus from calves.

Clinical signs and pathological changes. IN Under natural conditions, the disease can be caused by the genuine OK virus and the vaccine-induced VACV. The incubation period lasts 8-9 days. The prodromal period (fever, increase in temperature by 0.5-1 °C, lethargy, lack of appetite, decreased milk yield, liquefied milk) often goes unnoticed. The disease often occurs acutely and subacutely, less often chronically.

With smallpox in cows, roseola appears on the skin of the udder and nipples, and sometimes on the head, neck, back, thighs (in bulls, on the scrotum), and after 2-3 days, papules and vesicles turn into round or oblong (usually on the nipples of the udder) pustules with a reddish rim and a depression in the middle. With genuine smallpox, usually deeper tissues become necrotic, and the pockmarks look relatively flat, and if hemorrhage occurs, they become bluish-black. The subcutaneous tissue under the pustules is inflamed and hard to the touch. 10-12 days after the onset of the disease, brownish crusts (scabs) form in place of the pustules. Pockmarks appear gradually, over several days, and do not mature simultaneously, but in about 14-16 days. In calves, pockmarks usually appear on the head, mucous membranes of the lips, mouth and nose. The disease lasts 14-20 days, it can be accompanied by pronounced signs of generalization, complicated by ulcers and mastitis.

Cowpox, caused by the vaccinia virus, is milder and shorter lasting, although it sometimes affects all dairy cows in the herd. Pockmarks appear only in places of primary damage, affecting mainly the superficial layers of the skin, and they look more convex than in the disease caused by the true cowpox virus.

Pathological changes are characterized by the appearance of the lesions described above on the skin and mucous membranes. When the process generalizes (multiple pockmarks), signs of lymphadenitis and lymphangitis are found, and with complications, abscesses and phlegmons form in the subcutaneous tissue. At histological examination a specific mesh-nest structure of smallpox vesicles is noted and smallpox inclusion bodies are detected.

Animals get smallpox regardless of the time of year and climatic conditions. However, the disease is more often registered, and it is severe in winter and early spring, when the content of vitamins in the body of cows decreases, metabolism is disrupted, the permeability of the skin and mucous membranes increases and resistance decreases.

Morphology and chemical composition. VOC goes through several stages in the process of intracellular reproduction. Mature virions are cube-shaped with rounded edges. The sizes of virions are 170-350 nm, their elongated capsid has a helical type of symmetry. The surface protein layer of the virion consists of a network of hollow (channel 2-7 nm)

Thread-like structures - filaments with a diameter of 8-12 nm. At the center of the virion is a biconcave DNA-containing nucleoid. Sequencing and computer analysis of the nucleotide sequence of the DNA region of the cowpox virus strain GRI-90 (VOK-GRI) with a size of 52,283 bp, which is the left variable region of the viral genome, was carried out. 51 potential open translation frames were identified. The structural and functional organization of this DNA region of VOK-GRI is compared with previously published sequences of similar regions of the genome of vaccinia viruses of the Copenhagen (BB-COP) and WR (BB-VVR) strains; variola virus strains India-1967 (VNO-IND), Bangladesh-1975 (VNO-BAN) and Garcia-1966 (VNO-GAR). An extended DNA sequence unique to the cowpox virus (more than 14 kbp) was identified within the analyzed region. Multiple differences in the structure of homologous regions of the VOK-GRI genome and the genomes of the above-described orthopoxvirus strains were discovered. The intra- and interspecific homology of open translation frames (ORFs) is discussed, as well as the evolutionary relationships of the studied orthopoxviruses.

Type IB DNA topoisomerase, isolated from vaccinia virus, cleaves the phosphodiester backbone of duplex DNA according to the sequence 5 -(C/T)TTSS. forming a covalent 3"-phosphotyrosine adduct. Based on structural and biochemical data, it was assumed that in the structural rearrangement before cleavage, the enzyme forms a “buckle” around DNA. However, there is still no direct data confirming this assumption. Therefore, a new modification of the fluorescence assay was developed , which allows you to detect structural changes both in the enzyme and in the substrate DNA and determine the thermodynamic and kinetic mechanisms of DNA binding and phosphodiester bond cleavage.

Studies with this method have shown that buckle closure occurs at a rapid stage (>25 s-1), the rate of which is 14 times higher than the maximum rate of DNA cleavage. The rate of opening of the buckle to release the bound substrate is also 5-8 times faster than the rate of DNA cleavage. A model has been proposed in which DNA cleavage and reattachment are separated by a single high-energy transition state involving covalent bond cleavage. Alternative models involving slow rearrangement prior to fission do not fit well with the available data. The vaccinia virus protein, secreted from cells infected with this virus and controlling complement activation reactions (vaccinia virus complement control protein (VCP), was the first identified microbial protein with complement-binding activity. The VCPs of cowpox and vaccinia viruses are most similar to each other.

Significant differences in amino acid sequence from other studied orthopox viral VCPs were detected for variola virus. The unique structure of VCP is characteristic of monkeypox virus. Although this protein is very similar in amino acid sequence to the corresponding VCP of the vaccinia virus, it is significantly shorter due to the deletion of the C-terminal part. The identified differences in the VCP structure of orthopoxviruses pathogenic to humans reflect differences in their biological properties.

At a temperature of 4 °C the virus persists for up to 1.5 years, at 20 °C for 6 months, and at 34 °C for up to 60 days. Freezing preserves it. It quickly dies in decaying tissue, is sensitive to high temperature, exposure to sunlight and acids; when boiled, it dies in 2-3 minutes, at 70 °C - in 5, at 60 °C - in 10,

At 55 °C - for 20 minutes and at 39 °C - for 24 hours. Peptone increases its stability. Thermal resistance of virus strains varies. UV rays inactivate it in 4 hours, ultrasound quickly destroys it. At pH 3-3.6 it is inactivated within 1 hour. The optimal pH for storage is 7.5-8.5. From chemical substances The most destructive effect on the virus is 2.5-5% solutions of sulfuric, hydrochloric and carbolic acids, 1-4% solutions of chloramine, 5% solution of Lysol, potassium permanganate.

The AG structure is similar to the AG structure of the vaccinia virus. In the surface part of the virion there is a complex LS antigen with two serological reactive components: L (heat labil) and S (heat stable). The LS antigen is specific for the smallpox and vaccinia viruses and is identical to its samples obtained both from human smallpox crusts and CAO TBE infected with the smallpox virus, and from tissues of calves, rabbits, and guinea pigs infected with VACV. Both the L and S parts of the molecule can disintegrate.

Antigen NP is a nucleoprotein containing 6 % DNA is another immunologically specific part of VACV and cowpox. It can be isolated from elementary bodies by extraction with dilute alkalis. The NP antigen makes up at least half of the substance of the viral particle. After removal of the NP antigen, the neutralizing ability of the serum obtained by EQA does not change. LS and NP antigens make up a significant part of the surface of elementary bodies and are involved in reactions of precipitation, agglutination of elementary bodies and complement fixation. They are different from the GA of the smallpox virus.

In the blood serum of convalescents, VNA, CSA, PA, and GA-detaining antibodies are detected, the dynamics of increase and decrease in titers of which have not been studied. In terms of hypertension, VOC is very similar to the vaccinia virus, but differs from it in RSC and RDP.

VOK agglutinates erythrocytes of chickens at 37 "C. The agglutinability of erythrocytes of individual individuals varies significantly, up to complete insensitivity. When the virus multiplies, HA accumulates in CAO and in tissue cultures. During passages of the virus on transplanted L cells and Ehrlich ascites carcinoma cells, HA ability may be lost, but after passages on EC it is usually restored.The GA of the vaccinia and OK viruses differs from the elementary bodies and LS protein molecules and is a lipoprotein. It is separable from the elementary bodies and contains phospholipids.

Two types of GA were detected in suspensions of CAO infected with EC treated with ether-ethanol or subjected to chromatography in Sephadex LH-20. One of them (light component) is lipid. It precipitates at 30,000 min-", has non-specific GA activity, is thermolabile; its activity increases after treatment with trypsin and is suppressed by normal guinea pig serum. The other type of GA is heavier, thermostable, is not affected by trypsin, and GA is not suppressed by normal serum, it capable of blocking AT. The first GA is a tissue AG, and the second is a viral one.

The virus multiplies locally in epithelial cells of the skin and mucous membrane. Affected cells undergo ballooning and reticulating degeneration and dissolve. In their place, cavities are formed filled with transparent lymph. When the udder is severely affected, the virus is excreted in the milk. The timing of virus infection in OK has not been studied. In papules, the virus is usually found in the form of a pure culture; pyogenic bacteria and other microorganisms appear in vesicles. The virus enters the external environment with scabs that fall off. Experimental infection. VOC can infect calves (in scarified skin), rabbits (in testicles), guinea pigs, mice and monkeys. In infected animals, epithelial necrosis develops more slowly than when infected with the vaccinia virus, but the damage to the mesodermal tissue is more significant and the hemorrhages are larger. Mice infected with the virus intraperitoneally die more often than those infected with the vaccine virus. If infected subcutaneously, they die within 5-7 days. Mice do not die from the vaccinia virus. Lesions from VOC on the cornea of ​​rabbits are smaller compared to VOC.

In recent years, there has been an expansion of the range of animal hosts that may be carriers of VOC. The pathogen turned out to be the cause of smallpox in cats and various animals in zoos. It was also isolated from several species of rodents that are likely reservoirs for the infection. Infection of humans with cowpox from cats has been described. There is an increase in the incidence of orthopoxvirus infections in cats. The reservoir appears to be rodents. Cats develop ulcerative lesions on the head and front legs, usually without a tendency to generalize; after 3-5 weeks recovery occurs. Sometimes they are amazed internal organs(lungs, liver), which could lead to fatal outcome. In recent years, eight cases of human illness caused by VOC have been described; In six of these, domestic cats were the source. Lesions in humans were localized mainly on the face and hands. We studied 14 strains that caused Germany In 1985-1990 pox diseases of cats, humans and elephants; 11 of them turned out to be related to VOC.

For vaccinia and smallpox viruses, a single precursor is possible, which can be VOC or its analogue. This conclusion can be confirmed after sequencing the entire genome of the VACV and comparison with the genomes of the variola and VACV viruses.

The characteristics of lethal infection in outbred white mice aged 15-20 and 25-30 days infected intraperitoneally with the EP-2 strain of cowpox virus (CPV) at doses of 105, 106 and 107 PFU were studied. The virus causes a lethal infection (peritonitis) in 15-20 day old mice; 25-30 day old mice did not get sick or die. Virological, immunohistochemical and electron microscopic examination of 15-20-day-old mice revealed the multiplication of the EP-2 strain in the tissues adjacent to the site of virus injection; generalization of infection does not occur. The virus multiplies first in mesothelial cells, then in fibroblasts, endothelial, adipose, adventitial, striated and smooth muscle cells, as well as in myosatellites.

Cultivation. VOC differs from the vaccinia virus in the nature of its growth on CAO EC, the size and structure of inclusions, and forms diffuse and hemorrhagic pockmarks. Large infecting doses are detailed for embryos. Several strain variants have been identified that cause the formation of white pockmarks on CAO. EC infected with VOC in the allantoic cavity die; those infected with the vaccinia virus using a similar method do not die. In addition to EC, the virus can be cultivated in the culture of bovine kidney cells, EC and human embryonic kidney. Cloudy plaques form. The virus is characterized by inclusions of two types in the affected tissues: some are similar to Guarnieri bodies, others are hyaline bodies that do not react to DNA and do not react with specific sera in RIF. Ectromelia, vaccinia, and vaccinia viruses (EV, VACV, and VSV) cause secretion of a soluble interleukin-18 binding protein from infected cells. Soluble EV protein blocks the activation of the transcription factor NF-/eB and induces interferon-γ in response to interleukin-18. Highly attenuated BOB Ankara encodes a soluble protein whose gene deletion may improve the safety and immunogenicity of this vaccine strain. Molluscum contagiosum virus also encodes a soluble protein (MC54L gene) that may contribute to the lack of inflammatory response during infection with this virus. Soluble protein expression by various poxvirus genera causing local or systemic viral dissemination or persistent or acute infection highlights the importance of interleukin-18 in the response to viral infection.

Sources and routes of transmission of infection. The source of infection is sick animals, recovered animals and virus carriers located in incubation period diseases. The virus enters the external environment with sloughing epithelium (pockmarks) of the skin, discharge from the nasal and oral cavities, the eyes of sick animals and virus carriers. Service personnel are involved in the transmission of infection during the period of vaccination and revaccination with smallpox detritus if the rules of personal hygiene, as well as animal care items and feed are not observed. The main ways of infecting cows with smallpox are contact, aerogenic and nutritional. The virus can be transmitted by blood-sucking insects, in whose bodies it can persist for 100 days or longer.

In addition to cows, buffaloes, horses, donkeys, mules, pigs, camels, rabbits, monkeys and humans are susceptible to the virus. It is believed that VOC is the ancestor of smallpox viruses in animals of other species and humans. PC. Gen-86 VOC was isolated from sick cows; it turned out to be pathogenic for kittens when in different ways their infection. Obviously, domestic cats can be an intermediate host during the circulation of VOC in the rodent chain - Cattle.

Immunity and specific prevention. Immunity in smallpox is tissue-humoral (the latter is confirmed by the detection of specific ATs in the blood). Although AT is detected in the blood, tissue (skin) immunity is more pronounced. After animals naturally recover from the disease, immunity remains intact for life. For specific prevention use live vaccinia virus, applying it to freshly scarified skin in the perineal area or inner surface auricle.

Cowpox- an acute contagious disease caused by viruses, characterized by the formation of specific nodules, vesicles and pustules called pockmarks. The latter develop in stages, are localized mainly in the skin of the udder and teats of cows, and when the disease generalizes, on other parts of the body.

Etiology.
The causative agents are cowpox virus and vaccinia virus, which have morphological similarities but differ in biological properties. These viruses are classified as orthopoxviruses; they are detected by staining preparations according to Paschen, Morozov, Romanovsky, as well as by electron microscopy. Pathogenic for horses, camels, pigs, rabbits, chicken embryos, humans. During the eradication of human smallpox due to the use of vaccinia vaccine for human immunization, enzootic diseases caused by the vaccinia virus were often observed. After the eradication of human smallpox from the world in 1979, vaccination was stopped. Accordingly, cases of cowpox have decreased, but they are still periodically recorded on some farms. The reasons for their occurrence and the sources of preservation of cowpox pathogens in nature require further study.

Pathogenesis. Viruses enter the body through aerogenic and nutritional routes, through contact of sick animals with healthy ones, as well as through contaminated objects. Viruses are inactive outside the cell. Viruses that penetrate epithelial cells undergo deproteinization by cellular enzymes. The nucleoproteins and nucleic acids released during this process overcome the enzymatic activity of the cells, after which the reproduction of smallpox viruses begins in the epithelium of the skin and mucous membranes. Focal inflammation develops in areas where viruses are located. In the skin and mucous membranes, changes characteristic of smallpox occur: first, focal redness appears - roseola, from which, after 1-3 days, dense, raised nodules - papules - form. The latter turn into vesicles and pustules. Smallpox viruses from the primary focus spread to surrounding tissues. From the skin and mucous membrane of the organ, viruses penetrate into the regional lymph nodes, blood and internal organs. The period of viremia is usually short-term, characterized by fever, depression, changes in the blood and hematopoietic organs.

In the body of a susceptible animal, viruses, being antigens, stimulate immunological reactions. Anti-smallpox antibodies are produced in the spleen and lymph nodes. At the same time, in the lymph nodes regional to the areas of pockmark formation, proliferation of lymphoblasts that have antigenic information occurs and their transformation into plasma cells. Accordingly, during the body’s immune response, the number of plasmablasts, immature and mature plasma cells that produce specific anti-smallpox antibodies, increases in the lymph nodes and spleen. Lymph nodes increase in volume, become juicy and reddened.

An important role in smallpox is played by cellular protective factors - macrophages and T-lymphocytes. The latter, during reactions of cellular immunity, are transformed into immunoblasts and immune lymphocytes, which have a cytopathogenic effect and the property of destroying foreign antigens without the participation of antibodies. T lymphocytes act in conjunction with blood monocytes and macrophages. In addition, T lymphocytes secrete factors that stimulate cell proliferation and activate phagocytosis of macrophages.

In freeing the body from smallpox viruses, the role of macrophages of the reticulohistiocytic system is significant. It has been established that in the macrophages of non-immune animals, smallpox viruses multiply and cause the destruction of phagocytes, while in the cells of immune animals they do not multiply and disappear from the body relatively quickly. This is explained by the fact that in the macrophages of immune animals, smallpox viruses are neutralized, that is, complete phagocytosis occurs. However, the antiviral activity of micro- and macrophages is expressed differently. Polymorphonuclear neutrophils of immune animals do not destroy vaccinia viruses; only monocytes and lymphocytes have this property.

Some adult cattle have a fairly pronounced protective cellular reaction and, in the absence of predisposing factors, suffer from smallpox in a mild form. In this case, a small number of papules are formed. The epithelium in the latter is exposed to partial necrosis and hyperkeratosis under the influence of the virus, and soon dries out, forming a crust. The papule decreases in volume, the scab disappears, the infiltrate resolves, and the skin structure is quickly restored.

Metabolic and feeding hygiene disorders, influence of others harmful factors external environment reduce the activity of cellular elements, including immune defense cells; therefore, smallpox disease occurs in a severe form. Smallpox is also difficult for calves that have organs at birth immune defense do not reach functional and morphological maturity.

The smallpox process can be complicated by secondary bacterial processes, which often cause the development of mastitis in sick cows; gastroenteritis, bronchopneumonia - in calves.

Clinical signs.
In sick cows, smallpox nodules appear in the skin of the udder and teats, sometimes in the head, neck, back and thighs. In bulls it is more often noted latent course. In them, pockmarks form in the skin of the scrotum. Calves become infected through milk, and smallpox nodules often form in the mucous membrane of the mouth and near the edges of the lips. Sick cows show anxiety and do not allow staff to approach them. They stand with their limbs spread wide apart. When walking, put your feet to the side. The udder becomes painful, hard, milk production decreases, and the quality of milk deteriorates. In a severe generalized form of the disease with the formation of numerous pockmarks throughout the body, an increase in body temperature to 40-41 ° C, lethargy, and loss of appetite are noted. When milking, contact with bedding and other objects, the pockmarks are damaged, and bleeding wounds and scabs form in their place.

Pathological changes. IN skin smallpox lesions are detected. They are localized mainly on the udder and nipples, but often also in the head, neck, side surfaces of the body, chest, thighs, etc. The nodules that form are initially small, red or pink, and dense. Increasing in volume, they rise above the surrounding surface of the skin by 2-4 mm. The central part of the papules is covered with a thin gray crust, tightly attached to the skin. The incision shows that the scab is well demarcated from the underlying tissues. The cut surface is moist; when pressed, a little cloudy gray-yellowish or greenish exudate is released. Papules located at close distances merge. In these cases, the pathological process is spread over a large area, where the skin is covered with massive cracked scabs. The hair protruding from the depths of the crusts is stuck together and tousled. When the scab is removed, a reddened, uneven surface of the skin is exposed, covered with a thin layer of gray-greenish or gray-reddish cloudy sticky exudate. The hair is removed along with the scab. The epidermis under the scab is preserved in the marginal areas, and in the center of the nodules is separated along with the crust. Papules turn into vesicles and pustules. Vesicles are vesicles containing slightly cloudy serous exudate containing smallpox pathogens. The emigration of leukocytes and the formation of a large number of purulent bodies in the cavity of the vesicle is accompanied by the transformation of the vesicle into a pustule. The cavity of the latter contains purulent exudate. The pustule is surrounded by a red rim and has a depression in its center.

In the disease caused by the cowpox virus, deeper tissue necrosis occurs. The pockmarks look flat and, as a result of hemorrhages and hemorrhagic infiltration, have a reddish-bluish color, turning into bluish-black. Nodules located close to each other merge, and cracks form on their surface. The dermis and subcutaneous tissue under such pockmarks are infiltrated and dense to the touch. Next to the pockmarks there may be boils, abscesses, and phlegmon.

In sick calves, nodules and ulcers with slightly raised edges are found in the mucous membrane of the mouth and pharynx. The lymph nodes regional to the sites of pockmark formation (supraduperal, submandibular, retropharyngeal, cervical, prescapular) are enlarged, reddened, shiny, juicy when cut, the surrounding tissue is swollen.

Pathohistological changes. Typical changes in smallpox develop in the skin. At the roseola stage, hyperemia, moderate lymphoid-histiocytic infiltration in non-rivascular zones of the dermis, emigration of polymorphonuclear neutrophils, and swelling of epithelial cells of the epidermis are noted. The intensification of these processes leads to the formation of a nodule (papule) in place of roseola. It reveals swelling and proliferation of epithelial cells, as a result of which the epidermis is thickened, the number of rows of cells in it is increased, finger-like, tree-like and flat outgrowths appear, embedded in the dermis (acanthosis). In epidermocytes, cytoplasmic inclusions - Guarnieri bodies - are oval, round, sickle-shaped. When stained according to Romanovsky-Giemsa, as well as under an electron microscope, cowpox virions are detected in the cytoplasm of epithelial cells. The stratum corneum is massive, loose, some epidermocytes become keratinized while maintaining an elongated nucleus.

In the epidermis, individual epithelial cells and groups of cells are in a state of vacuolization. The latter are increased in volume, the cytoplasm is transparent, the nucleus is pyknotic and moved to the periphery. Vacuolization is replaced by reticulating degeneration. In such areas, the contours of the shell of epithelial cells are visible, the nucleus weakly perceives paints, or is lysed. Cell membranes, under the influence of accumulating transparent liquid, are stretched and create a kind of mesh structure in the cavity that appears in the thickness of the epidermis. Between the epithelial cells there are many polymorphonuclear leukocytes and lymphocytes. In the dermis, the exudative reaction is expressed in the form of hyperemia, stasis, increased vascular permeability, release of blood plasma from the vessels, and emigration of leukocytes. The collagen fibers in the subepidermal zone are swollen, separated from each other, between them there are plasma fluid, neutrophilic leukocytes, and macrophages. Epithelial vaginas hair follicles thickened, many cells are in a state of vacuolar degeneration. The lumens of some follicles are enlarged and contain varying numbers of purulent bodies. There are no hair shafts.

At the pustule stage, the epithelium and underlying connective tissue are subject to necrosis as a result of the toxic effects of smallpox viruses and accompanying microflora, as well as the enzymatic activity of leukocytes. Thus, pustules are purulent necrotizing pockmarks. On top they are covered with a crust formed as a result of hyperkeratosis and parakeratosis of the epidermis, sweating of exudate, necrosis of the cellular elements of the epidermis.

With smallpox caused by the true cowpox virus, necrosis of the epidermis is more pronounced, and the latter is absent in a significant area. The dermis is bare, infiltrated with erythrocytes, polymorphonuclear leukocytes, and lymphocytes. Vessels of all sizes are sharply dilated and overflowing with blood.

The diagnosis is made based on the results of clinical, pathomorphological and laboratory research taking into account epidemiological data. Detection of cytoplasmic inclusions - Guarnieri bodies and elementary viral particles from papules with characteristic pathomorphological changes in the skin is the basis for establishing smallpox. Imprint preparations are stained according to Morozov or Romanovsky-Giemsa. Viral particles are black or blue-violet in color, round in shape, located in groups or in large clusters.

Paravaccine should also be differentiated from smallpox. Foot and mouth disease is characterized by the formation of aphthae on the mucous membrane of the tongue, gums, cheeks, vestibule of the mouth, and skin of the fingers. Unlike smallpox, it is slow and benign.