Avian influenza (Grippus Avium, bird plague) is an acute, highly contagious viral disease characterized by septicemia, manifested by depression, edema, and damage to the respiratory and digestive organs.

History reference. The disease was described by Perroncino (1880) in Italy, where it was widespread under the name "exudative typhus of chickens", subsequently its devastating outbreaks were recorded in all parts of the world. The viral nature of classical (European) bird plague was established by the Italian scientist E. Chentania, and in Russia this disease was first registered and described by M. G. Tartakovsky (1902). In 1955, the pathogen was identified as Influenza virus A, which is why the disease has been called avian influenza since 1971. Currently, avian influenza in the form of classical plague is rare. Epizootic outbreaks caused by subtypes of the virus with lower virulence are more often recorded.

Pathogen- RNA-containing virus (Influenza virus subtype Hav-1), belonging to the genus influenza of the orthomyxovirus family. The size of the virion is 80-120 nm. All known influenza viruses are divided into 8 subtypes (A - A). The causative agent has a certain relationship with influenza A viruses of humans, horses, and pigs. In birds, the virus stimulates antihemapglutinins, neutralizing and complement-fixing antibodies. The virus reproduces in chicken embryos and cell culture> has hemagglutinating properties in relation to the erythrocytes of many species of birds, mammals and humans.

Sustainability- the virus is sensitive to ether, chloroform, heat and acidic environment (pH 3.0). At a temperature of 55 ° C, it is inactivated within one hour at 60 C in 10 minutes, and at 65-70 C - in 2-5 minutes. It is stored at low temperatures and in a lyophilized state for up to 2 years. The infectivity of the virus quickly disappears when treated with formaldehyde, detergents, oxidized agents (iodine), weak acids, hydroxylamine, ammonium ions. With deep freezing (-70 °C), the virus remains virulent in the material for more than 300 days, in 1% NaOH solution - 5-7 weeks. The virus is inactivated for 5 minutes with aqueous solutions of 5% HCl, 4% phenol, 3% bleach, 2% sodium hydroxide, 5% phenol.

epidemiological data. Influenza has been reported in many species of domestic and wild birds. Subtype A virus has been isolated from chickens, turkeys, pigeons and guinea pigs. Among the avian influenza virus, there are strains in the supercapsid shell of which contains neuraminidase, which is characteristic of human and equine influenza viruses. This testifies to the great diversity of the gene pool of the viral population circulating among birds. The circulation of the human influenza A2 virus among wild and domestic birds has also been proven. Among wild and domestic birds, several antigenic varieties of the influenza virus characteristic of humans, birds and domestic animals can simultaneously circulate. Stress reactions that occur in birds during long flights and changing climatic conditions lead to exacerbation of infection and the emergence of new epizootics.

In industrial-type farms, the causative agent of avian influenza is introduced with feed, inventory, equipment: infected containers for carcasses of chickens and eggs are of particular danger.

The first cases of the disease, as a rule, are recorded in chickens and adult weakened birds against the background of poor-quality feeding, transportation, and overcrowding. The passage of the virus through the weakened body of chickens increases its virulence and contributes to the subsequent disease of birds kept under normal conditions. As a rule, influenza infects all susceptible birds on the farm within 30-40 days -

Influenza virus causes disease in birds by respiratory, oral, intraperitoneal, subcutaneous and intramuscular infection. In industrial farms with a cellular system for keeping poultry, the aerogenic route and transmission with drinking water are of primary importance in the spread of the pathogen. From the body of a sick bird, the virus is excreted with all excretions and secrets, as well as with eggs. Rodents, cats, and especially free-living wild birds that penetrate or nest in poultry houses can take part in the spread of the pathogen within the farm.

Sources of the causative agent of influenza are sick and ill (virus carriers for 2 months) birds. The presence of curvirus-carriers maintains an epizootic focus in the farm with the continuous reproduction of new populations of susceptible birds and creates a stationary problem. The incidence of poultry varies from 80 to 100%, mortality - from 10 to 90%, depending on the virulence of the virus and the conditions of the poultry. In dysfunctional farms, influenza in chickens and hens is often complicated by pathogens of respiratory mycoplasmosis, colisepticemia, and infectious laryngotracheitis. An adult bird loses egg productivity by 40-60% within 2 months after a disease. There are frequent cases of loss of immunity against Newcastle disease, infectious laryngotracheitis, bronchitis, smallpox.

Pathogenesis. Depending on the virulence, tropism of the virus, the natural resistance of the bird, a generalized, or respiratory, form of the disease develops. After the virus enters the mucous membranes of the respiratory tract, it actively reproduces, followed by penetration into the circulatory system after 4-12 hours. The virus is adsorbed by red blood cells, spreads throughout the body, and as a result, septicemia occurs. The reproduction of the virus in parenchymal organs is accompanied by the formation of toxic products, intoxication, which leads to the death of the bird. This is usually observed in the acute course of influenza. The outcome of the subacute and chronic course (10-25 days) depends on the resistance of the organism.

All the most virulent strains of the virus, regardless of belonging to a particular subtype, cause a generalized form of infection. There is hypoplasia of lymphoid organs, lymphocytopenia and suppression of protective mechanisms, which contributes to viremia and virus replication in various cells of organs and tissues. The defeat of the walls of blood vessels leads to a violation of hemodynamics, hemorrhagic diathesis and exudative phenomena.

Course and symptoms. The incubation period is 3-5 days. The disease proceeds acutely, subacutely and chronically. Initially, anorexia, disheveled plumage, and loss of egg production are noted in birds. Chickens stand with their heads down and eyes closed. Visible mucous membranes are hyperemic and edematous, often viscous mucous exudates from a slightly ajar beak, nasal openings are sealed with inflammatory exudate. In some chickens, swelling of the earrings is noted. The comb and beards are dark purple. Breathing is hoarse and rapid, body temperature rises to 44 ° C, and drops to 30 C before death. The disease caused by subtype A1 leads to 100% death of the bird in acute course, and 5-20% in subacute and chronic. Along with the respiratory symptom complex, diarrhea occurs (liquid litter, colored brown-green), as well as ataxia, neurosis, convulsions, playpen movements, in the preagonal stage - tonic-clonic convulsions of the cervical and wing muscles. There may be cases of a chronic course of the disease without pronounced clinical signs.

pathological changes. Vary over a wide range depending on the course of the disease. The most typical are hemorrhagic diathesis and subcutaneous edema in the pharynx, larynx, neck, chest, legs. Massive subcutaneous hemorrhages are found in the muscles, heart, parenchymal organs and mucous membranes, rhinitis, pharyngitis and conjunctivitis are found in 35% of dead birds; hemorrhages in the stomach and intestines in 60% of cases. Gastroenteritis, peritonitis, pericarditis, bronchitis, aerosaculitis, pulmonary edema, congestion in internal organs are permanent pathological changes in avian influenza.

Changes in the brain are especially characteristic: hemorrhagic meningitis, diffuse hemorrhages, foci of edema in the softening of the medulla. Histopathological examination of birds that died on the 3rd-4th day of the disease, along with stasis and hemorrhages, reveals degenerative changes in neurons and multiple areactive necrobiotic foci in the gray and white matter of the brain.

Diagnosis. Based on the epidemiological features of influenza, the characteristic acute clinical signs of respiratory disease and pathological changes, only a presumptive diagnosis can be made. For the final diagnosis, it is necessary to conduct virological studies of pathological material (lungs, liver, brain, etc.) taken from dead birds in the acute course of the disease. The cadaveric material must be fresh or preserved cold (-60 C) in a 50% glycerol solution. For serological studies, paired blood sera are taken from chickens at different periods of the development of the disease.

Virus-containing material, prepared in the usual way, infect 9-12-day-old chicken embryos into the allantoic cavity. 48 hours after infection, the allantoic fluid is removed and examined for the presence of the virus in the hemagglutination reaction in chick embryo cell cultures (presence of CPD 36 hours after infection). For a biological sample, 2-4-month-old chickens are used, which are injected intramuscularly with 0.5-1 ml of the suspension. After 3-5 days in the presence of a virulent virus, the chickens develop respiratory symptoms of the disease, sometimes with a fatal outcome. The only evidence of the presence of a weakly virulent virus is the detection of an increase in antibody titer. From serological methods, RZGA, RA, RSK can be used. In practice, retrospective diagnosis is usually done using RPGA.

differential diagnosis. The generalized septicemic form of influenza is differentiated from Newcastle disease, and the respiratory form is differentiated from infectious bronchitis, mycoplasmosis, laryngotracheitis and other respiratory diseases.

Avian influenza, unlike Newcastle disease, affects all types of birds at any age and causes pronounced edema, catarrhal-hemorrhagic enteritis. With Newcastle disease, diphtheria often occurs. The respiratory form of influenza is characterized by a predominant lesion of the upper respiratory tract, all types of birds fall ill, and with infectious bronchitis - only chicken birds. Respiratory myxplasmosis of chickens and infectious sinusitis of turkeys are characterized by a chronic course of the disease, the absence of acute inflammatory processes and the development of fibrinous-diphtheritic aerosaculitis.

Treatment. Not designed and not practical. In view of the danger of the spread of the virus, the sick bird is destroyed.

Immunity. After recovering from influenza, the bird acquires non-sterile immunity lasting up to 6 months. For specific prophylaxis, inactivated hydro-aluminum hydroxylamine embryonic type A vaccine, liquid and dry inactivated vaccines against avian influenza are used. Vaccines are administered intramuscularly, inactivated - twice with an interval of 14 days. For preventive purposes, only clinically healthy birds (chickens, ducks, turkeys) are vaccinated in threatened farms. 14-21 days after vaccination, the bird acquires a strong immunity lasting up to 6 months. Its tension must be controlled on the 21st day after vaccination in the RZGA. If 80% of the 30 examined birds have an anti-hemagglutinin titer of at least 1:10, the immunity is considered strained.

Prevention and control measures. It is necessary to place separately different age groups of birds on the territory, while observing the necessary veterinarian gaps. Acquisition of poultry houses and zones is carried out only with birds of the same age. In the inter-cycle preventive break, a thorough cleaning and 3-fold disinfection of the premises are done. The well-being of farms supplying hatching eggs is systematically monitored for influenza: they disinfect transport, returnable packaging and strictly comply with veterinary and sanitary rules for poultry farms.

If the occurrence of avian influenza is suspected, the laboratory urgently clarifies the diagnosis. In a dysfunctional separate poultry house, a sick and suspicious bird is killed by a bloodless method and destroyed, and the rest (conditionally healthy) is killed for meat. The premises are thoroughly disinfected. When a disease appears in several poultry houses, a daily thorough culling and slaughter of sick and weakened birds is carried out. Eggs laid in the incubator from dysfunctional poultry houses are disposed of or destroyed. Eggs received from a sick bird must be checked within 10 minutes. For disinfection of objects against avian influenza, a 3% solution of caustic soda (16-20 ° C) is used with an exposure of 7 hours, 3% hot (70-80 ° C) - with an exposure of 3 hours, 1% formaldehyde solution - at an exposure of 1 hour, a clarified solution of bleach containing 3% active chlorine - at an exposure of 3 hours, a 1% solution of peracetic acid - at an exposure of 6 hours. Disinfection can be carried out with aerosols of a 38-40% solution of formaldehyde at consumption of 15 ml/m3 and exposure of 6 h. using a PVAN nozzle and compressed air at a working pressure of 3-4 atm or using an AGUD-2 generator.

Eggs for incubation are imported from influenza-free farms. Each batch of hatched young animals is grown in an isolated room and in a completely free from poultry and sanitized area. Before reaching 45 days of age, chickens are vaccinated with inactivated vaccines.

Down, feathers, obtained from the slaughter of a conditionally healthy bird, are dried in dryers at a temperature of 85-90 C for 15 minutes. In the absence of a drying unit, down, feathers are disinfected in any adapted containers with a 3% hot (45-50 ° C) formaldehyde solution for 30 minutes, followed by drying.

In the rehabilitated farm, systematic culling and slaughter of substandard and unproductive birds and aerosol disinfection of premises in the presence of a bird are carried out, with highly dispersed aerosols of lactic acid or chlorine turpentine in the presence of a bird. Quarantine from farms affected by influenza A1 is removed after the slaughter of all birds and the final disinfection.

Bird flu (Avian influenza Viruses). Synonyms: chicken typhus, Brunswick disease, classic bird plague.

Avian influenza is an acute septic illness caused by a virus. It is characterized by high infectiousness, high mortality among chickens, turkeys and poultry of other species, characterized by depression, edema, damage to the respiratory system, digestion.

Historical background, the spread of the disease and the damage it causes. Orthomyxovirus infection in birds was first described by Perroncito 125 years ago in Italy. A highly lethal disease for chickens and turkeys called “classical bird plague”, which has spread since then in various regions of the world, with a high epizootic index, has become a nosological form is not registered. With the emergence of new avian varieties of influenza A viruses, according to the recommendations of the 1st International Symposium on Avian Influenza (1981), the infection was named avian influenza (Avian Influenza), and its new variant with high mortality (at least 75%) is highly pathogenic avian influenza (Highly Pathogenic Avian Influenza).

Avian influenza has gained particular importance at the present time, due to the spread of highly pathogenic HSV H 5 N 1 in 10 countries of Southeast Asia at the end of 2003. In the spring of 2003, large outbreaks of highly pathogenic avian influenza H 7 N 7 occurred in Western Europe.

Epizootic situation of avian influenza in the world. According to OIE reports, there are very few countries in the world where avian influenza has not been reported. In recent years, outbreaks of avian influenza have periodically occurred in Africa (Senegal - 1993), America (Mexico - 1995, USA - 1984-2003, Chile - 2002, Guatemala - 2000, El Salvador - 2001 .), Asia (Pakistan - 2000, Kyrgyzstan, Laos - 1999, Lebanon, Myanmar, Nepal, Turkmenistan - 1996), Europe (Italy - 2000, Armenia - 1985, Turkey, Great Britain - 1992, Netherlands, Belgium, Germany - 2003), Oceania (Australia - 1997).

Avian influenza is most prevalent in the United States. The first outbreaks were noted in 1983-1985. in small poultry farms and in markets where live birds were traded.

The epizootic began in Pennsylvania in April 1983. Initially weakly pathogenic, the H5 N2 strain, which caused mild illness in chickens with respiratory symptoms, decreased egg production and insignificant mortality in the range of 0-15%, actively mutated and by October 1983 was characterized as highly pathogenic. Despite the measures taken, it was not possible to fully control the spread of the disease. In July 1983, a new wave of the disease began in Virginia. As a result, 17 million birds died, and the economic damage amounted to $60 million.

In 1986, the H 5 N 2 virus reappeared in five northeastern US states. Studies have shown that chickens in 26 out of 44 live bird markets in New York and 12 out of 26 in New Jersey were infected with HP H 5 N 2.

According to the results of virological and serological studies, avian influenza pathogen variants containing 11 of 15 known hemagglutinins (H1-7, 9-11, 13) and 8 of 9 known neuraminidase were isolated in 24 US states (D. J. Alexander, 2002) .

Since 1994, new varieties of influenza virus have been spreading in this country, initially caused by moderately pathogenic strains, and then highly pathogenic with the antigenic formula H 7 N 2, sometimes H 7 N 3. In a survey of 110 mentioned markets in New York and New Jersey HPV was found in 70% of cases, especially where ducks and rabbits were sold along with chickens.

In Virginia, 4.5 million birds were destroyed or disposed of (burned, buried, composted). The infection spread through transport and people keeping poultry in the household. in California in 2000-2001. There was an outbreak of influenza in turkeys caused by the H6 N2 strain, which was not accompanied by mass death, but was characterized by respiratory disorders and a decrease in productivity. In total, 195 affected farms were identified in 8 US states. The last outbreak of influenza in the United States was registered on 02.07.02.

The causative agent of the disease. The causative agent of the disease is a virus of the Orthomyxoviridae type A family. Virions are polymorphic, 80-120 nm in size, and are represented by two antigenic complexes. The outer V-antigen consists of hemagglutinin H and the enzyme neuraminidase N. The inner S-antigen is included in the core of the virus and determines the type.

According to the degree of virulence, 4 groups of pathogens are distinguished: high, medium, low and apathogenic, although this division is considered conditional, since strains often mutate, as a rule, in the direction of increasing pathogenicity.

Based on the antigenic features of the structure of the external antigen, all known strains of avian influenza virus are divided into 15 subtypes for hemagglutinin and 9 for neuraminidase. The pathogens with the 5th or 7th subtype of hemagglutinin (H5, H7) are considered the most virulent.

The RNA of the virus consists of 8 segments, which contributes to a rapid change in the antigenic composition through genetic recombinations, often occurring with the simultaneous circulation of influenza pathogens of various origins in the body.

The virus is well reduced in chicken embryos, has a wide spectrum of hemagglutination.

Formaldehyde, peracetic acid (in 0.5-1.0% concentration), sodium hypochlorite, 1-3% caustic alkali solutions reliably inactivate the pathogen when exposed for 1-6 hours.
epidemiological data. Influenza has been reported in all domestic and many species of wild birds. The widespread circulation of the human influenza virus in the bird population has been proven. The intercontinental transfer of the influenza virus is carried out by birds of the wild fauna, which are the natural reservoir of the infectious agent. Inter-farm transfer is possible in horizontal and vertical ways. Inside the farm, the virus is transmitted with the help of attendants, rodents, cats, synanthropic and wild birds. However, the main routes of spread of the pathogen are aerogenic and alimentary.

The most dangerous source of infection is an ill bird, which has been a virus carrier for at least 2 months. The virus remains in the body of convalescents in the presence of antibodies, forming a latent infection, and under the influence of extreme conditions can easily become activated and be released into the external environment for a long time. Therefore, influenza outbreaks most often occur after stressful conditions (poisoning, cooling, water starvation, etc.). Passing the virus through a weakened organism increases its virulence and contributes to the subsequent disease of birds kept under normal conditions.

The incidence of bird flu varies from 80 to 100%, mortality - from 10 to 90%, depending on the degree of virulence of the strains and the conditions of the susceptible livestock.

Pathogenesis. Depending on the virulence, tropism of the virus, the natural resistance of the bird, a generalized or respiratory form of the disease develops.

After the virus enters the mucous membranes of the respiratory tract, it actively reproduces and penetrates into the circulatory system. It takes from 4 to 12 hours. The virus is found in large quantities on the membrane and inside the erythrocyte, as well as in the blood serum. The development of the disease occurs in 4 phases: active reproduction of the virus and its accumulation in parenchymal organs, viremia - in this phase, the virus can be detected in the blood, then the formation of antibodies begins, which indicates the cessation of further reduction of the virus. The last stage is characterized by the active formation of antibodies and immunity.

Due to the fact that the virus releases toxic products in the viremia stage, intoxication and death of the bird occurs. This is usually observed in the acute course of GP. Under the acute and chronic course stretches for 10-25 days, the outcome depends on the resistance of the organism.

All the most virulent strains of the virus, regardless of belonging to a particular subtype, cause a generalized form of infection. With avian influenza, isolated by subtype A, hypoplasia of lymphoid organs, lymphocytopenia and suppression of protective mechanisms occur, which contributes to viremia and virus replication in various cells of organs and tissues. Violation of hemodynamics, hemorrhagic diathesis and exudative processes are associated with a violation of the porosity of the walls of blood vessels.

Clinical signs of the disease. Avian influenza usually occurs in an acute, and sometimes in a subacute form. The acute course of the disease is characterized by: a short latent period (2-4 days), fever up to 43-44 ° C, depression, cessation of oviposition, damage to the respiratory organs, stomach, intestines, diarrhea, pronounced cyanosis of the crest and wattles, fast (after 20- 40 h) and high mortality. The death of a bird reaches 80-100%.

Currently, individual small outbreaks of a subacute course of the disease are often recorded, in which they note: oppression, decreased egg production, damage to the respiratory system, stomach and intestines. In such cases, the disease lasts 2-3 weeks and the death of a sick bird is 5-10%.

In ducks, the main clinical signs of influenza are: frequent sneezing, massive rhinitis, conjunctivitis, keratitis with the release of serous-mucous exudate that sticks together the eyelids (infectious sinusitis of ducklings). With a complication of secondary infection, the waste of ducklings reaches 30-60%.

pathological changes. Pathological changes in influenza are not typical and vary depending on the severity of the disease, the type and age of the bird. The most common are: catarrhal-hemorrhagic gastroenteritis, peritonitis, pericarditis, splenitis, inflammation and edema of the lungs, oophoritis and nephritis. Find hemorrhages under the skin, in the skeletal muscles, heart, parenchymal organs. Differences between influenza and Newcastle disease in birds

Differentiating signs established in birds

The diagnosis is made according to the results of laboratory studies (virus isolation or retrospective serological studies), the detection of the genome in PCR, taking into account the indicated epizootological features, clinical signs and pathoanatomical changes with the obligatory exclusion of Newcastle disease - according to the hemagglutination delay reaction, using a diagnostic kit and a number of other distinctive features. properties of viruses (Table 1).

Differentiate from:

Pasteurellosis - according to the results of a bacteriological study with a bioassay on rabbits and by detecting foci of necrosis in the liver of dead birds; spirochetosis - based on the detection of the causative agent of this disease in blood smears of sick birds;

Infectious laryngotracheitis - according to the negative results of infection of chickens and the presence in sick birds of purulent plugs characteristic of laryngotracheitis and bloody-mucous exudate in the trachea;

Infectious bronchitis - according to the results of serological studies and autopsy results. All the necessary diagnostic tools are available in the country for the identification of isolated pathogens and serological studies. Two sets of antigens and sera for diagnosing avian influenza and Newcastle disease are biofabrically produced at the PZB, and the “Set of preparations based on monoclonal antibodies for the differential diagnosis of HP and NB by solid-phase ELISA” manufactured by VNIIVViM is undergoing extensive production tests.

LLC NPP AVIVAC has completed the development of the diagnostic ELISA test system “Influenza A serotest”, designed for express typing of antibodies to the HP virus by hemagglutinin and neuraminidase.

A PCR-based diagnostic test system for the detection of the genome of type A influenza virus (VGNKI) was tested with a positive result, research was begun on the creation of a PCR diagnosticum, which makes it possible to detect viral nucleic acid in samples of pathological material and in the allantoic fluid of infected chicken embryos, as well as to differentiate antigenic virus subtypes. One of the modern technologies is the creation of microchips (biochips) based on the hybridization of nucleic acids. This technology was developed by the staff of the Institute of Virology. D. I. Ivanovsky RAMS, the company "Narvak" and the Institute of Molecular Biology. Engelhard to identify and differentiate influenza A virus subtypes HI, H3, H5, H7 and H9. The technique allows in a short time not only to identify the influenza virus in materials from animals or humans, but also to identify its subtypes.

Immunity. Recovered chickens acquire immunity. Virus-neutralizing and anti-hemagglutinating antibodies are detected in the blood sera of recovered birds.

Treatment
The following drugs are recommended for treatment: rimantadine (adamantan), virazole (ribamidil), tamiflu (oseltamivir). Remantadine blocks the ion channels of the M-protein. Virazole inhibits the activity of the enzyme inosine dehydrogenesis, which synthesizes guanine monophosphate, as well as the RNA polymerase of the virus. Tamiflu inhibits the synthesis of neuraminidase.

Control measures and prevention. In 1992, the EEC Directive was adopted, requiring the complete destruction of all birds with influenza in the focus of infection and farms in the threatened zone (for example, the “stamping out” principle). According to American experts, this principle is the only effective and reliable one in the fight against influenza. However, the mass destruction of livestock in today's intensive poultry production is very costly and raises serious ethical issues, especially since the impact of avian influenza on human health is considered negligible. Therefore, the possibility of using biological protection measures in the fight against avian influenza is discussed more and more often and in more detail in the specialized literature. In the recent past, the use of influenza immunoprophylaxis in EEC countries was limited due to the justified risk of spreading the virus with infected vaccinated birds or poultry products obtained from such flocks. The development of available methods for differentiating vaccinated birds, infected with influenza or free from infection, has greatly reduced this risk, and a number of countries have begun to develop vaccines and implement an urgent livestock immunization program.

Inactivated vaccines from autogenous and heterogeneous strains were created on an emergency basis. The disadvantage of autogenous vaccines is the impossibility of differentiating vaccinated birds from naturally infected ones, so their use requires the use of groups of indicator birds, which is a rather complicated procedure and does not exclude the possibility of errors. Vaccines from heterogeneous strains are considered more promising, because in their

the composition is injected with a virus with a hemagglutinin subtype similar to the pathogen that caused the disease, but with a different neuraminidase subtype. The detection of antibodies against neuraminidase can be used as a marker of antibody response to vaccine and field virus.

Several types of recombinant vaccines based on smallpox and infectious laryngotracheitis virus vectors have also been developed (J. Capua, S. Marangon, 2002, 2003). Back in 1974, in the Russian Federation, a GOA vaccine was proposed for the prevention of avian influenza, which, 14-21 days after vaccination, provides intense immunity lasting 6 months. In our country, a differentiated approach is provided for in the organization of measures to combat this disease, set out in the "Temporary instructions on measures to combat bird flu", approved by the State Unitary Enterprise of the Ministry of Agriculture of the USSR on August 15, 1978 (Veterinary Legislation. M., 1981. V. 3 , p. 92).

So, in case of influenza caused by medium or low pathogenic strains, restrictions are introduced, and when highly pathogenic influenza appears, quarantine is imposed on the farm. The procedure for improving the economy is practically the same as the instructions on measures to combat Newcastle disease.

The variability of the avian influenza virus (AIV) makes it difficult to control avian influenza. The first thing to do after isolating a pathogen in a poultry farm is to determine the virulence of the isolate. An agent strain is considered virulent in poultry if it belongs to the H5 and H7 subtypes or has a high pathogenic index, as determined by the results of intravenous infection of 6-week-old chickens.

The International Epizootic Bureau (OIE), based on an analysis of information on outbreaks of avian influenza over the past 8 years and the results of measures taken to combat them, recommends that in a dysfunctional farm and on all poultry farms located at a distance of 1-10 km from it, to destroy all poultry with subsequent burial or burning of corpses (stamping out) or the organization of controlled sales of carcasses and other products of slaughter. The choice of any of these options should be based on taking into account the pathogenicity of the isolated AIV isolate, the density of the poultry population on farms located near the OI (center of infection), as well as the economic situation of the disadvantaged farm. For example, in Italy, stamping out is used mainly for broilers and young turkeys fattened for meat, and products obtained from the slaughter of adult birds are sold under careful control.

It is advisable to bring new batches of poultry from safe sources to farms no earlier than 2-3 weeks after the destruction of the infected livestock and the final disinfection.

Around the focus of infection (OI) of a highly contagious virulent strain of AIV, there is a zone of increased risk of infection spread. In this regard, the movement of birds, table and hatching eggs, vehicles and attendants is limited both in the very focus of infection and beyond. In the zone of increased risk of spreading the infection, the bird is vaccinated.

Currently, three types of vaccines are used to immunize birds against influenza - inactivated homologous, inactivated heterologous and recombinant.

In Russia, inactivated aluminum hydroxide vaccine against avian influenza has been produced since 1974. This drug creates a strong immunity 2-3 weeks after vaccination, which lasts for at least 6 months.

According to OIE regulations, fresh meat from poultry vaccinated against influenza is allowed to be sold to other countries if the well-being of the flock for this infection is regularly confirmed.

AVIAN INFLUENZA

Pathological and anatomical changes in the organs of birds with influenza:
1 - multiple pinpoint hemorrhages on the heart;
2 - hemorrhages on the serous membrane of the intestine;
3 - hemorrhages on the serous membrane of the glandular and muscular parts of the stomach;
4 - hemorrhages on the mucous membrane of the glandular and muscular parts of the stomach;
5 - hemorrhages in the muscular and glandular parts of the stomach;
6 - hemorrhages in the blind processes.

bird flu(Grippus avium), classic bird plague, duck sinusitis, South African tern virus, an acute viral disease characterized by damage to the digestive and respiratory organs, high mortality. Influenza of hens is established in France, Germany, the USA, Scotland and the USSR; influenza of ducks - in the USSR; quail and pheasant flu in Italy; flu terns - in the countries of North Africa; petrel flu in Australia. Antigenic variability of the virus G. p. and the presence of highly virulent strains make it possible to classify it as a particularly dangerous disease that can cause great economic damage. Various strains of the virus G. p. can cause from 10 to 100% death among the diseased and affect simultaneously from one to three species of birds.

Etiology. Pathogen G. p.- An RNA-containing virus belonging to the Orthomyxoviridae family, in terms of complement-binding antigen (RNP) is related to influenza A virus in humans and animals. The virion is characterized by polymorphism, a predominant spherical shape, and a size of 60–180 nm. The virion has a lipoprotein envelope with spines located radially on it, which contains a folded ring of RNP. The virion genome consists of 6 or more types of RNA. The virus has infectious, hemagglutinating and neuraminidase activity. It multiplies well in developing 10-11-day-old chicken embryos. Virus-containing allantoic fluid has the ability to agglutinate the erythrocytes of many animal species. When the virus is cultivated in tissue culture, many strains have a cytopathic effect and haemadsorbing properties. Virus strains G. p. isolated from different bird species may differ in virulence, pathogenicity spectrum and structure of surface antigens (hemagglutinin and neuraminidase). The virus is quickly inactivated under the action of a 3% solution of sodium hydroxide and phenol, 0.1% formaldehyde solution.

epizootology. Virus G. p. isolated from all types of poultry, as well as from quails, pheasants, terns and petrels. There are suggestions about the readaptation of strains of the human influenza virus to birds or other animals and vice versa. All strains of the virus, regardless of the animal species they affect, in the process of reproduction in one system, are capable of recombination, resulting in the formation of new antigenically modified virus subtypes. In some cases, the strains isolated in poultry farms during the mass death of chickens turned out to be non-virulent under laboratory conditions. The latter indicates a role in the disease G. p. additional stress: conditions of detention, the presence of secondary infections, such as mycoplasmosis, etc. The source of the infectious agent is sick birds, with excretions and secrets of which a large amount of active virus is released. The route of infection is airborne. Transmission factors of the virus are infected exchange containers (trays for carcasses and eggs), feed, commercial products (carcasses of birds, eggs, feathers) obtained during the incubation period or from a clinically sick bird. Wild birds (pigeons, sparrows, jackdaws and crows) can also play a certain role in the spread of the disease. G. p. occurs in the form of enzootic and epizootic.

Immunity. An ill or vaccinated bird acquires intense immunity only against the homologous subtype of the virus.

Symptoms and course. The incubation period is from 20-30 hours to 2 days. The disease is manifested by a sharp decrease in egg production, feed intake, thirst, depression, signs of respiratory damage, and diarrhea. In a sick bird, the feathers are ruffled, shortly before death, cyanosis of the crest and earrings.

Pathological changes. An autopsy reveals catarrhal and catarrhal-hemorrhagic lesions of the mucous membranes of the digestive tract and respiratory tract, multiple petechial hemorrhages on the spleen, liver, kidneys and heart (Fig.).

Diagnosis is based on the isolation of the virus and its identification in serological reactions. To identify the pathogen G. p. in the USSR sets of standard antisera and antigens are produced.

Treatment. Positive results have been obtained in the treatment of birds with amidantan, which is given to sick birds with food for 10-12 days.

Prevention and control measures. Veterinary-sanitary and zoohygienic measures are carried out in accordance with the instructions. For prevention G. p. Subtype A use a live vaccine from strains P y and P 5 . For other antigenic variants, killed vaccines prepared from homologous strains of the virus are used. G. p.

Literature:
Gorbunova A. S., Pysina T. V., Influenza of animals, M., 1973;
Syurin V. N., Osidze N. G. Bird flu, in the book: Little-known infectious diseases of animals, M., 1973;
Influenza viruses and influenza, trans. from English, M., 1978.

Veterinary encyclopedic dictionary. - M.: "Soviet Encyclopedia". Chief editor V.P. Shishkov. 1981 .

See what "BIRD FLU" is in other dictionaries:

bird flu- (lat. Grippus avium), classic bird plague is an acute infectious viral disease of birds, characterized by damage to the digestive and respiratory organs, high mortality. Antigenic variability of the avian influenza virus and the presence of highly virulent ... ... Wikipedia

animal flu- animal influenza, an acute contagious viral disease of pigs, horses, cattle and birds, caused by viruses of the Orthomyxoviridae family. Swine flu occurs in the cold season, is characterized by a sudden onset, abruptly ... ... Agriculture. Big encyclopedic dictionary

Influenza A birds (avian influenza)- 2. Characteristics of the disease. Influenza A birds (hereinafter referred to as avian influenza) is a disease of domestic and wild birds of various species, capable of occurring in the form of epizootics, which is called such a quantitative expression of the spread of contagious diseases ... Official terminology

ANIMAL FLU- acute contagious viral disease of pigs, horses, kr. horn. livestock and birds, caused by viruses of this family. Orthomyxoviridae. Swine flu occurs in the cold season, is characterized by a sudden onset, pronounced fever, general weakness ... ... Agricultural Encyclopedic Dictionary

animal flu- acute viral disease of pigs, horses, cattle and birds: fever, cough, rhinitis, conjunctivitis, sometimes diarrhea. * * * ANIMAL INFLUENZA ANIMAL INFLUENZA, an acute viral disease of pigs, horses, cattle and birds:… … encyclopedic Dictionary

- (Grippus suum), swine influenza, a highly contagious viral disease of pigs, characterized by catarrh of the respiratory tract, weakness and fever. G. s. registered in many countries of the world, including in the CCC. It causes ... ... Veterinary Encyclopedic Dictionary

ANIMAL FLU- an acute viral disease of pigs, horses, cattle and birds: fever, cough, rhinitis, conjunctivitis, sometimes diarrhea ... Big Encyclopedic Dictionary

FLU- an acute viral respiratory disease, which often acquires the character of an epidemic. The term flu is sometimes erroneously referred to as different forms of viral gastroenteritis, known to non-specialists as stomach flu, intestinal flu… Collier Encyclopedia

animal flu- an enzootic contagious disease of pigs, horses, ducks, chickens and other birds, characterized mainly by damage to the respiratory tract (in pigs, horses, ducks) or proceeding as a general septic acute disease (in chickens). Viruses... ... Great Soviet Encyclopedia

ANIMAL FLU- acute viral disease of pigs, horses, kr. horn. livestock and birds: fever, cough, rhinitis, conjunctivitis, sometimes diarrhea ... Natural science. encyclopedic Dictionary

Books

• Pandemics of the beginning of the XXI century. Avian influenza and the 2009 H1N1 swine flu pandemic, Kiselev Oleg Ivanovich. The monograph is devoted to the analysis of the structure, origin, genetic determinants of pathogenicity and transmissibility of pandemic influenza viruses. The properties and application schemes are described in detail ...

Avian influenza is an acute zoonotic infectious disease with a predominantly fecal-oral mechanism of pathogen transmission. It is characterized by a pronounced febrile-intoxication syndrome, lung damage with the development of RDS and high mortality.

ICD code 10

J10. Influenza caused by an identified virus.

Etiology (causes) of bird flu

The causative agent is influenza A virus of the genus Influenzavirus of the Orthomyxoviridae family. It is classified as an enveloped virus. The virion has an irregular or oval shape, covered with a lipid membrane pierced by glycoprotein spikes (spicules). They determine the hemagglutinating (H) or neuraminidase (N) activity of the virus and act as its main antigens. There are 15 known (according to some sources, 16) variants of hemagglutinin and 9 - neuraminidase. Their combination determines the presence of virus subtypes, and 256 combinations are theoretically possible. The modern "human" influenza virus has combinations of H1, H2, H3 and N1, N2 antigens. According to seroarchaeological studies, a severe pandemic of 1889-1890. was caused by the H2N2 subtype, a moderate epidemic of 1900–1903. - subtype H3N2, Spanish flu pandemic of 1918-1919. - H1N1 containing an additional protein derived from the avian influenza virus.

Epizootics of avian influenza in recent years are associated with subtypes H5N1, H5N2, H5N8, H5N9, H7N1, H7N3, H7N4, H7N7. Subtypes H1, H2, H3, N2, N4 circulate in wild bird populations; similar to the human influenza A virus. Under the lipid membrane is a layer of the matrix protein M-protein.

The nucleocapsid, located under the two-layer shell, is organized according to the type of helical symmetry. The genome is represented by single-stranded RNA, consisting of eight separate segments. One of the segments encodes non-structural proteins NS1 and NS2, the rest encode virion proteins. The main ones are NP, which performs regulatory functions, M-protein, which plays an important role in the morphogenesis of the virus and protects its genome, and internal proteins - P1-transcriptase, P2-endonuclease and B3-replicase. Differences in the structural proteins of the avian influenza virus and human influenza represent an insurmountable species barrier that prevents the replication of the avian influenza virus in the human body.

Different subtypes of this virus have different virulence.

The most virulent subtype is H5N1, which in recent years has acquired a number of unusual properties:

High pathogenicity for humans;
- the ability to directly infect people;
- the ability to cause hyperproduction of pro-inflammatory cytokines, accompanied by the development of acute RDS;
- the ability to cause multi-organ disorders, including damage to the brain, liver, kidneys and other organs;
- resistance to the antiviral drug rimantadine;
- resistance to interferon.

The avian influenza virus, in contrast to that of the human virus, is more stable in the environment. At a temperature of 36 ° C, it dies in three hours, 60 ° C - in 30 minutes, during the heat treatment of food (boiling, frying) - instantly. Tolerates freezing well. In bird droppings, it survives up to three months, in water at a temperature of 22 ° C - four days, and at 0 ° C - more than a month. It remains active in carcasses of birds for up to a year. Inactivated by common disinfectants.

Epidemiology of avian influenza

The main reservoir of the virus in nature are migratory waterfowl belonging to the orders Anseriformes (wild ducks and geese) and Charadriiformes (herons, plovers and terns). Wild ducks are of the greatest importance. Influenza viruses in Eurasia and America evolve independently, so migration between continents does not play a role in the spread of the virus, longitude flights are crucial. For Russia, the Central Asian-Indian and East Asian-Australian migration routes are important in this regard. They include routes to Siberia via Malaysia, Hong Kong and China, i.e. regions where there is an intensive formation of new variants of the virus. Less significant are the East-African-European and Western-Pacific routes.

In wild waterfowl, the virus does not cause clinically significant disease, although a large-scale severe influenza epizootopy has been described in Arctic terns. The replication of the virus in birds occurs mainly in the intestines and, accordingly, it is released into the environment with faeces, to a lesser extent with saliva and respiratory material. 1 g of faeces contains enough virus to infect 1 million poultry.

The main mechanism of transmission of the virus in birds- fecal-oral.

Waterfowl (ducks) are able to transmit the virus transovarially and thus serve as its natural reservoir and spread along their migration routes. They are the main source of infection for poultry, which, on the contrary, suffer from severe forms of influenza, accompanied by their mass death (up to 90%). The most dangerous subtype is H5N1. Infection occurs in conditions of free keeping and the possibility of contact with their wild counterparts. This is especially true for the countries of Southeast Asia (China, Hong Kong, Thailand, Vietnam and other states). There, along with large poultry farms, there are many small peasant farms.

The avian influenza virus can infect mammals: seals, whales, minks, horses and, most importantly, pigs. Cases of penetration of the virus into the population of the latter were noted in 1970, 1976, 1996 and 2004. These animals can also be affected by the human influenza virus. Human susceptibility to such avian viruses is currently low. All cases of infection were recorded in those who had long and close contact with a sick bird. An experiment conducted in the UK on the introduction of various subtypes of the virus into the body of volunteers gave a negative result.

In Thailand, with a population of 60 million, 12 human cases were reliably identified during an epizootic that affected two million birds. In total, by 2007, about 300 episodes of "bird" flu in humans were registered. Two cases of infection from a sick person have been officially recorded.

These data suggest that circulating strains of avian influenza virus do not pose a serious threat to humans. Thus, it can be concluded that the interspecies barrier is strong enough.

Even isolated cases of infection of people from birds and from patients indicate that the insurmountability of the interspecies barrier is not absolute.
The actual number of cases of infection from poultry, and possibly from sick people, given the real situation in regions where epizootics are rampant, can be many times higher. During the H7N7 influenza epizootic in Holland, 77 people fell ill, one died. High antibody titers were found in persons in contact with patients, which also indicates the possibility of transmission of the virus from person to person, but with a loss of virulence.

Secondly, the mutagenic potential of the avian influenza virus, especially the H5N1 subtype, is very high.

Thirdly, pigs are susceptible to avian influenza and human influenza viruses, so it seems theoretically possible for the pathogens to occur in the animal's body. Under these conditions, their hybridization and the emergence of assortant viruses with high virulence characteristic of the avian influenza virus, and at the same time capable of being transmitted from person to person, can occur. Due to the massive spread of avian influenza, this probability has increased dramatically.

Cases of human infection with swine flu have also been described, but the simultaneous penetration of two viruses into the human body is still less likely.

Fourth, it has been proven by genetic methods that the Spanish flu pandemic of 1918-1919. was of bird origin.

Fifth, in modern conditions, thanks to the processes of globalization, the availability of fast modes of transport, the possibility of spreading the assortant virus increases dramatically. Thus, it is fair to conclude that the likelihood of a new variant of the influenza A virus and the emergence of a severe pandemic is very high.

Mathematical modeling methods show that in a city with a population of seven million (Hong Kong), the number of cases at the peak of the epidemic can reach 365 thousand people daily (for comparison, in Moscow during the flu pandemic in 1957, this number did not exceed 110 thousand people a day ). According to WHO experts, it is possible that the rapid culling of birds during the epizootic in Hong Kong in 1997 prevented an influenza pandemic. US experts predict that in the event of a pandemic in America, from 314 to 734 thousand people will need to be hospitalized, from 89 to 207 thousand will die.

The pathogenesis of avian influenza in humans

Currently, the mechanism of development of influenza caused by the H5N1 virus in humans is not well understood. It has been established that the place of its replication is not only epithelial cells of the respiratory tract, but also enterocytes. Taking into account general biological and immunopathological processes, it can be assumed that the pathogenesis of influenza A (H5N1) in humans will develop according to the same mechanisms.

Various hemagglutinins of avian influenza viruses differ in their ability to recognize and bind to the receptor, sialic acid, bound in the oligosaccharide of cell membranes with galactose. The hemagglutinins of human influenza viruses interact with the residues of this acid, combined by a 2,6 bond with galactose, and the hemagglutinin of avian influenza viruses recognizes it in a 2,3 bond with galactose residues. The type of terminal sialic acid bond and the conformational mobility of surface lectin oligosaccharides are the main elements of the interspecies barrier for avian and human influenza viruses. Human tracheal epithelial cell lectins include lectins with the 2,6 linkage type and do not contain the 2,3 linkage type oligosaccharides characteristic of avian intestinal and respiratory epithelial cells. Changes in the biological properties of a highly pathogenic strain of the A virus (H5N1), the emergence of its ability to overcome the interspecies barrier can lead to damage to various cell types in humans with the development of more severe forms of the disease. In the clinical picture of such pathologies, along with the catarrhal syndrome, damage to the gastrointestinal tract develops.

Clinical picture (symptoms) of bird flu

The incubation period for influenza A (H5N1) is 2-3 days, with fluctuations from 1 to 7 days.

The main symptoms and dynamics of their development

The onset of the disease is acute. Symptoms of intoxication are expressed. Body temperature from the first hours of illness rises to 38 ° C, often reaching hyperpyretic values. The febrile period lengthens to 10-12 days, and in severe cases with a fatal outcome - until the last hours of the patient's life. Chills, muscle and joint pains are characteristic. At the height of the disease (2-3rd day), catarrhal syndrome joins, manifested by the development of bronchitis, bronchiolitis, laryngitis; there may be signs of rhinitis. Sore throat and "flaming" oropharyngitis are characteristic. During this period, most patients develop primary viral pneumonia. At the same time, shortness of breath, a wet cough with sputum, possibly with an admixture of blood, appear. Harsh breathing, wet rales of various sizes, crepitus are heard above the lungs.

On a chest x-ray in the early stages, nonspecific changes are determined in the form of diffuse, multifocal or individual infiltrates, tending to rapidly spread and merge. In some cases, segmental or lobar compactions may be detected. It is characterized by a progressive course, an increase in shortness of breath and the development of RDS. Along with intoxication and catarrhal syndrome, a gastrointestinal tract lesion develops, manifested by repeated vomiting, secretory diarrhea and abdominal pain. Perhaps an increase in the liver, accompanied by an increase in the activity of serum transferases. A third of patients develop acute renal failure, creatininemia.

In most patients, signs of damage to the nervous system are determined, impaired consciousness, and the development of encephalitis are possible.

Leukopenia, lymphopenia, thrombocytopenia are recorded in the hemogram.

There may be variants of the course of the disease with fever, diarrhea and no signs of respiratory damage.

Complications of bird flu

The infection is dangerous by the development of viral pneumonia, damage to the kidneys, liver, blood-forming organs. It is these consequences that often lead to the death of patients. It has been established that the place of replication of the H5N1 influenza virus in humans (at least in those who died as a result of the disease) is not only the respiratory tract, but also the intestines.

Risk factors for severe influenza A (H5N1) in humans:

Age of the patient (in children five years of age and younger, the symptoms of the disease are not pronounced);
- the duration of the manifestation of the disease before hospitalization (delay from hospitalization);
- anatomical level of damage to the respiratory tract;
- degree of peripheral blood leukopenia;
- the presence of multiple organ dysfunction.

Mortality and causes of death

Mortality is 50–80%. Most often, patients die from complications in the second week of illness.

Diagnosis of bird flu

The correct diagnosis at an early stage is the starting point for organizing targeted treatment, timely anti-epidemic measures and determining the prognosis. However, in the way of diagnosing avian influenza, there are certain objective difficulties associated with the similarity of the clinical picture of this disease and other acute respiratory viral infections.

A preliminary diagnosis of influenza A (H5N1) can be made on the basis of the following data from the epidemiological history and clinical manifestations:

The presence of reports of outbreaks of influenza A (H5N1) among the population of birds and animals or cases of death of poultry in the region of residence of the patient;
- contact with a sick person who is confirmed to be infected with the influenza virus (H5N1), seven days before the first clinical signs appear;
- contact with a patient with acute respiratory infections of unclear etiology, including fatal ones, seven days before the first clinical signs appear;
- an indication of the patient to travel to a country or territory where there are reports of an unfavorable epidemiological and / or epizootic situation for influenza A (H5N1);
- the presence of an occupational risk of infection of the patient;
- high fever combined with shortness of breath, cough;
- diarrhea (in the absence of blood in the feces).

The final diagnosis can be made after laboratory confirmation.

Laboratory diagnostics is based on the methods of virological research, serological reactions, immunofluorescent analysis and PCR.

Differential Diagnosis

Considering that influenza A (H5N1) causes symptoms of respiratory tract damage, it is necessary to carry out differential diagnostics with other acute respiratory viral infections: “traditional” influenza (A, B), severe acute respiratory syndrome, parainfluenza, respiratory syncytial, adenovirus and enterovirus infections, and also legionellosis and ornithosis.

Indications for consulting other specialists

With the development of ARF - consultation of a resuscitator.

Diagnosis example

J10. Influenza caused by the H5N1 virus, severe; complication - pneumonia, ODN.

Indications for hospitalization

The clinical picture of a respiratory infection in a patient who had contact with a sick bird.

Bird flu treatment

Mode. Diet

When the diagnosis of influenza A (H5N1) is confirmed, treatment is carried out in a boxed department of a hospital. During the entire acute period of the disease, bed rest must be observed. A complete diet rich in vitamins and containing sufficient fluids is recommended.

Medical therapy

Etiotropic therapy

Currently, oseltamivir (Tamiflu), an antiviral drug belonging to the class of neuraminidase inhibitors, is the most effective among etiotropic drugs. It is prescribed at a dose of 75 mg orally twice a day for seven days. It is possible to increase the dose to 300 mg. You can also use rimantadine (rimantadine, algirem).

Pathogenic agents

In pathogenetic therapy, the leading role belongs to detoxification. According to clinical indications, intravenous administration of crystalloid solutions is used to correct acid-base balance and electrolyte balance.

In severe clinical forms of the disease, glucocorticoids and aprotinins are indicated. With the development of ARDS, treatment is carried out in the intensive care unit with mandatory respiratory support, a surfactant is administered. Symptomatic therapy is carried out according to indications.

Convalescents are discharged from the hospital no earlier than seven days after the restoration of normal body temperature.

All contacts with influenza A (H5,N1) patients are shown medical observation for seven days, with body temperature measurement twice a day. With its increase, the appearance of a cough and difficulty breathing, you should immediately seek medical help.

Forecast

The prognosis of the disease is unfavorable. Mortality is 50-80% in the second week of illness.

Prevention measures

Specific

Global monitoring under the auspices of WHO allows you to quickly detect a dangerous virus and start mass production of a vaccine. Mass vaccination can be started in nine months. At present, it is important to carry out high-quality anti-epidemic measures aimed at reducing the spread of human influenza. In particular, it is necessary to increase the number of vaccinated, which will reduce the incidence rate, and possibly susceptibility to a new version of the virus. In some countries, a limited number of vaccines against antigenic variants of the virus are produced. According to forecasts, they are the most likely candidates for a new pandemic virus.

The main method of combating avian influenza is the complete extermination of the number of birds on infected farms, and those who come into contact with them and carry out their destruction must work in respirators and overalls. Great importance is attached to disinfection using quaternary ammonium compounds (acepur) that are non-toxic to humans. They are easily neutralized by soaps and other detergents. Carry out quarantine measures, prohibit the export of poultry and eggs from the affected regions. In the surrounding farms and poultry farms, vaccination is carried out, but its effectiveness and expediency are doubtful. The presence of antibodies in vaccinated birds makes monitoring difficult, as it does not allow differentiation from infection, and there is also evidence that vaccination contributes to virus mutation.

In Russia, the introduction of infection is possible with migratory birds. However, the conditions of agriculture in Russia (predominantly closed poultry keeping, low probability of contact with pigs, less close contact between people and animals than in Southeast Asia) make it possible to practically exclude the possibility of the emergence of an assortant virus. In this regard, the main activities should be aimed at preventing the transfer of the virus from countries where it may appear. To do this, it is necessary to tighten sanitary control at the border, recommend wearing respiratory masks, their preventive effectiveness reaches 98%.

Highly pathogenic avian influenza

Highly pathogenic avian influenza is an acute, highly contagious disease of birds accompanied by damage to the respiratory system, gastrointestinal tract and nervous phenomena. The disease can proceed without preliminary symptoms.

Etiology. The causative agent of the disease is a complexly organized RNA genomic virus belonging to the Orthomyxoviridae family, type A (Influenzaviruc A), which, by its serological properties, the most important of which is the surface antigen - hemagglutinin ( H) is subdivided into 15 subtypes currently known ( H1-H15). In addition, there is a similar intraspecific differentiation for the second surface antigen, neuraminidase ( N1-N9). All subtypes of the virus circulate among wild birds. The epizootic circulation of a highly pathogenic avian influenza virus can be quite long, in particular, in Mexico, a highly pathogenic H5N2 mutant caused the disease in birds with high mortality during 1992-1995.

The virus is resistant to low temperatures. However, it is characterized by high sensitivity to high temperature and traditional disinfectants.

Epizootic data. Under natural conditions, all types of birds are affected, and pigs and horses are also susceptible. Infection of people through meat products and eggs has not been recorded. Avian influenza is not registered in the Republic of Belarus. Human cases have been reported in Asia, the Middle East and some European countries. The main source of the pathogen is a sick bird and virus carriers, which actively excrete the virus with feces, nasal exudate and saliva. The transmission factors of the pathogen are virus-contaminated care items, inventory, feed, water, poultry products, etc. Waterfowl is the natural host of the virus. Infection occurs most often through the alimentary route. The transmission of the virus is carried out at a distance within a radius of 10 km from the epizootic focus or through indirect contact with wild, primarily waterfowl. No pronounced seasonality was found. However, the disease is more often recorded in the spring-summer period. The disease proceeds in the form of epizootics and panzootics.

Pathogenesis. By infecting epithelial cells, in the process of its reproduction, the virus causes their lysis and intoxication phenomena. The permeability of blood vessels increases, which leads to various forms of hemorrhage. In addition, the virus has a destructive effect on the immune system.

Symptoms and course. The incubation period is determined by the type and age of the bird and most often it is 2-7 days. Highly pathogenic influenza often occurs acutely and subacutely.

In chickens, with a mixed respiratory-intestinal form, the disease is accompanied by a coma, refusal to feed, thirst, atony goiter, discharge from the nasal cavity and beak, and shortness of breath. Body temperature rises to 44 ° C. Later diarrhea appears. The litter becomes frothy, a dirty yellow liquid consistency with an admixture of blood elements. Scallop and earrings with a bluish tinge. Edema appears in the head, neck, chest and larynx. The presence of edema is a characteristic sign of the disease. Violated coordination of movements due to paresis and paralysis.

In waterfowl, signs of pathology of the respiratory organs and the nervous system are noted. The bird is in deep prostration with an unnaturally positioned head and neck. In birds (ducks, geese) with influenza, the following were noted: head eversion by 180 0 hyperemia of the beak and legs, cracking and detachment of the stratum corneum of the beak, cyanosis of the oral mucosa, conjunctivitis, formation of a cloudy film on the cornea of ​​the eyes, anxiety, circular and aimless movements , hyperthermia, head trembling, drooping wings, diarrhea.

An autopsy of a bird allows you to establish the presence of catarrhal-hemorrhagic enteritis, aerosacculitis, tracheitis, conjunctivitis and hemorrhages in the serous integument, the digestive tract and parenchymal organs.

Diagnosis. Diagnosis is carried out comprehensively, taking into account a wide range of indicators such as: epizootological data, clinical signs, autopsy results with mandatory virological and serological testing. Of decisive importance in the diagnosis is the isolation of the virus with its mandatory typing.

Highly pathogenic influenza is differentiated from Newcastle disease, infectious laryngotracheitis, respiratory mycoplasmosis and other diseases with similar symptoms.

Treatment a sick bird is not carried out in view of the possible spread of the virus beyond the border of an unfavorable zone, it is destroyed.

Prevention and control measures. In order to create active immunity, inactivated whole-virion and recombinant vaccines are recommended for use.

To prevent the disease of birds with influenza, the heads of poultry farms, enterprises and organizations engaged in poultry breeding are obliged to: 1) ensure that all poultry farms (branches, poultry houses) have a strict sanitary-hygienic and veterinary regime to protect against the introduction of the pathogen; 2) poultry farms must operate in a closed regime with a strict access system; 3) barriers, barriers, disinfectants at the entrance to the farm, points for disinfection of returnable meat and egg containers and sanitary checkpoints for service personnel must be in working order; 4) exclude the possibility of penetration into poultry houses, feed shops, feed stores, ovipositors and other objects of wild birds.

Citizens who own a bird are obliged to strictly follow the recommendations of veterinarians on the conditions of keeping poultry. Avoid contact of poultry with wild birds, especially waterfowl.

If highly pathogenic influenza occurs in a bird, the head of the farm or the owner of the bird is obliged to immediately inform the veterinary specialist of the farm, district and take measures to prevent the spread of the disease in compliance with the rules of personal hygiene.

Veterinary specialists are obliged to immediately take the necessary measures to establish a diagnosis, at the same time to examine all the poultry of the farm and the given settlement.

After the diagnosis of influenza is established, quarantine is imposed on the unfavorable point on the proposal of the chief veterinary inspector of the district (city) in the manner prescribed by the legislation of the Republic of Belarus.

In poultry farms that are unfavorable for bird flu, all clinically ill, weak and suspicious birds in poultry houses that are unfavorable for the disease are immediately destroyed. When influenza is detected among birds belonging to the population, all sick and suspicious birds of dysfunctional yards are destroyed by burning.

In dysfunctional and adjacent poultry houses, paddocks, solariums, utility rooms, yards, thorough mechanical cleaning and disinfection is carried out. Litter, bedding, garbage, as well as perches of feeders with food residues and low-value wooden implements are burned. Means of transport (cars, carts, etc.) are also subject to disinfection.

Quarantine from settlements is removed after the last case of the destruction of a bird with influenza and the final veterinary and sanitary measures.

DISEASES OF OSTRICHES

(Sinitsa N.V., Soboleva I.V.)

ostrich flu

It is an acute contagious disease caused by a virus from the family Orthomyxoviridae, type A, characterized by damage to the respiratory and digestive organs, edema and depression. The disease occurs predominantly in South Africa.

Etiology. To date, several types of this virus have been identified in ostriches, in particular, H7N1, H5N9, H5N2, H9N2. The reservoir of the virus can be agricultural and wild birds.

The virus is not stable in the external environment at a temperature of 55 ºС it is inactivated within 1 hour, at 60 ºС - in 10 minutes, at 70 ºС - in 2-5 minutes, when boiled - instantly. Negative temperatures have a preservative effect. Disinfectants in normal concentrations have a detrimental effect on the pathogen.

epidemiological data. The source of the causative agent of infection are sick and recovered ostriches. A significant role in the occurrence and spread of the disease is given to wild birds, especially with their free access to food stores. The main route of transmission is airborne, but there is evidence of transovarial transmission of the virus. The appearance of the disease may also be favored by the lack of proper living conditions, underfeeding and, to a greater extent, an imbalance in the diet. Influenza can occur in ostriches usually between the 6th and 13th month of life. However, it is especially dangerous for chicks due to high morbidity and mortality, which in chicks a few days old can be up to 60% and even up to 80%.

Course and symptoms. Typical manifestations of the disease are weak appetite, general weakness, diarrhea, a noticeable change in the color of urine, which becomes greenish, bulging eyes and ailments in the respiratory system, an increase in body temperature by 1-2 ºС. Influenza viruses with low pathogenicity can not only reduce egg laying, but also stop it altogether.

pathological changes. At autopsy, hemorrhages are observed, mainly in the serous integument, parenchymal organs, skeletal muscles, and the digestive tract. Characterized by acute or subacute catarrhal inflammation of the gastrointestinal tract with thickening of the mucous membrane. There are focal necrosis in the spleen, liver, kidneys and central nervous system. At autopsy of the corpses of ostriches with a respiratory form of influenza, catarrhal conjunctivitis, rhinitis, sinusitis, tracheitis, aerosacculitis and interstitial pneumonia, nephritis are found. In some cases, in females, lesions of the oviducts and ovaries are noted.

Diagnostics. The diagnosis of influenza is made in a complex manner, taking into account epidemiological data, clinical signs and pathological changes. The final diagnosis is established by laboratory methods.

For research, samples from the respiratory tract (trachea, lungs, air sac, exudate from the sinuses) are sent to the laboratory. The virus can be isolated from the liver, spleen, blood, lavage from the cloaca. Samples from the trachea, exudate from the sinuses and material from the cloaca are taken with dry sterile swabs, which are placed in test tubes with 2 ml of sterile saline, to which antibiotics are added: penicillin - 10,000 U, streptomycin - 10 mg / ml, mycostatin - 200 U / ml. Fresh material should be delivered to the laboratory within 6 hours, and in a frozen state - within a day.

For the study, the method of infection of chicken embryos is used (to isolate a pure culture), and for identification - RTGA, RSK, ELISA, PCR.

Treatment. Not developed, due to the danger of the spread of sick ostriches, they are killed by a bloodless method and destroyed.

Prevention. It consists in observing zoohygienic and veterinary standards of feeding and keeping, preventing contact with wild birds, as well as importing ostriches and hatching eggs from safe farms for this disease.

Ostrich pox

Smallpox is a highly contagious disease caused by a dermotropic virus from the family Avipoxvirus, manifests itself in the form of smallpox exanthema or diphtheroid lesions, often in a mixed form (smallpox-diphtheroid), sometimes atypically and often with a chronic course.

Etiology. DNA containing virus, belongs to the genus Avipoxvirus, sensitive to high temperature, ethyl alcohol. Freeze-drying and low temperatures preserve it. Chemical disinfectants in normal concentrations have a detrimental effect on the pathogen.

epidemiological data. The disease is registered mainly in the USA, Israel, Mexico and Australia.

Outbreaks of smallpox occur in the form of enzootics, less often acquire the character of epizootics. The duration of the illness is about 6 weeks.

Ostriches are more likely to become infected when patients come into contact with healthy ones, through virus-contaminated feed, water, bedding, inventory, and clothing of attendants.

The virus enters the external environment with falling crusts, films, pieces of epithelium, secretions from the oral and nasal cavities, from the eyes, with droppings and infects the premises, containers, equipment, inventory and other items. The smallpox virus is carried not only by agricultural birds, but also by wild birds, as well as by rodents and blood-sucking insects.

Smallpox can occur at any time of the year, but more often and more severely it occurs in autumn, winter and early spring, since at this time the bird develops hypovitaminosis and mineral metabolism disorders. Crowding and stress also contribute to the long course of smallpox.

Ostriches are most susceptible to smallpox up to the 4th month of life. Morbidity is 10-50%, mortality - 15-25%.

Course and symptoms. Four forms of smallpox have been established: smallpox (skin), diphtheroid, mixed, and very rarely atypical or hidden with damage to internal organs. The course of the disease is predominantly subacute, sometimes chronic and rarely acute.

In the cutaneous form, infection of ostriches occurs through damaged skin and the mucous membrane of the nose and beak cavity. Sick birds have swollen eyelids, making it difficult to see. Warty tubercles of various sizes appear on the skin. There are also changes in the angle of the beak, which greatly complicates eating and even breathing. The cutaneous form proceeds, as a rule, benignly.

With the diphtheroid form, whitish, opaque, somewhat elevated nodules appear on the surface of the mucous membrane of the oral cavity, palate, tongue, larynx, bronchi, adnexal cavities, rarely appear on the intestinal mucosa. These lesions spread rapidly, increase in size, merge with each other and acquire a yellowish color. Diphtheroid overlays in the form of cheesy films of golden-white or yellow-brown necrotic tissue are connected to the submucosa. For smallpox films, their deep ingrowth into the submucosa is typical.

The larynx is most often affected. Breathing is usually very difficult. A sick bird stretches its neck, keeps its beak open or often opens it, makes whistling, groaning or wheezing sounds, and hardly inhales air. Feeding is difficult. The bird cannot close its jaws.

When the nasal cavity is damaged, a runny nose appears, serous, mucous, and later - mucopurulent outflows of a dirty yellow color are released from the nostrils, after which the nasal passages are sealed after drying. As a result of damage to the nasopharynx, the lacrimal canal and the infraorbital fossa are involved in the pathological process. The latter is filled with inflammatory exudate and a painful swelling of a dense consistency forms under the eye. The inflamed infraorbital sinus presses the eyeball up and back and presses on the palate, forcing it downward, making it difficult to close the beak and take food. The bird's head sometimes takes on an ugly shape.

Diphtheroid eye damage begins with photophobia, lacrimation, swelling and redness of the eyelids. Mucopurulent exudate dries up at the edges of the eyelids and sticks them together.

The mixed form of smallpox is characterized by a combination of cutaneous and diphtheroid forms, with the predominance of one of them. If there are no complications, a bird with smallpox recovers after 4-6 weeks. The diphtheroid form, in contrast to smallpox, is more severe, especially in young birds.

Pathological changes. In the smallpox form, smallpox nodules of a solid consistency with an elevated central part are found on the skin. The surface of small nodules is smooth, shiny, tense, light brown in color. Large nodules are rough, covered with dark brown cracked scabs that resemble warts. Histological examination of vertical sections of pockmarks establish a spike-like growth of the skin epithelium. In the affected cells of the epidermis, cytoplasmic viral bodies are found - Bollinger's inclusions, which is a pathognomonic sign.

With an atypical form, changes on the skin are not pronounced, while on the internal organs they are significant. Small yellowish foci are found in the liver, the lungs are edematous, petechial hemorrhages are visible on the epicardium and serous membranes, the intestinal mucosa is loosened with hemorrhages.

In the chronic course of the disease, the liver, kidneys, heart are reborn, the spleen is swollen, brown-gray in color. The corpses of dead birds are emaciated, which is also characteristic of the latent course of smallpox.

Diagnostics. The diagnosis of smallpox is made comprehensively, taking into account epizootological data, clinical signs and pathological changes. The final diagnosis is established by laboratory methods.

If there are typical smallpox skin lesions, the diagnosis is not difficult. In doubtful cases, the head, the affected areas of the skin and internal organs are sent to the laboratory for bioassay and histological examination.

Smallpox is differentiated from hypovitaminosis A, respiratory mycoplasmosis, aspergillosis, candidiasis, staphylococcosis and other skin lesions. Skin lesions are differentiated using a histological examination of the pathological material, which reveals the spherical degeneration of epithelial cells characteristic of smallpox and the formation of Bollinger bodies.

Prevention. It is possible to almost completely prevent the disease by inoculation at two weeks of age with the ostrich pox vaccine, which is injected into the wing membrane ( wing web).