Pullorosis chickens treatment with what antibiotic to drink. Pullorosis typhus in poultry. Therapeutic and preventive measures

Pulloroz(bacillary white diarrhea) of birds is an acute infectious contagious disease of chickens; at adult bird it proceeds in the form of a chronic latent infection. The causative agent of the disease is Salmonella pullorum.

Historical overview and prevalence. The birthplace of the infection, where it was discovered and studied, is considered the United States. Here Retger published in 1900 his research on septicemic epidemic disease in 2-3-week-old chickens. He isolated a microbe from them and became convinced of its pathogenicity.

Later, while studying the epizootic on chickens in Connecticut, Retger called the disease white-nosed.

Bacillary white diarrhea, or, as it came to be called, pullorosis, was found for a short time in most states of the United States, in Canada, in the South American republics, in Australia, Africa, Japan, and in colonial countries. Soon there were reports of pullorosis in most European countries. In this way, pullorosis proved to be one of the most common avian infections.

In the USSR, the infection was first established in 1926 in imported chickens; in subsequent years, pullorosis began to be recorded everywhere where the bird was imported from abroad.

Economic damage. In the United States, a country with a developed poultry industry, when measures to combat pullorosis had not yet been developed, this branch of the economy was brought to a catastrophic state due to the mass departure of chickens. The losses were so great that the government allocated large funds for the study of the disease. Losses were caused primarily by the mortality of chickens.

So, according to Retger, the death of chickens hatched from birds of an infected herd is 77%, while the total waste from various causes among chickens from a healthy herd is only 5.98%.

According to the Michigan College, the loss of chickens from a pullor flock of hens, even under the most favorable conditions, reached 29.6%, versus a waste of 1.02% among chickens bred from a healthy flock.

Infected flocks also produce 23.5% more weak chicks than healthy flocks. The fertility of eggs from pullor birds is reduced by 20%, and the yield of chickens is reduced by 12%. The death from pullorosis of chickens is also high in the embryonic period of their life (the so-called "suffocating"): 15-40% of vibrios are underdeveloped in the eggs.

The victims of pullorosis are not only chickens, but also an adult bird, among which a departure from the latent form of the disease is sometimes observed.

In addition, in a pullora adult bird, the number of eggs laid is reduced by 10–20%, and with a far advanced process, oviposition completely stops.

Etiology. Salmonella pullorum belongs to the coli-typhoid group of microbes. The microbe is a gram-negative, capsuleless, with rounded ends, a stick 1–2.5 r long. (according to American data - 3 - 5 rubles) and 0.3 - 0.8 ji in diameter, motionless, not forming a dispute. It stains well with ordinary paints, sometimes bipolar.

Cultivation. S. pullorum - facultative aerobe; it is easily cultivated at thermostatic temperature on conventional nutrient media. Its distinct growth appears during the first day and reaches a maximum on agar media by 17g - 2 days.

On ordinary agar slant, freshly isolated strains of S. pullorum produce cultures of two types: in the form of separate transparent horn-shaped small colonies and in the form of coarser, whitish-bluish colonies shining from the surface.

When bacteriological examination of the material from chickens or adult chickens that have died from pullorosis, they do not receive mucous, honey-like cultures typical of chicken typhus.

On direct agar, cultures of S. pullorum grow in separate colonies at the prick. Gelatin does not liquefy.

On potatoes, growth becomes distinct on the second day and appears as a greyish-white, not particularly abundant overlay. On Drygalski's agar - small bluish colonies.

In the broth, S. pullorum gives a uniform, rather abundant turbidity of the medium and a loose sediment, which easily breaks into a uniform turbidity when shaken; in aging cultures, a small parietal ring forms on the surface, and the sediment becomes denser.

Milk does not coagulate or peptonize; its reaction becomes slightly sour. Litmus milk first turns slightly pink and then turns blue. The most favorable temperature for the formation of hydrogen sulfide is 30 - - 34 ° C; at 37 CC, hydrogen sulfide is detected intermittently; this property is not well expressed in all strains of S. pullorum. Indole is not formed.

For practical diagnostics, when one often has to deal with stale corpses, the diamond-green medium deserves attention. Brilliantgreen, added to the medium at a concentration of 1: 60,000, does not inhibit the growth of pullor bacillus and S. gallinarum), but delays the development of saprophyte microbes.

Carbohydrates and alcohols ferment usually with acid release, and only some strains are capable of gas formation. S.pullorum ferments glucose, levulose, galactose, mannose, arabinose, rhamnose, mannitol; maltose, dulcit are fermented intermittently. Does not ferment lactose, sucrose, glycerin.

Serological properties. Due to the presence of groups of the same name in the somatic O-antigenic complex of S. pullorum (as well as in S. gallinarum), group agglutination is observed with the sera of some representatives of typhoparatyphoid bacteria (b. typhi abdom., S. enteritidis, etc.). The serological relationship between S. pullorum and S. gallinarum is fully revealed when, on the one hand, mucilaginous S. gallinarum cultures are used for the preparation of agglutinating sera and, on the other hand, S. pullorum cultures growing in the form of dewdrop colonies. In this case, the agglutination reaction differentiates S. gallinarum from S. pullorum.

S.gallinarum has S and R variants; S-forms are isolated in acute, and R-forms in chronic avian typhus.

Mucus-forming colonies from cultures of S. pullorum isolated from small chickens are of great interest. Through long-term selection, in the former dew-like colonies of S. pullorum, it is possible to obtain slimy, rampart-forming colonies that are completely identical in cultural and serological respects with S. gallinarum.

Experiments show that both microbes are close to each other, but they represent two variants with differences that are well expressed in their pathogenic characteristics for birds of different ages.

These biologically distinct variants can be reproduced not only experimentally; a similar dissociation takes place in nature. This is evidenced by the ongoing enzootics of pullorosis in all countries, while chicken typhus (causative agent - S. gallinarum) is an infection that appears only from time to time (quickly stopping outbreaks). These temporary enzootics of avian typhus are the result of "typhoid" variants that arose from the Pullor bacillus, which is widespread among birds.

In 5 to 15 day cultures of S. pullorum, toxic substances passing through the filters are formed, which are more pathogenic for guinea pigs than for chickens. Fresh, heat-killed agar cultures are also toxic, injections of which (into the blood or abdominal cavity) cause rapid death of rabbits.

Sustainability. In broth cultures in sealed pipettes, S. pullorum can be stored at room temperature for more than 7 years. In wet feces, the microbe survives for more than 100 days, in water - over 200 days, in wet substrates - about a year. A temperature of 60°C kills S. pullorum in 30 minutes. Under the action of potassium permanganate in a dilution of 1: 20,000, 4% bleach (in the presence of about 1% active chlorine in the solution), S. pullorum dies in 15 minutes; 1% formalin, 1% phenol, 0.1% sublimate kill it in 5 minutes.

Susceptibility. S. pullorum is pathogenic for guinea pigs that die after subcutaneous infection in 1-2 days with edema and necrosis at the injection site; in rabbits and mice, after subcutaneous or intra-abdominal infection, death occurs in 1-7 days.

Sparrows are susceptible, as well as canaries, pheasants, oatmeal with subcutaneous and oral infection; pigeon infection succeeds. The susceptibility of small free-living birds has been studied for laboratory purposes; their epizootological role is reduced to the mechanical spread of infection.

Pullorosis in ducks has been described many times in the literature. The strains isolated from ducklings are culturally and biochemically similar to S. pullorum. Sick chickens are considered the source of infection for ducklings. Yet, until now, there is little evidence to recognize ducks as susceptible to pullorosis as chickens. It can be assumed that ducks are only relatively susceptible to S. pullorum. Pullorosis as a duck infection has not been proven, and this issue is for further study.

Experimental infection of chickens with pullorosis was successful for many researchers. Chickens in the first days of their life are easily infected by feeding cultures, while after the 5th day of them, a smaller percentage of them become ill. With increasing age, the possibility of a fatal infection in chickens decreases. In adult chickens experimentally infected with cultures by feeding, usually it is not possible to cause a fatal disease, but only a chronic infection is achieved. As a rule, agglutinins appear in their blood on the 3rd - 42nd day after infection.

Sources of infection and ways of natural infection. Under normal natural conditions, chickens are susceptible to pullorosis, mainly in the first 20 days of life; susceptibility decreases with age. This is evidenced by the percentage of mortality from pullorosis of chickens of different ages.

So, in Germany, mortality in chickens at the age of 4 days reached 10.5%, 1 week - 20.9%, 2 weeks - 36.2%, 3 weeks - 24%, 5 weeks - 8.4%. The following data are available on observations of pullorosis in the USSR: at the age of 20-45 days, the incidence and withdrawal from pullorosis sharply decrease, and after I1/* months, mortality from pullorosis is calculated in isolated cases.

In adult birds, outbreaks of acute pullor infection are not observed, although they are described in the literature. The death of an adult bird (hens; roosters do not die) is the result of a latent chronic infection.

In this way, pullorosis in an epizootic form it affects young chickens, and in an adult bird it proceeds in a chronic latent form.

The main source of infection is an adult bird. She suffers from pullorosis in a chronic latent form and transmits the infection through eggs to hatching chickens. The infection can affect a chicken not only in the postembryonic period, but also at the stage of embryo development, in an infected laying egg (mainly the yolk is infected). Therefore, the infected laying hen represents the main reservoir of infection, spreading it through the eggs.

However, not all eggs laid by pullor hens are infected. The percentage of infection of eggs varies even in individual laying hens over a wide range, depending on the state of infection in the chicken and on its localization in the body of the bird. It is known that the ovary is the most frequent, but not a permanent location of the microbe (other places of its localization are the heart muscle, liver, etc.); in addition, even with the defeat of the ovary, not all of its follicles are seeded with the pathogen.

Infection of eggs varies widely - from 4 to 89%.

The number of chickens carrying the infection also varies considerably.

In Kansas (USA), when examining 16 million birds, 18% of carriers of the infection were identified. According to Retger, in the herds he studied, the infestation of birds ranged from 0 to 56%. Pullor laying hens (bacillus carriers), infecting the yolk of eggs (the ovary, in which the infection is localized, forms the yolk of the egg, and the protein and the shell are formed in the oviduct), they release the infection by mail exclusively with eggs. The ejection of an infectious agent with feces by adult chickens is a secondary factor that may be due to the localization of the microbe in the oviduct or infection of the intestines. Nevertheless, there are indications of the possibility of infection with pullorosis and adult chickens through their contact with patients.

Oral infection can be achieved after 11/2 - 2 months of infection in ovarian hens, which proves the susceptibility of adult birds. The same is also evidenced by the facts of the transfer of infection from chickens to the broodstock (due to sanitary omissions). In these cases, the disease occurs in chickens not in an acute, but in their usual latent form.

Due to the fact that the embryo is infected while still in the egg, feeding the bird of dead (as poultry farmers sometimes practice) embryos (“suffocators”) can be a dangerous source of infection. The latter is possible both with the shells of eggs from which sick chickens have hatched, and as a result of healthy hens pecking fresh eggs from pullor hens. The spread of infection with the shell of whole eggs is of secondary importance.

In addition to sick chickens, sick chickens spread the infection, abundantly excreting microbes with feces. Due to the relatively high resistance of S. pullorum, incubators, brooderhaus, soil infected with the feces of sick chickens (with careless cleaning of the shell from the incubator, litter from the premises, insufficient disposal of hatchery trays, etc.) are the most dangerous source of pullorosis both among chickens and among adult bird. In this regard, infected bedding, inventory and other items that can contribute to the mechanical transfer of the pathogen are of great importance.

Before the organization of modern control of pullorosis, it was especially widespread with the egg and even more with day-old chickens, which are bred in hundreds of thousands in incubators. Incubators, which replaced the mother hen and laid the foundation for the great growth of the poultry industry, were also the cause of great losses for many farms in the United States. As soon as one infected batch of chickens got into the hatchery, pullorosis covered a huge number of chickens (contact infection). The last ones with a latent form of the disease arrived at the farms at the age of one day, transporting the infection with them.

An infected laying hen, spreading the infection mainly through the eggs she laid and to a much lesser extent as a result of contact with a healthy bird, embryos that died from infection, sick chickens and the external environment infected by their feces - these are the sources of chicken pullorosis. Wild small birds, like many other factors, including roosters, play a mechanical role in spreading the infection. In the testes of roosters, S. pullorum is found in very rare, almost exceptional cases.

Pathogenesis. During the embryonic life of the chicken, the infection contained in the yolk is transmitted to the embryo and causes its death from sepsis or due to nutritional disorders and, possibly, as a result of the formation of toxic substances in the yolk sac.

In chickens hatched from infected eggs, the microbe also initially nests in the yolk sac and partly in the intestines. With the development of infection, the pathogen, spreading through the blood, causes sepsis (more often) or metastasizes to various organs (heart muscle, liver, spleen, partly to the lungs), forming pullor nodes in them (heart, lungs) or foci of necrosis (liver In addition, the infection may be accompanied by focal pneumonia.

The appearance of pneumonia is attributed by some to respiratory infection of chickens in incubators. However, the same lesions of the lungs are obtained by experimental infection through the mouth; therefore, the origin of pneumonias is not only respiratory; they can also be caused by the migration of the microbe from the main reservoir of infection - the yolk sac. Infection of healthy chickens occurs as a result of contact - direct with sick chickens (mainly) or indirectly with a contaminated environment (contaminated feed, inventory, bedding, etc.).

Thus, infection in chickens can be of both embryonic and post-embryonic origin. In both cases, its pathogenesis is basically the same.

Upon recovery, the infectious beginning does not always completely disappear from the body of chickens. In some pullets, the infection takes only a latent course, which does not manifest itself outwardly for a long time. The infection progresses very slowly. The causative agent is localized in this case only in separate foci of various organs (heart muscle, liver, spleen), more often in the ovary, and the rest of their parenchyma usually remains free from microbes. This form is accompanied by a slow intoxication of the bird's body, which is expressed in the degeneration of the liver, heart muscle and ovary.

Clinical picture and course. The main symptom of the disease in chickens is diarrhea (often profuse) with a high content of uric acid in the feces, which is why the liquefied feces turn whitish. The feces, polluting the fluff around the anus and drying on it, form a plug that prevents the free exit of feces that accumulate in the rectum in large quantities. Mechanical constipation occurs with the formation of stones. This undoubtedly accelerates the course of the disease and increases the number of deaths.

Sick chickens are little mobile, walk with a retracted neck, half-closed eyes, often squeak; their feathers are ruffled; anemia develops rapidly, growth slows down sharply.

In the first 3 - 4 days of a chicken's life, the disease is acute, ending in death in 1 - 3 days. Chickens are seriously ill even up to 10-20 days of age, although the disease takes a somewhat longer course during this period (2-8 days). After 20 days and up to 1% of months, the incidence and death from pullorosis, as we have already indicated, are sharply reduced; the disease is subacute or chronic. Recovered chicks recover so much that they appear clinically healthy.

With a latent form of infection in an adult bird, the disease lasts for many months and years; its signs are revealed only with a strong defeat of the body. They are expressed in the sagging of the abdomen, anemia, decreased oviposition, and shortly before death or with advanced myocarditis - in the cyanosis of the scalp and mucous membranes. Death often occurs from hemorrhage into the abdominal cavity, due to rupture of the degenerated tissue of the liver, and sometimes the ovary (follicle). Often, the so-called "yolk peritonitis" develops due to the loss of the yolk mass from a degenerated and ruptured follicle. These chickens often have a sagging abdomen.

Pathological and anatomical changes in chickens are expressed in exhaustion, catarrhal condition of the intestinal mucosa, the presence of grayish-whitish, small, the size of a needle prick, and sometimes almost the size of a pinhead, foci of necrosis in the liver, overflow of the gallbladder, detection of grayish-whitish foci in the lungs (sometimes pneumonic foci), whitish tubercles in the heart muscle, slight swelling of the spleen. Whitish nodules can also be in the wall of the stomach. The yolk is usually not resorbed; its contents are compacted or, conversely, liquefied, yellowish, greenish or grayish in color.

Often there is a bottle-shaped expansion of the rectum; the anus is closed with a fecal plug and is impassable.

Histologically, a focal histiocytic reaction is detected in the organs.

In an adult bird, the ovary is most often affected. The shell of the follicles (yolk balls) is either sharply hyperemic or hemorrhagic, or loosened and thinned, and in the areas of its thinning, the yolk mass protrudes, which is why the follicle acquires a cystic, bumpy appearance. The content of the altered follicles is liquefied and has a greenish, grayish-brown or red color (from the outflow of blood). Sometimes, on the contrary, the follicle contains a dense yolk mass, is deformed and, due to this, acquires a diverse shape.

The second most frequent organ is the liver. It is enlarged, softened, grayish in color, sometimes with a greenish tint; on it there are focuses of a grayish-brick color.

The spleen is mostly slightly enlarged. The muscle of the heart is reborn; often whitish tubercles the size of a pea are found in it. Often set "yolk" peritonitis. Salpingitis is also found, although they are unlikely to be specific to pullorosis. In some cases, pathological changes may be absent in the presence of a positive agglutination reaction and even in the isolation of cultures of S. pullorum.

In roosters, pathological and anatomical changes usually do not occur.

The diagnosis is based on clinical, pathological and anatomical data and bacteriological examination of the corpses of chickens, as well as adult birds. In bacteriological examination, it must be borne in mind that even in small chickens, and even more so in chickens at 15-30 days of age and older, sepsis is unstable. Therefore, for the accuracy of the diagnosis, several corpses should be opened and cultures should be taken from the blood of the heart, liver, spleen, unresorbed yolk, and also from the bone marrow (stale corpses). In an adult bird, crops are needed from the largest possible number of ovarian follicles; it is better to examine the entire ovary (immersion in a flask with liver broth containing brilliantgrun) and, of course, also other organs and affected tissue areas (tubercles in the heart, etc.).

In an adult bird, the intravital diagnosis of latent forms is of the greatest importance.

Agglutination reaction. Sanitation of pullor herds is based on the isolation of infection carriers from an infected herd by means of an agglutination reaction.

The agglutinating properties of the blood of pullor chickens were discovered in 1907, after which they began to use for practical diagnostics the study of chicken blood by the Wright method in test tubes. This method has become widespread in the USA and has been practiced for many years. However, studies of the multi-million bird population required a method that was more accessible for mass use.

In 1925, the possibility of using an accelerated method of agglutination was revealed, which consists in mixing a drop of chicken blood serum and a drop of pullor antigen on glass, as is done with brucellosis.

To eliminate false agglutinations and obtain a distinct reaction, various methods of preparing antigens (phenol, formalin, alkaline), standardizing the number of microbial bodies in an antigen, establishing a normal and diagnostic serum titer, feeding regimen for chickens before taking blood for research, etc., were also studied.

To identify carriers of pullor infection, an intradermal allergic diagnostic test was proposed (injections are made into the skin of the beard). The diagnostic preparation was prepared from broth cultures of S. pullorum by analogy with tuberculin or from killed microbial bodies.

This allergic test was tested both abroad and in the USSR. Due to the lack of: advantages over serological testing, the pullorin test was abandoned.

Serological methods for diagnosing pullor chickens have played a huge sanitary and economic role in all countries of intensive poultry farming. The accelerated method of research with fresh blood has acquired the greatest practical significance.

A drop of fresh blood immediately after taking is mixed on a glass slide with a drop of antigen. A positive reaction is expressed by the formation of whitish flakes consisting of agglutinated bacteria of the antigen and stand out in relief when viewed with the naked eye.

To improve the reading of the reaction, a stained antigen was tested. However, he did not give significant relief, since a positive test is clearly visible and without auxiliary means. This method has found wide application.

Some researchers preliminarily, before the study, dry the blood on the glass and dissolve it before setting up the reaction. This method does not provide advantages over others and at the same time requires a large number people, materials and time.

The rapid method with fresh blood (the so-called blood droplet agglutination) is somewhat inferior in efficiency to the Wright tube method. According to some data, their discrepancies are expressed in tenths of a percent, according to others, 4.8% (Kiur-Muratov, Koronny).

Both the one and the other methods of intravital diagnosis by different authors were unequally confirmed by the data of subsequent pathological-anatomical and bacteriological studies.

Some received 89% pathological and anatomical and 91% bacteriological confirmation of the serological lifetime diagnosis. In others, the consistency of indications: Wright's serological method with post-mortem bacteriological examination was established in 80% of cases, and fast method with fresh blood in 83%,

Some authors denied the diagnostic value of both test-tube and rapid agglutination, pointing out that agglutination either does not reveal some part of pullora chickens, or, conversely, its positive indications are not confirmed by any subsequent study of the responders (pathological-anatomical and bacteriological), or by the results hatching of chickens from the eggs of the studied hens (absence of lullorosis diseases).

In this regard, it was proposed to use, for example, only the Wright method and take into account the high titers of the studied sera. However, despite the fact that many issues of the pathogenesis of latent infection and its relationship with agglutinins in the blood have not yet been resolved, the agglutination reaction turned out to be a powerful method in the complex of measures for the sanitation of pullor herds.

So, for example, according to the data of the Massachusetts Agricultural Experimental Station, in this state for 1920 - 1921. 24178 birds in 108 farms were tested by agglutination test, and 12.5% ​​of the responders were isolated. In subsequent years, the number of responders decreased significantly.

According to 13 states, as a result of systematic health work for 1927 - 1941. out of 4431297 examined birds, 1582834 were free from pullora infection.

Some farms have been cleared of pullorosis and have not seen a responding bird for a number of years. Similarly, in Hungary, during a six-year work (isolation of pullor chickens by the agglutination reaction), up to 67 - 87% of the farms included in the experiment were improved.

Despite the shortcomings of the agglutination reaction, judging by the long-term data of poultry farming practice, it turned out to be a slow but quite reliable means of purifying pullor flocks from infection carriers.

To promote the method of rapid blood-drop agglutination into the widespread practice of poultry farms in the USSR, it was necessary to study some of its aspects.

Thus, the optimal temperature of 10–20°C recommended for the normal course of the reaction could not always be reached in the cold season (the studies are carried out in an unheated poultry house immediately after blood sampling). The microscopic verification of pseudo-reactions due to the loss of fibrin also made it difficult. The need for a long wait for the result of the reaction (b - 10 minutes) significantly influenced the number of birds under study.

The works of Soviet authors (Kiur-Muratov and Zasedateleva) established that agglutination readings do not change even at temperatures below -f 10 ° C; in addition, pseudo-agglutination is easily eliminated by adding sodium citrate to the antigen (eliminates blood clotting) and introducing a drop of the test blood into the drop of antigen already on the glass slide (and not vice versa, as recommended by foreign researchers). Further, by collecting blood from a chicken and an antigen with commensurate metal loops, it is possible to bring the blood dilution in the antigen to 1:20 or more, which eliminates non-specific indications (which are sometimes observed at a 1:1 dilution recommended by foreign works). The reaction is read with its usual reliability within 1 minute.

All this facilitates the mass use of the method of rapid blood-drop agglutination in the conditions of poultry farms in the USSR; as a method of in vivo diagnosis of pullor chickens, it has been widely used in the USSR since 1931.

To study chickens, a small cut of one of the protrusions of the comb or an injection into the comb is made; the first drop of blood that comes out is removed with cotton wool, and the second is taken with a metal loop and mixed well with a drop of antigen previously applied to a glass slide. Shaking the glass, determine the result within one minute (antigen is prepared from well agglutinable strains of S. pullorum); a positive reaction is the appearance in a drop of white flakes of agglutinated microbial bodies.

During the year, multiple studies of poultry are necessary due to the inconstancy of finding agglutinins in the blood of patients.

The best time to detect pullora chickens is considered to be the summer months, as they correspond to the period of the greatest activity of the ovary, in which the focus of infection often nests. Experiments have shown that the presence of agglutinins in the blood is most constant before the onset of oviposition and after its decline. In the economic life of state farms and poultry farms, this time coincides with the period of repair, acquisition of herds, which is also very convenient for research.

A bird that has reached puberty and has begun oviposition is subjected to research. Most researchers do not recommend the use of serodiagnosis at a younger age due to the inconsistency of indications. Agglutinins are also found in a young bird, but their fluctuations in the blood are more significant than in an adult, so the reaction gives more incorrect readings; nevertheless, the study of young animals can serve as an additional measure of sanitation.
Pullor birds are excluded from the breeding herd and isolated into an isolated productive group (food egg) or killed for meat.

In the USSR, as a result of these measures, the percentage of annually detected reacting birds and the disease of chickens with pullorosis has sharply decreased.

So, for the farms of the People's Commissariat of state farms for 1937 - 1940. the percentage of birds reacting to pullorosis was reduced by almost three times.

As the flock was cleared of pullor hens, not only did the percentage of responding birds decrease; parallel to this, the incidence of pullorosis in chickens also fell sharply; pullor epizootics in most farms stopped.

This health work, carried out by poultry doctors and veterinary laboratories, undoubtedly gave satisfactory results, saving the state many tens of millions of birds, significantly increasing the collection of eggs in herds freed from pullorosis.

Treatment. Of the therapeutic agents, yogurt is used, obtained by means of cultures b. bulgaricus or b. acidophilus. Bulgarian stick, not being a representative of the intestinal flora, usually quickly disappears from the intestine; acidophilus bacillus vegetates well in birds. Therefore, acidophilic “curdled milk and, moreover, fermented with bird strains b. acidophilus. The healing power of curdled milk is very small; however, if introduced into the diet from the first day of life (and up to one month), it significantly reduces the number of deaths from post-embryonic infections of chickens. Thus, the use of curdled milk in chickens of dysfunctional farms deserves great attention.

Serum therapy and prophylaxis have been unsuccessful. A bacteriophage was also tested, but also without satisfactory results (Korotich).

Immunity. The use of different vaccines did not lead to vaccine immunity. The difficulty of vaccination is also due to the onset of the disease in chickens in the embryonic period and their susceptibility at a very young age.

Control measures and prevention. The fight in pullorosis-infected bird flocks should be directed against the main reservoir of infection - adult birds - carriers of latent pullorosis. In pullor herds, the identification of cryptic patients is resorted to at least three times a year: in summer, after the period of maximum egg-laying, and twice in the autumn-winter season. All birds that react according to the agglutination reaction (rapid blood drop method) must be isolated in a separate group and used to obtain food eggs and, moreover, no longer than within a year. If there is no need to exploit this bird, it is killed for meat; export of pullor poultry from farms is not allowed. Birds from flocks that do not respond to agglutination cannot be combined with the livestock of those premises and farms (farms) in which reactants were found. When completing a breeding herd, in breeding breeding farms, chickens should be excluded from groups that have been ill with pullorosis.

The laying of eggs in incubators from groups of birds that are disadvantaged and prosperous in terms of pullorosis should be separate; chicks produced from eggs of these groups should also be reared separately.

In farms free from pullorosis, it is allowed to import poultry only from farms that are safe for this disease.

From the first day of life, it is advisable to include acidophilic yogurt in the feed regime of chickens from farms that are unfavorable for pullorosis. As a rule, sick chickens e!

In disadvantaged farms, it is necessary to completely abandon the use of incubation waste (dead embryos, etc.) in poultry feed. Feeding them to other animals (pigs) is allowed only after boiling. Litter from chickens with pullorosis is burned.

Disinfection of incubators is carried out with gaseous formalin (18-25 ml of formalin diluted with a small amount of water is taken per 1 m3 of the volume of the incubator, and 9.0-17.5 potassium permanganate is added; with the upper vent of the incubator closed, the duration of disinfection is at least 45 minutes); incubator trays are decontaminated after each hatch.

For the purposes of disinfection, other means are also suitable (solutions of creolin, lysol, as well as a 1% solution of the same formalin).

Great importance in prevention pullorose have hygienic and sanitary measures in relation to walking, premises, inventory.

Pullorosis (white bacillary diarrhea) is an acute, contagious, infectious disease of young chickens. It is characterized by an acute course in chickens, intestinal damage, internal organs and septicemia. In adult birds, the disease is chronic in the form of ovarian yolk peritonitis or asymptomatic.

The causative agent of pullorosis is a bacterium that is highly resistant in the external environment.

In the poultry house chicken manure the microbe can persist for more than three months, in water for more than 200 days, in the kidney for more than a year.

Disinfectants inactivate the causative agent of pullorosis: 1% solutions of formalin, creolin - after five minutes; clarified bleach solution containing 0.2% active chlorine - after 35 minutes. For disinfection, 1–2% solutions of caustic soda, xylonafta, a clarified solution of bleach containing 1–2% active chlorine and other preparations are used.

Chickens suffer from pullorosis in the first days of their lives. They can get sick at the age of 3-4 weeks. In addition to chickens, turkeys, pheasants, black grouse, pigeons, canaries, and sparrows are susceptible to pullorosis. The most susceptible are the young. The source of the pathogen is sick chickens and bacterial carriers, which release a large number of microbes into the external environment with litter. The pathogen can be transmitted through hatching eggs.

Chickens become infected through contaminated feed, water, bedding, inventory. The causative agent of pullorosis is often found in the organs of sick and recovered birds, on egg shells, so chickens can become infected with pullorosis when feeding untreated chicken slaughter waste, incubation waste, etc.

Signs and course of the disease

In chickens, signs of the disease appear after a 1 to 5 day incubation period. Chickens do not eat feed well, are lethargic, clog in dark places, sit with half-closed eyes, extended head and lowered wings. They breathe with an open beak, often lower their heads and fall.

Body temperature rises to 43-44 degrees Celsius. Profuse diarrhea appears, stools are liquid, whitish or greenish-brown in color, frothy with an unpleasant odor. Chickens of the first week of life die within two days, and the survivors are bacteria carriers. In 15–20 day old chicks, the disease proceeds subacutely and chronically. Mortality is declining.

In adult chickens, the disease is chronic for several months, often for life. In some birds, intestinal disorders, loss of appetite, depression, blue crest are possible.

As a result of the defeat of the ovary, egg production is sharply reduced, sagging of the abdomen is noted. If yolk peritonitis develops, then the body temperature rises to 42 degrees Celsius. Outwardly, in most diseased chickens, the disease is not observed. When the corpses of dead chickens are opened, an unresorbed yolk is found, of a dense consistency, painted brown or greenish. The liver is enlarged, light yellow. In older chickens, the liver is clay-colored; small, dotted, gray-colored small foci of necrosis are found on it.

The same lesions can be on the spleen, heart, lungs. The gallbladder is always enlarged, filled with a thick viscous dark green liquid. In the corpses of fallen chickens, changes are found in the ovaries. In them, the follicles acquire an irregular shape, become oblong, tuberous, yellowish-gray, brown or dark greenish in color.

The diagnosis of pullorosis is made on the basis of clinical, pathoanatomical, epizootological and laboratory studies. In addition, blood capillary agglutination reaction is widely used for diagnosis.

Prevention

In order to prevent chickens and adults, antibiotics are used:

biomycetin at the rate of 1 g per 1000 chickens from the 1st to the 30th day of life and 1.2 g each from the 10th to the 30th day, the daily dose of the drug is mixed with feed and divided into parts;

terramycin at a dose of 2–3 mg per chicken for 3–5 days;

furazolidol at a dose of 3 g per 1000 chickens, the drug is mixed with feed and fed daily from the 1st to the 10th day of life.

Of great importance for prevention are the incubation of eggs only from healthy laying hens and compliance with the incubation regimen. Eggs are disinfected before incubation. The incubator is thoroughly cleaned and disinfected before and after incubation. The veterinary and sanitary requirements for keeping and feeding chickens should be strictly observed.

For the prevention of intestinal function, it is useful for chickens to feed fresh yogurt, cottage cheese, ABA, PABA preparations. PABA is given once a day with food for 5–6 days in a row at a dose of 0.5–1 ml. From the first days of life, it is necessary to give finely chopped fresh herbs.

If pullorosis occurs among the young, all sick and suspected of the disease, as well as a weak bird, are destroyed. Clinically healthy birds are prescribed antibiotics and chemotherapy drugs for therapeutic and prophylactic purposes. Young animals, among which there was an outbreak of the disease, are fattened for meat. Before placing a new batch of chickens, the room is thoroughly cleaned and disinfected. Feeders, drinkers, and other equipment are cleaned, washed with a hot solution of a disinfectant and air-dried.

INTRODUCTION Bacteria of the genus Salmonella are one of the causes of acute and chronic infectious diseases. poultry. In addition to being a salmonella reservoir, infected poultry can transmit through food chain this pathogen to people. Based on the reported detection of Salmonella in food, it can be concluded that it is more often isolated from processed products than from any other animal species. This fact indicates the high prevalence of infectious diseases caused by salmonella in poultry, in particular among chickens and turkeys raised for sale. Therefore, nationwide programs to identify infected flocks of birds are of great importance.

Genus Salmonella(family Enterobacteriaceae) is named after the eminent veterinarian and bacteriologist Daniel E. Salmon. The genus includes more than 2,300 serologically distinct variants. These serotypes are named after the place where they were originally isolated.

PULLOROSIS AND TYPHUS IN POULTRY

Pullorosis and typhoid fever in poultry are very similar in clinical presentation, epizootology, damage caused, control and measures to combat these diseases also have much in common, so they are described together. Pulloroz (PT) is caused by the bacterium Salmonella pullorum, and poultry typhoid (PFT) is caused by S. gallinarum. This disease affects primarily chickens and turkeys, but other bird species (quail, pheasants, ducks, peacocks and guinea fowls) are also susceptible to them. In diseases, a transovarial route of infection is possible. The causative agents of both diseases have a well-defined host and rarely cause disease in other animals. In some parts of the world, including Europe, S. pullorum and "S. gallinarum" are considered to cause the same disease, salmonellosis.

Accidental infection of human PZ occurred as a result of mass consumption of contaminated food products experimental induction of disease in animals. The disease was manifested by acute enteritis, which stopped on its own - without treatment. 5. gallinarum is rarely isolated from humans and is not a public health problem. PATHOGENESIS AND EPIZOOTOLOGY natural hosts. The natural hosts of S. pullorum and S. gallinarum are chickens, however, outbreaks of both PAD and TDP have been described in turkeys, guinea fowls, quails, pheasants, sparrows and parrots. In addition, there are descriptions of outbreaks of PZ in canaries and bullfinches, and TDP - in ringed pigeons, ostriches and peacocks. Mortality from pullorosis is usually limited to 2-3 weeks of age. Some chickens and poults that survive the initial stage of the disease become carriers of the infection with or without injury. Although poultry typhoid is considered a disease of adult birds, there are many reports of morbidity in young chickens, accompanied by high mortality. Mortality from TDP is as high as, for example, among chickens of the first month of life)