Experience of specific prevention of gumboro disease. Gumboro disease in chickens: prevention, vaccination, measures in case of a disease outbreak. Modern methods of protection

gumboro disease(Disease Gamboro) (Infectious bursal disease - IBD, Infectious bursitis, infectious nephrosis) - bursa of Fabricius disease, a highly contagious viral disease of poultry of the chicken family, characterized by diarrhea, inflammation of the bursa of Fabricius, immunosuppression. It is registered in a number of US states, in certain countries of Africa and Asia, in France, Italy, Germany and in other countries with developed poultry farming.

Pathogen information. The causative agent is an RNA-containing virus of the Birnae Viridae or Picornaviridae family, cultivated on embryos, causing their death on the 5-7th day. The pathogen can withstand heating up to 60°C for 1 hour, is resistant to ether, chloroform, and is sensitive to solutions of formaldehyde and caustic soda.

Epizootiological characteristics. Chickens are most susceptible to the disease meat breeds at the age of 2-15 weeks. Infection occurs, as a rule, through the nutritional route.

Clinical signs and flow. The incubation period is very short. The chickens show drowsiness, trembling, diarrhea, they eat little and drink a lot, their feathers are ruffled, and they die on the 4th day from the onset of the disease (3-80%). Unlike clinical form, the subclinical form is observed in chickens less than 4 weeks of age, when the immune system is damaged. Early manifestations of IBD are characterized by the absence of clinical signs and damage to the bursa of Fabricius, where the number of B-lymphocytes sharply decreases and immunosuppression develops.

The corpses are dehydrated. At autopsy, intramuscular hemorrhages are found in the chest and lower leg and other muscle groups. The kidneys are colorless, the liver and spleen are hypertrophied. The bursa of Fabricius is enlarged, edematous, and necrotic areas are noted on its mucosa. With a longer course of the disease, the volume of the bag decreases, and when it is opened, a curdled mass is discovered.

Diagnosis set on the basis clinical picture and autopsy results, laboratory research(precipitation reaction in gelatin gel), which is based on the isolation of the virus, its identification, detection of antibodies in blood serum, and performing a bioassay on susceptible chickens. Differentiated from infectious bronchitis, sulfonamide poisoning, mycotoxicosis, Newcastle disease, lymphoid leukemia, Marek's disease, fatty toxicosis

Control measures. When a disease appears, the poultry house is isolated, and after slaughtering the birds, the premises are thoroughly cleaned and disinfected. For specific prevention vaccination is used.

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Infectious bursal disease of chickens

Infectious bursal disease (IBD, Gumboro disease) is an acute contagious disease of chickens, characterized by damage to the bursa of Fabricius, diarrhea, nephrosis, and intramuscular hemorrhages.

The disease was first registered in 1957 in the town of Gumboro (USA), which gave the disease a second name.

Currently, the disease is registered in all countries of the world. Infection of herds ranges from 2 to 100% and is manifested by outbreaks of the disease. Economic damage consists of losses associated with the death of chickens, forced culling of poultry, a decrease in the meat productivity of young animals, as well as the costs of preventive actions And low level response to vaccination due to immunosuppression caused by bursa pathology.

Characteristics of the pathogen. The causative agent of IBD is a virus belonging to the family Birnaviridae (from the English bi - double, rna - ribonucleic acid), the genus Avibirnavirus. Virions of the virus are non-enveloped and are spherical particles with a diameter of 55 and 18-22 nm. They consist of a core containing double-stranded linear RNA and a protein - an icosahedral capsid, built of 92 capsomers.

Resistance to physical and chemical influences. The virus is resistant to ether, chloroform, changes in pH (2-11), and UV irradiation. When exposed to a 0.5% formalin solution, it is inactivated in 6 hours, 0.5% chloramine in 10 minutes.

Antigenic structure. Five proteins were found in the structures of virions. One of them is responsible for group specificity, the other for type specificity and the induction of virus-neutralizing antibodies.

Antigenic variability. The virus has antigenic variability: one serotype with six subtypes is pathogenic for chickens, two serotypes are pathogenic for turkeys. The presence of antigenic variability of the virus requires the use as a vaccine of a strain that has the maximum degree of antigenic homology with the epizootic strain.

Hemagglutinating properties. Not installed.

Virus cultivation. The IBD virus can be propagated in chicken embryos free of maternal antibodies to a number of viruses, including the IBD virus. When infected in the allantoic cavity or yolk sac embryos die 3-8 days after infection. Signs of virus replication in a chicken embryo are necrosis and hemorrhages on the body of the embryo, in the liver, and kidneys. The virus reproduces well in culture kidney cells and fibroblasts of chicken embryos, causing CPD on the 3-5th day after infection. It can be cultivated on SPF chickens (free from pathogenic flora) 21-25 days of age.

Clinical signs. In chickens 3-6 weeks of age, the disease is acute, but depending on the immune state of the livestock, a subacute course or death is possible. The incubation period is 1-3 days, and the disease lasts 5-7 days.

Sick chickens exhibit diarrhea with the release of watery, whitish-yellowish droppings, then trembling of the head, neck, and deep prostration appear. Morbidity and mortality increase quickly and reach a maximum on the 3-4th day of illness, then within 5-7 days it usually declines. Features illness - suddenness, high level lesions and rapid recovery. The mortality rate is 6-37%. Subclinical infection is expressed mainly by growth retardation. When an adult bird becomes ill, only a slight decrease in the percentage of embryo viability is observed.

Pathological changes. On different stages They are different diseases. Initially, hypertrophy of the bursa and petechiae in its mucosa, exudate with fibrin flakes between its folds, hemorrhages in pectoral muscles and leg muscles, serous membranes. After a week, the lesions become different: serofibrous pericarditis, hepatitis and nephritis. A month after infection, the bursa atrophies and is 3-4 times smaller in size than in a healthy bird of the same age. Microscopic changes characteristic of IBD are found in the bursa of Fabricius of sick birds. They are mainly represented by necrosis of lymphoid and hyperplasia of reticuloendothelial cells, thickening of interfollicular connecting septa, and the formation of glandular structures instead of follicles.

Localization of the virus. The virus enters through digestive tract and affects lymphoid tissue. After 24-28 hours it is localized in the bursa of Fabricius. The most sensitive to the virus are lymphocytes, on the surface of which IgM is fixed. Therefore, the main target for the virus is the subclass of B lymphocytes, especially their immature forms. In addition, lymphocytes of the spleen, caecal glands of the blind processes, etc. are destroyed. lymphoid tissue explains the immunosuppressive effect caused by the virus.

CPD of immune complexes, including virus-infected lymphocytes, antibodies, and complement, leads to the appearance of hemorrhagic lesions in skeletal muscles, liver and other organs. Precipitation of immune complexes in the glomeruli and convoluted tubules of the kidneys reduces their filtration capacity, and urate accumulates in the kidneys.

Diarrhea with IBD develops due to the reproduction of the virus in the intestinal epithelial cells, which leads to dehydration of the body. Weakening immune status poultry leads to additional infection with viruses and bacteria.

Source of infection- a sick bird. The pathogen is transmitted through infected feed, water, aerogenously, as well as through equipment and through eggs. Helminths and lice are considered direct vectors of transmission. Wild birds can be direct and indirect vectors. IN natural conditions IBD only affects chickens, namely chickens 2-15 weeks of age. However, it was possible to isolate the virus from turkey poults, bats and mosquitoes.

Diagnostics. Only with a typical course is the disease relatively easily diagnosed based on clinical and pathological signs. On early stages or in subclinical cases, laboratory tests are necessary.

Laboratory diagnostics. For laboratory studies, the bursa of Fabricius, liver, and kidneys are taken from birds that died or were killed during the first 7 days of illness.

Virus detection in pathological material it is possible to establish using express methods: indirect version of ELISA, RIF and PCR.

Virus isolation carried out by bioassay with subsequent isolation of the virus on chicken embryos, in cell culture and infection of chickens. It is not always possible to isolate the virus from affected organs, so a more reliable method for diagnosing IBD is serodiagnosis. Blood serum is also examined at asymptomatic diseases. Important in the prevention of IBD has systematic monitoring of the immune state of the herd. Such control is carried out by examining paired blood sera.

Identification The isolated virus is carried out using PH on chicken embryos, in RIF and RDP.

Antibody detection to the IBD virus in the blood sera of sick and recovered birds is carried out in PH, RNGA, RDP, ELISA.

Virus-neutralizing antibodies reach maximum titers by the seventh day after infection and remain in the bird’s body for up to three months. Sera with a high titer of virus-neutralizing antibodies are usually positive in the RDP. RNGA detects antibodies already on the 3-5th day after infection with their maximum titers at 3-4 weeks. For a broad serological study, ELISA is used.

Differential diagnosis. IBD must be differentiated from infectious bronchitis of chickens, Newcastle disease, Marek's disease, Rous sarcoma, coccidiosis, nephritis, vitamin deficiency A. However, only the detection of antibodies does not allow a diagnosis; it is necessary to isolate the virus, establish its serotype, subtype and virulence.

Immunity and specific prevention. When carrying out specific prevention measures, it is necessary to take into account factors that negatively affect the formation of stable immunity in poultry. This is primarily the type of antigen, the method and frequency of its use in the vaccination process, the degree of attenuation or inactivation.

When immunizing against IBD with a live vaccine, it is necessary to establish the compliance of the drug used with the epizootic strain circulating among birds. In addition, vaccination should be carried out taking into account maternal antibodies.

Currently, live vaccines from naturally weakened strains, as well as those weakened by passage on EC and in cell culture, are widely used. Birds have different age groups The intensity and duration of post-vaccination immunity are not the same. Level specific antibodies in chickens corresponds to the concentration of virus-neutralizing antibodies in adult mother hens during the laying period.

Currently, dry live vaccines of the D-78 and Winterfield 2512 strains are used orally and in the form of a spray.

An inactivated vaccine is prepared from a virus propagated in EC and in cell cultures. The virus is inactivated with formalin or β-propiolactone, and aluminum hydroxide is added. The vaccine is used subcutaneously or intramuscularly, administered at the age of 2-4 months. Post-vaccination antibody titers are studied by ELISA and PH.

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Gumboro disease ( infectious bursitis chickens, infectious bursal disease)(Bursitis infectiosa galli - Latin, Infestiosus bursae disease - English) is an acute viral disease of chickens, characterized by apathy, anorexia, diarrhea, damage to the bursa of Fabricius, extensive intramuscular hemorrhages, and kidney damage.

Prevalence. The disease was first described in Gumboro, USA (A. Cosgrove, 1962). Currently, it is diagnosed in the USA, Mexico, Canada, England, Germany, France and other European countries, Israel, India, Japan, and South African countries.

Economic damage significant. Losses consist of the death of up to 10-20% of the livestock, a high percentage of carcasses being rejected as a result of subcutaneous, intramuscular hemorrhages and exhaustion. Large losses are caused by indirect factors: weakening of the livestock’s resistance to infectious agents, decreased efficiency preventive vaccinations, and therefore the possible occurrence of new outbreaks of disease (epizootics) and further restrictions, as well as bad influence on the productivity and reproduction of poultry during the egg-laying period.

The causative agent of Gumboro disease belongs to reoviruses. Its taxonomic position for a long time remained undefined and in a number of reports it was designated as picorna or adenovirus. For some period after registration, the disease was called avian nephrosis and was combined with nephroso-nephritis caused by the infectious bronchitis virus. No antigenic variants of the infectious bursitis virus have been detected.

The pathogen is relatively heat-stable (withstands 30 minutes at 70°C), resistant to acids and alkalis in the pH zone from 2 to 12, lipid solvents, and can last up to 120 days in a dried state in contaminated droppings. The virus is quickly destroyed by the action of disinfectants: formalin, iodine derivatives, chloramine.

The virus is well cultivated in chicken embryos of 9-11 days of age, causing their death 4-6 days after infection on the allantoic membrane or in the yolk sac. They have hemorrhages under the skin, in the kidneys, myocardial degeneration, necrosis and greenish staining of the liver, and hepatopathy is often accompanied by similar staining of the yolk and chlorioallantoic fluid.

Chicken embryo cell cultures are highly sensitive to the virus, in which a cytopathogenic effect is manifested in the form of eosinophilic cytoplasmic inclusions and the formation of syncytium. The virus affects only chickens, although, according to some authors, quails and sparrows are also affected (S. Edgar, 1965). Under experimental conditions, white mice are infected intracerebrally at the age of 1-1 days or intraperitoneally at 12-14 days. They die after 5-13 days with signs nervous disorders, encephalitis and myocarditis are noted at autopsy.

Epizootological data. The source of the pathogen is sick chickens. The disease is acute and subacute. It is also possible to have asymptomatic illness. Virus carriage was not observed in convalescents. The virus is spreading rapidly in poultry flocks. It is transmitted when sick and healthy chickens are kept together, through contaminated feed, water, bedding, droppings, and also mechanically - by people, other bird species, insects, especially the Coleoptera Alphetobius diaperinas (S. Snedeker et al., 1967). The pathogen enters the body through the mucous membranes of the nasal cavity, oral cavity, conjunctiva in natural conditions, apparently, the bird becomes infected through the nutritional route. Chicks 2-15 weeks old are susceptible, most sensitive at 3-5 weeks of age. The disease is not observed in adult chickens and chickens up to 14 days of age, even with artificial infection. The incidence ranges from 20 to 50;%, but can be extremely high (up to 80%), which to a certain extent depends on the breed, the individual state of the body, conditions of detention and feeding. Mortality ranges from 0.5 to 20%, sometimes up to 50%, depending on the age of the bird (Fig. 16).
Epizootic spread of infectious bursitis is observed mainly in regions with temperate climates, less often in tropical countries. The disease spreads especially widely in reproductive farms where poultry is present. of different ages. When the disease occurs, the first sign is a massive acute course; subsequently, a subacute and more latent course may predominate.

Pathogenesis. The causative agent of infectious bursitis, which enters the body orally, is found in the lymphoid cells of the intestine within 4-5 hours. The latter penetrate the circulating systems, bypassing the Kupffer cells of the liver, and ensure rapid dissemination of the virus. After 11 hours, it begins to multiply in the bursa of Fabricius. The resulting viremia is short-lived, lasting up to two days. Then the virus is detected in all parenchymal and lymphoid organs, in the most high concentrations in the bursa of Fabricius, where it persists for up to 2 weeks (N. Muller, 1979). The pathogen is excreted in excrement.

Damage to lymphoid tissue is accompanied by a pronounced immunosuppressive effect, consisting in a significant decrease in the number of lymphocytes up to the suppression of all B-dependent immune functions, especially the primary humoral response (antibody formation). The level of serum complement and blood clotting decreases, and immune complexes may be involved in the pathogenesis (L. Skeeles, 1979). This leads to a loss of effectiveness of immunization of the affected bird against Newcastle disease, Marek's disease, infectious bronchitis, and an increase in susceptibility to Marek's disease by 3-6 times. A sufficient level of protection against Newcastle disease is achieved only by immunizing one-day-old chicks or 2-3 weeks before infection with the infectious bursitis virus. Against the background of immunosuppression and the absence of lymphocytes, they often worsen or occur. various infections, for example colibacillosis, viral hepatitis with inclusions, gangrenous dermatitis, salmonellosis, coccidiosis (Y. Mogeai, N. Debreuil, 1979).

Clinical signs. The incubation period is from 2-3 days to 1-3 weeks (usually 1 week). Initially, the disease is hyperacute, reaches a maximum in a few days and lasts about 7 days. Clinically manifested by diarrhea (watery whitish discharge), severe apathy, refusal to feed, disheveled hair, trembling. These symptoms are approximately the same as for coccidiosis. The bird dies on the 4th-7th day; often dead chicks lie in a characteristic position: with straightened legs and neck.
With a successful outcome, the symptoms of the disease disappear after a week (M. Krasselt, I. Phillips, 1976).
Pathological changes. At autopsy, inflammation and hyperplasia of the bursa of Fabricius (increased 2 times), hemorrhagic lesions from petechiae to diffuse hemorrhages in the skin, muscles and connective tissue, nephritis of the “pale kidney” type. These three indicators are sufficient to make a diagnosis. In addition, erosions on the gastric mucosa, hepatitis and liver atrophy, nephritis without renal hypertrophy, atrophied dark or hypertrophied red spleen, serous pericarditis, sacculitis, perihepatitis, peritonitis are detected (from 10 to 90%) (P. Montlaur et al. , 1974).

At histological examination necrosis of lymphoid elements is detected, especially in the bursa of Fabricius, as well as foci of proliferative inflammation, hemorrhages in the stroma of the follicles, a general picture of purulent and necrotic inflammation with vacuolization in this organ.

Diagnosis and differential diagnosis . Peculiarities clinical course diseases and characteristic dependence curve deaths from age are important elements epizootological diagnosis of infectious bursitis. The typical pathological-anatomical triad and pathognomonic signs of damage to the bursa of Fabricius against the background of the course of the epizootic allow one to diagnose the disease. IN laboratory conditions The pathogen is isolated from pathological material of the bursa of Fabricius by infecting chicken embryos, cell cultures, healthy chickens and taking into account typical lesions.

For serological identification of the pathogen, various modifications of the precipitation reaction in the gel and the neutralization reaction in chicken embryos and cell culture are used. Since embryos from immune chickens are resistant to infection due to fapoovarian-transferred antibodies, the results of their infection can be used to characterize the well-being of egg supply farms.

Infectious bursitis is differentiated from the following diseases (I. Brugere-Picoux, 1974):
intestinal coccidiosis- clinically manifests approximately the same, can be excluded by scatological examination;
Newcastle disease- hemorrhagic lesions may be observed, characteristic respiratory symptoms, high contagiousness and lethality, birds of all ages are susceptible;
fatty liver and kidney syndrome- accompanied by hemorrhages and kidney damage, very rarely ends in death, chicken carcasses are pale pink;
nephrosonephritis- caused by the infectious bronchitis virus, similar in damage to parenchymal organs, but accompanied by respiratory disorders and does not affect the bursa of Fabricius;
hemorrhagic syndrome of toxic nature- occurs when poisoned by sulfonamides or mycotoxins, observed in birds of all ages, hemorrhages are concentrated in the visceral organs;
vitamin deficiency A- atrophy of the bursa of Fabricius is observed, the lesions are limited to the epithelium.

Means of specific prevention. Numerous live vaccines that are highly immunogenic have been developed abroad. For example, we can cite the preparations gumbo-vax (Italy), LZD-228 (Merrier, France), nobilis (Holland). These vaccines are harmless, do not have an immunosuppressive effect, are effective, stable during storage and passage, and are convenient for use.

Chickens are vaccinated intraocularly or by drinking the vaccine at one day of age, as well as intramuscularly in groups. over 12 weeks. The drugs can be used for complex vaccinations in combination with vaccines against Newcastle and Marek's diseases, infectious bronchitis. An inactivated emulsified vaccine is also available. In general, vaccination of chickens ensures the safety and usefulness of lymphoid tissue. High titres of maternal antibodies are transferred with the egg and protect the offspring during the first four weeks.

Prevention and control measures consist in preventing contacts of healthy chickens with sick ones - sources of the infectious agent and factors of transmission of the virus, in limiting contacts of birds of different ages. Affected herds may be c. depending on economic considerations, destroyed or stored in isolation in compliance with strict restrictions. It is necessary to carry out disinfection and general hygiene measures. In endangered and disadvantaged farms, poultry are vaccinated for preventive purposes.

Infectious bursal disease of chickens

Infectiosis Bursitis gallinarum (Gumboro disease) An acute viral disease of chickens and turkeys, mainly 2-15 weeks of age, characterized by inflammation of the bursa of Fabricius, joints, intestines and internal hemorrhages.

HISTORICAL REFERENCE- the disease was first recorded in 1956 in Gumboro County (USA). In 1962, Kostrov described Gumboro disease as a disease. Winterfeld and Hitchner (1962) isolated a virus from sick chickens that caused nephroso-nephritis in sick broilers. Therefore, this disease is sometimes called nephroso-nephritis. Later, Karnayup (1965) proved that the symptoms of nephroso-nephritis are concomitant, the main and permanent changes are found in the bursa of Fabricius, which is why the disease began to be called infectious bursitis.

The disease is widespread in many countries of America, Europe, and Asia, where industrial poultry farming is developed. Data from serological studies show that the infection rate of herds ranges from 2 to 100%. And the reason for this is considered to be the constant import of poultry.

PATIENT- RNA virus from the genus Aviovirus of the Reoviredae (reovirus) family. The virion size is 70-75 nm. When 9-day-old embryos are infected in the yolk sac, the virus causes their death after 6 days. In addition to growth retardation, it causes

the appearance of edema, necrotizing lesions in the liver, which are typical for all viruses of this group. 3 days after the introduction of virus-containing material into the fibricium bursa, changes characteristic of a natural infection occur. In chicken embryo fibroblast culture, the virus causes a cytopathic effect. Virus-neutralizing and precipitating antibodies are formed in recovered birds.

RESISTANCE - the virus is resistant to ether, chloramine and pH 2.0, sensitive to trypsin. Indoors, the virus persists in droppings for 52 days. At 56°C it does not die within an hour. A solution of chloramine (0.5%) inactivates the virus in 10 minutes, formaldehyde (0.5%) in 6 hours.

EPISOOTOLOGICAL DATA- chickens of all ages are susceptible to the pathogen, but especially broilers aged 2-15 weeks. The most sensitive are 3-6 week old White Leghorn chickens. In adult chickens the disease is asymptomatic.

The source of the infectious agent is sick chickens that shed the virus in their droppings.

Infectious bursitis is an extremely contagious disease that is easily transmitted when birds are housed in close quarters. Chickens become infected through contaminated feed and water. A vertical route of transmission of the virus through infected eggs cannot be ruled out. Infected care items, equipment, clothing, and personnel play a certain role in the transmission of the pathogen.

The possibility of spreading the virus through the air has been proven. The reservoir of the pathogen can be flour beetles.

In fresh epizootic foci, the disease is acute and subacute, and in stationary outbreaks it is chronic and asymptomatic. In a number of farms, an immunizing subinfection is mainly recorded among birds.

PATHOGENESIS- consists of damage to lymphoid tissues, and first of all, lymphocytes of the bursa of Fabricius, spleen, and caecal glands of the blind processes are destroyed. The virus penetrates the digestive tract and after 24-48 hours is localized in the bursa of Fabricius, infecting B lymphocytes.

CLINICAL SIGNS- incubation period 1-2 days. Occurs in chickens under 3 weeks of age in the form of immunosuppression, which is manifested by increased sensitivity to bacterial infections.

May leak into acute form in the first 5-7 days after the disease in chickens aged from 3 to 6 weeks of age. In case of low poultry resistance, mortality can reach 90%.

One of the first signs is diarrhea, with the release of yellow, liquefied droppings, or mucous-watery, white droppings, and feathering is impaired.

Then there is sudden apathy, trembling, signs of damage to the nervous system. The bird soon loses the ability to move and dies in a state of prostration.

Maximum mortality for 3-4 days from the beginning of the disease outbreak,

then the mortality rate decreases.

When the disease lasts 6-8 days, morbidity is 10-20% of birds, mortality is 1-15%.

Hematological changes are characterized by lymphopenia and erythrocytosis. Over 2 days of illness, the total number of leukocytes decreases, on the 5th day it increases and reaches a maximum on the 7th day after infection.

PATHOLOGANATOMICALCHANGES- the corpses are well-fed, but the muscles are dehydrated and pale, the goiter is empty, multiple pinpoint and striped hemorrhages are revealed, especially often under the skin of the thigh; the muscles are dark purple.

The bursa of Fabricius is greatly increased in volume, more than 2 times, and contains gelatin-like transudate; there are fibrinous deposits in the folds of the bursa, and in severe cases there is bloody fluid.

Swelling of the liver, necrotic foci, and atrophy of the spleen are noted. The pancreas is changed, nephrosis. In the final stage of the disease, swelling of the kidneys and atrophy of the bursa of Fabricius appear. Partial banded hemorrhages in the degenerated skeletal muscles of the myocardium, serous membranes, glandular stomach and intestines.

The most typical histological changes are necrosis

lymphoid elements of the bursa of Fabricius, thymus, spleen, renal degeneration.

DIAGNOSIS- infectious bursitis is a difficult-to-detect infection that spreads unnoticed, is masked by other diseases and physiological disorders, and only with a typical course is it relatively easily diagnosed based on clinical and pathological signs. They take into account the high percentage of morbidity, rapid spread and relapse within 5-7 days. The diagnosis can be confirmed by the detection of characteristic changes in the bursa of Fabricius.

For the final diagnosis, histological studies are carried out and a bioassay is performed by infecting 9-day-old chicken embryos on the chorioallantoic membrane. Embryos die within 3-5 days after infection.

The virus is identified in RN, RDP and ELISA.

DIFFERENTIAL DIAGNOSIS- exclude coccidiosis, poisoning, infectious bronchitis, hemorrhagic syndrome, mycoses, Newcastle disease.

TREATMENT- not developed.

IMMUNITY- use live and inactivated vaccines of the BG strain (Gumboro disease), IBD (infectious bursal disease), Winterfield-2512.

The first vaccine is administered twice at the age of 7-21 days with an interval of 10-14 days using the drinking method. Second time at the age of 110-120 days

once intramuscularly into the pectoral muscle area or into the thigh in a volume of 0.5 ml. Immunity occurs 14-21 days after vaccination and lasts up to a year.

In foreign practice, a vaccine made from a weakened strain of the infectious bursitis virus is used with drinking water and aerosolized. Among foreign vaccines, you can use Nobilis Gumboro D78 and 228E. Also developed inactivated vaccine Nobilis Gumboro inc.

PREVENTION AND CONTROL MEASURES- carry out general veterinary and sanitary measures to prevent the introduction of the pathogen into the farm.

The young animals of each technological batch are raised in isolation. The state of poultry resistance is controlled through targeted feeding and maintenance.

The air entering the poultry house is cleaned with filters and disinfected with ultraviolet rays.

When infectious bursitis appears, restrictions are introduced. Sick and suspicious birds are destroyed. Healthy people are vaccinated.

The premises are thoroughly disinfected with solutions of caustic soda, bleach (2-3%), and an aerosol of iodide preparations.

If the disease cannot be controlled by general veterinary and sanitary measures, the farm stops incubating eggs and carries out additional health measures.

There are no deadlines for lifting the restrictions; they are set by veterinarians, since it is difficult to get rid of this disease due to the rapid development of this disease as a permanent one.

Broilers are one of the most popular crosses. Alas, but fast growth and the precocity of these hens is associated with some health problems. In particular, it has become not uncommon for an entire population of broilers to be decimated by Gumboro disease. Let’s find out what it is and how to protect your household right now!

What is Gumboro disease?

Gumboro disease, also called infectious bursal disease, was first recorded in the United States in 1962 in the city of Gumboro, which gave the name to the disease. Later, outbreaks of a similar disease were recorded in Mexico, England, and Belgium. Currently, outbreaks have been recorded on all continents. The disease is caused by a virus of the Birnaviridae family.

The main “target” of Gumboro disease is leukocytes, which are actively destroyed in the bursa of Fabricius and other organs immune system (thyroid, spleen, amygdala), the kidneys are also severely affected.

Bursal disease can affect broilers at any age, but chickens between 2 and 9 weeks of age are particularly at risk.

Its danger is that it is very quickly transmitted from one individual to another, and infection can occur both by contact and through food, water, and equipment. Because of this, on large industrial enterprises there is a risk that the staff themselves may become carriers of the virus. Gumboro disease has a very severe consequences and is associated with significant financial losses. Not only does infection among livestock occur quite quickly, the destruction of leukocytes is associated with the onset of immune depression in birds. Sick broilers become very vulnerable and often begin to suffer from colibacillosis, coccidiosis, enteritis, which most often leads to the death of the bird.

The virus that causes this disease is quite stable and persists in the external environment for a long time. For example, in the droppings of infected birds, in water or feed, it persists for up to 56 days. On inventory and equipment of poultry farms even longer - more than 120 days.

Symptoms

There are two types of disease:

1. Clinical type.
2. Hidden (subclinical) type.

The clinical type of Gumboro disease is characterized by an acute course and obvious external manifestations. It is most often recorded in broilers at the age of 3-6 weeks. The incubation period does not last long - a maximum of 1-2 days; infection of the livestock occurs very quickly.

The main symptoms of Gumboro disease are:

• severe diarrhea, mostly white;
• ruffled plumage, weakness and depression of the bird;
• chills, significant loss of appetite, signs of incoordination may be observed;
• dehydration and susceptibility to pathogenic organisms.

Most often, outbreaks of the disease can be short-term nature– about 2-3 days. After recovery, the birds continue to experience a decrease in immunity for some time. Mortality from bursal disease, as a rule, reaches 5-6%, however, it can be much higher - 40% or more.

The hidden type, although it does not have such obvious external manifestations, is considered more insidious and dangerous. It can manifest itself in a general depressed state in birds. Hidden Current Gumboro disease is associated with deterioration in feed conversion, stunted growth of broilers and their immune vulnerability.

Treatment

There is no specific treatment for Gumboro disease. The best way The way to prevent an unwanted epidemic is vaccination. For these purposes, so-called live and inactivated vaccines are used.

It is very important to detect foci of the disease in time and isolate the sick bird. Particularly affected individuals are recommended to be killed.

Pathological changes that will help confirm the diagnosis are as follows:

• enlarged and edematous bursa of Fabricius, it can be yellowish to brown due to areas of hemorrhage;
• hemorrhages in the kidneys and muscles;
• dehydration and anemia.

Since the virus is very stable, it is recommended to “relocate” sick birds from the chicken coop to another place. And in the room, carry out repeated treatment with formaldehyde and phenol.

Video “Diseases of chickens”

The video below will tell you what ailments befall the feathered inhabitants of farmsteads!

Infectious bursitis (Gumboro disease) is an acute contagious viral disease of chickens, characterized by apathy, diarrhea, anorexia, damage to the bursa of Fabricius, extensive intramuscular hemorrhages and kidney damage.

Historical reference. For the first time, infectious chicken bursitis was described by researchers in 1962 in the city of Gumboro, USA. Today, the disease is diagnosed in many countries around the world - the USA, Canada, Mexico, England, Germany, France and other European countries, India, Japan, Israel, and South African countries.

Economic damage quite significant and is determined by losses from death of up to 10-20% of the poultry population, a large percentage of carcasses being rejected due to subcutaneous, intramuscular hemorrhages and exhaustion.

The causative agent of the disease belongs to reoviruses. The size of virions is 50-70nµ. They have icosahedral symmetry. The capsid consists of a single layer with 92 capsomeres. The virus is cultivated in chicken embryos of 9-11 days of age, causing their death 4-6 days after infection in the allantoic cavity in the CAO and in the yolk sac, as well as in the culture of kidney cells and fibroblasts of chicken embryos. The virus is relatively resistant to factors external environment. Indoors, on metal and wooden surfaces, the virus remains active for 122 days. The virus is viable in water, food and droppings for 52 days. The virus retains its infectivity when heated to 60°C for 90 minutes, at 56°C for 5 hours. Only at a temperature of 70°C the virus is destroyed in 30 minutes. The virus is resistant to chloroform, ether, trypsin, while 5% formalin kills it. Chloramine and sodium hydroxide solutions have an inactivating effect.

Epizootological data. Under natural conditions, 2-15 week old chickens are susceptible to the virus, 2-4 week old chickens are especially sensitive. There are reports of quail sensitivity to the virus. The disease is observed at any time of the year in different climatic zones, regardless of the breed of chickens. The disease is especially widespread in reproductive farms where there are birds of different ages. The source of the virus is a sick or recovered bird, a virus carrier, which sheds it in its droppings for up to 14 days. The virus is spreading rapidly in poultry flocks. It is transmitted when sick and healthy chickens are kept together, through contaminated feed, water, bedding, droppings, and the virus can also be transmitted mechanically - by service personnel, through care items contaminated with the virus, with slaughter products, other species of birds, insects, especially yellowwings. Ducks, turkeys, geese, guinea fowl, and quail can be carriers of the virus.

The pathogen enters the body through the mucous membranes of the nasal, oral cavities, and conjunctiva in natural conditions. The bird becomes infected through nutrition.

Pathogenesis. The causative agent of infectious bursitis that has entered the body of a bird orally can be detected in intestinal lymphoid cells within 4-5 hours. From lymphoid cells with the blood and lymph flow, bypassing the Kupffer cells of the liver, the virus enters all organs and tissues. After 11 hours, the virus begins to multiply in the bursa of Fabricius. In this case, the phenomena of viremia in the bird’s body are short-lived, lasting up to two days. Subsequently, we detect the virus in all parenchymal and lymphoid organs, but in the highest concentrations in the bursa of Fabricius, where it persists for up to 2 weeks.

Damage to the lymphoid tissue of a sick bird is accompanied by a pronounced immunosuppressive effect, manifested in a significant decrease in the number of lymphocytes in the bird’s blood, up to the suppression of all. In dependent functions of immunity, especially the primary humoral one responsible for the formation of antibodies. There is a decrease in the level of serum complement and blood clotting, with the possible involvement of immune complexes in the development of the disease. All this leads to a loss of effectiveness of immunization of the affected bird against, and Marek. Susceptibility to increases by 3-6 times. Wherein enough level protection against Newcastle disease can only be achieved by immunizing one-day-old chicks or 2-3 weeks before infection with infectious bursitis virus. Against such an immunosuppressive background, in the absence of lymphocytes in the blood of birds, various infections such as gangrenous dermatitis often worsen or reappear.

Clinical signs. The incubation period is 2-6 days. The disease begins super-acutely, symptoms of the disease in birds appear suddenly, from 10 to 20% of chickens fall ill with a mortality rate of 0.5-15%.
In sick chickens we note depression, disheveled behavior, refusal to feed, trembling, unsure gait, symptoms of diarrhea ( watery diarrhea with whitish-yellow feces), soiled feathers around the cloaca. Some chickens appear severe itching around the cloaca, which they try to calm down by pecking at this area. This is often the first sign of an onset of illness for service personnel; the patients drink a lot, their feathers are ruffled.

At acute course disease, the death of chickens is observed, which reaches its maximum on the 3-4th day of illness (3-80%). The mortality curve is very characteristic and must be taken into account when making a diagnosis. The duration of the disease in birds in the affected group is 4-8 days.
In the subacute course, the symptoms of the disease are less pronounced and the death rate is insignificant.

In poultry farms, where the disease is not registered for the first time, it can be asymptomatic. In such farms, chickens do not show signs of illness, and when examining blood serum, virus-neutralizing and precipitating antibodies are detected.

Pathological changes. We note anemia and dehydration in chickens muscle tissue; in the muscles of the leg, thigh, wings and chest we often find pinpoint and striped hemorrhages. We also find hemorrhages on the mucous membrane of the glandular stomach. The kidneys are enlarged, light gray in color (from the accumulation of salts in the tubules uric acid). The liver and spleen are hypertrophied. In some birds, the ureters may also be congested with urate. We note signs of catarrhal enteritis, serous pericarditis, and peritonitis. At the same time, the most characteristic changes for this disease are found in the bursa of Fabricius. In the first 2-4 days after the bird is infected, it increases 2-3 times. Its mucous membrane is swollen, hyperemic, with hemorrhages and necrotic areas, sometimes in its lumen we find fibrin clots, and later a cheesy mass. In asymptomatic cases, these changes are less pronounced and can only manifest themselves in the form mild hyperemia or completely absent.

From the 10-12th day after infection, signs of atrophy of the bursa of Fabricius, thinning of the folds of the mucous membrane, which are often hyperemic and have pinpoint hemorrhages, are observed.
The leading cytomorphological sign is necrosis of cells of the lymphoid tissue of the bursa of Fabricius. In place of the destroyed follicles, proliferation of corticomedullary epithelium is established, fermenting mucous glands. We observe a general picture of purulent and necrotic inflammation with vacuolization in the bursa of Fabricius.

Diagnosis and differential diagnosis are based on the analysis of epizootic, clinical data, pathological changes and the results of laboratory (serological and virological) studies, including isolation and identification of the virus. A study is carried out on the bursa of Fabricius, spleen, liver, and kidneys taken from dead or forcibly killed birds. All this is delivered to the veterinary laboratory in a thermos with ice. For serological testing, 20-25 blood serum samples are sent, from daily and over 60 days of age, obtained at the onset of the disease and after 21 days. The veterinary laboratory uses the following research methods: isolation of the virus in chicken embryos or in cell culture; bioassay on susceptible chickens; identification of the isolated virus in neutralization reactions (RN) and diffuse precipitation in agar gel (DPR); determination of specific antibodies in blood serum in RN and DNP; detection of histological changes in organs and tissues Research is carried out only on SPF embryos and SPF birds.

Infectious bursitis must be differentiated from the following diseases:

• , which clinically manifests itself in approximately the same way as infectious bursitis, we make an exception by conducting a scatological examination;
• which may cause hemorrhagic lesions and characteristic respiratory symptoms, is highly contagious and lethal, birds of all ages are susceptible;
• fatty liver and kidney syndrome, which is accompanied by hemorrhages and kidney damage, very rarely ends in death, chicken carcasses have a pale pink color;
• nephrosonephritis, which is caused by the infectious bronchitis virus, is similar in damage to parenchymal organs, but is manifested by respiratory disorders and does not affect the bursa of Fabricius;
• hemorrhagic syndrome of a toxic nature - occurs when poisoned by sulfonamides or mycotoxins, observed in birds of all ages, hemorrhages are concentrated in the visceral organs;
• — atrophy of the bursa of Fabricius is observed, the lesions are limited to the epithelium.

The disease additionally needs to be differentiated from lymphoid leukemia and.

Immunity and means of specific prevention. The recovered bird develops immunity, which is used for diagnostic test and vaccine development.

Numerous live vaccines that are highly immunogenic have been developed and used abroad. In Italy - gumbo-vax, LZD-228 (Merrier, France), Nobilis (Holland). These vaccines are harmless, do not have an immunosuppressive effect, are effective, stable during storage and transportation, and are convenient for use.
Chickens are vaccinated intraocularly or by drinking the vaccine at one day of age, as well as intramuscularly in groups older than 12 weeks. Vaccines can be used for complex vaccinations in combination with vaccines against diseases and infectious bronchitis. Inactivated emulsified vaccines are also used. Vaccination of chickens ensures the safety and usefulness of lymphoid tissue. High titres of maternal antibodies are transferred with the egg and protect the offspring during the first four weeks.

Disease prevention measures. To prevent Gambora disease, poultry farm owners must comply with the following requirements:

• strictly observe measures to protect the farm from the introduction of infection, and also supply bird flocks with hatching eggs and day-old young animals only from farms free from Gumboro disease;
• carry out preventive vaccination of young animals in all categories of farms with live vaccines from an intermediate strain, and vaccinate replacement young animals of the parent and breeding herds with an inactivated vaccine;
• create for the bird optimal conditions maintenance and provide them with nutritious feed;
• place birds of different age groups in geographically separate areas;
• equip poultry houses with birds of the same age;
• observe inter-cycle preventive breaks with thorough cleaning and disinfection of premises;
• disinfect imported breeding eggs, containers and transport used for their delivery;
• carry out separate incubation of breeding eggs imported to the farm and eggs received from one’s own parent flock;
• raise day-old chicks obtained from imported eggs separately from the rest of the poultry farm.

Each farm (farm) should ensure the necessary zoohygienic, veterinary and zootechnical requirements for keeping and feeding birds.

Measures to combat the disease.

When a diagnosis of infectious bursal disease (Gumboro disease) is made in accordance with the order of the Ministry Agriculture RF dated December 19, 2011 No. 476 “On approval of the list of contagious, including especially dangerous, animal diseases for which restrictive measures (quarantine) can be established.” By the Decree of the Governor of the region, restrictions are introduced on the farm and in accordance with” instructions for the prevention and elimination of infectious bird diseases bursal disease from October 25, 1995" on the farm prohibited:

• export hatching eggs. Day-old young animals, grown and adult birds, feed, equipment, inventory, etc. to other farms and sell to the public.

According to the restrictions allowed:

• sell eggs to the retail chain after disinfection;
• poultry should be slaughtered in the slaughterhouse (slaughterhouse) of the farm; in its absence, conditionally healthy birds should be sent for slaughter to the nearest meat processing plant only with special permission from the Chief State Veterinary Inspector of the region, in a separate batch within the time frame established by the State Veterinary Service and agreed upon with the poultry plant for immediate slaughter with compliance with current veterinary and sanitary rules and other veterinary regulatory documents preventing the spread of the pathogen.

Clinically healthy birds immunize against IBD in herds with subclinical disease using vaccines from intermediate strains; in herds with acute and subacute disease - vaccines from moderately pathogenic (“hot”) strains.

Along with vaccinations of young animals with live vaccines, immunization of breeding replacement young animals at the age of 100-130 days (one month before the start of egg laying) is carried out with an inactivated vaccine.

Vaccines are used in accordance with the instructions for their use.
Systematically culled. A weakened and sick bird. All poultry that have reached slaughter standards from premises in which the disease was recorded are killed for meat. Stop laying eggs for incubation, thoroughly clean and disinfect the hatchery, poultry houses, equipment, inventory, territory, transport, etc. Eggs are laid for incubation no earlier than 7 days after the departure of the last batch of incubated eggs.

Each poultry house is assigned maintenance personnel who are provided with special clothing, safety shoes, disinfectants. At the end of the working day, workwear is disinfected with formaldehyde vapor.
In premises with sick birds, aerosol disinfection is carried out in accordance with current instructions on carrying out aerosol disinfection of poultry premises in the presence of birds.

The farm is improving the feeding and maintenance of birds, and introducing anti-stress additives (drugs) into the diet.

For wet disinfection of bird-free premises, use one of the following drugs: 2% formaldehyde solution, 4% sodium hydroxide solution, clarified bleach solution containing at least 3% active chlorine. Exposure for at least 6 hours. Consumption of disinfectants is 0.5 l per 1 m² of surface area to be treated; ceilings, walls, floors, wooden surfaces are whitened with 20% freshly slaked lime twice with an interval of 1 hour.

Litter and deep litter are transported to a manure storage facility for biothermal neutralization.

Restrictions on the farm are lifted after the delivery for slaughter of all poultry from poultry houses in which IBD disease was observed, completion of final veterinary and sanitary measures, and in the absence of the disease in more than three batches of young animals raised up to 90 days of age in all poultry houses of the farm during the professional break.