In recent 50 years, due to the high concentration of chickens and the subsequent changes in feeding management conditions and environmental conditions, the harm of this respiratory infectious disease in chickens has become more and more prominent. This happens all over the world. Although the mortality rate is not high, it makes chickens grow poorly and lay fewer eggs, which causes great losses to the poultry industry.
1. epidemiology
(1) source of infection The infection of this disease is mainly through infecting chickens. In particular, the symptoms of infected chickens are not obvious, the course of disease is long, and it is not easy to be found in chickens, which is the most dangerous source of infection.
(2) Transmission route Pathogens can be transmitted through the air. When sick chickens cough and sneeze, pathogens in droplets can spread to other poultry. Contaminated feed and drinking water can also spread diseases. The disease can be transmitted vertically through eggs. Eggs laid by sick or infected chickens contain pathogens, and chicks hatched from infected eggs can become new sources of infection. In addition, pathogens were found in the semen of sick turkeys and the fallopian tubes of hens, so infection may also occur during reproduction.
(3) Chickens and turkeys of different ages in susceptible animals can be infected with this disease, especially 1 ~ 2 months old. Sometimes it is also found in quail, guinea fowl, peacock, partridge and pigeon. The epidemic is most likely to occur in a large group of chickens, while most adult chickens are recessive and sporadic.
(4) The disease can occur all the year round in the onset season, but it occurs most frequently in winter and spring, and its condition is also serious.
(5) The secondary infection of other bacteria and viruses by inducing factors is one of the main factors leading to the outbreak of the disease in chickens with recessive infection. Secondary pathogens mainly include Haemophilus parasuis, Pasteurella multocida, Escherichia coli, staphylococcus, pneumococcus, mold and so on. And infectious bronchitis virus, infectious laryngotracheitis virus and fowlpox virus.
Poor environmental sanitation, high feeding density, poor ventilation in chicken houses, lack of vitamin A in feed, long-distance transportation and mixed feeding of chickens of different ages can all be the causes of the disease. These inducements play an important role in promoting the occurrence and development of diseases.
When the attenuated Newcastle disease vaccine is immunized by aerosol method, it can also stimulate the incidence of chickens infected with Mycoplasma gallisepticum.
2. Clinical symptoms
The incubation period of the disease is about 4 ~ 12d, and the natural infection may be longer.
(1) Chickens infected with Mycoplasma gallisepticum usually show only mild respiratory symptoms, and occasionally pollutants can attach around the nostrils, but nasal discharge is rarely seen, and most of them are recessive infection processes. Due to poor feeding management and environmental conditions, especially when mixed with other pathogenic microorganisms, obvious respiratory symptoms may appear, such as increased nasal discharge, serous or purulent nasal discharge, blocked nostrils, blocked breathing, frequent shaking of the head or strange noises. If the turbinate or tracheal mucosa is inflamed, mucus will increase, breathing will be difficult, sneezing, coughing, breathing with the mouth open, and tracheal rales can be heard. Followed by rhinitis, sinusitis and conjunctivitis, nasal cavity and suborbital sinus accumulated exudates, moist eyes, tears, eyelid swelling, exophthalmos like tumors. Compression of one or both eyeballs leads to atrophy and blindness. Systemic symptoms are elevated body temperature, loss of appetite, growth retardation and gradual weight loss.
The disease usually has a chronic course, which can be as long as 1 month. The mortality rate of chicks can reach 30%. The symptoms of adult chickens are relatively mild, and hens also show a decrease in egg production, a decrease in hatching rate and an increase in weak sick chickens.
(2) The turkey has foamy secretion outside its nostrils, mucus on its head and wings, and tears. Then, sinus swelling, rales when breathing, cough, dyspnea, and significantly reduced egg production.
3. Lesions
(1) Cases of simple infection with Mycoplasma gallisepticum, pathological autopsy showed mild rhinosinusitis and suborbital sinusitis. Natural infections are mostly mixed infections, with edema, congestion and hypertrophy of respiratory mucosa, and sinus cavity filled with mucus and caseous exudate. When the symptoms are severe, inflammation can spread to the lungs and airbags, and the changes of airbags in the chest and abdomen are often obvious. At the early stage, the balloon was slightly turbid with gray edema and nodular lesions on the surface. With the development of the disease, the balloon membrane thickens and there is a lot of cheese-like exudate in the balloon cavity. Sometimes a certain degree of hepatitis lesions can be seen. In chronic severe cases, the mucosa of suborbital sinus is inflamed, and turbid mucus or cheese-like substances accumulate in the sinus cavity. If there is mixed infection of Escherichia coli and cellulose, purulent pericarditis and hepatic capsulitis may occur. Hens have salpingitis.
(2) Histological examination showed that the mucosa of the invaded tissue was obviously thickened, with monocyte infiltration, mucous gland hyperplasia and submucosal focal lymphoid tissue hyperplasia.
4. Diagnostic points
According to the epidemic situation, clinical symptoms and pathological changes, a preliminary diagnosis can be made. However, the diagnosis of this disease must be separated, confirmed and serologically examined.
(1) isolation and identification of pathogen can directly take trachea, air sac exudate, turbinate bone and lung tissue of sick chicken, add liquid culture medium, grind it into suspension, inoculate it on appropriate agar slant of mycoplasma culture medium containing liquid culture medium, and culture it at 37℃ for at least 5 ~ 7 days. In the initial separation process, 0.25ml 1% thallium acetate solution and 65438+ million units of penicillin should be added to all media to inhibit the growth of other miscellaneous bacteria. After the initial separation, there was no growth. It is necessary to suck 0.5 ~ 1.0 mL L of culture solution from the culture tube every 3 ~ 5 days, and then blindly transfer it to a new tube. After 2 ~ 3 consecutive times, the liquid medium with phenol red indicator turns yellow, and the growth of mycoplasma can be known. The culture can be used for staining, colony observation, hemagglutination, chick embryo and chick inoculation test, and can also be made into antigen and serological test with known antiserum to prove whether it is mycoplasma gallisepticum.
(2) There are two serological tests: agglutination test (including whole blood agglutination reaction and rapid plate agglutination reaction) and hemagglutination inhibition test.
The rapid plate method is to put 1 drop of chicken serum or whole blood on a white porcelain plate or glass plate, and then add 1 drop of known staining antigen to mix thoroughly. 1 ~ 2 minutes later can be judged as positive. This method is a simple and rapid laboratory diagnosis method, which can quickly determine the antibody agglutination value in serum.
(3) Attention should be paid to the difference between this disease and respiratory infectious diseases such as chicken infectious bronchitis, chicken infectious laryngotracheitis and infectious rhinitis. Infectious bronchitis spreads rapidly in chickens; Chicken infectious laryngotracheitis, the tracheal mucosa is hemorrhagic inflammation, and when the course of disease is prolonged, solidified cheese-like substances often appear on the surface of the tracheal mucosa; Simple infectious rhinitis, edema, swelling and tears on the face of sick chickens, its lesions generally do not invade the airbag.
5. Treatment methods
Tylosin is a specific therapeutic drug for this disease, especially for chickens with mild clinical symptoms.
Drinking water containing tylosin 500 mg/L for 5 ~ 7 days has a good curative effect. Broilers can be fed 500 ~ 1000 mg/kg, 1 ~ 5 days old for the first time, 1 ~ 2 times, and then used for 24 ~ 48 hours at 3 ~ 5 weeks old, which can effectively prevent and treat the disease. It is a contagious disease of pigs caused by mycoplasma pneumoniae. The disease is widely spread all over the world, and has occurred in major pig-raising countries and regions such as Europe, Asia, the United States, Africa and Oceania, which has caused serious harm to the pig industry.
1. epidemiology
(1) infected pigs and infected pigs are the main sources of infection. Most of the new epidemic areas are due to the introduction of infected pigs, which have not been strictly quarantined and observed, and have been mixed into healthy pigs, thus causing epidemic outbreaks. Sows with bacteria in old epidemic areas are the most important in transmission. This kind of sick sow carries bacteria and secretes bacteria to infect its piglets in a certain period of time, and most of them can get sick.
(2) Transmission route Mycoplasma exists in the secretions of sick pigs, and is excreted with coughing, sneezing and panting, forming aerosol floating in the air, and healthy pigs are infected by inhaling mycoplasma-containing aerosol. Experiments show that the lung suspension or culture solution of sick pigs can cause typical respiratory diseases by spraying, nasal dropping and intratracheal injection. Other routes rarely cause disease.
Mycoplasma exists in the secretions of the respiratory tract of sick pigs and can survive in pigs for a long time. Even after the symptoms disappear for half a year to one year, mycoplasma still exists in the body and continues to be excreted. Therefore, once the disease is introduced into pigs, it can continue to occur and is difficult to eliminate.
(3) The natural cases of susceptible animal Mycoplasma hyopneumoniae are only found in pigs, but not in other domestic animals, animals and people. Pigs of different ages, sexes and breeds are susceptible. However, suckling and weaning piglets are the most susceptible, followed by sows in the late pregnancy and lactation, and fattening pigs and adult pigs have less disease and mild illness. The incidence of local pigs is higher than that of hybrid pigs and imported purebred pigs.
(4) In the onset season, the disease can occur all year round. Although there is no obvious seasonality, it usually occurs in winter, spring and cold season, followed by autumn and summer.
(5) Pigs with improper feeding management, crowded piggery, damp piggery, poor ventilation and poor sanitary conditions have high morbidity and serious illness.
2. Clinical symptoms
The incubation period is generally 1 1 ~ 16 days, the shortest is 5 ~ 7 days, and the longest is over 1 month. According to the course of disease and clinical manifestations, symptoms can be roughly divided into three types: acute, chronic and recessive, among which chronic and recessive are the most common.
(1) At the initial stage of acute disease, the spirit is depressed and breathing is accelerated, reaching 60 ~ 120 times per minute. Unwilling to leave. After that, abdominal breathing appeared, and the two forelimbs were open, showing a dog sitting position. In severe cases, the mouth is panting and the mouth and nose are foaming. Sometimes I hear a continuous or even spasmodic cough. Body temperature generally does not change much, and only a few cases have slight fever. Appetite is generally normal, only when breathing is difficult, but rarely stop eating. This kind of disease has short course, severe symptoms and high mortality. It usually takes 1 ~ 2 weeks, and most of them die of suffocation. Resistant pigs turn chronic. This type is very common in new pigs with this disease.
(2) Most pigs with chronic type of the disease have a chronic course at the initial stage of the disease, and some of them are transformed from acute type. The main symptom is long-term cough, which often occurs in the morning, evening or during exercise and after meals. From light to heavy, it is a simple cough at first, and a persistent spasmodic cough often occurs in severe cases. Stand still when coughing, arch your back, straighten your neck and lower your head until respiratory secretions are coughed up or swallowed. If the course of the disease develops further, there will be dyspnea. It is characterized by shortness of breath, increased frequency and abdominal breathing. These symptoms often fluctuate due to changes in management and climate. Fattening pigs, hybrid pigs and reserve pigs will soon be improved and restored after improved feeding or under good environmental conditions. On the other hand, it gradually loses weight and grows slowly, becoming a stiff pig, especially a native pig. This kind of disease has a long course, which can be delayed for 2 ~ 3 months or even more than half a year, but the mortality rate is not high. This type is more common in pigs in old epidemic areas.
(3) Latent sick pigs usually have no obvious clinical manifestations, and occasionally have mild cough and asthma at night or after fleeing. Growth and development are basically normal. Only through X-ray examination or slaughter autopsy can we see the changes of pneumonia in the tip, tip and middle lobe of the lung. Some even can't see the pathological changes with naked eyes, only the pathological changes are found in histological examination, and mycoplasma pneumoniae is found in pathogen examination. This kind of sick pig is common in old epidemic areas, and it is often ignored by people and becomes a dangerous source of infection.
3. Lesions
(1) Pathological autopsy showed that chronic cases with long course of disease were stunted and extremely emaciated. Autopsy found that the main lesions were lung, hilum and mediastinal lymph nodes. When the disease is in the stage of inflammatory development, the whole lung is swollen, with different degrees of edema and emphysema; When the inflammation dissipates, the connective tissue between pulmonary lobules proliferates and hardens, the surface sinks, and the surrounding tissues are not fully expanded. Pulmonary lesions are mainly found in the heart lobe, pointed lobe, middle lobe and the leading edge of diaphragm. Interstitial pneumonia often occurs, and the lung lesions on both sides are roughly symmetrical. The boundary of the lesion is obvious, showing the appearance of substantial change, light gray color like pancreas, colloidal infiltration and translucent state. The cut surface is moist and smooth, the alveolar boundary is unclear, and it looks like tender meat, which is customarily called "meat degeneration". When the disease worsens, it can be seen that the color of the lesion deepens, showing lavender, deep purple or grayish white and grayish red. Translucency decreases and toughness increases, like pancreatic tissue, which is customarily called pancreatic change.
Hilar and mediastinal lymph nodes are swollen, gray and edema. The cut surface is moist, slightly everted, and the edge is sometimes slightly congested.
(2) Histological examination showed that a large number of lymphocytes infiltrated and follicles proliferated around bronchi and small vessels in the early stage, forming a tube sleeve. With the development of the disease, the alveoli around the bronchioles expand and the alveoli are filled with a lot of inflammatory exudates. The exudate is serous and contains lymphocytes and exfoliated alveolar epithelial cells. Most small lesions merge into large consolidation areas. The capillaries in the alveolar wall are slightly congested, the alveoli around the focus are swollen, a large number of lymphocytes accumulate around the bronchioles, the tracheal mucosa epithelium proliferates and thickens, and different amounts of exudates remain in the lumen. Lobular interstitial widening, edema and inflammatory cell infiltration.
Diffuse hyperplasia and edema of hilar and mediastinal lymph nodes.
4. Diagnostic points
According to epidemiological data, clinical manifestations and pathological changes, a preliminary diagnosis can be made, but both early pigs and recessive pigs can be diagnosed by X-ray examination.
(1)X-ray examination X-ray examination is of great value in diagnosing the disease and cultivating healthy pigs. The sick pigs showed irregular turbid and oozing shadows in the medial lung field and diaphragm angle. The shadow density is medium and the edges are blurred. According to the different stages of the disease, the characteristics of lesion shadow are different.
① Early stage: On dorsoventral examination, the lung field of diaphragm angle showed slight flocculent high-density shadow with uneven shadow and blurred edge. Then the shadows became more and more obvious, and large clouds of shadows could be seen, blurring the lower bound of the heart. During lateral examination, the shadow of the heart is uneven, and the flocculent shadow also appears in the trailing lung field.
② Severe stage: extensive diffuse turbid oozing shadow was seen in the central area of lung field in dorsal and abdominal position. Lateral view shows extensive and dense shadows in the abdominal lung field, and the heart is hidden.
③ Fading period: Shadow is characterized by both extensiveness and looseness. Diffuse exudation shadow turned into sparse shadow, lung field basically returned to the transparent state of expansion, and the outline of heart reappeared.
(2) Serological examination, indirect hemagglutination test, tube agglutination test, plate agglutination test, rapid serum plate agglutination test, indirect immunofluorescence test, tube complement binding reaction and trace complement binding reaction can all provide basis for diagnosis.
5. Treatment methods
Tylenol is the first choice for treatment. Tylosin powder for injection, chongchuankang (tylosin 1), 10 mg/kg body weight, was injected intramuscularly twice a day for 5 ~ 7 days, with good curative effect.