Common bacterial and parasitic diseases in laying hens mainly include pullorum, Escherichia coli, Staphylococcus aureus, Mycoplasma, Aspergillus, avian cholera, coccidiosis, etc.
1. Pullorum
(1) Pathogen and epidemic characteristics of chicken pullorum: the pathogen is Salmonella, Gram stain negative, elongated bacilli with slightly rounded ends, without capsule And spores also have no flagella and cannot move. It has strong resistance to the environment and can survive for 65 days on a wooden feeding trough at a temperature of 5 to 8°C. It can survive in the soil for 20 to 35 days in summer and 128 to 184 days in winter. It can survive in chicken manure suspension. It can survive for more than 3 months, and the bacteria attached to the villi can survive for about 1 year. The bacteria attached to the egg shell will die after 5 days and 3 days in the incubator. Bacteria multiply rapidly in egg yolks stored at 20°C.
Epidemic characteristics: Different breeds of poultry are infectious, and the susceptibility is related to age and breed. Chicks are the most popular, and chickens under 2 weeks old have high morbidity and mortality. Brown-shelled hens are more sensitive than white-shelled hens. Chickens, turkeys, ducks, pheasants, peacocks, quails, pigeons, sparrows, etc. can all be naturally infected. Sick chickens and infected chickens are the main sources of infection, which can be transmitted both horizontally and vertically. The excrement and secretions of sick chicks contaminate feed, drinking water and utensils, which can cause infection of chicks in the same group. Most of the infected chicks die, but some of them are in a bacterium-preserving state. When they lay eggs, they will produce bacterium-preserving eggs again, forming repeated infections and cycles. onset. Roosters can also pass the disease to hens during mating. Flies and sparrows are also vectors of infection. Poor feeding and management of chicks, sudden high and low temperatures, incomplete feed nutrition, long-distance transportation, etc. can all contribute to the prevalence of this disease and increased mortality. In chicken farms where the disease has always existed, the incidence rate of chicks is about 20% to 40%. However, in chicken farms where the disease is newly introduced, the incidence rate is significantly higher, sometimes even as high as 100%, and the fatality rate is also higher than in old epidemic farms.
(2) Symptoms and autopsy Symptoms: Most of the chicks hatched from bacteria-preserved eggs die within 7 days. Chicks infected in the same group will die within 2 to 3 weeks. Sick chicks are afraid of cold, often huddle together, have drooped wings, are listless, stop eating, and are lethargic. White feces are discharged, often sticking to the tail feathers, sometimes blocking the anus, making defecation difficult or even impossible. Screaming during defecation and abdominal distension. When the lungs are infected, breathing becomes difficult. It can also cause joint swelling and lameness. Most of the surviving chicks are stiff chickens. Most adult chickens are asymptomatic and tolerate it. When the ovary is diseased, it can cause a decrease in egg production, a decrease in the hatchability of infected eggs, and a decrease in the survival rate of hatched infected chicks. Some also suffer from lethargy, loss of appetite, shrunken necks, drooped wings, upside-down feathers, dark purple wattles, and loose feces.
Pathological changes: Chicks that die early have enlarged, congested or streaky livers and enlarged gallbladder containing a large amount of bile. Congestion or bleeding in the lungs. The yolk of long-term disease is malabsorbed and appears greasy or cheese-like. There are yellow necrotic spots or small nodules on the liver, lungs, heart, intestines and gizzard. When the nodules on the myocardium increase, they can significantly deform the heart. The cecum is enlarged and its contents are blocked like cheese. The color of the kidneys is dark red or pale, and the renal tubules and ureters are dilated and filled with urate.
It is common for adult hens to have ovaries that are shrunk, deformed, discolored, and cyst-like. Acute or chronic pericarditis. Some of the damaged follicles fall into the abdominal cavity, causing peritonitis, ascites, and abdominal organ adhesion. The testicles of the rooster are atrophied and blue-grey, and the vas deferens are filled and enlarged with cheese-like material. Some livers are significantly enlarged and brittle, often causing liver rupture, causing severe internal bleeding and sudden death of sick chickens.
(3) Diagnosis, prevention and treatment Diagnosis: A preliminary diagnosis can be made based on the epidemic characteristics, onset symptoms and autopsy changes. Further confirmation requires pathogen isolation, identification and serological examination.
Prevention: Do a good job in quarantine and purification of breeder chickens, as well as sanitation of the environment, feed, and drinking water, as well as disinfection of eggs and hatching processes. For drug prevention, you can use 14 ml of formalin and 7 grams of potassium permanganate per cubic meter after the chicks hatch, fumigate them in the hatcher for 15 minutes, and use 0.01% permanganate at 1 to 2 days old. Potassium solution in drinking water. Chicks can also be prevented with drugs such as norfloxacin, gentamicin and kanamycin. Or regularly feeding biological agents such as lactic acid bacteria to chickens, which has a good effect on preventing pullorum in chickens.
Treatment: Treatment with norfloxacin, gentamicin and kanamycin can be used.
2. Escherichia coli
(1) Pathogen and epidemic characteristics The pathogen is Escherichia coli, which is a common bacterium in the intestines of healthy livestock and poultry. It is divided into pathogenic and non- Two broad categories of pathogenicity. Colibacillosis is a conditional disease that is easy to develop under poor sanitary conditions and poor feeding and management. E. coli is highly resistant to the environment. E. coli can survive for a long time if it adheres to feces, soil, dust in chicken houses, incubator fluff, broken egg skins, etc.
Popular characteristics: Chickens of all ages can be infected, characterized by pericarditis, perihepatitis, airsacculitis, peritonitis, salpingitis, synovitis, Escherichia coli granuloma and omphalitis. , morbidity and mortality are affected by various factors, and chicks and chickens under 4 months old are highly susceptible. Poor feeding management, stress or concurrent infections with other pathogens can all be causes of colibacillosis. Chicks and young chickens mostly suffer from acute sepsis, while adult chickens mostly suffer from subacute airsacculitis and polyserositis. Transmissible through eggs, respiratory tract and mouth.
(2) Symptoms and necropsy Symptoms: ① Escherichia coli sepsis, the sick chicken is listless, eats less, becomes weak and dies. The abdomen is distended and yellow-green loose stools are discharged. In fibrinous pericarditis, the air sacs are cloudy and hypertrophic, with caseous exudate. The liver capsule is white and turbid, with fibrinous attachments, and sometimes white necrotic spots can be seen. The spleen is congested and swollen.
②The hatching rate of hatching eggs is reduced, the embryos die in the late hatching period, and the number of dead embryos increases. The chicks are weak, have poor yolk absorption, umbilical cord inflammation, and discharge white, yellow-green or earthy loose stools. The abdomen is distended and the baby dies 2 to 3 days after birth. The mortality rate generally decreases after 6 days of age. Even immortal chickens are stunted. The vitelline membrane of dead embryos and dead chicks becomes thinner, and the navel is swollen and inflamed. Pericarditis is common in infections after 4 days of age.
③ During fallopian tube inflammation, the fallopian tubes become thinner and filled with foul-smelling cheese-like substances, which block the fallopian tubes and cause the discharged eggs to fall into the abdominal cavity, causing peritonitis.
④ Hemorrhagic enteritis, sick chickens have rough feathers, drooping wings, lethargy and diarrhea. The intestinal mucosa in the upper third to half of the intestine becomes congested and thickened. In severe cases, blood vessels rupture and bleed, forming hemorrhagic enteritis.
⑤ Synovitis and arthritis, the sick chicken is lame or prone, and one or more tendon sheaths and joints are swollen.
⑥ During granuloma, nodular granuloma occurs along the intestines and liver, resembling tuberculosis.
⑦ Panophthalmitis, encephalitis, etc.
(3) Diagnosis, prevention and treatment Diagnosis: A preliminary diagnosis can be made based on epidemic characteristics, clinical symptoms and pathological changes. Bacterial isolation, pathogenicity testing and serological identification are required for confirmation. The diagnosis of secondary colibacillosis must be based on the isolation of E. coli from the primary disease.
Prevention: Do a good job in environmental sanitation and disinfection, strictly control the sanitation and disinfection of feed and drinking water, and do a good job in immunity against various diseases. Strictly control the breeding density, ventilate the house well, and carry out regular disinfection of chickens. Avoid contamination of eggs with feces and strictly disinfect eggs and the incubation process. Regularly feeding biological agents such as lactic acid bacteria to chickens is very effective in preventing colibacillosis. The oil emulsion inactivated vaccine made from the pathogenic Escherichia coli isolated on the farm to immunize the chickens on the farm has a certain effect on preventing colibacillosis. Two immunizations are required, the first at 4 weeks of age and the second at 18 weeks of age. It can also be used to immunize chicks.
Treatment: Antibiotics or sulfa drugs can be used for treatment, and gentamicin, kanamycin, streptomycin, oxytetracycline, cotrimoxazole, etc. are commonly used. However, E. coli can easily become resistant to drugs, so it is best to conduct a drug sensitivity test and use sensitive drugs for treatment.
3. Staphylococcus disease
(1) Pathogen and epidemic characteristics The pathogen is Staphylococcus aureus, which has no flagella and cannot move. No spores, except for a few strains, generally do not form capsules. Gram stain is positive. It is widely distributed in soil, air, water, feed, object surfaces, and feathers, skin, mucous membranes, intestines and feces of chickens in nature. It has strong resistance to the external environment, can survive in dry pus or blood for 2 to 3 months, and is resistant to many disinfectants.
Popular features: Staphylococcus aureus can infect all kinds of poultry. Chickens of any age and even chicken embryos can be infected. It is characterized by localized suppuration of tendon sheaths, joints, and synovial bursae, wound infection, sepsis, omphalitis, and bacterial endocarditis. Although chicks aged 4 to 6 weeks are extremely sensitive, the actual incidence rate is most among middle chicks aged 40 to 60 days. It is mainly transmitted through wounds on the skin and mucous membranes, but can also be transmitted through direct contact and air. Chicks can also be infected through the umbilical cord. No obvious seasonality.
(2) Symptoms and necropsy Symptoms: ①Acute septicemia type: The sick chicken is depressed, standing still, unwilling to move, and its wings are drooping. Neck shrinkage, half-closed eyes in a lethargic state, rough and dull feathers, loss of appetite or loss of appetite, some chickens have diarrhea, and the feces is watery, gray-white or yellow-green. There is subcutaneous edema in the chest, abdomen, and inner thighs, with varying amounts of blood-like exudate. The appearance is purple or purple-black, and there is a wavy feeling when touched, and local feathers are easy to fall off. After the skin ruptures, brown or purple-red fluid oozes out, making the surrounding feathers wet and dirty. Some chickens have bleeding spots of varying sizes on the dorsal and ventral surfaces of their wings, wing tips, tails, heads, faces, wattles, backs and legs. Local inflammation, necrosis or dry necrosis or dry scab (dark purple). Most people die within 2 to 5 days, with an average mortality rate of 5% to 10%, and the mortality rate in a few acute outbreak cases can be as high as 60%.
②Chronic arthritis type, multiple joints suffer from inflammatory swelling, the area is purple-red or purple-black, and black scabs form after ulceration. Due to swelling caused by puncture wounds to the foot pads, the chickens may become lame, unable to stand, and lie prone near the water trough or feeding trough. The chickens may gradually lose weight due to difficulty in eating, and eventually die of exhaustion.
③ In the omphalitis type, the abdomen of the sick chick is enlarged, the umbilical hole is inflamed, swollen, and moist, and the part is yellow or purple-black, and is hard to touch. Sick chicks suffering from omphalitis usually die within 2 to 5 days after hatching.
④ Eye type and lung type, enlarged head, swollen eyelids, and purulent secretions. If the disease lasts for a long time, the eyeballs will sag and become blind. The pulmonary type is characterized by pulmonary congestion, edema, and changes in lung parenchyma.
Neopsy changes: ①Acute sepsis type, the feathers on the chest and front abdomen fall off, the skin turns purple-black, and there is edema. Subcutaneous congestion, with a large amount of pink or yellow-red jelly-like exudate. The liver is enlarged, purple-red or mottled in color, with bleeding spots and white necrotic spots. The spleen is enlarged and has necrosis.
There was yellow turbid exudate in the pericardial cavity. Enteritis, intestinal contents become watery.
②Chronic arthritis type, the joints and synovial membrane are inflamed, the joints are swollen, the synovial membrane is thickened, and there are serous, mucinous or fibrous exudates in the joints.
③Omphalitis type, the umbilicus is inflamed and swollen, purple-red or purple-black, with dark red or yellow exudate. The yolk is poorly absorbed and appears dirty yellow, red or black, and its contents are thin, sticky, and tofu-like. The liver is enlarged and there are bleeding spots. The gallbladder is enlarged.
(3) Diagnosis, prevention and treatment Diagnosis: A preliminary diagnosis can be made based on the typical medical history, onset characteristics, clinical symptoms and pathological changes, and the absence of other respiratory diseases. Perform Gram staining on the exudate smear and microscopic examination. If Gram-positive bipolar stained cocci, some of which are filamentous or polymorphous, are found, the disease can be further suspected. Confirmation requires isolation, culture and identification of bacteria. To determine the pathogenicity of a pathogen, animal testing is required.
Prevention: Avoid trauma to chickens. Equipment in the chicken house must not contain any sharp objects. Be careful when trimming beaks, trimming toes, and immunizing; do a good job of disinfection, regularly spray disinfection of chickens in the chicken house with 0.3% peracetic acid, which can reduce the amount of bacteria in the environment; strengthen feeding management, timely ventilation, and maintain The chicken house should be dry and the density of the chickens should not be too large; the hatching eggs, hatching equipment and disinfection during the hatching process should be done well to reduce embryo infection and chick disease.
Treatment: Once staphylococcal disease occurs, it should be diagnosed immediately, and sensitive drugs should be selected for treatment based on the results of the drug sensitivity test. Such as gentamicin, kanamycin and other drugs.
4. Mycoplasmosis
(1) Pathogen and epidemic characteristics Pathogen: There are three kinds of mycoplasma that are pathogenic to poultry, Mycoplasma gallisepticum, Mycoplasma synoviae and turkey Mycoplasma. Mycoplasmas are tiny prokaryotic microorganisms that lack a cell wall. Mycoplasma gallisepticum is 0.25 to 0.5 nanometers, and Mycoplasma synoviae is 0.2 to 0.4 nanometers in the form of spherical and coccobacilli. It needs a special artificial culture medium to grow. Pathogenic mycoplasma can agglutinate chicken red blood cells and has weak resistance to the external environment. It quickly loses its vitality after being separated from the body and can be quickly killed by general disinfectants. It has weak resistance to heat and can survive in chicken manure at 20°C for 1 to 3 days. It will lose vitality in 1 hour at 45°C and 20 minutes at 50°C. Stores at room temperature for 6 days.
Popular characteristics: Most chickens in chicken farms in my country are infected with mycoplasma. Under normal circumstances, no obvious clinical symptoms appear, and the incidence rate is generally high and the mortality rate is low. Depending on the environmental factors, the severity of the disease and the mortality rate vary greatly, with the general mortality rate ranging from 10% to 30%. The disease can be transmitted through contact and through the egg. It can be transmitted through droplets from coughs and sneezes of infected chickens, or through contaminated feed and drinking water. Eggs produced by sick chickens contain pathogens, and chicks hatched from infected eggs carry mycoplasma. It can also be transmitted through mating. Chickens infected with mycoplasma alone often do not show symptoms under normal feeding and management conditions and have a latent process. This disease can be induced if you are reinfected with Newcastle disease, infectious bronchitis or infectious rhinitis, or if you are vaccinated. Poor ventilation in chicken houses, overly densely stocked chickens, and sudden changes in feed can be the predisposing factors for the disease. This disease can occur throughout the year, but is more common in cold seasons.
(2) Symptoms and necropsy symptoms: Chronic respiratory disease in young chickens includes runny nose, cough, sinusitis, conjunctivitis and airsacculitis, respiratory rales, often nasal mucus blocking the nostrils, frequent head shaking, Some chickens have foamy secretions in their eyes. Growth is stagnant, and the mortality rate of simple infection is low, while the mortality rate of concurrent infections reaches 30%. Infection in laying hens mostly occurs in a silent manner, with only a decrease in egg production and a decrease in hatchability. Newly hatched chicks are stunted in their weight gain. This disease is often co-infected with E. coli, causing symptoms such as fever and diarrhea. In the early stage of the disease, the chickens with infectious synovitis have pale crowns, changed gait, showed a slight splay, dull feathers, alienation, anemia, shrunken heads and closed eyes. Stunted growth, retarded growth, crown collapse, and in some cases the crown is blue-white. There is often swelling around the joints that can reach the size of a pigeon egg, and there are often blisters on the chest. The hock joints and soles of the feet are the main sites of infection.
Pathological changes: Mycoplasma septicarum lesions mainly manifest catarrhal inflammation of the nasal passages, trachea, bronchi and air sacs. The wall of the air sac is thickened, and there is often mucus or caseous exudate in the air sac. In mixed infections with E. coli, fibrinous pericarditis and perihepatitis can be seen. Pneumonia and salpingitis may also be seen. In the early stages of chickens with mycoplasma synovialis disease, there is sticky, gray-white to yellow exudate in the synovial membrane of joints and tendon sheaths. The exudate in chronic cases is cheese-like. The liver and spleen are enlarged, and the kidneys are enlarged, pale, and mottled.
(3) Diagnosis and prevention diagnosis: A preliminary diagnosis can be made based on epidemiology, clinical symptoms and pathological changes. The diagnosis requires pathogen isolation and identification and serological tests. Rapid serum plate agglutination test and hemagglutination are commonly used. Suppression tests monitor flocks. Pay attention to the differential diagnosis of avian influenza, infectious rhinitis, infectious bronchitis, infectious laryngotracheitis, mucosal fowlpox, and vitamin deficiency.
Prevention: ① Strengthen the environmental sanitation of the chicken house, clean and disinfect frequently, pay attention to ventilation, and get vaccinated in time to prevent the occurrence of other respiratory diseases. Avoid stress and other inducements and adopt an “all in, all out” feeding method.
② To block trans-oval transmission, give breeder chickens a course of sensitive drugs within 1 month before selecting hatching eggs to reduce the rate of bacteria in the eggs; warm the eggs to 37°C before hatching, and then Immerse in an antibiotic (tylosin or erythromycin 400-1000 mg per liter) solution at 2 to 4°C for 15 to 20 minutes to allow the antibiotics to be absorbed into the egg. The eggs are taken out and dried before hatching.
③Establishing a mycoplasma-free breeder flock is the most fundamental measure to control chicken mycoplasmosis. Comprehensive disease prevention and purification measures are adopted. Breeding chickens and brooding chickens are raised separately. All-in, all-out feeding methods are implemented throughout the site. Various means are adopted to block trans-oval transmission. Breeding chickens are raised separately, regularly administered drugs, and strictly disinfected. , conduct regular quarantine, and must persist and persevere.
④ Vaccination. Use sensitive drugs to prevent infection in chickens at 1 to 3 days of age, and immunize chickens with attenuated vaccines at 7 days of age, so that chickens can be well protected. Injecting oil emulsion inactivated vaccine into breeder flocks before laying eggs can greatly reduce egg-borne transmission.
Treatment: Mycoplasma gallisepticum is resistant to tylosin, tetracycline, mycotoxin, erythromycin, tetracycline, oxytetracycline, doxycycline, spiramycin, spectinomycin, and When the disease disappears and other sensitivities occur, these drugs can be used for treatment. Drug sensitivity testing can be performed if conditions permit. The mixture is used in the 1st and 3rd weeks, and the medicine is used throughout the week. Tylosin 0.1%, erythromycin 0.013% to 0.025%, enrofloxacin drinking water 75 mg/L (first 3 days), 50 mg/L (last 3 days), Beilinomycin 0.033% to 0.05%. Chlortetracycline, tetracycline, oxytetracycline: 250 g/ton of feed. Doxycycline 0.01% ~ 0.02%. The above-mentioned drugs can also be treated with drinking water, but the dosage should be reduced by half.
5. Aspergillosis
(1) Pathogen and epidemic characteristics Pathogen: Aspergillus fumigatus is generally common and the most pathogenic. Its spores are widely distributed in nature and often contaminate feed. In addition, in cases of mixed infection, there are Aspergillus flavus, Aspergillus niger, Aspergillus nidulans, Aspergillus terreus and Penicillium. Aspergillus fumigatus belongs to the incomplete fungi Aspergillaceae and is a thermophilic fungus suitable for temperatures of 37 to 40°C. Aspergillus fumigatus has a strong growth ability and a strong resistance to physical and chemical effects. On sterilized millet grains, it can still maintain its pathogenicity for up to 4 years under laboratory conditions. Dry heat at 120℃ for 1 hour or boil in boiling water at 100℃ for 5 minutes can make it lose its germination ability. It is highly resistant to general disinfectants, which can only weaken it but not kill it. It can be weakened by 2% formaldehyde for 10 minutes, 3% carbolic acid for 1 hour, and 3% caustic soda for 3 hours.
Epidemic characteristics: It usually occurs within 1 week of age, especially in chicks about 1 to 4 days old. It is an acute epidemic process with a mortality rate of up to 50%. In chronic cases, the mortality rate is not high. Adult poultry sufferers are rare and the disease is mainly chronic. The disease is almost always related to the environment where mold grows. It is often caused by feed or litter being contaminated by Aspergillus, coupled with excessive density of chickens and poor ventilation, which induces the disease in chicks. Infection in newborn chicks is caused by mold contamination during the incubation process. The disease is characterized by difficulty breathing, widespread inflammation and fungal nodules on the lungs and air sacs. Distributed around the world, the disease also exists in my country, especially in rainy and humid areas in the south, where it often breaks out among chickens.
(2) Symptoms and autopsy Symptoms: The sick chick has loss of appetite, fatigue, loose feathers, difficulty breathing, increased breathing times, and mouth breathing. Symptoms of diarrhea may also appear in the later stages. The course of the disease is usually about 1 week, and the mortality rate can be as high as 50% or more. Some were standing still or lying in a corner, stretching their necks and gasping for air. Death eventually occurred from exhaustion and convulsions. If the pathogen infects the eyeballs, it can cause gray-white opacity, corneal ulcers and other lesions; if the brain is infringed, neurological symptoms such as torticollis and difficulty walking will occur; when the spinal cord is infringed, symptoms of paralysis will occur. After adult chickens are infected, their symptoms are similar to those of chickens suffering from laryngotracheitis, but there is no abnormal death and egg production continues to decrease by 10% to 20%.
Pathological changes: Yellow-white or off-white nodules the size of millet grains can be seen scattered in the lungs, and sometimes nodules of varying sizes can also be seen on the walls of the air sacs. In severe cases, there are nodules or round gray-green plaques on the surface of the abdominal cavity, serosa, liver or other parts. In pulmonary aspergillosis, lesions appear in the lungs, air sacs, bronchi and trachea, and lesions may also appear in other organs. Chicks aged 1 to 5 days show acute symptoms, with no nodules but only congestion. The walls of the air sacs are thick, with scattered nodules, and some become large mound-like bulges or yellow-white discs. Disc-shaped nodules can also be found on the surfaces of the liver, spleen, kidneys, and ovaries. Sometimes bluish hyphae can be seen attached to the surface of the disc-shaped nodules.
(3) Diagnosis, prevention and treatment Diagnosis: When the above symptoms and acute death occur in 1 to 4-day-old chicks, bronchial embolism, pulmonary congestion, and nodules are found, and the disease can be suspected. If a disc-shaped nodule appears with hyphae attached, mix it with 1 drop of lactic acid phenol (20 ml of crystallized carbolic acid, 20 ml of lactic acid, 40 ml of glycerin, 20 ml of water) and conduct a microscopic examination. If there are apical cysts and stems found, , spores, etc., it can be determined as aspergillosis. However, to determine the species of Aspergillus, identification must be carried out by culture.
Prevention: ① Strengthen feeding management, clean feeding troughs and drinking fountains frequently to avoid mold breeding, strengthen ventilation, and reduce humidity; especially in closed chicken houses in winter, moldy feed and litter should be removed , reduce the content of mold spores in the environment. ②Do not use moldy bedding, and feeding moldy feed is strictly prohibited.
③Prevent the incubator from being contaminated by mold. ④ If the poultry house is found to be contaminated by mold, the sick chicks must be isolated immediately and the bedding must be removed. Thoroughly disinfect with 20% milk of lime, replace with new litter, and add 0.1% copper sulfate solution to the feed.
Treatment: Oral potassium iodide can be used to treat sick chickens. Add 5 to 10 grams of potassium iodide per liter of drinking water, which has certain curative effects. Nystatin has a certain effect on this disease. The dosage is 15 to 20 mg for adult chickens and 3 to 5 mg for chicks. It should be mixed with feed and fed for 3 to 5 days. In addition, a 1:2000-3000 copper sulfate solution can be used instead of drinking water for 2-3 days, which has a therapeutic effect.
6. Avian cholera
(1) Pathogen and epidemic characteristics Pathogen: Pasteurella multocida, a short bacterium with blunt ends and a slightly convex center, Gram Staining negative. It does not form spores, has no flagella, is stained by Wright's stain, and is stained at both ends, much like two cocci side by side. It is present in various tissues, body fluids, secretions and excretions of sick chickens. A few chronic cases are present in diseased tissues. Healthy chickens can also carry bacteria. This bacterium contains bacterial antigens and capsular antigens and is divided into many serotypes. This bacterium has weak resistance to the outside world and can be killed by ordinary disinfectants. It is sensitive to a variety of antibiotics and chemotherapeutic drugs.
Popular characteristics: It is generally sporadic. Ducks are the most susceptible, followed by chickens, geese and turkeys. Wild birds, wild birds and various experimental animals can all be infected and die. Young chickens are resistant and rarely get sick before 16 weeks of age. The peak period of the disease is during sexual maturity, mostly in sporadic form. The disease is more likely to occur in autumn and early winter, followed by winter and spring, and rarely occurs in summer. Unfavorable factors such as sudden changes in weather, poor ventilation of chicken houses in winter, and crowding of chickens can all induce this disease. Sick poultry and infected poultry are the main sources of infection of this disease. It is mainly spread through the respiratory tract, digestive tract and wounds. The disease can be spread by staff, feed and sick chicken carcasses.
(2) Symptoms and necropsy Symptoms: ① The most acute type, common in the early stages of the epidemic, most common in chickens with high egg production. Sometimes death occurs at night and is discovered in the morning. There are no prodromal symptoms before death, but the chickens die in the house. Sometimes the chickens are seen depressed, falling to the ground, struggling, flapping their wings and twitching, and die quickly. The course of the disease is a few minutes to a few hours.
②Acute type: sick chickens are depressed, lethargic, have loose feathers, drooped wings, neck and eyes closed, head tucked under the wings, unwilling to move, stand alone, and often have diarrhea. Passage of grey-white, yellow or green loose feces. Loss of appetite, difficulty breathing, and mucus mixed with foam coming from the nose and mouth. Severe diarrhea, discharge of yellow, gray or light green loose feces. The combs and beards of the sick chickens turn blue-purple, and the beards of some sick chickens are swollen, the laying hens stop laying eggs, the body temperature of the sick chickens rises to 43 to 44°C, and finally collapses and dies. The course of the disease is 0.5 to 3 days.
③Chronic type, often occurs in the later stages of the epidemic, and is more common in chronic pneumonia, chronic respiratory inflammation and chronic gastroenteritis. Sick chickens become increasingly emaciated, with pale crowns and beards, swollen leg joints and lameness, difficulty breathing, diarrhea, and finally become emaciated and die or become carriers after recovery. The course of the disease is more than 1 month, and growth and development are blocked and egg production cannot be restored for a long time.
Lesions: ① The most acute type, no special lesions, occasionally a few bleeding points in the epicardium. ② Acute type, acute epicardial and coronary fat have obvious bleeding points. Lung congestion and hemorrhage, liver enlargement, brittle texture, brown or yellow-brown color, with many gray-white, needle-tip-sized necrotic spots. Duodenal hemorrhagic inflammation is severe. The mature follicles of laying hens are flaccid, the immature follicles and the interstitium of the ovary are often congested, and sometimes ruptured yolk material is found in the abdominal cavity. ③Chronic type, it can be seen that there is a large amount of viscous secretions in the lungs and respiratory tract, pulmonary sclerosis; joint swelling and deformation, inflammatory exudate and caseous necrosis; ovarian bleeding or solid, yellow caseous material around the ovary, etc. .
(3) Diagnosis and prevention diagnosis: Based on the epidemiological characteristics of mutual infection among chickens, ducks and geese, and the clinical characteristics of fat and high-yielding chickens, rapid onset, rapid death, and discharge of gray or green loose feces. , the autopsy features of many white necrotic spots on the liver surface can make a preliminary diagnosis, and laboratory diagnosis is required for a confirmed diagnosis. Pay attention to the differential diagnosis of Newcastle disease.
Prevention and treatment: ① In areas where it often occurs, chickens over 60 days old should be given intramuscular injection of avian cholera propolis cholera inactivated vaccine, and a second vaccination should be carried out 6 months later.
② Strengthen feeding and management, eliminate stress factors, and pay attention to frequently adding microecological preparations to feed or drinking water.
③Sensitive antibiotics should be selected for sick chickens. This bacterium is prone to develop drug resistance, so drug susceptibility testing is necessary. The disease is easy to relapse. The drug should be administered again after 3 to 5 days, and then microecological preparations should be added to the feed or drinking water to restore the normal intestinal flora and completely restore the chickens to a healthy state.
7. Coccidiosis
(1) Pathogen and epidemic characteristics Pathogen: Eimeria, including Eimeria tenella, Eimeria virulentus, Eimeria aeruginosa, Eimeria maxima, Eimeria harveyi, Eimeria mitis, and Eimeria precoccus. The first two are more pathogenic. Coccidia of the genus Eimeria are characterized by the formation of 4 sporangia within the endospore cells of the oocyst, each containing 2 sporozoites. The oocysts of coccidia are very resistant and can remain viable in the soil for 4 to 9 months. When the temperature is 22 to 30°C, it usually only takes 18 to 26 hours to become infectious. Oocysts are less resistant to heat and desiccation.
The development of coccidia in chickens goes through three stages: the asexual reproduction and sexual reproduction stages are carried out in the epithelial cells of the intestinal mucosa, and the sporogenous stage is the formation of sporangia and spores in vitro, which become infectious coccidia eggs.
Pandemic characteristics: It mainly occurs in chickens under 3 months old, especially chicks between 15 and 45 days old. Coccidiosis rarely occurs in chicks under 11 days old. The epidemic season has a great relationship with the external environmental conditions and feeding and management on the occurrence of coccidiosis, with the most cases from May to August. The occurrence of this disease can be promoted when the stocking density is too high, hot and humid, damp, poor ventilation, lack of vitamin A and vitamin K in the feed, and poor sanitary conditions. Sick chickens are the main source of infection. Eggs are present in feed, drinking water, soil or utensils contaminated by infected chickens. People, their clothes, utensils, etc. can become mechanical communicators. Flies, beetles, cockroaches, rodents and wild birds can all act as mechanical vectors. The main route of infection is eating infectious oocysts.
(2) Symptoms and autopsy Symptoms: ① Acute type, the course of disease is usually 2 to 3 weeks, and it is more common in chicks. Mental fatigue, lethargy, loose coat, eyes closed, head shrunken, standing still, like to squeeze together, burps filled with fluid, bloody stools, diarrhea, perianal feathers adhesion due to excrement pollution. If the cecum is infected with coccidia, the feces will be brown-red and later turn into bloody stools. The mortality rate of chicks is as high as 100%. Visible mucosa, crown, and beard are pale. In the later stage, there is coma, with the legs turned outward, stiff or spasmodic. ②Chronic type, which is more common in 2 to 4-month-old chicks or adult chickens. It has no obvious symptoms and is characterized by anorexia, lack of movement, weight loss, slow growth, paraparesis of the legs and wings, and occasionally intermittent diarrhea. The course of the disease is long, lasting several weeks or months. Sick chickens gradually lose weight, produce fewer eggs, and have intermittent diarrhea, but they rarely die.
Pathological changes: weight loss, pale or blue mucous membranes and combs. The pericloacal feathers are contaminated with feces, often with blood. The lesions are generally concentrated in the intestines, and lesions in other organs are not obvious. The degree and location of lesions caused by different types of coccidia are also different. Eimeria tenella mainly infects the cecum, manifesting as intestinal dilation, intestinal wall relaxation, thickening, necrosis, pale white spots, a large number of white spots on the mucosa, and coagulated blood in the intestinal wall and intestinal lumen, making the intestinal appearance It is light red. Eimeria maxima damages the middle part of the small intestine, manifesting as intestinal dilation, thickening of the intestinal wall, and intestinal contents that are light gray or light brown, mucusy, and occasionally have small blood clots. Eimeria aeruginosa develops on the surface of the duodenal epithelium, and worms at the same stage gather together to form a large number of pale gray-white spots, sometimes forming a band. Eimeria brucei invades the junction of the posterior segment of the small intestine and the cecum, manifesting as epithelial cell shedding, mucosal hemorrhage, pinpoint hemorrhage, and gray-white spots. Eimeria harveyi mainly damages the duodenum and the anterior part of the small intestine, and the characteristic change is the appearance of red, round bleeding spots as big as a needle on the intestinal wall.
(3) Diagnosis and prevention diagnosis: According to symptoms and epidemiological data, it mostly occurs in the warm season, and chicks aged 3 weeks to 1.5 months are susceptible, with high morbidity and mortality. The chicks are weak and emaciated, the combs and mucous membranes are pale, the feathers around the cloaca are adhered to feces, and bloody diarrhea can be initially diagnosed as coccidiosis. The diagnosis can be confirmed by microscopic examination of feces or scrapings from intestinal lesions. A large number of oocysts, schizonts, merozoites and young gametes can be found. When no oocysts are found in the feces, it is not enough to rule out coccidiosis, because the chicken often becomes sick or dies before oocysts appear in the feces.
Prevention and treatment: ① Do a good job of sanitation and disinfection of the chicken house, keep the chicken house dry and well ventilated, and chicken manure should be fermented. Young chickens should be kept separately from adult chickens to reduce the chance of infection. Maintain appropriate temperature, humidity and stocking density. ② During the epidemic season of this disease, feed vitamin A and vitamin K to enhance the body’s immunity and increase antibody levels. ③Drug prevention and treatment. Drugs can be used for prevention at 10 to 45 days of age. Commonly used anti-coccidioidal drugs include chlorpheniramine, globohydrin, tribacterial sulfonamide mixture, San'an coccidia powder, globulin powder, and Kelzuril, coccidiodine, amprolium, etc. You can choose any one. The preventive dose of amprolium is 40 to 250 mg per kilogram of feed, fed for 7 days, and then halved, and used for another 14 days. The therapeutic amount is 500 mg per kilogram of feed for 7 days, and then reduced to 250 mg for 10 days. The preventive dose of sulfadimethoxine is 0.05% added to feed or drinking water for 6 days; the therapeutic dose is double the preventive dose mixed with feed or drinking water for 3 to 7 consecutive days. Add 35 grams of chlorpheniramine per ton of feed, mix well, and feed for 1 to 2 months. Sulfaquinoxaline is best treated with intermittent administration, 0.1% mixed feeding, continuous use for 2 to 3 days, stopped for 3 days, and then mixed with 0.05% fed for 2 days. The dosage of Sudan (Changshanone) is 3 mg per kilogram of feed. Mix Taifenzhi at a concentration of 0.1% and use it for 5 days. Salinomycin is mixed into the feed at 0.007%. Prevention begins at 15 days of age and is administered continuously for 30 to 45 days. Diclazuril, with a concentration of 0.02 to 0.05 ml/L in drinking water, is taken continuously for 5 to 7 days, and the effect is significant.