What is swine lockjaw disease? Detailed explanation of prevention and control methods
This disease is a common swine respiratory infectious disease caused by Pasteurella multocida, characterized by the peracute type presenting as septicemia and pharyngitis, the acute type presenting as fibrinous pleuropneumonia, and the chronic type being relatively rare, presenting as chronic pneumonia.
This bacterium exists in all tissues, body fluids, secretions and excretions of the diseased animal, and the upper respiratory tract of healthy livestock may also carry the bacterium. Its resistance to physical and chemical factors is relatively low, and it dies quickly under natural drying conditions. Common disinfectants at conventional concentrations all have good disinfecting power against this bacterium; 1% carbolic acid or bleaching powder, and 5% lime milk can kill it within a few minutes to a dozen or so minutes. Sunlight has a strong bactericidal effect on this bacterium; a thin bacterial layer exposed to sunlight is killed within 10min. This bacterium is not heat-resistant; heating at 60°C for 1min can kill the 24h culture of Martin broth.
1. Clinical symptoms
The occurrence of this disease has no obvious seasonality. When environmental hygiene conditions are poor, or due to cold and damp, cold waves, sudden climate changes, poor ventilation, stuffy and crowded conditions, nutritional deficiency, feed contaminated feed, drinking water, utensils and the external environment, healthy pigs can be infected through the digestive tract; diseased pigs expel the pathogen through coughing and sneezing, and can also infect healthy pigs through droplets via the respiratory tract; in addition, transmission can also occur through blood-sucking insects as vectors and through wounds of the skin and mucous membranes. The incubation period of this disease is 1-5d, and it is generally divided by disease course into the peracute type, acute type and chronic type. The first two types mostly manifest as septicemia and pleuropneumonia, while the lesions of the chronic type are concentrated in the respiratory tract, presenting as chronic pneumonia.
1.1 The peracute type is mostly seen in the early stage of an outbreak, commonly known as “lockjaw disease”. Often the pig eats normally in the evening and dies suddenly the next morning, with no clinical symptoms observed. Those with a slightly longer disease course have high fever (41°C-42°C), general weakness, complete loss of appetite, inability to stand, difficulty breathing, accelerated heartbeat, and restlessness. The pharynx is hot, red and swollen and hard; in severe cases the local swelling can extend to the base of the ears and the neck. When breathing is extremely difficult, it often shows a dog-sitting posture with the neck extended, and bloody foam flows from the mouth and nose; the visible mucous membranes are congested and cyanotic, and red spots appear on the skin at the base of the ears, neck, abdomen and inner sides of the limbs. The disease course is 1-2d; after respiratory symptoms appear, the condition deteriorates rapidly and death occurs quickly, and the mortality rate can be as high as 100%.
1.2 The acute type is the main and common disease type. In addition to septicemia, there are also symptoms of acute pleuropneumonia. Body temperature rises (40-41°C); in the early stage there is a spasmodic dry cough, nasal discharge of mucus, and difficulty breathing, which later becomes a wet cough. Palpation of the chest is painful, and auscultation reveals rales and friction sounds. As the disease progresses, breathing becomes more difficult, with the mouth open and tongue extended, in a dog-sitting posture; the visible mucous membranes are cyanotic, with purulent conjunctivitis. First constipation, then diarrhea; in the terminal stage there is heart weakness, accelerated heartbeat, and skin congestion or small hemorrhagic spots. Diseased pigs lie down and cannot rise, and most die from suffocation. The disease course is 5-8d, and those that survive turn into the chronic type.
1.3 The chronic type shows symptoms of chronic pneumonia and gastroenteritis. There is often persistent coughing and difficulty breathing, with mucus-like nasal discharge. Sometimes scab-like eczema appears, joints swell, appetite is poor, and there is often diarrhea. Diseased pigs show progressive malnutrition, emaciation and weakness; those not treated in time mostly die of exhaustion after more than 2 weeks.
2. Pathological changes
2.1 In the peracute type, there is hemorrhagic serous infiltration of the systemic mucous membranes, serous membranes and subcutaneous tissue. A large amount of pale yellow gelatinous edematous fluid can be seen under the skin of the neck, and the edema can spread to the forelimbs. Acute pulmonary edema. Systemic lymph nodes and spleen hemorrhage, but the spleen is not enlarged; there are small hemorrhagic spots on the epicardium and pericardium; the gastrointestinal mucosa shows hemorrhagic inflammatory changes.
2.2 In the acute type, there is hemorrhage of the systemic mucous membranes, serous membranes, parenchymal organs and lymph nodes, and the characteristic lesion is fibrinous pneumonia. The lungs show hepatization, edema and emphysema; in long-standing cases the hepatized areas have necrotic foci, the lung "bni- interstitium has serous infiltration, and the cut surface shows marble-like change. The pleura often has fibrinous material attached; in severe cases the chest and lungs adhere, and there is pleural and pericardial effusion. The thoracic lymph nodes are enlarged, and the cut surface is red and juicy. There is a large amount of frothy mucus in the trachea and bronchi, and the mucosa is inflamed.
2.3 Chronic type. The carcass is extremely emaciated and anemic. The hepatized areas of the lungs are extensive, and the necrotic foci are encapsulated by connective tissue and contain caseous material, with some forming cavities. There is pericardial and thoracic effusion, and fibrinous material is deposited in the thoracic cavity, often adhering to the lungs.
3. Clinical diagnosis
A preliminary diagnosis can be made based on epidemiological characteristics, clinical symptoms and pathological change features, and a definitive diagnosis should be made by etiological examination. Materials can be collected, such as lung lymph nodes, spleen and liver, or body fluids such as cervical edematous fluid and thoracic fluid; during life, ear vein blood can be collected for smear staining and microscopic examination. If large numbers of Gram-negative, bipolar-staining small bacilli are found, a definitive diagnosis can be made, and when necessary, bacterial culture, isolation and identification should be carried out.