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Edematous skin disease (ESD) Pseudotuberculosis in Egyptian buffaloes Definition It is a mild contagious acute, subacute or chronic disease of buffaloes which caused by corynbacterium pseudotuberculosis (C. ovis). It is characterized by swelling and suppurative in one or more of superficial lymph nodes and/or its related lymphatic or general edema in the four legs, intracutaneous nodules and ulceration of the skin Etiology It is caused by C. Pseudotuberculosis alone or with other pyogenic bacteria as Staphylococcus, Streptococcus and Pseudomonas. It is believed that the disease might be caused by C. pseudotuberculosis and filarial worms. Morphology and staining: C. pseudotuberculosis is facultative intracellular, Gram positive, non-capsulated coccoid or filaments. It is arranged in the form of palisade or Chinese letter. Growth requirements and characteristics: It grows well in media containing blood and serum. Epidemiology Distribution: It is endemic disease and appears regularly in Egypt. It was diagnosed for the first time in April 1960 at Senbellawene, Dakahalia province. Animal susceptibility: Buffaloes are the main susceptible animals. Transmission: The main source of infection is discharged pus from infected animals. The disease is transmitted through the skin wounds and abrasion. Also, insects are playing a major role in the transmission of this disease. Factors affecting on susceptibility The disease is common in autumn and summer seasons. All ages of buffaloes are susceptible and the age group from 8 months to 3 years is more susceptible. Both sexes are affected but females are more susceptible. Animal crowding in muddy or dirty unhygienic stable are more susceptible. Pathogenesis After infection of skin wound or abrasion, the organism multiplies and secrets exotoxins and invade lymphatic vessels with formation of subcutaneous swelling, nodules or abscesses along course of lymph vessels (lymph vessels appear corded). These lesions appear mainly on chest, abdomen and legs or may be developed all over body. Edematous swellings develop due to increase of permeability of blood vessels and impaired drainage through early damaged lymphatics. Subcutaneous lesions along with draining lymph nodes are then undergo suppuration and rupture discharging serosanginous fluid or creamy pus stained with blood. Occasionally, bacteremia develops with localization of the organism in other internal organs. Clinical signs The incubation period is long, morbidity is high, mortality is low and the course is long about 2-3 weeks and may extend to 12 months Acute form: It is characterized by mild fever, mild systemic disturbance, decrease of appetite, decrease of milk production painful local edema in one or both forelimbs, slight lameness and enlargement and swelling of prescapular and/or the precural lymph nodes. The lymph nodes are firm, hot and painful. Puncture of these swellings revealed serosanginous fluid or thick creamy green pus tinged with blood. Subacute form: It is characterized by appearance of one or more pimple-like nodules subcutaneously at any part of the body. There is swelling and cording of the lymphatics with formation of small abscesses along their course on fore limbs, abdomen and thigh. These abscesses are spontaneously opened discharging creamy pus tinged with blood. Chronic form; There are circumscribed nodules which gradually develop into closed abscess containing thick yellowish pus with formation of small area of skin necrosis on the lateral or ventral aspect of the trunk. Sloughing of the necrosed skin leaves crusts or dried bloody exudates containing pus. Occasionally, bacteremia develops with localization of the organisms in other internal organs resulting debilitation and death Postmortem lesions Carcasses show skin nodules, edematous swellings and ulcerations. Skin and subcutaneous tissues thickened, edematous and adhered to each other and to the underlying muscles. There is enlargement and suppuration of the superficial lymph nodes. There is congestion in liver, spleen and kidneys and hemorrhagic foci in heart. Diagnosis Field diagnosis: It can be suspected on the basis of history, epidemiology, clinical signs and PM Laboratory Diagnosis Samples: Samples includes pus from closed lesions of untreated animals, swabs or biopsy, slices from skin and parenchymatous lesions, lymph nodes, blood and serum. Procedures: Direct microscopic examination of pus smears to demonstrate short Gram positive Chinese letter bacilli. Isolation and identification of the organism: inoculation of the suspected material on the blood agar. The colonies can be identified by biochemical reactions. Serological examinations: They include CFT, FAT and toxin neutralization test Differential diagnosis: It can be confused with all skin affections as skin abscess caused by Staphylococcus, skin lesions of actinobacillosis, dermatophytosis, dermatphilosis, lumpy skin disease, pseudolumpy skin disease, pox. Ephemeral fever, filariasis and hypoderma. Treatment Systemic administration of large doses of antibiotics such as pencillin (20,000-80,000 IU/kg for 5-7 days), tetracycline, gentamycin and cephalosporin reduce the severity of the infection. Also, supportive treatment is recommended such as antipyretics, anti-inflammatory, antihistaminic, fluid therapy and vitamins The closed lesions should be locally dressed with iodine or icthyol ointment (5-10%) for ripening. The open lesions should be completely evacuated from pus and irrigated daily with antiseptics as betadin until complete healing. Control Proper management and hygiene: The infected animal should be isolated and treated either locally or systemically or both with the early treatment of the skin abrasions. All possible sources of the infection should be destroyed such as removal of the contaminated surface soil of the animal yard, Hygienic disposal of animal carcass, frequent cleaning and disinfection of the stables, especially during the season of the disease and insect control. Vaccination: Vaccination trials were conducted by bacterin and toxoid or vaccination of calves at 6 months of age by BCG which enhance the non-specific immunity.