The economic appraisal of the control of chronic respiratory disease in meat chickens.
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There is increased recognition of hypersensitivity lung disease among workers with laboratory animals as an occupational disease. Symptoms of asthma in 44 of 78 workers with laboratory animal dander allergy reflected the serious consequences of this occupational ailment. Affected employee profiles induced family history of atopy; immediate (Type I) allergic reaction; symptoms of rhinitis, asthma, and cough; hypersensitivity to one or more species, most often rats, mice, and rabbits. Diagnosis depends on history and physical, radiologic, and laboratory examinations, including skin tests with relevant antigens. Control and treatment depend on environmental change (reemployment or reduction of antigen contact); mechanical devices (masks and filters); chemotherapy (bronchodilators, steroids), prophylaxis and immunotherapy (hyposensitization). Standardization of medico-legal criteria covering occupational asthma is needed.
National and international awareness of the heavy burden of chronic disease has led to the development of new strategies for managing care. Elisabeth Bryant explains how self-care, education and support for more patients with complex needs should be built into planned care delivery, and emphasises that the patient is the key member of the care team.
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A candidate breeder flock of turkeys was studied during and after an outbreak of rhinotracheitis. Laboratory studies revealed the presence of three pathogens during the acute phase of the disease. These agents were hemorrhagic enteritis virus (HEV), paramyxovirus type 2 (PMV2), and chlamydia. Twenty-five turkeys in the flock were individually identified, and blood samples from these birds were collected for serological studies each week for 21 weeks. The serological results revealed high titers for HEV and chlamydia but very low titers for PMV2.
Specific-pathogen-free chickens were infected via the trachea when 4 weeks old with 2000 plaque-forming units (PFU) of the virulent Australian infectious laryngotracheitis (ILT) virus strain CSW-1. Titers of ILT virus in the trachea were greatest (10(7.0) PFU/ml in washings, 10(6.0) PFU/g of tissue) 2-4 days postinfection (PI). Infectivity then declined rapidly, to become undetectable by 7 days PI, although highly localized areas of ILT antigen in the tracheal epithelium were occasionally observed by fluorescent antibody staining at 7 and 8 days PI. Tracheal organ cultures established 7 and 8 days PI provided no evidence of latent ILT virus infection at this immediate post-acute stage of pathogenesis. ILT virus was not isolated from peripheral blood leukocytes or lymphoid organs (spleen, bursa, thymus). ILT virus was found in the trigeminal ganglia and/or brain in 14 of 36 chickens (40%) examined between 4 and 7 days after intratracheal inoculation, but it was not in these tissues in five chickens examined at 8 days PI. Virus was also detected at 6 days PI in the trigeminal ganglia in one of five chickens infected by the conjunctival route. These data indicate that the early pathogenesis of ILT (CSW-1) infection frequently involves the tissues of the nervous system. In acute ILT in 4-week-old chickens, interferon-alpha/beta activity was not detectable in serum or tracheal exudates within 14 days PI, but tracheal washings contained significant virus-neutralizing activity by 7 and 8 days PI. In 3-day-old chickens infected via the trachea with 200 PFU of ILT CSW-1, the clearance of ILT virus from the trachea was similar to that observed in 4-week-old chickens, but ILT virus spread systemically to the livers of 20% by 5-7 days PI.
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