• Title/Summary/Keyword: Pulmonary Oxalosis

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Pulmonary Aspergillosis and Renal Oxalosis in an Elk (엘크의 폐장 아스퍼질러스증 및 신장 옥살산증)

  • Kim, Jae-Hoon;Kang, Kyung-Il;Kim, Won-Il;Sohn, Hyun-Joo;Lee, Sang-Kyung;Jean, Young-Hwa
    • Korean Journal of Veterinary Research
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    • v.42 no.3
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    • pp.383-387
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    • 2002
  • A four-year-old male elk (Cervus elaphus nelsoni) was diagnosed as pulmonary aspergillosis and renal oxalosis. Clinical signs were coughing, sneezing, respiratory distress, salivation, moderate anorexia, and progressive emaciation. Main gross lesions were fibrinopurulent tonsillitis, diffusely fibrinous pleuritis, and distinct lobar pneumonia with purple red in color. Most of the pulmonary lobes had numerous well demarcated 0.5 to 2 cm yellowish white discrete or confluent nodules that were surrounded by pale red zones. Histopathologically, the affected lungs were disseminated necrotizing pyogranulomas including fungal hypae, vasculitis, and diffusely fibronecrotic pleuritis. The renal lesions were composed of extensive tubular necrosis with large numbers of rosette-formation by birefringent oxalate crystals. Aspergillus fumigatus was isolated from lesions of the lungs. It seems to be a first report for pulmonary aspergillalis and renal oxalosis of a farmed elk in Korea.

Pulmonary Oxalosis Caused by Aspergillus Niger Infection (Aspergillus Niger 감염에 의한 폐옥살산염 1예)

  • Cho, Gye Jung;Ju, Jin Young;Park, Kyung Hwa;Choi, Yoo-Duk;Kim, Kyu Sik;Kim, Yu Il;Kim, Soo-Ok;Lim, Sung-Chul;Kim, Young-Chul;Park, Kyung-Ok;Nam, Jong-Hee;Yoon, Woong
    • Tuberculosis and Respiratory Diseases
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    • v.55 no.5
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    • pp.516-521
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    • 2003
  • The Aspergillus species produces metabolic products that play a significant role in the destructive processes in the lung. We experienced a case of chronic necrotizing pulmonary aspergillosis caused by an Aspergillus niger infection, which contained numerous calcium oxalate crystals in the necrotic lung tissue. A 46-year-old man, who had a history of pulmonary tuberculosis, presented with high fever, intermittent hemoptysis and pulmonary infiltrations with a cavity indicated by the chest radiograph. Despite being treated with several antibiotics and anti-tuberculosis regimens, the high fever continued. The sputum cultures yielded A. niger repeatedly, and intravenous amphotericin B was then introduced. The pathological specimen obtained by a transbronchial lung biopsy revealed numerous calcium oxalate crystals in a background of acute inflammatory exudates with no identification of the organism. Intravenous amphotericin B was continued at a total dose of 1600 mg, and at that time he was afebrile, although the intermittent hemoptysis continued. On the $63^{rd}$ hospital day, a massive hemoptysis (about 800 mL) developed, which could not be controlled despite embolizing the left bronchial artery. He died of respiratory failure the next day. It is believed that the oxalic acid produced by A. niger was the main cause of the patient's pulmonary injury and the ensuing massive hemoptysis.