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Invasive pulmonary aspergillosis (IPA) is often a lethal entity in transplant recipients (up to 90%). We report the successful treatment of a case of IPA in a renal transplant recipient whose only risk for exposure was habitual marijuana smoking. Although marijuana smoking has been linked to the development of IPA in patients immunosuppressed for a variety of reasons, this case is the first report involving a solid organ transplant recipient. The patient's clinical course and treatment are described and the literature is reviewed with respect to environmental and patient risk factors. In this case, IPA was associated with the patient's heavy usage of marijuana during the immediate posttransplant period. Treatment was successful and included the experimental amphotericin product amphotericin B colloidal dispersion. Contemporaneous exposure to a large amount of inocula of Aspergillus within 30 days of receiving high doses of steroids appeared to be the most important factor that predisposed this patient to IPA. Transplant recipients should be specifically proscribed from marijuana use during periods of high steroid administration.

The mechanisms controlling vagally induced 5-HT and SP release into the jejunal lumen were studied in the cat. In control animals, electrical vagal nerve stimulation doubled the rate of endoluminal secretion of 5-HT and SP. Propranolol pretreatment did not alter luminal secretion of these hormones. Atropine suppressed motor function and induced dose-related inhibition of vagal release of endoluminal 5-HT, but not of SP; the response to hexamethonium pretreatment was similar to that of atropine. In contrast, superior cervical ganglionectomy did not alter stimulated endoluminal 5-HT release but it completely abolished release into the portal vein. The portal 5-HT release was not affected by ganglionic blockade. The data suggest that vagally mediated 5-HT release into the lumen and the portal circulation are mediated by different neural mechanisms, the former cholinergic, the latter presumably adrenergic; and release of feline 5-HT and SP are independent, suggesting two intestinal sources, the EC cell for 5-HT and peptidergic neurons for SP.

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