Histoplasmosis around the world: A global perspective on the presentation, virulence factors, and treatment of histoplasmosis.

Histoplasmosis is a systemic infection caused by an endemic dimorphic fungus, Histoplasma capsulatum. Though prevalent in the eastern United States of America, near the Ohio and Mississippi River Valleys, the evidence underlying the global prevalence of histoplasmosis, especially in immunocompromised populations, is underappreciated. This article highlights the global epidemiology, risk factors, microbiology and pathophysiological characteristics, pulmonary and extrapulmonary manifestations, prevention measures, radiographic patterns, diagnostic techniques, and antifungal treatment approaches for Histoplasma capsulatum.

Arachidonic acid products in airway nociceptor activation during acute lung injury.

We have reported that airway nociceptors [C fibre receptors (CFRs) and high-threshold Aδ fibre receptors (HTARs)] are activated during oleic acid (OA)-induced acute lung injury. In the present studies, we tested the hypothesis that this nociceptor activation is mediated by arachidonic acid products. In anaesthetized, open-chest, mechanically ventilated rabbits, we examined the response of the nociceptors to intravenous injection of OA before and after blocking the cyclo-oxygenase pathways with indomethacin. Pretreatment with indomethacin (20 mg kg(-1)) decreased the background activities of both CFRs (from 0.48 ± 0.12 to 0.25 ± 0.08 impulses/s, n = 7, P < 0.05) and HTARs (from 0.54 ± 0.14 to 0.23 ± 0.08 impulses/s, n = 10, P < 0.01). It also blocked the response of the nociceptors to OA. Likewise, pretreatment with thromboxane synthase inhibitor (ketoconazole) also blocked the nociceptor response to OA. In addition, local microinjection or intravenous injection of a thromboxane mimetic stimulated CFRs and HTARs. The present results clearly indicate that arachidonic acid metabolites mediate airway nociceptor activation during OA-induced acute lung injury and suggest that thromboxane may be a key mediator.

Pulmonary Aspergillosis: Spectrum of Disease.

Aspergillus species are ubiquitous in the environment. Aspergillosis is acquired by inhalation of Aspergillus spores. In normal hosts, spore inhalation rarely causes lung disease. Pulmonary Aspergillosis covers a wide spectrum of clinical syndromes depending on the interaction between Aspergillus and the host (immune-status, prior bronchopulmonary disease). It runs the gamut from invasive Aspergillosis to Aspergillus bronchitis. Invasive Aspergillosis usually occurs in severely immunocompromised patients, typically in neutropenic but also in non-neutropenic patients. Chronic pulmonary Aspergillosis affects patients with chronic structural lung disease such as COPD or previous mycobacterial lung disease, but without other significant immunocompromise. Aspergillus bronchitis affects patients with bronchial disease such as bronchiectasis. Allergic bronchopulmonary Aspergillosis affects patients with bronchial asthma or cystic fibrosis, and is due to an allergic response to Aspergillus.