Tracheobronchial mycosis in a retrospective case-series study of five status asthmaticus patients.

The etiology of status asthmaticus (SA), a complication of severe asthma, is unknown. Fungal exposure, as measured by fungal atopy, is a major risk factor for developing asthma, but the relationship of fungi in SA per se has not previously been reported. In this five patient retrospective case series study, lower respiratory tract cultures were performed on bronchoalveolar lavage or tracheal aspirate fluid, comparing standard clinical laboratory cultures with a specialized technique in which respiratory mucus was removed prior to culture. We show that mucolytic treatment allows an increased detection of fungal growth, especially yeast, from the lower airways of all SA patients. We also demonstrate that inhalation of the yeast Candida albicans readily induces asthma-like disease in mice. Our observations suggest that SA may represent a fungal infectious process, and support additional prospective studies utilizing anti-fungal therapy to supplement conventional therapy, broad-spectrum antibiotics and high-dose glucocorticoids, which can promote fungal overgrowth.

Bronchial neutrophilia in patients with noninfectious status asthmaticus.

Cellular events that occur in status asthmaticus (SA) remain poorly investigated. Autopsy studies frequently emphasized about the presence of eosinophils in bronchial airway wall, whereas recent studies reported increased number of neutrophils in patients dying of sudden-onset fatal asthma. Mucus plugs occluding the bronchial lumen are almost constant features during SA. Bronchial lavage (BL) may be useful to remove mucus plugs in cases of atelectasis and/or refractory SA. We investigated the contribution of different cell types and cellular mediators (neutrophil elastase, eosinophil cationic protein [ECP], histamine, interleukin-8 [IL-8]) to the pathogenesis of SA. We studied 16 BL from eight patients undergoing mechanical ventilation (MV) for SA (time interval from onset of MV = Day 0 to Day 11), four BL from patients undergoing MV without preexisting respiratory disease (V), 11 BL from patients with stable asthma (A) and eight BL from healthy controls (C). SA exhibited higher number and percentage of neutrophils (81.5 +/- 4.5%) than V (44.3 +/- 12.2) (p < 0.05), A (6.9 +/- 2.7) and C (9.5 +/- 3.8) (p < 0.0001), and higher number of eosinophils than V, A, and C (p < 0.01). Neutrophil elastase, ECP, and IL-8 levels were dramatically increased in SA. Histamine was higher in SA than in C and V (p < 0.05). Bronchial neutrophilia was not related to concomitant bacterial infection as bacteriological cultures were positive in only three BL. Eosinophils, mast cells and histamine were higher in BL performed within the first 48 h of MV (p < 0.05) than in BL performed later on. Our results indicate that bronchial inflammation in SA differs from bronchial inflammation in mild asthma. Persistent bronchial neutrophilia is associated with increased eosinophils and mast cells in the early phase of SA. Neutrophils may result in tissue damage and participate to the shedding of the epithelium in SA.

Los virus como desencadenante de crisis asmáticas / Virus as unchainments of asthmatic crisis

Estudio realizado con 45 pacientes en el servicio de alergia del Instituto Nacional de Pediatría, con el propósito de analizar la participación de los virus como desencadenantes de crisis asmáticas en niños que vivían en el suroeste de la Ciudad de México. Los sujetos fueron incluidos en el estudio si presentaban datos de atopia o infección de vías aéreas superiores. Se excluyó a los pacientes con alergia a pólenes, rinosinusitis, familiares con hábitos tabáquicos o que tuviesen mascotas. En este grupo de población la participación de los virus como desencadenantes de crisis asmaticas es muy significativo y los virus predominantes fueron VSR, influenza B y parainfluenza

[Infectious agents associated with exacerbations of chronic obstructive bronchopneumopathies and asthma attacks]. / Agents infectieux associés aux décompensations des bronchopathies chroniques obstructives et aux attaques d'asthme.

Infections of the respiratory airways are frequently responsible for exacerbations of chronic obstructive pulmonary disease (COPD) and attacks of asthma. However, the causal infectious agents in practice are rarely precisely identified. We have undertaken a prospective study with the aim of researching into the bacteria and viruses associated with these exacerbations. Forty-seven patients who were in hospital between 1987 and 1989 for attacks of asthma (13 episodes) or exacerbations of COPD (35 episodes) were included in this study. The microbiological analysis consisted of: 1) the bacteriology of expectorated material or the products aspirated by fibroscopy with direct examination, quantitative cytology and culture; 2) samples taken from the nasal airways to identify and isolate pneumotropic viruses and mycoplasma; 3) serial serology looking for antibodies against pneumotropic bacteria and viruses. One of more infectious agents were shown in 47% of the episode studies of which 57% were exacerbations of COPD and treated 23% attacks of asthma. In the cases COPD bacteria were identified in 13 cases including Haemophilus influenzae [3], Streptococcus pneumoniae [3], Pseudomonas aeruginosa [3]. Amongst the 14 viruses recovered, the influenza virus [8] and the respiratory syncytial virus (VRS) [4] predominated. In 14 cases of acute asthma only 4 infectious agents were shown; Mycoplasma pneumoniae, influenza A, VRS and parainfluenza virus. The influenza virus was the agent most frequently discovered (26%) during the course of exacerbation of COPD and of asthma.