Organizing pneumonia mechanisms

Interferon alfa was also suspected to be involved in one case of biopsy-proven bronchiolitis obliterans-organizing pneumonia (41). Clinical symptoms of pneumonitis appeared 3-12 weeks after the onset of interferon alfa therapy, and after withdrawal of treatment they usually completely resolved, either spontaneously or after a short course of glucocorticoid treatment. Immune-mediated pulmonary toxicity involving the activation of T cells was considered as a likely mechanism. The uncommon features of bronchiolitis obliterans-organizing pneumonia have been reported in three other patients who received interferon alfa together with ribavirin or cytosine arabino-side (42,43). 

Infectious complications of EN include aspiration pneumonia and infections related to delivery of contaminated EN formula. Aspiration is a complication with GI, mechanical, and infectious implications. Although GI infections owing to contamination of enteral formulas have been reported uncommonly, there is ample opportunity for these formulas to be seeded with organisms during the processes of transferring from the can to the delivery bag with ready-to-use formulas and during the process of reconstitution with powdered formulas. The so-called closed systems of delivery, wherein the formulas come from the manufacturer premixed in a delivery bag, should help to decrease the chance of formula contamination. 

An additional mechanism of antibiotic resistance involves an alteration of PBPs. Resistant bacteria, usually gram-positive organisms, produce PBPs with low affinity for p-lactam antibiotics. The development of mutations of bacterial PBPs is involved in the mechanism for p-lactam resistance in Streptococcus pneumoniae. Enterococcus faecium, and methicillin-resistant S. aureus (MRS A). 

Other synergistic antimicrobial combinations have been shown to be more effective than monotherapy with individual components. Trimethoprim-sulfamethoxazole has been successfully used for the treatment of bacterial infections and Pneumocystis jiroveci (carinii) pneumonia. 3-Lactamase inhibitors restore the activity of intrinsically active but hydrolyzable 3-lactams against organisms such as S aureus and Bacteroides fragilis. Three major mechanisms of antimicrobial synergism have been established ... 

So what are nitrogen oxides Where does they come from And why is there a concern about the amount that enters the atmosphere Nitrogen dioxide (NO2) is a brownish, highly reactive gas that is present in all urban atmospheres. N02 can irritate the lungs, cause bronchitis and pneumonia, and lower resistance to respiratory infections. Nitrogen oxides are an important precursor both to ozone (Oj) and acid rain, and may affect both terrestrial and aquatic ecosystems. The major mechanism for the formation of NO2 in the atmosphere is the oxidation of the primary air pollutant, nitric oxide (NO). NOx plays a major role, together with VOCs (Volatile Organic Compounds), in the atmospheric... 

In addition to S. pneumoniae, the viridans group of streptococci is also developing resistance to penicillin through the same mechanism, altered penicillin-binding proteins. In contrast, resistance has not developed in Streptococcus pyogenes, and both penicillins G and V are antibiotics of choice for systemic infections caused by this organism. 

Pneumocystis carinii is a common organism ibiit is probably inhaled in early life and lies dormant in the lungs. In immunosuppressed patients (steroids, immunosuppressive drugs, AIDS) it may cau.se an interstitial pneumonitis. P. carinii pneumonia is the most common presentation of AIDS in Western countries. Il is treated with co-trimoxazolc (Chapter 37), atovaquone or pentamidine given parentcrally or by inhalation. Hie mechanism of action of pentamidine is unknown. It has many side-effects, which are sorneiime.s fatal. 

The mechanisms responsible for postoperative pneumonia are similar to the etiologies of other types of nosocomial pneumonia. The most frequent mechanism for bacteria to enter the lower respiratory tract is via aspiration of contaminated oropharyngeal or gastric fluids. Less commonly, organisms can be transmitted via contaminated anesthesia or respiratory therapy equipment or may spread hematogenously from a distant site of infection. As described later, both general anesthesia and postoperative alterations in pulmonary mechanics may increase the likelihood of infection after bacterial contamination of the lower respiratory tract. 

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