Nosocomial pneumonia: trying to make sense of the literature.

Nosocomial pneumonia is hard to diagnose with any certainty. Widely accepted concepts regarding the infection are based on data that are far from conclusive. Published recommendations for diagnosis and treatment often reflect a concentrated effort to consolidate these data. According to the authors of this article, initial empirical treatment may be defined by dividing patients into specific host groups. However, this approach should always be supplemented by earnest attempts at identifying the cause with microbial cultures.

Tuberculosis in the 1990s.

The steady decline in tuberculosis case rate reversed in the mid-1980s, and tuberculosis cases have increased dramatically since that time. Important factors contributing to this increase are the human immunodeficiency virus (HIV) epidemic and tuberculosis occurring in foreign-born persons. Tuberculosis outbreaks have occurred in HIV clinics and wards, prisons, homeless shelters, nursing homes, and health care facilities. Some of the outbreaks have involved strains of tuberculosis resistant to multiple antituberculosis drugs. Recent recommendations for initial therapy of tuberculosis include the use of four drugs and directly observed therapy in an effort to prevent the emergence of further drug resistance.

Treatment of tuberculosis and tuberculosis infection in adults and children. American Thoracic Society and The Centers for Disease Control and Prevention.

Treatment of Tuberculosis. 1. A 6-mo regimen consisting of isoniazid, rifampin, and pyrazinamide given for 2 mo followed by isoniazid and rifampin for 4 mo is the preferred treatment for patients with fully susceptible organisms who adhere to treatment. Ethambutol (or streptomycin in children too young to be monitored for visual acuity) should be included in the initial regimen until the results of drug susceptibility studies are available, unless there is little possibility of drug resistance (i.e., there is less than 4% primary resistance to isoniazid in the community, and the patient has had no previous treatment with antituberculosis medications, is not from a country with a high prevalence of drug resistance, and has no known exposure to a drug-resistant case). This four-drug, 6-mo regimen is effective even when the infecting organism is resistant to INH. This recommendation applies to both HIV-infected and uninfected persons. However, in the presence of HIV infection it is critically important to assess the clinical and bacteriologic response. If there is evidence of a slow or suboptimal response, therapy should be prolonged as judged on a case by case basis. 2. Alternatively, a 9-mo regimen of isoniazid and rifampin is acceptable for persons who cannot or should not take pyrazinamide. Ethambutol (or streptomycin in children too young to be monitored for visual acuity) should also be included until the results of drug susceptibility studies are available, unless there is little possibility of drug resistance (see Section 1 above). If INH resistance is demonstrated, rifampin and ethambutol should be continued for a minimum of 12 mo. 3. Consideration should be given to treating all patients with directly observed therapy (DOT). 4. Multiple-drug-resistant tuberculosis (i.e., resistance to at least isoniazid and rifampin) presents difficult treatment problems. Treatment must be individualized and based on susceptibility studies. In such cases, consultation with an expert in tuberculosis is recommended. 5. Children should be managed in essentially the same ways as adults using appropriately adjusted doses of the drugs. This document addresses specific important differences between the management of adults and children. 6. Extrapulmonary tuberculosis should be managed according to the principles and with the drug regimens outlined for pulmonary tuberculosis, except for children who have miliary tuberculosis, bone/joint tuberculosis, or tuberculous meningitis who should receive a minimum of 12 mo of therapy.(ABSTRACT TRUNCATED AT 400 WORDS)

The treatment of tuberculosis.

Short-course chemotherapy has made the treatment of TB easier and better than ever, but it works only when patients take the drugs regularly. Compliance is a must for therapy to be successful. Physicians treating patients with tuberculosis should be acutely aware of noncompliance, and every effort to ensure adequate treatment must be put forth. Directly supervised therapy is an excellent option when enough resources are available. Intermittent regimens markedly reduce the manpower required for observed therapy. New agents are being tested for in vitro activity against M. tuberculosis, and clinical studies of those found to be potentially effective are needed to formulate new regimens against the ever-increasing threat of multidrug-resistant TB.

The role of bacterial super infection in extensive pulmonary tuberculosis. Data from protected brush cultures in untreated patients from the University of South Alabama Medical Center, Mobile, Alabama, USA.

Pulmonary tuberculosis (TB) and bacterial pneumonia are both characterized by fever, cough, and purulent sputum production. Although TB alone can cause these symptoms, the possibility of a concomitant bacterial pneumonia has led some clinicians to treat these patients empirically with antibacterial agents. Neither the benefit of such empiric antibiotic therapy nor transtracheal aspirate cultures from patients with pulmonary TB have yielded consistent results. Consequently, we performed a prospective study to obtain lower airway secretions via a bronchoscopic protected specimen brush (PSB) technique for quantitative aerobic and anaerobic cultures from untreated patients with extensive pulmonary TB (defined as cavitary disease or involvement of > or = 3 segments). We obtained bronchoscopic samples from 3 untreated men aged 21, 61, and 60 years with extensive pulmonary TB. There was no significant bacterial growth (aerobic or anaerobic) from the specimens obtained. These results, therefore, do not support the hypothesis that bacterial pneumonia is a common concomitant of extensive pulmonary TB.

Bronchoscopic protected specimen brush and bronchoalveolar lavage in the diagnosis of bacterial pneumonia.

Despite marked improvements in antibiotic therapy, the accurate diagnosis and treatment of bacterial lower respiratory tract infection remain a challenge. The bronchoscopic protected specimen brush and bronchoscopic bronchoalveolar lavage combined with quantitative bacterial cultures can provide sensitive and relatively specific information about lower airway flora. Both of these methods require strict observance of the required protocol, careful processing of the obtained specimens, and the absence of prior antibiotic therapy to obtain best results. These procedures are also of some utility in sickle cell acute chest syndrome, bronchiectasis, and in the immunocompromised host.

Hemoglobin potentiates oxidant injury in isolated rat lungs.

Isolated perfused rat lungs were subjected to oxidant injury induced by tert-butyl hydroperoxide (t-buOOH), which caused a significant increase in capillary permeability as assessed by the change in the capillary filtration coefficient. t-buOOH caused an increase in the change in the capillary filtration coefficient (delta Kfc) of 0.27 +/- 0.05 ml.min.cmH2O-1.100 g lung tissue-1 (mean +/- SE) that was accompanied by an increase in thiobarbituric acid reactive products of lipid peroxidation in the lung perfusate. The addition of hemoglobin to the perfusate potentiated t-buOOH-induced lung injury as evidenced by a significantly greater (P = 0.007) delta Kfc of 0.43 +/- 0.05. t-buOOH also caused hemoglobin to release large quantities of free iron in vitro. The potentiation of t-buOOH-induced lung injury by hemoglobin was prevented by apotransferrin as evidenced by a significant reduction (P = 0.001) in delta Kfc to 0.13 +/- 0.02. No statistically significant (P greater than 0.05) changes in segmental resistances or pulmonary vascular pressures occurred in any of the lungs injured with t-buOOH when compared with time controls. These results demonstrate that t-buOOH causes an oxidant injury in isolated rat lungs that can be potentiated by free iron released from hemoglobin.

Tuberculous pleural effusion. Twenty-year experience.

We reviewed the records of 1,738 cases of tuberculosis seen during the period from 1968 to 1988 in Mobile, Alabama. Seventy cases of tuberculous pleural effusion were identified and constituted 4.9 percent of all disease due to Mycobacterium tuberculosis during this period. Tuberculous pleural effusion was diagnosed if the patient had M tuberculosis cultured from sputum, pleura, or pleural fluid and had a roentgenographic pleural effusion without an alternative explanation for the presence of the effusion. The diagnosis of tuberculous pleural effusion was made in the absence of a positive culture if the patient had an undiagnosed lymphocytic exudative pleural effusion and all clinical and roentgenographic abnormalities resolved on antimycobacterial chemotherapy. The mean age of all patients was 47 +/- 18.4 years. The 70 cases were evenly divided between 35 that were accompanied by roentgenographic pulmonary parenchymal infiltrates and 35 that occurred in the absence of parenchymal infiltrates. We conclude that cultures of all potentially diagnostic specimens (sputum, pleural fluid, and pleura) and an intermediate-strength skin test, are sensitive tests for the diagnosis of tuberculous pleural effusion. In addition, the age of patients with tuberculous pleural effusion appears to be increasing.

Results of bronchoscopically obtained lower airway cultures from adult sickle cell disease patients with the acute chest syndrome.

PURPOSE: The purpose of this study was to determine the frequency of bacterial pneumonia as a cause of the acute chest syndrome in adult patients with sickle cell disease based on bronchoscopically obtained lower airway cultures and to describe the clinical, laboratory, and roentgenographic features of the acute chest syndrome in a series composed entirely of adult patients with sickle cell disease. PATIENTS AND METHODS: We reviewed the hospital records from 19 episodes (18 patients) of acute chest syndrome in adult patients with sickle cell disease (greater than or equal to 19 years of age) who had undergone flexible bronchoscopy to obtain lower airway cultures between January 1979 and July 1987. We also recorded patients' clinical, laboratory, and roentgenographic characteristics. RESULTS: Pneumonia was diagnosed in four of 19 episodes (21%) of acute chest syndrome based on quantitative cultures obtained at bronchoscopy. The pneumonia was caused by Streptococcus pneumoniae in two patients and mixed aerobic and anaerobic organisms in the other two patients. Forty-four of 45 blood cultures were negative, and one grew Staphylococcus epidermidis, which was considered a contaminant. Chest roentgenograms revealed lower lobe involvement in 17 episodes (90%) and bilateral infiltrates in six (32%). Pleural effusions occurred in seven episodes (37%), and pleural fluid samples obtained from five of these revealed sterile exudates. CONCLUSION: The results of this retrospective study suggest that bacterial pneumonia is an uncommon cause of acute chest syndrome in adult patients with sickle cell disease. These results are consistent with previous retrospective studies using noninvasive techniques to diagnose pneumonia. Nevertheless, there appeared to be no reliable noninvasive variables that could accurately differentiate between patients with and without pneumonia and, consequently, we recommend empiric antibiotic therapy in addition to usual supportive care of these patients.

U74500A inhibition of oxidant-mediated lung injury.

Toxic oxygen species are thought to play a primary role in the pathophysiological mechanisms responsible for a diverse group of lung diseases. In this study, isolated perfused rat lungs were subjected to oxidant injury induced by ischemia-reperfusion (IR) and t-butyl hydroperoxide (t-buOOH) challenge. Both forms of injury caused large increases in capillary permeability as assessed by the capillary filtration coefficient (Kfc). IR and t-buOOH challenge caused increases in the Kfc of 0.95 +/- 0.22 and 0.30 +/- 0.06 ml.min-1.cmH2O-1.100 g lung tissue-1, respectively. U74500A, a potent inhibitor of iron-mediated lipid peroxidation, significantly attenuated the endothelial damage seen in both forms of injury. In lungs pretreated with U74500A, the Kfc increased 0.01 +/- 0.02 and 0.11 +/- 0.03 ml.min-1.cmH2O-1.100 g lung tissue-1 following IR and t-buOOH challenge, respectively. In lungs pretreated with the iron binding protein transferrin the Kfc increased 0.31 +/- 0.11 and 0.19 +/- 0.03 ml.min-1.cmH2O-1.100 g lung tissue-1 following IR and t-buOOH challenge, respectively. In these studies, transferrin significantly attenuated permeability in the IR group only. However, the attenuation of injury in IR due to U74500A was significantly greater (P less than 0.05) than the attenuation provided by transferrin. Both forms of injury also caused small but statistically significant increases in pulmonary artery pressure. These results suggest that the increase in capillary permeability seen after IR and t-buOOH is in part mediated by iron-dependent mechanisms.

Quantitative bacterial cultures of bronchoalveolar lavage fluids and protected brush catheter specimens from normal subjects.

Bronchoalveolar lavage (BAL) is quite useful in the diagnosis of nonbacterial lung infections, especially in immunocompromised patients, and recent studies have suggested that BAL may be useful in the diagnosis of bacterial pneumonia as well. Because previous studies indicated that bronchoscopic aspirates are usually contaminated by oropharyngeal flora, we anticipated that BAL fluid would also likely be contaminated. Therefore, the purpose of this study was to perform quantitative bacterial cultures on BAL fluids obtained from eight normal subjects. Prior to each procedure, saline was aspirated through the bronchoscope and submitted for culture. A protected brush catheter (PBC) specimen was obtained from each subject's right middle lobe, and then a BAL specimen was obtained from the same location. All specimens were quantitatively cultured for aerobic and anaerobic organisms. In addition, lidocaine concentrations were measured in the BAL fluids and the PBC specimens. Six of the eight bronchoscope cultures were sterile. Seven of the eight PBC specimens were sterile and one yielded less than 10(3) cfu/ml of normal oropharyngeal flora. One BAL fluid specimen was sterile and seven yielded from one to four bacterial strains each; however, quantitation revealed less than 10(4) cfu/ml in all specimens. Lidocaine concentrations (mean +/- 1 SD) were as follows: PBC specimen, 0.81 microgram/ml (+/- 0.62); BAL fluid specimen, 62.6 micrograms/ml (+/- 43). We conclude that BAL fluid obtained from normal subjects is frequently contaminated by oropharyngeal bacterial flora.(ABSTRACT TRUNCATED AT 250 WORDS)

Physiologic effects and serum lidocaine concentrations after inhalation of lidocaine from a compressed gas-powered jet nebulizer.

The physiologic effects, efficacy, and serum lidocaine concentrations were determined in 10 normal volunteers who inhaled nebulized lidocaine from a compressed gas-powered jet nebulizer. Physiologic variables and serial venous serum lidocaine concentrations were measured during and after lidocaine inhalation. All 10 subjects experienced loss of the gag reflex, which returned to normal at 32 +/- 5.9 min (mean +/- 1 SD), with a range of 20 to 40 min. There were no significant changes in systolic or diastolic blood pressures or heart rates. There were no significant changes from baseline in any of the measured spirometric variables (FVC, FEV1, peak expiratory flow rate, peak inspiratory flow rate). The peak mean serum lidocaine concentration measured at 20 min after beginning lidocaine inhalation was 0.52 microgram/ml, and the highest single value measured was 1.05 micrograms/ml. We conclude that inhalation of lidocaine from a compressed gas-powered jet nebulizer can produce safe and effective oropharyngeal anesthesia with minimal drug absorption.