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Fibronectin (FN) has been postulated to prevent gram-negative bacillary (GNB) colonization of the oropharynx by covering epithelial cell GNB receptors. We investigated the distribution of FN along the luminal surface of oropharyngeal epithelium in animals and humans. Examination of buccal epithelial biopsies obtained from normal rats revealed no luminal surface FN by either immunofluorescent or immunoperoxidase staining. Extraction of epithelial surface proteins and quantitation of FN by rocket immunoelectrophoresis and electrophoretic transfer to nitrocellulose followed by immunologic detection also detected no FN from normal animals' oropharyngeal biopsies. Buccal epithelial biopsies from three normal humans were examined for FN using electrophoretic transfer to nitrocellulose followed by immunologic detection, and no FN was demonstrable. Our results suggest that FN is not present on the oral epithelial surface of healthy rodents or humans, and that FN may not be involved in the pathogenesis of bacillary colonization.

Intrapulmonary deposition of the proteolytic enzyme papain produces a lesion resembling emphysema in experimental animals. The natural history of this lesion has not been well defined. The present study was performed to evaluate changes in lung structure and function with aging in normal rats and rats exposed to an aerosol of papain at 2 mo of age. Groups of control and papain-exposed animals were studied at 4, 8, and 18 mo of age. The parameters of lung function studied were specific airways' conductance (G(aw)/TGV), diffusing capacity per unit of alveolar volume (D(Lco)/V(A)), diffusing capacity (D(Lco)), and functional residual capacity (FRC). Morphometric parameters were the postfixation lung volume (V(L)) and mean chord length (L(M)); internal surface area (ISA) and ISA extrapolated to both the mean V(L) of the corresponding papain group and a V(L) of 10 ml (ISA(10)) were calculated. At 4 mo of age L(M) and FRC were significantly increased and ISA, D(Lco)/V(A), and D(Lco) were significantly reduced in the papain group. At 8 mo of age L(M) was significantly increased and ISA was significantly decreased in the papain group: physiologic studies were not performed in this group. At 18 mo of age L(M) was significantly increased and D(Lco)/V(A), D(Lco), and ISA were significantly decreased. Neither progression nor healing of the lesion was observed despite similar lung growth in both groups. This study demonstrates that a single proteolytic lung injury produces a fixed deficit of lung parenchyma. Progressive lung destruction may require repeated or continuous lung injury.

In seven of 30 consecutive patients with the adult respiratory distress syndrome, disseminated intravascular coagulation (DIC) developed. Increasing respiratory dysfunction characterized by decreased effective static compliance and increased hypoxemia coincided with the development of DIC. Patients in whom DIC developed were characterized by a high incidence of bleeding, gangrene of the extremities, renal dysfunction, mortality and autopsy evidence of fibrin microthrombi in the lungs, kidney and skin. In 12 of 23 patients who did not meet the criteria for DIC, the platelet count decreased by at least 50 per cent of the initial values at some time during their illness. Fibrin microthrombi were found in the lungs in the majority of the patients subjected to autopsy. These data support the concept that depostion of platelet on damaged pulmonary capillary endothelium may be more common in the adult respiratory distress syndrome than the DIC syndrome.

The determinants of the lung clearance of Streptococcus pneumoniae, Klebsiella pneumoniae, Escherichia coli, and Staphylococcus aureus were studied in normal mice after exposure to an aerosol of viable bacteria and 99mTc-labeled dead bacteria. The fraction of bacteria in lungs that remained viable 4 h after exposure were: S. pneumoniae, 7.3%; K. pneumoniae, 121%; E. coli, 88.5%; S. aureus, 27.6%. The rate of physical removal of bacterial particles (Kmc) was determined from the change in lung 99mTc counts with time: Kmc ranged between 7 and 12%/h and and was similar in all species. The rate of mucociliary clearance and of intrapulmonary bacterial killing (Kk + Kmc) was calculated from the change in bacterial counts with time in animals that had received tetracycline to inhibit bacterial multiplication. Kk, the rate of intrapulmonary killing, was obtained by subtraction of Kmc from (Kk + Kmc). The calculated values for Kk were: S. pneumoniae, - 87%/h; K. pneumoniae, - 17%/h; E. coli, - 18%/h; S. aureus, - 22%/h. The rate of intrapulmonary bacterial multiplication (Kg) was estimated from the relationship of bacterial counts in tetracycline and nontetracycline-treated animals, assuming that tetracycline altered only Kg. Kg, expressed as the doubling time, was: S. pneumoniae, 310 min; K. pneumoniae, 217 min; E.coli, 212 min; S. aureus, infinity (no multiplication). The data indicate that the marked differences in the clearance of these species from the normal mouse lung result from the interaction of differing rates of in vivo bacterial multiplication and killing.

Controlled oxygen therapy may aggravate carbon dioxide retention during acute exacerbations of chronic obstructive pulmonary disease (COPD). Of 50 consecutive patients with COPD and acute respiratory failure, 13 required intubation because of carbon dioxide narcosis. With discriminant analysis of their arterial oxygen tension (PaO 2 ) and pH on admission, a diagram separated patients into those at high risk and those at low risk for carbon dioxide narcosis. This diagram was then used to predict carbon dioxide narcosis in 73 patients with COPD and acute respiratory failure who were treated with controlled oxygen. In 16 of these patients carbon dioxide narcosis developed. Thirteen (81 per cent) were predicted by the diagram to be at high risk for this complication. Only two (4 per cent) patients judged by the diagram to be at low risk for carbon dioxide narcosis required mechanical ventilation. Utilizing an oxygen tension (PO 2 ), carbon dioxide tension (PCO 2 ) diagram a patient's ventilatory response was compared to that of ambulatory patients with COPD. These data suggest that hypoxemia and acidosis are more discriminatory for "carbon dioxide narcosis" than hypercapnia.

Using histologic techniques, we have quantified the amount of infiltration of bronchi and alveoli by polymorphonuclear leukocytes during the 4 hours after an aerosol inoculation of mice with bacteria. Although the lungs of animals challenged with Staphylococcus aureus differed little from those of animals exposed only to a water aerosol, the lungs of animals exposed to Klebsiella pneumoniae or to Escherichia coli demonstrated significantly greater polymorphonuclear leukocyte infiltrations in bronchi and alveoli 2 and 4 hours afer exposure. These results suggest that the polymorphonuclear leukocyte may contribute to the early defense of the lung against some bacteria.

Patients with a history of chronic debilitating disease due to a variety of causes are known to be at risk for infection with coliform gram-negative bacilli when they present with community-acquired pneumonia. Empiric treatment with broad-spectrum parenteral antibiotics is often begun in such patients pending the result of blood and other cultures. The optimal duration of broad-spectrum empiric therapy in such patients when cultures fail to reveal a specific pathogen is unknown. Review was made of the charts of 131 patients with community-acquired pneumonia admitted to the hospital and treated with broad-spectrum parenteral antibiotics in whom a specific pathogen was never isolated. Overall, 89 percent of these patients were cured without complication or relapse. Patients receiving broad-spectrum therapy for four days or less due to rapid clinical improvement had a successful outcome in 95 percent of cases. It is concluded that broad-spectrum parenteral antibiotic therapy can safely be abbreviated provided response to therapy is prompt.

Net lung bacterial clearance in normal mice is determined by the balance of in vivo bacterial multiplication on the one hand, and the defense mechanisms of mucociliary clearance and phagocytosis and killing by the oxygen-dependent alveolar macrophage on the other. The bactericidal function of the macrophage is the major component of the defense mechanism. The effect of acute hypoxia on the defense mechanism was studied in mice exposed to aerosols of Staphylococcus aureus, Escherichia coli, Klebsiella pneumoniae, and Streptococcus pneumoniae. Physical clearance was not impaired by acute hypoxia, and bacterial replication was not stimulated by the low oxygen atmosphere. Clearance of Staphylococcus aureus, Klebsiella pneumoniae, and Escherichia coli was impaired during acute hypoxia due to decreased phagocytosis or killing by the alveolar macrophage. The important human pathogen Streptococcus pneumoniae was cleared normally in the presence of acute hypoxia. This observation suggests that an oxygen-independen...

1. Patients should be divided preoperatively into low- or high-risk categories, depending on their probability of developing postoperative pulmonary complications. The evaluation should include spirometry as well as an assessment of the previously defined risk factors. 2. Patients in a low-risk category need only instruction in deep breathing pre- and postoperatively. Routine use of supplemented oxygen postoperatively is reasonable until it can be demonstrated whether such is necessary. 3. High-risk patients should be as free as possible of respiratory secretions at the time of surgery. A regimen for this purpose includes cessation of smoking, and administration of inhaled bronchodilators followed by chest percussion and postural drainage. 4. High-risk patients should be carefully instructed in deep breathing and coughing preoperatively. A mechanical device such as an incentive spirometer may be beneficial in this regard. If it is not possible to achieve spontaneous deep breathing, an attempt to accomplish this by IPPB may be undertaken. The tidal volume desired should be ordered. If IPPB does not result in large tidal volumes, it should be discontinued. 5. The deep breathing procedure found to be most successful preoperativelly should be continued postoperatively. 6. The patient should be as mobile as possible while in bed and ambulated as soon as is feasible. 7. Patients with preoperative expiratory flows of less than 20% of predicted values or with chronic hypercapnia should be carefully observed for postoperative ventilatory failure.

Lung clearance of Diplococcus pneumoniae was markedly reduced in rats with acute hemorrhagic pulmonary edema produced by instillation of hydrochloric acid. Bacterial clearance was enhanced in both control and acid-instilled animals by pretreatment with a bacteriostatic antibiotic, tetracycline, 30 mg/kg. From these data the contributions of bacterial multiplication and bacterial elimination to net lung bacterial clearance were estimated. In control animals the constant for exponential bacterial elimination was -1.4283 (fractional clearance = 76% per h), and the doubling time for the pneumococcus was 170 min. In acid-instilled rats the elimination constant was -0.5336 (fractional clearance = 41% per h), and the doubling time of the pneumococcus was 47 min, approximating the doubling time of 42 min observed with pneumococci grown in broth. These results indicate that, in the case of pneumococci, both bacterial elimination and bacterial growth contribute to lung bacterial clearance in normal animals as well as animals with damaged lungs. In the present study changes in both parameters were required to explain the observed results in acid-instilled animals. The pulmonary pathogenicity of some bacterial species may be determined by their capacity for growth in the lung, since infection of the lung occurs when bacterial multiplication exceeds the rate of elimination of viable organisms.

This study correlated levels of activated fibrinolysis with the presence, extent, and rate of resolution of angiographically documented pulmonary emboli. Pulmonary emboli demonstrable by angiography were associated with detectable fibrin split products in the serum of 24 of 25 patients. In the absence of increased fibrin split products, pulmonary emboli large enough to be demonstrated by angiography were found in only 2 of 25 positive pulmonary angiograms. Spontaneous resolution of pulmonary emboli could not be correlated with the the concentration or persistence of fibrin split products but did correlate well with the presence of a reversible precipitating cause. Thrombophlebitis in the absence of clinical evidence of pulmonary embolism was not associated with increased concentrations of fibrin split products in eight of nine patients. The one patient with increased fibrin split product concentration had evidence on lung scan of silent pulmonary embolism.

The Henderson apparatus (D. W. Henderson, J. Hyg. 50:53, 1952; 0. T. Miller and G. G. Gremillion, In Technical Manuscript 39, U.S. Army Biological Laboratories, Fort Detrick, Md., 1963) has become standard equipment for exposing a variety of animals to microbiological aerosols. When small animals such as mice are used, it is advantageous to aerosolize many animals in a single study. The standard small-animal exposure chamber supplied with the Henderson apparatus accommodates only 16 mice, necessitating repeated periods of nebulization. This produces an unavoidable variation in the character of the aerosol delivered to the different groups of mice. To circumvent this problem, we have devised a small-animal exposure chamber which holds 66 mice. It is designed for use with I.

Elastase activity generated during lung defense against aerobic bacteria was studied in an animal model. Bronchoalveolar lavage (BAL) fluid from hamsters inoculated with bacteria was assayed for elastase activity at 0, 2, 4, 6, and 8 h after inoculation using a synthetic substrate of elastase, succinyl-trialanine-nitroanilide (SLAPN). Streptococcus pneumoniae type 25 inoculation led to a peak elastase activity of 0.72 +/- 0.27 X 10(-3) units, not significantly different from baseline (0.41 +/- 0.08 X 10(-3) units) or saline control (0.33 +/- 0.18 X 10(-3) units). In contrast, inoculation with Pseudomonas aeruginosa strain PAO-1 (a species known to produce elastase as well as other virulence factors) produced peak elastase activity of 3.0 +/- 1.2 X 10(-3) units in BAL fluid, significantly higher than either pneumococcus type 25 or saline control (p less than 0.025). Inoculation with Pseudomonas aeruginosa strain E-64, an isogenic mutant of PAO-1 that produces a nonfunctional elastase, led to peak levels similar to the PAO-1 strain, suggesting that the presence of bacterial elastase was not the primary factor in BAL fluid elastase activity. Total numbers of granulocytes in BAL fluid from pneumococcus-inoculated animals (144 +/- 31 X 10(6] was significantly higher (p less than 0.05) than from either the PAO-1 (74 +/- 31 X 10(6] or E-64 (99 +/- 27 X 10(6] strains of Pseudomonas, Use of selective enzyme inhibitors of elastase, diisopropyl fluorophosphate and disodium ethylenediaminetetraacetate, implied that the majority of elastase activity in BAL fluid was due to a serine protease, of which granulocyte elastase is the primary source.(ABSTRACT TRUNCATED AT 250 WORDS)

Two sets of phagocytic cells are available to defend the lung against inhaled bacteria. Both resident alveolar macrophages and granulocytes from the circulation have been observed in pulmonary air spaces after the deposition of bacteria; their functional roles, however, have been defined. We rendered mice selectively granulocytopenic with heterologous antiserum in order to ascertain the relative contributions of these two groups of cells in intrapulmonary bacterial killing. The clearance of Staphylococcus aureus was unimpaired in granulocytopenic animals, confirming the primary role of the alveolar macrophages in the killing of these organisms. In contrast, granulocytopenic animals cleared only 10.0+/-7.0% of an inoculum of Klebsiella pneumoniae compared with 33.0+/-4.0% clearance in normal animals (P < 0.02), and Pseudomonas aeruginosa proliferated to 513% of baseline levels in granulocytopenic animals, whereas normal mice cleared 26.8+/-10.6% of the inoculum. These findings indicate that circulating granulocytes play a major role in the clearance of the latter two organisms. This variation in cellular response to different bacterial species suggests that the defense of the lung against pathogenic bacteria is more complex than has been previously assumed.

We have studied the clearance from murine lungs of two strains of Staphylococcus aureus, one possessing high and the other possessing low levels of protein A.S. aureus FDA 209 and S. aureus Wood 46 were assayed for their ability to bind mouse immunoglobulin G, using an indirect radioimmunoassay. S. aureus FDA 209 binding of mouse immunoglobulin was significantly greater than that of S. aureus Wood 46 (118,909 versus 37,845 cpm). Clearance of these two strains from the lung after a 30-min aerosol inoculation period was not significantly different. The percentage of bacteria remaining in the lung was 49.2 and 55.0% at 2h, 31.8 and 33.2% at 3 h, and 25.4 and 17.2% at 4 h for protein A-rich and protein A-poor strains, respectively (P greater than 0.20 at each time). These data suggest that the previously demonstrated in vitro antiphagocytic effect of protein A may not be relevant to pulmonary clearance mechanisms.

When two sets of phagocytic cells participate simultaneously in the inflammatory process and bacterial killing, the relative contribution of each cell type is difficult to ascertain. The use of cell-specific antibody will permit selective depletion of one phagocyte population. We describe an experimental model of granulocytopenia which utilizes the immunoglobulin G fraction of an antigranulocyte serum. This material markedly depleted circulating polymorphonuclear leukocytes (PMN); within 2 h after injection of antigranulocyte globulin, PMN counts were at 19% of original levels and remained significantly depressed for 24 h. Granulocyte recruitment was also impaired, with only 5 x 10(3) PMN appearing in the lungs in response to an aerosol of Klebsiella, compared to 4.17 x 10(5) PMN in control animals (P less than 0.01). Most importantly, alveolar macrophages retained normal viability (97% versus 94% for control value, P not significant) normal phagocytic function, and normal bactericidal capacity. Antigranulocyte globulin is thus a valuable tool for the study of bacterial defense mechanisms.

The prevalence of respiratory symptoms and chest radiographic and spirometric abnormalities was assessed among 397 employees of an activated carbon plant. Definite radiographic findings of pneumoconiosis, consisting of p-type, rounded opacities in the lower lung fields without firbosis or coalescence, were present in 9.6% of men and were related to cumulative dust exposure. Lesser degrees of radiographic abnormality suggesting pneumoconiosis were present in 11% of men and 2% of women. Spirometric values were substantially lower in blacks than in whites. However, cumulative dust exposure was not an important determinant of pulmonary function in either race. Review of lung biopsy speciments that had been obtained previously in two employees revealed extensive carbon depositiion but minimal associated fibrosis. Prolonged inhalation of activated carbon dust leads to pulmonary deposition of carbon and raciographic signs of pneumoconiosis; such deposition has little, if any, effect on respiratory symptoms or pulmonary function.

A sensitive technic using indium111 chloride was devised to investigate the occurrence of pharyngeal aspiration. Twenty normal subjects and 10 patients with depressed consciousness were studied. Forty-five per cent of the normal subjects aspirated during deep sleep. Normal subjects who did not aspirate were noted to sleep poorly. Seventy per cent of the patients with depressed consciousness aspirated. Aspiration of pharyngeal secretions occurs frequently in patients with depressed sensorium and also in normal adults during deep sleep. Bacterial pneumonia may result when aspirated bacteria are not effectively cleared. This may result when clearance mechanisms are impaired or when they are overwhelmed by large volumes of aspirated secretions.

After aerosol deposition of Serratia marcescens in mice, initial delayed pulmonary clearance was followed between 4 and 24 hr later by progressive elimination.

The prevalence of gram-negative bacilli among the oropharyngeal bacterial flora was low in physiologically normal subjects despite hospital exposure but rose markedly in patients with illnesses of varying severity. This increased prevalence was not correlated with antibiotic administration or inhalation therapy, was not dependent on duration of hospitalization and correlated best with the clinical severity of illness. Increased exposure to these organisms alone does not adequately explain these findings, suggesting that pharyngeal clearance mechanisms are impaired in these patients. Since most bacterial pneumonias begin with the aspiration into the lung of bacteria present in the upper respiratory tract, this alteration in the pharyngeal flora of ill patients may represent an important initial step in the pathogenesis of pneumonia due to gram-negative bacilli.

An area-sampling device for obtaining quantitative samples of the oropharyngeal bacterial flora is described and illustrative data are presented.

The stress imposed by exercise is usually considered deleterious to patients with cardiopulmonary disorders. For this reason limitation of activity is often recommended for patients with chronic obstructive pulmonary disease. However, Barach and associates 1,2 have repeatedly reported a clinical observation similar to ours, that patients with chronic obstructive pulmonary disease who continue to be active remain in relatively better health for a longer period of time than their more sedentary counterparts. Such observations prompted the present study to assess the physiological responses to progressive exercise training. Methods Patients with severe obstructive pulmonary disease and evidence of generalized physical disability were selected for the study. Patients with manifestations of left ventricular disease were excluded. In addition, patients who developed either multiple premature ventricular contractions or marked cyanosis during exercise were not included in the study. These latter excluded patients, subsequently trained while breathing supplemental oxygen, will form the basis of

CHRONIC, obstructive pulmonary disease is the most frequent cause of physical disability associated with pulmonary disorders. The pathogenesis of disability arising from pulmonary disease can be summarized as follows: either pulmonary ventilatory or circulatory insufficiency may be responsible for exertional dyspnea which, in turn, causes fear and inactivity. Fear, itself, tends to promote further inactivity. Inactivity promotes diminished muscle tone, decreased muscle efficiency, easy fatigability, and progressive physical debility. All of these in turn lead again to more inactivity and exertional dyspnea. Thus a vicious cycle of events is established which eventually leads to even more serious difficulties, such as venostasis with the threat of phlebothrombosis and pulmonary embolization, increased bone resorption which may result in fractures and deformity, and decreased cardiac function. Having recognized the existence of debility, then the need for rehabilitation becomes apparent. The execution of a complete physiological treatment program,' prior to the active physical rehabilitation, must be considered as a prime requisite to a successful rehabilitation program. It is first necessary to improve ventilatory function to an optimum. The initial step consists of removal of all irritants, especially cigarette smoking and other pollutants. The existence of bronchial infection must be identified and treated with appropriate antibiotics. Bronchial edema and bronchospasm can be treated with oral and aerosol bronchodilator agents. When the cause of the obstruction is retained inflammatory exudate or secretions, as is so often the case, then bronchial hygiene becomes essential. The latter is probably the single most neglected aspect of treatment. The methods for achieving effective bronchial hygiene, which have been presented elsewhere,2-5 deserve much more comment than space will permit. Intensive use of saline or detergent aerosols (particularly heated aerosols), deep breathing, rotary postural drainage, with chest clapping or vibration and occasionally potassium iodide as an expectorant, will be necessary. Finally, in those situations where the inflammatory reaction is resistant to protracted and diligent therapy as outlined, the administration of steroids, either orally or by aerosol, may be indicated in order to improve bronchial integrity to an optimum. Patient edqgatiozm is one of the most important components of rehabilitation programs. The patient must be informed concerning the mechanical nature of his disease and the factors responsible for his breathing difficulty. In ventilatory obstructive disease, the work of breathing is done largely in overcoming the resistance to airflow.6 Thus it becomes essential that the patient maintain the slowest feasible respiratory pattern. In addition, because of the tendency for the airways to collapse during rapid ex

Inhalation-therapy equipment incorporating reservoir nebulization was sampled for bacterial contamination during a four-year period after the introduction of routine daily decontamination with 0.25 per cent acetic acid. The incidence of contamination was found to be less than 10 per cent during the last three study years, as compared to 84 per cent before the use of the acetic acid regimen. Residual contamination was related to personnel error or corrosion of nebulizer jets. During the "preacetic acid era" the prevalence of necrotizing pneumonia due to gram-negative bacilli at autopsy was 7.9 per cent, whereas in the last two years studied, the incidence was 2.2 and 2.1 per cent. This prevalence is similar to that found before the use of reservoir nebulizers. These data indicate that daily decontamination of reservoir nebulizer equipment with 0.25 per cent acetic acid is effective and practical in routine hospital use.

Hospital-acquired respiratory infections develop in approximately 5% of patients admitted to a general hospital [1, 2]. In a previous study [3] we analyzed factors predisposing to hospitalacquired necrotizing pneumonia. That study was based on the work of Fraenkel [4], which indicated that Pseudomonas aeruginosa produces a specific necrotizing hemorrhagic pneumonia recognizable by histologic appearance. Subsequently, other investigators have confirmed that such lesions occur in patients dying with gram-negative bacillary pneumonia [5, 6]. However, other histologic descriptions have been reported in pneumonias caused by gram-negative bacilli [7-10], and necrotizing pneumonia has been reported with infection caused by other types of bacteria [11]. The present study was undertaken to define the microbiologic spectrum of necrotizing pneumonia and to determine whether histopathologic criteria are sufficient to make a diagnosis of gramnegative bacillary pneumonia.

After aerosol deposition of Pseudomonas aeruginosa strains in mice and rats, completely different patterns of pulmonary bacterial clearance were observed in each animal species.

Excerpt Gram-negative bacilli are assuming an increasing role in nosocomial infections, having surpassed staphylococci in frequency of occurrence. In addition to the well-recognized syndromes of py...

The following article on nebulization equipment calls attention to the fact that there is no single simple method of humidification which does not carry at least some risk of contamination. A study is made of several mechanical devices that are in common use and well known by their trade names. It is shown that techniques for decontamination are not equally effective in all cases. Strongly implied is the conclusion that all such pieces of mechanical equipment should in their distribution be accompanied by carefully specified instructions for effective decontamination.—Ed.

Endotracheal tubes have been used with increasing frequency to avoid the use of tracheostomies in patients with respiratory depression. Use of the tubes seems justified in decreasing patient morbidity when an episode of respiratory depression is transient or when episodes of respiratory failure are unlikely to recur. The use of endotracheal tubes, however, may be associated with certain complications with which the attending physician should be familiar.1-5This communication describes one such complication, namely, the tendency of some types of endotracheal tubes to collapse and thus obliterate the lumen when the cuff is excessively inflated. Report of a Case A 42-year-old woman was admitted to a local hospital with a one-week history of increasing cough, yellow sputum, and dyspnea, all of which were unresponsive to antibiotics. She had had a long-standing cough and exertional dyspnea despite a lower lobectomy on the right side in 1960 for bronchiectasis. On examination

Inhalation therapy equipment may potentially act as a vector of hospital-acquired pneumonia due to gram-negative bacilli. The major mechanism by which bacteria are disseminated is aerosolization of organisms in particle sizes that are sufficiently small to be deposited in terminal lung units. Ventilators and humidifiers are relatively innocuous in this regard, and small-volume Venturi nebulizers (medications nebulizers) are not frequently incriminated in nosocomial epidemics. Large-volume nebulizers of all designs (Venturi, spinning disk, or ultrasonic) are the primary source of aerosolized bacteria. The method of decontamination differs with nebulizer design, but any system of decontamination must be carried out at least once every 24 hours while the equipment is in use. No hospital can consider its procedure of decontamination satisfactory unless it has a continuing monitoring program to demonstrate that the degree of contamination does not exceed that of hospital air.