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Background: The role of Ureaplasma urealyticum in the development of chronic lung disease (CLD) in preterm infants continues to be disputed. Recently U. urealyticum has been found to consist of two species, U. urealyticum and Ureaplasma parvum, a finding that has not been considered in previous studies of CLD. This study examined the possible relationships between development of CLD and respiratory colonization by these newly redefined species, their concentrations in lower respiratory secretions and the effect of pulmonary surfactant treatment on these relationships in preterm infants with birth weights < 1500 g., Methods: Endotracheal aspirates (ETA) were collected from intubated infants when airway suctioning was medically required. ETA were stored at -80 degrees C until quantitative cultures for ureaplasmas and Mycoplasma hominis were performed. Culture results were correlated with development of CLD., Results: Of 475 infants (birth weights < 1500 g) admitted during the 2-year study period, 272 were excluded because they were not intubated or were extubated before ETA could be obtained. An additional 28 infants died, were discharged or were transferred before they could be assessed for CLD. From the remaining 175 infants ureaplasmas were isolated from 66 (38%). No statistically significant associations were identified between development of CLD and the Ureaplasma species isolated, or concentration of ureaplasmas in lower respiratory secretions. These findings were not altered by treatment with pulmonary surfactant (Survanta)., Conclusion: Lower respiratory colonization by ureaplasmas does not appear to be a contributory cause of CLD in preterm infants.

To investigate the pathogenicity of Ureaplasma urealyticum and Mycoplasma hominis in preterm infants, we conducted a study to determine (1) frequency of isolation from cerebrospinal fluid and tracheal aspirate specimens and (2) clinical outcomes and effect of erythromycin treatment in ureaplasma-colonized infants. From the cerebrospinal fluid of 920 infants, U. urealyticum was isolated from 2 (0.2%) and M. hominis from none. From tracheal aspirate specimens from 224 infants, U. urealyticum was recovered from 37 (17%) and M. hominis from 4 (2%). Demographic characteristics and clinical outcomes were compared in very low birth weight infants (< 1500 gm) who were culture-positive or -negative for U. urealyticum. Although infants with positive results were less mature than their cohorts with negative results, there were no substantive differences in clinical outcomes between the two groups. Initiation of erythromycin treatment of infants with positive ureaplasma culture results at a mean age of 16.4 days did not appear to alter the clinical outcome. We conclude that in preterm infants (1) infection of the cerebrospinal fluid by U. urealyticum is infrequent, (2) ureaplasma organisms are frequently present in tracheal aspirate specimens but do not appear to be related to the presence or the subsequent development of respiratory disease, and (3) initiation of erythromycin treatment at 1 to 3 weeks of age does not alter the clinical course.

US military recruits receive benzathine penicillin prophylaxis because of endemicity of group A beta-hemolytic streptococcal (GABHS) infections. GABHS prevalence in Navy recruits receiving single-dose benzathine penicillin prophylaxis was assessed during spring and fall 1989 by culturing throat specimens from randomly selected groups of approximately 230 men before and 2, 4, and 7 weeks after prophylaxis and from men with pharyngitis diagnosed at sick call. Of 60 GABHS isolates, 75% were serotype M-3. The pharyngitis rate increased from 0.18% in the spring to 1.55% in the fall with a concurrent increase in serotype M-3 prevalence from 35% to 91%. The GABHS prevalence rate was three- to fourfold lower after prophylaxis. There were no cases of acute rheumatic fever (ARF) despite predominance of M-3, a rheumatogenic serotype. It was concluded that penicillin prophylaxis continues to be effective for control of GABHS infections and prevention of ARF in Navy recruits.

Clinical isolates of Pseudomonas aeruginosa from patients with cystic fibrosis were studied in an effort to determine the unique characteristics of the infecting strains and to elucidate the pattern of colonization. Of 413 patients studied, 81% were chronically infected with P. aeruginosa. Patients from whom P. aeruginosa was never or only occasionally isolated were in better clinical condition than the chronically infected patients. Isolates were classified into six morphologic varieties: classic, rough, mucoid, gelatinous, dwarf, and enterobacter. Most patients had two or more of these varieties. Such multiple varieties from the same individual were of the same serotype but often differed in antibiotic susceptibility as determined by both the disk and the minimal inhibitory concentration methods. These differences were apparent when mucoid strains were compared with nonmucoid strains and when nonmucoid strains were compared with one another. Studies of antibiotic susceptibility should be performed on each morphologically different type of P. aeruginosa obtained from patients with cystic fibrosis.

Recent reports indicate that methicillin-resistant Staphylococcus aureus (MRSA) may be emerging as a significant pediatric nosocomial pathogen. Children with cystic fibrosis (CF) pulmonary disease are subject to many of the risk factors for MRSA colonization and/or infection. We retrospectively investigated the prevalence and significance of MRSA from sputum and throat cultures in 452 patients with CF followed during 1986. No MRSA had been isolated during 1984 or 1985. Although S. aureus was isolated from 212 patients (47%) in 1986, only 14 (3%) showed MRSA. The MRSA strains had 11 different antimicrobial susceptibility patterns. Neither age, clinical condition, nor recent prior hospitalization correlated with MRSA acquisition. Acquisition did not appear to directly affect the course of the pulmonary disease in these patients even though no patient received any treatment for their MRSA. The prevalence of MRSA is low, although patients with CF are subject to many risk factors. MRSA appears to be mainly community-acquired and to represent colonization rather than infection. However, the potential for nosocomial MRSA infection is present, and vigilance is required in monitoring any changes in frequency of isolation or infection with these organisms.

In the neonate, fungal infections result in significant morbidity and mortality. For very low birth weight (less than 1,500 g) infants, we prospectively determined the fungal colonization rate to be 26.7%. In one third of infants with fungal colonies, mucocutaneous candidiasis developed, and in 7.7%, systemic disease developed. Two thirds of the infants had colonies in the first week of life. This colonization was probably acquired during labor and delivery, because those infants who had colonization were more often delivered vaginally than by cesarean section. Early colonization, commonly from the gastrointestinal or respiratory tract, featured Candida albicans and Candida tropicalis. Late colonization, occurring after 2 weeks of life (15.0% of patients), was more likely to be cutaneous and was associated with either Candida parapsilosis or such poor growth that the organism could not be identified. Infants with colonization only rarely had budding yeasts (6.1%), whereas more than half of the infants with either a urinalysis showing budding yeasts or a urine culture growing fungi had invasive disease. Fungal contamination was not found on either thoracotomy tubes or catheter tips. In the low birth weight infant, fungal colonization represents a significant risk factor for cutaneous or systemic candidiasis in these infants.

Systemic infection with Malassezia furfur was first reported in 1981 as a specific complication of Intralipid therapy in a neonate. Six additional patients, including three older than 16 years of age, were identified subsequently. All had received prolonged Intralipid infusion through central venous catheters. Pulmonary infection was documented in tissue in three cases, the clinical presentation was characterized by pulmonary infiltrates, fever, and, in the infants, thrombocytopenia. Two subgroups of patients appear to be at the greatest risk for Malassezia infection: neonates with cardiopulmonary disease and adults with severe gastrointestinal disease and immunosuppression. The documentation of pulmonary arterial lipid deposits in vessels that had been infiltrated by Malassezia organisms and the observation of organisms in small pulmonary thromboemboli suggest that these lipophilic and lipid-dependent organisms are introduced into the bloodstream from venous catheters and require high lipid concentrations to proliferate in tissue.

This report presents experimental observations indicating the presence of an inhibitory activity in cystic fibrosis (CF) serum which impairs phagocytosis of Pseudomonas aeruginosa by rabbit as well as human alveolar macrophages. Of the 49 patient serum samples studied, 40 consistently showed greater than or equal to 60% inhibition, 3 showed no inhibition and 6 were in the range of 20-60% inhibition of Pseudomonas phagocytosis. In parallel studies, the phagocytosis of S. aureus and S. marcescens was found not to be inhibited by CF serum. Mixing of CF serum with normal serum could not overcome the inhibitory effect, indicating the presence of an inhibitory factor rather than the lack of a necessary component. The inhibitory activity is not lost upon exposure of serum to glass, upon freezing the serum once, or upon heating at 56 degrees C for 30 minutes.

Alveolar macrophages were isolated from three cystic fibrosis patients, and the structure and function of these cells were compared to that of normal alveolar macrophages. The cystic fibrosis (CF) and normal alveolar macrophages were able to phagocytize Pseudomonas in the presence of normal serum, but cells from both sources had decreased phagocytosis of Pseudomonas in the presence of CF serum. Phagocytosis of Staphylococcus was not inhibited. Ultrastructural studies showed CF macrophages to be morphologically normal, however, in contrast to CF polymorphonuclear cells, they had not been heavily engaged in phagocytosis. The similarities between CF and normal macrophages suggest that the chronic pulmonary infection of CF may be due to an extrinsic factor in an altered lung environment rather than to any intrinsic cellular defect of the alveolar macrophage.

Among 302 infants and children with acute bacterial meningitis, the syndrome of cerebral herniation occurred in 3 of 10 fatal cases and in 15 patients who survived. The interval from time of admission to herniation was 8 hours or less, and no predictive factors could be determined. Seizures occurring immediately prior to cerebral herniation made diagnosis more difficult. Early recognition of cerebral herniation and prompt treatment with osmotic diuretics can reduce the mortality of bacterial meningitis.

Despite the decrease in the incidence and severity of rheumatic fever and rheumatic heart disease in the United States, overzealous emphasis on proper diagnosis and treatment of group A streptococcal pharyngitis in order to prevent these illnesses may often result in a frustrating, anxiety-provoking condition known as "streptococcal neurosis." Physicians, parents, and patients may all suffer from this condition, which often occurs even after all possible and appropriate treatment has been used to eradicate the group A streptococci. "Streptococcal neurosis" and the perplexing problem of treatment failure can be avoided or alleviated by utilizing knowledge of the interrelationship of the human host, the group A streptococcus, and nonsuppurative sequelae.

A practical concern of the working mother is the bacteriostatic quality of human milk over time without benefit of refrigeration. Therefore, quantitative cultures of human milk stored at room temperature were performed at 0, 2, 4, 6, and 24 hours after expression. Milk from 10 mothers less than six days postpartum (colostrum) and from 10 mothers 7 to 42 weeks postpartum (mature milk) was studied. The number of colony-forming units per milliliter of milk cultured at 0 time did not significantly increase in mature milk after 6 hours nor in colostrum after 24 hours of storage at room temperature. Thus, mothers who express milk for their own infants while at work may assume that the bacterial contamination of their milk will not increase significantly for up to but no longer than 6 hours after expression, even if they have no access to refrigeration.

A.S.O. titers were determined in 93 children with various kidney diseases. In addition, 52 children without renal disorders were investigated as controls. In the children with renal disease, 38 suffered from the "idiopathic", "primary" nephrotic syndrome of childhood. Thirteen had acute, post-infectious glomerulonephritis, 16 had "primary" chronic glomerulonephritis, 3 had pyelonephritis, and 1 had disseminated lupus nephritis. In acute glomerulonephritis, with or without N.S., the titers were higher than in the controls, which is known and consistent with the frequency of preceding streptococcal infections. Children with chronic glomerulonephritis, with and without associated N.S., did not show a similar tendency to increased values. All patients but one with "primary", , "idiopathic" N.S. of childhood had titers of less than 100. They were between 50 and 12 Todd units. These titers were observed early during the course of the disease and persisted for years in spite of remissions. They were not related to concomitant antimicrobial therapy, nor to corticosteroid administration. In "idiopathic" nephrotic syndrome of childhood a titer of less than 100 does not, in itself, lead to the diagnosis of a N.S. of childhood. However, a greater than 100 titer speaks against it and may well serve as a valid indication for a renal biopsy, in order to differentiate this disease from acute glomerulonephritis, and also from R.P.G.N. whenever they are associated with a N.S. The low titers are only of value in differentiating the "primary" form of the N.S. from the "secondary" forms which are preceded by chronic renal disease or which are due to another underlying, systemic disease. In nephrotic children less than 6 years of age, the less than 100 A.S.O. titers may also be due to their age.