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Summary: 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 ≥ 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 C for 30 minutes.Speculation: The serum of cystic fibrosis patients selectively inhibits alveolar macrophage function in vitro; the expression of this inhibitory activity in vivo may compromise effective host control of infection. Investigation of the origin, nature and pathophysiologic role of the activity may suggest new approaches to the control of Pseudomonas pulmonary infection.Pultionary infection is a major factor in the morbidity and mortality associated with cystic fibrosis (CF) (6). Pseudomonas, a uhrquitous organism in the environment, is cystic fibrosis (CF) (6). Pseudomonas, a uhrquitous organism in the environment, is usually not pathogenic for healthy individuals. However, individuals with the chronic lung disease of CF are particularly susceptible to opportunistic Pseudomonas aeruginosa infections. The frequency of this organism in CF pulmonary infections is inadequately explained. It is well known that most CF patients have elevated levels of Pseudomonas antibodies in their sera and pulmonary secretions (l2,14). While recently there has been an indication that a lymphocyte unresponsiveness to Pseudomonas may be acquired as the infection progresses (18,19), no other immunologic abnormality has been consistendy observed (5.10). Extrapulmonary infection is extremely rare and sepsis is almost never, seen after the first months of life (22). This unusual susceptibility to Pseudomonas despite apparently normal systemic humoral and cellular immunity. suggests that local pulmonary host defense mechanisms are defective in CF. Several recent studies have indicated that lung defenses can, to a certain extent, function independently of systemic humoral and cell mediated immune systems (9,15,20,21).Lung defenses include mucociliary transport as well as phagocytic cells, lymphocytes, and immunoglobulin secretion. Since mucociliary transport in some CF patients is compromised (5). clearing of the bacteria becomes more dependent on the efficient action of the phagocytic cells. Previous studies in our laboratory (2) and by Biggar, et al. (I) have shown that CF serum impairs phagocytosis of Pseudomonas by rabbit alveolar macrophages. This report presents experimental observations indicating the presence of an inhibitory activity in CF serum which impairs phagocytosis of Pseudomonas by human as well as rabbit alveolar macrophages.

The complex, frustrating problem of the failure to eradicate group A streptococci in a patient with streptococcal pharyngitis even after appropriate treatment and apparent clinical recovery is explored. Utilizing knowledge of the interrelationship of the human host, the group A streptococcus, and nonsuppurative sequelae is suggested as a means to alleviate or avoid “streptococcal neurosis” and the problem of treatment failure.

Summary: 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 seram. 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.Speculation: Functional and morphologic observations indicate that cystic fibrosis alveolar macrophages are not providing an adequate phagocytic defense against Pseudomonas. This defective phagocytosis does not appear to arise from an intrinsic problem with the macrophages, but rather appears to be due to extrinsic factors, i.e.. an altered lung environment together with a substance(s) present in cystic fibrosis serum which selectively inhibit Pseudomonas phagocytosis.

IN THE prechemotherapeutic era gonococcal arthritis in the newborn Was not uncommon.1,2 In 1905, Holt reviewed 26 cases in children from Babies Hospital in New York, two of which had occurred in neonates, and one of these patients had associated conjunctivitis.1 In 1927, Cooperman reported 53 cases out of 182 births in an outbreak in the newborn nursery of a maternity hospital in Philadelphia.2 It was unclear who was the original source of the infection, but it was most likely introduced into the nursery through an infant who had some of the contaminated discharges on its body. The disease was then disseminated unknowingly to the other infants probably by means of contaminated rectal thermometers, wash basins, or laundry. Since then only occasional reports have appeared.3-6 This is in contrast to neonatal gonococcal ophthalmia in thechemotherapeutic era; the highest rate for those who received no treatment at

THIS REPORT presents the evaluation of a prematurely born male infant who was infected with herpes simplex virus (HSV) near or at term and who developed generalized infection with central nervous system involvement and chorioretinitis. At 4 months of age he was recognized to have adrenocortical insufficiency. His unique clinical presentation, together with the prospective accumulation of relevant ophthalmologic, virologic, and metabolic findings prompted this report.The isolation of HSV from CSF served to help establish the pathogenesis of his eye lesions. Although the adrenal cortices of infants having generalized herpes simplex infection have been judged to be infected,1-3 functional impairment of this organ has not been recorded previously. REPORT OF A CASE The patient was born on March 17, 1964, after a 34-week gestation of a 21-year-old woman who had developed extensive genital herpes simplex infection, first noted 20 days prior to delivery. After meconium-stained amniotic fluid was noted

MIGRATORY polyarthritis as a complication of mumps is a rare entity which is merely mentioned in textbooks and described in detail only in the adult medical and foreign literature.1-4We know that acute rheumatic fever may be a frequently over-diagnosed disease,5 and that therefore many children are unnecessarily subjected to a long-term program of antibiotic prophylaxis which may be expensive, inconvenient, and frequently psychologically damaging. The arthritis observed in mumps is self-limited and resolves completely without any residual joint damage or recurrence. Its importance to pediatricians lies in differentiating this entity from the polyarthritis of acute rheumatic fever.Despite its application to pediatrics, the association of mumps and arthritis has not been described in the pediatric literature. This can probably be explained by the fact that the great majority of the 19 cases reported in detail have occurred in adults.The following report illustrates the association of arthritis

US military recruits receive benzathine penicillin prophylaxis because of endemicity of group A β-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 ∼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.