Volume 121 Number 1

E d i t o r i a l correspondence

suits; warming the saline solution to 37 ~ C wilI help reduce the risk of inducing bronchospasm when performing the lavage. M. L. Everard, M R C P Lecturer in Child Health Department o f Child Health Queens Medical Centre Nottingham NG2 5AN, United Kingdom

A. D. Milner, FRCP Professor o f neonatology Department o f Pediatrics St. Thomas's Hospital London S E l 7EH, United Kingdom REFERENCES

I. Derish MT, Kulbanjian JA, Frankel LR, Smith DW. Value of bronchoalveolar lavage in diagnosing severe respiratory syncytial virus infections in infants. J PEDIATR 1991; 119:761- 3. 2. Domurat F, Roberts N J, Walsh EE, Dagan R. Respiratory syncytial virus infection of human mononuclear [eukocytes in vitro and in vivo. J Infect Dis 1985;152:895-902. 3. Midulla F, Huang YT, Gilbert IA, Cirino N M , McFadden ER, Panuska JR. Respiratory syncytial virus infection of human cord and adult blood monocytes and alveolar macrophages. Am Res Respir Dis 1989;140:77i-7.

Reply To the Editor: We appreciate Dr. Lipson's and Dr. Krilov's concern about the temporal relationship between our nasopharyngeal (NP) specimens and our bronchoalveolar lavage (BAL) specimens. Because our initial results with BAL were of clinical importance, but an actual study had not been planned, we did not resubmit N P swab specimens for direct fluorescent antibody (DFA) and viral culture after the BAL specimens showed a positive reaction. Our original article bad a table that was deleted, at the Editor's request, for the sake of brevity. This table gave dates of cultures; the longest time lapse between collection of an NP specimen and collection of a BAL specimen was 1 day, because if patients' initial N P specimen had no respiratory syncytial virus (RSV), another N P specimen was obtained a few days later. When these culture and DFA results proved negative as well, then diagnostic BAL was the next step. Since publication of this article, we have had two more critically ill patients receiving mechanical ventilation whose NP swab cultures were negative and whose BAL specimens were positive for RSV. These patients all had NP swab specimens obtained at referring hospitals and then at our hospital before BAL. Additional NP swab specimens were obtained after the BAL specimens were found to have RSV. Although all BAL specimens were positive, all NP swab specimens had negative culture and DFA results. One of us (D.W.S.) has moved to another large pediatric intensive care unit and has seen two additional patients whose clinical course indicated a possible RSV infection, but whose N P swab specimens had no RSV; within l day, culture of a BAL specimen was positive for RSV. The second point raised was that we were "attempting to justify

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the use of N P swab collection." We were not; rather, a brief review of N P swab and nasal aspirate sensitivity and specificity seemed relevant as a baseline to discussing missed RSV infection diagnoses. We do use N P swabs in our institution. Our laboratory will process an NP swab for DFA and culture only if the slides show adequate numbers of ciliated epithelial cells when screened by phase microscopy, as pointed out in our Methods section. By using this screening technique, we have attained an acceptable DFA sensitivity. Any intensive care clinician has cared for many RSV-infected infants with severe lower respiratory tract disease along with, or separate from, bronchiolitis. Although wandering atelectasis is a hallmark of the disease, for many patients serial chest radiographs show persistent pneumonia. The entire conclusion of the pathology study quoted by Lipson and Kritov was as follows: "In our study of respiratory deaths we noted how easily R.S. virus could be isolated from the lungs in pneumonia and how difficult this was in bronchiolitis. ''1 Thus we agree with this early study by Gardner et al., and indeed they may be describing some of the same patients in whom RSV is detected only if BAL is done. Gardner's speculation in 1970 is similar to ours: Are there some RSV-infected infants who have the bulk of infection in their lower respiratory tract? We must point out an error: The next to last sentence of our article's introduction says that "influenza A and B viruses, RSV, and parainfluenza virus were not detected on routine bacterial cultures and NP DFA assay." The word should be viral. Melinda T. Derish, MD Lorry R. Frankel, MD Department o f Pediatrics Division o f Critical Care Medicine Julie T. Kulhanijian, MD Department o f Pediatrics Division o f Infectious Diseases Stanford University School of Medicine Stanford, CA 94305

David W. Smith, MB, ChB Pediatric Intensive Care Sutter Memorial Hospital Sacramento, CA 95819 REFERENCE

1. Gardner PS, McQuillin J, Court SDM. Speculation of pathogenesis in death from respiratory syncytial virus infection. BMJ 1970;1:327-30.

Group B streptococcal latex agglutination testing in neonates To the Editor." I read with interest the article by Ascher et al. t These authors reported on six neonates with sterile blood cultures and urine specimens with a positive latex particle agglutination (LPA) reaction to group B streptococcus (GBS). They speculated that GBS anti-

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Editorial correspondence

The Journal of Pediatrics July 1992

gen was absorbed from the gastrointestinal tract and excreted in the urine. In 1991, ten neonates admitted to our neonatal intensive care unit had positive LPA reactions to GBS in the cerebrospinal fluid specimen. Four of these neonates had sterile cerebrospinal fluid cultures, and the urine specimens from two of these four had positive LPA reactions to GBS. These four neonates also had sterile blood and urine cultures but were treated for GBS meningitis. It is possible that these neonates also had GBS antigen in the cerebrospinal fluid and urine without the organism. Although a positive urine LPA reaction, with cultures remaining sterile, is not uncommon, a positive cerebrospinal fluid LPA reaction with sterile cultures is rare. 2 Until better tests are available to differentiate between infectious and noninfectious presence of antigen in the cerebrospinal fluid, it appears prudent to consider a diagnosis of meningitis whenever the CSF LPA reaction is positive for GBS.

These cases underscore the possible causes of LPA+CSF - status, although most of the reported infants also had abnormal CSF findings, or blood or urine LPA positive reactions. The sensitivity of GBS CSF LPA is reported to range from 105 to 107 colonyforming units (CFU) of GBS per milliliter) The sensitivity of the Gram stain is also dependent on the number of organisms: 60% with 103 to 105 C F U / m l , and 97% with >105 C F U / m l , 6 although there have not been comparison studies between LPA and Gram stain. We agree with Dr. Rathore that the infant with a positive CSF LPA reaction but a sterile CSF culture is uncommon, and it appears prudent to consider a diagnosis of meningitis whenever CSF LPA reactions are positive for GBS.

David P. Ascher, MD Department of Pediatrics Wilford Hall Medical Center San Antonio, TX 78236

Mobeen H. Rathore, MD Department of Pediatrics University of Florida Health Science Center Jacksonville, FL 32209 REFERENCES

1. Ascher DP, Wilson S, Mendiola J, Fischer GW. Group B streptococcal latex agglutination testing in neonates. J PEDIATR 1991;119:458-61. 2. Sfinchez P J, Seigel JD, Cushion NB, Threlkeld N. Significance of a positive urine group B streptococcal latex agglutination test in neonates. J PEDIATR 1990;116:601-6.

Reply To the Editor: Dr. Rathore reports four neonates who had sterile urine, blood, and cerebrospinal fluid (CSF) cultures with positive latex particle agglutination (LPA) reactions to group B streptococcus (GBS) on cerebrospinal fluid (CSF) specimens. The several possible explanations for the clinical situation when the GBS CSF LPA is positive and the CSF culture is negative for GBS (LPA+CSF - ) include the following: (I) Nonspecific agglutination with LPA can occur from high protein concentration, which may require heat treatment. (2) Other bacteria may have antigens that cross-react with GBS (e.g., pneumococci, group G streptococci, proteus). (3) Intrapartum antibiotics may sterilize cultures, but sufficient GBS antigen may persist to be detected by LPA. (4) A traumatic bloody lumbar puncture may result in serum antigen detection. (5) Culture-negative GBS infection may be present. It is not known whether putative GBS antigen absorption from the gastrointestinal tract in the absence of infection can diffuse into the CSF. 1 Blecker et al. 2 reported on one infant who had a blood culture positive for GBS and a sterile CSF culture but ~h~6 had a CSF LPA that was positive. Friedman et al) reported on three infants who were GBS LPA+CSF -. One of these infants had a CSF culture positive for GGS; the two others had CSF pleocytosis, one of whom had had prior treatment with antibiotics. Rabalais et al. 4 reported on two LPA+CSF - infants, one of whom had GBS LPA positive urine, CSF, and sera and had not been pretreated with antibiotics.

Gerald W. Fischer, MD Department of Pediatrics Uniformed Services University Bethesda, MD 20814 REFERENCES

1. Ascher DP, Wilson S, Mendiola J, Fischer GW. Group B streptococcal latex agglutination testing in neonates. J PEDIATR 1991;119:458-61. 2. Blecker DL, Zimbro M J, Erbe MB, Mortensen JE. Polyclonal anti-group B streptococcus latex antigen detection test. Pediatr Infect Dis J 1989;8:251-2. 3. Friedman CA, Wender DF, Rawson JE. Rapid diagnosis of group B streptococcal infection utilizing a commercially available latex agglutination assay. Pediatrics 1984;73:27-30. 4. Rabalais GP, Bronfin DR, Daum RS. Evaluation of a commercially available latex agglutination test for rapid diagnosis of group B streptococcal infection. Pediatr Infect Dis J 1987;6:177-81. 5. Ascber DP, Wilson S, Fischer GW. Comparison of commercially available group B streptococcal agglutination assays. J Clin Microbiol 1991;29:2895-6. 6. LaScolea LJ Jr, Dryja D. Quantitation of bacteria in cerebrospinal fluid and blood of children with meningitis and its diagnostic significance. J Clin Microbiol 1984;19:187-90.

Intrapartum asphyxia and cerebral palsy To the Edito'r: Our article "Intrapartum Asphyxia: A Rare Cause of Cerebral Palsy ''1 concluded that "in only 8.2% (of spastic cerebral palsy [CP] cases) was it thought possible or very likely that the recorded events in and around delivery were the cause of the CP." We now present a pedigree (Figure) in which subject IV.1 was one of the nine cases of CP assessed as verylikely to be caused by birth asphyxia. This pedigree was collected during a subsequent study of moderate and severe quadriplegia that included only 5 of the 15 cases originally assessed as having a reasonable likelihood

Group B streptococcal latex agglutination testing in neonates.

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