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“Nonpathogenic” Neisseria and meningitis
10 12
Editorial correspondence
Sodium overload from Karo syrup To the Editor: The clinical report by Hopp and WoodrutP of an infant who received a "sodium overload" from Karo syrup is flawed, both in its content and conclusions. The sodium content of dark Karo syrup presented by the authors, (980 mg sodium/480 ml, or 89 mEq/l) is over twice the content indicated in a standard reference of food composition 2 (68 mg sodium/100 gm, or 39.4 mEq/l). This source gives values for sodium in sugar syrups which vary from negligible quantities up to 55 mEq/l for blackstrap molasses. Even the authors' unsubstantiated value indicates only a modest sodium content in Karo in relation to calories fed. The authors provide no clear data on the infant's daily Karo intake. If I assume this infant received 85 mEq of sodium from Karo over a two-week period (955 ml Karo total; 68 ml/day or 14 teaspoonsauthors' value for sodium in Karo assumed), then he received 6 mEq sodium from Karo daily. Since daily total sodium was t5 mEq, 9 was from formula. This required ingestion of 818 ml formula daily. Assuming an average weight of 3.4 kg, total daily intake was 240 ml of formula, 20 ml Karo, and 240 kCal/kg. This is fairly gross overfeeding, especially with calories, but did not receive comment by the authors. The sodium load totals 4.4 mEq/kg daily on this intake, but would be only 3.4 mEq/kg if the reference value for sodium in Karo obtains. Also, since 60% of the sodium is from the formula, why blame the Karo? Finally, the authors .provide no data, and cite none, that daily sodium loads of 4 to 5 mEq/kg will cause generalized edema. The infants studied by Gamble and coworkers ~ received 10 mEq sodium/kg daily for eight days. They showed modest fluid retention but no clinical edema. In a review of salt intake by the Committee on Nutrition of the American Academy of Pediatrics, ' average intakes of 6 mEq/day obtained at age 6 months before 1970, and tolerance of intakes as high as 10 mEq/kg in infancy is implied. Karo has been around a long time. It is a safe and effective caloric supplement to evaporated milk formulas. It is my opinion that overdosage with Karo would produce diarrhea before salt overload. Michael K. Wald, M.D., EA.A.P. Ebnira Medical Arts Center Elmira, N Y 14901 REFERENCES
1. Hopp R, and Wooruff C: Sodium overload from Karo syrup, J PEDIATR 93:883, 1978. 2. Watt BK, and Merrill AL: Composition of foods. Agriculture Handbook No. 8 Washington, DC, U. S. Government Printing Office. 3. Gamble JL, Wallace WM, et al: Effects o~r large loads of electrolytes, Pediatrics 7:305, 1951. 4. American Academy of Pediatrics Committee on Nutrition, Holliday MA chairman; Salt intake and eating patterns of infants and children in relation to blood pressure, Pediatrics 53:115, 1974.
The Journal of Pediatrics June 1979
RepZy To the Editor: Since the introduction of nutritional labeling of foods in 1973, information listed on the label of a specific product is the most reliable source for its nutrient content. The data we reported was obtained from the label in 1978, rather than from data for all such products published in 1963. The reason for reporting this unusual result from an accidentally large overdose of a product commonly used in infant feeding was to emphasize two facts. (1) That dark Karo syrup contains 89 mEq/l of sodium and (2) that about 5 mEq/kg/day of sodium for two weeks can result in edema although the majority of infants do not retain sodium on intakes even larger. The infant's intake was apparently high in both volume and calories, as Dr. Wald points out. This may also be within outside limits of normal variation. Infants under 41 days of age tend to control their intake by volume rather than calories; older infants tend to do the opposite. 1 The dramatic disappearance of his scrotal and periorbital edema in 36 hours after restricting both fluid and sodium intakes could only be interpreted as isotonic expansion of the extracellular space. A similar edematous episode in a 7V2-week-old infant of 35 weeks' gestation has been brought to my attention by Drs. L. Cohen and M. Stein of the St. Vincent Family Practice Program in Indianapolis, Ind. Russell Hopp, D.O. Calvin Woodruff, M.D. Department o f ChiM Health School of Medicine University of Missouri-Columbia Columbia, MO 65201 REFERENCE
1. Foman SI: Infant nutrition, ed 2, Philadelphia, 1974, WB Saunders, p 28.
"Nonpathogenic" Neisseria and meningitis To the Editor: A case of Neisseria lactamica meningitis in an infant was recently described by Greenberg and Kleinerman.' We have recently encountered another example of meningitis due to a chromogenic Neisseria species. CASE REPORT A 14-year-old boy was admitted to the hospital with fever, myalgia, and nuchal rigidity. On examination, he had pharyngitis and nuchal rigidity. CSF examination revealed 63 WBC/mm:' (72% polys); CSF protein and glucose were normal; no organisms were seen. The patient was treated with penicillin iv for 72 hours. At that time the examination was normal, WBC 5,300, and all
Volume 94 Number 6
Editorial correspondence
cultures were sterile. Twenty-four hours later, a chromogenic, oxidase-positive, gram-negative diplococcus was isolated from one of three blood cultures. The microbiologic characteristics were those of a Neisseria sp. but not consistent with N. meningitidis. A repeat blood culture, off antibiotic therapy, was sterile. The patient was discharged, asymptomatic. Three weeks later he presented with fever and abdominal pain. Examination revealed only mild guarding of the abdomen. Soon after admission he developed headache and nuchal rigidity. CSF examination showed 20,130 WBCs, protein 224 MG/dl, and no glucose. Intracellular gram-negative diplococci were seen. The patient was treated with penicillin and chloramphenicol iv and did well. A single colony of a gram-negative, oxidase positive, chromogenic Neisseria was isolated from one of two blood cultures after seven days. A presumptive identification of Neisseria perflava was made but could not be confirmed due to low viability of the organism. Sinus and mastoid radiographs were normal. Computerized axial tomography of the head and a radioisotope brain scan were also normal. CSF culture did not grow the organism. This case is a reminder that the chromogenic Neisseria species may be pathogens. 2 Richard L. Weiner, M.D. Coordinator, Pediatric Medical Education New Rochelle Hospital Medical Center Instructor in Pediatrics Albert Einstein College of Medicine 1165 Morris Park Ave. Bronx, N Y 1046I
holding o f antihistamine medication for 48 hours, and withholding of sodium cromoglycate for 24 hours. Mitchell et al ~ withheld antihistamine agents for 24 hours and sodium cromoglycate for 12 hours preceding each bronchial challenge. Fig. 2 of the current work 1 shows greater than complete reversibility back to baseline in the asthmatic group and a return to 90% of baseline in the CF group. One can interpret these data as suggesting a common reversible component in both patient groups, and perhaps a common denominator in mechanism. Table III shows that the P value of the data presented in Fig. 2 is < 0.001. Bronchial hyperreactivity is a complicated issue, with multiple etiologic triggers? Because of certain problems with baseline measurements and withholding of medication, it seems that the conclusion of Mitchell et al may not be well supported. The data showing significant reversibility would lead one to believe that there might be a common mechanism in the bronchial hyperreactivity seen in the two patient groups. Lawrence S. Mihalas, M.D. Clinical Instructor Department of Pediatrics UCLA School of Medicine Los Angeles, CA 90024 REFERENCES 1.
2. REFERENCES 1.
Greenberg LW, and Kleinerman E: Neisseria lactamica meningitis, J PEDIATR 93:1061, 1978. Gold R, Goldschneider I, Lepow ML, Draper TF, and Randolph M: Carriage of Neisseria meningitidis and Neisseria lactamica in infants and children, J Infect Dis 137:112, 1978.
Bronchial hyperreactivity in cystic fibrosis To the Editor Mitchell and co-workers 1 conclude that bronchial hyperreactivity is common in cystic fibrosis (CF) but is different from that in asthma (A). Their data were interesting, but I do not agree with their conclusion. A baseline forced expiratory volume in one second (FEV1) of at least 80% of the average best FEV~ was required in order to qualify for bronchial challenge by the method of Spector and Farr? Chai et al 3 similarly have stressed the importance of a baseline FEV 1 o f at least 80% of the highest previously observed value. In the current work, ~ Fig. 1 gives the distribution of baseline FEV~ values in CF patients to be 10 to 120% of predicted. Chai et aV have recommended a prebronchial challenge with-
10 13
3.
Mitchell I, Corey M, Woenne R, Krastins IRB, and Levison H: Bronchial hyperreactivity in cystic fibrosis and asthma, J PEDIAIR 93:744, 1978. Spector SL, Farr RS: Bronchial inhalation procedures in asthmatics, Med Clin North Am 58:71, 1974. Chai H, Farr RS, Froehlich LA, et al: Standardization of bronchial inhalation challenge procedures J Allergy Clin Immunol 56:323, 1975.
Reply To the Editor: The bronchial challenges were performed according to the method of Chai et al, except that many of our patients had a baseline FEV1 less than 80% predicted. We felt justified in studying those patients with a low baseline F E V , since a subject's bronchial response to methacholine remains stable even if there is moderate fluctuation both in initial specific airway conductance and in the severity of the disease. ~ It is difficult to know how long to withhold a drug before bronchial challenge, but the same restrictions were placed on all subjects. We feel, therefore, that withholding the drug for a longer period would not have affected the comparisons. Although there might be a common underlying mechanism in bronchial hyperreactivity in asthma and cystic fibrosis, our data showed a number o f differences between the two groups of patients. Both the subjects with asthma and those with cystic fibrosis showed reversibility. As Mihalas pointed out, the asthmatic patients achieved a mean FEV~ at the end of the study greater than their baseline value, whereas the patients with cystic fibrosis did not quite reach their baseline value. There were other
Editorial correspondence
Sodium overload from Karo syrup To the Editor: The clinical report by Hopp and WoodrutP of an infant who received a "sodium overload" from Karo syrup is flawed, both in its content and conclusions. The sodium content of dark Karo syrup presented by the authors, (980 mg sodium/480 ml, or 89 mEq/l) is over twice the content indicated in a standard reference of food composition 2 (68 mg sodium/100 gm, or 39.4 mEq/l). This source gives values for sodium in sugar syrups which vary from negligible quantities up to 55 mEq/l for blackstrap molasses. Even the authors' unsubstantiated value indicates only a modest sodium content in Karo in relation to calories fed. The authors provide no clear data on the infant's daily Karo intake. If I assume this infant received 85 mEq of sodium from Karo over a two-week period (955 ml Karo total; 68 ml/day or 14 teaspoonsauthors' value for sodium in Karo assumed), then he received 6 mEq sodium from Karo daily. Since daily total sodium was t5 mEq, 9 was from formula. This required ingestion of 818 ml formula daily. Assuming an average weight of 3.4 kg, total daily intake was 240 ml of formula, 20 ml Karo, and 240 kCal/kg. This is fairly gross overfeeding, especially with calories, but did not receive comment by the authors. The sodium load totals 4.4 mEq/kg daily on this intake, but would be only 3.4 mEq/kg if the reference value for sodium in Karo obtains. Also, since 60% of the sodium is from the formula, why blame the Karo? Finally, the authors .provide no data, and cite none, that daily sodium loads of 4 to 5 mEq/kg will cause generalized edema. The infants studied by Gamble and coworkers ~ received 10 mEq sodium/kg daily for eight days. They showed modest fluid retention but no clinical edema. In a review of salt intake by the Committee on Nutrition of the American Academy of Pediatrics, ' average intakes of 6 mEq/day obtained at age 6 months before 1970, and tolerance of intakes as high as 10 mEq/kg in infancy is implied. Karo has been around a long time. It is a safe and effective caloric supplement to evaporated milk formulas. It is my opinion that overdosage with Karo would produce diarrhea before salt overload. Michael K. Wald, M.D., EA.A.P. Ebnira Medical Arts Center Elmira, N Y 14901 REFERENCES
1. Hopp R, and Wooruff C: Sodium overload from Karo syrup, J PEDIATR 93:883, 1978. 2. Watt BK, and Merrill AL: Composition of foods. Agriculture Handbook No. 8 Washington, DC, U. S. Government Printing Office. 3. Gamble JL, Wallace WM, et al: Effects o~r large loads of electrolytes, Pediatrics 7:305, 1951. 4. American Academy of Pediatrics Committee on Nutrition, Holliday MA chairman; Salt intake and eating patterns of infants and children in relation to blood pressure, Pediatrics 53:115, 1974.
The Journal of Pediatrics June 1979
RepZy To the Editor: Since the introduction of nutritional labeling of foods in 1973, information listed on the label of a specific product is the most reliable source for its nutrient content. The data we reported was obtained from the label in 1978, rather than from data for all such products published in 1963. The reason for reporting this unusual result from an accidentally large overdose of a product commonly used in infant feeding was to emphasize two facts. (1) That dark Karo syrup contains 89 mEq/l of sodium and (2) that about 5 mEq/kg/day of sodium for two weeks can result in edema although the majority of infants do not retain sodium on intakes even larger. The infant's intake was apparently high in both volume and calories, as Dr. Wald points out. This may also be within outside limits of normal variation. Infants under 41 days of age tend to control their intake by volume rather than calories; older infants tend to do the opposite. 1 The dramatic disappearance of his scrotal and periorbital edema in 36 hours after restricting both fluid and sodium intakes could only be interpreted as isotonic expansion of the extracellular space. A similar edematous episode in a 7V2-week-old infant of 35 weeks' gestation has been brought to my attention by Drs. L. Cohen and M. Stein of the St. Vincent Family Practice Program in Indianapolis, Ind. Russell Hopp, D.O. Calvin Woodruff, M.D. Department o f ChiM Health School of Medicine University of Missouri-Columbia Columbia, MO 65201 REFERENCE
1. Foman SI: Infant nutrition, ed 2, Philadelphia, 1974, WB Saunders, p 28.
"Nonpathogenic" Neisseria and meningitis To the Editor: A case of Neisseria lactamica meningitis in an infant was recently described by Greenberg and Kleinerman.' We have recently encountered another example of meningitis due to a chromogenic Neisseria species. CASE REPORT A 14-year-old boy was admitted to the hospital with fever, myalgia, and nuchal rigidity. On examination, he had pharyngitis and nuchal rigidity. CSF examination revealed 63 WBC/mm:' (72% polys); CSF protein and glucose were normal; no organisms were seen. The patient was treated with penicillin iv for 72 hours. At that time the examination was normal, WBC 5,300, and all
Volume 94 Number 6
Editorial correspondence
cultures were sterile. Twenty-four hours later, a chromogenic, oxidase-positive, gram-negative diplococcus was isolated from one of three blood cultures. The microbiologic characteristics were those of a Neisseria sp. but not consistent with N. meningitidis. A repeat blood culture, off antibiotic therapy, was sterile. The patient was discharged, asymptomatic. Three weeks later he presented with fever and abdominal pain. Examination revealed only mild guarding of the abdomen. Soon after admission he developed headache and nuchal rigidity. CSF examination showed 20,130 WBCs, protein 224 MG/dl, and no glucose. Intracellular gram-negative diplococci were seen. The patient was treated with penicillin and chloramphenicol iv and did well. A single colony of a gram-negative, oxidase positive, chromogenic Neisseria was isolated from one of two blood cultures after seven days. A presumptive identification of Neisseria perflava was made but could not be confirmed due to low viability of the organism. Sinus and mastoid radiographs were normal. Computerized axial tomography of the head and a radioisotope brain scan were also normal. CSF culture did not grow the organism. This case is a reminder that the chromogenic Neisseria species may be pathogens. 2 Richard L. Weiner, M.D. Coordinator, Pediatric Medical Education New Rochelle Hospital Medical Center Instructor in Pediatrics Albert Einstein College of Medicine 1165 Morris Park Ave. Bronx, N Y 1046I
holding o f antihistamine medication for 48 hours, and withholding of sodium cromoglycate for 24 hours. Mitchell et al ~ withheld antihistamine agents for 24 hours and sodium cromoglycate for 12 hours preceding each bronchial challenge. Fig. 2 of the current work 1 shows greater than complete reversibility back to baseline in the asthmatic group and a return to 90% of baseline in the CF group. One can interpret these data as suggesting a common reversible component in both patient groups, and perhaps a common denominator in mechanism. Table III shows that the P value of the data presented in Fig. 2 is < 0.001. Bronchial hyperreactivity is a complicated issue, with multiple etiologic triggers? Because of certain problems with baseline measurements and withholding of medication, it seems that the conclusion of Mitchell et al may not be well supported. The data showing significant reversibility would lead one to believe that there might be a common mechanism in the bronchial hyperreactivity seen in the two patient groups. Lawrence S. Mihalas, M.D. Clinical Instructor Department of Pediatrics UCLA School of Medicine Los Angeles, CA 90024 REFERENCES 1.
2. REFERENCES 1.
Greenberg LW, and Kleinerman E: Neisseria lactamica meningitis, J PEDIATR 93:1061, 1978. Gold R, Goldschneider I, Lepow ML, Draper TF, and Randolph M: Carriage of Neisseria meningitidis and Neisseria lactamica in infants and children, J Infect Dis 137:112, 1978.
Bronchial hyperreactivity in cystic fibrosis To the Editor Mitchell and co-workers 1 conclude that bronchial hyperreactivity is common in cystic fibrosis (CF) but is different from that in asthma (A). Their data were interesting, but I do not agree with their conclusion. A baseline forced expiratory volume in one second (FEV1) of at least 80% of the average best FEV~ was required in order to qualify for bronchial challenge by the method of Spector and Farr? Chai et al 3 similarly have stressed the importance of a baseline FEV 1 o f at least 80% of the highest previously observed value. In the current work, ~ Fig. 1 gives the distribution of baseline FEV~ values in CF patients to be 10 to 120% of predicted. Chai et aV have recommended a prebronchial challenge with-
10 13
3.
Mitchell I, Corey M, Woenne R, Krastins IRB, and Levison H: Bronchial hyperreactivity in cystic fibrosis and asthma, J PEDIAIR 93:744, 1978. Spector SL, Farr RS: Bronchial inhalation procedures in asthmatics, Med Clin North Am 58:71, 1974. Chai H, Farr RS, Froehlich LA, et al: Standardization of bronchial inhalation challenge procedures J Allergy Clin Immunol 56:323, 1975.
Reply To the Editor: The bronchial challenges were performed according to the method of Chai et al, except that many of our patients had a baseline FEV1 less than 80% predicted. We felt justified in studying those patients with a low baseline F E V , since a subject's bronchial response to methacholine remains stable even if there is moderate fluctuation both in initial specific airway conductance and in the severity of the disease. ~ It is difficult to know how long to withhold a drug before bronchial challenge, but the same restrictions were placed on all subjects. We feel, therefore, that withholding the drug for a longer period would not have affected the comparisons. Although there might be a common underlying mechanism in bronchial hyperreactivity in asthma and cystic fibrosis, our data showed a number o f differences between the two groups of patients. Both the subjects with asthma and those with cystic fibrosis showed reversibility. As Mihalas pointed out, the asthmatic patients achieved a mean FEV~ at the end of the study greater than their baseline value, whereas the patients with cystic fibrosis did not quite reach their baseline value. There were other