episodes. Recommended protocols for the management of parenteral nutri¬ tion'
were
maintained, but it
was
acknowledged that occasional lapses occurred, especially in the routine of changing intravenous tubing. Similar mechanisms explained an outbreak of
Klebsiella infections related to in-use contamination of conventional intra¬ venous fluid in a neonatal intensive care unit."' Parenteral nutrition with soybean oil emulsion remains an effective and safe mode of therapy. However, extreme care must be exercised in the preparation and delivery of all paren¬ teral nutrition solutions.4·" If sepsis due to contaminated fluids is sus pected, guidelines have been compiled to assist in evaluating the circum¬ stances.7
KELLY T. MCKEE, JR, MD Department of Pediatrics M. ANN MELLY, PHD Department of Medicine HARRY L. GREENE, MD Department of Pediatrics WILLIAM SCHAFFNER, MD Department of Medicine
Children's Hospital Vanderbilt University School of Medicine Nashville, TN 37232
1. Melly MA, Meng HC, Schaffner W: Microbial growth in lipid emulsions used in parenteral nutrition. Arch Surg 110:1479-1481, 1975. 2. Allen JR: The incidence of nosocomial infection in patients receiving total parenteral nutrition, in Johnston IDA (ed): Advances in Parenteral Nutrition. Lancaster, England, MTP Press Ltd, 1978, pp 339-377. 3. Silberman H, Freehauf M, Fong G, et al: Parenteral nutrition with lipids. JAMA 238:1380-1382, 1977. 4. Goldmann DA, Maki DG: Infection control in total parenteral nutrition. JAMA 223:1360\x=req-\ 1364, 1973. 5. Ross BS, Peter G, Dempsey JM, et al: Klebsiella pneumoniae nosocomial epidemic in an intensive care nursery due to contaminated intravenous fluid. Am J Dis Child 131:712, 1977. 6. Maki DG: Preventing infection in intravenous therapy. Hosp Prac 11:95-104, 1976. 7. National Coordinating Committee on Large Volume Parenterals: Recommended procedures for in-use testing of large volume parenterals suspected of contamination or of producing a reaction in a patient. Am J Hosp Pharm 35:678\x=req-\ 682, 1978.
Lung Abscess due to influenzae Type C
Haemophilus
Haemophilus influenzae type B is responsible for approximately 95% of serious H influenzae infections in children.1 However, other typeable H
influenzae strains also have been reported to cause serious infections. Types A, E, and F have been isolated
from the CSF of children with meningitis.2-4 Type E has been associated with septic arthritis.5 Types C, D, and F have been isolated from the blood or pleural fluid of adults with pneumonia.6 Sell et al7 recovered H influenzae type C from the nasopharynx of normal children and from Three children with upper respiratory tract illnesses. We report a child in whom H influenzae type C was isolated from a lung abscess.
Report of a Case.\p=m-\A5\m=1/2\-year-old boy by his private physician following a one-day history of fever and abdominal pain. A chest roentgenogram revealed a right lower lobe abscess, and therapy with cloxacillin sodium, 45 mg/kg/day, was initiated. The fever persisted for the next three days and a repeat chest roentgeno¬ was seen
gram indicated an increase in the amount of fluid in the abscess. The patient was admitted for further evaluation. The patient had been in excellent health and had no history of chronic cough, aspi¬
ration,
or
a
previous chest roentgeno¬
gram.
On admission to the hospital, the physi¬ cal examination revealed a rectal tempera¬ ture of 39.2 °C and a respiratory rate of 50/min. Abnormal physical findings were confined to the base of the right lung. This area was dull to percussion, and on auscul¬ tation decreased breath sounds and inspiratory rales were heard. The admission chest roentgenogram at this time (Figure) showed a large abscess with an air fluid level in the right lower lobe. Aspiration of the lung abscess was performed under direct fluoroscopy, and 5 mL of purulent non-foul-smelling material was obtained. Gram stain of this fluid revealed abundant polymorphonuclear leu¬ kocytes and numerous pleomorphic Gramnegative bacilli. Countercurrent immuno-
electrophoresis (CIE) was negative using and antiserum to H influenzae type Streptococcus pneumoniae, but was posi¬
tive with // influenzae type C antiserum. The organism isolated by routine bacterial culture techniques was a Gram-negative pleomorphic rod that required X and V factors for growth and also formed a single precipitin band with influenzae type C antiserum in CIE. Anaerobic, fungal, and mycobacterial cultures of the lung aspirate were negative. Three blood cultures also were sterile. This strain of influenzae type C produced /3-lactamase, and the minimal inhibitory concentration to ampicillin was 12.5 /xg/mL. The minimal inhibitory con¬ centrations to chloramphenicol and cephalothin were 3.125 n¿g/mL and 0.2 µg/mL, respectively. The minimum bactericidal
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/10/2015
Admission genogram fluid level.
posterior-anterior chest roent¬ showing large abscess and air
concentrations to ampicillin, chlorampheni¬ col, and cephalothin were 25.0, 6.25, and 0.8
µg/mL, respectively. The patient initially received nafcillin and gentamicin and then ampicillin, but
remained febrile. When the identification and sensitivities of the organism were available, the antibiotic therapy was changed to chloramphenicol succinate in a dose of 100 mg/kg/day intravenously. Five days after chloramphenicol therapy was initiated, the patient became afebrile. A repeat chest roentgenogram after ten days of chloramphenicol therapy showed a decrease in the size of the lung abscess. After 12 days of chloramphenicol therapy, the patient was discharged, receiving oral cephalexin monohydrate (Reflex) at a dose of 50 mg/kg/day. After two months of therapy the abscess resolved almost entire¬
ly.
Comment.—Lung
abscesses in chil¬
frequently Staphylococcus aureus, H in¬ fluenzae type B, and S Pneumoniae.' We describe a child with a lung abscess due to H influenzae type C. Although severe H influenzae infec¬ tions (especially type B) appear to be increasing in incidence, reports of H influenzae type C infections are extremely limited. Lowe" reported the isolation of H influenzae type C at necropsy from the lungs of an elderly man with pneumonia. Denis et al'" reported meningitis caused by H influenzae type C in four children. To our knowledge, our report is the first known pulmonary infection due to H influenzae type C in a child. The strain of H influenzae type C that was isolated from the lung abscess produced ß-lactamase and was dren with
are
associated most
resistant to ampicillin. In addition, the patient did not have any clinical response to therapy until chloram¬ phenicol therapy was initiated. Cephalexin monohydrate was administered at discharge since this specific orga¬ nism was very sensitive to cephalosporins by tube dilution sensitivity test¬ ing. However, we do not know the value of cephalexin therapy in this particular patient, and we certainly do not recommend cephalosporins in gen¬ eral for the treatment of infections due to H influenzae. Typing of H influenzae strains can be performed by agglutination, immunofluorescent techniques, and CIE; however, certain strains of H influen¬ zae cannot be typed by agglutination because the organism autoagglutinates." The value of CIE for estab¬
etiologic diagnosis rapidly was illustrated by the present case. Type C antigen was detected in the material obtained by lung aspiration. lishing
an
SEIJI KITAGAWA, MD SHELDON L. KAPLAN, MD DAN K. SEILHEIMER, MD Divisions of Infectious Diseases and Pulmonary Medicine Department of Pediatrics Baylor College of Medicine and Texas Children's Hospital Houston, TX 77030
Nicholas E.
pate in the
Tengg, MD, allowed of his patient.
us
to
partici¬
care
1. Weinstein LS: Type b Haemophilus influeninfections in adults. N Engl J Med 282:221\x=req-\ 222, 1970. 2. Fine RN, Kiertz HM, Krieger G: Haemophilus influenzae type A meningitis. J Pediatr 70:962-963, 1967. 3. Buck LL, Douglas GW: Meningitis due to Haemophilus influenzae type E. J Clin Microbiol 4:381, 1976. 4. Gray BM: Meningitis due to Haemophilus influenzae type F. J Pediatr 90:1031, 1977. 5. Harlow M, Chung SMK, Plotkin SA: Haemophilus influenzae septic arthritis in infants and children. Clin Pediatr 14:1146-1149, 1975. 6. Quintiliani R, Hymons PJ: The association of bacteremic Haemophilus influenzae pneumoniae in adults with typeable strains. Am J Med 50:781-786, 1971. 7. Sell SH, Turner DJ, Federspiel CF: Natural zae
infections with Haemophilus influenzae in children: "Types identified," in Sell SHW, Karzon DT (eds): Haemophilus influenzae. Nashville, 1973, Vanderbilt University Press, pp 3-12. 8. Mark PH, Turner JAP: Lung abscess in childhood. Thorax 23:216-220, 1968. 9. Lowe MB: Haemophilus influenzae type C bronchopneumonia. Pathol Bacteriol 88:315-316, 1964. 10. Denis FA, Chiron JP, Cadoz M, et al: Meningitis caused by Haemophilus influenzae type C. J Pediatr 93:1064-1065, 1978. 11. Myhre EB: Typing of Haemophilus influenzae by counterimmunoelectrophoresis. Acta Pathol Microbiol Scand 82:164-166, 1974.
Neonatal Meningococcal and Meningococcemia
Meningitis
Meningococcal meningitis and meningococcemia are relatively common
entities in children. Neonatal menincaused by Neisseria meningitidis is quite rare, however, and the outcome is often fatal. Furthermore, to our knowledge, recovery from meningococcemia has yet to be reported in a neonate. We describe a 2-week-old boy with meningococcemia and meningococcal meningitis whose condition was successfully treated, but in whom a colonized contact was never identified.
gitis
Report of a Case.\p=m-\A2,250-g boy, first of pair of monozygotic twins, was born by spontaneous vaginal delivery after a 38\x=req-\ week gestation to a 31-year-old, gravida 4, para 3 woman. Apgar scores were 7 and 9 at one and five minutes, respectively. A previous full-term pregnancy resulted in the unexplained birth of a stillborn male infant. This pregnancy, labor, and delivery a
unremarkable. The infant was discondition at 7 with his twin brother. He was well until 15 days of age when he was noted to have nasal conges¬ tion. A 3-year-old sibling had bronchitis at this time, and both parents complained of upper respiratory tract infections. The twin was clinically well. Two days later, seven hours after the onset of fever of 40.8 °C, the child was first examined. The examination showed mild, bilateral con¬ junctivitis and right otitis media; however, no nuchal rigidity, irritability, or skin rash was noted. He was immediately admitted to a community hospital. Laboratory studies disclosed the following values: WBCs, 7,900/cu mm, with 18% polymorphonuclear leukocytes, 44% band forms, 20% lympho¬ cytes, 8% monocytes, 1% basophils, and 3% metamyelocytes; hemoglobin, 14 mg/dL; blood glucose, 61 mg/dL. Cerebrospinal fluid showed the following values: WBCs, 100/cu mm (all polymorphonuclear leuko¬ cytes); glucose, 39 mg/dL; protein, 85 mg/ dL. Serum electrolyte level was normal. were
charged in apparently good days of age to his parents,
Gram-negative diplococci were seen on Gram's stain. A diffuse, erythematous rash was seen
at the time the lumbar
puncture
performed and soon became purpuric. Penicillin G potassium and kanamycin sulfate therapy was started, and he was transferred to St Joseph's Hospital and
was
Medical Center, Paterson, NJ. On arrival, he was found to be irritable, with a slightly bulging anterior fontanel, poor peripheral perfusion, and numerous 1 X 1-cm ecchymotic lesions on his lower extremities (Figure). Blood pressure was 70/40 mm Hg; heart rate, 160 beats per minute; and respiratory rate, 50/min. The rest of the physical examination showed no abnormalities, and in particular, there was
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/10/2015
At admission, diffuse purpura area and lower extremities.
on
perineal
other evidence of bleeding. Pertinent laboratory values were as follows: platelets, 249,000/cu mm; prothrombin time, 15.4 seconds; partial thromboplastin time, 54.1 seconds; fibrinogen, 175 mg/dL, with no detectable fibrin-split products. A diagno¬ sis of meningococcal meningitis with meningococcemia and early shock was no
made. The patient was transfused with fresh whole blood (10 mL/kg). Fluids were restricted, and antibiotics were changed to penicillin G potassium (200,000 units/kg/24 hr), gentamicin sulfate (7.5 mg/kg/24 hr), and chloramphenicol sodium succinate (50 mg/kg/24 hr). The hydrocortisone methyl prednisolone sodium succinate (50 mg/kg/ day) was added to the regimen. After 24 hours, there were no new ecchymotic lesions; however, generalized seizure activ¬ ity was noted. Serum electrolyte, glucose, and calcium levels were all normal at this time, and the seizures were controlled with phénobarbital sodium. A repeated lumbar puncture disclosed the following values: WBCs, 373/cu mm, with 52% polymorpho¬ nuclear leukocytes, and 48% lymphocytes; glucose, 79 mg/dL; protein, 117 mg/dL. No organisms were seen on Gram's stain. A culture of this CSF was later reported as
negative.
After 48 hours of treatment, the infant
began to improve, and the remainder of his course was
uneventful. He
was
treated for
days with penicillin alone. The original CSF, conjunctival, throat, and blood cul¬ tures showed meningitidis, group B. Throat cultures performed on the parents and siblings of the patient showed no evidence of meningitidis, and the vagi¬ nal culture taken after delivery from the mother indicated no Neisseria species. 14
There
were no
other known caretakers.
Hospital personnel were not cultured. The patient's parents and 3-year-old sibling were treated prophylactically with rifampin, and the twin with penicillin since rifampin and sulfonamides are contraindicated in newborns. Results of a repeated CSF examination two days after discontin¬ uation of the antibiotic therapy were normal. Follow-up at 8 months of age showed him to be developmentally identi¬ cal to his twin brother. His EEG reported to be normal.
was
Comment—Meningococcal meningi-
were
maintained, but it
was
acknowledged that occasional lapses occurred, especially in the routine of changing intravenous tubing. Similar mechanisms explained an outbreak of
Klebsiella infections related to in-use contamination of conventional intra¬ venous fluid in a neonatal intensive care unit."' Parenteral nutrition with soybean oil emulsion remains an effective and safe mode of therapy. However, extreme care must be exercised in the preparation and delivery of all paren¬ teral nutrition solutions.4·" If sepsis due to contaminated fluids is sus pected, guidelines have been compiled to assist in evaluating the circum¬ stances.7
KELLY T. MCKEE, JR, MD Department of Pediatrics M. ANN MELLY, PHD Department of Medicine HARRY L. GREENE, MD Department of Pediatrics WILLIAM SCHAFFNER, MD Department of Medicine
Children's Hospital Vanderbilt University School of Medicine Nashville, TN 37232
1. Melly MA, Meng HC, Schaffner W: Microbial growth in lipid emulsions used in parenteral nutrition. Arch Surg 110:1479-1481, 1975. 2. Allen JR: The incidence of nosocomial infection in patients receiving total parenteral nutrition, in Johnston IDA (ed): Advances in Parenteral Nutrition. Lancaster, England, MTP Press Ltd, 1978, pp 339-377. 3. Silberman H, Freehauf M, Fong G, et al: Parenteral nutrition with lipids. JAMA 238:1380-1382, 1977. 4. Goldmann DA, Maki DG: Infection control in total parenteral nutrition. JAMA 223:1360\x=req-\ 1364, 1973. 5. Ross BS, Peter G, Dempsey JM, et al: Klebsiella pneumoniae nosocomial epidemic in an intensive care nursery due to contaminated intravenous fluid. Am J Dis Child 131:712, 1977. 6. Maki DG: Preventing infection in intravenous therapy. Hosp Prac 11:95-104, 1976. 7. National Coordinating Committee on Large Volume Parenterals: Recommended procedures for in-use testing of large volume parenterals suspected of contamination or of producing a reaction in a patient. Am J Hosp Pharm 35:678\x=req-\ 682, 1978.
Lung Abscess due to influenzae Type C
Haemophilus
Haemophilus influenzae type B is responsible for approximately 95% of serious H influenzae infections in children.1 However, other typeable H
influenzae strains also have been reported to cause serious infections. Types A, E, and F have been isolated
from the CSF of children with meningitis.2-4 Type E has been associated with septic arthritis.5 Types C, D, and F have been isolated from the blood or pleural fluid of adults with pneumonia.6 Sell et al7 recovered H influenzae type C from the nasopharynx of normal children and from Three children with upper respiratory tract illnesses. We report a child in whom H influenzae type C was isolated from a lung abscess.
Report of a Case.\p=m-\A5\m=1/2\-year-old boy by his private physician following a one-day history of fever and abdominal pain. A chest roentgenogram revealed a right lower lobe abscess, and therapy with cloxacillin sodium, 45 mg/kg/day, was initiated. The fever persisted for the next three days and a repeat chest roentgeno¬ was seen
gram indicated an increase in the amount of fluid in the abscess. The patient was admitted for further evaluation. The patient had been in excellent health and had no history of chronic cough, aspi¬
ration,
or
a
previous chest roentgeno¬
gram.
On admission to the hospital, the physi¬ cal examination revealed a rectal tempera¬ ture of 39.2 °C and a respiratory rate of 50/min. Abnormal physical findings were confined to the base of the right lung. This area was dull to percussion, and on auscul¬ tation decreased breath sounds and inspiratory rales were heard. The admission chest roentgenogram at this time (Figure) showed a large abscess with an air fluid level in the right lower lobe. Aspiration of the lung abscess was performed under direct fluoroscopy, and 5 mL of purulent non-foul-smelling material was obtained. Gram stain of this fluid revealed abundant polymorphonuclear leu¬ kocytes and numerous pleomorphic Gramnegative bacilli. Countercurrent immuno-
electrophoresis (CIE) was negative using and antiserum to H influenzae type Streptococcus pneumoniae, but was posi¬
tive with // influenzae type C antiserum. The organism isolated by routine bacterial culture techniques was a Gram-negative pleomorphic rod that required X and V factors for growth and also formed a single precipitin band with influenzae type C antiserum in CIE. Anaerobic, fungal, and mycobacterial cultures of the lung aspirate were negative. Three blood cultures also were sterile. This strain of influenzae type C produced /3-lactamase, and the minimal inhibitory concentration to ampicillin was 12.5 /xg/mL. The minimal inhibitory con¬ centrations to chloramphenicol and cephalothin were 3.125 n¿g/mL and 0.2 µg/mL, respectively. The minimum bactericidal
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/10/2015
Admission genogram fluid level.
posterior-anterior chest roent¬ showing large abscess and air
concentrations to ampicillin, chlorampheni¬ col, and cephalothin were 25.0, 6.25, and 0.8
µg/mL, respectively. The patient initially received nafcillin and gentamicin and then ampicillin, but
remained febrile. When the identification and sensitivities of the organism were available, the antibiotic therapy was changed to chloramphenicol succinate in a dose of 100 mg/kg/day intravenously. Five days after chloramphenicol therapy was initiated, the patient became afebrile. A repeat chest roentgenogram after ten days of chloramphenicol therapy showed a decrease in the size of the lung abscess. After 12 days of chloramphenicol therapy, the patient was discharged, receiving oral cephalexin monohydrate (Reflex) at a dose of 50 mg/kg/day. After two months of therapy the abscess resolved almost entire¬
ly.
Comment.—Lung
abscesses in chil¬
frequently Staphylococcus aureus, H in¬ fluenzae type B, and S Pneumoniae.' We describe a child with a lung abscess due to H influenzae type C. Although severe H influenzae infec¬ tions (especially type B) appear to be increasing in incidence, reports of H influenzae type C infections are extremely limited. Lowe" reported the isolation of H influenzae type C at necropsy from the lungs of an elderly man with pneumonia. Denis et al'" reported meningitis caused by H influenzae type C in four children. To our knowledge, our report is the first known pulmonary infection due to H influenzae type C in a child. The strain of H influenzae type C that was isolated from the lung abscess produced ß-lactamase and was dren with
are
associated most
resistant to ampicillin. In addition, the patient did not have any clinical response to therapy until chloram¬ phenicol therapy was initiated. Cephalexin monohydrate was administered at discharge since this specific orga¬ nism was very sensitive to cephalosporins by tube dilution sensitivity test¬ ing. However, we do not know the value of cephalexin therapy in this particular patient, and we certainly do not recommend cephalosporins in gen¬ eral for the treatment of infections due to H influenzae. Typing of H influenzae strains can be performed by agglutination, immunofluorescent techniques, and CIE; however, certain strains of H influen¬ zae cannot be typed by agglutination because the organism autoagglutinates." The value of CIE for estab¬
etiologic diagnosis rapidly was illustrated by the present case. Type C antigen was detected in the material obtained by lung aspiration. lishing
an
SEIJI KITAGAWA, MD SHELDON L. KAPLAN, MD DAN K. SEILHEIMER, MD Divisions of Infectious Diseases and Pulmonary Medicine Department of Pediatrics Baylor College of Medicine and Texas Children's Hospital Houston, TX 77030
Nicholas E.
pate in the
Tengg, MD, allowed of his patient.
us
to
partici¬
care
1. Weinstein LS: Type b Haemophilus influeninfections in adults. N Engl J Med 282:221\x=req-\ 222, 1970. 2. Fine RN, Kiertz HM, Krieger G: Haemophilus influenzae type A meningitis. J Pediatr 70:962-963, 1967. 3. Buck LL, Douglas GW: Meningitis due to Haemophilus influenzae type E. J Clin Microbiol 4:381, 1976. 4. Gray BM: Meningitis due to Haemophilus influenzae type F. J Pediatr 90:1031, 1977. 5. Harlow M, Chung SMK, Plotkin SA: Haemophilus influenzae septic arthritis in infants and children. Clin Pediatr 14:1146-1149, 1975. 6. Quintiliani R, Hymons PJ: The association of bacteremic Haemophilus influenzae pneumoniae in adults with typeable strains. Am J Med 50:781-786, 1971. 7. Sell SH, Turner DJ, Federspiel CF: Natural zae
infections with Haemophilus influenzae in children: "Types identified," in Sell SHW, Karzon DT (eds): Haemophilus influenzae. Nashville, 1973, Vanderbilt University Press, pp 3-12. 8. Mark PH, Turner JAP: Lung abscess in childhood. Thorax 23:216-220, 1968. 9. Lowe MB: Haemophilus influenzae type C bronchopneumonia. Pathol Bacteriol 88:315-316, 1964. 10. Denis FA, Chiron JP, Cadoz M, et al: Meningitis caused by Haemophilus influenzae type C. J Pediatr 93:1064-1065, 1978. 11. Myhre EB: Typing of Haemophilus influenzae by counterimmunoelectrophoresis. Acta Pathol Microbiol Scand 82:164-166, 1974.
Neonatal Meningococcal and Meningococcemia
Meningitis
Meningococcal meningitis and meningococcemia are relatively common
entities in children. Neonatal menincaused by Neisseria meningitidis is quite rare, however, and the outcome is often fatal. Furthermore, to our knowledge, recovery from meningococcemia has yet to be reported in a neonate. We describe a 2-week-old boy with meningococcemia and meningococcal meningitis whose condition was successfully treated, but in whom a colonized contact was never identified.
gitis
Report of a Case.\p=m-\A2,250-g boy, first of pair of monozygotic twins, was born by spontaneous vaginal delivery after a 38\x=req-\ week gestation to a 31-year-old, gravida 4, para 3 woman. Apgar scores were 7 and 9 at one and five minutes, respectively. A previous full-term pregnancy resulted in the unexplained birth of a stillborn male infant. This pregnancy, labor, and delivery a
unremarkable. The infant was discondition at 7 with his twin brother. He was well until 15 days of age when he was noted to have nasal conges¬ tion. A 3-year-old sibling had bronchitis at this time, and both parents complained of upper respiratory tract infections. The twin was clinically well. Two days later, seven hours after the onset of fever of 40.8 °C, the child was first examined. The examination showed mild, bilateral con¬ junctivitis and right otitis media; however, no nuchal rigidity, irritability, or skin rash was noted. He was immediately admitted to a community hospital. Laboratory studies disclosed the following values: WBCs, 7,900/cu mm, with 18% polymorphonuclear leukocytes, 44% band forms, 20% lympho¬ cytes, 8% monocytes, 1% basophils, and 3% metamyelocytes; hemoglobin, 14 mg/dL; blood glucose, 61 mg/dL. Cerebrospinal fluid showed the following values: WBCs, 100/cu mm (all polymorphonuclear leuko¬ cytes); glucose, 39 mg/dL; protein, 85 mg/ dL. Serum electrolyte level was normal. were
charged in apparently good days of age to his parents,
Gram-negative diplococci were seen on Gram's stain. A diffuse, erythematous rash was seen
at the time the lumbar
puncture
performed and soon became purpuric. Penicillin G potassium and kanamycin sulfate therapy was started, and he was transferred to St Joseph's Hospital and
was
Medical Center, Paterson, NJ. On arrival, he was found to be irritable, with a slightly bulging anterior fontanel, poor peripheral perfusion, and numerous 1 X 1-cm ecchymotic lesions on his lower extremities (Figure). Blood pressure was 70/40 mm Hg; heart rate, 160 beats per minute; and respiratory rate, 50/min. The rest of the physical examination showed no abnormalities, and in particular, there was
Downloaded From: http://archpedi.jamanetwork.com/ by a University of Iowa User on 06/10/2015
At admission, diffuse purpura area and lower extremities.
on
perineal
other evidence of bleeding. Pertinent laboratory values were as follows: platelets, 249,000/cu mm; prothrombin time, 15.4 seconds; partial thromboplastin time, 54.1 seconds; fibrinogen, 175 mg/dL, with no detectable fibrin-split products. A diagno¬ sis of meningococcal meningitis with meningococcemia and early shock was no
made. The patient was transfused with fresh whole blood (10 mL/kg). Fluids were restricted, and antibiotics were changed to penicillin G potassium (200,000 units/kg/24 hr), gentamicin sulfate (7.5 mg/kg/24 hr), and chloramphenicol sodium succinate (50 mg/kg/24 hr). The hydrocortisone methyl prednisolone sodium succinate (50 mg/kg/ day) was added to the regimen. After 24 hours, there were no new ecchymotic lesions; however, generalized seizure activ¬ ity was noted. Serum electrolyte, glucose, and calcium levels were all normal at this time, and the seizures were controlled with phénobarbital sodium. A repeated lumbar puncture disclosed the following values: WBCs, 373/cu mm, with 52% polymorpho¬ nuclear leukocytes, and 48% lymphocytes; glucose, 79 mg/dL; protein, 117 mg/dL. No organisms were seen on Gram's stain. A culture of this CSF was later reported as
negative.
After 48 hours of treatment, the infant
began to improve, and the remainder of his course was
uneventful. He
was
treated for
days with penicillin alone. The original CSF, conjunctival, throat, and blood cul¬ tures showed meningitidis, group B. Throat cultures performed on the parents and siblings of the patient showed no evidence of meningitidis, and the vagi¬ nal culture taken after delivery from the mother indicated no Neisseria species. 14
There
were no
other known caretakers.
Hospital personnel were not cultured. The patient's parents and 3-year-old sibling were treated prophylactically with rifampin, and the twin with penicillin since rifampin and sulfonamides are contraindicated in newborns. Results of a repeated CSF examination two days after discontin¬ uation of the antibiotic therapy were normal. Follow-up at 8 months of age showed him to be developmentally identi¬ cal to his twin brother. His EEG reported to be normal.
was
Comment—Meningococcal meningi-
