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Splenic function after nonsurgical management of splenic rupture
Volume 105 Number 2
In contrast to findings in previous studies, in which a significant number of systemic and severe local reactions were observed when a booster was given 1 to 2 years after the primary immunization, few reactions were experienced by our 17 patients. The occurrence of marked local reactions correlates with large amounts of circulating antibody and may represent an arthus-like reaction. 7 Although it is possible that more severe reactions might occur in a larger patient population, we believe that this is unlikely because of the low level of antibodies found in both interval and pre-booster sera. This long-term follow-up of patients with sickle cell anemia given primary immunization in 1973-1974 showed that antibody levels had fallen by 3 to 5 years after immunization and were similar at the time of booster vaccination. Mean antibody levels after booster immunization were significantly increased, and no serious reactions were noted. We therefore recommend that children with sickle cell anemia who received primary immunization at or after 2 years of age should be given booster immunization not sooner than 3 nor later than 5 years after primary immunization. W e would expect this to add significant protection against pneumococcal infections, while reducing the high reaction rates seen in earlier booster trials. We thank Ann Earles, R.N., Marva Hijazi, R.N., and Carol Dahlstrom for assistance. REFERENCES 1. Ammann A J, Addiego J, Wara DW, Lubin B, Smith WB, Mentzer WC: Polyvalent pneumococcal polysaccharide immunization of patients with sickle cell anemia and patients with splenectomy. N Engl J Med 297:897, 1977. 2. Carlson A J, Davidson WL, McLean AA, Vella PP, Weibel RE, Woodhour AF, Hilleman MR: Pneumococcal vaccine: Dose, revaccination and coadministration with influenza vaccine (40596). Proc Soc Exp Biol Med 161:558, 1979.
Clinical and laboratory observations
263
3. Schiffman G, Douglas RM, Bonner M J, Robbins M, Austrian R: A radioimmunoassay for immunologic phenomena in pneumococcal disease and for the antibody response to pneumococcal vaccines. I. Method for the radioimmunoassay of anticapsular antibodies and comparison with other techniques. Immunol Meth 33:133, 1980. 4. Heidelberger M, diLapi MM, Siegel M, Walter A: Persistence of antibodies in human subjects injected with pneumococcal polysaccharides. J Immunol 65:535, 1950. 5. Mufson MA, Krause HE, Schiffman G: Long-term persistence of antibody following immunization with pnenmococcal polysaccharide vaccine (41643). Proc Soc Exp Biol Med 173:270, 1983. 6. Vella PP, McLean AA, Woodhour AF, Weibel RE, Hilleman MR: Persistence of pneumococcal antibodies in human subjects following vaccination (40891). Proc Soc Exp Biol Med 164:435, 1980. 7. Borgono JM, McLean AA, Vella PP, Woodhour AF, Canepa I, Davids0n WL, Hilleman MR: Vaccination and revaccination with polyvalent pneumococcal polysaccharide vaccines in adults and infants (40010). Proc Soc Exp Biol Med 157:148, 1978. 8. Rigau-Perez JG, Overturf GD, Chan LS, Weiss J, Powars D: Reactions to booster pneumococcal vaccination in patients with sickle cell disease. Pediatr Infect Dis 2:199, 1983. 9. Lawrence EM, Edwards KM, Schiffman G, Thompson JM, Vaughn WK, Wright PF: Pneumococcal vaccine in normal children. Am J Dis Child 137:846, 1983. 10. Schiffman G: Immune response to pneumococcal vaccine: Two uses. Clin Immunol News 3:33, 1981. 11. Overturf GD, Field R, Edmonds R: Death from type 6 pneumococcal septicemia in a vaccinated child with sickle-cell disease (Letter). N Engl J Med 300:143, 1979. 12. Ahonkhai VI, Landesman SH, Fidrib SM, Schmalzer EA, Brown AK, Cherubin CE, Schiffman G: Failure of pneumococcal vaccine in children with sickle cell disease. N Engl J Med 301:25, 1979. 13. Broome CV, Facklam RR, Fraser DW: Pueumococcal disease after pneumococcal vaccination: An alternative method to estimate the efficacy of pneumococcal vaccine. N Engl J Med 303:549, 1980.
Splenic function after nonsurgical management of splenic rupture Tommy Linn6, M.D., Margareta Eriksson, M.D., Karin L~innergren,M.D., Paul Tordai, M.D., Birgit Czar-Weidhagen, and Kerstin Swedberg Stockholm, Sweden
From the Department of Pediatrics and Pediatric Surgery, Karolinska Institute, St. G6ran's Hospital. Supported by a grant from S~llskapet Barnavi~rd. Submined for publication Dec. 30, 1983; accepted Feb. 24, 1984. Reprint requests: Tommy Linnb, M.D., Department of Pediatrics, St. GOran's Hospital, S-112 81 Stockholm, Sweden.
SPLENECTOMY CARRIES AN INCREASED RISK of overwhelming septicemia and meningitis later in life L2; therefore, nonsurgical management of traumatic splenic rupture has become increasingly common, particularly among pediatric surgeons? This study was performed to evaluate the function of the spleen after nonoperative management.
264
Clinical and laboratory observations
The Journal of Pediatrics August 1984
Table. Hematologic data
1 Nonsurgical management (n = 22) 2 Sp|enectomy (n = 20) 3 Healthy controls (n = 17)
Hemoglobin (graiL)
Hematocrit ( %)
WBC count (XlO,/L)
Neutrophil count (•
135.8 • 11.0
40.6 • 3.6
5.8 • 1.3
3.1 • 0.9
138.3 +_11.9 144.4 • 9.0
42.4 • 42.8 • 3.0
8.5* +3.1 6.8 -!-_1.9
Lymphocyte count (XlOTL)
2.4 • 3.4
4.3~" •
•
3.6 • 1.4
•
2.8
Platelet count (•
"'Pocked'" RBC count (%)
263.5 • 344.3~ • 265.2 •
HowellJolly bodies
3.6
0/22
31.1~
13/20
•
• 4.1 •
0/17
Values are mean +- SD. *Group 2 vs 1, P < 0.01. tGroup 2 vs I, P < 0.05. :~Group2 vs 1 and 3, P < 0.001. Hematologic measurements known to quantify splenic function were investigated, as well as serum immunoglobulin levels.
METHODS The study was approved by the Ethical Committee of the Karolinska Institute. Informed consent was given by parents. Hematologic studies were performed in 22 patients (mean age 11.9 • 3.0 years) who had received nonsurgical management of splenic rupture at least 6 months before the investigation (rupture had been verified by 99mTcscan in 19 patients, and the diagnosis in the remaining three was based on a typical clinical course), in 20 patients (age 15.2 _ 2.1 years) who had undergone splenectomy after a traumatic rupture more than 6 months prior to the investigation, and in 17 healthy control subjects (age 12.5 • 2.9 years). Analysis of serum immunoglobulins was performed in slightly different patient groups: 21 patients who had received nonsurgical management '(mean age 10.1 +_ 3.1 years), 28 patients after splenectomy (age 14.0 ___3.5 years), and 22 healthy controls (age 12.9 • 2.1 years). Patients were selected from periods with different principles of management after splenic rupture, nonsurgical and splenectomy, respectively. The incidence of splenic rupture was about the same during the two periods. As judged from clinical signs and spleen scan findings, there is no reason to believe that the degree of splenic damage was less severe during the nonsurgical management period. Hemoglobin concentration, hematocrit, total leukocyte count with differential, and platelet count were analyzed. Red blood cells (3000 consecutive RBC) were examined for Howell-Jolly bodies and-for inclusion vesicles, which give the surface of the RBC a pocked appearance under interference phase-contrast microscopy?.5
For analysis of "pocked" RBC, 100 t~l capillary or fresh venous blood was mixed with 2 ml buffered (pH 7.4) 3% glutaraldehyde solution (290 mOsm/kg) and examined as a wet preparation with a Zeiss interference phase-contrast microscope with Nomarski optics. One thousand consecutive RBC were examined for the presence of one or more round indentations (pocks). The evaluations were performed without knowledge of the diagnosis. Serum concentrations of IgG, IgA, and IgM were determined by radial immunodiffusion (NOR-Partigen, Behring). Statistical evaluation was performed by one-way analysis of variance. In some cases the medians were compared by chi-square test. The method of linear contrasts was used for multiple comparisons between groups. Data are presented as mean +_ SD. P values <0.05 were considered significant. RESULTS The hemoglobin concentration and hematocrit did not differ in the three groups (Table). The total number of WBC and the neutrophil counts were significantly higher after splenectomy than in patients given nonsurgical treatment. There was no significant difference in the counts of lymphocytes, monocytes, eosinophils, or basophils. The number of platelets was significantly higher (P < 0.001) after splenectomy, whereas the nonoperatively managed and the healthy controls did not differ, Howell-Jolly bodies were found in >~I/3000 RBC in 13 of 20 patients who had had splenectomy; none was found in any of the other subjects. The percentages of "pocked" RBC were generally high after splenectomy; the values after nonoperative management were as low as in the healthy controls (Table). However, in a few patients after splenectomy they were within the same range as after nonoperative management or in controls. All 10 patients
Volume 105 Number 2
with >30% "pocked" RBC also had Howell-Jolly bodies. The mean serum concentrations of IgG and IgA were the same in all three groups of patients. Serum IgM, however, was significantly lower in the patients after splenectomy (0.8 _+ 0.4 gm/L) than after nonoperative management (1.2 + 0.4 gm/L, P < 0.05) and in the controis (1.5 + 0.5 gm/L, P < 0.01), and did not differ after nonoperative management from those in controls. DISCUSSION
An increased risk for overwhelming septicemia, primarily caused by pneumococci but also by Haemophilus influenzae and Neisseria meningitidis, has been found in asplenic patients (congenital or after splenectomy) and under hyposplenic conditions (e.g., sickle cell disease. L2,6 The spleen is involved both in the clearing of bacteria from the blood7 and in the formation of antibodies; serum levels of IgM become lower after splenectomy.2 Many surgeons now try to preserve the spleen after a traumatic rupture, either by nonoperative management3 or by ~uturing the spleen? Such spleen-saving principles were introduced in our clinic in 1978, and of 46 patients with splenic rupture, splenectomy was necessary in only one.9 The results of this study indicate that splenic function is well preserved after the healing of a traumatic rupture. After nonsurgical management no patients had signs of hyposplenism, and serum Ig values were normal. After splenectomy, however, significantly higher platelet counts, high percentages of "pocked" RBC, and Howell-Jolly bodies were found in more than half of the patients; in addition, the serum IgM concentration was significantly lower. The percentage of "pocked" RBC has been used as an index of splenic function in neonates,4 patients with sickle cell disease, 5'6 and patients with splenectomy after a traumatic rupture? ~ Our study showed an increased pro-
Clinical and laboratory observations
265
portion of "pocked" RBC in most patients after splenectomy. When this percentage was high, Howell-Jolly bodies were also found. The percentages of "pocked" RBC in some of these patients were within the range of those found after nonoperative management and in healthy controls. This may reflect a partial restoration of splenic function, possibly related to heterotopic autotransplantation?~ Our data provide evidence for a normal function of the healed traumatically damaged spleen and supports nonsurgical management whenever possible.
REFERENCES 1. Singer DB: Postsplenectomy sepsis. Perspect Pediatr Pathol 1:285, 1973. 2. Spirer Z: The role of the spleen in immunity and infection. Adv Pediatr 27:55, 1980. 3. Wesson DE, Filler RM, Ein SH, Shandling B, Simpson JS, Stephens CA: Ruptured spleen: When to operate? J Pediatr Surg 16:324, 1981. 4. Holroyde CP, Oski FA, Gardner FH: The "pocked" erythrocyte: Red-cell surface alterations in reticuloendothelialimmaturity of the neonate. N Engl J Med 281:516, 1969. 5. Pearson HA, Mclntosh S, Ritchey AK, Lobel JS, Rooks Y, Johnston D: Developmental aspects of splenic function in sickle cell diseases. Blood 53:358, 1979. 6. Buchanan GR, Smith SJ, Holtkamp CA, Fuseler JP: Bacterial infection and splenic reticuloendothelial function in children with hemoglobin SC disease. Pediatrics 72:93, 1983. 7. Brown EJ, Hosea SW, Frank MM: The role of the spleen in experimental pneumococcalbacteremia. J Clin Invest 67:975, 1981. 8. Buntain WL, Lynn HB: Splenorrhaphy: Changing concepts for the traumatized spleen. Surgery 86:748, 1979. 9. Tordai P, L~innergrenK, Linn6 T: Avoiding splenectomy in the treatment of children with splenic injury (Submitted for publication.) 10. Pearson HA, Johnston D, Smith KA, Touloukian RJ: The born-again spleen: Return of splenic function after splenectomy for trauma. N Engl J Med 298:1389, 1978.
Varicella pneumonitis." Immunodiagnosis with a monoclonal antibody Kristen A. Weigle, M.D., and Charles Grose, M.D. San Antonio, Texas
From the Departments of Pediatrics and Microbiology, The University of Texas Health Science Center at San Antonio. Supported in part by grants from the Morrison Trust (San Antonio, Texas) and the National Institute of Allergy and Infectious Diseases (Al14604). Submitted for publication Dec. 12, 1983; accepted Feb. 24, 1984. Reprint requests: Charles Grose, M.D., Department of Pediatrics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284.
CHICKENPOX IS CAUSED BY PRIMARY INFECTION with varicella zoster virus, one of the human herpes group agents (the others are herpes simplex virus types 1 and 2, cytomegalovirus, and Epstein-Barr virus). Childhood CMV HSV VZV
Cytomegalovirus Herpessimplex virus Varicellazoster virus
In contrast to findings in previous studies, in which a significant number of systemic and severe local reactions were observed when a booster was given 1 to 2 years after the primary immunization, few reactions were experienced by our 17 patients. The occurrence of marked local reactions correlates with large amounts of circulating antibody and may represent an arthus-like reaction. 7 Although it is possible that more severe reactions might occur in a larger patient population, we believe that this is unlikely because of the low level of antibodies found in both interval and pre-booster sera. This long-term follow-up of patients with sickle cell anemia given primary immunization in 1973-1974 showed that antibody levels had fallen by 3 to 5 years after immunization and were similar at the time of booster vaccination. Mean antibody levels after booster immunization were significantly increased, and no serious reactions were noted. We therefore recommend that children with sickle cell anemia who received primary immunization at or after 2 years of age should be given booster immunization not sooner than 3 nor later than 5 years after primary immunization. W e would expect this to add significant protection against pneumococcal infections, while reducing the high reaction rates seen in earlier booster trials. We thank Ann Earles, R.N., Marva Hijazi, R.N., and Carol Dahlstrom for assistance. REFERENCES 1. Ammann A J, Addiego J, Wara DW, Lubin B, Smith WB, Mentzer WC: Polyvalent pneumococcal polysaccharide immunization of patients with sickle cell anemia and patients with splenectomy. N Engl J Med 297:897, 1977. 2. Carlson A J, Davidson WL, McLean AA, Vella PP, Weibel RE, Woodhour AF, Hilleman MR: Pneumococcal vaccine: Dose, revaccination and coadministration with influenza vaccine (40596). Proc Soc Exp Biol Med 161:558, 1979.
Clinical and laboratory observations
263
3. Schiffman G, Douglas RM, Bonner M J, Robbins M, Austrian R: A radioimmunoassay for immunologic phenomena in pneumococcal disease and for the antibody response to pneumococcal vaccines. I. Method for the radioimmunoassay of anticapsular antibodies and comparison with other techniques. Immunol Meth 33:133, 1980. 4. Heidelberger M, diLapi MM, Siegel M, Walter A: Persistence of antibodies in human subjects injected with pneumococcal polysaccharides. J Immunol 65:535, 1950. 5. Mufson MA, Krause HE, Schiffman G: Long-term persistence of antibody following immunization with pnenmococcal polysaccharide vaccine (41643). Proc Soc Exp Biol Med 173:270, 1983. 6. Vella PP, McLean AA, Woodhour AF, Weibel RE, Hilleman MR: Persistence of pneumococcal antibodies in human subjects following vaccination (40891). Proc Soc Exp Biol Med 164:435, 1980. 7. Borgono JM, McLean AA, Vella PP, Woodhour AF, Canepa I, Davids0n WL, Hilleman MR: Vaccination and revaccination with polyvalent pneumococcal polysaccharide vaccines in adults and infants (40010). Proc Soc Exp Biol Med 157:148, 1978. 8. Rigau-Perez JG, Overturf GD, Chan LS, Weiss J, Powars D: Reactions to booster pneumococcal vaccination in patients with sickle cell disease. Pediatr Infect Dis 2:199, 1983. 9. Lawrence EM, Edwards KM, Schiffman G, Thompson JM, Vaughn WK, Wright PF: Pneumococcal vaccine in normal children. Am J Dis Child 137:846, 1983. 10. Schiffman G: Immune response to pneumococcal vaccine: Two uses. Clin Immunol News 3:33, 1981. 11. Overturf GD, Field R, Edmonds R: Death from type 6 pneumococcal septicemia in a vaccinated child with sickle-cell disease (Letter). N Engl J Med 300:143, 1979. 12. Ahonkhai VI, Landesman SH, Fidrib SM, Schmalzer EA, Brown AK, Cherubin CE, Schiffman G: Failure of pneumococcal vaccine in children with sickle cell disease. N Engl J Med 301:25, 1979. 13. Broome CV, Facklam RR, Fraser DW: Pueumococcal disease after pneumococcal vaccination: An alternative method to estimate the efficacy of pneumococcal vaccine. N Engl J Med 303:549, 1980.
Splenic function after nonsurgical management of splenic rupture Tommy Linn6, M.D., Margareta Eriksson, M.D., Karin L~innergren,M.D., Paul Tordai, M.D., Birgit Czar-Weidhagen, and Kerstin Swedberg Stockholm, Sweden
From the Department of Pediatrics and Pediatric Surgery, Karolinska Institute, St. G6ran's Hospital. Supported by a grant from S~llskapet Barnavi~rd. Submined for publication Dec. 30, 1983; accepted Feb. 24, 1984. Reprint requests: Tommy Linnb, M.D., Department of Pediatrics, St. GOran's Hospital, S-112 81 Stockholm, Sweden.
SPLENECTOMY CARRIES AN INCREASED RISK of overwhelming septicemia and meningitis later in life L2; therefore, nonsurgical management of traumatic splenic rupture has become increasingly common, particularly among pediatric surgeons? This study was performed to evaluate the function of the spleen after nonoperative management.
264
Clinical and laboratory observations
The Journal of Pediatrics August 1984
Table. Hematologic data
1 Nonsurgical management (n = 22) 2 Sp|enectomy (n = 20) 3 Healthy controls (n = 17)
Hemoglobin (graiL)
Hematocrit ( %)
WBC count (XlO,/L)
Neutrophil count (•
135.8 • 11.0
40.6 • 3.6
5.8 • 1.3
3.1 • 0.9
138.3 +_11.9 144.4 • 9.0
42.4 • 42.8 • 3.0
8.5* +3.1 6.8 -!-_1.9
Lymphocyte count (XlOTL)
2.4 • 3.4
4.3~" •
•
3.6 • 1.4
•
2.8
Platelet count (•
"'Pocked'" RBC count (%)
263.5 • 344.3~ • 265.2 •
HowellJolly bodies
3.6
0/22
31.1~
13/20
•
• 4.1 •
0/17
Values are mean +- SD. *Group 2 vs 1, P < 0.01. tGroup 2 vs I, P < 0.05. :~Group2 vs 1 and 3, P < 0.001. Hematologic measurements known to quantify splenic function were investigated, as well as serum immunoglobulin levels.
METHODS The study was approved by the Ethical Committee of the Karolinska Institute. Informed consent was given by parents. Hematologic studies were performed in 22 patients (mean age 11.9 • 3.0 years) who had received nonsurgical management of splenic rupture at least 6 months before the investigation (rupture had been verified by 99mTcscan in 19 patients, and the diagnosis in the remaining three was based on a typical clinical course), in 20 patients (age 15.2 _ 2.1 years) who had undergone splenectomy after a traumatic rupture more than 6 months prior to the investigation, and in 17 healthy control subjects (age 12.5 • 2.9 years). Analysis of serum immunoglobulins was performed in slightly different patient groups: 21 patients who had received nonsurgical management '(mean age 10.1 +_ 3.1 years), 28 patients after splenectomy (age 14.0 ___3.5 years), and 22 healthy controls (age 12.9 • 2.1 years). Patients were selected from periods with different principles of management after splenic rupture, nonsurgical and splenectomy, respectively. The incidence of splenic rupture was about the same during the two periods. As judged from clinical signs and spleen scan findings, there is no reason to believe that the degree of splenic damage was less severe during the nonsurgical management period. Hemoglobin concentration, hematocrit, total leukocyte count with differential, and platelet count were analyzed. Red blood cells (3000 consecutive RBC) were examined for Howell-Jolly bodies and-for inclusion vesicles, which give the surface of the RBC a pocked appearance under interference phase-contrast microscopy?.5
For analysis of "pocked" RBC, 100 t~l capillary or fresh venous blood was mixed with 2 ml buffered (pH 7.4) 3% glutaraldehyde solution (290 mOsm/kg) and examined as a wet preparation with a Zeiss interference phase-contrast microscope with Nomarski optics. One thousand consecutive RBC were examined for the presence of one or more round indentations (pocks). The evaluations were performed without knowledge of the diagnosis. Serum concentrations of IgG, IgA, and IgM were determined by radial immunodiffusion (NOR-Partigen, Behring). Statistical evaluation was performed by one-way analysis of variance. In some cases the medians were compared by chi-square test. The method of linear contrasts was used for multiple comparisons between groups. Data are presented as mean +_ SD. P values <0.05 were considered significant. RESULTS The hemoglobin concentration and hematocrit did not differ in the three groups (Table). The total number of WBC and the neutrophil counts were significantly higher after splenectomy than in patients given nonsurgical treatment. There was no significant difference in the counts of lymphocytes, monocytes, eosinophils, or basophils. The number of platelets was significantly higher (P < 0.001) after splenectomy, whereas the nonoperatively managed and the healthy controls did not differ, Howell-Jolly bodies were found in >~I/3000 RBC in 13 of 20 patients who had had splenectomy; none was found in any of the other subjects. The percentages of "pocked" RBC were generally high after splenectomy; the values after nonoperative management were as low as in the healthy controls (Table). However, in a few patients after splenectomy they were within the same range as after nonoperative management or in controls. All 10 patients
Volume 105 Number 2
with >30% "pocked" RBC also had Howell-Jolly bodies. The mean serum concentrations of IgG and IgA were the same in all three groups of patients. Serum IgM, however, was significantly lower in the patients after splenectomy (0.8 _+ 0.4 gm/L) than after nonoperative management (1.2 + 0.4 gm/L, P < 0.05) and in the controis (1.5 + 0.5 gm/L, P < 0.01), and did not differ after nonoperative management from those in controls. DISCUSSION
An increased risk for overwhelming septicemia, primarily caused by pneumococci but also by Haemophilus influenzae and Neisseria meningitidis, has been found in asplenic patients (congenital or after splenectomy) and under hyposplenic conditions (e.g., sickle cell disease. L2,6 The spleen is involved both in the clearing of bacteria from the blood7 and in the formation of antibodies; serum levels of IgM become lower after splenectomy.2 Many surgeons now try to preserve the spleen after a traumatic rupture, either by nonoperative management3 or by ~uturing the spleen? Such spleen-saving principles were introduced in our clinic in 1978, and of 46 patients with splenic rupture, splenectomy was necessary in only one.9 The results of this study indicate that splenic function is well preserved after the healing of a traumatic rupture. After nonsurgical management no patients had signs of hyposplenism, and serum Ig values were normal. After splenectomy, however, significantly higher platelet counts, high percentages of "pocked" RBC, and Howell-Jolly bodies were found in more than half of the patients; in addition, the serum IgM concentration was significantly lower. The percentage of "pocked" RBC has been used as an index of splenic function in neonates,4 patients with sickle cell disease, 5'6 and patients with splenectomy after a traumatic rupture? ~ Our study showed an increased pro-
Clinical and laboratory observations
265
portion of "pocked" RBC in most patients after splenectomy. When this percentage was high, Howell-Jolly bodies were also found. The percentages of "pocked" RBC in some of these patients were within the range of those found after nonoperative management and in healthy controls. This may reflect a partial restoration of splenic function, possibly related to heterotopic autotransplantation?~ Our data provide evidence for a normal function of the healed traumatically damaged spleen and supports nonsurgical management whenever possible.
REFERENCES 1. Singer DB: Postsplenectomy sepsis. Perspect Pediatr Pathol 1:285, 1973. 2. Spirer Z: The role of the spleen in immunity and infection. Adv Pediatr 27:55, 1980. 3. Wesson DE, Filler RM, Ein SH, Shandling B, Simpson JS, Stephens CA: Ruptured spleen: When to operate? J Pediatr Surg 16:324, 1981. 4. Holroyde CP, Oski FA, Gardner FH: The "pocked" erythrocyte: Red-cell surface alterations in reticuloendothelialimmaturity of the neonate. N Engl J Med 281:516, 1969. 5. Pearson HA, Mclntosh S, Ritchey AK, Lobel JS, Rooks Y, Johnston D: Developmental aspects of splenic function in sickle cell diseases. Blood 53:358, 1979. 6. Buchanan GR, Smith SJ, Holtkamp CA, Fuseler JP: Bacterial infection and splenic reticuloendothelial function in children with hemoglobin SC disease. Pediatrics 72:93, 1983. 7. Brown EJ, Hosea SW, Frank MM: The role of the spleen in experimental pneumococcalbacteremia. J Clin Invest 67:975, 1981. 8. Buntain WL, Lynn HB: Splenorrhaphy: Changing concepts for the traumatized spleen. Surgery 86:748, 1979. 9. Tordai P, L~innergrenK, Linn6 T: Avoiding splenectomy in the treatment of children with splenic injury (Submitted for publication.) 10. Pearson HA, Johnston D, Smith KA, Touloukian RJ: The born-again spleen: Return of splenic function after splenectomy for trauma. N Engl J Med 298:1389, 1978.
Varicella pneumonitis." Immunodiagnosis with a monoclonal antibody Kristen A. Weigle, M.D., and Charles Grose, M.D. San Antonio, Texas
From the Departments of Pediatrics and Microbiology, The University of Texas Health Science Center at San Antonio. Supported in part by grants from the Morrison Trust (San Antonio, Texas) and the National Institute of Allergy and Infectious Diseases (Al14604). Submitted for publication Dec. 12, 1983; accepted Feb. 24, 1984. Reprint requests: Charles Grose, M.D., Department of Pediatrics, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284.
CHICKENPOX IS CAUSED BY PRIMARY INFECTION with varicella zoster virus, one of the human herpes group agents (the others are herpes simplex virus types 1 and 2, cytomegalovirus, and Epstein-Barr virus). Childhood CMV HSV VZV
Cytomegalovirus Herpessimplex virus Varicellazoster virus