- Email: [email protected]
Bacterial infections in children withglucose-6-phosphate dehydrogenase deficiency
850
Clinical and laboratory observations
Given the exploratory nature of this study and the relatively small sample sizes, it is reasonable to interpret the findings with caution. On the other hand, analyses done with a less stringent definition of abnormal concentration (10% change, raising number of abnormal formulas from 15 to 29) and analyses done using total solids (rather than fat concentration) confirmed the above findings. Stepwise multiple regressions (with fat content as the dependent variable) also were entirely consistent. Future research should be longitudinal, include infants with failure to thrive, and seek to develop an inexpensive rapid screen for significant deviations in formula concentration.
The Journal of Pediatrics December 1987
REFERENCES
1. Calle E, Ayoub E, Raile R. Hypernatremic dehydration: the role of feedings high in solute. Pediatrics 1958;22:5-12. 2. Taitz LS, Byers HD. High calorie/osmolar feeding and hypertonic dehydration. Arch Dis Child 1972;47:257-60. 3. Coodin FJ, Gabrielsen IW, Addiego JE. Formula fatality. Pediatrics 1971;47:438-43. 4. Chambers TL, Steel AE. Concentrated milk feeds and their relation to hypernatremic dehydration in infants. Arch Dis Child 1975;50:610-5. 5. Abrams CAL, Phillips LL, Berkowitz C, Blackett PR, Priebe CJ. Hazards of overconcentrated milk formula: hyperosmolality, disseminated intravaseular coagulation, and gangrene. JAMA 1975;232:1136-40. 6. Beaton GH. Nutritional needs during the first year of life. Pediatr Clin North Am 1985;32:275-88. 7. Morbidity and Mortality Weekly Report. Racial and educational factors associated with breastfeeding--United States, 1969 and 1980. MMWR 1984;33:153-4.
We acknowledge the Robert Wood Johnson Foundation (who supported Dr. McJunkin's fellowship), Ross Laboratories (especially Dewey Sehring and Mark Williams), and Kevin Lawlor.
Bacterial infections in children with glucose-6-phosphate dehydrogenase deficiency A h m a d A. Mallouh, MD, a n d Y. K. A b u - O s b a , MD From the Department of Pediatrics, Dhahran Health Center, Dhahran, Saudi Arabia
G6PD deficiency affects more than 130 million persons worldwide. The main deleterious effects are shortened red blood cell survival when exposed to an oxidative stress. A few patients with severe leukocyte G6PD deficiency have been reported to have a clinical picture similar to that of chronic granulomatous disease of childhood, with an increased susceptibility to infections by catalase-positire bacteria; chemotaxis and phagocytosis are normal but there is defective bactericidal activity of the leukocytes. ~-s Because G6PD activity is usually decreased in the leukocytes of patients with the Mediterranean and Chinese variants, we studied the possibility that increased susceptibility to bacterial infections might be present in G6PDdeficient children. METHODS Clinic files and inpatient charts of all Saudi children (1 month to 14 years of age) who were treated at Dhahran
Submitted for publication May 1, 1987; accepted Aug. 20, 1987. Reprint requests: A. Mallouh, MD, FAAP, Pediatric Hematologist/Oncologist, c/o ARAMCO 31311, Dhahran, Saudi Arabia.
Health Center, Saudi Arabia, for meningitis, septicemia, osteomyelitis, or typhoid fever between January 1977 and December 1985 were reviewed. Only culture-proved infections were included. The types of the organism and G6PD status were recorded. Patients with conditions that may increase susceptibility to infection were excluded.
See related article, p. 852.
[
G6PD
Glucose-6-phosphatedehydrogenase
[
G6PD status. Because G6PD deficiency is prevalent in our population, comprehensive neonatal screening was started in August 1980. Most of those who were born before this date had undergone G6PD determinations on previous clinic visits or at the time of hospitalization. The rest of the children were contacted and G6PD studies were done. The results of screening of 8808 consecutively born neonates were used to indicate the prevalence of G6PD deficiency in our population. G6PD was studied with a commercially available kit (BM test, G6PD screening, Boehringer-Mannheim GmbH Diagnostic, West Germany) based on the procedure
Volume 111 Number 6, part 1
Clinical and laboratory observations
8 51
Table. G6PD status in patients with infection vs control G6PD status (deficient) total Patients with bacterial infection (%)
All infections Catalase-positive infections (both sexes) Catalse-negative infections (both sexes) Males (total) Males with catalase-positive infections Males with catalase-negative infections Females (total) Females with catalase-positive infections Females with catalase-negative infections
described by Beutler and Mitchell 6 and recommended for use in all ages, including newborn infants. Statistical analysis. The X2 method was used to compare the observed vs the expected incidence of G6PD deficiency. RESULTS Two hundred thirty-six patients with one of the abovementioned diagnoses were identified. Thirty-six were excluded from analysis: four patients could not be located, 28 had sickle cell disease, two had immune deficiency, one had non-Hodgkin lymphoma, and one was severely malnourished. Two hundred patients (126 males) were included in the final analysis. There were 69 cases of meningitis (37 males), 49 cases of septicemia (32 males), 28 cases of osteomyelitis (21 males), and 54 cases of typhoid fever (36 males). There were 102 infections by catalase-positive organisms (salmonella, coagulase-positive staphylococci, Escherichia coli, and Klebsiella pneumoniae) and 98 by catalase-negative organisms (Streptococcus pneumoniae, Haemophilus influenzae, meningococcus, and a-hemolytic streptococci). The observed incidence of G6PD deficiency was significantly higher than that expected for the entire group, for females with both catalase-positive and catalase-negative infection, and for males with catalase-positive infections (Table). DISCUSSION Deficiency of G6PD results in short survival of red blood cells when they are exposed to an oxidative stress. Even though the enzyme activity is deficient in other tissue cells, including leukocytes,7-9the significance of this deficiency is not known. A few examples of severe leukocyte G6PD deficiency, defective bactericidal function, and recurrent infection by catalase-positive bacteria have been reported. 1-5 On the other hand, several population studies have indicated that G6PD deficiency might lead to increased
75/200 (37.5) 57/102 (46) 28/98 (28.5) 50/126 (40) 38/76 (50) 12/50 (24) 25/74 (34) 9 I29 (31) 16/45 (35.5)
Control (%)
P value
1448/8808 (16.4)
<0.001 <0.001
969/4490 (21.6) 479/4318 (11)
susceptibility to bacterial infections. Schlegel and Bellanti 1~ suggested that the increased susceptibility of males to infection might be related to G6PD deficiency. Petrakis et al. 11 reported a decline in the frequency of G6PD deficiency with age and postulated that the effects of the environmental factors on these patients might be more significant than currently considered. In this study of 200 Saudi children with severe bacterial infection, G6PD deficiency was significantly more common than expected. The difference was statistically significant for the entire group and for each sex regardless of the organisms. However, when both sex and type of infection (catalase positive or negative) were taken into consideration, the difference was significant for catalase-positive infections in males and for both catalase-positive and catalase-negative infections in females. We conclude that Saudi children with G6PD deficiency are at increased risk of bacterial infections. The mechanism might be related to absent or decreased stimulation of the initial step of the hexose monophosphate shunt of the metabolic pathway, but other mechanisms could also be involved. Previous studies suggested that leukocyte G6PD activity must be extremely low for the deleterious clinical or biochemical effects of its deficiency to be observed. 1-5,7-9 Because the level of leukocyte G6PD activity varies in each individual family and according to ethnic background, ~2it is necessary to study leukocyte G6PD activity in different ethnic groups and, if necessary, in individual families. Bellanti et al. ~3 found that patients with chronic granulomatous disease had reduced G6PD activity in leukocytes with accelerated decay of the enzyme; a similar phenomenon of accelerated decay has been reported in certain variants of G6PD deficiency,7,12 so that an initially high level of the enzyme in a fresh leukocyte preparation from a clinically stable patient might not reflect the true level in a sick febrile patient. Further studies are needed to confirm our findings, to study leukocyte G6PD activity in patients with serious infections, and to study in vitro leukocyte function under these circumstances.
852
Clinical and laboratory observations
The Journal of Pediatrics December 1987
REFERENCES 1. Baehner RL, Johnston RB, Nathan DG. Reduced pyridine nucleotide content in G6PD deficiency granulocytes (RMN): an explanation for their defective bactericidal function (abstr). J Clin Invest 1971;50:4. 2. Baehner RL, Johnston RB, Nathan DG. Comparative study of the metabolic and bactericidal characteristics of severely glucose-6-phosphate dehydrogenase deficient polymorphonuclear leukocytes and leukocytes from children with chronic granulomatous disease. J Reticuloendothel Soc 1972;12: 150-69. 3. Cooper MR, DeChatelet LR, McCall CE, LaVia MF, Spurr CL, Baehner RL. Complete deficiency of leukocyte glucose6-phosphate dehydrogenase with defective bactericidal activity. J Clin Invest 1972;51:769-78. 4. Gray GR, Klebanoff SJ, Stamatocyannopoulos G, et al. Neutrophil dysfunction, chronic granulomatous disease and non-spherocytic haemolytic anemia caused by complete deficiency of glucose-6-phosphate dehydrogenase. Lancet 1973; 2:530-4. 5. Vives Corrons JL, Feliu E, Pujades MA, et al. Severe glucose-6-phosphate dehydrogenase (G6PD) deficiency associated with chronic hemolytic anemia, granulocyte dysfunction, and increased susceptibility to infections: description of a new molecular variant (G6PD Barcelona). Blood 1982; 59:428-34. 6. Beutler E, Mitchell M. Special modifications of the fluores-
7.
8.
9.
10. 11.
12.
13.
cent screening method for glucose-6-phosphate dehydrogenase deficiency. Blood 1968;32:816-8. Ramot B, Fisher S, Szeinberg A, Adam A, Sheba C, Gafni D. A study of subjects with erythrocyte glucose-6-phosphate dehydrogenase deficiency: investigation of leukocytes enzymes. J Clin Invest 1959;38:2234-7. Rodey GE, Jacob HS, Holmes B, MeArthur JR, Good RA. Leukocyte glucose-phosphate dehydrogenase levels and bactericidal activity. Lancet 1970;1:355-6. Miller DR, Wollman MR. A new variant of glucose-6phosphate dehydrogenase deficiency hereditary hemolytic anemia, G6PD Cornell: erythrocyte, leukocyte, and platelet studies. Blood 1974;44:323-31. Schlegel R J, Bellanti JA. Increased susceptibility of males to infection. Lancet 1969;2:826-7. Petrakis NL, Wiesenfeld SL, Sams BJ, Collen MF, Cutler JL, Siegelaub AB. Prevalence of sickle-cell trait and glucose6-phosphate dehydrogenase deficiency: decline with age in the frequency of G6PD-deficient Negro males. N Engl J Med 1970;282:767-70. Justice P, Shih L, Gordon J, Grossman A, Hsia DY. Characterization of leukocyte glucose-6-phosphate dehydrogenase in normal and mutant human subjects. J Lab Clin Med 1966; 68:552-9. Bellanti JA, Cantz BE, Schlegel RJ. Accelerated decay of glucose-6-phosphate dehydrogenase activity in chronic granulomatous disease. Pediatr Res 1970;4:405-11.
Glucose-6-phosphate dehydrogenase deficiency, neutrophil dysfunction and Chromobacterium violaceum sepsis Robert J. Mamlok, MD, Viviane Mamlok, MD, Gordon C. Mills, PhD, C, W. Daeschner III, MD, Frank C. Schmalstieg, MD, PhD, and Donald C. Anderson, MD From the Departments of Pediatrics. Pathology, and Human Biological Chemistry and Genetics, the University of Texas Medical Branch, Galveston, and the Department of Pediatrics, Baylor College of Medicine, Houston, Texas
Polymorphonuclear leukocyte glucose-6-phosphate dehydrogenase (EC1.1.1.49) deficiency is rare v5 compared with red blood cell G 6 P D deficiency, a relatively common cause of hemolytic anemia. Patients with severe P M N G 6 P D deficiency have increased susceptibility to infections and abnormal phagocyte function that resembles that of
Supported by the James W. McLaughlin Fellowship Fund. Submitted for publication May 11, 1987; accepted July 21, 1987. Reprint requests: Robert J. Mamlok, MD, Department of Pediatrics, Division of Immunology and Allergy, Room C2-3 I, Child Health Center, the University of Texas Medical Branch, Galveston, TX 77550.
patients patients reported life. We
with chronic granulomatous disease, except that with P M N G 6 P D deficiency have not been to have infections during the first decade of describe a case of fatal Chromobacterium vio-
See related article, p. 850.
G6PD CGD PMN PMA NBT
Glucose-6-phosphate dehydrogenase Chronic granulomatous diseases Polymorphonuclear leukocyte Phorbol myristate acetate Nitroblue tetrazolium
Clinical and laboratory observations
Given the exploratory nature of this study and the relatively small sample sizes, it is reasonable to interpret the findings with caution. On the other hand, analyses done with a less stringent definition of abnormal concentration (10% change, raising number of abnormal formulas from 15 to 29) and analyses done using total solids (rather than fat concentration) confirmed the above findings. Stepwise multiple regressions (with fat content as the dependent variable) also were entirely consistent. Future research should be longitudinal, include infants with failure to thrive, and seek to develop an inexpensive rapid screen for significant deviations in formula concentration.
The Journal of Pediatrics December 1987
REFERENCES
1. Calle E, Ayoub E, Raile R. Hypernatremic dehydration: the role of feedings high in solute. Pediatrics 1958;22:5-12. 2. Taitz LS, Byers HD. High calorie/osmolar feeding and hypertonic dehydration. Arch Dis Child 1972;47:257-60. 3. Coodin FJ, Gabrielsen IW, Addiego JE. Formula fatality. Pediatrics 1971;47:438-43. 4. Chambers TL, Steel AE. Concentrated milk feeds and their relation to hypernatremic dehydration in infants. Arch Dis Child 1975;50:610-5. 5. Abrams CAL, Phillips LL, Berkowitz C, Blackett PR, Priebe CJ. Hazards of overconcentrated milk formula: hyperosmolality, disseminated intravaseular coagulation, and gangrene. JAMA 1975;232:1136-40. 6. Beaton GH. Nutritional needs during the first year of life. Pediatr Clin North Am 1985;32:275-88. 7. Morbidity and Mortality Weekly Report. Racial and educational factors associated with breastfeeding--United States, 1969 and 1980. MMWR 1984;33:153-4.
We acknowledge the Robert Wood Johnson Foundation (who supported Dr. McJunkin's fellowship), Ross Laboratories (especially Dewey Sehring and Mark Williams), and Kevin Lawlor.
Bacterial infections in children with glucose-6-phosphate dehydrogenase deficiency A h m a d A. Mallouh, MD, a n d Y. K. A b u - O s b a , MD From the Department of Pediatrics, Dhahran Health Center, Dhahran, Saudi Arabia
G6PD deficiency affects more than 130 million persons worldwide. The main deleterious effects are shortened red blood cell survival when exposed to an oxidative stress. A few patients with severe leukocyte G6PD deficiency have been reported to have a clinical picture similar to that of chronic granulomatous disease of childhood, with an increased susceptibility to infections by catalase-positire bacteria; chemotaxis and phagocytosis are normal but there is defective bactericidal activity of the leukocytes. ~-s Because G6PD activity is usually decreased in the leukocytes of patients with the Mediterranean and Chinese variants, we studied the possibility that increased susceptibility to bacterial infections might be present in G6PDdeficient children. METHODS Clinic files and inpatient charts of all Saudi children (1 month to 14 years of age) who were treated at Dhahran
Submitted for publication May 1, 1987; accepted Aug. 20, 1987. Reprint requests: A. Mallouh, MD, FAAP, Pediatric Hematologist/Oncologist, c/o ARAMCO 31311, Dhahran, Saudi Arabia.
Health Center, Saudi Arabia, for meningitis, septicemia, osteomyelitis, or typhoid fever between January 1977 and December 1985 were reviewed. Only culture-proved infections were included. The types of the organism and G6PD status were recorded. Patients with conditions that may increase susceptibility to infection were excluded.
See related article, p. 852.
[
G6PD
Glucose-6-phosphatedehydrogenase
[
G6PD status. Because G6PD deficiency is prevalent in our population, comprehensive neonatal screening was started in August 1980. Most of those who were born before this date had undergone G6PD determinations on previous clinic visits or at the time of hospitalization. The rest of the children were contacted and G6PD studies were done. The results of screening of 8808 consecutively born neonates were used to indicate the prevalence of G6PD deficiency in our population. G6PD was studied with a commercially available kit (BM test, G6PD screening, Boehringer-Mannheim GmbH Diagnostic, West Germany) based on the procedure
Volume 111 Number 6, part 1
Clinical and laboratory observations
8 51
Table. G6PD status in patients with infection vs control G6PD status (deficient) total Patients with bacterial infection (%)
All infections Catalase-positive infections (both sexes) Catalse-negative infections (both sexes) Males (total) Males with catalase-positive infections Males with catalase-negative infections Females (total) Females with catalase-positive infections Females with catalase-negative infections
described by Beutler and Mitchell 6 and recommended for use in all ages, including newborn infants. Statistical analysis. The X2 method was used to compare the observed vs the expected incidence of G6PD deficiency. RESULTS Two hundred thirty-six patients with one of the abovementioned diagnoses were identified. Thirty-six were excluded from analysis: four patients could not be located, 28 had sickle cell disease, two had immune deficiency, one had non-Hodgkin lymphoma, and one was severely malnourished. Two hundred patients (126 males) were included in the final analysis. There were 69 cases of meningitis (37 males), 49 cases of septicemia (32 males), 28 cases of osteomyelitis (21 males), and 54 cases of typhoid fever (36 males). There were 102 infections by catalase-positive organisms (salmonella, coagulase-positive staphylococci, Escherichia coli, and Klebsiella pneumoniae) and 98 by catalase-negative organisms (Streptococcus pneumoniae, Haemophilus influenzae, meningococcus, and a-hemolytic streptococci). The observed incidence of G6PD deficiency was significantly higher than that expected for the entire group, for females with both catalase-positive and catalase-negative infection, and for males with catalase-positive infections (Table). DISCUSSION Deficiency of G6PD results in short survival of red blood cells when they are exposed to an oxidative stress. Even though the enzyme activity is deficient in other tissue cells, including leukocytes,7-9the significance of this deficiency is not known. A few examples of severe leukocyte G6PD deficiency, defective bactericidal function, and recurrent infection by catalase-positive bacteria have been reported. 1-5 On the other hand, several population studies have indicated that G6PD deficiency might lead to increased
75/200 (37.5) 57/102 (46) 28/98 (28.5) 50/126 (40) 38/76 (50) 12/50 (24) 25/74 (34) 9 I29 (31) 16/45 (35.5)
Control (%)
P value
1448/8808 (16.4)
<0.001 <0.001
969/4490 (21.6) 479/4318 (11)
susceptibility to bacterial infections. Schlegel and Bellanti 1~ suggested that the increased susceptibility of males to infection might be related to G6PD deficiency. Petrakis et al. 11 reported a decline in the frequency of G6PD deficiency with age and postulated that the effects of the environmental factors on these patients might be more significant than currently considered. In this study of 200 Saudi children with severe bacterial infection, G6PD deficiency was significantly more common than expected. The difference was statistically significant for the entire group and for each sex regardless of the organisms. However, when both sex and type of infection (catalase positive or negative) were taken into consideration, the difference was significant for catalase-positive infections in males and for both catalase-positive and catalase-negative infections in females. We conclude that Saudi children with G6PD deficiency are at increased risk of bacterial infections. The mechanism might be related to absent or decreased stimulation of the initial step of the hexose monophosphate shunt of the metabolic pathway, but other mechanisms could also be involved. Previous studies suggested that leukocyte G6PD activity must be extremely low for the deleterious clinical or biochemical effects of its deficiency to be observed. 1-5,7-9 Because the level of leukocyte G6PD activity varies in each individual family and according to ethnic background, ~2it is necessary to study leukocyte G6PD activity in different ethnic groups and, if necessary, in individual families. Bellanti et al. ~3 found that patients with chronic granulomatous disease had reduced G6PD activity in leukocytes with accelerated decay of the enzyme; a similar phenomenon of accelerated decay has been reported in certain variants of G6PD deficiency,7,12 so that an initially high level of the enzyme in a fresh leukocyte preparation from a clinically stable patient might not reflect the true level in a sick febrile patient. Further studies are needed to confirm our findings, to study leukocyte G6PD activity in patients with serious infections, and to study in vitro leukocyte function under these circumstances.
852
Clinical and laboratory observations
The Journal of Pediatrics December 1987
REFERENCES 1. Baehner RL, Johnston RB, Nathan DG. Reduced pyridine nucleotide content in G6PD deficiency granulocytes (RMN): an explanation for their defective bactericidal function (abstr). J Clin Invest 1971;50:4. 2. Baehner RL, Johnston RB, Nathan DG. Comparative study of the metabolic and bactericidal characteristics of severely glucose-6-phosphate dehydrogenase deficient polymorphonuclear leukocytes and leukocytes from children with chronic granulomatous disease. J Reticuloendothel Soc 1972;12: 150-69. 3. Cooper MR, DeChatelet LR, McCall CE, LaVia MF, Spurr CL, Baehner RL. Complete deficiency of leukocyte glucose6-phosphate dehydrogenase with defective bactericidal activity. J Clin Invest 1972;51:769-78. 4. Gray GR, Klebanoff SJ, Stamatocyannopoulos G, et al. Neutrophil dysfunction, chronic granulomatous disease and non-spherocytic haemolytic anemia caused by complete deficiency of glucose-6-phosphate dehydrogenase. Lancet 1973; 2:530-4. 5. Vives Corrons JL, Feliu E, Pujades MA, et al. Severe glucose-6-phosphate dehydrogenase (G6PD) deficiency associated with chronic hemolytic anemia, granulocyte dysfunction, and increased susceptibility to infections: description of a new molecular variant (G6PD Barcelona). Blood 1982; 59:428-34. 6. Beutler E, Mitchell M. Special modifications of the fluores-
7.
8.
9.
10. 11.
12.
13.
cent screening method for glucose-6-phosphate dehydrogenase deficiency. Blood 1968;32:816-8. Ramot B, Fisher S, Szeinberg A, Adam A, Sheba C, Gafni D. A study of subjects with erythrocyte glucose-6-phosphate dehydrogenase deficiency: investigation of leukocytes enzymes. J Clin Invest 1959;38:2234-7. Rodey GE, Jacob HS, Holmes B, MeArthur JR, Good RA. Leukocyte glucose-phosphate dehydrogenase levels and bactericidal activity. Lancet 1970;1:355-6. Miller DR, Wollman MR. A new variant of glucose-6phosphate dehydrogenase deficiency hereditary hemolytic anemia, G6PD Cornell: erythrocyte, leukocyte, and platelet studies. Blood 1974;44:323-31. Schlegel R J, Bellanti JA. Increased susceptibility of males to infection. Lancet 1969;2:826-7. Petrakis NL, Wiesenfeld SL, Sams BJ, Collen MF, Cutler JL, Siegelaub AB. Prevalence of sickle-cell trait and glucose6-phosphate dehydrogenase deficiency: decline with age in the frequency of G6PD-deficient Negro males. N Engl J Med 1970;282:767-70. Justice P, Shih L, Gordon J, Grossman A, Hsia DY. Characterization of leukocyte glucose-6-phosphate dehydrogenase in normal and mutant human subjects. J Lab Clin Med 1966; 68:552-9. Bellanti JA, Cantz BE, Schlegel RJ. Accelerated decay of glucose-6-phosphate dehydrogenase activity in chronic granulomatous disease. Pediatr Res 1970;4:405-11.
Glucose-6-phosphate dehydrogenase deficiency, neutrophil dysfunction and Chromobacterium violaceum sepsis Robert J. Mamlok, MD, Viviane Mamlok, MD, Gordon C. Mills, PhD, C, W. Daeschner III, MD, Frank C. Schmalstieg, MD, PhD, and Donald C. Anderson, MD From the Departments of Pediatrics. Pathology, and Human Biological Chemistry and Genetics, the University of Texas Medical Branch, Galveston, and the Department of Pediatrics, Baylor College of Medicine, Houston, Texas
Polymorphonuclear leukocyte glucose-6-phosphate dehydrogenase (EC1.1.1.49) deficiency is rare v5 compared with red blood cell G 6 P D deficiency, a relatively common cause of hemolytic anemia. Patients with severe P M N G 6 P D deficiency have increased susceptibility to infections and abnormal phagocyte function that resembles that of
Supported by the James W. McLaughlin Fellowship Fund. Submitted for publication May 11, 1987; accepted July 21, 1987. Reprint requests: Robert J. Mamlok, MD, Department of Pediatrics, Division of Immunology and Allergy, Room C2-3 I, Child Health Center, the University of Texas Medical Branch, Galveston, TX 77550.
patients patients reported life. We
with chronic granulomatous disease, except that with P M N G 6 P D deficiency have not been to have infections during the first decade of describe a case of fatal Chromobacterium vio-
See related article, p. 850.
G6PD CGD PMN PMA NBT
Glucose-6-phosphate dehydrogenase Chronic granulomatous diseases Polymorphonuclear leukocyte Phorbol myristate acetate Nitroblue tetrazolium