Severe Mycoplasma Pneumonia in Children with Down Syndrome
Young
Shari L. Orlicek, M.D. Michael S. Walker, M.D. Thomas L. Kuhls, M.D.
Summary: Three young children with Down syndrome developed fever, cough, wheezing, irritability, and tachypnea. They had bilateral infiltrates on their chest radiographs and developed respiratory distress, which required their hospitalization. Laboratory studies suggested that the children had mycoplasma pneumonia. These children may have experienced severe mycoplasma infections early in life because of their Down syndrome-associated immune abnormalities. When young children with Down syndrome develop pneumonia, physicians should consider Mycoplasma pneumoniae as the possible etiologic agent. Introduction
been
reported to develop respirarequiring their hospitalization.2-4 Thus, M. pneumoniae is not often suspected to be the cause of clinically severe pneumonia in young tory distress
he
organism Myco~lasma pneumoniae generally causes a
mild, self-limiting
illness in children between 5 and 15 years of age. Symptoms associated with lower respiratory tract disease are usually nonspecific and include cough, malaise, fever, coryza, vomit-1 ing, abdominal pain, and headache. Children less than 5 years of age who develop a mycoplasma infection are almost always asymptomatic; in this age group only three otherwise healthy children and a child with sickle-cell hemoglobinopathy have From the Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City.
Address correspondence to: Thomas L. Kuhls, M.D., Department of Pediatrics, Room 2B283, Children’s Hospital of Oklahoma, Oklahoma City, 0K 73104
(405)271-6788
children. We describe three young children with Down syndrome who developed severe respiratory distress. In each case, laboratory studies suggested that the children had
mycoplasma pneumonia. Case
Reports
Patient 7
A 2-year-old male with Down syndrome and mild mitral regurgitation after atrioventricular canal repair at 14 months of age was admitted to Children’s Hospital of Oklahoma for evaluation and treatment of respiratory distress. He had no previous history of frequent infections. Seven days earlier he had developed fever, cough,
congestion, tachypnea, and wheezing. His symptoms became worse despite two days of oral amoxicillin/clavulanate for left lower lobe pneumonia diagnosed by his local physician. At the time of admission, he had a temperature of 36.5°C and a respiratory rate of 38 breaths per minute. Auscultation of the chest revealed expiratory wheezes from both lungs and rales from the lower portion of the left lung. A chest radiograph revealed left upper-lobe, right upper-lobe, and left lower-lobe consolidations. An arterial blood gas determined while he received 2 liters of oxygen per minute by nasal cannula
revealed: pH 7.48, PC02 42 mm Hg, and P02 97 mm Hg. A blood culture obtained at the time of admission was sterile. Capsular
antigens of Haemophilus influStreptococcus pneumoniae, and Neisseria meningitidis were not deenzae,
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
409
tected in his urine. Respiratory viruses and adenovirus were not cultured from nasopharyngeal secretions, and rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. Despite intravenous cefuroxime, his respiratory distress worsened, and he required increasing amounts of oxygen. On day 12 of his hospitalization, the hematology laboratory reported the presence of cold agglutinins in his blood. A Mycoplasma complement-flxation titer (Whittaker Bioproducts, Walkersville, Maryland), obtained 19 days into his illness, was >_1:512. He went home three days after receiving oral erythromycin, with dramatic improvement in his condition.
46 mm Hg, and P02 38 mm Hg. Since he required 100% oxygen by face mask to adequately sustain oxygenation, he was transferred to the critical-care unit. Blood culture at the time of admission was sterile, and respiratory viruses and adenovirus were not isolated from his nasopharyngeal secretions. Rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. However, his cold agglutinin titer was 1:128, and a
Mycoplasma complement-fixation titer, obtained 15 days into his illness,
was
1:512.
He was given oral erythromycin and intravenous cefotaxime. He
had rapid clinical improvement, with resolution of his respiratory symptoms in three days.
Patient 2 A
5-year-old
male with Down
chanically ventilated. A blood culture obtained on admission was sterile, and capsular antigens of H. influenzae, S. pneumoniae, and N. meningitidis were not detected in his urine. Respiratory viruses and adenovirus were not cultured from his nasopharyngeal secretions. Rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. His tracheal aspirate had moderate numbers of white blood cells, but no organisms were visualized, and culture of the secretions was sterile. However, his cold agglutinin titer was 1:512, and his Mycoplasma complement-fixation titer (obtained 11 days into his
syndrome was transferred to Children’s Hospital of Oklahoma for evaluation and treatment of respiratory distress. He had no underlying cardiac anomalies and did not have a history of frequent infec-
A 4-year-old male with Down syndrome was admitted to a regional hospital because of respiratory distress. He had no underlying cardiac anomalies or history of fre-
tions. Two weeks earlier he had
for
started on oral erythroand continued on intravemycin nous cefotaxime. He also received
and
irritability. He was given intravenous cefotaxime after being diagnosed with left lower-lobe and right lower-lobe pneumonia. Due to his increasing respiratory dis-
lone, and terbutaline. Eight days
tress, he was transferred to Children’s Hospital of Oklahoma after receiving two days of antibiotics. Upon arrival, he was in moderate respiratory distress. He had a temperature of 37.2°C and a respiratory rate of 38 breaths per minute. He was grunting and had poor air movement in all lung fields. Scattered rhonchi and rales were auscultated throughout the lungs, while wheezing was heard in the left anterior chest. A chest radiograph revealed infiltrates in the right middle lobe and left lingula, bilateral perihilar infiltrates, and a
formed. He went home after resolution of his respiratory symptoms, but he was found to be tra-
developed fever, cough, irritability, tachypnea, and wheezing. Despite receiving six days of intravenous cefotaxime at a regional hospital because his chest radiograph had demonstrated infiltrates in both
lungs, his respiratory status continued to worsen. At the time of admission, he had a temperature of 37.6°C and a respiratory rate of 68 breaths per minute. He had prominent subcostal and intercostal retractions with nasal flaring. Auscultation of the chest revealed diffuse bilateral expiratory wheezes and rales in his left lung field. A chest radiograph demonstrated right upperlobe, right lower-lobe, and left lingula infiltrates. His arterial blood gas, obtained while breath-
ing
410
Patient 3
small, right-sided pleural effusion. An arterial blood gas, obtained while he breathed 5 liters of oxygen per minute via face mask, revealed : pH 7.30, PC02 71 mm Hg, and P02 61 mm Hg. He was transferred to the critical-care unit and later intubated and me-
room
air,
was:
pH 7.41, PC02
quent infections but had been ill seven days with symptoms of tachypnea, cough, fever, wheezing,
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
illness) He
was
1:512.
was
aminophylline,
methylpredniso-
after intubation he required minimal ventilatory support; however,
multiple attempts at extubation failed, and a tracheostomy was per-
cheostomy-dependent. Discussion These children with Down syndrome had illnesses with multiple characteristics in common, including the presenting symptoms of fe-
cough, wheezing, irritability, tachypnea. Also, they developed respiratory distress, with bi-
ver,
and
lateral infiltrates
on
their chest
radiographs. Two of the patients required intensive care due to the severity of their disease. In each case, there was a prolonged duration of symptoms before M. pneumoniae was identified as the probable cause of their illnesses. This probably occurred because M. pneumoniae was not considered to be a cause of respiratory distress in children of their age group. Since M. pneumoniae is difficult to culture, infections caused by this microorganism are often diagnosed by documenting a fourfold rise or fall in complement-fixing
antibody titers.5 Only
acute sera
obtained from our patients because the children did not live in the surrounding area and were lost to follow-up. However, M. pneumoniae infections have been diagnosed by a single complement-fixing antibody titer of >_1:256 in patients with respiratory illness. 1 All of our patients had acute complement-fixation titers of >_1:512. Complement-fixing antibodies to M pneumoniae will develop in 72% to 92% of patients with pneumonia who have serum cold agglutinins. Since our patients had serum cold agglutinins and elevated M. pneumoniae complement-fixation titers at the time of their respiratory distress, and since a dramatic improvement in each child’s condition was observed after erythromycin therapy was instituted, it is likely that our patients had mycoplasma pneumonia. Also, cultures for viruses and bacteria that commonly cause childhood pneumonia were sterile at the time of maximal illness ; however, each patient had received antimicrobials prior to the time cultures were obtained. Severe M. pneumoniae respiratory infections have been described in otherwise healthy older were
children; however, only two
severe
infections have been reported in healthy children under 5 years of
age. 3,7 Certain groups of children with immune abnormalities have been reported to develop respiratory distress due to M. pneumoniae comparatively frequently. It has been postulated that patients with sickle-cell disease are at risk for severe infection because they have functional asplenia and defects in opsonization.4,8,9 Also, four patients with antibody deficiencies and a child receiving cancer chemotherapy have developed severe
children’s illnesses, and appropriconvalescent serologic studies should also be done. ate
Acknowledgment We thank Rose Stursa for her administrative assistance.
REFERENCES
mycoplasma pneumonia.lo°l Children with Down syndrome have been shown to have multiple immune defects, possibly placing them at high risk for mycoplasma infection. They have
1.
2.
chemotaxis and phagocytosis and deficiency of IgG4 antibodies have been described. 16,17 Institutionalized children with Down syndrome may develop more respiratory infections than noninstitutionalized Down syndrome children because they are
3.
1001.
5.
Foy HM, Kenney CE, McMahen R, et al. Mycoplasma pneumoniae, pneumonia in an urban area. JAMA. 1970 ;214 :16661672.
6.
7.
pneumoniae infection, including bedside cold agglutinins, acute antibody titers, and culture, early in the course of the
Broughton RA: Infections due to Mycoin plasma pneumoniae childhood. Pediatr Infect Dis. 1986;5:71-83. Grix A, Giammona ST. Pneumonitis pleural effusion in children due to Mycoplasma pneamoniae. Am Rev Respir
with Dis. 8.
9.
1974;109:665-671.
Solanki PL, Berdoff RL. Severe mycoplasma pneumonia with pleural effusions in a patient with sickle cell-hemoglobin C (SC) disease. Am J Med. 1979;66:707710. Chusid
MJ, Lachman BS, Lazerson J.
Severe mycoplasma pneumonia and vesicular eruption in SC hemogloJ Pediatr. 1978 ;93 :449binopathy. 451. 10.
Foy HM, Ochs H, Davis SD, et al. Mycoplasma pneumoniae infections in patients with immunodeficiency syndromes : report offour cases. J Infect Dis.
11.
Ganick
tress in these children, clinicians should carry out diagnostic stud-
ies for M.
Singer J, DeVoe WM. Severe Mycoplasma pneumoniae infection in otherwise Shulman ST, Bartlett J, Clyde WA, et al. The unusual severity of mycoplasma pneumonia in children with sickle-cell disease. N Engl J Med. 1972 ;287 :164167.
not
pneumoniae as a possible etiologic agent of pneumonia in young children with Down syndrome. Due to the development of respiratory dis-
Pediatrics.
4.
frequently exposed to respiratory pathogens. Our patients
exposed to each other prior to the onset of their illnesses, suggesting that the children were not infected with a single, highly virulent strain of M. pneumonias. Physicians should consider M.
childhood.
healthy siblings. J Pediatr. 1979 ;95 :999-
more
and were
in
1967;40:669-682.
a
were not institutionalized
Clyde WA, Denny FW. Mycoplasma infections
diminished delayed hypersensitivity reactions following skin testing, and they have impaired
blastogenic responses to phytohemagglutinin, probably because of decreased interleukin-2 production.12-15 Also, defects in neutrophil
Stevens D, Swift PCF, Johnston PCB, et al. Mycoplasma pneumoniae infection in children. Arch Dis Child. 1978;53:38-42.
1973;127:388-393. DJ, Wolfson J,
Mycoplasma suppressed
Gilbert EF, et al. infection in the immuno-
leukemic patient. Arch Pathol Lab Med . 1980;104:535-536.
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
411
12.
Pediatrics.
al. Altered cellular immune functions in patients with Down syndrome. Am J Dis
Spina CA, Smith D, Korn E,
14.
Fekete C, Kulcsar C, Dan P,
et
15.
Ugazio AG, Maccario R, Notorangelo LD, et al. Immunology of Down syndrome : a review. Am J Med Genet Suppl.
16.
Khan
Child. 1981;135:251-255.
412
1975;87:87-89.
1982;138:59-62.
1979;63:80-87.
13.
fective neutrophil chemotaxis in patients with Down syndrome. J Pediatr.
munological and virological investigations in Down syndrome. Pediatrics.
Levin S, Schlesinger M, Hanzel F, et al. Thymic deficiency in Down syndrome.
et
al. Im-
1990;7:S204-S212. AJ, Evans HE, Glass L,
et
al. De-
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
17.
Loh RKS, Harth SC, Thong VH, et al. Immunoglobulin G subclass deficiency and predisposition to infection in Down syndrome. Pediatr Infect Dis J
1990;9:547-551.
Young
Shari L. Orlicek, M.D. Michael S. Walker, M.D. Thomas L. Kuhls, M.D.
Summary: Three young children with Down syndrome developed fever, cough, wheezing, irritability, and tachypnea. They had bilateral infiltrates on their chest radiographs and developed respiratory distress, which required their hospitalization. Laboratory studies suggested that the children had mycoplasma pneumonia. These children may have experienced severe mycoplasma infections early in life because of their Down syndrome-associated immune abnormalities. When young children with Down syndrome develop pneumonia, physicians should consider Mycoplasma pneumoniae as the possible etiologic agent. Introduction
been
reported to develop respirarequiring their hospitalization.2-4 Thus, M. pneumoniae is not often suspected to be the cause of clinically severe pneumonia in young tory distress
he
organism Myco~lasma pneumoniae generally causes a
mild, self-limiting
illness in children between 5 and 15 years of age. Symptoms associated with lower respiratory tract disease are usually nonspecific and include cough, malaise, fever, coryza, vomit-1 ing, abdominal pain, and headache. Children less than 5 years of age who develop a mycoplasma infection are almost always asymptomatic; in this age group only three otherwise healthy children and a child with sickle-cell hemoglobinopathy have From the Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma City.
Address correspondence to: Thomas L. Kuhls, M.D., Department of Pediatrics, Room 2B283, Children’s Hospital of Oklahoma, Oklahoma City, 0K 73104
(405)271-6788
children. We describe three young children with Down syndrome who developed severe respiratory distress. In each case, laboratory studies suggested that the children had
mycoplasma pneumonia. Case
Reports
Patient 7
A 2-year-old male with Down syndrome and mild mitral regurgitation after atrioventricular canal repair at 14 months of age was admitted to Children’s Hospital of Oklahoma for evaluation and treatment of respiratory distress. He had no previous history of frequent infections. Seven days earlier he had developed fever, cough,
congestion, tachypnea, and wheezing. His symptoms became worse despite two days of oral amoxicillin/clavulanate for left lower lobe pneumonia diagnosed by his local physician. At the time of admission, he had a temperature of 36.5°C and a respiratory rate of 38 breaths per minute. Auscultation of the chest revealed expiratory wheezes from both lungs and rales from the lower portion of the left lung. A chest radiograph revealed left upper-lobe, right upper-lobe, and left lower-lobe consolidations. An arterial blood gas determined while he received 2 liters of oxygen per minute by nasal cannula
revealed: pH 7.48, PC02 42 mm Hg, and P02 97 mm Hg. A blood culture obtained at the time of admission was sterile. Capsular
antigens of Haemophilus influStreptococcus pneumoniae, and Neisseria meningitidis were not deenzae,
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
409
tected in his urine. Respiratory viruses and adenovirus were not cultured from nasopharyngeal secretions, and rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. Despite intravenous cefuroxime, his respiratory distress worsened, and he required increasing amounts of oxygen. On day 12 of his hospitalization, the hematology laboratory reported the presence of cold agglutinins in his blood. A Mycoplasma complement-flxation titer (Whittaker Bioproducts, Walkersville, Maryland), obtained 19 days into his illness, was >_1:512. He went home three days after receiving oral erythromycin, with dramatic improvement in his condition.
46 mm Hg, and P02 38 mm Hg. Since he required 100% oxygen by face mask to adequately sustain oxygenation, he was transferred to the critical-care unit. Blood culture at the time of admission was sterile, and respiratory viruses and adenovirus were not isolated from his nasopharyngeal secretions. Rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. However, his cold agglutinin titer was 1:128, and a
Mycoplasma complement-fixation titer, obtained 15 days into his illness,
was
1:512.
He was given oral erythromycin and intravenous cefotaxime. He
had rapid clinical improvement, with resolution of his respiratory symptoms in three days.
Patient 2 A
5-year-old
male with Down
chanically ventilated. A blood culture obtained on admission was sterile, and capsular antigens of H. influenzae, S. pneumoniae, and N. meningitidis were not detected in his urine. Respiratory viruses and adenovirus were not cultured from his nasopharyngeal secretions. Rapid viral diagnostic tests for influenza, parainfluenza, and respiratory syncytial viruses were negative. His tracheal aspirate had moderate numbers of white blood cells, but no organisms were visualized, and culture of the secretions was sterile. However, his cold agglutinin titer was 1:512, and his Mycoplasma complement-fixation titer (obtained 11 days into his
syndrome was transferred to Children’s Hospital of Oklahoma for evaluation and treatment of respiratory distress. He had no underlying cardiac anomalies and did not have a history of frequent infec-
A 4-year-old male with Down syndrome was admitted to a regional hospital because of respiratory distress. He had no underlying cardiac anomalies or history of fre-
tions. Two weeks earlier he had
for
started on oral erythroand continued on intravemycin nous cefotaxime. He also received
and
irritability. He was given intravenous cefotaxime after being diagnosed with left lower-lobe and right lower-lobe pneumonia. Due to his increasing respiratory dis-
lone, and terbutaline. Eight days
tress, he was transferred to Children’s Hospital of Oklahoma after receiving two days of antibiotics. Upon arrival, he was in moderate respiratory distress. He had a temperature of 37.2°C and a respiratory rate of 38 breaths per minute. He was grunting and had poor air movement in all lung fields. Scattered rhonchi and rales were auscultated throughout the lungs, while wheezing was heard in the left anterior chest. A chest radiograph revealed infiltrates in the right middle lobe and left lingula, bilateral perihilar infiltrates, and a
formed. He went home after resolution of his respiratory symptoms, but he was found to be tra-
developed fever, cough, irritability, tachypnea, and wheezing. Despite receiving six days of intravenous cefotaxime at a regional hospital because his chest radiograph had demonstrated infiltrates in both
lungs, his respiratory status continued to worsen. At the time of admission, he had a temperature of 37.6°C and a respiratory rate of 68 breaths per minute. He had prominent subcostal and intercostal retractions with nasal flaring. Auscultation of the chest revealed diffuse bilateral expiratory wheezes and rales in his left lung field. A chest radiograph demonstrated right upperlobe, right lower-lobe, and left lingula infiltrates. His arterial blood gas, obtained while breath-
ing
410
Patient 3
small, right-sided pleural effusion. An arterial blood gas, obtained while he breathed 5 liters of oxygen per minute via face mask, revealed : pH 7.30, PC02 71 mm Hg, and P02 61 mm Hg. He was transferred to the critical-care unit and later intubated and me-
room
air,
was:
pH 7.41, PC02
quent infections but had been ill seven days with symptoms of tachypnea, cough, fever, wheezing,
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
illness) He
was
1:512.
was
aminophylline,
methylpredniso-
after intubation he required minimal ventilatory support; however,
multiple attempts at extubation failed, and a tracheostomy was per-
cheostomy-dependent. Discussion These children with Down syndrome had illnesses with multiple characteristics in common, including the presenting symptoms of fe-
cough, wheezing, irritability, tachypnea. Also, they developed respiratory distress, with bi-
ver,
and
lateral infiltrates
on
their chest
radiographs. Two of the patients required intensive care due to the severity of their disease. In each case, there was a prolonged duration of symptoms before M. pneumoniae was identified as the probable cause of their illnesses. This probably occurred because M. pneumoniae was not considered to be a cause of respiratory distress in children of their age group. Since M. pneumoniae is difficult to culture, infections caused by this microorganism are often diagnosed by documenting a fourfold rise or fall in complement-fixing
antibody titers.5 Only
acute sera
obtained from our patients because the children did not live in the surrounding area and were lost to follow-up. However, M. pneumoniae infections have been diagnosed by a single complement-fixing antibody titer of >_1:256 in patients with respiratory illness. 1 All of our patients had acute complement-fixation titers of >_1:512. Complement-fixing antibodies to M pneumoniae will develop in 72% to 92% of patients with pneumonia who have serum cold agglutinins. Since our patients had serum cold agglutinins and elevated M. pneumoniae complement-fixation titers at the time of their respiratory distress, and since a dramatic improvement in each child’s condition was observed after erythromycin therapy was instituted, it is likely that our patients had mycoplasma pneumonia. Also, cultures for viruses and bacteria that commonly cause childhood pneumonia were sterile at the time of maximal illness ; however, each patient had received antimicrobials prior to the time cultures were obtained. Severe M. pneumoniae respiratory infections have been described in otherwise healthy older were
children; however, only two
severe
infections have been reported in healthy children under 5 years of
age. 3,7 Certain groups of children with immune abnormalities have been reported to develop respiratory distress due to M. pneumoniae comparatively frequently. It has been postulated that patients with sickle-cell disease are at risk for severe infection because they have functional asplenia and defects in opsonization.4,8,9 Also, four patients with antibody deficiencies and a child receiving cancer chemotherapy have developed severe
children’s illnesses, and appropriconvalescent serologic studies should also be done. ate
Acknowledgment We thank Rose Stursa for her administrative assistance.
REFERENCES
mycoplasma pneumonia.lo°l Children with Down syndrome have been shown to have multiple immune defects, possibly placing them at high risk for mycoplasma infection. They have
1.
2.
chemotaxis and phagocytosis and deficiency of IgG4 antibodies have been described. 16,17 Institutionalized children with Down syndrome may develop more respiratory infections than noninstitutionalized Down syndrome children because they are
3.
1001.
5.
Foy HM, Kenney CE, McMahen R, et al. Mycoplasma pneumoniae, pneumonia in an urban area. JAMA. 1970 ;214 :16661672.
6.
7.
pneumoniae infection, including bedside cold agglutinins, acute antibody titers, and culture, early in the course of the
Broughton RA: Infections due to Mycoin plasma pneumoniae childhood. Pediatr Infect Dis. 1986;5:71-83. Grix A, Giammona ST. Pneumonitis pleural effusion in children due to Mycoplasma pneamoniae. Am Rev Respir
with Dis. 8.
9.
1974;109:665-671.
Solanki PL, Berdoff RL. Severe mycoplasma pneumonia with pleural effusions in a patient with sickle cell-hemoglobin C (SC) disease. Am J Med. 1979;66:707710. Chusid
MJ, Lachman BS, Lazerson J.
Severe mycoplasma pneumonia and vesicular eruption in SC hemogloJ Pediatr. 1978 ;93 :449binopathy. 451. 10.
Foy HM, Ochs H, Davis SD, et al. Mycoplasma pneumoniae infections in patients with immunodeficiency syndromes : report offour cases. J Infect Dis.
11.
Ganick
tress in these children, clinicians should carry out diagnostic stud-
ies for M.
Singer J, DeVoe WM. Severe Mycoplasma pneumoniae infection in otherwise Shulman ST, Bartlett J, Clyde WA, et al. The unusual severity of mycoplasma pneumonia in children with sickle-cell disease. N Engl J Med. 1972 ;287 :164167.
not
pneumoniae as a possible etiologic agent of pneumonia in young children with Down syndrome. Due to the development of respiratory dis-
Pediatrics.
4.
frequently exposed to respiratory pathogens. Our patients
exposed to each other prior to the onset of their illnesses, suggesting that the children were not infected with a single, highly virulent strain of M. pneumonias. Physicians should consider M.
childhood.
healthy siblings. J Pediatr. 1979 ;95 :999-
more
and were
in
1967;40:669-682.
a
were not institutionalized
Clyde WA, Denny FW. Mycoplasma infections
diminished delayed hypersensitivity reactions following skin testing, and they have impaired
blastogenic responses to phytohemagglutinin, probably because of decreased interleukin-2 production.12-15 Also, defects in neutrophil
Stevens D, Swift PCF, Johnston PCB, et al. Mycoplasma pneumoniae infection in children. Arch Dis Child. 1978;53:38-42.
1973;127:388-393. DJ, Wolfson J,
Mycoplasma suppressed
Gilbert EF, et al. infection in the immuno-
leukemic patient. Arch Pathol Lab Med . 1980;104:535-536.
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
411
12.
Pediatrics.
al. Altered cellular immune functions in patients with Down syndrome. Am J Dis
Spina CA, Smith D, Korn E,
14.
Fekete C, Kulcsar C, Dan P,
et
15.
Ugazio AG, Maccario R, Notorangelo LD, et al. Immunology of Down syndrome : a review. Am J Med Genet Suppl.
16.
Khan
Child. 1981;135:251-255.
412
1975;87:87-89.
1982;138:59-62.
1979;63:80-87.
13.
fective neutrophil chemotaxis in patients with Down syndrome. J Pediatr.
munological and virological investigations in Down syndrome. Pediatrics.
Levin S, Schlesinger M, Hanzel F, et al. Thymic deficiency in Down syndrome.
et
al. Im-
1990;7:S204-S212. AJ, Evans HE, Glass L,
et
al. De-
Downloaded from cpj.sagepub.com at MICHIGAN STATE UNIV LIBRARIES on April 7, 2015
17.
Loh RKS, Harth SC, Thong VH, et al. Immunoglobulin G subclass deficiency and predisposition to infection in Down syndrome. Pediatr Infect Dis J
1990;9:547-551.
