Mycoplasma pneumoniae

Mycoplasma pneumoniae is a cell wall–deficient pleomorphic bacterium and well-reported cause of respiratory tract infection in the school-aged child. Symptoms are variable, and clinical presentations run the gamut from upper respiratory (usually self-limited) and lower respiratory tract involvement (pneumonia) to unusual manifestations including nervous system disease (encephalitis, cerebellar ataxia, transverse myelitis), hemolytic anemia, Stevens-Johnson syndrome, and myocarditis/pericarditis.

Pneumonia occurs in 10% of infected school-aged children, and cough can persist for 3-4 weeks; some children wheeze in the setting of Mycoplasma infection. Radiographic patterns of disease are variable; patchy alveolar infiltrates with small pleural effusions are often described. Consolidated pneumonia, large effusions, and hilar adenopathy are uncommonly reported, and severe disease has been described in certain patient populations, including those with sickle cell disease, children with Down syndrome, and those with immunodeficiencies. The acute chest presentation has been associated with M. pneumoniae in children with sickle cell anemia and prolonged hospitalizations (mean, 10 days), and the need for transfusion and mechanical ventilation was noted in 82% and 6%, respectively, in one study (Pediatrics 2003;112(1 Pt 1):87-95). Community clusters of pneumonia are reported in school-aged children, and in Rhode Island, an outbreak was reported in children from four schools; 76 had pneumonia and 3 had encephalitis (J. Infect. Dis. 2008;198:1365-74).

Considering this is a common pathogen, there are a number of questions regarding the scope of disease and impact of treatment that are incompletely answered. The first problem is that it is hard to confirm diagnostically. Culture is technically difficult, the organism takes up to 3 weeks to grow, and the diagnostic test is offered in very few labs. The old-fashioned cold agglutinin test has a low sensitivity and specificity; an increase in titers can be seen during a variety of viral infections. Polymerase chain reaction (PCR) on respiratory secretions is increasingly available; sensitivity and specificity are said to be 80% and 100%, respectively. The organism can persist in the respiratory tract for several weeks though, even after treatment, so PCR can remain positive for 2-3 weeks. This makes it hard to use PCR to confirm M. pneumoniae as the etiologic agent, especially in the setting of unusual clinical presentations. Serologic testing is often ordered and hard to interpret. False positive IgM antibody tests are not uncommon, and IgM antibody can persist for months. Outside of PCR and culture, acute and convalescent specimens can be used diagnostically, and a fourfold IgG antibody rise is consistent with acute infection.

Macrolides are regarded as the preferred treatment for M. pneumoniae pneumonia, but several studies question whether treatment impacts the clinical course. This may be due to the inherent difficulty of confirming M. pneumoniae as the etiologic agent, as most studies used serology to confirm the diagnosis. In countries outside the United States, macrolide resistance is well reported, and this may be underappreciated in the United States. We recently cared for a teenager with Down syndrome with pneumonia caused by M. pneumoniae who had a protracted clinical course. Fever and hypoxemia were persistent over a several-week period despite two courses of azithromycin and exclusion of virus, bacteria, and fungal pathogens. Bronchoalveolar lavage was performed, M. pneumoniae was detected by PCR, and macrolide resistance was confirmed. Levofloxacin was given, and she recovered over the next week.

Macrolide resistance is commonly reported outside the United States; rates in China are reported to be greater than 90%, in Japan 80%, and in Europe, between 15% and 25%. A recent study from Greg Storch and his colleagues (Pediatr. Infect. Dis. J. 2012;31:409-10) documented macrolide resistance in 8% of respiratory samples collected between 2007 and 2010 (49 patients; mean age, 10 years), noting the resistance rate was 3% in 2007-2008 and 15% in 2009-2010. A recently published study of data from Canada reported that 12.1% of M. pneumoniae–positive specimens collected between 2010 and January 2012 carried nucleotide mutations associated with macrolide resistance in the 23S rRNA gene (Emerg. Infect. Dis. 2013 September [doi: 10.3201/eid1909.121466]). Anecdotal studies suggest that patients with macrolide-resistant M. pneumoniae infection clinically improve when given doxycycline (or minocycline) or levofloxacin.

A number of clinical questions regarding M. pneumoniae may be answered more definitively in the future, but we need more easily available diagnostics (PCR is a good start), routinely accessible susceptibility data, and a good randomized controlled study to investigate the question of whether treatment shortens the course of disease.

Dr. Jackson is chief of pediatric infectious diseases at Children’s Mercy Hospital, Kansas City, Mo., and professor of pediatrics at the University of Missouri-Kansas City. She said she has no conflicts of interest to disclose. E-mail her at pdnews@frontlinemedcom.com.

Mycoplasma pneumoniae is a cell wall–deficient pleomorphic bacterium and well-reported cause of respiratory tract infection in the school-aged child. Symptoms are variable, and clinical presentations run the gamut from upper respiratory (usually self-limited) and lower respiratory tract involvement (pneumonia) to unusual manifestations including nervous system disease (encephalitis, cerebellar ataxia, transverse myelitis), hemolytic anemia, Stevens-Johnson syndrome, and myocarditis/pericarditis.

Pneumonia occurs in 10% of infected school-aged children, and cough can persist for 3-4 weeks; some children wheeze in the setting of Mycoplasma infection. Radiographic patterns of disease are variable; patchy alveolar infiltrates with small pleural effusions are often described. Consolidated pneumonia, large effusions, and hilar adenopathy are uncommonly reported, and severe disease has been described in certain patient populations, including those with sickle cell disease, children with Down syndrome, and those with immunodeficiencies. The acute chest presentation has been associated with M. pneumoniae in children with sickle cell anemia and prolonged hospitalizations (mean, 10 days), and the need for transfusion and mechanical ventilation was noted in 82% and 6%, respectively, in one study (Pediatrics 2003;112(1 Pt 1):87-95). Community clusters of pneumonia are reported in school-aged children, and in Rhode Island, an outbreak was reported in children from four schools; 76 had pneumonia and 3 had encephalitis (J. Infect. Dis. 2008;198:1365-74).

Considering this is a common pathogen, there are a number of questions regarding the scope of disease and impact of treatment that are incompletely answered. The first problem is that it is hard to confirm diagnostically. Culture is technically difficult, the organism takes up to 3 weeks to grow, and the diagnostic test is offered in very few labs. The old-fashioned cold agglutinin test has a low sensitivity and specificity; an increase in titers can be seen during a variety of viral infections. Polymerase chain reaction (PCR) on respiratory secretions is increasingly available; sensitivity and specificity are said to be 80% and 100%, respectively. The organism can persist in the respiratory tract for several weeks though, even after treatment, so PCR can remain positive for 2-3 weeks. This makes it hard to use PCR to confirm M. pneumoniae as the etiologic agent, especially in the setting of unusual clinical presentations. Serologic testing is often ordered and hard to interpret. False positive IgM antibody tests are not uncommon, and IgM antibody can persist for months. Outside of PCR and culture, acute and convalescent specimens can be used diagnostically, and a fourfold IgG antibody rise is consistent with acute infection.

Macrolides are regarded as the preferred treatment for M. pneumoniae pneumonia, but several studies question whether treatment impacts the clinical course. This may be due to the inherent difficulty of confirming M. pneumoniae as the etiologic agent, as most studies used serology to confirm the diagnosis. In countries outside the United States, macrolide resistance is well reported, and this may be underappreciated in the United States. We recently cared for a teenager with Down syndrome with pneumonia caused by M. pneumoniae who had a protracted clinical course. Fever and hypoxemia were persistent over a several-week period despite two courses of azithromycin and exclusion of virus, bacteria, and fungal pathogens. Bronchoalveolar lavage was performed, M. pneumoniae was detected by PCR, and macrolide resistance was confirmed. Levofloxacin was given, and she recovered over the next week.

Macrolide resistance is commonly reported outside the United States; rates in China are reported to be greater than 90%, in Japan 80%, and in Europe, between 15% and 25%. A recent study from Greg Storch and his colleagues (Pediatr. Infect. Dis. J. 2012;31:409-10) documented macrolide resistance in 8% of respiratory samples collected between 2007 and 2010 (49 patients; mean age, 10 years), noting the resistance rate was 3% in 2007-2008 and 15% in 2009-2010. A recently published study of data from Canada reported that 12.1% of M. pneumoniae–positive specimens collected between 2010 and January 2012 carried nucleotide mutations associated with macrolide resistance in the 23S rRNA gene (Emerg. Infect. Dis. 2013 September [doi: 10.3201/eid1909.121466]). Anecdotal studies suggest that patients with macrolide-resistant M. pneumoniae infection clinically improve when given doxycycline (or minocycline) or levofloxacin.

A number of clinical questions regarding M. pneumoniae may be answered more definitively in the future, but we need more easily available diagnostics (PCR is a good start), routinely accessible susceptibility data, and a good randomized controlled study to investigate the question of whether treatment shortens the course of disease.

Dr. Jackson is chief of pediatric infectious diseases at Children’s Mercy Hospital, Kansas City, Mo., and professor of pediatrics at the University of Missouri-Kansas City. She said she has no conflicts of interest to disclose. E-mail her at pdnews@frontlinemedcom.com.

Mycoplasma pneumoniae is a cell wall–deficient pleomorphic bacterium and well-reported cause of respiratory tract infection in the school-aged child. Symptoms are variable, and clinical presentations run the gamut from upper respiratory (usually self-limited) and lower respiratory tract involvement (pneumonia) to unusual manifestations including nervous system disease (encephalitis, cerebellar ataxia, transverse myelitis), hemolytic anemia, Stevens-Johnson syndrome, and myocarditis/pericarditis.

Pneumonia occurs in 10% of infected school-aged children, and cough can persist for 3-4 weeks; some children wheeze in the setting of Mycoplasma infection. Radiographic patterns of disease are variable; patchy alveolar infiltrates with small pleural effusions are often described. Consolidated pneumonia, large effusions, and hilar adenopathy are uncommonly reported, and severe disease has been described in certain patient populations, including those with sickle cell disease, children with Down syndrome, and those with immunodeficiencies. The acute chest presentation has been associated with M. pneumoniae in children with sickle cell anemia and prolonged hospitalizations (mean, 10 days), and the need for transfusion and mechanical ventilation was noted in 82% and 6%, respectively, in one study (Pediatrics 2003;112(1 Pt 1):87-95). Community clusters of pneumonia are reported in school-aged children, and in Rhode Island, an outbreak was reported in children from four schools; 76 had pneumonia and 3 had encephalitis (J. Infect. Dis. 2008;198:1365-74).

Considering this is a common pathogen, there are a number of questions regarding the scope of disease and impact of treatment that are incompletely answered. The first problem is that it is hard to confirm diagnostically. Culture is technically difficult, the organism takes up to 3 weeks to grow, and the diagnostic test is offered in very few labs. The old-fashioned cold agglutinin test has a low sensitivity and specificity; an increase in titers can be seen during a variety of viral infections. Polymerase chain reaction (PCR) on respiratory secretions is increasingly available; sensitivity and specificity are said to be 80% and 100%, respectively. The organism can persist in the respiratory tract for several weeks though, even after treatment, so PCR can remain positive for 2-3 weeks. This makes it hard to use PCR to confirm M. pneumoniae as the etiologic agent, especially in the setting of unusual clinical presentations. Serologic testing is often ordered and hard to interpret. False positive IgM antibody tests are not uncommon, and IgM antibody can persist for months. Outside of PCR and culture, acute and convalescent specimens can be used diagnostically, and a fourfold IgG antibody rise is consistent with acute infection.

Macrolides are regarded as the preferred treatment for M. pneumoniae pneumonia, but several studies question whether treatment impacts the clinical course. This may be due to the inherent difficulty of confirming M. pneumoniae as the etiologic agent, as most studies used serology to confirm the diagnosis. In countries outside the United States, macrolide resistance is well reported, and this may be underappreciated in the United States. We recently cared for a teenager with Down syndrome with pneumonia caused by M. pneumoniae who had a protracted clinical course. Fever and hypoxemia were persistent over a several-week period despite two courses of azithromycin and exclusion of virus, bacteria, and fungal pathogens. Bronchoalveolar lavage was performed, M. pneumoniae was detected by PCR, and macrolide resistance was confirmed. Levofloxacin was given, and she recovered over the next week.

Macrolide resistance is commonly reported outside the United States; rates in China are reported to be greater than 90%, in Japan 80%, and in Europe, between 15% and 25%. A recent study from Greg Storch and his colleagues (Pediatr. Infect. Dis. J. 2012;31:409-10) documented macrolide resistance in 8% of respiratory samples collected between 2007 and 2010 (49 patients; mean age, 10 years), noting the resistance rate was 3% in 2007-2008 and 15% in 2009-2010. A recently published study of data from Canada reported that 12.1% of M. pneumoniae–positive specimens collected between 2010 and January 2012 carried nucleotide mutations associated with macrolide resistance in the 23S rRNA gene (Emerg. Infect. Dis. 2013 September [doi: 10.3201/eid1909.121466]). Anecdotal studies suggest that patients with macrolide-resistant M. pneumoniae infection clinically improve when given doxycycline (or minocycline) or levofloxacin.

A number of clinical questions regarding M. pneumoniae may be answered more definitively in the future, but we need more easily available diagnostics (PCR is a good start), routinely accessible susceptibility data, and a good randomized controlled study to investigate the question of whether treatment shortens the course of disease.

Dr. Jackson is chief of pediatric infectious diseases at Children’s Mercy Hospital, Kansas City, Mo., and professor of pediatrics at the University of Missouri-Kansas City. She said she has no conflicts of interest to disclose. E-mail her at pdnews@frontlinemedcom.com.