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Mycoplasma pneumoniae infection in children

Mycoplasma pneumoniae infection in children
Author:
Jesus G Vallejo, MD
Section Editor:
Morven S Edwards, MD
Deputy Editor:
Diane Blake, MD
Literature review current through: Jan 2024.
This topic last updated: Jan 08, 2024.

INTRODUCTION — Mycoplasma pneumoniae is one of the few species of Mycoplasma that frequently cause infection in humans. M. pneumoniae predominantly causes respiratory tract infection but has a wide variety of clinical manifestations.

The clinical features, diagnosis, and treatment of M. pneumoniae infection in children will be reviewed here. M. pneumoniae infection in adults, Mycoplasma genitalium, Mycoplasma hominis, and Ureaplasma urealyticum infections are discussed separately. (See "Mycoplasma pneumoniae infection in adults" and "Mycoplasma genitalium infection" and "Mycoplasma hominis and Ureaplasma infections".)

MICROBIOLOGY AND PATHOGENESIS — The term "mycoplasma" is used to refer to any organism within the class Mollicutes, which is composed of five genera (Mycoplasma, Ureaplasma, Acholeplasma, Anaeroplasma, and Asteroloplasma).

M. pneumoniae lacks a cell wall, which differentiates it from other pathogenic bacteria [1]. Although it grows under both aerobic and anaerobic conditions and can be isolated on media supplemented with serum, it is a fastidious organism, and isolation is not commonly performed in clinical laboratories.

The mechanisms by which mycoplasmas produce infection are becoming better understood. They include direct effects of the bacteria, indirect immune-mediated effects, and effects mediated through vasculitis or thrombosis secondary to cytokines, chemokines, or immunomodulation [2,3].

Pathogenic mycoplasmas have specialized tip organelles that mediate their interactions with host cells through transmembrane proteins (eg, P1, P30) that contribute to adherence and gliding motility along the respiratory epithelium [2,4-7]. Toll-like receptor 2 is also believed to be important for binding of Mycoplasma and activation of inflammatory mediators, including cytokines [8-10].

The adherence proteins of M. pneumoniae have a particular affinity for respiratory tract epithelium [11,12]. Once attached, M. pneumoniae produces hydrogen peroxide and superoxide, causing injury to epithelial cells and their associated cilia. Survival is achieved by surface parasitism of target cells, acquisition of essential biosynthetic precursors, and, in some cases, cell entry and intracellular survival [13]. After acute infection, prolonged asymptomatic carriage may be mediated by intracellular invasion, bacterial-induced cytoskeleton rearrangement, and tissue remodeling [14-16].

The clinical manifestations of M. pneumoniae infection are affected by the immune competence and immune response of the host, suggesting that some of the pathogenic features of M. pneumoniae infection, particularly extrapulmonary manifestations (eg, hemolysis, encephalitis), are immune mediated [2,12]. The antibodies produced against the glycolipid antigens of M. pneumoniae cross-react with human red cells and brain cells and may act as autoantibodies [17].

TRANSMISSION — M. pneumoniae is transmitted from person to person by infected respiratory droplets during close contact. The incubation period after exposure is approximately 23 days [2]. The cumulative attack rate in families approaches 90 percent [18]. Immunity is not long-standing, although immunoglobulin (Ig)G antibodies may persist for years [2].

EPIDEMIOLOGY — M. pneumoniae infection occurs most frequently during the summer and early fall but may develop year-round [2,19].

M. pneumoniae infection occurs in children of all ages. In a series of 353 children hospitalized with M. pneumoniae infection between 2007 and 2017, approximately one-half of patients were <6 years old [20]. In population-based surveillance, the rate of hospitalization for M. pneumoniae pneumonia among children (<18 years) was 1.4 per 10,000 children per year and was similar across age groups [21].

M. pneumoniae is a common cause of community-acquired pneumonia (CAP) in children. In population-based surveillance from 2010 to 2012, M. pneumoniae was the most frequently detected bacterial pathogen in >2200 children (age <18 years) hospitalized with radiographically confirmed CAP in the United States, accounting for 8 percent of cases [21,22].

The relative importance of M. pneumoniae as a cause of CAP in children increases during the school-age years (even though the overall incidence of pneumonia declines). In prospective population-based surveillance, the median age of children hospitalized with CAP was 7 years [22]. The proportion of cases caused by M. pneumoniae increased with age (2 percent in children age <2 years, 5 percent in children age 2 to 4 years, 16 percent in children age 5 to 9 years, and 23 percent in children age 10 to 17 years) [21].

Other pathogens are frequently detected in children with M. pneumoniae infection [22-24]. In two reviews of children hospitalized with M. pneumoniae, codetection of viral pathogens occurred in approximately 30 percent of children, most frequently in children younger than two to five years. Viral copathogens may account for some of the clinical manifestations attributed to M. pneumoniae in young children [23].

CLINICAL MANIFESTATIONS — M. pneumoniae causes a wide spectrum of illness [25]. Many M. pneumoniae infections are asymptomatic [14,26]. The clinical manifestations of symptomatic M. pneumoniae infection are typically divided into respiratory tract (most common) and extrapulmonary manifestations (less common) [2,26]. None of the manifestations is unique to M. pneumoniae [27,28]. Although M. pneumoniae infections generally are mild and self-limiting, patients of all ages can develop severe community-acquired pneumonia (CAP) or extrapulmonary manifestations [19].

Asymptomatic carriage — Asymptomatic carriage is common and may play a role in M. pneumoniae transmission [14,15,29]. Following symptomatic infection, asymptomatic carriage of M. pneumoniae can persist for weeks to months, even in patients who received antimicrobial therapy [14,15,30]. In studies using polymerase chain reaction (PCR)-based assays, the reported rates of M. pneumoniae detection in the respiratory secretions of children range from ≤3 to 56 percent [14,21,31,32]. The wide range may be due to different definitions for asymptomatic controls, testing methods, and M. pneumoniae activity with time and geographic location.

Pneumonia — Pneumonia is the most common clinical manifestation of M. pneumoniae in school-age children [20].

Clinical features – The signs and symptoms of M. pneumoniae pneumonia vary according to the stage of illness (figure 1). The onset is gradual and usually is heralded by headache, malaise, and low-grade fever [17,26]. Physical examination abnormalities are often minimal.

Among children with PCR-documented, radiographically confirmed M. pneumoniae pneumonia in two studies, commonly reported symptoms and signs included [20,22]:

Fever (86 to 96 percent)

Cough (85 to 96 percent); cough is usually nonproductive and may persist for weeks to months [19,28]

Fatigue (78 percent)

Dyspnea (67 percent)

Headache (11 to 48 percent)

Sore throat (12 to 47 percent)

Abnormal auscultation (75 percent)

Extrapulmonary manifestations (26 percent)

Clinical features that were more frequently associated with M. pneumoniae than other pathogens include age 5 through 17 years, rales, decreased breaths sounds, headache, and sore throat [22]. However, these findings are nonspecific and do not definitively distinguish M. pneumonia from other CAP pathogens [22,28].

Other clinical findings related to the respiratory tract include sinus tenderness, rhinorrhea, mild erythema of the posterior pharynx, ear pain, erythema or bullae of the tympanic membrane, and nonprominent cervical adenopathy [20,26].

M. pneumoniae CAP can be severe [33,34]. In a prospective study of 182 children (age <18 years) with M. pneumoniae CAP, 26 percent had pleural effusion and 12 percent required intensive care [22]. Empyema is a rare complication of M. pneumoniae pneumonia [35]. (See "Epidemiology, clinical presentation, and evaluation of parapneumonic effusion and empyema in children" and "Management and prognosis of parapneumonic effusion and empyema in children".)

Radiographic findings – Radiographic findings of M. pneumoniae pneumonia are variable, nonspecific, and may be difficult to appreciate [20,22,36].

In a prospective study of 182 children (age <18 years) hospitalized with M. pneumoniae CAP, radiographic findings (which were not mutually exclusive) included consolidation (59 percent), single lobar infiltrate (32 percent), unilateral multilobar infiltrates (11 percent), bilateral multilobar infiltrates (image 1) (12 percent), pleural effusion (26 percent), and hilar adenopathy (10 percent) [22]. The finding of hilar adenopathy in children with suspected M. pneumoniae infection should also prompt consideration of tuberculosis. (See "Tuberculosis disease in children: Epidemiology, clinical manifestations, and diagnosis".)

Although high-resolution computed tomography may be more sensitive than chest radiography for detection of air space abnormalities in patients with M. pneumoniae pneumonia [36], it is not necessary in the routine evaluation. Given the radiation exposure, it should only be obtained if the results will affect management. (See "Radiation-related risks of imaging", section on 'Children and adolescents'.)

Laboratory findings – Laboratory findings in children with M. pneumoniae pneumonia are nonspecific.

The total white blood cell count, neutrophil count, and platelet count may be slightly elevated [2,20]. In a review of 182 cases of PCR-documented M. pneumoniae pneumonia in children, 25 percent had leukocytosis and 9 percent had thrombocytosis [22].

C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) also may be elevated [2,20]. In a cohort of 194 children with radiographically confirmed M. pneumoniae pneumonia, the median ESR was 51 mm/h (interquartile range [IQR] 23 to 73 mm/h) and the median CRP was 4 mg/dL (IQR 2 to 8 mg/dL) [20].

Some patients have subclinical evidence of hemolytic anemia (eg, positive Coombs test, elevated reticulocyte count). (See 'Hemolysis' below.)

Other respiratory manifestations — M. pneumoniae may cause a nonspecific respiratory illness similar to an upper respiratory tract infection (eg, nonexudative sore throat, coryza, headache, ear pain, prolonged cough) [2,20].

M. pneumoniae infection can worsen asthma symptoms and may be associated with wheezing in children who do not have asthma [2,20,22]. Whether M. pneumoniae has a pathogenic role in asthma is discussed separately. (See "Risk factors for asthma", section on 'Respiratory infections'.)

Extrapulmonary manifestations — Extrapulmonary manifestations may occur with respiratory manifestations or independently [19,20]. When present, they support the diagnosis. In a review of children hospitalized with PCR-documented M. pneumoniae infection, 26 percent of the 332 children with complete clinical information had extrapulmonary manifestations; 11 percent had only extrapulmonary manifestations [20].

Hemolysis — M. pneumoniae-associated hemolysis usually is not clinically significant, although it can be severe, particularly in patients with underlying sickle cell disease [17,37]. (See "Autoimmune hemolytic anemia (AIHA) in children: Classification, clinical features, and diagnosis".)

IgM antibodies to the I antigen on erythrocyte membranes appear during the course of mycoplasma infection and produce a cold agglutinin response in approximately 50 percent of patients [2]. Why mycoplasma infections promote the production of such antibodies and their significance in pathogenesis is not known. (See 'Laboratory tests' below and "Cold agglutinin disease", section on 'Pathogenesis'.)

Mucocutaneous disease — Mucosal or cutaneous eruptions are a common extrapulmonary manifestation of M. pneumoniae infection, occurring in as many as 25 percent of patients [20,38,39].

Dermatologic manifestations range from a mild erythematous maculopapular or vesicular rash (which is most commonly seen accompanying respiratory tract infections), to bullous papular purpuric gloves and socks syndrome, to reactive infectious mucocutaneous eruption (a Stevens-Johnson-like syndrome) [39]. (See "Reactive infectious mucocutaneous eruption (RIME)", section on 'Clinical manifestations'.)

Central nervous system manifestations — Central nervous system (CNS) manifestations occur in approximately 0.1 percent of all patients with M. pneumoniae infections and approximately 6 percent hospitalized patients [2,20,40].

CNS involvement occurs most frequently in children and includes [20,41-51]:

Meningoencephalitis (which may be complicated by postencephalitic epilepsy)

Acute disseminated encephalomyelitis (ADEM)

Transverse myelitis

Cerebellar ataxia

Guillain-Barré syndrome

Cerebellar infarct

Peripheral neuropathy

Cranial nerve palsies

In patients with CNS involvement, the cerebrospinal fluid (CSF) typically reveals a lymphocytic pleocytosis, elevated protein, and normal glucose [50]. Detection of M. pneumoniae in the CSF occurs relatively infrequently [40,52,53].

In a retrospective study of 365 children with M. pneumoniae detected in the CSF or respiratory tract by PCR between 1996 and 2013, neurologic disease was attributable to M. pneumoniae in 11.5 percent [47]. Among the 42 children with neurologic disease, encephalitis, ADEM, transverse myelitis, and cerebellar ataxia were most common. CSF PCR was positive for M. pneumoniae in 14 of the 35 children in whom it was obtained. Two distinct patterns of neurologic disease were noted: a prodrome of ≥7 days, respiratory manifestations, chest radiograph abnormalities, reactive IgM in acute serum, and detection of M. pneumoniae in the respiratory tract, but not the CSF; and a prodrome of <7 days, fewer respiratory manifestations, nonreactive IgM response, and detection of M. pneumoniae in the CSF only.

Although uncommon, CNS involvement is associated with significant morbidity and mortality [40,47,50]. In the retrospective study described above, 20 of 42 children with M. pneumoniae neurologic disease had adverse neurologic outcomes (eg, epilepsy, focal neurologic deficits, persistent headaches), but no deaths were reported [47]. In another retrospective study of 61 patients with M. pneumoniae neurologic disease, 14 had severe sequelae and 8 patients died [40].

Other manifestations — M. pneumoniae can also cause gastrointestinal, rheumatologic, cardiac, and renal disease [2,17,54].

In a review of 353 children hospitalized with PCR-documented M. pneumoniae infection, 38 percent had abdominal pain, vomiting, and diarrhea; 10 percent had elevated liver enzymes; 3 percent had more serious gastrointestinal involvement (eg, splenomegaly, intussusception, hepatomegaly, pancreatitis); 3 percent had arthritis or arthralgia; and 4 percent had cardiovascular involvement (eg, heart failure, myocarditis, pericardial effusion) [20]. Clinically significant glomerulonephritis is a rare complication that is presumed to be secondary to immune complex deposition [55-57].

DIAGNOSIS

Criteria for confirmation — M. pneumoniae should be suspected in children with a compatible clinical syndrome. (See 'Clinical manifestations' above.)

Confirmation of M. pneumoniae requires detection of M. pneumoniae or antibody response to M. pneumoniae in conjunction with a compatible clinical syndrome. Laboratory results must be interpreted with caution because they may not differentiate between M. pneumoniae disease and asymptomatic colonization or clinical manifestations of a concomitant viral pathogen [14,58-60]. The diagnosis may be confirmed in retrospect (eg, by convalescent serology or clinical improvement with M. pneumoniae-specific therapy).

Indications for testing — Laboratory confirmation should only be pursued if it will alter management (eg, in patients with life-threatening disease, such as encephalitis, or if antimicrobial therapy is necessary and the empiric regimen does not include an agent with activity against M. pneumoniae, such as a macrolide, tetracycline, or quinolone antibiotic). (See 'Management' below.)

Approach to testing — The approach to laboratory testing for M. pneumoniae varies with the clinical findings.

Pneumonia

Outpatients – Laboratory testing usually is not performed in outpatients with community-acquired pneumonia (CAP) because empiric treatment is almost always successful, whether or not it includes activity against M. pneumoniae [61,62]. (See "Community-acquired pneumonia in children: Clinical features and diagnosis", section on 'Indications for microbiologic testing'.)

Hospitalized children – Laboratory testing for M. pneumoniae generally is warranted for children hospitalized with CAP, particularly if they have compromised immunity, risk factors (eg, close exposure during an outbreak), or associated extrapulmonary manifestations (eg, mucocutaneous eruption, hemolysis) [19].

Laboratory testing also may be warranted for hospitalized children who do not improve as expected with supportive care for presumed viral pneumonia or with beta-lactam antibiotics for presumed typical bacterial pneumonia.

Testing approach – When testing is necessary, we prefer M. pneumoniae polymerase chain reaction (PCR), including multiplex PCR panels, from a respiratory specimen (eg, nasopharyngeal or throat swab) [63]. PCR can be performed rapidly and has high sensitivity and specificity. If PCR is not available, serology (M. pneumoniae IgM and IgG enzyme immunoassay [EIA]) is a reasonable alternative. M. pneumoniae culture is not available in most clinical laboratories [58]. We do not routinely obtain cold agglutinin antibody titers or bedside cold agglutinins in children with pneumonia. (See 'Laboratory tests' below.)

Mucocutaneous disease — Detection of M. pneumoniae is necessary to definitively attribute mucocutaneous disease to M. pneumoniae [64]. Diagnosis of reactive infectious mucocutaneous eruption (RIME) is discussed separately. (See "Reactive infectious mucocutaneous eruption (RIME)", section on 'Diagnosis'.)

If not already obtained, chest radiograph also may be warranted given the frequency of prodromal respiratory symptoms in patients with RIME. (See "Reactive infectious mucocutaneous eruption (RIME)", section on 'Diagnosis'.)

Encephalitis — Encephalitis is an acute, life-threatening emergency, and a systematic approach is necessary for prompt recognition and appropriate management. The complete evaluation is discussed in detail separately and summarized in the table (table 1). (See "Acute viral encephalitis in children: Clinical manifestations and diagnosis", section on 'Evaluation'.)

Our approach to the evaluation for M. pneumoniae in children with encephalitis is consistent with that of the International Encephalitis Consortium [65].

Children with respiratory symptoms – For children with suspected M. pneumoniae meningoencephalitis and concomitant respiratory symptoms, we obtain M. pneumoniae PCR from the throat and cerebrospinal fluid (CSF) and serology (M. pneumoniae IgM and IgG). (See 'Laboratory tests' below.)

Children without respiratory symptoms – For children with suspected M. pneumoniae meningoencephalitis without respiratory symptoms, we obtain a throat sample for M. pneumoniae PCR and serology (M. pneumoniae IgM and IgG); we obtain CSF PCR only if either of the initial tests is positive. (See 'Laboratory tests' below.)

Other extrapulmonary disease — For other types of extrapulmonary disease, the confirmation of M. pneumoniae may be established by detection of M. pneumoniae at the affected site (eg, M. pneumoniae PCR from vesicular fluid, oral lesions, synovial fluid) or by the M. pneumoniae antibody response [66-70]. However, lack of detection or antibody response does not exclude the diagnosis [14,58,59,71].

Laboratory tests — Available tests for acute diagnosis of M. pneumoniae include nucleic acid amplification tests (NAATs) and serology. Culture, performed in specialized reference laboratories, is not widely available. Each of these methods has advantages and disadvantages [72].

Nucleic acid amplification tests NAATs, including PCR-based assays, are highly sensitive and specific for M. pneumoniae in patients with respiratory tract infections and results are available in less than one day [2,73,74]. However, they may not reliably distinguish active M. pneumoniae infection from coinfection with other pathogens or from asymptomatic carriage [14]. (See 'Asymptomatic carriage' above.)

Single and multiplex PCR assays for M. pneumoniae are commercially available for respiratory tract samples (eg, nasopharyngeal or throat swab, sputum sample, bronchoalveolar lavage fluid) [63,72,75,76]. Although the sensitivity and specificity of US Food and Drug Administration (FDA)-cleared assays is generally >90 percent for respiratory samples (using various reference standards including serology, culture, or another NAAT) [76-79], the sensitivity and specificity of PCR assays that are used by individual institutions (which may not be cleared by the FDA) are not generalizable.

Single and multiplex assays for M. pneumoniae in the CSF are also available, but the diagnostic yield of CSF PCR is low relative to serology. (See "Molecular diagnosis of central nervous system infections", section on 'Bacteria'.)

Serology – Serology is an adjunct to PCR or as an alternative to PCR if PCR is not available. IgM antibody titers begin to rise approximately seven to nine days after infection, peak at three to six weeks, and persist for months [52]. IgG antibody titers begin to rise and peak approximately two weeks after IgM titers and persist for years. Both IgM and IgG antibodies may be negative early in the disease course.

In general, a fourfold or greater increase in titer in paired sera (separated by four weeks) is indicative of infection [19]; a single titer is not definitive for diagnosis, but convalescent titers are only necessary if they will change management [80-82].

Although serologic tests provide evidence of infection, definitive diagnosis is delayed by the need to assay acute and convalescent serum. In addition, serologic tests may not distinguish M. pneumoniae disease from asymptomatic carriage [14].

Among the available serologic tests, EIA is preferred to complement fixation tests because EIA is more readily available and more specific [52]. EIA is more sensitive in detecting acute infection than culture and has sensitivity comparable to the PCR if there has been sufficient time to develop an antibody response [81].

A number of studies evaluating commercially available serologic tests note a lack of comparability among the tests and among different laboratories [82-85].

Antigen detection –Antigen detection can be performed by antigen capture-EIA (Ag-EIA), which may detect 104 colony-forming units/mL (a level which should be present in the majority of infections) [86]. Antigen detection tests have largely been replaced by molecular testing methods but continue to be used in some countries [2]. One problem with Ag-EIA is that the ability to detect antigen may vary with the time of sampling; the test is most often positive within seven days of onset.

Culture – Most clinical laboratories do not attempt to culture M. pneumoniae [58]. Although isolation is possible, it takes two to three weeks and requires a specialized media. M. pneumoniae is not visible on Gram stain because it lacks a cell wall.

Cold agglutinins – The formation of cold agglutinins is a nonspecific early IgM reaction against the erythrocyte I antigen.

We do not routinely obtain cold agglutinin antibody titers in children because the accuracy of cold agglutinins in detecting M. pneumoniae in children is not known [58], nor do we suggest performing bedside cold agglutinins because bedside cold agglutinins are neither sensitive nor specific for M. pneumoniae infection in children. A variety of other respiratory pathogens have been associated with increased cold agglutinins. (See "Cold agglutinin disease", section on 'Infections and autoimmune disorders'.)

MANAGEMENT

Pneumonia

Empiric therapy — Initial treatment for M. pneumoniae pneumonia typically is initiated based on clinical suspicion. Confirmation of M. pneumoniae is often lacking because of the difficulty with definitive diagnosis early in the course of infection and because microbiologic testing is not recommended for community-acquired pneumonia (CAP) in children who are treated in the outpatient setting. Empiric treatment of CAP in children, including M. pneumoniae pneumonia, is discussed separately. (See 'Diagnosis' above and "Pneumonia in children: Inpatient treatment" and "Community-acquired pneumonia in children: Outpatient treatment", section on 'Empiric therapy'.)

Documented M. pneumoniae — For children with documented M. pneumoniae pneumonia, we suggest antimicrobial therapy with an agent with activity against M. pneumoniae (eg, macrolide, tetracycline, or fluoroquinolone antibiotics). M. pneumoniae is resistant to antibiotics that inhibit cell wall synthesis (eg, beta-lactam antibiotics) [19]. Limited evidence suggests that M. pneumoniae-specific therapy may be associated with decreased rates of hospitalization or shorter length of stay.

For immunocompetent children we typically use a macrolide or tetracycline antibiotic for initial therapy. Fluoroquinolones are reserved for children in whom there is no safe or effective alternative [87,88]. The regimens are as follows [58,89,90]:

Azithromycin 10 mg/kg in one dose (maximum dose 500 mg) orally or intravenously (IV) on the first day and 5 mg/kg in one dose (maximum dose 250 mg) for the next four days.

Clarithromycin 15 mg/kg per day orally in two divided doses (maximum daily dose 1 g) for 7 to 10 days.

Doxycycline 2 to 4 mg/kg per day orally or IV in one or two divided doses (maximum daily dose 200 mg) for 7 days.

Compared with other tetracycline antibiotics, doxycycline is unlikely to cause permanent tooth discoloration in young children [91-94]. It can be administered for ≤21 days to children of all ages [94].

Erythromycin 40 to 50 mg/kg per day orally in three or four divided doses (maximum daily dose 2 g) for 7 to 10 days.

Erythromycin 20 mg/kg per day IV in four divided doses (maximum daily dose 2 g) for 7 to 10 days.

For children ≥8 years of age – Tetracycline 25 to 50 mg/kg per day orally in four divided doses (maximum daily dose 2 g) for 7 to 10 days.

Azithromycin, clarithromycin, doxycycline, and tetracycline are preferred to erythromycin because they require less frequent dosing and have fewer gastrointestinal adverse effects. Azithromycin has a longer half-life than clarithromycin and usually is better tolerated [23].

For immunocompromised children, fluoroquinolones (eg, levofloxacin) are an alternative initial agent, especially if the patient has a history of exposure to a macrolide antibiotic [24]. Fluoroquinolones are bactericidal rather than bacteriostatic. Dosing for levofloxacin varies according to age:

≥6 months and <5 years – Levofloxacin 8 to 10 mg/kg per dose orally or IV every 12 hours (maximum daily dose 750 mg/day) for 7 to 10 days.

≥5 years – Levofloxacin 10 mg/kg per dose once per day orally or IV (maximum daily dose 750 mg/day) for 7 to 10 days.

Macrolide, tetracycline, and fluoroquinolone antibiotics are active against M. pneumoniae in vitro, and macrolide antibiotics may have anti-inflammatory effects [2]. Macrolide and tetracycline antibiotics have a lower risk of severe adverse effects than fluoroquinolones.

Studies supporting antibiotic treatment of documented M. pneumoniae pneumonia in children are limited [95-97]. Support is provided predominantly by in vitro studies [98,99], a randomized trial in military recruits [100], and observational studies in which inclusion of M. pneumoniae-specific therapy was associated with decreased risk of treatment failure (ie, change in antimicrobial therapy or hospital admission) or length of stay in children with CAP (etiologic data were not available) [62,101]. A systematic review of 17 studies (4294 patients) found insufficient evidence for efficacy of antimicrobial treatment of M. pneumoniae lower respiratory tract infection in children ≤17 years [97]. However, the included trials were limited by publication bias, heterogeneity, and lack of blinding [97,102].

Whether administration of antibiotics decreases the incidence or severity of associated mucocutaneous disease is unclear [103].

Macrolide resistance — The possibility of macrolide resistance should be considered in children with suspected M. pneumoniae infection who do not respond as expected to macrolide therapy, particularly if the child is severely ill and/or has a history of exposure to a macrolide [24].

M. pneumoniae resistant to macrolides has been reported in Asia, Europe, and North America [104-112]. In the United States, in studies published from 2010 to 2019, macrolide resistance ranges from 3.5 to 13.2 percent of M. pneumoniae isolates [22,24,111,113]. In a 2015 to 2018 study, the overall rate of macrolide resistance from eight hospitals in the United States was 7.5 percent [24]. However, resistance varied geographically, from 2 percent in the West to 18 percent in the South and East.

In some studies, prolonged fever (ie, ≥48 hours after the initiation of therapy) has been reported in children with macrolide-resistant isolates who were treated with macrolide antibiotics [107,114-117]. Another study found no differences in clinical features or outcome between patients with macrolide-resistant and macrolide-susceptible M. pneumoniae, but there were few children with macrolide-resistant M. pneumoniae (21 versus 285) [24].

Rapid testing methods for detection of macrolide resistance have been developed and are available in some clinical laboratories [2].

For children with documented or suspected M. pneumoniae pneumonia who do not respond as expected to macrolide therapy, we suggest a tetracycline antibiotic (eg, tetracycline, doxycycline) or fluoroquinolone (eg, levofloxacin) antibiotic [98,109]. We suggest one of the following regimens [88,90,118]:

Doxycycline 2 to 4 mg/kg orally or IV per day in one or two divided doses (maximum daily dose 200 mg) for 10 days; compared with other tetracycline antibiotics, doxycycline is unlikely to cause permanent tooth discoloration in young children [91-94]. It can be administered for ≤21 days to children of all ages [94].

Levofloxacin

≥6 months and <5 years – 8 to 10 mg/kg per dose every 12 hours (maximum daily dose 750 mg/day) for 7 to 10 days

≥5 years – 10 mg/kg per dose once per day (maximum daily dose 750 mg/day) for 7 to 10 days

Although fluoroquinolones are not routine first-line agents for children, they may be reasonable if no other safe and effective alternative is available [87,88]. (See "Fluoroquinolones", section on 'Children'.)

Other clinical syndromes

Upper respiratory tract infections – We do not treat M. pneumoniae upper respiratory tract infections with antibiotics. The benefits of antimicrobial therapy for the treatment of upper respiratory tract symptoms caused by M. pneumoniae have not been adequately studied in children.

Mucocutaneous disease – Consultation with a specialist in dermatology or infectious diseases may be warranted to differentiate reactive infectious mucocutaneous eruption (RIME) from other mucocutaneous eruptions [119].

The management of RIME is discussed separately. (See "Reactive infectious mucocutaneous eruption (RIME)", section on 'Management'.)

Treatment of associated pneumonia (if present) is discussed above [120]. (See 'Pneumonia' above.)

Central nervous system disease – Treatment of M. pneumoniae central nervous system (CNS) disease is individualized according to the clinical syndrome (eg, encephalitis, Guillain-Barré syndrome) and severity of illness. Consultation with an expert in pediatric infectious diseases and/or pediatric neurology is suggested.

Antibiotics and adjunctive therapies to address immune-mediated symptoms may have a therapeutic role and are frequently administered given concern for long-term neurologic sequelae. However, randomized trials evaluating antimicrobial and/or adjunctive therapies for M. pneumoniae CNS disease are lacking. In observational studies, glucocorticoids, anti-inflammatory drugs, diuretics, intravenous immune globulin, and plasma exchange have been used in addition to antibiotics without clear indication of benefit [12,42,47,121,122]. As an example, in a retrospective analysis of 42 children with definite, probable, or possible M. pneumoniae CNS disease (eg, encephalitis, transverse myelitis, acute disseminated encephalomyelitis), 29 children received macrolide therapy and 17 received glucocorticoids [47]. Adverse neurologic outcome (eg, epilepsy, focal neurologic deficit) occurred in 15 of those who received macrolides and 9 of those who received glucocorticoids.

Hemolytic anemia – The management of M. pneumoniae-related hemolytic anemia is discussed separately. (See "Cold agglutinin disease", section on 'Management'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pediatric pneumonia" and "Society guideline links: Infectious encephalitis".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword[s] of interest.)

Basics topics (see "Patient education: Pneumonia in children (The Basics)" and "Patient education: Mycoplasma pneumonia in children (The Basics)")

SUMMARY AND RECOMMENDATIONS

Mycoplasma pneumoniae is fastidious bacteria that lacks a cell wall. It is transmitted from person to person by infected respiratory droplets. The incubation period is approximately three weeks and the cumulative attack rate in families approaches 90 percent. (See 'Microbiology and pathogenesis' above and 'Transmission' above.)

M. pneumoniae infection occurs in children of all ages and is a common cause of community-acquired pneumonia (CAP) in children, particularly those ≥5 years of age. (See 'Epidemiology' above.)

M. pneumoniae CAP has a gradual onset and usually is heralded by headache, malaise, and low-grade fever (figure 1). M. pneumoniae CAP may be accompanied by other respiratory tract findings (eg, pharyngitis) and extrapulmonary manifestations (eg, hemolysis, mucocutaneous eruption, central nervous system involvement). Clinical, radiographic, and laboratory features are nonspecific and do not definitively distinguish M. pneumoniae from other CAP pathogens. (See 'Clinical manifestations' above.)

M. pneumoniae mucocutaneous disease is increasingly recognized in adolescents. It predominantly affects the mucous membranes and usually is associated with atypical CAP. (See 'Mucocutaneous disease' above.)

M. pneumoniae should be suspected in children with a compatible clinical syndrome. Laboratory confirmation requires detection of M. pneumoniae or antibody response to M. pneumoniae but should only be pursued if it will alter management (eg, if antimicrobial therapy is necessary and the empiric regimen does not include an agent with activity against M. pneumoniae, such as a macrolide or tetracycline antibiotic). (See 'Indications for testing' above.)

The approach to testing varies with the clinical syndrome. When testing is necessary, we generally prefer M. pneumoniae polymerase chain reaction (PCR) from a respiratory specimen. It can be performed rapidly and has high sensitivity and specificity. If PCR is not available, serology (IgM and IgG enzyme immunoassay) is a reasonable alternative. (See 'Approach to testing' above.)

For children with documented M. pneumoniae pneumonia, we suggest antimicrobial therapy with an agent with activity against M. pneumoniae (eg, macrolide, tetracycline, or fluoroquinolone antibiotics) (Grade 2C). Limited evidence suggests that M. pneumoniae-specific therapy may be associated with decreased rates of hospitalization or shorter length of stay. For immunocompetent children, we prefer macrolide or tetracycline antibiotics to fluoroquinolones. For immunocompromised children, fluoroquinolones (eg, levofloxacin) are another alternative, especially if the patient has a history of exposure to a macrolide antibiotic. (See 'Documented M. pneumoniae' above.)

The regimens are as follows:

Azithromycin 10 mg/kg in one dose (maximum dose 500 mg) orally or intravenously (IV) on the first day and 5 mg/kg in one dose (maximum dose 250 mg) for the next four days

Clarithromycin 15 mg/kg per day orally in two divided doses (maximum daily dose 1 g) for 7 to 10 days

Doxycycline 2 to 4 mg/kg per day orally or IV in one or two divided doses (maximum daily dose 200 mg) for 7 days

Erythromycin 40 to 50 mg/kg per day orally in three or four divided doses (maximum daily dose 2 g) for 7 to 10 days

Erythromycin 20 mg/kg per day IV in four divided doses (maximum daily dose 2 g) for 7 to 10 days

For children ≥8 years of age: tetracycline 20 to 50 mg/kg per day orally in four divided doses (maximum daily dose 2 g) for 7 to 10 days

Levofloxacin:

-≥6 months and <5 years – Levofloxacin 8 to 10 mg/kg per dose orally or IV every 12 hours (maximum daily dose 750 mg/day) for 7 to 10 days

-≥5 years – Levofloxacin 10 mg/kg per dose once per day orally or IV (maximum daily dose 750 mg/day) for 7 to 10 days

Doxycycline or a fluoroquinolone (eg, levofloxacin) antibiotic should be used if macrolide resistance is suspected or documented, particularly if the child is severely ill. (See 'Macrolide resistance' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Dori Zaleznik, MD, who contributed to an earlier version of this topic review.

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Topic 6070 Version 45.0

References

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