Mycoplasma pneumoniae infection and asthma in children

Abstract

A clinical association between exacerbation of asthma symptoms and Mycoplasma pneumoniae (M. pneumoniae) infection has long been suspected. We studied 80 children aged 5–15 years; 50 with asthma (Group 1) and 30 without an acute exacerbation of asthma (Group 2) for detection of M. pneumoniae by serology and polymerase chain reaction (PCR) on nasopharyngeal aspirates. Our study confirms that lower respiratory tract infections with M. pneumoniae are frequently associated with exacerbations of asthma in children.

Keywords

Asthma bacterial infection diagnosis disease respiratory tract infections

Introduction

Mycoplasma pneumoniae (M. pneumoniae) causes 6–20% of lower respiratory tract infections (LRTIs) and community-acquired pneumonia (CAP) in both older children and adults.¹ It has been suspected for >20 years that there is a clinical association between exacerbation of asthma symptoms and M. pneumoniae infection, but the nature of this correlation is still far from clear. The aim of our study was to analyse the role of M. pneumoniae as a cause of exacerbation of asthma in children by using serology and polymerase chain reaction (PCR).

Material and methods

Our study included children aged 5–15 years: Group 1 (50 cases of known asthma presenting as paediatric emergencies) and Group 2 (30 cases of asthmatic children under control without acute exacerbation). Exclusion criteria were the presence of a chronic disease of the pulmonary or cardiovascular system, metabolic disorders, immunosuppression, genetic or neurological disorders. Nasopharyngeal aspirates (NPA) were collected for the diagnosis of M. pneumoniae by PCR assay. Serum samples were obtained for IgM and IgG antibodies to M. pneumoniae by commercially available ELISA-based kits (Novatech Immunodiagnostica, GmbHD, Germany). All the samples were taken at admission before treatment. M. pneumoniae PCR was performed on DNA extracted from NPA by the centrifugation proteinase-K method of Williamson et al.² A 543 base pair (bp) region on the P1 gene of M. pneumoniae was amplified employing primers Mpn1 CAA GCC AAA CAC GAG CTC CGG CC and Mpn 2 CCA GTG TCA GCT GTT TGT CCT TCC CC.²

Analysis of the data was performed and the difference of proportion between qualitative variables tested by χ² test and Fisher's exact with SPSS version 12 software. All statistical tests were performed for determining any significant difference at 5% level.

Results

Neither age group 5–8 years compared to 9–15 years, within Group 1 and Group 2 children, nor sex ratio was significant for differences in M. pneumoniae infection. All clinical characteristics were comparable in Group 1 and Group 2 children (Table 1).

Table 1.

Baseline characteristics of the study groups.

	Group 1* (n = 50)			Group 2^† (n = 30)
Characteristic	M. pneumoniae positive	M. pneumoniae negative	P	M. pneumoniae positive	M. pneumoniae negative	P
Age group (years)
5–8	12 (24)	15 (30)	0.81	2 (6.7)	6 (20)	0.28
9–15	11 (22)	12 (24)	0.81	2 (6.7)	20 (66.7)	0.28
Gender
Male	16 (32)	13 (26)	0.12	3 (10)	14 (46.7)	0.61
Female	7 (14)	14 (28)	0.12	1 (.3.3)	12 (40)	0.61
Family history of asthma	2 (4)	Nil	0.20	Nil	Nil	–
History of allergy	1 (2)	Nil	0.46	Nil	Nil	–
Seasonal variation	3 (3)	1 (2)	0.32	Nil	Nil	–

Values are presented as n (%).

Children with asthma.

^†Asthmatic children without acute exacerbation and controlled.

IgM antibodies to M. pneumoniae were documented in 21 patients (42%) in Group 1 and 4 patients (13.3%) in Group 2, this being statistically significant (P < 0.0005). Serological evidence of M. pneumoniae (IgM + IgG antibodies) was observed in 23 patients (23%) in Group 1 and four patients (13.3%) in Group 2, also being statistically significant (P < 0.0005). M. pneumoniae PCR was positive in three patients (6%) in Group 1 and no patients in Group 2, likewise statistically significant (P < 0.0005) (Table 2).

Table 2.

M. pneumoniae serology and PCR in the study group.

Characteristic	Group 1* (n = 50)	Group 2^† (n = 30)
	M. pneumoniae positive	M. pneumoniae negative	P
Microbiological tests
IgM antibodies	21 (42)	4 (13.3)	<0.0005
Immunoglobulin M + G (IgM + IgG) antibodies	23 (46)	4 (13.3)	<0.0005
Polymerase chain reaction	3 (6)	Nil	<0.0005

Values are presented as n (%).

Children with asthma.

^†Asthmatic children without acute exacerbation and controlled.

Considering serology as the diagnostic standard, sensitivity and specificity of PCR were 13.0% and 100%, respectively, while positive and negative predictive values were 100% and 13.0%, respectively.

Discussion

Respiratory infections associated with wheezing are reported in all ages. None of the clinical parameters were found to be significantly associated with M. pneumoniae infection. Immunoglobulin M (lgM) serology for M. pneumoniae was significantly associated with M. pneumoniae infection in acute exacerbations of bronchial asthma.

Low sensitivity of PCR (13.0%) in our study may be attributed to the presence of PCR inhibitors in nasopharyngeal aspirates as reported earlier,³ such as primer impairing, errors in DNA extraction or low copy number of target genome. Sensitivity is probably higher if bronchoalveolar lavage fluid samples are used for PCR assay, but such specimens are difficult to obtain routinely in children.

A limitation of this study relates to the time point of collection of serum as specific IgM emerges only within one week after initial infection and approximately two weeks before IgG. Although IgG-paired sera sero-conversion and/or rise in antibody titre is a definitive diagnosis of M. pneumonae infection, convalescent phase sera are not always available.

Conclusions

Our study confirms an association of M. pneumoniae infection with exacerbations of asthma frequently in nearly 50% of children, indicating an urgent need to search for M. pneumoniae infection in such cases.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

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