Because Mycoplasma pneumoniae is hypothesized to play an important role in reactive airway disease/asthma, a comprehensive murine model of M. pneumoniae lower respiratory infection was established. BALB/c mice were intranasally inoculated once with M. pneumoniae and sacrificed at 0 to 42 days postinoculation. All mice became infected and developed histologic evidence of acute pulmonary inflammation, which cleared by 28 days postinoculation. By contrast, M. pneumoniae persisted in the respiratory tract for the entire 42 days studied. Tumor necrosis factor alpha, gamma interferon, interleukin-6 (IL-6), KC (functional IL-8), MIP-1␣, and MCP-1/JE concentrations were significantly elevated in bronchoalveolar lavage samples, whereas IL-4 and IL-10 concentrations were not significantly elevated. Pulmonary airflow resistance, as measured by plethysmography, was detected 1 day postinoculation and persisted even after pulmonary inflammation had resolved at day 28. Serum anti-M. pneumoniae immunoglobulin G titers were positive in all mice by 35 days. This mouse model provides a means to investigate the immunopathogenesis of M. pneumoniae infection and its possible role in reactive airway disease/asthma.

Because chronic Mycoplasma pneumoniae respiratory infection is hypothesized to play a role in asthma, the potential of M. pneumoniae to establish chronic respiratory infection with associated pulmonary disease was investigated in a murine model. BALB/c mice were intranasally inoculated once with M. pneumoniae and examined at 109, 150, 245, 368, and 530 days postinoculation. M. pneumoniae was detected in bronchoalveolar lavage fluid by culture or PCR in 70 and 22% of mice at 109 and 530 days postinoculation, respectively. Lung histopathology was normal up to 368 days postinoculation. At 530 days, however, 78% of the mice inoculated with M. pneumoniae demonstrated abnormal histopathology characterized by peribronchial and perivascular mononuclear infiltrates. A mean histopathologic score (HPS) at 530 days of 5.1 was significantly greater (P < 0.01) than that for controls (HPS score of 0). Serum anti-M. pneumoniae immunoglobulin G was detectable in all of the mice inoculated with M. pneumoniae and was inversely correlated with HPS (r ‫؍‬ ؊0.95, P ‫؍‬ 0.01) at 530 days postinoculation. Unrestrained whole-body plethysmography measurement of enhanced pause revealed significantly elevated airway methacholine reactivity in M. pneumoniae-inoculated mice compared with that in controls at 245 days (P ‫؍‬ 0.03) and increased airway obstruction at 530 days (P ‫؍‬ 0.01). Murine M. pneumoniae respiratory infection can lead to chronic pulmonary disease characterized by airway hyperreactivity, airway obstruction, and histologic inflammation.While Mycoplasma pneumoniae is known to be a significant cause of acute respiratory illness in children and adults, the significance of chronic infection is undetermined. In humans, M. pneumoniae is reported to commonly be detectable by culture of the respiratory tract for up to several months after clinical recovery from acute pneumonia (5). Even after therapy with effective antibiotics, such as erythromycin or tetracycline, M. pneumoniae can still be cultured from respiratory secretions (6, 18). After receiving macrolides for 14 days, children have been found to have pulmonary structural abnormalities, by high-resolution computed tomography, suggestive of small airway obstruction 1 to 2 years after M. pneumoniae pneumonia with significantly increased frequency compared with that of controls. In these children, a greater antimycoplasma antibody titer was a significant risk factor for the development of abnormal pulmonary sequelae, suggesting that the host immune response may play a pathogenic role in this condition (10). The duration of M. pneumoniae infection in the human lower respiratory tract after acute pneumonia as determined by a method more sensitive than culture, such as PCR, has not been investigated in a controlled fashion.Of potentially greater relevance, chronic M. pneumoniae respiratory infection has been hypothesized to play a role in asthma. By PCR, M. pneumoniae has been detected in the lower airways of chronic, stable asthmatics with significantly greater frequency than in ...

The objective of this article is to examine the association of teen motherhood and long-term physical and mental health outcomes. The physical and mental health components (PCS and MCS) of the SF-12 Healthy Survey in the NLSY79 health module were used to assess long-term health outcomes of women who experienced teenage motherhood. Various familial, demographic, and environmental characteristics were indentified and controlled for that may have predicted teen motherhood and long-term health outcomes. The two comparison groups for teen mothers were women who experienced teen-pregnancy only and women who were engaged in unprotected sexual activity as a teenage but did not experience pregnancy. Multivariate ordinary least squares regression was used for analysis. The average PCS and MCS for teen mothers was 49.91 and 50.89, respectively. Teen mothers exhibited poorer physical health later in life compared to all women as well as the comparison groups. When controlling for age, teen mothers had significantly lower PCS and MCS scores compared to all other women. Furthermore, when controlling for familial, demographic, and environmental characteristics, teen mothers exhibited significantly lower PCS and MCS scores. When comparing teen mothers to the two comparison groups, PCS was not statistically different although MCS was significantly lower in the teen-pregnancy group. Teen motherhood does lead to poorer physical health outcomes later in life. On the other hand, poorer mental health outcomes in later life may be attributed to the unmeasured factors leading to a teen pregnancy and not teen motherhood itself. Additional research needs to be conducted on the long-term consequences of teen motherhood.

A PCR assay was used to analyze endotracheal aspirates from preterm infants for Ureaplasma parvum versus U. urealyticum. U. parvum was detected more often than U. urealyticum. There was no significant difference or trend in the prevalence of either species between infants with or without bronchopulmonary dysplasia when isolated alone.The major factor leading to high morbidity and mortality of preterm infants is pulmonary immaturity. This manifests as respiratory distress in the early neonatal period and can develop into bronchopulmonary dysplasia (BPD), currently defined as a supplemental oxygen requirement at 36 weeks postmenstrual age, with characteristic radiographic findings (2). A recent survey reported that the incidence of BPD ranged from 67% among infants with birth weights of 500 to 750 g to Ͻ1% in infants weighing 1,250 to 2,500 g (2).Development of BPD is multifactorial and is related to pulmonary immaturity, oxidant injury due to high levels of inspired oxygen, and volutrauma associated with mechanical ventilation. However, recent research has focused on the roles of perinatal infection and the inflammatory response as critical factors influencing chronic lung injury (7, 16). Particular attention has been paid to the role of Ureaplasma species, fastidious bacteria found in the lower genital tracts of 40 to 80% of asymptomatic women (4). Rates of vertical transmission range from 18 to 88%, varying inversely with gestational age (6,8,12,24,25). Ureaplasma spp. are the most common microorganisms isolated from inflamed placentas and the lower respiratory tracts of neonates and are proven causes of neonatal pneumonia (4). Since initial reports associating ureaplasmal colonization and development of BPD were published in 1988 (5, 23, 26), more than 30 studies have been conducted. Most, but not all, have supported this association, despite major changes in the pulmonary management of very-low-birth-weight infants, such as exogenous surfactant, antenatal corticosteroid administration, and high frequency ventilation.

To investigate the pathogenesis of acute Mycoplasma pneumoniae infection, BALB/c mice were anesthetized with metofane, and M. pneumoniae was introduced intranasally on days 0, 1, and 2. Mice were sacrificed on days 0-15. A histopathologic scoring system defined inflammatory changes in the lungs on a scale of 0-26 (least to most severe). Broth cultures were positive for all nasal passage and bronchoalveolar lavage (BAL) specimens. Histopathologic scores ranged from 0 to 21. The mean log10 (cfu/mL) were 4.1-6.4 on days 1-10 and >/=1.7 on days 13-15 for nasal passage and BAL specimens. Serum polymerase chain reaction was negative. ELISA for serum IgM and immunoblots for M. pneumoniae antibody were positive in 21 (62%) of 34 and 33 (97%) of 34 infected animals, respectively, at days 8-15. ELISA for IgG antibody was negative. This mouse pneumonia model can be used to study the immunologic and therapeutic responses to acute M. pneumoniae infection.