Mycoplasma Pneumonia

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Jerry W. Simecka - One of the best experts on this subject based on the ideXlab platform.

  • Regulatory CD4+CD25+ T Cells Dampen Inflammatory Disease in Murine Mycoplasma Pneumonia and Promote IL-17 and IFN-γ Responses
    2016
    Co-Authors: Adam N. Odeh, Jerry W. Simecka
    Abstract:

    Mycoplasmas cause respiratory diseases characterized by persistent infection and chronic airway inflammation. Mycoplasma lung disease is immunopathologic, with CD4+ Th cells determining both disease severity and resistance to infection. Th2 cell responses promote immunopathology, while Th1 cells confer resistance to infection. However, regulatory CD4+ T cells may also have a role in the pathogenesis of Mycoplasma respiratory diseases. We hypothesized Treg cells control the severity of the inflammatory lesions and may also promote persistence of infection. To examine this, BALB/c mice were depleted of CD25+ cells, and had increased disease severity due to Mycoplasma pulmonis infection. Increases in Mycoplasma antibody responses and lymphocyte infiltration into lungs also occurred after CD25+ cell depletion. CD4+CD25+ regulatory T cells promoted IFN-γ and IL-17 Mycoplasma-specific CD4+ T cell responses in vitro and in vivo, while dampening IL-13+ Th responses. Neither IL-10 nor TGF-ß expression was detected in CD4+CD25+ T cells from lymph nodes. Thus, a regulatory T cell population plays an important role in controlling damaging immune responses in Mycoplasma respiratory disease but does not contribute to persistence of infection. It appears that a regulatory T cell population preferentially dampens Th2 cell-mediated inflammatory responses to Mycoplasma through a mechanism independent of IL-10 or TGF-ß characteristic of “classic” Treg cells.

  • cytokine and chemokine transcription profile during Mycoplasma pulmonis infection in susceptible and resistant strains of mice macrophage inflammatory protein 1β ccl4 and monocyte chemoattractant protein 2 ccl8 and accumulation of ccr5 th cells
    Infection and Immunity, 2006
    Co-Authors: Xiangle Sun, Harlan P Jones, Lisa M Hodge, Jerry W. Simecka
    Abstract:

    The progression of murine Mycoplasma Pneumonia is dependent on T cells and other immune cells. The role of cytokines in immunity are complex, and identifying the network of cytokines produced after infection of mice is essential in dissecting the key cytokine cascades involved Mycoplasma disease pathogenesis. In the present study, mRNA expression of 143 different cytokines, chemokines, or receptors were evaluated in lung tissues from both susceptible (BALB/c and C3H/HeN) and resistant (C57BL/6) mice after Mycoplasma pulmonis infection. To accomplish this, membrane-based cDNA microarrays were used to monitor changes mRNA expression in lungs. There was a clear association with disease susceptibility and development of cytokine mRNA expression. In addition to proinflammatory cytokines, mRNA expression of an anti-inflammatory cytokine, interleukin-10, increased with disease severity, suggesting an attempt to moderate the severity of the inflammatory response. Furthermore, it is clear that an array of chemokines produced in susceptible mice could contribute to the recruitment and maintenance of inflammatory cells at the site of disease. In support of this, there was an increase in macrophage inflammatory protein 1beta (MIP-1beta; CCL4) and monocyte chemoattractant protein 2 (MCP-2; CCL8) mRNA levels from Mycoplasma-infected mice and a corresponding accumulation of CD4+ Th cells expressing the MIP-1beta/MCP-2 receptor, CCR5, in the lungs of mice. Furthermore, MIP-1beta- and MCP-2-producing cells and CD4+ T cells were found to be in close association in pulmonary lesions. Thus, there was a significant cytokine response associated with disease pathogenesis, and these studies provide important leads and insights into ongoing cytokine- and chemokine-mediated processes in this persistent inflammatory disease.

Yuko Kunimi - One of the best experts on this subject based on the ideXlab platform.

  • statistical analysis of stevens johnson syndrome caused by Mycoplasma Pneumonia infection in japan
    Allergology International, 2011
    Co-Authors: Yuko Kunimi, Yuko Hirata, Michiko Aihara, Yumiko Yamane, Zenro Ikezawa
    Abstract:

    ABSTRACT Background Stevens-Johnson syndrome (SJS) associated with Mycoplasma Pneumoniae (M. Pneumoniae) infection is mainly observed in children. In adults, drugs are a major cause of SJS, but some adult patients with SJS are infected with M. Pneumoniae. We analyzed patients with SJS associated with M. Pneumoniae infection to elucidate the differences between drug-induced SJS and M. Pneumoniae-associated SJS and also to study differences between M. Pneumoniae-associated SJS in children and adults. Methods This is a retrospective review of Japanese patients who have been reported as M. Pneumoniae- associated SJS in medical Journals published from 1981 to 2009, compared with data of Japanese patients with drug-induced SJS reported from 2000 to 2009. Results Thirty-eight cases of M. Pneumoniae-associated SJS and 78 cases of drug-induced SJS were analyzed in this study. Ocular lesions were observed more frequently in M. Pneumoniae-associated SJS than in drug-induced SJS (p 0.01), and adult patients showed a higher ratio of sequelae in their eyes than did patients under 20 years of age (p 0.01). Sixty-six percent of adult patients with M. Pneumoniae-associated SJS developed fever/respiratory symptoms and mucocutaneous lesions on the same day. In contrast, most of the patients under 20 years of age developed fever/respiratory symptoms before mucocutaneous involvement. This means that these adult patients were infected and immunized previously and developed allergic reactions to M. Pneumoniae soon after the later infection. Conclusions In order to prevent ocular sequelae in adult patients when M. Pneumoniae infection is suspected, more intensive treatment may be needed in adult patients than in younger patients.

Christoph Wenisch - One of the best experts on this subject based on the ideXlab platform.

  • Laboratory diagnosis of Mycoplasma Pneumoniae infection
    Clinical Microbiology and Infection, 2003
    Co-Authors: Florian Daxboeck, R Krause, Christoph Wenisch
    Abstract:

    Diagnosis of Mycoplasma Pneumoniae infection is challenging due to the fastidious nature of the pathogen, the considerable seroprevalence, and the possibility of transient asymptomatic carriage. During recent years, various new techniques have been adapted for the diagnosis of M. Pneumoniae infection, notably in the field of molecular biology. Standard polymerase chain reaction (PCR) is currently the method of choice for direct pathogen detection, but several PCR-related methods provide enhanced sensitivity or more convenient handling procedures, and have been successfully applied for research purposes. Among these techniques are real-time PCR, nested PCR, reverse transcriptase PCR (RT-PCR) and multiplex PCR. Generally, amplification-based methods have replaced hybridization assays and direct antigen detection. Serology, which is the basic strategy for Mycoplasma diagnosis in routine clinical practice, has been improved by the widespread availability of sensitive assays for separate detection of different antibody classes. For the diagnosis of Mycoplasma Pneumonia, serology and direct pathogen detection should be combined. Extrapulmonary diseases may be diagnosed by direct pathogen detection alone, but the value of this diagnostic approach is limited by the probably immunologically mediated pathogenesis of some manifestations. This review summarizes the current state of Mycoplasma Pneumoniae diagnosis, with special reference to molecular techniques. The value of different methods for routine diagnosis and research purposes is discussed.

Qing Wu - One of the best experts on this subject based on the ideXlab platform.

  • detection of viruses and atypical bacteria associated with acute respiratory infection of children in hubei china
    Respirology, 2014
    Co-Authors: Zegang Wu, Hongyun Zheng, Yongqing Tong, Jian Gu, Yan Li, Qing Wu
    Abstract:

    Background and objective Acute respiratory infection is the major cause of disease and death in children, particularly in developing countries. However, the spectrum of pathogenic viruses and atypical bacteria that exist in many of these countries remains incompletely characterized. The aim of this study was to examine the spectrum of pathogenic viruses and atypical bacteria associated with acute respiratory infection in children under the age of 16. Methods A total of 10 435 serum sera specimens were collected from hospitalized children presenting with acute respiratory infection symptoms. Indirect immunofluorescence assays were performed to detect immunoglobulin M antibodies against nine common pathogens: Mycoplasma Pneumonia, influenza virus B, respiratory syncytial virus, parainfluenza virus, adenovirus, influenza virus A, legionella pneumophila, coxiella burnetii and chamydophila Pneumonia. Results Of the 10 435 specimens examined, 7046 tested positive for at least one pathogen. Among all of the tested pathogens, Mycoplasma Pneumonia had the highest detection rate (56.9%). Influenza virus A and influenza virus B epidemics occurred during both winter and summer. The detection rate of respiratory syncytial virus and adenovirus was higher in spring. Cases of mixed infection were more complex: 4136 specimens (39.6%) tested positive for ≥2 pathogens. There were statistically significant difference in detection rates of Mycoplasma Pneumonia, influenza virus B, respiratory syncytial virus, parainfluenza virus, adenovirus, influenza virus A, legionella pneumophila and chamydophila Pneumonia among different age groups (P < 0.05). Conclusions The most common pathogens causing acute respiratory infection among children in Hubei of China were Mycoplasma Pneumonia, influenza virus B and respiratory syncytial virus. The detection rates for each pathogen displayed specific seasonal and age group variations.

Chihyung Chiu - One of the best experts on this subject based on the ideXlab platform.

  • Mycoplasma Pneumoniae infection complicated by necrotizing pneumonitis with massive pleural effusion
    European Journal of Pediatrics, 2006
    Co-Authors: Chihyung Chiu, Linmei Chiang, Tzuping Chen
    Abstract:

    Mycoplasma Pneumoniae is recognized as an important and frequent cause of community-acquired respiratory illness in school-aged children [4]. The clinical course of Mycoplasma Pneumonia is typically mild and self-limited. Pleural effusion is not a common feature of M. Pneumoniae, and when it occurs there is usually a small amount of effusion which does not require chest tube insertion [6]. We report here on a child with M. Pneumoniae infection complicated by necrotizing pneumonitis (NP) who presents with respiratory distress secondary to massive pleural effusion. A 7-year-old – previously healthy – girl presented to our hospital with a 10-day history of fever and cough. Shortness of breath developed on the day before admission. Antibiotics had not been administered by mouth previously, and no known allergy to drug or food was elicited. Upon arrival to our Emergency Department, she appeared to be acutely ill with respiratory distress. Her body temperature was 39.5°C, pulse rate was 163 beats/min, respiratory rate was 50/min with a blood pressure of 107/55 mmHg. Tachypnea with subcostal retraction was present, and examination of the chest revealed dullness to percussion, with decreased breath sounds to auscultation over the left lower lung field. A chest roentgenogram showed consolidation of the left lower lobe and partial atelectasis of left upper lobewith massive pleural effusion. Complete blood cell counts and biochemical examination revealed a white blood cell count of 17,600/μl with 89% neutrophils and 5% lymphocytes and an increased C-reactive protein level of 337.8 mg/l (normal: <5 mg/l). A chest ultrasonography with diagnostic thoracocentesis was performed, and yellow, not turbid fluid was aspirated. Analysis of the pleural effusion showedwhite blood cells at 980/mm (neutrophils: 54%; lymphocytes: 29%; monocytes: 11%), red blood cells at 70/mm, protein at 3.6 g/ dl, glucose at 105 mg/dl and lactate dehydrogenase at 2,002 U/l. No organisms were found on Gramand acid faststained smears. The latex agglutination test of the pleural fluid for Streptococcus Pneumoniae, Haemophilus influenzae type b and group B Streptococcus was negative. Empiric ceftriaxone (100 mg/kg body weight per day) was prescribed, but spiking high fever and pleural effusion with respiratory distress persisted for 1 week. Cultures for bacteria, Mycobacterium tuberculosis, fungi and viruses were all negative. A computed tomography (CT) of the chest was performed for further evaluation, and the scan revealed consolidation of the left lower lobe with multiple low attenuation areas and a massive pleural effusion with left lung entrapment (Fig. 1a). Subsequent video-assisted thoracic surgery (VATS) with pleural decortication was performed, and a chest tube was placed with effective drainage of the pleural effusion. Initially, the cold hemagglutinin titer was 1:4 and the complement-fixation immunoglobulin G (IgG) titer for M. Pneumoniae was 1:160. One week later, the tests were repeated; the second time the cold hemagglutinin titer was 1:16 and complement-fixation IgG titer had increased to 1:2,560. Mycoplasma IgM by enzyme immunoassay (EIA) was positive on two occasions. The earlier prescribed antibiotics were continued, and azithromycin (10 mg/kg body weight per day) was administered concomitantly for 10 days until the fever had subsided as well as vigorous postural drainage. Multiple pneumatoceles were present on the chest roentgenogram taken 14 days after admission (Fig. 1b). The young patient recovered completely from this acute episode and was discharged with a hospital stay of 22 days. M. Pneumoniae Pneumonia usually follows a benign course and the patient normally does not require hospitalization. The most common radiographic features of C.-Y. Chiu (*) . L.-M. Chiang Department of Pediatrics, Chang Gung Memorial Hospital, 222, Mai-chin Road, Keelung, Taiwan e-mail: pedchest@adm.cgmh.org.tw Tel.: +886-2-24313131 Fax: +886-2-24335342