Mycoplasma pneumoniae (Mp) is a leading cause of community acquired pneumonia. Knowledge regarding Mp pneumonia obtained from animal models or human subjects has been discussed in many different reports. Accumulated expertise concerning this critical issue has been hard to apply clinically, and potential problems may remain undiscovered. Therefore, our multidisciplinary team extensively reviewed the literature regarding Mp pneumonia, and compared findings from animal models with those from human subjects. In human beings, the characteristic pathological features of Mp pneumonia have been reported as alveolar infiltration with neutrophils and lymphocytes and lymphocyte/plasma cell infiltrates in the peri-bronchovascular area. Herein, we demonstrated the novel aspects of Mp pneumonia that the severity of the Mp pneumonia seemed to depend on the host innate immunity to the Mp, which might be accelerated by antecedent Mp exposure (re-exposure or latent respiratory infection) through up-regulation of Toll-like receptor 2 expression on bronchial epithelial cells and alveolar macrophages. The macrolides therapy might be beneficial for the patients with macrolide-resistant Mp pneumonia via not bacteriological but immunomodulative effects. This exhaustive review focuses on pathogenesis and extends to some therapeutic implications such as clarithromycin, and discusses the various diverse aspects of Mp pneumonia. It is our hope that this might lead to new insights into this common respiratory disease.

BackgroundPleural separation, the “split pleura” sign, has been reported in patients with empyema. However, the diagnostic yield of the split pleura sign for complicated parapneumonic effusion (CPPE)/empyema and its utility for differentiating CPPE/empyema from parapneumonic effusion (PPE) remains unclear. This differentiation is important because CPPE/empyema patients need thoracic drainage. In this regard, the aim of this study was to develop a simple method to distinguish CPPE/empyema from PPE using computed tomography (CT) focusing on the split pleura sign, fluid attenuation values (HU: Hounsfield units), and amount of fluid collection measured on thoracic CT prior to diagnostic thoracentesis.MethodsA total of 83 consecutive patients who underwent chest CT and were diagnosed with CPPE (n=18)/empyema (n=18) or PPE (n=47) based on the diagnostic thoracentesis were retrospectively analyzed.ResultsOn univariate analysis, the split pleura sign (odds ratio (OR), 12.1; p<0.001), total amount of pleural effusion (≥30 mm) (OR, 6.13; p<0.001), HU value≥10 (OR, 5.94; p=0.001), and the presence of septum (OR, 6.43; p=0.018), atelectasis (OR, 6.83; p=0.002), or air (OR, 9.90; p=0.002) in pleural fluid were significantly higher in the CPPE/empyema group than in the PPE group. On multivariate analysis, only the split pleura sign (hazard ratio (HR), 6.70; 95% confidence interval (CI), 1.91-23.5; p=0.003) and total amount of pleural effusion (≥30 mm) on thoracic CT (HR, 7.48; 95%CI, 1.76-31.8; p=0.006) were risk factors for empyema. Sensitivity, specificity, positive predictive value, and negative predictive value of the presence of both split pleura sign and total amount of pleural effusion (≥30 mm) on thoracic CT for CPPE/empyema were 79.4%, 80.9%, 75%, and 84.4%, respectively, with an area under the curve of 0.801 on receiver operating characteristic curve analysis.ConclusionThis study showed a high diagnostic yield of the split pleura sign and total amount of pleural fluid (≥30 mm) on thoracic CT that is useful and simple for discriminating between CPPE/empyema and PPE prior to diagnostic thoracentesis.

c Candida glabrata strains sequentially isolated from blood developed resistance to micafungin (MICs from <0.015 to 4 g/ml). A novel mutation identified in micafungin-resistant strains at bp 262 of FKS2 (containing a deletion of F659 [F659del]) was inserted into the homologous region in FKS1. CASE REPORTA 93-year-old man was admitted to our hospital with a diagnosis of pulmonary tuberculosis (day 1). The patient had been receiving treatment for essential hypertension with chronic renal failure for a decade. On admission, the patient's vital signs were normal; however, serum laboratory data showed a marked elevation of creatinine (Cr) (4.7 mg/dl) and blood urea nitrogen (BUN) (74.5 mg/dl). After initiation of antituberculous therapy with oral isoniazid (300 mg/day) plus rifampin (450 mg/day), renal failure progressed (Cr, 7.0 mg/dl) due to drug-induced myoglobinemia (1,000 ng/ml) with uremic symptoms. Although an urgent flexible double lumen (FDL) catheter was introduced into the internal jugular vein, readministration of isoniazid (day 18) caused severe rhabdomyolysis (myoglobinemia, 25,650 ng/ml), with a recurrence of the uremic symptoms.On day 27, the patient suddenly went into a state of shock with high fever and was empirically treated with intravenous meropenem (0.5 g/day), vancomycin (0.5 g, every 48 h [q48h]), and fluconazole (200 mg/day) based on a tentative diagnosis of aspiration pneumonia or catheter-related bloodstream infection complicated by sepsis. On the same day, two sets of blood cultures and serum endotoxin antigen were negative except for an elevation of ␤-D-glucan (133 pg/ml). On day 32, the patient's serum value of ␤-D-glucan rose to 530 pg/ml, and he had a positive result for serum galactomannan (Aspergillus antigen) of 4.5, thrombocytopenia (6.4 ϫ 10 3 platelets/l), and leukocytopenia (2.0 ϫ 10 3 leukocytes/l). Therefore, the fluconazole was changed to voriconazole (6 mg/kg of body weight/day, q12h) with the intent of targeting Aspergillus spp. However, on day 35, a blood culture collected on day 32 (strain NO1) was identified as Candida glabrata; therefore, voriconazole was changed to intravenous micafungin (100 mg/day) according to the Infectious Diseases Society of America (IDSA) 2009 guidelines (1). A blood culture taken on day 34 (NO2) also was positive for C. glabrata; however, after initiation of treatment with micafungin, the persistent fever subsided, and a blood culture taken at day 37 was negative for the yeast. Both strain NO1 and strain NO2 were susceptible to micafungin (MIC, Ͻ0.015 g/ml) but susceptible-dose dependent to fluconazole (MIC Ͻ8 g/ml) by Clinical and Laboratory Standards Institute (CLSI) broth microdilution (BMD) methods (CLSI document M27-S4). With regard to voriconazole, no breakpoint was determined for C. glabrata. In spite of two rounds of replacement of the FDL catheter, the serum value of ␤-D-glucan remained high (Ͼ600 pg/ml), and blood cultures taken on day 48 (NO3) and day 51 (NO4) again yielded C. glabrata. Based on the suspicion of a micafungin-resista...

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BackgroundThe presence of “mechanic’s hands” is one of the clinical clues for collagen vascular diseases. However, the exact relevance of “mechanic’s hands” in collagen vascular diseases has not been well documented. The aim of this study was to clarify the relevance of “mechanic’s hands” to collagen vascular diseases including various skin lesions and interstitial pneumonia.MethodsA retrospective review of the medical records of patients with “mechanic’s hands” at our hospital between April 2011 and December 2012 was conducted. A PubMed search was also conducted using the term “mechanic’s hands”.ResultsFour patients in our institution and 40 patients obtained from PubMed who had “mechanic’s hands” were identified. The most frequent diseases were DM/amyopathic DM (n = 24, 54.5%) and anti-ARS syndrome (n = 17, 38.6%). In these patients, the major skin lesions associated with “mechanic’s hands” were periungual erythema (n = 23, 52.3%), Gottron’s sign (n = 17, 38.6%), heliotrope rash (n = 10, 22.7%), Raynaud’s phenomenon (n = 9, 20.5%), and anti-ARS syndrome (n = 17, 38.6%). Six cases (2 DM, 4 anti-ARS syndrome) had only “mechanic’s hands”. Antibodies to anti-ARS (n = 24) were Jo-1 (n = 19), PL-7 (n = 3), OJ (n = 1), and PL-12 (n = 1).ConclusionThe presence of “mechanic’s hands” together with diverse skin lesions could be a clinical clue to the diagnosis of lung involvement associated with collagen vascular diseases, especially in anti-ARS syndrome or DM/amyopathic DM.

A 31-year-old woman was referred due to a 1-month history of low-grade fever and dry cough. Physical examination showed a bilateral, erythematous, scaly eruption occurring in a symmetric fashion over the metacarpophalangeal and interphalangeal joints, knees, and elbows, suggestive of Gottron's papules. She also had late inspiratory crackles mainly over the right upper lung field, but no muscle weakness. Laboratory examination revealed negative anti-Jo-1 antibodies and high antinuclear antibody titer (1 : 80), KL-6 (3,050 U/mL). Thoracic computed tomography showed subpleural patchy ground glass attenuation and consolidation in both lobes, with bronchiectasis (Picture 1A). She was diagnosed as having amyopathic dermatomyositis and treated with oral prednisolone plus cyclosporine. Although her condition seemed to improve, one month later, massive pneumomediastinum (Picture 1B, arrowhead) and subcutaneous emphysema (Picture 1B, arrow) suddenly developed, and compressed major vessels and main bronchi. Thereafter, her lung disease showed rapid deterioration, and she died three weeks later. Le Goff et al (1) reported that the prevalence of pneumomediastinum in polymyositis/dermatomyositis (PM/DM) may be estimated at approximately 2.2%, and in most cases, it occurs within one year of the initial onset of signs and symptoms of PM/DM. They also described that the one of the factors associated with poor survival was an absence of muscle weakness and the overall mortality rate was 34.4%, with up to 25% of patients dying during the first month of respiratory distress, as in the present case.

A 51-year-old man was transferred to our hospital due to acute respiratory failure that had progressed over four days. A chest X-ray and thoracic computed tomography scan showed multiple faint micronodules randomly distributed throughout both lungs with ground glass opacity, suggesting miliary tuberculosis or Pneumocystis jirovecii pneumonia with acute respiratory distress syndrome. Six hours after admission, the patient died of septic shock. Later, the cryptococcal antigen titer was found to be markedly elevated (1/65,536), with a positive result for anti-human immunodeficiency virus and a low CD4 cell count (12/μL). The present case is reminder that disseminated cryptococcosis with HIV infection can be misdiagnosed as miliary tuberculosis based on radiological findings.

A 55-year-old man was transferred to our hospital with unilateral lung lesions, a persistent fever and vague chest pain with arthralgia lasting for three months. He had been treated for end-stage renal disease with hemodialysis for 15 years and had a medical history of recurrent subcutaneous calciphylaxis due to secondary hyperparathyroidism. Transbronchial biopsied specimens demonstrated metastatic pulmonary calcification, and a bone marrow biopsy showed Philadelphia chromosome-positive acute lymphoblastic leukemia. Although metastatic calcification often lacks specific symptoms, the lungs is a primary site for deposition. This is the first report of unilateral metastatic pulmonary calcification associated with secondary hyperparathyroidism.