Background: The contemporary guidelines have recommended multiple antimicrobial therapies along with oral macrolides for the treatment of Mycobacterium abscessus complex lung disease (MABC-LD). However, there is little evidence supporting the parenteral tigecycline-containing regimens against MABC-LD. Therefore, we conducted this study to evaluate the effect of intravenous tigecycline-containing regimens on the treatment of MABC-LD. Methods: A retrospective study was conducted in 6 medical centers. Patients with MABC-LD that were followed up at ≥12 months were enrolled. Mycobacterium abscessus subspecies were identified by hsp65, rpoB, secA1 gene PCR, and sequencing. Antimicrobial susceptibility was determined for 34 patients using broth microdilution methods following the Clinical and Laboratory Standards Institute (CLSI) guideline. The microbiology and treatment outcomes were defined as either success or failure. The impacts of tigecycline and amikacin were adjusted for age, comorbidities, surgical resection, and radiologic scores. Results: During the study period, seventy-one patients were enrolled for final analysis. The microbiology failure rate was 61% (43/71) and the treatment failure rate was 62% (44/71). For M. abscessus complex, 97% (33/34) of tigecycline MIC were ≤1 mg/L. Amikacin also demonstrated great susceptibility (94.1%; 32/34). Treatment with regimens containing tigecycline plus amikacin provided better microbiology success (adjusted OR 17.724; 95% CI 1.227–267.206) and treatment success (adjusted OR 14.085; 95% CI 1.103–166.667). Conclusion: The outcome of MABC-LD is always unsatisfactory. Treatment regimens with oral macrolide in combination with tigecycline and amikacin were correlated with increased microbiology success and less treatment failure.

After the concept of healthcare associated pneumonia (HCAP) was introduced in 2005 by the American Thoracic Society/Infectious Disease Society of America (ATS/IDSA), pneumonia in hemodialysis patients has been classified as HCAP. Even though there are several risk factors and scoring systems of drug-resistant pathogens (DRPs) in HCAP, the risk factors for DRPs in hemodialysis-associated pneumonia are unclear. Patients who were admitted to our tertiary care hospital from January 2005 to December 2010 were screened by a discharge diagnosis of pneumonia. Patients were enrolled if they fulfilled the definition of HCAP according to the 2005 ATS/IDSA guidelines. A total of 530 subjects were diagnosed with HCAP, of whom 48 (9.1 %) received regular hemodialysis (HD group) and the other 482 did not (non-HD group). The most common pathogens in HD group were Pseudomonas aeruginosa and methicillin resistant Staphylococcus aureus (MRSA). There was a similar distribution of Gram-negative bacilli infections between the two groups except for Haemophilus influenzae and Citrobacter species. The incidence of DRPs was not significantly different between the two groups (HD vs. non-HD, 35.4 vs. 39.2 %, p = 0.607). Wound care, severe pneumonia and an age of more than 70 years were significant risk factors for DRPs. The area under the operating cure of predicting DRPs was 0.727 (0.575–0.879, p = 0.01). P. aeruginosa and MRSA were the most important pathogens in hemodialysis-associated pneumonia. Wound care, severe pneumonia and old age were significant risk factors for DRPs.

Controlling latent tuberculosis infection (LTBI) is important for preventing tuberculosis (TB). However, the immune regulation of LTBI remains uncertain. Immune checkpoints and CD14+ monocytes are pivotal for immune defense but have been scarcely studied in LTBI. We prospectively enrolled participants with LTBI and controls from January 2017 to December 2019. We measured their CD14+ monocytes and the expression of immune checkpoints, including programmed death-1 (PD-1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4), and T cell immunoglobulin mucin domain-containing-3 (TIM3) on T lymphocytes in peripheral blood mononuclear cells before and after LTBI treatment. A total of 87 subjects were enrolled, including 29 IGRA-negative healthy controls (HC), 58 in the LTBI group (19 without chronic kidney disease (non-CKD), and 39 with end-stage renal disease (ESRD)). All PD-1, CTLA-4, and TIM3 on lymphocytes and monocytes were higher in the LTBI group than that in the HC group. Total CD14+ monocytes were higher and PD-L2+CD14+ over monocytes were lower in patients with LTBI-non-CKD than that in the HC group. After LTBI treatment, CD14+ monocytes, TIM3+ on CD4+ and monocytes, and CTLA-4 on lymphocytes decreased significantly. Multivariable logistic regression indicated that CD14+ monocytes was an independent factor for LTBI-non-CKD from the HC group, whereas PD-L2+CD14+ monocytes and TIM3+ monocytes were significant for LTBI-ESRD from the HC group. In conclusion, LTBI status was associated with increasing CD14+ monocytes plus low PD-L2 expression. By contrast, increased expression of immune checkpoints over all immune cells might be due to Mycobacterium tuberculosis related immune exhaustion, which decreased after treatment.

Background: Low handgrip strength (HGS) is independently associated with a higher exacerbation risk in stable chronic obstructive pulmonary disease (COPD); however, the relationship between HGS while being admitted for COPD exacerbation and further exacerbation risk after discharge remains unclear. Methods: We enrolled patients admitted for COPD exacerbation between January 2018 and June 2019. HGS tests were done within 3 days after admission. The primary endpoint was exacerbations within 12 months after the index admission, which needed emergency room visits or hospital admission. We analyzed the relationships among demographics, HGS, pulmonary function parameters, and acute exacerbation events. Results: Among 43 enrolled patients, 31 (72.1%) participants (HGSw) had HGS weakness (22.1 ± 4.1 kg). The other 12 (27.9%) participants (non-HGSw) had the strength of handgrips 33.7 ± 3.1 kg. HGSw group showed a significantly higher rate of emergency room visits within 6, 9, and 12 months after the index admission than non-HGSw group (0.81 ± 1.30 vs. 0.08 ± 0.29, p = 0.045; 1.26 ± 1.59 vs. 0.17 ± 0.38, P = 0.019; 1.48 ± 1.86 vs. 0.25 ± 0.62, P = 0.027, respectively). There was a trend to have higher admission rate within 9 and 12 months in HGSw group, which did not achieve statistical significance (0.77 ± 1.38 vs. 0.08 ± 0.29, P = 0.064; 0.94 ± 1.56 vs. 0.08 ± 0.29, P = 0.062, respectively). Conclusions: HGS weakness measured upon admission for COPD exacerbation was associated with a higher risk of exacerbation in the next year. Trial registration ClinicalTrials.gov Identifier: NCT04885933.

Early detection of lung cancer has a higher likelihood of curative treatment and thus improves survival rate. Low-dose computed tomography (LDCT) screening has been shown to be effective for high-risk individuals in several clinical trials, but has high false positive rates. To evaluate the risk of stage I lung cancer in the general population not limited to smokers, a retrospective study of 133 subjects was conducted in a medical center in Taiwan. Regularized regression was used to build the risk prediction model by using LDCT and health examinations. The proposed model selected seven variables related to nodule morphology, counts and location, and ten variables related to blood tests and medical history, achieving an area under the curve (AUC) value of 0.93. The higher the age, white blood cell count (WBC), blood urea nitrogen (BUN), diabetes, gout, chronic obstructive pulmonary disease (COPD), other cancers, and the presence of spiculation, ground-glass opacity (GGO), and part solid nodules, the higher the risk of lung cancer. Subjects with calcification, solid nodules, nodules in the middle lobes, more nodules, and diseases related to thyroid, liver, and digestive systems were at a lower risk. The selected variables did not indicate causation.

Clinical deterioration during the treatment of tuberculosis remains a diagnostic challenge. We describe the case of a 46-year-old man with a history of oral cancer status after a radical operation who had pulmonary tuberculosis with pleura and neck lymph node involvement. The clinical condition improved after antituberculosis therapy. However, the patient suffered from low-grade fever, progressive dyspnea, and cough after 7 weeks of the therapy. The findings of chest plain films were relapse and progression of left lung haziness. The deterioration was caused by disseminated Penicillium marneffei infection. Disseminated P. marneffei in a non-HIV patient with tuberculosis is rarely seen, and the manifestations are similar to a paradoxical response and relapse of pulmonary tuberculosis, thereby making it difficult to establish a diagnosis.