Secondary Pulmonary Infection Research Articles

IgG4-related nephritis and interstitial pulmonary disease complicated by invasive pulmonary fungal infection: a case report

BackgroundIgG4-related kidney disease (IgG4-RKD) can affect multiple organs, which was first reported as a complication or extra-organ manifestation of autoimmune pancreatitis in 2004. It is characterized by abundant IgG4-positive plasma cells infiltration in tissues involved.Case presentationA 69-year-old man presented with cough and renal dysfunction with medical history of hypertension and diabetes. Pathological findings revealed interstitial nephritis and he was initially diagnosed with IgG4-RKD. Prednisone helped the patient to get a remission of cough and an obvious decrease of IgG4 level. However, he developed invasive pulmonary fungal infection while steroid theatment. Anti-fungal therapy was initiated after lung puncture (around cavitary lung lesion). Hemodialysis had been conducted because of renal failure and he got rid of it 2 months later. Methylprednisolone was decreased to 8 mg/day for maintenance therapy. Anti-fungal infection continued for 4 months after discharge home. On the 4th month of follow-up, Chest CT revealed no progression of lung lesions.ConclusionsThe corticosteroids are the first-line therapy of IgG4-RD and a rapid response helps to confirm the diagnosis. This case should inspire clinicians to identify IgG4-related lung disease and secondary pulmonary infection, pay attention to the complications during immunosuppressive therapy for primary disease control.

Phage Therapy to Prevent Nosocomial Bacterial Pneumo-nia in Patients with Severe COVID-19 in 2020

The COVID-19 was reported to be a pandemic, according to the World Health Organization (WHO). Secondary bacterial pneumonia exacerbates respiratory problems and increases mortality in patients with COVID-19. Recently, 50% of the causes of death in these patients have been reported as nosocomial pneumonia in these cases. These bacteria have become multidrug-resistant. Phage production is a cost-benefit. Inhalation of phage cocktail with mesh nebulizer can be suitable to prevent secondary bacterial pulmonary infection in patients with severe COVID-19. To prevent secondary bacterial pneumonia and reduce mortality in patients with severe type COVID-19 and patients who are under a ventilator for a long time, the use of phage cocktail product by inhalation with mesh nebulizer device is recommended.

COVID-19 INFECTION IN A CANDIDATE FOR AUTOLOGOUS HEMATOPOIETIC STEM CELL TRANSPLANTATION: A CASE REPORT

The pandemic for the new coronavirus SARS-CoV-2 has been the causeof enormous challenges for the entire health system, especially in programs who dealwith Hematopoietic Stem Cell Transplantation (TCTH), since sequelae related to COVID-19 can be a hindrance to a possible HSCT. In case report, VBF, 61 years old, diagnosis of classic lymphocyte-rich Hodgkin'slymphoma in 2018 with initial treatment with ABVD, due to the return of the disease, an ICE regimen was started, but with disease progression after 5 cycles. Then, an IGEV scheme was started with a schedule of autologous hematopoietic cell transplantation, which took place in the third cycle in May / 2020. However, at the end of May / 2020, he was admitted to the emergency department with confirmation of SARS-Cov-2 infection by means of PCR of the nasal and oropharyngeal swab. He evolved during hospitalization with hypoxemic respiratory failure, mechanical ventilation and signs of secondary pulmonary infection, using multiple antimicrobial regimens, showing improvement and finally being extubated. However, he presented important pulmonary sequelae, with chest CT showing extensive cavitation in the left upper lobe and reticular opacities, with distortion of the pulmonary architecture. He was reassessed as to the possibility of autologous hematopoietic cell transplantation, but this was contraindicated due to pulmonary sequelae. In the case reported, the patient complied with the formal indication for HSCT, which would be refractoriness or relapse in a second remission in patients up to 70 years old with sensitivity to rescue schemes. However, due to pulmonary sequelae acquired after COVID-19, HSCT was contraindicated. This case leads us to the conclusion that the pandemic by the SARS-CoV-2 coronavirus can directly affect HSCT services and that in addition to preventing infection in this group of patients, they should be reevaluated after the recovery of COVID-19 for evaluation of structural and functional respiratory sequelae.

Pulmonary and cardiac pathology in African American patients with COVID-19: an autopsy series from New Orleans

BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spread rapidly across the USA, causing extensive morbidity and mortality, particularly in the African American community. Autopsy can considerably contribute to our understanding of many disease processes and could provide crucial information to guide management of patients with coronavirus disease 2019 (COVID-19). We report on the relevant cardiopulmonary findings in, to our knowledge, the first autopsy series of ten African American decedents, with the cause of death attributed to COVID-19.MethodsAutopsies were performed on ten African American decedents aged 44–78 years with cause of death attributed to COVID-19, reflective of the dominant demographic of deaths following COVID-19 diagnosis in New Orleans. Autopsies were done with consent of the decedents' next of kin. Pulmonary and cardiac features were examined, with relevant immunostains to characterise the inflammatory response, and RNA labelling and electron microscopy on representative sections.FindingsImportant findings include the presence of thrombosis and microangiopathy in the small vessels and capillaries of the lungs, with associated haemorrhage, that significantly contributed to death. Features of diffuse alveolar damage, including hyaline membranes, were present, even in patients who had not been ventilated. Cardiac findings included individual cell necrosis without lymphocytic myocarditis. There was no evidence of secondary pulmonary infection by microorganisms.InterpretationWe identify key pathological states, including thrombotic and microangiopathic pathology in the lungs, that contributed to death in patients with severe COVID-19 and decompensation in this demographic. Management of these patients should include treatment to target these pathological mechanisms.FundingNone.

Pulmonary Alveolar Proteinosis Syndrome.

Pulmonary alveolar proteinosis (PAP) is a syndrome characterized by progressive accumulation of pulmonary surfactant. This results in dyspnea, secondary pulmonary and systemic infection, and in some cases respiratory failure. PAP syndrome occurs in distinct diseases, classified according to pathogenetic mechanism; these include primary PAP (due to disruption of granulocyte-macrophage colony-stimulating factor [GM-CSF] signaling), secondary PAP (due to reduction in alveolar macrophage numbers/functions), and congenital PAP (due to disruption of surfactant production). In primary PAP, the most common cause is autoimmune PAP, which accounts for over 90% of all PAP syndrome. The pathogenesis is driven by reduced GM-CSF-signaling causing abnormal alveolar macrophage function which subsequently results in impaired alveolar surfactant clearance. Autoimmune PAP can be accurately diagnosed by serum GM-CSF autoantibody levels and there now exist other diagnostic tests for rare causes of PAP syndrome. The current standard treatment is whole lung lavage; however, there is emerging evidence to support the use of novel therapeutic approaches, including inhaled GM-CSF, immune modulation, gene and cell therapy, and targeting macrophage cholesterol homeostasis. Furthermore, several innovative approaches to monitor disease severity and response to therapy have recently been developed.

Pilot Study of the Difference C-TBNA with EBUS-TBNA in Mediastinal Bronchial-Derived Cysts

Objective: To investigate the difference value of conventional transbronchial needle aspiration (C-TBNA) and endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) in mediastinal bronchogenic cysts. Method: A retrospective analysis of clinical data and follow-up data of 27 patients using conventional TBNA and EBUS-TBNA techniques diagnosed as mediastinal bronchogenic cysts from May 2008 to December 2016 in the First Affiliated Hospital of Soochow University was done. Results: In 8 years, there were 13 cases of C-TBNA and 14 cases of EBUS-TBNA-diagnosed mediastinal bronchogenic cysts. C-TBNA extracted clear liquid and its volume was 8.9 ± 1.5 ml. The 14 patients examined by EBUS had a homogenous anechoic signal. Clear liquid was extracted, and its volume was 29.1 ± 7.5 ml. The cyst liquid extracted with EBUS-TBNA was significantly more than that extracted with CTBNA (P < 0.05). During follow-up, 1 patient had cyst rupture after being punctured by C-TBNA, secondary pulmonary infection and right pleural effusion, followed by surgical treatment. The recurrence rate for C-TBNA was 100.00% (13/13), and that for EBUS-TBNA was 14.29% (2/14) (P < 0.05). Conclusion: The C-TBNA and EBUS-TBNA technologies have high diagnostic value for the mediastinal bronchogenic cysts. Both C-TBNA and EBUS-TBNA technologies have the risk of secondary infection and recurrence of cysts.

Surgical treatment of benign mediastinal teratoma: summary of experience of 108 cases

BackgroundMediastinal teratoma is a rare disease, many cases were reported before, but few articles focus on large case analyses. The objective of this article is to summarize the clinical characteristics of benign mediastinal teratoma and the experience of surgical treatment, especially thoracoscopic surgery for benign mediastinal teratoma.MethodsThe clinical data of 108 patients with benign mediastinal teratoma confirmed by operation and pathology from January 1992 to January 2018 were analyzed retrospectively. The clinical symptoms, imaging examination, surgical methods and prognosis of all patients were analyzed. We compared the difference of thoracoscopic surgery and thoracotomy surgery using 102 patients underwent only chest surgery. Normally distributed continuous variables were compared by independent sample t test. Categorical variables were analyzed by chi-square test.ResultsImaging examination showed that all 108 cases of mediastinal teratoma were located in the anterior region of mediastinum. All cases underwent surgical resection, postoperative pathology confirmed that all cases were benign. 1 case was taken simple neck collar incision, 5 case was taken median thoracotomy combined with neck incision, other 102 cases were taken thoracoscopic surgery (22) or thoracotomy surgery (80). 4 cases were treated with partial pericardial resection due to adhesions, 12 cases underwent partial pericardial resection, 5 cases underwent lobectomy, 9 cases underwent wedge resection of lobe, and 2 patients underwent anonymous vein angioplasty. 1 case underwent second operation because of postoperative bleeding, 1 case of chylothorax, 1 case of recurrent laryngeal nerve injury, 2 cases of wound infection, 1 case of secondary pulmonary infection. 106 cases were followed up, period from 12 months to 10 years, no recurrence of tumor was found. Comparing to take thoracotomy surgery, patients underwent thoracoscopic surgery has strong advantage on intraoperative blood loss and hospital stay days after surgery (P < 0.05). tumor maximum diameter is larger for thoracotomy surgery group, as well as more patients suffer estimated adhesions from preoperative imaging. so we compared above parameters in patients with tumor diameter less than 10 cm with or without estimated adhesions from preoperative imaging, a strong advantage still can be found in thoracoscopic surgery group, inpatients with estimated adhesions from preoperative imaging, intraoperative blood loss (38.75 ± 15.53 vs 169.17 ± 208.82., P = 0.04) and hospital stay days after surgery (5.50 ± 0.93 vs 9.43 ± 6.54., P = 0.04) were better. In patients without estimated adhesions from preoperative imaging, intraoperative blood loss (46.67 ± 10.00 vs 110.53 ± 123.13., P = 0.06) and hospital stay days after surgery (4.70 ± 1.16 vs 7.53 ± 2.32., P = 0.01) were better. Especially, in thoracoscopic surgery group, hospital stay days after surgery was significantly shorter.ConclusionThe clinical manifestations and imaging performance of benign mediastinal teratoma were complicated, and the surgical treatment was effective. Compared with traditional thoracotomy surgery, thoracoscopic surgery can improve patients’ quality of life, less intraoperative blood loss, and less hospital stay days after surgery, so if condition is permitted, thoracoscopic surgery should be a better choice.

The Clinical Implication of Secondary Pulmonary Bacterial Infection for the Outcome of Critically Ill Patients with COVID-19

The Clinical Implication of Secondary Pulmonary Bacterial Infection for the Outcome of Critically Ill Patients with COVID-19

Analysis of related factors of secondary pulmonary infection in children with tracheobronchial foreign body

Objective:To analyze the secondary pulmonary infection and the distribution of pathogenic bacteria in children with tracheobronchial foreign body, and to guide the clinical treatment. Method:The clinical data of 197 children with tracheobronchial foreign bodies confirmed by rigid bronchoscopy were reviewed. According to the clinical manifestations and signs, blood routine, chest CT and airway endocrine pathogen distribution, the secondary pulmonary infection was analyzed. Result:Seventy-five of 197 children with foreign bodies in tracheobronchial had secondary pulmonary infections. Among them, 32 cases of airway endocrine cultured pathogenic bacteria, mainly including Streptococcus pneumoniae and Haemophilus influenzae. Children with long preoperative history, fever, and with a history of using antibiotics are more likely to have secondary pulmonary infections. Conclusion:The duration of disease history, preoperative fever and the use of antibiotics are related to secondary pulmonary infection. The third generation of cephalosporins can effectively control the infection.

Fatal Vitamin K-Dependent Coagulopathy Associated with Cefoperazone/Sulbactam: A Case Report.

This case report describes a suspected and fatal adverse reaction involving vitamin K-dependent coagulopathy that might be associated with cefoperazone/sulbactam (CPZ/SAM), a combined antimicrobial formulation. We reported a patient diagnosed with acute cerebral infarction and secondary pulmonary infection who was treated with an intravenous infusion of CPZ/SAM at 3 g twice daily. After receiving treatment with CPZ/SAM, the patient developed a fatal adverse reaction of CPZ-induced hemorrhage. The Naranjo assessment score in this report was 5, suggesting that the patient’s coagulation function disorder was potentially associated with the use of CPZ/SAM. To prevent vitamin K-dependent coagulopathy caused by CPZ/SAM, it is suggested to avoid cephalosporins in patients with a high risk of bleeding unless the need for cephalosporins is compelling.

Medication analysis and pharmaceutical care for one case of secondary invasive pulmonary aspergillus infection

Medication analysis and pharmaceutical care for one case of secondary invasive pulmonary aspergillus infection

侵袭性肺部真菌感染103例临床分析

Objective: To analyze the clinical features of invasive pulmonary fungal infection (IPFI), and to explore the prevention and treatment of IPFI. Methods: Clinical data of 103 cases with IPFI diagnosed in our hospital were retrospectively analyzed. Results: COPD, bronchial lung cancer, and the abuse of antibiotics were the main risk factors of IPFI, among which Candida albicans accounted for 57.3% and Aspergillus species accounted for 32%in all cases. The mortality of IPFI patients was 20.4%. Conclusions: IPFI is a secondary pulmonary infection because of variety of predisposing factors, and its mortality rate is high. Early diagnosing, effective treatment for the fungus and enhancing the nutrition are good for IPFI.

Transcription levels of Cyp450s, H99, Hsps and Dmp53 in Drosophila melanogaster larvae treated with zearalenona

Cryptococcus neoformans is an opportunistic fungal pathogen that threatens individuals with impaired cell-mediated immunity (CMI). Presently, there are no standardized vaccines available to prevent cryptococcal infections and conventional anti-fungal drug therapy does not induce host immune reactivity and thus cannot efficiently resolve C. neoformans infections in immunocompromised individuals. The present study was designed to characterize pulmonary immune responses following infection with an avirulent temperature-sensitive (ts) mutant, calcineurin A1 (cna1) compared to the pathogenic C. neoformans strain H99 and its potential to induce protective anti-cryptococcal immunity. Host CMI responses in cna1-inoculated mice were observed to be dose-dependent, and comprise increases in pulmonary macrophages and CD4+ T lymphocytes. However, cytokine analysis demonstrated a mixed pulmonary cytokine response (increases in IL-4, and MCP-1) with no induction of IFN-γ. Also, pre-immunization with the ts cna1 mutant did not result in protection from a subsequent secondary pulmonary infection with the pathogenic C. neoformans strain H99. Taken together, these results suggest that host pulmonary CMI responses to the ts cna1 mutant that is eventually eliminated from the host without the induction of IFN-γ appear to be dose-dependent, diverse, and require further stimulation to induce C. neoformans-specific Th1-type cytokine responses to resolve subsequent experimental pulmonary cryptococcal infections.

Does hyperoxia enhance susceptibility to secondary pulmonary infection in the ICU?

Hyperoxia is common practice in the acute management of circulatory shock, and observational studies report that it is present in more than 50 % of mechanically ventilated patients during the first 24 h after intensive care unit (ICU) admission. On the other hand, “oxygen toxicity” due to the increased formation of reactive oxygen species limits its use due to serious deleterious side effects. However, formation of reactive oxygen species to boost bacterial killing is one of the body’s anti-microbial auto-defense mechanisms and, hence, O2 has been referred to as an antibiotic. Consequently, hyperoxia during the peri-operative period has been advocated for surgical patients in order to reduce surgical site infection. However, there is ample evidence that long-term exposure to hyperoxia impaired bacterial phagocytosis and thereby aggravated both bacterial burden and dissemination. Moreover, a recent retrospective study identified the number of days with hyperoxia, defined as a PaO2 > 120 mmHg only, as an independent risk factor of ventilator-associated pneumonia in patients needing mechanical ventilation for more than 48 h. Since so far the optimal oxygenation target is unknown for ICU patients, “conservative” O2 therapy represents the treatment of choice to avoid exposure to both hypoxemia and excess hyperoxemia.

IFN-?, but not IL-17A, is required for survival during secondary pulmonary Francisella tularensis Live Vaccine Stain infection

IL-17 and IFN-? production by Th17 and Th1 cells, respectively, is critical for survival during primary respiratory infection with the pathogenic bacterium, Francisella tularensis Live Vaccine Strain (LVS). The importance, however, of these T cell subsets and their soluble mediators is not well understood during a secondary or memory response. We measured the number of CD4+ T cells producing IFN-? or IL-17 in the spleen and lungs of vaccinated mice on day four of the secondary response using intracellular cytokine staining in order to identify protective T cell subsets participating in the memory response. Few bacteria were present in spleens of vaccinated mice on day four and a T cell response was not observed. In the lung, where more bacteria were present, there was a robust Th1 response in vaccinated mice but Th17 cells were not present at higher numbers in vaccinated mice compared to unvaccinated mice. These data show that the lung is the dominant site of the secondary immune response and suggest that Th17 cells are not required for survival during secondary challenge. To further investigate the importance of IFN-? and IL-17 during the secondary response to F. tularensis, we neutralized either IFN-? or IL-17 in vivo using monoclonal antibody treatment. Vaccinated mice treated with anti-IFN-? lost more weight and had higher bacterial burdens compared to vaccinated mice treated with isotype control antibody. In contrast, treatment with anti-IL-17A antibody did not alter weight loss profiles or bacterial burdens compared to mice treated with isotype control antibody. Together, these results suggested that IFN-? is required during both primary and secondary respiratory F. tularensis infection. IL-17, on the other hand, is only critical during the primary response to respiratory F. tularensis but dispensable during the secondary response.

Influenza A/H1/N1/09 infection in patients with cirrhosis has a poor outcome: A case series

Seasonal influenza is often unsuspected in cirrhotic patients admitted with pneumonia and acute hepatic decompensation. We report five consecutive patients with influenza A subtype H1N1 2009 strain (influenza A/H1N1/09) admitted to our intensive care unit. All had a short history of rapidly worsening respiratory symptoms, but there were no characteristic clinical or radiographic features. Secondary pulmonary infection was universal. All five patients died, despite prompt institution of oseltamivir and intensive supportive care. A high index of suspicion is needed for influenza infection among patients with decompensated cirrhosis.

Toll-Like Receptor 2 Deficiency Increases Resistance to Pseudomonas aeruginosa Pneumonia in the Setting of Sepsis-Induced Immune Dysfunction

Sepsis is characterized by a dysregulated inflammatory response followed by immunosuppression that favors the development of secondary infections. Toll-like receptors (TLRs) are major regulators of the host's response to infections. How variability in TLR signaling may impact the development of sepsis-induced immune dysfunction has not been established. We sought to establish the role of TLR2, TLR4, and TLR5 in postseptic mice with Pseudomonas aeruginosa pneumonia. We used an experimental model of sublethal polymicrobial sepsis induced by cecal ligation and puncture (CLP). Wild-type, tlr2(-/-), tlr4(-/-), tlr5(-/-), tlr2 4(-/-) mice that underwent CLP were secondarily subjected to P. aeruginosa pulmonary infection. Postseptic wild-type and tlr4(-/-) and tlr5(-/-) mice displayed high susceptibility to P. aeruginosa pneumonia. In contrast, TLR2-deficient mice, either tlr2(-/-)or tlr2 4(-/-), that underwent CLP were resistant to the secondary pulmonary infection. As compared to wild-type mice, tlr2(-/-) mice displayed improvement in bacterial clearance, decreased bacteremic dissemination, and attenuated lung damage. Furthermore, tlr2(-/-) mice exhibited a pulmonary proinflammatory cytokine balance, with increased production of tumor necrosis factor α and decreased release of interleukin 10. In a model of secondary P. aeruginosa pneumonia in postseptic mice, TLR2 deficiency improves survival by promoting efficient bacterial clearance and restoring a proinflammatory cytokine balance in the lung.

Lung injury in acute pancreatitis: Mechanisms underlying augmented secondary injury

Acute lung injury (ALI) and its more severe form, the acute respiratory distress syndrome (ARDS), are common complications of acute pancreatitis (AP). ALI/ARDS contribute to the majority of AP-associated deaths, particularly in the setting of secondary infection. Following secondary pulmonary infection there can be an exacerbation of AP-associated lung injury, greater than the sum of the individual injuries alone. The precise mechanisms underlying this synergism, however, are not known. In this review we discuss the main factors contributing to the development of augmented lung injury following secondary infection during AP and review the established models of AP in regard to the development of associated ALI.

Role of regulatory T cells in long-term immune dysfunction associated with severe sepsis

To investigate the role of regulatory T cells in the modulation of long-term immune dysfunction during experimental sepsis. It is well established that sepsis predisposes to development of a pronounced immunosuppression. Nevertheless, the mechanisms underlying the immune dysfunction after sepsis are still not well understood. Prospective experimental study. University research laboratory. Wild-type mice underwent cecal ligation and puncture and were treated with antibiotic during 3 days after surgery. On days 1, 7, or 15 after cecal ligation and puncture, the frequency of regulatory T cells, proliferation of CD4 T cells and bacterial counts were evaluated. Fifteen days after cecal ligation and puncture, surviving mice underwent secondary pulmonary infection by intranasal inoculation of nonlethal dose of Legionella pneumophila. Some mice received agonistic glucocorticoid-induced tumor necrosis factor receptor antibody (DTA-1) before induction of secondary infection. Mice surviving cecal ligation and puncture showed a markedly increased frequency of regulatory T cells in thymus and spleen, which was associated with reduced proliferation of CD4 T cells. Fifteen days after cecal ligation and puncture, all sepsis-surviving mice succumbed to nonlethal injection of L. pneumophila. Treatment of mice with DTA-1 antibody reduced frequency of regulatory T cells, restored CD4 T cell proliferation, reduced the levels of bacteria in spleen, and markedly improved survival of L. pneumophila infection. These findings suggest that regulatory T cells play an important role in the progression and establishment of immune dysfunction observed in experimental sepsis.

Dendritic Cells Modulate Lung Response toPseudomonas aeruginosain a Murine Model of Sepsis-Induced Immune Dysfunction

Host infection by pathogens triggers an innate immune response leading to a systemic inflammatory response, often followed by an immune dysfunction which can favor the emergence of secondary infections. Dendritic cells (DCs) link innate and adaptive immunity and may be centrally involved in the regulation of sepsis-induced immune dysfunction. We assessed the contribution of DCs to lung defense in a murine model of sublethal polymicrobial sepsis (cecal ligature and puncture, CLP). In this model, bone marrow-derived DCs (BMDCs) retained an immature phenotype, associated with decreased capacity of IL-12p70 release and impaired priming of T cell lymphocytes. Eight days after CLP surgery, we induced a secondary pulmonary infection through intratracheal instillation of 5 x 10(6) CFUs of Pseudomonas aeruginosa. Whereas all sham-operated mice survived, 80% of post-CLP mice died after secondary pneumonia. Post-CLP mice exhibited marked lung damage with early recruitment of neutrophils, cytokine imbalance with decreased IL-12p70 production, and increased IL-10 release, but no defective bacterial lung clearance, while systemic bacterial dissemination was almost constant. Concomitant intrapulmonary administration of exogenous BMDCs into post-CLP mice challenged with P. aeruginosa dramatically improved survival. BMDCs did not improve bacterial lung clearance, but delayed neutrophil recruitment, strongly attenuated the early peak of TNF-alpha and restored an adequate Il-12p70/IL-10 balance in post-CLP mice. Thus, adoptive transfer of BMDCs reversed sepsis-induced immune dysfunction in a relevant model of secondary P. aeruginosa pneumonia. Unexpectedly, the mechanism of action of BMDCs did not involve enhanced antibacterial activity, but occurred by dampening the pulmonary inflammatory response.