Chlamydia pneumoniae respiratory infection after allogeneic stem cell transplantation

Chlamydia pneumoniae is a common cause of upper and lower respiratory tract infections in immunocompetent patients; however, its role as a respiratory pathogen in immunocompromised hosts has been infrequently recognized. We describe C. pneumoniae lower respiratory tract infection in a 19-year-old male after allogeneic stem cell transplantation. The patient developed fever on day +14, and a subsequent computed tomography scan of the chest revealed a right lateral pleural-based opacity, which was then resected during thoracoscopy. Diagnosis was made by culture and staining of the resected tissue with C. pneumoniae-specific monoclonal antibodies, and azithromycin was administered. To the best of our knowledge, this is the first report of C. pneumoniae respiratory infection after stem cell or marrow transplantation. C. pneumoniae often coexists with other etiologic agents of pneumonia in immunocompromised patients. Considering the infrequency of infections from this organism in this clinical setting, one must still rule out other more likely respiratory pathogens.     

Viral infection after lung transplantation

We experienced 3 cases of viral infections after lung transplantation. Case 1: Fifty-two-year-old male with pulmonary emphysema underwent left single lung transplantation from a cadaveric donor. Three months after transplantation he presented Epstein-Barr virus (EBV) viremia, resulting in multiple lymphadenopathy. Biopsy showed post-transplant lymphproliferative disorder, and he was treated successfully with rituximab. He is well without recurrence around 1 and a half years after treatment. Case 2: Thitry-eight-year-old male with pulmonary emphysema underwent double lung transplantation from a cadaveric donor. Four months after transplantation he showed multiple nodules in both lungs. Percutaneous biopsy showed post-transplant lymphproliferative disorder, and he was treated successfully with rituximab. He is well without recurrence more than 2 years after treatment. Case 3 : Twenty-four-year-old woman with lymphangioleiomyomatosis underwent living-related bilateral lobar lung transplantation. Three months after lung transplantation she presented cytomegalovirus viremia. Since it proved to be ganciclovir-resistant cytomegalovirus infection, she was treated with foscarnet successfully. She is well without recurrence about 2 and a half years after treatment.     

Chlamydia pneumoniae serology in donors and recipients and the risk of bronchiolitis obliterans syndrome after lung transplantation

BACKGROUND: Bronchiolitis obliterans syndrome (BOS) is a common late complication in lung transplant recipients (LTR). Chlamydia pneumoniae (C. pneumoniae) is a common but difficult to diagnose respiratory pathogen with a propensity to latency. METHODS: We studied the impact of C. pneumoniae on BOS development using donor-recipient serology obtained before transplantation in a cohort of 76 LTR. RESULTS: BOS was present in 29.9% patients (mean follow-up 866 days). High donor C. pneumoniae immunoglobulin (Ig)G titers were associated with BOS in the recipient (area under the curve [AUC] 0.71, 95% confidence interval [CI] 0.52-0.91, P=0.027), whereas high recipient titers were inversely associated with BOS (AUC 0.27, 95% CI 0.11-0.44, P=0.018). The risk of developing BOS was 75.0% in the case of a primary seromismatch for C. pneumoniae (D+/R-), whereas a reverse mismatch had a risk of 4.6% (likelihood ratio 9.8, P=0.02). In a multivariate model that included human leukocyte antigen matching, acute rejection and cytomegalovirus pneumonitis, C. pneumoniae IgG donor 32 or greater and C. pneumoniae IgG recipient 32 or greater remained positive and negative independent risk factors, respectively, for BOS in LTR. In the freedom from BOS analysis, BOS occurred more frequently and earlier in C. pneumoniae seropositive donors, and the reverse was true in seronegative recipients. CONCLUSION: C. pneumoniae serology in donor and recipient is associated with the development of BOS in LTR.     

Autoantibodies and anti-factor VIII and Chlamydia pneumoniae infection

We report the case of a 64-year-old man without hemorrhagic history experiencing epistaxis. The standard hemostasis assessment including prothrombin index, activated partial thromboplastin time (APTT) and platelet count found an isolated abnormal APTT (105 sec vs 33 sec). Therefore, coagulation factors were explored. An acquired factor VIII deficiency (5%) with anti-FVIII antibody (4.5 Bethesda unit.mL-1) was recognised. This anti-FVIII antibody was related to a Chlamydia pneumoniae pulmonary infection. Treatment consisted of: i) Four successive anterior packing and activated factor VII infusion (Novoseven); ii) steroids injection and bi-antibiotherapy. The time course of the epistaxis was favourable under treatment.     

Chlamydia trachomatis infection as a cause of pneumonia after human marrow transplantation

Seventy-two marrow transplant patients were studied to assess the role of Chlamydia trachomatis infection in the etiology of pneumonia in the compromised host. Sixty-four patients had pneumonia from various causes and eight died of causes other than pneumonia. Chlamydial serologies and cultures of lung tissue, or other sites, or both, were obtained from all patients. C trachomatis was recovered from a single sputum specimen obtained at the onset of pneumonia in one patient, and three patients developed sustained IgG and IgM antibody responses to chlamydiae during their pneumonia. Two of the four patients died of pneumonia. These data further confirm that C trachomatis infection occurs in immunosuppressed patients in association with pneumonia. The source of the organism and the frequency of infection remain to be determined.     

Early COVID‐19 infection after lung transplantation

COVID‐19, the clinical syndrome caused by the novel coronavirus, SARS‐CoV‐2, continues to rapidly spread, leading to significant stressors on global healthcare infrastructure. The manifestations of COVID‐19 in solid organ transplant recipients are only beginning to be understood with cases reported to date in transplant recipients on chronic immunosuppression. Herein, we report the first case of COVID‐19 in a lung transplant recipient in the immediate posttransplant period, and we describe the epidemiologic challenges in identifying the source of infection in this unique situation.     

The impact of ganciclovir-resistant cytomegalovirus infection after lung transplantation

BACKGROUND: Cytomegalovirus (CMV) resistance to ganciclovir has become increasingly common in acquired immunodeficiency syndrome patients but has only rarely been reported in recipients of solid organ transplants. METHODS: A retrospective study of ganciclovir susceptibility testing of CMV isolates recovered from lung transplant recipients was performed. Patients with CMV isolates having partial (1 or =3 microg/ml) to ganciclovir determined by plaque reduction assay were included in a case-control study to identify risk factors for ganciclovir resistance. RESULTS: Between 2/91 and 5/98, 18 patients (5.2% of patients transplanted) were found to have CMV infections with some degree of ganciclovir resistance (4 partially, 14 fully resistant). More positive viral blood cultures (3.2+/-2.5 vs. 1.6+/-1.4 CMV positive cultures, P=0.02) and more episodes of CMV pneumonitis (0.24+/-0.23 vs. 0.10+/-0.17 episodes/bronchoscopy, P=0.02) occurring before the detection of resistance were seen among resistant patients than controls. Ganciclovir-resistant patients received more antithymocyte globulin during induction (70+/-44 vs. 45+/-39 mg/kg, P=0.03) and received ganciclovir for a greater number of days (79+/-52 vs. 64+/-53 days, P=0.005) before the detection of resistance than controls. Ganciclovir-resistant patients had a shorter survival and an earlier onset of bronchiolitis obliterans syndrome compared with patients in the transplant database at Washington University. CONCLUSIONS: Ganciclovir-resistant CMV infection is a serious complication of solid organ transplantation associated with more episodes of viremia, more frequent disease, earlier onset of bronchiolitis obliterans and shorter survival. The use of antithymocyte globulin and prolonged exposure to ganciclovir are risk factors for the development of ganciclovir resistance.     

No evidence of acute Chlamydia pneumoniae infection in patients with Bell's palsy.

The cause of Bell's palsy remains unknown even though available evidence suggests that infection could be a factor. In recent studies, Chlamydia pneumoniae has been associated with neurologic diseases such as multiple sclerosis. In the present study, the association of C pneumoniae with Bell's palsy was studied with the use of serology and polymerase chain reaction to test tear fluid and peripheral blood mononuclear cells from 21 patients with Bell's palsy and 21 control subjects. C pneumoniae DNA was detected from tear fluid samples in 1 patient with Bell's palsy and in 2 healthy control subjects. Whether this indicates earlier disease or subclinical infection remains to be studied. However, an association between Bell's palsy and acute C pneumoniae infection could not be shown.     

Lymphocytic myocarditis after lung transplantation.

This study reports the development of lymphocytic myocarditis in a bilateral lung allograft recipient. A 23-year-old woman developed congestive heart failure and severe left ventricular dysfunction 32 months after a bilateral lung allograft for cystic fibrosis. She had taken oral acyclovir for infectious mononucleosis that was diagnosed 11 months previously. Her viral load for Epstein-Barr virus (EBV) increased, and an echocardiogram revealed a left ventricular ejection fraction of 25% and endomyocardial biopsy revealed lymphocytic myocarditis. She received valacyclovir (1 g x 3 times daily) and made a full recovery 6 months later.     

Weight gain after lung transplantation.

BACKGROUND: Weight gain is frequently observed after lung transplantation, but the magnitude, predictors and implications of weight gain after lung transplant are unknown. METHODS: This retrospective cohort study included 826 lung transplant recipients randomly selected from 12 international transplant centers. We included adult patients with available weight data at baseline and 1 year post-transplant. We examined demographic and clinical predictors of first year weight gain using a multiple linear regression model (n = 579) with percent weight change as the dependent variable. To study the association between first year weight gain and subsequent survival, we performed a Cox proportional hazards analysis. p < 0.05 was considered statistically significant. RESULTS: The median weight change was 10% (range -32% to 84%). On multi-variate analysis, increasing age and prolonged mechanical ventilation were inversely associated with weight gain; obstructive disease, interstitial disease and increasing ischemic time were positively associated with weight gain. Increasing baseline weight was negatively associated with weight gain in patients with obstructive and interstitial disease. The model accounted for 14% of the variance in weight gain. Patients with weight gain above the median had better subsequent survival (adjusted hazard ratio 0.61, 95% confidence interval 0.41 to 0.90). Infection was a more common cause of death in these patients, whereas malignant deaths were more frequent in patients with below-median weight gain. CONCLUSIONS: Substantial weight gain occurs in the first year after lung transplantation. The predictors of weight gain may be used to target high-risk patients for early intervention. Higher weight gain is associated with better subsequent survival.     

Chlamydia pneumoniae infection and ischemic heart disease in hemodialysis patients

INTRODUCTION: Ischemic heart disease and other atherosclerotic complications are the prominent causes of death among hemodialyzed end-stage renal disease (ESRD) patients and renal transplant recipients. Numerous articles in recent years have raised the possibility of an infective factor, especially Chlamydia pneumoniae, in the development of atherosclerosis and its complications. The aim of this study was to assess the incidence of chronic C pneumoniae infection and its association with ischemic heart disease and atherosclerosis in a population of patients with ESRD awaiting renal transplantation. MATERIAL AND METHODS: The studied group consisted of 164 subjects: 99 ESRD patients (heart disease [HD] group) who were hospitalized for vascular access creation (27), pretransplantation nephrectomy (47), or kidney transplantation (25), and a control group of 65 subjects consisting of 50 healthy blood donors and 15 multiorgan donors. C pneumoniae was detected in vascular wall fragments, kidney biopsy specimens and peripheral blood monocytes using real time polymerase chain reaction (PCR). Serum immunoglobulin IgG and IgA anti-C pneumoniae antibodies were detected using Enzyme-linked immunosorbent assay (ELISA) and a lipid profile (cholesterol, high-density lipoprotein [HDL], low-density lipoprotein [LDL], and triglycerides [TG]) was obtained. Data on cardiovascular disease events, smoking history, diabetes, hypertension, cause, and length of renal failure were collected and analyzed. The existence of atherosclerotic lesions was detected using ultrasound (US) Doppler examination of aortic bifurcation. Chronic C pneumoniae infection was diagnosed on the basis of detection of both IgA and IgG antibodies and/or the detection of C pneumoniae DNA in vascular wall fragments or peripheral blood monocytes. After a follow-up of 32 months, data on cardiovascular events and patient history were collected again. RESULTS: Chronic C pneumoniae infection affected 46.5% (46/99) of HD patients and 9% (6/65) of controls (P < .05). Among HD patients, 26.3% (26/99) had ischemic heart disease (IHD) versus 6% in the control group. Among C pneumoniae-infected HD patients, IHD was more frequent (39.1%) than in noninfected HD patients (15%; P < .05). Within the 32-month observation period of the HD group, cardiac pain was observed in 11 (24%; 11/46) infected patients versus 3 (5.7%; 3/53) patients without C pneumoniae infection (P < .05). Exacerbation of previously diagnosed IHD was observed in 8 (44%; 8/18) cases in the C pneumoniae-infected group versus 0 (0%; 0/8) in the uninfected patients (P < .05). CONCLUSIONS: Chronic C pneumoniae infection affects hemodialysis patients more frequently than healthy subjects. Hemodialysis patients with C pneumoniae infection are at the greater risk of exacerbation of existing IHD.