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Pulmonary strongyloidiasis causing septic shock in a patient with Crohn's disease.

ABSTRACT: A 58 years old male who was admitted to the intensive care unit for septic shock secondary to pneumonia, he has Crohn's disease currently treated with Vedolizumab and previously with infliximab. He was started on broad spectrum antibiotics and vasopressors for treatment of septic shock without improvement in the following days, sputum & blood cultures were negative. Bronchoscopy was done for non-resolving pneumonia work up, broncheoalveolar lavage smears and cultures were negative for bacteria, tuberculosis and Fungi. Bronchial washings cytology showed filariform larvae and serology was positive for Strongyloides, He was started on ivermectin and his condition improved significantly.

SUBMITTER: Abdalla M

PROVIDER: S-EPMC6010665 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Pulmonary strongyloidiasis causing septic shock in a patient with Crohn's disease.

Abdalla Mohammed M Sinyagovskiy Pavel P Mohamed Wiam W Abdelghani Amro A

Respiratory medicine case reports 20180406

A 58 years old male who was admitted to the intensive care unit for septic shock secondary to pneumonia, he has Crohn's disease currently treated with Vedolizumab and previously with infliximab. He was started on broad spectrum antibiotics and vasopressors for treatment of septic shock without improvement in the following days, sputum & blood cultures were negative. Bronchoscopy was done for non-resolving pneumonia work up, broncheoalveolar lavage smears and cultures were negative for bacteria, ...[more]

PMID: 29977759

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Pulmonary Strongyloidiasis Masquerading as Exacerbation of Chronic Obstructive Pulmonary Disease.

Project description:Pulmonary strongyloidiasis is an uncommon presentation of Strongyloides infection, usually seen in immunocompromised hosts. The manifestations are similar to that of acute exacerbation of chronic obstructive pulmonary disease (COPD). Therefore, the diagnosis of pulmonary strongyloidiasis could be challenging in a COPD patient, unless a high index of suspicion is maintained. Here, we present a case of Strongyloides hyperinfection in a COPD patient mimicking acute exacerbation, who was on chronic steroid therapy.

| S-EPMC5077736 | biostudies-literature

Fatal strongyloidiasis after corticosteroid therapy for presumed chronic obstructive pulmonary disease.

Project description:Introduction:Strongyloidiasis is a neglected tropical disease with global prevalence. Under some cases of immune suppression (especially with corticosteroid administration), the nematode involved disseminates, leading to an amplified, possibly lethal hyper-infection syndrome. Case presentation:A 56-year-old Nepalese man presenting with chief complaints of nausea, vomiting, joint pain and abdominal cramps was admitted to Sumeru Hospital. His past history revealed: chronic obstructive pulmonary disease (COPD), systemic hypertension and previously treated pulmonary tuberculosis. The patient had been treated with oral prednisolone (60?mg gl-1) for 8?days due to a presumed exacerbation of his COPD. Sequentially, he developed haemoptysis, chest tightness, frequent wheezing and worsening cough. Bronchoscopy showed severe diffuse alveolar haemorrhage; microbiological examination of broncho-alveolar lavage (BAL) was recommended. Examination of an acid fast bacilli stain preparation of BAL revealed filariform larvae of Strongyloides. Stool specimen examination revealed larvae of Strongyloides. The physical condition of the patient began to deteriorate; a few days after admission, vancomycin-sensitive Enterococcus faecium was isolated from a blood sample. He was treated with ivermectin and albendazole for strongyloides and linezolid plus vancomycin for E. faecium. However, the patient failed to recover from the illness and died. Conclusion:The findings of our study suggest that corticosteroid administration in strongyloidiasis can lead to the development of fatal strongyloides hyper-infection syndrome. Hence our experience suggests the need for early diagnosis of strongyloidiasis to avoid such an outcome. A deterioration of the patient's condition after the initiation of corticosteroid therapy in endemic areas should raise the possibility of strongyloidiasis.

| S-EPMC6230759 | biostudies-literature

Point-of-care Ultrasound Diagnosis of Pulmonary Hydatid Cyst Disease Causing Shock: A Case Report.

Project description:IntroductionPoint-of-care ultrasound (POCUS) is accepted as an important tool for evaluating patients presenting to the emergency department (ED) with dyspnea1 and undifferentiated shock.2 Identifying the etiology and type of shock is time-critical since treatments vary based on this information. Clinicians typically rely on the history, exam, and diagnostics tests to identify the etiology of shock. In resource-limited settings where there is reduced access to timely laboratory and diagnostic studies. The use of POCUS enables rapid classification and directed treatment of shock. Additionally, POCUS can aid in the diagnosis of rarer tropical diseases that can be important causes of shock in resource-limited settings.Case reportWe discuss a case of a pediatric patient who presented to an ED in Cusco, Peru, with acute dyspnea and shock. Point-of-care ultrasound was used to expedite the diagnosis of a ruptured pulmonary hydatid cyst, guide proper management of septic and anaphylactic shock, and expedite definitive surgical intervention.ConclusionIn resource-limited settings where there is reduced access to timely laboratory and diagnostic studies, the use of POCUS enables rapid classification and directed treatment of shock.

| S-EPMC8610475 | biostudies-literature

Pediatric septic shock

Project description:In an ongoing translational research program involving microarray-based expression profiles in pediatric septic shock, we have now conducted longitudinal studies focused on the temporal expression profiles of canonical signaling pathways and gene networks. Genome-level expression profiles were generated from whole blood-derived RNA samples of children with septic shock (n = 30 individual patients) corresponding to days 1 and 3 of admission to the pediatric intensive care unit. Based on sequential statistical and expression filters, day 1 and day 3 of septic shock were characterized by differential regulation of 2,142 and 2,504 gene probes, respectively, relative to normal control patients. Venn analysis demonstrated 239 unique genes in the day 1 data set, 598 unique genes in the day 3 data set, and 1,906 genes common to both data sets. Analyses targeted toward derivation of biological function from these data sets demonstrated time-dependent, differential regulation of genes involved in multiple canonical signaling pathways and gene networks primarily related to immunity and inflammation. Notably, multiple and distinct gene networks involving T cell- and MHC antigen-related biological processes were persistently downregulated from day 1 to day 3. Further analyses demonstrated large scale and persistent downregulation of genes corresponding to functional annotations related to zinc homeostasis. These data represent the largest reported cohort of patients with septic shock, which has undergone longitudinal genome-level expression profiling. The data further advance our genome-level understanding of pediatric septic shock and support novel hypotheses that can be readily tested at both the experimental and translational levels. Keywords: Inflammation; sepsis; innate immunity; T cells; MHC antigen Keywords: to be updated

2007-06-14 | GSE8121 | GEO

Pulmonary infections prime the development of subsequent ICU-acquired pneumonia in septic shock.

Project description:PURPOSE:To investigate the determinants and the prognosis of intensive care unit (ICU)-acquired pneumonia in patients with septic shock. METHODS:This single-center retrospective study was conducted in a medical ICU in a tertiary care center from January 2008 to December 2016. All consecutive patients diagnosed for septic shock within the first 48 h of ICU admission were included. Patients were classified in three groups: no ICU-acquired infections (no ICU-AI), ICU-acquired pneumonia and non-pulmonary ICU-AI. The determinants of ICU-acquired pneumonia and death were investigated by multivariate competitive risk analysis. RESULTS:A total of 1021 patients were admitted for septic shock, and 797 patients were alive in the ICU after 48 h of management. The incidence of a first episode of ICU-AI was 31%, distributed into pulmonary (17%) and non-pulmonary ICU-AI (14%). Patients with septic shock caused by pneumonia were at increased risk of further pulmonary ICU-AI with a cumulated incidence of 34.4%. A pulmonary source of the initial septic shock was an independent risk factor for subsequent ICU-acquired pneumonia (cause-specific hazard 2.33, 95% confidence interval [1.55-3.52], p < 0.001). ICU-AI were not associated with a higher risk of ICU mortality after adjustment in a multivariate-adjusted cause-specific proportional hazard model. CONCLUSION:Septic shock of pulmonary origin may represent a risk factor for subsequent ICU-acquired pneumonia without affecting mortality.

| S-EPMC6420540 | biostudies-literature

Novel XIAP mutation causing enhanced spontaneous apoptosis and disturbed NOD2 signalling in a patient with atypical adult-onset Crohn's disease.

Project description:X-linked inhibitor of apoptosis (XIAP) is the most potent human inhibitor of apoptosis, and is also involved in NOD2-dependent NF?B and MAPK signalling cascade activation. The absence or defective function of XIAP leads to the development of a rare and severe primary immunodeficiency known as X-linked lymphoproliferative syndrome type 2 (XLP-2), which is characterized by a triad of clinical manifestations, including a high incidence of haemophagocytic lymphohistiocytosis (HLH), lymphoproliferation and inflammatory bowel disease (IBD), usually with very early onset. Here, we present a novel XIAP mutation identified in a patient with atypical adult-onset IBD complicated by relapsing HLH, splenomegaly and sarcoid-like disease. The c.266delA mutation in the XIAP gene creates a premature stop codon, and causes a severe reduction in XIAP protein expression. The mutation is also associated with impaired spontaneous and staurosporine- and PMA-induced apoptosis accompanied by significantly increased expression of pro-apoptotic genes. We also confirmed the negative impact of this particular XIAP mutation on NOD2-dependent NF?B and MAPK activation, while NOD2-independent activation was found to be unaffected. Moreover, we assume that the mutation has an impact on the overproduction of IL-12 and IFN?, the shift towards the Th1 immune response and increased numbers of central memory and effector memory CD4+ and CD8+ T cells. All these changes contribute to immune dysregulation and the clinical manifestation of XLP-2.

| S-EPMC7280281 | biostudies-literature

Sepsis and septic shock.

Project description:For more than two decades, sepsis was defined as a microbial infection that produces fever (or hypothermia), tachycardia, tachypnoea and blood leukocyte changes. Sepsis is now increasingly being considered a dysregulated systemic inflammatory and immune response to microbial invasion that produces organ injury for which mortality rates are declining to 15-25%. Septic shock remains defined as sepsis with hyperlactataemia and concurrent hypotension requiring vasopressor therapy, with in-hospital mortality rates approaching 30-50%. With earlier recognition and more compliance to best practices, sepsis has become less of an immediate life-threatening disorder and more of a long-term chronic critical illness, often associated with prolonged inflammation, immune suppression, organ injury and lean tissue wasting. Furthermore, patients who survive sepsis have continuing risk of mortality after discharge, as well as long-term cognitive and functional deficits. Earlier recognition and improved implementation of best practices have reduced in-hospital mortality, but results from the use of immunomodulatory agents to date have been disappointing. Similarly, no biomarker can definitely diagnose sepsis or predict its clinical outcome. Because of its complexity, improvements in sepsis outcomes are likely to continue to be slow and incremental.

| S-EPMC5538252 | biostudies-other

Transcriptome of the septic shock

Project description:Septic shock by pneumopathy was studied in prospective way in 20 patients and compared to normal blood. Blood samples were taken within 12 hours of diagnosis and the resulting transcritomes were compared to 42 normal control samples (selected samples from series GSE10715, GSE12711, GSE16728 and GSE7400). keywords: patient cohort study, septic shock, transcription-profile, blood

2017-09-08 | GSE33118 | GEO

Angiotensin II in septic shock.

Project description:This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2015 and co-published as a series in Critical Care. Other articles in the series can be found online at http://ccforum.com/series/annualupdate2015. Further information about the Annual Update in Intensive Care and Emergency Medicine is available from http://www.springer.com/series/8901.

| S-EPMC4360936 | biostudies-literature

Serum citrullinated histone H3 concentrations differentiate patients with septic verses non-septic shock and correlate with disease severity.

Project description:PurposeMicrobial infection stimulates neutrophil/macrophage/monocyte extracellular trap formation, which leads to the release of citrullinated histone H3 (CitH3) catalyzed by peptidylarginine deiminase (PAD) 2 and 4. Understanding these molecular mechanisms in the pathogenesis of septic shock will be an important next step for developing novel diagnostic and treatment modalities. We sought to determine the expression of CitH3 in patients with septic shock, and to correlate CitH3 levels with PAD2/PAD4 and clinically relevant outcomes.MethodsLevels of CitH3 were measured in serum samples of 160 critically ill patients with septic and non-septic shock, and healthy volunteers. Analyses of clinical and laboratory characteristics of patients were conducted.ResultsLevels of circulating CitH3 at enrollment were significantly increased in septic shock patients (n = 102) compared to patients hospitalized with non-infectious shock (NIC) (n = 32, p < 0.0001). The area under the curve (95% CI) for distinguishing septic shock from NIC using CitH3 was 0.76 (0.65-0.86). CitH3 was positively correlated with PAD2 and PAD4 concentrations and Sequential Organ Failure Assessment Scores [total score (r = 0.36, p < 0.0001)]. The serum levels of CitH3 at 24 h (p < 0.01) and 48 h (p < 0.05) were significantly higher in the septic patients that did not survive.ConclusionCitH3 is increased in patients with septic shock. Its serum concentrations correlate with disease severity and prognosis, which may yield vital insights into the pathophysiology of sepsis.

| S-EPMC7527151 | biostudies-literature

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