Background. This study aims to describe the characteristics of tuberculosis (TB) patients requiring intensive care and to determine the in-hospital mortality and the associated predictive factors.Methods. Retrospective cohort study of all TB patients admitted to the ICU of the Infectious Diseases Department of Centro Hospitalar de São João (Porto, Portugal) between January 2007 and July 2014. Comorbid diagnoses, clinical features, radiological and laboratory investigations, and outcomes were reviewed. Univariate analysis was performed to identify risk factors for death.Results. We included 39 patients: median age was 52.0 years and 74.4% were male. Twenty-one patients (53.8%) died during hospital stay (15 in the ICU). The diagnosis of isolated pulmonary TB, a positive smear for acid-fast-bacilli and a positive PCR forMycobacterium tuberculosisin patients of pulmonary disease, severe sepsis/septic shock, acute renal failure and Multiple Organ Dysfunction Syndrome on admission, the need for mechanical ventilation or vasopressor support, hospital acquired infection, use of adjunctive corticotherapy, smoking, and alcohol abuse were significantly associated with mortality ().Conclusion. This cohort of TB patients requiring intensive care presented a high mortality rate. Most risk factors for mortality were related to organ failure, but others could be attributed to delay in the diagnostic and therapeutic approach, important targets for intervention.
Artemisinin-based therapy is the current standard treatment for non-severe malaria due to Plasmodium falciparum. The potential for asymptomatic liver toxicity of this therapy and its implication in clinical practice is currently unknown. The aim of this study is to assess the hepatic function in patients treated with a standard three-day artemisinin-based regimen and to compare it with the quinine-doxycycline regimen. Retrospective and comparative study of returned adult travellers admitted with non-severe P. falciparum malaria. Fifty-seven patients were included: 19 treated with artemisinin-based therapy and 38 with quinine-doxycycline therapy. During treatment, when compared with quinine-doxycycline group, the artemisinin-lumefantrine group presented a higher proportion of significant liver enzyme abnormalities (42 vs. 5%, p < 0.01) and a higher peak value of aspartate aminotransferase (131 vs. 64 U/L, p < 0.01) and alanine aminotransferase (99 vs. 75 U/L, p = 0.05). None of the patients was symptomatic, there were no treatment interruptions and all patients achieved clinical cure. Treatment of uncomplicated falciparum malaria with artemisinin-based therapy might cause asymptomatic liver enzyme abnormalities in the first days of treatment. Nevertheless, these liver enzyme abnormalities seem to be harmless, asymptomatic and self-limited.
1 October 2018 in Journal of Microbiology, Immunology and Infection
CD4 cell-count has been regarded as the key surrogate marker for prognostic staging and therapeutic monitoring of HIV-infected individuals. Our purpose was to assess the probability of maintaining a CD4 count >200 cells/μL in patients with continuous viral suppression and CD4 cell counts >200 cells/μL. Retrospective cohort study of HIV-infected patients, treatment naïve, who started antiretroviral therapy between 2007 and 2011. We estimated the probability of maintaining CD4 counts >200 cells/μL during continuous viral suppression using the Kaplan-Meier method. The hazard ratios of a CD4 count 200 cells/μL was 40.5 months. Ninety-three percent of patients maintained CD4 counts ≥200 cells/μL during the period of continuous viral suppression. Compared with those with an initial CD4 count ≥350 cells/μL, patients with initial CD4 count <300 cells/μL had a significantly higher risk of a CD4 count <200 cells/μL. Patients with viral suppression and CD4 counts ≥350 cells/μL had a 97.1% probability of maintaining CD4 cell counts ≥200 cells/μL for 48 months. The probability of a CD4 count <200 cells/μL in an HIV-infected patient with viral suppression and CD4 ≥350 cells/μL was very low. These data suggests less frequent monitoring of CD4 counts in these patients.
Cytomegalovirus (CMV) reactivation with neurological involvement in patients with acquired immunodeficiency syndrome (AIDS) is increasingly rare since the introduction of antiretroviral therapy (ART). Manifestations include encephalitis, myelitis, polyradiculopathy and, less commonly, mononeuritis multiplex (MNM). We report a case of disseminated CMV disease with gastrointestinal and peripheral and central nervous system involvement in a patient with AIDS, manifesting primarily as MNM. A 31-year old woman with AIDS presented with a clinical picture of MNM. Electromyography confirmed the clinical findings. CMV DNA was detected in cerebrospinal fluid (CSF) and blood. Gastrointestinal involvement was histologically documented. HIV RNA was also detected in CSF and brain MRI was consistent with HIV encephalopathy. A diagnosis of disseminated CMV disease (with esophagitis, colitis, encephalitis and MNM) and HIV encephalopathy was made. Treatment consisted of ganciclovir and foscarnet, followed by maintenance therapy with valganciclovir. Evolution was favorable and valganciclovir was stopped after sustained immune recovery following ART initiation. We discuss the diagnostic approach to CMV neurological disease, with a focus on MNM and CMV encephalitis. Combination therapy with ganciclovir and foscarnet should be considered for all forms of neurological involvement, although available data are scarce. Since there is significant overlap between CMV encephalitis and HIV encephalopathy, ART drugs with higher CSF penetration may have to be considered. ART and immune recovery are essential to improve outcomes.
Pleural aspergillosis (PA) is a rare but potentially fatal disease. Most cases are secondary to bronchopleural fistulae or pleural intervention and can occur in the absence of immunosuppression. We report a case of PA in a young patient after pleurodesis for recurrent pneumothorax. Clinical resolution was achieved with systemic and local antifungal therapy combined with surgical debridement. Hepatotoxicity led to a switch from voriconazole to isavuconazole, with a successful outcome.
Panton-Valentine leukocidin-producing Staphylococcus aureus (PVL-SA) is associated with relapsing multifocal skin and soft tissue infections (SSTI), necrotizing pneumonia (NP) and severe musculoskeletal infections. Epidemiology is underknown and underdiagnosis is likely. Recent travel abroad, case clustering and relapsing disease are often reported. We reviewed all cases of PVL-SA infection diagnosed at our center, and found 21 cases over a 43-month period. Most patients were adult males, had relevant travel history, reported recurrent disease and presented with SSTI. Etiologic diagnosis took up to five years; meanwhile, 42% of patients had antibiotic treatments. Draining procedures were required in 43% of patients and intensive care support in 19%. All patients recovered. Methicillin-resistance prevalence was 24%. Only 2/13 decolonized patients had posterior relapsing SSTI, both with likely infected contacts. PVL-SA infection’s severity and impact are clear, even in small case series as ours. Physician awareness and active PVL-gene search are crucial for an adequate management.