Overall, 25% and 13% of isolates were MDR and multi-azole resistant, respectively. The most common resistance combination was azoles and 5-flucytosine in 14% followed by azoles and amphotericin B in 7% and azoles and echinocandins in 2% of isolates.
Tuberculosis (TB) has been a human disease for centuries. Its frequency is increased manyfold in patients with liver cirrhosis. The gold standard of TB management is a 6-mo course of isoniazid, rifampicin, pyrazinamide and ethambutol. Although good results are seen with this treatment in general, the management of patients with underlying cirrhosis is a challenge. The underlying depressed immune response results in alterations in many diagnostic tests. The tests used for latent TB have many flaws in this group of patients. Three of four first-line antitubercular drugs are hepatotoxic and baseline liver function is often disrupted in patients with underlying cirrhosis. Frequency of hepatotoxicity is increased in patients with liver cirrhosis, frequently leading to severe liver failure. There are no established guidelines for the treatment of TB in relation to the severity of liver disease. There is no consensus on the frequency of liver function tests required or the cut-off used to define hepatotoxicity. No specific treatment exists for prevention or treatment of hepatotoxicity, making monitoring even more important. A high risk of multidrug-resistant TB is another major worry due to prolonged and interrupted treatment.
Introduction: Candida pericarditis is a rare clinical entity with a high fatality, primarily attributed to difficulty in diagnosis. Unfortunately, the diagnosis is made post-mortem in more than 50 % of cases, and thus a high index of clinical suspicion is crucial.Case presentation: We report a rare case of fungal pericardial effusion caused by the recently recognized multidrug-resistant Candida auris, which was cultured from pericardial fluid, blood, bronchoalveolar lavage and urine of a chronic liver disease patient while on empiric fluconazole therapy. The yeast was misidentified as Candida haemulonii by the VITEK2 commercial identification system, and was confirmed as C. auris by internal transcribed spacer and large ribosomal subunit sequencing. In addition, the VITEK2 AST card erroneously revealed a high amphotericin B MIC (16 mg ml 21 ) and low caspofungin MIC (0.25 mg ml 21 ) that did not correlate with results from the reference Clinical and Laboratory Standards Institute (CLSI) microbroth dilution method. Based on VITEK2 MIC data, the patient was administered caspofungin. However, in vitro antifungal susceptibility data for C. auris by the CLSI method exhibited high MICs to fluconazole (64 mg ml 21 ) and caspofungin MIC (1 mg ml 21 ) but low MICs to amphotericin B (MIC range, 0.12520.5 mg ml 21 ). The patient's repeat pericardial fluid culture, despite caspofungin therapy for 12 days, grew C. auris and he died on day 13 of therapy.Conclusion: C. auris is a recently reported agent of fungaemia and deep-seated infections and is notable for its antifungal resistance. Although early species identification and rapid antifungal susceptibility testing are needed in cases of critical infections, the reporting of rare yeast isolates exhibiting high MICs to antifungals by automated systems needs a cautionary approach.
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