Cardiac surgery for infective endocarditis has acceptable early postoperative results among intravenous drug users. The 2- and 5-year survival were 79 and 59%, respectively. The number of reinfections was high within 2 years, as continued drug use seems to be a major challenge for this group.
dWe present a case of infective endocarditis caused by Streptococcus dysgalactiae subsp. dysgalactiae, a major cause of bovine mastitis and previously thought to be an animal-restricted pathogen. The patient reported no direct contact with animals, and the clinical course was severe and complicated. CASE REPORTA 65-year-old male patient was admitted to Haukeland University Hospital in western Norway with radiating pain in his left shoulder, fever, and muscle ache. One month earlier, he had been admitted to a hospital in Spain with similar symptoms but was rapidly discharged with a diagnosis of shoulder tendinitis. He had a family history of sudden cardiac death, and his previous medical history included hypertrophic obstructive cardiomyopathy and a normal coronary angiography 7 years prior to the actual admission.Upon admission, he had a pulse rate of 100/min, a temperature of 39°C, and a respiratory frequency of 24/min, thus fulfilling the criteria of systemic inflammatory response syndrome (SIRS). He was pale, with a blood pressure of 118/59 mm Hg, and a holosystolic murmur was heard at the apex. No local signs of infection were observed over his left shoulder.The initial blood chemistry results were as follows, with normal range values in parentheses: hemoglobin, 8.5 g/dl (13.4 to 17.0 g/dl); C-reactive protein, 277 mg/liter (Ͻ5 mg/liter); leukocytes, 20.8 ϫ 10 9 /liter (3.5 ϫ 10 9 to 11.0 ϫ 10 9 /liter); neutrophils, 18.5 ϫ 10 9 /liter (1.7 ϫ 10 9 to 8.2 ϫ 10 9 /liter); sedimentation rate, 102 mm/h (0 to 20 mm/h); procalcitonin, 12.1 g/liter (Ͻ0.10 g/ liter); and troponin T, 896 ng/liter (Ͻ25 ng/liter). Thrombocytes were within the normal range. The electrocardiogram (ECG) demonstrated ST segment elevation in leads V 1 and V 2 and T inversion in leads V 4 to V 6 , indicative of ischemia.Antibiotic therapy was started on day 1 and included meropenem and vancomycin. A broader initial regimen than that recommended in the Norwegian National Antibiotic Guidelines was chosen since the patient had recently been admitted to a hospital in Spain. The following day, all four blood cultures grew nonhemolytic bacteria on blood agar. Species identification was performed using matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and showed that the isolate was Streptococcus dysgalactiae. Subsequently, group C carbohydrate specificity was documented using a slide agglutination test (Oxoid, Cambridge, United Kingdom). The antimicrobial susceptibility testing showed that the group C streptococcus (GCS) isolate was fully susceptible to all tested antibiotics, with the following MICs: penicillin G, 0.008 mg/liter; ceftriaxone, Ͻ0.016 mg/liter; clindamycin, 0.25 mg/liter; vancomycin, 0.25 mg/liter; teicoplanin, 0.25 mg/liter; and linezolid, 1 mg/liter.A more thorough anamnestic interview revealed a history of weight loss of 6 kg, bloody stools, increasing pain in the left shoulder, and inaccuracy of vision. On examination, he had no peripheral vascular phenomena indicative of septic emboliz...
The incidence of IE increased significantly. Non-viridans streptococci, enterococci and S. aureus were all significantly associated with increased mortality. The increased number of enterococcal IE and the increased number of IVDUs with left-sided IE constituted new challenges. Biological implants were preferred in a majority of patients requiring surgery.
We herein describe the first novel species within the genus Eikenella since it was established in 1972 by the reclassification of ‘Bacteroides corrodens’ to Eikenella corrodens . From a polymicrobial brain abscess, we encountered an Eikenella isolate, PXXT, that could not validly be named E. corrodens . The isolate grew on blood agar with small, translucent, pitting colonies after 3 days of anaerobic incubation. By reviewing previously collected invasive isolates, we found an additional Eikenella strain, EI-02, from a blood culture exhibiting the same properties as PXXT. Phylogenetic analyses based on both whole genome and individual house-keeping genes confirmed that the two strains allocate in a phylogenetic cluster separate from E. corrodens . Using specific amplification and sequencing of the Eikenella nusG gene, we further detected the novel Eikenella species in six historic brain abscesses previously reported to contain E. corrodens based on 16S metagenomics. Out of 24 Eikenella whole-genome projects available in GenBank, eight cluster together with PXXT and EI-02. These isolates were recovered from brain abscess (n=2), blood (n=1), bone/soft tissue (n=3), parotid gland (n=1) and unknown (n=1). It remains to be investigated whether the new species can cause endocarditis. The average nucleotide identity value between strain PXXT and the E. corrodens type strain ATCC 23834T was 92.1 % and the corresponding genome-to-genome distance value was 47.1 %, both supporting the classification of PXXT as a novel species. For this species we propose the name Eikenella exigua. The type strain of E. exigua is PXXT (DSM 109756T, NCTC 14318T).
COVID-19 infection primarily causes severe pneumonia complicated by acute respiratory distress syndrome and multiorgan failure requiring a ventilator support. We present a case of a 55-year-old male, admitted with COVID-19. He was obese but had no other medical conditions. His blood pressure was measured by his general physician on several occasions in the past, all values being normal (<140/90 mmHg). He developed multiorgan failure, requiring vasopressor and ventilator support for 17 days. A prone positioning improved the arterial oxygenation, and reduced the need for supplemental oxygen. After recovery, he showed persistently elevated blood pressure and sinus tachycardia both in clinic and out-of-clinic. The activation of the renin–angiotensin–aldosterone and sympathetic systems, volume-overload, hyperreninemia and cytokine storm might have contributed to the exaggerated cardiovascular response.
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