First Report of Granulicatella sp. Endocarditis in a Kidney Transplant Patient
Flávio Jota de PaulaPrecil Diego Miranda de Menezes NevesRamaiane Aparecida BridiAlice Tung Wan SongElias David‐Neto
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Abstract:
Granulicatella and Abiotrophia are genera of fastidious Gram-positive cocci commensal of the oral, genitourinary, and intestinal flora. We report the first case of infective endocarditis caused by Granulicatella sp. in a kidney transplant recipient. A 67-year-old male kidney transplant recipient was admitted to the hospital for investigation of fever, abdominal pain, and diarrhea. On physical examination, he was dehydrated. Laboratory tests identified impaired renal function (creatinine level of 15.5 mg/dl; reference, 3.0 mg/dl), metabolic acidosis, and electrolyte disturbances. Cryptosporidium sp. was identified as the cause of the diarrhea, and the infection was treated with nitazoxanide. On admission, cultures of blood, urine, and stool samples were negative. Echocardiography results were normal. Despite the antimicrobial treatment, the fever persisted. A transthoracic echocardiogram revealed infective endocarditis of the mitral valve, and Granulicatella spp. were isolated in blood cultures. Although the patient was treated with penicillin and amikacin, he evolved to septic shock of pulmonary origin and died. Infective endocarditis caused by Granulicatella sp. should be suspected in cases of culture-negative endocarditis.Keywords:
Infective Endocarditis
Amikacin
Blood Culture
SummaryIn a 15 month period we have studied the epidemiology of aminoglycoside resistance in ai general hospital. We determined the effect of preferential amikacin usage on the resistance levels of amikacin, gentamicin, tobramycin, netilmicin and dibekacin. The resistance levels’ to each of these antibiotics were monitored in a> 3 month baseline phase during which amikacin usage was less than 1 %. During the remainder 12 months, amikacin was the aminoglycoside of choice and in this period no significant change in aminoglycoside resistance was noted. Nevertheless some changes in the combined resistance were found. From the aminoglycoside resistant strains only 8.8 % showed resistance to amikacin. Isolated amikacin resistance was not found and amikacin resistant strains showed cross-resistance to nearly all the other aminoglycosides.
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• During a 36-month period, 28 patients treated for infections due to amikacin-susceptiblePseudomonas aeruginosasubsequently developed infections or colonization with amikacin-resistant P aeruginosa at the same site. Eleven amikacin-susceptible/-resistant pairs of isolates were analyzed for aminoglycoside-inactivating enzymes, plasmid profiles, cellular proteins, outer membrane proteins (OMPs), lipopolysaccharide (LPS) profiles, and amikacin uptake. While clearly distinct from isolates of other patients, sensitive and resistant isolates from the same patients were indistinguishable in plasmid profile, LPS profiles, and OMPs. These results suggest that the resistant Paeruginosaisolates were derived from the sensitive isolates. None of the resistant isolates produced enzymes known to inactivate amikacin. In nine of 11 resistant isolates tested, transport of amikacin into Paeruginosawas reduced. A major mechanism of in vivo development of amikacin resistance in Paeruginosais alteration in permeability to amikacin, but the aquisition of plasmids or changes in OMPs or LPS profile may not account for this phenomenon. (Arch Intern Med1989;149:630-634)
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Two cases of infective endocarditis are reported. In both, vegetations on the cardiac valves characteristic of endocarditis were documented by echocardiography and confirmed at surgery in one of them. The various features of vegetative endocarditis on the echocardiogram are described. Differentiation of these echoes from those produced by other morbid states is discussed. Echocardiography is considered a useful non-invasive technique in the diagnosis of infective endocarditis. Cardiac surgery is usually found to be necessary in addition to medical therapy, when echoes characteristic of vegetative endocarditis are recorded by echocardiography.
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Amikacin sulfate was first used sparingly at our cancer center in 1976; since 1979, it has been the only aminoglycoside used for systemic cancer therapy for patients with granulocytopenia. As the development of resistance has been correlated with antibiotic use over time, we wished to determine if prolonged use of amikacin in our patients had led to increased amikacin resistance. A total of 1,129 strains were recovered from 315 patients during a 13-month period. Each species isolated per patient was considered once. Seven percent of the patients had amikacin-resistant strains (2.7% of isolates), and 10% of patients had gentamicin-resistant strains (4% of isolates). Amikacin resistance was significantly less than in an earlier study. Unrestricted use of amikacin has not led to a concomitant increase in amikacin resistance in gram-negative bacilli. (JAMA1982;248:1199-1202)
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• During a 36-month period, 28 patients treated for infections due to amikacin-susceptiblePseudomonas aeruginosasubsequently developed infections or colonization with amikacin-resistant P aeruginosa at the same site. Eleven amikacin-susceptible/-resistant pairs of isolates were analyzed for aminoglycoside-inactivating enzymes, plasmid profiles, cellular proteins, outer membrane proteins (OMPs), lipopolysaccharide (LPS) profiles, and amikacin uptake. While clearly distinct from isolates of other patients, sensitive and resistant isolates from the same patients were indistinguishable in plasmid profile, LPS profiles, and OMPs. These results suggest that the resistant Paeruginosaisolates were derived from the sensitive isolates. None of the resistant isolates produced enzymes known to inactivate amikacin. In nine of 11 resistant isolates tested, transport of amikacin into Paeruginosawas reduced. A major mechanism of in vivo development of amikacin resistance in Paeruginosais alteration in permeability to amikacin, but the aquisition of plasmids or changes in OMPs or LPS profile may not account for this phenomenon. (Arch Intern Med1989;149:630-634)
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Aerosolized amikacin reaches high concentrations in lung fluids, which are well above the minimum inhibitory concentrations (MICs) of resistant strains of Pseudomonas aeruginosa. However, P. aeruginosa can gain resistance to amikacin through different cumulative mechanisms; amikacin MICs are seldom reported beyond values of 1,000 μg/ml, as tested in clinical microbiology assays. To assess how high amikacin MICs can be reached by graded exposure, four amikacin-resistant P. aeruginosa isolates were grown in a 4-step increased exposure to amikacin; derivative strains were further characterized by measuring their comparative growth rate, biofilm-forming ability, and susceptibility to other antibiotics. In addition, the mechanism underlying the MIC increase was assessed phenotypically, using a set of 12 aminoglycoside disks, and measuring the effect of Phe-Arg-β-naphthylamide, an efflux pump inhibitor. Graded exposure to amikacin increased MICs of resistant strains up to 10,000-20,000 μg/ml, without apparent fitness cost, and having variable consequences on their biofilm-forming ability, and on their susceptibility to other antibiotics. Decreased permeability may have contributed to hyper-resistance, although evidence was inconclusive and variable between strains. Amikacin-resistant P. aeruginosa is able to gain in vitro hyper-resistance with minimal changes in the specific phenotypes that were tested; the ability to achieve high-level amikacin (AMK) resistance may confound the clinical utility of this aerosolized AMK, but clinical data would be required to assess this.
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Objective To develop the catheter with slow-release amikacin for decreasing the catherter-associated urinary tract infection(CAUTI).Methods Taking chitosan as a carrier,the amikacin was added to the surface of catheters.The density of amikacin in leach liquor,the element components and the antibacterial activity of amikacin in the membrane were determined by spectrophotometric method,energy spectrum analysis technology(EDAX) and direct antibacterial experiment respectively.Results The antibacterial amikacin was added to the the surface of catheters by the method described in this paper.Meanwhile,the antibacterial activity of amikacin was maintained.The slow-release time of amikacin exceeded 15 days.Conclusion The method described in the paper can be used for developing the catheter with slow-release amikacin.The catheter can also be used to prevent the CAUTI.
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