Please note, due to essential maintenance online transactions will not be possible between 02:30 and 04:00 BST, on Tuesday 17th September 2019 (22:30-00:00 EDT, 17 Sep, 2019). We apologise for any inconvenience.
To send this article to your account, please select one or more formats and confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send this article to your Kindle, first ensure firstname.lastname@example.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about sending to your Kindle.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
Candida species are seldom considered as a cause of suppurative peripheral thrombophlebitis. During a 15-month period in a 291-bed acute-care hospital, candidal suppurative peripheral thrombophlebitis developed in seven patients. All patients had fever, a tender palpable cord, and Candida species isolated from resected veins and/or pus expressed at the catheter entrance site. Four patients had candidemia. None were neutropenic or recipients of corticosteroids. All had concomitant or preceding bacterial infections, and had received a median of 5 antibiotics (range 3 to 9) for at least 2 weeks. Five of seven had documented preceding candidal colonization associated with broad spectrum antibiotic therapy. Catheter sites had not been routinely rotated and local catheter site care was deficient. Risk factors of antibiotics and duration of hospitalization were fewer in patients with bacterial suppurative thrombophlebitis. Combined segmental venous resection and intravenous amphotericin B appears to be the most rational therapy for this nosocomial fungal infection.
One hundred fifty-three critical care patients with documented cimetidine and antacid use were prospectively studied with serial gastric pH determinations and semiquantitative gastric fluid cultures. This study documents the abnormal gastric colonization of patients with therapeutically altered gastric acidity by hospital acquired gram negative rods (GNR). Three hundred twenty-four gastric fluid cultures from 153 patients revealed 152 (47%) positive cultures for GNR, 78 (24%) sterile specimens, and 94 (29%) positive for mixed oropharyngeal flora. One hundred forty (59%) of the 236 cultures at a pH of 4 or greater were positive for GNR. In contrast, only 12 (14%) of the 88 cultures at a pH of less than 4 were positive for GNR (p<.001). Forty-six (52%) of 88 cultures at a pH of less than 4 were sterile as compared to only 32 (14%) of 236 sterile cultures at a pH of 4 or greater (p<.001). At low pH, cultures are predominately sterile and at a pH of 4 or greater the flora dramatically changes to hospital acquired GNR. This artificially maintained reservoir of gram negative rods in the critically ill patient is a potential reservoir of organisms causing nosocomial bacteremia or pneumonia in this high risk population.
Sera from 275 employees of three hospitals were tested for the presence of antibodies to polio virus. Immunity was found to increase with age, and was higher in personnel directly involved in patient care than in the others. Previous exposure to poliomyelitis as well as a history of previous immunization did not correlate with the immunological status of the employee. When antibodies against one of the three polio types or more could not be demonstrated, the employee was vaccinated by an inactivated polio virus vaccine.
On May 17, 1984, a 67-year-old woman with endometrial carcinoma underwent an uneventful abdominal hysterectomy. Suddenly, 18 hours later she was in septic shock, short of breath, restless and oliguric. The wound appeared intact without erythema. Intraabdominal sepsis was postulated and the patient was given full dosages of intravenous cefotaxime, metronidazole and netilmicin. At 48 hours postoperative, the abdominal wound showed areas of necrosis and the patient died. The wound, peritoneal fluid, urine and blood yielded group A (β-hemolytic streptococci (Streptococcus pyogenes). Shortly before death, intravenous penicillin had been administered. An epidemiologic study was promptly initiated.
Why are blood cultures drawn? Is there a purpose to the blood culture or is it a reflex reaction to a fever? Nurse says, “patient has fever,” Doctor replies “draw blood culture.” I fear that the latter is all too often the scenario that exists in the hospital today. As we enter an era where the extra laboratory tests do not “make money, keep the techs employed and justify the lab,” we must re-examine the rationale for blood cultures.
It is thought that the first person to describe the organism subsequently known as Eikenella corrodens was Sverre Henriksen, who in 1948 reported the isolation of three gram-negative anaerobic rods with concentrically spreading colonies and a tendency to pit the agar. This corroding of the agar was seen most reliably with strain AJ, a nonmotile organism isolated from a perineal abscess. Two years later, Per Holm found that a gram-negative anaerobic organism resembling the influenza bacillus was often isolated from specimens of pus, examined for the presence of actinomycetes. Because of its appearance on blood agar, Holm proposed calling this organism the “corroding bacillus.” In 1958, Eiken studied 1,097 anaerobes isolated from 798 patients; of these, 61 corresponded in colony and microscopic morphology with the corroding bacillus.