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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nearly 50 per cent of patients with acute bacterial pneumonia have an accompanying pleural effusion (parapneumonic effusion). With appropriate antibiotic therapy, the pleural effusion will resolve along with the pneumonia in the majority of patients. However, in a small fraction, the pleural effusion will not resolve unless drainage of the pleural space is instituted. Such patients are said to have complicated parapneumonic effusions. It is important to identify patients with complicated parapneumonic effusions as early as possible, since tube drainage of the pleural space becomes increasingly difficult the longer its institution is delayed. The possibility of a complicated parapneumonic effusion should be considered in every patient with bacterial pneumonia. If both diaphragms cannot be distinctly identified throughout their length on the lateral chest radiograph, decubitus chest radiographs should be obtained. If the thickness of the fluid on the decubitus radiograph is greater than 10 mm, a diagnostic thoracentesis should be performed. Only pleural fluid analysis can identify patients with complicated parapneumonic effusions. Complicated parapneumonic effusions are characterized by low pleural fluid pH and glucose levels, a high pleural fluid LDH, and a positive Gram stain of the pleural fluid. Tube thoracostomy should be performed immediately in a patient with an acute bacterial pneumonia if the pleural fluid glucose is below 40 mg per 100 ml, the pleural fluid pH is below 7.00, or if the Gram stain of the pleural fluid is positive. Patients with pleural fluid pH above 7.20, pleural fluid LDH below 1000 IU per L, and pleural fluid glucose levels above 40 mg per 100 ml respond well to only the administration of appropriate antibiotics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Parapneumonic effusions and empyema. 384 2

We describe what appears to be the first reported case of nosocomial pneumonia caused by Neisseria cinerea. The isolate metabolized glucose when tested in BACTEC Neisseria Differentiation Kits (Johnston Laboratories), but did not produce detectable acid in cystine-Trypticase (BBL Microbiology Systems) agar medium or in modified oxidation-fermentation medium. Clinical laboratories that rely on the BACTEC method for differentiation of pathogenic neisseriae should be aware of the fact that N. cinerea may mimic N. gonorrhoeae when tested in BACTEC Neisseria Differentiation kits. The ability of N. cinerea to grow well on tryptic soy and Mueller-Hinton agars and its inability to grow on modified Thayer-Martin medium are characteristics which help to distinguish N. cinerea from N. gonorrhoeae.
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PMID:Nosocomial pneumonia caused by a glucose-metabolizing strain of Neisseria cinerea. 388 66

Amikacin (AMK) by intravenous drip infusion was given to patients with infections in the field of internal medicine and the results were followings: AMK was administered to 19 patients. Diagnosis included sepsis or suspected sepsis (11 cases), pneumonia (2 cases), chronic respiratory tract infections (3 cases) and urinary tract infections (3 cases). Underlying disease included hematologic disease (13 cases), lung fibrosis (1 case), chronic respiratory insufficiency (1 case), diabetes mellitus (1 case), hepatic coma and bronchial asthma (1 case) and prostatic hypertrophy (1 case). Nineteen episodes responded to single therapy (2 cases) or combined therapy with other antibiotics (17 cases). AMK by intravenous drip infusion (dissolved in not less than 100 ml of saline or glucose) was administered at the dose of 200 mg/day to 600 mg/day divided into 2 or 3 times, over 1 hour to 2 hours. The mean duration of therapy was 10 days and the mean total dose was 4.3 g. Clinical effects: Excellent in 7 cases, good in 7 cases, fair in 3 cases and poor in 2 cases, and efficacy rate was 74%. Bacteriological effects: Disappeared in 3 cases, partly disappeared and unchanged in 3 cases, superinfection in 1 case and newly appeared in 1 case. Four strains out of 7 cases of which were detected the causative bacteria were disappeared. GM resistant bacteria (S. marcescens in 2 strains and C. diversus in 1 strain) were disappeared by the administration of AMK, also some clinical symptoms and signs were improved. No side effects and no abnormalities in laboratory findings were noted in any cases attributed to AMK. In conclusion, high efficacy rate was obtained without any side effects, intravenous drip infusion of AMK seemed to be useful for infections in patients with bleeding tendency (e.g. leukemia) or malignant disease.
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PMID:[Clinical evaluation of amikacin by intravenous drip infusion for infections in the field of internal medicine]. 407 2

Chronically diabetic nonketotic rats were shown to be more susceptible to experimental Type 25 pneumococcal pneumonia than nondiabetic rats. The cumulative mortality in the diabetic group was significantly higher at infecting doses of 10(3), 10(4), 10(5), and 10(6) organisms, and the LD(50) was less than one twentieth of that for the nondiabetic group. More than ten times as many viable pneumococci were found in the pneumonic lesions of the diabetic animals at 24 and 36 hr as were present in the lesions of the nondiabetic controls, and serial histologic studies revealed that phagocytosis was strikingly depressed in the alveolar exudates of the diabetic animals. The diabetic state was also found to cause a similar depression of in vivo phagocytosis in preformed peritoneal exudates. The results of in vitro experiments indicated that the principal defect in the diabetic animals resided in their serum rather than in their polymorphonuclear leukocytes. The depressive factor in the serum was identified as the abnormally high concentration of glucose. Since equivalent molar concentrations of unmetabolized sugars added to normal serum caused a similar depression of phagocytosis, it was tentatively concluded that the action of the glucose on the leukocytes was primarily osmotic. The sensitivity of the granulocytes to the glucose effect, however, depended upon the conditions of the phagocytic test. Only when the pneumococci were encapsulated and the leukocytes derived from inflammatory exudates were crowded together, as in vivo, was the depressive action of the glucose clearly demonstrable.
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PMID:Studies on the effect of experimental nonketotic diabetes mellitus on antibacterial defense. I. Demonstration of a defect in phagocytosis. 438 Jun 70

Mycoplasma pulmonis, an etiological agent of murine pneumonia, produced about 0.065 mumoles of hydrogen peroxide (H(2)O(2)) per hr per 10(10) colony-forming units. When glucose was present at a concentration of 0.01 m, H(2)O(2) production was increased by 50%. To determine if H(2)O(2) production by M. pulmonis could be correlated with virulence, normal, acatalasemic, and acatalatic mice were infected with the organism. Three days after infection with M. pulmonis significantly more acatalatic mice had pneumonia than did normal or acatalasemic mice. The pneumonia in acatalatic mice was also more severe than in the other two groups. Five days after infection, pneumonia in the acatalatic mice was resolved, whereas normal mice were severely affected. The presence of pneumonia and the severity were correlated with the recovery of M. pulmonis from the lesions. In vitro studies of the effect of catalase on M. pulmonis showed that exogenously supplied catalase stimulated the growth of M. pulmonis at 37 C and prolonged its survival at 25 C. Hemolysis of sheep blood, guinea pig blood, rabbit blood, and normal and acatalasemic mouse blood by M. pulmonis was inversely related to the catalase activity of the erythrocytes. These findings suggest that H(2)O(2) secretion contributes to the virulence of M. pulmonis and to the death of the microorganism in the absence of host catalase.
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PMID:Relationship of hydrogen peroxide production by Mycoplasma pulmonis to virulence for catalase-deficient mice. 578 95

We have reviewed ten children who underwent surgical therapy for persistent neonatal hypoglycemia over a 5-year period. All had inappropriately high insulin levels in the face of hypoglycemia, and all failed medical management with intravenous glucose, frequent feeds, diazoxide and glucagon. Two groups of five patients each were analysed retrospectively. Group 1 underwent 95% pancreatectomy, leaving a small amount of pancreatic tissue on the duodenum and common bile duct. The only major complication in this group was in one patient with common duct obstruction requiring choledochoduodenostomy. All these children are developing normally, without diabetes, steatorrhea, or recurrent hypoglycemia. Group 2 underwent 85% pancreatectomy, leaving the uncinate process in situ. Two of these children are well. Two required conversion to 95% resection because of recurrent hypoglycemia; one of these required a subsequent total pancreatectomy, at which time the pancreatic remnant had significantly regenerated. The other Group II patient was normoglycemic but died at age 3 from pneumonia. Pathology in nine cases showed islet cell dysplasia; 5 of these also had microadenomatosis. One case had a histologically normal pancreas. We conclude that 95% pancreatectomy is a safe operation with a lower failure rate than less radical resections, and should be used early in the management of this condition.
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PMID:Surgical management of persistent neonatal hypoglycemia due to islet cell dysplasia. 639 33

A 6-week-old female infant presented in a severe metabolic crisis from propionic acidaemia. The condition was aggravated by pneumonia and heart insufficiency. In addition to the general supportive measures and caloric intake exclusively from glucose, intravenous L-carnitine treatment (2 g L-carnitine/24 h) was started to enhance propionic acid excretion as a carnitine conjugate. Despite the therapeutic efforts the patient died about 48 h after admission in sudden respiratory arrest and bradycardia. Serum propionic acid concentration was increased to 0.3 mumol/ml. Propionylcarnitine excretion was measured and about 55% of the overall excretion during the 48 h treatment period was attributed to an effect of carnitine administration. 2-methylcitrate and 2-methyl-3-oxovaleric acid excretion decreased during the same period. Obviously carnitine was not able to prevent metabolic deterioration but may provide some additional "buffer capacity" during long-term dietary treatment.
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PMID:The effect of intravenous L-carnitine on propionic acid excretion in acute propionic acidaemia. 651 Apr 34

Four patients, treated with pentamidine because of Pneumocystis carinii pneumonitis, displayed severe fasting hypoglycemia during this treatment. Diabetes mellitus appeared later, requiring insulin therapy in the three of them who survived more than a few weeks. The metabolic study, performed in two cases during the hypoglycemic period, demonstrated inappropriately high insulin levels in the postabsorptive state. 28 +/- 1 microunits/ml (blood glucose 41 +/- 4 mg/dl) and 86 +/- 5 microunits/ml (blood glucose 15 +/- 5 mg/dl) vs. 15 +/- 3 microunits/ml in 10 control subjects and 55 +/- 3 microunits/ml in 6 patients with a verified B-cell tumor, respectively. Poor B-cell secretory responses followed the stimulations by oral glucose (maximal increment over basal: +5 microunits/ml vs. + 40 microunits/ml in control group and +77 microunits/ml in the insulinoma group), by i.v. arginine (maximal increment + 10 and +28 microunits/ml, respectively, vs. +55 in the controls and +90 microunits/ml in the insulinoma group) and by i.v. glucagon (+10 and +23 microunits/ml, respectively) vs. +40 microunits/ml in both the control and the insulinoma groups). Plasma cortisol and glucagon, and the A-cell response to arginine were higher than normal. These high, nonsuppressible, nonstimulable insulin levels and the sequence of hypoglycemia followed by insulin-dependent diabetes mellitus is consistent with the hypothesis of a selective toxicity turned towards the B-cells. In vitro incubation of islets with pentamidine 10(-10) M produced a passive release of insulin, followed by a significant decrease in B-cell response to glucose + theophylline. It is suggested that pentamidine can induce hypoglycemia because of an early cytolytic release of insulin, and then diabetes mellitus because of B-cell destruction and insulin deficiency.
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PMID:Diabetes mellitus following pentamidine-induced hypoglycemia in humans. 675 11

The course of 61 infants admitted for treatment of chronic diarrhea and malnutrition was reviewed. 30 children had (M) marasmus, 18 (K) kwashiorkor, and 13 (MK) marasmic kwashiorkor. After initial rehydration, infants were managed with a predominantly oral nutrition regimen utilizing a formula based on whole protein (casein), vegetable oil, glucose, and sucrose. Intravenous fluids were required for 38 infants (62%) for a median duration of 6 days, principally for the delivery of antibiotics, although amino acids were added in many instances. Feedings were started at 25 kcal/kg/day and were increased 35 kcal/kg/day every other day until acceptable steady weight gain ensued, provided that stool ouput did not exceed 100-50 gm/day and stool character was improving. Infants with M and MK reached a maximum intake of 151 + or - 21 kcal/dg/day after 5 weeks of treatment. Weight gain had been occurring for 2 weeks prior to this time. Infants with K were purposely not advanced past 75 kcal/kg/day until edema had cleared; a maximum intake of 135 + or - 16 kcal/kg/day was reached at 5 weeks. Mean initial serum albumin concentration in these infants with K was 1.8 + or - 0.3 gm/day and required 20 + or - 13 and 53 + or - 24 days to exceed 2.0 and 3.6 gm/dl, respectively. 14 of the 61 infants were moribund on arrival and died within the first 3 days; the remaining 8 died of overwhelming infection (6 generalized and 2 pneumonia). Data suggest that once infection is controlled, infants with chronic diarrhea and malnutrition can usually be effectively managed by enteral feeding without resorting to parenteral alimentation.
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PMID:Nutritional management of chronic diarrhea and malnutrition: primary reliance on oral feeding. 677 51

A 26-year-old man presented with progressive pneumonia, and Aspergillus was grown from cultures of lung, cutaneous nodules, and urine. His PMNs had a poor CL response after exposure to phagocytic stimuli (S. aureus, latex, aggregated IgG and IgG-coated latex) (p less than 0.01 vs. controls) and soluble stimuli (PMA, sodium fluoride, and Con A) (p less than 0.05). His PMNs failed to reduce NBT, oxidize 14C-1 glucose (p less than 0.001), or iodinate proteins (p less than 0.001), normally, compared with controls, and his PMNs killed Candida albicans and Staphylococcus aureus abnormally (p less than 0.05). The patient was anergic; his plasma inhibited responsiveness of his lymphocytes to stimulation with Aspergillus and Candida antigens. His lymphocytes failed to produce the lymphokine LMIF normally. The patient's 10-month-old daughter was demonstrated to have the same defects of PMN metabolism and function. The findings in this patient were similar to those in CGd, but transmission of the defect from father to daughter and the presence of lymphocyte abnormalities make this diagnosis unlikely. Inhalation of Aspergillus by patients with defective PMN oxidative metabolism may be associated with development of significant infection.
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PMID:A genetic defect of granulocyte oxidative metabolism in a man with disseminated aspergillosis. 678 13


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