Control of methicillin-resistant Staphylococcus aureus outbreak involving several hospitals.

This population-based, retrospective, cohort study describes a large methicillin-resistant Staphylococcus aureus (MRSA) epidemic caused by one strain (E1) in the greater Helsinki region. The epidemic comprised 210 cases at several hospitals, but was finally controlled. The study period ranged from June 1991 to December 2000. The epidemic peaked in 1993-1995 with 143 cases (68% of total cases). From August 1993, all MRSA-positive cases at the eight municipal hospitals were isolated and barrier nursed. Contacts were cohorted and screened for MRSA colonization. Decolonization treatment was administered to some chronic carriers. MRSA cases and contacts were identified in the joint patient register of the municipal hospitals from August 1993. The annual incidence of MRSA E1 in Helsinki City area per 100,000 inhabitants rose from 0.2 in 1991 to 13.6 in 1994. It decreased from 1995, reaching 0.7 per 100,000 in 2000. A jointly agreed policy on MRSA and timely co-operation between all units were essential for control of this epidemic.

Lipoproteins and acute phase response during acute infection. Interrelationships between C-reactive protein and serum amyloid-A protein and lipoproteins.

To study the interrelations between the changes of acute phase proteins and those of serum lipoproteins in acute infections we measured the concentrations of different lipoproteins, serum amyloid-A protein and C-reactive protein and activities of lipoprotein lipase and hepatic lipase during acute and convalescence phase and after complete recovery in 64 patients with infectious diseases (30 with viral infection and 34 with bacterial infection). The maximal decrements of both low density lipoprotein and high density lipoprotein cholesterol correlated significantly with the acute phase levels of C-reactive protein and serum amyloid-A protein. The acute phase concentration of very low density lipoprotein triglyceride correlated inversely to C-reactive protein level (r = -0.31, P less than 0.05) but not to serum amyloid-A protein level. Regression analysis showed that the concentration of C-reactive protein was a significant predictor of very low density lipoprotein triglyceride level in the acute phase of infection but not during convalescence. These results and the previous findings that C-reactive protein binds to low and very low density lipoproteins and that serum amyloid-A protein is associated with high density lipoprotein give credence to the view that C-reactive protein and serum amyloid-A protein interfere with the metabolism of serum lipoproteins during acute phase of infection.

Severity, duration, and mechanisms of insulin resistance during acute infections.

Acute infections provoke insulin resistance. These experiments were designed to study the severity, duration, and mechanisms of insulin resistance caused by acute infections. First, we studied eight patients [mean age, 29 +/- 11 (+/- SD) yr; body mass index, 23 +/- 2 kg/m2] with acute viral or bacterial infections during the acute stage of their infection and 1-3 months after recovery. The rate of glucose infusion required to maintain normoglycemia during hyperinsulinemia (approximately 500 pmol/L) was used as a measure of insulin action. During infection, the glucose requirements in the patients [21 +/- 2 (+/- SE) mumol/kg.min] were 52% less than those in weight- and age-matched normal subjects (44 +/- 2 mumol/kg.min; P less than 0.001). Compared to data from a large group of normal subjects, the resistance to insulin during infection corresponded to that predicted for a weight-matched 84-yr-old normal person or an age-matched obese person with a body mass index of 37 kg/m2. One to 3 months after recovery, the patients' glucose requirements were still significantly lower (37 +/- 3 mumol/kg.min; P less than 0.02) than those in matched normal subjects. To assess the mechanism of insulin resistance, seven additional patients were studied during the acute stage of infection using a low dose insulin infusion (plasma insulin, 215 pmol/L) combined with a [3-3H]glucose infusion and indirect calorimetry. Again, the glucose requirements were 59% lower in the patients (14 +/- 2 mumol/kg.min) than in matched normal subjects (34 +/- 2 mumol/kg.min; P less than 0.001). This decrease was due to a defect in glucose utilization (18 +/- 2 vs. 37 +/- 1 mumol/kg.min; P less than 0.001, patients vs. normal subjects) rather than impaired suppression of glucose production (4 +/- 1 vs. 3 +/- 1 mumol/kg.min, respectively). Total carbohydrate oxidation rates were similar in both groups (16 +/- 2 vs. 14 +/- 1 mumol/kg.min, respectively), whereas the apparent glucose storage was neglible in the patients (2 +/- 1 mumol/kg.min) compared to that in normal subjects (22 +/- 2 mumol/kg.min; P less than 0.001). We conclude that acute infections induce severe and long-lasting insulin resistance, which is localized to glucose-utilizing pathways. The rate of carbohydrate oxidation is normal during infections, whereas the rate of nonoxidative glucose disposal, as determined by indirect calorimetry, is nearly zero. The apparent blockade in glucose storage could result from diminished glycogen synthesis, accelerated glycogenolysis, or both.

Glucose intolerance in acute infections.

To evaluate the influence of an infective agent, severity of infection and the age of the patient on infection-induced glucose intolerance, concentrations of fasting blood glucose, serum insulin (n = 31) and plasma glucagon (n = 22) were measured and the oral glucose tolerance test (OGTT) was carried out (n = 26) during acute and convalescence phases and after complete recovery in patients with viral (n = 17) or bacterial (n = 14) infections. Serum insulin was increased (P less than 0.001) but plasma glucagon was decreased (P less than 0.01) both during acute infection and the convalescence period. In the acute stage, 2-h values of blood glucose (P less than 0.01) and serum insulin concentrations (P less than 0.001) during OGTT were elevated. The index of insulin resistance (glucose x insulin) was increased by 33% during infection and by 28% during convalescence (P less than 0.001). The observed changes did not correlate with the severity of infection, were more pronounced in younger patients than in older ones and were not dependent on the infective agent. It is clinically important to recognize that the restoration of insulin sensitivity takes longer than the immediate recovery period from the infection.

Changes in serum lipoprotein pattern induced by acute infections.

To study the effects of acute infections on serum lipids and lipoproteins we measured the concentration and composition of different lipoproteins, apoproteins A-I, A-II, and B, and the activities of plasma postheparin lipolytic enzymes, lipoprotein lipase (LPL) and hepatic lipase (HL) during acute and convalescence phase and after complete recovery in 72 infectious patients (33 with viral infection and 39 with bacterial infection). The mass concentrations of both low density lipoprotein (LDL) (P less than .001) and high density lipoprotein (HDL)2 (P less than .002) were reduced during acute infections due to the lowering of their cholesterol, phospholipid, and protein contents. The reduction of LDL cholesterol was maximal at the acute stage of infection (change -15%, P less than .001) while the reduction of HDL2 cholesterol was maximal during the convalescence (change -35%, P less than .001). During acute infections LDL became triglyceride-enriched (11.8 v 8.6%, P less than .0001) but cholesterol-poor (36.6 v 39.3%, P less than .0001). The ratio of HDL cholesterol/LDL cholesterol was significantly reduced during the convalescence (0.42 +/- 0.15 v 0.53 +/- 0.19, P less than .0001). The concentrations of apo A-I and apo A-II were decreased during acute infections (changes -22%, P less than .001, and -16%, P less than .001, respectively). The very low density lipoprotein (VLDL) was 18% higher during the convalescence period than after the recovery due to the elevations of VLDL triglycerides, cholesterol, and phospholipids. The activity of LPL was reduced both in the acute and convalescence phase, whereas that of HL was reduced only in the acute phase of infections.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum selenium in acute infections.

We measured the serum selenium concentration in 64 patients with uncomplicated viral (n = 33) or bacterial (n = 31) infections during the acute state of infection, during the early convalescent phase and after a minimum recovery period of three weeks and compared it to serum iron values. Both selenium (mean +/- SEM: 70.3 +/- 2.3 micrograms/l vs 79.4 +/- 2.2 micrograms/l, p less than 0.0001) and iron (8.4 +/- 0.8 micrograms vs 16.7 +/- 0.9 micrograms/l, p less than 0.0001) concentrations showed significant depressions in the acute stage of infection compared with the values after the recovery. The reduction of serum selenium did not correlate with the severity of infection measured by fever. We conclude that acute infections decrease serum levels regardless of the infective agent. The changes are of interest because of the possible connection between selenium and the immune system.

Delta agent in Finland.

We report for the first time the occurrence of infection with delta agent in Finland. One out of 121 HbsAg-positive sera, collected in Finland in 1983-84, had antibodies against delta agent.