Molecular epidemiology of Staphylococcus epidermidis isolates in a hematological unit during a 4-month survey.

In order to study the strain variety, clonal stability and epidemiology of Staphylococcus epidermidis, isolates from all bacterial cultures taken when clinically indicated in 2 wards of the hematological unit of Helsinki University Hospital, during a 4-month period, were characterized by 3 typing methods: antibiogram, plasmid profile and ribotype. A total of 141 distinct S. epidermidis colonies, from 28 blood cultures and 37 cultures from other sources in 32 patients were studied. Plasmid profiles and ribopatterns revealed 47 different strains of which 16 were bacteremic. One of these strains caused bacteremia in 4 different patients over a 3-month period and it was isolated from blood on 7 different sampling occasions. The occurrence of this clone was constant; it was usually found in both of 2 blood culture bottles inoculated (6/7 pairs) and dominated among the 17 distinct S. epidermidis colonies studied from the positive bottles (94% of the total). The clones causing bacteremias in the 2 wards were distinct. These findings indicate that certain clones of S. epidermidis can predominate in hematological wards and that nosocomial transmission of S. epidermidis strains may occur among patients, particularly within the same ward.

Persistence of a multiresistant clone of Staphylococcus epidermidis in a neonatal intensive-care unit for a four-year period.

A cluster of cases of Staphylococcus epidermidis bacteremia in a neonatal intensive-care unit (NICU) during 1991 raised the question of whether these infections were caused by a single strain. Sixty-seven isolates of S. epidermidis from blood cultures of 56 neonates treated in the NICU between 1986 and 1992 and 54 control strains from other patients with bacteremia were characterized by three typing methods: antibiogram, plasmid profile, and ribotype. Plasmid profiles and ribotype patterns indicated that 11 (16%) of the 67 episodes of S. epidermidis bacteremia in the NICU were caused by a single strain. Although this epidemic strain did not account entirely for the increase in the incidence of bacteremia in the NICU, it did persist for 4 years during the study period. Other clones responsible for smaller outbreaks were also found. These results suggest that S. epidermidis cross-infections are very common in the NICU setting.

Cold exposure decreases the effectiveness of atropine-oxime treatment in organophosphate intoxication in rats and mice.

1. The effect of cold environment on the acute toxicity of organophosphates (OP), without and with atropine-oxime treatment, was studied in rats and mice by exposing them to +5 and -5 degrees C temperature. The tested OPs and oximes (given intraperitoneally) were diisopropylfluorophosphate (DFP), isopropyl methylphosphonofluoridate (sarin) and dichlorovinyl phosphate (DDVP), pralidoxime (PAM) and obidoxime. 2. An exposure to low environmental temperature decreased the effectiveness of atropine-oxime therapy in OP poisoned rats and mice, evaluated by means of acute LD50 values. 3. The lowering of environmental temperature did not influence the ability of PAM to reactivate tissue cholinesterase in rats intoxicated by 0.5 x LD50 doses of DFP. 4. The acute toxicity of atropine and oximes was not affected by cold environment in rats, but in mice it was increased by 1.1-2.1 times. 5. The decrease in the effectiveness of atropine-oxime therapy at cold environment may be explained by the observation that the cold temperature sensitizes the animals to the inhibition of brain acetylcholinesterase by OP.

Effect of the cold environment on organophosphate toxicity and inhibition of cholinesterase activity.

1. Rats were used for studies on organophosphate (OP) toxicity both in acute and chronic cold exposure. Furthermore the effects of OPs on tissue acetyl- and butyrylcholinesterase activities were studied in the cold environment. 2. No change in the toxicity of dichlorovinyl phosphate (DDVP) was observed whereas that of diisopropylphosphofluoridate (DFP) increased 1.5-fold at +5 degrees C. 3. Chronic exposure to cold produced no change in DFP toxicity. 4. The survival time in acute cold exposure (1.1 x LD50 DFP) was longer than in chronic exposure or at +20 degrees C. 5. In control rats, chronic cold exposure increased blood BuChE and decreased BuChE in lungs. 6. A dose-dependent inhibition of cholinesterases was observed. 7. AcChE in the liver of chronically cold exposed rats was more sensitive to DFP inhibition compared to acute exposure. 8. Blood AcChE activity correlated only to AcChE in brain and lungs in rats.

Physical exercise affects cholinesterases and organophosphate response.

1. Cholinesterase activities in blood and tissues of control and exercising rats with and without organophosphate (OP) exposure were studied. 2. Physical exercise increased total cholinesterase and butyrylcholinesterase activities in rats without OP exposure in blood and diaphragm. In brain physical exercise had no effect on acetylcholinesterase activity. 3. Physical exercise diminished cholinesterase inhibition in blood and tissues after OP exposure.

A simple method for the measurement of blood cholinesterase activities under field conditions.

A new separation method using a hand-driven discoidal micro-centrifuge was developed. It is suitable for separating red cells from plasma in field conditions. The amounts of plasma produced are sufficient to be used for the dip-stick estimation of pseudocholinesterase activity. The strip estimations of plasma pseudochoninesterase activity correlated well with the spectrophotometric method of plasma cholinesterase. The test paper methods seem to be reliable under field conditions in acute organophosphate poisonings. To verify the results of the paper strip methods the blood method absorbed on paper can be used. This method is applicable for the measuring of blood cholinesterase activities and thus monitoring humans exposed to organophosphates under field conditions.

Relationship between serum lipids, lipoproteins and pseudocholinesterase during organophosphate poisoning in rabbits.

The activities of serum pseudocholinesterase, lecithin: cholesterol acyltransferase (LCAT) and gamma-glutamyltransferase in rabbits were investigated before and after dichlorvos administration in vivo. The effects of this organophosphate on some serum lipids and lipoprotein fractions were also determined. LCAT activity remained almost unaffected after organophosphate administration. However, serum gamma-glutamyltransferase and pseudocholinesterase activities markedly decreased. Dichlorvos markedly lowered both serum low density lipoprotein (LDL) and cholesterol contents, whereas high density lipoprotein (HDL) concentration increased and very low density lipoprotein (VLDL) remained unaffected. Triglycerides as well as esterified fatty acids increased significantly but the statistical changes in free fatty acid concentrations were not significant, because individual variations in fatty acid concentrations were high.

Serum lipids and hepatic microsomal enzymes with special reference to serum cholinesterase in Wistar rats.

Serum pseudocholinesterase in accordance with indicators revealing the lipid metabolism and liver function was studied in rats exposed to phenobarbital, bis-p-nitrophenylphosphate and disulfiram in vivo. Phenobarbital markedly induced the hepatic microsomal drug-metabolizing enzymes and tended to decrease the triglyceride content in serum. Serum lipids remained almost unaffected after the treatment of bis-p-nitrophenylphosphate. However, serum gamma-glutamyltransferase activity showed a marked decrease to this organophosphorus compound. Disulfiram activated the microsomal UDP-glucuronosyltransferase (p-nitrophenol) activity, and caused an enhancement of serum total cholesterol, which suggests that this drug might be atherogenic.

Pseudocholinesterase activity in some human body fluids.

Pseudocholinesterase activity of sweat, lacrimal fluid, urine, parotid saliva, whole saliva, whole blood and plasma was estimated using butyrylthiocholine iodide and propionylthiocholine iodide as substrates. There was similarity in activity between erythrocytes and plasma, but considerable differences between whole blood and other body fluids. The level of enzyme activity was approximately the same in sweat, lacrimal fluid, urine, parotid fluid and whole saliva, but it was only about 1/1500 of that of plasma. The enzyme activity in either whole blood or plasma is a good measure of organophosphate exposure but in other fluids activity can hardly give more than an approximate indication of acute poisoning.

Pseudocholinesterase activity and its origin in human oral fluid.

Pseudocholinesterase (PCE) activity in oral fluid of 31 male and 24 female subjects was determined using butyrylthiocholine iodide as substrate. Males had approximately twice as much salivary PCE activity as did females [4.8 +/- 2.4 (S.D.) U/1 and 2.2 +/- 1.5 (S.D.) U/1, respectively]. The activity was not much affected by salivary flow rate, although in men it was a little higher in stimulated than in unstimulated saliva. Salivary PCE activity showed diurnal variation. Accordingly, activities were about three times greater at four a.m. than at four p.m. Parotid PCE activity correlated with that of whole saliva in both men and women. PCE activity in crevicular fluid (four subjects) was 120 +/- 48 (S.D.) U/1. An elevation of PCE activity in oral fluid was found after experimental induction of gingival inflammation. However, the mean PCE activity of patients with clinical gingivitis was not significantly higher than that of healthy subjects, although some exceptionally high values were found. Sonicated samples of plaque did not contain any PCE activity. No correlation existed between PCE activities in saliva and serum.