Abstract in English:Toxic shock syndrome is a staphylococcal disease caused by toxins produced by the staphylococci, toxic shock syndrome toxin-1 and enterotoxin B. The disease results from staphylococci growing in the vagina with the use of tampons during menstruation, primarily in young women. However, any staphylococcal infection can result in toxic shock syndrome if the staphylococci produce the appropriate toxins and the individual has no antibodies to the toxins. The symptoms can be quite severe, with high fever, low blood pressure, diffuse macular erythroderma, orthostatic dizziness, vomiting and or diarrhea at the onset, severe myalgia, peeling of the skin of the palms of the hands and the soles of the feet after seven to ten days, and death in some cases. The disease is not contagious as it is necessary for the toxin producing organisms to infect a cut or incision or be inserted into the vagina with a tampon. A high percentage of individuals have protective antibody titers to the toxins, with the percentage of individuals with titers increasing with age. Anyone colonized with a toxin-producing staphylococci will have a protective antibody titer. The source of the disease causing staphylococci is difficult to determine although it can be transferred from other family members or from a surgeon during operations. The disease is more or less accidental. The toxins are classed as superantigens because they react with many more T-cells than do conventional antigens. They stimulate the production of cytokines which may be directly involved in toxic shock syndrome.
Abstract in English:In the present study, we demonstrate that the volumes in which a given protein mass of Crotalus durissus terrificus venom or of a lyophilized stabilized aqueous extract (LSAE) of Peschiera fuchsiaefolia, an antivenom agent injected intramuscularly, have a decisive influence on the results. The LD50 of C. d. terrificus venom injected i.m. in a final volume of 200µl (2µl/g) (saline solution, 0.9% NaCl) was 180µg/100g rat body weight (p<0.05, 161 to 202µg/100g body weight) and the LD50 of the venom injected i.m. in a volume of 50µl (0.5µl/g) was 120µg/100g body weight (p<0.05, 107 to 134 µg/100g body weight). The reduction of the final volume injected i.m. also required a reduced mass of LSAE necessary to neutralize the lethal effect of C. d. terrificus venom. The dose of 60mg LSAE/100g rat body weight in a final volume of 200µl administered i.m. 20 seconds after venom injection, and that of 40mg LSAE/100g body weight/200µl mixed and incubated with the venom for 1 h at 25ºC before i.m. injection were able to neutralize the lethal activity of 2LD50. However, the LSAE doses that neutralized the 2LD50 were reduced to 20mg LSAE/100g body weight in a final volume of 50µl when administered i.m. 20 seconds after venom injection and to 2.5mg LSAE/100g body weight/50µl when mixed and incubated for 1 h at 25ºC with the venom before i.m. injection. The LD50 of C. d. terrificus venom and the doses of P. fuchsiaefolia LSAE that neutralized the venom lethal activity were, therefore, significantly lower when the final volume injected i.m. was reduced.
Abstract in English:very sensitive method for estimating the concentration of crotamine in a solution was developed. This method was based on the time required for the appearance of permanent hyperextension of the rear legs of mice as a function of the dose administered. This method can be used to determine toxin doses as low as 0.32 mg/kg<img SRC="http:/img/fbpe/jvat/v3n1/image2875.gif"> . Its high specificity for crotamine means that it can be used to measure toxin concentrations in the presence of other proteins and polypeptides.
Abstract in English:The present study demonstrates that Vipera ammodytes venom is a potent inhibitor of human complement activation. Crude venom was fractionated by ion-exchange chromatography and each fraction was then tested for proteolytic, hemolytic and anti-complement activities. Three peaks decreased the hemolytic activity of human serum when measured using assays for the classical and alternative pathways of activation. One of the anti-complement peaks contains a protease capable of cleaving the C3 component of complement.
Abstract in English:Bothrops alternatus venom was intramuscularly inoculated (3 mg/kg) into 12 dogs, 30 to 65 days old. Spontaneous bleeding commenced twenty minutes later. Blood samples obtained 3 and 20 minutes after venom inoculation presented spontaneous clotting formation. Plasmatic fibrinogen decreased within 3 minutes. Partial thromboplastin time (PTT) and one-stage prothrombin time (PT) were found. Plasma did not coagulate 40 minutes after inoculation. Platelet counts did not vary but their function was altered. Histopathology pointed out severe muscular necrosis and massive hemorrhage in the inoculation area. Regional ganglia showed intense hemorrhage. The 45 and 65-day-old animals showed alveolar thickening of the septum and generalized congestion, but the 30-day-old animals showed thrombosis of small arteries and arterioles. Renal lesions were different with the age. Cortical tubular necrosis was present in puppies, and intense cortical tubular hydropic degeneration was present in adult dogs. Thymus hemorrhage and necrosis were present.