Toxic shock syndrome

Platelet activating factor (PAF) was first identified by its ability (at low levels) to cause platelet aggregation and dilation of blood vessels, but it is now known to be a potent mediator in inflammation, allergic responses, and shock. PAF effects are observed at tissue concentrations as low as 10 M. PAF causes a dramatic inflammation of air passages and induces asthma-like symptoms in laboratory animals. Toxic-shock syndrome occurs when fragments of destroyed bacteria act as toxins and induce the synthesis of PAF. This results in a drop in blood pressure and a reduced... 

Suggested Alternatives for Differential Diagnosis Anthrax, brucellosis, dengue, ehrlichiosis, infectious mononucleosis, Kawasaki disease, leptospirosis, malaria, meningitis, men-ingococcemia, relapsing fever, Rocky Mountain spotted fever, syphilis, toxic shock syndrome, toxoplasmosis, tularemia, typhoid fever, rubella, measles. 

The cervical cap, smaller and less messy than the diaphragm, fits over the cervix like a thimble. Caps can be inserted 6 hours prior to intercourse, and women should not wear the cap for longer than 48 hours to reduce the risk of toxic shock syndrome. 

HIV, human immunodeficiency virus STD, sexually transmitted disease TSS, toxic shock syndrome UTI, urinary tract infection. 

Dmytryshin JR, Gribble MJ, Kassen BP. 1983. Chemical face peel complicated by toxic shock syndrome. Arch Otolaryngol 109-170ff. 

S. R. Monday G. A. Bohach, Properties ot Staphylococcus aureus Enterotoxins and Toxic Shock Syndrome Toxin-1. in The Comprehensive Sourcebook of Bacterial Protein Toxins, 2nd ed. J. E. Aiout, J. H. Freer, Eds. Academic Press London, 1999 pp 589-610. 

Staphylococcus aureus is an important human pathogen that causes a variety of clinical manifestations, ranging from benign skin infections to life-threatening infections such as septicemia, endocarditis, osteitis, and toxic shock syndrome. The virulence has been ascribed to a coordinated production of a large set of different toxins,... 

In addition to SFPs, enterotoxins may participate in the development of atopic eczema (Morishita et ah, 1999 Wehner and Neuber, 2001) and menstrual toxic-shock syndrome (MTSS) (Morishita et ah, 1999). 

De Boer, M.L., Kum, W.W. and Chow, A.W., Staphylococcus aureus isogenic mutant, deficient in toxic shock syndrome toxin-1 but not staphylococcal enterotoxin A production, exhibits attenuated virulence in a tampon-associated vaginal infection model of toxic shock syndrome, Can. J. Microbiol., 45, 250-256,... 

McLauchlin, J., Narayanan, G.L., Mithani, V. and O Neill, G., The detection of enterotoxins and toxic shock syndrome toxin genes in Staphylococcus aureus by polymerase chain reaction, J. Food Prot., 63, 479-88, 2000. 

Wieneke, A.A., The detection of enterotoxin and toxic shock syndrome toxin-1 production by strains of Staphylococcus aureus with commercial RPLA kits, Int. J. Food Microbiol., 7, 25-30, 1988. 

The relatively acidic thiol on serum albumin forms a fairly stable S-nitroso adduct with nitric oxide, which may serve to preserve and carry NO throughout the circulatory system [162,163]. Bacterial toxins released in toxic-shock syndrome induce excessive NO-synthase activity in macrophages. The resulting arterial expansion may induce the cardiovascular collapse associated with toxic shock syndrome [164]. Nitrous acid reacts with DNA to form dG-N2-dG interstrand crosslinks at the sequence 5 CG [165]. NO can also deaminate cytidine [166] and deoxyguanosine [167] and so may function as a mutagen. The rate law for NO reacting with O2 has been measured electrochemically as [168] ... 

For parenteral therapy, nafciUin and oxacillin offer comparable efficacy and antimicrobial spectra of activity. Although both drugs undergo hepatic metabolism, only nafcillin requires dose adjustment in patients with combined hepatic and renal insufficiency. Other pharmacokinetic data for nafcillin and oxacillin appear in Table 45.1. Indications for nafcillin or oxacillin include severe staphylococcal infections like cellulitis, empyema, endocarditis, osteomyelitis, pneumonia, septic arthritis, and toxic shock syndrome. 

Sudden infant death syndrome. Water-soluble smoke extract, in cell culture supernatants of mouse fibroblasts (L-929 cell line), produced an increase in TNF-a from respiratory syncytial virus-infected cells. It decreased TNF-a from cells incubated with toxic shock syndrome toxin. Incubation with cigarette smoke extract decreased the NO production from respiratory syncytial virus-infected cells and increased the NO production from cells incubated with toxic shock syndrome toxin. Monocytes from a minority of individuals demonstrated extreme TNF-a responses and/or very high or very low NO. The proportion of samples in which extreme responses with a very high TNF-a and very low NO were detected was increased in the presence of the three agents to 20% compared with 0% observed with toxic shock syndrome toxin. One to 4% was observed with cigarette smoke extract or respiratory syncytial virus L Symphatomimetic activity. Water extract of the dried leaf, administered intravenously to cats at doses of 0.05 and 10-20 mg/kg. 

There were four deaths in previously healthy women due to endometritis and toxic shock syndrome within 1 week after medically induced abortions with oral mifepristone 200 mg and vaginal misoprostol 800 micrograms in two cases Clostridium sordellii was found (19). Another similar case was reported in Canada in 2001. Endometritis and toxic shock syndrome associated with C. sordellii are rare. Of 10 cases identified by authors in the previous literature, eight occurred after the delivery of live-born infants, one after a medical abortion, and one was not associated with pregnancy. The cases produced an FDA alert with a Dear Health Care Provider letter from the manufacturer and publication of a Dispatch in the Morbidity and Mortality Weekly Report (20). 

Fischer M, Bhatnagar J, Guarner J, Reagan S, Hacker JK, Van Meter SH, Poukens V, Whiteman DB, Iton A, Cheung M, Dassey DE, Shieh WJ, Zaki SR. Fatal toxic shock syndrome associated with Clostridium sordellii after medical abortion. N Engl J Med 2005 353(22) 2352-60. 

Centers for Disease Control and Prevention. Clostridium sordellii toxic shock syndrome after medical abortion with mifepristone and intravaginal misoprostol—United States and Canada, 2001-2005. MMWR Morb Mortal Wkl Rep 2005 54 724. 

Toxic shock syndrome is a very damaging, often fatal condition caused by toxins from Staphylococcus aureus or Streptococcus pyogenes. First reported in children in 1978, it is manifested by high fever, erythroderma (a skin rash condition), and severe diarrhea.6 Patients may exhibit confusion, hypotension, and tachycardia, and they may go into shock with failure of several organs. Survivors often suffer from skin desquamation (flaky skin). 

In 1980, toxic shock syndrome in menstruating women was linked to the use of a new superabsorbent tampon that altered the vaginal environment, including sequestration of magnesium ion, in a way that greatly increased susceptibility to the infection. The tampons were quickly withdrawn from the market, and now most cases occur in surgical patients infected by the bacteria that cause the syndrome. 

The bacterial toxins responsible for toxic shock syndrome are proteins that are classified as superantigens. These proteins bypass some of the steps normally involved in antigen-mediated immune response, thereby activating 5 to 30% of the T cell population, compared to 0.01 to 0.1% activated by conventional antigens. The consequence of the huge numbers of activated T cells is release of cytokines that cause capillaries to leak, resulting in many of the symptoms of the syndrome. 

Issa, N.C. and Thompson, R.L., Staphylococcal toxic shock syndrome suspicion and prevention are keys to control, Postgraduate Medicine, Oct. 1, 2001, p. 55. 

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