antibiotic treatment, s. aureus bacteremia has a case fatality rate around 80%. with antibiotic treatment, case fatality rates range from 15% to 50% depending on the age and health of the patient, as well as the antibiotic resistance of the s. aureus strain. medical implant infections s. aureus is often found in biofilms formed on medical devices implanted in the body or on human tissue. it is commonly found with another pathogen, candida albicans, forming multispecies biofilms. the latter is suspected to help s. aureus penetrate human tissue. a higher mortality is linked with multispecies biofilms. s. aureus biofilm is the predominant cause of orthopedic implant-related infections, but is also found on cardiac implants, vascular grafts, various catheters, and cosmetic surgical implants. after implantation, the surface of these devices becomes coated with host proteins, which provide a rich surface for bacterial attachment and biofilm formation. once the device becomes infected, it must by completely removed, since s. aureus biofilm cannot be destroyed by antibiotic treatments. current therapy for s. aureus biofilm-mediated infections involves surgical removal of the infected device followed by antibiotic treatment. conventional antibiotic treatment alone is not effective in eradicating such infections. an alternative to postsurgical antibiotic treatment is using antibiotic-loaded, dissolvable calcium sulfate beads, which are implanted with the medical device. these beads can release high doses of antibiotics at the desired site to prevent the initial infection. novel treatments for s. aureus biofilm involving nano silver particles, bacteriophages, and plant-derived antibiotic agents are being studied. these agents have shown inhibitory effects against s. aureus embedded in biofilms. a class of enzymes have been found to have biofilm matrix-degrading ability, thus may be used as biofilm dispersal agents in combination with antibiotics. animal infections s. aureus can survive on dogs, cats, and horses, and can cause bumblefoot in chickens. some believe health-care workers' dogs should be considered a significant source of antibiotic-resistant s. aureus, especially in times of outbreak. in a 2008 study by boost, o’donoghue, and james, it was found that just about 90% of s. aureus colonized within pet dogs presented as resistant to at least one antibiotic. the nasal region has been implicated as the most important site of transfer between dogs and humans. s. aureus is one of the causal agents of mastitis in dairy cows. its large polysaccharide capsule protects the organism from recognition by the cow's immune defenses. virulence factors main article: virulence factor enzymes s. aureus produces various enzymes such as coagulase (bound and free coagulases) which facilitates the conversion of fibrinogen to fibrin to cause clots which is important in skin infections. hyaluronidase (also known as spreading factor) breaks down hyaluronic acid and helps in spreading it. deoxyribonuclease, which breaks down the dna, protects s. aureus from neutrophil extracellular trap-mediated killing. s. aureus also produces lipase to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and beta-lactamase for drug resistance. toxins depending on the strain, s. aureus is capable of secreting several exotoxins, which can be categorized into three groups. many of these toxins are associated with specific diseases. superantigens antigens known as superantigens can induce toxic shock syndrome (tss). this group comprises 25 staphylococcal enterotoxins (ses) which have been identified to date and named alphabetically (sea - sez), including enterotoxin type b as well as the toxic shock syndrome toxin tsst-1 which causes tss associated with tampon use. toxic shock syndrome is characterized by fever, erythematous rash, low blood pressure, shock, multiple organ failure, and skin peeling. lack of antibody to tsst-1 plays a part in the pathogenesis of tss. other strains of s. aureus can produce an enterotoxin that is the causative agent of a type of gastroenteritis. this form of gastroenteritis is self-limiting, characterized by vomiting and diarrhea 1–6 hours after ingestion of the toxin, with recovery in 8 to 24 hours. symptoms include nausea, vomiting, diarrhea, and major abdominal pain. exfoliative toxins