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Staphylococci (staph) are Gram-positive spherical bacteria that occur in microscopic clusters resembling grapes. Bacteriological culture of the nose and skin of normal humans invariably yields staphylococci. In 1884, Rosenbach described the two pigmented colony types of staphylococci and proposed the appropriate nomenclature: Staphylococcus aureus (yellow) and Staphylococcus albus (white). The latter species is now named Staphylococcus epidermidis. Although more than 20 species of Staphylococcus are described in Bergey's Manual (2001), only Staphylococcus aureus and Staphylococcus epidermidis are significant in their interactions with humans. S. aureus colonizes mainly the nasal passages, but it may be found regularly in most other anatomical locales, including the skin, oral cavity and gastrointestinal tract. S epidermidis is an inhabitant of the skin. Taxonomically, the genus Staphylococcus is in the Bacterial family Staphylococcaceae, which includes three lesser known genera, Gamella, Macrococcus and Salinicoccus. The best-known of its nearby phylogenetic relatives are the members of the genus Bacillus in the family Bacillaceae, which is on the same level as the family Staphylococcaceae. The Listeriaceae are also a nearby family. Staphylococcus aureus forms a fairly large yellow colony on rich medium; S. epidermidis has a relatively small white colony. S. aureus is often hemolytic on blood agar; S. epidermidis is non hemolytic.
The test should not be done on blood agar because blood itself contains catalase. The bacteria are catalase-positive and oxidase-negative. skin and mucous membranes pathogen of humans. aureus can grow at a temperature range of 15 to 45 degrees and at NaCl concentrations as high as 15 percent. The staphylococci grow in clusters because the cells divide successively in three perpendicular planes with the sister cells remaining attached to one another following each successive division. The shape and configuration of the Gram-positive cocci helps to distinguish staphylococci from streptococci. Streptococci are slightly oblong cells that usually grow in chains because they divide in one plane only. and the cells may change position slightly while remaining attached. aureus should always be considered a potential pathogen. Nearly all strains of S. as well as food poisoning and toxic shock syndrome . the result is formation of an irregular cluster of cells. S. causes a wide range of suppurative infections. Staphylococcus epidermidis may be a pathogen in the hospital environment. Catalase-positive cultures produce O2 and bubble at once. The test is performed by adding 3% hydrogen peroxide to a colony on an agar plate or slant. cluster-forming coccus nonmotile. Without a microscope. the catalase test is important in distinguishing streptococci (catalase-negative) from staphylococci. Table 1. most strains of S. similar to a bacillus. Important phenotypic characteristics of Staphylococcus aureus Gram-positive. S. epidermidis) catalase positive coagulase positive golden yellow colony on agar normal flora of humans found on nasal passages. epidermidis lack this enzyme. aureus produce the enzyme coagulase: nearly all strains of S.Staphylococci are facultative anaerobes that grow by aerobic respiration or by fermentation that yields principally lactic acid. which are vigorous catalase-producers. epidermidis are nonpathogenic and may even play a protective role in humans as normal flora. nonsporeforming facultative anaerobe fermentation of glucose produces mainly lactic acid ferments mannitol (distinguishes from S. Since the exact point of attachment of sister cells may not be within the divisional plane. Staphylococci are perfectly spherical cells about 1 micrometer in diameter.
aureus infections Staphylococcus aureus causes a variety of suppurative (pus-forming) infections and toxinoses in humans. (7) exotoxins that damage . leukocidin. aureus expresses many potential virulence factors: (1) surface proteins that promote colonization of host tissues. meningitis.MRSA( (CA-MRSA) or superbug strains of the organism. S. kinases. which now account for the majority of staphylococcal infections seen in the ER or clinic. It causes superficial skin lesions such as boils. MRSA strains have recently emerged outside the hospital becoming known as community associated. (2) invasins that promote bacterial spread in tissues (leukocidin. leukotoxin. coagulase). hyaluronidase). aureus causes food poisoning by releasing enterotoxins into food. aureus is a major cause of hospital acquired (nosocomial) infection of surgical wounds and infections associated with indwelling medical devices. (4) biochemical properties that enhance their survival in phagocytes (carotenoids. (5) immunological disguises (Protein A.Pathogenesis of S. (3) surface factors that inhibit phagocytic engulfment (capsule. and deep-seated infections. mastitis. catalase production). such as osteomyelitis and endocarditis. more serious infections such as pneumonia. (6) membrane-damaging toxins that lyse eucaryotic cell membranes (hemolysins. Protein A). and urinary tract infections. phlebitis. styes and furuncules. S. S. Although methicillin-resistant Staph aureus (MRSA) have been entrenched in hospital settings for several decades. and toxic shock syndrome by release of superantigens into the blood stream.
The application of molecular biology has led to advances in unraveling the pathogenesis of staphylococcal diseases. including sutures. which may make infections difficult to control. there are correlations between strains isolated from particular diseases and expression of particular virulence determinants. which suggests their role in a particular diseases. and necrosis of tissue. More serious infections of the skin may occur. Human staphylococcal infections are frequent. Staphylococcal pneumonia is a frequent complication of influenza. the accumulation of pus. Virulence determinants of Staphylococcus aureus For the majority of diseases caused by S. The localized host response to staphylococcal infection is inflammation. so it is difficult to determine precisely the role of any given factor. TSST. However. pathogenesis is multifactorial. With some staphylococcal toxins. characterized by an elevated temperature at the site. but usually it is a break in the skin which may be a minute needle-stick or a surgical wound. Around the inflamed area. walling off the bacteria and leukocytes as a characteristic pus-filled boil or abscess. Genes encoding potential virulence factors have been cloned and sequenced. such as furuncles or impetigo. Foreign bodies. Serious . ET). aureus. and (8) inherent and acquired resistance to antimicrobial agents. are readily colonized by staphylococci. The portal may be a hair follicle. lending an understanding of their mechanism of action. but usually remain localized at the portal of entry by the normal host defenses. a fibrin clot may form. swelling.host tissues or otherwise provoke symptoms of disease (SEA-G. Localized infection of the bone is called osteomyelitis. and many protein toxins have been purified. Another portal of entry is the respiratory tract. symptoms of human disease can be reproduced in animals with the purified protein toxins. FIGURE 2.
skeletal muscle or meninges. most strains express a fibrin/fibrinogen binding protein (clumping factor) which promotes attachment to blood clots and traumatized tissue. Most strains of S.consequences of staphylococcal infections occur when the bacteria invade the blood stream. Mutants defective in binding to fibronectin and to fibrinogen have reduced virulence in a rat model for endocarditis. Interaction with collagen may also be important in promoting bacterial attachment to damaged tissue where the underlying layers have been exposed. kidney. heart. other skin lesions. Sites of infection and diseases caused by Staphylococcus aureus Adherence to Host Cell Proteins S. or infections in the lung. a bacteremia may result in seeding other internal abscesses. Evidence that staphylococcal matrix-binding proteins are virulence factors has come from studying defective mutants in adherence assays. FIGURE 3. an adhesin that promotes attachment to collagen has been found in strains that cause osteomyelitis and septic arthritis. In addition. and mutants lacking the collagen-binding protein have reduced virulence in a mouse . aureus express both fibronectin and fibrinogen-binding proteins. In addition. A resulting septicemia may be rapidly fatal. aureus cells express surface proteins that promote attachment to host proteins such as laminin and fibronectin that form the extracellular matrix of epithelial and endothelial surfaces.
suggesting that bacterial colonization is ineffective. aureus isolates express leukocidin. It is expressed as a monomer that binds to the membrane of susceptible cells. some of which may occur also as cell-associated proteins. epidermidis. aureus. The classical test for ß-toxin is lysis of sheep erythrocytes. Subunits then oligomerize to form heptameric rings with a central pore through which cellular contents leak. The role of delta toxin in disease is unknown. Leukocidin is hemolytic. A lysogenic bacteriophage is known to encode the toxin. but nearly 90% . It is also produced by S. The mode of action of alpha hemolysin is likely by osmotic lysis. Invasion The invasion of host tissues by staphylococci apparently involves the production of a huge array of extracellular proteins. In humans. These proteins are described below with some possible explanations for their role in invasive process. Leukocidin forms a hetero-oligomeric transmembrane pore composed of four LukF and four LukS subunits. Leukocidin is a multicomponent protein toxin produced as separate components which act together to damage membranes. the isolated ligand-binding domain of the fibrinogen. Only 2% of all of S. Susceptible cells have a specific receptor for alpha toxin which allows the toxin to bind causing small pores through which monovalent cations can pass. thereby forming an octameric pore in the affected membrane. fibronectin and collagen receptors strongly blocks attachment of bacterial cells to the corresponding host proteins. ß-toxin is a sphingomyelinase which damages membranes rich in this lipid. The majority of human isolates of S. but less so than alpha hemolysin.model for septic arthritis. aureus is alpha toxin. delta toxin is a very small peptide toxin produced by most strains of S. Furthermore. Membrane-damaging toxins alpha toxin (alpha-hemolysin) The best characterized and most potent membrane-damaging toxin of S. platelets and monocytes are particularly sensitive to alpha toxin. aureus do not express ß-toxin.
Staphylokinase Many strains of S aureus express a plasminogen activator called staphylokinase. However. Specific mutants lacking coagulase retain clumping factor activity. which is used in medicine to treat patients suffering from coronary thrombosis. which suggests that it is an important factor in necrotizing skin infections. This factor lyses fibrin. aureus cell surface. a lipase. Other extracellular enzymes S. Coagulase is a traditional marker for identifying S aureus in the clinical microbiology laboratory. while clumping factor mutants express coagulase normally.of the strains isolated from severe dermonecrotic lesions express this toxin. a deoxyribonuclease (DNase) and a fatty acid modifying enzyme (FAME). resulting in the conversion of fibrinogen to fibrin. although it seems reasonable to imagine that localized fibrinolysis might aid in bacterial spreading. The protease activity characteristic of thrombin is activated in the complex. The first three probably provide nutrients for the bacteria. aureus can express proteases. genetic studies have shown unequivocally that coagulase and clumping factor are distinct entities. although it is reasonable to speculate that the bacteria could protect themselves from phagocytic and immune defenses by causing localized clotting. There is some confusion in the literature concerning coagulase and clumping factor. Partly the confusion results from the fact that a small amount of coagulase is tightly bound on the bacterial cell surface where it can react with prothrombin leading to fibrin clotting. there is no strong evidence that staphylokinase is a virulence factor. However. there is no overwhelming evidence that it is a virulence factor. The mechanism is identical to streptokinase. the fibrinogen-binding determinant on the S. The genetic determinant is associated with lysogenic bacteriophages. Coagulase and clumping factor Coagulase is an extracellular protein which binds to prothrombin in the host to form a complex called staphylothrombin. As with coagulase. A complex formed between staphylokinase and plasminogen activates plasmin-like proteolytic activity which causes dissolution of fibrin clots. and it is unlikely that they .
aureus can express several different types of protein toxins which are probably responsible for symptoms during infections. Avoidance of Host Defenses S. aureus lacking protein A are more efficiently phagocytosed in vitro. In serum. aureus strains isolated from infections express high levels of the polysaccharide but rapidly lose the ability when cultured in the laboratory. However. This has been called a microcapsule because it can be visualized only by electron microscopy unlike the true capsules of some bacteria which are readily visualized by light microscopy. the FAME enzyme may be important in abscesses. perhaps by masking adhesins. This includes both structural and soluble elements of the bacterium. Phagocytosis is an important defense against staphylococcal infection so leukocidin should be a virulence factor. Although it does impede phagocytosis in the absence of complement. S. Those which damage the membranes of cells were discussed previously under Invasion. aureus expresses a number of factors that have the potential to interfere with host defense mechanisms. aureus which binds IgG molecules by their Fc region. Mutants of S. Capsular Polysaccharide The majority of clinical isolates of S aureus express a surface polysaccharide of either serotype 5 or 8. Leukocidin S. The function of the capsule in virulence is not entirely clear. and mutants in infection models have diminished virulence. aureus can express a toxin that specifically acts on polymorphonuclear leukocytes. but it is . Protein A Protein A is a surface protein of S. which disrupts opsonization and phagocytosis. Some will lyse erythrocytes. the bacteria will bind IgG molecules in the wrong orientation on their surface. Exotoxins S. causing hemolysis.have anything but a minor role in pathogenesis. it also impedes colonization of damaged heart valves. where it could modify antibacterial lipids and prolong bacterial survival.
C. When expressed systemically. causing the symptoms of TSS. TSST-1 is weakly related to enterotoxins. This complex recognizes only the Vb element of the T cell receptor. Superantigens bind directly to class II major histocompatibility complexes of antigen-presenting cells outside the conventional antigen-binding grove. and the host lacks appropriate neutralizing antibodies. ETA and ETB. The toxins have esterase and protease activity and apparently target a protein which is involved in maintaining the integrity of the epidermis. and toxic shock syndrome toxin (TSST-1). E and G). There are two antigenically distinct forms of the toxin. whereas normally. but it does not have emetic activity. which results in widespread blistering and loss of the epidermis. including all menstrual cases. enterotoxins. of which there are six antigenic types (named SE-A.000 are stimulated during a usual antigen presentation. Up to one in five T cells may be activated. Thus any T cell with the appropriate Vb element can be stimulated. Superantigens stimulate T cells non-specifically without normal antigenic recognition (Figure 4). aureus secretes two types of toxins with superantigen activity. whereas only 1 in 10. TSST-1 is expressed systemically and is the cause of toxic shock syndrome (TSS). enterotoxins B and C cause 50% of non-menstrual cases of TSS. Leukocidin causes membrane damage to leukocytes. enterotoxins can also cause toxic shock syndrome. B. but is not hemolytic. D. TSS can occur as a sequel to any staphylococcal infection if an enterotoxin or TSST-1 is released systemically. Cytokines are released in large amounts. The exfoliatin toxin causes scalded skin syndrome in neonates. while enterotoxins and TSST-1 are superantigens that may cause toxic shock. Enterotoxins cause diarrhea and vomiting when ingested and are responsible for staphylococcal food poisoning. In fact. antigen specificity is also required in binding. Superantigens: enterotoxins and toxic shock syndrome toxin S. Staphylococcal enterotoxins cause emesis (vomiting) when ingested and the bacterium is a leading cause of food poisoning (intoxication). . Systemic release of alpha toxin causes septic shock.unlikely that hemolysis is a relevant determinant of virulence in vivo. TSST-1 is responsible for 75% of TSS.
A characteristic of many pathogenic strains of S. Superantigens bind directly to class II major histocompatibility complexes (MHC II) of antigen-presenting cells outside the normal antigen-binding groove. Exfoliatin toxin (ET) The exfoliatin toxin. epidermidis is the production of a slime resulting in biofilm formation. epidermidis will bind to fibronectin. aureus. Resistance of Staphylococci to Antimicrobial Drugs . Superantigens and the non-specific stimulation of T cells. normally found in the cell wall of the staphylococci. Bacteria-plastic interactions are probably important in colonization of catheters. associated with scalded skin syndrome. This is probably why healing occurs with little scarring although the risks of fluid loss and secondary infections are increased. epidermidis infections.FIGURE 4. between the living layers and the superficial dead layers. Cytokines are released in large amounts. The slime is predominantly a secreted teichoic acid. The separation is through the stratum granulosum of the epidermis. a cadherin that is found in desmosomes in the epidermis. little is known about mechanisms of pathogenesis of S. Staphylococcal exfoliative toxin B has been shown to specifically cleave desmoglein 1. Adherence is obviously a crucial step in the initiation of foreign body infections. when host proteins deposit on the implanted device S. Pathogenic Staphylococcus epidermidis In contrast to S. This ability to form a biofilm on the surface of a prosthetic device is probably a significant determinant of virulence for these bacteria. and a polysaccharide adhesion (PS/A) has been identified. In addition. causing the symptoms of toxic shock. causes separation within the epidermis. Up to one in five T cells may be activated.
Methicillin resistance is widespread and most methicillin-resistant strains are also multiply drug-resistant. especially in surgical wounds. A plasmid associated with vancomycin resistance has been detected in Enterococcus faecalis which can be transferred to S. then developing inhibitors of the specific target molecule. Beginning with the use of the penicillin in the 1940's.Hospital strains of S. S. A few strains are resistant to all clinically useful antibiotics except vancomycin. The term MRSA refers to Methicillin resistant Staphylococcus aureus. such as quaternary ammonium compounds.g. transposons. Gram-negative bacilli (e. and vancomycin-resistant strains are increasingly-reported. this approach will turn up new antimicrobial agents for the battle against staph infections. which may aid its survival in the hospital environment. coli and Pseudomonas aeruginosa) have replaced staph as the most frequent causes of nosocomial infections. Some strains are now resistant to most conventional antibiotics. alternatives to vancomycin have been approved for treatment of MRSA. or other types of DNA inserts. aureus in the laboratory. MRSA . aureus are usually resistant to a variety of different antibiotics. Staphylococcal disease has been a perennial problem in the hospital environment since the beginning of the antibiotic era. staphylococcal infection was synonymous with nosocomial infection.g. and there is concern that new antibiotics have not been forthcoming. E. Hopefully. transducing particles. S aureus responded to the introduction of antibiotics by the usual bacterial means to develop drug resistance: (1) mutation in chromosomal genes followed by selection of resistant strains and (2) acquisition of resistance genes as extrachromosomal plasmids. in the gastrointestinal tract). aureus exhibits resistance to antiseptics and disinfectants. S. During the 1950's and early 1960's. although the staphylococci have remained a problem. New strategies in the pharmaceutical industry to find antimicrobial drugs involve identifying potential molecular targets in cells (such as the active sites of enzymes involved in cell division). aureus expresses its resistance to drugs and antibiotics through a variety of mechanisms. In addition. drug resistance has developed in the staphylococci within a very short time after introduction of an antibiotic into clinical use. and it is speculated that this transfer may occur naturally (e. Indeed. since 2003.
and other pus-filled lesions. especially healthcare workers' hands. such as abscesses. The main mode of transmission to other patients is through human hands. Reports of VRSA (Vancomycin-Resistant Staph aureus) or VRSA are troublesome in the ongoing battle against staph infections. and can affect vital organs leading to widespread infection (sepsis). MRSA are often sub-categorized as Hospital-Associated MRSA (HAMRSA) or Community-Associated MRSA (CA-MRSA). such as bloodstream infections. amoxacillin). It is not known why some healthy people . CA-MRSA strains display enhanced virulence. MRSA infections that occur in otherwise healthy people who have not been recently (within the past year) hospitalized or had a medical procedure (such as dialysis. the bacteria can be spread when the healthcare worker touches other patients. spread more rapidly and cause more severe illness than traditional HA-MRSA infections. However. including vancomycin. catheters) are categorized as community-associated (CA-MRSA) infections. MRSA in healthcare settings commonly causes serious and potentially life threatening infections. surgical site infections or pneumonia. depending upon the circumstances of acquiring disease. but to several classes of antibiotics. surgery. Some MRSA are resistant to all but one or two antibiotics.g. MRSA have evolved resistance not only to beta-lactam antibiotics. HA-MRSA occurs most frequently among patients who undergo invasive medical procedures or who have weakened immune systems and are being treated in hospitals and healthcare facilities such as nursing homes and dialysis centers. In the case of HA-MRSA.MRSA are strains of the Staphylococcus aureus that are resistant to the action of methicillin and related beta-lactam antibiotics (e. patients who already have an MRSA infection or who carry the bacteria on their bodies but do not have symptoms (are colonized) are the most common sources of transmission. boils. About 75 percent of CA-MRSA infections are localized to skin and soft tissue and usually can be treated effectively. Based on current data. If appropriate hand hygiene such as washing with soap and water or using an alcohol-based hand sanitizer is not performed. toxic shock syndrome and pneumonia. Hands may become contaminated with MRSA bacteria by contact with infected or colonized patients. penicillin. these are distinct strains of the bacterial species. These infections are usually skin infections. oxacillin.
as reported by CDC in the Oct.000 life-threatening infections and 18.000 people in the U. Studies have shown that rates of CA-MRSA infection are growing fast.S. the average age of people with MRSA in a hospital or healthcare facility was 68. The national estimate is more than double the invasive MRSA prevalence reported five years earlier.650 deaths in 2005. 17. especially in certain geographic regions. CA-MRSA are infecting much younger people. 2007 issue of The Journal of the American Medical Association. fatal infections. That same year. But the average age of a person with CAMRSA was only 23. roughly 16. now die from MRSA infection than from AIDS. four children in Minnesota and North Dakota were reported to have died from fulminant CA-MRSA infections One study of children in south Texas found that cases of CA-MRSA increased 14-fold between 1999 and 2001. More people in the U. Also. CA-MRSA skin infections have been identified among certain populations that share close quarters or experience more skin-to-skin contact. However. In 1999. CA-MRSA was the most frequent cause of skin and soft-tissue infections seen in emergency departments in the United States. some are more serious with septicemia and pneumonia.S. and prisoners. Two-thirds of the 85% of MRSA infections that could be traced to hospital stays or other health care exposures occurred among people who were no longer hospitalized. Examples are team athletes. died from AIDS. Although most MRSA cases are skin and soft-tissue infections. military recruits. Methicillin-resistant Staphylococcus aureus was responsible for an estimated 94. By 2007.develop CA-MRSA skin infections that are treatable whereas others infected with the same strain develop severe. according to CDC. more and more. CA-MRSA infections are being seen in the general community as well. People over age 65 were four times more likely than the . While most invasive MRSA infections could be traced to a hospital stay or some other health care exposure. about 15% of invasive infections occurred in people with no known health care risk. It was reported in 2005 that previously healthy adolescents without any predisposing risk factors presented more frequently with severe Staph infections (mostly the USA 300 strain) since 2002. In a study of Minnesotans published in The Journal of the American Medical Association.
general population to get an MRSA infection.g. Incidence rates among blacks were twice that of the general population. many of the community associated (CA) staphylococcal infections are now methicillin resistant. aureus bacterial infections. Over 60% of abscess isolates from the emergency department of an Austin. Hyperimmune serum or monoclonal antibodies directed towards surface components (e. capsular polysaccharide or surface protein adhesions) could theoretically prevent bacterial adherence and promote phagocytosis by opsonization of bacterial cells. Host Defense against Staphylococcal Infections Phagocytosis is the major mechanism for combating staphylococcal infection. Particularly in Georgia. Vaccines No vaccine is generally available that stimulates active immunity against staphylococcal infections in humans. Texas hospital yielded MRSA. the bacterial capsule and protein A may interfere with phagocytosis. These organisms are uniformly resistant to penicillins and cephalosporins. However. The infections have been treated with combination therapy using sulfa drugs and minocycline or rifampin. However.. Texas. MRSA) and can only be treated with vancomycin or an alternative. vaccine therapies represent a new and innovative approach in broadening the available clinical tools against the global health problem of community and healthcare-associated S. Antibodies are produced which neutralize toxins and promote opsonization. which are primary phagocytic killing mechanisms within the phagolysosome. However. the prevalence of CA-MRSA is widespread. Biofilm growth on implants is also impervious to phagocytes. and rates were lowest among children over the age of 4 and teens. infections acquired outside hospitals have been treated with penicillinase-resistant ß-lactams. Until recently. Also.g. human hyperimmune serum could be given to hospital patients before surgery . Staphylococci may be difficult to kill after phagocytic engulfment because they produce carotenoids and catalase which neutralize singlet oxygen and superoxide. Treatment Hospital acquired infection is often caused by antibiotic resistant strains (e. A vaccine based on fibronectin binding protein induces protective immunity against mastitis in cattle and might also be used as a vaccine in humans. and California.
aureus. A decrease in vaccine efficacy after week 40 correlated with a decrease in S. The 336 conjugate vaccine. S. One of the . was shown to be safe and to generate antibodies in humans that are specific and mediate protection against 336-positive strains of S. In randomized trials. Since toxins are major contributors to the virulence of S. The vaccine called StaphVAX is composed of S. conjugated to nontoxic recombinant Pseudomonas exotoxin A. a surface polysaccharide. aureus bacteremia were diagnosed in the vaccinated group compared with 26 cases in a control group. Such patients do not require protection for the rest of their lives. aureus Type 336 accounts for the approximately 20% of S. aureus causing infections in the hospital as well as the community. An experimental bivalent vaccine against Staphylococcus aureus is reported to be safe and immunogenic for approximately 40 weeks in patients with end-stage renal disease undergoing hemodialysis. evaluated in a phase I/II human trial. Together.as a form of passive immunization. such as a joint replacement. For example. aureus strains. 336. To enhance the efficacy of this vaccine. The pharmaceutical company Nabi has developed a trivalent staphylococcal polysaccharide conjugate vaccine called TriStaph™. aureus infections that do not form a polysaccharide capsule in the human bloodstream. these three polysaccharide conjugates cover all clinically-significant serological types of S. aureus. Nabi identified two vaccine candidates that cover relevant toxins. is added. Between weeks 3 and 40. These could be administered systemically or topically. 11 cases of S. what they need is protection for a short period while they are in the hospital. it might be possible to design compounds that block the interactions and thus prevent bacterial colonization. found in the outer coating of more than 80% of S. When the precise molecular basis of the interactions between staphylococcal adhesins and host tissue receptors is known. aureus type 5 and 8 capsular polysaccharides conjugated to nontoxic recombinant Pseudomonas aeruginosa exotoxin A. aureus antibodies. 5 and 8. the vaccine might be used in cases where healthy individuals come into the hospital for elective surgery. The investigators did not believe that use of StaphVAX would be limited to hemodialysis patients. one injection of the vaccine was administered to 892 hemodialysis patients. Nearly 90% of patients receiving the vaccine generated antibodies to the two capsular polysaccharides. It contains the two main capsular types.
hemolysins. Table 2. carotenoids. nucleases. elastase. lipases. collagenase. hyaluronidase Other extracellular enzymes (proteases. etc. Adding these two components to Tristaph produces a multi-targeted S. aureus polysaccharide conjugate vaccine and toxoid vaccine called PentaStaph™. etc. Possible virulence determinants expressed in the pathogenesis of Staphylococcus aureus infections boils and pimples (folliculitis) Colonization: cell-bound (protein) adhesins Invasion: Invasins: staphylokinase Other extracellular enzymes (proteases. carotenoids. leukocidin. protein A. growth at low pH .toxins in animal models is produced by almost all clinical isolates and the other is a toxin associated with severe skin and soft tissue infections caused by the newly emerging multi-drug resistant community-acquired MRSA strains. hemolysins. collagenase. catalase. etc. antigenic variation Toxigenesis: Cytotoxic toxins (hemolysins and leukocidin) food poisoning (emesis or vomiting) Toxigenesis: Enterotoxins A-G septicemia (invasion of the bloodstream) Invasion: Invasins: staphylokinase. superoxide dismutase. growth at low pH Resistance to immune responses: coagulase. leukocidin Resistance to immune responses: coagulase Toxigenesis: cytotoxic toxins (hemolysins and leukocidin) pneumonia Colonization: cell-bound (protein) adhesins Invasion: Invasins: staphylokinase. Genetic engineering technology was used to render the toxins nontoxic so they can be used safely. catalase. elastase.) Resistance to phagocytosis: coagulase. superoxide dismutase. elastase. nucleases. lipases. hyaluronidase Other extracellular enzymes (proteases. nucleases. collagenase. lipases. leukocidin.) Resistance to phagocytosis: coagulase.) Resistance to phagocytosis: coagulase.
nucleases. hyaluronidase Other extracellular enzymes (proteases. protein A.Resistance to immune responses: coagulase. antigenic variation Toxigenesis: cytotoxic toxins (hemolysins and leukocidin) osteomyelitis (invasion of bone) Colonization: cell-bound (protein) adhesins Invasion: Invasins: staphylokinase.) Resistance to phagocytosis: coagulase.) Resistance to phagocytosis: coagulase. collagenase. superoxide dismutase. carotenoids. etc. elastase. antigenic variation Toxigenesis: cytotoxic toxins (hemolysins and leukocidin) scalded skin syndrome Colonization: cell-bound (protein) adhesins Invasion: Invasins: staphylokinase. leukocidin. hyaluronidase Other extracellular enzymes (proteases. Enterotoxins A-G surgical wound infections Colonization: cell-bound (protein) adhesins Invasion: Invasins: staphylokinase. antigenic variation Toxigenesis: Exfoliatin toxin . etc. protein A. collagenase. growth at low pH Resistance to immune responses: coagulase. carotenoids. superoxide dismutase. leukocidin. catalase.) Resistance to phagocytosis: coagulase. hyaluronidase Other extracellular enzymes (proteases. lipases. protein A. collagenase. lipases. nucleases. etc. leukocidin. protein A. protein A. elastase. catalase. antigenic variation Toxigenesis: TSST toxin. hemolysins. hemolysins Resistance to immune responses: coagulase. lipases. growth at low pH Resistance to immune responses: coagulase. nucleases. elastase. hemolysins. antigenic variation Toxigenesis: cytotoxic toxins (hemolysins and leukocidin) toxic shock syndrome Colonization: cell-bound (protein) adhesins Resistance to immune responses: coagulase.
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