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Staphylococci Ass.Prof. Dr. Huda H. AL-Hassnawi Staphylococci are Gram-positive cocci about 0.5 – 1.0 μm in diameter. They grow in clusters, pairs and occasionally in short chains. The clusters arise because staphylococci divide in two planes, catalase positive, oxidase negative, non-motile, non-spore forming. Traditionally they were divided into two groups on the basis of their ability to clot blood plasma (the coagulase reaction). The coagulase-positive staphylococci constitute the most pathogenic species S. aureus. The coagulase-negative staphylococci (CNS) are now known to comprise over 30, other species such as S. epidermidis and S. saprophyticus. The CNS are common commensals of skin, although some species can cause infections. Staphylococcus aureus:Phenotypic characteristics of Staphylococcus aureus:Gram-positive, cluster-forming coccus, non-motile, non-spore forming facultative anaerobe, fermentation of glucose produces mainly lactic acid, ferments mannitol (distinguishes from S. epidermidis), catalase positive, coagulase positiv, golden yellow colony on agar, normal flora of humans found on nasal passages, skin and mucous membranes pathogen of humans, causes a wide range of suppurative infections, as well as food poisoning and toxic shock syndrome. Pathogenesis of S. aureus:S. aureus infections can spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroys tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person. Deeply penetrating S. aureus infections can be severe. Prosthetic joints put a person at particular risk of septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia. S. aureus expresses many potential virulence factors: (1) surface proteins that promote colonization of host tissues:S. 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. In addition, most strains express a fibrin/fibrinogen binding protein (clumping factor) which promotes attachment to blood clots and traumatized tissue. Most strains of S. aureus express both fibronectin and fibrinogen-binding proteins. In addition, an adhesin that promotes attachment to collagen has been found in strains that cause osteomyelitis and septic arthritis (2) invasins that promote bacterial spread in tissues such as (leukocidin, staphylokinases, hyaluronidase), leukocidin a toxin that specifically acts on polymorphonuclear leukocytes. Hyaluronidase breaks down hyaluronic acid and helps 1 in spreading of Staphylococcus aureus. also staphylokinase which activates plasminogen to form plasmin, which digest fibrin clots. This disrupts the fibrin meshwork which can often form to keep an infection localized. (3) surface factors that inhibit phagocytic engulfment (capsule, Protein A): Capsular Polysaccharide :-The majority of clinical isolates of S. aureus express a surface polysaccharide of either serotype 5 or 8. 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. Protein A:- Protein A is a surface protein of S. aureus which binds IgG molecules by their Fc region. In serum, the bacteria will bind IgG molecules in the wrong orientation on their surface, which disrupts opsonization and phagocytosis. (4) biochemical properties that enhance their survival in phagocytes (carotenoids, catalase production). (5) immunological disguises (Protein A, coagulase):Coagulase is an extracellular protein which binds to prothrombin in the host to form a complex called staphylothrombin. The protease activity characteristic of thrombin is activated in the complex, resulting in the conversion of fibrinogen to fibrin. (6) membrane-damaging toxins that lyse eucaryotic cell membranes:1-alpha toxin (alpha-hemolysin):- The best characterized and most potent membranedamaging toxin of S. aureus is alpha toxin. In humans, platelets and monocytes are particularly sensitive to alpha toxin. Susceptible cells have a specific receptor for alpha toxin which allow low concentrations of toxin to bind, causing small pores through which monovalent cations can pass. At higher concentrations, the toxin reacts nonspecifically with membrane lipids, causing larger pores through which divalent cations and small molecules can pass. 2-ß-toxin is a sphingomyelinase which damages membranes rich in this lipid. The classical test for ß-toxin is lysis of sheep erythrocytes. The majority of human isolates of S. aureus do not express ß-toxin. A lysogenic bacteriophage is known to encode the toxin. 3-delta toxin is a very small peptide toxin produced by most strains of S. aureus. It is also produced by S. epidermidis. The role of delta toxin in disease is unknown. 4- Panton and Valentine (PV) leukocidin: It causes dermonecrosis when injected subcutaneously in rabbits. Furthermore, at a concentration below that causing membrane damage, the toxin releases inflammatory mediators from human neutrophils, leading to degranulation. So is associated with severe necrotizing pneumonia in children. (7) exotoxins that damage host tissues or otherwise provoke symptoms of disease:Superantigens: enterotoxins and toxic shock syndrome toxin :- 2 S. aureus secretes two types of toxins with superantigen activity, enterotoxins, of which there are six antigenic types (named SE-A, B, C, D, E and G), and toxic shock syndrome toxin (TSST-1). Enterotoxins cause diarrhea and vomiting when ingested and are responsible for staphylococcal food poisoning. TSST-1 is expressed systemically and is the cause of toxic shock syndrome (TSS). When expressed systemically, enterotoxins can also cause toxic shock syndrome. In fact, enterotoxins B and C cause 50% of non-menstrual cases of TSS. TSST-1 is weakly related to enterotoxins, but it does not have emetic activity. TSST-1 is responsible for 75% of TSS, including all menstrual cases. TSS can occur as a sequel to any staphylococcal infection if an enterotoxin or TSST-1 is released systemically, and the host lacks appropriate neutralizing antibodies. TSS is characterized by high fever , vomiting, diarrhea, sore throat and muscle pain, within 48h it may progress to sever shock with evidence renal and hepatic damage Epidermolytic (exfoliative) toxin (ET) EF toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS) or Ritter disease , which occurs most commonly in infants and young children which results in widespread blistering with clear fluid that contains no bacteria or leukocytes and loss of the epidermis. There are two antigenically distinct forms of the toxin, 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. . It also may occur as epidemics in hospital nurseries Figure (2):- Virulence determinants of Staphylococcus aureus Clinical Manifestations of S. aureus Staphylococcus aureus causes a variety of suppurative (pus-forming) infections and toxinoses in humans. It causes superficial skin lesions such as boils, styes and furuncules; more serious infections such as pneumonia, mastitis, phlebitis, meningitis, and urinary tract infections; and deep-seated infections, such as osteomyelitis and 3 endocarditis. S. aureus is a major cause of hospital acquired (nosocomial) infection of surgical wounds and infections associated with indwelling medical devices. S. aureus causes food poisoning by releasing enterotoxins into food, and toxic shock syndrome by release of super-antigens into the blood stream, scalded skin syndrome, septicemia. Collection of specimens This depends on the area of the body affected. For example, those with a skin infections or throat, nostrils and wound infections need to swabbed for pus and other discharge with the bacteria. Swabs consist of a sterile absorbent cotton tipped sticks. Those with a urinary tract infection need to provide a urine samples in sterile containers and those with a generalized blood infection need to provide blood samples. Blood samples are then transferred to blood culture bottle. Identification of the bacteria A small portion of the sample is swabbed onto a glass slide. This is then stained with Gram stain or dyes like crystal violet and basic fuschin and viewed under the microscope. S. aureus is Gram positive and stains blue or purple and appears as small round cocci or short chains and most commonly as grape-like clusters. Since S. aureus may be normally present on skin and mucous membranes, this test is not always confirmatory. Coagulase positive is performed to distinguish it from coagulase negative sp. Treatment Staphylococcus aureus causes a variety of manifestations and diseases. The treatment of choice for S. aureus infection is penicillin. In most countries, S. aureus strains have developed a resistance to penicillin due to production of an enzyme by the bacteria called penicillinase. The first line therapy is penicillinase-resistant penicillins like oxacillin, flucloxacillin, nafcillin, cefazolin etc.. Therapy is often given in combination with aminoglycosides like gentamicin for more serious infections. The duration of treatment depends on the site of infection and on severity. Hospital acquired infection is often caused by antibiotic resistant strains (e.g. MRSA) and can only be treated with vancomycin or an alternative. Methicillin resistant Staphylococcus aureus (MRSA):MRSA are strains of the Staphylococcus aureus that are resistant to the action of methicillin and related beta-lactam antibiotics (e.g. penicillin, oxacillin, amoxacillin). MRSA have evolved resistance not only to beta-lactam antibiotics, but to several classes of antibiotics. Some MRSA are resistant to all except one or two antibiotics, including vancomycin. Reports of VRSA (Vancomycin-Resistant S. aureus) or VRSA are troublesome in the ongoing battle against Staphylococcus infections. So Choice of antibiotics for MRSA includes Linezolid, Vancomycin, Clindamycin, Quinupristin/dalfopristin, tetracyclines, Doxycycline, Minocycline etc. are chosen. 4 Staphylococcus epidermidis Staphylococcus epidermidis is a gram-positive, coagulase-negative cocci that is a part of our normal flora. Consequently, it is a true opportunistic pathogen, as it requires a major breach in the host’s innate defenses. It is one of the leading pathogens of nosocomial infections, particularly associated with foreign body infections. Those most susceptible to infection are intravenous drug users, newborns, elderly, and those using catheters or other artificial appliances. The organism produces slime layers, which forms a hydrophobic biofilm. This film is adhesive to hydrophobic biopolymers of prosthetics, creating diseases such as endocarditis. The biofilm of S. epidermidis consists of clusters of cells that are embedded in extracellular slime substance that is up to 160 micrometers thick, exceeding 50 cells Disease Infections are associated with intravascular devices (prosthetic heart valves, shunts, etc.) but also commonly occur in prosthetic joints, catheters, and large wounds. Catheter infections along with catheter-induced UTIs lead to serious inflammation and pus secretion. In these instances, urination is extremely painful. Septicemia and endocarditis are also diseases associated with S. epidermidis. Their symptoms run the gamut from fever, headache, and fatigue to anorexia and dyspnea. Septicemia is especially prevalent resulting from neonatal infections, particularly in very low birth weights. Endocarditis is an infection of the heart valves and parts of the inside lining of the heart muscle. Treatment The drug of choice is often vancomycin, to which rifampin or aminoglycoside can be added Staphylococcus saprophyticus is a gram positive and coagulase-negative species of Staphylococcus bacteria. S. saprophyticus is often implicated in urinary tract infections Symptoms of infection:S. saprophyticus is implicated in 10-20% of urinary tract infections (UTIs). In females between the ages of about 17-27 it is the second most common causative agent of acute UTIs, after Escherichia coli. Some of the symptoms of infection by these bacteria are burning sensation when passing urine, the urge to urinate more often than usual, a 'dripping effect' after urination, weak bladder, a bloated feeling with sharp razor pains in the lower abdomen around the bladder and ovary areas, and razor-like pains during sexual intercourse. Antibiotic susceptibility:S. saprophyticus is resistant to the antibiotic novobiocin, a characteristic that is used in laboratory identification to distinguish it from S. epidermidis. Quinolones are commonly used in treatment of S. saprophyticus urinary tract infections. 5