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True bacteria –Cocci- Gram positive cocci Staphylococci Staphylococci are members of the normal flora of the skin and mucous membranes of humans; others cause abscess formation, a variety of pyogenic infections, and even fatal septicemia.The pathogenic Staphylococci often hemolyze blood, coagulate plasma, and produce a variety of extracellular enzymes and toxins. The most common type of food poisoning is caused by a heat-stable staphylococcal enterotoxin. Staphylococci rapidly develop resistance to many antimicrobial agents and present difficult therapeutic problems.The genus Staphylococcus has at least 35 species: (A)The coagulase-positive staphylococci: as Staphylococcus aureus , the most common causes of bacterial infections ,food poisoning and toxic shoke syndrome. (B)The coagulase-negative staphylococci: as Staphylococcus epidermidis, and Staphylococcus saprophyticu,are normal human flora and sometimes cause infection. (A)- Coagulase-positive staphylococci:Staphylococcus aureas: is G+ cocci, spherical cells arranged in irregular clusters, single cocci, pairs, tetrads, and chains are also seen in liquid cultures, non motile, non spore forming and non capsulated. Its facultative anaerobic grow readily on most bacteriologic media at 37 °C, but form endopigment(from golden-yellow to cream in color)under anaerobic condition at room temperature (20–25 °C). Colonies on solid media are round, smooth,opaque,shining surfaces and low convex.Catalase + Staphylococcus, which differentiates them from the catalase - Streptococci. Its slowly ferment many carbohydrates, producing lactic acid but not gas, and produce many extracellular substances. Its resists drying, heat (50°C for 30 minutes), and 9% sodium chloride. Host compromise is required for It's infection. Epidemiology It's carried by healthy individuals on the skin and mucous membranes, serves as a source of infection to themselves and others (direct contact, contamination of food). Pathogenesis Staph. aureus produces many enzymes and toxins which are responsible for pathogenisty as well as virulence factors (figure1).So the pathogenesis depend on the combined actions of several virulence factors and it ś difficult to determine the role of any given factor. 1 Enzymes 1. catalase →E. that convert hydrogen peroxide (H2O2) to water and oxygen. Under aerobic condition, this E. become toxic. 2. coagulase →) invasive pathogenic potential factor) converts fibrinogen→fibrin in plasma causes clot preventing the bacterial cell from being killed by the immune cells. coagulase includes two types: a. bond b. free. 3. hyaluronidase →)spreading factor) degrades hyaluronic acid in connective tissue. 4.staphylokinase→E .causes fibrinolysis by degrading fibrin, and facilitates in spreading of bacteria cells. 5. β-lactamase. 6. proteinase. 7. lipase. 8. nuclease. Figure:(1)virulence factors that may play a role in the pathogenesis of staphylococcal infections. Toxins Staph. aureus produces exotoxins:(1)- cytolytic exotoxins or haemolysin→ toxin that lyses the R.B.Cs as: α-haemolysin =which partially (in completely) lyses R.B.Cs. β-haemolysin =which lyses R.B.Cs completely. ȣ-haemolysin =which lyses R.B.Cs of animals & some times human. δ- haemolysin=causes distribution of biologic membrane which results in diarrhea. (2)- leucocidin → toxin that lyses the W.B.Cs. 2 (3)- superantigen exotoxins → these toxins have an affinity for the T cell receptor MHC class П antigen complex. They stimulate an enhanced T lymphocyte response . T cell activation can cause toxic shock syndrome by release large amounts of T cell cytokines, such as interleukin-2(IL2), interferon-ȣ(IFNȣ) and Tumor necrosis factorα(TNF-α). (A)- enterotoxins:They are at least six (A-F) soluble toxins produced by 50% of Staph. aureus, differ in chains of a.a.s. and responsible for gastroenteritis, food poisoning. They cause vomiting and diarrhoea after (1-8 hour).Enterotoxins are heat stable, resist boiling for 30min,and resistance to the action of gut enzyme. (B)- exfoliative toxin (ET)(epidermolytic toxin):Causes staphylococcal scalded skin syndrome (ssss) this disease mainly occurs in young children. (C) - toxic shock syndrome toxin-1 (TSST-1):This toxin is structurally similar to endotoxins (B) and (C) also this toxin is the same as the enterotoxin (F) and the pyogenic exotoxins (C).This toxin is associated with fever, shock, rash ,desquamative of the skin. (TSST-1) is the classic cause of toxic shock syndrome, because of similarities in molecular structure.This toxin does not cause food poisoning when ingested. Cell wall virulence factors (a)- protein A:Is a major component of the Staph. aureus cell well, it binds to the Fc of IgG therefore strongly antiphagocytic effect. (b)- fibronectin-binding protein (FnBP):Staphylococcal surface proteins promote binding to mucosal cells and tissue matrixes. Clinical significance S. aureus causes disease by infecting tissues and /or by producing toxins (figure2) A common entry to the body:(A)-is a break in the skin. (B)-is the respiratory tract (as a complication of influenza). (C)-is a digested contaminated food. The localized host response to Staph. infection is inflammation ,creates a "abscess". Serious consequences of Staph. infections occur when the bacteria invade the blood stream, resulting septicemia (the presence and persistence of pathogenic microorganisms or their toxins in the blood) may be fatal.Bacteremia (the presence of viable bacteria circulating in the blood stream)may result in seeding internal abscesses, skin lesions, or infections in the lung, kidney, heart, skeletal muscle or meninges. 3 (1)Localized skin infections: → folliculitis = the most common Staph. aureus infections, superficial abscess involving hair follicles. → lmpetigo = a localized superficial spreading crusty skin lesion seen in children (by staph. aureus or strep. pyogenes or both). → furunclosis = subcutaneous abscesses form around foreign bodies (local therapy as removal of the foreign body, soaking, drainage). → carbunclosis = larger deeper skin Infections lead to bacteremia (antibiotic therapy). (2)- deep, localized infections:These may be metastatic from superficial infections or skin carriage, or may result from trauma. → acute and chronic infection of the bone marrow. → acute infection of joint space in children (treated by drainage + an antibiotic). (3)- acute endocarditis:associated with intravenous drug abuse, caused by:(A)-injected of contaminated preparations. (B)-needles contaminated with staph. aureus . (C)-skin a round the injection site which is contaminated with staph. aureus ,which can be introduced into soft tissue and the blood stream, even when a sterilized needle is used. (4)- septicema:Is a generalized infection with sepsis or bacteremia, itś fatal. (5)- pneumonia:Causes of severe, necrotizing pneumonia. (6)- nosocomial infections:Its one of the most common causes of hospital-acquired infections often of wounds (surgical) or bacteremia associated with catheters. Progression to septicemia . (7)- toxinoses:a)-toxic shock syndrome (TSST-1);Results in high fever, rash, vomiting, diarrhea, hypotension and multiorgan involvement (especially GI., renal, and /or hepatic damage)by TSST-1 positive strains of staph. aureus resulting in entry of the toxin into the circulation in the absence of true infection. Currently, 50 % are associated with staph. aureus infections from a circulating enterotoxin rather than TSST. (b)-staphylococcal gastroenteritis (food poisoning):Is caused by ingestion of food contaminated with enterotoxin producing Staph. aureus (such as proteins-rich egg salad, cream pastry refrigerated). 4 Symptoms = nausea, vomiting and diarrhea are acute following a short incubation period (<6hs) and are caused by local actions of the toxin on GI tract rather than from infection. (C)- scalded skin syndrome (ssss):Resulting from the action of an exofoliative toxin that attacks the intercellular adhesive of the stratum granulosum causing epithelial desquamation. (8)- other pyogenic infections:→ cystitis =inflammation in urinary bladder. → cellulites = occurs in skin and soft tissue. → osteomyelitis = occurs in the bone. → bronchopheumonia = usually after influenza. →lung abscess. →post operative wound infections. →arthritis. Figure:(2)Diseases caused by staph.aureus Laboratory identification → specimens:- as surface swab, pus, blood, tracheal aspirate or spinal fluid depending upon localization of process. 5 → microscopic examination :- G+ cocci, staining darkly round cocci occur like grapes cluster. → macroscopic examination (culture and biochemical tests):- on the blood agar, give rise of typical colonies in 18hs at 37co .Staph. aureus colonies lend to be yellow, hemolytic rather than gray and non haemolytic in coagulase –ve Staph. on selective and differential media called mannitol salt agar( which includes selective agents are mannitol + 7.5% Nacl) produces acid that lower ph when ferments mannitol sugar, then the ph indicator turns the color from pink to yellow, but others types of Staph. spp. will increase the ph turning the color from pink to deep pink. biochemical reactions → coagulase +ve while other S. spp. coagulase – ve, catalase +ve, Mannitol + ve . → serological and typing tests:- Abs to teichoic acid can be detected in prolonged deep infections, like osteomylelitis and arthritis.Phage typing is used in severe out breaks of Staph. aureus infection as might occur in hospital. Immunity Staph. aureus infections do not be strong or long-lasting immunity,as demonstrated by the continuing susceptibility of individuals to Staph. aureus infections. Treatment (see figure-3-) Require aggressive treatment including incision and drainage of localized lesions as well as systemic antibiotics. Choice of antibiotics is complicated by the frequent presence of acquired antibiotic resistance determinants. All community and hospital-acquired Staph. aureus infections are now resistant to penicillin G due pencillinase-encoding plasmids or transposons.This has required the replacement of the Initial agent of choice, penicillin G, by β-lactamase-resistance penicillins such as methicillin or oxacillin. Increase use of methicillin and related antibiotics has resulted in methicillin-resistant- Staph. aureus. (1)- hospital-acquire methicillin-resistant- Staph. aureus (MRSA): A high percentage (50%) of hospital Staph. aureus isolates has been found to be resistant to methicillin or oxacillin. Antibiotics resistance is caused by chromosomal acquisition of the gene for a nodified pencillin-binding protein (PBP),(PBP-2a),which codes for new peptidoglycan transpeptidase with a low affinity for all currently available β-lactam antibiotics,and thus renders infections with methicillin-resistant S. aureus unresponsive to β-lactam therapy.Compared with methicillin-sensitive Staph. aureus, MRSA infections are associated with longer hospital and ICU stays,longer durations of mechanical ventilation and higher mortality rates. MRSA strains are also resistant to many other antibiotics, some being sensitive only to glycopeptides such as vancomycin. (2)- community acquired MRSA (CA-MRSA). The most common clinical manifestations of CA-MRSA are skin and soft tissue infections (abscesses or cellulitis). Less commonly, can cause severe disease such as necrotizing pneumonia, posteomyelitis, septicemia. CA-MRSA distinguish from hospital-associated MRSA((1)has DNA fragments obtained upon enzymic cleavage and electrophoresis and(2)it produce specific toxin). CA-MRSA also a(3)unique 6 Antibiotic resistance pattern,that is CA-MRSA is(4)sensitive to Many antibiotics that do not shoe much activity against hospital-associated MRSA, include Ciprofloxacin clindamycin , with some CA-MRSA sensitive to erythromycin, gentamicin, Rifampin, tetracycline, and for trimethoprim-sulfamethoxazole. (3)- Vancomycin resistance:Vancomycin has been the great of choice for treatment of life threatening Staph. aureus infections.in 1997 several MRSA when isolated had acquired low-level Vancomycin Resistance, and itś increased prompting the use of alternative drugs, such as quinupristin dalfopristin, linezolid, daptomycin. So, Clinical strains of Staph. aureus are resistant to benzyl penicillin due to the production of Pencillinase, a βlactamase. Penicillin & amoxicillin are susceptible to S. β-lactamase. Combination of amoxicillin and clavulanic acid is used in therapy. Prevention There is no effective vaccine against Staph. aureus infection control like barrier precautions, disinfection of hands and fomites. are need in nosocomial Staph. aureus epidemics. (B)- coagulase-negative staphylococci:Twelve coagulase-ve Staph. spp. have been recovered as a normal flora of skin and anterior nares. S. epidermidis. and S. saprophyticus both of them are important agents of hospital-acquired infections. (1)-S.epidermidis: Present in large numbers of the normal flora of the skin, recovered from blood contaminant from skin. Despite itś low virulence, itś cause infection of heart valves and catheters. Acquired drug resistance by S. epidermidis is more frequent than by Staph.aureus. Vancomycin sensitivity remains the rule (but also reported vancomycin-resistant isolates). S.epidermidis produced slime that facilitates adherence to intravenous catheters acts as barrier antimicrobial agents. (2)-S. saprophyticus: Cause cystitis in women, probably related to its occurrence as a part of normal vaginal flora. Sensitive to penicillin G. its can be distinguished from S. epidermidis and most coagulase –ve staph. by its resistance to novobiocin. 7