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Staphylococcus in Hospital Practice


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Staphylococcus in Hospital Practice

Staphylococcus in Hospital Practice

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  • 2. STAPHYLOCOCCUS• Sir Alexander Ogston, a Scottish surgeon, first showed in 1880 that a number of human pyogenic diseases were associated with a cluster-forming micro-organism. He introduced the name staphylococcus (Greek: staphyle = bunch of grapes; kokkos = grain or berry), now used as the genus name for a group of facultatively anaerobic, catalase-positive, Gram- positive cocci.DR.T.V.RAO MD 2
  • 3. DR.T.V.RAO MD 3
  • 4. INTRODUCTION• Staphylococci - derived from Greek “stapyle” (bunch of grapes)• Gram positive cocci arranged in clusters• Hardy organisms surviving many non physiologic conditions• Include a major human pathogen and skin commensalsDR.T.V.RAO MD 4
  • 5. Staphylococci: Gram positive Cocci ( from Greek staphyle, means bunch of grapes ) that occur singly and in pairs, short chains and irregular grape-like clusters.DR.T.V.RAO MD 5
  • 6. STAPHYLOCOCCUS= nonmotile, grapelike clusters, nonsporeformers= nonencapsulated but few strains form capsules= aerobic or facultative anaerobes= catalase positive 2H 202  2H20 + 02= most strains --- heat stable (60oC x 30 mins.)SPECIES: Staphylococcus aureus coagulase ( + ) (clots citrated plasma) Staphylococcus epidermidis coagulase ( - )TOXINS: hemolysins 6 enterotoxins Leukocidin exfoliatin DR.T.V.RAO MD 6
  • 7. ALEXANDER FLEMINGPenicillin: is the antibiotic agent that Alexander Fleming a Scottish physician discovered in 1929. In 1950 only 15% of S.aureus was susceptible to penicillin. Approximately only 5% of S. aureus today are sensitive to penicillin.DR.T.V.RAO MD 7
  • 8. • Family CLASSIFICATION• Genus Micrococcaceae• Species Micrococcus and Staphylococcus S. aureus S. saprophyticus S. epidermidis more M. luteus than 20 speciesDR.T.V.RAO MD 8
  • 9. STRUCTURE AND PHYSIOLOGY• Gram-positive cocci, nontitle, facultative anaerobes• Cells occur in grapelike clusters because cells division occurs along different planes and the daughter cells remain attached to one another• Salt-tolerant: allows them to tolerate the salt present on human skin• Tolerant of desiccation: allows survival on environmental surfaces (fomites)DR.T.V.RAO MD 9
  • 10. S. AUREUS A UNIQUE ORGANISM PVLAdapted from: Lowy. N Engl J Med. 1998;339:520-532. DR.T.V.RAO MD 10
  • 11. STRUCTURE AND PHYSIOLOGY• Two species are commonly associated with staphylococcal diseases in humans • Staphylococcus aureus-The more virulent strain that can produce a variety of conditions depending on the site of infection • Staphylococcus epidermidis- Normal micro biota of human skin that can cause opportunistic infections in immunocompromised patients or when introduced into the bodyDR.T.V.RAO MD 11
  • 12. GENERAL CULTURAL CHARACTERISTICS Staphylococcusspecies, mostnotably S. aureus,produce a hemolysisthat completely lysesred blood cells ofhumans and someother mammals(sheep blood). Thisis referred to as“beta” hemolysis.DR.T.V.RAO MD 12
  • 13. Staphylococcus aureus: is the staphylococcus which has the ability to clot plasma, which is coagulase positive. More than 80% of Staphylococcus aureus strains produce beta-lactamases.DR.T.V.RAO MD 13
  • 14. OTHER S. AUREUS CHARACTERISTICSMannitol fermentation is another useful characteristic – it is unique to, and consistent among S. aureus strains. Virtually all strains of S. aureus ferment mannitol.Bright yellow colonies on a yellow background indicates mannitol fermentation on mannitol salt agar. DR.T.V.RAO MD 14
  • 15. PATHOGENICITY• Staph’ infections result when staphylococci breach the “ body’s physical barriers• Entry of only a few hundred bacteria can result in disease• Pathogenicity results from 3 features • Structures that enable it to evade phagocytosis • Production of enzymes • Production of toxinsDR.T.V.RAO MD 15
  • 16. CELL-ASSOCIATED VIRULENCE FACTORS • Capsule or slime layer (glycocalyx) • Peptidoglycan (PG) • Teichoic acid is covalently linked to PG and is species specific: • S. aureus ribitol teichoic acid (polysaccharide A) • S. epidermidis glycerol teichoic acid (polysaccharide B) • Protein A is covalently linked to PG • Clumping factor (bound coagulase) DR.T.V.RAO MD 16
  • 17. VIRULENCE FACTORS EXTRACELLULAR ENZYMES • Coagulases (bound or free) • Antigenic • Hyaluronidase • “spreading factor” of S. aureus • Nuclease • Cleaves DNA and RNA in S. aureus • Protease • Staphylokinase (fibrinolysin) • Lipases • EsterasesDR.T.V.RAO MD 17
  • 18. BIOCHEMICAL CHARACTERISTIC• Staphylococcus species can be differentiated from Micrococcus species based upon oxygen requirements: Staph is facultative and Micrococcus species are obligate aerobesDR.T.V.RAO MD 18
  • 19. STRUCTURAL DEFENSES AGAINST PHAGOCYTOSIS1. Protein A coats the cell surface • Interferes with humoral immune responses by binding to class G antibodies • Inhibits the complement cascade2. Clumping Factor (Bound coagulase) • Converts the soluble blood protein fibrinogen in insoluble fibrin molecules that form blood clots • Fibrin clots hide the bacteria from phagocytic cellsDR.T.V.RAO MD 19
  • 20. VIRULENCE FACTORS: EXOTOXINS• Cytolytic (cytotoxins; cytolysins) • Alpha toxin - hemolysin • Reacts with RBCs • Beta toxin • Sphingomyelinase • Gamma toxin • Hemolytic activity • Delta toxin • Cytopathic for: • RBCs • Macrophages • Lymphocytes DR.T.V.RAO MD 20
  • 21. Virulence Factors: Exotoxin• Enterotoxin• Exfoliative toxin (epidermolytic toxin)• Pyrogenic exotoxinsDR.T.V.RAO MD 21
  • 22. STAPHYLOCOCCAL TOXINS ENTEROTOXINS• Enterotoxins, types A-E, G, H, I and J, are commonly produced by up to 65% of strains of Staph. aureus, sometimes singly and sometimes in combination. These toxic proteins withstand exposure to 100°C for several minutes.DR.T.V.RAO MD 22
  • 23. DISEASE MANIFESTATIONS• Boils, carbuncles Scalded skin syndrome Wound infection Pemphigus neonatroum Abscesses Toxic shock syndrome Impetigo Food poisoning Mastitis Bacteraemia Osteomyelitis Pneumonia Endocarditis DR.T.V.RAO MD 23
  • 24. CLINICAL MANIFESTATIONS/DISEASE• SKIN • folliculitis • boils (furuncles) • carbuncles  impetigo (bullous & pustular)  scalded skin syndrome •Neonates and children under 4 years DR.T.V.RAO MD 24
  • 25. A painful cluster of boils with a central well of pus, often found on the neck. take a long time to heal and often leave a scar. caused by infections of the skin StaphylococcusDR.T.V.RAO MD aureus 25
  • 26. • Bedsores or pressure sores, local loss of skin and softDECUBITUS tissue as a result of pressureULCER OR from prolonged bed rest. • Also known as decubitus ulcers, BEDSORE bedsores • common on the buttocks, and on bony points such as the heels, elbows, shoulders, and the back of the head. • affect elderly or infirm people who are confined to bed for long periods, including comatose patients, whose condition prevents them from moving freely.DR.T.V.RAO MD 26
  • 27. MASTITIS Inflammation of the breast especially during nursing. also a frequent site of both benign and malignant tumors.DR.T.V.RAO MD 27
  • 28. MENINGITIS• Involving the covering of the brain & the spinal cord (meninges). DR.T.V.RAO MD 28
  • 29. CYSTITIS inflammation of the urinary bladder, usually from bacterial infection originating in the urethra, vagina, or, in the kidneys.DR.T.V.RAO MD 29
  • 30. • most common form• usually associated with adolescence but may also occur in adults.• primarily from hormonal changes taking place in the body• Other factors include stress, drugs, bacteria, and certain foodstuffs. DR.T.V.RAO MD 30
  • 31. SKIN LESIONS• Boils• Styes• Furuncles(infection of hair follicle)• Carbuncles (infection of several hair follicles)• Wound infections(progressive appearance of swelling and pain in a surgical wound after about 2 days from the surgery)• Impetigo(skin lesion with blisters that break and become covered with crusting exudate)DR.T.V.RAO MD 31
  • 33. DEEP ABSCESSSES• Can be single or multiple• Breast abscess can occur in 1-3% of nursing mothers in puerperiem• Can produce mild to severe disease• Other sites - kidney, brain from septic foci in blood• Needs special investigationsDR.T.V.RAO MD 33
  • 34. PATHOLOGY - PREDISPOSING FACTORS • This list is virtually true for all pathogens • Immune system suppressed or otherwise compromised. Specifically… • Skin injuries (e.g. burns, surgical incisions, cuts, etc) • Presence of foreign bodies (e.g intravenous lines, prosthetic devices, sutures, tampons-)DR.T.V.RAO MD 34
  • 35. Pre-existing infections • Chronic underlying conditions (e.g. auto- immune conditions, malignancies, alcoholism, heart disease, etc.) • Compromised micro biota via antimicrobial therapy • Infants susceptible: oral, skin: impetigo, “scalded skin”, respiratory, otherDR.T.V.RAO MD 35
  • 36. PRE-EXISTING INFECTIONS• With obvious focus • Osteomyelitis, septic arthritis• 2. No obvious focus • heart (infective endocarditis) • Brain(brain abscesses)• 3. Associated With predisposing factors • multiple abscesses, septicemia(IV drug users) • Staphylococcal pneumonia (Post viral)DR.T.V.RAO MD 36
  • 37. FACTORS THAT FACILITATE TRANSMISSION Frequent Contact Crowding Antimicrobial Use Contaminated SurfacesCompromised Skin and Shared Items Cleanliness DR.T.V.RAO MD 37
  • 38. TOXIN MEDIATED DISEASES• 1 . Staphylococcal food poisoning • Due to production of entero toxins • heat stable entero toxin acts on gut • produces severe vomiting following a very short incubation period • Resolves on its own within about 24 hoursDR.T.V.RAO MD 38
  • 39. TOXIC SHOCK SYNDROME TOXIN (TSST-1)This was discovered in the early 1980s as a result of epidemiological and microbiological investigations in the USA of toxic shock syndrome, a multi-system disease caused by staphylococcal TSST-1 or enterotoxin, or both. A link was established with the use of highly absorbent tampons in menstruating women, although non-menstrual cases are now as common. The absence of circulating antibodies to TSST-1 is a factor in the pathogenesis of this syndrome.DR.T.V.RAO MD 39
  • 40. TOXIC SHOCK SYNDROME TOXIN (TSST-1)• TSST-1 and the enterotoxins are now recognized as super antigens, that is, they are potent activators of T lymphocytes resulting in the liberation of cytokines such as tumour necrosis factor, and they bind with high affinity to mononuclear cells. These characteristics partly explain the florid and multi-system nature of the clinical conditions associated with these toxins.DR.T.V.RAO MD 40
  • 41. TOXIC SHOCK SYNDROME• High fever, diarrhea, shock and erythematous skin rash which desquamate• Mediated via „toxic shock syndrome toxin‟• 10% mortality rate• Described in two groups of patients • ass. With young women using tampons during menstruation • Described in young children and menDR.T.V.RAO MD 41
  • 42. ENZYMES1. Coagulase • Triggers blood clotting2. Hyaluronidase • Breaks down hyaluronic acid, enabling the bacteria to spread between cells3. Staphylokinase • Dissolves fibrin threads in blood clots, allowing Staphylococcus aureus to free itself from clots DR.T.V.RAO MD 42
  • 43. ENZYMES (CONT.). Lipases • Digest lipids, allowing staphylococcus to grow on the skin’s surface and in cutaneous oil glands5. -lactamase • Breaks down penicillin • Allows the bacteria to survive treatment with - lactam antimicrobial drugsDR.T.V.RAO MD 43
  • 44. TOXINS• Staphylococcus aureus produces toxins more frequently than S.epidermidis1. Cytolytic toxins • Disrupts the cytoplasmic membrane of a variety of cells • Leukocidin can lyse leukocytes specifically2. Exfoliative toxins • Causes the patient’s skin cells to separate from each other and slough off the body DR.T.V.RAO MD 44
  • 45. FOOD POISONING• S. aureus is the #1 most common cause of food poisoning although it is comparatively mild in most cases.• Symptoms include nausea, vomiting, diarrhea, abdominal cramping and mild fever.• Symptom onset can be within minutes or hours of ingestion, with similar duration• Foods: handled foods: wet, sugary or salty, handled after some preparation – cooked, mixed, then served cold, at least initially DR.T.V.RAO MD 45
  • 46. COAGULASE• Coagulase (staphylocoagulase) is a fibrinogen activating enzyme produced by some staph species - it has thrombin- like activity. In situ, coagulase combines with “coagulase reacting factor” (CRF) to catalyze the formation of fibrin clots around cells as a barrier to host immune components – it is a virulence factor.• Clinically significant staphylococci are usually divided into two groups: those that produce coagulase and those that do not• Coagulase positive species include S. aureus, S. intermedius and S. hyicus• S. intermedius and S. hyicus mostly inhabit animals and are only rarely found as a cause of human infections DR.T.V.RAO MD 46
  • 47. COAGULASE TESTING• The tube is observed hourly during the four hour incubation period• The formation of a fibrin clot or gel indicates a positive test DR.T.V.RAO MD 47
  • 48. EMERGING MULTI-DRUG RESISTANCE IN USA300? • Clusters of USA300 isolates with multiple resistance to erythromycin, clindamycin, tetracycline, ciprofloxacin, and mupirocin 1 • Resistance to ≤ one class of antibiotics other than beta-lactams is still the most common resistance pattern in MRSA USA300 • TMP/SMX resistance rare in MRSA USA3001Diep et al Lancet 2006. Han et al J Clin Micro 2007. DR.T.V.RAO MD 48
  • 49. BETA LACTAMS:Beta lactams: are the antibiotics that contain the beta lactam ring. These are : penicillins, cephamycins, cephalosporins, carbapenems monobactams. The ring structure is common to all beta-lactams and must be intact for antibacterial action. They are cell wall synthesis inhibitors.DR.T.V.RAO MD 49
  • 50. COMMUNITY-ASSOCIATED MRSA:CDC POPULATION-BASED SURVEILLANCE DEFINITION• MRSA culture in outpatient setting or 1 st 48 hours of hospitalization AND patient lacks risk factors for healthcare-associated MRSA: • Hospitalization • Surgery • Long-term care • Dialysis • Indwelling devices DR.T.V.RAO MD 50
  • 51. ANTIMICROBIAL SUSCEPTIBILITY• Penicillin resistance (possession of penicillnase) is coded on a plasmid – the enzyme is also known as beta-lactamase: inactivates the beta-lactam ring of penicillins and other beta-lactam antibiotics such as the cephalosporins• Semi-synthetic drugs (modified penicillins) such as methicillin and oxacillin were developed for treating beta lactamase positive S. aureus infections• Some strains are now resistant to these drugs – MRSA, etc. A recent survey indicated that as many as 34% of S. aureus isolates were MSRA. DR.T.V.RAO MD 51
  • 52. ANTIMICROBIAL SUSCEPTIBILITY• Penicillin resistance (possession of penicillnase) is coded on a plasmid – the enzyme is also known as beta-lactamase: inactivates the beta-lactam ring of penicillins and other beta-lactam antibiotics such as the cephalosporins• Semi-synthetic drugs (modified penicillins) such as methicillin and oxacillin were developed for treating beta lactamase positive S. aureus infections• Some strains are now resistant to these drugs – MRSA, etc.. DR.T.V.RAO MD 52
  • 53. EPIDEMIOLOGY OF S AUREUS INFECTIONS • Predominant reservoir of organisms = human beings • Approximately 15% – 35% of normal people harbor S aureus in nares or pharynx at a given point. Longitudinal view of carriage: • 30% prolonged, 50% intermittent, 20% never • Vaginal carriage in ~10% of premenopausal women • Rectal and perineal carriage also occurSheagren. N Engl J Med. 1984;310:1368-1373.Rimland et al. J Clin Microbiol. 1986;24:137-138.Centers forMD DR.T.V.RAO Disease Control (CDC). MMWR Morb Mortal Wkly Rep. 1982;31:605-607. 53
  • 54. HAND WASHING• Cross-infection is an important method of spread of staphylococcal disease, particularly in hospitals, and scrupulous hand washing is essential in preventing spread. Food handlers may similarly introduce enterotoxin- producing food poisoning strains into food.DR.T.V.RAO MD 54
  • 55. PREVENTION • Hand antisepsis is the most important measure in preventing Nosocomial infections • Also important is the proper cleansing of wounds and surgical openings, aseptic use of catheters or indwelling needles, an appropriate use of antisepticsDR.T.V.RAO MD 55
  • 56. PREVENTION• Proper hygiene, segregation of carrier from highly susceptible individuals• Good aseptic techniques when handling surgical instruments• Control of Nosocomial infectionsDR.T.V.RAO MD 56
  • 58. WHY ARE MRSA IMPORTANT?1. Hospital –acquired infections. MRSA are common Nosocomial pathogens around the world.2. The treatment is very difficult. Vancomycin often is the only drug of choice for severe infections.DR.T.V.RAO MD 58
  • 59. WHY ARE MRSA IMPORTANT?3. MRSA with reduced susceptibility to glycopeptides. Since 1996 has been identified in Europe, Asia and United States. That increases the possibility some strains became fully resistant to glycopeptides.4. MRSA are easily transmissible between patients.DR.T.V.RAO MD 59
  • 60. CONTROL OF MRSA IN HOSPITALSGeneral Principles:• Prevention of acquisition and spread of infection by patients and staff• Priorities are high risk units, such as intensive care units and patients who are susceptible to infection.DR.T.V.RAO MD 60
  • 61. CONTROL OF MRSA IN HOSPITALS• Hand washing. Health care workers should wash their hands before and after contact with all patients, even when gloves are worn. A written protocol detailing proper hand wash technique should be available for reference.DR.T.V.RAO MD 61
  • 62. CONTROL OF MRSA IN HOSPITALS• Gloves should be worn when in contact with any body substance. Gloves should be changed and hands washed immediately after contact with each resident.• Appropriate use of antimicrobials. Monitoring and auditing of drug use.DR.T.V.RAO MD 62
  • 63. CONTROL OF MRSA IN HOSPITALS• Isolation is necessary for infected patients and possible carriers in a single room or preferably in an isolation unit with designated staff. Isolation reduce staphylococcal cross-infection.DR.T.V.RAO MD 63
  • 64. CONTROL OF MRSA IN HOSPITALS• Carriage of MRSA by health care workers. During outbreaks staff should be reminded of the hand washing and transient carriage of MRSA. Staff with infected or colonized lesions should not be at work especially in critical areas, as intensive care units, cardiothoracic words e.t.c.DR.T.V.RAO MD 64
  • 65. CONTROL OF MRSA IN HOSPITALS • Treatment of carriers. Nasal carriage is treated topical with mupirocin. • Systemic treatment of infections The glycopeptide antibiotics are currently the agents of choice for treatment. • Microbiological characterization of MRSA.DR.T.V.RAO MD 65
  • 66. COAGULASE NEGATIVE STAPHYLOCOCCUS• Coagulase negative staphylococci (Cons) are generally less virulent that S. aureus• Cons are inherently difficult to speciate even using modern clinical products and methods• Unless a Cons isolate is cultured repeatedly from a normally sterile body site (e.g. Blood, CSF), identification to species level is usually not attempted• Isolates that must be definitively identified to species level are sent to reference labsDR.T.V.RAO MD 66
  • 67. CONS – S. EPIDERMIDIS• The most common Cons species in clinical samples is S. epidermidis, comprising 50-80% of these isolates.• S. epidermidis can be presumptively differentiated from other Staph species on the basis of the following observations • It does not ferment mannitol or trehalose • Coagulase negative • It is sensitive to novobiocin • It is resistant to polymyxin B• Pathology of S. epidermidis is almost exclusively associated with skin penetration in the hospital setting DR.T.V.RAO MD 67
  • 68. CONS – S. EPIDERMIDIS• S. epidermidis produces a capsule that adheres to plastic devices such as intravenous catheters, prosthetic heart valves, and shunts• S. epidermidis and other Cons are cause of native valve endocarditisDR.T.V.RAO MD 68
  • 70. DR.T.V.RAO MD 70
  • 72. • Programme created by Dr.T.V.Rao MD for Medical and Paramedical Professionals in the Developing World • Email • doctortvrao@gmail.comDR.T.V.RAO MD 72