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Gram Positive Pyogenic Cocci (Streptococcus, staphylococcus, Pneumococcus) Yewande Dayo Student Pharmacist 1 Objectives Upon completion of this section, students should be able to 2 Describe characteristics of different gram-positive bacteria Differentiate between different bacteria based on unique features and characteristics Describe pathogenic characteristics of different gram-positive bacteria Identify infections caused by different gram-positive bacteria General Characteristics of Staphyloccoci They grow characteristically in irregular groups like clusters of grapes. They are facultative anaerobic, nonmotile, non-spore forming, and catalase test positive. Common inhabitant of the skin and mucous membranes Lack flagella May have capsules 31 species 3 major pathogens in this genus: S. aureus, S. epidermidis, and S. saprophyticus. S. aureus is the only coagulase-positive species. 3 4 Staphylococcal Infections There are three clinically relevant members of the staphyloccocal bacteria species 5 S. aureus S. epidermidis S. saprophyticus Unique Characteristics of S. aureus • It is -hemolytic on blood agar plates. • Its cell wall has a unique protein A. 6 Sources and Routes of Infection Carriage nasal carriage: 35% of normal adult skin carriage: 10-20% of normal person Air-borne dissemination from droplet of respiratory tract from desquamated skin scales Disseminated by contact 7 Virulence factors of S. aureus Enzymes: Coagulase – coagulates plasma and blood; produced by 97% of human isolates; diagnostic Hyaluronidase – digests connective tissue Staphylokinase – digests blood clots DNase – digests DNA Lipases – digest oils; enhances colonization on skin Penicillinase – inactivates penicillin 8 Virulence factors of S. aureus Toxins: Hemolysins (α, β, γ, δ) – lyse red blood cells Leukocidin – lyses neutrophils and macrophages Enterotoxin – induce gastrointestinal distress Exfoliative toxin – separates the epidermis from the dermis Toxic shock syndrome toxin (TSST) - induces fever, vomiting, shock, systemic organ damage 9 Local (Skin) Pathologic Effect Folliculitis, acne, stye, paronychia Furuncle, carbuncle Bullous impetigo 10 Disseminated Pathologic Effect Bacteremia: Osteomyelitis, endocarditis, arthritis, cerebral, pulmonary and renal abscess. Toxemia: 1. Scalded skin syndrome. 2. Staphylococcal toxic shock syndrome 11 Toxemia Staphylococcal scalded skin syndrome Bullous Impetigo Ritter's disease Staphylococcal Toxic Shock Syndrome 12 Menstrual TSS (TSST 1) Non-menstrual TSS (TSST-1, enterotoxins) Treatment: aggressive fluid replacement with saline and intravenous administration of oxacillin or nafcillin, 8-10 g/day. Coagulase-negative staphylococci (CONS) They are opportunistic or nosocomial pathogens. Infections by CONS are always associated predisposing factors such as immunosuppression, surgery, and indwelling devices. S. epidermidis is the organism most frequently associated with CONS endocarditis, wound infections, and urinary tract infections in elderly hospitalized men. S. saprophyticus is an agent for the primary urinary tract infection in women. 13 Identification of Staphylococcus in Samples Frequently isolated from pus, tissue exudates, sputum, urine, and blood Cultivation, catalase, biochemical testing, coagulase 14 15 Comparison between S. aureus and S. epidermidis 1. 2. 3. 16 Coagulase assay Hemolysis Growth on mannitol salt plate Treatment for Staphylococcal Diseases Simple drainage of abscess usually suffices for superficial lesion. Deep-infections require intensive prolonged chemotherapy. Most clinical isolates are penicillin resistant. In acute and serious staphylococcal infection, cephalosporin or vancomycin are usually used in therapy. Systemic infections require intensive lengthy therapy. 17 Emergening Problems of S. aureus infections (Antibiotic Resistant S. aureus) Penicillin-resistant S. aureus (PRSA). Resistance is due to the production of plasmid encoded -lactamase. Penicillinase-resistant -lactam cephalosporin was used. Methicillin-resistant S. aureus (MRSA). Some of these strains further develop resistance to cephalosporin due to expression of unusual chromosomal encoded PBP which is peptidoglycan transpeptidase and has a lowaffinity for -lactam antibiotics. Vancomycin-resistant S. aureus (VRSA). 18 Prevention of Staphylococcal Infections Universal precautions by healthcare providers to prevent nosocomial infections Hygiene and cleansing 19 General Characteristics of Streptococci Gram-positive spherical/ovoid cocci arranged in long chains; commonly in pairs Non-spore-forming, nonmotile Can form capsules and slime layers Facultative anaerobes Do not form catalase, but have a peroxidase system Most parasitic forms are fastidious and require enriched media. Small, nonpigmented colonies Sensitive to drying, heat and disinfectants 25 species 20 21 Streptococci Lancefield classification system based on cell wall Ag – 17 groups (A,B,C,….) Another classification system is based on hemolysis reactions. β-hemolysis – A,B,C,G and some D strains α-hemolysis – S. pneumoniae and others collectively called viridans 22 23 Human Streptococcal Pathogens S. pyogenes S. agalactiae Viridans streptococci S. pneumoniae Enterococcus faecalis 24 β-hemolytic S. pyogenes Most serious streptococcal pathogen Strict parasite Inhabits throat, naso-pharynx, occasionally skin 25 Virulence Factors of β-hemolytic S. pyogenes Produces surface antigens: 26 C-carbohydrates – protect against lysozyme Fimbriae - adherence M-protein – contributes to resistance to phagocytosis Hyaluronic acid capsule – provokes no immune response 27 Virulence Factors of β-hemolytic S. pyogenes Extracellular toxins: 28 streptolysins – hemolysins; streptolysin O (SLO) and streptolysin S (SLS) – both cause cell and tissue injury pyogenic toxin (erythrogenic) – induces fever and typical red rash superantigens – strong monocyte and lymphocyte stimulants; cause the release of tissue necrotic factor Virulence Factors of b-hemolytic S. pyogenes Extracellular enzymes 29 streptokinase – digests fibrin clots hyaluronidase – breaks down connective tissue DNase – hydrolyzes DNA Epidemiology and Pathogenesis Humans only reservoir Inapparent carriers Transmission – contact, droplets, food, fomites Portal of entry generally skin or pharynx Children predominant group affected for cutaneous and throat infections Systemic infections and progressive sequelae possible if untreated 30 Scope of Clinical Disease Skin infections Impetigo (pyoderma) – superficial lesions that break and form highly contagious crust; often occurs in epidemics in school children; also associated with insect bites, poor hygiene, and crowded living conditions Erysipelas – pathogen enters through a break in the skin and eventually spreads to the dermis and subcutaneous tissues; can remain superficial or become systemic Throat infections Streptococcal pharyngitis – strep throat 31 32 33 Scope of Clinical Disease Systemic infections Scarlet fever strain of S. pyogenes carrying a prophage that codes for pyrogenic toxin; can lead to sequelae Septicemia Pneumonia Streptococcal toxic shock syndrome 34 Long-Term Complications of Group A Infections Rheumatic fever Follows overt or subclinical pharyngitis in children; carditis with extensive valve damage possible, arthritis, chorea, fever Acute glomerulonephritis 35 Nephritis, increased blood pressure, occasionally heart failure; can become chronic leading to kidney failure Group B: Streptococcus agalactiae Regularly resides in human vagina, pharynx and large intestine Can be transferred to infant during delivery and cause severe infection most prevalent cause of neonatal pneumonia, sepsis, and meningitis 15,000 infections and 5,000 deaths in US Pregnant women should be screened and treated. Wound and skin infections and endocarditis in debilitated people 36 Group D Enterococci and Groups C and G Streptococci Group D: Enterococcus faecalis, E. faecium, E. durans normal colonists of human large intestine cause opportunistic urinary, wound, and skin infections, particularly in debilitated persons Groups C and G: 37 common animal flora, frequently isolated from upper respiratory; pharyngitis, glomerulonephritis, bacteremia Identification Cultivation and diagnosis ensure proper treatment to prevent possible complications. Rapid diagnostic tests based on monoclonal antibodies that react with C-carbohydrates Culture using bacitracin disc test, CAMP test 38 39 40 Treatment and Prevention Groups A and B are treated with penicillin. Sensitivity testing needed for enterococci No vaccines available 41 α-Hemolytic Streptococci: Viridans Group Large complex group Streptococcus mutans, S. oralis, S. salivarus, S. sanguis, S. milleri, S. mitis Most numerous and widespread residents of the gums and teeth, oral cavity and also found in nasopharynx, genital tract, skin Not very invasive; dental or surgical procedures facilitate entrance 42 Viridans Group Bacteremia, meningitis, abdominal infection, tooth abscesses Most serious infection – subacute endocarditis – bloodborne bacteria settle and grow on heart lining or valves Persons with preexisting heart disease are at high risk. Colonization of heart by forming biofilms 43 Viridans Group S. mutans produce slime layers that adhere to teeth, basis for plaque. Involved in dental caries Persons with preexisting heart conditions should receive prophylactic antibiotics before surgery or dental procedures. 44 Streptococcus pneumoniae: The Pneumococcus Causes 60-70% of all bacterial pneumonias Small, lancet-shaped cells arranged in pairs and short chains Culture requires blood or chocolate agar. Growth improved by 5-10% CO2 Lack catalase and peroxidases 45 cultures die in O2 46 S. pneumoniae All pathogenic strains form large capsules – major virulence factor. Specific soluble substance (SSS) varies among types. 84 capsular types have been identified Causes pneumonia and otitis media 47 Epidemiology and Pathology 5-50% of all people carry it as normal flora in the nasopharynx; infections are usually endogenous. Very delicate, does not survive long outside of its habitat Young children, elderly, immune compromised, those with other lung diseases or viral infections, persons living in close quarters are predisposed to pneumonia Pneumonia occurs when cells are aspirated into the lungs of susceptible individuals. Pneumococci multiply and induce an overwhelming inflammatory response. Gains access to middle ear by way of eustachian tube 48 49 Cultivation and Diagnosis Gram stain of specimen – presumptive identification α -hemolytic; optochin sensitivity Quellung test or capsular swelling reaction 50 Treatment and Prevention Traditionally treated with penicillin G or V Increased drug resistance Two vaccines available for high risk individuals: 51 capsular antigen vaccine for older adults and other high risk individuals-effective 5 years conjugate vaccine for children 2 to 23 months The Genus Clostridium Gram-positive, spore-forming rods Anaerobic and catalase negative 120 species Oval or spherical spores produced only under anaerobic conditions Synthesize organic acids, alcohols, and exotoxins Cause wound infections, tissue infections, and food intoxications 52 53 Gas Gangrene Clostridium perfringens most frequent clostridia involved in soft tissue and wound infections myonecrosis Spores found in soil, human skin, intestine, and vagina Predisposing factors – surgical incisions, compound fractures, diabetic ulcers, septic abortions, puncture wounds, gunshot wounds 54 Virulence Factors Virulence factors toxins – 55 α-toxin – causes RBC rupture, edema and tissue destruction collagenase hyaluronidase DNase Pathology Not highly invasive; requires damaged and dead tissue and anaerobic conditions Conditions stimulate spore germination, vegetative growth and release of exotoxins, and other virulence factors. Fermentation of muscle carbohydrates results in the formation of gas and further destruction of tissue. 56 57 Treatment and Prevention Immediate cleansing of dirty wounds, deep wounds, decubitus ulcers, compound fractures, and infected incisions Debridement of disease tissue Large doses of cephalosporin or penicillin Hyperbaric oxygen therapy No vaccines available 58 Clostridium difficile-Associated Disease (CDAD) Normal resident of colon, in low numbers Causes antibiotic-associated colitis relatively non-invasive; treatment with broad-spectrum antibiotics kills the other bacteria, allowing C. difficile to overgrow Produces enterotoxins that damage intestines Major cause of diarrhea in hospitals Increasingly more common in community acquired diarrhea 59 Treatment and Prevention Mild uncomplicated cases respond to fluid and electrolyte replacement and withdrawal of antimicrobials. Severe infections treated with oral vancomycin or metronidazole and replacement cultures Increased precautions to prevent spread 60 Tetanus Clostridium tetani Common resident of soil and GI tracts of animals Causes tetanus or lockjaw, a neuromuscular disease Most commonly among geriatric patients and IV drug abusers; neonates in developing countries 61 Pathology Spores usually enter through accidental puncture wounds, burns, umbilical stumps, frostbite, and crushed body parts. Anaerobic environment is ideal for vegetative cells to grow and release toxin. Tetanospasmin – neurotoxin causes paralysis by binding to motor nerve endings; blocking the release of neurotransmitter for muscular contraction inhibition; muscles contract uncontrollably Death most often due to paralysis of respiratory muscles 62 63 Treatment and Prevention Treatment aimed at deterring degree of toxemia and infection and maintaining homeostasis Antitoxin therapy with human tetanus immune globulin; inactivates circulating toxin but does not counteract that which is already bound Control infection with penicillin or tetracycline; and muscle relaxants Vaccine available; booster needed every 10 years 64 Clostridial Food Poisoning Clostridium botulinum Rare but severe intoxication usually from home canned food Clostridium perfringens 65 Mild intestinal illness; second most common form of food poisoning worldwide Botulinum Food Poisoning Botulism Intoxication associated with inadequate food preservation Clostridium botulinum Spore-forming anaerobe; commonly inhabits soil and water 66 Pathogenesis Spores are present on food when gathered and processed. If reliable temperature and pressure are not achieved air will be evacuated but spores will remain. Anaerobic conditions favor spore germination and vegetative growth. Potent toxin, botulin, is released. Toxin is carried to neuromuscular junctions and blocks the release of acetylcholine, necessary for muscle contraction to occur. Double or blurred vision, difficulty swallowing, neuromuscular symptoms 67 68 Infant and Wound Botulism Infant botulism Caused by ingested spores that germinate and release toxin; flaccid paralysis Wound botulism 69 Spores enter wound and cause food poisoning symptoms Treatment and Prevention Determine presence of toxin in food, intestinal contents or feces Administer antitoxin; cardiac and respiratory support Infectious botulism treated with penicillin Practice proper methods of preserving and handling canned foods; addition of preservatives. 70 Clostridial Gastroenteritis Clostrium perfringens Spores contaminate food that has not been cooked thoroughly enough to destroy spores. Spores germinate and multiply (especially if unrefrigerated). When consumed, toxin is produced in the intestine; acts on epithelial cells, acute abdominal pain, diarrhea, and nausea Rapid recovery 71