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Bacterial Infections of the Skin Bacterial Organisms  Staphylococcus  Streptococcus Gram (+) cocci -- Catalase test: (+) Staphylococcus (-) Streptococcus Staphylococci

 “staphyle”: bunch of grapes  Non-motile, non spore former  Relatively resistant to heat & drying  Can persist for long periods in fomites  Facultative anaerobes  Fermenting carbohydrates  Inhibited by certain chemicals (hexachlorophene)  Suppuration, abscess formation, a variety of pyogenic infections, & even fatal septicemia  Pathogenic staphylococci: hemolyze blood, coagulate plasma & produce a variety of extracellular enzymes & toxin  Heat-stable staphylococcal enterotoxin  Develop resistance Staphylococcus – Coagulase test: (+) S. aurues (-) S. epidermis, S. saprophyticus Staphylococci – 40 species 1. Staphylococcus aureus  Major pathogen for humans 2. Staphylococcus epidermidis  90% of normal flora  Potentially pathogenic 3. Staphylococcus saprophyticus  Immunocompromised patients  Common cause of UTI in young women Staphylococci Cell Wall Major Components:  antigenic structures

Peptidoglycan  rigid exoskeleton of the cell wall  N acetyl muramic acid with tetrapeptide chains cross-linked by pentaglycine bridges  Tight structure; survival in environment of host tissue  Destroyed by strong acid or exposure to lysozyme  Important in the pathogenesis of infection  Elicits production of interleukin-1 (endogenous pyrogen) and opsonic antibodies by monocytes  Chemoattractant for polymorphonuclear leukocytes  Endotoxin-like activity  Activate complement Teichoic acids  Polymers of glycerol or ribitol phosphate  Linked to the peptidoglycan  Component of phage receptor  Antiteichoic acid antibodies detectable in patients with active endocarditis  Controls activity of autolytic enzymes(growth of cell wall & separation of daughter cells) Protein A  Surface protein; specific for S.aureus  adhesins (MSCRAMMS) – microbial surface component recognizing matrix molecules): virulence factor  covalently linked with peptidoglycan  binds to the Fc portion of IgG molecules except IgG3  important reagent in immunology and diagnostic laboratory technology  “coagglutination”  Anticomplimentary: antiphagocytic; elicits HPS reaction; platelet injury Capsules  inhibit phagocytosis by PMNs Coagulase, or clumping factor  binds nonenzymatically to fibrinogen, yielding aggregation of the bacteria 1

renal cortex Beta toxins – degardes sphingomyelin. shock & multisystem involvement. invasion of healthy skin. Panton-Valentine Leukocidin  Fast & slow components  Kill white blood cells of humans & rabbits  Synergistically on the white blood cell membrane to form pores and increase cation permeability  Associated with MRSA 6. leukotriene. heat stable (resists boiling for 20 minutes)  Epidermolytic B . Toxic Shock Syndrome Toxin (TSST)  Superantigen  Binds to MHC Class II molecules – T cell stimulation  Protean manifestations of the toxic shock syndrome-1 (TSST-1) .Binds to prothrombin – enzymatically active and initiate fibrin polymerization .Fever.fibrinolytic. correlation with boils 1. histamine 5. including a desquamative skin rash Gene for TSST-1: 20% of S.Clots plasma . fats & oils. enterotoxin  group IV: enterotoxin Determinants of pathogenecity:  surface antigens: antiphagocytic  extracellular enzymes: ability to multiply and spread widely in tissues  coagulases: clots plasma  lipases: active on plasma.Chromosomal gene product. activation of plasma plasminogen to fibrinolytic enzyme plasmin  Nucleases – cleaves DNA or RNA  Proteinases. RBCs Delta toxins Gamma toxins – diarrheal diseases  Lysing WBCs by causing pore formation  Release IL8.Staphylococci Grouping of stains: susceptibility of S. cytotoxic to tissues Injury to circulatory system.Invasive pathogenic potential Clumping factor: adherence of the organisms to fibrinogen & fibrin 3.Converts hydrogen peroxide into water and oxygen 2. Exotoxins Alpha toxins – hemolysis. pemphigus of NB)  group III: methicillin resistant.Plasmid-mediated and heat-labile  Superantigens  EXOTOXIN & EXFOLIATIVE TOXINS: Clinical Manifestations  Histologically: intraepidermal cleavage plane at stratum granulosum (S. aureus to temperate bacteriophage  group I  group II: skin infections (impetigo.Protects organism from phagocytosis and isolate from defenses . Coagulase and Clumping Factor . intense colonization in sebaceous areas. lipases and lactamase 4.hydrolyzes hyaluronic acid in intracellular ground substance (spreading factor)  Staphylokinase . Aureus group II) 7. muscle tissues. lethal & dermonecrotic  Disrupts lysosomes. Catalase . Exfoliative toxins (epidermolytic toxins)  Generalized exfoliation (Ritter’s syndrome)  Toxic epidermal necrolysis (adult)  Staphylococcal Scalded Skin syndrome (SSS) or Generalized scarlatiniform eruptions: children  Epidermolytic toxin A . aureus isolates 2  . Other enzymes  Hyaluronidase .

SCCmec typeIV: community acquired MRSA Staphylococci Clinical Findings  Wall prevent spread of the organisms  Direct contamination of a wound . ampicillin.Associated with thrombosis . and hypotension with cardiac & renal failure . vomiting.Bacteremia. piperacillin & similar drugs) 2.Staphylococcal cassette chromosome SCCmecA gene . meningitis. a scarlatiniform rash. acute hematogenous osteomyelitis. Beta-Lactamse producing: .Pathogenesis  Nasal carriage of S aureus: 20-50% of humans  Found in clothing. tracheal aspirate.Plasmid mediated. or spinal fluid for culture Smears  Not possible to distinguish saprophytic from pathogenic Culture  Blood agar plates Catalase Test  A drop of hydrogen peroxide solution plus a small amount of the bacterial growth  Positive test: formation of bubbles (the release of oxygen) Coagulase Test  Citrated rabbit (or human) plasma mixed with growth colonies on agar and incubated at 37°C  Positive: clots form in 1-4 hours  Coagulase (+): pathogenic Susceptibility Testing  Broth microdilution or disk diffusion susceptibility testing  Gene detection by polymerase chain reaction Serologic and Typing Tests  Little value  Molecular typing techniques Resistance Classes .Associated with the use of tampons .Spread via the lymphatics & bloodstream . genetic 1. ticarcillin.In wounds or other localized infections. or pulmonary infection Toxic shock syndrome . or in the throat but virtually never in the blood stream 3 .Abrupt onset of high fever. bed linens & other fomites in human environments  Combined effect of extracellular factors and toxins together with the invasive properties of the strain Pathology:  Penetrate sebaceous gland or hair shaft  Proteases: chemotaxis  Tissue necrosis (dermonecrotic factor)  Coagulase: coagulates fibrin around the lesion & within the lymphatics (formation of a wall)  Accumulation of inflammatory cells  Fibrous tissue (avascular fibroblastic wall)  Liquefaction of the necrotic tissue  Abscess “points” in the direction of least resistance  Granulation tissue and eventual healing     Folliculitis Furunculosis Carbuncle Abscess Diagnostic Laboratory Tests Specimens  Surface swab. blood.Resistant to many penicillins (penicillin G. myalgias. Resistance to nafcillin (and to methicillin and oxacillin): . pus. endocarditis. diarrhea.

Colony growth characteristics 2. R antigens)  Carbohydrates (group-specific)  Peptidoglycans  Hair-like pili project through the capsule 4 - .S. Biochemical reactions 4. T. mitior) Group-Specific Cell Wall Antigen  Lancefield groups A-H.milleri.Glossy colonies: often nonvirulent Streptotcoccus Pyogenes Cell wall:  Proteins (M. K-U: Carbohydrate-cell wall.mutans. agalactiae  C. Vancomycin-resistant S aureus (VRSA) strains – gene vanA from enterococci . and C strains: produce capsules of hyaluronic acid-impede phagocytosis  A.Patients with complex infections on prolonged vancomycin therapy .Difference between minimal inhibitory and minimal lethal concentrations of an antimicrobial drug .S. S. basis of serologic grouping  Specificity of the group-specific carbohydrate: determined by an amino sugar  Group A streptococci (GAS): rhamnose-Nacetylglucosamine Group A. virulent and insusceptible to phagocytosis by human leukocytes . heavy encapsulation.S.pyogenes: Human pathogen Local or systemic Poststreptococcal disorders  B. Plasmid-mediated resistance to tetracyclines.hemolytic streptococcus  Rigid cell wall  Capsule: hyaluronic acid identical to that of humans: binds to hyaluronic acid binding protein CD44 in human epithelial cells  Produces hyaluronidase  Fuzzy surface: type specific M protein  Energy: principally from the utilization of sugars (lactic acid as end product)  Facultative anaerobes  Oxidase (-)  Variants of the same streptococcus strain may show different colony forms . B.Attributed to lack of activation of autolytic enzymes in the cell wall Streptococci  Gram-positive cocci in pairs or chains  20 species  Pasteur: in puerperal sepsis  Kochs: wound infection  1883: pure culture  1930: Lancefield classification Classification based on: 1.equi  D.Major concern worldwide 5.Associated with increased cell wall synthesis and alterations in the cell wall 4. Cell wall group-specific cell substance and capsular antigens 3.enterococci Streptococcus Pyogenes Group A b --. aminoglycosides 6. Vancomycin-Intermediate S Aureus or “VISA” .Nafcillin resistance gene mecA . S. “Tolerance”: inhibited but not killed by the drug . erythromycins. clearing of blood around growth culture Alpha hemolysis: incomplete lysis (S.pneumoniae)  Viridans Group (S.Matt colonies: M proteins-rich. sanguis. Ecologic features  Catalase negative  Hemolysis: Beta Hemolysis: complete disruption of erythrocytes. S.- Lack or inaccessibility or penicillin-binding proteins (PBPs) in the organisms 3.

Pyrogenic Exotoxins (Erythrogenic Toxin) .Antistreptokinase: specific antibody  Given for the treatment of pulmonary emboli and coronary artery and venous thromboses 2.Streptococcal toxic shock syndrome .Active proteolytic enzyme that digests fibrin and other proteins (dissolves clots) . secondary hypersensitivity Exotoxin A . serodiagnosis  Streptodornase and streptokinase: in “enzymatic debridement” 3.Scarlet fever Exotoxin C . Streptokinase (Fibrinolysin): . Streptolysin O (SLO): potent antigen  Inactivated by oxygen. myocardial cells  Immunogenic  Antistreptolysin O (ASO) – antibody vs.Increases permeability of BBB to endotoxin. Diphosphopyridine Nucleotidase  Elaborated into the environemtn by some streptococci  Ability to kill leukocytes  Serodiagnosis of pharyngeal and skin infections  Proteinases and amylase 6.Rash in scarlet fever.Transforms that plaminogen of human plasma into plasmin . DNAse: develops after skin infection. SLO . little antigenic significance  Enhances virulence Toxins & Enzymes 1.induces antibodies that cross react with human cardiac muscle tissue (virulence determinant for rheumatic fever) T Substance  No relationship to virulence  Determined by agglutination with specific antisera R protein  Destroyed by pepsin not trypsin Nucleoproteins  P substances: streptococcal cell body No serologic activity Capsular antigens:  Hyaluronic acid. Hemolysins: a.    Streptodornase: Streptotococcal deoxyribonuclease Depolymerizes DNA Purulent exudates: deoxyribonucleoprotein Antibody vs. pyrogenicity.Quantitative test for the antibody 5 . dermal reactivity. Hyaluronidase  Spreading infecting microorganisms (spreading factor)  Splits hyaluronic acid: ground substance of connective tissue  Antigenic and specific  Serodiagnosis 4. Pili – M protein and covered with lipoteichoic acid (attachment of streptococci to epithelial cells) Streptococcus Pyogenes: Antigenic Structure M Protein  Major virulence factor  Hair-like projections in the cell wall  Able to resist phagocytosis by PMNs  Prevents activation of complement  150 types  Presence of type-specific antibodies to M protein: immunity  Two major structural classes of M protein: Classes ! & II  Important role in the pathogenesis of rheumatic fever Class I M protein . inactivated by cholesterol  Toxic for RBCs. WBCs. pyretic effect on hypothalamus Exotoxin B: unclear 5.

hypertension  Chronic GN.57. following pharyngitis or skin or soft tissue infection 6 . antihyaluronidase.60  Antigen-antibody complexes on the glomerular membrane  Hematuria. or pointed ends. pyogenes Portal of entry: determines the principal clinical picture  Diffuse and rapidly spreading infection  Minimal local suppuration  Infection can extend to the bloodstream Streptococcal Pyoderma: Impetigo  Superficial layer of the skin  Highly communicable  Hot & humid climates  M types 49.- Serum titer: >160-200 units: recent infection with streptococci or earlier exposure in a hypersensitive person b. muscles. showing curved. lymphadenopathy Streptococcus Pyogenes Necrotizing Fascitis  Streptococcal gangrene  Soft tissue. gm (+) anaerobe  Highly pleomorphic. antiM Treatment:  Penicillin G  Erythromycin  Vary in their susceptibility  Aminoglycosides often enhance the rate of bactericidal action of penicillin Propionibacterium  Normal flora of the skin. 12 and 28 producing exotoxin A or B Poststreptococcal Acute Glomerulonephritis (PSGN)  1-4 weeks after skin infection  M types 2. 57. 59-61  May lead to glomerulonephritis Streptococcus Pyogenes: Erysipelas  Skin & subcutaneous tissues  Face Cellulitis: Lymphangitis. clubbed. Streptolysin S:  Oxygen stable. antiDNAse. respiratory and multiorgan failure following soft tissue infection  M types 1 or 3. long forms with beaded uneven staining and occasionally coccoid or spherical forms  Contaminates blood or cerebrospinal fluid cultures  Metabolic products include propionic acid  Acne: produces lipases split fatty acids – tissue inflammation  Post surgical infections Streptococcus Pyogenes Diseases: Invasion by S. non antigenic  Responsible for the hemolytic zones around colonies growing in blood agar plates  Elaborated in the presence of serum  Hemolysis by direct cell to cell contact (RBCs and WBCs)  Independent of past infection  Rash trunk to extremities Streptococcal Toxic Shock Syndrome  Bacteremia. fascia  “flesh eating bacteria”  Associated with diabetes. antistreptokinase.49.56. edema. proteinuria. PVD  Usually mixed infections  Exotoxin A Scarlet Fever  Strep producing exotoxin A-C. renal failure Diagnosis:  Smears  Culture: blood agar  Antigen detection  Serologic tests: ASO. 42.

slender. imipenem  Quinolones (ciprofloxacin)  Ceftazidime and cefoperazone  Susceptibility tests Mycobacterium Leprae  Leprosy. water  Normal stools. urinary tract infection necrotizing pneumonia  Fatal sepsis Diagnostic Laboratory Tests Specimens: from site of infection Smears  Gram-negative rods  No specific morphologic characteristics Culture  Blood agar  Does not ferment lactose  Specific test Treatment  Should not be treated with single-drug therapy  Ticarcillin or piperacillin plus aminoglycoside  Aztreonam. long. soil. generation time 12 days  Preferred sites: temp 30°C (nose. 1400 BC  Hebrew writings  Old testament stories  Hansen in 1873 Mycobacterium Leprae  Obligate intracellular organism  Acid-fast. Verdoglobin  Ecthyma gangrenosum  Meningitis. metabolic diseases. gram-negative  Resistant to chemical disinfection  Gram negative obligate aerobe  In culture sweet or grape-like or corn tacolike odor  Forms smooth round colonies with a fluorescent greenish color  Pyocyanin  Pyoverdin  Pyorubin  Pyomelanin  Can produce multiple colony types  Different biochemical and enzymatic activities and different antimicrobial susceptibility patterns  Oxidase-positive  Oxidize glucose Pseudomonas Aeruginosa Antigen Structure & Toxins  Somatic or O antigen: grouping of strains  Pili (fimbriae): attachment to host epithelial cells  Exopolysaccharide: for the mucoid colonies  Lipopolysaccharide: endotoxic properties Pathogenesis  Burns.Pseudomonas Aeruginosa  Widely distributed I n nature. invades locally and produces systemic disease Clinical Findings:  Pseudomonas dermatitis  Otitis externa: “swimmer’s ear”  Infection of wounds and burns: blue-green pus. non-motile bacilli  Resistant to drying but not to heat or ultraviolet irradiation  Cell walls: contain long chain bhydroxylated fatty acids (mycolic acids) complexed with carbohydrates and proteins creating a waxy hydrophobic surface  Multiplies slowly.feet)  Strong predilection for nerves  Found within the endothelial cells of blood vessels or in mononuclear cells (histiocytes of the skin. instrumentation/manipulation (intravenous or urinary catheters)  Attaches to and colonizes the mucous membranes or skin. malignancy. skin  Commonly present in moist environments in hospitals  Saprophyte  Opportunistic pathogen  Primarily a nosocomial pathogen  Motile and rod-shaped. Schwann cells of nerves)  “lepra cells”  “packet of cigars” 7 .

protracted incubation period (years)  Chronic granulomatous condition of peripheral nerves and mucocutaneous tissue Clinical findings:  Insidious onset (3 months to 40 years)  Hypopigmented macules trunk and distal extremities  Skin. Man is the only host  Armadillos: naturally infected  O-diphenoloxidase: to differentiate from other mycobacterium and nocardia  Lepromin test a. eyes and testicles  Anesthetic macular lesions  Diffuse or discrete erythematous. larynx. abrasions  Low infectivity. neuritis. paresthesia. superficial nerves. lymphadenopahty. trophic ulcers. Intermediate stages Diagnosis  Scrapings: skin or mucous membranes (nasal septum) in lepromatous leprosy  Biopsy of earlobe skin  Ziehl-Neelsen technique  Histopath  No serologic tests  Nontreponemal serologic tests for syphilis: false-positive results in leprosy Laboratory Identification  Cannot be grown in artificial medium  Animal inoculation o Footpads of mice o Armadillo  PCR Treatment  Sulfones such as dapsone: first-line therapy  Rifampin  Clofazimine  Minocycline  Clarithromycin  Fluoroquinolones  Several years of therapy Epidemiology  Prolonged periods of exposure to heavy shedders  Incubation period: 2-10 years Prevention & Control  Identification & treatment of patients  Chemophrophylaxis 8 . Delaye d HPS reaction (Mitsuda reaction): 3-4 weeks Pathogenesis  Transmitted from human to human: exudates of skin lesions. infiltrated nodules  Diffuse skin infiltration  Anesthesia. nose. testicles). ear lobes. eye involvement  Amyloidosis 3. and bone resorption and shortening of digits Lepromatous Leprosy:  Progressive and malignant  Nodular skin lesions/erythema nodosum. Early reaction (Fernandez reaction): 24-48 hours b. pharynx. neuritis (anesthesia)  Macular skin lesions  Asymmetric nerve involvement  Few bacilli present in the lesions  Positive lepromin skin test  Cell-mediated immunity: intact  Helper T cells in the lesions  Anemia. Tuberculoid:  Benign and nonprogressive  Large maculae in cooler body parts (nose. multiple skin lesions  Symmetric nerve involvement  Leonine facie  Abundant acid-fast bacilli in the skin lesions  Continuous bacteremia  Negative lepromin (extract of lepromatous tissue) skin test  Cell-mediated immunity: deficient  Suppressor T cells in the lesions 2.

singly or pairs.Gram (+) bacillus. trimethoprim-sulfamethoxazole. Experimental BCG vaccination and an M leprae vaccine Erysipelothrix rhusiopathiae . acid fast Chronic suppurative & granulomatous infection Pyogenic lesions with interconnecting sinus tracts that contain granules – actinomycetoma granule Streptomycin. human accidental exposure . bacillary chains or filaments. and dapsone  Clostridium perfringens  Gas gangrene  Produce the alpha toxin: necrotizing.Erysipeloid: “seal fingers” or “whale fingers” . brasiliensis  Streptomyces somaliensis  Actinomadura madurae     Saprophytes Gram-positive anaerobic bacilli.Land and sea animals . :hemolytic .Causes erysipelas in swines.Non suppurative painless swelling violaceous lesions at the site of inoculation . hemolytic exotoxin – lecithinase  Present throughout the environment  Wound contamination (trauma.abortion). fatal bacteremia  CO2 and H2 detectable as gas  Surgical removal of the infection  Penicillin G 9 .Penicillin. erythromycin Actinomycetoma (Mycetoma/Madura Foot)  Nocardia asteroids  N.