Bacterial Skin Infections PDF Microbiology and Parasitology

MICROBIOLOGY AND PARASITOLOGY 09/03/2024. MOD 5: BACTERIAL SKIN INFECTIONS...

MICROBIOLOGY AND PARASITOLOGY 09/03/2024. MOD 5: BACTERIAL SKIN INFECTIONS Dr. Vendale Jon D. Figuerres; Dr. Ma. Teresa A. Barzaga Trans Group/s: 3A, 4A I. STAPHYLOCOCCI A. GENERAL CHARACTERISTICS Gram-positive (+) spherical cells Arranged in grape-like irregular clusters Aerobic or facultative anaerobic Non-motile Non-spore forming Key characteristic: can produce catalase as their by-product Normal flora of skin and mucous membranes Multisystem involvement of TSST-1. Primary reservoir: human nares 2. EXFOLIATIVE TOXIN B. VIRULENCE FACTORS Serine protease that splits the intracellular bridges of the epidermis VIRULENCE FACTORS Two distinct proteins: ○ Exfoliative toxin A: encoded by eta gene located 1 Toxic Shock Syndrome Toxin-1 (TSST-1) on a phage; heat stable ○ Exfoliative toxin B: plasmid-mediated; heat-labile 2 Exfoliative toxins When activated, this superantigen causes generalized desquamation of staphylococcal scalded skin 3 Hemolysins syndrome (SSSS) or Ritter Disease ○ This is common in newborn and infants 4 Panton-Valentine Leukocidin (PVL) This also plays a major role in bullous impetigo. 5 Coagulase 6 Clumping Factor 7 Enzymes (i.e. Hyaluronidase, Lipase, Beta-lactamase) 8 Protein A 9 Enterotoxin SSSS or Ritter Disease. 1. TOXIC SHOCK SYNDROME TOXIN-1 (TSST-1) 3. HEMOLYSINS Enterotoxin F Cytolytic toxins that are regulated by agr gene Chromosomal-mediated toxin Affects erythrocyte (RBCs) and leukocytes (WBCs) When activated, it becomes a superantigen that Has four major types stimulates T-cell proliferation and the subsequent ○ alpha(⍺)-hemolysin production of cytokines ○ beta(ꞵ)-toxin ○ Binds to MHC II molecules → T-cell stimulation ○ delta(δ)-toxin Associated with fever, shock and multi-organ system ○ gamma(γ)-hemolysin involvement Gene is found in about 20% of S. aureus isolates. Causes majority of menstruation-associated toxic TYPES OF HEMOLYSIN shock syndrome ⍺-HEMOLYSIN Heterogeneous protein Can cause tissue damage due to its lytic activity in erythrocytes, platelets, and macrophages Disrupts smooth muscle in blood vessels Microbio and Para - Mod 5 Bacterial Skin Infections 1 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  ○ It is unlikely that PVL has a direct necrotic effect on ꞵ-TOXIN Degrades the epithelial cells. (SPHINGOMYELINASE C) sphingomyelin Hydrolase enzyme that catalyzes hydrolysis of membrane phospholipids resulting in cell lysis Hemolytic activity is enhanced when incubated at 37°C and subsequent exposure to lower temperature (~4°C) Exhibited in CAMP laboratory test to identify Group B Streptococci δ-TOXIN Heterogeneous protein and dissociated into Diagram of PVL mechanism on polymorphonuclear cells subunits in non-ionic agents 5. COAGULASE Cytolytic to erythrocytes and demonstrates Enzyme-like protein that clots oxalated or citrated non-specific membrane plasma toxicity to other Agglutination occurs when bound to prothrombin and mammalian cells becomes enzymatically active to initiate fibrin May have a role in polymerization producing diarrhea when Due to this occurrence, fibrin may deposit on the surface the gut is infected by S. of S. aureus which results to the organisms aureus anti-phagocytic characteristic (resisting phagocytosis) Synonymous with invasive pathogenic potential γ-HEMOLYSIN Leukocidin that lyses or 6. CLUMPING FACTOR primarily affects the leukocytes (WBCs) A microbial surface component recognizing adhesive Has a great association matrix molecules (MSCRAMM) responsible for with Panton-Valentine adherence of S. aureus to fibrinogen and fibrin, thereby Leukocidin causing agglutination when mixed with plasma 7. OTHER ENZYMES 4. PANTON-VALENTINE LEUKOCIDIN (PVL) Lethal exotoxin that affects polymorphonuclear leukocytes (or PMNs) Hyaluronidase Permits bacteria to spread ○ Primarily affects the neutrophils and monocytes through connective tissues Encoded on a mobile phage Also called spreading factor Two components: protein S and protein F ○ Acts synergistically on WBCs together with Lipase Degrades lipids on skin surface, gamma-hemolysin to form six potential permitting bacterial entry into the two-component toxins epidermis ○ These proteins can cause pore-formation in the cellular membranes that increase cation Beta- Enzyme that cleaves the ring permeability which leads to massive release of lactamase structure of penicillin inflammatory mediators Significant virulence factor of S. Contributes to invasiveness of S. aureus by aureus since this makes the suppressing phagocytosis organism resistant to penicillin Important virulence factor in Community-Acquired Methicillin-Resistant Staphylococcus aureus (CA-MRSA) 8. PROTEIN A The 2 main components of PVL are LukS-PV (protein Cell wall component of S. aureus that is S) and LukF-PV (protein F) which are secreted from S. characterized among MSCRAMMS aureus before they assemble into a pore-forming Binds to Fc portion of IgG molecules except IgG3 heptamer on PMN membranes with the help of ○ Blocks phagocytosis and negate the protective γ-hemolysin. effects of IgG ○ High concentrations of PVL causes PMN lysis Fab portion of IgG-Protein A complex is free to ○ Low concentrations of PVL mediate PMN combine with a specific antigen apoptosis by directly binding to mitochondrial membranes 9. ENTEROTOXIN Tissue necrosis could result from the release of Heat-stable exotoxins reactive oxygen species (ROS) from lysed PMNs. Superantigens that have the ability to interact with Alternately, release of granule contents from lysed many T cells, causing an aggressive, overreactive PMNs could set in motion an inflammatory response immune response which eventually leads to tissue necrosis. Resistant to actions of the gut enzymes Microbio and Para - Mod 5 Bacterial Skin Infections 2 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  15 types (A-E, G-P) Important cause of food poisoning: most commonly caused by Enterotoxins A, B, and D ○ Enterotoxin B: results in vomiting and diarrhea; linked to staphylococcal pseudomembranous enterocolitis MEDICALLY IMPORTANT SPECIES OF STAPHYLOCOCCI 1 Staphylococcus aureus Folliculitis. 2 Staphylococcus epidermidis 1.2 Furuncle 3 Staphylococcus saprophyticus Extension of a folliculitis into deep tissue of the skin 4 Staphylococcus lugdunensis (i.e. dermis) Lesion: large, raised, violaceous to erythematous, tender lesion containing abscess II. STAPHYLOCOCCUS AUREUS Risk factors: diabetes mellitus, obesity, Most clinically important species immunocompromised state Important community-acquired pathogen Treatment: incision and drainage, empirical Coagulase-producing organism antibiotics against staphylococcal agents Can cause superficial (i.e. impetigo, furunculosis) or systemic (i.e. septicemia, bacteremia) illnesses Common cause of infective endocarditis and toxin-induced illnesses (i.e. TSS – toxic shock syndrome, food poisoning) Furuncle. 1.3 Carbuncle Larger, more invasive lesions that develop from Staphylococcus aureus. multiple furuncle Extends to the subcutaneous fat A. PATHOGENESIS Consists of multiple coalescing abscesses that can Determined by: drain at several adjacent sites along hair follicles ○ Virulence of the strain Patients can have systemic symptoms (i.e. fever, ○ Size of infectious dose chills), indicating systemic spread of the bacteria ○ Status of host’s immune system Most common sites: nape, back of the thighs Superficial staphylococcal infections are initiated when Treatment: incision and drainage, empirical there is a breach in skin or mucosal barrier antibiotics ○ As the organism enters the deeper layers of the skin, its virulence factors activate the host’s acute inflammatory response. Toxins and enzymes secreted by the organism are resistant to inflammatory cell actions (i.e. phagocytosis) → (+) focal lesion B. SKIN INFECTIONS CAUSED BY S. AUREUS May be superficial or toxin-mediated 1. SUPERFICIAL INFECTIONS Suppurative Carbuncle. Abscess is filled with pus surrounded by necrotic tissues and damaged leukocytes 2. TOXIN-MEDIATED CUTANEOUS DISEASE Usually occur as a result of previous skin injuries Caused by toxins of S. aureus: ○ Exfoliative toxins A and B 1.1 Folliculitis ○ Toxic shock syndrome toxin-1 Mild inflammation of a hair follicle or sebaceous gland May start primarily from skin or as secondary skin Lesion: small, erythematous papules; may be pruritic; manifestation due to circulating bacterial toxins in the often evolve to form pustules blood ○ Frequently associated with shaving Microbio and Para - Mod 5 Bacterial Skin Infections 3 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 2.1 Bullous Impetigo Pustules are larger as compared with streptococcal non-bullous impetigo, and is surrounded by a small zone of erythema Formation of bullae – caused by exfoliative toxins A and B of S. aureus Easily spread by direct contact with patients, fomites, or autoinoculation Diagnosis: gram-stain and culture of the bullous contents Treatment: cephalosporins, topical antibiotics (i.e. Mupirocin) Normal skin vs. SSSS. Mortality: 1-5% in children; 50-60% in adults ○ Adults have much higher mortality rate compared to children when contracted with SSSS Treatment: ○ Immediate administration of antibiotics ○ Hydration ○ Wound care Differential diagnosis: Toxic Epidermal Necrolysis (TEN) ○ Split skin tissue occurs BETWEEN the dermis and epidermis Bullous Impetigo. ○ Caused by systemic reaction to antibiotics, barbiturates or other drugs 2.2 Staphylococcal Scalded Skin Syndrome (SSSS) ○ NOT caused by a bacterial agent Another essential and more serious dermolytic condition caused by exfoliative toxins A and B of S. aureus May occur in children and adults, but newborns and infants are the most vulnerable Transmission: direct contact, droplet contact, nosocomial Characterized by fever, skin tenderness, scarlatiniform rash, followed by extensive formation of bullae and exfoliation Comparison between SSSS and TEN. 3. TOXIC SHOCK SYNDROME (TSS) Systemic syndrome caused by exotoxins/superantigens of S. aureus (less common) and Group A Streptococcus (more common) ○ Superantigens: TSST-1, Staphylococcal Staphylococcal Scalded Skin Syndrome (SSSS). enterotoxins, Streptococcal pyrogenic exotoxins TSST-1: staphylococcal infections Nikolsky Sign: the pathognomonic sign for SSSS; Enterotoxins: streptococcal infections elicited by stroking the skin upon which the epidermal Presents as a diffuse sunburn-like erythroderma in its layer is easily separated from the rest of layers of the early stage, accompanied by fever, hypotension and skin evidence of multiorgan dysfunction ○ Toxins act exclusively on stratum granulosum of Cutaneous desquamation on palms and soles occurs epidermis – no mucosal involvement (they do not during convalescent phase (1-2 weeks after rash onset) act on mucosal surfaces) Commonly occurs in children and in young women Toxins may enter the bloodstream from an initial site who use superabsorbent tampons and may interact with the skin of other areas of the Treatment plans: body ○ Systemic antibiotics ○ Hydration ○ Vasopressors ○ Debridement of infected tissue IVIG – may be helpful in neutralizing superantigens Streptococcal toxic shock syndrome is more common than staphylococcal toxic shock syndrome. Microbio and Para - Mod 5 Bacterial Skin Infections 4 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  Colonies of Used for contaminated Staphylococcus specimens with mixed species appear after microbiota incubating for 18 Used to screen for hours at 37°C nasal carriers of S. Hemolysis and aureus and to recover pigment production S. aureus from may occur several days respiratory specimens later since S. aureus can Three hemolysis ferment mannitol patterns are reported: Mannitol can inhibit the ○ alpha-hemolysis growth of other ○ beta-hemolysis organisms, including ○ gamma- non-aureus hemolysis Staphylococci. HEMOLYSIS PATTERNS Cutaneous desquamation on palms and soles. Alpha- Shows partial hemolysis of an III. INFECTIONS CAUSED BY OTHER hemolysis organism STAPHYLOCOCCUS SP. It will appear as areas of small discoloration surrounding the cultured organism Staphylococcus May infect orthopedic or epidermidis cardiovascular prosthesis Beta- Shows complete hemolysis of an infection hemolysis organism in which there are large areas May be refractory to treatment of discoloration surrounding the because of formation of biofilms cultured organism Staphylococcus aureus is a prime Staphylococcus Causes urinary tract infections example of an organism that exhibits saprophyticus in young women beta-hemolysis. Large areas of golden yellow discoloration will be seen Staphylococcus Causes disease spectrum surrounding the colonies. lugdunensis similar to S. aureus Gamma- Do not show hemolytic reaction from Shares hemolysis and hemolysis the cultured colonies clumping factor with S. aureus This is exemplified by Staphylococcus epidermidis. IV. DIAGNOSTIC LABORATORY TESTS FOR STAPHYLOCOCCI Specimens that may be submitted to the laboratory to confirm the etiologic agent of an infection: ○ Surface swab pus ○ Aspirate from an abscess ○ Blood ○ Endonasotracheal aspirate ○ Expectorated Sputum ○ Spinal fluid Blood agar plates of S. aureus and S. epidermidis. Techniques and Tests used: ○ Gram-stain Smears ○ Culture ○ Catalase Test ○ Coagulase Test ○ Susceptibility Testing A. SMEARS Staphylococcus species may appear as gram-positive cocci organisms arranged in clusters in smear slides. Mannitol salt agar. A great limitation: CANNOT DIFFERENTIATE between S. aureus and non-aureus organisms (one C. CATALASE staphylococcus species to another) A cytochrome oxidase enzyme that converts hydrogen peroxide into water and oxygen through the process B. CULTURE of hydrolyzation A definitive diagnostic technique for identifying Staphylococcus species is through bacterial culture. 1. CATALASE TEST A simple test to detect the presence of cytochrome TYPES OF CULTURE oxidase enzymes BLOOD AGAR PLATES MANNITOL SALT AGAR Microbio and Para - Mod 5 Bacterial Skin Infections 5 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  ○ This is done by simply applying a drop of hydrogen peroxide on the specimen slide or tube 2. BROTH MICRODILUTION containing the organism Either oxacillin or cefoxitin may be used to detect ○ A positive result will produce bubbles since the oxacillin resistance catalase has hydrolyzed hydrogen peroxide into ○ 2% of NaCl is added to the medium if cefoxitin is to water and oxygen be used, and the test must be incubated for a full 24 This test is used to differentiate Staphylococcus sp, a hours at 35°C catalase-positive organism, from Streptococcus sp., a Done by adding a certain amount of microbial catalase-negative bacteria. sample into a series of broth tubes containing serial dilution of a specific drug The minimal inhibitory concentration (MIC) is then recorded 2.1 Penicillin G Resistance (+) for beta-lactamase Approximately 90% of S. aureus produce beta-lactamase; hence, majority are penicillin-resistant 2.2 Nafcillin Resistance Catalase test. (+) mecA or mecC genes: genes that encode for PB2a Occurs in about 65% of S. aureus and approximately D. COAGULASE 75% of S. epidermidis An exoenzyme that clots blood plasma by a ○ mecA or mecC-positive organisms are also mechanism similar to normal clotting resistant to all extended spectrum penicillin, Two forms: carbapenems, and cephalosporins (except ○ Free coagulase – secreted extracellularly ceftaroline) ○ Bound coagulase – cell wall-associated protein V. EPIDEMIOLOGY AND CONTROL FOR 1. COAGULASE TEST STAPHYLOCOCCI Used to detect the presence of coagulase, the exoenzyme present ONLY in S. aureus A. EPIDEMIOLOGY Differentiates S. aureus from other Staphylococcus sp. Done by applying a drop of blood plasma on a slide or tube of specimen sample CHIEF SOURCES OF INFECTION ○ Positive result: presence of agglutination after 1-4 hours 1 Shedding Human Lesions TYPES OF COAGULASE TEST 2 Fomites SLIDE COAGULASE Detects bound coagulase 3 Human Respiratory Tract TUBE COAGULASE Detects free coagulase 4 Skin Antibiotic-resistant Staphylococci may be carried in the nose or on the skin B. CONTROL OF MICROBE CONTROL MEASURES FOR STAPHYLOCOCCUS IN THE HOSPITAL 1 Proper hygiene 2 Strict adherence to infection-control policies Slide and tube coagulase test. 3 Exclusion of individuals and personnel with E. SUSCEPTIBILITY TESTING active infection in vulnerable areas such as Broth microdilution or disk diffusion susceptibility nurseries, ICUs, operating rooms, and chemotherapy testing wards Should be done routinely on staphylococcal isolates from clinically significant infections 4 Frequent screening for anterior nares colonization among high risk patients 1. DISK DIFFUSION Also known as cefoxitin disk test 5 Strict adherence of health care workers to infection Recommended for S. aureus, S. lugdunensis, and S. control policies by wearing gloves and proper hand saprophyticus hygiene before and after patient contact A zone of inhibition less than 22 mm in diameter indicates resistance for cefoxitin Microbio and Para - Mod 5 Bacterial Skin Infections 6 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  CONTROL MEASURES FOR STAPHYLOCOCCUS Streptococcus agalactiae OUTSIDE THE HOSPITAL GAMMA Non-hemolytic organisms 1 Proper hygiene Ex. some strains of Streptococcus salivarius 2 Avoidance of long-term usage of tampons Aerosols and UV irradiation of air in hospitals have little to no effect for control. VI. STREPTOCOCCI A. GENERAL CHARACTERISTICS Gram-positive (+) spherical to ovoid cells Arranged in pairs or chains Catalase-negative Most are facultative or aerotolerant anaerobes Can ferment glucose, with lactic acid as the Different hemolytic patterns on blood agar. end-product 2. LANCEFIELD CLASSIFICATION Based on carbohydrate antigen found in the cell wall of the organism ○ This is identified by an agglutination reaction on a specific antibody preparation Basis of serological specificity: amino sugar Lancefield Groups A-H and K-U Medically important groups for Streptococci: A, B, C, D, F, G LANCEFIELD GROUPS OF MEDICALLY IMPORTANT STREPTOCOCCUS ORGANISMS AMINO SUGAR PRESENT REPRESENTATIVE ORGANISM Streptococci. A Rhamnose-N- S. pyogenes acetylglucosamine B. CLASSIFICATION OF STREPTOCOCCI Based on the following B Rhamnose-glucosamine S. agalactiae ○ Colony morphology and hemolytic reactions on polysaccharide blood agar ○ Lancefield classification or serologic specificity C Rhamnose-N- S. dysgalactiae sub. of the cell wall group-specific substance (Lancefield acetylgalactosamine equisimilis Antigens) and other cell wall or capsular antigens Majority of streptococcal bacteria are classified according to their Lancefield classification D Glycerol teichoic acid with S. bovis ○ Biochemical reactions and resistance to D-alanine and Glucose physical and chemical factors F Glucopyranosyl-N- S. anginosus 1. HEMOLYSIS acetylgalactosamine Many streptococcal organisms are able to hemolyze G Rhamnose-N- S. canis erythrocytes. acetylgalactosamine with Galactose TYPES OF HEMOLYSIS ALPHA Incomplete lysis of erythrocytes with reduction of hemoglobin Result in the formation of a green pigment surrounding the colonies Ex. Streptococcus pneumoniae, Streptococcus mutans BETA Complete disruption of erythrocytes Clearing of blood around bacterial colonies Ex. Streptococcus pyogenes, Lancefield Classification. Microbio and Para - Mod 5 Bacterial Skin Infections 7 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 3. BIOCHEMICAL REACTIONS Used for species that do not react with commonly used antibody preparations for group-specific substances (A, B, C, F, and G) Organism will undergo to a battery of biochemical test Include: ○ Sugar fermentation reactions ○ Test for presence of enzymes ○ Test for susceptibility to specific chemical substance Streptokinase (fibrinolysin). C. VIRULENCE FACTORS 3. DEOXYRIBONUCLEASES (DNases) VIRULENCE FACTORS Enzymes that degrade DNA. Facilitates the spread of Streptococci in the tissue by 1 M protein liquefying pus Can be measured by the decrease in viscosity of DNA 2 Streptokinase (Fibrinolysin) solutions Used in enzymatic debridement together with 3 Deoxyribonucleases (DNases) streptokinase 4 Hyaluronidase 5 Pyrogenic Exotoxins (Erythrogenic Toxin) 6 Hemolysins 1. M-PROTEIN Major virulence factor of Streptococci Filamentous structure anchored to the cell membrane that penetrates and projects from the cell wall Inhibits the activation of alternative complement pathway Deoxyribonucleases. 4. HYALURONIDASE TWO MAJOR STRUCTURAL CLASSES Acts as a spreading factor Splits hyaluronic acid of the tissue which enables the CLASS I Contains antigenic epitopes infecting microbes to spread throughout the body system CLASS II DOES NOT possess epitopes Antigenic and specific Specific antibodies of hyaluronidase-producing organisms are seen in the serum after infection M-Protein. Hyaluronidase. 2. STREPTOKINASE (FIBRINOLYSIN) 5. PYROGENIC EXOTOXINS (ERYTHROGENIC TOXIN) Transforms plasminogen of human plasma into plasmin Analogous to exfoliative toxins (A and B) of ○ Allows escape of bacteria from blood clots Staphylococcus ○ Interfered with non-specific serum inhibitors & Associated with streptococcal toxic shock syndrome antistreptokinase and scarlet fever Produced by group A, β-hemolytic Streptococci Act as superantigens which stimulate T cells by binding to the MHC II complex in Vb region of the T-cell receptor → release of cytokines that mediate shock and tissue injury Microbio and Para - Mod 5 Bacterial Skin Infections 8 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  THREE ANTIGENICALLY DISTINCT STREPTOCOCCAL PYROGENIC EXOTOXINS (Spe) ERYSIPELAS SpeA Produced by Group A Strep. that carry a Characterized Painful, indurated, lysogenic phage by erythematous areas of inflammation with raised SpeB Cysteine protease borders that are sharply Interferes with phagocytosis demarcated from the adjacent normal skin SpeC Similar with SpeA Risk Factors in Diabetes mellitus Adults Alcohol abuse Venous stasis Trauma Skin ulcers Chronic inflammatory skin conditions Lymphatic obstruction Drug of Choice Penicillin 1st Gen Cephalosporins (i.e. cefalexin, erythromycin) Pyrogenic Exotoxins (Erythrogenic Toxins). 6. HEMOLYSINS (STREPTOLYSINS) Lyse erythrocyte membranes and cause damage to other cells Produced by S. pyogenes 6.1 Streptolysin O Hemolytically active in reduced state Erysipelas. Rapidly inactivated in the presence of oxygen Easily detected with anti-streptolysin O (ASO) titers 1.2 Cellulitis Diffuse inflammation and infection of the superficial 6.2 Streptolysin S skin layers and subcutaneous tissues Responsible for the hemolytic zones produced around Extends deeper into the soft tissues the streptococcal colonies growing on the surface of blood agar plates NOT antigenic CELLULITIS Characterized Painful, erythema, warmth, by and edema of the skin with poorly defined margins Drainage of pus may sometimes occur Risk Factors Surgery Trauma Skin ulcer Dermatitis Treatment Broad spectrum antibiotics that may cover for Hemolysins (Streptolysins). Streptococcus, Staphylococcus, and other gram-positive or D. SKIN DISEASES CAUSED BY STREPTOCOCCI gram-negative organisms, including anaerobes 1. SUPERFICIAL INVASION AND SPREADING OF S. PYOGENES 1.1 Erysipelas Superficial infection that involves the epidermis, dermis and lymphatic system Usually seen in children and older adults Sometimes preceded by a respiratory beta-hemolytic streptococcal infection Microbio and Para - Mod 5 Bacterial Skin Infections 9 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  Surgery Childbirth IV Drug Use Treatment Immediate surgical exploration of the wound Excision of all devitalized tissue Empiric broad-spectrum antibiotics Drug Choices Vancomycin Cellulitis. Combination regimen: Daptomycin + 1.2.1 Recurrent Cellulitis Piperacillin-tazobactam Combination regimen: Usually predisposed to patients with lymphedema, Carbapenem + Clindamycin obesity, venous stasis, and untreated tinea pedis 1.3 Necrotizing Fasciitis 2. LOCAL INFECTION WITH S. PYOGENES AND THEIR Often begin at a site of trauma and progress from BY-PRODUCTS superficial involvement to deep involvement in a rapid manner 2.1 Non-Bullous Impetigo (Impetigo Contagiosa) May occur as a bacteremia with secondary involvement Purulent skin infection involving face and extremities. of skin and soft tissues More contagious than Bullous Impetigo. Loss of sensation in the involved area may occur due Initial lesions begin as small vesicles and progress to to extensive tissue damage. pustules Prominent honey-colored crust lesions are due to NECROTIZING FASCIITIS ruptured pustules that produce purulent discharge, which eventually dries out Characterized Painful, erythematous lesions ○ Ruptured pustules → purulent discharge and dries by which progress to hemorrhage, out → honey-colored crusts ischemia and necrosis Approximately 10% of cases are caused by Group A afterwards streptococci while the majority are caused by S. Bullae and palpable gas aureus. (crepitus) may also occur due Group B streptococci occasionally cause impetigo in to tissue ischemia from newborns acquired through vaginal delivery. thrombosed blood vessels Common in hot and humid climates. Most common skin infection in children. NON-BULLOUS IMPETIGO (IMPETIGO CONTAGIOSA) Risk Factors Overcrowding Diabetes mellitus Treatment Oral penicillin** (for streptococcal impetigo) Cefalexin (for MRSA impetigo) Dicloxacillin (for MRSA impetigo) ** — drug of choice Necrotizing Fasciitis. 1.3.1 Polymicrobial Necrotizing Fasciitis (Type I) Caused by Enterobacterales and anaerobes 1.3.2 Monomicrobial Necrotizing Fasciitis (Type II) Caused by S. pyogenes (more common) or S. aureus (less common) Honey-colored crust lesions. Usually involve the extremities 3. INVASIVE GROUP A STREPTOCOCCAL INFECTIONS MONOMICROBIAL NECROTIZING FASCIITIS (TYPE II) Diseases caused by invasive Group A streptococcal infections: Risk Factors Blunt Trauma ○ Scarlet Fever ○ Streptococcal Toxic Shock Syndrome Microbio and Para - Mod 5 Bacterial Skin Infections 10 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 3.1 Scarlet Fever tissues IVIG (as adjunct therapy) Caused by release of streptococcal pyrogenic exotoxin. Most commonly occurs in children with concomitant pharyngeal infection Rash starts on the chest and spreads outward Does NOT involve the face. SCARLET FEVER Lesion Erythematous Petechial to maculopapular Sandpaper textured rashes Other Signs & Flushed skin Symptoms Circumoral pallor Strawberry tongue Streptococcal Toxic Shock Syndrome. Treatment Penicillin VII. DIAGNOSTIC LABORATORY TESTS FOR Macrolides STREPTOCOCCI Cephalosporin Streptococcal infections may be detected through throat swab, pus, CSF, and other sterile body fluid via culture. Detection through blood is via serum for antibody determination. A. SMEARS Positive (+) smear samples often show single cocci or pairs rather than definite chains. Sometimes, the organism may appear as gram-negative cocci due to loss of viability. Throat swab smears are rarely contributory. ○ This is because viridans streptococci are always present and have the same appearance as group A streptococci. Scarlet Fever. 3.2 Streptococcal Toxic Shock Syndrome Presented similarly as staphylococcal toxic shock syndrome Portal of entry is through skin with cellulitis that progresses rapidly Streptococci Smear. Most cases involve young adults Same signs and symptoms as with the Staphylococcal B. CULTURE Toxic Shock Syndrome Specimens suspected of streptococcal infection are cultured in blood agar plates/ Incubation in 10% CO2 increases the rate of hemolysis/ STREPTOCOCCAL TOXIC SHOCK SYNDROME ○ Streptolysins are active in the absence of oxygen. Alpha-hemolytic streptococci and enterococci may Risk Factors Lack of immunization grow slowly. Prolonged skin Streptococcus pyogenes are beta-hemolytic. infection/chronic dermatitis Bacitracin sensitivity test is used for detection of Group A streptococci. Diagnosis Blood cultures are more often ○ Group A streptococci may be presumptively positive, yielding more growth in identified by inhibition of growth by bacitracin. Streptococcal TSS than in Staphylococcal TSS Treatment Antimicrobial therapy Debridement of infected Microbio and Para - Mod 5 Bacterial Skin Infections 11 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  VIII. EPIDEMIOLOGY AND CONTROL FOR STREPTOCOCCI A. EPIDEMIOLOGY Humans can be asymptomatic carriers via nasopharynx or perineum. Nasal discharges harboring S. pyogenes are the most dangerous source of spread. Viridans streptococci and enterococci are part of normal flora of the body. Bacitracin Sensitivity Test. B. PREVENTION C. ANTIGEN DETECTION TESTS Prophylactic antibiotics prior surgical procedures, Commercially-available rapid test kits that use especially to patients with known heart valve deformity enzymatic or chemical methods to extract antigen and to those prosthetic valves or joints from the swab, then use enzyme immunoassay or agglutination tests to demonstrate the presence of C. CONTROL antigen Detection and early antimicrobial therapy of 60-90% sensitive and 98-99% specific as compared with respiratory and skin infections with group A culture methods streptococci. Antistreptococcal chemoprophylaxis in persons who have suffered an attack of rheumatic fever Eradication of S. pyogenes from carriers. X. BACILLUS A. GENERAL CHARACTERISTICS Large (size = 1.0 x 3.0-4.0 um), gram-positive, rod-shaped Arranged in long chains Pathogenic species possess virulent plasmids Antigen Detection Tests. Most are saprophytic Spores are located at the center of the bacilli and are resistant to environmental changes. D. SEROLOGIC TESTS Used to detect antibody titers in the serum It is done by making serial dilution of the patient’s serum and adding a drop of RBC in the diluted samples The test is positive (+) if there is a agglutination reaction SEROLOGIC TESTS ASO For respiratory infections Most widely used Bacillus. Anti-DNase B & For skin infections Antihyaluronidase MEDICALLY IMPORTANT SPECIES OF BACILLUS SP. Anti-Streptokinase NOT frequently utilized compared to ASO and 1 Bacillus anthracis Causes anthrax Anti-M Anti-DNase B & Type-Specific Antihyaluronidase 2 Bacillus cereus Causes food poisoning Bacillus cereus. Serologic Test. Microbio and Para - Mod 5 Bacterial Skin Infections 12 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited.  XI. BACILLUS ANTHRACIS Primary hosts: herbivores Humans are just incidental hosts Endemic in developing countries (i.e., Africa, Middle East, and Central America) Portal of entry is through the mouth of herbivores. In humans, infection is acquired through the following: ○ Cutaneous anthrax — injured skin ○ Inhalation anthrax — inhalation of the organism ○ Gastrointestinal anthrax (rare) — gut mucosa via consumption of an infected ○ May also be acquired through injection or bite of an infected insect (rare) Bacillus Anthracis. B. VIRULENCE FACTORS Aid in the survival of the bacteria as they spread via the lymphatics Bacteria may propagate freely in the blood and in tissues before and after the host‘s death 2 primary virulence factors: capsule and exotoxins 1. CAPSULE Composed of Poly-gamma D-glutamic acid Antiphagocytic Bacillus Anthracis. Genes responsible for its formation are encoded on pXO2 plasmid A. THE ANTHRAX CYCLE 2. EXOTOXINS Herbivores acquire them through ingestion of bacteria from the soil. Compounds released by the bacteria responsible for Humans may acquire the disease through contamination tissue edema and death of injured skin, inhalation, or consumption of Genes are encoded on pXO1 plasmid infected meat. Anthrax may also be considered as a vector borne THREE IMPORTANT EXOTOXINS infection (rare). Protective Binds to specific cell receptors Agent (PA) and mediates entry of EF and LF Edema Factor An adenylate cyclase that becomes (EF) an edema toxin when combined with the protective agent PA + EF = edema toxin The edema toxin is responsible for cell and tissue edema Lethal Factor Lethal factor when combined with (LF) the protective agent, it produces lethal toxin PA + LF = lethal toxin Lethal toxin: major virulence factor The Anthrax Cycle. of Anthrax that causes death Once the anthrax bacteria enters the body, spores germinate in the tissue at the portal of entry. The human immune system will try to eradicate the bacterial spore, however, due to the formation of the gelatinous edema and congestion, the growth of vegetative cells will ensue. Capsule and Exotoxins. C. DISEASES CAUSED BY BACILLUS ANTHRACIS Microbio and Para - Mod 5 Bacterial Skin Infections 13 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 1. CUTANEOUS ANTHRAX Most common form of anthrax (approx. 95%) Most common sites: upper extremities, face, neck Lesion begins as a pruritic papule which initially develops 1-7 days after entry of the anthrax spores through skin Papule rapidly changes into vesicle or small ring of vesicles Coalescence of vesicles → development of necrotic ulcer Prominent lesion: central black eschar; 1-3 cm in diameter Inhalation Anthrax. 3. GASTROINTESTINAL ANTHRAX Rare in humans Can be due to ingestion of infected meat or hematologic spread of inhalation anthrax to the GIT, causing bowel ulceration May be difficult to detect clinically since it can mimic other GIT diseases Signs and symptoms: abdominal pain, vomiting, bloody diarrhea Cutaneous Anthrax. 4. INJECTION ANTHRAX Eschar fully develops after 7-10 days Characterized by extensive, painless, subcutaneous Lesion healing occurs by granulation and leaves a edema scar NO production of eschar Mildest form of anthrax, although 20% can lead to May progress to hemodynamic instability if left sepsis and eventually, death untreated Antibiotic therapy does NOT appear to change the progression of disease but prevents dissemination of the D. DIAGNOSTICS BY B. ANTHRACIS infection. Specimen may be extracted from pus from local lesion, blood, pleural fluid, and CSF 1. SMEAR Will show chains of large, gram-positive rods 2. CULTURE In Blood Agar Plates (BAP), B. anthracis will appear non-hemolytic, gray to white, tenacious colonies with rough texture and ground glass appearance; comma-shaped ("Medusa head", "curled hair") outgrowths may be seen projecting from the colony Cutaneous Anthrax. 2. INHALATION ANTHRAX Also known as “Woolsorter’s Disease” Characterized by marked hemorrhagic necrosis and edema of the mediastinum Manifested as severe substernal pain Incubation period of spores when inhaled can be as long as 6 weeks Chest X-ray: pronounced mediastinal widening Deadliest form of anthrax = high mortality rate B. anthracis colony exhibiting the Medusa head or curled hair outgrowth. Microbio and Para - Mod 5 Bacterial Skin Infections 14 of 22 The use of trans, practice questions, and evals ratio must be used discreetly and social media/public exposure of the aforementioned shall be strictly prohibited. 2.1 Blood Agar Plate Cell culture with sodium bicarbonate – used for demonstrating capsule; incubated in 5-7% CO2 3. DEFINITIVE IDENTIFICATION Cell lysis by anthrax gamma-bacteriophage Detection of capsule by fluorescent antibody Identification of toxin genes by PCR XII. TREATMENT, PREVENTION AND CONTROL FOR BACILLUS A. TREATMENT Drug of choice (DOC): ○ Ciprofloxacin: for cutaneous anthrax ○ Raxibacumab: for inhalational anthrax Species of Clostridium Sp. B. EPIDEMIOLOGY XIV. CLOSTRIDIUM PERFRINGENS Primary source of infection: direct contact with Spores reach tissue by contamination of traumatized infected soil or animal wool area or from GIT Soil is contaminated through carcasses of infected Spore germination ensue at low oxidation-reduction animals potential Contact with infected animals or with their hides, hair Vegetative cells ferment carbohydrates present in and bristles is the source of infection in humans. tissue and produce gas Distention of tissue and interference with blood C. PREVENTION AND CONTROL supply together with secretion of necrotizing toxins Disposal of animal carcasses by burning or by deep and hyaluronidase favor the spread of infection burial in lime pits Bacterial growth is increased when tissue necrosis Decontamination by autoclaving of animal products extends. Protective clothing and gloves for handling potentially infected animals Active immunization of domestic animals with live attenuated vaccine Persons with high occupational risk should be immunized XIII. CLOSTRIDIUM A. GENERAL CHARACTERISTICS Large, gram-positive (+) rods Motile; (+) peritrichous flagella Obligate or aerotolerant anaerobes Clostridium perfringens. Natural habitat: soil, marine sediments, sewage, GIT of animals and humans A. VIRULENCE FACTORS Spores are usually wider than the diameter of rods Spores may be centrally, subterminally, or terminally 1. TOXINS located Saccharolytic and/or proteolytic organisms Alpha Toxin Lecithinase Prothrombotic, lethal necrotizing MEDICALLY IMPORTANT SPECIES OF toxin caused by type A strain CLOSTRIDIUM SP. Beta Toxin Lethal necrotizing toxin produced Clostridium perfringens Causative agent of gas by type B