Bacterial Dysentery-I (Gram Positive) PDF

Tile Bacterial Dysentery-I (Gram Positive) Department: Microbiology Topic/Subject Staphylococcus aureus Staphylococcus epidermidis AMBOSS Cases References Staphylococci: Staphylococcus aureus (S. aureus) Important properties Three species of staphylococci are important human pathogens:...

Tile Bacterial Dysentery-I (Gram Positive) Department: Microbiology Topic/Subject Staphylococcus aureus Staphylococcus epidermidis AMBOSS Cases References Staphylococci: Staphylococcus aureus (S. aureus) Important properties Three species of staphylococci are important human pathogens: - S. aureus, S. epidermidis & S. saprophyticus. - S. aureus is the most important Gram-positive cocci arranged in grapelike clusters. All staphylococci produce catalase* (virulence factor) survive the killing effect of H2O2 within neutrophils *Catalase degrades H2O2 into O2 & H2O Staphylococci: Staphylococcus aureus (S. aureus) Important properties 1.Coagulase enzyme* Coagulase enzyme clot of plasma by activating prothrombin to form thrombin catalyzes the activation of fibrinogen form fibrin clot S. epidermidis & S. saprophyticus are coagulase-negative Staphylococci: Staphylococcus aureus (S. aureus) Important properties 2. Staphyloxanthin Staphyloxanthin (carotenoid pigment) golden color colonies. It enhances pathogenicity of S. aureus by inactivating microbicidal effect of superoxides within neutrophils.  Staphylococci: Staphylococcus aureus (S. aureus) Important properties 3. Mannitol fermentation S. aureus grow on Mannitol salt agar & ferment mannitol yellow colonies with yellow zones 4. Hemolyzes of red blood cells Hemolysins is source of iron required for S. aureus growth Iron in hemoglobin is recovered by S. aureus & utilized in synthesis of cytochrome enzymes used to produce energy. NB.S. epidermidis & S. saprophyticus do not ferments mannitol or hemolyzes red blood cells. Staphylococci: Staphylococcus aureus (S. aureus) Important properties S. aureus has several important cell wall components & antigens: 1. Protein A: Major protein in cell wall & important virulence factor Protein A binds to Fc portion of IgG at complement-binding site preventing activation of complement No C3b production great reduction of opsonization & phagocytosis of S. aureus S. epidermidis & S. saprophyticus do not produce protein A. Staphylococci: Staphylococcus aureus (S. aureus) Important properties S. aureus has several important cell wall components & antigens: 2. Teichoic acids Mediate adherence to mucosal cells. 3. Lipoteichoic acids Induction of septic shock by inducing cytokines (interleukin-1 (IL-1) & tumor necrosis factor (TNF) from macrophages 4. Surface receptors for specific staphylococcal bacteriophages Phage typing of strains for epidemiologic purposes.  Staphylococci: Staphylococcus aureus (S. aureus) Important properties 5. Polysaccharide capsule* Important virulence factor. Strains with small amount of polysaccharide capsule microcapsule Poorly immunogenic capsule difficult to produce effective vaccine 6. Peptidoglycan It has endotoxin-like properties** stimulate macrophages cytokines & activate complement & coagulation cascades *There are 11 serotypes based on the antigenicity of the capsular polysaccharide, but types 5 and 8 cause 85% of infections. **This explains the ability of S. aureus to cause the clinical findings of septic shock yet not possess endotoxin Staphylococci: Staphylococcus aureus (S. aureus) Transmission Humans are the reservoir for staphylococci 1. Nose is the main site of colonization. Chronic carriers of S. aureus in nose increase risk of skin infections 2. Skin, especially of hospital personnel & patients. Hand contact is an important mode of transmission. 3. Vagina toxic shock syndrome. * approximately 5% of women Staphylococci: Staphylococcus aureus (S. aureus) Transmission Disease caused by S. aureus is favored by: 1. Heavily contaminated environment 2. Compromised immune system 3. Reduced humoral immunity (low levels of antibody, complement, or neutrophils) 4. Diabetes 5. Foreign bodies: Intravenous drug & sutures 6. Chronic granulomatous disease (defect in neutrophils ability to kill bacteria) Staphylococci: Staphylococcus aureus (S. aureus) Pathogenesis S. aureus causes disease both by: 1. Inducing Pyogenic Inflammation Abscess is the typical lesion Abscesses undergo central necrosis & drain to outside e.g., furuncles & boils, but S. aureus may disseminate via bloodstream. 2. Producing Toxins Enterotoxin Toxic shock syndrome toxin Exfoliatin Staphylococci: Staphylococcus aureus (S. aureus) Pathogenesis 1.Enterotoxin Food poisoning with prominent vomiting & watery, non-bloody diarrhea It act as superantigen within gastrointestinal tract stimulate release of large amounts of IL-1 from macrophages & IL-2 from helper T cells. Prominent vomiting caused by cytokines released from lymphoid cells, stimulate enteric nervous system to activate vomiting center in brain Toxin is Heat-resistant & not inactivated by brief cooking. It is resistant to stomach acid & enzymes in stomach & jejunum. There are six immunologic types of enterotoxin, types A–F. Staphylococci: Staphylococcus aureus (S. aureus) Pathogenesis 2. Toxic shock syndrome toxin (TSST) Disease: Toxic shock syndrome in - Tampon-using menstruating women - Individuals with wound infections. - Patients with nasal packing used to stop bleeding from nose. TSST is produced locally in vagina, nose (or other infected sites). TSST enters bloodstream toxemia. It is superantigen polyclonal T cell activation by binding to MHC II & T-cell receptors massive release of IL-2, IFN-γ &TNF-α toxic shock (high fever, rash, altered mental status & shock) Approximately 5% to 25% of isolates of S. aureus carry the gene for TSST. Toxic shock occurs in people who do not have antibody against TSST. Staphylococci: Staphylococcus aureus (S. aureus) Pathogenesis 3. Exfoliatin Disease: scalded skin syndrome It is epidermolytic & acts as protease cleaves desmoglein in desmosomes separation of epidermis at granular cell layer. 4. Enzymes Coagulase, staphylokinase, hyaluronidase, proteases, nucleases & lipases. Coagulase: clotting plasma, serves to wall off infected site retarding the migration of neutrophils into the site. Staphylokinase: fibrinolysin lyse thrombi. Staphylococci: Staphylococcus aureus (S. aureus) Pathogenesis 5. Leukocidins: Exotoxins kill leukocytes & necrosis of tissues in vivo. 1.Alpha toxin It causes marked necrosis of skin & hemolysis. Forms holes in cell membrane loss of low-molecular-weight substances from damaged cell. 2. P-V leucocidin Pore-forming toxin that kills cells, especially white blood cells, by damaging cell membranes. Two subunits of toxin assemble in cell membrane to form pore through which cell contents leak out. Staphylococci: Staphylococcus aureus (S. aureus) Clinical picture Clinical manifestations caused by S. aureus are divided into two groups: Staphylococcus aureus: Pyogenic Diseases 1. Skin & soft tissue infections Abscess, impetigo, furuncles, carbuncles Abscess on foot. Note central raised area of whitish pus surrounded by erythema. An abscess is the classic lesion caused by Staphylococcus aureus. (Reproduced with Impetigo. Lesions of impetigo are crops of vesicles with a “honey- colored” crust. Impetigo is caused by either Staphylococcus aureus or Carbuncle. A carbuncle is a multiheaded abscess often located on the back permission from Wolff K, Johnson R eds. Fitzpatrick’s Color Folliculitis. Note the multiple, small pustules on the chin and neck. Staphylococcus aureus is of the neck. Note drop of yellowish pus near the center of the lesion. Streptococcus pyogenes. (Reproduced with permission from Wolff K, the most common cause of folliculitis. (Reproduced with permission from Wolff K, Goldsmith Carbuncles are caused by Staphylococcus aureus. (Reproduced with Atlas & Synopsis of Clinical Dermatology. 6th ed. New Johnson R eds. Fitzpatrick’s Color Atlas & Synopsis of Clinical LA, Katz SI, et al eds. Fitzpatrick’s Dermatology in General Medicine. 7th ed. New York, NY: permission from Wolff K, Johnson R eds. Fitzpatrick’s Color Atlas & Synopsis York, NY: McGraw-Hill; 2009.) Dermatology. 6th ed. New York, NY: McGraw-Hill; 2009.) McGraw-Hill; 2008, pg 1699.) of Clinical Dermatology. 6th ed. New York, NY: McGraw-Hill; 2009.) Staphylococci: Staphylococcus aureus (S. aureus) Clinical picture Staphylococcus aureus: Pyogenic Diseases 1. Skin & soft tissue infections: Impetigo Non-bullous Impetigo Painless, nonpruritic, papular/pustular lesions with serous oozing that dry & form characteristic honey- colored crusts (without vesicles) on face Bullous Impetigo Vesicles that grow to form large flaccid bullae filled with clear yellow fluid, which rupture & form thin brown crusts, on trunk & upper extremities. Exfoliative toxin A is the most common cause Staphylococci: Staphylococcus aureus (S. aureus) Clinical picture Staphylococcus aureus: Pyogenic Diseases 2. Septicemia (sepsis): from wound infection or intravenous drug abuse 3. Endocarditis: on normal or prosthetic heart valves 4. Osteomyelitis & septic arthritis - Hematogenous spread from distant infected focus - Introduced locally at the wound site. 5. Postsurgical wound infections 6. Pneumonia: postoperative or after viral respiratory infection (influenza) 7. Conjunctivitis 8. Metastatic Abscesses* *S. aureus circulates in the bloodstream (bacteremia). These abscesses occur by spread of bacteria from original site of infection, often in skin. It can affect any organ. Staphylococci: Staphylococcus aureus (S. aureus) Clinical picture Staphylococcus aureus: Toxin-Mediated Diseases (1) Food poisoning (gastroenteritis) Ingestion of performed enterotoxin in foods Short incubation period (1-8 hours) (rapid onset of symptoms) Vomiting is more prominent than diarrhea. (2) Toxic shock syndrome Fever, hypotension, diffuse, macular, sunburn-like rash that goes on to desquamate Involvement of 3 or more organs: liver, kidney, gastrointestinal tract, central nervous system, muscle, or blood. Staphylococci: Staphylococcus aureus (S. aureus) Clinical picture Staphylococcus aureus: Toxin-Mediated Diseases (3) Scalded skin syndrome (young children