Medical Microbiology Lecture 1 - Gram Positive Cocci PDF

Medical Microbiology Lecture 1 Gram positive cocci  ‫رؤيــــــــــــة الكليـــــــــــــة‬ ‫الريادة محلياً واقليمياً ودولياً لالرتقاء بصحة االنسان من خالل استخدام االبتكارات فى‬ ‫مجال التعليم والبحوث العلمية والممارسات التطبيقية‪.‬...

Medical Microbiology Lecture 1 Gram positive cocci  ‫رؤيــــــــــــة الكليـــــــــــــة‬ ‫الريادة محلياً واقليمياً ودولياً لالرتقاء بصحة االنسان من خالل استخدام االبتكارات فى‬ ‫مجال التعليم والبحوث العلمية والممارسات التطبيقية‪.‬‬ ‫رســـــــــــــــالة الكليــــــــــــة‬ ‫توفير أفضل الممارسات في مجال التعليم والتعلم والتدريب وإستمرارية خلق فرص‬ ‫للطالب والخريجين بإبتكار ونشر وتطبيق المعرفة الحديثة المرتكزة على البحوث‬ ‫والتطبيقات في العلوم الصيدلية واإلكلينيكية واإلجتماعية للنهوض بالصحة‬ Week Course Topics Key elements Lect. 1: Introductory host-parasite relationship-commensalism and parasitism 1-1-2.1, 1-1-2.2,1-1-4. W1 Lab. 1: Lab-safety and orientation Lect. 2: Bacterial classification, Gram(+) Staphylococci & Streptococci, & pneumococcus 1-1-2 , 1-1-4,1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-3, 3-1- W2 Lab. 2: Microscopic, BRs,& cultures characters of Staphylococci, Streptococci,& Pneumococcus 2, 3-1-3, 3-1-4. Lect. 3: Gram (+) Cocci-Enterococci & Gram (-) cocci Neisseria menigitidis, N.gonorrhoeae,& Moraxella spp.&Acinetobacter 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W3 spp. 2, 3-1-3, 3-1-4. Lab 3: Microscopic, BRs,& cultures characteristics Lect. 4: The acid fast Mycobacterium-TB, MOTT& M.leprae, Nocardia spp. & ,Actinomyces Israeli (Actinomycosis) & Gram(-) 1-1-2, 1-1-4,1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W4 Fastidious: Hemophilus (HACEK) & Bordetella spp.& Brucella spp 2, 3-1-3, 3-1-4, 4-3-2. Lab. 4: Microscopic, BRs & cultures characteristics + Periodical-1 Lect. 5: The Gram (+) None-spore forming bacilli-Corynebacterium, Listeria, and & Lactobacilli, and Erysipelothrix. The Gram 1-1-2, 1-1-4,1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W5 (+) spore forming Bacilli (aerobic) 2, 3-1-3, 3-1-4. Lab. 5: Microscopic, BRs,& cultures characteristics Lect. 6 Gram (+) spore forming Clostridia (anaerobic) & other anaerobes-Bacteroides (and Peptococcus & 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W6 Propionibacterium), The microaerophilic fastidious- Gram (-) curved rods, Helicobacter & Campylobacter spp. 2, 3-1-3, 3-1-4. Lab. 6: Lab diagnosis -antigenicity Lect. 7 The Gram (-) Enterobacteriaceae family: the LF: E coli –Klebseilla,Enterobacter, Serratia (Coliform bacilli) & NLF: 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W7 Shigella spp., Salmonella spp., Proteus spp. 2, 3-1-3, 3-1-4, 4-3-2 Lab. 7: Microscopic, BRs, & cultures characteristics. Lect. 8 The facultative anaerobes Vibrio cholera O1 gp &O139gp & V. parahemolyticus, vulnificus, and Non glucose 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W8 fermenters: Pseudomonas aeruginosa, Acinetobacter, Xanthomonas maltophilia & Ps. cepacia & putida 2, 3-1-3, 3-1-4. Lab. 8: Microscopic, BRs & cultures characteristics + Periodical 2 Lect.9: Gram -ve Rods zoonotic bacteria (Yersinia spp. Brucella, Pasteurella, Francisella, & the environmental 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- Legionella pneumophila). 2, 3-1-3, 3-1-4. W9 Lab.9- Microscopic, BRs,& cultures characteristics Lect. 10: The spirochetes (Treponema, Borrelia & Leptospira, & The Wall-less Mycoplasma spp., and intracellular bacteria: 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W10 Chlamydia and Rickettsia spp. plus Ecto-parasites (Scabies and human louse). 2, 3-1-3, 3-1-4. Lab. 10: Microscopic, BRs & cultures characteristics. Lect. 11: Mycology (superficial, cutaneous, Systemic and opportunistic fungal infection) 1-1-2, 1-1-4,1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W11 Lab. 11: Yeasts & filamentous fungi-microscopic exam. 2, 3-1-3, 3-1-4. Lect. 12: The DNA viruses (Smallpox) –Parvo, Papova HPV, Herpes and Hepatitis viruses 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-4, 3-1- W12 Lab. 12: Viruses Lab diagnosis. 2, 3-1-3, 3-1-4, 4-3-2. + Periodical-3 Lect. 13 The RNA viruses: Rhinoviruses- Corona viruses-Influenza/Parainfluenza-Mumps-RSV-Measles (HIV, Rabies, Picorna- 1-1-2, 1-1-4, 1-1-7, 1-1-8, 2-3-2, 2-3-3, 2-5-3, 3-1- W13 Polio-virus- & ROTA & Norwalk viruses) and Rhabdo Rabies /viruses. 2, 3-1-3, 3-1-4, 4-2-2. Overall Aims of this lecture 1-1-1.1- Describe the classification, morphology, and physiology of different categories of microorganisms. 1-1-1.2- Identify common infections and infectious diseases (etiology, clinical manifestation and routes of transmission). 1-1-2- Use proper medical and pharmaceutical terms and abbreviations in pharmacy practice. 1-1-6- Articulate knowledge of principles of basic medical sciences to understand the rational and proper pharmacotherapeutic approaches of different medical problems 2-3-1- Handle and dispose chemical and biological specimens according legal and ethical guidelines. 2-3-2- Apply the laboratory safety instructions and regulations. 2-5-3- Retrieve, analyze, assess and interpret experimental results, microbiological, pathological laboratory records. 3-1-2- Use the principles of medical microbiology to choose and evaluate suitable methods of infection control of infectious bacterial and mycobacterial diseases. 3-1-3- Employ different laboratory tests for investigation of bacterial and mycobacterial infectious diseases and estimate the microbial growth. 3-1-4- Select proper, safe and effective lines of treatment and prevention of different bacterial and mycobacterial diseases.  Staphylococci They are spherical cocci, arranged characteristically in grape-like clusters. They are non sporing, nonmotile and usually non capsulate except for rare strain Species Species of staphylococci are initially differentiated by the coagulase test and are classified into two groups: coagulase-positive and coagulase-negative staphylococci. Coagulase-positive staphylococci: Staphylococcus aureus Coagulase-negative staphylococci (CNS): S. epidermidis and S. saprophyticus. Resistance S. aureus and the other Micrococcaceae are among the hardiest of the non sporing bacteria. They retain their viability for 3–6 months. Most strains grow in the presence of 10% NaCl.  Cell Surface Proteins Protein A: is a group-specific antigen unique to S. aureus. Protein A binds IgG molecules, nonspecifically, through Fc region leaving specific Fab sites free to combine with specific antigen. When suspension of such sensitized cells is treated with homologous (test) antigen, the antigen combines with free Fab sites of IgG attached to staphylococcal cells.  Toxins and Enzymes: They are the virulence factors. A. Toxins 1. Cytolytic Toxins i. Alpha (a) hemolysin: is the most important. ii. Beta (b) hemolysin: kills experimental animals only when injected in large doses. iii. Gamma (γ) hemolysin, Delta (d) hemolysin, Leukocidin. 2. Enterotoxins This toxin is responsible for the manifestations of staphylococcal food poisoning nausea, The toxin is believed to act directly on the autonomic nervous system to cause the illness, rather than on the gastrointestinal mucosa 3. Toxic Shock Syndrome Toxin-I (TSTT-1) a severe and often fatal disorder characterized by multiple organ dysfunction. 4. Epidermolytic Toxins (Exfoliative Toxins) This is responsible for the ‘staphylococcal scalded skin syndrome’ (SSSS). SSSS is seen mostly in young children and only rarely in older children and adults. B. Extracellular Enzymes Staph. aureus produces a number of enzymes such as coagulase catalase, hyaluronidase, fibrinolysin, lipases, nucleases and penicillinase. Coagulase: Coagulase test is the standard criterion for the identification of Staph. aureus isolates.  Epidemiology Staphylococcus is a normal component of man’s indigenous microflora and is carried asymptomatically in several body sites.  About 10–30% healthy persons carry staphylococci in the nose.  Vaginal carriage is about 5–10%, which rises greatly during menses, a factor relevant in the pathogenesis of TSS related to menstruation. Staphylococci are a common cause of postoperative wound infection and other hospital infections.. Staphylococcal Diseases S. aureus causes disease through the direct invasion and destruction of tissue or through the production of toxin. A. Cutaneous infections: These include wound and burn infection, pustules, furuncles or boils carbuncles, impetigo. B. Deep infections: These include osteomyelitis, periostitis, tonsillitis, pharyngitis, sinusitis, bronchopneumonia,septicemia, meningitis, endocarditis, breast abscess, renal abscess and abscesses in other organs. C. Toxin-mediated diseases i. Food poisoning: Staphylococcal food poisoning may follow 2–6 hours after the ingestion of food in which S. aureus has multiplied and formed enterotoxin. ii. Toxic shock syndrome (TSS): Most cases occur in menstruating women who use tampons. However, non menstruating women, children, and men with boils or staphylococcal infections of wounds can also have TSS. the syndrome occurs in other infections of the skin, mucosa and other sites and in some surgical wounds. iii. Exfoliative diseases: These lesions are produced by the strains of S. aureus which produce epidermolytic toxins. This toxin is responsible for the ‘staphylococcal scalded skin syndrome’ (SSSS), exfoliative skin diseases in which the outer layer of epidermis gets separated from the underlying tissues. SSSS is seen mostly in young children and only rarely in older children and adults.  o Coagulase-negative Staphylococci are commonly found on the surface of healthy persons. They are opportunistic pathogens that cause infection in debilitated or compromised patients. Various species are Staph. epidermidis, Staph. Saprophyticus o Staphylococcus epidermidis Staph. epidermidis is invariably present on normal human skin. It is nonpathogenic ordinarily but can cause disease when the host defenses are breached. S. epidermidis has a distinct predilection for foreign bodies, such as artificial heart valves, indwelling intravascular catheters and hip prostheses. Clinical Infection Stitch abscesses; endocarditis of native and prosthetic valves; intravenous catheter infections etc. o Staphylococcus saprophyticus S. saprophyticus is a common cause of urinary tract infections in sexually active young women. It may also cause urethritis in men and women, catheter associated urinary tract infections, etc.  This coagulase-negative Staphylococcus can be distinguished from S. epidermidis by its resistance to novobiocin and by its failure to ferment glucose anaerobically.  It is nonhemolytic and does not contain protein A.   Methicillin-resistant Staphylococcus aureus (MRSA) methicillin resistant strains of Staph. aureus (MRSA) became common, which were resistant not merely to penicillin, but also to all other beta lactam antibiotics and many others besides. Isolates that are resistant have been traditionally termed methicillin-resistant staphylococci, with S. aureus being called MRSA and S. epidermidis referred to as MRSE. When any staphylococcus isolated is identified as being resistant to methicillin, this implies that it is also resistant to nafcillin and oxacillin and to all β-lactam antibiotics, including the cephalosporins. MRSA is also becoming more common in the community, especially in long-stay institutions.  Micrococci Micrococci are catalase-positive, gram-positive, coagulase-negative and usually oxidase-positive. They may occasionally colonize the skin or mucous membrane of humans, but they are only rarely associated with infections. Only two species, Micrococcus luteus and Micrococcus lylae, remain in the genus. Treatment Benzyl penicillin is the most effective antibiotic, if the strain is sensitive but most clinical isolates of S.aureus are resistant to benzyl penicillin due to production of beta lactamase. Cloxacillin, oxacillin, flucloxacillin and methicillin are penicillinase resistant penicillins. Methicillin-resistant Staphylococcus aureus (MRSA) are also resistant to other penicillins and cephalosporins. Glycopeptides (vancomycin or teicoplanin) are the agents of choice in the treatment of systemic infection Control 1. The focus of infection (e.g. abscess) must be identified and drained. 2. Treatment is symptomatic for patients with food poisoning. 3. Proper cleansing of wounds and use of disinfectant. 4. Thorough hand washing and covering of exposed skin helps medical personnel prevent infection or spread to other patients. 5. Asymptomatic nasopharyngeal carriage— the use of chemoprophylaxis consisting of vancomycin and rifampin to prevent spread of oxacillin-resistant organisms Staphylococcus aureus Virulence factors Virulence factors of S aureus –mechanisms of Immune Evasion Proteins Protein A Binds Fc in IgG to escape opsonization and phagocytosis Coagulase Fibrin formation around the bacteria to sequester it from phagocytes Hemolysins Lyse RBCs, neutrophils, macrophages, and platelets Leukocidins Destroy WBCs Penicillinase Secreted b-lactamase against natural penicillins Penicillin-binding -Cell wall peptidoglycan formation- is-Inhibited by penicillin. proteins -Some strains of S. aureus have new penicillin-binding proteins ( PBP2’) that are resistant (MRSA) to (transpeptidase) All Beta Lactam antibiotics : penicillins and cephalosporins,& MonoBactam- & Carbapenicillins. (B) Tissue Invasion Proteins Hyaluronidase- Break down connective tissue & DNA act as spreading factors upon necessity DNase Staphylokinase Lyses fibrin clots Lipase Vs. lipids (S. aureus colonize sebaceous glands) Protease Vs. proteins (C) Exotoxins Exfoliatin Causes skin to slough off (scalded skin syndrome) Enterotoxin Heat-stable, food poisoning toxin (100 C stable 30 minutes (intoxication-food) -Analogous to the pyrogenic toxin produced by Lancefield group A beta-hemolytic streptococci, but far more deadly (20-60% Mr) 50% bacteremia or 50% fasciitis. The TSST-1 is Found in 20% of S. aureaus Toxic Shock isolates. -Called superantigens and bind to the MHC class II molecules on antigen presenting cells (e.g., Syndrome Toxin macrophages). The toxin-MHC II complex causes a massive T cell response and out-storming of (TSST-1) cytokines, resulting in TSS described above. Note : (QQs between S aureus & Strept pyogenes (GAS) mortality due to TSS Summary of Staphylococcus aureus-Features: 1. Catalase-positive, coagulase or DNase-positive, beta-hemolytic, Gram-positive coccus found in grapelike clusters. (Halo-duric /Selective medium is MSA medium. 2. Human reservoir, it colonizes mucosa (40% of adults are carriers, in nose). Increased cutaneous numbers are found on ‘‘needle users.’’ drug up-useers Transmitted by direct contact, aerosols and fomites/often from health care workers Diseases: 1. Causes skin (boils, abscesses, furuncles, carbuncles ,sty, impetigo, & surgical infections, acute endocarditis, toxic shock syndrome, septicaemias, scalded skin syndrome, food poisoning, infective arthritis, it causes ( 80%) of acute osteomyelitis,(post/influenza pneumonia, & pneumonia in very young cystic fibrosis (CF) children-patients. Pathogenesis: a. Hemolysins/ Leucocidins and other WBCs-cytolytic toxins. b. Coagulase activates fibrinogen to self-fibrin coating S. aureus, slowing clearance. c. Fibrinogen-binding allows S. aureus to bind to heart tissue/ causing damage(endocarditis). d. Protein A on its surface binds the Fc portion of antibody, reducing opsonization. e. Teichoic acids (lipoteichoic and cell-wall–bound) play a role in adherence and, upon cell lysis released lipoteichoic acids with peptidoglycan trigger shock via the same pathways as endotoxin. Lab ID: positive catalase and coagulase tests; beta-hemolytic; halo-duric (tolerate salts) (7%) (No plasmolysis) and ferments mannitol-in selective MSA((mannitol salt agar positive). Treatment: required susceptibility testing: it is (S) to oxacillin but -all hospital strains Must be tested for methicillin resistance (MRSA) on MHA at 30 not 37 C.because modified PPP2’ is active at 30C &(+) patients must be room isolated and treated with vancomycin.  Streptococci The genus Streptococcus comprises a large and biologically diverse group of gram-positive cocci that grow in pairs or chains. They are normal flora of humans and animals. They inhabit various sites, notably the upper respiratory tract, and live harmlessly as commensals. Classification  Hemolytic Activity The aerobic and facultative anaerobic streptococci are classified based on their hemolytic properties. A. Alpha-hemolytic (α) Streptococci They produce a zone of partial hemolysis with a greenish discoloration around the colonies on blood agar. The streptococci producing a-hemolysis are also known as viridans streptococci. B. Beta (β) Hemolytic Streptococci They produce a sharply defined, clear, colorless zone of hemolysis (2–4 mm wide) around the colony, caused by complete lysis of red blood cells in the agar medium induced by bacterial hemolysins. C. Gamma (γ) or Non-hemolytic Streptococci They produce no hemolysis on blood agar. Enterococcus faecalis is an important organism of this group.  Serological Properties Lancefield Grouping The work of Rebecca Lancefield in 1933 laid the groundwork for the serological classification of β - hemolytic streptococci. based on group specific carbohydrate (C) antigens in the cell wall, β -hemolytic streptococci are divided into 21 serological groups from A to W (without I and J). These are known as Lancefield groups. Groups A, B, C, D, and G are most found associated with human infections.  Type-specific Antigens Several proteins antigens have been identified in the outer layer of the cell wall.  Streptococcus pyogenes can be typed, based on the surface proteins M, T and R. i. M protein: The M protein is the most important of these three. It acts as virulence factor by inhibiting phagocytosis. ii. T protein iii. R protein Some strains of S. pyogenes. R protein has no relation to virulence. Toxins and Enzymes Str. pyogenes forms several exotoxins and enzymes which contribute to its virulence. A. Toxins 1. Hemolysins Two hemolytic and cytolytic toxins—streptolysin O (SLO) and streptolysin S (SLS)—are produced by most strains of group A streptococci and many strains of groups C and G. i. Streptolysin O Streptolysin O is so called because it is oxygen labile hemolysin. cytolytic and capable of lysing erythrocytes, leukocytes, platelets ii. Streptolysin S (SLS) Streptolysin S is an oxygen-stable. It is protein but nonantigenic. It is cell bound hemolysin that can lyse erythrocytes, leukocytes, and platelets. 2. Pyrogenic Exotoxins (Erythrogenic, Dick, Scarlatinal Toxin) The primary effect of the toxin is induction of fever and so it was renamed streptococcal pyrogenic exotoxin (SPE). SPEs act as ‘superantigens’ interacting with both macrophages and helper T cells with the release of inflammatory cytokines. These cytokines cause important effects, including the fever, shock, the organ failure and the rash observed in patients with scarlet fever. B. Enzymes 1. Deoxyribonucleases (streptodornase DNAase) These enzymes can depolymerize the highly viscous DNA which accumulates in thick pus as a result of disintegration of polymorphonuclear leukocytes. 2. Streptokinase (Fibrinolysin) Streptokinase, also known as fibrinolysin, is another spreading factor. 3. Hyaluronidase Hyaluronidase splits hyaluronic acid, and might favor the spread of streptococcal infection along the intercellular spaces. 4. Proteinase It destroys several proteins formed by the Streptococcus itself. Pathogenesis Acute diseases associated with Streptococcus pyogenes occur in the respiratory tract, bloodstream, the skin. A. Suppurative Streptococcal Disease 1. Respiratory Infections i. Sore throat is the most common of streptococcal disease. It may be localized as tonsillitis or may involve the pharynx more diffusely (pharyngitis). ii. Scarlet fever: It is a complication of streptococcal pharyngitis that occurs when the infecting strain is lysogenized by a temperate bacteriophage that stimulates production of a pyrogenic exotoxin. iii. Suppurative complications: The infection may spread to the surrounding tissues which may cause suppurative complications of streptococcal pharyngitis, such as peritonsillar or retropharyngeal abscess, otitis media, suppurative adenitis and disseminated infections to brain, heart, bone, and joints. 2. Skin and Soft Tissue Infections. i. Erysipelas: Erysipelas is an acute infection of the skin. ii. Pyoderma (impetigo): is seen primarily in young children. iii. Cellulitis: Typically involves the skin and deeper subcutaneous tissues. iv. Necrotizing fascitis (Streptococcal gangrene). v. Streptococcal Toxic Shock Syndrome. 3. Other Suppurative Infections a. Puerperal sepsis: Streptococcal puerperal sepsis used to take a heavy toll of life before antibiotics became available. b. Abscesses in internal organs, such as the brain, lungs, liver and kidneys. c. Septicemia. B. Nonsuppurative Sequelae These complications ensue 1–5 weeks after the acute infection. 1. Acute Rheumatic Fever (ARF) Rheumatic fever is a nonsuppurative inflammatory reaction Typically, rheumatic fever follows persistent or repeated streptococcal throat infection with a strong antibody response. The disease is caused by specific M types. Pathogenesis The disease is autoimmune in nature and is believed to result from the production of antibodies and T lymphocytes induced by cross reactive components of the bacteria and host tissues. Antibodies produced in response to the streptococcal infection could cross-react with myocardial and heart value tissues, causing cellular destruction. 2. Acute Poststreptococcal Glomerulonephritis (AGN) In contrast to rheumatic fever, which occurs only after pharyngitis, AGN may be seen after either a pharyngeal or a cutaneous infection. Specific nephritogenic strains of group A streptococci are associated with this disease. AGN is most often seen in children Pathogenesis 1. Immune complex deposition in the glomeruli. 2. Reaction of antibodies cross-reactive with streptococcal and glomerular antigen. 3. Alterations of glomerular tissues by streptococcal products such as streptokinase. 4. Direct complement activation by streptococcal components that have a direct affinity for glomerular tissues. Treatment S. pyogenes is very sensitive to penicillin. Erythromycin or an oral cephalosporin can be used in patients with a history of penicillin allergy. Adequate treatment during acute infection prevents the complications of acute rhematic fever. Prophylaxis Patients with a history of rheumatic fever require long-term antibiotic prophylaxis to prevent recurrence of the disease. Those persons who have recovered from ARF are given oral penicillin for many years to prevent recurrence. o Group B Streptococci: Streptococcus agalactiae Streptococcus agalactiae belongs to Lancefield group B. It has become the leading cause of neonatal infections Strept. agalactiae is found in the vaginocervical tract of female carriers. Transmission occurs from an infected mother to her infant at birth. Clinical Diseases 1. Infection in the neonate A. Early-onset disease : It develops during the first week of life and disease is characterized by bacteremia, pneumonia, or meningitis and is often fatal. B. Late-onset disease: It develops between second and twelfth weeks of life. The predominant manifestation is bacteremia with meningitis, but septic arthritis. 2. Infections in the adult: Puerperal sepsis, pneumonia endometritis, urinary tract infection, wound infection, and bacteremia. o Group C Streptococci Streptococci of this group are predominantly animal pathogens o Group D Streptococci Until the mid-1980s, the group D streptococci were divided into the two groups: 1. Enterococcus group (enterococci or fecal streptococci) which have been reclassified as a separate genus called Enterococcus. 2. Non enterococcal group, for example, Str. bovis, Str. equinus.   Enterococcus Enterococcus faecalis (“pertaining to feces”) is the Enterococcus most often isolated from human sources.  Characteristics of Enterococci The enterococci are gram-positive cocci typically arranged in pairs and short chains. The cocci are facultatively anaerobic  Identification E. faecalis can be identified by its ability to ferment mannitol, sucrose, sorbitol and aesculin, and to grow on tellurite blood agar producing black colonies with gas production.  Clinical Infections The enterococci inhabit the gastrointestinal tract and the genitourinary tract in humans and other animals. Enterococci are frequent causes of nosocomial infections and may cause urinary tract infection, bacteremia, infective endocarditis, biliary tract infection, intra-abdominal abscess, peritonitis and wound infection.  Treatment Most strains of enterococci are resistant to penicillin. They are also resistant to sulfonamides. Recently they have developed resistance to newer penicillins and cephalosporins, streptomycin and gentamicin.  o Viridans streptococci The viridans streptococci are commensals of mouth and upper respiratory tract. The viridans group of streptococci are a heterogeneous collection of α-hemolytic and nonhemolytic streptococci. The term viridis means “green.” because many of these bacteria produce a green pigment on blood agar media. Classification The current classification assigns streptococci species in the viridans group to one of the four groups: 1. Anginosus group (S. anginosus, S. constellatus, and S, intermedius) 2. Mitis group (S. sanguis, S. mitis, etc.) 3. Mutans group (S. mutans, etc.) 4. Salivarius groups (S. salivarius). Clinical Infections The viridans streptococci are opportunistic pathogens but can, on occasion, cause disease. 1. Dental Caries S. mutans is the principal cause of dental caries (tooth decay). 2. Subacute Endocarditis Viridans streptococci are the most common cause of subacute bacterial endocarditis. About two thirds of the viridans-associated cases are due to S. sanguis and S. mutans. Transient bacteremia is associated with endocarditis. o Pneumococcus (Streptococcus Pneumoniae)  Virulence Factors 1. Capsule: The capsule is antiphagocytic, inhibiting complement deposition and phagocytosis. Noncapsulated strains are avirulent. 2. IgAI protease: that specifically cleaves human IgA. 3. Pneumolysin: A cytotoxin like the streptolysin O in S. pyogenes  Pathogenesis 1. Pneumonia i. Lobar pneumonia: In adults, types 1–8 are responsible for about 75% of cases ii. Bronchopneumonia: It is almost always a secondary infection. 2. Acute Exacerbations in Chronic Bronchitis 3. Meningitis: it is among the leading causes of bacterial meningitis. 4. Bacteremia: occurs in 25–30% of patients with pneumococcal pneumonia and in more than 80% of patients with meningitis. 5. Other Infections: pericarditis, otitis media, sinusitis, conjunctivitis, suppurative arthritis and peritonitis Prophylaxis Immunity is type-specific and associated with antibody to the capsular polysaccharide. The existence of some 90 serotypes makes a complete polyvalent vaccine impracticable. The current vaccine contains 23 different capsular polysaccharides which is stated to give 80–90% protection. Vaccination is contraindicated in young children and elderly with lymphoreticular malignancies and immunosuppressive therapy. Treatment  Penicillin is the drug of choice for susceptible strains, although resistance is increasingly common. Cephalosporins, erythromycin, chloramphenicol, or vancomycin are used for patients allergic to penicillin or for treatment of penicillin-resistant strains. THANK YOU