Mkgrady8 Host Streptococci And Enterococci

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streptococci general features

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the streptococci are gram positive cocci characteristically growing in chains (greek for a necklace of berries) or as dipococci; cause a wide variety of diseases including strep throat (acute pharyngitis, sore throat), rheumatic fever, scarlet fever, acute glomerulonephritis (AGN), pneumonia, tooth decay, endocarditis, and other diseases like necrotizing fasciitis

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classification schemes for the streptococci based on

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serological properties (Lancefield grouping)- specific cell wall antigens (carbohydrates)/group specific antigens; hemolytic (red blood cell bursting) patters= alpha (incomplete hemolysis), beta (complete hemolysis), or gamma (no hemolysis); biochemical (physiologic) properties- susceptibility to optochin, ability to grow in the presence of bile, and ability to withstand high salt concentration

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hemolytic reactions observed on 5% sheep blood agar plates (what do you see with alpha, beta, and gamma)

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alpha hemolysis see green discoloration of agar around colony due to incomplete hemolysis (viridans streptococci and streptococcus pneumoniae); beta hemolysis see clear zones around colony due to complete destruction of red blood cells (streptolysin O inactivated by atmospheric oxygen anaerobic environment, streptolysin S- oxygen stable)(S. pyogenes and S. agalactiae); gamma hemolysis see no hemolysis either within the agar or on the surface (S. bovis and enterococcus faecalis)

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streptococcus pyogenes (aka group A strep or GAS) physiology and structure

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cellular antigens; group specific carbohydrate (Lancefield group A antigen) N acetylglucosamine and rhamnose, outer hyaluronic acid capsular antigenically indistiguishable from hyaluronic acid in mammalian connective tissue, M protein is the major type specific protein associated with virulent strains; M like surface proteins, lipoteichoic acid, and F proteins

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group specific carbohydrate (Lancefield group A antigen) N acetylglucosamine and rhamnose

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used for classification and antibodies to the group specific carbohydrate are not protective in man

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outer hyaluronic acid capsular antigenically indistinguishable from hyaluronic acid in mammalian connective tissue

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interferes with phagocytosis and encapsulated strains cause severe systemic infections

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M protein is the major type specific protein associated with virulent strains

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anchored in the cell membrane, M protein protrudes above the cell surface as fimbriae; class I M proteins share exposed antigens, RHEUMATIC FEVER IS CAUSED ONLY BY STRAINS WITH CLASS I M PROTEINS; class II M proteins do not have shared antigens; interferes with phagocytosis by blocking the binding of the C3b complement component; anti-M protein antibody is protective

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M like surface proteins

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also encoded by the emm gene super family; interfere with phagocytosis by binding either Fc fragment of antibody (just like what? protein A of staphylococci) of fibronectin

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lipoteichoic acid and F protein bind

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to fibronectin which is present on host cell surface; together these proteins facilitate binding to host cell (trying to get taken inside to invade); initial weak adherence involves teichoic acid; subsequent adherence involves M like and F proteins; M and F proteins also mediate invasion of epithelial cells; this also helps them avoid being phagocytosed because they are in a host cell avoiding detection

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streptococcus pyogenes toxins and enzymes

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streptococcal pyrogenic exotoxins (Spe) or erythrogenic toxin; streptolysin S; streptolysin O; streptokinase (A and B); deoxyribonucleases (DNases A-D)

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streptococcal pyrogenic exotoxins (Spe) or erythrogenic toxin

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produced by LYSOGENIZED STRAINS of streptococci; FOUR immunologically distinct heat labile toxins; toxins function as SUPERANTIGENS which results in the enhanced release of pro inflammatory cytokines; responsible for many of the clinical manifestations of SEVERE streptococcal diseases

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streptolysin S

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oxygen stable, responsible for hemolysis; non immunogenic (cannot be used as a marker to identify this bac), cell bound hemolysin; lyses erythrocytes, leukocytes, and platelets

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streptolysin O

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oxygen labile hemolysin (needs to be in low O2 conditions to be active); irreversibly inhibited by cholesterol in skin lipid; antibodies to streptolysin O (ASO) useful for documenting recent streptococcal infection (so can use this to identify the bac)

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streptokinase (A and B)

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mediate cleavage of plasminogen releasing plasmin which cleaves fibrin and fibrinogen and lyse blood clots; facilitate the spread of S pyogenes in infected tissues

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deoxyribonucleases (DNases A-D)

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depolymerize free DNA in the pus reducing viscosity of the abscess materials; facilitate the spread of S. pyogenes; they are lysing cells right? so there is a bunch of vine like DNA floating around and they use a DNase to cut through it; CAN DETECT STREP PYOGENES BY DETECTING ANTIBODIES FOR DNASE B AND STREPTOLYSIN O

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streptococcus pyogenes epidemiology

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recently acquired strains may transiently (asymtomatically) colonize the upper respiratory tract; isolation of the bacteria in a pt with pharngitis is significant; person to person spread by either respiratory droplets (pharyngitis) or through skin breaks by direct contact with infected person or fomite; S. pyogenes pharyngitis is primarily a disease of children between 5-15 yrs old; soft tissue infection is usually proceeded by initial skin colonization; organisms are introduced into superficial or deep tissues through a break in the skin

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streptococcal pyogenes clinical diseases: suppurative infections

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pharyngitis; scarlet fever (a complication of pharyngitis); pyoderma or impetigo; erysipelas; cellulitis; necrotizing fasciitis; streptococcal toxic shock syndrome (multisystem toxicity); bacteremia

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pharyngitis

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abrupt onset of sore throat, fever, and malaise; posterior pharynx may appear erythematous with exudates; children 5-15 are at highest risk for this

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scarlet fever

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a complication of pharyngitis; caused by S. pygenes strains that are lydogenized with bacteriophage carrying the gene for the pyrogenic exotoxin (Spe); within 1-2 days of initial pharyngitis symptoms a diffuse erythematous rash appears on the chest and spreads to the extremities; a yellowish white coating covers the tongue and is later shed revealing a red raw surface underneath (strawberry tongue); the rash disappears within a few days and is followed by desquamation of the superficial skin layer; will NOT see rash on palms or soles

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pyoderma or impetigo

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a confined purulent infection of the skin primarily affects the exposed areas (face, arms, legs); vesicles develop and progress into pustules that later rupture and crust over (honey colored crust); regional lymph nodes may enlarge but systemic infection is uncommon; occurs primarily in children (2-5 yrs old) and people with poor hygeine during the summer moist months

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erysipelas

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an acute infection of the skin characterized by localized inflammation, enlargement of the lymph nodes, and signs of a systemic infection (chills, fever); the affected skin is typically raised and distinctly differentiated from the uninvolved skin; occurs in young children and older adults

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cellulitis

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involves skin and deeper subcutaneous tissues; no distinction between infected and uninfected skin; these features distinguish cellulitis from erysipelas

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necrotizing fasciitis

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streptococcal gangrene (still streptococcus pyogenes); flesh eating bacteria disease; occurs deep in the subcutaneous tissues and spreads along the fascial planes; characterized by extensive destruction of muscle and fat; bacteria reach the tissues through a break in the skin (minor cut, trauma, burn injury); initial cellulitis followed by development of bullae and gangrene (tissue necrosis associated with blood flow obstruction); hallmark of the disease includes toxicity, multi organ failure, and death; surgical debridement of the infected tissue is essential to halt progress of the infection

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streptococcal toxic shock syndrome

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multisystem toxicity starts as soft tissue inflammation at the site of the infection; progresses to shock and organ failure; similar to staphylococcal toxic shock syndrome; pts with streptococcal toxic shock syndrome are bacteremic and many have necrotizing fasciitis; pts at an increased risk of streptococcal toxic shock syndrome are HIV infected individuals, cancer pts, pts with diabetes mellitus, intravenous drug abusers, pts with soft tissue infection, and those who abuse alcohol; the production of exotoxins (particularly speA and speC) is a prominent feature of the disease

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bacteremia

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S. pyogenes is one of the most common beta hemolytic streptococci isolated in blood cultures; bacteremia rarely occurs in pts with pharyngitis, pyoderma, and erysipelas; however blood cultures are positive for pts with necrotizing fasciitis or toxic shock syndrome; the mortality rate in those pts reaches 40%

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streptococcus pyogenes clinical diseases: non suppurative diseases

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rheumatic fever and acute glomerulonephritis

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rheumatic fever

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a complication of S. pyogenes pharyngitis; anti streptococcal antibody also attacks heart proteins; characterized by inflammatory changes in the heart (pancarditis), joint, blood vessels, and subcutaneous tissues, class I M proteins; not associated with cutaneous streptococcal infections; most common in young school aged children; occurs primarily during the cooler months; occurs at a low rate in US but more common in developing countries

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acute glomerulonephritis

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associated with specific nephritogenic strains S. pyogenes- antibody antigen complexes; characterized by acute inflammation of the renal glomeruli with edema, hypertension, hematuria, and proteinuria; may occur following either pharyngeal or pyodermal streptococcal infection

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streptococcal pyogenes lab diagnosis using

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gram stain and microscopy; antigen detection; DNA amplification based tests (PCR); cultures; typing with antisera against group specific carbohydrate antigen (Lancefield group A); biochemical tests; antibody detection

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what do you see with gram stain and microscopy

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gram positive cocci in pairs and chains associated with leukocytes; USEFUL FOR SKIN AND SOFT TISSUE INFECTIONS(streptococci are not observed in gram strain of uninfected skin) BUT NOT FOR PHARYNGEAL INFECTIONS (streptococci are part of the normal oro-pharyngeal flora)

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what do you see with antigen detection

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immunological tests based on antibodies that react with group specific antigens in the cell wall; detect S. pyogenes in throat swab; rapid, inexpensive, and specific BUT NOT VERY SENSITIVE

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what do you see with DNA amplification based tests (PCR)

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high cost limits their use

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how do you do a culture for phyngitis

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throat swabs must be obtained from posterior oropharyns; swabs from the anterior areas of the mouth may be contaminated with other bacteria that inhibit the growth of S. pyogenes

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how do you do a culture for pyoderma (impetigo)

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to avoid super infection with staphylococci culture specimens should not be obtained from open draining skin pustules rather the material may be obtained from the base of the lesion

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how do you do a culture for necrotizing fasciitis

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organisms are readily recovered from tissues and blood cultures

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what biochemical tests would you do

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catalase negative; susceptible to bacitracin; L-pyrrolidonyl arylamidase (PYR) enzyme positive (hydrolyzes L-pyrrolidonyl-beta-naphthalamide releasing beta naphthylamine which in the presence of an indicator forms a red compound (in less than one minute)

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antibody detection

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antistreptolysin O test (ASO) is useful to confirm rheumatic fever or glomerulonephritis resulting from streptococcal pharyngitis; anti DNase B test is important to confirm glomerulonephritis associated with either pharyngitis or soft tissue infection

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streptococcus pyogenes treatment

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oral penicillin V or amoxicillin for pharyngitis; macrolide or cephalosporin for PCN allergic pts

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streptococcal pyogenes prevention

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to prevent rheumatic fever, antibiotic therapy must start within 10 days in pts with pharyngitis; for pts with a history of a rheumatic fever, antibiotic prophylaxis must be given before any procedure that may induce bacteremias (e.g. oral surgery); no antibiotic treatment or prophylaxis is recommended for pts with glomerulonephritis

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summary for streptococcus pyogenes (group A): biology, virulence, and disease

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rapidly growing gram positive cocci arranged in chains; group specific carbohydrate (A antigen) and type specific proteins (M protein) in cell wall; virulence determined by ability to avoid phagocytosis (mediated primarily by capsule, M and M like proteins, C5a peptidase), adhere to and invade host cells (M protein, lipoteichoic acid, F protein), and produce toxins (streptococcal pyrogenic exotoxins, streptolysin S, streptolysin O, streptokinase, DNases); responsible for suppurative diseases (pharyngitis, soft tissue infections, streptococcal toxic shock) and non suppurative diseases (rheymatic fever, glomerulonephritis)

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summary for streptococcus pyogenes (group A): epidemiology

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transient colonization in upper respiratory tract and skin surface with disease caused by recently acquired strains (before protective antibodies are produced); pharyngitis and soft tissue infections typically caused by strains with different M proteins; person to person spread by respiratory droplets (pharyngitis) or through breaks in skin after direct contact with infected person, fomite, or arthropod vector; individuals at higher risk for disease include children 5-15 yrs old (pharyngitis), children 2-5 yrs old with poor personal hygiene (pyoderma), pts with soft tissue infection (streptococcal toxic shock syndrome), pts with prior streptococcal pharyngitis (rheumatic fever, glomerulonephritis) or soft tissue infection (glomerulonephritis)

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summary for streptococcus pyogenes (group A): diagnosis

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microscopy is useful in soft tissue infections but not pharyngitis or nonsuppurative complications; direct tests for the group A antigen are useful for the diagnosis of streptococcal pharyngitis but negative results must be confirmed by culture or molecular assays; isolates identified by catalase (negative), positive PYR (L-pyrrolidonul arylamisae) reaction, susceptibility to bacitracin, and presence of group specific antigen (group A antigen) antistreptolysin O test is useful for confirming rheumatic fever or glomerulonephritis associated with streptococcal pharyngitis; anti DNase B test should be performed for glomerulonephritis associated with pharyngitis or soft tissue infections

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summary for streptococcus pyogenes (group A); treatment, prevention, and control

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PCN V or amoxicillin used to treat pharyngitis; oral cephalosporin or macrolide for PCN allergic pts; intravenous PCN plus clindamycin used for systemic infections; oropharyngeal carriage occurring after treatment can be re treated; treatment is not indicated for prolonged asymtomatic carriage because antibiotics disrupt normal protective flora; starting antibiotic therapy within 10 days in pts with pharyngitis prevents rheumatic fever; for pts with a history of rheumatic fever antibiotic prophylaxis is required before procedures (e.g. dental) that can induce bacteremias leading to endocarditis; for glomerulonephritis no specific antibiotic treatment or prophylaxis is indicated

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streptococcus agalactiae (aka group B streptococci or GBS): characterisitic growth on sheep blood agar and 3 serological markers

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large colonies with a narrow zone of beta hemolysis; 3= GROUP SPECIFIC CELL WALL POLYSACCHARIDE B ANTIGEN (LANCEFIELD GROUPING ANTIGEN), type specific capsular polysaccharide (9 types), and surface proteins (especially c protein or c antigen)

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streptococcus agalactiae: virulence

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the polysaccharide capsule interferes with phagocytosis until type specific antibodies develop; neonates with no maternal antibodies are at risk; sialic acid interferes with phagocytosis by inhibiting the activation of the complement pathway; REMEMBER VIRULENCE= CAPSULE AND SIALIC ACID AND THAT BABIES WITHOUT ANTIBODIES ARE AT RISK

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streptococcus agalactiae: immunity

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functional complement system (classical and alternative) is required to kill GBS); physiologically low complement in premature infants increases the risk of systemic infection

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streptococcus agalactiae: epidemiology

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neonates are at higher risk for infection if there is premature rupture of membranes, prolonged labor, preterm birth, or the mother is without type specific antibodies and has low complement levels; women with genital colonization are at risk for postpartum disease; men and non pregnant women with DM, cancer, or alcoholism are at increased risk for disease; S. agalactiae is the most common cause of septicemia and meningitis in new borns

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streptococcus agalactiae clinical diseases

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early onset neonatal disease; late onset neonatal disease; pregnant women; men and non pregnant women

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early onset neonatal disease

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acquired in utero or at birth; characterized by bacteremia, pneumonia, or meningitis; examination of cerebrospinal fluid is required because meningeal involvement may not be initially apparent; some infants who survive the meningitis develop blindness, deafness, or mental retardation

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late onset neonatal disease

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acquired from an exogenous source after birth (mother or another infant); characterized by bacteremia with meningitis

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pregnant women

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occurs during and immediately after pregnancy; postpartum endometriosis, wound infection, urinary tract infection

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men and non-pregnant women

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older people with debilitating conditions such as DM, cancer, or alcoholism; characterized by bacteremia, pneumonia, joint infection, soft tissue infection

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streptococcus agalactiae diagnosis

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microscopy= cerebrospinal fluid (meningitis), lower respiratory secretions (pneumonia), exudate (wound infection); antigen= less sensitive than microscopy; DNA= PCR; culture= selective broth with antibiotics added (LIM broth with collistin and nalidixic acid) to prevent the growth of other bacteria; recommended by the CDC to detect GBS in the vaginal secretions of women between 35-37 weeks of pregnancy

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streptococcus agalactiae: treatment

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PCN G is drug of choice; add aminoglycoside for pts with serious complications

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streptococcus agalactiae: prevention

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no vaccine is available; GBS positive mothers should be treated with PCN for at least 4 hrs before delivery to prevent GBS infection in neonate

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summary for streptococcus agalactiae (group B): biology, virulence, and disease

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rapidly growing gram positive cocci arranged in chains; group specific carbohydrates (B antigen) and type specific capsular carbohydrates (Ia, Ib, II-VII); virulence determined primarily by ability to avoid phagocytosis (mediated by capsule); responsible for neonatal disease (early onset and late onset disease with meningitis, pneumonia, bacteremia), infections in pregnant women (endometritis, wound infections, urinary tract infections), and other adults (bacteremia, pneumonia, bone and joint infections, skin and soft tissue infections); early onset disease acquired by neonates from mother during pregnancy or at time of birth

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summary for streptococcus agalactiae: epidemiology

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asymtomatic colonization of the upper respiratory tract and genitourinary tract; neonates are at higher risk for infection is there is premature rupture of membranes, prolonged labor, preterm birth, or disseminated maternal group B streptococcal disease, and mother is without type specific antibodies and has low complement levels; women with genital colonization are at risk for postpartum disease; men and nonpregnant women with DN, cancer, or alcoholism are at increased risk for disease; no seasonal incidence

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summary for streptococcus agalactiae (group B); diagnosis

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microscopy useful for meningitis (cerebral fluid), pneumonia (lower respiratory secretions), and wound infections (exudates); antigen tests are less than microscopy and should not be used; culture most sensitive test; a selective broth (i.e. LIM) is needed for optimal detection of vaginal carriage; polymerase chain reaction based assays to detect vaginal carriage in pregnant women are commercially available as sensitive as culture and rapid; isolates identified by demonstration of group specific cell wall carbohydrate or positive nucleic acid amplification test

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summary for streptococcus agalactiae (group B): treatment, prevention, and control

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PCN G is the drug of choice; empiric therapy with broad spectrum antibiotics (broad spectrum cephalosporin plus aminoglycoside) used until specific pathogen identified; combination of PCN and aminoglycoside is used in pt with serious infections; a cephalosporin or vancomycin is used for pts allergic to PCN; for high risk babies PCN is given at least 4 hrs before delivery; no vaccine is currently available

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viridans streptococci

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a heterogeneous collection of alpha hemolytic and non hemolytic gamma streptococci many of them produce a green pigment on blood agar ('viridans'=green); they colonize the oropharynx, GI tract, and GU tract; several groups and species are clinically important= S. anginosus group (abscess in brain or peritoneal cavity), S. mitis group (sepsis in neutropenic pts, meningitis), S. mitis and S. salivarius (subacute endocarditis), S. mutans group (dental caries), S. bovis group (bacteremia associated with gastrointestinal cancer)

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streptococcus pneumoniae characteristics

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gram positive cocci in pairs (diplococci) or short chains; often described as 'lancet shaped' often appearing encapsulated

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streptococcus pneumoniae physiology

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grow only on enriched media containing blood as alpha hemolytic colonies that vary in morphology; encapsulated strains form large colonies and non encapsulated strains form small colonies; all colonies undergo autolysis with aging; catalase negative; alpha hemolysis results from the production of Pnemolysin which degrades hemoglobin

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streptococcus pneumoniae structure

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capsule- virulent strains are covered with a complex polysaccharide capsule; peptidoglycan; teichoic acid in 2 forms= C polysaccharide (extends through the capsule and is exposed on the cell surface, it precipitates a serum globulin fraction, C reactive protein, in the presense of calcium) and F antigen (is bound to plasma membrane lipid, cross reacts with Forssman antigen on mammalian cells); phosphorylcholine= unique to the cell wall of S. pneumoniae and both forms of teichoic acid are associated with phosphorylcholine

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streptococcus pneumoniae: colonization

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bacteria bind to the epithelial cells of orpharynx through surface protein adhesins; host mucus and ciliated epithelial cells prevent S. pneumoniae migration to the lower respiratory tract; secretory IgA in mucus traps the bacteria; the bacteria responds to that by producing secretory IgA protease and pneumolysin (a cytotoxin that destroys ciliated cells)

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streptococcus pneumoniae: tissue destruction

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bacterial peptidoglycan fragments, teichoic acid, and penumolysin active the alternative and classical complement pathways leading to migration of inflammatory cells to the infection site and subsequent tissue damage; bacterial phosphoylcholine binds to receptors for platelet activating factor expressed on surface of endothelial cells of respiratory tract and meninges and lung alveolar cells leading to bacterial internalization

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streptococcus pneumoniae: avoidance of phagocytosis

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the capsule protects the bacteria from phagocytosis; the virulence of S. pneumoniae in human and experimental animals is directly linked to encapsulated strains

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streptococcus penumoniae: survival within the phagocytic cells

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through the pneumolysin mediated suppression of the phagocytic cell oxidative burst thereby preventing intracellular killing of S. pneumoniae; internalized bacteria are protected from the host immune response

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streptococcus pneumoniae: epidemiology

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common inhabitant of the throat and nasopharynx of healthy individuals; colonization is more common in children; disease results when the bacteria migrate from the nasopharynx to adjacent areas the bloodstream or the meninges; circumvention of natural clearing mechanisms in those with viral respiratory infection such as influenzae, congestive heart failure, and chronic pulmonary diseases; aspiration of endogenous oral bacteria into the lower respiratory tract results in pneumonia; persons with splenic dysfunction are at higher risk for bacteremia

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streptococcus pneumoniae clinical diseases

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pneumonia, sinusitis and otitis media, meningitis, bacteremia

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pneumonia

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results from bacterial multiplication within the alveolar space; abrupt onset of severe shaking chills and sustained high fever plus productive cough with blood tinged sputum often following viral infection; generally localized to the lower lobe of the lung (lobar pneumonia); children may have a generalized bronchopneumonia; mortality rate is high among elderly and bacteremia pts; severe pneumococcal disease may occur in pts with splenectomy; abcesses develop in pts infected with specific serotypes

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sinusitis and otitis media

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usually follow viral infection of the upper respiratory tract as polymorphonuclear neutrophils obstruct the sinuses or ear canal; middle ear infection primarily occurs in children, sinusitis in all ages

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meningitis

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bacteria reach the CNS during bacteremia, ear or sinus infection, or head trauma; mortality and neurological deficits in survivors are common

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bacteremia

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occurs in pts with pneumococcal pneumonia and at a higher rate in pts with meningitis; it generally does not occur in pts with sinusitis; in pts with previously damaged heart valves endocarditis may occur

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streptococcus penumoniae lab diagnosis microscopy and gram stain

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gram positive cocci with unstained capsule; may be confirmed by the quellung reaction in which bacteria mixed with anti capsular antibody appear more refractive microscopically due to capsular swelling

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streptococcus pneumoniae antigen testing

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penumococcal C polysaccharide is excreted in urine and commercially available immunoassay to test for pneumococcal polysaccharide antigens is available; highly sensitive when testing CSF of pts with pneumococcal meningitis; less sensitive if urine is tested

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streptococcus pneumoniae PCR

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tests have been developed for identification of S. penumoniae isolates but are not used with clinical samples

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streptococcus pneumoniae culture

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requires an enriched medium supplemented with blood (sheep blood agar, BA); may be difficult to recover from sputum samples as S. pneumoniae is overgrown by other contaminating oral micro flora; readily cultures from blood or CSF if the pt has not been treated with antibiotics; cultures may be negative in antibiotic treated pts

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streptococcus penumoniae identification

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bile solubility test: bile activates autolysins and S. pneumoniae colonies dissolve in minutes; optochin susceptibility disk diffusion assay: bacteria are streaked on an agar plate and a disk saturated with optochin is placed in the middle of the plate, a zone of inhibition indicated S. pneumoniae

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streptococcus pneumoniae treatment

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PCN for susceptible strains; many strains are PCN resistant through decreased affinity of PCN to the PCN binding protein in the cell wall; empiric treatment involves a combination of vancomycin and ceftriazone

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streptococcus penumoniae prevention

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WANTS YOU TO REMEMBER THESE VACCINES; vaccines for the most epidemiologically important peumococcal serotypes; a 23 valent (23 capsular types) polyvalent pneumococcal polysaccharide (PS) vaccine is recommended for children older than 2 yrs and adults (PPSV23); 13 valent conjugated (PS carrier protein) pneumococcal vaccine is recommended for infants younger than 2 yrs of age (PCV13); young children (less than 2 yrs) do not produce antibodies against polysaccharides alone (T independent antigens, addition of protein changes PS to T dependent antigen)

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summary of streptococcus penumoniae: biology, virulence, and disease

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elongated gram positive cocci arranged in pairs (diplococci) and short chains; cell wall includes teichoic acid rich in phosphorylcholine (C polysaccharide) which is required for the activity of an autolytic enzyme, amidase; virulence determined by ability to colonize oroharynx (surface protein adhesion), spread into normally sterile tissue pneumolysin, IgA protease, stimulate local inflammatory response (teichoic acid, peptidoglycan fragments, pneumolysin), and evade phagocytic killing (polysaccaride capsule); responsible for pneumonia, sinusitis and otitis media, meningitis, and bacteremia

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summary for streptococcus penumoniae: epidemiology

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most infections are caused by endogenous spread from the colonized nasopharynx or oropharynx to distal site (e.g. lungs, sinuses, ears, blood, meninges); person to person spread through infectious droplets is rare; colonization is highest in young children and their contacts; individuals with antecedent viral respiratory tract disease or other conditions that interfere with bacterial clearance form respiratory tract are at increased risk for pulmonary disease; children and the elderly are at greatest risk for meningitis; people with hematologic disorder (e.g. malignancy, sickle cell disease) or functional asplenia are at risk for fulminant sepsis; although the organism is ubiquitous disease is more common in cool months

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summary for streptococcal pneumoniae diagnosis

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microscopy is highly sensitive as is culture unless the pt has been treated with antibiotics; antigen tests for pneumococcal C polysaccharide are sensitive with cerebrospinal fluid (meningitis) but not with urine (meningitis, pneumonia, other infections); nucleic acid based tests are not commonly used for diagnosis; culture requires use of enriched nutrient media (e.g. sheep blood agar); organism highly susceptible to many antibiotics so culture can be negative in partially treated pts; isolates identified by catalase (negative), susceptibility to optochin, and solubility in bile

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summary for streptococcus penumoniae treatment, prevention, and control

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PCN is the drug of choice for susceptible strains although resistance is increasingly common; vancomycin combined with ceftriazone is used for empiric therapy; monotherapy with a cephalosporin, fluoroquinolone, or vancoycin can be used in pts with susceptible isolates; immunization with 13 valent conjugated vaccine is recommended for all children younger than 2 yrs of age; a 23 valent polysaccharide vaccine is recommended for adults at risk for disease

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enterococci: what are the most important species

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E. faecalis, E. faecium, E. gallinarum

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enterococci: physiology, structure, and virulence

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gram positive cocci, pairs and short chains; grow under wide range of temp and in the presence of high concentrations of bile salts; virulence= adherence to different tissues and biofilm development (adherence factors are surface proteins, membrane glycolipids, and pili), antibiotic resistance (both inherent resistance (chromosomal) and acquisition of resistance genes) REMEMBER THE 2 ANTIBIOTIC RESISTANCE MECHANISMS FOR ENTEROCOCCI

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enterococci: epidemiology

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colonizes the GI tract; utilization of bread spectrum antibiotics allows it to spread to other mucosal surfaces

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enterococci clinical diseases

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nosocomial infections, UTI, peritonitis, bacteremia, endocarditis

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nosocomial infections

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one of the most common causes of nosocomial infections

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UTIs

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associated with indwelling urinary catheters; frequently follows use of broad spectrum antibiotics

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peritonitis

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usually presents as abdominal swelling following leakage of intestinal bacteria due to trauma or surgery; often present in polymicrobial infections

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bacteremia

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associated with dissemination from a local infection site (wound, urinary tract, or peritoneum) or primary infection of the endocardium (endocarditis)

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endocarditis

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infection of heart endothelium or valves associated with persistent bacteremia; may be acute or chronic; serious infection due to the resistance of enterococci to most commonly used antibiotics

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enterococci diagnosis

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enterococci grow on non selective media; frequently non hemolytic, catalase negative; can be differentiated from streptococci by chemical reactions= optochin and bile resistant, hydrolyze bile esculin, grow in presence of 6.5% NaCl, L-pyrrolidonyl arylamidase (PYR) positive

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enterococci treatment

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synergistic combination of aminoglycoside and cell wall active antibiotics such as PCN oc vancomycin (NOT cephalosporins or oxacillin- no activity); aminoglycoside and vancomycin resistance (VRE) strains, sspecially E. faecium can be treated with linexolid, daptomycin, quinupristin/dalfopristin, or tigecycline

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enterococci prevention

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restrict antibiotic usage (cephaloscporins, vancomycin); implement appropriate infection control practices such as isolating pts with VRE, use of gloves, and good hand hygiene

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summary for enterococcus biology, virulence, and disease

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gram positive cocci arranged in pairs and host chains (morphologically similar to streptococcus pneumoniae); cell wall with group specific antigen (group D glycerol teichoic acid); virulence mediated by ability to host surfaces and form biofilms and by antibiotic resistance; diseases include urinary tract infections, peritonitis (usually polymicrobic), wound infections, and bacteremia with or without endocarditis

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summary for enterococcus epidemiology

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colonizes the GI tracts of humans and animals; spreads to other mucosal surfaces if broad spectrum antibiotics eliminate the normal bacterial population; cell wall structure typical of gram positive bacteria, which allows survival on environmental surfaces for prolonged periods; most infectious endogenous (form pts bacterial flora); some caused by pt to pt spread; pts at increased risk include those hospitalized for prolonged periods and treated with broad spectrum antibiotics (particularly cephalosporins to which enterococci are naturally resistant)

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summary for enterococcus diagnosis

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grows readily on common, nonselective media; differentiated form related organisms by simple tests (catalase negative, L-pyrrolidonyl arylamidase positive, resistant to bile and optochin)

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summary for enterococcus treatment, prevention, and control

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therapy for serious infections requires combination of an aminoglycoside with a cell wall active antibiotic (PCN, ampicillin, or vancomycin); newer agents used for antibiotic resistant bacteria include linezolid, daptomycin, tigecycline, and quinyprinstin/dalfopristin; antibiotic resistance to each of these drugs is becoming increasingly common, and infections with many isolates (particularly entercoccus faecium) are not treatable with any antibiotics; prevention and control of infections require careful restriciton of antibiotic use and implementation of appropriate infection control practices

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a 62 yr old man with a history of chronic obstructive pulmonary disease (COPD) came to the ER because of a fever of 40Cchills, nausea, vomiting, and hypotension; the pt also produced tenacious yellowish sputum that had increased in quantity over the preceding 3 days; chest radiographic exam showed extensive infiltrates in the left lower lung that involved both the lower lobe; multiple blood cultures and culture of the sputum yielded S. pneumoniae; the virulence of S. pneumoniae is a direct result of: a. oxygen stable streptolysin b. its polysaccharide capsule c. protein A d. streptococcal pyrogenic exotoxins (Spe) E e. P-V leukocidin

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B its polysaccharide capsule