Micro Strep and Staph Trans 1

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Microbiology 1: Strep and Staph

Dr. Bibera

August 8, 2010

2nd Shifting Period, Trans #1

Genus Streptococcus I. Morphology Individual cocci: spherical, ovoid Arrangement: chains (may appear as diplococci) Gram positive

II. Physical Properties Capsular polysaccharide

- capsules more noticeable in young cultures - impede phagocytosis - group A, B, C stains (capsules are composed of hyaluronic

acid) Cell Wall

- Proteins: M, T, R antigens - Carbohydrates - Peptidoglycan Pili project through the capsule

III. Culture Solid media: discoid colonies (1-2 mm diameter) Strains with capsular material give rise to mucoid colonies

IV. Growth Characteristics Energy: utilization of sugars Poor growth on solid media or in broth unless enriched with

blood or tissue fluids Incubation in 10% CO2 supports growth and hemolysis Most pathogenic strep grow best at 37oC

- Group D enterococci: 15oC-45oC (enterococci also grow in high NaCl concentrations, in 0.1% methylene blue and in bile-esculin agar)

Most strep are facultative anaerobes V. Antigenic Structure A. Group-Specific Cell Wall Antigen Carbohydrate in the cell wall Basis of serologic grouping: Lancefield groups A-H, K-U Serologic specificity of the group specific carbohydrate

determined by an amino sugar - Group A Strep: rhamnose-N-acetylglucosamine - Group B: rhamnose-glucosamine polysaccharide - Group C: rhamnose-N-acetylgalactosamine - Group D: glycerol teichoic acid containing D-alanine and

glucose - Group F: glucopyranosyl-N-acetylgalactosamine

B. M Protein A major virulence factor of Group A Strep (S. pyogenes)

- Group C and G strep have genes homologous to the genes for M protein of group A

Appears as hair-like projections of the strep cell wall More than 80 types of M protein M protein molecule

- 2 major structural classes of M protein: class I and class II Role in the pathogenesis of rheumatic fever (RF)

- Cell wall of selected M types induces antibodies that react with cardiac muscle tissue (Class I M protein: virulence determinant for RF)

C. T substance Has no relationship to virulence Acid-labile and heat-labile Permits differentiation of certain streptococcal types by

agglutination with specific antisera D. Nucleoproteins Proteins and other substances of little serologic specificity (P

substances) make up most of the streptococcal cell body

VI. Toxins and Enzymes Group A strep elaborates > 20 extracellular enzymes that are

antigenic and includes: - Streptokinase - Streptodornase - Hyaluronidase - Pyrogenic Exotoxins - Diphosphopyridine Nucleotidase - Hemolysins A. Streptokinase (Fibrolysin) Produced by many strains of Group A ß hemolytic

streptococcus Transforms plasminogen to plasmin Streptokinase therapeutic use: given IV for the treatment of

pulmonary emboli and coronary artery and venous thromboses

B. Streptodomase (Streptococcal Deoxyribonuclease) Depolymerizes DNA Streptodornase together with streptokinase are used in

enzymatic debridement - Liquefy exudates and facilitates removal of pus and necrotic

tissue - Antibody to DNase develops after strep infections esp. after

skin infections

C. Hyaluronidase Splits hyaluronic acid Aids in spreading infecting microorganisms (spreading

factor) Are antigenic and specific for each bacterial or tissue source

D. Pyrogenic Exotoxins (Erythrogenic Toxins) Elaborated by Group A Strep Strep pyrogenic exotoxins A, B, and C Associated with strep toxic shock syndrome and scarlet

fever

E. Diphosphopyridine Nucleotidase This substance may be related to the ability of the organism

to kill leukocytes

F. Hemolysin Many streptococci are able to lyse rbc’s in varying degrees ß (beta) hemolysis: complete disruption of erythrocytes

with release of hemoglobin α (alpha) hemolysis: incomplete hemolysis with formation of

green pigment γ (gamma) hemolysis The ß hemolytic group A S. pyogenes elaborates 2

hemolysins (streptolysins) a. Streptolysin O - A protein responsible for hemolysis seen when growth is in

cuts deep into the BAP - Combines quantitatively with antistreptolysin O (ASO) - ASO is an antibody that appears in humans following any

strep infection: blocks hemolysis by streptolysin O (ASO serum titer in excess of 160 to 200 units is considered suggestive of a recent strep infection)

b. Streptolysin S - Agent responsible for the hemolytic zones around colonies

growing on the surface of BAP - Elaborated in the presence of serum - Not antigenic but may be inhibited by an inhibitor present in

the sera of humans and animals - Is independent of past experiences with streptococci

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VII. Classification Based On:

- Colony morphology and hemolytic reactions on blood agar - Serologic specificity of the cell wall group – other specific

substance (Lancefield classification) and other cell wall or capsular antigens

- Biochemical reactions and resistance to physical and chemical factors

- Ecologic features ***Medically Important Streptococci (Table 15-1 – trans) A. Group A streptococcus – Streptococcus pyogenes a. contains the group A antigen b. beta hemolytic c. main human pathogen associated with local or systemic

invasion and post streptococcal immunologic disorders d. typically produces large (1 cm diameter) zones of ß

hemolysis around colonies > 0.5 mm diameter e. PYR positive (hydrolysis of L-pyrrolidonyl-2-napthylamide) f. usually susceptible to bacitracin B. Group B Streptococcus – Streptococcus agalactiae a. contains the group B antigen b. members of the normal flora of the female genital tract c. an important cause of neonatal sepsis and meningitis d. beta hemolytic e. hydrolyzes sodium hippurate f. gives a positive response to CAMP test C. Groups C and G Streptococci a. occur sometimes in the nasopharynx b. may cause sinusitis, bacteremia, or endocarditis c. beta hemolytic d. identified by reactions with specific antisera for groups C or

G e. looks like Group A strep on BAP D. Enterococcus faecalis (E. faecium, E. durans) a. Part of the normal enteric flora b. Usually nonhemolytic; occasionally alpha hemolytic c. PYR positive d. Grow in the presence of bile e. Hydrolyze esculin (bile esculin positive) f. grow in 6.5% NaCl g. Resistant to penicillin G h. Many strains are vancomycin resistant E. Streptococcus bovis: non-enterococcal group D streptococci a. Part of the enteric flora b. Occasionally cause endocarditis c. Sometimes cause bacteremia in patients with colon

carcinoma d. Nonhemolytic and PYR negative e. Grow in the presence of bile f. Hydrolyze esculin (bile esculin-positive) g. Do not grow in 6.5% NaCl h. often classified as viridians streptococci F. Streptococcus anginosus group (Streptococcus anginosus or Streptococcus milleri, Streptococcus intermedius, Streptococcus constellatus) a. part of the normal flora b. may be beta, alpha or nonhemolytic c. includes: 1. Beta hemolytic streptococci that form minute colonies (<0.5

mm in diameter) and react with groups A, C, or G antisera 2. All beta hemolytic group F streptococci d. Voges Proskauer test positive e. Those that are group A are PYR negative f. May be classified as Viridans streptococci

G. Group N Streptococci a. rarely found in human disease states b. produce normal coagulation (souring) of milk H. Groups E, F, G, H and K-U streptococci a. occur primarily in animals I. Streptococcus pneumoniae a. alpha hemolytic b. growth inhibited by optochin (ethylhydrocupreine

hydrochoride) c. colonies are bile soluble J. Viridans streptococci (Streptococcus mitis, Streptococcus salivarius, Streptococcus

sanguis (Group H), Streptococcus mutans)

- typically alpha hemolytic; may be nonhemolytic - growth not inhibited by optochin - colonies are not soluble in bile (deoxycholate) - most prevalent members of the normal flora of the upper

respiratory tract - important for the healthy state of the mucous membranes - may reach the bloodstream due to trauma - a principal cause of endocarditis on abnormal heart valves - Streptococcus mutans – synthesizes large polysaccharides

(dextrans and levans) from sucrose which may lead to dental carries

K. Nutritionally variant streptococci or pyridoxal-dependent streptococci

Streptococcus defectives (Abiotrophia defectiva) Streptococcus adjacens (Abiotrophia adjacens) a. require pyridoxal or cysteine for growth on blood agar b. grow as satellite colonies around colonies of staphylocci and

other bacteria c. usually alpha hemolytic; may be nonhemolytic d. part of the normal flora e. occasionally cause bacteremia or endocarditis f. can be found in brain abscesses and other infections L. Peptostreptococcus a. grow only under anaerobic or microaerophilic conditions b. variably produce hemolysis c. part of the normal flora of the mouth, upper respiratory

tract, bowel and female genital tract d. often participate in mixed anaerobic infections in the

abdomen, pelvis, lung, or brain Epidemiology Streptococci are widely distributed in nature and frequently

form part of the normal human flora Approximately 5-15% of humans carry S. pyogenes or S.

agalactiae in the nasopharynx S. pneumoniae infects humans exclusively, and no reservoir

is found in nature - carrier rate of S. pneumoniae in the normal human

nasopharynx is 20-40% A. Group A Streptococcal Infections Strep pharyngitis occurs at all ages but is most common

among school-aged children and adolescents Pharyngitis and pyoderma are less common in adults than

children Pharyngitis and impetigo: associated with crowding Invasive group A strep infections is highest in infants and

older people - Varicella is the most commonly identified risk factor in

children; others include IV drug abuse, HIV, Dm and chronic cardiac or pulmonary disease

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Acute rheumatic fever was previously common among the poor; susceptibility may be partly genetic

1. Pharyngitis - Transmission: infected respiratory tract secretions - Communicability is highest during acute infection

(contagiousness is until 24 hours after antimicrobial therapy)

- Incubation period: 2 to 5 days 2. Streptococcal Impetigo Acquired from another person by direct contact Lesions occur at sites of breaks in the skin (e.g. insect bites) Incubation period: 7 to 10 days

B. Group B Streptococcus Common inhabitants of the GIT and GUT Occasionally cause invasive neonatal infection Transmission from the mother to the infant occurs shortly

before or during delivery After delivery, person to person transmission can occur At risk for early onset disease

a. Infants born < 37 weeks gestation b. Mother has high genital GBS inoculums c. GBS bacterium during pregnancy d. Previous infant with invasive GBS disease e. Intrauterine fetal monitoring f. PROM (18 hours or more) g. Intrapartum fever h. Chorioamniotis i. Maternal age < 20 years old j. Black or Hispanic origin C. Viridans strep Many streptococci (viridans) are members of the normal

flora and produce disease only when established in body parts where they do not normally occur (e.g. heart valves)

PATHOGENESIS: Group A Streptococci Group A Streptococci (Streptococcus pyogenes) cause disease

by three mechanisms: a. Pyogenic inflammation – induced locally at the site of the organisms in tissue b. Exotoxin production – can cause widespread systemic symptoms in areas of the body

where there are no organisms c. Immunologic – occurs when antibody against a component of the organism

cross-reacts with normal tissue or forms immune complexes that damage normal tissue

Inflammation-related enzymes produced by Group A

Streptococcus (Streptococcus pyogenes) a. Hyaluronidase (spreading factor) 1. Degrades hyaluronic acid which is the ground substance of the

connective tissue 2. Facilitates spread of the microorganisms 3. Antigenic – specific antibodies are found in the serum after

infection with hyaluronidase-producing organisms b. Streptokinase (fibrinolysin) 1. Transforms plasminogen of human plasma into plasmin (an

active proteolytic enzyme that digests fibrin and other proteins)

2. Given intravenously for treatment of pulmonary emboli and of coronary artery and venous thromboses

c. Streptodornase (streptococcal deoxyribonuclease) 1. Depolymerizes DNA in exudates or necrotic tissue

2. With streptokinase – used in enzymatic debridement; helps liquefy exudates and facilitates removal of pus and necrotic tissue

3. Antibody to DNAse develops after streptococcal skin infection (normal limit – 100 units)

Toxins and hemolysins produced by Group A Streptococci

(Streptococcus pyogenes) A. Streptococcal pyrogenic toxins Three antigenically distinct toxins

a. Exotoxin C – classic erythrogenic toxin 1. Causes the rash in scarlet fever 2. Produced only by strains lysogenized by a bacteriophage

carrying the gene for the toxin 3. Dick test: the injection of a skin test dose of erythrogenic toxin

gives a positive result (an erythematous reaction in the skin of non-immune persons who lack antitoxins)

4. Schultz Charlton reaction: antitoxin injected into the skin of a patient with scarlet fever causes localized blanching as a result of neutralization of erythrogenic toxin

b. Exotoxin B – cysteine protease that rapidly destroys tissue and is produced by strains that cause necrotizing fasciitis

c. Exotoxin A – may cause streptococcal toxic shock syndrome B. Hemolysins 1. Streptolysin S oxygen stable, non-immunogenic cell bound hemolysin

capable of lysing erythocytes, leukocytes and platelets stimulate release of lysosomal contents after engulfment responsible for the hemolytic zones around streptococcal

colonies growing on the surface of blood agar not antigenic

2. Streptolysin O a protein that is hemolytically active in the reduced state responsible for the hemolysis seen when growth cuts

deep into the medium in blood agar antigenic – antibodies are formed against Streptolysin O

following infection with streptococci that produce Streptolysin O

ASO serum titer in excess of 160-200 units – suggests: 1. recent infection with streptococci 2. persistently high antibody levels due to an exaggerated

immune response to an earlier exposure in a hypersensitive person

PATHOGENESIS: Group B Streptococci (Streptococcus agalactiae) based on the ability of the organism to induce an

inflammatory response no cytotoxic exotoxins produced role of enzymes in the pathogenesis of infection is unknown

– deoxyribonucleases, hyaluronidase, neuraminidase, proteases, hippurase and hemolysins

no evidence for any immunologically- induced disease has a polysaccharide capsule – antiphagocytic anticapsular antibody is protective

PATHOGENESIS: Viridans streptococci, including non-

groupable streptococci of the oral and gastrointestinal cavities and urogenital tract

Important etiologic agents of bacterial endocarditis Predisposing factors for bacterial endocarditis: - Dental manipulation and dental disease with associated

transient bacteremia

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- Risk for endocarditis increases especially if with damaged heart valves (previous rheumatic fever or by congenital cyanotic heart disease)

S. mutans and S. sanguis - odontopathogens responsible for formation of dental plaque - linked to caries and other human oral disease - S. mutans is more cariogenic – virulence is directly related to its

ability to synthesize glucan CLINICAL FINDINGS: Group A Streptococcus Types of diseases produced by Streptococcus pyogenes 1. Pyogenic diseases a. pharyngitis b. cellulites and erysipelas c. impetigo (pyoderma) 2. Toxigenic diseases a. scarlet fever b. toxic shock syndrome 3. Immunologic diseases a. rheumatic fever b. acute glomerulonephritis Pharyngitis 1. Streptococcus pyogenes is the major cause of bacterial

pharyngitis 2. A disease of children 5-15 years old 3. Spread by person to person by respiratory droplets 4. Characterized by sore throat, fever, malaise, headache and

nausea; beefy red tonsils; palatal petechiae 5. Posterior pharynx erythematous with an exudate; cervical

lymphadenopathy present 6. Can result to complications (tonsillar abscesses, mastoiditis,

septicemia, osteomyelitis, rheumatic fever) Cellulitis 1. Cardinal features – erythema, swelling, heat and pain 2. Erythema may be pink or red but lacks the intense, fiery red or

salmon colored appearance of erysipelas. 3. Initiated by infection through a small break in the skin 4. Can invade the subcutaneous tissue and advance rapidly

through lymphatics – septicemia Erysipelas 1. Characteristic appearance – bright red or salmon red painful

confluent erythema in a “butterfly” distribution involving the nasal eminence, cheeks and nose with abrupt borders along the nasolabial folds

2. Erythema increases over a course of 3-6 days and usually resolves in 7-10 days

3. Erysipelas usually occur on the face, although any skin surface such as the leg, can be affected. Note the sharp line of demarcation and bright red color; features that distinguish it from cellulitis.

Scarlet fever *diffuse erythema and circumoral pallor 1. The primary site of the infection is usually the pharynx, with

the distinctive rash resulting from an erythrogenic toxin produced by the streptococcus.

2. The rash appears within 2 days after the onset of the sore throat and disappears in 6-10 days.

Impetigo 1. A superficial infection that usually begins as small vesicles

progressing to weeping lesions with amber crust and slightly cloudy purulent exudate

2. Serotypes implicated: M types 2, 49, 55 and 57 3. May result to nephritis as a complication

Streptococcal toxic shock syndrome (also called Toxic Shock like Syndrome) *Desquamation of skin occurs 10-14 days after infection at sites

that where erythematous during the initial phase. 1. Characterized by hypotension, diffuse erythroderma,

hypoalbuminemia and multi-organ failure (kidney, lungs, liver, heart)

2. Serotypes implicated: M1, M3 or M18 3. Due to the production of pyrogenic exotoxins – exotoxin A

Rheumatic fever 1. Most serious sequelae of hemolytic streptococcal infection

because it results in damage to heart muscle and valves 2. Occurs 2 weeks after a group A streptococcal infection, usually

pharyngitis 3. Results in a systemic inflammatory process involving the

connective tissue, heart, joints and CNS 4. Characterized by fever, migratory polyarthritis and carditis 5. Due to an immunologic reaction between cross-reacting

antibodies to certain streptococcal M proteins and certain antigens of joint and heart tissue

6. Treat promptly with Penicillin which is continued prophylactically to prevent recurrence and increased damage

Revised Jones Criteria for the Diagnosis of Rheumatic Fever The diagnosis of rheumatic fever is highly likely if supported

by evidence of a preceding group A streptococcal infection and the presence of two major manifestations or one major and two minor manifestations.

Supporting evidence of antecedent Group A streptococcal infection

1. Positive throat culture 2. Positive streptococcal antigen test 3. Elevated or rising streptococcal antibody titer Major manifestations Carditis Polyarthritis Chorea Erythema marginatum Subcutaneous nodules Minor manifestations

Clinical findings: arthralgia, fever Laboratory findings

Elevated acute phase reactants (ESR-erythrocte sedimentation rate, C-reactive protein)

Prolonged P-R interval on electrocardiography Acute glomerulonephritis 1. Typically occurs 2-3 weeks after streptococcal skin infections

with M types 2, 4, 12 or 49 (49 -most frequent) 2. More frequent after skin infections than after phrayngitis 3. Characterized by hypertension, edema of the face (especially

periorbital edema) and ankles, and “smoky” urine 4. Complete recovery; reinfection with streptococci rarely leads

to recurrence 5. Initiated by deposition of soluble streptococcal antigen-

antibody complexes and complement on the glomerular basement membrane – lumpy-bumpy pattern on immunofluorescence

6. Can be prevented by early eradication of nephritogenic streptococci from skin colonization sites

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CLINICAL FINDINGS: Group B Streptococcus Diseases produced by Streptococcus agalactiae NEONATAL GROUP B STREPTOCOCCAL DISEASE Features Early-onset

disease Late-onset

disease Age of onset Obstetrical

complications Time of acquisition Clinical disease Mortality rate Streptococcal

serotype

<7 days Yes In utero or at

delivery Bacteremia,

pneumonia, meningitis

High I, II, or III

1 week to 3 months

Infrequent Post- partum Bacteremia, meningitis, osteomyelitis Low (<20%) III – most

common LABORATORY DIAGNOSIS for Streptococcus pyogenes 1. Microscopy – Gram Stain Gram stain of streptococci in a positive broth culture (Gram

[+] cocci in chains) 2. Cultures Colonies of Group A streptococci on 5% sheep blood agar

(small colonies with a wide zone of beta hemolysis) Streptococcus selective agar – contains sulfamethoxazole

and trimethoprim which inhibits the growth of non-Group A beta hemolytic streptococci, staphylococci, viridans streptococci and gram negative bacilli

3. PYR Test - L-pyrrolidonyl-2-naphthylamide - the presence of an aminopeptidase enzyme that degrades the

substrate is a 10-minute presumptive test for Group A streptococci (beta hemolytic) and Aerococcus, Enterococcus and Gemella (alpha or non-hemolytic)

Positive rxn – red color Negative – colorless 4. Bacitracin susceptibility test - an alternative to PYR Test for the presumptive identification of

Group A beta hemolytic streptococci - 0.04 units of bacitracin disk is placed on an inoculum of the

microorganism on sheep blood agar Positive test – zone of inhibition LABORATORY DIAGNOSIS for Group B Streptococcus Streptococcus agalactiae – Group B beta hemolytic streptococcus 1. Microscopy - Gram stain of vaginal secretions Gram positive cocci in pairs: suggestive of Streptococcus

agalactiae which colonize the genitor-urinary tract of women

2. Culture Colonies of Group B streptococcus on 5% sheep blood agar

- colonies are larger than other beta hemolytic streptococci - hemolytic zone surrounding the colony is smaller 3. Hippurate hydrolysis test a. Incubate a suspension of the microorganism for 2 hours at

35oC in a hippurate solution. b. Add ninhydrin (indicator). c. Hydrolysis of sodium hippurate leads to the formation of

glycine and sodium benzoate. d. Deamination of glycine – purple color (positive test) *colorless – negative test

4. CAMP test (Christie, Atkins, Munich-Peterson) An alternative to Hippurate hydrolysis Demonstrates the arrowhead shaped enhancement of beta

hemolysis that occurs when the hemolytic beta toxin produced by S. Aureus Acts synergistically with the CAMP factor.

Group D Streptococcus-Enterococcus 1. Microscopy 2. Cultures Colonies of Enterococcus spp. On 5% sheep Blood agar Colonies are raised, white to gray white ranging from 0.5 to

1.5 mm in size and are usually non-hemolytic 3. Bile esculin and 6.5% NaCl (+) black (+) turbidity yellow a. Bile esculin slant- indicates that the microorganism can

grow in the presence of bile and hydrolyzes esculin. b. 6.5% NaCl broth- growth is indicated by turbidity and change

in the indicator from pink to yellow. 4. PYR Test The presence of an aminopeptidase enzyme that degrades the

substrate PYR (L-pyrrolidonyl-B napthylamide) is a 10 minute presumptive test for group A streptococci (beta hemolytic) and Aerococcus, enterococcus and Gemella (alpha or nonhemolytic)

Viridans Streptococcus 1. Microscopy - Gram stain of V. streptococci in blood culture broth: appear in

long chains especially when recovered from a blood culture broth.

2. Cultures 3. Optochin Susceptibility Test - No zone of inhibition - A paper disc containing optochin (ethylhydrocupreine

hydrochloride) is applied to the surface of an inoculated 5% sheep blood agar plate.

*Definitive identification requires several substrates including:

bile esculin, arginine decarboxylase, 6.5% NaCl, lactose, mannitol, raffinose, sorbitol, arabinose, inulin, sucrose and esculine.

Treatment 1. All Group A streptococci are susceptible to

Penicillin G. Mild- oral Penicillin V If allergic- erythromycin or its derivatives (Azithromycin

2. Endocarditis caused by Viridans streptococci is curable by prolonged penicillin treatment

3. Enterococcal endocarditis- eradicated only by a penicillin or vancomycin combined with an aminoglycoside

4. vancomycin resistant enterococci-Linezolid (Zyvox) and Quinupristin/Dalforpristin (Synercid)

5. Nonenterococcal Streptococcus bovis- Penicillin G 6. Group b streptococcal infections- Penicillin G or

Ampicillin in combination with an aminoglycoside 7. Peptostreptococci- Penicillin G Prevention and control 1. Rheumatic Fever can be prevented by prompt

treatment of Group A Streptococcal pharyngitis with Penicillin.

2. Penicillin prophylaxis for acute rheumatic fever patients to prevent recurrence of the disease; not neede in acute glumerulonephritis.

3. In patients with damaged heart valves who undergo invasive dental procedures, endocarditis can be prevented by using amoxicillin perioperatively.

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4. In patients with damaged heart valves who undergo gastrointestinal or urinary tract procedures, endocarditis caused by enterococcus can be prevented by using ampicillin and gentamicin perioperatively.

5. neonatal sepsis caused by group B streptococcus can be prevented by administration of parenteral ampicillin perinatally to women who experienced prolonged (longer than 18 hours) rupture of membranes, whose labor begins before 37 weeks gestation or who have a fever at the time of labor.

Streptococcus pneumoniae Physical Properties and Morphology 1. Gram positive lancet-shaped cocci arranged in pairs

(diplococcus) or in short chains 2. Possesses a capsule of polysaccharide that permits

typing with specific antisera 3. Produces alpha-hemolysis in blood agar 4. lysed by surface active antigens such as bile or

deoxycholate 5. Growth is inhibited by optochin 6. Normal inhabitants of the upper respiratory tract of

humans 7. Most common cause of pneumonia and otitis media 8. An important cause of meningitis and

bacteremia/sepsis. Antigenic Structure 1. Polysaccharide capsule or specific soluble

substances a. virulence factors- interferes with

phagocytosis and favor invasiveness b. specific antibody to capsule 1. opsonizes the organism 2. facilitates phagocytosis 3. promotes resistance c. Quellung Reaction- swelling of capsule when type specific antiserum is added to the organism. d. elicits a B-cell response. 2. C- substance a. carbohydrate in the cell wall b. reacts with a normal serum protein made by the liver- CRP

(non-specific indicator of inflammation and is elevated in response to the presence of many organisms)

Epidemiology *Pneumococci are ubiquitous - Upper respiratory tract of many people are colonized. *Transmission: person to person via respiratory droplet

contact *Period of communicability: may be as long as the organism is

present in the respiratory tract but probably <24 hours after effective antimicrobial therapy.

*Pre-disposingg factors - viral URTI including influenza - infection rate highest among infants, young children, elderly,

black, Alaskan natives, American-Indian populations - Severe infections: Congenital or acquired humoral

immunodeficiency, HIV, congenital or surgical asplenia, sickle cell disease, abnormal innate immune responses

Pathogenesis 1. The most important virulence factor is the capsular

polysaccharide, and anticapsular antibody is protective. 2. Lipoteichoic acid, which activates complement and induces

inflammatory cytokine production, contributes to the inflammatory response and to the septic shock syndrome that occurs in some immunocompromised patients.

3. Pneumolysin (the hemolysin that causes alpha-hemolysis) may also contribute to the pathogenesis.

4. Pneumococci produce IgA protease that enhances the organism’s ability to colonize the mucosa of the upper respiratory tract.

5. Pneumococci multiply in tissues and cause inflammation. 6. When they reach the alveoli, there is outpouring of fluid and

red and white blood cells, resulting in consolidation of the lung.

7. During recovery, pneumococci are phagocytized, mononuclear cells ingest debris, and consolidation resolves.

Streptococcus pneumoniae virulence factors

Virulence Factor Action Capsule Pneumolysin Purpura-producing Principle Neuraminidase Amidase

Inhibits phagocytosis in absence of antibodies

Hemolysin, dermotoxic Cause dermal hemorrhage Spreading factor Autolysin important for celll

division Factors that lower resistance and predispose to pneumococcal infection 1. Alcohol or drug intoxication or other cerebral impairment that

can depress the cough reflex and increase aspiration of secretions.

2. Abnormality of the respiratory tract (eg. Viral infections, pooling of mucus, bronchial obstruction and respiratory tract injury and movement of the mucociliary blanket)

3. Abnormal circulatory dynamics (eg. Pulmonary congestion and heart failure)

4. Splenectomy 5. Certain chronic diseases such as sickle cell anemia and

nephrosis. Clinical Findings 1. Pneumococcal pneumonia a. infections are caused by aspiration of the endogenous oral

organisms b. most commonly associated with an antecedent viral

respiratory disease such as influenza and measles c. abrupt onset of fever, chills, chest pain and productive cough

with blood tinged sputum or rusty sputum followed by a crisis on days 7-10.

d. pleural effusion is seen in 25% of patients; empyema is a rare complication.

2. Sinusitis and Otitis media - preceeded by a viral infection of the upper respiratory tract,

leading to infiltration with polymorphonuclear leukocytes and obstruction of the sinuses and the middle ear.

3. Meningitis - spread of S. Pneumonia into the central nervous system can

folloe bacteremia, infections of the ear and sinuses, or head trauma with communication between the subarachnoid space and nasopharynx.

4. Bacteremia - occurs in 25% to 30% of patients with pneumococcal

pneumonia and more than 80% of patients with meningitis. Laboratory Diagnosis 1. Microscopy Gram stain of respiratory secretions: Gram positive lancet

shaped diplococci suggestive of Streptococcus pneumoniae 2. Culture

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Colonies of S. Pneumoniae on 5% sheep blood agar: - young colonies are round with complete edges,

- somewhat mucoid, and about 1mm in diameter - surrounded by a zone of alpha hemolysis. Slightly older colonies show the central indentation caused

by the easily induced autolysis. Occasionally, colonies may simply flatten out as they age. Colonies of S. Pneumoniae ion chocolate agar:

- If the medium was incubated in CO2 it will result in fairly large zones of alpha hemolysis.

- Colonies are quite flat on Chocolate agar.

3. Optochin Susceptibility test A paper disc containing optochin (ethylhydrocupreine

hydrochloride) is applied to the surface of an inoculated 5% sheep blood agar.

Zone of greater than or equal to 14 mm in diameter is presumptive identification of S. Pneumoniae. If less than 14 mm in diameter, confirm with bile solubility test.

4. Bile Solubility Test A drop of 2% sodium deoxycholate is applied directly to the

colonies. Pertaining to the picture in the lecture:

- Left- lysis of the colonies; Right- colonies remain intact - After the bile has evaporated, only the zone of hemolysis

remains.

5. Capsule Swelling Test - Quellung reaction - Capsules of S. Pneumoniae swell in the presence of specific

pneumococcal antiserum. Treatment Drug of Choice- Penicillin G Non-susceptible strains

- Cefotaxime - Centriaxone - Vancomycin Prevention and Control Immunization

- Pneumococcal conjugate vaccine - Pneumococcal polysaccharide vaccine

Additional table for Staphylococci Trans: Characteristics distinguishing major species of the Genus

Staphylococcus Coagulase S.

aureus

S. epidermidis

S. saprohyticus

Anaerobe growth and fermentation of glucose

+ - -

mannitol + + - Acid aerobically + - Acid anaerobically + - α Toxin + - - Heat-resistant

endonucleases + - -

Biotin-required for growth

- + NT

Cell wall Ribitol + - + Glycerol - + Protein A + - - Novobiocin

sensitivity S S R

Genus Staphylococcus 1. Gram positive spherical cells, usually arranged in grapelike

irregular clusters 2. Grows readily on many types of media and are active

metabolically 3. Ferments carbohydrates and produce pigments that vary

from white to deep yellow 4. Some are members of the normal flora of the skin and

mucous membranes of humans 5. Others cause suppuration , abscess formation, a variety of

pyogenic infection and even fatal septicemia 6. Pathogenic staphylococci hemolyze blood, coagulate plasma

and produce a variety of extracellular enzymes and toxins 7. Most common type of food poisoning is caused by heat

stable staphylococcal enterotoxin 8. Rapidly develops resistance to many antimicrobial agents 9. Three main species of clinical importance a. Staphylococcus aureus- most significant pathogen for man;

infection ranges from food poisoning or minor skin infections to severe life threatening infection

b. Staphylococcus epidermidis- normal human flora but can cause infection often associated with implanted devices especially in very young, old and immunocompromised patients

c. Staphylococcus saprophyticus- relatively common cause of urinary tract infection in young women.

10. Coagulase production- most important criterion for the recognition of Staphylococcus sp.

a. Coagulase positive i. Staphylococcus aureus

b. Coagulase negative i. Staphylococcus epidermidis

ii. Staphylococcus saprophyticus Staphylococcus aureus

1. Morphology a. Microscopic morphology - Gram positive, non motile coccus, 0.8 to 1.0 um in diameter in irregular grapelike clusters - Smears from pus- singly, pairs, clusters or in short chains - Smears from cultures grown on solid media- irregular clusters

GRAM+ COCCI ↓

+ Catalase -

Staphylococcus (clusters) Streptococcus (pairs and chains) ↓ ↓

Coagulase Hemolysis Beta: (+) Bacitracin S.pyogenes ( A)

(+) cAMP/Hippurate S. agalactiae (B) Alpha:

Optochin/Bile solubility S. pnneumoniae

Gamma: (+) Beta Esculin + 6.5% NaCl Grp D* Enterococcus

(-) Beta Esculin + 6.5% NaCl Grp D* Non-enterococcus *can also be Beta or Alpha hemolytic

(+) S. aureus hemolytic mannitol

yellow

(-) S. epidermidis Nonhemolytic

(usually) Mannitol

White

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- Broth cultures- short chains and diplococcal forms - Few Strains produce a capsule or slime layer b. Colonal morphology

1. Agar plates - Colonies are smooth, opaque, round, low convex, 1 to 4 mm

in diameter - Most strains produce golden yellow colonies on primary

isolation due to carotenoid pigments ranging from deep orange to pale yellow

2. Blood agar- zone of beta hemolysis surrounds colonies of organisms that produce soluble hemolysins *Microscopic morphology reveals gram positive cocci in grapelike clusters *Blood agar- Zone of beta hemolysis around the colonies

3. Physiology a. Cultural characteristics

- Facultative anaerobe but grows more abundant under aerobic conditions - Some strains require increased carbon dioxide tension - Wide temperature range from 4.2 to 9.3; optimum of 7.0 to 7.5 - Complex nutritional requirements - Grows well on most routine laboratory media such as nutrient agar and trypticase soy agar - Sheep blood agar- primary isolation media b. Metabolism - Energy is obtained via both respiratory and fermentive pathways - Exists under conditions of both high and low oxidation-reduction potential - Catalase is produced aerobically - Wide range of sugars and other carbohydrates are used - Mannitol fermentation differentiates Staphylococcus aureus (which ferments mannitol) from Staphylococcus epidermidis (which does not ferment mannitol) 3. Antigenic structure a. Capsule - A loose fitting polysaccharide layer - Protects bacteria by inhibiting chemotaxis and phagocytosis by polymorphonuclear leukocytes and proliferation of mononucelar cells following mitogen exposure - Facilitates adherence of bacteria to catheters and other synthetic materials like graft, prosthetic valves and joints and shunts - Interferes with the interaction between the underlying teichoic acid-peptidoglycan complex and complement b. Peptidoglycan layer - Elicits the production of interleukin-1 which is an endogenous pyrogen and opsonic antibodies by monocytes - Chemoattractant for polymorphonuclear leukocytes - Has endotoxin like activity - Produces a localized Shwartzman phenomenon - Activates complement - Elicits both humoral and cellular immune response - Increased antipeptidoglycan IgG level in infections accompanied by bacteremic phase c. Protein A - A group specific antigen unique to S. aureus - Consists of a single polypeptide chain - Has five regions

1. Four highly homologous domains-Fc binding 2. Fifth, c terminal domain- bound to cell wall and does not

bind Fc

- Binds to the Fc portion of the IgG molecules except Ig3 - Provokes a variety of biologic effects:

1. Chemotactic 2. Anticomplementary 3. Antiphagocytic 4. Elicits hypersensitivity reactions 5. Platelet injury

d. Teichoic acid - Complex, phosphate containing polysaccharides bound to both peptidoglycan and cytoplasmic membrane - Species specific:

S. aureus- ribitol teichoic acid with N-acetyl-D-glucosamine residues (polysaccharide A)

S. epidermidis- glycerol teichoic acid with glucosyl residues (polysaccharide B) - Mediates attachment of staphylococci to mucosal surfaces through their specific binding to fibronectin - Antigenic- teichoic antibodies are used to detect systemic staphylococcal disease e. Clumping factor - Component in the cell wall that results in the clumping of the whole staphylococci in the presence of plasma - Protein which binds fibrinogen and differs from free coagulase in both its mechanism of action and its antigenic properties f. Cytoplasmic membrane - A complex of protein, lipids and a small amount of carbohydrate forming an osmotic barrier for the cell - Provides an anchor site for the cellular biosynthetic and respiratory enzymes 4. Epidemiology - Widespread in the environment - Can be cultured form various objects and environmental surfaces - May be transmitted by multiple routes, including contact with infected persons, contact with asymptomatic carriers, airborne spread, and contact with contaminated objects - Colonizes the skin and mucous membranes of 30 to 50% of healthy adults and children - Usual body sites of colonization: anterior nares, throat (infants and children), axilla, perineum, vagina, or rectum - Anterior nares are the most densely colonized and can persist for years in 10 to 20% of affected people - From 25 to 50% of nasal carriers transiently carry the organism in their hands and other skin areas - Rates of carriage of more than 50% occur in children with desquamatting skin disorders of burns, and in people with frequent needle use (ex. Diabetes mellitus, hemodialysis, allergy shots) *Determinants of Pathogenicity 1. Surface receptors

a. Polysaccharides - Surface components that posses antiphagocytic activity are advantageous to the staphylococcus in its initial establishment in the host - Encapsulated staphylococci are able to spread rapidly through tissue by protecting the organisms from the complement mediated attack of polymorphonuclear leukocytes - Adhesion of the organisms to a biosurface-essential initiating event for colonization to occur b. Protein receptors

- Specific binding sites on the staphylococcal cell surface

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- Provide the organism with an adhesion mechanism by which infective foci become established

- Plasma proteins that bind specifically to S. aureus include fibronectin, fibrinogen, IgG, C1q

- Also binds to components of the extracellular matrix like laminin, collagen, fribronectin

1. Fibronectin a. A glycoprotein ubiquitous in wounds b. Mediates the adherence of vital cells such as fibroblasts,

epithelial cells and monocytes to an injured site c. May serve as a bridge between the organism and the host

wound tissue

2. Laminin a. Major glycoprotein in human basement membrane b. Metastasis like potential staphylococci to breach the normal

barriers between host tissues may be related to its ability to bind specifically to basement membrane 2. Extracellular enzymes a. Coagulase - An enzyme which clots plasma - Used as a marker for virulence of S. aureus - May cause the formation of a fibrin layer around a staphylococcal abscess thus localizing the infection and protecting the organism from phagocytosis b. Lipases - Lipid hydrolyzing enzymes - Required for the invasion of staphylococci into the cutaneous and subcutaneous tissues and the formation of superficial skin infections c. Hyaluronidase (spreading factor) - Hydrolyzes the hyaluronic acid present in the intracellular ground substance of connective tissue—facilitating spread of infection d. Staphylokinase (fibrinolysin) - A proteolytic enzyme with fibrinolytic activity - Can dissolve fibrin clots- proenzyme plasminogen is converted to the fibrinolytic enzyme plasmin e. Nucleases - A phosphodiesterase with both endonucleolytic and exonucleolytic properties and can cleave either DNA or RNA 3. Toxins a. Cytolytic toxins- a group of toxins which includes:

1.Streptolysin O and S 2.Various toxins of Clostridium 3.Hemolysins and leokocidin of S. aureus -Proteins -Extracellular -Induce the formation of neutralizing antibodies

*Four distinct hemolysins produced by S. aureus

1. Alpha toxin 2. Beta toxin 3. Delta toxin 4. Gamma toxin

1. Alpha toxin a. exhibits a wide range of biologic activities including hemolytic, lethal and dermonecrotic b. disrupts lysosomes c. cytotoxic for a variety of tissue culture cells d. human macrophages and platelets are damaged; monocytes resistant

e. causes injury to the circulatory system, muscle tissue and tissue to the renal cortex f. contributes to pathogenicity by producing tissue damage after the establishment of a focus of infection 2. Beta toxin (sphingomyelinase C) a. a heat labile protein that is toxic for a variety of cells, including erythrocytes, macrophages and fibroblasts b. catalyzes the hydrolysis of membrane phospholipids in susceptible cells c. with alpha toxin – responsible for the tissue destruction and abscess formation characteristic of staphylococcal diseases and the ability of Staphylococcus aureus to proliferate in the presence of a vigorous inflammatory response 3. Delta toxin a. a relatively thermostable surface active toxin b. detergent like properties- have damaging effects on membrane c. exhibits a high degree of aggregation d. high content of hydrophobic amino acids—when localized, becomes amphipathic and strongly surface active e. inhibits water absorption by the ileum f. stimulates accumulation of adenosine monophosphate g. alters ion permeability in the guinea pig ileum h. influences human polymorphonuclear leukocyte functions and platelet activating factor metabolism 4. Gamma toxin a. has pronounced hemolytic activity b. contains two protein components that act synergistically both essential for hemolysis and toxicity c. elevated specific neutralizing antibodies in human staphylococcal bone disease- suggestive of its role in the disease state b. Leukocidin- Panton- Valentine leukocidin 1. Attacks polymorphonuclear leukocytes and macrophages but no other cell type 2. Two protein components (S and F) that act synergistically to induce cytolysis 3. Unique response of leukocyte to leukocidin- altered permeability to cation b. Pyrogenic protein toxins- includes 1. Enterotoxins 2. Toxic shock syndrome toxin – 1 3. Streptococcal pyrogenic exotoxin A through C - all are pyrogenic and immunosuppressive as a result of their ability to induce nonspecific T lymphocyte mitogenicity and enhance host susceptibility to lethal endotoxin shock 1. Enterotoxins a. unique feature- ability to provoke vomiting and diarrhea in humans after oral ingestion b. Six serological types, A,B,C,C2,D and E Enterotoxin A – most frequently associated with staphylococcal food poisoning c. Emetic receptor sites – abdominal viscera from which site the sensory stimulus reaches the vomiting center via the vagus and sympathetic nerves d. Enterotoxin induced diarrhea- due to inhibition of water absorption from the lumen of the intestine and to increased transmucosal fluid flux into the lumen e. Biologic response modifiers which affect host immune defense mechanisms – SUPERANTIGENS

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2. Toxic shock syndrome toxin- 1 (formerly pyrogenic exotoxin C and enterotoxin F) a. an exotoxin with pronounced and diverse immunologic effects 1. Induction of interleukin – 2 2. Receptor expression 3. Interleukin synthesis 4. Proliferation of human T lymphocytes 5. Stimulation of interleukin- 1 synthesis by human monocytes b. Mediates toxic shock syndrome- characterized by fever, hypotension, rash followed by desquamation and multiple organ dysfunction c. Exfoliative toxin 1. Mediates staphylococcal scalded syndrome 2. Produced by bacteriophage group II strain 3. Does not elicit an inflammatory response 4. Does not primarily cause cell death 5. Potent mitogen primarily of T cells 6. A sphingomyelinase different from Beta toxin 5. Clinical infections a. epidemiology 1. Habitat (reservoir) a. normal flora of human anterior nares, nasopharynx, perineal area, and skin b. can colonize various epithelial or mucosal surfaces 2. Mode of transmission 1. Spread of patients endogenous strain to normally sterile site by traumatic introduction 2. Also may be transmitted person to person by fomites, air, or unwashed hands of health care workers 3. May be transmitted from infected lesion of health care worker to patient b. Pathogenesis 1. Typical staphylococcal skin infection – organisms penetrate a sebaceous gland of hair shaft where the environment is suitable for growth 2. Likelihood of infection is determined by: a. defense mechanisms of the host b. size and virulence of the infective dose 3. Precipitating causes of staphylococcal disease a. third degree burns b. traumatic wounds c. surgical incisions d. Decubitus or trophic ulcers e. certain viral infections c. Clinical manifestation 1. Localized skin infections a. folliculitis 1. superficial folliculitis- raised domed pustules form around hair

follicles 2. deep folliculitis – microorganisms Invades the deep portion of the follicle and dermis

b. Furuncle or boils – an extension into the

subcutaneous tissue resulting in the formation of a focal suppurative lesion c. Carbuncles 1. result from the coalescence of furuncles and extend to the deeper subcutaneous tissue 2. with multiple sinus tracts 3. associated fever and chills

d. Impetigo 1. A superficial infection affecting mostly young

children 2. Manifested primarily on the face and limbs 3. Starts initially as a small macule that develops

into a pus filled vesicle on an erythematous base 4. Crusting when pustules rupture

2. Deep, localized infections a. osteomyelitis

1. Follows hematogenous spread from a primary focus, usually a wound or furuncle

2. Organisms localize at the diaphysis of long bones 3. Acute osteomyelitis – fever, chills, pain over the

bone and muscle spasm around the area of involvement 4. Secondary osteomyelitis – associated with a

penetrating trauma or surgery and frequent in patients with diabetes mellitus and peripheral vascular disease b. Pyoarthrosis

1. May occur after orthopedic surgery in conjunction with osteomyelitis or local skin infections

2. May result from direct inoculation of staphylococci into the joint during intra-articular injections, especially in patients with rheumatoid arthritis

3. Destroys the articular cartilage resulting to permanent joint deformity 3, Bacteremia and endocarditis a. bacteremia may occur with any

localized staphylococcal infection b. primary focus – infections of the skin, the

respiratory tract or the genitourinary tract c. commonly seen in persons with diabetes

mellitus, cardiovascular disease, granulocyte disorders and immunologic deficiency

d. symptoms – fever, shaking chills and systemic toxicity

e. frequent complication – endocarditis with heart valve destruction 4. Pneumonia a. primary 1. most often seen in: a. Patients with impaired host defense b. Children with cystic fibrosis or measles c. influenza patients d. debilitated, hospitalized persons being treated with antimicrobials, steroids, cancer chemotherapy or immunosuppressants

2. necrosis, with formation of multiple abscesses- characteristics of the infection

3. usually patchy and focal b. Secondary

1. Results from staphylococcal bacteremia from a focus elsewhere

5. Metastatic staphylococcal infections

a. production of metastatic abscesses – characteristic feature of staphylococcal bacteremia b. most frequent sites – skin, subcutaneous tissues and the lungs; also kidneys, brain and spinal cord

6. Toxinoses ( Toxin mediated) – diseases caused by

the action of toxin a. toxic shock syndrome 1. Mediated by toxic shock syndrome toxin-1 2. A multisystem disease that primarily affects young women who use tampons

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during menstruation 3. Symptoms – fever, marked hypotension, Diarrhea, conjunctivitis, myalgia and a scarlatiniform rash followed by fine desquamation b. Food poisoning (gastroenteritis) 1. Due to the ingestion of food that contains the performed toxin elaborated by enterotoxin producing strains of S. aureus 2. Foods implicated – custard or cream filled bakery products, ham, processed meats, ice cream, cottage cheese, hollandaise sauce and chicken salad 3. Onset – 2 to 6 hours after ingestion of food 4. Symptoms: severe cramping abdominal pain nausea, vomiting and diarrhea, sweating and headache; no fever 5. Recovery within 6 to 8 hours c. Scalded skin syndrome 1. Mediated by staphylococcal exfoliative toxin 2. Three distinct entities a. Generalized exfoliative dermatitis (Ritters disease, toxic epidermal necrolysis) 1. Most severe form

2. Characterized by generalized painful erythema and dramatic bullous desquamation large areas of the skin

3. Positive Nikolsky sign – skin is displaced under slight pressure b. Bullous impetigo – a localized form of SSS 1. Produced by phage type 71 2. Associated with superficial skin blisters 3. Negative Nikolsky sign c. Staphylococcal scarlet fever – a mild generalized form of the scalded skin syndrome, clinically similar to streptococcal scarlet fever d. Laboratory diagnosis 1. Microscopic morphology – Gram stain

b. Culture 1. Blood agar plate – primary isolation media c. Catalase test – differentiate Staphylococci from streptococci a. staphylococci – catalase positive b. streptococci – catalase negative 1. Add H2O2 to a colony in a slide. Add colony paste on a wooden stick to a drop of H202 on a slide 2. Catalase hydrolyzes H2O2 into oxygen and water d. Coagulase test – to distinguish pathogenic staphylococci from nonpathogenic staphylococci 1. Coagulase positive – pathogenic; S. aureus 2. Coagulase negative – nonpathogenic Two forms of coagulase 1. bound coagulase (clumping) – can directly convert fibrinogen to insoluble fibrin and causes the staphylococci to clump together 2. free coagulase – reacts with a globulin plasma factor (caogulase reacting factor – CRF) to form a thrombinlike factor, staphylothrombin – catalyzes the conversion of fibrinogen to insoluble fibrin

1. Slide coagulase test – detects bound coagulase a. a drop of plasma is added to a drop of bacterial suspension 2. Tube coagulase test – detects free coagulase a. Microorganisms are incubated in plasma for 2 to 4 hours e. Mannitol fermentation – differentiates S. aureus from other catalase positive gram- positive cocci f. Susceptibility testing – broth microdillution or disk diffusion susceptibility testing g. Serologic and typing tests 1. Antibodies to teichoic acid can be detected in prolonged, deep infections (endocarditis) 2. Phage typing – used for epidemiologic tracing of infection only in severe outbreaks of S. aureus infections e. Treatment 1. Localized staphylococcal infections a. adequate drainage b. debriment c. antibiotics – may control the spread of the organisms from the abscess but less effective on bacteria within the abscess and do not facilitate its resolution Initial drug of choice – penicillinase – resistant drugs since most isolates are resistant to penicillin G, penicillin V and ampicillin If sensitivity testing shows staphylococcus to be sensitive to penicillin continue treatment with penicillin because it is more active and less expensive 2. cutaneous infections 1. Oral therapy with a semisynthetic penicillin such as cloxacillin or dicloxacillin; not nafcillin and oxacillin – not well absorbed orally 2. Erythromycin if allergic to penicillin 3. Serious systemic staphylococcal disease a. parental administration of nafcillin or oxacillin b. alternative drugs – vancomycin or cephalosporins c. duration of treatment – 4 to 6 weeks to prevent later emergence of metastatic abscesses 4. Methicillin – drug used in testing the resistance of these organisms If resistant to methicillin, also resistant to nafcillin, oxacillin and all B lactam antibiotics; also to gentamicin, tobramycin and clindamycin Recommended treatment for MRSA – vancomycin alone or in combination with rifampin f. Prevention 1. Staphylococcal infection will never be controlled because of the carrier state in humans 2. Home and hospital setting a. proper hygienic care b. disposal of contaminated materials 3. Hospital setting a. Segregate persons with staphylococcal lesions from newborn infants and from highly susceptible adults b. Avoid indiscriminate use of antibiotics to prevent establishment of resistant strains c. Perform all surgical procedures and instrumentation observing aseptic techniques d. In the newborn infant 1. proper care of the umbilical stump 2. Screen personnel in the nursery for staphylococcal carriers e. The infection committee should provide effective surveillance and follow through problems encountered.

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STAPHYLOCOCCUS EPIDERMIS 1. Identification a. Staphylococcus epidermis characteristically produce white colonies on blood agar b. It may be distinguished from S. aureus and from other coagulase negative staphylococci in biochemical properties. 2. Epidemiology a. Host specific for humans which serve as an: a. endogenous source b. exogenous source of contamination for infection to others b. Most frequent sites – axillae, head, arms, nares and legs c. All infections are hospital acquired and result from contamination of a surgical site by organisms from the patient’s skin or naso-pharynx or from hospital personnel d. Resistant to multiple antibiotics including methicillin and penicillin G 3. Pathogenesis a. In the normal host, S. epidermidis is an organism with low virulence, but when host defenses are breached, it may cause serious often life threatening infections b. has a distinct predilection for foreign bodies like artificial heart valves, indwelling intravascular catheters, central nervous system shunts and hip prostheses c. initiating step for infection – adhesion of organisms to the surface of the prosthetic device d. some produce a viscous extracellular substance that facilitates colonization on smooth surfaces e. Glycocalyx 1. facilitates adhesion to the smooth prosthetic surfaces 2. Protects them from antibiotics and natural host defenses f. adherence of S. epidermidis causes erosive changes in the inert surface of polyethylene catheters 4. Clinical infection a. single mist common isolate from infectious associated with cardiac valve or hip replacement and central nervous system shunt insertion b. causes infections of pacemakers, vascular grafts and prosthetic joints and also peritonitis in patients undergoing peritoneal dialysis c. single most common organism infecting intravenous catheters d. bacteremia e. urinary tract infections especially in elderly hospitalized men f. natural valve endocarditis in intravenous drug abusers g. produces toxins in toxic shock syndrome 5. Treatment 1. multiple antibiotic resistance, including methicilin 2. choice of appropriate therapy – based on the local antibiogram 3. Initial regimen – if no antibiogram a. aminoglycoside (gentamicin or tobramycin) with cephalothin + penicillinase resistant penicillin b. vancomycin alone or vancomycin + aminoglycoside Prevention

- Difficult due to ubiquitous nature of organism - Measures taken

*handwashing * reducing transmission rate from staff to patient or patient to patient *proper surgical techniques help minimize infections associated with installation of indwelling medical devices

STAPHYLOCOCUS SAPROPHYTICUS 1. This coagulase negative staphylococci can be distinguished from S. epidermidis by its: a. resistance to novobiocin b. failure to ferment glucose anaerobically 2. It is nonhemolytic and does not contain Protein A. 3. Most strains have the ability to agglutinate sheep erythrocytes 4. Occurs on the normal skin and in the periurethral and urethral flora 5. Common cause of urinary tract infections in sexually active young women second to Escherichia coli – upper urinary tract is involved 6. Shows tropism for the epithelial lining of the urinary tract 7. Selectively adheres to urothelial cells via specific oliogosaccharide receptors on the cell membrane 8. Certain strains are able to suppress growth of other bacteria such as Neisseria gonorrhea and S. aureus attributed to an extracellular enzyme complex. Although we stumble everyday The Lord is always there To lift us up, forgive our sin, And show His love and care.

Micro Strep and Staph Trans 1

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