Gram-Positive Cocci

Published on 18/02/2015 by admin

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Gram-Positive Cocci

I Staphylococcus Species

Trigger words:

S. aureus: catalase, coagulase, grape-like clusters, MRSA, pus, 3-hour gastroenteritis, toxins, TSST

S. epidermidis: catalase, catheters, coagulase negative, shunts

• Three staphylococcal species commonly cause human disease: S. aureus (most virulent), S. epidermidis, and S. saprophyticus.

A Shared staphylococcal properties

1. Gram-positive cocci in grape-like clusters

2. Catalase positive; growth in 7.5% salt

3. Ubiquitous distribution; part of normal flora; responsible for many nosocomial infections

B Coagulase-positive staphylococci (S. aureus)

S. aureus: major cause of nosocomial and wound infections

S. aureus ferment mannose, other staph don’t.

• S. aureus is normal flora of skin and the anterior nares.

1. Pathogenesis

• Table 9-1 summarizes the major contributors to the virulence of S. aureus.

TABLE 9-1

Major Virulence Factors of Staphylococcus Aureus

ADCC, antibody-dependent cellular cytotoxicity.

2. Diseases caused by S. aureus (Box 9-1)

BOX 9-1 Staphylococcus Aureus Diseases: Quick Cases

Toxin-Mediated Diseases

Food poisoning due to enterotoxin (A-E): Individual with severe nausea, vomiting, and diarrhea developing 4 hours after eating potato salad and ham sandwiches at a picnic in July. Complete recovery after bed rest for 2 days and drinking plenty of fluids

Scalded skin syndrome due to exfoliative toxin: Young child with blister-like lesions widely disseminated over the body. Large areas of desquamated epithelium but no scarring

Toxic shock syndrome due to TSST-1 (superantigen): Young woman with rapid onset of fever, diarrhea, desquamating rash, multisystem organ involvement, kidney failure, shock with generalized flushing of the skin and mucous membranes. Examination shows a tampon lodged in her vagina.

Toxic shock syndrome due to TSST-1: Child or adolescent develops shock with multiorgan failure and generalized flushing of the skin and mucous membranes within days of sustaining a deep wound.

Suppurative Infections

CA-MRSA: A high school football player with necrotizing fasciitis is treated with clindamycin. Other members of the team also have skin infections (boils and abscesses).

Carbuncle: Diabetic patient whose blood glucose is under poor control with a large swollen area of redness on one leg

Endocarditis: Recent onset of fever, petechial lesions, and detection of a new heart murmur in a patient with an intravascular catheter

Impetigo: Child with honey-colored or clear crusts over ruptured pustules (usually bullous lesions) on the face; intense itching

Osteomyelitis and septic arthritis: Child with fever and localized pain and swelling below the right knee following orthopedic surgery; positive blood culture for S. aureus

Pneumonia: Individual suddenly develops fever, difficulty breathing, and empyema (intrapleural abscesses) soon after recovering from influenza.

Wound infection: Elderly man with fever and redness and swelling at the site of recent surgery

• Toxin-mediated diseases

a. Food poisoning, toxic shock syndrome (TSS), scalded skin syndrome

Staphylococcal food poisoning due to preformed toxin is quick acting (<3 hours).

Staphylococci are salt tolerant and grow on picnic meats and other foods.

• Community-acquired methicillin resistant S. aureus (CA-MRSA) carries resistance plasmids that also have the Panton valentine leukocidin gene and may be more virulent.

CA-MRSA also carries Panton valentine leukocidin gene.

• Inflammatory diseases mediated by pyogenic and necrotic activities of S. aureus

a. These suppurative (pus-forming) infections range from benign skin lesions (e.g., folliculitis, furuncles, and carbuncles) to life-threatening systemic diseases (osteomyelitis, pneumonia, and endocarditis) and bacteremia.

S. aureus uses many different virulence mechanisms to degrade tissue.

Staphylococci and streptococci cause pus-forming (suppurative) infections.

3. Transmission of S. aureus

• Person-to-person contact and via fomites

• Endogenous spread via blood or aspiration of nasal secretions

• Ingestion of preformed enterotoxins in food

a. S. aureus can multiply and make toxin in salted and smoked meats (cold cuts), as well as creamy foods (potato or egg salads), if they are unrefrigerated for extended periods. Reheating does not destroy the heat-stable enterotoxins.

Antibiotics and staphylococci: most staphylococci are resistant to penicillin (produce a β-lactamase). Resistance to methicillin means resistance to all β-lactams.

Staphylococci = catalase (positive); streptococci = catalase (negative).

• Most staphylococci produce penicillinase (a β-lactamase) and are commonly treated with a penicillinase-resistant β-lactam penicillin derivative, such as nafcillin, oxacillin, or methicillin.

• MRSA strains (hospital acquired) are treated with vancomycin, linezolid, daptomycin, tigecycline, trimethoprim sulfa, or clindamycin.

• CA-MRSAs are becoming more common.

a. Treatment is with trimethoprim-sulfamethoxazole.

• Methicillin- and vancomycin-resistant S. aureus was acquired from an Enterococcus plasmid.

C Coagulase-negative staphylococci (S. epidermidis and S. saprophyticus)

1. These bacteria are normally benign colonizers of the skin.

2. They are less virulent than S. aureus, although their virulence factors are similar (except for lack of coagulase).

3. S. epidermidis can adhere to artificial heart valves, vascular catheters, shunts, and prosthetic joints, colonizing the implant area and causing tissue destruction mediated by degradative enzymes.

• Vancomycin is the drug of choice.

4. S. saprophyticus is a frequent cause of urinary tract infections (UTIs) in sexually active young women.

• Treatment: oral cephalosporin or amoxicillin clavulanate

II Streptococcus Species

• Most common streptococcal pathogens in humans are S. pyogenes, S. agalactiae, viridans group, and S. pneumoniae.

Trigger words:

S. pyogenes: Bacitracin (A disk-group A) sensitivity, β hemolysis, gram-positive cocci in chains, necrotizing fasciitis, pus, streptolysin O and S

A Shared streptococcal properties

1. Gram-positive spherical or football-shaped cocci in pairs or chains

2. Catalase negative

3. Species-dependent hemolysis in blood agar (Table 9-2)

TABLE 9-2

Streptococcal Hemolysis

Hemolytic reaction	Organism	Differentiating property
α (Incomplete) hemolysis	S. pneumoniae	Optochin sensitive
(greenish zone around colony)	Viridans streptococci	Optochin resistant
	Enterococcus (some)	—
β (Complete) hemolysis	S. pyogenes (group A)	Bacitracin sensitive
(clear zone around colony)	S. agalactiae (group B)	Bacitracin resistant
γ (No) hemolysis	Enterococcus (some)	—

4. Lancefield classification

• Groups based on serologic identification of group-specific C-carbohydrates on cell wall

B Group A streptococci (S. pyogenes)

S. pyogenes: causes pharyngitis, scarlet fever, toxic shock, rheumatic fever, acute glomerulonephritis

1. Identification

• β-Hemolytic

• Sensitive to bacitracin (A disk)

• Hyaluronic acid–containing capsule

a. Spreading factor that helps bacteria extend through subcutaneous tissue (cellulitis)

• Antibodies to streptolysin O appearing 3 or 4 weeks after primary infection

a. Antistreptolysin O titer is useful in the diagnosis of acute rheumatic fever.

• Anti-DNase B antibodies

a. Useful in the diagnosis of acute rheumatic fever, streptococcal skin infections (e.g., scarlet fever), poststreptococcal glomerulonephritis

2. Pathogenesis

• Table 9-3 summarizes the major contributors to the virulence of S. pyogenes and other group A streptococci.

TABLE 9-3

Major Virulence Factors of Group A Streptococci

3. Group A streptococcal diseases (Box 9-2)

BOX 9-2 Group a Streptococcal Diseases: Quick Cases

Suppurative Infections

Erysipelas: Elderly woman or young child with well-demarcated swollen, erythematous area on face; has fever, headache, and swollen lymph nodes

Impetigo: Child with honey-crusted skin lesions over face or trunk, itching, and possible regional lymphadenopathy. S. pyogenes is the second most common cause of impetigo.

Pharyngitis: Child with fever, inflamed throat with possible exudates, general malaise, cervical lymphadenopathy, and no coryza (acute rhinitis); often indistinguishable from viral infection

Pyoderma: Young child (2-5 years) with multiple 1- or 2-mm abscesses over the body, palpable regional lymphadenopathy, and evidence of skin abrasions or insect bites. Most commonly occurs during warm, humid weather and among children in close contact with each other (e.g., in day care centers)

Necrotizing fasciitis: Patient with rapidly expanding area of erythema, bulla formation, and anesthesia around a recent wound on the arm, which leads to tissue destruction; accompanied by fever and other evidence of systemic toxicity (possible shock and multisystem organ failure)

Toxin-Mediated Diseases

Scarlet fever: Child with strawberry tongue and diffuse sandpaper-like erythematous rash over the body within 24 to 48 hours after onset of streptococcal pharyngitis. Rash fades in 5 to 7 days with desquamation.

Streptococcal toxic shock syndrome: Adult man with cellulitis, shock, multisystem organ failure, and generalized skin flushing

Autoimmune Sequelae

Acute glomerulonephritis: Child or teenager with hematuria, red blood cell casts, proteinuria, hypertension, and periorbital edema with history of recently treated skin infection

Rheumatic fever: Child with fever, heart failure, migrating inflamed joints that are not symmetrically involved, and a history of a recent sore throat (see Box 9-3)

• Localized suppurative diseases: pharyngitis (strep throat), skin infections, postsurgical cellulitis, puerperal (at childbirth) sepsis

• Toxin-mediated diseases

a. Streptococcal TSS, scarlet fever

• Nonsuppurative autoimmune sequelae

a. Acute glomerulonephritis, rheumatic fever (Box 9-3)

Group A streptococci must be treated to prevent sequelae.

Sequelae of group A streptococci are rheumatic fever and acute glomerulonephritis.

4. Transmission of S. pyogenes

• Pharyngitis is spread primarily by respiratory droplets.

a. Most common in fall and winter

b. Children 5 to 15 years of age are most susceptible.

• Skin infections are commonly spread by contact of skin breaks with an infected person, fomite, or insect vector.

• Other diseases are complications of primary S. pyogenes infection.

• S. pyogenes is sensitive to penicillin G.

• Treatment of group A pharyngitis prevents potential sequelae (e.g., rheumatic fever and glomerulonephritis).

Group A streptococci are still sensitive to penicillin.

C Group B streptococci (S. agalactiae)

• S. agalactiae is a normal inhabitant of the gastrointestinal and lower genital tracts.

1. Identification

• β-Hemolytic

• Resistant to bacitracin

• Positive CAMP test in which group B hemolysin enhances β hemolysis by S. aureus

2. Pathogenesis

• Antiphagocytic capsule is immunogenic.

• Anticapsular antibodies are important in host defense.

• Hemolysins and various degradative enzymes mediate cellular and tissue destruction.

3. Group B streptococcal diseases

Group B streptococci acquired at birth cause bacteremia, pneumonia, and meningitis within first week.

• Early-onset neonatal disease begins within 7 days of birth.

a. Acquired in utero or at delivery (infection in mother’s vagina)

b. Most common in premature infants

c. High mortality rate

d. Symptoms: bacteremia, pneumonia, meningitis

• Late-onset neonatal disease begins 1 week to 3 months after birth.

a. Acquired postpartum

b. Low mortality rate (<20%)

c. Symptoms: bacteremia, meningitis

• Postpartum sepsis is usually acquired via wound inflicted during parturition.

a. Symptoms: endometritis, fever, chills, wound infection, possible UTI

• Wound infections occur in other adults, especially immunocompromised patients.

• Penicillin G alone or in combination with aminoglycosides

• Passive immunization in serious cases

D Viridans streptococci (S. mutans, S. sanguis)

• These constitute a major part of normal flora of the mouth and teeth.

1. Identification

• α-Hemolytic

• Resistant to Optochin

• No Lancefield antigens

2. Viridans streptococcal diseases

Viridans streptococci cause dental plaque, caries.

Damaged heart valves are a risk factor for viridans strep endocarditis.

• Streptococcal endocarditis occurs most commonly in patients with damaged heart valves, to which bacteria adhere.

a. Symptoms include prolonged fever, heart murmur, microembolization (vegetations), immunocomplex disease (e.g., glomerulonephritis, splinter hemorrhages under nails)

b. Bacteria enter the bloodstream during dental work or after oral trauma, causing transient bacteremia that can initiate disease.

• Dental caries are caused primarily by S. mutans.

a. Adheres to tooth enamel and erodes teeth by converting sucrose to acetic and lactic acids

3. Treatment of streptococcal endocarditis

• Antibiotic prophylaxis of at-risk individuals (e.g., patient with valvular heart disease who has dental work)

E S. pneumoniae (pneumococcus)

Trigger words:

S. pneumoniae: α-hemolytic, capsule, gram-positive diplococci, meningitis, otitis media, P disk (Optochin) sensitive, polysaccharide vaccine, pneumonia

• S. pneumoniae is normally present in the throat and nasopharynx.

1. Identification

• α-Hemolytic

• Sensitive to Optochin (P disk)

• No Lancefield antigens

• Positive quellung reaction (capsular swelling in the presence of specific anticapsular antibody)

Strep pneumo; Optichin sensitive (P-disk; pneumoniae)

Quellung reaction indicates capsule on S. pneumoniae.

2. Pathogenesis

• Aspiration of nasopharyngeal secretions into lower airways leads to rapid growth of pneumococci in alveolar spaces.

a. Reduced clearance of airways due to disruption of ciliated epithelium in upper respiratory tract by viral infection or smoking promotes aspiration.

• Antiphagocytic capsule is required for virulence (See Box 9-4).

• Pneumolysin (similar to streptolysin O) lyses cells.

• Pneumococcal immunoglobulin A (IgA) protease cleaves secretory IgA, increasing adherence to mucosal surfaces.

• Neuraminidase (spreading factor) promotes bacterial spread into tissue.

3. Pneumococcal diseases

• Typical community-acquired pneumonia

a. Marked by abrupt onset, high fever (102° to 105°F), rigor, productive cough, and pleuritic chest pain from pleural inflammation from either bronchopneumonia (patchy pneumonia) or lobar pneumonia (involvement of one or more lobes)

• Bacteremia, found in 25% to 30% of pneumonia patients, may lead to pneumococcal meningitis.

a. S. pneumoniae is the leading cause of bacterial meningitis in people older than 18 years.

• Most common cause of acute otitis media and sinusitis

• Most common cause of sepsis in children with sickle cell disease and dysfunctional spleen

a. Functioning spleen is required for normal elimination of bloodborne S. pneumoniae

• Most common cause of spontaneous peritonitis in children with nephrotic syndrome and ascites

S. pneumoniae and Haemophilus influenzae: most common bacterial causes of acute otitis media and sinusitis

S. pneumoniae, H. influenza, Neisseria meningitidis, and Cryptococcus neoformans (yeast) have capsules and cause meningitis.

4. Epidemiology of pneumococcal infection

• Transmission of pneumococci occurs via aerosol droplets from infected person followed by aspiration into lower airways. Infection is most common in winter and spring.

• At-risk groups include young children, elderly people, asplenic patients (Box 9-4), and other immunocompromised individuals.

BOX 9-4 Infection Risks Associated with Splenectomy

Splenectomy increases the risk for infections by encapsulated bacteria (e.g., S. pneumoniae, H. influenzae, Salmonella species). Factors implicated include a drop in the concentration of IgM (spleen is a synthetic site) and decreased complement activation and production of C3b, an opsonizing agent that is required to phagocytose encapsulated bacteria. Pneumovax immunization is important in preventing S. pneumoniae sepsis.

5. Prevention and treatment

• Polysaccharide capsular vaccines (with or without conjugated protein) for at-risk populations and children

• Increasing pneumococcal resistance to penicillin, especially in isolates from children attending day care centers

a. Macrolides (erythromycin), cephalosporins, and fluoroquinolones are effective alternatives to treatment with penicillin for pneumonia, otitis media, and sinusitis.

• Cefotaxime or ceftriaxone for meningitis

III Enterococcus (E. faecalis, E. faecium)

• These organisms are normal flora of the large bowel and feces. Antibiotic resistance is common among enterococci and contributes to their pathogenicity.

A Identification

1. Gram-positive cocci in twisted chains

2. Catalase negative

3. Bacitracin resistant

4. Variable hemolysis

5. Bile and salt tolerant (growth in media containing 6.5% NaCl)

Enterococci grow in bowel and resistant to bowel conditions: bile and salt.

B Enterococcal diseases

• Risk factors include catheterization and administration of broad-spectrum antibiotics.

1. UTIs, particularly in hospitalized patients

2. Endocarditis (similar to viridans streptococci)

3. Wound infections

C Treatment

1. Ampicillin can be used for sensitive strains

2. Combination of an aminoglycoside and vancomycin for resistant strains.

• Vancomycin-resistant enterococci (VRE) have a substitute for the D-Ala-D-Ala in peptidoglycan that is the target for vancomycin.

Enterococci are inherently resistant to many antibiotics.

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