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105 Cards in this Set
- Front
- Back
Genus streptococcus
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a. Gram positive cocci in pairs or chains
b. Facultative and capnophilic c. Fastidious |
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Serology of strep
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a. Lancefield groupings
b. A-W |
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Strep hemolysis
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a. β
b. α c. γ |
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S. pyogenes
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a. Associated with pyogenic infections
b. Catalase-negative c. β hemolysis d. Requires enriched medium (blood and serum) |
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S. pyogenes epidemiology
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a. Asymptomatic URT and transient skin colonization
b. Person to person spread by respiratory droplets c. Crowding facilitates spread d. .5 deaths/yr due to GAS infections |
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Patients with soft-tissue infections and bacteremia with s. progenies
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i. TSS
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5-15 y/o risk
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i. Pharyngitis
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2/5 y/o with poor hygiene
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i. Pyoderma
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Seasonal risk
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i. Pharyngitis--winter
ii. Pyoderma--summer |
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S. pyogenes virulence
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a. Capsulated
b. LTA c. M protein d. M-like protein e. F protein |
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M-proteins in s. pyogenes
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a. >120 serotypes
b. Anchored in cell wall and extends to surface c. Phagocytic resistance neutralized by M-protein antibody d. Plasma fibrinogens binds to M-proteins |
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Plasma fibrinogens binding to M-proteins causes....
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i. A prevention of complement activation and opsonization
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Increase of M-antibodies
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i. Protection from only that serotype
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S. pyogenes pharyngitis
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a. Strep throat
b. Primarily in 5-15y/o age group c. Adults and very young also susceptible d. Spreads via respiratory droplets and close contact |
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Peak of s. pyogenes pharyngitis
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i. Winter
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Incubation period of s. pyogenes
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i. 1-4 days
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Symptoms of s. pyogenes pharyngitis
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i. Mild throat discomfort to severe swelling of pharyngeal mucosa with exudate
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Suppurative complications of s. pyogenes
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i. Peritonsillar or retropharyngeal abscess
ii. Rheumatic fever |
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Non-suppurative complications of s. pyogenes
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i. Acute glomerular nephritis
ii. Suppuration rare due to timely antibiotic treatment |
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What toxins produce scarlet fever?
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1. Pyrogenic exotoxins A, B, and C
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Toxin spread in scarlet fever
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1. Through the blood
2. Localizes in the skin 3. Induce a diffuse erythematous rash on upper chest |
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Initial presentation of scarlet fever
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1. Tongue initially furred and red later
2. Rash spreads to extremities 3. Rash disappears in 5-7 days followed by desquamation 4. Disease is now rare |
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Scarlet fever and subsequent s. pyogenes infection
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1. Rash not serious in scarlet fever, but signals infection by a harmful S. pyogenes
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Scarlet fever rash
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1. Discrete
2. Pinhead-sized 3. Desquamation follows |
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Streptococcal impetigo/pyoderma
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i. More common in summer
ii. Most common in children w/ poor hygiene iii. Skin colonization precedes clinical infection iv. Minor trauma introduces GAS into skin |
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Usual site of impetigo/pyoderma
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1. Around nose and mouth
2. Legs |
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Progression of impetigo/pydoerma
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1. Vesicle→ pustule→ ruptures and crusts over
2. Lesion usually not painful and patients do not appear ill |
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Culture of lesion in streptococcal impetigo/pyoderma
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1. Yields S. aureus and S. pyogenes
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Cellulitis
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i. Infection involving skin and subcutaneous tissues
ii. Infection due to traumatic/surgical wound or insect bite iii. Often no entry site is apparent |
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Ersyipelas
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i. A form of cellulitis
ii. Bright and red appearance of skin iii. Usually on malar area of face iv. Extends over bridge of nose to contralateral malar region v. “Butterfly rash” |
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Necrotizing fasciitis
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i. GAS responsible for ~60% of cases
ii. Starts like cellulitis→ gangrene, bullaes, and systemic signs iii. Requires extensive debridement and antibiotic treatment iv. Obstructed blood supply along the fascial planes |
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Extensive necrosis
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1. Requires surgical exploration
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What is another name for necrotizing fasciitis?
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1. Hemolytic streptococcal gangrene
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Streptococcal TSS
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i. Likely in patients bacteremic with GAS
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Bacteremia causes....
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1. Pharyngitis→ rare
2. Cellulitis→ occasional 3. NF→ always |
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streptococcal toxins in TSS
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1. Always involved
2. SpeA and SpeC-- super antigens |
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Symptoms of streptococcal TSS
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1. Fever
2. Malaise 3. HT 4. Multiple organ failure |
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Acute rheumatic fever and rheumatic heart disease
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i. 1-3 wk after acute illness
ii. Almost exclusively after a URT infection (pharyngitis) iii. Less common in developed countries |
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Rheumatogenic GAS
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1. Encapsulated and rich in M proteins
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Presentation of rheumatogenic GAS
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1. S/C nodules
2. Arthralgia 3. Frank arthritis |
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Ig and rheumatogenic GAS
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1. Anti-M IgG cross-react with heart proteins
2. Produce pancarditis |
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Prevention of rheumatogenic GAS
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1. Antibiotic prophylaxis needed to prevent subsequent GAS infection
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Acute glomerulonephritis
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i. Can be seen after pharyngitis and also after skin infections
ii. Only 4-5 M strains cause AGN, recurrences are unlikely iii. Ag-Ab complexes on glomerular basement membrane iv. Glomerular capillaries are filled with monocytes and PMNs |
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Antibiotic prophylaxis for acute glomerulonephritis
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1. Not recommended
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Symptoms of AGN
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1. Acute inflammation
2. Hypertension 3. Hematuria 4. Proteinuria |
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Identification of s. pyogenes
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1. Chains of cocci
2. Β-hemolytic 3. Catalase-negative |
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PYR test in s. pyogenes
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1. Only streptococci that gives a positive test
2. Forms pink to cherry-red pigment |
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A disk in s. pyogenes
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1. Bacitracin
2. S pyogenes is sensitive but S agalactiae is resistant |
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P disk in s. pyogenes
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1. Optochin
2. Most viridian streptococci are α hemolytic 3. S. pneumoniae- sensitive 4. Other viridans-resistant |
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Two immunogenic toxins of s. pyogenes
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1. Streptolyisn O
2. DNase B |
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Group B strep
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a. Streptococcus agalactiae
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S. agalactiae characteristics
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1. Gram positive cocci
2. Long chains 3. β hemolytic |
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S. agalactiae epidemiology
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1. Native to female urogenital tract and rectum
2. Women with genital colonization--risk for postpartum sepsis 3. Babies acquire from other or babies in nursery |
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Nine capsular polysaccharide types of s. agalactiae
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a. Ia, Ib, II-VIII
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Most commonly capsular polysaccharides associated with disease
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i. Ia
ii. III iii. V |
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Affects of GBS on fetus
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1. Genital colonization increases risk of premature birth
2. Premature infants are at greater risk of disease |
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GBS in men and non-pregnant women
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1. Disease usually in older and IC
2. Bacteremia, pneumonia, bone, skin and soft tissue infections 3. High mortality due to IC |
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GBS in pregnant women
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1. UTI during and immediately after pregnancy
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Puerperal sepsis in GBS
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a. Serious septiciemia during or shortly after childbirth
b. Rare due to improved hygiene during delivery |
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GBS disease in newborns
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1. Major cause of neonatal meningitis
2. Acquired by aspiration of infected amniotic fluid 3. Few alveolar Mψ, poor PMN chemotaxis and phagocytosis 4. Low complement levels which are needed for GBS killing |
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Early-onset GBS disease in newborns
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a. >5% motality due to better dx and supportive care
b. Clinical presentation i. Bacteremia, pneumonia, and meningitis |
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Late-onset GBS disease in newborns
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a. Acquired from infected mother or nosocomial
b. Bacteremia with meningitis |
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Identification of s. agalactiae
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i. Catalase-negative
ii. β hemolytic iii. Coccus |
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Biochemical tests for s. agalactiae
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1. Hydrolysis of sodium hippurate (99% positive)
2. Hydrolysis of bile esculin (99-100% positive) 3. Bacitracin susceptibility (92% resistant) 4. CAMP test (98-100% positive) |
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CAMP test for s. agalactiae
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1. Christie, Atkins, Munch, Petersen test
2. CAMP factor is a phospholipase 3. Causes synergistic hemolysis with S. aureus β-lysin |
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Prevention of s. agalactiae
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i. Screen anogenital region @ 35-37 weeks of pregnancy
ii. Chemoprophylaxis for culture positive cases iii. Treat women with history of GBS+ irrespective of test result |
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Viridans streptococci
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a. Non-pyogenic
b. 5 groups c. *Mitis, *anginosus, *salivarius, mutans, bovis d. *-- Core of group |
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Prevalence of viridans streptococci
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i. Oral cavity
ii. URT iii. Female genital tract iv. Can cause cavities |
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Viridans spread to blood
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i. Through disruption of oral mucosa
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Important viridans
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i. S. mitis
ii. s. mutans iii. s. salivarius iv. s. sanguis |
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Viridis
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i. Green
ii. Produce a green pigment on blood agar |
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Mitis group
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1. Includes s. pneumonia and 12 other species
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S. pneumoniae characteristics
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a. Gram positive coccus (lancet shaped)
b. Diplococci (pairs) c. Fastidious d. Capsulated e. Capnophilic f. α hemolytic g. Bile salt susceptible |
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s. pneumoniae epidemiology
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i. Colonizes nasopharynx
ii. 5-10% of adults and 20-40% of children iii. Mostly endogenous spread iv. URT to middle ear, sinuses, meninges, lungs, and blood |
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Colonization and migration of s. pneumoniae
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i. Colonization of URT is mediated by surface adhesins
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sIgA and s. pneumoniae
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i. SIgA trap bacteria in mucus and prevent migration to lower LRT
ii. Produce sIGA protease and pneumolysin (ply) |
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Ply
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1. Kills ciliated epithelial cells and phagocytes
2. Lysis of host cells causes edema, hemorrhage, bacterial growth 3. Helps in penetration through epithelium into interstitium and blood |
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S. pneumoniae removed from airways by...
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1. Ciliated epithelial cells
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Capsule of s. pneumoniae
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i. Primary virulence factor
ii. Non-encapsulated strains are almost harmless iii. Inhibits phagocytosis and complement iv. >90 serotypes |
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Vaccines for s. pneumoniae
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1. Mixture of capsular polysaccharides
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Disease of s. pneumoniae
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i. Occur worldwide
ii. Frequently seen in co-infection with influenza |
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Three major clinical diseases of s. pneumoniae
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i. Pneumonia
ii. Meningitis iii. Otitis media |
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S. pneumoniae pneumonia
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i. Often preceded by viral illness
ii. Viruses up-regulate adhesion factors in respiratory epithelium |
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PG and TA in pneumonia
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1. PG and TA induce invasion
2. PG/TA also induce inflammatory cytokines (IL1, IL6, TN F) |
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Symptoms of s. pneumoniae pneumonia
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1. Acute onset, high fever with rigors, productive cough
2. Pleural pain, dyspnea, tachypnea, tachycardia, sweats 3. PMNs and lance-shaped diplococcic in rusty sputum 4. Rusty sputum as blood leaks from capillaries |
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Localization of pneumonia
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1. Only affects a section/lobe
2. No significant protease-- seldom destroys parenchyma 3. Consolidation is less obvious in dehydrated patients |
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Otitis media symptoms
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1. Severe and continuous earache often with fever of 39C or more
2. Pain and fever more common than OM caused by other bacteria 3. Rare cases-- may spread from middle ear to cause meningitis |
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Bacterial pathogens in OM
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1. Negative culture-- 33.7%
2. S. pneumonia-- 29.4% 3. Moraxella catarrhalis--25.2% 4. H. influenzae-- 20.5% |
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Meningitis
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i. Most common cause in children and adults in US
ii. Severe neurological defects in survivors |
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Predisposing conditions to meningitis
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1. Pneumonia
2. OM |
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Fatality compared to other bacterial meningitis
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1. Higher
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Bacteremia/endocarditis from s. pneumoniae
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i. ~30% pneumonia and 80% meningitis patients are bacteremic
ii. Sub-acute endocarditis iii. Common in those with previous damaged heart valves |
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Identification of s. pneumoniae
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i. α hemolytic
ii. Lancet-shaped iii. Gram positive iv. Diplococcic v. Catalase negative vi. Bile soluble vii. Optochin-sensitive viii. TA in urine |
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Enterococcus characteristics
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i. E. faecalis predominates
ii. Gram positive cocci (pairs and short chains) iii. High salt, bile, temp, and antibiotic resistance |
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Enterococcus epidemiology
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i. Enteric pathogen, can also colonize the GUT
ii. Most infections are endogenous iii. Frequent cause of nosocomial infections iv. Cross-infection in nosocomial settings |
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Enterococcus virulence
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i. Many secreted factors, adhesins, and a dynamic genome
ii. Use of avoparcin-- a GP/growth promoter in animal husbandry iii. Proliferaiton after antibiotic use--especially in those that target anaerobes/gram negative rods iv. Loss of normal flora suppresses signals that control enterococci |
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Enterococcus UTI
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i. Mainly nosocomial
ii. Significant cause of UTI iii. Dysuria and pyuria iv. Common in those with indwelling catheter or on broad antibiotics |
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Peritonitis from enterococcus
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i. Abdominal swelling and tenderness after abdominal trauma or surgery
ii. Patients are typically acutely ill and febrile |
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Endocarditis from enterococcus
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i. In patients with persistent bacteremia
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Identification of enterococcus
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i. High salt, bile, and temp tolerance
ii. Optochin resistant distinguishes it form s. pneumonia iii. Do not lyse sheep RBCs (white colonies on blood agar) iv. Usually lytic for human RBCs |
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Anaerobic cocci
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a. Part of normal flora
b. Colonize oral cavity, GIT, genitourinary tract, and skin |
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Anaerobic cocci in URT
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i. Sinusitis
ii. Pleuropulmonary infections |
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Anaerobic cocci in GIT
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i. Intra-abdominal infections
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Anaerobic cocci in GUT
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i. Endometritis
ii. Pelvic abcesses iii. Salpingitis |
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Anaerobic cocci on skin
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i. Cellulitis
ii. Soft tissue infections |