Streptococcal Infections Flashcards

1
Q

Pharyngitis

A

essentials of DX:

  • abrupt onset of sore throat, fever, malaise, N, and HA
  • throat red and edematous, w/ or w/o exudate; cervical nodes tender
  • DX confirmed by cx of throat

etiology:

  • Group A beta-hemolytic streptococci (Streptococcus pyogenes) are most common bacterial cause of pharyngitis
  • transmission = droplets of infected secretions

S:

  • “strep throat”
    • characterized by sudden onset of fever, sore throat, pain on swallowing, tender cervical adenopathy, malaise, N
    • pharynx, soft palate, and tonsilas are red and edematous
    • may be purulent exudate
    • Centor clinical criteria for dx of Strep pharyngitis = T>38 degrees C, tender ant cervical adenopathy, lack of cough, pharyngotonsillar exudate
  • rash of scarlet fever:
    • diffusely erythematous, resembling a sunburn, w/ superimposed fine red papules and is most intense in groin and axillae
    • blanches on pressure, may become petechial, fades in 2-5 days, leaving fine desquamation
    • face is flushed, with circumoral pallor and tongue is coated with enlarged red papillae (strawberry tongue)

A:

  • Leukocytes with neutrophil predominence is common
  • throat cx onto single blood agar has sensitivity of 80-90%
  • Clinical criteria ie Centor criteria are useful for identifying pts who should receive rapid antigen test or throat cx (pts who meet 2 or more merit further testing)
  • DDX:
    • Strep sore throat resembles and cannot be reliably distinguished clinically from pharyngitis caused by viruses such as adenoviruses, Epstein-Barr virus, primary HIV, or other bacteria such as *Fusobacterium necrophorum *and *Arcanobacterium haemolyticum *(which may also cause rash)
    • pharyngitis and lymphadenopathy are common findings in primary HIV infection
    • generalized lymphadenopathy, splenomegaly, atypical lymphocytosis, and positive serologic test distinguich mononucleosis from strep
    • Diptheria is categorized by pseudomembrane
    • oropharyngeal shows white patches of exudate and less erythema
    • necrotizing ulcerative gingivostomatitis (Vincent fusospirochetal gingivitis or stomatitis) presents with shallow ulcers in the mouth
    • retropharyngeal abscess or bacterial epiglottis should be considered when odynophagia and difficulty in handling secretions are present and when severity of sxs is disproportionate to findings on exam of pharynx
    • F necrophorum pharyngitis is ass w/ Lemierre syndrome, suppurative thrombophlebitis of the internal jugular vein, bacteremia, and metastatic infections

P/TX:

  • antimicrobial therapy has modest effect on resolution of sxs and is primarily used for prevention of complications; abx therapy can be safely delayed until dx est based on positive antigen test or cx
  • macrolides not reliable against F necrophorum infection, so adolescents and adults (where pharyngitis has not been confirmed to be of group A beta-hemolytic strep) should be given Penicillin or amoxicillin
  • if pharyngitis does not quickly resolve, consider suppurative complications, i.e. peritonsillar abscess and the Lemierre syndrome
  • Benzathine Penicillin G (1.2 million units IM, single dose)
  • Penicillin VK (250 mg QID or 500mg BID PO x 10 days)
  • Amoxicillin (1000mg QD or 500 mg BID PO x 10 days)
  • Cephalosporins (cephalexin, cefdinir, cefpodoxime)
  • Macrolides (erythromycin, azithromycin, clindamycin)
  • prevention of rheumatic fever is very important
  • when to refer:
    • peritonsillar or retropharyngeal abscess should be referred to ENT
  • when to admit:
    • odynophagia resulting in dehydration
    • suspected or known epiglottitis
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2
Q

Strep Skin Infections

A

etiology:

  • Group A beta-hemolytic strep are not normal skin flora
  • strep skin infections resultsfrom colonization of normal skin by contact with other infected individuals or by preceding strep respiratory infection

S/O:

  • Impetigo
    • focal, vesicular, pustular lesion with thick, amber-colored crust wth a “stuck-on” appearance
  • Erysipelas
    • painful superficial cellulitis frequently involves the face
    • well demarcated
    • affects skin with impaired lymphatic drainage ie edematous LE or wounds

A:

  • cx obtained from wound or pustule are likely to grow group A strep

P/TX:

  • parenteral abx are indicated for pts with facial erysipelas or evidence of systemic infection
  • Penicillin (2 million units IV every 4 hours) is drug of choice
  • hard to distinguish between staph and strep infections
  • Nafcillin
  • cefazolin
  • in pt at risk for methicillin-resistant *S aureus *infection or with serious penicillin allergy, vancomycin (1g IV every 12 hrs) or daptomycin (4mg/kg IV daily) can be used
  • pts who do not require parenteral therapy may be treated with amoxicillin, cephalexin, or clindamycin orally
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3
Q

Arthritis

A

etiology:

  • group A Streptococcal infection
  • generally occurs in association with celluitis

P/TX:

  • In addn to IV therapy with penicillin G, 2 million units every 4 hours (or cefazolin orvancomycin in doses recommended above for penicillin-allergic patients), frequent percutaneous needle aspiration should be performed to remove joint effusions
  • Open surgical drainage may be necessary in many cases
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4
Q

Pneumonia and empyema

A

etiology:
* other group A Strep infections

S/O:

  • extensive tissue destruction and aggressive, rapidly progressive clinical course ass w/ significant morbidity and mortality

P/TX:

  • high-dose PCN and chest tube drainage are indicated for tx of empyema (vancomycin to sub for PCN in allergic pts)
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5
Q

Endocarditis

A

Subacute bacterial endocarditis (SBE)

etiology

  • Group A strep

P/TX:

  • PCN G IV
  • vancomycin 1g IV every 12 hours for PCN allergy
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6
Q

Necrotizing fascitis

A

etiology:

  • Group A Strep
  • rapidly spreading infection involving fascia of deep muscle
  • enter via break in skin caused by trauma

S/O:

  • w/n a day pt develops swelling, heat, and rednessthat moves rapidly from initial infection site
  • a day later skin changes from red to purple to blue and bullae form
  • later skin dies and muscle may become infected
  • severe cellulitis but presence of systemic toxicity and severe pain which may be followed by anesthesia of involved area due to destruction of nerves as infection advances through the fascial planes (clue to DX)

P/TX:

  • must be recognised early and fascia surgically removed
  • surgical exploration is mandatory when this is expected early and extensive debridement is essential for survival
  • rapid abx tx is crucial (PCN G and add clindamycin)
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7
Q

Streptococcal Toxic Shock Syndrome

A

etiology:

  • any strep infection (necrotizing fascitis in particular) can be ass w/ Strep TSS
  • invasion of skin or soft tissues, acute respiratory distress syndrome, and kidney failure
  • bacteremia occurs in most cases
  • skin rash and desquamation may not be present
  • due to elaboration of pyrogenic erythrotoxin, a superantigen that stimulates massive release of inflamm cytokines believed to mediate the shock
  • outbreaks of invasive disease have been ass w/ colonization by invasive clones that can be transmitted to close contacts who, though asx, may be resevoir for disease

epidemiology:

  • the very young, elderly, and those with underlying medical conditions are at high risk in particular for invasive disease
  • mortality rates can be up to 80%

P/TX:

  • beta-lactam, ie PCN, remains drug of choice for tx of serious strep infections but Clindamycin (which is potent inhibitor of toxin production) should also be administered at dose of 600mg every 8 hrs IV
  • IV immune globulin has also been recommended for strep TSS for presumed therapeutic benefit from specific antibody to strep exotoxins in immune globulin preparations
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8
Q

Non Group A Streptococcal Infections

A
  • Non-Group A homelytic strep (eg groups B, C, and G) produce spetrum of diseases similar to Group-A diseases
  • TX for them is same as TX for Group-A infections

Group B

  • cause of sepsis, bacteremia, and meningitis in neonate
  • part of normal vaginal flora
  • may cause septic abortion, endometritis, peripartum infections and, less commonly, cellulitis, bacteremia, and endocarditis in adults

Viridans strep

  • nonhemolytic or alpha-hemolytic
  • part of normal oral flora
  • may produce focal pyogenic infection
  • most notable as leading cause of native valve endocarditis

Group D

  • *Streptococcus bovis *and enterococci
  • *S bovis *is cause of endocarditis in ass w/ bowel neoplasia or cirrhosis and is treated like viridans strep
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9
Q

Streptococcal/Enterococcal

A

Physiology= Growth and Morphology:

  • Gram positive cocci
  • rapid growth of sharply defined, smooth, translucent colonies on nonselective media
  • not as large as Staph (has to do with mode of metabolism)
  • O2 tolerant anaerobic mode of metabolism
  • formation of pairs and chains

Characteristics:

  • Gram stain = Gram positive cocci, usually in pairs or chains (purple)
  • Catalase test = negative
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10
Q

Streptococcus pyogenes (Group A)

A

How to Identify:

  • wide-zone beta-hemolysis on 5% sheep blood agar
  • Bacitracin (A disk) susceptible (no one does this anymore)
  • PYRase positive
  • detection of Lancefield Group A antigen in colonies

Toxins:

  • Pyrogenic (erythrogenic) exotoxins A, B, and C (act as superantigens resulting in massive cytokine release)
  • erythrogenic toxin
  • TSS toxin

Epidemiology:

  • lives on mucous membranes
  • preferentially colonizes the upper respiratory tract

Infections:

  • Respiratory Tract Infections and Sequelae
    • Pharyngitis
      • O/PE findings: enlarged/erythematous tonsils and uvula, and the palatal petechiae; presence of erythema, uvulitis, and tonsillar exudates
    • Scarlet fever
      • O/PE findings: Scarlatiniform Sandpaper Rash (feels like fine grade sand paper) and Strawberry Tongue
    • Suppurative sequelae
      • tonsillar abscess
      • retropharyngeal abscess
    • Nonsuppurative sequelae
      • Acute rheumatic fever
      • Acute glomerulonephritis
  • Other Infections
    • Impetigo
      • highly contagious superficial skin infection
      • also caused by Staph aureus
      • epidemiology: often outbreaks in daycare centers or in institutionalized pops
      • O/PE findings: usually involves face (self inoculation from nose to face) and skin nearby nose
      • P/TX: can treat topically with abx; no scars left behind
    • Ecthyma
      • O/PE findings: punched-out ulcers covered by greenish yellow crusts that extend deeply into the dermis and are surrounded by raised violaceous margins
    • Cellulitis
      • etiology: an acute spreading infection of the skin that extends deeper than erysipelas and involves the subQ tissues
      • O/PE findings: diffuse erythema and inflammation of the skin
    • Erysipelas
      • etiology: distinctive type of superficial cellulitis w/ prominent lymphatic involvement
      • O/PE findings: almost always on face (cheeks); edematous, indurated (peau d’orange) appearance of the skin w/ raised advancing edges and sharp borders
    • Toxic shock syndrome
      • S: pts present w/ fever, hypotension, tachycardia, and tachypnea followed later by desquamation

Worrisome Antimicrobial Resistance:

  • Inducible clindamycin resistance in beta-hemolytic strep
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11
Q

Streptococcus agalactiae (Group B)

A

aka (Group B beta-hemolytic)

Epidemiology:

  • lives on mucous membranes
  • preferentially colonizes the vagina and respiratory tract

Infections:

  • Neonatal sepsis/meningitis
    • early onset (in first 7 days of living)
    • late onset (7-30 days after birth)
    • outcome for both as well as tx options differ for wach onset
    • presence of Gram positive cocci in chains
  • Postpartum sepsis

P:

  • PCN G

Worrisome Antimicrobial Resistance

  • Inducible clindamycin resistance in beta-hemolytic strep
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12
Q

Streptococcus pneumoniae

A

How to Identify:

  • Alpha hemolysis (green zones of discoloration around colonies) on blood agar
  • Optochin (P disk) susceptible (filter paper disk impregnated by optochin detergent)
    • strep pneumo is only one inhibited by this
  • Quellung reaction positive (antibody binds to capsular antigen and produces halos)
  • Bile solubility test
  • lancet-shaped Gram positive diplococci (some have rod like appearance)

Toxin:

  • pneumolysin (binds to cholesterol in host cell membranes); effect unknown

Epidemiology:

  • lives on mucous membranes
  • preferentially colonizes the upper respiratory tract

Infections:

  • Pneumonia (Pneumococcal Pneumonia) in adults
    • O: occurs suddenly w/ rigors, high fevers, CP w/ respirations, SOB’ productive cough with green sputum
      • diffuse b/l pulmonary infiltrates on chest XR
    • alveoli of one or more lung lobes fill w/ WBCs (consolidated lobe on Chest XR)
    • sputum Gram stain = lancet-shaped gram positive diplococci and inflammatory cells
    • pneumovax for immunocompromised or elderly pts
  • Bacteremia/Sepsis
  • Meningitis (Pneumococcal Meningitis) in adults
    • pus coating the brain
    • most common cause of bacterial meningitis
    • O: stiff neck (nuchal rigidity)
  • Otitis Media in kids
    • O: bulging TM on otoscope examination
  • Sinusitis (can also be caused by a number of other organisms)

P:

  • PCN G (IM)
  • erythromycin
  • ceftriaxone
  • vaccine

Worrisome Antimicrobial Resistance

  • Fluoroquinolone resistance
  • PCN resistance!
  • cephalosporin resistance
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13
Q

Viridans Streptococci

A

(e.g., S. mitis, S. mutans, S. sanguis)

How to identify:

  • alpha hemolysis on blood agar
  • Optochin (P disk) resistant
  • Quellung reaction negative
  • Bile solubility negative

Epidemiology:

  • Lives on mucous membranes
  • preferentially colonizes the upper respiratory tract (part of normal flora)
  • can be found in nasopharynx and gingiva

Infections:

  • endocarditis (dental manipulations send it into bloodstream and can implant on heart endocardium)
    • subacute bacterial endocarditis (SBE)
      • O: pt slowly develops low-grade fevers, fatigue, anemia, heart murmurs secondary to valve obstruction
  • dental caries
  • abscesses (in brain or abd organs)

Worrisome Antimicrobial Resistance

  • PCN/cephalosporin resistance
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14
Q

Pneumococcal Pneumonia

A

Essentials of DX:

  • productive cough, fever, rigors, dyspnea, early pleuritic CP
  • consolidating lobar pneumonia on chest radiograph
  • Gram positive diplococci on Gram stain of sputum
  • Strep pneumoniae

etiology:

  • pneumococcus is most common cause of community-acquired pyogenic bacterial pneumonia
  • alcoholism, asthma, HIV, sickle cell disease, splenectomy, and hematologic disorders are predisposing factors

S:

  • high fever, productive cough, occassionally hemoptysis, pleuritic CP
  • rigors occur w/n first few hrs of infection but are uncommon thereafter
  • bronchial breath sounds are an early sign

O:

  • classically lobar pneumonia w/ radiographic findings of consolidation and occassionally effusion
  • complications:
    • parapneumonic (sympathetic) effusion is common and may cause recurrence or persistance of fever; these sterile fluid accumulations need no specific therapy
    • empyema occurs in 5% or less cases and is differentiated from sympathetic effusion by presence of organisms on Gram-stained fluid or positive pleural fluid cavities
    • pneumococcal pericarditis is rare complication that can cause tamponade
    • pneumococcal arthritis is also uncommon
    • pneumococcal endocarditis usually involves aortic valve and often occurs in ass w/ meningitis and pneumonia (sometimes referred to Austrian or Osler triad)
    • early heart failure and multiple embolic events are typical

A:

  • not possible to differentiate from other pneumonias radiographically or clinically b/c of overlap in presentations
  • DX requires isolation of organism in cx (sputum and blood cxs should be obtained prior to initiation of antimicrobial therapy)

P/TX:

  • Initial antimicrobial therapy for pneumonia is empiric pending isolation and identification of the causative agent
  • Once S pneumoniae is identified as pathogen, any of several antimicrobial agents may be used depending on the clinical setting, community patterns of PCN resistance, and susceptibility
  • Uncomplicated pneumococcal pneumonia caused by PCN-susceptible strains => outpt tx with amoxicillin
    • for PCN allergic pts = azithromycin, clarithromycin, doxycycline, levofloxacin
  • pts should be closely monitored due to increasing resistance of strains to PCN and second-line agents
  • parenteral therapy recommended for hospitalized pt until clinical improvement at least
    • IV PCN or ceftriaxone effecive for strains not highly PCN-resistant
    • for PCN allergy or highly PCN-resistant = Vancomycin IV or respiratory fluoroquinolone
  • TX of complications
  • PCN-resistant Pneumococci
    • Resistance breakpoints for parenterally administered PCN and high-dose oral amoxicillin are: susceptible, penicillin MIC ≤ 2 mcg/mL; intermediate, MIC = 4 mcg/mL; resistant, MIC ≥ 8 mcg/mL
    • In cases of pneumococcal pneumonia where the isolate has a PCN MIC > 2 mcg/mL, cephalosporin cross-resistance is common, and a non–beta-lactam antimicrobial, such as vancomycin or a fluoroquinolone with enhanced gram-positive activity is recommended
    • PCN-resistant strains of pneumococci may be resistant to macrolides, trimethoprim-sulfamethoxazole, and chloramphenicol, and susceptibility must be documented prior to their use=> all blood and CSF fluid isolates should be tested for PCN resistance
  • when to refer:
    • To ID specialist = all pts with suspected pneumococcal endocarditis or meningitis
    • extensive disease
    • seriously ill pt w/ pneumonia particularly w/ comorbid conditions (ie liver disease)
    • progression of pneumonia or failure to improve on abx
  • when to admit
    • All pts with suspected or documented pneumococcal endocarditis or meningitis should be admitted for observation and empiric therapy
    • all pts w/ multilobar infection or ass w/ significant hypoxemia
    • failure of outpt therapy, including inability to maintain oral intake and meds
    • exacerbation of underlying disease (ie heart failure) by pneumonia that would benefit from hospitalization
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15
Q

Pneumococcal Meningitis

A

essentials of DX:

  • fever, HA, alterned mental status
  • meningismus
  • gram-positive diplococci on Gram stain of CSF

etiology:

  • S pneumoniae is most common cause in adults
  • head trauma w/ CSF fluid leaks, sinusitis, and pneumonia may precede it

S:

  • rapid onset w/ fever, HA, meningismus, and altered mentation
  • pneumonia may be present
  • in comparison to meningococcus = pneumococcal lacks rash and focal neurologic defecits, cranial nerve palsies, and obtundation are more prominent features

O:

  • CSF typically has > 1000 WBCs per microliter, over 60% of which are polymorphonuclear leukocytes
    • glc concentration is < 40 mg/dL or < 50% of the simultaneous serum concentration
    • the protein usually exceeds 150 mg/dL
  • Gram stain of CSF shows gram positive cocci in 8–90% of cases

P/TX:

  • Abx should be given as soon as DX is suspected
  • if LP should be delayed, pt should be treated empirically for presumed meningitis with IV ceftriaxone plus vancomycin plus dexamethasone administered concomitantly after blood cx have been obtained
  • PCN given once PCN susceptibility has been confirmed or ceftriaxone
  • best method for PCN-resistant strains is not known as they are often cross-resistant to third-generation cephalosporins as well as other abx
  • Susceptibility testing is essential to proper management of this infection
  • If a pt with a PCN-resistant organism is slow to respond clinically, repeat lumbar puncture may be indicated to assess bacteriologic response
  • Dexamethasone administered w/ abx to adults and recommended IV should be given immediately prior to or concomitantly with the first dose of appropriate antibiotic and continued in those with pneumococcal disease every 6 hours thereafter for a total of 4 days
    • Patients with pneumococcal meningitis and AIDS who do not have access to resources may not benefit from dexamethasone
    • effect on outcome in meningitis caused by PCN-resistant organisms is not known
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