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Bacteriology > Streptococci > Flashcards

Streptococci Flashcards

1
Q

Key characteristics of Streptococci

A
  • gram positive cocci arranged in pairs or chains
  • most species are facultatively anaerobic
  • ferment carbohydrate, resulting in lactic acid production
  • require blood or serum enriched medium for growth
  • catalase negative as opposed to Staphylococcus
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2
Q

Is streptococci catalase negative or positive

A

Catalase negative

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3
Q

How are the different Streptococci classified

A

Classification is based on 3 overlapping schemes
1. Cell wall carbohydrate antigens recognized by specific antibodies aka Lancefield typing
ex Group A streptococci=S. pyogenes and Group B streptococci is S. agalactiae

  1. hemolytic pattern on agar containing blood cells
    - Alpha: partial hemolysis or “greening”
    - Beta: complete clearing
    - Gamma: no change in red blood cells
  2. Biochemical properties
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4
Q

Which species of Streptococci are B hemolytic

A
  • group A: S. pyogenes
  • group B:S. agalactiae
  • group C: S. dysgalactiae
  • group F: S. anginosus
  • Group G: S. absesses
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5
Q

How are the B hemolytics further classified

A

Lancefield types

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6
Q

How are the alpha and gamma hemolytics further classified

A

biochemical tests

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7
Q

which strains are alpha or gamma hemolytic

A

S. pneumoniae

S. mutans

S. bovis

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8
Q

Describe the physiology and structure of the surface proteins for Streptococcus pyogenes

A
  • group specific antigen=Lancefield Group A carbohydrate
  • Type specific antigen= M proteins encoded by emm genes-epidemiologic markers
  • contains M-like surface proteins
  • Lipteichoic acid and F protein to help mediate adherence to fibronectin
  • hyaluronic acid capsule

C5a peptidase

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9
Q

mechanism of pathogenesis Streptococcus pyogenes

A
  1. Avoidance of opsonization and phagocytosis
  2. Adherence to host cells
  3. Invasion of host cells
  4. Toxins and Enzymes
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10
Q

How does S pyogenes avoid opsonization and phagocytosis

A
  • hyaluronic capsule
  • M proteins block C3b binding (complement)
  • M-like proteins bind the Fc fragment of antibodies which in turn reduces bound C3b and blocks complement activation by the alternative pathway
  • C5a peptidase degrades C5a and prevents it from acting as a chemo attractant
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11
Q

how does S pyogenes adhere to host cell

A

-lipoteichoic acid, M proteins, F protein-mediate attachment

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12
Q

How does S pyogenes invade host cells

A

M protein and F protein

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13
Q

How does S pyogenes use toxins and enzymes for pathogenesis (cytokine storm)

A
  • streptococcal pyogenic exotoxins SpeA, B, C, F-phage encoded, act as a superantigens
  • mediate a cytokine storm by nonspecifically crosslinking T cell receptors to APC class II MHC
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14
Q

How do Spe toxins mediate several clinical manifestations of S. pyogenes infections

A
  1. cytokine release may be key to the severity o necrotizing fasciitis and streptococcal toxic shock syndrome
  2. responsible for the rash in patients wiht scarlet fever
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15
Q

Streptolysin S

A

oxygen and serum stable cell-bound hemolysin, responsible for
complete lysis of red blood cells (β hemolysis) and likely kills macrophages and
neutrophils in vivo.

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16
Q

Streptolysin O

A

oxygen labile hemolysin

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17
Q

Streptokinase

A

mediates the cleavage of plasminogen, the release of plasmin

and subsequent cleavage of fibrin and fibrinogen

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18
Q

Dnases

A

depolymerize released DNA from lysed cells aiding the spread of
streptococci through infected tissues

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19
Q

Streptococcus pyogenes epidemiology

A
  • S. pyogenes is a transient colonizer of the oropharynx of healthy children and adults
  • it is considered significant if isolated from a patient with pharyngitis
  • *****Patients with antibodies to M proteins are protected
  • the pathogen is spread by droplet transmission
  • pharyngitis affect children between 5 and 15 years
  • soft tissue infections (pyoderma, cellulitis, fasciitis, erysipelas) are mediated by organisms that transiently colonize the skin and are introduced into the superficial or deep tissues through a wound
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20
Q

List the clinical diseases associated with S. pyogenes

A
  • streptococcal pharyngitis
  • scarlet fever
  • impetigo or pyoderma
  • erysipelas
  • streptococcal toxic shock
  • endocarditis
  • necrotizing fasciitis
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21
Q

streptococcal pharyngitis -

A

redness and edema of the mucous membranes, fever, purulent exudate, tonsilitis 2-4 days

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22
Q

scarlet fever -

A

streptococcal pharyngitis and an erythematous punctiform rash due to the Spe toxins

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23
Q

impetigo or pyoderma

A

infection of the superficial layers of the skin

in children. Vesicles develop into pustules, rupture and crust over

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24
Q

erysipelas -

A

infection of the skin and subcutaneous tissues edema, induration with a distinct advancing border

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25
Q

streptococcal toxic shock

A

focal infection, bacteremia, shock hypotension, in conjunction with 2 or more of the following: ARDS, renal impairment, liver abnormality, coagulopathy, rash with desquamating soft tissue necrosis

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26
Q

endocarditis

A

streptococcal bacteremia allows access to normal, injured or congenitally deformed heart tissue, particular the valves

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27
Q

necrotizing fasciitis

A

infection of the deeper subcutaneous tissues and fascia, extensive necrosis and gangrene, progresses to acute toxicity, multiorgan failure and death

28
Q

group A late sequelae

A

-rheumatic fever -glomerulonephritis

29
Q

rheumatic fever

A

follows respiratory infections, hypersensitivity response to streptococcal antigens the cross react with human heart tissue antigens; fever, polyarthritis, and carditis

30
Q

glomerulonephritis

A

can follow either pharyngeal or cutaneous infections, deposition of antigen-antibody complexes in the glomerular basement membrane; fever, blood in urine, edema, sometimes hypertension and elevated blood urea nitrogen

31
Q

How can you detect S pyogenes in a lab

A
  • Gram stain of samples from infected tissues, particularly soft tissue infections
  • Antigen detection
  • Nucleic acid amplification: pharyngeal specimens
  • Culture: throat swab
  • Gram stain of blood bottles
  • Cultures of draining pustules
32
Q

Antigen Detection S pyogenes

A

rapid immunologic tests for the Group A carbohydrate
directly from throat swabs. Antigen tests are not used for cutaneous
or late sequelae manifestations of S. pyogenes

33
Q

if you get a positive culture for S pyogenes

A

Gram positive cocci in chains, catalase negative, group specific
carbohydrate positive, susceptible to bacitracin

34
Q

How do you confirm rheumatic fever or glomerulonephritis

A

Antibodies to streptolysin O (ASO titer)

35
Q

treatment for S pyogenes pharyngitis

A

penicillin, penicillin V amoxicillin

-if allergic to penicillin take cephalosporin or macrolide

36
Q

Severe or systemic infections S pyogenes:

A

Penicillin I.V. + a protein-synthesis inhibitor antibiotic (clindamycin)

37
Q

Serious soft tissue infections: S pyogenes

A

Surgical debridement and antibiotics

38
Q

Physiology and structure of Streptococcus agalactiae- group B

A

expresses Group B carbohydrate antigen

39
Q

Pathogenesis and Immunity group B strep- Streptococcus agalactiae

A

avoids phagocytosis by expressing a capsule

40
Q

Epidemiology of S agalactiae–Group B

A

Asymptomatic colonization of the lower gastrointestinal tract and
genitourinary tract; risk for neonates increases if labor is prolonged, premature
rupture of membranes, premature birth, or mother has disseminated group B
disease or lacks type specific antibodies

41
Q

Clinical Diseases associated with S agalactiae Group B

A

– Neonatal disease, early and late onset of meningitis, pneumonia
bacteremia; infections in pregnant women (endometritis, wound, urinary tract,);
infections in other adults (bacteremia, pneumonia, bone and joint infections,
skin and soft tissue infections)

42
Q

Laboratory diagnosis S agalactiae group B

A

Gram stain of CSF for meningitis, pneumonia and wound infections
Culture, PCR, and group specific antigen test for vaginal carriage

43
Q

Treatment, Prevention and control – S agalactiae

A

drug of choice penicillin G for serious infections

penicillin and aminoglycoside

44
Q

S pneumniae Physiology and structre

A
  • encapsulated gram positive, elongated or oval coccus arranged in pairs or chains
  • α-hemolytic colonies on blood agar (aerobic incubation)
  • Capsular polysaccharides are the basis for classification of strains
  • Possesses a unique cell wall composition
45
Q

what is the basis for classification of strains of s pneumoniae

A

Capsular polysaccharides

46
Q

Describe the unique cell wall composition of S pneumoniae

A

-phosphorylcholine + species specific teichoic acids
*C polysaccharide-C polysaccharide binds to serum
C-reactive protein a marker for acute inflammation.
*F antigen. F antigen cross reacts with Forssman surface
antigens on mammalian cells

47
Q

What is the major difference between pathology of S pyogenes and of S pneumonia

A

pathology related to S pneumonia infection is due mostly to host response rather than the expression of bacterial toxins like it is with S pyogenes

48
Q

Mechanisms of pathology for S pneumonia

A
  1. colonization
  2. resistance to phagocytosis
  3. release of toxic cell wall components that trigger an intense inflammatory response
49
Q

Colonization as a pathogenic mechanism S pneumonia

A

bacterial colonization is mediated by surface protein adhesins that allow binding to epithelial cells of the oropharynx

50
Q

Resistance to phagocytosis as apathogenic mechanism S pneumonia

A

S. pneumonia produces a secretory IgA
protease that cleaves the Fc portion of IgA and prevents the association with host mucins. It also expresses pneumolysin a pore forming toxin that kills ciliated epithelial cells and phagocytes. Finally the capsule is anti-phagocytic.

51
Q

Release of toxic cell wall components that trigger an intense
inflammatory response as a mechanism of pathogenesis S pneumonia

A

teichoic acids, peptidoglycan and pneumolysin
activate complement pathways, resulting in IL-1 and TNF α production. Bacteria migrate to deeper tissues by bacterial cell wall phosphorylcholine binding to receptors on endothelial cells.

52
Q

Epidemiology of S pneumonia

A

-S. pneumonia transiently colonizes normal healthy individuals
-Pneumonia can occur when endogenous oral organisms are aspirated
into the lower airways
-Disease is associated with the breakdown of natural defense
mechanisms (epiglottal reflex, failure to remove the bacteria
by the ciliated respiratory epithelium, failure of the cough reflex)
-Pneumococcal pneumonia is associated with antecedent viral
respiratory disease, like influenza, chronic pulmonary disease,
alcoholism, congestive heart failure, diabetes, chronic renal
disease, splenectomy
-In children it is a common cause of otitis media

53
Q

S pneumonia clinical diseases

A
  • Pneumococcal pneumonia
  • Sinusitis and Otitis media
  • Meningitis
  • Bacteremia
  • Endocarditis
54
Q

Pneumococcal pneumonia –

A

replication of bacteria in the alveolar spaces
abrupt onset, severe chill, sustained fever (39˚C- 41˚C), productive cough,
blood-tinged sputum, chest pain (pleurisy).

55
Q

Sinusitis and Otitis media –

A

infection of the

paranasal sinuses and ear.

56
Q

Meningitis -

A

S. pneumoniae spreads to the CNS
after bacteremia or after infections of the
ear or sinuses or after head trauma.

57
Q

Bacteremia –

A

occurs in 25-30% of the patients
with pneumonia and 80% of patients
with meningitis.

58
Q

Endocarditis –

A

can occur in patients with abnormal heart valves or vegetations.

59
Q

Lab diagnosis of S pneumonia

A

-Gram stain of sputum or CSF is rapid.

-Quellung reaction: detection of capsule with antibodies in
a microscopic assay

-Pneumococcal C polysaccharide in urine with ELISA

-Culture: sputum or CSF is cultivated on rich medium supplemented
with blood

-Specimen from middle ear or sinus has too many contaminants for
culture and identification of S. pneumonia

-Isolate is tested for bile solubility (+), optochin sensitive colony should exhibit α-hemolysis on a blood agar plate

60
Q

describe resistance with S pneumonia

A

-many strains are now resistant to penicillin as opposed to S pyogenes
-resistance is also documented for macrolides and cephalosporins
-For serious infections: vancomycin + ceftriazone followed by monotherapy
with an effective cephalosporin, fluoroquinolone or vancomycin

61
Q

What is protective for S pneumonia

A

Anti-capsular antibody

62
Q

Vaccine for S pneumonia

A

Adults and Children > 2 y – immunize with vaccine containing
23-different capsular polysaccharides

For children < 2 y – immunize with 13-valent conjugated vaccine

63
Q

S pygogenes summary

A
  • Bacitracin sensitive β Hemolytic
  • Skin and soft tissue Strep throat
  • M proteins, hyaluronic acid capsule, Spe toxins, enzymes that promote tissue dissemination
  • Antibodies to M proteins are protective but no vaccine
64
Q

S pneumonia summary

A
  • Optochin sensitive α Hemolytic
  • Lobar pneumonia Meningitis, otitis media
  • Resistance to phagocytosis, release of cell wall components leading to inflammation

-23-valent capsular polysaccharide 13-valent capsular polysaccharide
conjugate

65
Q

Overall are streptococci gram positive or gram negative and are they catalase positive or catalase negative

A

Gram-positive cocci in chains, catalase negative

Bacteriology (15 decks)

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