Streptococci Flashcards
Key characteristics of Streptococci
- 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
Is streptococci catalase negative or positive
Catalase negative
How are the different Streptococci classified
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
- hemolytic pattern on agar containing blood cells
- Alpha: partial hemolysis or “greening”
- Beta: complete clearing
- Gamma: no change in red blood cells - Biochemical properties
Which species of Streptococci are B hemolytic
- group A: S. pyogenes
- group B:S. agalactiae
- group C: S. dysgalactiae
- group F: S. anginosus
- Group G: S. absesses
How are the B hemolytics further classified
Lancefield types
How are the alpha and gamma hemolytics further classified
biochemical tests
which strains are alpha or gamma hemolytic
S. pneumoniae
S. mutans
S. bovis
Describe the physiology and structure of the surface proteins for Streptococcus pyogenes
- 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
mechanism of pathogenesis Streptococcus pyogenes
- Avoidance of opsonization and phagocytosis
- Adherence to host cells
- Invasion of host cells
- Toxins and Enzymes
How does S pyogenes avoid opsonization and phagocytosis
- 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
how does S pyogenes adhere to host cell
-lipoteichoic acid, M proteins, F protein-mediate attachment
How does S pyogenes invade host cells
M protein and F protein
How does S pyogenes use toxins and enzymes for pathogenesis (cytokine storm)
- 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
How do Spe toxins mediate several clinical manifestations of S. pyogenes infections
- cytokine release may be key to the severity o necrotizing fasciitis and streptococcal toxic shock syndrome
- responsible for the rash in patients wiht scarlet fever
Streptolysin S
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.
Streptolysin O
oxygen labile hemolysin
Streptokinase
mediates the cleavage of plasminogen, the release of plasmin
and subsequent cleavage of fibrin and fibrinogen
Dnases
depolymerize released DNA from lysed cells aiding the spread of
streptococci through infected tissues
Streptococcus pyogenes epidemiology
- 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
List the clinical diseases associated with S. pyogenes
- streptococcal pharyngitis
- scarlet fever
- impetigo or pyoderma
- erysipelas
- streptococcal toxic shock
- endocarditis
- necrotizing fasciitis
streptococcal pharyngitis -
redness and edema of the mucous membranes, fever, purulent exudate, tonsilitis 2-4 days
scarlet fever -
streptococcal pharyngitis and an erythematous punctiform rash due to the Spe toxins
impetigo or pyoderma
infection of the superficial layers of the skin
in children. Vesicles develop into pustules, rupture and crust over
erysipelas -
infection of the skin and subcutaneous tissues edema, induration with a distinct advancing border
streptococcal toxic shock
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
endocarditis
streptococcal bacteremia allows access to normal, injured or congenitally deformed heart tissue, particular the valves
necrotizing fasciitis
infection of the deeper subcutaneous tissues and fascia, extensive necrosis and gangrene, progresses to acute toxicity, multiorgan failure and death
group A late sequelae
-rheumatic fever -glomerulonephritis
rheumatic fever
follows respiratory infections, hypersensitivity response to streptococcal antigens the cross react with human heart tissue antigens; fever, polyarthritis, and carditis
glomerulonephritis
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
How can you detect S pyogenes in a lab
- 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
Antigen Detection S pyogenes
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
if you get a positive culture for S pyogenes
Gram positive cocci in chains, catalase negative, group specific
carbohydrate positive, susceptible to bacitracin
How do you confirm rheumatic fever or glomerulonephritis
Antibodies to streptolysin O (ASO titer)
treatment for S pyogenes pharyngitis
penicillin, penicillin V amoxicillin
-if allergic to penicillin take cephalosporin or macrolide
Severe or systemic infections S pyogenes:
Penicillin I.V. + a protein-synthesis inhibitor antibiotic (clindamycin)
Serious soft tissue infections: S pyogenes
Surgical debridement and antibiotics
Physiology and structure of Streptococcus agalactiae- group B
expresses Group B carbohydrate antigen
Pathogenesis and Immunity group B strep- Streptococcus agalactiae
avoids phagocytosis by expressing a capsule
Epidemiology of S agalactiae–Group B
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
Clinical Diseases associated with S agalactiae Group B
– 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)
Laboratory diagnosis S agalactiae group B
Gram stain of CSF for meningitis, pneumonia and wound infections
Culture, PCR, and group specific antigen test for vaginal carriage
Treatment, Prevention and control – S agalactiae
drug of choice penicillin G for serious infections
penicillin and aminoglycoside
S pneumniae Physiology and structre
- 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
what is the basis for classification of strains of s pneumoniae
Capsular polysaccharides
Describe the unique cell wall composition of S pneumoniae
-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
What is the major difference between pathology of S pyogenes and of S pneumonia
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
Mechanisms of pathology for S pneumonia
- colonization
- resistance to phagocytosis
- release of toxic cell wall components that trigger an intense inflammatory response
Colonization as a pathogenic mechanism S pneumonia
bacterial colonization is mediated by surface protein adhesins that allow binding to epithelial cells of the oropharynx
Resistance to phagocytosis as apathogenic mechanism S pneumonia
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.
Release of toxic cell wall components that trigger an intense
inflammatory response as a mechanism of pathogenesis S pneumonia
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.
Epidemiology of S pneumonia
-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
S pneumonia clinical diseases
- Pneumococcal pneumonia
- Sinusitis and Otitis media
- Meningitis
- Bacteremia
- Endocarditis
Pneumococcal pneumonia –
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).
Sinusitis and Otitis media –
infection of the
paranasal sinuses and ear.
Meningitis -
S. pneumoniae spreads to the CNS
after bacteremia or after infections of the
ear or sinuses or after head trauma.
Bacteremia –
occurs in 25-30% of the patients
with pneumonia and 80% of patients
with meningitis.
Endocarditis –
can occur in patients with abnormal heart valves or vegetations.
Lab diagnosis of S pneumonia
-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
describe resistance with S pneumonia
-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
What is protective for S pneumonia
Anti-capsular antibody
Vaccine for S pneumonia
Adults and Children > 2 y – immunize with vaccine containing
23-different capsular polysaccharides
For children < 2 y – immunize with 13-valent conjugated vaccine
S pygogenes summary
- 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
S pneumonia summary
- 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
Overall are streptococci gram positive or gram negative and are they catalase positive or catalase negative
Gram-positive cocci in chains, catalase negative
