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Microbiology and Immunology
Microbiology and Immunology 2500A/B

Streptococci – Feb. 27, 2013 - It is a gram-positive; coccus shaped & aerotolerant anaerobes that grow in chains - Oxygen is not used by Streptococci (anaerobic), but it does not kill them (they are tolerant to it, unlike Clostridia which are strict anaerobes) - The word “Streptos” is a Greek word for bent or twisted – the bent or twisted shape can be seen on the gram strain - They are non-motile & non-endospore forming - They are initially classified by their pattern of hemolysis on blood agar α-hemolytic  They can cause partial hemolysis: erupt cells partially  S. pneumoniae  pneumococcus  S. viridans  endocarditis: infection of heart valves  S. mutans  tooth decay  S. thermaphilus (not a pathogen)  Daily foods  Not all Strep are pathogenic β-hemolytic  S. pryogenes (Group A Strep)  S. agalactiae (Group B Strep) Lancefield Classification  S. equi (Group C Strep); it causes infection in horses  These are classified on the basis of surface γ-hemolytic carbohydrates antigens  Enterococcus species (Group D Streptococcus)  Lactococcus (Group N Streptococcus) – not a pathogen Streptococcus pyogenes: Pathogen  It is a common human specific pathogen; humans are the only reservoir for this pathogen; an extracellular pathogen – inside the cells but generally outside the host cells  “Pyo” means pus – this occurs to inflammation, neutrophils leading to pus  In 5-15% cases there is asymptomatic carriage; in this situation, the patient is a carrier of the disease or infection, however, they do not experience any symptoms  It was a major cause of mortality from scarlet fever, puerperal sepsis & wound infections in soldiers  In the modern day, this pathogen causes pharyngitis & impetigo; it also causes severe invasive streptococcal disease and the streptococcal toxic shock syndrome (Flesh eating disease)  It is an important cause of “post infection sequelae” including acute rheumatic fever; something happens after the infection, infections goes away and then it develops the disease  It is capable of producing an arsenal of key virulence factors  Master of hiding from the immune system and capable to causing severe damage  M – Protein - An anti-phagocytic cell surface expressed protein - Binds “Factor H” (host protein) of the complement system - Factor H is a complement regulatory protein that protects self-cells from C3b deposition  Strep binds to Factor H so that the complement system is unable to detect it because it is being protected by Factor H - Greater than 100 M protein serotypes - Hypervariable N-terminus  Basis for M protein serotypes (antigenically distinct)  Different M protein serotypes will cause different disease (Linkage of specific M protein to a specific disease)  Ex. M1, M3 typically cause pharyngitis & invasive disease  Ex. M18 typically cause acute rheumatic fever - However, if you have antibodies to a particular M protein serotype, you will opsonize and kill these bacteria - S. pyogenes makes 2 hemolysins (they target red blood cells as well as other cells; ex. leukocytes)  Streptolysins (O & S)  Streptolysin S produced β-hemolysis  Streptolysin O is Oxygen sensitive and can be seen under anaerobic conditions  Hyaluronic acid capsule  A polysaccharide (sugar capsule)  Hyaluronic acid is a major component of host tissues – bacteria “look like self”  This is why we are unable to make the capsule vaccine because then it would target our healthy cells  Can also block opsonization through C3b (typical of other capsules)  Streptococcal Pryogenic Exotoxins (Spe’s) - Secreted exotoxins - Known as “superantigens” (Recall S. Aureus) - All S. pyogenes strains make between 4 and 8 different superantigens - Function as potent activators of T cells resulting in a cytokine storm disease known as the toxic shock syndrome - NOT emetic like the staphylococcal  DNAse (Streptodornase) - Enzyme that degrades DNA - Secreted exotoxin - Targets (NETs) – Neutrophil extracellular traps 1) Activation of the neutrophil leads to formation of reactive O s2ecies 2) Loss of nuclear structure  nucleus contents spills into cytoplasm 3) DNA mixes with the granules 4) Loss of cell membrane integrity (it blows up) and release of NETs  The DNA becomes like a net/web; this will sit there and trap bacteria that are coming through The Disease: Pharyngitis (Strep throat)  It is most common in school aged children & teenagers  Fever & Severe sore throat  Typically absence of cough (coughing is not a symptom)  Swollen cervical lymph nodes  Tonsillar exudate (pus) – tonsils get infected and they form this pus  Skin Rash  Is it strep or viral? Not easy to tell and if it is viral, there is no point in giving antibiotics  Diagnosed by a rapid strep test – swallow this piece of gum; gagging  Positive test = strep throat  antibiotics  Negative test  throat culture  Treated with antibiotics  Penicillins (no documented resistance)  Erythromycin (resistant strain exist); still came out with this erythromycin for those who are allergic to penicillin  Untreated pharyngitis can lead to a number of complications including acute rheumatic fever The Disease: Impetigo  Most common
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