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33 Cards in this Set

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Streptococcus Morphology:

Group A strep:
Gram + cocci, often in chains, aerotolerant but grow anaerobically

S. pyogenes - Beta hemolytic, cause variety of systemic infections sometimes with severe sequelae
ID and classification of Step (focus on S. Pyogenes):
Microscopically - observe chains of G+ cocci

Plate on Medium with intact RBCs observe zone of hemolysis -
Gamma hemolysis = none
Alpha hemolysis = green, cloudy zone (intact RBCs with altered green heme pigment)
Beta hemolysis = *S. pyogenes* clear zone, lysed RBCs (note: a small zone of hemolysis may look cloudy if it does not penetrate agar)

Detect cell wall carb Ags -
C-carbohydrate, use complex carbs extracted from bacteria as Ags in precipitation test with with rabbit antisera
(this test groups beta hemolytic strep in groups A *S. pyogenes* -O)

Detect cell wall protein Ags -
Immunological analysis of M (finbriae) proteins (~80 types) subdivides group A strep (S. pyogenes)
S. pyogenes structure inside to outside:
Bacterial membrane with M protein embedded -> cell wall made of peptidoglycans and C carbohydrate -> Hyaluronic acid capsule with M-proteins from the memb
Acute diseases caused by group A beta hemolytic strep:

1) Puerperal fever:

2) Acute pharyngitis and tonsilitis:
uterine infection immediately following birth - frequently fatal - uncommon in developed countries

Mild form = strep throat, other symptoms -> headache, fever-chills, malaise, elevated WBC count *diagnosis and treatment with penicillin necessary to prevent rheumatic fever*
3) Scarlet fever:
cutaneous rash that sometimes accompanies pharyn-tonsilitis, caused by exotoxin

streptococcal pyrogenic exotoxin -
probably causes rash by acting as superAg
3 antigenic types speA, speB, speC
Lysogenic bacteriophage confers ability to produce toxin
Used to be a major cause of mortality, now toxigenic strains are less common
Possible to be immune to the toxin, but not immune to infection
4) Impetigo (pyoderma):

5) Erysipelis:
Minor, superficial skin infection
usually in children
strep enter through pre-existing skin lesion
most common cause = staph aureus

severe cellulitis of dermis and underlying tissues
6) Streptococcal toxic shock syndrome:
Life threatening syndrome
Symptoms - severe hypotension plus two or more of -> impaired renal or liver function, DIC, resp distress, generalized rash, soft tissue necrosis
cause - strep exotoxins (speA, speB, speC)
process - exotoxins act as superAgs, enhance interaction between TCR and MHC II on APC, cause massive lymphokine overproduction
7) Necrotizing faciitis:
highly invasive S. pyogenes
causes rapid and destructive muscle infections, may involve poorly defined proteolytic exotoxin
Life-threatening
Treatment - antibiotics and may need surgery
8) Others:
Sinusitis, mastoiditis, otitis media, pneumonia (rare, generally only after influenza), meningitis
S. pyogenes infection pathogenesis:

factors that stop spread:
1) Very invasive, tends to spread rather than be walled off

Potential factors:
Streptolysins - hemolysins (cause B hemolys) that lyse other cells as well
a)O: antigenic, oxygen-labile, only functions in reduced atmosphere, Ab measurements (with ASO) important in lab diagnosis
b)S: poor Ag, oxygen stable

Streptokinase - triggers blood proteolytic system to destroy fibrin clots

DNAase
S. pyogenes infection pathogenesis:

Factors with antiphagocytic activity:
Hyaluronic acid capsule: capsuleless bacteria aren't pathogenic

M proteins: major role in adherence to mucosal surfaces, resistant to phagocytosis, Ab to M protein confers immunity to strep of that type
S. pyogenes infection pathogenesis:

3 factors with roles in specific clinical presentations:
SpeA, B, C - causes scarlett fever rash (ab against an exotoxin prevents scarlett fever by that exotoxin, but not infection)

Spe A, B, C: also cause strep TSS (Ab against an exotoxin will prevent TSS by that toxin
Sequelae of S. pyogenes:

Rheumatic fever
Rheumatic fever -
Timing: 2-3 wks post recovery from strep sore throat
Path: heart and skin lesions, joint pains
Cause: Ab to M protein cross react with self Ag at heart (especially mitral and aortic valves) and joints
Not all strains cause this and some are worse than others
Unknown which strains are more likely to cause RF, therefore penicillin treatment of all strep throat is necessary
Treatment: protected against reinfection by prophylactic penicillin
Sequelae of S. pyogenes:

Acute glomerulonephritis:
timing: 1 week post infection of throat or skin
Caused by: a few M-protein types
Symptoms: hematuria, edema, glomerulonephritis symptoms
Pathogenesis: deposition of immune complexes containing bacterial Ags in kidney

*NOTE - viable bacteria not found in damaged tissue of either
Lab diagnosis of S. pyogenes:
1) Elaborate Ag typing (not routine)

2) Labs: beta hemolysis on blood agar, G+ streptococci, Bacitracin sensitivity (correlates well to group A, and other groups are relatively resistant)

3) Physician's office: Small plastic beads coated with anti-strep A Ab (agglutinate joined by bacteria when incubated with pharyngeal exudate), alternative = ELISA based Ag recognition assay with colored product

4) ASO titer: High titer of Ab to streptolysin O (>160) suggests recent infection
Better indication: increase in titer comparing acute and convalescent sera
Also used: titer of Ab against other extracell proteins
S. pyogenes epidemiology:

Treatment:
Pharyngitis Mode of transmission = respiratory droplets
Inoculum: large inoc for infection
Carriers: ~5-10% normal indiv carry group A B-hemolytic strep in pharynx and/or nose (Nasal is more infectious!)
Chronic/carried strains: usually less pathogenic because strains without M protein are selected for (since those with M are opsonized and phagocyt)


NO strains are resistant to Penicillin
Group B beta hemolytic Strep:

Most important strain -

Why?
S. agalactiae

causes up to 1/3 neonatal infections -> septicemia, meningitis, pneumonia, death
Epidemiology of neonatal S. agalactiae:
*neonatal illness correlated with lack of maternal Ab during delivery

1) early onset (w/in first week):
correlated with vaginal bacterial infection
Despite prompt antibiotic therapy, may be rapidly fatal ~40%
Prevention by vaginal and rectal cultures of mother late in term -> treat with intrapartum (during labor) parenteral (into body not mouth) penicillin or ampicillin

2) Late onset:
correlated with infant to infant spread in nursery
Less rapid, less mortality
Age specific highest incidence of Child and adult Group B strep infections:
> 65 yrs
Enterococci (group D strep):
most important -
Hemolysis Pattern -
Resistance to -
Cause what?
Enterococcus faecalis (common GI inhabitant)

differs strain to strain

severe growth conditions (high salt, temp, nearly all antibiotics), and "last resort" vancomyocin

UTIs
Viridans Streptococci:
inhabit where -
most frequent cause of -
pathogenesis -
characteristics of disease -
alpha-hemolytic
nearly universally in mouth, nose, pharynx

Infective endocarditis: bact in mouth enter through minor oral trauma -> transient bacteremia -> focus of infection occurs on preexisting heart lesion -> multiply within fibrin mass and platelets (= vegetation)

can detect vegetation with echocardiogram (ultrasound)

often subacute with intermittent bacteremia and often fatal if untreated
Streptococcus pneumoniae:
aka -
Organism characteristics -
Lab ID -
ID pneumococcal type -
pneumococus

-G+ diplococci with shorter side adjacent (neisseria longer side is adjacent)
- large polysacch capsule, nearly 100 types ID'd via capsule Ags,

alpha hemolytic on blood agar, Optochin sensitivity test to distinguish from viridans (viridans is resistant)

Quellung reaction - if specific Ab binds to capsule, it swells (can be observed microscopically)
Pneumococcus pathogenesis:
1) most typical disease
2) commonly inhabit
3) what prevents resp tract infection?
1)pneumonia
2)throat - these are usual source of pulmonary infection
3) Rare mucous aspiration, when it occurs, cilia bring up mucous to cough out, alveolar macrophages can phagocytose a limited # of bacteria
Pneumococci pathogenesis:
Grow intracellularly -> may be phagocytosed (if unencapsulated=non pathogenic! or Abs to capsule) -> phagocytosis without Ab requires bacteria trapped against a surface="surface phagocytosis" -> bacteria escape phagocytosis -> alveoli seeded with pneumococci -> multiple, cause entry of serous fluid (good growth med and hinders surface phag) -> PMNs infiltrate -> produce consolidation -> may progress throughout entire lobe (Lobar pneumonia) -> this process halted by Ab and antibiotics

*a lytic enzyme may contribute to pathogenesis
Most frequent cause of bact pneumonia =

symptoms:
Leukocytosis:
Prognosis:
Untreated cases:
Higher risk patients:
pneumococcal

nonspecific prodromal -> shaking chills, high fever, severe pleuritic pain and cough, production of blood-tinged sputum

commonly high circulating lymphocytes

5-20% hospital cases fatal even with antibiotics
bacteremia, leukopenia, multilobar distribution and extrapulmonary spread indicate poor prognosis

immune response causes decreased fever and sense of well-being

1) Defect in humoral immunity because type specific opsonizing Ab is important
2) Splenectomized pts and Sickle cell anemia
Pneumococcal pneumonia:

Lab Diagnosis:
Treatment:
microscopic exam of sputum - pneumococcal type generally not determined

Frequent multiple antibiotic resistance - requires sensitivity testing
Other Pneumococcal infections:
may be secondary to pneumonia by seeding during bacteremia or direct extension of lung infection

in children - prominent role in middle ear infections and severe or fatal meningitis
Pneumococcal prevention:
Vaccine:
PneumovaxTM - first vaccine, 17 capsular polysaccharides, T cell independent Ag, no booster response, recommended for <65 (not young children, elderly or certain native american groups!)

PrevnarTM - conjugated vaccine, 7 capsular polysacch conjugated to highly immunogenic protein -> T cell dependent immune response in infants, prevents pneumococcal meningitis

Neither substantially protective against community acquired pnemococc. pneum, but both prevent invasive disease associated with high mortality
Listeria monocytogenes:

characteristics -
location -
Transmission -
small, G + rod, related to diptheroids although it is beta hemolytic

widespread, soil and water, infected animals and humans

usally animal -> human, also dairy products and meat (potent food pathogen - grows well at refrigerator temp)
Listeria monocytogenes:

High-risk patients -
Why?
What to avoid -
Immunosuppressed patients
Pregnant women: can cause bacteremia -> transplacental infection
Early in term -> abortion and still birth
Late term -> live birth but newborn may die of early onset neonatal septicemia and meningitis

pregnant women probably more susceptible b/c:
decrease cell mediated immunity

avoid unpasteurized milk, unprocessed soft cheese

processed soft cheeses (cottage, cream) and yogurt are SAFE
Listeria monocytogenes:

Types of adult infections -

Fatality and infection rate -
meningitis, septicemia, urethritis, endocarditis

20% hospitalized cases, 500 deaths/yr in US, 2500 serious infections/yr in US
Facultative intracellular Listeria monocytogenes:

list the 3 obligate intracell bacteria:

growth preferences of facultative intracell bacteria:
Rickettsia, chlamydia, Mycobacterium leprae

can be grown on medium, but take advantage of intracell growth during infection
Facultative intracellular Listeria monocytogenes:

process of entering cell -
extracell bact promotes phagocyt -> taken up into phagolysosome -> secretes hemolysin that lyses phagolysosomal membrane -> bacteria released into cytoplasm -> one end of bacterium induces host cell actin to polymerize and form a long tail for the bacterium -> propels within cytoplasm to host cell projection -> enters second cell -> lyses into second cell cytoplasm -> repeat cycle

*THUS evades Ab in extracellular fluid!