Gram Positive Bacteria Test Questions – Flashcards

gram positive coccus (pairs or chains)

facultative anaerobes

capnophilic

fastidious (complex nutritional requirements)

1. serologic properties (lancefield groupings: A-W)

2. hemolysis (alpha-partial; beta-complete; gamma-absent)

3. biochemical & physiological properties

group A antigen in cell wall (plus other additional type-specific (M & T) antigens)

PYR positive

catalase negative

bacitracin susceptible

beta hemolytic

associated w/ pyogenic (pus generating) infections

asymptomatic URT colonization; transient skin colonization

person --> person via respiratory droplets

incr risk: crowding in daycare/classrooms

"flesh-eating bacteria"

pharyngitis: 5-15 yoa; winter (RF/AGN)

pyoderma: 2-5 yoa (w/ poor hygiene); summer

TSS: pts w/ soft tissue infection & bacteremia

1. capsule (antiphagocytic)

2. LTA (binds epithelial cells ~60% of adhesion)

3. M protein (adhesion; antiphagocytic; degrades C3b)

4. M-like protein (bind IgG & IgM; antiphagocytic)

5. F protein (mediate adhering to epithelial cells & internalization)

most important virulence factor for GAS infection

>120 serotypes (some w/ epitopes similar to heart tissue proteins)

structure: fibrillar (anchored in cell wall --> surface --> binds plasma fibrinogen => prevent complement activation/opsonization)

sequence: constant proximally, variable distally

*PCR/sequencing of variable region used to serotype

M antibody (only for particular serotype): may overcome phagocytic resistance

1. suppurrative

pharyngitis, scarlet fever, pyoderma, erysipeias, cellulitis, necrotizing fasciitis, streptococcal toxic shock syndrome

2. non-suppurrative

rheumatic fever & acute glomerulonephritis

common age groups: 5-15 (20-40% of cases)

transmission: respiratory droplets & close contact (esp winter)

progression: 1-4 d incubation --> sore throat; fever; chills; malaise

suppurative complications: peritonsillar OR retropharyngeal abscess *rare w/ early antibiotic treatment

non-supp complications: RF & AGN

diagnosis: rapid strep test + culture

*collecting sample: rub swab over both tonsillar pillars

streptococcus pyogenes disease (erythrogenic toxin encoded by lysogenic)

cause: streptococcal pyrogenic exotoxins A, B, & C

(toxins spreads via blood --> localizes in skin => diffuse erythematous rash)

progression: initially, rash on upper chest & tongue is furred --> later, tongue is white/red/strawberry --> rash to extremities (esp abdomen & skin folds) --> rash disappears (5-7 d) --> desquamation

*rash rarely on perioral, palm, & sole areas; suppuration rare

it is generally not serious except that it signals a harmful S. pyogenes infection AND is evidence that a hypersensitivity reaction is occurring (requires prior toxin exposure)

*scarlet fever currently rare (unknown) however toxin producing GAS still prevalent

1. staphylococcus aureus (perhaps due to penicillin resistance)

2. streptococcus pyogenes

*skin colonization w/ GAS (minor trauma) precedes clinical infection

similarities: local signs of inflammation (warmth, erythema, & pain); fever; lymphangitis; lymphadenitis *streptococcus pyogenes

differences: 

cellulitis - infection of skin/subcut tissue <= traumatic/surgical wound/insect bite; no apparent entry site

erysipelas - a form of cellulitis; more erythema/elevation; malar area of face => butterfly rash

hemolytic streptococcal gangrene (streptococcus pyogenes) *GAS infection ~60% NF cases

affected areas: superficial and/or deep fascia

progression: like cellulitis --> bullaes gangrene; systemic signs (extensive necrosis, obstructed blood supply, inflam fluid along fascial lines)

treatment: extensive debridement & antibiotic treatment

*seen in bacteremic pts w/ GAS

cause: streptococcal toxins (superantigens)

presentation: like StaphTTS (fever, malaise, hT, multiple organ failure)

diagnostic criteria existis to differentiate bt/w staph and GAS TSS (created in 1993)

1. acute rheumatic fever/rheumatic heart disease (RF/RHD)

2. acute glomerulonephritis (AGN)

*1-3 wks after acute illness

*nearly ONLY after URT infection (pharyngitis- SLO not inactivated in pharynx => antibody response)

multisystem disease (autoimmune rxn to GAS)

all symptoms resolve EXCEPT cardiac valvular dmg (in RHD)

more common location: under-developed/developing countries

rheumatogenic GAS: encapsulated; rich in immunogenic M proteins (many epitopes are similar to human tissue proteins) 

human ex. myosin, tropomyosin, laminin, actin, keratin

*anti-M IgG cross react w/ heart proteins => pancarditis

ARF presentation: subcut nodules/arthralgia --> arthritis

tx: antibiotic phrophylaxis (to prevent subseq GAS infect) 

dx: evidence of recent GAS infection; modified Jones Criteria; anti-SLO for RF

pharyngitis AND skin infections (streptolysin O inactivated in skin => NO antibody response

dx: anti-DNaseB for AGN

recurrence unlikely, as only 4-5 M strains => AGN

therefore, do NOT use antibiotic prophylaxis (will not likely be necessary to prevent subseq infe)

mechanism: Ag-Ab-complement complexes on glomerular basement membrane --> glom cap filled w/ monocytes & PMN

presentation: acute inflamm, HT, hematuria, proteinuria, etc.

PYR test positive (pyogenes is the only streptococci to => positive result)

optochin resistant (P disk)

bacitracin sensitive (A disk)

GBS

gram+, facultative, beta-hemolytic, long chains

normal flora of GIT/GUT

mothers-->babies<--other babies

women w/ genital colonization: higher risk for postpartum sepsis

virulence: undefined (capsule, PG, DNases, hyaluronidase, hemolysins)

bacteremia, pneumonia, bone/skin/soft tissue infections

higher risk: older; pts w/ debilitating underlying disease

UTI: during/immediately following pregnancy

endometritis: after delivery

chorioamnionitis: w/ heavy 2nd trimester colonization

puerperal sepsis (rare serious septicemia in pregnant mother): during/shortly after childbirth; starts w/ puerperal fever

mortality rates now decr (5%)

15-30% of survivors from meningitis have lasting complications (eg. blindness, deafness)

time of acquisition => early or late onset

(happens @ time of birth OR w/ aspiration of infected amniotic fluid)

newborns have few alveolar macrophages, poor PMN chemotaxis/phagocytosis

bacterial cell wall components => sepsis (systemic hT, hypoxia)

> 7 d after birth

transmission: from infected mother or nosocomial

characterized by: bacteremia w/ meningitis; high survival rate; neurologic sequelae

large buttery, beta-hemolytic colonies on blood agar

gram+, catalase-, bacitracin-resistant, CAMP test+

sodium hippurate+ (does hydrolyze)

bile esculin- (does NOT hydrolyze)

streptococcus agalactiae is the ONLY streptococcus w/ positive CAMP test (note the enhanced zone of hemolysis)

CAMP factor is a phospholipase => synergistic hemolysis w/ beta-lysin from certain S. aureus

streptococcus pneumoniae capnophilic, mucoid (capsule producing) colonies on blood agar

alpha-hemolysis

gram+, catalase-, produce green pigment on blood agar, optochin resistant 

*streptococcus pneumoniae is the ONLY optochin sensitive viridans streptococcus

most prevalent: oral cavity

=> life-threatening diseases: subacute endocarditis, meningitis, pneumonia

fastidious and facultative (requires blood or serum)

enhanced w/ CO2

alpha hemolysis on blood agar

bile salt susceptible

endogenous (URT --> middle ear, sinuses, meninges, lungs, & blood)

infections from new strains (resp droplets/fomites) are rare

1. PspA (protect from host's complements)

;

2. hyaluronate lyase (surf protein acts on ECM; incr tissue perm, essential for virulence in pneumon, bacteremia, ; meningitis)

;

3. neuaminidase (cleaves sialic acid from cell surf glycans; change glycosylation ; expose host surf (by incr receptors)

;

4. capsule *primary VF-those w/o are harmless (inhib phago/complement activation)

;

5. proteases (degrade SIgA =; enhance oral/intestinal mucosal infections)

;

6. pneumolysin (Ply) those w/o are less harmful (binds cholesterol of ciliated bronchial epithelia/phagocytes =; pores =; edema; hemorrhage; bacterial growth; penetration via epithel --> interstitium/blood

streptococcus pneumonia don't produce sig proteases

presentation: lobar consolidation (seldom destroy parenchyma); often preceded by viral illness; acute onset of high fever; rigors common; productive cough; pleural pain, dyspnea, tachypnea, tachycardia, sweats, malaise

sputum (rusty-from blood leaking out of capillaries) + for: PMN & lancet shaped diplococci

streptococcus pneumoniae

most sinusitis has viral origin, but acute sinusitis is usually bacterial

presentation: facial pain, headache, tenderness, fever, nasal discharge

streptococcus pneumoniae

predisposing conditions: pneumonia, otitis media

>4-20xs fatal/severe neurologic defects than meningitis by other bacteria

> 35 species, most common E. faecalis & faecium

gram+ coccus (pairs and short chains), more ovate than streptococci

facultative

high salt/bile/heat stress tolerant

optochin resistant

large white colonies on blood agar 

usually non-hemolytic

enteric

present in human/animal feces/lg intestine/GUT

MOST infections: endogenous

nosocomial: due to cross infection

not well defined

antibiotic resistance

*UTI (less common than E. coli)

presentation: dysuria & pyuria

higher risk: w/ indwelling catheter OR use of broad-spectrum antibiotics

*Peritonitis

presentation: typically acutely ill; febrile; abdominal swelling/tenderness after abdominal trauma/surgery

~Endocarditis (occasionally)

associated w/: persistent bacteremia (acute or chronically)

Peptostreptococcus

part of normal flora, infections due to spread of these organisms to normally sterile places

colonizations: oral cavity, GIT, GUT, & skin

usually susceptible to penicillin; metronidazole; imipenem; & chloramphenicol

dx: presence of anaerobic coccus assoc w/ infection