Microorganisms Flashcards
Types of Gram + Cocci
Staphylococci; Streptococci; Enterococci
Differentiate Staph from Strep via Catalase Test
Staph + ; Strep -
Basic features of Staphylococci
- Gram + (purple)
- Looks like cluster of grapes
- Golden yellow colonies on culture
- Hardy
- Persist on fomites (inorganic objects)
- Normal as skin and nasal flora
- Common wound infections
- Facultative Anaerobes
How do you differentiate between subclasses of Staph?
Coagulate Test
(whether or not it clots)
S. Aureus: Coagulase + ; All others: Coagulase -
All others include S. Epidermidis & S. Saprophyticus
S. Aureus
Virulence Factors
- Major pathogen/most virulent
- Cytotoxic: Hemolysis; PVL
- Superantigen toxins: TSST-1; Enterotoxin; Exfolatin
- cause T cell explosions and systemic disease
- Protien A: binds to and neutralizes antibody (binds in reverse orientation)
- Microcapsules
- Adhesions
- Invasins: Stapylokinase: Collagenase; Lipase
- Enzymes which help to go deep into and penetrate tissue
- Spreading factors
- just remember invasins and think enzymes
S. Aureus
Epidemiology
- Carry rate: 20-30%
- Infection surrounding open wounds; diabetes; IV drug use (aka things that cause open wounds like injections)
- Infection can be localized or systemic
-
Very common hospital infection
- especially because it survives on fomites!
S. Aureus
Clinical Manifestations
- Most commonly presents as SSTIs (skin and soft tissue infection)
- Infections of other tissues, potentially from metastatsis from other superficial infections
- Osteomyelitis
- Septic Joint (especially in children)
- Pneumonia
-
Acute Endocarditis (heart infection)
- frequently associated with IV drug use
- Septicemia (blood infection)
- Toxinoses caused by superantigens
- Toxic Shock Syndrome from TSST-1 exotoxin
- results in high fever, sunburn like rash, and multi-organ failure
- systemic reaction
-
Enterotoxins causing food poisoning or gastroenteritis
- Heat stable enterotoxins
- acute onset of GI distress post incubation
-
Exfollatin toxin causing Scalded Skin Syndrome
- bullae look like sunburn
- Toxic Shock Syndrome from TSST-1 exotoxin
S. Aureus
Resistance
>90% seen in clinic resistant to penicillins
MRSA
S. Epidermidis
- Gram +, Staphylococci Family
- Coagulase -
- Novobiocin Sensative
- Highly resistant to antibiotics
- Major component of skin flora
- Cause wound infections through broken skin
- Less virulent
- Produces slime as barrier to antibiotics (virulence factor)
- slime adheres to bioprosthetic
-
Frequently involved in nosocomial and opportunistic infections
- catheters, medical devices, IVs
- Most are highly resistant to penicillins and methicillins
S. Saprophyticus
- Gram +; Staphylococci Family
- Coagulase -
- Novobiocin Resistance
- Normal vaginal flora
- UTI, cystitis in women
- Distingued from others because naturally resistant to Novobiocin
- Sensative to penicillin G
Streptococcus Cell Wall Classification
Lancefield Groups
Based on C Substance (antigenic cell wall polysaccharide)
A-U react
Common human Pathogens:
A, B, D, “none”
S. Pyogenes
- Group A Streptococci (GAS)
- Gram +
- Catalase -
- B-hemolytic
- Bacitracin Sensative
S. Pyogenes
Virulence Factors
-
M-Protein
- ~80 types
- surface, antiphagocytic protein
- many different types to evade & confuse body
- highly variable antigenic
- Streptolysin O and S
- lyse RBCs
- ASO titer Abs
- Exotoxins
S. Pyogenes
Clinical Manifestations
1. Streptococcal Pharyngitis
- Strep Throat
- Associated with scarlet fever
2. Streptococcal Skin Infections
- Flesh-eating bacteria
3. Streptococcal Toxic Shock Syndrome
- Full body systemic response
S. Pyogenes
Post-Infection Sequelae of GAS Infections
Antibody-mediated
1. Acute Rheumatic Fever (ARF): Heart and Joints
- Ab to M proteins cross react and cause damage
2. A true PostStreptococcal Glomerulonephritis (APSGN): Kidney
- develop Ab/Ag complexes which get trapped in the kidney and cause damage
S. Pyogenes
Epidemiology
Inhabits throat, nasopharynx, occasionally skin in humans
Transmission: contact, droplets, food
Spreads easily
Children predominantly affected
(~30% of all bacterial pharyngitis in children’s is due to GAS)
S. Agalactiae
- Gram +
- Streptococcal Group B
-
Bacitracin Resistant
- distinguishes from S. pyogenes (Bacitracin sensative)
-
Normal flora of female reproductive tract
- not problematic to the mother, but can be very problematic to the child
- leading cause of neonatal sepsis
Alpha-Hemolytic Steptococci
Viridans (many different species): Optochin RESISTANCE
S. Pneumoniae: Optochin SENSITIVE
*Non-Lancefield Group*
Beta-Hemolytic Streptococcus
S. Pyogenes: Bacitracin SENSATIVE; Group A
S. Agalactiae: Bacitracin RESISTANCE; Group B
Viridans Group Streptococci
- Large complex group
- Widespread residents of the oral cavity
- Not very invasive; inter through surgical facilitation
- Clinical Manifestations
- Dental Caries
- Subacute Endocarditis (heart infection)
Streptococcus pneumoniae
High Level
- Small, lancet-shaped cells arranged in pairs and short chains
- Also know as pneumoncocci
- Very serious
- causes 30-60% of all pneumonias
Streptococcus pneumoniae
Virulence Factors
-
Polysaccharide Capsule
- heavily encapsulated forms are more frequently associated with severe, invasive disease
- Antiphagocytic and antigenic
- Many different capsule serotypes
S. Pneumoniae
Epidemiology
- Normal flora in nasopharynx in carriers; infections often endogenous
- Fastidious
- Young children, elderly, immune compromised, alcoholics, those with lung diseases or viral infections, smokers and persons living in close quarters are predisposed to pneumonia
- Patients with sickle cell disease or those who have had a splenectomy are particularly susceptible
- when spleen becomes compromised v. problematic
S. Pneumoniae
Clinical Manifestations
-
Lobar pneumonia
- pneumococci in lungs
-
Otitis Media (ear infection)
- most frequent bacterial ear infection in children
-
Meningitis
- common cause of adult meningitis
-
Bacteremia and Sepsis
- blood infection; high mortality
S. Pneumoniae
Laboratory Tests
Alpha-hemolysis
Optochin SENSATIVE
Gamma-hemolytic Streptococci
S. Bovis
Group D
S. Bovis
- Group D Streptococci
- Component of normal GI flora
- Bacteremia caused by S. Bovis associated with GI malignancy and colon cancer
- Can grow in 40% bile
Enterococci
- Gram +
- Group D Antigen
- Genetically distinct from Streptococci but referred to as “Group D Strep”
- Infrequently Beta-Hemolytic, can be others
-
Most concerning: cause >90% of bacterial infections
- E. faecalis
- E. faecium
- Can grow in 40% bile
Enterococci
Epidemiology
- Opportunistic infection
- component of normal GI flora
- rarely causes infections in normal healthy individuals
- Resistant to chemical agents and persist on fomites
- Not very virulent; significant nosocomial papthogens due to multidrug resistant phenotype
- naturally resistance/learned resistance to most drugs
- Cause opportunistic urinary of biliary infections or intra-abdominal abscesses in immune compromised individuals
- Infections can lead to endocarditis (heart infection)
VRE
Vancomycin Resistant Enterococci
Of increasing concern due to ability to pass resistance
Laboratory Identification of Enterococci
- Bile Esculin Test
-
Ability to grow in 40% bile and hydrolyze esculin
- ^characteristic feature of Group D streptococci and enterococci
- group D grows in black; all else die
-
Ability to grow in 40% bile and hydrolyze esculin
-
Enterococci are salt resistant
- Grow in 6.5%. NaCl broth
- Differentiates group D streptococci (S. Bovis) from enterococci
Neisseria
Subclasses
Gram negative cocci
-
N. Gonorrheoeae
- 2nd most common STI in the US
-
N. Meningitidis
- Very dangerous, very aggressive
- one of the most common causes of bacterial meningitis
Nisseria spp
High Level
- Gram negative (pink)
- Kidney shaped
- Aerobic
- Fastidious
N. Gonorrhoeae
- Unencapsulated
- Gene conversion and phase variation mechanisms: cell surface proteins change
- Antigenically heterogenous: every population’s below attributes are different to help escape immune system
- Pili: facilitate attachment to host mucosa/epithelia
- Opa
- LOS: like LPPS but shorter more branched
N. Gonorrhoeae
Epidemiology and Pathogenesis
- STD
- Attack mucus membranes
- Incident rates high in teens/young adults
- Many infected are asymptomatic
N. Gonorrhoeae
Clinical Manifestations
- Genitourinary tract infections
- Pharingitis and rectal infections
- Opthalmia neonatorum
- Bloodstream invasions relatively rare and can lead to DGI (disseminated go coco cal infection)
- common cause of septic arthritis in young sexually active adults
N. Gonorrhoeae
Diagnosis
- Specimens plus mucus secretions must be plated promptly
- Smears
- intracellular Gram negative diplococci
- Culture - Complex nutritional requirements
- modified Thayer-Martin medium contains anti microbial agents to suppress normal flora
- oxidase positive
- NAATs (nuclei acid amplification tests)
- primary method for diagnosing gonococci infection
N. Meningitidis
Virulence Factors
-
Antigenic Capusle
- Serogroup B most common in US!
- Pili, LOS, Opa (similar to gonorrhoeae
N. Meningitidis
Epidemiology
- Epidemic waves in closed communities
- Carrier rate 5-10%; found in nasopharynx
-
Rapid onset and progression within 12-24 hours; very dangerous/life threatening
- can infect young and healthy individuals
- Vaccine available
Meningococci
Clinical Manifestation
-
Meningococcemia
- rapidly multiplying in bloodstream
- Petechial rash
Meningitis
Symptoms
- Severe headache
- Stiff neck
- Sensativity to light
- Vomiting
- Altered mental state or coma
Fulminant Septicemia
Meningococci
Septic Shock
Gram -
Meningococci
Treatment
- Antibiotics prophylacticly administered before confirmation if meningitis is suspected
- also prophylactic antibiotics to surrounding peeps
N. Meningitidis
Clinical Diagnosis
- Gram Stain
- Oxidase +
- Rapid latex agglutination tests for capsular antigen
- Culture to differentiate from N. Gonorrhoeae
- Maltose is differentiating factor
- leads to fermentation and pH color change
- Maltose is differentiating factor
