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Microorganisms Flashcards

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1
Q
A
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2
Q

Types of Gram + Cocci

A

Staphylococci; Streptococci; Enterococci

Differentiate Staph from Strep via Catalase Test

Staph + ; Strep -

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3
Q

Basic features of Staphylococci

A
  • 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
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4
Q

How do you differentiate between subclasses of Staph?

A

Coagulate Test

(whether or not it clots)

S. Aureus: Coagulase + ; All others: Coagulase -

All others include S. Epidermidis & S. Saprophyticus

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5
Q

S. Aureus

Virulence Factors

A
  • 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
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6
Q

S. Aureus

Epidemiology

A
  • 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!
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7
Q

S. Aureus

Clinical Manifestations

A
  • ​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
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8
Q

S. Aureus

Resistance

A

>90% seen in clinic resistant to penicillins

MRSA

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9
Q

S. Epidermidis

A
  • 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
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10
Q

S. Saprophyticus

A
  • 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
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11
Q

Streptococcus Cell Wall Classification

A

Lancefield Groups

Based on C Substance (antigenic cell wall polysaccharide)

A-U react

Common human Pathogens:

A, B, D, “none”

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12
Q

S. Pyogenes

A
  • Group A Streptococci (GAS)
  • Gram +
  • Catalase -
  • B-hemolytic
  • Bacitracin Sensative
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13
Q

S. Pyogenes

Virulence Factors

A
  • 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
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14
Q

S. Pyogenes

Clinical Manifestations

A

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
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15
Q

S. Pyogenes

Post-Infection Sequelae of GAS Infections

A

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
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16
Q

S. Pyogenes

Epidemiology

A

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)

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17
Q

S. Agalactiae

A
  • 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
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18
Q

Alpha-Hemolytic Steptococci

A

Viridans (many different species): Optochin RESISTANCE

S. Pneumoniae: Optochin SENSITIVE

*Non-Lancefield Group*

19
Q

Beta-Hemolytic Streptococcus

A

S. Pyogenes: Bacitracin SENSATIVE; Group A

S. Agalactiae: Bacitracin RESISTANCE; Group B

20
Q

Viridans Group Streptococci

A
  • Large complex group
  • Widespread residents of the oral cavity
  • Not very invasive; inter through surgical facilitation
  • Clinical Manifestations
    • Dental Caries
    • Subacute Endocarditis (heart infection)
21
Q

Streptococcus pneumoniae

High Level

A
  • Small, lancet-shaped cells arranged in pairs and short chains
  • Also know as pneumoncocci
  • Very serious
  • causes 30-60% of all pneumonias
22
Q

Streptococcus pneumoniae

Virulence Factors

A
  • Polysaccharide Capsule
    • ​heavily encapsulated forms are more frequently associated with severe, invasive disease
  • Antiphagocytic and antigenic
  • Many different capsule serotypes
23
Q

S. Pneumoniae

Epidemiology

A
  • 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
24
Q

S. Pneumoniae

Clinical Manifestations

A
  • 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
25
Q

S. Pneumoniae

Laboratory Tests

A

Alpha-hemolysis

Optochin SENSATIVE

26
Q

Gamma-hemolytic Streptococci

A

S. Bovis

Group D

27
Q

S. Bovis

A
  • 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
28
Q

Enterococci

A
  • 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
29
Q

Enterococci

Epidemiology

A
  • 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)
30
Q

VRE

Vancomycin Resistant Enterococci

A

Of increasing concern due to ability to pass resistance

31
Q

Laboratory Identification of Enterococci

A
  • 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
  • Enterococci are salt resistant
    • ​Grow in 6.5%. NaCl broth
    • Differentiates group D streptococci (S. Bovis) from enterococci
32
Q

Neisseria

Subclasses

A

Gram negative cocci

  1. N. Gonorrheoeae
    1. ​2nd most common STI in the US
  2. N. Meningitidis
    1. ​Very dangerous, very aggressive
    2. one of the most common causes of bacterial meningitis
33
Q

Nisseria spp

High Level

A
  • Gram negative (pink)
  • Kidney shaped
  • Aerobic
  • Fastidious
34
Q

N. Gonorrhoeae

A
  • 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
35
Q

N. Gonorrhoeae

Epidemiology and Pathogenesis

A
  • STD
  • Attack mucus membranes
  • Incident rates high in teens/young adults
  • Many infected are asymptomatic
36
Q

N. Gonorrhoeae

Clinical Manifestations

A
  • 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
37
Q

N. Gonorrhoeae

Diagnosis

A
  • 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
38
Q

N. Meningitidis

Virulence Factors

A
  • Antigenic Capusle
    • ​Serogroup B most common in US!
  • Pili, LOS, Opa (similar to gonorrhoeae
39
Q

N. Meningitidis

Epidemiology

A
  • 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
40
Q

Meningococci

Clinical Manifestation

A
  • Meningococcemia
    • ​rapidly multiplying in bloodstream
    • Petechial rash
41
Q

Meningitis

Symptoms

A
  • Severe headache
  • Stiff neck
  • Sensativity to light
  • Vomiting
  • Altered mental state or coma
42
Q

Fulminant Septicemia

A

Meningococci

Septic Shock

Gram -

43
Q

Meningococci

Treatment

A
  • Antibiotics prophylacticly administered before confirmation if meningitis is suspected
    • also prophylactic antibiotics to surrounding peeps
44
Q

N. Meningitidis

Clinical Diagnosis

A
  • 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

Microbiology (7 decks)

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