Microorganisms Flashcards
1
Q
A
2
Q
Types of Gram + Cocci
A
Staphylococci; Streptococci; Enterococci
Differentiate Staph from Strep via Catalase Test
Staph + ; Strep -
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
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
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
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!
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
- Toxic Shock Syndrome from TSST-1 exotoxin
8
Q
S. Aureus
Resistance
A
>90% seen in clinic resistant to penicillins
MRSA
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
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
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”
12
Q
S. Pyogenes
A
- Group A Streptococci (GAS)
- Gram +
- Catalase -
- B-hemolytic
- Bacitracin Sensative
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
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
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
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)
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
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
S. Pneumoniae
Laboratory Tests
Alpha-hemolysis
Optochin SENSATIVE
26
Gamma-hemolytic Streptococci
S. Bovis
Group D
27
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
28
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**
29
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)
30
VRE
Vancomycin Resistant Enterococci
Of increasing concern due to ability to pass resistance
31
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
* **Enterococci are salt resistant**
* **Grow in 6.5%. NaCl broth**
* **Differentiates group D streptococci (S. Bovis) from enterococci**
32
Neisseria
Subclasses
**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
Nisseria spp
High Level
* Gram negative (pink)
* Kidney shaped
* Aerobic
* Fastidious
34
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
35
N. Gonorrhoeae
Epidemiology and Pathogenesis
* **STD**
* **Attack mucus membranes**
* Incident rates high in teens/young adults
* Many infected are **asymptomatic**
36
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**
37
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
38
N. Meningitidis
Virulence Factors
* **Antigenic Capusle**
* **Serogroup B most common in US!**
* Pili, LOS, Opa (similar to gonorrhoeae
39
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
40
Meningococci
Clinical Manifestation
* **Meningococcemia**
* ****rapidly multiplying in bloodstream
* **Petechial rash**
41
Meningitis
Symptoms
* Severe headache
* Stiff neck
* Sensativity to light
* Vomiting
* Altered mental state or coma
42
Fulminant Septicemia
Meningococci
Septic Shock
Gram -
43
Meningococci
Treatment
* Antibiotics prophylacticly administered before confirmation if meningitis is suspected
* also prophylactic antibiotics to surrounding peeps
44
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
