First Aid 2015 Micro G+ Organisms pp. 127-134 Flashcards

(97 cards)

0
Q

How do you differentiate Viridans strep and S. pneumoniae?

A

Optochin
Viridans is resistant
S. pneumoniae is sensitive
(OVRPS “overpass”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

How do you differentiate S. epidermidis and S. saprophyticus?

A

Novobicin
S. epidermidis is sensitive
S. saprophyticus is resistant
(NO StRESs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do you differentiate group A strep (pyogenes) from group B strep (agalactiae)?

A

Bacitracin (BRASitracin)
Group B strep are resistant
Group A strep are sensitive
(B-BRAS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What defines alpha hemolytic bacteria? Which bacteria are alpha hemolytic?

A

They perform partial hemolysis causing a green ring around the colony on blood agar.

S. pneumoniae and Viridans strep (S. mutans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What defines beta hemolytic bacteria? Which bacteria are beta hemolytic?

A

They perform complete hemolysis causing a clear ring around the colony on blood agar.

S. aureus, S. pyogenes, S. agalactiae, L. monocytogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Catalase +, Coagulase +, B-hemolytic

A

S. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Catalase +, Coagulase -, Novobiocin sensitive

A

S. epidermidis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Catalase +, Coagulase -, Novobiocin resistant

A

S. saprophyticus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Catalase -, a-hemolytic, Optochin sensitive

A

S. pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Catalase -, a-hemolytic, Optochin resistant

A

Viridans strep (S. mutans)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Catalase -, B-hemolytic, Bacitracin sensitive

A

S. pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Catalase -, B-hemolytic, Bacitracin resistant

A

S. agalactiae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Catalase -, Growth in bile and NaCl

A

Group D Enterococcus - E. faecalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Catalase -, Growth in bile only

A

Group D NonEnterococcus - S. bovis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

S. aureus - microscopic appearance and normal site of colonization

A

Gram + cocci in clusters

Commonly colonizes nares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

S. aureus - virulence factor(s) and toxins/diseases

A

V: Protein A - binds FcIgG –> inhibit complement activation and phagocytosis
T: TSST-1 –> toxic shock syndrome - fever, rash, shock
T: Exfoliative Toxin –> scaled skin syndrome
T: Enterotoxin –> rapid onset food poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MRSA Significance and Mechanism of Resistance

A

Important cause of nosocomial and community acquired infections.

Resistant to nafcillin and methicillin because of altered penicillin binding protein.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Toxic Shock Syndrome - Etiology, Mechanism, Symptoms

A

E: Prolonged use of tampons or nasal packing
M: TSST1 is a superantigen - binds constant region of MHC II and T cell receptor resulting in polyclonal T cell activation
Sxs: fever, vomiting, rash, desquamation, shock, end-organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Contrast S. pyogenes mediated TSS with S. aureus mediated

A

S. pyogenes mediated presents with a painful skin infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

S. aureus food poisoning - Pathophysiology

A

Ingestion of preformed toxin –> short incubation (2-6 hrs) –> non-bloody diarrhea and emesis

Heat stable - not destroyed by cooking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does coagulase allow S. aureus to do?

A

It allows it to form a fibrin clot around itself, and better form an abscess.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does S. epidermidis cause infection?

A

Infects prosthetic devices (implants, heart valves) and IV catheters by producing adherent biofilms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where is S. epidermidis normally found? What does it often contaminate?

A

Normal skin flora

Contaminates blood cultures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the main infection caused by S. saprophyticus?

A

it is the second most common cause of uncomplicated UTI in young women.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
S. pneumo is the most common cause of:
Meningitis Otitis media (in children) Pneumonia Sinusitis
25
What is the gross appearance of S. pneumo?
It is a lancet shaped diplococcus.
26
What virulence factors does S. pneumo produce?
IgA protease (also encapsulated - not virulent without capsule)
27
S. pneumo is associated with what color of sputum?
Rusty
28
S. pneumo causes sepsis in what patient subset?
Patients with sickle cell disease
29
Where are viridans strep normally found?
Oropharynx
30
What species of viridans strep causes dental caries?
S. mutans
31
What species of viridans strep causes endocarditis of previously damaged valves?
S. sanguinis
32
How does S. sanguinis cause endocarditis?
It makes dextrans which bind to fibrin-platelet aggregates on damaged valves. (Sanguinis=blood)
33
What pyogenic disease states are caused by S. pyogenes (group A strep)?
Pharyngitis - also tonsilitis Cellulitis Impetigo Erysipelas (more superficial than cellulitis)
34
What toxigenic disease states are caused by S. pyogenes (group A strep)?
Scarlet fever Toxic shock like syndrome Necrotizing fasciitis
35
What immunologic disease states are caused by S. pyogenes (group A strep)?
``` Rheumatic fever (mediated by M protein) Acute glomerulonephritis ```
36
Which B hemolytic bacterium is pyrrolidonyl arylamidase (PYR) +?
S. pyogenes
37
Titers of what antibody can be used to detect recent S. pyogenes infection?
ASO antibodies - anti-streptolysin O | could also check anti DNAse B antibody
38
What are the criteria for acute rheumatic fever?
``` JONES Criteria Joints - polyarthritis O (heart shaped) - carditis Nodules - subcutaenous Erythema marginatum Sydenham chorea ```
39
Is post strep glomerulonephritis more likely to occur after pharyngitis or impetigo?
Impetigo
40
What bacteria causes scarlet fever and how does it present?
S. pyogenes Scarlet rash with sandpaper texture Strawberry tongue Circumoral pallor Subsequent desquamation
41
Where is group B strep most commonly found?
In the vagina
42
What population is most commonly affected by group B strep? What are the common conditions seen?
Babies Pneumonia, meningitis, and sepsis
43
What bacterium produces CAMP factor? What does it do?
S. agalactiae (Group B strep) | It enlarges the area of hemolysis produced by S. aureus
44
What bacterium has a positive Hippurate test?
S. agalactiae (Group B strep)
45
Who should be screened/treated for group B strep?
Pregnant women should be screened at 35-37 weeks of gestation. If culture is positive, they should receive intrapartum penicillin prophylaxis.
46
Where are Enterococci (group D strep) normally found?
Part of the normal colonic flora
47
What disease states are caused by Enterococci (group D strep)?
UTI, biliary tract infections, and subacute endocarditis following GI/GU procedures
48
Enterococci (group D strep) are resistant to what antibiotic?
Penicillin G
49
Enterococci and Non-enterococci strep are both group D based on what system?
Lancefield grouping - based on C carbohydrate of cell wall
50
Which group of enterococci are most commonly seen in nosocomial infections?
Vancomycin resistant enterococci
51
Where are non-enterocci (Group D strep) normally found?
In the gut
52
What species/subspecies of non-enteroccus (Group D strep) causes bacteremia and endocarditis in the setting of colon cancer?
S. gallolyticus (S. bovis biotype 1)
53
How does C. diphtheriae cause diphtheria?
Exotoxin encoded by B-prophage inhibits protein synthesis by ADP-ribosylation of EF2 (elongation factor)
54
How does diphtheria present?
Pseudomembranous pharyngitis (gray-white membrane) Lymphadenopathy Myocarditis Arrhythmias
55
How do you identify C. diphtheriae in the lab?
G+ rods with blue/red metachromatic granules Forms black colonies on cystine-tellurite agar Can also do an Elek test for the toxin
56
Characteristics of spores
Contain dipicolinic acid No metabolic activity Must be autoclaved to kill
57
Which bacteria produce spores?
``` Bacillus anthracis Bacillus cereus Clostridium botulinum Clostridium difficile Clostridium perfringens Clostridium tetani Coxiella burnetii ```
58
How does C. tetani cause tetanus?
Produces tetanospasmin which cleaves SNARE proteins and prevents exocytosis of GABA and glycine from the Renshaw cells of the spinal cord.
59
What are the symptoms of tetanus?
Spastic paralysis, trismus (lockjaw), risus sardonicus (raised eyebrows and open grin)
60
Treatment of tetanus
Antitoxin +/- vaccine booster and diazepam for muscle spasms Prevent with vaccine
61
How does C. botulinum cause botulism?
Produces a preformed heat-labile toxin that cleaves SNARE proteins and inhibits ACh release
62
How does botulism differ between adults and babies?
In babies, ingestion of spores (in honey) is enough to cause disease. In adults disease only occurs with ingestion of preformed toxin. Can also be found in bad bottles of food.
63
How does C. perfringens cause disease?
It produces alpha toxin (lecithinase) that causes myonecrosis (gas gangrene) and hemolysis.
64
How does C. difficile cause disease?
Produces two toxins. Toxin A (enterotoxin) binds to the gut brush border. Toxin B (cytotoxin) depolymerizes the actin cytoskeleton ---> pseudomembranous colitis --> diarrhea.
65
Which two antibiotics classically lead to C. difficile infection?
Clindamycin and ampicillin
66
What is the treatment for C. difficile? What about recurrent cases?
Metronidazole or oral vancomycin Recurrent cases may require a repeat treatment, fidaxomicin, or fecal transplant.
67
What is special about Bacillus anthracis structure?
It is the only bacteria with a polypeptide capsule. The capsule contains D-glutamate.
68
What are the symptoms of cutaneous anthrax?
Painless papule surrounded by vesicles --> painless ulcer with black eschar --> bacteremia/death (uncommon)
69
What are the symptoms of pulmonary anthrax?
Flu-like symptoms with rapid progression to fever, pulmonary hemorrhage, mediastinitis, and shock. (Requires spore inhalation)
70
How is Bacillus cereus commonly contracted?
Keeping rice warm causes spore germination. Spores survive the cooking and cause food poisoning. "Reheated rice syndrome"
71
What are the two types of Bacillus cereus poisoning and what are the symptoms?
Emetic type: Seen with rice and pasta. N/V w/in 1-5 hours. Caused by cereulide, a preformed toxin. Diarrheal type: Watery non-bloody diarrhea and GI pain w/in 8-18 hours.
72
What type of bacteria (metabolically) is Listeria? How is it usually acquired?
Facultative intracellular microbe Unpasturized dairy, deli meats, transplacental, vaginal birth
73
How does Listeria move?
It forms "rocket tails" by rapid polymerization of actin that allow intracellular and cell-to-cell movement with a characteristic tumbling motility.
74
What is special about the membrane/wall structure of Listeria?
It is the only G+ bacteria to produce endotoxin.
75
What are the disease manifestations associated with Listeria infection during pregnancy?
Amnionitis, septicemia, and spontaneous abortion
76
What are the disease manifestations associated with Listeria infection in an immunocompromised patient? How do you treat it?
Meningitis Treat with ampicillin
77
What conditions does Listeria infection cause in newborns? How do you treat it?
Granulomatosis infantiseptica, neonatal meningitis Treat with ampicillin
78
What are the symptoms of Listeria infection in a healthy adult?
Mild gastroenteritis (self limited)
79
Both actinomyces and nocardia form branching filaments resembling fungi. Differentiate them based on: Metabolism Staining (most important) Normal location
Actinomyces is anaerobic Nocardia is aerobic Actinomyces is not acid fast Nocardia is acid fast Actinomyces is a normal part of oral flora Nocardia is found in the soil
80
What are the manifestations of actinomyces infection? How do you treat it?
Causes oral/facial abscesses that drain through sinus tracts | Treat with penicillin Tx is a SNAP - Sulfonamide - Nocardia - Actinomyces - Penicillin
81
What are the manifestations of nocardia infection? How do you treat it?
Pulmonary infections in immunocompromised Cutaneous infection after trauma in immunocompetent Treat with sulfonamides (Tx is a SNAP - Sulfonamide - Nocardia - Actinomyces - Penicillin)
82
Describe the initial process of TB infection? What are the four possible outcomes?
Pulmonary infection forming Ghon complex of hilar lymphadenopathy and lower lobe infiltrates. Outcomes - Heal by fibrosis --> hypersensitized --> + PPD - Progressive lung disease --> Death (usu. w/HIV) - Bacteremia --> Miliary TB --> Death - Dissemination with dormancy --> reactivate as adult
83
What is the pathologic manifestation of reactivated/reinfected TB in a previously sensitized person?
Caseating granuloma in upper lobe of lung
84
Reactivated TB can disseminate to many organs. What is disease of the vertebral body called?
Pott disease
85
When will a PPD be a true positive? What are causes of false positives? What test should be used to evaluate false positives?
True: current infection or past exposure False: BCG vaccination Evaluate FPs with IGRA assay
86
When will a PPD be negative? When will it be a false negative?
Negative if no infection or past exposure False: - Anergy (steroids, immunocompromised, malnutrition) - Sarcoidosis
87
What are the classic symptoms of TB?
Fever, night seats, weight loss, cough (may be productive), hemoptysis
88
What two virulence factors does TB possess?
Cord factor: inhibits macro maturation and induces TNFa release Sulfatides on surface inhibit phagolysosome fusion
89
Who is infected by M. avium-intracellulare? How do you prevent this?
HIV patients - disseminated non-TB disease Often resistant to multiple drugs so best strategy is to prevent it by giving prophylactic azithromycin when CD4+ count <50 cell/mm3.
90
All mycobacteria stain with:
acid fast stain
91
What are the manifestations of M. scrofulaceum infection?
Cervical lymphadenitis in children
92
What are the manifestations of M. marinum infection?
Hand infection in aquarium handlers
93
What disease is caused by M. leprae? What is its pathogenesis?
Leprosy or Hansen's Disease Infects skin and superficial nerves of hands and feet causing a "glove and stocking" loss of sensation
94
Describe the disease manifestations and pathophysiology of lepromatous M. leprae infection.
Diffuse skin lesions with leonine facies Damage is caused by low cell mediated immunity with humoral Th2 response It is communicable.
95
Describe the disease manifestations and pathophysiology of tuberculoid M. leprae infection.
Limited disease with a few hypoesthetic hairles skin plaques. Characterized by high cell mediated immunity with Th1 response.
96
What is the treatment for tuberculoid M. leprae infection? What about lepromatous?
Dapsone and rifampin for tuberculoid | Add clofazimine for lepromatous