Microbiology 3 Flashcards

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1
Q

Which organisms are Gram +ve?

A

BACILLI: Clostridium, Bacillus, Listeria, Coryne
COCCI: Staph, Strep

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2
Q

How is C.Diff treated?

A

Metronidazole
Vancomycin

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3
Q

What are the Sx of tetanus?

A

Autonomic overactivity
Spasms of voluntary muscles

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4
Q

Do you need a vaccination against tetanus?

A

5 childhood vaccines should give life-long immunity
If infected & showing Sx need immunoglobulins

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5
Q

Which organisms are gram -ve?

A
  • ENTEROBACTERIA: E.Coli, Klebsiella, Salmonella, Shigella, Proteus
    -Pseudomonas
    -Neisseria
  • Haemophilus
  • Legionella
  • H.Pylori
  • Campylobacter
  • Gonorrhoe
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6
Q

What’s the difference between gram +ve & Gram -ve?

A

Thick peptidoglycan layer in gram +ve cells wall which takes up staining
Gram -ve has lipopolysaccharide layer outside of this so staining can’t reach

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7
Q

Which type of E.Coli is the most severe?

A

E.Coli Verotoxin (0157)
Through contaminated food
10% causes HUS

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8
Q

Why is E.Coli UTI difficult to get rid of?

A

Form biofilm over urothelial cells

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9
Q

How does Klebsiella acquire resistance?

A

Through plasmids
Particularly seen in gram -ve bacteria

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10
Q

How helpful are leukocytes/nitrites on a urine dipstick?

A

Nitrite: High specificity
Leukocytes: Low specificity, high sensitivity

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11
Q

How is H.Pylori treated?

A

PPI, 2 antibiotics (amoxicillin & Macrolide)

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12
Q

What are the Sx of Typhoid?

A

High fever
Cough
Abdominal pain
Relative bradycardia
Rose spots in pale skin
3rd week: Necrosis of Peyer’s patches & peritonitis

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13
Q

How is Typhoid treated?

A

Fluoroquinolones
Vaccination 30-70% effective

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14
Q

Where does Shigella affect?

A

Large bowel
Invades colonic epithelial cells
Causes bloody diarrhoea

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15
Q

How is Campylobacter treated?

A

Clarithromycin

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16
Q

What is a complication of Campylobacter?

A

Guillan-Barre Syndrome

17
Q

What is the triad of reactive arthritis?

A

Arthritis
Conjunctivitis
Urethritis

18
Q

What are the causes of reactive arthritis?

A

Diarrhoea: Salmonella, Campylobacter, Shigella
STD: Chlamydia, Gonorrhoea

19
Q

What are the other Sx of reactive arthritis?

A

Iritis
Circular balanitis
Keratoderma blenorrhagia

20
Q

How long does immunity to Norovirus last?

A

4-10/52

21
Q

How is gonorrhoea treated?

A

IM Ceftriaxone
Plus Azithromycin

22
Q

What are the complications of gonorrhoea?

A

Chronic (men = strictures, women = PID)
Septic arthritis
Epididymo-orchitis
Bacterial endocarditis
Reactive arthritis

23
Q

What is the complication of chronic Chlamydia in women?

A

Half of asymptomatic women progress to PID

24
Q

What are the Sx of Chlamydia in men?

A

Discharge
Urethritis

25
Q

How is Chlamydia diagnosed?

A

NAATs

26
Q

How is Chlamydia treated?

A

Doxycycline

27
Q

What is the difference between aerobic, anaerobic & facultative anaerobic bacteria?

A
  • Aerobic: Use O2 for metabolism, can only survive if O2 present but needs enzymes to detoxify O2
    -Anaerobic: Metabolise without O2, Cannot survive in presence of O2
  • Facultative: Can survive with/without O2 but prefer with
28
Q

What are the 3 mechanisms of action of antibacterials?

A

1) Action on cell wall synthesis: B-lactams, Glycopeptides
2) Inhibition of protein synthesis: Tetracyclines, Aminoglycosides, Macrolides, Chloramphenicol
3) Inhibition of nucleic acid synthesis: Metro, Rifampicin, Trimethoprim

29
Q

How do B-Lactams work?

A

1) Rely on integrity of B-lactam ring
2) Bind to & inhibit enzymes that catalyse link preventing cross-bridges between peptidoglycan polymer chains
Examples: Penicillins, Ceph, carbapenems

30
Q

How do Glycopeptides act as antibacterials?

A

Interfere with cell wall synthesis by binding to peptidoglycan chains preventing formation of cross-links
Examples: Vanc, Teic

31
Q

How to antibacterials that inhibit protein synthesis generally work?

A

Selectively toxic
Tend to be bacteriostatic
Bacterial ribosomes consist of 50S & 30S subunit

32
Q

How do Macrolides, Tetracyclines, Aminoglycosides, Clindamycin & Chloramphenicol work?

A

M: Bind to 50S subunit inhibiting peptide chain translocation
T: Bind to 30S subunit & inhibit binding of aminoacyl-tRNA
A: Same as tetracyclines but cause misreading of mRNA
Cl: Disrupt function of 50S subunit inhibiting bacterial protein synthesis
Ch: Inhibit peptidyl transferase activity of 50S subunit stopping transpeptidation

33
Q

How does Trimethoprim, Quinolones, Metro, Rifampicin inhibit nucleic acid synthesis?

A

T: Inhibitor of dihydrofolate reductase needed for purine synthesis
Q: Inhibit DNA gyros (compresses DNA into coils)
M: Inhibits & damages DNA synthesis
R: Prevents RNA transcription by inhibiting DNA dependent RNA polymerase

34
Q
A