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med 2a > microbiology > Flashcards

microbiology Flashcards

1
Q

Define pathogen.

A

An organism capable of causing disease.

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2
Q

Define commensal.

A

An organism that colonises the host but causes no disease.

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3
Q

Define opportunist pathogen.

A

An organism that only causes disease if host defences are compromised.

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4
Q

Define virulence.

A

The degree to which a given organism is pathogenic.

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5
Q

Define asymptomatic carriage

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease

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6
Q

Gram positive vs Gram negative bacteria under a microscope?

A

Gram +ve = purple/blue

Gram -ve = red/pink

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7
Q

Gram positive vs Gram negative bacteria:

structure?

A

Gram +ve = 1 cell membrane and large peptidoglycan area

Gram -ve = double membrane (aka diderms) and small peptidoglycan area and LPS (endotoxin area)

pilli and flagella

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8
Q

Gram staining method?

A
  1. Apply crystal violet to heat fixed bacteria.
  2. Treat with Gram’s iodine solution.
  3. Decolourise the sample
  4. Then counterstain with safranin or fuchsine
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9
Q

Between what temperatures and what pH range can bacteria grow?

A

Between -80 to +80°C. And from a pH of 4 to 9.

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10
Q

What test can be done to distinguish between staphylococcus and streptococcus?

steps of the test?
what is the positive test sign?

A

The catalase test; detects the presence of catalase enzyme using hydrogen peroxide. Staph = catalase + ve.
Strep = catalase - ve.

add H2O2 to bacteria and see is there’s bubbling

bubbling

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11
Q

What test could be done to further distinguish between staphylococci bacteria.

steps briefly?

A

Coagulase test; looks at whether a fibrin clot is produced.

slide test: detects bound coagulase

tube test: detects free coagulase (staphylocoagulase) which reacts with coagulase-reacting factor (CRF). CRF is a thrombin-like molecule.

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12
Q

Give an advantage and a disadvantage of the slide coagulase test as opposed to the tube test.

A

Advantage: quicker and easier. Disadvantage_ less sensitive as it only detects bound coagulase and not free coagulase too_

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13
Q

Examples of gram +ve cocci vs gram +ve bacilli

A

Cocci = Staphylococci Streptococci Enterococci
Anaerobic Streptococci e.g. peptostreptococci

Bacilli = Bacillus e.g. B. anthrancis Corynebacteria e.g. C diptheriae Listeria monocytogenes
Anaerobic bacilli: e.g. Clostridia Propionibacteria

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14
Q

Examples of gram -ve cocci vs gram -ve bacilli?

A

Cocci = Neisseria Moraxella
Anaerobic cocci e.g. veillonella spp

Bacilli = E. coli Campylobacter Pseudomonas Salmonella Shigella Proteus

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15
Q

Exotoxins vs endotoxins?

A

Exotoxins:
Secreted proteins of Gram positive and Gram negative bacteria
(proteins!!)

Endotoxins:
Componentof the outer membrane of bacteria, eg lipopolysaccharide in Gram negative bacteria
(LPS!!)

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16
Q

why are mycobacteria difficult to treat with antibiotics?

A

bc they are v slow growing and they have very lipid rich cell wall

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17
Q

example of slow growing vs fast growing bacteria?

A 
slow = TB
fast = E.coli and S.aureus.
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18
Q

mycobacterium TB: body’s immune response to it?

Cell response?

A

phagocytosed by macrophages and they bring them to phagolysosomes

BUT it adapts and escapes t the cytosol

BUT then is DEGRADED by proteases
-> which leads to T cell activation and intracellular killing by macrophages

(T cell response is after 3-9 weeks following 1st exposure)

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19
Q

what are the positives of M. TB?

A

the M. TB can be killed - infection has been contained and a tissue granulomata has formed in response to the chronic infection

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20
Q

Primary TB vs Latent TB vs. Pulmonary TB?

A

Primary TB:

  • Inhale bacilli which settles in the apex of the lung & forms a granuloma
  • bacilli are taken to the hilar lymph nodes via lymphatics & leads to a T cell response [primary complex!]

Latent TB:

  • contained primary infection but the cell mediated immune response persists.
  • No clinical disease As there is a clear chest x-ray but detectable CMI (cell-mediated immunity) to TB on tuberculin skin test

Pulmonary TB:

  • Could occur immediately following primary infection (post-primary) or after later reactivation
  • which leads to a cell mediated immune response from T cells
  • In apex of lung there is more air and less blood supply (fewer defending white cells to fight)
  • which can cause necrosis in lesions → results in caseous material being coughed up & results in a cavity (hole) – it can also spread to lungs thus increasing lesions
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21
Q

How could you detect whether an individual has had previous exposure to TB?

A
  1. Tuberculin skin test (mantoux). (which measures reactivity following injection of a protein [thus looking for an immune response to the protein].)
  2. Interferon gamma release assays.
    (bc effective immunity requires CD4 T-cells which generate interferon gamma and this helps activate intracellular killing by macrophages)
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22
Q

3 main mechanisms of antibiotics?

A
  1. inhibit cell wall synthesis - The cell wall or membranes that surrounds the bacterial cell
  2. inhibit nuclei acid synthesis - The machineries that make the nucleic acids DNA and RNA (inhibits topoisomerases - which interfere with DNA unwinding)
  3. inhibit protein synthesis - The machinery that produce proteins (the ribosome and associated proteins)(binds to the 30S subunit of ribosome) = inhibits bacterial protein synthesis
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23
Q

MIC?

A

Minimum Inhibitory concentration (MIC)

the lowest concentration of an antimicrobial that will inhibit the visible growth of a microorganism after overnight incubation

The best antibiotic = time and concentration dependent killing
so the antimicrobial concen would remain above the MIC for a sufficient amount of time AND also the antimicrobial needs to occupy an adequate no of binding sites

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24
Q

bacteriostatic vs bactericidal?

A

Bacteriostatic:
• Prevent the growth of bacteria but not necessarily kill it
• However in more than 90% they kill in 18-24 hours
• Antibiotics that inhibit protein synthesis, DNA replication or metabolism are bacteriostatic

Bactericidal:
• These agents kill the bacteria
• They kill more than 99% in 18-24 hours
• Antibiotics that generally inhibit cell wall synthesis
• Useful if there is poor penetration e.g. endocarditis or difficult to treat infections or need to eradicate infection quickly e.g. meningitis

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25
Q

antibiotics?

A

Antibiotics are molecules that work by binding a target site on a bacteria

The crucial binding site will vary with the antimicrobial class

Antimicrobial = antibiotic

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26
Q

Narrow spectrum vs broad spectrum antibiotics?

A

Narrow-spectrum antibiotics are more specific and only active against certain groups or strains of bacteria.

Broad-spectrum antibiotics instead inhibit a wider range of bacteria

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27
Q

which classes of antibiotics inhibit cell wall synthesis?

give eg of antibiotics within each ab class

A

beta lactams eg penicillins, cephalosporins, carbapenems

glycopeptides eg vancomycin and teicoplanin

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28
Q 
which classes of antibiotics inhibit nucleic acid synthesis:
in particular:
- inhibit folate synthesis?
- inhibit DNA gyrase?
- binds to RNA polymerase?
- DNA strand breaks?
A
  • inhibit folate synthesis - trimethoprim and sulfonamides
  • inhibit DNA gyrase - fluoroquinolones - …floxacin eg
  • binds to RNA polymerase - rifampacin
  • DNA strand breaks - nitroidimazoles or metronidazole
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29
Q

which classes of antibiotics inhibit protein synthesis?

A
  • chloroamphenicol
  • macrolides eg clarithromycin and erythromycin - ce…mycin
  • tetracyclines - eg tetracycline and doxycycline - …cycline
  • aminoglycosides eg gentamycin and streptomycin - gs… mycin
30
Q

how do bacteria resist antibiotics?

A
  1. Target site mutation - Bacteria changes the molecular configuration of its antibiotic binding site or masks it
2. Destruction of antibiotic - The antibiotic is destroyed or inactivated:
Some bacteria produce the bacterial enzyme ‘beta lactamase’ which hydrolyses beta lactam ring of penicillins and cephalosporins
meaning the antibiotics in beta lactams class are unable to bind to penicillin binding proteins and inhibit cell wall synthesis = resistance

3.

31
Q

how do bacteria resist antibiotics?

A
  1. Target site mutation - Bacteria changes the molecular configuration of its antibiotic binding site or masks it
2. Destruction of antibiotic - The antibiotic is destroyed or inactivated:
Some bacteria produce the bacterial enzyme ‘beta lactamase’ which hydrolyses beta lactam ring of penicillins and cephalosporins
meaning the antibiotics in beta lactams class are unable to bind to penicillin binding proteins and inhibit cell wall synthesis = resistance
  1. Prevention of antibiotic entry: Bacteria modifies its bacterial membrane porin channel size, numbers or selectivity
  2. Remove antibiotic from bacterium: Proteins in bacterial membranes can act as an export or efflux pump so → the antibiotic is pumped out of the bacteria/microbe resulting in reduced levels and thus reduced effect of antibiotic on bacteria/microbe:
32
Q

antibiotic resistance:

give an irl eg of Destruction of antibiotic

A

Staphylococci produce penicillinase so penicillin but not flucloxacillin is inactivated

33
Q

How does resistance develop?

A
  1. Intrinsic: natural resistance.
  2. Acquired:
    - Spontaneous mutation.
    - Horizontal gene transfer.
34
Q

How can spontaneous mutation lead to antibiotic resistance?

A
  • Change in AA sequence.
  • Change to cell structure.
  • Decrease affinity/activity of antibiotic.
  • New nucleotide base pair.
35
Q

Give 3 methods of horizontal gene transfer.

A
  1. Conjugation. - Sharing of extra chromosomal DNA plasmids - ‘bacterial sex’
  2. Transduction. - Insertion of DNA by bacteriophages (viral vector)
  3. Transformation. -Picking up naked DNA
36
Q

What are antibiotics used for?

A
  • Treatment.
  • Prophylaxis.
  • Prevention of post-surgical infection.
37
Q

What are protozoa?

A

Single celled eukaryotic organisms.

Eaten by invertebrates.
Important parasitic and symbiotic relationships: Vertebrates, Invertebrates & Plants.

38
Q

why are protozoa hard to identify in body?

A

They evade the immune response by specific antigenic variation thus making it difficult to identify & produce a response.

They also have an intracellular phase whereby they cannot be identified. They carry out outer coat sloughing which increases antigenic variation.

39
Q

Protozoa: Classification into which 5 major groups?

and what diseases/conditions do each of the 5 major groups cause?

A

Mastigophora (Flagellates) - Usually reproduce by binary fission
It causes:
- Giardiasis → contact w/ contaminated food & water [foreign travel] & causes offensive diarrhoea, flatulence & abdominal cramps.
- African trypanosomiasis [sleeping sickness] → Bitten on arm by insect: lesion developed 2 weeks later → Self-resolved. 2 years later: fever, lethargy, myalgia, Weight loss ++, Personality change, Irritability, Increasing daytime somnolence [strong desire to sleep], Coma

Sarcodina (Amoebae)
Moves by means of flowing cytoplasm & production of pseudopodia E.g. Entamoeba histolytica
it causes:
Amoemiasis → visit abroad & has bloody diarrhoea, fever, cramps. On return has RUQ pain

Apicomplexa (Sporozoans)
No locomotory extensions, all species parasitic, most intracellular parasites, reproduce by multiple fission.
it causes:
Toxoplasmosis → Recent HIV +ve diagnosis: CD4 count 70, 2-week history of progressive left sided weakness, Headaches, visual disturbance
Malaria → 4 species cause human disease:

Ciliophora (Ciliates)
Very large group, has cilia that beat rhythmically at some stage in lifecycle,
It causes: Severe diarrhoea +/- ulceration of colon

Microsporidia
Little known about human disease but it causes diarrhoea in immunocompromised

40
Q

Give 2 examples of protozoa that can cause diarrhoea.

A
  1. Cryptosporidium.

2. Giardia lamblia.

41
Q

4 species of Protozoa cause malaria?

A
  • Plasmodia falciparum
  • Plasmodia ovale
  • Plasmodia vivax
  • Plasmodia malariae, (P. knowlesi).
    Transmitted by bite of female Anopheles mosquitoes [the vector]
42
Q

Malaria: investigations?

A

Diagnosis via blood film (thick and thin) w/ light microscopy ->
Thick: sensitive

Thin: identify morphological features & quantification of parasitaemia. Identification of species on thin film: Trophozoite most commonly used and rapid antigen test

Non-specific features:

  • Anaemia
  • Low platelets
  • Hyperbilirubinaemia
  • Mildly raised transaminases (ALT, AST)
43
Q

Malaria signs?

A

Fever, haemolysis, chills, sweats, headaches etc.

  • Anaemia - (haemolytic anaemia) - malaria parasites infect rbc - at the end of that infection cycle, red blood cell ruptures - process lowers the amount of red blood cells and can in a severe stage cause severe anemia.
  • Jaundice
  • Hepatosplenomegaly
  • Black water Fever - darkened urine - bc of all the haemolysis (baso excreting Hv out of kidneys)
44
Q

life cycle of malaria?

A

see goodnotes

45
Q

Describe the pathogenesis of p.falciparum?

A

Unique cerebral malaria, fatal infection.

Parasites mature in RBC’s,
‘knobs’ on RBC surface → bind to receptors on endothelial cells in capillaries & venules
RBC’s collect in these small vessels and cause blockage of cerebro-microvasculature = hypoxia!

aka they also bind to non-infected RBCs = ‘Rosetting’ -> sequestration in small vessels (including brain, lung) → microcirculation obstructed: tissue hypoxia

46
Q

ziehl neelsen staining:
aka?
function?
results?

A

acid-fast test
function:
for acid -fast bacilli like mycobacteria
Gram staining can differentiate most bacteria but not mycobacteria bc High lipid content with mycolic acids in cell wall makes Mycobacteria resistant to Gram stain (it’s the mycolic acid in the cell wall that makes it difficult to stain)

results; acid-fast bacilli = red eg mycobacteria
non-acid fast bacilli = blue eg e.coli

47
Q

can Mycobacteria withstand phagolysosome killing?

A

Yes. The bacterium has adapted to the intracellular environment can can withstand phagolysosome killing and escape to the cytosol.

48
Q

Stages of viral replication?

A
  1. ATTACHMENT 🡪 viral and cell receptors e.g. HIV (gp120 and CD4). [IgA blocks this]
  2. CELL ENTRY 🡪 only central viral ‘core’ carrying the nucleic acid and some associated proteins which act as enzymes to assist viral replication and negate intracellular host defence factors are freed into the host cell cytoplasm.
  3. INTERACTION WITH HOST CELLS 🡪 use cell materials (enzymes, amino acids, nucleotides) for their replication; subvert host cell defence mechanisms [GAM blocks virus-host cell fusion]
  4. REPLICATION 🡪 may localise in nucleus, cytoplasm or both; production of progeny viral nucleic acid and proteins.
  5. ASSEMBLY 🡪 occurs in nucleus (e.g. herpesviruses); in cytoplasm (e.g. poliovirus); or at cell membrane (e.g. influenza virus).
  6. RELEASE 🡪 by bursting open (lysis) of cell (e.g. rhinoviruses); or by ‘leaking’ (exocytosis) from the cell over a period of time (e.g. HIV, influenza virus) [GM activates complement which causes lysis & opsonisation]
49
Q

What category of bacteria do salmonella and shigella fall under?

A

Gram negative bacilli.

50
Q

Give 2 functions of pili.

What is the primary function of flagelli?

A
  1. Help adhere to cell surfaces.
  2. Plasmid exchange.

Locomotion.

51
Q

Name 2 gram negative bacilli that will give a positive result with MacConkey agar.

A
  1. E.Coli.

2. Klebsiella pneumoniae.

52
Q

Does shigella give a positive result with MacConkey agar?

A

No. Shigella does not ferment lactose and so gives a negative result.

53
Q

Does e.coli give a positive result with MacConkey agar?

A

Yes. E.coli does ferment lactose and so you would see a red/pink colour indicating a positive result.

–

54
Q

Oxidase test:
function?

positive result?

Name 2 bacteria that give a positive result with the oxidase test.

A

Detects the presence of cytochrome oxidase in bacteria.

A positive test is indicated by the disk turning blue.

  • Pseudomonas.
  • Neisseria.
55
Q

xld agar:
function?

results?

A

to differentiate between shigella and salmonella

Salmonella: Red/pink colonies some with black spots

shigella: Red/pink colonies

56
Q

optochin test:
function?

results?

A

Test to differentiate between streptococcus pneumoniae (causes lobar pneumonia and meningitis) - identification of Streptococcus pneumoniae

SENSITIVE: Streptococci pneumoniae - clear zone of no growth
around disc
RESISTANT: Viridans streptococci and other alpha haemolytic
streptococci - there will be growth around the disc

57
Q

haemolysis on blood agar:
Function?

Results of alpha haemolysis?
Example of alpha haemolysis?

Results of beta haemolysis?

How to test further for the streptococci in the ß haemolysis group?

A

To distinguish between different streptococci

It’s a partial erythrocyte lysis
A green colour
Streptococcus pneumoniae

 A complete erythrocyte lysis 
    You see a complete area
    Group A strep
    Group B strep
    Group G strep

Serogrouping - detecting surface antigens eg lance field grouping

58
Q

Give an example of a gram negative diplococci?

A

Neisseria e.g. N.meningitidis and N.gonorrhoeae.

59
Q

Describe the appearance of the meningococcal bacteria on microscopic
examination?

A

Gram negative diplococci.

(Neisseria meningitidis).

60
Q

Name 4/5 diseases that haemophilus influenzae can cause.

A
  1. Meningitis.
  2. Otitis media.
  3. Pharyngitis.
  4. Exacerbations of COPD.
    and pneumonia

(H influenzae is a gram negative ‘cocco-bacillus’ - a short pink rod responsible for many types of respiratory tract infection. It does not cause gastroenteritis.)

61
Q

Name 6 sterile sites in the body.

A
  1. Urinary tract.
  2. CSF.
  3. Pleural fluid.
  4. Peritoneal cavity.
  5. Blood.
  6. Lower respiratory tract.
62
Q

What are the 5 ways by which viruses can cause disease?

A
  1. Damage by direct destruction: cell lysis.
  2. Damage by modification of cell structure.
  3. ‘Over-reactivity’ of the host as a response to infection: immuno-pathological damage.
  4. Damage via cell proliferation and immortalisation.
  5. Evasion of host defences.
63
Q

What does the HIV envelop contain?

A

RNA, caspid, reverse transcriptase.

64
Q

Chains of purple cocci are seen on a gram film. They appear as above (green) when grown on blood agar. They don’t grow near the optochin disc (not shown). These are probably *

Streptococcus pneumoniae
Staphylococcus epidermidis
Viridans Streptococci
Group A streptococci (S. pyogenes)
Neisseria meningitidis
A

S pneumoniae are gram positive alpha haemolytic streptococci that give blood agar a green appearance. Their growth is inhibited by optochin. Staphylococci don’t cause haemolysis, viridans streptococci are resistant to optochin, Group A Streptococci cause (complete) beta haemolysis, Neisseria meningitidis are gram negative cocci.

65
Q

Give all characteristics of s. pneumoniae

A

S pneumoniae are

  • gram positive
  • alpha haemolytic
  • streptococci
  • that give blood agar a green appearance.
  • Their growth is inhibited by optochin.
66
Q

Give all characteristics of E. coli

A
  • pink colony is picked off this MacConkey plate bc E.coli ferments lactose
  • pink staining bacilli with Gram’s staining.
67
Q

When diagnosing viral infections which is true?

A

The sample must come from a sterile site
Electron microscopy is most appropriate
A black charcoal swab maintains virus better
PCR results take a week or more
A detectable IgM in serum may be diagnostic

68
Q

Which pair is correct? *

Toxoplasma = bacteria
Ringworm = helminth
Aspergillus fumigatus = mycobacteria
Falciparum malariae = filarial worm
Giardia lamblia = protozoa
A

Giardia lamblia = protozoa

69
Q

Mycobacteria vs Bacteria?

A

Mycobacteria:

  • Resist destaining by acid and alcohol
  • Cell wall contains lipoarabinomannan
  • They usually withstand phagolysosomal killing

bacteria:

  • They divide every 30-60 minutes
  • May cause meningitis
70
Q

A 21 year old complains of myalgia, sore throat and tiredness. He is febrile and has an enlarged spleen. Which is the best answer? *

  1. He has sepsis and needs broad spectrum antimicrobial therapy with cefotaxime
  2. A charcoal throat swab will confirm the diagnosis
  3. Tests show atypical lymphocytes and detectable EBV IgM in serum
  4. PCR on a viral throat swab will confirm the diagnosis
  5. This is a viral upper respiratory tract infection and doesn’t warrant investigation
A

Correct answer
Tests show atypical lymphocytes and detectable EBV IgM in serum

Your answer was incorrect. Have another look at the Diagnosis of Viral infections practical. This is consistent with acute infectious mononucleosis from EBV infection and typically leads to the development of atypical lymphocytes on a blood film and detectable IgM against EBV. None of the criteria for sepsis have been suggested in the clinical story. Although bacterial throat infections such as those from S pyogenes can be diagnosed with a charcoal swab, and acute viral respiratory infections can be diagnosed with PCR, neither cause enlarged spleens acutely. EBV can be detected with a viral PCR but it is often shed asymptomatically in the throat in people who have long since recovered, so not helpful for diagnosing an acute infection.

med 2a (13 decks)

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