Microbiology Flashcards

1
Q

Give the 2 main species of mycobacteria

A

M. Tuberculosis (1/4th leading infection that results in death. - wasting, fever & bloody cough)

M. Leprae (affects skin, mucous membranes & nerves, can lead to disformaties and disfigurement in severe cases)

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2
Q

How do you stain for mycobacteria?

A

Ziehl-Neelsen stain

Their cell wall has a thick lipid layer which is pale staining in gram stains due to the mycolic acids in the wall.

Need acid fast stain

Ziehl-Neelsen: carbon fuchsin, acid alcohol, methylene blue.

AFB are resistant to destaining so stay pink/red

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3
Q

Explain how the immune system tries to prevent an infection due to a mycobacterium

A

Mycobacterium (AFB) phagocytosed by macrophages & enter a phagolysosome.

Host aims to degrade AFB and display the antigens for T-cells.

CD4 cells generate IFN-gamma for macrophages for intracellular killing. IL-12 stimulates T Helper and IFN-gamma.

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4
Q

Explain how a mycobacterium can lead to in infection

A

Signalling pathways are required to attract macrophages for killing.

Problems in the signalling pathways can lead to infection.

  • genetic defects in IL-12/INF-g/signaling
  • CD4 (HIV)
  • TNF inhibitors (rheumatoid arthritis, inflammatory bowel disease)
  • Immunosuppresed patients
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5
Q

Explain how granulomas form in mycobacterial infections

A

Lesions that try and contain mycobacteria

Macrophages:

  • become epitheliod cells
  • M0 fuse to form giant multinucleated cells ‘langhans giant cells’

Central part may necrose = caseating granuloma

Granuloma? Rule out TB

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6
Q

Which of the following is true?

a) Mycobacteria are not immunogenic
b) Mycobacteria are highly immunogenic

A

Mycobacteria are highly immunogenic

Due to mycobacterial lipids

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7
Q

How can you test exposure to TB?

Which is the most useful test and why?

A

Tuberculin skin test - intradermal injection of purified proteins, difficult to tell if immunitiy to BCG/TB

Interferon gamma release assays IGRAs - ELLISPOT/TSOT use antigens specific for M. tuberculosis. Demonstrate exposure but not active infection. - more useful

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8
Q

For the following give the main reason for the tissue damage

a) Tuberculoid leprosy
b) Lepromatous leprosy

A

a) Tuberculoid leprosy - too much immune response -tissue hypersensitivity and granulomata
b) Lepromatous leprosy - Too little immune response - tissue damage to uncontrolled bacilli & poorly formed granulomata

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9
Q

What are the principles of mycobacterial treatment?

A

Prolonged treatment as slow growing bacteria

Can grow in different locations - intra/extracellular

Combination of drugs

Resistance (big problem) - need to target all populaions and mutants - MDR & XDR

Compliance is essential

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10
Q

In primary tuberculosis where are the bacilli most likely to settle and why?

a) Carina of trachea
b) Apex of lung
c) Lower legft and right lobes
d) Right main broncus

A

Bacilli settle in the apex of the lung and form granuloma.

This is because the apex has more air and less blood supply (fewer defending WBC)

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11
Q

With TB which doesn’t makes up the primary complex?

a) granuloma
b) lymphatics
c) lymphnodes
d) capillary beds

A

Primary Complex = Granuloma + Lymphatics + Lymph nodes

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12
Q

Describe how laten TB can become active

A

Latent TB = no clinical disease

Vigorous T cell control

Detectable cell mediated immunity of IGRA/tuberculin test

May become active if there is a compromise to the immune system - aging, HIV, malnutrition, diabetes

Control lost by the T cells

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13
Q

Which bacteria is being described?

Purple on gram stain. Negative catalase test with chains of cocci. Appears yellow on a haemolysis test.

a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus

A

Beta haemolytic stretococcus

Purple on gram stain = +ve

Negative catalase test with chains of cocci = Streptococcus

Appears yellow on a haemolysis test = beta haemolytic

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14
Q

Which of the following are being described?

Purple on gram stain. Clusters of cocci that are catalase +ve and coagulase +ve.

a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus

A

Staphlococcus aureus

Purple on gram stain = gram postive

Clusters of cocci that are catalase +ve = Staphlococcus

Coagulase +ve = S. aureus

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15
Q

Which of the following are being described?

Purple on gram stain. Catalase test -ve. Green haemolysis test. Optochin sensative.

a) Beta haemolytic stretococcus
b) Streptococcus pneumoniae
c) Staphlococcus pneumonia
d) Staphlococcus aureus

A

Streptococcus pneumoniae

Purple on gram stain = +ve

Catalase test -ve = Streptococcus

Green haemolysis test = alpha haemolysis

Optochin sensative = S.pneumoniae

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16
Q

Name the sterile parts of the body?

A

Sterile parts of the body

Blood, CNS, joints, peritoneal cavity, pleura fluid, lower respirary tract, urinary tract

17
Q

Which of the following could be being described here?

Pink on gram film. Yellow appearence on MacConkey agar. Oxidase test +ve.

a) Shigella / salmonella
b) Pseudomonas
c) E.coli

A

Pseudomonas

Pink on gram film = -ve

Yellow appearence on MacConkey agar = non-lactose fermentors

Oxidase test +ve = Pseudomonas

18
Q

Which of the following could be being described?

Pink on gram stain. Pink/red appearence on MacConkey agar

a) Shigella / salmonella
b) Pseudomonas
c) E.coli
d) Staphlococcus

A

Pink on gram stain = GNB

Pink/red appearence on MacConkey agar = lactose fermentors = enterobacteriaceae = E.coli

19
Q

What are protozoa?

A

Protozoa are single cells eukaryotic organisms

Consumers of bacteria, algae + microfungi

20
Q

What type of infection is malaria?

A

Parasitic protozoa

Sporozona -> plasmodium spp.

21
Q

How is malaria transmitted?

A

On the bite of an anophele mosquito

22
Q

Which is the most dangerous type of malaria?

A

Plasmodia falciparum

23
Q

Explain the life cycle of malaria

A

Malaria bites an infected human - takes up gametocytes

Gamaetocytes to sporozoites in mosquito salivary gland

Mosquito bites human

Human liver into merozites - released into blood stream

Merozites invade RBC, divide and destroy them

24
Q

Explain the difference in lifecycles of P.ovale and P.vivax

A

P.ovale & P.vivax have an additional hypnozoite stage in the liver

They are also not eradicated by conventional anti-malarial treatments

25
Q

P.falciparum is known as ‘cerebral malaria’ and can be fatal.

Explain how it can cause tissue hypoxia.

A

The parasite matures in RBC and forms knobs on the surface.

These bind to receptors on endothelial cells & other RBC (rosetting)

Sequestration in small vessels (including brain, lung)

= Microcirculation obstructed: tissue hypoxia

26
Q

A 32 year old presents with fever, chills and sweats, fatigue, headaches and diarrhea.

On history you find that they have been in Kenya 2 months ago.

What could be the diagnosis?

A

Malaria

Fever and they have been to a tropical contry… think Malaria

27
Q

What are the following clinical features describing?

Fever, coma, ARDS, renal failure and shock

A

P.falciparum malaria

28
Q

Broadly explain how antimicrobials work

A

Antimicrobials work by binding to target sites on a bacteria.

Defined as points of bichemical reactions that are crucial to the survival of the bacteria.

The crucial binding site varies with each class of antimicrobials.

29
Q

Give examples of beta lactams and explain how they act as antimicrobials

A

Beta-lactams:

Penicillin based - penicillin, amoxicillin - cephamycin, cephalosporins …

They bind to penicilin binding proteins in the cell wall and prevent cell wall synthesis

Glycoptpties also work by this mechanism

30
Q

Give the correct antimicrobial mechanism of action for the fluroquinolones

a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)

A

The antimicrobial mechanism of action for the fluroquinolones =

Inhibition of DNA gyrase (topoisomerase II)

31
Q

Give the correct antimicrobial mechanism of action for the aminoglycosids and tetracyclins

a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)

A

The antimicrobial mechanism of action for the aminoglycosids and tetracyclins =

Inhibition of ribosomal acivity & protein synthesis

32
Q

Give the correct antimicrobial mechanism of action for metronidazole & rifampicin

a) Inhibition of ribosomal acivity & protein synthesis
b) Interference with nucleic acid synthesis/function
c) Binding to cell wall and inhibiting cell wall synthesis
d) Inhibition of DNA gyrase (topoisomerase II)

A

The antimicrobial mechanism of action for metronidazole & rifampicin =

b) Interference with nucleic acid synthesis/function

33
Q
A