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Medical Immunology > Intracellular Pathogens > Flashcards

Intracellular Pathogens Flashcards

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USMLE® Step 1 flashcards
0
Q

What are some of the pros of an intracellular pathogen?

A
  • gain access to protected env.
  • protection from immune response
  • protection from bacterial competitors
  • nutrient rich env.
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1
Q

What are some of the cons of being an intracellular pathogen?

A

They have to:

  • overcome host barriers
  • resist innate immunity
  • resist adaptive immune responses
  • adapt to life in a hostile env.
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2
Q

Viruses by their nature can be referred to as what?

A

Obligate intracellular parasites

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3
Q

Briefly describe what happens in immediate innate immune

A

0-4 hours

  • recognition by preformed, non-specific and broadly specific effectors
  • removal of infectious agent
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4
Q

Briefly describe what happens during the early induced innate response

A

4-96 hours

  • Recognition of microbial-associated molecular patterns
  • inflammation recruitment and activation of effector cells
  • removal of infectious agent
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5
Q

Briefly describe what happens during the adaptive immune response

A

> 96 hours

  • Transport of antigen to lymphoid organs
  • recognition by naive B and T cells
  • clonal expansion and differentiation to effector cells
  • removal of infectious agent
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6
Q

Describe the microbiology of mycobacterium tuberculosis

A

Acid-fast rod

24-30 hours doubling time

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7
Q

What are the routes of infection for mycobacterium tuberculosis?

A

Aerosolised bacterium
May need repeated exposure
Infectious dose approx. 1-10CFU in animals
Repeated infection

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8
Q

What are some of the risk factors for mycobacterium tuberculosis?

A 
Confined spaces
Overall poor health and immune status
Poverty/unemployment
Homelessness
Alcoholism/drug use
HIV co-infection
Steroid immunosupression
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10
Q

Briefly describe measuring the pathology of pulmonary tuberculosis

A

Sputum or smear culture

Pathology : KC8 caseating granuloma, necrosis, cavity formation

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11
Q

How does pulmonary tuberculosis cause death?

A

cachexia (constant weight loss when not trying)
respiratory failure
dissemination
massive haemoptysis

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12
Q

What is the infectivity of tuberculosis?

A

infects 1 in 3 of 2 billion
latent carriers harbour a 2-23% risk of developing TB
risk increases 10% annually should the immune system become suppressed

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13
Q

How does Mtb infect lung resident phagocytes?

A

(i) passes through epithelial layers in alveoli
(ii) enters phagocytes through natural mechanism
(iii) forms a phagolysosome
(iv) divides until cell lyses

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14
Q

What are some of the antimicrobial activities of phagolysosomes? And what substances cause them?

A

(i) nutrient deprivation - lactoferrin
(ii) membrane permeabilisation - defesins
(iii) hydrolases - lysozyme, phospholipases, proteases
(iv) production of reactive oxygen and nitrogen species
(v) acidification

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15
Q

In what 2 ways can mycobacterium tuberculosis evade macrophage engulfing?

A

(i) SapM hydrolyses phosphatidylinositide-3-phosphate and phosphatidylinositide mannoside which promote fusion of early endosomes with Mtb containing phagosomes
(ii) Rab5 is present on arrested phagosomes but fails to recruit other proteins onto the membrane

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16
Q

How are mycobacterium identified for phagocyte engulfing?

A

ABCs express toll-like receptor to detect PAMPs
pro-inflammatory cytokines causes Vitamin D pathway activation = upregulates expression of vitamin D hydrolase producing the antibacterial peptide cathelicidin

17
Q

What antimicrobial functions and cytokines released by the following receptor activation?

(i) MHCI and II
(ii) CD40/B7
(iii) TNF/IFNgamma
(iv) Fas

A

(i) toxic oxygen radicals - IL-12
(ii) Toxic nitrogen radicals - TNF
(iii) Lysosomal enzymes - IL-1
(iv) numbers of granules - IL-18

18
Q

How are cytokines involved in the response to mycobacterium?

A

Produces IFNgamma which superactivates macrophages

19
Q

In mycobacterium infection, what is the difference between antigen presentation on dendritic cells and macrophages

A

Dendritic - peptide MHC complex is stabilised and persist for T cell priming in LN
Macrophages - presentation is transient and lost in later stages - when bacterium enters latent phase with decreased CD4+ T cell response

20
Q

Can T cells respond to a whole organism?

A

No, only to processed antigen fragments

*also very efficient at destroying cancer cells and foreign organs (transplant issues)

21
Q

What’s the difference between Th1 and Th2 cells?

A

Th1 - intracellular pathogens (cytotoxic)
requires IFNgamma and IL12
Th2 - extracellular pathogens (Th17 helper cells)
IL-2 essential for skewing Th1 response

22
Q

Briefly describe Tuberculoid leprosy

A

Organisms present at low to undetectable levels
Low infectivity
Granulomas and local inflammation (peripheral nerve damage)
Normal serum Ig levels
Normal T-cell responsiveness, specific response to M. leprae antigens

23
Q

Briefly describe Lepromatous leprosy

A

Organisms show florid growth in macrophages
High infectivity
Disseminated infection - bone/cartilage/diffuse nerve damage
Hypergammaglobulinemia
low or absent T-cell responsiveness and no response to M. leprae antigens

24
Q

How do the 2 forms of leprosy arise in different organisms?

A

Tuberculoid caused by Th1, the milder form
Th2 is the incorrect immune response to mycobacterium infection
causes dissemination to the rest of the body

25
Q

How are CD4 T cells involved in response to Mtb infection?

A

Th1 provide stimulus to further activate macrophages:
(i) CD40 sensitises macrophages to IFNgamma
(ii) Th1 cell produce IFNgamma
(also TNFalpha is produced to enhance macrophage response)
*cytokine delivery is polarised for efficiency

26
Q

What is the last resort against mycobacterium infections?

A

Formation of a granuloma

- organised aggregates of immune cells surround foci of infected tissues limiting disssemination

27
Q

Briefly describe research and potential ideas for HIV and biological therapies

A

Using small antibodies
Targets immune system aspected towards inflammatory diseases (e.g. MS)
e.g. cytokine tumour necrosis factor alpha (major factor for fighting TB)

28
Q

Briefly describe the properties of herpesviruses

A 
Enveloped, dsDNA
Long and short fragment (4 isomers)
3 subfamilies: alpha, beta and gamma
Set up latent/persistent infection
Reactivation during immunosuppression
29
Q

What do alpha herpesviruses cause?

A

HSV-1/2, VZV

Medical Immunology (6 decks)

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