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Microbiology and Immunology > Week 8 > Flashcards

Week 8 Flashcards

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Biology 101 flashcards
1
Q

Spanish Flu - number of deaths

A

50-100 million

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2
Q

Spanish Flu when

A

May 1918 after WWI

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3
Q

Spanish Flu - where it replicates + consequence (2)

A
  • Deep inside lungs
  • triggers a very strong immune response = recruit immune cells and fluid = difficulty breathing
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4
Q

Spanish Flu - symptoms

A
  • “people drowned in their own phlegm”
  • spurting blood from ears and noses
  • people turning blue = cyanotic
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5
Q

Spanish Flu - age group

A

20-40 years (unusual)

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6
Q

Spanish Flu - how they caused death (2)

A

1) death in initial infection
2) death by extremely strong immune response where lungs filled with fluid

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7
Q

How the spanish flu spread

A
  • initially in army camp, then spread by war
  • but how did it spread to places outside of war?
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8
Q

Spanish Flu - initial animal

A
  • a bird flu
  • but this bird flu was commonly in pigs at this same time
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9
Q

Spanish Flu - move from animal virus to human virus

A
  • likely not an accident
  • from first wave, it was animal flu
  • from second wave, it began to evolve intentionally and become more pathogenic
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10
Q

Spanish Flu - vaccines

A
  • predict evolutionary trends and artificially evolve virus
  • predict variants that we see
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11
Q

Influenzae/Flu - why it is different to erradicate

A
  • it is constantly evolving
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12
Q

Most recent influenzae pandemic

A

2009

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13
Q

Spanish Flu - type of microbe

A

H1N1 Influenzae A virus

an orthomyxovirus

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14
Q

Spanish Flu - vector

A

Avian (birds)

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15
Q

Spanish Flu - mode of transmission among humans

A
  • respiratory droplets/secretions of infected people
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16
Q

The Black Plague - conditions leading to its spread (7)

A
  • overcrowded cities
  • poor sanitation
  • population expansion
  • trade
  • political networks
  • powerful bacterium
  • powerful vectors
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17
Q

The Black Plague - type of microbe

A

Yersina Pestis

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18
Q

The Black Plague - vector

A
  • Rats
  • xenopsylla cheopis (fleas)
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19
Q

The Black Plague - how much of europe died

A

30-40%

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20
Q

The Black Plague - how many people died worldwide

A

200 MILLION (world pop of 500 million)

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21
Q

The Black Plague - where does it originate?

A

near the Eurasian steppe and the Gobi Desert???

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22
Q

The Black Plague - spread by (3)

A
  • trade routes - silk roads
  • crusades
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23
Q

The Black Plague - The black rat as a vector (8)

A
  • impressive powers of reproduction
  • can climb nearly vertical surfaces
  • quarter inch thick
  • survive a fall of 5 stories
  • powerful jaw (lead adobe concrete)
  • problem solving skills
  • reconnaissance
  • reservoir for fleas
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24
Q

The Black Plague - the flea as a vector (5)

A
  • aka the rat flea
  • can live for a month without a host
  • can live on almost any surface (clothing, corpses, fur)
  • jump 1/2 a meter
  • exceptional bite (regurgitate plague bacteria)
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25
Q

Yersinia pestis

A

the black plague

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26
Q

Yersinia pestis - what microbe

A

bacteria

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27
Q

Yersinia pestis - how it causes harm in body

A
  • replicates rapidly
  • produces destructive enzymes
  • invades the lymphatic system (role in immune defence
  • plague is adaptive (to invade immune system)
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28
Q

Yersinia pestis - transmission among humans

A
  • respiratory droplets/secretions
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29
Q

Yersinia pestis - gram status

A

gram negative

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30
Q

Yersinia pestis - movement

A

non-motile

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31
Q

Yersinia pestis - shape

A

rod-shapped coccoaccillus

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32
Q

Yersinia pestis - oxygen status

A

facultative anaerobic

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33
Q

HIV - Stigmatization groups (4)

A
  • men who have sex with men
  • Haitians
  • IV drug uses
  • haemophiliacs
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34
Q

Global HIV prevalence in 2017

A

africa carries most of this burden (67% of all HIV positive people lived in Africa)

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35
Q

Africa - demographics affected by HIV (2)

A
  • more women than men
  • heterosexual transmission
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36
Q

Why has HIV/AIDS disproportionately affected Africans?

A
  • Time: pre-history, the longest exposure
  • inequality: the last to receive antiretrovirals
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37
Q

HIV - Transmission (4)

A
  • transmitted sexually,
  • donated blood,
  • injection drug use,
  • pregnant women to their babies
38
Q

AIDS - first report

A
  • pneumocystis pneumonia in previously healthy gay men
39
Q

AIDS - common presentation diseases

A

1) pneumocystis pneumonia
2) Kaposi sarcoma

  • note: both are markers of a immune system loss of competence
40
Q

HIV/AIDS - name of virus

A

Human Immunodeficiency Virus

41
Q

HIV - family class

A
  • lentivirus subgroup of retroviridae family
42
Q

Retroviridae family - characteristics

A
  • latency
  • persistent viremia
  • infection of nervous system
  • weakened immune responses
43
Q

HIV - targets which cells

A
  • destroys CD4T lymphocytes
44
Q

HIV - how disease progresses

A
  • virus targets immune cells, leaving the body vulnerable to infection and cancer
45
Q

HIV - how it spreads through the body

A

1) HIV uses protein spikes embeded in its two layer lipid outer coat envelope to enter cells
2) HIV binds to CD4 cells and becomes internalized. The virus then replicates itself by generating a DNA copy by reverse transcriptase
3) Viral DNA becomes incorporated into host DNA enabling further replication

46
Q

Steps of how HIV multiplies in the body (7)

A

1) binding
2) fusion
3) reverse transcription
4) integration
5) replication
6) assembly
7) budding

47
Q

HIV - Binding (5)

A
  • step 1
  • HIV binds to a molecule on the surface of a CD4 cell
  • HIV binds to first a CD4 receptor
  • HIV then binds to a CCR5 or CXCR4 co-receptor
  • by binding to two cites on the cell, HIV can enter the host cell successfully
48
Q

HIV - Fusion (4)

A
  • step 2
  • HIV viral envolope fuses with the CD4 cell membrane
  • HIV enters the CD4 cell
  • HIV then releases its RNA and enzymes (transcriptase, integrase)
49
Q

HIV - Reverse Transcription (3)

A
  • step 3
  • HIV releases and uses reverse transcriptase (enzyme) to convert its genetic material (HIV RNA) to (HIV) DNA
  • this allows HIV DNA to enter the CD4 cell nucleus
50
Q

HIV - Integration (2)

A
  • step 4
  • HIV releases integrase (enzyme) to insert its viral DNA into the DNA of the host cell
51
Q

HIV - replication (2)

A
  • step 5
  • virus uses machinery of CD4 cell to create long chains of HIV proteins (which are the building blocks for more HIV(
52
Q

HIV - assembly (3)

A
  • step 6
  • New HIV RNA and HIV proteins made by host CD4 cell move to the surface of the cell
  • they then assemble into immature (noninfectious) HIV
53
Q

HIV - Budding (5)

A
  • step 7
  • immature (noninfectious) HIV pushes itself out of the host cell
  • outside the cell, HIV releases protease (enzyme) which breaks up the long protein chains that form non-infectious virus
  • smaller HIV proteins combine to form mature, infectious HIV
54
Q

Stages of an HIV infection (3)

A

1) acute HIV infection
2) Chronic HIV infection
3) AIDS

55
Q

Acute stage of HIV infection (3)

A
  • HIV multiplies rapidly
  • 2-4 weeks
  • highly infectious
56
Q

Chronic HIV infection (3)

A
  • HIV multiplies much less rapidly and levels start to drip
  • progresses with higher HIV levels and lower CD4 cell levels
57
Q

human immunodeficiency virus - what

A

the virus that causes AIDS

58
Q

HIV - types

A

HIV-1 and HIV-2

59
Q

HIV - which type is present mostly in US

A

HIV-1

60
Q

Acute HIV infection - how is it detected

A
  • rapid increase in HIV viral load first
  • HIV antibodies present later
61
Q

Chronic HIV infection - treatment?

A
  • antiretroviral therapy (ART) can prevent HIV from destroying immune system and advancing to AIDS
62
Q

Viral latency

A
  • when a virus is present in the body but exists in a resting (latent) state without producing more virus
  • no noticeable symptoms for a long time
  • HIV is capable of this (reservoirs despite ART therapy)
63
Q

Acquired immunodeficiency syndrome (AIDS) - what

A
  • most advanced stage of HIV infection
64
Q

Aquired immunodeficiency syndrome (AIDS) - diagnosis

A

1) have an AIDS-defining condition
OR
2) have a CD4 count less than 200 cells/mm3

65
Q

Clinical manifestation of AIDS - immunologic (4)

A
  • low white cell count CD4 (less than 200mm3)
  • opportunistic infectdions
  • lymphadenopathy
  • fatigue
66
Q

Clinical manifestation of AIDS - integumentary (3)

A
  • poor wound healing
  • skin lesions
  • night sweats
67
Q

Clinical manifestation of AIDS - respiratory (2)

A
  • cough
  • SOB
68
Q

Clinical manifestation of AIDS - gastrointestinal (3)

A
  • diarrhea
  • weight loss
  • nausea and vomitting
69
Q

Clinical manifestation of AIDS - central nervous system (7)

A
  • confusion
  • dementia
  • headache
  • visual changes
  • personality changes
  • pain
  • seizures
70
Q

Clinical manifestation of AIDS - opportunistic infections (4)

A
  • protozoal infections (pneumocystic pneumonia, encephalitis, etc.)
  • fungal infections
  • bacterial infections (TB, mycobacterium)
  • Viral infections (Herpes simplex, varicella)
71
Q

Clinical manifestation of AIDS - malignancies

A
  • Kaposis’s sarcoma
  • non-hodkin’s lymphoma
  • hodkin’s lymphoma
  • invasive cervical carcinoma
72
Q

Clinical manifestation of AIDS - AIDS dementia complex - what

A
  • cognitive, motor, behavioural impairments (70% of AIDS clients)
73
Q

HIV testing (3)

A
  • point of care test
  • self test
  • confirmatory testing - bloodwork
74
Q

HIV - point of care testing

A
  • results within minutes
  • INSTI HIV-1/HIV-2 antibody test (POC test)
  • finger prick of blood
75
Q

HIV - point of care testing is NEGATIVE

A

no further follow up (unless indicated by client exposure)

76
Q

HIV point of care testing is POSITIVE

A

follow up blood work for confirmatory testing (1-2 weeks)

77
Q

HIV - self test

A
  • INSITI HIV Self-Test
  • same technology POC test
  • allows the person to do the test alone
78
Q

Confirmatory testing: bloodwork

A

1) HIV1/2 confirmatory assay (positive or negative result)
2) P24 antigen (major protein in HIV viral core)
3) NAAT (nucleic acid amplification tests

79
Q

Clinical markers of HIV infection (2)

A
  • viral load (amount of HIV in blood)
  • CD4 count - measure CD4 T lymphocytes in a sample of blood
80
Q

why we monitor clinical markers of HIV infection (2)

A

1) a viral load to an undetectable level = effectiveness of Antiretroviral therapy (ART)
2) CD3 monitors HIV progression of the infection and a person’s response to ART

81
Q

HIV genotyping (4)

A
  • HIV is highly mutable virus = many antigenic variations
  • NOTE: differences between HIV in different ethnicities/persons AND between isolates from same person
  • great variability = error prone nature of reverse transcriptase
  • medication non-compliance –> mutatoins
82
Q

HIV - type of vector

A
  • chimpanzees
83
Q

Malaria - first symptoms

A
  • high fever
  • vomiting
84
Q

Old Anti-malaria drugs -how do they work

A
  • kill the parasite in the patient’s blood
85
Q

Malaria - vector

A

mosquito carries parasite and passes it on when it bites the next host

86
Q

Malaria - why are antimalaria drugs failing

A

the parasites are able to be resistant and avoid these drugs
- random mutations, only takes one mutation for one parasite to have a selective advantage
- this parasite is free to grow and colonize the whole human, transmit to other mosquitos, and transmit to other humans

87
Q

Tools to control Malaria spread (3)

A
  • different than other diseases (vaccines, drugs)
  • genetically engineered male mosquitos, released them to wild (they don’t bite), and instead of the females having thousands of eggs, the offspring instead die (reduce population of mosquitos to reduce risk of disease) = slow process
  • a vaccine that blocks the transmission of malaria to others
88
Q

Malaria - type of microbe

A
  • plasmodium parasite
  • P. Falciparum and P. Vivax
89
Q

Malaria - vector

A

mosquito

90
Q

Malaria - mode of transmission between humans

A

1) mosquito bites infected person
2) mosquito transfers parasite to other humans through subsequent bites

Microbiology and Immunology (10 decks)

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