Human Impact on Zoonoses Flashcards

1
Q

How does deforestation affect mosquitoes? Use examples.

A
  • ·Plasmodium knowlesi: deforestation positively associated with infection rates –> more shallow pools in your backyard
  • Anophelese gambiae larvae prefer well lit pools (more sunlight –> warmer –> reproduce at a higher rate)
  • Anophelese durlingi have been found to bite 287X more in deforested areas (more mosquitoes present)
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2
Q

Does zoonoses affect deforestation?

A

In the amazon a 1% increase in malaria incidence was correlated with a 1.4% decrease in cleared forest area (nature fighting back)

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3
Q

How does deforestation affect wildlife?

A

puts wildlife in closer proximity with humans and mosquitos

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4
Q

Describe the transmission cycle of hantavirus? Include hosts and mode of transmission

A
  1. chronically infected rodent
  2. horizontal transmission of infection between rodents
  3. virus is present in aersolized excreta, particulary urine
  4. human infection by inhalation of aersolized rodent excreta
  5. human to human transmission is not possible
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5
Q

What causes hemorrhagic fever with renal syndrome? What are some symptoms? What is the treatment?

A
  • caused by hantavirus
  • symptoms: headache, back and abdominal pain, fever, chills, nausea, and blurred vision
  • treatment: supportive therapy (electrolytes, fluids, oxygen) and IV ribavarin
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6
Q

Describe the trend that occured in china between urbanization and hantavirus infections. Why?

A
  • inital urbanization –> lots of cases (lots of people living together + inadequate infrastructure)
  • further urbanization –> fewer cases (better infrastructure that reduced rodent exposure as cities develop)
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7
Q

Describe how urbanization affects zoonoses?

A
  • income inequality plays a role (e.g. access to clean water)
  • urbanization results in proliferation of many types of animals from which zoonotic diseases often emerge - birds, bats, and rodents (love living near humans)
  • initial urbanization can result in more zoonotic spill over events - much to do with sanitary conditions
  • more prosperity associated with urbanization helps alleviate some of the damage caused by zoonotic disease
  • greater animal density can result in more pathogen diversity
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8
Q

How did urbanization affect the parasitic load of macaques? Why?

A

urbanization increases parasite species in these monkeys

from eating human garbage

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9
Q

Describe three ways in which alterations in ecosystems can impact zoonotic disease transmission in several ways

A
  1. altered suitability for reservoir hosts
  2. altered suitability for disease vectors
  3. increased or decreased contact with humans
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10
Q

Rank the following bodies of water in terms of area suitable for mosquitos in most to least suitable: 1km river, 100 x 100m lake, 100 x 100 rice paddy

A

rice paddy > lake > river

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11
Q

Does the dilution effect or diversity begets pathogen diversity hypothesis apply better to specialist pathogens? Generalists? Why?

A
  • specialists: the dilution effect –> if their host diversity decreases then they have fewer options
  • generalists: diversity begets pathogen diversity –> not affected as much from biodiversity loss
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12
Q

Describe how biodiversity loss of birds affected WNV transmission? Does this support the dilution effect or diversity begets pathogen diversity hypothesis?

A

more bird diversity –> less WNV infections

supports the diltution effect hypothesis

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13
Q

Describe how habitiat size affects vertebrate diversity, and conversely how biodiversity loss affects the amount of LD found in ticks, and LD transmission to humans? Does this support the dilution effect or diversity begets pathogen diversity hypothesis?

A

smaller habitats tend to have less vertebrate diversity, less diversity –> more infected ticks, rodents (the reservoir for LD) live closer to humans –> more LD transmission to humans

supports the dilution effect

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14
Q

Describe the pathogen that causes Q fever: type of pathogen, species name, intracellular vs extracellular

A
  • bacteria
  • Coxiella burnetti
  • obligate intracellular parasite
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15
Q

What are the two variants of C burnetti? Describe each one

A
  1. SCV - small cell variant: sporelike, survives well in the environment, passively enters phagosome and blocks its fusion with lysosomes
  2. LCV - large cell variant: arises from SCV in phagosome, multiplies inside macrophages
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16
Q

Describe entry of C burnetti into macrophages

A
  1. binds to integrins
  2. phagocytosis in actin-dependent matter
  3. blocks fussion with lysosome
  4. acidification of phagosome
  5. decreases the presence of cathepsins
  6. induces expansion of the phagolysosome
17
Q

What are two common sources for Q fever outbreaks?

A

abattoirs and wool-processing plants

18
Q

How does testosterone affect the immune system?

A

immunosuppressive: energy expenditure on getting bigger and reproducing –> less energy on IS

19
Q

Describe chronic Q fever

A
  • infection that persists for > 6 months
  • more serious disease
  • manifests as endocarditis
  • incubation period depends on the number of organisms that infect the patients
20
Q

Describe the diagnostics, treatment, and control of Q fever

A
  • treatment: doxycycline (inhibits 30S ribosome) and hydroxychloroquine (acidifies phagolysosome)
  • diagnostics: detect serum Ab using ELISA, PCR
  • control: vaccines available for high risk occupation groups, bury placenta from sheep/goats
21
Q

What was the seasonality trend of Q fever infections that occured in the Netherlands? Why?

A

trend: increase incidence during birthing season

closer proximity to goats and sheep giving birth

22
Q

Why is it important to monitor zoo and farm animals for diseases?

A

helps predict outbreaks

23
Q

What gene is responsible for conferring resistance to common antibiotics, such as penicillin?

A

extended-spectrum B-lactamase genes

24
Q

What is the reservoir host for ebola?

A

bats

25
Q

What mistake did the Dutch make when trying to control Q fever during the outbreak?

A

didn’t implement stricter policies fast enough

26
Q

Describe the human behaviours that contributed to the spread of ebola

A
  1. traditional funeral practices
  2. unprotected healthcare workers
  3. unprotected contact with blood and body bluids
27
Q

Briefly describe how ebola enters cells (also what cells does it infect?)

A
  1. taken up by micropinocytosis
  2. glycoproteins removed by cathepsins
  3. co-opts NPC1 to facilitate release of genetic material

infects: monocytes, MFs, DCs, endothelial cells, fibroblasts, hepatocytes, adrenal cortex cells, and epithelial cells

28
Q

How does ebola cause pathology?

A

trigger release of pro-inflammatory cytokines with subsequent vascular leak and impairment of clotting, ultimately resulting in multi organ failure or shock…usually in the spleen, liver, adrenal gland

29
Q

Describe the treatment and prevention of ebola

A
  • treatment: inmazeb and ebanga (mAbs), vaccine
  • prevention: proper burial of bodies, PPE for healthcare workers, burning of bedding/clothing
30
Q

Give two reasons why bats harbour so many zoonotic diseases

A
  1. bats constituvely express type 1 IFNs and their associated proteins, humans do not have similar basal levels
  2. bats have a greater Ig repertoire: greater repertoire of heavy chain combinations –> don’t require affinity maturation?