Environmental Zoonotic Diseases Flashcards

1
Q

What factors affect the following pathogens to survive in the environement?

  • viruses
  • bacteria
  • protozoan parasites
  • helminths
  • prions
A
  • Viruses: humidity, temperature, light, matrix – general rule: soft surfaces kill viruses more quicly as does low himidity and exposure to sunlight
  • bactera: matrix, persistence within feces or animal tissues, spore-formation
  • protozoans: matrix, persistence within feces or animal tissues, ability to encyst
  • helminths: ability of eggs to survive harsh conditions
  • prions: transmission via consumption of tissues, exposure to bodily fluids (pretty hardy)
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2
Q

What makes anthrax persistent in the environment?

A

exists as an endospore

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3
Q

Describe the transmission cycle of anthrax

A

infected animal –> biting fly –> bites human (cutaneous)

ingestion of contaminated meat

animal decomposition –> anthrax spores in environment –> inhalation or gets into an open wound in humans

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4
Q

Describe the anatomy of an athrax spore and the function of each structure

A
  • core (Cr): houses chromosomes + SARPs –> protection against UV and heat
  • cortex (Cx): layer of PG –> keeps spore dry
  • coat (Ct): multilayered protein shell –> prvents entry of toxins and attack by other microbes
  • interspace (IS)
  • exosporium (Exo): interacts with the environment
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5
Q

What are the three forms of anthrax disease in domestic animals?

A
  • apoplectic
  • acute and subacute
  • chronic
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6
Q

What happens to anthrax is dead animals and in oozing blood?

A
  • dead animal: readily destroyed by anaerobic bacteria
  • blood: develops into spores
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7
Q

What are the 3 forms of athrax disease in humans? Describe the tranmittence of each

A
  1. pulmonary – inhaling spores
  2. gastrointestinal – ingestion of spores
  3. cutaneous – contact with infected caracasses, contaminated wool, hides, etc
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8
Q

In anthrax pulmonary disease, how does the bacteria gain access to the pulmonary draning lymph nodes and thus go systemic?

A
  1. trojan horse model: hitches a ride in lung phagocytes to PLNs where it escapes
  2. jailbreak model: breaches the epithelial/endothelilar barrier –> enters PLN
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9
Q

What are the two plasmids in athrax? what do they encode for?

A
  1. PX01: encodes edema factor, lethal factor and protective Ag
  2. PX02: encodes antiphagocytic capsule
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10
Q

Describe the effects of the following antrax virulence factors:

  • poly D glutamic acid capsule
  • edema factor
  • lethal factor
A
  • capsule: inhibits phagocytosis, linear polymer that is weakly antigenic
  • edema factor: inactivates neutrophils via adenyl cyclase which cleaves ATP –> cAMP and floods cells with cAMP to disrupt signaling pathways
  • lethal factor: targets endotherial cells –> vasuclar leakage –> low blood volume –> septic shock; proteases that cleaves MAPK kinases –> disrupts signaling pathways
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11
Q

What does anthrax’s protective Ag do?

A

creates a pore that facillitates entry of EF and LF into cells

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12
Q

How can anthrax be diagnosed?

A
  • microscopic examination of blood smears
  • PCR amplification of EF or LF
  • inoculation of lab animals
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13
Q

What are the treatments for anthrax?

A

early antibiotic treatment

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14
Q

what do old world vs new world hantavirsuses cause?

A

old world –> HFRS
new world –> HPS

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15
Q

Why is there seasonality with HFRS?

A
  • harvesting of wheat in summer
  • harvesting rice in late fall

fields with rodent excreta –> harvesting kicks up a lot of dust

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16
Q

What is the primary agent of HPS?

A

Sin nombre virus

17
Q

What is the transmission route for hantaviruses?

A

aersolized animal excreta (salvia, feces, urine)

18
Q

Why does hantaviruses horizontally transmit around male rodents more efficiently?

A

fighting and aggressive behaviours (e.g. urinating closer to each other)q

19
Q

What is the significance of andesvirus? What is worrisome about this?

A

linked to person-to-person tranmsision (only hantavirus that can do this

ANDV and SNV have (in lab) reassorted their M segments

20
Q

Describe the different strands of hantaviruses

A
  • (S)mall: nuclecapsid
  • (M)edium: glycoproteins G1/G2
  • (L)arge: viral transcriptase/replicase
21
Q

Describe hantavirus viral entry

A
  1. binds to B3 integrin R
  2. endocytosis
  3. nucleocapsid empty into cytoplasm via pH-dependent fusion with endosome
  4. targeted to ER-Golgi
22
Q

What is the main difference between HFRS and HPS causing hantaviruses?

A

G1/G2 composition

23
Q

Briefly describe some pathogenic characterisitics of hantaviurses

A
  • dysregulate B3 functions
  • high [IL], [TNF], [IFN], and activated T cells –> pro-inflam immuine response
24
Q

How can we prevent HFRS and HPS?

A
  • education: caution about rodent infested areas
  • early treatment
  • reduce rodent population
25
Q

what are some risk factors for contracting new world hantaviruses?

A
  • greatest risk is rodents in the house (mostly farmers)
  • entrance to rarely used building
26
Q

What are virinos?

A

postulated idea that the scrapie’s agent is a nucleid acid-PrPsc complex – nucleic acid transmits genetic info for transmitting disease and PrPsc serves as protective coat

27
Q

What is PrPc?

A

normal host protein expressed on neurons,, glia, and other peripheral cells

28
Q

how do prions replicate?

A

mut –> shifts –> misfold –> misfolded PrPc (PrPsc) converts normal PrPc to misfold –> aggregates –> fragments to convert more protein

29
Q

Which tissue is most highly infected by prions?

A

brain, sc, eye (CNS)

30
Q

How can prions be tranmitted into the environment?

A
  • nasal secretions
  • saliva – salt blocks can trasmit
  • skin and mucous membrane lesions
  • feces and urine
  • in utero tranmission
  • milk
31
Q

Why was BSE so prevelant in cows?

A

high use of ruminant animal protein in dairy feeds

32
Q

lDescribe the different kinds of human prion diseases (i.e. how they are acquired)

A

sporadic

  • sCJD
  • random mutation

inherited

  • autosomal dominant mutation
  • familial CJD (fCJD)

acquired:

  • lCJD from contaminated surgical tools and tissues grafts
  • Kuru: from endoconnibalism
  • vCJD: consumption of BSE prion strain
33
Q

What are there more sCJD cases in elderly folks?

A

elders – longer life –> greater chance of mutation

34
Q

For the following treatments of inactivating prions, describe their effectiveness:

  • standard autoclaving
  • boiling
  • phenol
  • 50% bleach
A
  • autoclave = reduces infectivity
  • boiling = reduces
  • phenol = effective
  • bleach = effective