Environmental Zoonotic Diseases Flashcards
What factors affect the following pathogens to survive in the environement?
- viruses
- bacteria
- protozoan parasites
- helminths
- prions
- 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)
What makes anthrax persistent in the environment?
exists as an endospore
Describe the transmission cycle of anthrax
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
Describe the anatomy of an athrax spore and the function of each structure
- 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
What are the three forms of anthrax disease in domestic animals?
- apoplectic
- acute and subacute
- chronic
What happens to anthrax is dead animals and in oozing blood?
- dead animal: readily destroyed by anaerobic bacteria
- blood: develops into spores
What are the 3 forms of athrax disease in humans? Describe the tranmittence of each
- pulmonary – inhaling spores
- gastrointestinal – ingestion of spores
- cutaneous – contact with infected caracasses, contaminated wool, hides, etc
In anthrax pulmonary disease, how does the bacteria gain access to the pulmonary draning lymph nodes and thus go systemic?
- trojan horse model: hitches a ride in lung phagocytes to PLNs where it escapes
- jailbreak model: breaches the epithelial/endothelilar barrier –> enters PLN
What are the two plasmids in athrax? what do they encode for?
- PX01: encodes edema factor, lethal factor and protective Ag
- PX02: encodes antiphagocytic capsule
Describe the effects of the following antrax virulence factors:
- poly D glutamic acid capsule
- edema factor
- lethal factor
- 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
What does anthrax’s protective Ag do?
creates a pore that facillitates entry of EF and LF into cells
How can anthrax be diagnosed?
- microscopic examination of blood smears
- PCR amplification of EF or LF
- inoculation of lab animals
What are the treatments for anthrax?
early antibiotic treatment
what do old world vs new world hantavirsuses cause?
old world –> HFRS
new world –> HPS
Why is there seasonality with HFRS?
- harvesting of wheat in summer
- harvesting rice in late fall
fields with rodent excreta –> harvesting kicks up a lot of dust
What is the primary agent of HPS?
Sin nombre virus
What is the transmission route for hantaviruses?
aersolized animal excreta (salvia, feces, urine)
Why does hantaviruses horizontally transmit around male rodents more efficiently?
fighting and aggressive behaviours (e.g. urinating closer to each other)q
What is the significance of andesvirus? What is worrisome about this?
linked to person-to-person tranmsision (only hantavirus that can do this
ANDV and SNV have (in lab) reassorted their M segments
Describe the different strands of hantaviruses
- (S)mall: nuclecapsid
- (M)edium: glycoproteins G1/G2
- (L)arge: viral transcriptase/replicase
Describe hantavirus viral entry
- binds to B3 integrin R
- endocytosis
- nucleocapsid empty into cytoplasm via pH-dependent fusion with endosome
- targeted to ER-Golgi
What is the main difference between HFRS and HPS causing hantaviruses?
G1/G2 composition
Briefly describe some pathogenic characterisitics of hantaviurses
- dysregulate B3 functions
- high [IL], [TNF], [IFN], and activated T cells –> pro-inflam immuine response
How can we prevent HFRS and HPS?
- education: caution about rodent infested areas
- early treatment
- reduce rodent population
what are some risk factors for contracting new world hantaviruses?
- greatest risk is rodents in the house (mostly farmers)
- entrance to rarely used building
What are virinos?
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
What is PrPc?
normal host protein expressed on neurons,, glia, and other peripheral cells
how do prions replicate?
mut –> shifts –> misfold –> misfolded PrPc (PrPsc) converts normal PrPc to misfold –> aggregates –> fragments to convert more protein
Which tissue is most highly infected by prions?
brain, sc, eye (CNS)
How can prions be tranmitted into the environment?
- nasal secretions
- saliva – salt blocks can trasmit
- skin and mucous membrane lesions
- feces and urine
- in utero tranmission
- milk
Why was BSE so prevelant in cows?
high use of ruminant animal protein in dairy feeds
lDescribe the different kinds of human prion diseases (i.e. how they are acquired)
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
What are there more sCJD cases in elderly folks?
elders – longer life –> greater chance of mutation
For the following treatments of inactivating prions, describe their effectiveness:
- standard autoclaving
- boiling
- phenol
- 50% bleach
- autoclave = reduces infectivity
- boiling = reduces
- phenol = effective
- bleach = effective
