zoonotic illness
originates in animals and ends up in humans (MUST be animal to human) ex. rabies- typically in rodents, bats, pigs
vector-borne
an intermediate is involved between animal to human OR human to human; ex. lyme disease- mouse to tick to human; malaria- human to mosquito to human; typically arthropods, mosquitoes, ticks
what are spillover events
movement from one species to another; when does it spill into the human population?
how can vectors lead to transmission that would otherwise not occur
serve as "bridges" for transmission events that otherwise wouldn't occur; person to person, animal to person; details of transmission by vector can lead to further evolution by pathogens
what are general characteristics of most emerging diseases
new diseases to humans are from RNA genome viruses; zoonotic/vector borne; occurring because of more contact with insects/animals than ever before
what groups of people will need to collaborate in order to keep these emergence events under control?
all professionals- doctors, public health, ecologists, environmentalists, wildlife vets; west nile virus spread across US because we didn't connect dead birds tot he virus
what are factors leading to increased contact between humans and/or vectors?
economic impact of wildlife- ecotourism/farming; human population explosion- population growth= encroachment on wildlife/crowding; changes in agricultural practices- we are taking land from animals for agriculture; live animal markets; climate change- cha
nipah virus land use changed
switched wild areas to agricultural areas and moved fruit trees and pig farms out there; noticed pigs getting respiratory/neuro illness and death; pigs infected humans taking care of them, went from bats to pigs to humans
hantavirus outbreak- climate change
impacts from el nino led to prolonged drought then followed by periods of heavy rain; drought affected larger animals and heavy rain increased plant and insect populations; decrease in predators increase in food sources, led to explosion of rodent populat
what is known or suspected about the emergence and spillover of the 2019 nCoV
80k infected; started in seafood/animal market; lower mortality than MERS/SARS only about 2 %; have now found a virus 95-96% similar to corona that started in bats; what was the intermediate? pangolins?
what were components of plague doctor uniform? why were they included?
coat and hat made of heavy material hooded in wax- barrier from person; beak- filled with herbs/fragrant items- prevent from smelling Miasma; stick-kept patients at arms length
which country typically reports the highest # of plague infections each year? why?
madagascar- high rats/flea population there
what is the story behind the case of the plague in Illinois
attenuated strain of Y. pestis defective in iron acquisition; a university had 2 labs dealing with the plague; one lab had weakened attenuated y. pestis and the other lab had a virulent plague; man working in lab with attenuated strain died in hospital fr
plague infection in the US can be divided into two distinct trends based on time periods since the introduction in 1900, what characteristics define each trend?
1900-1925 was first big wave/outbreak (urban areas); 1965- started the endemic, reported cases every year but typically only 8-10 cases per year (rural areas)
enzootic cycle
endemic disease in animals; primarily the cycle is just between rodents and fleas; could be due to high diversity in rodent population, some rodents resistant to dying from plague; low animal deaths, persisting plague; territorial animals
epizootic cycle
epidemic in animal population which has high animal deaths meaning fleas need to branch out and infect new hosts (humans)
what are the transmission possibilities for the plague? what is the role of flea blockage?
bubonic transmission through flea bites or contaminated fluids/tissues; blockage occurs when induction of biofilm production forms large plugs in the digestive tract of a flea; forms clotted blood with a lot of y. pestis in it; flea can then no longer eff
bubonic characteristics
flu like symptoms- 10% mortality rate but it can develop into 2 more serious forms of plague; transmission- flea bites, contaminated tissue/fluid
septicemic characteristics
flu like, pain, shock, bleeding, skin/tissue death, can turn black; without treatment=90% mortality; transmission through flea bites, contaminated tissues/fluids, or untreated bubonic
pneumonic symtpoms
fever, headache, weakness, pneumonia; very rare and transmission is through inhaling infectious droplets person-person or untreated bubonic/septicemic
what are some measures madagascar took to help the 2017 plague epidemic under control?
contact tracing- finding someone who has plague and tracing everyone they had contact with, make a map of people and their exposure levels; offered large #s of possible infected people with prophylactic antibiotics; public education to reduce stigma, airp
what was unique about the arthritis outbreak in Old Lyme, Connecticut
arthritis is not contagious; thought it was rheumatoid arthritis- autoimmune disorders- not based on season or geography; affected 40 kids, 10 adults; all lived in the same town on the outskirts in a rural part backed up against forest; seasonality was ju
why is it interesting that B. burgdorferi does not appear to require iron?
no/low levels of iron required; uses manganese as a cofactor and accumulates higher levels; typically infections limited by need for iron/ iron levels in body
why are co-infections problematic with B. burgdorferi
tick can carry 2 species of borrelia (anaplasma and babosia), and peowassan virus; likely that you will get infected with more than one disease from the tick because other viruses are transferred much faster than borrelia (24-36 hrs)
why does human infection take up to 36 hours for B. burgdorferi
infection spreads into body from 24-48 hrs
why is vaccine for lyme disease no longer offered in US
stopped being made in early 2000s because immunity didn't last very long and wasn't overly effective, needed boosters every year
does chronic borrelia infection exist (lyme)? why
most insurance companies/CDC do not recognize this as life-long disease; if you are retested you don't get consistent positive results and you can't successfully culture borrelia from person; antibiotics don't work after initial infection gone
how many serotypes of dengue exist
flavivirus group- 4 serotypes and strains within these serotypes; labeled 1-4;
disease progression for dengue
febrile--critical--convalescent
febrile stage (dengue)
fever lasts multiple days; might see biphasic presentation (fever not present in morning and climbs as the day goes on); very nonspecific= hard to diagnose
critical stage (dengue)
24-48 hours; difficult to access because everyone appears to be improving but actually you are either getting ready to a actually improve or completely crash; leakage of capillaries occurring and virus invaded endothelial cells (lining blood vessels); lea
convalescent (dengue)
you are recovering but it can last for months; residual pain/fatigue/etc.; hemorrhagic illness can occur; can the body handle the plasma leakage
why is the second dengue infection often more severe than the first in an individual? what does this phenomenon mean for areas where multiple flaviviruses circulate?
if you are bitten and infected first time, you are immune to that serotype only; at second infection your body should fight it off immediately but if you are infected with a second type of serotype antibody dependent enhancement occurs; your antibodies re
describe what is known about vaccines for dengue. controversy?
dengvaxia- controversy; children at high risk for death because they are at high risk of second infection, 2014-2015 vaccine came out and was supposed to protect against all 4 serotypes; gave antibody response to all 4 at first; 2016 did mass vac. in phil
seronegative individuals at vac.
at time of vaccination they never had dengue before; vac. gave low rate of immunity and it wass short-term/promoted antibody dependent enhancement if they did get infected later on; increased hospitalization if infected
seropositive individuals at vac.
you have had prior infection then vaccine works how it should; you get immunity, decent/long-lasting, no increased risk of ADE
what does this mean for other flavivirus vacc.
large # of flaviviruses overlap, need protection from all types or no vac. at all
what are the main risks for human exposure to rabies globally and in the US
need at least 70% vacc. in dogs, 30-50%; our major risk in US is wildlife (foxes, raccoons, skunks, bats)
how is rabies transmitted to humans
animal-human; saliva (biting), rare cases from contact with brain/nervous system
how is rabies treated before/after the development of clinical symptoms?
before: vaccine quickly stimulates immune response; after symptoms: 98% fatality rate, nothing helps
why did investigators think the risk of rabies for the individuals in this study was fairly low? why was post-exposure prophylaxis recommended regardless?
reduced risk due to no rabies found in specimen, bat's cranium intact, salad was rinsed before packaging, mucous membrane exposure not proven to result in rabies and virus doesn't survive more than few days outside host; post-exposure prophylaxis- more ef