Zoonotic or Vector Borne Infections of the CNS Flashcards

(75 cards)

1
Q

disease of vertebrate animals that can be transmitted to man; either directly or indirectly through an insect vector

A

zoonoses

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2
Q

if an insect vector is involved the disease is also known as an

A

arboviral disease

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3
Q

are all arboviral diseases zoonosis

A

no

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4
Q

two examples of viral zoonoses

A

rabies, hantaviruses

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5
Q

Rabies and Lymphocytic Choriormeningitis are viruses that are

A

directly transmitted to humans from other mammals

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6
Q

What form of vector transmission is most common.

A

Animal to Human, not Human to Human

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7
Q

Transmitted by mosquitoes (4)

A

West Nile, Dengue, Yellow Fever, St. Louis Encephalitis

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8
Q

cause of febrile illness and encephalitis in man and horses

A

West Nile Virus

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9
Q

West Nile was first discovered in the US

A

in New York in 1999

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10
Q

most common arboviral infection that we worry about in the US now

A

West Nile Virus

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11
Q

% of cases that are neuro-invasive

A

50%

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12
Q

Why might west nile cases vary year to year?

A

Amount of rain, mosquito populations, perhaps other factors

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13
Q

West Nile is transmitted by mosquitoes from this organism to humans and horses and other mammals (cattle, dogs, and cats).

A

Birds

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14
Q

Are humans and horses a normal part of the west nile life cycle or the SLE life cycle?

A

No, they normally go back and forth between birds and mosquitoes.

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15
Q

Are humans a good host for the west nile virus or SLE virus?

A

No, there is no viremia-so it is hard for mosquitoes to feed on us and pick up some of the virus (dead end host)

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16
Q

Only cases of human to human transmission of WNV found are from these behaviors

A

transfusions, organ transplant, breast feeding

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17
Q

West Nile Fever

A

mild illness 1/5 infected with WNV

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18
Q

symptoms of west nile fever

A

malaise, anorexia, nausea, vomiting, headache (eye pain), myalgia, rash, lymphadenopathy

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19
Q

symptoms of neurological disease from WNV

A

encephalitis (mostly) and meningitis, fever, headache, weakness, GI disturbance, change in mental status, ataxia, seizures, disorientation, visual distrubances (progress to coma, paralysis)

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20
Q

WNV progression to neurological disease usually occurs in this population

A

the elderly

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21
Q

Dx: WNV

A

suspected in older adults who develop unexplained encephalitis or meningitis in summer or early fall, do serology of CSF fluid, usually against a panel of summertime arboviruses

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22
Q

Tx: WNV

A

treatment is supportive

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23
Q

Vaccine available for WNV?

A

vaccine for horses, but not humans

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24
Q

transmitted to humans by Culex mosquitoes that acquire virus from infected birds, horses can also serve as reservoirs

A

SLE

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25
Found in temperate areas of the US in the late summer, early fall and year round in the southern US
SLE
26
SLE vaccine available?
no
27
Tx: SLE
supportive care (90% of severe disease requires hospitalization)
28
Leading cause of viral encephalitis in Asia most are seropositive due to high exposure rate
Japanese Encephalitis Virus
29
transmitted to humans and other animals by mosquitoes that obtain the virus by infected rodents and birds-horses are major reservoirs
Togaviruses (alphaviruses)
30
significant causes of vector borne viral encephalitis in the US
Eastern Equine Encephalitis, Western Equine Encephalitis
31
primarily occurs in South and Central America, but sporadic cases occur in the US
Venezuelan Equine Encephalitis
32
usually preceed EEE human infection
equine epidemics
33
30% fatality rate of those that develop clinical encephalitis, nay suffer permanent brain damage w/ some requiring permanent institutional care
EEE
34
important cause of encephalitis in horses and humans in N. America mainly in Western parts of US and Canada
WEE
35
WEE which populations are affected most severely
children affected more severely than adults and may be left with permanent neurological sequelae (mortality 3%)
36
has caused large epidemics in both horses and humans and is predominatly found in South and Central America
Venezuelan Equine Encephalitis
37
most infections are symptomatic-initially present with flu-like symptoms, children are more likely to have CNS involvement
Venezuelan Equine Encephalitis
38
spread by inhalation of dried feces and urine from infected rodents
Hantaviruses
39
Bunyaviruses
Hantaviruses, LaCrosse (California) Encephalitis Virus
40
arbovirus that is transmitted by the bite of mosquitoes and is a bunyavirus
LaCrosse Encephalitis Virus
41
infections primarily occur in Midwestern and Mid-Atlantic states, mostly in children
LaCrosse Encephalitis Virus
42
chipmunk and tree squirrel resevoirs
LaCrosse Encephalitis Virus
43
prior to vaccination in the US hundreds of deaths occurred each year
rabies
44
worldwide distribution excluding australia, great britain, and hawaii
rabies
45
Why has there been such a decrease in the number of rabies cases in the US?
animal control and vaccination
46
Often rabid in the US
skunks, fox, raccoon, mongoose (puerto rico)
47
transmission of rabies
saliva-bites, contamination of mucous membranes, aerosol transmission, corneal transplants, exposure to infected dogs or bats
48
prevention
post-exposure prophylaxis
49
Is Rabies fatal?
Yes, once the patient has symptoms the patient will die it is just a matter of how quickly, usually within 2 weeks. (99.9% fatal)
50
virus enters peripheral nerves and is transported to the CNS (sensory and motor nerves)
rabies virus
51
incubation period of a few days to months starting with nonspecific flu-like signs and the virus rapidly disseminates within the CNS and spreads to peripheral nerves
rabies
52
During cerebral infection, behavioral changes are seen-anxiety, confusion, agitation, delirium, abnormal behavior, hallucinations, insomnia, hydrophobia (50%), ending in coma and death
Rabies
53
Prevention
vaccination of animals and high risk individuals (animal handlers, veterinarians)
54
Tx:
1 dose of immune globulin and 5 doses of vaccine over a 28-day period.
55
Dx:
usually post-mortum, presence of Negri bodies (distinct intracytoplasmic inclusions) in infected neurons, also serology and viral identification
56
example of an arenavirus
lymphocytic choriomeningitis virus (LCMV)
57
rodent-borne virus that can cause aseptic meningitis,encephalitis, or meningoencephalitis but most infections are asymptomatic or produce mild febrile illnesses
Lymphocytic choriomeningitis virus (LCMV)
58
pregnancy-related infection has been associated with abortion and neurological deficits
Lymphocytic choriomeningitis virus (LCMV)
59
transmission of LCMV
inhalation of rodent urine/feces/saliva, or ingesting food contaminated with the virus
60
spread by the house mouse Mus musculus
LCMV
61
biphasic: first phase includes fever, malaise, anorexia, muscle aches, headache, nausea, and vomiting. remission for a few days and then followed by a second phase including symptoms of meningitis or encephalitis
LCMV
62
most patients recover completely and some have temporary or permanent neurological damage
LCMV
63
cause slowly developing neurodegenerative diseases (spongiform encephalopathies)
prions
64
cannabalistic tribes in New Guinea acquire this prion disease from ingesting brain and other neuronal tissue or handled it
Kuru ( a human spongiform encephalopathy)
65
human spongiform encephalopathies
kuru, creutzfeldt-jakob disease, gestermann-straussler-scheinker disease, fatal familial insomnia
66
animal spongiform encephalopathis
scrapie, transmissible mink encephalopathy, bovine spongiform encephalopathy (mad cow), chronic wasting disease (mule deer, elk)
67
infectious form of prion protein that has a globular conformation with beta-pleated sheets
PrPSC
68
normal cellular prio-related protein that has an extended conformation containing numerous alpha-helicies
PrPC
69
what happens to PrPc when exposed to PrPSc
Its released from the cell surface and converted to PrPSc-aggregates form and are internalized by neurons-neurons become vacuolated and amyloid plaques are deposited, also causes astrocyte and glial cell proliferation
70
some spongiform encephalopathies are not infectious, but
inherited or spontaneously formed (thought to be due to mutations in the PrPc
71
it is believed that those with vCJG became infected through their consumption of
cattle products contaminated with the agent of BSE
72
incubation period of prion diseases
long-years to decades, death ensues rapidly (months) after symptoms appear
73
symptoms include loss of muscle control, shivering, jerks, tremors, behavioral changes and dementia and is associated with an infectious protein
prion diseases
74
Dx: prion diseases
postmortem histological examination of brain tissue-serological tests (difficult to distinguish PrPc from PrPsc)
75
Tx: prion diseases
no current treatment for transmissible spongiform encephalopathies