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Emerging infectious diseases Flashcards

1
Q

Characteristics of emerging infectious diseases

A

Have not occurred in humans before
Have occurred previously but only affected a small number of people in isolated areas
Have occurred throughout human history but have only been recognized as distinct diseases due to an infectious agent

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2
Q

Diseases that once were major health problems globally or in a particular country, and then declined dramatically, but are again becoming health problems for a significant proportion of the population.

A

Re-emerging infectious diseases

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3
Q

New new diseases

A

Lyme disease

Legionnaire’s disease

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4
Q

New-old diseases

A

Campylobacter food borne disease
Whipple disease
Cat scratch disease

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5
Q

Old-new diseases

A

TB, Cholera, diptheria, antibiotic resistant bacteria,

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6
Q

Old-old diseases

A

Gonorrhea, C. Trachomatis

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7
Q

Family: Flaviviridae
Genus: Flavivirus

A

ZIKA VIRUS

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8
Q

Vector of zika virus

A

Aedes species mosquito (also dengue and chikungunya)

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9
Q

Modes of transmission of zikv

A

Sexual transmission
Perinatal (rare)
Blood transfusion
Body fluids

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10
Q

T OR F: No post-transfusion ZIKAV infection has been reported in recipients of ZIKAV (+) blood

A

True in french polynesia study

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11
Q

T or F: Breast milk transmission in zikv has been confirmed

A

False

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12
Q

T or F: zikv has negative ssrna

A

False, icosahedral positive ssrna

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13
Q

T or F: ZIKV spreading to the americas is associated with african lineage

A

False, asian

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14
Q

Increases viral replication rate in humans in the asian lineage of zikv

A

non-structural protein (NS1) codon

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15
Q

IP of zikv

A

3-12 days

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16
Q

Symptoms associated with ZIKV (2 of the ff)

A

Low-grade fever (lasts for about 4-7 days) Maculopapular rash
Transient arthritis or arthralgia
Non-purulent conjunctivitis
Headache, asthenia, vomiting, myalgia

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17
Q

Family filoviridae

A

Marburg, Ebola

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18
Q

How do you get marburg virus?

A

Direct contact with blood, tissues, and body fluids of infected persons
Handling of ill or dead infected wild animals (fruit bats and monkeys)
Via contaminated needles (higher fatality rate)
aerosol or airborne transmission ????
Prolonged exposure to mines or caves with Rousettus bat colonies

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19
Q

What is the reservoir host of Marburg Virus

A

Rousettus aegyptiacus (asymptomatic)

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20
Q

IP of Marburg

A

2-21 days

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21
Q

Which phase of MARBURG exhibits “ghost-like” features with deep set eyes, expressionless face and extreme lethargy

A

Early phase

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22
Q

Symptoms of MARBURG which arise 2-21 days after exposure

A

→ severe malaise and headache
→ Fever, abdominal pain, vomiting
→ Diarrhea – persists for a week
→ red eyes, raised lashes
→ Chest pain and cough
→ Severe hemorrhagic manifestations (days 5-7)
§bleeding internally, eyes, nose, rectum, bruising

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23
Q

Which symptom appears in the late phase (15days) of MARBURG?

A

Orchitis

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24
Q

Treatment for MARBURG

A

IV fluids and oral rehydration with electrolytes

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25
Indicator for fatal cases (8-9) [MARBURG]
Blood loss and shock (precedes it)
26
True or false: zika and marburg are related viruses that cause hemorrhagic fevers
False, ebola and marburg
27
What are the 5 subtypes of ebola virus
``` Zaire Sudan Bundibugyo Tai Forest Reston (fatal to monkeys) ```
28
How do you acquire EBOLA?
Close contact with bodily fluids of infected animals (Gorillas, chimpanzees, monkeys, Forest antelope, Porcupines, Bats of family PTEROPODIDAE (megabat or fruit bats): the natural ebola virus hosts) Direct contact through broken skin or mucous membranes with bodily fluids and contam. surface ONLY INFECTIOUS WHEN SYMPTOMATIC
29
When and where first EVD outbreak
1976 | Nzara, South Sudan, Democratic repub of congo, yambuku
30
EVD shape
Baciliform
31
Describe the EVD envelope
Long, crooked, branching filament
32
What is the capsid of EVD
Helical nucleocapsid
33
Describe the genome of EVD
nonsegmented, linear, (-) ssRNA
34
What makes up the nucleocapsid of EVD?
Nucleoprotein, VP35 (polymerase cofactor) and Polymerase (L)
35
Primary matrix protein in EVD
VP40
36
VP40 and VP 24 in EVD function to
Forms the virus matrix Helps viral entry once envelope is removed Manipulates host cell machinery Enables virus production Helps in viral reassembly during virion maturation
37
What are the attachment factors of EVD?
Lectins (binding to sugars in Dendritic cells, Alveolar macrophages, Peripheral blood cells and platelets, Cells of the liver, lymph, and bone marrow) T-cell Ig Mucin (TIM) (binding to the eye epithelia, lung epithelia, blood cells, and kidney tubule epithelia) Tyro3, Axl, Mer (TAM) (adhesion, reproduction, and cytokines (for entry to different cells) Integrins (Unique to different Ebola entry as attachment factors)
38
Symptoms 7-9 days after EVD exposure
Joint pain, headache,fever, sore throat, weakness, muscle soarness
39
10th day symptom EVD
Vomiting blood, high fever, diarrhea, extreme fatigue,
40
11th day symptoms of EVD
Brain damage, bleeding from nose, mouth and anus
41
12th day of EVD symptoms
Coma, shock, massive internal bleeding, organ failure, death
42
What places a person under investigation for ebola
Fever (>38.6°C or 101.5°F) + symptoms + epidemiologic factors within past 21 days prior to symptom onset
43
A physiologic endocytic mechanism done by cells used by ebola virus wherein a very large vacuole (macropinosome) is made to engulf solutes((evd))
Macropinocytosis
44
What does the ebola virus use to trick apoptosis inducing micropinocytosis?
Glycoproteins: also target of antibodies
45
T or F: there is No effective treatment available for EVD
True **same supportive treatment with marburg + Maintaining renal function and electrolyte balance and Preventing hemorrhage and shock
46
Diseases that are transmissible and causes spongiform pathological changes in the brain that results to encephalopathy (brain damage) Also includes fatal neurodegenerative disorders
Transmissible spongiform encephalopathies
47
Where is kuru found
Fore people of new guinea
48
Coined the term prion
Dr. Stanley Prusiner
49
Why will cases of CJD due to exposure to bovine spongiform encephalopathy from british beef will likely occure itf?
CJD has a long incubation period.
50
What are the unique characteristics of TSE?
Inherited and infectious , sporadic?? do not contain nucleic acids or the genetic material, unlike other infectious agents (diseased prion infects normal prion)
51
How is TSE transmitte?
contaminated neural tissue | → can be interspecies (inoculation/oral)
52
CJD usually occurs in people aged??
50-75 years old
53
What arethe three forms of CJD?
Sporadic disease 85%- unknown origin Iatrogenic – <1% of cases (Accidental transmission of the agents through contaminated instruments, Dural and corneal grafts, Administration of cadaveric pituitary hormones) Familial – ~10-15% of cases (gene mutation) vCJD- Strongly linked to exposure through food and to infected cattle
54
What differentiates vCJD from CJD
Age of patients (younger in vcjd) Presence of behavioral or sensory problems -depression or occasionally schizophrenia-like psychosis Delayed onset of neurological signs -unsteadiness, involuntary movements, and difficulty in walking Longer duration of illness Difference in pathology (Madcows->humans)??
55
Blood donors develop vCJD after donating. They take longer to develop in recipients
True
56
Most widely accepted theory on nature of prps
Protein only
57
T or F: prions ar susceptible to protein modifying agents but resistant to nucleic acid modifying agents
Truth
58
PRNP is located in which chromosome?
Chromosome 20
59
2 protein structures of prion proteins
``` Cellular isoform (normal or healthy animals) (may be involved in the communication between neurons, controlling sleep patterns, cell death, or copper metabolism) involves PrPc (cellular) or PrP-sen (sensitive to being broken down) PrPSc (scrapie) or PrP-res (resistant) Disease-causing form, Have a tendency to stick to each other due to their shape abnormality = amyloid fibers (long chains)-cytotoxic and lethal to cells − Astrocytes digest the dead neurons creating holes but the amyloid fibers stay ```
60
TSE exhibits host immune response
False
61
Seen in neuropath of tse infx
Neuronal loss Accumulation of prp Amyloid plaques
62
Neurologic symptoms in all prion diseases
``` → Psychiatric symptoms → Rapidly progressive dementia → Cerebellar symptoms → Involuntary movements → Ultimately fatal disease ```
63
Animal diseases of TSE
Scrapie BSE Chronic wasting disease
64
Human prion diseases
CJD (cerebrum: most prevalent spongiform disease) Kuru Gertsman-Straussler-Scheinker Disease-inherited, ataxia +dementia Fatal familial insomnia (Thalamus: 36-61 y.o.)
65
Marked by Personality changes, progressive dementia, muscle twitching, and vision problems
CJD
66
Marked by "shivering” or “trembling in fear” Studied by Carleton Gadjusek in 1957 transmitted by ritual cannibalism as part of funeral ceremonies
Kuru/laughing disease
67
T or F: all tses involve dementia
True
68
T or F: FFI is the only human tse with ataxia
False, FFI only without ataxia
69
Infectious TSEs (Exogenous PrPSc induces conformational change of the host’s PrPc into PrPSc)
Kuru and CJD
70
Inherited TSEs (Follows an autosomal disease pattern)
CJD (except vCJD), FFI, GSS
71
How can you diagnose Prion diseases?
Brain Tissue Examination (Immunostaining for PrPSc, Gold standard) • Study of CSF Proteins (checks for elevated Tau protein (vCJD) and 14-3-3 (sCJD)) • Neuro-imaging Tests (hockey stick sign in MRI and pulvinar sign in vCJD) • Serial Electroencephalogram (CJD, sCJD) → Abnormality not seen in vCJD • Biopsy of Lymphoreticular Tissue (Tonsil biopsy-vCJD-early diagnosis)
72
What is seen in serial EEC of sCJD patients?
Periodic slow wave complexes

Medical microbiology (14 decks)

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