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Emerging infectious diseases Flashcards

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Biology 101 flashcards USMLE® Step 1 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
Q

Indicator for fatal cases (8-9) [MARBURG]

A

Blood loss and shock (precedes it)

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26
Q

True or false: zika and marburg are related viruses that cause hemorrhagic fevers

A

False, ebola and marburg

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27
Q

What are the 5 subtypes of ebola virus

A 
Zaire
Sudan
Bundibugyo
Tai Forest
Reston (fatal to monkeys)
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28
Q

How do you acquire EBOLA?

A

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

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29
Q

When and where first EVD outbreak

A

1976

Nzara, South Sudan, Democratic repub of congo, yambuku

30
Q

EVD shape

A

Baciliform

31
Q

Describe the EVD envelope

A

Long, crooked, branching filament

32
Q

What is the capsid of EVD

A

Helical nucleocapsid

33
Q

Describe the genome of EVD

A

nonsegmented, linear, (-) ssRNA

34
Q

What makes up the nucleocapsid of EVD?

A

Nucleoprotein, VP35 (polymerase cofactor) and Polymerase (L)

35
Q

Primary matrix protein in EVD

A

VP40

36
Q

VP40 and VP 24 in EVD function to

A

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
Q

What are the attachment factors of EVD?

A

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
Q

Symptoms 7-9 days after EVD exposure

A

Joint pain, headache,fever, sore throat, weakness, muscle soarness

39
Q

10th day symptom EVD

A

Vomiting blood, high fever, diarrhea, extreme fatigue,

40
Q

11th day symptoms of EVD

A

Brain damage, bleeding from nose, mouth and anus

41
Q

12th day of EVD symptoms

A

Coma, shock, massive internal bleeding, organ failure, death

42
Q

What places a person under investigation for ebola

A

Fever (>38.6°C or 101.5°F) + symptoms + epidemiologic factors within past 21 days prior to symptom onset

43
Q

A physiologic endocytic mechanism done by cells used by ebola virus wherein a very large vacuole (macropinosome) is made to engulf solutes((evd))

A

Macropinocytosis

44
Q

What does the ebola virus use to trick apoptosis inducing micropinocytosis?

A

Glycoproteins: also target of antibodies

45
Q

T or F: there is No effective treatment available for EVD

A

True

**same supportive treatment with marburg + Maintaining renal function and electrolyte balance and Preventing hemorrhage and shock

46
Q

Diseases that are transmissible and causes spongiform pathological changes in the brain that results to encephalopathy (brain damage)
Also includes fatal neurodegenerative disorders

A

Transmissible spongiform encephalopathies

47
Q

Where is kuru found

A

Fore people of new guinea

48
Q

Coined the term prion

A

Dr. Stanley Prusiner

49
Q

Why will cases of CJD due to exposure to bovine spongiform encephalopathy from british beef will likely occure itf?

A

CJD has a long incubation period.

50
Q

What are the unique characteristics of TSE?

A

Inherited and infectious , sporadic??
do not contain nucleic acids or the genetic material, unlike other infectious agents (diseased prion infects normal prion)

51
Q

How is TSE transmitte?

A

contaminated neural tissue

→ can be interspecies (inoculation/oral)

52
Q

CJD usually occurs in people aged??

A

50-75 years old

53
Q

What arethe three forms of CJD?

A

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
Q

What differentiates vCJD from CJD

A

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
Q

Blood donors develop vCJD after donating. They take longer to develop in recipients

A

True

56
Q

Most widely accepted theory on nature of prps

A

Protein only

57
Q

T or F: prions ar susceptible to protein modifying agents but resistant to nucleic acid modifying agents

A

Truth

58
Q

PRNP is located in which chromosome?

A

Chromosome 20

59
Q

2 protein structures of prion proteins

A 
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
Q

TSE exhibits host immune response

A

False

61
Q

Seen in neuropath of tse infx

A

Neuronal loss
Accumulation of prp
Amyloid plaques

62
Q

Neurologic symptoms in all prion diseases

A 
→ Psychiatric symptoms
→ Rapidly progressive dementia 
→ Cerebellar symptoms 
→ Involuntary movements
→ Ultimately fatal disease
63
Q

Animal diseases of TSE

A

Scrapie
BSE
Chronic wasting disease

64
Q

Human prion diseases

A

CJD (cerebrum: most prevalent spongiform disease)
Kuru
Gertsman-Straussler-Scheinker Disease-inherited, ataxia +dementia
Fatal familial insomnia (Thalamus: 36-61 y.o.)

65
Q

Marked by Personality changes, progressive dementia, muscle twitching, and vision problems

A

CJD

66
Q

Marked by “shivering” or “trembling in fear” Studied by Carleton Gadjusek in 1957 transmitted by ritual cannibalism as part of funeral ceremonies

A

Kuru/laughing disease

67
Q

T or F: all tses involve dementia

A

True

68
Q

T or F: FFI is the only human tse with ataxia

A

False, FFI only without ataxia

69
Q

Infectious TSEs (Exogenous PrPSc induces conformational change of the host’s PrPc into PrPSc)

A

Kuru and CJD

70
Q

Inherited TSEs (Follows an autosomal disease pattern)

A

CJD (except vCJD), FFI, GSS

71
Q

How can you diagnose Prion diseases?

A

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
Q

What is seen in serial EEC of sCJD patients?

A

Periodic slow wave complexes

Medical microbiology (14 decks)

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