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Microbiology > 3.32 > Flashcards

3.32 Flashcards

1
Q

Coronaviruses characteristics (3)

A

+ strand RNA viruses
enveloped
• Cause up to 30% of common colds

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2
Q

— is agent of COVID-19

A

SARS-CoV-2

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3
Q

§ SARS outbreak:

A

late 2002 -

2003

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4
Q

§ SARS =

A

atypical pneumonia

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5
Q

§ SARS-CoV jumped from
— to humans and the same is
true for SARS-CoV-2

A

animals

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6
Q

middle east respiratory syndrome (MERS) is a

A

viral respiratory illness

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7
Q

–% mortality rate for MERS-CoV infection

A

30-40

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8
Q

clinical presentation of people with sars-cov-2 infection

A

Asymptomatic or Presymptomatic Infection
Mild Illness
Moderate Illness

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9
Q

skipped

Asymptomatic or Presymptomatic Infection

A

Individuals who test positive for SARS-CoV-2 using a virologic
test (i.e., a nucleic acid amplification test or an antigen test), but who have no symptoms that are
consistent with COVID-19.

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10
Q

skipped

Mild Illness

A

Individuals who have any of the various signs and symptoms of COVID-19 (e.g., fever, cough,
sore throat, malaise, headache, muscle pain, nausea, vomiting, diarrhea, loss of taste and smell) but who
do not have shortness of breath, dyspnea, or abnormal chest imaging

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11
Q

skipped

Moderate Illness

A

Individuals who show evidence of lower respiratory disease during clinical assessment or
imaging and who have saturation of oxygen (SpO2) 294% on room air at sea level.

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12
Q

Severe Illness:

A

Individuals who have SpO2 <94% on room air at sea level, a ratio of arterial partial pressure
of oxygen to fraction of inspired oxygen (PaO2/FiO2) <300 mmHg, respiratory frequency >30 breaths per
minute, or lung infiltrates >50%.

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13
Q

Critical Illness:

A

Individuals who have respiratory failure, septic shock, and/or multiple organ dysfunction.

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14
Q

SARS -

A

Severe acute respiratory syndrome in severe/critical illness

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15
Q

PaO,/FIO2 =

A

arterial partial pressure of oxygen/fraction of inspired oxygen
(PaO2/FIO2) ratio
at sea level, the normal Pa02/FiO2 ratio is ~ 400-500 mmHg

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16
Q

ACE2 –

A

angiotensin converting enzyme (cleaves angiotensin II (vasoconstrictor) to angiotensin 1-7 (vasodialator)
ACE2 activity lowers blood pressure

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17
Q

TMPRSS2 –

A

transmembrane protease, serine 2 (cleaves (“primes”) Spike protein)

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18
Q

RAAS –

A

renin angiotensin aldosterone system (blood pressure regulation)

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19
Q

— manifestations of COVID-19

A

Extrapulmonary

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20
Q

covid 19 is associated with — effects on many other organ systems

A

deleterious

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21
Q

Picornaviruses (Chapter 32)
— stranded RNA viruses
do not have —

A

+

envelope

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22
Q

enteroviruses
habitat =
include:

A

gastrointestinal tract

poliovirus and coxsackievirus
echoviruses - enteric cytopathic human orphan viruses

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23
Q

rhinoviruses

habitat =

A

respiratory epithelium

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24
Q

Rhinoviruses:

A

Sensitive to acidic pH

Replicate poorly above 33 C

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25
Q

Enteroviruses:

A

very stable in food and water

also stable at pH 3 (stomach)

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26
Q

Organ involvement for enteroviruses:
only occurs if — persists
usually does not; <—% typically

A

viremia

5

27
Q

poliovirus

3 antigenic types

A

PV1, PV2, PV3
Capsid differences
between types

28
Q

Poliovirus replication

A

However, PV exhibits restricted tissue tropism,
the basis for which is not clear
RNA alone can cause infection!
-shown by researchers

29
Q

Poliovirus replication

lytic virus -

A 
destruction of host cells
virus is shed into stool
up to 10,000 virus per infected cell)
even weeks to months after symptoms
gone
30
Q

Poliovirus replication

transmission:

A

fecal-oral

31
Q

Poliovirus IRES

A

Internal Ribosome Entry Site
IRES serves as the “cap” of the viral RNA, promoting translation
of viral RNA into viral proteins
Because of IRES, translation starts far from the 5’ end of
poliovirus RNA (normal mRNA translation starts near 5’ end)

32
Q

Pathogenesis of poliovirus.
central nervous system disease
flaccid paralysis

A

results from destruction of anterior horn cells in spinal cord

33
Q

Pathogenesis of poliovirus.
central nervous system disease
bulbar poliomyelitis

A

most severe form
respiratory muscle paralysis (medulla oblongata)
~25% mortality

34
Q

factors increasing severity of poliovirus infections (2)

A

physical exertion and trauma

tonsillectomy

35
Q

Poliovirus vaccines:
— mimics the normal infection process of
poliovirus

A

Live oral vaccine (Sabin)

36
Q

Coxsackieviruses

group A coxsackieviruses (3)

A

aseptic meningitis
herpangina
coxsackievirus type A16

37
Q

Coxsackieviruses
group A coxsackieviruses

herpangina

A

sudden onset of fever

vesicles/ulcers on tonsils and palate

38
Q

Coxsackieviruses
group A coxsackieviruses

coxsackievirus type A16 (2)

A

hand, foot, and mouth disease

blisters on hand, feet, and palate

39
Q

Coxsackieviruses

group B coxsackieviruses (3)

A

heart (myocarditis)
respiratory tract (pleurodynia)
mucous membranes of eye
(hemorrhagic conjunctivitis)

40
Q

Rhinoviruses
~— serotypes
account for ~— the cases of the common cold

A

100

1/2

41
Q

Rhinoviruses

bind to respiratory epithelial cells (2)

A

ICAM-1 (most) or VLDL receptor (some)

42
Q

replication details very similar to poliovirus

A

Acid sensitive and 33oC optimum for replication

no tissue destruction

43
Q

Rhinoviruses

sometimes infection has complications (3)

A

sinusitis, otitis media

worsening of asthma (assoc. with 50% of attacks)

44
Q

Rhinoviruses

vaccine

A

prospects poor (too many variants)

45
Q

Arboviruses (arthropod-borne viruses) (2)

A

viruses transmitted by arthropods

multiply in tissues of vector, often without producing disease

46
Q

For many arboviruses humans
are
“dead-end” hosts:

A

viremia of short duration

virus levels in blood are low

47
Q 
Togaviruses
characteristics (2)
A

plus stranded RNA (single linear molecule)

enveloped

48
Q

Togavirus
replication
2 phases of translation

A

-first produce early proteins
and then late proteins
-like coronavirus

49
Q

Figure 63-2 Replication of a togavirus. Semliki Forest virus. 1, Semliki Forest virus binds to cell receptors
and is internalized in a coated vesicle. 2, On acidification of the endosome, the viral envelope fuses with
the endosomal membrane to release the nucleocapsid into the cytoplasm. 3, Ribosomes bind to the
(1) RNA genome, and the p230 or p270 (full-length) (2). 4, The
polyproteins are cleaved to produce nonstructural proteins 1 to 4 (NSP1 to NSP4), which include a
polymerase to transcribe the genome into a (3) RNA template. 5, The template is used to
produce a (4) for the structural proteins.
6, The C (capsid) protein is translated first, exposing a protease cleavage site and then a signal peptide
for association with the endoplasmic reticulum. 7, The E glycoproteins are then synthesized,
glycosylated, processed in the Golgi apparatus, and transferred to the plasma membrane. 8, The capsid
proteins assemble on the 42S genomic RNA and then associate with regions of cytoplasmic and plasma
membranes containing the E1, E2, and E3 spike proteins. 9, Budding from the plasma membrane releases
the (5).

A 
positive-sense 
early polyproteins are made
negative-sense
full-length 42S positive-sense mRNA genome and a late 26S mRNA
virus
50
Q

Rubella virus (2)

A

Member of Togavirus family
Rubivirus genus
but not arthropod-borne

51
Q

Rubella =

A

German measles
one of the 5 childhood exanthems
(along with measles, roseola, chickenpox,
and fifth disease)

52
Q

Figure 63-6 Spread of rubella virus within the host.

A

Rubella enters and infects the nasopharynx and lung and then spreads to the lymph nodes and monocytemacrophage system. The resulting viremia spreads the virus to other tissues and the skin. Circulating antibody can block the transfer of virus at the indicated
points (X). In an immunologically deficient pregnant woman, the virus can infect the placenta and spread to the fetus.

53
Q 
Flaviviruses
characteristics (2)
A

plus stranded RNA (single linear molecule)

enveloped

54
Q

Figure 63-4 Disease syndromes of the alphaviruses and flaviviruses.

A

Primary viremia may be associated with mild systemic disease. Most infections are
limited to this. If sufficient virus is produced during the secondary viremia to escape immune protection and to reach critical target tissues, severe systemic
disease or encephalitis may result. For dengue virus, rechallenge with another strain can result in severe dengue hemorrhagic fever (DHF), which can cause
dengue shock syndrome (DSS) because of the loss of fluids from the vasculature.

55
Q

Zika virus (a Flavivirus) (3)

A

mostly mild illness (Zika fever) except for congenital infection of fetus,
which leads to microcephaly and other birth defects
transmitted by mosquitos from person to person (most common)
Aedes aegypti mosquito (worldwide distribution of A. aegypti below)
also transmitted sexually

56
Q

Dengue fever (caused by a Flavivirus) (4)

A

most prevalent disease caused by arboviruses
does not cause significant mortality
generally not a zoonosis
when partial immunity exists due to prior infection

57
Q

generally not a zoonosis:

A

transmitted by mosquitos from person to person

58
Q

when partial immunity exists due to prior infection (4)

A 
dengue hemorrhagic shock (DHS)
dengue shock syndrome (DSS)
due to immune enhancement
virus forms immune complex/readily enter macrophages
increases viral load
59
Q

Activates memory T cells, which release cytokines and initiate hypersensitivity reactions.
These reactions cause

A

weakening and rupture of vasculature, internal bleeding, loss of plasma.

60
Q 
Yellow Fever (caused by a Flavivirus)
• historical importance (3)
A

– first human disease found to be caused by a virus
– first viral disease confirmed to be spread by insect vector
– Mosquito: Aedes aegypti

61
Q 
Yellow Fever (caused by a Flavivirus)
• spread by two methods (via mosquito) (2)
A

– human to human

– monkey to human

62
Q 
Yellow Fever (caused by a Flavivirus)
clinical manifestations (2)
– severe cases
•
A

jaundice

• lesions and hemorrhaging of infected organs

63
Q 
Yellow Fever (caused by a Flavivirus)
tx
A

– attenuated live vaccine and insect control measures

Microbiology (42 decks)

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