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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
Enteroviruses:
very stable in food and water | also stable at pH 3 (stomach)
26
Organ involvement for enteroviruses: only occurs if --- persists usually does not; <---% typically
viremia | 5
27
poliovirus | 3 antigenic types
PV1, PV2, PV3 Capsid differences between types
28
Poliovirus replication
However, PV exhibits restricted tissue tropism, the basis for which is not clear RNA alone can cause infection! -shown by researchers
29
Poliovirus replication | lytic virus -
``` 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
Poliovirus replication | transmission:
fecal-oral
31
Poliovirus IRES
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
Pathogenesis of poliovirus. central nervous system disease flaccid paralysis
results from destruction of anterior horn cells in spinal cord
33
Pathogenesis of poliovirus. central nervous system disease bulbar poliomyelitis
most severe form respiratory muscle paralysis (medulla oblongata) ~25% mortality
34
factors increasing severity of poliovirus infections (2)
physical exertion and trauma | tonsillectomy
35
Poliovirus vaccines: --- mimics the normal infection process of poliovirus
Live oral vaccine (Sabin)
36
Coxsackieviruses | group A coxsackieviruses (3)
aseptic meningitis herpangina coxsackievirus type A16
37
Coxsackieviruses group A coxsackieviruses herpangina
sudden onset of fever | vesicles/ulcers on tonsils and palate
38
Coxsackieviruses group A coxsackieviruses coxsackievirus type A16 (2)
hand, foot, and mouth disease | blisters on hand, feet, and palate
39
Coxsackieviruses | group B coxsackieviruses (3)
heart (myocarditis) respiratory tract (pleurodynia) mucous membranes of eye (hemorrhagic conjunctivitis)
40
Rhinoviruses ~--- serotypes account for ~--- the cases of the common cold
100 | 1/2
41
Rhinoviruses | bind to respiratory epithelial cells (2)
ICAM-1 (most) or VLDL receptor (some)
42
replication details very similar to poliovirus
Acid sensitive and 33oC optimum for replication | no tissue destruction
43
Rhinoviruses | sometimes infection has complications (3)
sinusitis, otitis media | worsening of asthma (assoc. with 50% of attacks)
44
Rhinoviruses | vaccine
prospects poor (too many variants)
45
Arboviruses (arthropod-borne viruses) (2)
viruses transmitted by arthropods | multiply in tissues of vector, often without producing disease
46
For many arboviruses humans are “dead-end” hosts:
viremia of short duration | virus levels in blood are low
47
``` Togaviruses characteristics (2) ```
plus stranded RNA (single linear molecule) | enveloped
48
Togavirus replication 2 phases of translation
-first produce early proteins and then late proteins -like coronavirus
49
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).
``` positive-sense early polyproteins are made negative-sense full-length 42S positive-sense mRNA genome and a late 26S mRNA virus ```
50
Rubella virus (2)
Member of Togavirus family Rubivirus genus but not arthropod-borne
51
Rubella =
German measles one of the 5 childhood exanthems (along with measles, roseola, chickenpox, and fifth disease)
52
Figure 63-6 Spread of rubella virus within the host.
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
``` Flaviviruses characteristics (2) ```
plus stranded RNA (single linear molecule) | enveloped
54
Figure 63-4 Disease syndromes of the alphaviruses and flaviviruses.
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
Zika virus (a Flavivirus) (3)
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
Dengue fever (caused by a Flavivirus) (4)
most prevalent disease caused by arboviruses does not cause significant mortality generally not a zoonosis when partial immunity exists due to prior infection
57
generally not a zoonosis:
transmitted by mosquitos from person to person
58
when partial immunity exists due to prior infection (4)
``` dengue hemorrhagic shock (DHS) dengue shock syndrome (DSS) due to immune enhancement virus forms immune complex/readily enter macrophages increases viral load ```
59
Activates memory T cells, which release cytokines and initiate hypersensitivity reactions. These reactions cause
weakening and rupture of vasculature, internal bleeding, loss of plasma.
60
``` Yellow Fever (caused by a Flavivirus) • historical importance (3) ```
– first human disease found to be caused by a virus – first viral disease confirmed to be spread by insect vector – Mosquito: Aedes aegypti
61
``` Yellow Fever (caused by a Flavivirus) • spread by two methods (via mosquito) (2) ```
– human to human | – monkey to human
62
``` Yellow Fever (caused by a Flavivirus) clinical manifestations (2) – severe cases • ```
jaundice | • lesions and hemorrhaging of infected organs
63
``` Yellow Fever (caused by a Flavivirus) tx ```
– attenuated live vaccine and insect control measures

Microbiology (42 decks)

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