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D&D Unit IV > Common Viral Pathogens > Flashcards

Common Viral Pathogens Flashcards

1
Q

What viruses are in the Herpesviridae family?

A

Herpes simplex type 1 (HSV1)
Herpes simplex type 2 (HSV2)
Varicella zoster virus (VZV)
Cytomegalovirus (CMV)

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2
Q

Herpesvirus: General structure and classification

A

double-stranded DNA genome that is protected by an icosahedral capsid

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3
Q

Herpesvirus replication

A
  • Attach to surface proteins, fuse viral and host membrane, release nucleocapsid cytoplasm
  • Immediate early (IE) genes need to be brought in
  • Virus assembly occurs in nucleus;
  • Nucleocapsids assembled in the nucleus bud through
    the nuclear membrane and acquire their glycoprotein-rich envelope as they pass through the Golgi complex
  • Virions leave the cell through exocytosis or cell lysis
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4
Q

Herpes simplex type 1 (HSV1)

A

a. Type: double stranded DNA
b. Cells targeted: mucosal epithelium
Latency: Neuron (ganglia)
c. Transmission: usually occurs through close contact with a person who is shedding virus at a peripheral site, mucosal surface, or in genital or oral secretions
Incubation period: 2-12 days (average is 4 days)
d. Clinical presentations: Orofacial lesions (Gingivostomatitis) and (some) genital lesions, Encephalitis, Herpes whitlow, Herpes keratitis, Neonatal herpes
e. Diagnosis: Viral culture of lesions, Direct fluorescent antibody stain of lesions, PCR of lesions
f. Treatments: acycloguanosine (acyclovir)
g. Prophylaxis-including vaccines: In certain patients who will be compliant, oral antiviral suppressive therapy is considered

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5
Q

Herpes simplex type 2 (HSV2)

A

a. Type: double stranded DNA
b. Cells targeted: mucosal epithelium
Latency: Neuron (ganglia)
c. Transmission: usually occurs through close contact with a person who is shedding virus at a peripheral site, mucosal surface, or in genital or oral secretions
Incubation period: 2-12 days (average is 4 days)
d. Clinical presentations: Genital lesions and (some) orofacial lesions (Gingivostomatits), Encephalitis, Herpes whitlow, Herpes keratitis, Neonatal herpes
e. Diagnosis: Viral culture of lesions, Direct fluorescent antibody stain of lesions, PCR of lesions
f. Treatments: acycloguanosine (acyclovir)
g. Prophylaxis-including vaccines: In certain patients who will be compliant, oral antiviral suppressive therapy is considered

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6
Q

Varicella zoster virus (VZV)

A

a. Type: double stranded DNA
b. Cells targeted: mucosal epithelium
Latency: Neuron (ganglia)
c. Transmission
Incubation: 10-21 days
d. Clinical presentations: Chickenpox (aka varicella);
Shingles (aka zoster> reactivation)
e. Diagnosis: Direct fluorescent antibody, VZV PCR, Viral culture
f. Treatments
g. Prophylaxis-including vaccines

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7
Q

Cytomegalovirus (CMV)

A

a. Type: double stranded DNA
b. Cells targeted: Epithelia, monocytes, lymphocytes, others
Latency: Monocytes, lymphocytes and possibly others
c. Transmission: Contact w/ body fluids: (saliva, breast milk, sexual contact, blood, tears, respiratory secretions, urine, stool), blood transfusions, transplantation, congenital
Incubation period: 2 weeks to 2 months
d. Clinical presentations: Infectious mononucleosis-like
syndrome;In immunocompromised: retinitis, pneumonia, colitis;
In newborns: congenital CMV
e. Diagnosis: Viral culture, PCR, Fluorescent antibody staining, Serology, Histology (“owl’s eye” appearance)
f. Treatments: Treatment of CMV disease in persons with normal immune systems is not indicated resolution without sequelae is expected
Immunocompromised persons with CMV infections are treated with an antiviral (Ganciclovir)
g. Prophylaxis-including vaccines: no vaccine, CMV-IG to immunocompromised

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8
Q

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A

a. Type:
b. Cells targeted:
Latency:
c. Transmission:
Incubation period
d. Clinical presentations:
e. Diagnosis:
f. Treatments:
g. Prophylaxis-including vaccines

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9
Q

Chickenpox

A
  • varicella zoster virus
  • Transmission: primarily transmitted by the
    respiratory route via droplet or aerosolized secretions; direct contact with lesions
  • fever, malaise, headache and sometimes cough
  • lesions: dew drop on a rose petal
  • Vesicles mature to pustules, which then rupture and scab
  • more severe in adults and adolescents
  • Complications: secondary infection or cellulitis, pneumonia, necrotizing fascitis, encephalitis or encephalomyelitis, hepatitis, congenital varicella syndrome
  • Treatment: typically self limited, can be treated with antiviral therapy (acyclovir)
  • vaccine: Live attenuated varicella zoster virus vaccine (chickenpox vaccine)
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10
Q

Shingles

A
  • varicella zoster virus
  • virus reactivation
  • varicella-form rash in the distribution of a dermatome w/ neuropathic pain
  • virus is shed only from the shingles lesions
  • major complication is chronic burning, itching, or shooting pain called post-herpetic neuralgia
  • treatment: Acyclovir
  • shingles vaccine (Zostavax) is approved for individuals 50 years of age or older
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11
Q

Influenza:

Basic structure, Important proteins, Pathogenesis

A
  • Basic structure: segmented genome made up of 8 different pieces of single-stranded RNA; lipid envelope
  • Important proteins: hemagglutinin (H) and neuraminidase (N) glycoproteins (both surface proteins)
  • Pathogenesis: Type A and B circulate every year; Type A can infect other animals
    ~ incubation period is relatively short, typically 1-3 days
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12
Q

Influenza:

Route of entry, Affected cells/organs, Mechanism, Presentation

A
  • Route of entry: respiratory route; droplet and small particle aerosols generated by coughing and sneezing are the primary mechanisms of spread
  • Affected cells/organs:
  • Mechanism:
  • Presentation: acute onset of fever, chills, myalgias, headache and cough
    ~ Infants/toddlers: GI symptoms (nausea, vomiting
    and diarrhea); fever; anorexia; and various respiratory syndromes
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13
Q

Influenza:

Transmission, Prevention

A
  • Transmission: respiratory route; droplet and small particle aerosols generated by coughing and sneezing are the primary mechanisms of spread
    ~ contact with infectious particles can occur by contamination of hands or inanimate objects (fomites)
  • Prevention: hand-washing; sneeze into arm rather than hand
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14
Q

Influenza:

Vaccines

A
  • Vaccines: 2 types
    1) Inactivated influenza vaccine (IIV): injectable, killed vaccine; 6 mos and older
    2) Live attenuated influenza vaccine (LAIV): delivered intranasally via a small, needle-free syringe that delivers a fine mist into the nose; live, attenuated (weakened strain) vaccine; licensed for healthy persons 2 yrs through 49 years of age
  • Efficacy: TIV has been shown to be 70-90% effective in preventing influenza in a well-matched year; declines in the elderly population
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15
Q

Influenza: Antigenic Drift and Antigenic Shift

A
  • Antigenic Drift: gradual change in the virus that occurs through a slow series of mutations, substitutions or
    deletions in amino acids constituting the hemagglutinin or neuraminidase surface antigens
    ~ represents an adaptation to the development of host antibodies
  • Antigenic Shift: occurs when a type A influenza virus with a completely novel hemagglutinin or
    neuraminidase gene segment is introduced into humans (usually acquired from other host species)
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16
Q

Influenza: H1N1

Origin, Epidemiology, Morbidity/Mortality

A
  • Origin: created from reassortment (antigenic shift) from pigs
  • Epidemiology: pandemic on 2 continents, highest pandemic level
  • Morbidity/Mortality: highest among children/young adults <24 y/o
17
Q

Influenza: newly emerging (e.g. H5N1)

A
  • Geographic Occurrence: SE Asia, some in Mongolia, Russia, Eastern Europe and Africa
  • Importance to public health: highly virulent strain of avian flu; close contact to infected birds is biggest risk factor; H gene might mutate and preferentially infect humans
18
Q

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A

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19
Q

Respiratory Syncytial Virus (RSV):

Basic structure, Important proteins, Pathogenesis

A
  • Basic structure: single stranded, non-segmented RNA virus
  • Important proteins:
    1) F protein: fusion of viral envelope to host cell; fusion of membranes of infected cells to each other to cause “syncytia”
    2) G protein: initial binding of virus to the host cell
  • Pathogenesis: invades conjunctiva/nasopharynx; 3-5 day incubation; initially replicates in the nasopharynx
    ~ Primarily replicates in respiratory epithelium
    ~ Spreads to lower respiratory tract by inhalation of secretions or spread by the respiratory epithelium
20
Q

Respiratory Syncytial Virus (RSV):

Route of entry, Affected cells/organs, Mechanism, Presentation

A
  • Route of entry: Invades conjunctiva/nasopharynx
  • Affected cells/organs:
  • Mechanism: invades conjunctiva/nasopharynx; 3-5 day incubation; causes constriction of smooth muscles in bronchioles
  • Presentation: viral lower respiratory tract infection in all ages, but particularly in young children
    ~ is most common cause of bronchiolitis
    ~ Respiratory distress, wheezing/rhonchi on auscultation, hypoxia, copious secretions; causes constriction of smooth muscles in bronchioles; collection of fluid in the bronchioles and alveoli
21
Q

Respiratory Syncytial Virus (RSV):

Vaccines

A
  • Antibody/immune protection is incomplete for infection, but previous infection may prevent more severe disease
  • Vaccine in the 1960s, formalin-inactivated RSV vaccine; did not produce protective immunity and children who were immunized has worse disease
  • RSV immunoprophylaxis
    ~ Respigam is a human pooled antibody with high RSV titers, shown to have a decrease in disease severity and hospitalization
    ~ A mouse monoclonal anti-RSV antibody: Palavisumab
    (Synagis)
22
Q

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A

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23
Q

Ebola:

Basic structure, Important proteins, Pathogenesis

A
  • Basic structure: enveloped, negative-strand RNA, replicates in the cytoplasm
  • Important proteins: Matrix proteins VP40 and VP24; VP30 and nucleoproteins form the nucleocapsid; Polymerase complex VP35 and L
    ~ VP35 and VP24 both interfere with the cell’s interferon production, which plays a role in signaling for “help” and also inhibits the cell from apoptosis
  • Pathogenesis: enters phagocytic cells, sends signal for more cells to come, which facilitates infecting those cells; also spreads efficiently when cells go to lymph
    nodes, which allows ebola to infect more immune cells
    ~ Once in the cell, induces a massive cytokine storm; induce disseminated intravascular coagulation; infect many other cells/organs in the body including: endothelial cells, liver, spleen, lungs
    ~ infection of endothelial cells, get leakage of fluids, severe fluid loss, hypovolemic shock, organ failure
24
Q

Ebola:

Route of entry, Affected cells/organs, Mechanism, Presentation

A
  • Route of entry: mucosal surfaces or cuts to the skin
  • Affected cells/organs: endothelial cells, liver, spleen, lungs
  • Mechanism: enters phagocytic cells, sends signal for more cells to come, which facilitates infecting those cells; also spreads efficiently when cells go to lymph
    nodes, which allows ebola to infect more immune cells
    ~ Once in the cell, induces a massive cytokine storm; induce disseminated intravascular coagulation; infect many other cells/organs in the body including: endothelial cells, liver, spleen, lungs
    ~ infection of endothelial cells, get leakage of fluids, severe fluid loss, hypovolemic shock, organ failure
  • Presentation: GI, fever, fatigue/weakness; spacing, loose a lot of fluids through capillary leak, vomiting and diarrhea
    ~ People die from hypovolemia +/- organ failure
25
Q

Ebola:

Transmission, Prevention

A
  • Transmission: outbreaks result from spillover events from animal reservoirs with subsequent human-to-human transmission
  • Prevention: avoid bodily fluids of infected
26
Q

Ebola:

Vaccines

A
  • After someone is infected, it is believed that he/she is protected from future infections
  • Antibodies from Ebola survivors – we used this in the US, not clear that it works
  • Vaccines in Phase I/II studies currently, plan large Phase III study soon
  • Management is symptomatic – there are no Ebola tratments
27
Q

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D&D Unit IV (4 decks)

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