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Unit 3 D&D > DD 02-26-14 08-10am Common Viral Pathogens - Curtis > Flashcards

DD 02-26-14 08-10am Common Viral Pathogens - Curtis Flashcards

1
Q

Infection vs. Disease

A 
Infection = virus has replicated in host
Disease = infection that causes symptoms
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2
Q

Lab Tests to Dx Viral Infection

A
  • Culture: can grow SOME viruses in TISSUE
  • Antigen assays
  • PCR
  • ELISA (Enzyme-Linked Immunosorbent Assay)
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3
Q

Antigen assays for viral Dx

A
  • various assays using enzymatic rxns or immunofluorescence to detect specific Ags of virus in question (ex: rapid flu test)
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4
Q

PCR for viral Dx

A
  • copying & amplifying portion of viral genome
  • very sensitive & specific
  • can be done on blood, nasal wash, CSF, biopsies

Results may be…

  • qualitative (+ or -)
  • quantitative (# of copies/mL)
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5
Q

ELISA (Enzyme-Linked Immunosorbent Assay to Dx virus

A
  • to look for host’s immune response to viral infection by looking for Abs specific for that virus

Most commonly, ELISA would…

  • Coat plate w/ viral Ag (whole virus or part)
  • Incubate host’s serum on plate to let Abs attach to Ag on bottom of wells
  • Then incubate plate w/ an antibody that detects the host antibody (i.e., a secondary antibody)
  • Then incubate plate w/ a substrate that will allow visualization of the secondary antibody
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6
Q

Herpes virus (type of virus, who they infect)

A
  • double-stranded DNA viruses

- infect most animals.

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7
Q

Hallmark of a herpes infection

A

Once a host is infected, the host is always infected.

  • establishes latency after infection
  • latent virus can become reactivated
  • reactivated infection doesn’t always cause disease
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8
Q

Antiviral medications for Herpes Viruses

A
  • work against some of the human herpes viruses

Acyclovir
= most common
= works by inhibiting the viral DNA polymerase
= indicated for HSV and VZV infections

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9
Q

Herpes Viruses that infect humans (8)

A
  • HHV-1: Herpes Simplex Virus-1 (HSV-1)
  • HHV-2: HSV-2
  • HHV-3: Varicella Zoster Virus (VZV)
  • HHV-4: Epstein Barr Virus (EBV)
  • HHV-5: Cytomegalovirus (CMV)
  • HHV-6: Roseola (HHV-6a, HHV-6b)
  • HHV-7: Roseola
  • HHV-8: HHV-8
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10
Q

Clinical Manifestations of Herpes Simplex viruses 1 & 2 (HSV-1, HSV-2)

A
  • Oral and genital herpes
  • Neonatal herpes
  • Herpes keratitis (eye)
  • Herpes encephalitis
  • Herpetic whitlow (finger lesion)
  • Herpes gladiotorum (“wrestlers”)
  • Encephalitis
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11
Q

Clincal Manifestations of Varicella zoster virus

VZV

A
  • Chickenpox,

- In immunocompromised: vasculitis, encephalitis, pneumonia

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12
Q

Clincal Manifestations of Epstein-Barr virus

EBV

A
  • Infectious mononucleosis
  • Burkitt’s lymphoma-
  • Encephalitis
  • In immunocompromised: lymphoma
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13
Q

Clincal Manifestations of Cytomegalovirus

CMV

A
  • Infectious mononucleosis-like syndrome
  • In immunocompromised: retinitis, pneumonia
  • In newborns: congenital CMV
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14
Q

Clincal Manifestations of Human herpesvirus 6 & 7

A
  • Roseola or exanthem subitum

- In immunocompromised: fever, encephalitis

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15
Q

Clincal Manifestations of Human herpesvirus 8

A
  • Kaposi’s sarcoma (only occurs in immunocompromised)
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16
Q

Signs/Symptoms of Herpes Simplex viruses 1 & 2 (HSV-1, HSV-2)

A

-painful vesicles at the site of inoculation

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17
Q

Differences between of HSV-1 & HSV-2

A

Though both can cause oral & genital herpes…

  • HSV-1 is predominantly oral lesions
  • HSV-2 is predominantly genital lesions
  • These differences are becoming less strong with time, mainly as a result of oral sex allowing the two viruses to now infect other body sites
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18
Q

Incubation Period of HSV-1 & -2

A

2-12 days

typically ~4 days

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19
Q

Transmission of HSV-1 & -2

A

Transmission occurs through inoculation from someone who is shedding virus into a mucosal surface or cut of another person.

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20
Q

Clinical patterns of HSV-1 & HSV-2 depend on…

A

whether infection is primary or recurrent

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21
Q

Primary infection vs. Latent infection vs. Reactivation infection with HSV-1/HSV-2: Clinical pattern

A

Primary:

  • most are asymptomatic
  • usually worse than recurrent infection
  • If symptomatic, lesions usually develop 1-3 days after inoculation
  • Vesicular rash +/- fever
  • Usually occurs during childhood w/ HSV gingivostomatitis (historically HSV-1)

Latent:
- asymptomatic

Reactivation:

  • Contagious, though may be asymptomatic
  • If symptomatic, usually less than primary infection
  • Can be infrequent or very frequent
  • Provoked by variety of stimuli
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22
Q

HSV-1 & -2 Rash in Immunocompromised vs. Immunocompetent Hosts

A

Immune competent hosts:
- area of vesicular rash stays contained to area of inoculation
Immunocompromised host:
- Infection may involve larger areas of skin
- Can disseminate to specific/multiple organs (systemic)
- EX: encephalitis, hepatitis

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23
Q

Neonatal HSV-1 & -2 infection: Locations

A 
Skin
Eye
Mucous Membrane
CNS
Disseminated
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24
Q

Latent infection with HSV-1/HSV-2: where infection occurs

A

Occurs in sensory ganglia of areas infected w/ the primary infection

  • Orofacial infection: trigeminal ganglia
  • Genital infection: sacral ganglia
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25
Q

HSV-1/-2 Diagnosis:

A

Often clinical Dx

If need definitive Dx:

  • Tzanck smear
  • HSV culture
  • Direct Fluorescent Antigen stain
  • PCR of lesions
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26
Q

Triggers of Reactivation of HSV-1/HSV-2 Infection

A
  • sunlight
  • stress
  • febrile illness
  • menstruation
  • immunosuppression
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27
Q

HSV Treatment

A

Severe HSV infections:
<– IV acyclovir
= for neonatal HSV, HSV in immunocompromised hosts, encephalitis/meningoencephalitis

Oral antiviral therapy (acyclovir or related antiviral)
= for oral or genital outbreaks
= standing Rx for ppl w/ frequent outbreaks not on suppressive therapy, so they can fill it & start treatment at very onset of reactivation / outbreak

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28
Q

Tzanck smear to Dx HSV-1/-2 infection

A
  • direct specimen (scrape base of lesion)
  • put specimen on slide & stain
  • look for multinucleated giant cells
  • not specific for HSV (also VZV and CMV)
  • rarely used in favor of easier & more sensitive / specific testing
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29
Q

HSV-1/-2 Prevention of Reactivation Infection (& what warrants it)

A

Prophylactic Acyclovir

  • in lower doses than used for treatment
  • difficult to maintain

Used for pts with:

  • frequent outbreaks of oral / genital lesions
  • recurrent keratitis & encephalitis
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30
Q

HSV-1/-2 Prevention of Primary Infection

A
  • NO vaccine available
  • Hand hygiene
  • Physical barriers: gloves, condoms
  • Avoid contact
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31
Q

Varicella Zoster Virus (VZV) - Clinical Syndrome

A

VZV causes 2 clinical syndromes of importance:
• Chickenpox (varicella)
• Shingles (zoster)

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32
Q

Primary Varicella Zoster Virus (VZV) Infection

A

= Varicella, or Chicken pox

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33
Q

Clinical Pattern of Primary VZV infection (Chickenpox/Varicella)

A
  1. Fever, malaise, headache, +/- cough
  2. Rash develops, in successive waves
    - Typically lasts 7 days
    - No longer contagious when lesions all crusted over
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34
Q

Primary VZV Infection (Chickenpox / Varicella) Rash

A
  • itchy
  • vesicular
  • “dew drop on rose petal” = clear fluid + red base
  • Usually starts on trunk & spreads to face & limbs
  • Lesions appear in successive waves, so lesions will be in various stages on physical exam
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35
Q

Pathogenesis of Primary VZV Infection (Chickenpox / Varicella)

A
  1. Virus gains entry via respiratory tract
  2. Spreads to regional lymphoid system & replicates over next 2-4 days
  3. Causes primary viremia (~4-6 days after incoc.)
  4. Replicates in liver, spleen & other organs causing secondary viremia.
  5. Secondary viremia spreads viral particles to skin 14-16 days after initial exposure & causes typical vesicular rash.
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36
Q

Primary VZV Infection - Age, Spread, Incubation, Prevention

A
  • common childhood disease
  • highly contagious
  • incubation of 10-21 days
  • preventable by vaccination (introduced in 1995)
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37
Q

Varicella Treatment

A
  • Typically self-limited & requires no treatment
  • Treatment accelerates resolution of chickenpox & decreases symptoms
  • Immunocompromised patients should always receive treatment
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38
Q

Varicella Prevention/Prophylaxis

A

Varicella vaccine: is a live-attenuated vaccine

  • Beware in immunocompromised hosts
  • 2-dose series at 12-15 mo & 4-6 yo
  • Can be used post-exposure in certain situations

Varicella-zoster immune globulin (Varizig)
- for reducing severity of varicella in high-risk individuals if given w/in 4 days of exposure
= pooled Abs from ppl w/ high VZV Ab titers

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39
Q

Pathogenesis of Latency and Reactivation of VZV

A
  • Latent in cranial, dorsal root and/or trigeminal ganglia
    = Only herpes virus w/out asymptomatic viral shedding in normal hosts
  • Reactivation is ALWAYS SYMPTOMATIC
  • Reactivates in ganglion & tracks down sensory nerve to skin innervated by the nerve
  • Causes dermatomal rash that is pathognomonic for Zoster
40
Q

Zoster (Shingles) Infection = Reactivation of Primary VZV

A
  • in up to 30% of population
  • 1st symptom is pain at site where vesicles will erupt in a few days.

Lesions

  • develop in single dermatome.
  • itchy, but main symptom is pain
  • usually crust over within 2 weeks
41
Q

Complications of Zoster (Shingles):

A
  • Similar to Varicella
  • Secondary skin infections
  • VZV ophthalmicus
  • Encephalitis
  • CNS vasculitis
  • Myelitis (spinal cord inflammation)
  • Cranial-nerve palsies: Ramsay-Hunt syndrome, Bell’s palsy
  • Peripheral nerve palsies
  • Post-herpetic neuralgia (PHN): can be very debilitating & last weeks to months after lesions resolve
42
Q

Immune response to VZV reactivation

A
  • Cell-mediated immunity is crucial to maintaining latency & preventing reactivation of VZV
  • Cell-mediated immunity decreases w/ age & is often affected by immunosuppression and HIV
43
Q

Complications of Varicella (Primary VZV)

A

Secondary infection:

  • Group A Strep
  • Necrotizing fasciitis
  • Pneumonia (bacterial or viral)
  • Encephalitis or encephalomyelitis
  • Hepatitis
  • Congenital varicella (TORCH infection, severe)

Adolescents & adults have more severe disease

Pregnant / immunocompromised ppl have higher morbidity / mortality from primary VZV

44
Q

Zoster treatment

A

Acyclovir

  • decreases number & duration of lesions
  • decreases pain

PAIN
= often worst part of shingles
- can be treated w/ NSAIDS & opiates, occasionally with steroids

45
Q

Zoster Prevention/Prophylaxis:

A
  • Live-attenuated vaccine, Zostavax (ZOS)
  • One dose age 60+ recommended by ACIP
  • Boosts immune response to VZV, thereby preventing reactivation
  • Can also use acyclovir for people w/recurrent shingles (usually the immunocompromised)
46
Q

Epstein Barr Virus - Primary Infection

A
  • very common (almost all ppl infected by age 40)
  • primary infections often occur in early childhood
  • either asymptomatic or are a mild febrile illness
  • incubation period is 4-6 weeks
  • Transmission via saliva: kissing, sharing utensils/food/drink
47
Q

Infectious mononucleosis

A

= clinical syndrome that occurs when older child, adolescent or adult gets primary EBV infection (or less commonly CMV)
= in ~40-50% of primary infections in this age group
= “kissing disease”

Symptoms include:

  • fever
  • sore throat
  • swollen lymph nodes
  • fatigue

Physical exam:

  • Exudative tonsillitis
  • Enlarged cervical nodes
  • Splenomegaly, occasionally hepatomegaly

Symptoms usually resolve in 4-8 weeks

48
Q

Pathogenesis of EBV infection

A
  1. Infects nasopharyngeal epithelium
  2. Results in cell lysis & viral spread to adjacent structures (salivary glands, oropharyngeal lymphoid tissue, etc.)
  3. Viremia occurs w/ distribution to liver, spleen, & infection of B lymphocytes
  4. Remains dormant/latent in nasopharyngeal epithelium & B cells
  5. Periodically, can reactivate (normally asymptomatic) & is commonly found intermittently in saliva of infected persons
49
Q

Diagnosis of EBV (Infectious Mono)

A
  • Often clinical diagnosis
  • Atypical lymphocytes on peripheral blood smear & often are >10% on the differential
  • Monospot/heterophile tests
  • If definitive Dx needed, can do EBV serology
50
Q

Monospot/heterophile tests for EBC/Infectious mononucleosis

A
  • Detects presence of Abs that agglutinate horse / sheep / cattle RBCs
  • After acute infection w/EBV, 75-90% of pts develop Abs that cross-react & agglutinate RBCs
  • Heterophile Abs highest during 1st four weeks of infection
51
Q

EBV serology

A
  • used if definitive Dx of EBV is needed
  • measures development of Abs to EBV antigens: EBNA and VCA (viral capsid antigen)

IgM response to VCA indicates recent infection:

  • appears early in infection & disappears in 4-6 wks
  • seen by the time symptoms appear

IgG response to VCA indicates prior infection:
- appears at 2-4 weeks after symptoms begin & persists for life

EBNA (IgG) indicates past infection:

  • infection at least a few months back
  • NEVER positive in an acute infection
52
Q

EBV Prevention/Prophylaxis

A
  • NO vaccine available

- Prevention of primary infection through preventing contact w/ infectious saliva

53
Q

Cancers associated with EBV

A
  • Not part of a primary infection, but occur later

Burkitt’s Lymphoma:

  • endemic in Africa & sporadic elsewhere
  • B cell tumor often affecting the jaw

Hodgkin’s lymphoma

Nasopharyngeal carcinoma: esp. in Chinese

Lymphoproliferative disease:
- in immunocompromised patients
<– uncontrolled proliferation of EBV-infected B cells

54
Q

EBV Treatment

A

In normal hosts
- treated supportively (fluids, antipyretics)

Steroids

  • for pts w/impending tonsillar enlargement threatening to occlude airway
  • for pts w/ severe hepatitis

In immunocompromised hosts

  • very difficult to treat
  • mainstay is restoring immune function (reducing immunosuppression) if possible
55
Q

Cytomegalovirus (CMV) Transmission

A

Transmission through contact w/ infected body fluids

  • Saliva, milk, sexual contact, blood, tears, urine
  • Blood transfusions & organ transplantation

Infected pregnant women can pass the virus to their unborn babies (in utero or perinatally)

56
Q

Zoster/Shingles diagnosis

A
  • Usually diagnosed clinically

- can use Direct IFA, PCR, or culture

57
Q

Pathogenesis of CMV:

A
  1. Infects epithelial cells of salivary gland or genital tract
  2. Persistent infection & intermittent viral shedding
    * All cells where CMV becomes latent UNKNOWN
  3. Likely viremia causing wide distribution of virus to other organs & tissues
    * Infection of GU system leads to shedding in urine
58
Q

Primary Infection with CMV in normal, healthy people

A

In most healthy persons acquiring CMV after birth:

  • Almost always asymptomatic
  • Sometime mild febrile illness
  • Sometimes mono-like syndrome (similar to EBV) w/ fever, swollen lymph nodes, & mild hepatitis
  • no longterm consequences

Incubation period 2 weeks to 2 months

59
Q

Primary Infection with CMV in Immunocompromised

A
  • serious & can infect most organs
  • severity parallels degree of impairment of cell-mediated immunity
  • severe disease most common in pts with organ / marrow transplants or HIV (w/very low CD4 counts)
  • -> CMV pneumonia, colitis, retinitis, hepatitis, encephalitis
  • -> CMV retinitis & colitis in HIV patients
60
Q

Pregnancy & CMV

A
  • Most common in utero infection in US
  • When pregnant woman develops primary CMV infection, 3-5% chance that child will be born w/ congenital CMV infection.
  • Infection of fetus can also occur if pregnant women reactivates CMV, but much lower risk (<1% infected & even fewer symptomatic)
61
Q

Congenital CMV Syndrome

A
  • Most congenitally infected infants asymptomatic
  • Only 10-15% have symptoms at birth (this is 3-5% of infants born to mothers w/ primary infections)

Syndrome:

  • Low birth weight
  • Microcephaly
  • Hearing loss
  • Mental impairment
  • Hepatosplenomegaly & Jaundice
  • Skin rash (blueberry muffin spots)
  • Chorioretinitis
62
Q

Latency and Reactivation of CMV:

A
  • Latent in monocytes & lymphocytes

- May reactivate from time to time, during which infectious virions appear in urine & saliva

63
Q

Reactivation of CMV in Pregnant Women

A
  • can lead to vertical transmission (mom to fetus)

- more common in mothers w/ primary infection

64
Q

Epidemiology of CMV Infection

A
  • In developed countries w/ high standard of hygiene, 50-80% of entire population is infected by 40 yo
  • In developing countries, over 90% are infected
65
Q

Reactivation of CMV in immunocompromised individuals

A
  • may produce serious disease w/ high morbidity & mortality

Disease can be…

  • non-focal viral syndrome
  • organ-specific infection (ex:hepatitis, pneumonitis)
66
Q

Diagnosis of CMV infection

A
  • Serology (CMV IgM & IgG)
  • Viral culture (easy to grow, takes several days)
  • PCR
  • Direct fluorescence test
  • Tissue histology
67
Q

Reactivation of CMV in persons with normal immune systems

A
  • asymptomatic

- BUT virus is being shed in bodily secretions

68
Q

Tissue histology in CMV infection

A

“Owl’s Eye” appearance of infected cells
= densely staining body surrounded by a halo
- due to intranuclear inclusion bodies (viral proteins or particles)

Intracytoplasmic inclusions (multiple smaller inclusions) are also seen in CMV infection

69
Q

Treatment of CMV in Immunocompetent hosts

A

No treatment indicated

70
Q

Treatment of CMV in Pregnant woman

A
  • Some protection offered by immunoglobulin preparation w/ high titer of CMV Abs (CMV-IG)
71
Q

Treatment of CMV in Infants w/ Congenital CMV

A
  • Gancyclovir in infants w/congenital CMV is currently being studied
  • NEW standard of practice will likely be treatment of symptomatic congenital CMV infection for first 6 mos of life w/ oral valganciclovir
72
Q

Prevention of CMV

A
  • NO vaccines available

In Immunocompromised pts at very high risk for severe CMV disease:

  • IV CMV-IG once a month as prophylaxis
  • Ganciclovir or valganciclovir as prophylaxis in some circumstances (ex: post-transplant)
73
Q

Respiratory Syncytial Virus (RSV) – Family & Structure

A
  • Paramyxoviridae family
  • Enveloped
  • ssRNA genome
  • 2 important surface proteins: G-protein & F-protein
74
Q

2 Important Surface Proteins in RSV

A

G-protein - for viral attachment to host cells

F-protein (Fusion protein)
- fusion of infected cells to neighboring cells to form syncytia (multinucleated giant cells)

75
Q

Primary Infection w/ RSV (w/ ages)

A
  • Usually Symptomatic
  • lasts 7-21 days
  • Acute respiratory disease in patients of all ages
  • Bronchiolitis: children <1 yr of age
  • Viral pneumonia: young children & elderly
  • Upper respiratory tract infection: children & adults
76
Q

Transmission of RSV & Incubation period

A
  • By contact w/ droplets (respiratory secretions) on fomites, with subsequent contact w/eye, nose, or mouth
  • By aerosol droplets also possible
  • Incubation period is 5 days
77
Q

Clinical patterns of RSV in premature infants & young children

A

Most frequent cause of bronchiolitis & viral pneumonia

Almost all children infected at least once by 2yo
Symptoms include:
- fever
- runny nose
- cough
- wheezing w/ involvement of lower respiratory tract

78
Q

Clinical patterns of RSV infection (seasonality, hospitalizations)

A
  • Seasonal illness, peaking in Winter

- Up to 125,000 hospitalizations annually

79
Q

Reinfection w/ RSV

A
  • In adults and older children
  • Rarely Asymptomatic
  • Generally resembles severe cold
  • Usually confined to upper respiratory tract
80
Q

Bronchiolitis w/ RSV

A
  1. URI w/ congestion, sore throat, fever
  2. Cough deepens & becomes more prominent
  3. Lower respiratory tract involvement develops w/
    - increased respiratory rate
    - intercostal muscle retraction
    - wheezing

Wheezing in child <2 yr of age is most likely bronchiolitis

81
Q

Pathogenesis of RSV infection

A
  1. Entry through mucosa of eye & nose
  2. Infects respiratory tract locally
  3. Cell-to-cell transfer of virus leads to spread from upper to lower respiratory tract
  4. Syncytia formed through fusion of adjacent cell membranes
82
Q

Pathogenesis of Bronchiolitis in RSV infections

A

Bronchiolitis results from:

  • Mucosal edema
  • Cell necrosis & sloughing
  • Increased mucous secretion & plugging of bronchiolar lumina w/ epithelial debris & mucous

Airway hyper-reactivity & bronchoconstriction also occur as a result of inflammation –> wheezing

83
Q

High-risk patients for RSV infections

A

Infants at high risk for severe RSV bronchiolitis

  • Premature infants (< 32 weeks gestation)
  • Pts w/ Chronic lung disease
  • Pts w/Complicated congenital heart disease

Adults & older children at high risk for severe RSV disease are those w/significant immunosuppression (bone marrow or solid organ transplant)

84
Q

High risk infants vs. Non-high risk infants with RSV infection

A

High risk (premature) infants:

  • 8-10 x higher hospitalization rates
  • Higher need for ICU care & mechanical ventilation
  • 2-6 x higher Mortality rates
85
Q

Treatment of CMV in Immunocompromised hosts:

A
  • Treat with gancyclovir or valganciclovir

- Choice of med & duration of treatment depends on the disease

86
Q

Treatment of RSV

A

-Mostly supportive

Can use inhaled bronchodilators (albuterol)

Ribavirin = only antiviral available for Tx of RSV

  • Currently limited use (only in dire circumstances – bone marrow transplant, complicated congenital heart disease, etc.)
  • Controversial efficacy / safety
  • Modest effects in studies
  • Given as an aerosol
  • VERY Expensive
87
Q

RSV Prevention

A
  • Humoral immunity (antibodies)
  • NO licensed vaccine available
  • Primary prevention via avoiding infected secretions
88
Q

Humoral immunity (antibodies) in Prevention of RSV infection

A

Infants w/ high levels of maternal Abs to RSV are less likely to be infected

RSV F-protein mAb prep

  • can be given IM to high risk infants
  • -> ~50% reduction in hospitalizations due to RSV
  • Administered monthly during RSV season
  • Very expensive
89
Q

Rotavirus (Family, Structure, etc.)

A

Reoviridae family

Double stranded RNA virus w/ segmented genome
–> Allows for reassortment & genetic diversity

Several serotypes (strains) of rotavirus
- 5 strains responsible for >90% of rotavirus disease in the U.S.
90
Q

Diagnosis of RSV:

A
  • usually clinical
  • Viral culture
  • Serology
  • Direct fluorescent antibody
91
Q

Transmission of Rotovirus

A
  • Fecal oral transmission most common
  • Kids excrete 100 billion rotavirus particles per mL of feces
  • Infectious dose is 10-100 virus particles
  • 43% of rotavirus virions survive on human fingers for 60 minutes
  • Rotavirus in feces may survive for days to weeks on environmental surfaces
92
Q

Pathogenesis of Rotavirus & Recovery

A
  1. Infects mature absorptive epithelial cells or enterocytes (at tips of villi) in proximal 2/3 of ileum
  2. Cell death leads to:
    - Reduced absorptive surface area of sm. intestine
    - Loss of enzymes that break down complex sugars
    - Increased fluid & osmotic load –> diarrhea

Regeneration of villi takes 7-10 days (recovery period)

93
Q

Natural Immunity to Rotovirus

A
  • 1st infections –> severe gastroenteritis
  • Subsequent infections –> milder or asymptomatic
  • Protective immunity develops after each infection which protects against symptomatic disease
94
Q

Epidemiology of Rotovirus infection

A
  • Leading single cause of severe diarrhea and/or gastroenteritis in infants & young children
  • Prior to vaccine, nearly every child had been infected at least once w/ rotavirus by age 5
95
Q

Rotovirus Treatment

A
  • No antivirals available
  • Supportive management
    = Attention to fluids (Pedialyte, 50/50 Gatorade / water, IV fluids for severe dehydration)
96
Q

Rotovirus Prevention/Prophylaxis

A

2 oral, live-attenuated rotavirus vaccines licensed for use in infants:

  • RotaRix (2 doses): monovalent human
  • RotaTeq (3 doses): pentavalent human-bovine reassortment

Both vaccines roughly equivalent in safety & efficacy

Both highly protective in prevention of moderate & severe rotavirus disease
- ~90% reduction in all types of health care visits

97
Q

Diagnosis of rotavirus

A

ELISA on stool samples

Unit 3 D&D (18 decks)

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