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Viral Infections Flashcards

1
Q

Symptoms of Influenza

A
  • Headache
  • Fever (usually high)
  • Extreme Muscle Tiredness
  • Joint Aches
  • Runny or stuffy nose
  • Sore Throat
  • Nasopharygeal Aches
  • Coughing
  • Vomiting
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2
Q

What is the most common consequence of influenza infection?

A

Secondary Bacterial Pneumonia

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3
Q

Risk Factor for Secondary Bacterial Pneumonia

A

Age 65+

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4
Q

Presentation of Secondary Bacterial Pneumonia

A

Improvement followed by a period of worsening

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5
Q

CXR of Secondary Bacterial Pneumonia

A

Consolidation

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6
Q

Sputum Results of Secondary Bacterial Pneumonia

A
  • Pneumococcus
  • Staphylococcus
  • Haemophilus influenzae
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7
Q

CBC Results of Secondary Bacterial Pneumonia

A

Left Shift

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8
Q

Secondary Bacterial Pneumonia Treatment

A
  • Will respond to antibiotics
  • Low Mortality Rates
  • No Viral Isolation
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9
Q

Risk Factors for Primary Viral Pneumonia

A
  • Young adult
  • Underlying Comorbid Conditions
  • Preggo
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10
Q

Symptoms of Primary Viral Pneumonia

A
  • Relentless progression beyond 3 days

- Patchy Infiltrates

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11
Q

Sputum Results of Primary Viral Pneumonia

A

Normal Flora

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12
Q

Primary Viral Pneumonia Treatment

A
  • No response to antibiotics
  • Mortality is high
  • Viral isolation
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13
Q

What is antigenic variation?

A
  • Involves hemaglutinin or neuraminidase
  • High frequency of antigenic change (reason for changing vaccines)
  • Leads to a reduction or absence of immunity
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14
Q

H1N1 differs from the “normal” influenza.

A

Quadruple Re-assortment

  • 2 swine strains (most of genome)
  • Human strain
  • Avian strain
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15
Q

Rapid Diagnosis of Influenza

A
  • Immunologic detection of viral antigen in respiratory secretions
  • Can differentiate between A and B
  • Can be a dipstick that has a color change in the presence of viral antigen
  • 30 min test time
  • 40-80% sensitive (Highest in early stages due to viral shedding)
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16
Q

PCR in checking for Influenza

A
  • 95-98% sensitive

- Depends on the area swabbed and can be positive for long periods in immunocompromised patients

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17
Q

Gold Standard of Influenza Testing

A

Culture

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18
Q

Treatment of Influenza

A
  • Rimantadine annd Amantadine

- Oseltamivir and Zanamivir

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19
Q

MOA of Rimantadine and Amantadine

A
  • Inhibits M2 Protein Pore Formation
  • Inhibits Viral Uncoating
    • Drug resistance occurs rapidly
    • Nor used anymore alone
  • Only influenza A
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20
Q

MOA of Oseltamivir and Zanamivir

A
  • Block neuraminidase
    • Required for virus release from cell
  • Little resistance develops
  • Both influenza A and B
  • Reduction in viral shedding and symptom scores
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21
Q

Who should be vaccinated?

A
  • All persons aged 6 months and older
  • Two types:
    • Live attenuated
    • Killed vaccine
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22
Q

Things to know about the Influenza Vaccine

A

Trivalent Defense!

  • Type A (H1N1 and H3N2)
  • Type B
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23
Q

Properties of Herpes

A
  • Enveloped double stranded DNA viruses
  • 3 subfamilies
  • Once infected, a lifelong carrier state develops whereby a low grade infection is kept in check by the immune defenses
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24
Q

3 subfamilies of herpes

A
  • Alphaherpesviruses - HSV-1, HSV-2, VZV
  • Betaherpesviruses - CMV, HHV-6, HHV-7
  • Gammaherpesviruses - EBV, HHV-8
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25
Properties of Herpes Simplex
- Alphaherpesvirus subfamily - The genome of HSV-1 and HSV-2 share 50-70% homology - Man is the ONLY natural host for HSV
26
Epidemiology of Herpes Simplex
- Generally HSV-1 causes infection above the belt and HSV-2 below the belt - This data is complicated by oral sexual practices - Following primary infection, 45% of orally infected individuals and 60% of patients with genital herpes will experience recurrences.
27
Pathogenesis of Herpes Simplex
1. Primary Infection 2. Latent Infection 3. Reactivation
28
Primary Infection of HSV
Spread locally and a short-lived viremia occurs, whereby the virus is disseminated in the body
29
Latent Infection of HSV
Establishes latency in the cranio-spinal ganglia
30
Reactivation of HSV
Physical or Psychological stress, infection, fever, irradiation and menstruation
31
Clinical Manifestations of HSV
1. Acute Gingivostomatitis 2. Herpes Labialis (cold sore) 3. Ocular Herpes 4. Herpes Geitalis 5. Other forms of cutaneous herpes 6. Meningitis 7. Encephalitis 8. Neonatal Herpes
32
This is the most common manifestation of primary herpetic infection. The patient experiences pain and bleeding of the gums with 1-8 mm ulcers with necrotic bases present. Neck glands are commonly enlarged accompanied by fever. It is usually a self-limiting disease which lasts about 14 days.
Acute Gingivostomatitis
33
This infection of herpes affects the outer lips. Sometimes referred to as a cold sore. 45% of orally infected individuals will experience reactivation after the primary infection. A prodrome of tingling, warmth, or itching at the site usually heralds the recurrence.
Herpes Labialis
34
This infection of herpes has lesions that are vesicular, pustular, or ulcerative involving the penis, vagina, or cervix. Lesions have a clean base, are painful, and patients have tender adenopathy. Primary infection is typically worse than reactivation.
Herpes Genitalis
35
This is the most serious clinical manifestation of HSV.
Herpes Simplex Encephalitis
36
This type of Herpes Simplex Encephalitis has global involvement and the brain is almost liquefied.
Neonatal
37
Focal Disease of Herpes Simplex Encephalitis.
The temporal lobe is most commonly affected. This form of the disease appears in children and adults. The mortality rate is high (70%) without treatment.
38
What is the drug of choice given to patients suspected of HSE before lab results are available?
IV Acyclovir
39
Management of HSV
Tx is indicated for: - Primary infection (usually severe) - Dissemination - Sigh is threatened - HSE - Acyclovir - Other older agents (highly toxic and is commonly used for topical use for ophthalmic infection only): idoxuridine, trifluorothymidine, vidarabine (ara-A)
40
Properties of Varicella/Herpes Zoster Virus
- Alphaherpesvirus subfamily - Double stranded DNA enveloped virus - One antigenic serotype only, although there is some cross reaction with HSV
41
Epidemiology of Varicella/Herpes Zoster Virus
- Primary infection in 4 - 10 years old age group - Varicella is highly communicable, with an attack rate of 90% in close contacts - Herpes zoster, in contrast, occurs sporadically and evenly throughout the year.
42
Difference b/t lesions in Small Pox vs. Varicella
- Small Pox lesions are localized to periphery | - Varicella lesions are more centrally located
43
Management of Uncomplicated Varicella
Self-limiting dx and requires no specific tx.
44
Management of Varicella in Immunocompromised Patients
Acyclovir (given promptly)
45
Management of Varicella in Normal Individuals with Serious Complications such as PNA and Encephalitis.
Acyclovir (given promptly)
46
Management of Herpes Zoster
Not normally a cause of concern. However, post-herpetic neuralgia. -- Antiviral therapy should be offered routinely to all pts over 50 yo presenting with Herpes zoster
47
Treatment of Herpes Zoster
- Acyclovir - Valicyclovir - Famciclovir ***Little difference in efficacy between them
48
Properties of Epstein-Barr Virus (EBV)
- Gammaherpesvirus subfamily - Genome is a linear double stranded DNA molecule with 172 kbp - The virus is transmitted by contact with saliva
49
Epidemiology of EBV
- In developed countries, 2 peaks of infection are seen : the first in very young preschool children aged 1 - 6 and the second in adolescents and young adults aged 14 - 20 Eventually 80-90% of adults are infected. - In developing countries, infection occurs at a much earlier age so that by the age of two, 90% of children are seropositive.
50
Pathogenesis of EBV
- Low grade virus replication and shedding can be demonstrated in the epithelial cells of the pharynx of all seropositive individuals. - EBV is able to immortalize B-lymphocytes in vitro and in vivo - Furthermore a few EBV-immortalized B-cells can be demonstrated in the circulation which are continually cleared by immune surveillance mechanisms. - EBV is associated with several very different diseases where it may act directly or one of several co-factors.
51
EBV and B-Cell Transformation
1. Fever - cytokine release consequent to B-lymphocyte invasion 2. Pharyngitis - proliferation of EBV-infected B lymphocytes in the lymphatic tissue of the oropharynx 3. Lymphocytosis - proliferation of EBV-infected B lymphocytes
52
Clinical Manifestations of EBV
- Infectious Mononucleosis - Burkitt's lymphoma - Nasopharyngeal carcinoma - Lymphoproliferative disease and lymphoma in the immunosuppressed. - X-linked lymphoproliferative syndrome - Chronic infectious mononucleosis - Oral leukoplakia in AIDS patients - Chronic interstitial pneumonitis in AIDS patients.
53
Effect of EBV on Immunology
- The humoral immune response directed against EBV structural proteins is the basis for the test used to diagnose EBV infectious mononucleosis - T-lymphocyte response is essential in the control of EBV infection; natural killer (NK) cells and predominantly CD8+ cytotoxic T cells.
54
Diagnosis of EBV
- Based on Clinical Suspicion - Increased number of atypical lymphocytes on blood smear (Downey Cells) - Monospot Test
55
What is the Monospot Test?
- Heterophile antibodies - Positive in 90% of primary infections - Can be negative in the early course of the dz in children.
56
Treatment of EBV
- More than 95% of cases resolve without specific therapy - Antibiotics should be avoided - -- Ampicillin causes rash - Corticosteroids - -- Reduce fever and shorten duration of symptoms - -- Usually not given due to possibility of side effects and because disease is usually self limited - -- Reserved for patients with mononucleosis complicated by airway obstruction, severe thrombocytopenia, or severe hemolytic anemia - Antivirals - -- Acyclovir or Ganciclovir for severe cases
57
Acyclovir and Valacyclovir
- Guanosine analogs - Requires viral thymidine kinase - Valacyclovir is converted to acyclovir in the liver during 1st pass metabolism - - Serum concentrations 3-5X that of acyclovir - - Dosing therefore less frequent - Blocks DNA synthesis by 2 steps - - Chain termination - - Competitive inhibition of DNA polymerase (Blocks incorporation of guanosine triphosphate) - Active against HSV-1, HSV-2 and VZV
58
Ganciclovir
- Guanosine analog - Requires viral thymidine kinase - Inhibits the incorporation of guanosine triphosphate by viral DNA polymerase - Is not a chain terminator - Reaches intracellular levels 10X that of acyclovir - Effective against CMV, EBV, HSV, and VZV
59
Cidofovir
- Analog of cytosine nucleotide analog - Does not require viral kinase for activity (helps limit resistance) - Mechanism of action - --- Chain terminator - --- Competitive inhibitor - CMV, HSV, VZV, EBV, adenovirus, poxviruses, and papilloma viruses
60
Ribavirin
- Guanosine analog - Inhibits DNA and RNA viruses - Mechanism of action not completely understood - --- Interferes with viral mRNA production - --- Interferes with guanosine monophosphate production - --- Inhibit the viral RNA dependant polymerase - RSV, influenza, parainfluenza, hepatitis, adenovirus, ans pox viruses

Infectious Disease (6 decks)

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