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Infectious Disease > Viral Infections > Flashcards

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
Q

Properties of Herpes Simplex

A
  • Alphaherpesvirus subfamily
  • The genome of HSV-1 and HSV-2 share 50-70% homology
  • Man is the ONLY natural host for HSV
26
Q

Epidemiology of Herpes Simplex

A
  • 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
Q

Pathogenesis of Herpes Simplex

A
  1. Primary Infection
  2. Latent Infection
  3. Reactivation
28
Q

Primary Infection of HSV

A

Spread locally and a short-lived viremia occurs, whereby the virus is disseminated in the body

29
Q

Latent Infection of HSV

A

Establishes latency in the cranio-spinal ganglia

30
Q

Reactivation of HSV

A

Physical or Psychological stress, infection, fever, irradiation and menstruation

31
Q

Clinical Manifestations of HSV

A
  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
Q

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.

A

Acute Gingivostomatitis

33
Q

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.

A

Herpes Labialis

34
Q

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.

A

Herpes Genitalis

35
Q

This is the most serious clinical manifestation of HSV.

A

Herpes Simplex Encephalitis

36
Q

This type of Herpes Simplex Encephalitis has global involvement and the brain is almost liquefied.

A

Neonatal

37
Q

Focal Disease of Herpes Simplex Encephalitis.

A

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
Q

What is the drug of choice given to patients suspected of HSE before lab results are available?

A

IV Acyclovir

39
Q

Management of HSV

A

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
Q

Properties of Varicella/Herpes Zoster Virus

A
  • Alphaherpesvirus subfamily
  • Double stranded DNA enveloped virus
  • One antigenic serotype only, although there is some cross reaction with HSV
41
Q

Epidemiology of Varicella/Herpes Zoster Virus

A
  • 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
Q

Difference b/t lesions in Small Pox vs. Varicella

A
  • Small Pox lesions are localized to periphery

- Varicella lesions are more centrally located

43
Q

Management of Uncomplicated Varicella

A

Self-limiting dx and requires no specific tx.

44
Q

Management of Varicella in Immunocompromised Patients

A

Acyclovir (given promptly)

45
Q

Management of Varicella in Normal Individuals with Serious Complications such as PNA and Encephalitis.

A

Acyclovir (given promptly)

46
Q

Management of Herpes Zoster

A

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
Q

Treatment of Herpes Zoster

A
  • Acyclovir
  • Valicyclovir
  • Famciclovir

***Little difference in efficacy between them

48
Q

Properties of Epstein-Barr Virus (EBV)

A
  • Gammaherpesvirus subfamily
  • Genome is a linear double stranded DNA molecule with 172 kbp
  • The virus is transmitted by contact with saliva
49
Q

Epidemiology of EBV

A
  • 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
Q

Pathogenesis of EBV

A
  • 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
Q

EBV and B-Cell Transformation

A
  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
Q

Clinical Manifestations of EBV

A
  • 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
Q

Effect of EBV on Immunology

A
  • 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
Q

Diagnosis of EBV

A
  • Based on Clinical Suspicion
  • Increased number of atypical lymphocytes on blood smear (Downey Cells)
  • Monospot Test
55
Q

What is the Monospot Test?

A
  • Heterophile antibodies
  • Positive in 90% of primary infections
  • Can be negative in the early course of the dz in children.
56
Q

Treatment of EBV

A
  • 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
Q

Acyclovir and Valacyclovir

A
  • 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
Q

Ganciclovir

A
  • 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
Q

Cidofovir

A
  • 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
Q

Ribavirin

A
  • 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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