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Year 3 Infection & Immunology > Dermatological viruses > Flashcards

Dermatological viruses Flashcards

1
Q

What is varicella zoster?

A

Primary infection is called varicella (chickenpox). Reactivation of the dormant virus in the dorsal root ganglia causes zoster (shingles). AKA herpes zoster or HHV-3.

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2
Q

What is the aetiology of varicella zoster?

A

Varicella zoster virus (VZV) is a herpes ds-DNA virus that is transmitted by aerosol inhalation or direct contact with vesicular secretions.

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3
Q

What is the pathophysiology of varicella zoster?

A
  1. PRIMARY VIRAEMIC PHASE: Virus spreads to regional lymph nodes then the liver, spleen and other cells in the reticuloendothelial system
  2. SECONDARY VIRAEMIC PHASE: mononuclear cells (such as lymphocytes and monocytes) transport the virus to the skin and mucous membranes causes classic vesicular rash. It also causes vasculitis of small blood vessels and degeneration of epithelial cells leading to vesicles filled with fluid with high levels of the virus
  3. DORMANCY: resides in dorsal root or cranial nerve ganglia. Evades immune system through reduction of, and downregulation of the expression of, MHC Class I antigens on the surface of the infected neuronal cells 4. REACTIVATION: leads to herpes zoster
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4
Q

What are the risk factors for varicella zoster? (x2)

A

Immunocompromised (decline in cell-mediated immunity; HIV, malignancy, chemotherapy, chronic corticosteroid use, or high dose immunosuppressants), pregnant women, and neonates.

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5
Q

What is the pathophysiology of herpes zoster?

A
  • Reactivation leads to ganglionitis: inflammation and destruction of the neurons and supporting cells.
  • Movement of the virus down the axons leads to local inflammation of the subsequent cutaneous dermatome. This causes the characteristic symptom sequela of 2–3-day prodromal period of burning pain, followed by vesicular eruption.
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6
Q

What is the epidemiology of varicella zoster: Age? When?

A

Most are infected before the age of 10. More prevalent in late winter and early spring.

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7
Q

What is the epidemiology of herpes zoster: Age? Gender? Common?

A

Over 50 years old. More common in women. One third get herpes zoster.

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8
Q

What are the signs and symptoms of chickenpox (disseminated varicella)? (x3) Where?

A
  • Macular popular rash evolving into crops (different stages of acuity/healing) of vesicles with areas of exudate and crusting. Can also occur on mucosa, usually nasopharynx
  • Pruritis
  • Mild pyrexia (up to 39 degrees)
  • First on face and trunk, then spreading to extremities
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9
Q

What are the signs and symptoms of shingles? (x5) Where? Disease course?

A
  • Most commonly T1 to L2; mostly sensory neurones, though 5-15% have motor neurones affected
  • Typically around 4 weeks
  • Prodromal burning dermatomal pain
  • Erythematous maculopapular rash followed by vesicular eruption. Vesicles eventually pustulate and crust
  • May also be associated with pruritus
  • Corneal ulceration: pain and reduced vision, from trigeminal nerve
  • Mild pyrexia
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10
Q

How may signs and symptoms of shingles differ in high-risk patients?

A

For example, immunocompromised or pregnant women, appears in more than one dermatome i.e. disseminated infection.

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11
Q

What is zoster sine herpete?

A

Patients develop pain without rash.

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12
Q

What are the signs and symptoms of motor zoster? q

A

Muscle weakness of myotome at similar level as involved dermatome.

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13
Q

What are the investigations for varicella zoster? (x2)

A
  • Clinical diagnosis
  • VESICULAR FLUID: PCR is diagnostic with viral DNA, can also do viral culture, direct fluorescent antibody testing (which is positive for the viral antigen; aka DFA)
  • HIV: consider in adults with HZ (herpes zoster), as this is an indicator infection of HIV
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14
Q

How is chickenpox managed? (x2)

A
  • CHILDREN: supportive therapy with analgesics, oral and topical diphenhydramine (antihistamine) and calamine lotion (relieve itching)
  • MODERATE/HIGH RISK patients or SEVERE DISEASE such as in adults: oral antiviral therapy (acyclovir). IV in patients who are high risk or disease is severe.
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15
Q

How is shingles managed? (x2)

A
  • Oral antiviral therapy: famciclovir or valaciclovir (acyclovir is second line). IV acyclovir if eye involvement, disseminated disease or immunocompromised
  • Supportive care: analgesics and calamine lotion
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16
Q

What are the complications of varicella zoster (chickenpox)? (x7)

A

Secondary bacterial infection (of lesions; characterised by fever lasting more than 3 days), scarring, pneumonia, encephalitis, hepatitis, cerebellar syndrome, congenital varicella syndrome.

17
Q

What is congenital varicella syndrome?

A

Characterised by scarring, ophthalmic defects, limb dysplasia (abnormally shaped bones, hindered growth) and CNS abnormalities.

18
Q

What are the complications of herpes zoster? (x6)

A

Postherpetic neuralgia, secondary bacterial infection, zoster ophthalmic (rash involves ophthalmic division of trigeminal nerve), Ramsay Hunt’s syndrome, sacral zoster may lead to urinary retention, disseminated zoster (involves more than one dermatome)

19
Q

What is Ramsay’s Hunt syndrome?

A

Reactivation of virus in geniculate ganglion (CNVII) leading to zoster of the ear and facial nerve palsy. Vesicles may be seen preauricular or in the ear canal.

20
Q

How is postherpetic pain treated?

A

Treated with analgesics and topical capsaicin (for pain relief)

21
Q

What is herpes simplex virus?

A

Disease resulting from HSV1 and HSV2

22
Q

What is the aetiology of HSV: Type of virus? Transmission? Reactivation?

A

Alpha-herpes virus with dsDNA. Transmitted through symptomatic or asymptomatic reactivation of the virus via close contact (kissing, sex). Reactivation means that an individual is shedding the virus. Following primary viral infection, reactivation may occur in response to physical or emotional stresses or immunosuppression.

23
Q

What is the pathophysiology of HSV? Where?

A
  1. PRIMARY INFECTION: virus acquired at mucosal surfaces or breaks in skin and replicates in epidermis then infects sensory or autonomic nerve endings. From here, it travels by retrograde axonal transport to sensory ganglia. During primary infection, there is no host antibody response, and it is usually asymptomatic
  2. LATENT STATE: allows the virus to evade the immune system, usually in trigeminal and sacral root ganglie
  3. REACTIVATION: most activations are asymptomatic. Leads to cytolysis of epithelial cells and vesicle formation. Associated with CD4+ and CD8+ T cell response and antibody production
24
Q

What is HSV1 and HSV2 associated with?

A
  • HSV1 (aka HHV-1 (human herpes virus)): most commonly associated with herpes labialis (mouth and lips), though can also cause genital herpes. Also associated with encephalitis and ocular ulcers
  • HSV2: (aka HHV-2) genital herpes, though can also cause herpes labialis
25
Q

What is the epidemiology of HSV: Prevalence? (x2) Gender?

A

70% adults are seropositive for HSV1 by 50 years worldwide. Over one third has recurrent HSV infections. HSV is higher among women.

26
Q

What are the signs and symptoms of HSV-1 PRIMARY infection? (x5)

A
  • Primary infection often asymptomatic
  • Pharyngitis
  • Gingivostomatitis: infection of mouth and gums filled with yellow slough
  • Herpetic whitlow: small blisters on fingers
  • Tender cervical lymphadenopathy
  • Pyrexia
27
Q

What are the signs and symptoms of HSV-1 reactivation?

A
  • Usually asymptomatic
  • Prodrome (6 hours) of peri-oral tingling and burning
  • Vesicles appear over 48 hours, ulcerate and crust over. Typically only a single vesicle. Complete healing after 10 days.
28
Q

What are the signs and symptoms of HSV-2? (x3)

A
  • Maculopapular rash, multiple painful vesicles and ulcers on external genitalia, anal margin and upper thighs, that progress to crusting
  • Dysuria in women in primary, not often recurrent disease
  • Fever and malaise
29
Q

What are the signs and symptoms of HSV ocular ulcers?

A

Keratoconjunctivitis (pain) with epiphora (watering) and photophobia. Characteristic lesion is a dendritic ulcer which may be visualised by staining with 1% fluorescin.

30
Q

What are the investigations for HSV?

A
  • Clinical diagnosis
  • VESICLE FLUID: PCR is diagnostic. Can also use viral culture and direct immunofluorescence

Year 3 Infection & Immunology (6 decks)

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