5. Varicella Zoster Virus 5
• Mode of spread
• Airborne droplets/direct contact
• Entry through the respiratory tract
• Incubation period: 10 to 12 days [2 weeks]
6. PATHOPHYSIOLOGY – PRIMARY INFECTION
Vesicle formation
Intercellular edema and intracellular edema
Infection of cells of the malpighian layer
Diffuse viral invasion of capillary endothelial cells and the epidermis
Secondary viremia 14-16 days post infection
Second round of viral replication – Liver & spleen
Primary viremia on postinfection days 4-6
Viral proliferation - regional lymph nodes - upper respiratory tract 2-4 days after infection
Virus infects the conjunctivae or the mucosae of the upper respiratory tract
Contaminated respiratory droplets
6
7. • LONG TIME IMMUNITY - Production of antibodies
[IgG, IgM, and IgA]
7
8. PATHOPHYSIOLOGY –
SECONDARY INFECTION
After primary
infection
VZV spreads from
mucosal and
epidermal lesions to
local sensory nerves
Remains latent in
the dorsal ganglion
cells of the sensory
nerves
Reactivation of
VZV results in
herpes zoster
(shingles)
8
9. CLINICAL FEATURES
• Prodromal symptoms
• Triad - Rash, malaise, low-grade fever
• 3 or more successive crops over several days
• Each crop usually progresses within less than 24 hours from macules
to papules, vesicles, pustules and crusts so that on any part of the
body there are lesions in different stages of development
• Starts on face and trunk, then spreads to extremities
• Secondary infection – Scar formation
9
11. ORAL MANIFESTATIONS
• White opaque vesicles – raised
vesicle with surrounding erythema –
3 to 4 mm
• Later form ulcers with red margin –
1 to 3 mm
11
12. COMPLICATIONS
• Secondary bacterial infection of skin lesions
• Central nervous system manifestations
• Pneumonia (viral or bacterial)
• Myocarditis
• Hepatitis
• Hemorrhagic complications – thrombocytopenia
• Nephritis
12
21. PATHOPHYSIOLOGY
VZV is activated at
the spinal root or
cranial nerve neurons
Inflammatory
response occurs
Hemorrhagic
necrosis of nerve cells
Neuronal loss and
fibrosis
Neuronal necrosis
Severe neuralgia
Virus travel down
through the nerve
Dermatologic
involvement
21
24. ACUTE ERUPTIVE PHASE
• Vesicular eruptions - Erythematous macules and
papules
• Cluster of vesicles on an erythematous base – classical
sign
• Vesicles rupture, release their contents, ulcerate, and
finally crust over and become dry
• Associated symptom - pain (acute neuritis)
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26. CHRONIC PHASE (PHN)
• Post herpetic neuralgia
• Dermatomal pain – Zoster sine herpete
• Deep burning or aching pain, paresthesia,
dysesthesia, hyperesthesia, or electric shock–
like Long time to resolve – upto 12 months
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27. ORAL MANIFESTATIONS
• Buccal mucosa, tongue, uvula,
pharynx, larynx
• 1-4mm vesicles or pustules, which
rupture to from ulcers
• Loss of taste sensation
• Teeth – pulpitis, pulpal necrosis,
pulpal calcification or root
resorption
27
28. • LONG TIME IMMUNITY – Zoster Immune Globulin
[ZIG]
28
29. COMPLICATION
• CNS
• Muscular weakness, cranial nerve palsies
• Guillain-Barré syndromeM
• Meningoencephalitis or encephalitis
• Ophthalmic
• Herpes zoster ophthalmicus (HZO
• Hutchinson sign – lesion in tip of nose –
nasociliary branch
• Auditory system
• Herpes zoster oticus/Ramsay Hunt
syndrome/Geniculate neuralgia/Herpes zoster
auricularis
29