I. Introduction
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| Pathogensis of varicella zoster virus |
Varicella-zoster virus ( VZV ) is a ubiquitous human which causes varicella ( chickenpox ) and herpes zoster ( shingles ). It is a common childhood illness associated with fever and a generalized pruritic vesicular rash. VZV establishes latency in cells of the dorsal root ganglia after primary infection. Herpes zoster is a localized, painful, vesicular rash involving one or adjacent dermatomes and caused by VZV reactivation. The incidence of herpes zoster increases with age or immunosuppression. Varicella lesions are scattered, whereas zoster lesions are localized.
II. Epidemiology
VZV is found in worldwide geographic distribution, but annual epidemics are more prevalent in temperate climates, occurring most often during late winter and spring. Varicella is a less common childhood disease in tropical areas. Herpes zoster occurs only in individuals who have had primary VZV infection. Most cases of herpes zoster occur in individuals who are more than 45 years old. Risk factors for herpes zoster in childhood include varicella acquired during the first year of life and VZV infection in utero as a result of maternal varicella during gestation. Herpes zoster is common in patients treated with immunosuppressive drugs for malignant diseases or to prevent rejection of bone marrow or organ transplants and in individuals with human immunodeficiency virus ( HIV ) infection.VZV reactivation is particularly frequent among patients with leukemia, Hodgkin’s disease, non-Hodgkin’s lymphoma, and oat cell carcinoma of the lung.
Systemic steroid therapy for chronic diseases such as rheumatoid arthritis or systemic lupus erythematosus also predisposes to VZV reactivation.
III. Pathogenesis
+ Varicella :
Although VZV can be transmitted by the respiratory route, the infectious virus has rarely been isolated from respiratory mucosal sites. The PCR data are consistent with the epidemiologic evidence that VZV is transmissible for 24 to 48 h before the exanthem begins.VZV lesions in the oropharynx are common and may facilitate the transfer of the virus in respiratory secretion. The virus is then through to spread to regional lymph nodes, resulting in a primary viremic phase that carries the virus to the liver or other cells of the mononuclear phagocyte system during the incubation period. The incubation period usually lasts about 14 days.
VZV viremia can be detected during the last 4 or 5 days before the onset of symptoms and for a few days after the appearance of the rash. Both lymphocytes and monocyte/macrophage cell types may harbor infectious viruses. Cell-associated viremia provides the virus with access to epidermal cells, and replication in these cells causes the typical varicella rash. Viral inclusions are detected in capillary endothelial cells and in adjacent fibroblasts, as well as in epithelial cells.
Varicella lesions evolve through maculopapular, vesicular, and crusting phases. The cells lining the lymphatics of the superficial dermis are also affected. showing dilatation and intranuclear inclusions. The evolution to vesicles is associated with progressive ‘ballooning‘ degeneration of epithelial cells, the appearance of fluid-filled spaces between cells, and increases numbers of infected cells at the base of the lesion.
Varicella lesions usually do not scar, because the infected epithelial cells are relatively superficial, but damage to the germinal layer of the epithelium may occur.
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| maculopapular, vesicular, and crusting phases |
Varicella pneumonia is characterized by active infection of the epithelial cells of the pulmonary alveoli, mononuclear cell infiltration, and edema of the alveolar septae.Transient hepatitis probably occurs in most healthy individuals with primary VZV infection, but extensive viral replication in the liver, with widespread hepatocellular destruction due to virus-induced cell lysis, is a complication of progressive varicella, causing fulminant hepatic failure.Varicella encephalitis and cerebellar ataxia are the most common neurologic complications of varicella. VZV can infect vascular endothelial cells and may cause central nervous system disease by inducing vasculitis.Other pathologic complications of VZV infection include thrombocytopenia, which causes coagulopathy and hemorrhage, particularly when associated with severe hepatitis.+ Herpes Zoster :
VZV infection of cells in the dorsal root ganglia is probably a consequence of all primary VZV infections. VZV DNA is detected by in situ hybridization and PCR in these tissues obtained at autopsy from individuals who have serologic evidence of prior VZV infection but no signs of VZV disease.
VZV may reach dorsal root ganglia from mucocutaneous lesions by an ascending route along neuronal cell axons. Symptomatic VZV reactivation causes a vesicular rash, usually involving the dermatomal distribution of a single sensory nerve. Infections virus may be carried by multiple axons since clusters of lesions appear in scattered areas of the involved dermatome. Histopathologic studies of ganglia during VZV reactivation show inflammation, necrosis, and disruption of the morphology of neuronal and nonneuronal cells. Inflammation and necrosis from VZV reactivation sometimes extend into the anterior horn cells, producing myelitis and deficits of motor function. VZV is detected within neurons and satellite cells during reactivation. VZV reactivation often causes postherpetic neuralgia syndrome (PHN). VZV reactivation in the immunocompromised host is usually associated with a more extensive local rash than in immunocompetent individuals and is often accompanied by cell-associated viremia. VZV viremia can result in progressive varicella, with the spread of the virus to the lungs, liver, central nervous system, and other organs.
IV. Clinical features
+ Varicella:
Primary VZV infection is characterized by a prolonged incubation period, ranging from 10 to 21 days, with the usual duration being 14 to 16 days. About half of the cases begin with a prodrome of fever, malaise, headache, and abdominal pain. The prodromal symptoms last about 24 to 48 h before the first skin lesions appear and are more common in older children and adults. Fever associated with uncomplicated
varicella is usually less than 38.68C (101.58F) but maybe
as high as 418C (1068F).
The initial cutaneous lesions of varicella often involve the scalp, face, or trunk and are pruritic, erythematous macules; the maculopapular phase evolves to a vesicular phase, during which small, fluid-filled vesicles appear in existing or new erythematous lesions. Ulcerative and often painful lesions appear on mucous membranes, including the oropharynx, conjunctivae, and vagina. The crusting phase begins with the clouding of the vesicular fluid, within about 24 to 48 h after the appearance of each lesion. Lesions heal as new epithelial cells form at the base of the lesion; hypopigmentation is common during healing. Scarring is rare except where the first lesions appeared, usually along the hairline or eyebrows. The differential diagnosis of varicella includes vesicular rashes associated with infections caused by other common pathogens, such as enteroviruses or Staphylococcus aureus, rashes due to drug reactions, and contact dermatitis and insect bites.
Secondary bacterial infection of varicella lesions is most
obvious as bullous progression or cellulitis surrounding one or
more lesions. Regional lymphadenitis and subcutaneous
abscesses may occur. Varicella gangrenous, which is usually
due to S. pyogenes, is diagnosed when an area of rapidly extending erythema with pain and induration appears around a single lesion, often on the trunk or an extremity. The common manifestations include staphylococcal or streptococcal pneumonia, arthritis, or osteomyelitis. Varicella lesions often involve the eyelids and bulbar conjunctivae,
but serious ocular complications are rare; unilateral anterior
uveitis or corneal lesions occur occasionally but usually resolve without sequelae. Infants of these mothers may be born with cutaneous varicella lesions or may develop lesions within the first 5 days of life, but they are not at risk for serious complications. Infants exposed to varicella by nonmaternal contact rarely have the neonatal disease, because most are born to seropositive mothers and have passively acquired antibodies to VZV. Herpes zoster in pregnancy does not appear to result in congenital varicella syndrome.
+ Herpes Zoster :
The reactivation of VZV from latency causes a localized,
pruritic, vesicular rash that usually appears unilaterally in the
distribution of one or more adjacent sensory nerves. The initial lesions in the affected dermatome are usually clustered at a few sites anteriorly and posteriorly; as the cutaneous disease evolves, the vesicles often coalesce into larger, fluid-filled lesions. The rash is often preceded by several days of localized neuropathic pain. Acute neuritic pain and hypersensitivity frequently accompany the appearance of vesicular lesions. Herpes zoster most often involves the thoracic dermatomes, particularly T5 to T12; 14 to 20% of patients have disease in the distribution of a cranial nerve, and lumbosacral dermatomes, especially L1 to L2, are affected in 16% of patients. The most common and debilitating
a complication of herpes zoster is PHN.In a population-
the based study, 9% of cases of herpes zoster were associated
with PHN lasting 4 weeks to more than 10 years; pain persisted
for more than 1 year in 22% of individuals who developed the
syndrome. The motor deficits that accompany some cases of herpes zoster, including facial palsies, usually resolve over time (143). Elderly patients are at the highest risk for prolonged weakness, which may occur in 10 to 15% of cases.
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| Zonna herpes virus |
V. Diagnosis
Rapid diagnosis of VZV infection can sometimes be accomplished by using direct fluorescent antibody (DFA) testing on scraping from active vesicular skin lesions that have not yet crusted.
Viral culture or viral isolation is sometimes available but is insensitive and associated with low yield (approximately 50 to 75 percent ). Specific VZV culture isolation from a swab of a vesicular skin lesion or sterile body fluid, such as CSF, typically requires prolonged incubation with a turnaround time of one to two weeks.
The presence of IgG antibodies to VZV correlates both with a history of varicella and protection against subsequent infection.
Some experts have concluded that commercial ELISA assays are suitable for screening for VZV susceptibility among healthcare workers.
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