Varicella Zoster Virus (VZV) is one of 8 human herpes viruses and the cause of varicella (chickenpox) and herpes zoster (shingles).
Before 1995, approximately 90% of children under 10 years of age showed symptoms of being infected with the virus.
Shingles is a reactivation of latent VZV infection and develops in approximately 20% of healthy adults and 50% of immunocompromised persons. Early treatment with antivirals can reduce or eliminate the serious sequelae caused by VZV infections.
Epidemiology of the VZV.
The virus is cosmopolitan and it is estimated that 98% of adults are carriers.
Before the introduction of the varicella vaccine in 1995, 4 million children under 10 years of age were affected, only in the United States, concentrating the outbreaks in winter and early spring.
After the vast vaccination campaigns, the cases were reduced by approximately 85%, showing the effectiveness of the vaccine in stimulating the immunological system. After the vaccination, the peak age changed to 10-14 years, causing varicella outbreaks in children already immunized, which made another vaccination campaign necessary to reinforce the immunological level of children at later ages.
Although the incidence and severity of herpes zoster infection increases between the middle and late adults, it can occur at any age and is more likely to appear in young people who have had chickenpox in the first year of life.
The person who has had varicella, has a 20% chance of developing herpes zoster. An estimate from WHO states that among 1000 people aged 20 to 50 years, 2.5 will develop herpes zoster. This figure doubles in the age range of 51 to 70 years and quadruples for over 80 .
How the varicella zoster virus spreads?
The virus spreads mostly by air, although direct contact with the fluid of the vesicles is another way of contagion.
The period of incubation of the virus is 11 to 20 days, and is highly contagious, with 80 to 90% of presenting clinical evidence of infection then being exposed to the virus. The infected can spread the virus from 2 days before presenting symptoms until the vesicles have crusted.
Varicella Zoster virus pathogenesis
During varicella infection, primary viremia appears during the first 2 to 4 days of viral replication within the lymph nodes. The replication of the virus to other organs such as the liver, spleen and other organs it reflects in the second viremia, which culminates with its full spread in a period of 14 to 16 days after the exposure.
During this time, the zoster virus travels to the epidermis, invading capillary cells of the endothelium. Subsequently, VZV travels from mucocutaneous lesions to the root of the lymph node system where it remains dormant until reactivation.
Herpes Zoster appears after it is reactivated. This reactivation can be spontaneous or induced by stress, fever, radioactive therapy, local traumas or immunosuppression. During the outbreak of herpes zoster, it continues to replicate by the ganglion system, producing painful ganglionitis. Neural inflammations and necrosis can appear as a result of severe neuralgia, which intensifies as the virus spreads through the sensory nerve.
The contact with the Herpes Zoster fluid in individuals not carrying the virus leads to infection by Varicella (not Herpes Zoster) in 15% of cases compared to more than 70% probability of infection in the case of contacts with fluids of chickenpox.
Common varicella lesions
Varicella (Chickenpox) symptoms.
Chickenpox can start (in adults > children) with moderate fever, malaise and myalgia (muscle pains). This continue with an eruption of erythematous and pruritic papules and maculae. It may starts at the scalp, the face, and then spreading along the trunk and the extremities.
The lesions evolve rapidly in only 12 to 14 hours, forming clear vesicles, surrounded by narrow pink halos similar to drops of dew or rose petals. the number of vesicles varies from only a few to hundreds of them, with the oral mucosa frequently being affected, as opposed to areas far from the face, which are usually not affected. The oldest lesions form pustules and scabs, healing completely after 7 or 10 days. These lesions are present in all stages of the infection and are characteristic of varicella infection.
This disease is usually self-limited and benign in healthy children, with bacterial infections being the product of the most common complications in this disease. Chickenpox in adolescents and adults is always much more severe than in children, with a considerable increase in injuries and a more frequent development of pneumonia. Occasional complications include thrombocytopenia, hepatitis, optic neuritis, arthritis, pancreatitis, myocarditis and vasculitis.
There is a 2% risk of developing congenital varicella syndrome in pregnant women who suffer from varicella in the first 20 weeks of pregnancy. Possible congenital defects may occur including low birth weight, ocular abnormalities, cotical atrophy, psychomotor retardation, ect. Children whose mothers had chickenpox during pregnancy have a high probability of suffering from herpes zoster without having suffered extra-uterine varicella.
In immunosuppressed individuals, varicella can lead to high morbidity and mortality. These patients frequently have atypical and greater skin rashes, sometimes of the purpura and hemorrhagic type.
Common Herpes Zoster lesions
Herpes zoster (Shingles) symptoms.
The reactivation of the VZV can happen at any time after having developed Varicella. it starts with pruritus( itching), tingling, tenderness, hyperesthesia and/or intense pain (which can mimic a myocardial infarction, abdominal pain or a toothache) in 90% of patients. these symptoms can appear without skin lesions, a phenomenon named “Zoster sine herpete”.
However, most patients develop a rash formed by a group of erythematous-based vesicles with a dermatomal distribution. Lesions may involve more than one contiguous dermatomy and occasionally cross the midline. Edematous papules and plaques may precede the appearance of vesicles, and progression to pustules or bullae may occur. Any part of the body can be affected by herpes zoster, with the trunk having the highest incidence, followed by the face. The DNA of the virus can be detected in saliva and peripheral blood, even before starting antiviral treatment.
Children and young adults with intact immune systems, who suffered from herpes zoster do not have sequelae. However, pain, skin lesions and complications from herpes zoster are much more severe in elderly patients and weakened immune systems. The most frequent complications in these cases are postherpetic neuralgia, characterized by dysesthetic pain (sensation of stabbing or burning, allodynia) that persist after the injuries have healed
Varicella and herpes zoster treatment and prevention
Varicella in immunocompetent children can be treated symptomatically with antipyretics (acetaminophen), antihistaminics, calamine lotion, and topical baths. It has been found that by administering acyclovir after 24 to 72 hours from the onset of skin rashes, the duration and severity of varicella diminishes. Oral acyclovir and valaciclovir are drugs approved by the FDA for the treatment of chickenpox in children 2 to 17 years of age. while acyclovir is approved in adults.
These antivirals are recommended against varicella in adolescents and healthy adults as well as in children with pulmonary disorders.
Intravenous acyclovir is indicated in immunocompromised patients, including those receiving steroid therapy for chronic systemic diseases, due to their high risk of complications.
Administration of immunoglobulin against herpes zoster virus (125 U-10 kg, 625 U maximun) within 96 hours of exposure to chickenpox is recommended to provide preventive prophylaxis to patients with immunological system in good condition, women pregnant women and newborns (protection lasts only 3 weeks), this medication is only available in the United States under the new FDA approval protocol. Another option for prophylactic protection is intravenous immunoglobulin injection (IVIg> = 400 mg / kg).
VARICELLA – ZOSTER VIRUS INFECTIONS
|Varicella||Acyclovir: 20 mg/kg (800 mg max) Oral, one doses every 6 hrs. x 5 days.|
Valacyclovir: 20 mg/kg (1 g max) one doses every 6 hrs. x 5 days.
|Zoster||Acyclovir: 20 mg/kg (800 mg max) Oral, 5 doses/day x 7-10 days.|
Famcyclovir: 500 mg, Oral, 3 doses/day x 7 days.
Valacyclovir: 1 g, Oral, 3 doses/day x 7 days.
|Immunocompromised||Acyclovir: 10 mg/kg (500 mg/m2) intravenous, one dose every 8 hrs. x 7-10 days or until cropping has ceased(depending on the setting, consider continuing until lesion are healed)|