INFECTIONS BY THE

HERPES ZOSTER VIRUS

Dr. Catalina Torres M.
 DEFINITION
The varicella-zoster virus (VZV) produces two clinical entities.
different: chickenpox and shingles. Chickenpox, a universal and highly
contagious, it is usually a benign childhood disease, characterized by a
vesicular rash. When the latent VZV reactivates (which is more common
after the sixth decade of life) shingles appears as a
vesicular rash circumscribed to a dermatome and generally accompanied by pain
intense.
 PATHOGENESIS
PRIMARY INFECTION
Transmission is easy by respiratory route; replication is confined to a location not
involved (probably the nasopharynx) produces dissemination in the system
reticuloendothelial and, finally, viremia. The vesicles affect the dermis and the
epidermis, with degenerative changes characterized by bulging, cells
multinucleated giants and eosinophilic intranuclear inclusions. The infection may
reach the local cutaneous vessels, causing necrosis and epidermal hemorrhage.
As the disease progresses, the fluid in the vesicles becomes cloudy.
Finally, they break and release their liquid content (which contains infectious viruses).
they are gradually absorbed.
 PATHOGENESIS
RECURRENT INFECTION
The mechanism of reactivation of VZV that leads to shingles is unknown.
Viruses are supposed to infect the dorsal root ganglia during the
chickenpox and there they remain latent until they are reactivated.

The histology of the corresponding ganglia of the dorsal roots during the
active herpes zoster shows the presence of hemorrhages, edema, and infiltration.
lymphocytic.
During chickenpox or shingles, active replication of VZV can occur.
in other organs, such as the lung or the brain, but it is rarely found in
sick with intact immunity.
 PATHOGENESIS
RECURRENT INFECTION
Pulmonary affection is characterized by interstitial pneumonitis, formation
of multinucleated giant cells, intranuclear inclusions and
pulmonary hemorrhage.
Infection of the CNS leads to histopathological images of cuffs.
perivascular similar to those found in measles and others
viral encephalitis. The focal hemorrhagic necrosis of the brain,
characteristics of encephalitis due to HSV are rare in the infection by
the varicella-zoster virus.
 HERPES ZOSTER
Shingles is an sporadic disease caused by reactivation.
of the latent virus situated in the dorsal root ganglia.
Most patients do not have a history of recent exposure.
to other people with VZV infection.
The condition occurs at all ages, but its incidence is
maximum (five to 10 cases per 1,000 inhabitants) among the subjects who
they are found in the sixth decade of life or beyond.
 HERPES ZOSTER
Recent data suggests that in the United States, 1.2 appear each year.
millions of cases.
Recurrent herpes zoster is very rare, except in hosts.
immunocompromised individuals, particularly those with AIDS.
It is characterized by a unilateral vesicular rash in a dermatome.
minute associated with intense pain. The dermatomes T3 to L3 are the most
frequently involved.
If the ophthalmic branch of the trigeminal nerve is involved, shingles occurs.
ophthalmic.
 HERPES ZOSTER
Causative factors for the reactivation of VZV are not known. In children, the
reactivation is usually benign: in adults, it can be debilitating
due to the pain.
The onset of the disease is announced by pain in a dermatome, which
may precede the lesions by 48 to 72 hours; a erythematous rash
maculopapular quickly evolves into vesicular lesions
In the normal host, these lesions can remain in number.
reduced and continue training for only three to five days.
 HERPES ZOSTER
The total duration of the illness is generally seven to 10 days; without
embargo, it can take two to four weeks for the skin to return to
normality.
Patients with shingles can transmit the infection to individuals.
seronegative with the consequent chickenpox
In few patients, the characteristic location of pain has been reported.
in a dermatome with serological signs of herpes zoster without lesions
cutaneous, an entity
What is known as zoster without herpes.
 HERPES ZOSTER
If there is an attack on the branches of the trigeminal nerve, lesions may arise in
the face, mouth, eye or tongue.
Ophthalmic zoster is usually a debilitating condition that sometimes culminates in
blindness if antivirals are not administered.
In Ramsay Hunt syndrome, pain and vesicles appear on the
external auditory canal and the individual shows ageusia in the two thirds
anterior to the tongue, and facial paralysis on the same side.
There is an attack on the geniculate ganglion of the sensory branch of the facial nerve.
 HERPES ZOSTER
The most debilitating complication of shingles, both in hosts
healthy as in immunocompromised, it is the pain that accompanies neuritis
acute and postherpetic neuralgia.
Postherpetic neuralgia is rare in young people; however,
at least 50% of patients over 50 years old with shingles report
to feel pain in the affected dermatome months after it has
skin lesions have disappeared. Skin alterations are common.
sensory in the dermatome, causing hyperesthesia or hypoesthesia.
 HERPES ZOSTER
After a localized zoster, central nervous system involvement may occur.
Many patients without signs of meningeal irritation will have pleocytosis and elevation.
moderate levels of proteins in the CSF.
Symptomatic meningoencephalitis is characterized by headache, fever, photophobia,
meningitis and vomiting.

An uncommon manifestation of CNS involvement is vasculitis.

granulomatous with contralateral hemiplegia, which can be diagnosed by
cerebral arteriography.
Another neurological manifestation is transverse myelitis, with or without motor paralysis.
 HERPES ZOSTER
The formation of lesions continues for more than a week in most of the
sick people and the scabs do not appear until three weeks have passed since the
disease.
Patients with Hodgkin's disease and non-Hodgkin lymphoma have the risk
higher risk of suffering from progressive shingles. About 40% of these patients
they are characterized by a cutaneous spread of the disease
Patients with cutaneous dissemination have a 5 to 10% higher risk of suffering
neumonitis, meningoencephalitis, hepatitis, and other serious complications. Without
embargo, even in immunocompromised patients, disseminated zoster rarely
it is lethal.
 Shingles
People who receive hematopoietic stem cell transplants are
exposed to particularly high risk of infection by VZV. Of all cases of
infection by that virus after the transplant, 30% arose within a period of 12
months (half of them, in a period of nine months); 45% of the patients
those affected had dissemination to the skin or the viscera.
In such a situation, the mortality rate is 10%. Postherpetic neuralgia, the
scars and bacterial superinfection are especially common in the
infections by VZV suffered in the first nine months after the transplant.
In infected patients, the simultaneous onset of graft disease
host rejection (reverse rejection) increases the possibility of dissemination or of
death.
 DIFFERENTIAL DIAGNOSIS
Unilateral vesicular lesions distributed in a dermatome should lead to
ready for the diagnosis of shingles, although cases of shingles without have been described
rash.
Both infections by the herpes simplex virus and those caused by
Coxsackievirus can produce vesicular lesions in a dermatome. In such
cases, the studies of virological diagnosis and the fluorescent staining with
monoclonal antibodies are useful for achieving the correct diagnosis.
In the prodromal phase of shingles, the diagnosis may be
extraordinarily difficult and is established only when lesions appear or
through retrospective serological studies.
 LABORATORY
Confirmation is only possible through the isolation of VZV, or detection.
the VZV DNA by PCR
It can also be achieved with the Tzanck smear, although this method has little
sensitivity (around 60%).
Direct immunofluorescent staining of base cells can be used.
the lesions or the identification of viral antigens by other methods, although these
tests are not marketed.
The most widely used serological tests to assess the response of
host are the identification of immunofluorescent antibodies against the
membrane antigens of VZV, the fluorescent antibody test against the
membrane antigen (FAMA, immune adherence hemagglutination or
ELISA. The most sensitive ones seem to be FAMA and ELISA.
 TREATMENT
The baths with aluminum acetate for the management of shingles may
calm discomfort and clean.
Patients with shingles benefit from antiviral treatment, such as
it is demonstrated by the accelerated healing of injuries and the resolution of pain
associated with shingles using acyclovir, valacyclovir, or famciclovir. Acyclovir is
Administer a dose of 800 mg 5 times a day for seven to 10 days. Without
embargo, valaciclovir and Famciclovir are better
Famciclovir; the dose is 500 mg orally three times a day for seven days.
Valaciclovir accelerates the healing and resolution of pain associated with shingles.
faster than acyclovir. The dosage is 1 g orally three times a day for five to seven
days. Compared to acyclovir, both Famciclovir and valacyclovir
they offer the advantage of less frequent administration. These three drugs
they are currently off patent.
 TREATMENT
Severely immunocompromised hosts should be treated at the outset with
aciclovir IV, which reduces the occurrence of visceral complications but does not have
effect on the healing of skin lesions or pain. The dose is 10 mg/kg
every 8 hours for seven days.

For low-risk immunocompromised patients, the oral treatment with

Valaciclovir or Famciclovir seems beneficial.
If it is medically possible, it is desirable to reduce the immunosuppressive treatment.
together with the administration of acyclovir IV.
 TREATMENT
People with ophthalmic shingles should be referred immediately to a
ophthalmologist.
The treatment for this condition consists of the administration of analgesics.
for intense pain and the use of atropine. Acyclovir, valacyclovir, and famciclovir, all
they accelerate healing. Decisions about the use of glucocorticoids must be
taken by the ophthalmologist
The management of acute neuritis, postherpetic neuralgia, or both can be
particularly difficult.
In addition to the judicious use of analgesics, from non-narcotics to derivatives of
narcotics, various drugs such as Gabapentin, Pregabalin, hydrochloride of
amitriptyline, lidocaine (patches) and fluphenazine hydrochloride have been reported
as benefits to relieve pain.
 TREATMENT
In a study, early treatment with glucocorticoids administered in the
the course of localized shingles significantly accelerated improvements in quality
of life, such as returning to normal activities and doing without painkillers.
The orally administered dose of prednisone was 60 mg/day on days one to
seven, 30 mg/day on days eight to 14, and 15 mg/day on days 15 to 21. This regimen
it is suitable only for relatively healthy elderly with moderate pain or
intense in the presentation.
Patients with osteoporosis, diabetes mellitus, glucosuria, or hypertension may not
to be suitable candidates. Glucocorticoids should not be used without
combined antiviral treatment.
 PROPHYLAXIS
There are three methods for the prophylaxis of infections caused by VZV.
First
A live attenuated varicella vaccine is recommended.
The inactivation of the vaccine virus significantly reduces the occurrence of
herpes zoster after hematopoietic stem cell transplant.
individuals over 50 years, a VZV vaccine with 18 times the viral content of the
Oka vaccine reduced the incidence of shingles by 51%, the disease burden in
61% and the incidence of postherpetic neuralgia at 66%.
 PROPHYLAXIS

SECOND METHOD
Administer varicella-zoster immunoglobulin (VZIG) to individuals
susceptible individuals, who are at high risk of developing complications from chickenpox and
they have had significant exposure.
This product should be administered within 96 hours (preferably within
the 72 h) of the exposure.
 PROPHYLAXIS
Finally, antiviral administration can be undertaken for purposes.
prophylactics in high-risk individuals who are not eligible to receive the vaccine or
when the 96-hour interval since direct contact has been exceeded.
The treatment is started seven days after intense exposure. In that
the host is at a midpoint in relation to the period of
incubation.
The mentioned strategy notably decreases the intensity of the
disease, although it does not completely prevent it.