Herpes Zoster

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I. Introduction
II. Etiology
III. Pathogenesis
IV. Clinical Manifestations
V. Diagnosis
VI. Treatment
VII. Conclusion
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Scientists proved the infectious genesis of this disease through clinical data in
the 19th century. They determined that Herpes Zoster was accompanied by an increase
in body temperature, cyclic flow, and infectious nature (more than one person with the
virus in a family). As scientists have investigated, Varicella Zoster belongs to the group
of DNA-containing viruses, and its size is approximately 120-250 microns (Cohen et al.,
2013). The virion of this pathogen consists of DNA with a protein coat (the virion can
contain up to 30 proteins). The reproduction begins in the nucleus and is neutralized by
the serum of the convalescent (Cohen et al., 2013). It is crucial to note that serums
obtained during the acute period have the greatest activity, which may be because this
virus is a secondary manifestation of chicken pox. Moreover, at present, it is believed
that varicella causes this condition.
After assessing the nervous system of patients suffering from the virus and
carrying out pathomorphological and virological studies, scientists came to a conclusion
that Herpes Zoster infection was widely disseminated in the human body (Kuchar et al.,
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2016). Not only the spinal and cerebral ganglia are involved in the process but also the
substance of the spinal cord and brain. In addition, the shells of the brain are also
affected. When the spinal cord is infected, both the posterior and the anterior horns are
In addition, the virus can be found in saliva, tear fluid, and other secretions of the
mucous membranes. This manifestation of the disease allows concluding that Herpes
Zoster can infect parasympathetic effector cells and penetrate directly into the skin, and
when entering the nervous system, the virus localizes within the peripheral sensory
neuron and spreads to the central nervous system (Ferri, 2014). When Herpes Zoster
enters motor cells, myelitis occurs in the gray substance.
In general, this virus occurs in people who are exposed to the effects that
weaken their immunity. For instance, people suffering from leukemia,
lymphogranulomatosis, those receiving chemotherapy, people with AIDS, and many
others often develop Herpes Zoster (Kuchar et al., 2016). Older people also frequently
fall ill with this virus due to age-related decline in immune protection. The virus, which
has been in the human body for many years, proceeds from the latent phase to the
active one without causing any clinical manifestations (Cohen et al., 2013). During this
process, intervertebral ganglia and posterior roots are affected. In addition, the virus can
have an impact on vegetative ganglia, provoke meningoencephalitis, and influence the
functioning of internal organs (Cohen et al., 2013). Consequently, the nature of the
pathogenesis of Herpes of this type is complex since the virus shows not only
epitheliotropic but also neurotropic features.
Clinical Manifestations
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The clinical picture of the condition includes skin lesions and neurological
disorders. Many patients also exhibit common infectious symptoms such as fever,
enlarged lymph nodes, and alterations in cerebrospinal fluid. On the skin of the patient,
a specialist can observe erythematous spots of various shapes and small papules that
can also be felt when palpating the tissue (Juel-Jensen and Maccallum, 2013). In the
course of the disease, lesions of different sizes appear on the affected areas. They can
merge into one large vesicle or be isolated from each other. In some cases, a red rim
(irritation) can surround small bubbles. It is crucial that all elements of the rash are
always at the same stage of development; however, rashes can occur within a few
weeks in groups (Cohen et al., 2013). In this case, the groups will be at different stages
of disease evolvement.
As a rule, vesicles contain a transparent liquid, which gradually becomes turbid
and then turns into a crust. If this process has another course, then it is possible to
assume that the patient has the easy abortive form of Herpes Zoster, in which the
papules do not evolve into vesicles (Swash and Schwartz, 2013). Also, there is a
hemorrhagic form of the virus, in which lesions have a bloody liquid since the process
penetrates deep into the skin. With gangrenous course of the virus, the bottom of the
vesicles is necrotic, and it gradually transforms into a scar. Experts in the field suggest
that layering of bacterial infection plays a role in the genesis of this form (Cohen et al.,
2013). Nevertheless, further research is needed to confirm this hypothesis.
It is important to note that in addition to the symptoms of general into 

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