Herbal Remedies for Shingles

Fast Shingles Cure Ebook

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Herpes Zoster Shingles

Etiology Varicella zoster virus (VZV) causes chickenpox after primary infection, VZV remains dormant in sensory nerve roots for life, and reactivation results in herpes zoster (shingles). Reactivation may be idiopathic, but may occur with immunosuppression or stress. Increased incidence with increasing age more common in HIV & hematologic malignancy. Physical W i 3 4 d of onset of symptoms, clusters of erythema-tous papules and vesicles develop in a dermatomal distribution (thoracic cranial lumbar) new groups of lesions continue to appear over several days, eventually followed by crusting and desquamation over a 2 4-wk period. Generalized zoster Lesions involve several nonadjacent dermatomes and cross the midline. Complications Post-herpetic neuralgia (PHN), scarring, secondary bacterial infection. PHN occurs in 50 of pts 60 yr, & is present at 1 yr in 10 25 characterized by shooting or burning pain in the previously involved sites more common in older patients and when the trigeminal...

Herpes and Varicella Zoster

Dermis Multinucleated Cells Neutrophils

INTRODUCTION Herpes zoster (shingles) and varicella zoster (chickenpox) are both systemic infections with manifestations caused by herpes virus varicellae. The virus is an obligate human parasite requiring person-to-person transmission for its survival. Varicella most commonly occurs in children and is almost always a mild, self-limited disease however, when the disease occurs in adults it is often a much more severe process. Zoster, meaning belt or girdle in Greek, is felt to be a reactivation of a previous varicella infection within a single dermatome. Herpes zoster is most prevalent in middle to late adulthood however, it can occur in children and rarely even in infants, in whom it is usually a mild disease. Eyelid symptoms result from involvement of the first or ophthalmic division of the trigeminal (5th cranial) nerve and are seen in up to 10 of cases of zoster infections. Adults with herpes zoster are contagious during the early stages and often transmit the virus to susceptible...

Conditions That May Simulate Herpes Zoster

HSV in a linear distribution may be clinically impossible to distinguish from herpes zoster. Linear lesions are more common in children and with HSV on the extremities. Groups of lesions in different stages of evolution and pain or dysesthesia favor zoster. Culture, RIF, and PCR testing will distinguish the two. Vesicular poison oak (ivy, etc.) can be very similar to early zoster with minimal acute neuritis. Both may be linear and segmental, both may itch, and the morphology of the primary lesions is virtually identical. Pain or lack of pruritus favors zoster. Satellite lesions outside the primary dermatome or at distant sites favor rhus dermatitis. Tzanck smear helps to rapidly distinguish many cases, but it is not infallible. If the Tzanck smear is negative, RIF testing is indicated.

Isolation And Identification

The selection, transport, storage, and processing of the specimen are crucial for isolation attempts to be meaningful. The ideal specimen is taken from the site of the lesion or symptoms as early in the course of the illness as possible. The risk of fetal exposure or infection is determined by the status of the mother. Herpes I or II, enterovirus, rubella, and varicella-zoster virus (VZV) are some of the viruses that may be isolated and that are clinically relevant to the fetus or newborn. Other important agents such as hepatitis B virus, HIV, and parvovirus B-19 are either extremely difficult to culture or cannot be cultured.

Clinical Evaluation Of The Infant

The vesicular rash that occurs with HSV infection may be confused with the cutaneous manifestations of other infectious diseases, such as varicella-zoster virus infection, postnatally acquired enteroviral disease, and disseminated cytomegalovirus infection. Such distinctions are especially difficult when HSV assumes an atypical cutaneous presentation. Definitive confirmation of HSV disease can be achieved by culture of the skin vesicles. Noninfectious cutaneous conditions such as incontinentia pigmenti, acrodermatitis enteropathica, erythema toxicum, and neonatal melanosis should also be considered. Lesions associated with these diseases can often be distinguished rapidly from those caused by HSV by the presence of eosinophils on staining of a tissue scraping, by peripheral eosinophilia, and by appropriate viral cultures.

Natural Antibodies To Cytokines

Natural Ab against IFN in humans were first reported in 1981 as a case of neutralizing IFN-a Ab in a patient with varicella-zoster (13). Later, IFN-a Ab were found in patients with other viral infections, with neoplastic and autoimmune diseases, and in a patient with chronic graft versus host disease (6,7,13-24). The prevalence of IgG anti-IFN-a Ab in these patients is about 10 .

Timing And Routes Of Transmission

The usual incubation period for varicella is 14 days, with extremes of 10-28 days (1). The virus is transmitted by the airborne route its source is thought to be the respiratory tract and skin of an infected individual. Although the virus spreads within the body mainly by cell-to-cell contact, cell-free virus is required for transmission from one patient to another. The skin blisters of varicella and zoster are full of cell-free infectious virus. Fortunately, the virus is rather labile, so it is not spread on clothing or other fomites. Transmission requires direct contact with an infected individual in the early stages of illness. Persons with zoster are capable of transmitting VZV to varicella susceptibles, although zoster patients are thought to be less infectious than varicella patients. Persons who have had varicella who are exposed to patients with VZV infections may have a boost in immunity to VZV in one study, about one-third of parents exposed to their children with varicella...

Diagnostic Assays For Evaluation Of Infant And Mother

As mentioned in the preceding section, it is possible to make a diagnosis of VZV infection by laboratory means if the illness seems atypical. Usually, however, the clinical presentation is characteristic enough to make laboratory confirmation of chickenpox or zoster unnecessary. PCR is the best means for documenting the congenital varicella syndrome (7). This might be performed on a skin biopsy of an affected area or cerebrebrospinal fluid. It is also possible to detect VZV antigens when children thought to have this syndrome develop zoster (7). Some of these infants may develop very mild manifestations of zoster, consisting of only a few vesicular lesions. Laboratory confirmation of VZV infection may be very useful in such situations. 2. Lungu O, Panagiotidis C, Annunziato P, Gershon A, Silverstein S. Aberrant intracellular localization of varicella-zoster virus regulatory proteins during latency. Proc Natl Acad Sci U S A 1998 95 7080-7085. 4. Wharton M. The epidemiology of...

Discharge And Home Healthcare Guidelines

Herpes Zoster DRG Category 272 (Shingles) I I erpes zoster, also known as shingles, is a common viral skin eruption that is estimated to affect 300,000 to 500,000 persons a year in the United States. Approximately 95 of adults in the United States have antibodies to the varicella zoster virus (VZV), which means they have been exposed to it. The virus causes acute unilateral inflammation of a dorsal root ganglion. Each nerve innervates a particular skin area on the body called a dermatome, which bends around the body in a pattern that has been mapped corresponding to the vertebral source. Generally, herpes zoster eruptions occur in the thoracic region and, less commonly, affect a single cervical, facial (trigeminal nerve), lumbar, or sacral ganglion. 422 Herpes Zoster (Shingles)

Gender Ethnicracial And Life Span Considerations

Herpes zoster can occur at any age and in both genders, although it is uncommon in healthy children or young adults. Prevalence doubles in patients over the age of 50, and approximately 80 of all cases occur in people older than 20 years. It is hypothesized that 50 of all people who live to the age of 85 will have an attack and that 10 may suffer from more than one occurrence. Of those people who have been exposed to chickenpox, African Americans are 25 less likely than whites to develop herpes zoster.

Conditions That May Simulate Toxicodendron Dermatitis

Herpes Zoster Peculiar as it may seem, early acute zoster can be very similar to early toxicodendron dermatitis. Both eruptions can show a linear dermatomal pattern. Zoster with minimal acute neuritis may be pruritic rather than painful. Early toxicodendron dermatitis may exhibit only modest itching. Both conditions may have an orange-peel surface and similar-sized vesicles (see Photo 28). History of recreational exposure helps. Dysesthesia rather than itching, unilateral distribution, and umbilication of the vesicles suggest zoster. Intense pruritus, widespread satellites, and extension over the midline favors toxicodendron dermatitis. When in doubt, a Tzanck smear or rapid immunofluorescence (RIF) test for herpesvirus will help distinguish between them.

Chemical structure of virustatic antimetabolites

Because it undergoes bioactivation only in infected cells, where it preferentially inhibits viral DNA synthesis. (1) A virally coded thymidine kinase (specific to H. simplex and varicella-zoster virus) performs the initial phosphorylation step the remaining two phosphate residues are attached by cellular kinases. (2) The polar phosphate residues render acyclo-vir triphosphate membrane impermeable and cause it to accumulate in infected cells. (3) Acyclovir triphosphate is a preferred substrate of viral DNA polymerase it inhibits enzyme activity and, following its incorporation into viral DNA, induces strand breakage because it lacks the 3'-OH group of deoxy-ribose that is required for the attachment of additional nucleotides. The high therapeutic value of acyclovir is evident in severe infections with H. simplex viruses (e.g., encephalitis, generalized infection) and varicella-zoster viruses (e.g., severe herpes zoster). In these cases, it can be given by i.v. infusion. Acy-clovir may...

Risk Of Fetalneonatal Infection

Maternal Varicella

In addition to postnatal spread by the airborne route, varicella may spread by the transplacental route from mother to infant. The transmission rate by this route is thought to be 25-50 this is lower than the rate of transmission following household exposure, which is closer to 90 (7). Women with active varicella at term are at risk of infecting their infants by the transplacental route as well as from exposure to external lesions following the baby's birth. It appears, however, that infants infected transpla-centally are most at risk to develop severe varicella (see below). Fortunately, the immune response of the mother can have an impact in mitigating the course of varicella in the infant. Administration of varicella-zoster immune globulin (VZIG) can also compensate for this response in the infant. The risk of infection of the offspring if the mother has gestational zoster appears to be minimal. This probably reflects the fact that individuals with zoster usually have high titers of...

Clinical manifestation

Zoster oticus (geniculate zoster, zoster auris, Ramsay-Hunt syndrome, Hunt syndrome) Meniere disease, Bell palsy, cer-brovascular accident or abscess of the ear beginning with otalgia and herpetiform vesicles on the external ear canal, with or without features of facial paralysis, resulting from facial nerve involvement, auditory symptoms (e.g., deafness), and vestibular symptoms Disseminated zoster generalized eruption of more than i5-25 extradermatomal vesicles, occurring 7-i4 days after the onset of dermatomal disease occurs rarely in the general population, but commonly in elderly, hospitalized, or immunocompromised patients often an indication of depressed cell-mediated immunity caused by various underlying clinical situations, including malignancies, radiation therapy, cancer chemotherapy, organ transplants, and chronic use of systemic corticosteroids dissemination sometimes includes involvement of the lungs and central nervous system

Trigeminal Function and Pathology

Trigeminal neuralgia is the term given to the occurrence of intense pain, often in patients over 60 years, within one or more of the peripheral territorial divisions of the trigeminal system. The diagnosis involves the localization of the pain using a trigeminal sensory map this is useful in differentiating the pain from that involving, for example, the facial nerve. Infection of sensory nerve roots by herpes zoster causes painful shingles-like symptoms. In winter, inflammatory conditions cause nociceptive activity in afferents from the mucosa of the middle ear, larynx, pharynx, and pharyngotympanic tube. Dental pain is ascribed to nociceptive activity in trigeminal afferents, and frontal headache may be due to activation of trigeminal afferents activated by lesions distorting cerebral arteries.

Clinical Features

Specific skin lesions of AMoL and AMMoL present as violaceous to red-brown papules, nodules, and plaques (Figs. 1 and 2) (4,5,8). They are most commonly located on the trunk and extremities, but they can occur anywhere in either a grouped or a generalized pattern. Occasionally, a solitary red, sometimes, necrotic or ulcerated, nodule is found. The eruption may also involve the face and scalp. Mucocutaneous leukemic infiltrates were found in 24 of 81 patients with AMMoL (6). Leukemic gingival hyperplasia is a striking feature of AMoL and AMMoL. The infiltrated gingiva appear swollen, glazed, firm in consistency, and bright red to deep purple in color (6,8). The gums may completely cover the teeth. Deep oral ulcerations may occur in areas subjected to trauma such as the hard palate and tongue (Fig. 3). Specific skin lesions tend to localize at sites of trauma, burns, herpes zoster scars, and catheter placement (3,4,9). Unusual manifestations of AMoL and AMMoL include hemorrhagic bulla...

Indicated Supporting Diagnostic Data

A smear of material from a fresh, ruptured blister base is placed on glass slide and immediately stained with Giemsa or some similar stain. A positive smear will show her-pesvirus effect by the presence of keratinocytes with balloon nuclei and multinucleated giant cells with similar changes (see Photos 13,14). This test is rapid, inexpensive, and can be performed with equipment that is readily accessible. Sensitivity in experienced hands using material from a fresh vesicle approaches or exceeds 70 . In pustular lesions, sensitivity diminishes. This test does not distinguish between HSV-1, HSV-2, or herpes zoster virus. Biopsy of a herpetic lesion shows pathognomonic features, but is usually done only to investigate a lesion that is clinically atypical. Biopsy does not distinguish HSV-1 from HSV-2 or herpes zoster virus (HZV), and adds nothing if the lesions are clinically diagnostic.

Clinical Application Questions

A 75-year-old man in good general health presents at your office regarding a blistering rash on the right face and nose of 48 hours' duration. Lancinating pain was noted for 2 or 3 days before the rash. He also complains of diminished visual acuity in the right eye. You diagnose herpes zoster of the ophthalmic division of the trigeminal nerve. 1. What are the primary lesions of herpes zoster 2. What secondary lesions occur in herpes zoster

Postherpetic Neuralgia

This is a common and severe form of neuropathic pain in the elderly, caused by reactivation of the varicella zoster virus, usually a childhood infection. The incidence of postherpetic neuralgia (PHN) after herpes zoster varies between 9 and 15 , with 35-55 of patients continuing to have pain three months later, and 30 having intractable pain for one year. The dermatomal distribution and frequencies of PHN are as follows.

Face and Head Neuralgias

Paroxysmal deep ear pain with a trigger point in the ear of unknown etiology. It may be related to varicella zoster virus infection Continuous trigeminal pain in the hypalgesic or analgesic territory of the nerve. It occurs after percutaneous radiofrequency lesions or ophthalmic herpes zoster

Patients with Concomitant Disease Neurologic Diseases

Subsequent analysis revealed the largest group of conditions associated with constipation was neurologic and psychiatric disorders. A number of dramatic associations between constipation and neuropsychiatric and spinal diagnoses were observed, including herpes zoster (OR 5.1), depression (OR 6.5), multiple sclerosis (OR 3.9), Parkinson's disease (OR 3.2), vertebral column fracture (OR 10.1), and sprains and strains of the sacroiliac (OR 7.7) region.24 These associations suggest a potential link between central nervous system (CNS) function and constipation. Of particular interest was the strong association between herpes zoster and constipation. The zoster virus resides in the posterior root ganglia and can damage the ganglionic or spinal neurons. This association hints at a possible viral contribution to the onset of constipation among some patients with idiopathic constipation.

Lupus Erythematosus and Neutrophilic Dermatosis Sweets Syndrome

Neutrophilic dermatosis was first reported in association with SCLE by Goette in 1985. The next patient, described by Levenstein et al. (Levenstein et al. 1991), had a simultaneous appearance of both SCLE and Sweet's syndrome. The patient was later investigated for SS, and the latter was diagnosed in him. Therefore, the authors recommended that each patient with the clinical picture of both diseases be investigated for SS. Their suggestion is based on the article by Katayama et al. (Katayama et al. 1991), who found clinical evidence of annular erythema resembling Sweet's syndrome in 14 of 22 patients with SS. Choi and Chung (Choi and Chung 1999) described a patient with SLE, Sweet's syndrome and herpes zoster. SLE preceded for 3 months the appearance of Sweet's syndrome. Choi and Chung presumed that antibodies of SLE may have a role in the development of Sweet's syndrome because autoantibodies are incriminated in the pathogenesis of Sweet's syndrome. The patient described by Choi and...

Aging Effects by Disease Process

Eczemas Asteatotic dry skin, contact, seborrheic Infections Candidiasis, herpes zoster, onychomycosis, scabies Photodamage Actinic elastosis, colloid milium, Favre-Racouchot syndrome, freckling, photoaging (wrinkling, solar lentigo), poikiloderma of Civatte Premalignant Actinic keratosis, Bowen disease Malignancies BCC, lentigo maligna melanoma, MF, SCC Ulcerations leg, pressure decubitus Other Cutaneous horn, pruritus

Risk Of Maternal Infection During Pregnancy

There is little information on the risk of developing zoster during pregnancy. A few studies have suggested that the incidence is about the same as that of varicella in pregnancy (7). The course of illness is not more severe in pregnant women, and as is discussed next, there is little if any risk to the fetus and newborn infant. Fig. 1. Diagrammatic representation of transmission of varicella-zoster virus (VZV) and VZV antibody to the fetus in maternal varicella near term. (1) When the infant is born during the maternal incubation period, no varicella occurs unless the infant is exposed postnatally to the infection. (2) When the infant is born 0-4 days after onset of maternal varicella, disseminated varicella may develop because the infection will not be modified by maternal antibody. The onset of the varicella occurs between 5 and 10 days of age. (3) Infants born 5 days or more after maternal varicella receive maternal antibody, which leads to mild infection. This diagram is based on...


People infected with HIV may experience a flulike illness within a month or two of exposure to the virus many have no symptoms. This symptom-free period lasts from a few months to a decade, although the virus is actively multiplying, infecting, and killing immune system cells during this time. The only sign of this virulent activity may be a decline in blood levels of CD4 cells from a normal level of about 1,000. Once a person's CD4-cell count falls below 200, he or she is considered to have AIDS. By that time, other signs of the immune system's deterioration have appeared swollen glands, lack of energy, weight loss, frequent fevers and sweats, persistent or frequent yeast infections, skin rashes, short-term memory loss, frequent and severe herpes infections, or a painful nerve disease called shingles.

Clinical notes

1 Shingles and varicella-zoster The trigeminal ganglion, as any sensory ganglion, may be the site of infection by the herpes zoster virus causing shingles, a painful vesicular eruption in the sensory distribution of the nerve. The virus may have been latent in the ganglion following chickenpox (varicella).

Herpes Simplex

Herpes Zoster Lamina Histologica

HISTOPATHOLOGY The histological features of herpes simplex virus (HSV), varicella, and herpes zoster virus skin infections are similar. In HSV, the earliest changes are seen in the epidermal cell nuclei, which enlarge, develop a homogenous ground glass appearance, and have peripherally clumped chromatin. Changes begin along the basal epidermal layer and progress to involve all layers. Intraepidermal vesicles soon form secondary to ballooning and acantholysis of keratinocytes. Subepidermal vesicles may result from destruction of the basal layer of epidermis. Multinucleated keratinocytes are more conspicuous in lesions that have been present for several days. The histopathological clue to diagnosis is eosinophilic nuclear inclusions, which are more common in the multinucleated cells. Diagnosis is confirmed using immunohistochemistry. DIFFERENTIAL DIAGNOSIS The differential diagnosis includes acute stye, insect bite, chickenpox, herpes zoster, contact dermatitis, and ulcerative...

EE 477 Lung

Alveoli Electron Microscope

The cytoplasmic processes of adjacent endothelial cells partially overlap like shingles. The endothelium of the capillaries is not fenestrated. Note the numerous pinocytotic vesicles. Intercellular junctions seal the intercellular spaces. The alveolar epithelium spreads out in a thin layer ( anuclear layer of light microscopy). The cytoplasm contains few organelles.


Varicella zoster virus (VZV) - The virus causes chickenpox (varicella) in childhood, becomes latent in the dorsal root ganglia, and reactivates decades later to produce shingles (zoster) in adults. Subacute encephalitis develops against a background of cancer, immunosuppression, and AIDS, and death is common

Specific History

Zoster attacks may occur in children and young adults, but are quite rare. The incidence starts to climb during the fifth decade of life and peaks in the seventh and eighth decades. Severe or prolonged attacks, especially in young persons, should raise concern about concomitant illness and immune status. An attack usually confers lifelong immunity in an otherwise healthy person. Most cases of herpes zoster present with pain that is variously described as shock-like or a continuous burning sensation with hyperalgesia. Other patients experience less Uncomplicated zoster in children usually is mild and often painless. It can run its entire course in 2 weeks or less, and normally clears without sequelae. In young adults, the average course is 2 to 3 weeks long, pain is mild to moderate, and sequelae are rare. Elderly, debilitated, or immunologically compromised patients often have a course of 3 to 4 weeks or longer, and are more prone to complications. In uncomplicated cases, the...

Neonatal Evaluation

Infants with CCC typically present on the first day of life with a generalized rash consisting of erythematous macules, papules, or pustules on a 5- to 10-mm erythematous base. Generalized erythema can be seen initially, which then can evolve into a severe skin eruption with discrete papules or vesicles and sometimes bullae. The eruption occurs predominantly on the back, extensor surfaces, skin folds, palms, and soles, but the perineum area is spared. The rash in very low birth weight infants can rapidly progress to bullae, erosion, and desquamation resembling burns or scalded skin. This is associated with an extreme leukemoid reaction. The nails may also be involved and appear opaque, raised, and rough. With the loss of the skin barrier, the preterm infant is at risk for dehydration and secondary bacterial infections. The differential includes staphylococcal pustulosis, bullous impetigo, syphilis, neonatal pustular melanosis, toxic epidermolysis bullosa, incontinentia pigmenti,...


Sarcoid Granuloma Uveitis

DIFFERENTIAL DIAGNOSIS The differential diagnosis includes discoid lupus erythematosus, chalazia, hordeola, epidermal inclusion cyst, xanthelasma, lipoid proteinosis, amyloidosis, sebaceous cyst, lichen planus, erythema nodosum, tuberculosis, leprosy, syphilis and parasitic, fungal, viral (molluscum contagiosum, herpes simples and herpes zoster), or bacterial infections.

Infective stomatitis

Ballooning Degeneration Herpes

Herpes zoster of the trigeminal area Aetiology Reactivation of varicella-zoster infection, usually in the elderly long after the initial infection (chickenpox). The condition is especially common and severe in immunodeficiencies life-threatening in AIDS. Acyclovir is an effective anti-herpetic drug, but must be given in heavy dosage, especially to immunodeficient patients, and preferably intravenously. Trigeminal zoster affects the sensory area of skin and mucosa of the affected division, usually unilaterally and typically with aching pain.

Viral Infections

Herpes zoster (shingles) is caused by a reactivation of the varicellar-zoster virus which causes childhood chickenpox. Following an attack of chickenpox, the virus may remain dormant in a sensory root ganglion and may become reactivated at a later date, often many years later. Shingles is more common in the elderly, those with lymphoma, AIDS, or other causes of immunosuppression. The attacks often start with unilateral paresthesiae or pain and there may be accompanying systemic upset and fever. Vesicular lesions similar to those seen in varicella (chickenpox) develop within the course of the cutaneous nerve. Approximately 25 of patients develop a distressing postherpetic neuralgia that may persist for months, or sometimes years, after the rash has settled. Although topical therapy has little role in treating acute herpes zoster, topical antiseptics, such as Betadine paint may prevent secondary bacterial infection. Recently, a counterirritant cream containing capsaicin at a...


Since herpes simplex virus, cytomegalovirus, Epstein-Barr virus and varicella-zoster do not play an etiologic role in CL and since HTLV-I virus, due to its lack of thymidine kinase, cannot activate ACV, the drug does not act in its usual antiviral role. Instead, the following mechanisms may explain its possible effectiveness in lympho-proliferative diseases a direct cytopathic effect activation of ACV by the thymidine kinase of viruses not yet detected in cutaneous lymphoproliferative disorders or ACV activation by cellular thymidine kinase, which has been found to be elevated in lymphoproliferative disorders (40). We are aware of 23 patients (10 of our own, 13 reported in personal communications and in the literature) suffering from lymphoproliferative diseases who were treated with ACV. In 5 patients (3 of 18 with cutaneous T-cell lymphomas, 2 of 5 with lymphomatoid papulosis) , partial remission was achieved (40). Intravenous acyclovir for treatment of disseminated herpes zoster...

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