Friday, December 26

Congenital hypertrichosis

   ›      ›   Congenital hypertrichosis.
What is congenital hypertrichosis?
Hypertrichosis is the excessive growth of hair over the body. Congenital hypertrichosis (CH) is the presence of excessive hair growth at birth.
Congenital hypertrichosis may be present as an inherited genetic disorder. Congenital hypertrichosis may also occur as a result of spontaneous mutation during fetal growth. CH may concur and coexist with many hereditary medical conditions.

Types of congenital hypertrichosis

The excessive growth of hair is classified as congenital hypotrichosis when it is present at birth. Acquired hypotrichosis is the appearance of excessive hair growth later in the life. CH may involve terminal, Vellus or lanugo hair. CH may be generalised covering the entire body or localized and circumscribed. Some of the many forms of congenital hypertrichosis are discussed below.

Generalized congenital hypertrichosis (GCH)

Various types of genetic inheritance and spontaneous mutation can cause GCH. The entire body may be covered sparing, mucous membranes, palms and soles. The excessive growth of hair may involve either terminal hair or lanugo hair.

Congenital hypertrichosis lanuginosa (CHL)

In congenital hypertrichosis lanuginosa, the entire body of the newborn is covered by the lanugo hair.
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Only the mucous membranes, palms, soles, dorsal terminal phalanges, labia minora, prepuce, and glans penis are spared. The CHL may occur as an autosomal dominant inheritance or as a sporadic mutation. It is believed that mutations of gene in 8q22 of chromosome 8 is the cause.

Ambras Syndrome is an extremely rare type of congenital hypertrichosis lanuginosa, characterized by the vellus-type hair covering the entire body. Abnormalities like dental anomalies, triangular, coarse face, bulbous nasal tip, delayed tooth eruption, absence of teeth, glaucoma, pyloric stenosis, photophobia are associated with Ambras syndrome.

X-linked generalized congenital hypertrichosis (X-GCH)

X-GCH occurs very rarely. The excessive terminal hair growth was mapped to chromosome Xq24-q27.1 in a Mexican family. Terminal hair covers the face, trunk and limbs, sparing mucosa, soles and palms. It may be associated with medical conditions such as, gingival hyperplasia, scoliosis, and spina bifida.

Cornelia de Lange Syndrome (CDLS)

CDLS is a genetic disorder present from birth. The disorder can occur due to mutation in genes NIPBL, SMC1A or SMC3. The disorder is characterized by thick and convergent eyebrows (synophrys), thick and long eyelashes, and low hairline. Vellus hair hypertrichosis of trunk, posterior neck, sacrum and elbows is seen. It may be associated with abnormalities such as cutis marmorata, upturned nostrils, depressed nasal bridge, low set ears, small and irregular teeth, high palate and bifid uvula. The patients may have short and abnormal arms, hands and feet. They may suffer from severe mental retardation.

Localized congenital hypertrichosis

Congenital localized hypertrichosis is a notable feature of congenital melanocytic nevus, congenital Becker nevus, Hypertrichosis cubiti, smooth muscle hamartoma and nevoid hypertrichosis. The localized abnormal hair growth may be at a single site or just a few sites.

Congenital melanocytic nevus (CMN)

Congenital melanocytic nevus (CMN) is a type of melanocytic nevus found in newborns. CMN is usually larger than the acquired melanocytic nevus. The lesion may be covered by excessive growth of terminal hair. There are three types of CMN. Small-sized congenital nevocytic nevus has a diameter less than 2 cm. Medium-sized CMN has a diameter more than 2 cm but less than 20 cm. Nevus pigmentosus et pilosus (giant nevus) is more than 20 cm in diameter with dark pigment and terminal hypertrichosis.

In about 2% to 45% of patients with giant melanocytic nevi at birth, neurocutaneous melanosis is involved. Neurocutaneous melanosis (NCM) is characterized by melanocytic nevi on the skin and melanocytic tumors in the leptomeninges of the central nervous system. Nearly half of the patients with neurocutaneous melanosis may develop malignancy in the form of leptomeningeal melanoma. Early embryonic, postzygotic somatic mutations in the NRAS gene are implicated in the pathogenesis of NCM.

Hypertrichosis cubiti

Hypertrichosis cubiti, also known as hairy elbows syndrome, is a rare symmetric, localized, congenital, circumscribed hypertrichosis with long vellus hair occurring on the elbow (extensor surfaces). Both familial and sporadic forms have been reported. Partial or complete resolution during puberty is reported. A very high percentage of hair in the elbow appear to be in the anagen phase.

The hairy elbows syndrome may in some cases have associated abnormalities. Short stature or other physical abnormalities such as dysmorphic facial features, microcephaly, joint hyperlaxity, thin-long-webbed neck and mental retardation have been associated with hypertrichosis cubiti. Autosomal dominant as well as autosomal recessive inheritance is postulated in the pathogenesis.

Congenital smooth muscle hamartoma

Smooth muscle hamartomas are caused by the benign proliferation of smooth muscle bundle within the dermis. It is an uncommon malformation of the pilar smooth muscle, often involving the back and lower limbs. These lesions typically appear as a skin colored or lightly pigmented patch or plaque with hypertrichosis of vellus hair.

Becker's nevus

Becker's nevus is due to an overgrowth of the epidermis, melanocytes and hair follicles. Though most often it is seen as an acquired disorder with terminal hypertrichosis, it may also be present at birth. The pathophysiology of Becker's nevus remains unclear. A case was reported wherein the disorder had genetic association. A 16 month boy had a lesion on his right shoulder and a similar lesion existed on the right shoulder of his father.

Nevoid Hypertrichosis

Nevoid Hypertrichosis usually appears as a solitary patch of terminal hair without other abnormalities anywhere in the body. If present in lumbosacral area, differential diagnosis is required to rule out faun tail deformity conditions like, spina bifida occulta and diastematomyelia.

Lumbosacral hypertrichosis

Lumbosacral hypertrichosis is also known as faun tail deformity. This malformation is associated with cutaneous anomalies such as sacral dimple, lipoma, port-wine stain, hypertrichosis or dermoid cyst. It is also associated with bone and spinal cord defects such as spina bifida occulta, diastematomyelia, myelomeningocele, and vertebral abnormalities.

Hairy palms and soles

Hairy palms and soles is a bilaterally symmetric, hereditary hypertrichosis affecting the palms and soles. It is an autosomal dominant inheritance. The hair follicles are normal and the children and women have vellus hair. The excessive hair growth is androgen-sensitive and in boys the vellus hair becomes terminal at puberty.

Anterior cervical hypertrichosis

The cause of this congenital disorder can be autosomal dominant, autosomal recessive or X-linked chromosomal mutations. Excessive hair growth is observed on the neck of the affected individuals. In the autosomal recessive mutation, peripheral neuropathy is observed.
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Reference:
1.Trüeb RM. Causes and management of hypertrichosis. Am J Clin Dermatol. 2002;3(9):617-27.
2.Goel N, Rajaram S, Gupta B, Gupta K. Familial congenital generalized hypertrichosis. Indian J Dermatol Venereol Leprol 2013;79:849.
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Current topic in natural skin care: Congenital hypertrichosis.
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Sunday, December 21

Hypertrichosis causes

   ›      ›   Hypertrichosis causes.
Hypertrichosis, excessive growth of hair, is caused by several factors. Hypertrichosis may be congenital, being present at birth. It may also be acquired later in the life.
Hypertrichosis presence at birth is caused by congenital syndromes, autosomal mutations and hereditary diseases. Acquired hypertrichosis is induced by malignancies, endocrine anomalies and certain therapeutic medications.

The excess hair growth may be generalized, affecting the whole of the body or localized to form well defined patches. Hypertrichosis may involve all the three types of hairs; vellus hair, lanugo hair or terminal hair. The various types of excess hair growth and their causes are discussed below.

Common causes of hypertrichosis

Common health conditions like hormonal, endocrine disturbances, systemic illness and certain diseases can induce excessive growth of hair.
Some of the common factors inducing acquired hypertrichosis are:
  • hypothyroidism,
  • hyperthyroidism,
  • anorexia nervosa,
  • porphyria cutanea tarda,
  • pituitary abnormalities,
  • hypothalamic abnormalities,
  • HIV/AIDS,
  • Becker’s nevus,
  • cancers,
  • head injury,
  • injury,
  • friction and
  • inflammation.

(CH)

Congenital syndromes, autosomal mutations and hereditary diseases cause CH.
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  • Congenital erythropoietic porphyria (Gunther disease) is a rare, autosomal recessive metabolic disorder affecting heme, caused by deficiency of the enzyme uroporphyrinogen cosynthetase. Exposure to long-wave ultraviolet light causes vesiculobullous lesions, hyperpigmentation and excessive growth of hair.
  • CH lanuginosa is considered to be due to autosomal dominant mutation on chromosome 8q.
  • Generalized CH is considered to be due to autosomal dominant mutation on chromosome x24-q27.1.
  • CH generalized terminalis is due to a mutation in MAP2K6 on chromosome 17.
  • Localized CH may be associated with nevus, especially melanocytic naevus.
  • Abnormal localized lumbosacral hypertrichosis or faun-tail nevus is usually a marker for spinal dysraphism like spina bifida occulta or diastematomyelia.

Drug induced hypertrichosis

Many medications have been found to induce excessive hair growth. Some of the medications and chemicals inducing excessive hair growth are listed below:
  • Topical minoxidil,
  • Glucocorticoids,
  • Anticonvulsants,
  • Cyclosporine,
  • Diazoxide,
  • Psoralen,
  • Streptomycin,
  • Latanoprost,
  • Acetazolamide and
  • Phenytoin.

Treatment options

There is no treatment for congenital forms of excessive hair growth. Acquired forms resolve when the factors responsible excessive hair growth are removed or discontinued. Hair removal methods like shaving, waxing, laser hair removal and electrolysis are the treatment options available for congenital excessive hair growth.
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Reference:
1.Trüeb RM. Causes and management of hypertrichosis. Am J Clin Dermatol. 2002;3(9):617-27.
2.Goel N, Rajaram S, Gupta B, Gupta K. Familial congenital generalized hypertrichosis. Indian J Dermatol Venereol Leprol 2013;79:849.
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Friday, December 19

Lanugo hair - Lanugo baby

   ›      ›   Lanugo hair - Lanugo baby.
What is lanugo hair?
Lanugo is the fine, soft and downy hair found on the body of a fetus or newborn baby.
The word lanugo is derived from the Latin word "lana", meaning wool. It is the first hair produced by the fetal hair follicles at about five months of gestation. Lanugo may also appear as a congenital defect in a baby or as an after effect of eating disorders.

The development of fetal lanugo

During fetal development, ectoderm forms the surface epidermis and contributes to different associated skin structures like hair follicles, nails and glands. By the forth month of gestation, cords of ectoderm cells extend into mesoderm forming epithelial columns. These cells give rise to hair follicles, sebaceous and sweat glands. At the same time the melanocyte stem cells, which have neural crest origin move into the base of the follicle forming cord.

During fifth month of gestation, lanugo growth gets initiated at the base of the cord and the lateral outgrowths of the cord give rise to sebaceous glands. The sebaceous glands start producing vernix (vernix caseosa).
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Other ectoderm cords elongate and coil to form the sweat glands. By the sixth month of gestation, the body is fully covered by lanugo and has considerable deposit of vernix caseosa.

The lanugo growth over the entire body is at the same rate and the hairs appear to be of the same length. By the eighth month of gestation, the fetal skin is completely coated with vernix and the lanugo starts disappearing. By the ninth month of pregnancy, most of the embryonic hair is shed. Premature babies born before the complete shedding are seen still covered with embryonic hair.

Sometimes in full term babies also the lanugo is seen which may eventually disappears of its own accord within a few days or weeks. The persisting fine downy hair is completely shed when the baby is three to four months old. It is usually replaced by short, soft and near transparent vellus. It is also interesting to note that babies nearing their term in the womb swallow the lanugo along with amniotic fluid. The meconium (first stool) from newborn babies contains lanugo.
hair development stages

Function of fetal lanugo

Vernix caseosa is the waxy, cheese-like substance secreted by the fetal sebaceous glands to cover the fetal skin. Its secretion starts around 18 weeks into pregnancy and is seen coating the newborn babies. Vernix functions as a protective coating against the watery environment. Lanugo has the important role of binding the vernix to fetal skin.

Lanugo and eating disorders

Lanugo is observed in patients suffering from malnutrition and eating disorders like anorexia nervosa. Anorexia nervosa is characterized by a fierce quest for thinness in addition to having an intense fear of gaining weight. Most of the anorexia nervosa patients are adolescents, especially girls. Excessive preoccupation with body shape, self-image, perfectionism and negative self-evaluation leads to unregulated dieting, weight loss and malnutrition.

These patients require medical, nutritional and psychiatric support. Anorexia nervosa patients are known to grow fine, downy lanugo on the sides of the face, arms, and back. The condition differentiated from hirsutism, as in hirsutism only terminal hair is involved. Completely treating the anorexia nervosa can resolve the skin condition.

Lanugo in malignancy

Acquired lanugo-type hypertrichosis or hypertrichosis lanuginosa acquisita is sometimes associated with malignancy. Some patients affected by cancers have been observed to have such manifestations, though they may be lanugo-free as babies. The study by Slee PH et al concluded that malignancy associated lanugo is predominant in female patients in the age group of forty years to seventy years. It is observed in patients with colorectal cancer, lung cancer and breast cancer. They stressed that "the appearance of lanugo-type hypertrichosis in body areas previously perceived by patients as 'hairless' is highly indicative of internal malignancy."

Congenital lanugo in babies?

Hypertrichosis lanuginosa congenita, congenital lanugo-type hypertrichosis, is a rare skin disorder seen in some newborn babies. Vibhu Mendiratta et al in their case study on "Hypertrichosis lanuginosa congenita" reported about a three months old male baby. Babies born with this autosomal dominant cutaneous disorder, present lanugo hair covering the entire body. The palms, soles of the feet and mucous membranes are spared.

In these babies the hypertrichosis condition may increase or decrease with age. Lanugo babies may continue to have this type of hypertrichosis even after puberty. Hypertrichosis lanuginosa congenita may be associated with several other congenital defects in babies. In this particular case the baby was without any other manifestations of congenital defects.
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Reference:
1.Jeffrey M Brown, Philip S Mehler, R Hill Harris. Medical complications occurring in adolescents with anorexia nervosa. West J Med. Mar 2000; 172(3): 189–193.
2.Mendiratta V1, Harjai B, Gupta T. Hypertrichosis lanuginosa congenita. Pediatr Dermatol. 2008 Jul-Aug;25(4):483-4.
3.Slee PH, van der Waal R, Schagen van Leeuwen JH, Tupker RA, Timmer R, Seldenrijk CA, van Steensel MA. Paraneoplastic hypertrichosis lanuginosa acquisita: uncommon or overlooked? Br J Dermatol. 2007 Dec;157(6):1087-92. Epub 2007 Oct 17.
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Image source: https://embryology.med.unsw.edu.au/embryology/index.php/File:Hair_development_stages.jpg | Dr Mark Hill | Creative Commons Attribution License
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Thursday, December 18

Herpes zoster infection

   ›      ›      ›   Herpes zoster infection.

Herpes zoster (shingles) infection

Zoster infection is caused by the chickenpox virus, known as varicella-zoster virus (VZV). When a person is exposed to VZV for the first time, he develops chickenpox with symptoms of fever, widespread rash and blisters.
The individual develops partial immunity and the symptoms resolve by 10-15 days. However the virus is not completely eliminated from the body. The virus enters the nerve cells and lies dormant.

Once a person contracts chickenpox, he remains infected for life, though being asymptomatic. In some individuals the dormant virus gets reactivated causing blisters and pain in the dermatomic area. The exact cause of the reactivation of the virus is not known. Recurrent outbreaks of herpes zoster are rare and their occurrence indicates certain underlying serious multiple medical problems.

The reactivated virus starts replicating itself and the virions move along the nerve and reach the dermatome. After reaching the skin they cause rash and then blisters. The infection damages the nerve fibers and causes neuralgic pain. Though the blisters rupture and heal by about 2-3 weeks, the postherpetic neuralgia may last for several days, or last many months, even years.

shingles on neck
herpes zoster infection on neck
Zoster infection can cause chickenpox in people who have not contracted chickenpox by that time. Skin injury at the dermatome sometimes revives the zoster. Secondary bacterial/fungal diseases can occur if the blister area is injured by scratching.

Herpes zoster in old age

Old age associated conditions and overall decrease in immunity may be the primary triggering factors for the revived infection. Old age conditions involving poor nutrition, protein malnutrition, decreased absorption and assimilation can lead to high susceptibility. With the increase in age the severity of the episode and intensity of neuralgic pain may increase many fold.

Immunosuppression

Individuals with immunosuppressive diseases and immunodeficiency disorders, such as hypogammaglobulinemia, agammaglobulinemia, HIV/AIDS and many types of cancers can suffer from recurrent VZV infection. Individuals with generalized autoimmune diseases are also vulnerable.

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Patients taking immunosuppressive medicines as in the case of organ transplant are also vulnerable to shingles attack. The long term use of corticosteroids can also trigger zoster.

Complications

VZV infection sometimes involves nerves supplying the face and serious condition like herpes zoster ophthalmicus occur causing ophthalmic complications. The eye infection is a medical emergency which can lead to vision loss. Similarly affecting the inner ear, herpes zoster oticus can lead to hearing loss. Manifestation on facial nerves can also lead to partial/total facial paralysis.
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1.Zostavax (Herpes Zoster Vaccine) Questions and Answers (FDA)
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1.Image source: http://en.wikipedia.org/wiki/File:Herpes_zoster_neck.png
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Saturday, December 13

Herpes zoster symptoms

   ›      ›   Herpes zoster signs and symptoms.
Herpes zoster (shingles) is a contagious disease caused by the varicella zoster virus (VZV). Herpes zoster manifests with typical symptoms.
It is characterized by a group of small inflammatory blisters with neuralgic pain. The primary infection by varicella zoster virus manifests as varicella (smallpox) with the symptoms of widespread vesicular rash and fever.

Though the patient recovers from the chickenpox after 10-15 days, the virus is not completely eliminated from the body. The herpes zoster virus enters the nervous system and lodges itself in the cerebral ganglia or dorsal root ganglia. It attains dormancy, without causing any symptoms, lasting for a few months to several years or even a lifetime.

The varicella zoster virus, due to unknown reasons, reemerges as shingles in some individuals. About 20% of those who had chickenpox in their childhood develop zoster. Zoster blisters erupt unilaterally along the path of innervation by the affected ganglia, affecting one side of the body, most often affecting the torso, neck, arms, and legs.

diagram showing the progression of symptoms of herpes zoster infection
Herpes zoster symptoms
The above diagram shows the stages in the progression of herpes zoster symptoms.
1. Itching and burning sensation followed by inflamed patches of bumps.
2. The bumps turn into blisters.
3. The blisters fill with fluid and burst.
4. healing phase starts and the blisters crust and disappear.
5. Persisting postherpetic neuralgia for a few days to several months.
Zoster with its symptoms can develop in varicella affected children as well as adults.
shingles on neck
herpes zoster infection on neck
However individuals above fifty years of age are more prone for , probably due to their decreasing immunity. With increase in age there may be recurrent episodes. Individuals with weakened immune system, under immunosuppressive medications and newborn are under high risk.

Herpes zoster symptoms

The reactivated virus particles move along the nerve and reach the skin dermatome causing a stripe of blisters and pain. The usual sequence of events and symptom progression in herpes zoster are as follows.
  • Pain, inflammation near the region of affected nerve roots. Some individuals may develop fever.
  • Within a few hours the nerve supplying to the skin from the nerve root gets inflamed with symptoms of pain and burning sensation along its length.
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  • After two or three hours the patch of skin where the bumps and blisters will emerge becomes itchy with slight burning sensation. This area of skin is most likely to be the most affected area during the earlier varicella episode.
  • If the itchy skin is left alone without scratching bumps may appear within two or three hours. If the itchy skin is scratched, bumps will appear immediately.
  • Symptoms like severe burning pain (due to nerve damage) and itching are followed by the bumps turning into blisters.
  • Getting filled up with lymph, the blisters grow, become hard and then burst, spilling the contents.
  • The VZV virus can travel along the nerves and cause similar symptoms in the adjacent area of skin.
  • The burst blisters form crust and the crust may fall off in a week.
  • After the herpes zoster episode the symptoms like neuralgic pain along the nerve and the blister area may continue for sometime.
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Reference:
1.Zostavax (Herpes Zoster Vaccine) Questions and Answers (FDA)
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1.Image source: http://en.wikipedia.org/wiki/File:A_Course_of_Shingles_diagram.png
Author: FDA | License: public domain.
2.Image source: http://en.wikipedia.org/wiki/File:Herpes_zoster_neck.png
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Friday, December 12

Is herpes zoster contagious? - Herpes zoster causes and transmission

   ›      ›   Herpes zoster causes.
Herpes zoster, also known as shingles, zona or zoster is a contagious skin infection caused by the varicella-zoster virus (VZV or human herpesvirus type 3).
The primary infection caused by the VSV is the chickenpox (varicella). Varicella usually occurs in the childhood manifesting as widespread vesicular rash. Later on reactivated virus causes herpes zoster. The zoster rash appears on the respective dermatome, i.e., the area of skin to which the affected spinal nerve is supplying.

Herpes zoster is contagious

The virus after causing highly contagious chickenpox enters the nervous system and remains for life in a dormant condition in the sensory dorsal root ganglia or cranial nerve ganglia. The affected individuals develop partial immunity and the virus is not totally eliminated by the immune system. The virus may get reactivated anytime and cause zoster in the affected person and cause varicella in others coming under direct contact with lesions.

Cause of herpes zoster

After years of dormancy, VZV may get reactivated in some persons and cause vesicles. The exact cause of relapse to active phase is not known. However the main triggering factor may be immunodeficiency and immunosuppression. After activation, the virus particles move down the nerve and reach the area of skin supplied by the nerve and cause blisters. The occurrence of this contagious disease is more common in old age. Before the advent of vaccination for VZV, most of the adults might have contracted chickenpox in their childhood. Though the virus is dormant in them, they are carriers of the virus.
diagram showing the stages in the course of herpes zoster infection
course of herpes zoster infection
Stages in the progression of herpes zoster are given in the above image.
shingles on neck
herpes zoster on neck

  • 1.Initially there is itching and burning sensation followed by the appearance of a cluster of small bumps.
  • 2.These swellings turns into small blisters.
  • 3.The blisters fill with lymph and break open exuding the contents. They may get infected and pus may form.
  • 4.The blisters start healing, crust over and disappear.
  • 5.Postherpetic neuralgia may occur due to nerve damage and persist for sometime after healing.

Herpes zoster transmission

The transmission of either chickenpox or zoster is by direct or indirect contact with fluids exuding from the blisters or with crust formed during healing. The varicella may also get transmitted by breathing infected coughed droplets. Transmission of the infection to others occurs when the virus gets reactivated. Transmission of the VZV to those who did not have chickenpox earlier in their life will cause chickenpox in them.
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Transmission of this contagious disease commonly occurs from affected grandparents to unimmunized grandchildren resulting in varicella.

Risk factors

  • The occurrence of zoster is most common after 50 years of age. The risk of developing the contagious blisters increases with the increase in age.
  • Patients taking high-dose corticosteroids for some other health condition are at risk.
  • Patients taking immunosuppressant drugs for some other condition like organ transplant are also at risk.
  • Patient affected by cancers, AIDS and autoimmune diseases are at risk.
  • Patients undergoing chemotherapy or generalised radiotherapy are at the risk of reactivated herpes zoster.

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Reference:
1.Zostavax (Herpes Zoster Vaccine) Questions and Answers (FDA)
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1.Image source: http://en.wikipedia.org/wiki/File:A_Course_of_Shingles_diagram.png
Author: FDA | License: public domain.
2.Image source: http://en.wikipedia.org/wiki/File:Herpes_zoster_neck.png
Author: John Pozniak | License: CC BY-SA 3.0
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