Your SlideShare is downloading. ×
0
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Dermatology 5th year, 2nd lecture (Dr. Ali El-Ethawi)

1,883

Published on

The lecture has been given on Oct. 31st, 2010 by Dr. Ali El-Ethawi.

The lecture has been given on Oct. 31st, 2010 by Dr. Ali El-Ethawi.

Published in: Health & Medicine, Technology
0 Comments
2 Likes
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
1,883
On Slideshare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
92
Comments
0
Likes
2
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Viral diseases of the skin &mucous membrane DR. Ali El-ethawi Specialist Dermatologist M.B.CH.B , F.I.C.M.S, C.A.B.D 5th class lecture
  • 2.  Viruses are not cellular organism because they do not have functional ribosome's or other cellular organelles,  i.e; obligate intracellular parasite because their replication depend on host cell Viral genome consist of only single type of nucleic acid (RNA ,DNA) Two main groups of viruses are distinguished: DNA and RNA.  DNA virus types are herpesvirus, poxvirus ,parvovirus, papovavirus and adenovirus.  RNA viruses are picornavirus, coronavirus paramyxovirus, orthomyxovirus, togavirus, reovirus, retrovirus, arenavirus and rhabdovirus  Some viruses are distinguished by their mode of transmission: arthropod-borne viruses, respiratory viruses, fecal-oral or intestinal viruses, venereal viruses, and penetrating wound viruses.
  • 3.  Viral infections of skin and mucosa produce a wide spectrum of clinical manifestations.  Some Viruses not causing any clinical lesions. (produce latent, but lifelong infection)  Some cause benign epithelial proliferations, i.e., warts.  Some viruses cause febrile illness with exanthems.  In the setting of immunocompromise, these viruses can become active and cause disease with significant morbidity and mortality rates.
  • 4. •are medium-sized viruses dsDNA replicate in the cell nucleus. •produce latent, but lifelong infection by infecting immune cells and nerves. •Intermittently have replicative episodes with amplification of the viral numbers in anatomic sites from one host to the next (genital skin, orolabial region). The vast majority of infected persons remain asymptomatic. Viruses in this group are ; herpes simplex virus (HSV)1,2 varicella zoster virus (VZV) cytomegalovirus (CMV) Epstein-Barr virus (EBV) Human herpesviruses (HHV)-6, -7, and -8 Herpesvirus simiae (B virus) HERPESVIRUS GROUP
  • 5. Herpes simplex viruses (HSV)  are common human DNA viral pathogens that intermittently re-activate.  The virus is ubiquitous and carries continue to shed virus particles in their saliva &tears.  There are two types of HSV: HSV-1 and HSV-2.  HSV-2 usually causes genital infection, whereas HSV-1 is mostly are extragenital ,but both can infect oral and genital areas.  cause acute and recurrent infections.  Most of the adult population is seropositive for HSV-1, and the majority of infections are acquired in childhood while acquisition of HSV-2 correlates with sexual behavior.
  • 6. Clinical presentation HSV infections are classified as either primary “(first episode )“ or "recurrent." 1. primary infections It is often asymptomatic or not recognized in most cases, but they can also cause severe disease as acute gingivostomatitis ; is the recognizable manifestation of primary type-1 infection in children. The onset is often accompanied by high fever, malaise and cervical lymphadenopathy,. The herpetic lesions in the mouth are usually broken vesicles that appear as erosions or ulcers covered with a white membrane. The erosions may become widespread on the oral mucosa, tongue, and tonsils., The duration is 1 to 2 weeks. Primary type -2 virus infection Usual transmitted sexually often asymptomatic or , cause multiple & painful Genital & perianal blisters which rapidly ulcerate
  • 7. 2.Recurrent infections Most recurrences are not symptomatic (asymptomatic shedding), with most transmissions occurring by asymptomatic shedding. These strike in roughly the same place each time .They may ppt. by RTI, UVR ,menstruation or even stress Common site face ,lips (HSV-1) and the genitals (HSV-2) But lesions can occur any where .  HSV can also cause diseases involving the eye, central nervous system, and neonatal infection. Cellular immunity defects are a risk factor for severe and disseminated disease.
  • 8.  Genital herpes ;is the most prevalent sexually transmitted disease worldwide and is the most common cause of ulcerative genital disease, and it is an important risk factor for acquisition and transmission of human immunodeficiency virus. is spread by skin-to-skin contact, usually during sexual activity. The incubation period averages 5 days. Active lesions of HSV-2 contain live virus and are infectious .  Herpetic Whitlow Herpes simplex of the fingertip  HSV infection may uncommonly occur on the fingers or periungually.  Herpes Gladiatorum ; Cutaneous herpes, HSV-1 infection is highly contagious occur in athletes involved in contact sports is transmitted via direct skin-to-skincontact. This is a recognized health risk for wrestle
  • 9. Complications 1.Eczema herpeticum (Kaposi's varicelliform eruption) 2. Recurrent Erythema multiforme 3. Disseminated herpes simplex 4.Herpes encephalitis or meningitis 5. Herpes simplex infection of the eye can cause recurrent dendritic ulcer leading to corneal scarring Diagnosis; depending on the clinical presentation and no need for investigation ( Direct Microscopy (tzanck smear) ,viral culture, polymerase chain reaction and serology). Treatment; Regimens and dosages vary with the clinical setting by acyclovir, valacyclovir, or famciclovir. Resistance is rare in other than immunocompromised patients. Recurrence can be prevented by long term of treatment at lower dose (400mg/d)
  • 10. Varicella-Zoster Virus Infections (VZV)  It is a human herpes virus that infects 98% of adult populations.  Primary VZV infection (varicella or chickenpox) is nearly always symptomatic  characterized by disseminated pruritic vesicles.  During primary infection, VZV establishes lifelong infection in sensory ganglia.  When immunity to VZV declines, VZV reactivates within the nerve cell, traveling down the neuron to the skin, where it erupts in a dermatomal pattern [herpes zoster (HZ), or shingles].  In the immunocompromised host, primary and reactivated VZV infection is often more severe, associated with higher morbidity rates and some mortality.
  • 11. Chickenpox (Varicella) Varicella is the highly contagious primary infection caused by varicella-zoster virus.  It is characterized by successive crops of pruritic vesicles that evolve to pustules, crusts, and occur at the same times, scars.  This infection is often accompanied by mild constitutional symptoms;  the primary infection occurring in adulthood may be complicated by pneumonia and encephalitis.
  • 12.  Incubation Period;14 days (range, 10 to 23 days).  Prodrome; Characteristically absent or mild. Uncommon in children, more common in adults: headache, general aches and pains, severe backache, malaise. Exanthem appears within 2 to 3 days.  Skin Lesions;  In most children, illness begins with appearance of exanthem, vesicular lesions evident in successive crops.  Often single, discrete lesions or scanty in number in children and much more dense in adults.  Initial lesions are papules (often not observed) quickly evolve to vesicles and initially appear as small "drops of water "on a rose petal" .  Vesicles become umbilicated and rapidly evolve to pustules and crusts over an 8- to 12-h period.  With subsequent crops, all stages of evolution may be noted simultaneously, i.e., papules, vesicles, pustules, crusts.
  • 13. COMPLICATIONS  Secondary bacterial Skin infection.; it is the most common complication in children .  Neurologic complications. Encephalitis and Reye's syndrome are complications of chickenpox.  Reye's syndrome is an acute, noninflammatory encephalopathy associated with hepatitis or fatty metamorphosis of the liver; 20% to 30% of Reye's syndrome cases preceded by varicella. The fatality rate is 20%. Salicylates used during the varicella infection may increase the risk of the development of Reye's syndrome.  Pneumonia.; Pneumonia is rare in normal children, but it is the most common serious complication in normal adults.
  • 14. Herpes zoster (HZ) ,Shingles is an acute dermatomal infection associated with reactivation of endogenous VZV that had persisted in latent form within sensory ganglia after an earlier attack of varicella  Age of Onset; More than 66% are >50 years of age; 5% of cases in children <15 years.  c/f  Pre eruptive pain (preherpetic neuralgia), unilateral, dermatomal, precedes the eruption by 4 to 5 days.  Prodromal symptoms may be absent, particularly in children.  ERUPTIVE PHASE. The eruption begins with red, swollen plaque of varying sizes and spreads to involve part or all of a dermatome  The vesicles arise in clusters from the erythematous base and become cloudy with purulent fluid by day 3 or 4.  Successive crops continue to appear for 7 days.  Vesicles either umbilicate or rupture before forming a crust, which falls off in 2 to 3 weeks.  The elderly or debilitated patients may have a prolonged and difficult course.  The major morbidity is postherpetic neuralgia (PHN).
  • 15. R x  The aim of treatment is the suppression of inflammation, pain, and infection.  Oral antiviral agents are recommended in all patients over 50 with pain in whom blisters are still present, even if they are not given within the first 96 h of the eruption.  Antiviral therapy and analgesics aid acute pain control;  lidocaine patch (5 %), gabapentin, pregabalin, opioids, and tricyclic antidepressants reduce postherpetic neuralgia  Oral analgesia should be maximized using acetaminophen, nonsteroidal anti-inflammatory drugs (NSAIDs), and opiate analgesia as required.  Local anesthetics, such as 10% lidocaine in gel form, 5% lidocaine- prilocaine, or lidocaine patches (Lidoderm), may acutely reduce pain. Gabapentin starting at 100 mg three times
  • 16. Exanthems were previously consecutively numbered according to their historical appearance Diseases that begin with exanthems may be caused by bacteria, viruses, or drugs 1. first disease, measles; 2.second disease, scarlet fever; (bacterial) 3.third disease, rubella; 4. fourth disease, "Dukes' disease" (probably coxsackievirus or echovirus); 5.fifth disease, erythema infectiosum; 6.sixth disease, roseola infantum
  • 17. MEASLES( Rubeola)  Measles is a highly contagious childhood viral infection.  Significant morbidity and mortality occur in acute and chronic course.  Childhood immunization by combined MMR vaccine is highly effective at preventing infection.  Epidemic disease; worldwide distribution.  Etiology; Measles virus which is RNA paramyxovirus  Incubation Period;10 to 15 days.  Prodromal symptoms ;Fever, malaise, conjunctivitis,,photophobia ,URT catarrh ( coryza, cough), Koplik spots ;Pathognomonic. Appear before exanthem.( Cluster of tiny bluish-white spots on red background, on buccal mucosa opposite premolar teeth).  exanthem ;Generalized erythematous macules and papules that spread from the forehead and behind the ears to the trunk and extremities; begins to fade in 4 to 5 days.  More severe disease in immunocompromised or malnourished individuals.  Treatments;  First line  Supportive care  Treat secondary infections  Vitamin A  Immune globulin, IM  Measles vaccine  Second line  Ribavirina
  • 18. German measles( RUBELLA)  3-day measles.  Epidemic disease; worldwide distribution.  Cause; is an enveloped RNA virus in the Togaviridae family  Incubation period ;about 18 days  Short prodrome; pink macular rash ,which fades ,first on the turnk over the course of few days.  Enlargement of cervical, suboccipital, and postauricular glands.  rubella during the first trimester carries high risk of fetal malformations with congenital infection (microcephaly, congenital heart disease, deafness).  Prevention by vaccination with the combined MMR vaccine
  • 19. erythema infectiosum (fifth disease)  is caused by the B19 parvovirus.  It is relatively common and mildly contagious  appears sporadically or in outbreaks, often in the spring.  children between 5 and 14 years of age.  Incubation period; is 13 to 18 day  Asymptomatic infection is common.  Prodromal; Symptoms are usually mild or absent.  ERUPTIVE PHASE. There are three distinct, overlapping stages.  Facial erythema ("slapped cheek").  Reticular erythema of the shoulder.  Recurrent phase. The eruption may fade and then reappear in previously affected sites on the face and body during the next 2 to 3 weeks.
  • 20. GIANOTTI-CROSTI SYNDROME (Papular acrodermatitis of childhood)  Common, self-limited dermatosis.  presenting as discrete non-pruritic, erythematous monomorphic dome-shaped or flat-topped papules symmetrically distributed on face, buttocks and extensor extremities.  Typically, the trunk is spared  Associated with multiple viral triggers and immunizations.  Historically associated with hepatitis B infection, but now more often triggered by Epstein-Barr virus.  The exanthem occurs in children 1 to 6 years old,  Duration is 2 to 3 weeks.
  • 21. Roseola Infantum (Exanthem Subitum, Sixth Disease) a common cause of sudden, unexplained high fever in young children between 6 and 36 months of age. Prodromal fever is usually high and convulsions and lymphadenopathy may accompany it. Suddenly, on about the fourth day, the fever drops. a morbilliform erythema consisting of rose-colored discrete macules sites ; the neck, trunk, and buttocks, and sometimes on the face and extremities. The eruption may also be papular or, rarely, even vesicular. The mucous membranes are spared. Complete resolution of the eruption occurs in 1 to 2 days.
  • 22. Human Papillomavirus Infections (HPV)  are very widespread-to-ubiquitous in humans, causing subclinical infection or a wide variety of benign clinical lesions on skin and mucous membranes.  They also have a role in the oncogenesis of cutaneous and mucosal premalignancies [squamous cell carcinoma (SCC) and SCC in situ (SCCIS)] and malignancies (invasive SCC).  More than 150 types of HPV have been identified and are associated with various clinical lesions and diseases .
  • 23. wart  Transmission; Skin-to-skin contact.  Other Factors; Immunocompromise, such as occurs in HIV disease or after iatrogenic immunosuppression with solid organ transplantation, is associated with an increased incidence of and more widespread cutaneous warts. Occupational risk associated with meat handling.  Duration of Lesions; Warts often persist for several years if not treated.  Symptoms; Cosmetic disfigurement. Plantar warts act as a foreign body and can be quite painful during normal daily activities such as walking if located over pressure points.  More aggressive therapies such as cryosurgery often result in much more pain than that caused by the wart itself. Bleeding, especially after shaving.  Verruca Vulgaris (Common Warts)  Firm papules, 1 to 10 mm or rarely larger , hyperkeratotic, clefted surface, with vegetations. Palmar lesions disrupt the normal line of fingerprints. Return of fingerprints is a sign of resolution of the wart.  Characteristic "red or brown dots" are better seen with hand lens and are pathognomonic, representing thrombosed capillary loops.  Isolated lesion, scattered discrete lesions. Annular at sites of prior therapy. Occur at sites of trauma: hands, fingers, knees. Butcher's warts: large cauliflower-like lesions on hands of meat handlers.  Filiform warts have relatively small bases, extending out with elongated cap.
  • 24. Common warts (Verruca vulgaris)  first begin as smooth, flesh colored papules,  lesion enlarge into dome-shaped, gray-brown irregular growths with rough hyperkeratotic surface, studded with brown-black dots (thrombosed capillaries). are a useful diagnostic sign  The hands are the most commonly involved areas, but warts may be found on any skin surface.  They are more often multiple than single  Pain is rare
  • 25. R x  Aims of therapy are  1) to remove the wart;  2) not toproduce scarring;  3) to induce lifelong immunity to prevent recurrence.  Cryotherapy is a reasonable first line therapy for most common warts.  Products containing salicylic acid with or without lactic acid  Simple occlusion with a relatively impermeable tape can be effective in eradicating warts.  Surgical destruction with cautery or ablation of warts can be effective treatment, but even complete destruction of a wart and the surrounding skin does not guarantee the wart will not recur. for warts that are refractory  Bleomycin has high efficacy and is an important treatment for recalcitrant common warts.
  • 26. plane Warts (Verruca Plana)  Sharply defined, flat papules (1 to 5 mm); "flat" surface, skin-colored or light brown.  Round, oval, polygonal, linear lesions (inoculation of virus by scratching).  There may be only a few, but in general they are numerous & painless  Lesions that arise after trauma may have a linear arrangement.  Occur on face (,forehead , about the mouth) , the backs of the hands, beard area, shins.
  • 27. Flat Warts  Flat warts frequently undergo spontaneous remission, so therapy should be as mild as possible, and potentially scarring therapies should be avoided.  Treatment with topical tretinoin  Tazarotene cream or gel may also be effective If lesions are few, light cryotherapy is a reasonable consideration.  Imiquimod 5 % cream used up to once a day can be effective.  5-FU cream 5%  applied twice a day may be very effective.  For refractory lesions, laser therapy in very low fluences or photodynamic therapy  might be considered before electrodesiccation because of the reduced  risk of scarring.
  • 28. Plantar Warts  Warts of the soles are called plantar warts .  These have a rough surface which protrude only slightly from the skin & surrounded by bony collar .  On paring , the presence of the bleeding capillary loops allows planter warts to be distinguish from corns .  Often multiple .  It can be painful  A cluster of many warts that appears to fuse is referred to as amosaic wart
  • 29. Plantar Warts  In general, plantar warts are more refractory to any form of treatment  than are common warts.  Initial treatment usually involves daily application of salicylic acid in liquid, film, or plaster form after soaking.  In failures, cryotherapy or cantharidin application may be attempted, alone or in combination.  A second freeze-thaw cycle is beneficial when treating plantar warts with cryotherapy.  Bleomycin injections, laser therapy, or topical immunotherapy, may be used in refractory cases.  Surgical destruction with cautery or blunt dissection should be reserved for failures with nonscarring techniques, since a plantar scar may be persistentlypainful.  CO2 laser may also result in plantar scars.
  • 30. Genital warts Condylomata Acuminata  Genital warts are the most common STD Among sexually-active young adults in the US and Europe, are pale pink with numerous, discrete, narrow-to-wide projectionson a broad base. The surface is smooth or velvety, moist, and lacks the yperkeratosis of warts found elsewhere  Can appear any where in genital area .  The warts may coalesce to form a large, cauliflower-like masses in moist, occluded areas such as the perianal skin, vulva, and inguinal folds.  Another type is seen most often in young, sexually active patients. Multifocal, often bilateral, red- or brown pigmented slightly raised, smooth papules .  The presence of anogenital warts in children raise the spectra of sexual abuse ,but is usually caused by auto inoculation from common wart elsewhere
  • 31. Genital wart  Because no effective virus-specific agent exists for the treatment of genital warts, their recurrence is frequent.  Podophyllin is more effective in treating warts on occluded or moist surfaces, such as the mucosa or under the prepuce. as a crude extract, usually in 25 % in tincture of benzoin.  Purified podophyllotoxin 0.5% solution or gel is applied by the patient twice a day for 3 consecutive days of each week in 4- to 6-week treatment cycles.   Imiquimod, an immune response modifier which induces IFN locally at the site of application,  Trichloroacetic acid (TCA) 35 % to 85 % weekly or biweekly. TCA is safe for use inpregnant patients.  Cryotherapy with liquid nitrogen  Electrofulguration or electrocauterization  The use of CO2 laser in the treatment of genital warts has not been demonstrated to be more effective than simpler surgical methods.  Any surgical method that generates a smoke plume is potentially infectious to the surgeon.  5-FU 5% cream applied twice a day may be effective, 5-FU is not commonly recommended for the treatment of typical external genital warts because other methods of  treatment are available.  The efficacy of systemic and intralesional IFN-a therapy has been  found to be relatively low in eradicating genital warts.
  • 32. Molluscum Contagiosum  Molluscum contagiosum (MC), is a self-limited epidermal viral infection.  Etiology; a double-stranded DNA poxvirus , with 30% homology with smallpox virus.  Types MCV-1 and MCV-2.  Age, Sex; Children; sexually active adults; males > females.  Transmission ;Skin-to-skin contact. spreads via autoinoculation, scratching, or touching a lesion and fomites  clinically ; skin-colored papules that are often umbilicated, occurring in children and sexually active adults.  In HIV-infected individuals, however, numerous large mollusca often arise on the face, causing significant cosmetic disfiguremen  Sites; most commonly involved are the face, trunk, axillae, extremities in children, and the pubic and genital areas in adults  Unlike warts, the palms and soles are not involved  Classification by Risk Groups  Children;exposed skin sites. Child-to-child transmission relatively low. Resolve spontaneously. Usually caused by MCV-1.  Sexually Active Adults; Occur in genital region. Virus transmitted during sexual activity. Resolve spontaneously.  HIV-Infected Individuals; Most commonly occur on the face, spread by shaving. Usually caused by MCV-2
  • 33. Most lesions are self-limiting and clear spontaneously in 6 to 9 months; however, they may last 2 to 4 years or longer.  Genital molluscum contagiosum may be a manifestation of sexual abuse in children.
  • 34. Treatment  Treatment must be individualized.  Conservative non scarring methods should be used for children who have many lesions. Genital lesions in adults should be definitively treated to prevent spread by sexual contact .  Treatment are;  Curettage  Imiquimod (Aldara cream) ,  podophyllotoxin 0.5% (Condylox) ,  Tretinoin (Retin-A) cream ,  Salicylic acid (Occlusal)
  • 35. Human Orf; Ecthyma contagiosum  Human orf ;  is a parapoxvirus infection that normally occurs in ungulates but occurs in humans exposed to the virus; it is characterized by nodular lesions on exposed cutaneous sites. (hands, arms, legs, face); most common site is dorsum of right index finger.  Other Findings; Ascending lymphangitis and lymphadenopathy may occur.  Bacterial superinfection may occur.  More extensive infection may occur in the immunocompromised host  Course; lesion resolves spontaneously in 4 to 6 weeks, healing without scar formation  Management; Antiviral agents are not effective.  Treat bacterial superinfection; manage pain.

×