皮膚性病學(xué)課件：Viral Dermatoses

1、Viral Dermatoses Objective: 1) To master the clinical features, diagnosis and treatment of herpes zoster. 2) To understand the clinical features of varicella. 3) To understand the clinical features of verrucae. 4) To master the pathogens of varicella and herpes zoster. Introduction of viral dermatos

2、es Viral dermatoses are a group of cutaneous and mucosal lesions caused by viruses. According to the clinical features, viral dermatoses are divided into three groups: 1) Herpes group: herpes simples, varicella, herpes zoster 2) Eruptive group: rubella, measles, erythema infectiosum 3) Neoplastic gr

3、oup: verrucae, molluscum contagiosum Varicella and herpes zoster Varicella, commonly known as chickenpox, is primary infection with the varicella-zoster virus (VZV) Herpes zoster is a common, predominantly dermal and neurological disorder caused by VZV Etiology Varicella-zoster virus (VZV) Pathogene

4、sis (1)The relation of varicella and herpe zoster VZV No immunized people Varicalla(70%) Latent infections(30%) Latent viral carriers Inducing factors Herpes zoster (2) Pathogenesis of varicalla 1) Entry of virus is probably through the mucosa of the upper respiratory tract and oropharynx. 2) Initia

5、l viral multiplication at this portal of entry results in dissemination of small amounts of virus via the blood and lymphatics (the primary viremia). 3) A secondary viremia occurs at days 11 to 20, resulting is infection of the epidermis and the appearance of the characteristic skin lesions. 4) The

6、incubation period is 10 to 21 days (usually 14 to 15 days) 5) Transmission is by direct contact with the lesions and by the respiratory route. 6) Individuals are infectious for at least 4 days before and 5 days after the appearance of the exanthem. (3) Pathogenesis of herpes zoster The pathogenesis

7、of herpes zoster is not fully understood. But clinical epidemiologic and pathologic ata support the following model. 1) VZV passes from lesions in the skin and mucosal surfaces into the contiguous endings of sensory nerves. 2) VZV is transported centripetally up the sensory fibers to the sensory gan

8、glia. 3) A latent infection is established in the ganglia, and the virus persists silently and harmlessly. But the latent virus in the ganglia retains its potential for full infectivity. 4) Virus multiplies and spreads within the ganglion, causing neuronal necrosis and intense inflammation, when hos

9、t resistance falls below a critical level. This process is often accompanied by severe neuralgia. 5) The virus travels down the sensory nerve into the skin, where it produces the characteristic cluster of zoster vesicles. 6) Infection of motor neurons in the anterior horn and inflammation of the ant

10、erior nerve root account for the local palsies Clinical manifestations (1) Clinical manifestations of varicella 1) Varicella tends to be a disease of children. 90 percent of cases occur in children less than 10 years of age and fewer than 5percent in individuals over the age of 15. 2) The incubation

11、 period is 10 to 21 days. 3) Prodrome: the rash is often preceded by 2 to 3 days of fever, chills, malaise, headache, anorexia, severe backache, and, in some patients, sore throat and dry cough. 4) Rash of varicella The rash begins on the face and spreads rapidly to trunk, with relative sparing of t

12、he extremities. It is not uncommon to have a few lesions on the palms and soles. The distribution remains central. Varicella is characterized by a vesicular eruption consisting of delicate “teardrop” vesicles on an erythematous base. The eruption starts with faint macules, then they develop rapidly

13、into vesicles, pustules, and crusts. The typical vesicle of varicella is superficial and thin-walled, usully 2 to 3mm in diameter and elliptical. Successive fresh crops of vesicles appear for a few days after the onset. The lesion dries, beginning in the center, first producing an umbilicated vesicl

14、e or pustule and then a crust. Crusts fall off spontaneously in 1 to 3 weeks, depending upon the depth of the skin involvement. Scarring is rare ,but larger lesions and those that become secondarily infected may heal with a characteristic round, depressed scar. Healing lesions may leave hypopigmente

15、d spots that persist for weeks to months. Vesicles also develop in the mucous membranes of the mouth, nose, pharynx, larynx, gastrointestinal tract, trachea, urinary tract and vagina as well as on the conjunctivae. varicella varicella 5) Subjective symptoms: fever, headache, myalgia, anorexia, pruri

16、tus. 6) Varicella is more severe in adults and most severe in patients of any age with impaired cell-mediated immunity. 7) Complications of varicella In the normal child, varicella is a benign disease rarely attended by secondary complications. The severity of the disease is age dependent, with adul

17、ts having more severe disease and a greater risk of visceral disease. Secondary bacterial infection with staphylococcus aureus or a streptococcal organism is the most common complication of varicella. Pneumonia is seen in 1 in 400 adults with varicella. Cerebellar ataxia and encephalitis are the mos

18、t common neurologic complications. Reyes syndrome, a syndrome of hepatitis (fatty degeneration of the liver) and acute encephalopathy, is associated with the use of aspirin to treat the symptoms of varicella. Although its pathogenesis is not understood, there is no inflammatory response in the CNS,

19、and the studies have ruled out direct virus infection of the liver or brain. Reyes syndrome may be caused by some circulating toxin. Reyes syndrome occur in association with varicella, particularly when aspirin has been taken for fever. Aspirin is absolutely contraindicated in patients with varicell

20、a. Any child with varicella and severe vomiting should be referred immediately to exclude Reyes syndrome. The mortality of Reyes syndrome may be as high as 40 percent. (2) Clinical manifestations of herpes zoster 1) The prodromes include a low-grade fever, adynamia, malaise, and anorexia. 2) Predile

21、ction age: adults The incidence of zoster increases with age. Below age 45, the annual incidence is less than 1 in 1000 persons. Among patients older than 75 years of age, the rate is more than four times greater. 3) Rash of herpes zoster: It is nearly always unilateral, does not cross the midline,

22、and is generally limited to the area of skin innervated by a single sensory ganglion. The eruption initially presents as papules and plaques of erythema in the dermatome. Within hours the eruptions usually consist of closely grouped vesicles on an erythematous base. The content of vesicle is clear,

23、and the wall of vesicle is tense. Lesions may become hemorrhagic, necrotic, or bullous. Lesions continue to appear for several days Regional lymphadenopathy occurs in many cases of herpes zoster. Herpes zoster 4) Zoster sine herpete: Rarely, the patient may have pain, but no skin lesions. 5) Predile

24、ction sites: dermatomes: thoracic (55%), cranial(20%,with the trigeminal nerve being the most common single nerve involved), lumbar(15%), sacral(5%) 6) Neuralgia: Pain is a major symptom of herpes zoster. It often precedes and generally accompanies the rash, and it frequently persists after the rash

25、 has healed (postherpetic neuralgia, PHN). The elderly persons tend to have more pain. 7) Duration of illness: The total duration of the eruption depends on three factors: patient age severity of eruption presence of underlying immunosuppression. In younger patients, the total duration is 2 to 3 wee

26、ks. In elderly patients, the cutaneous lesions may require 6 weeks or more to heal. The relapse is rare. 8) Scarring is uncommon. 9) Mucous membrane lesion: lesions may develop on the mucous membranes within the mouth in zoster of the maxillary or mandibular division of the facial nerve, or in the v

27、agina in zoster in the S2 or S3 dermatome. 10）Postherpetic neuralgia: The pain persists after the rash has healed, so this complication is known as postherpetic neuralgia (PHN). 11) Special types: Disseminated herpes zoster: It is a generalized varicelliform eruption accompanying the segmental erupt

28、ion. It has been defined as more than 20 lesions outside the affected dermatome. It occurs chiefly in old or debilitated individuals, especially in patients with lymphoreticular malignancy or AIDS. Ophthalmic zoster: In herpes zoster ophthalmicus, the ophthalmic division of the fifth cranial nerve i

29、s involved. Ocular involvement is most commonly in the form of uveitis(92%) and keratitis (50%). Ramsay Hunt syndrome: Ramsay Hunt syndrome results from involvement of the facial and auditory nerves by the varicella zoster virus. Herpetic inflammation of the geniculate ganglion is felt to be the cau

30、se of this syndrome. The presenting features include: zoster of the external ear pain of ear ipsilateral facial paralysis auditory symptoms Auditory symptoms include mild to severe tinnitus, deafness, vertigo, nausea and vomiting, and nystagmus. Pathology (1) cytopathology: A Tzanck smear from a ves

31、icle will usually show characteristic multinucleate giant cells and inclusion bodies in the nuclei. (2)Histopathology: The vesicles are intraepidermal. The large, swollen cells called balloon cells are found. Acidophilic inclusion bodies are present in the nuclei of the cells of the vesicle epithliu

32、m. Diagnosis Differential Diagnosis The diagnosis of varicella is easily made clinically. In atypical cases, a Tzanck smear from a vesicle will usually show characteristic multinucleate giant cells and inclusion bodies in nuclei. Characteristic diagnosis features include: 1) The development, after a

33、 brief and mild (or absent) prodrome, of a papulovesicular eruption accompanied by fever and mild constitutional symptoms; 2) The appearance of lesions in crops, with a predominantly central distribution (including the scalp); 3) The rapid evolution of individual lesions from macules to papules to d

34、elicate thin-walled vesicles to pustules and finally to crust 4) The presence of lesions in all stages of development in any one anatomic area throughout the acute disease; 5) The presence of lesions in the mucous membranes of the mouth. Varicella should be differentiated from smallpox, impetigo and

35、 papular urticaria. The diagnosis of herpes zostor Characteristic diagnosis features include: 1) Grouped vesicles on an erythematous base; 2) Herpes zoster classically occurs unilaterally with in the distribution of a sensory nerve; ( along a dermatome) 3) The lesions arrange in zoster 4) Neuralgia

36、Differential Diagnosis of herpes zoster: Segmental cutaneous paresthesias or pain may precede the eruption by 4 or 5days. In such patients, prodromal symptoms are easily confused with the pain of angina pectoris, duodenal ulcer, biliary or renal colic, appendicitis, pleurodynia, or early glaucoma. T

37、reatment (1) Treatment of varicella 1) Antiviral agents: The first choice of antiviral agent is Acyclovir. The dose in children 10-15mg/kg.d (maximum 800mg per dose) five times daily for 5 days. In adolescents and adults (13 and older), the dose is 800mg-1000mg four or five times daily for 5 days. S

38、evere, fulminant cutaneous disease and visceral complication are treated with intravenous acyclovir 10mg/kg every 8 hours, adjusted for creatinine clearance. Famciclovir, valaciclorir, and vidarabine are also chosen. 2) Aspirin and other salicylates should not be used as antipyretics in varicella, b

39、ecause their use increases the risk of Reyes syndrome. 3) Antihistamines orally may help control the intense pruritus of the rash. 4) Topical treatment: calamine lotion, acyclovir ointment, cool compresses, etc. (2) Treatment of herpes zoster 1) Middle-aged and elderly patients are urged to restrict

40、 their physical activities or even stay home in bed for a few days. Bed rest may be of importance in the prevention of neuralgia. Younger patients may usually continue with their customary activities. 2) Antiviral therapy: Acyclovir at a dose of 800mg five times daily for 7 days was used. Valacyclovir(1000mg) famciclovir (500mg) may be given only three times daily for 7 days In immunosuppressed patients with ophthalmic zoster or Ramasay Hunt syndrome, and in pati