Guideline for self-study of students for practical lesson

Module I . Dermatology and Venereology

Thematic module 3. Сontagious Dermatoses

LESSON 6

Diseases due to virus infection. Etiology, pathogenesis. Classification. Clinical features. Diagnostics. Treatment. Prevention..

1. Theme urgency

Dermatoses of virus etiology form a rather large and frequently encountered group of skin diseases. It includes herpes, warts, molluscum contagiosum, and condyloma acuminatum. These diseases are quite common among children, particularly from the age of 5 years (virus dermatoses are recorded most in 5- to 8-year-old children). Virus diseases of the skin account for 3 to 4 per cent of adult and 9.5 per cent of child cases with dermatoses. Though the virus flora may be transmitted by the intrauterine route, during delivery or in the first days of the infant's life, the disease does not develop then because antivirus antibodies are transferred in the mother's blood, which causes passive immunity in the fetus and the infant. This immunity weakens by the beginning of the second year of life, owing to which virus dermatoses may develop. The virus enters the body by various routes: through the skin, contaminated articles or mucous membranes (during sexual intercourse with a sick person or virus carrier, through kissing) and with droplets. In the absence of or reduced immunity, the incubation period ranges from a few days to two or three weeks.

The subject-matter:

Herpes simplex

Herpes simplex virus (HSV) infection is one of the most commonly encountered human viral infections. HSV is a double-stranded DNA virus that is subdivided into two closely related types: HSV-1 and HSV-2. Oral-facial herpes is most commonly caused by HSV-1, while HSV-2 is most frequently implicated in genital lesions. It has been estimated that there are more than 500 000 new cases of genital HSV per year in the United States. Infection most often results from direct mucous membrane or skin contact between an infected individual and an uninfected individual. The risk factors for primary infection therefore include unprotected sexual contact and kissing. Other well described but less commonly encountered modes of transmission include nonsexual rubbing, as occurs with wrestlers and rugby players, and herpetic whitlow, acquired when health or dental workers have contact with an infected patient.

Infections with either HSV-1 or HSV-2 occur either at mucosal surfaces or at sites of abraded skin. The virus infects epidermal and dermal cells, causing vesicles as a result of an influx of fluid containing free virus and degenerated epithelial cells. Sensory and autonomic nerve endings also are infected, with the virus traveling to the nucleus through retrograde axonal flow. In the sensory ganglia, the virus establishes latent infection for the lifetime of the host. During reactivation, the virus actively replicates, leading to lesions in the distribution of the affected nerve.

Once a patient has undergone primary infection, he or she may experience intermittent recurrences. Although they are not necessary for a recurrence to occur, certain factors put a patient at risk of a recurrence, including ultraviolet (UV) radiation, tissue injury, stress, and menstruation.

In recent years, it has been determined that asymptomatic virus shedding occurs with greater frequency than was previously recognized. Indeed, asymptomatic viral expression is much more common that are symptomatic episodes. Patients infected with HSV who have no sings or symptoms of active infection have cultures positive for virus between 1 and 7 percent of the days when they are tested. This asymptomatic shedding may result in infection of the sexual partners of an affected individual.

The disease is characterized by eruption, on a hyperemic area, of grouped vesicles filled with a clear and then cloudy content. The favoured sites are the lips (herpes labialis), cheeks (herpes facialis), the wings of the nose (herpes nasalis), oral mucosa (herpes buccalis), cornea (herpes cornealis), and genitals (herpes genitalis). The vesicles dry into crusts which leave no scars when they drop off. Ruptured vesicles on the oral mucosa leave painful erosions with hyperemic swollen edges (aphthous stomatitis).

The eruption tends to recur, which is facilitated by stress reactions to cooling, infectious diseases, overstrain, neuro-psychic and physical traumas, and insolation. Herpes simplex occurs after disorders of gastro-intestinal activity, pneumonia, toxicosis, insolation, febrile diseases (herpes febrilis), and in dysmenorrhea (herpes menstrualis).

The eruption is often preceded by indisposition, a chill, restlessness, a sensation of burning, poor appetite, and insomnia. The regional lymph nodes are enlarged. The following clinical forms are distinguished: (1) mild (abortive) variety with rapid resolution of the few lesions that had erupted; (2) edematous form accompanied with bright hyperemia and marked swelling (e.g. on the cheeks); (3) severe form (herpes simplex ulcerosa); (4) zosteriform (herpes simplex zosteriformis); (5) frequently recurring form localized on the lips (vermilion border), buttocks, and external genitals.

Histopathology. The characteristic findings are ballooning and, to a lesser extent, reticular degeneration of the epidermal cells and acantholysis. Intranuclear eosinophilic inclusions are found in the ballooning cells and dilated blood vessels, oedema, and mild perivascular infiltration in the dermal papillary layer.

Diagnosis. In a typical clinical picture the diagnosis is easily made. Herpes simplex zosteriformis is distinguished from herpes zoster by the absence of pain irradiating along the distribution of the peripheral nerves. In aphthae the edges are not polycyclic. Polycyclic edges of the erosive surfaces, absence of sclerosis in the base, negative results of laboratory tests, and the medical history allow differential diagnosis with erosive hard chancre when herpes simplex is found on the genitals. The history of an acute onset of new or recurrent vesiculobullous lesions on an erythematous base is often highly suggestive of the diagnosis of HSV infection. However, adjunctive tests often are needed to confirm or establish the diagnosis. With any of the following techniques, the sensitivity of the test is highly dependent on the type of lesion sampled, with new vesicles giving the highest yield. Tzanck smear may be performed rapidly in the office and should demonstrate vitropathic multinucleated giant cells. This technique requires a great deal of training. In brief, a sharp sterile blade is used to gently scrape cells from the bottom of an erosion or from the lower portion of a vesicle roof, and this material is smeared onto a microscope slide. A Giemsa, or similar staining technique allows one to see the viropathic cells. This technique does not differentiate HSV from varicella zoster virus.

Viral culture should grow HSV within 48 h. It is capable of differentiating HSV-1, HSV-2, and varicella zostervirus (VZV). As in the Tzanck procedure, a sharp sterile blade is used to gently scrape cells from the bottom of an erosion or from the lower portion of a vesicle roof, and this material is placed into a viral transport medium. Immediate transportation to a viral laboratory improves diagnostic sensitivity.

In certain institutions, polymerase chain reaction (PCR) may also be used to detect HSV DNA. This is the fastest, most reliable, and most sensitive technique. In contrast to viral culture, PCR is less subject to specimen degredation, which quickly occurs if specimens are not immediately inocculated into culture media. Accordingly, the PCR technique is rapidly becoming the criterion standard for diagnosis and may replace all other techniques except Tzanck examination.