Viruses are obligate intracellular parasites. Viruses attack the skin in 3 ways: direct inoculation, systemic infection, or local spread from an internal focus. Dermatologically, viral diseases are generally caused by DNA viruses, while RNA viruses cause illnesses accompanied by general symptoms.
Viruses can have 3 different types of effect on skin cells:
1. Cytolytic-cytopathic effect: through this effect they can cause the formation of vesicles and bullae.
2. Proliferative effect: as a result of this effect they can lead to benign tissue hyperplasia.
3. Oncogenic effect: they can cause the development of various malignant diseases.
Viral Infections Causing Skin Rashes
In general, there are countless viral infections, mostly seen in childhood, that cause rashes. Examples include:
* Measles (morbilli)
* German measles (rubella)
* Chickenpox (varicella virus)
* Fifth disease (fifth disease caused by parvovirus)
* Roseola (exanthem subitum, caused by human herpesvirus type 6)
* Pityriasis rosea (the cause is unknown but is thought to be human herpesviruses types 6 and 7)
* Echovirus and adenovirus infections commonly produce a rash.
* Infectious mononucleosis (Epstein-Barr virus, or glandular fever) can cause a rash, but if amoxicillin or ampicillin is given, a rash is almost inevitable
* Primary HIV infection (often associated with a rash)
Other Viral Infections with Skin Involvement
Hand, foot and mouth disease
Hand, foot and mouth disease, which mostly affects young children in the summer months, is common, mild and short-lived. Although it can be caused by enterovirus 71, coxsackievirus A16 is also a cause. Many members of a family or class may be affected. The incubation period of the virus is 3–5 days. The infection is recognised by small, flat blisters on the hands and feet accompanied by mouth ulcers. These are sometimes painful, so children eat little and reluctantly. There may be a mild fever. A rash sometimes appears on the buttocks of young children. After a few days the blisters and mouth ulcers clear without scarring. Secondary infections are rare. Parents may be worried by the name, associating it with the serious veterinary consequences of foot-and-mouth disease; they should be reassured appropriately (that it is caused by a different and completely unrelated virus).
Non-Specific Viral Rashes
This is a widespread erythematous rash sometimes seen in viral infections. It is accompanied by the common symptoms of a viral infection such as fever, headache and malaise. The rash usually develops quickly. Its appearance varies, but it commonly takes the form of an erythematous, blotchy, heat-rash-like eruption.
Gianotti-Crosti syndrome
* This is a skin response to a viral infection in which there is a papular rash lasting several weeks.
* Other names include papulovesicular acrodermatitis of childhood, papular acrodermatitis of childhood and acrodermatitis papulosa infantum.
Causes of Gianotti-Crosti syndrome:
* Hepatitis B virus
* Epstein-Barr virus
* Coxsackieviruses
* Echoviruses
* Respiratory syncytial virus
It affects children aged 6–12 months. It can occur in clusters, and a preceding upper respiratory tract infection is not uncommon.
A profuse eruption of dull red spots develops over 3–4 days, usually in a symmetrical pattern, first on the thighs and buttocks, then on the outer arms and finally on the face.
The spots are about 5–10 mm in diameter and dark red in colour. Later they often turn purple, especially on the legs, because of blood leaking from the capillaries. They may become fluid-filled blisters.
Kaposi's sarcoma
This is thought to be a malignancy caused by a virus. It usually occurs in association with HIV infection, which should be looked for if the diagnosis is made. Kaposi's sarcoma is more aggressive with HIV.
Viral infections and sport
Sport generally increases the risk of transmission of skin infections.
The following factors can predispose to transmission of disease:
* Direct skin-to-skin contact (in contact sports such as rugby and wrestling)
* Excessive sweating softens the skin and provides a point of entry.
* Sharing wet areas, meaning showers and swimming pools, favours the passing of infections from the feet. In judo, as in other martial arts and gymnastics, bare but dry feet reduce the risk of transmitting the virus.
Papillomavirus Infections
Human papillomavirus (HPV) causes a disease characterised by benign epithelial proliferation of the skin and mucous membranes, which produces no acute signs or symptoms and follows a slow course; these lesions are known as warts (verrucae). They cause disease in different locations (such as verruca vulgaris, verruca plantaris and verruca genitalis). Some types cause clinical pictures such as epidermodysplasia verruciformis (EV) in immunosuppressed patients. EV and some HPV types that involve the genital mucosa can lead to the development of epithelial malignancy. HPV, of which there are more than 80 types, causes infection by entering through damaged epidermis. Trauma and autoinoculation are other routes of transmission. The incubation period of HPV ranges from 2 to 9 months. HPV produces disease by infecting the epithelial cells above the basal layer of the epidermis.
Verruca vulgaris (Common Wart): This presents as round, skin-coloured papules causing no subjective symptoms, characterised by a cauliflower-like keratotic surface. The lesions, averaging 5 mm in diameter, can merge to form large plaques. Most patients are aged 5–20. Warts are most often located on the hands and fingers. On the scalp, cheeks and around the eyes they take on a slightly elongated, brush-like appearance (verruca filiformis). Placement around the nails (periungual) can cause tenderness due to fissures and deformity of the nail.
The lesions develop over weeks or months. Usually a single large papule (the mother wart) appears first, followed by many new warts. Black dots on the wart surface, caused by thrombosed, dilated capillaries, are an important diagnostic criterion. Warts resolve spontaneously within one year in half of patients and within 2 years in two-thirds. Because warts are located in the epidermis, they do not leave scars when they heal.
Verruca plantaris (Plantar Wart): These can develop anywhere on the sole of the foot, but the mid-metatarsal area is their most common site. A hard, horn-like ring develops around the warty papule. Sometimes many warts come together and appear as a single plaque (mosaic wart). The normal skin lines (dermatoglyphics) are disrupted. Squeezing from the side causes more pain. While 30–35% resolve spontaneously in children, in adults they can last for years. They are confused with calluses; in a callus the skin lines are not disrupted, thrombosed capillaries are not seen, and more pain is felt when pressed from above.
Verruca filiformis (Filiform Wart): These appear on the face and neck as few or many small, skin-coloured, thread-like projections. They are particularly common in men.
Verruca genitalis (Condyloma acuminatum): This is regarded as a venereal disease. In Western countries it has been detected in about half of the adult age group. The infection may sometimes be subclinical or latent. The disease can cause squamous cell carcinoma in the anogenital region in both sexes. It also considerably increases the risk of cervical dysplasia in women. It is estimated that there are 630 million people worldwide infected with HPV, a virus that is extremely common, especially in developed countries. In a study published in our country in 2007, in which 1,353 women were screened, HPV was detected in 20% of participants, and preinvasive cervical lesions caused by HPV were found in 0.7%. The prevalence of cervical HPV colonisation in Türkiye is reported as 2.1%. The lesions appear as numerous lobulated papules (condylomata) about 2–5 mm in diameter and of highly variable height. In men they are seen more often on the penis and perianal area, and in women on the vulva, cervix, perineum and around the anus. In the perianal area, the groin folds and the vulva, the papules merge and grow to take on a cauliflower-like appearance. An unpleasant odour may arise from purulent material accumulating between the vegetative structures. The vegetative papules have a narrow base (they are pedunculated). If condylomata acuminata reach a large size, they are called verrucous carcinoma (Buschke-Löwenstein tumour). Treatment: this depends on the location and extent of the disease. The disease is resistant to treatment and recurs frequently, so some treatments are applied in combination. Cryotherapy, electrocautery, laser and surgical curettage or excision can be performed. Topical imiquimod or intralesional interferon is used to support these treatments.
Focal Epithelial Hyperplasia
Focal epithelial hyperplasia (FEH) is a rare disease caused by human papillomavirus (HPV). In this disease, small papules or nodules of mucosal colour or whiter appear inside the mouth. Lesions associated with FEH are usually asymptomatic, but in some cases they can be painful and cause cosmetic concern. Spontaneous regression or progression may occur. Treatment options for localised lesions include electrocautery, cryotherapy, surgical excision and laser, while in cases with widespread involvement successful results have been reported with topical interferon-β, imiquimod, retinoids and systemic treatments such as interferon-α2b.
Verruca plana (Plane Wart, Juvenile Wart): This is commonly seen in children and young adults. The disease, which produces no subjective symptoms, is mostly located on the face and less often on the hands and forearms. The lesions are slightly raised, flat-topped, mostly round, sometimes polygonal papules ranging from pinhead to lentil size, skin-coloured or grey-yellow. The papules, which spread through autoinoculation, are usually numerous and tend to spread with irritation (positive Koebner phenomenon).
Epidermodysplasia Verruciformis: This is a widespread, persistent HPV infection inherited in an autosomal recessive manner. It is caused particularly by HPV types 5 and 8. It takes the form of a combination of countless papules and plaques resembling verruca plana or pityriasis versicolor. It spreads rapidly over the face, trunk and limbs in childhood. Squamous cell carcinoma (SCC) may develop on sun-exposed areas.
Bowenoid Papulosis
Bowenoid papulosis is a sexually transmitted disease caused by human papillomavirus, manifesting as erythematous patches, papules or plaques on the genital skin, perineum, perianal area or thighs. Bowenoid papulosis is regarded as a precancerous skin condition. The diagnosis of bowenoid papulosis is based on the clinical picture, negative serological tests for syphilis, detection of human papillomavirus by PCR and the results of histological examination. Treatment of bowenoid papulosis consists of antiviral therapy and complete removal of the affected skin cells by laser, electrocoagulation, excision or cryodestruction.
Herpes Simplex Virus Infections
HSV is one of the most common infection-causing viruses in the world. There are two types of HSV: type 1 (HSV-1) and type 2 (HSV-2). HSV-1 infection, the most common (85% of the population), causes disease of the skin and mucous membranes outside the genital area. HSV-2 causes disease of the mucosa and skin of the genital and anal areas. However, in varying proportions of around 10–20%, infection with the other HSV type develops depending on the site. The infection is transmitted through close personal contact. Virus particles pass to a new host through mucous membranes or traumatised epithelium. Primary infection usually occurs in children. After this transmission, either a clinical infection appears (1%) or the infection is subclinical (99%). The sign of subclinical infection is the presence of antibodies in the serum. After "primary herpes simplex infection" the person becomes a carrier. In carriers the virus remains latent in the dorsal root ganglia. From time to time it reactivates, travels via the peripheral nerve to the skin at the site of entry and causes recurrences. Recurrences can be contagious even when they produce no clinical signs (such as the infectiousness of saliva in a person with labial herpes).
Triggering factors: emotional stress, physical trauma, sunburn, focal infections, menstruation, malignant diseases, fever and systemic infections, etc. Herpes simplex infections are divided into primary and recurrent, depending on whether the person has previously been in contact with the virus.
Primary Gingivostomatitis: This is the most common form of primary HSV infection, seen mostly in children aged 1–5. A prodromal period of malaise and fever is followed by the appearance of lesions inside the mouth and on the lips. The lesions, initially vesicles grouped like bunches of grapes, quickly turn into aphthous lesions. Widespread painful erosions are accompanied by drooling, bad breath, fever, general malaise and regional lymphadenopathy. Dehydration may occur in young children. Ulcerative and exudative lesions of the posterior pharynx may cause pharyngitis. Systemic antiviral treatment should be given to those diagnosed with primary HSV infection. In untreated cases it usually resolves on its own within 1–2 weeks, and rarely may last up to 2–6 weeks.
Primary Herpes Genitalis: This infection mostly develops due to HSV-2 (70–90%). A previous HSV-1 infection is partly protective against HSV-2 infection. Primary genital herpes is often sexually transmitted. Vesicles appearing 3–14 days after contact quickly become pustules and then merge to form irregular erosions and ulcers. Grouped vesicles and erosions are seen on the vagina, rectum or penis, and new lesions may continue to develop for 7–14 days (average 8 days). Patients have bilateral, widespread lesions, fever, malaise and bilateral painful lymphadenopathy. In addition, women may have vaginal pain and dysuria, and men burning, aching and urethral discharge from the penis; if there is a lesion at the anus, severe proctitis may be seen. The infection can last 3 weeks or longer. It does not leave scars. After the infection the virus remains latent in the sacral root ganglia. HSV IgM becomes positive 2–4 weeks after infection. Infection arising in the third trimester of pregnancy is risky for the foetus. Because there is a risk of transmission in the womb or during birth, systemic treatment should be given. Aciclovir 1 g/day, valaciclovir 1 g/day and famciclovir 500 mg/day are given. In pregnant women, intravenous aciclovir is preferred.
Herpetic Whitlow (herpetic infection of the fingers): This is an infection due to the HSV-1 and HSV-2 viruses that can be primary or recurrent. It is common in children who suck their fingers, adults who habitually bite their nails, and dentists and other dental and medical staff who work in and around the mouth without habitually wearing gloves. It is a very painful condition that arises when the virus enters through small abrasions on the fingertips and beside the nails. It is characterised by small, deep-seated vesicles grouped on an erythematous, oedematous base around the nail. It can heal on its own. In the acute stage, oral aciclovir 1 g/day may be given for 5–7 days.
Recurrent Oral-Labial Herpes Simplex: This is the most common form. After primary infection, HSV-1 enters the trigeminal ganglion, and more rarely the inferior and superior ganglia, and remains latent there. From time to time it is activated by triggering factors, replicates and travels along the axons to the skin and mucous membranes, causing new lesions. It appears as vesicles grouped on an erythematous base at the corners of the lips, together with itching, burning and stinging. The vesicles, clear at first, become cloudy over time and crust over in 4–5 days. The regional lymph nodes may be swollen and painful. Lesions without secondary infection heal without scarring within 7 days, leaving a faint red macule. There is no effective treatment for latent viruses. The most common trigger of herpes labialis is UV light, especially UVB.
Recurrent Herpes Genitalis: This arises spontaneously or as a result of reactivation, under the influence of triggering factors, of the virus lying latent in the sacral ganglia. In most cases the causative agent is HSV-2; however, in lesions occurring in children and in people with no history of sexual contact, the agent may be HSV-1. It begins with prodromal symptoms such as burning, itching or stinging. Red papular lesions usually appear within 24 hours and turn into vesicles filled with clear exudate on an erythematous base. Because of the nature of the genital area they quickly erode, leaving a moist, itchy erosion with irregular edges. They are seen as small groups of vesicles or superficial ulcers on the glans or shaft of the penis in men, and on the labia, vagina or cervix in women. It recurs on average 3–4 times a year. If not secondarily infected, it heals spontaneously in 7 days. Many patients may complain of pain in the skin and thighs.
Because a person with one sexually transmitted disease is more likely to have a second, tests for syphilis and AIDS should be requested in these patients. It should not be forgotten that recurrent genital herpes infection can be contagious through subclinical viral excretion (asymptomatic viral shedding) even when there are no active lesions. The effect of topical antivirals is limited. Suppressive treatment is recommended for those who have 6 or more attacks a year, are immunosuppressed or are under intense emotional stress.
Recurrent Lumbo-Sacral Herpes Simplex: Without genital lesions, this is characterised by grouped vesicles located on one side of the lumbosacral area (lower back, buttocks), triggered by triggering factors. Because it causes sciatica-like pain, it may be mistaken for shingles. Treatment is similar.
Eczema Herpeticum (Kaposi's Varicelliform Eruption): This is a widespread, severe skin infection caused by the herpes virus. It occurs particularly in people with atopic dermatitis, and in those with keratinisation disorders such as Darier's disease, ichthyosis vulgaris and pemphigus foliaceus. Patients are usually children. Grouped umbilicated vesicles appear, especially in eczematous areas. The condition, which may become generalised within 5–10 days, is accompanied by fever, malaise and lymphadenopathy. Most of the vesicles are haemorrhagic. When merging vesicles break open, large ulcerated areas appear. The lesions most often involve the face, neck and trunk. The infection may become systemic and lead to conditions such as encephalitis. In this disease, which heals within 2–6 weeks, mortality ranges from 10% to 50%. The causes of death are viraemia and serious secondary infection.
Erythema Multiforme
Erythema multiforme is a skin disease that develops suddenly on the skin and mucous membranes in response to various triggers (such as viral and/or bacterial infectious diseases and medicines) and tends to recur.
How is it treated?
Treatment may vary according to the severity of the disease. Inpatient or outpatient treatment may be recommended depending on the patient's clinical condition. One of the most important steps in treatment is to eliminate the cause that has predisposed to the disease, if it can be identified (infection and/or medicine). Your doctor will recommend treatment according to your symptoms. Do not use any medicine without consulting your doctor.
What should be considered during and after treatment?
If a medicine has been found to be responsible for the development of the disease, the person must never use that medicine again. It should not be forgotten that the disease may recur.
Chickenpox
Chickenpox, caused by the virus known medically as varicella zoster, is a contagious disease that appears as small red blisters on the body and is accompanied by tiredness, malaise and fever. These red blisters first appear on the face or trunk, and it is mostly seen in children.
How Does Chickenpox Develop?
The varicella zoster virus can survive in the air for 1–2 hours and multiplies rapidly. Spread into the air when an infected person coughs or sneezes, the virus is transmitted when other people breathe that air. Once transmitted to another person, within the first 4 days the virus settles in the lymph nodes via the upper respiratory tract and starts to multiply there. On day 7 it continues to multiply, spreading to other organs, chiefly the liver and spleen. On day 14 red blisters begin to appear on the patient's body, together with symptoms such as headache, fever, abdominal pain and malaise.
Treatment of Chickenpox
If the immune system of the person with chickenpox is working normally, treatment is given to relieve the itching and to prevent infection of the lesions. If the itching is mild, treatment is started in lotion form; if it is severe, in tablet form. In addition, attention should be paid to hygiene: hands should be washed more often and nails should be kept short. If there is a high temperature, fever-reducing medicines should also be used.
Herpes Zoster (Shingles)
The causative agent is varicella-zoster virus (VZV) from the herpesvirus group. This neurotropic and dermotropic virus is acquired in childhood and remains in the body for life. The primary infection is chickenpox. When chickenpox heals, the viruses settle in the spinal ganglia of the dorsal roots of the spinal cord. Whichever dermatome had the most lesions (and therefore the most virus) while the child had chickenpox, the most virus settles in the corresponding spinal ganglion, and later only the ganglion carrying the most virus is activated. During the course of chickenpox, the primary infection, the viruses enter through nerve endings in the skin and mucous membranes and reach the sensory ganglia. Viruses lying latent in the ganglia (trigeminal or dorsal root ganglia) are reactivated in connection with local trauma and reduced body resistance, and reach the skin via the sensory nerves. Before shingles appears, there may be subjective symptoms in the area corresponding to the affected dermatome, ranging from superficial itching to severe, stabbing pain. These pains are sometimes mistaken for a heart attack, pleurisy or renal colic. They may be accompanied by burning, stinging, tenderness and hyperaesthesia. Subjective symptoms are milder in young people. The first skin signs are pinhead-sized papules grouped on an erythematous base in the area corresponding to the dermatome. These papules turn into vesicles within 24 hours. The vesicular lesions contain live virus. Within two to three days they become pustules, and within another two to three days they show central umbilication. They then begin to dry, and crusts form within 7–10 days. Over the course of a week, new lesions may develop as separate foci along the dermatome. The lesions in one group differ in appearance from those in another group.
In severe cases the skin lesions may become haemorrhagic and gangrenous. The regional lymph nodes are usually swollen and painful. If the skin lesions do not become secondarily infected, they heal without scarring within 2–4 weeks; in older people this period may be longer than 6 weeks. Herpes zoster is had only once because it leaves immunity. The disease is usually one-sided, but in immunosuppression it may be bilateral or generalised. The most common location is the intercostal area, and most cases are seen in dermatomes supplied by the spinal nerves between T3 and L2. In ophthalmic zoster there may be eye involvement. The particular condition involving the trigeminal nerve and accompanied by facial paralysis is called Ramsay Hunt syndrome. Rarely, shingles may present only with dermatomal pain without any skin lesions.
Ophthalmic Zoster (Shingles Involving the Eye): The trigeminal nerve (5th cranial nerve) has 3 branches: the 1st division (ophthalmic), running around the eye, forehead and along the nose; the 2nd division (maxillary), running along the lower nose, cheeks, upper teeth, palate and upper jaw; and the 3rd division (mandibular), running along the lower jaw, lower teeth and lower lip. In ophthalmic zoster, the first branch of the trigeminal nerve is affected. This can cause lesions to appear on the forehead and eyelids. Eyelid oedema may be seen, and the shingles lesions tend to be painful and to bleed. It should also be followed by ophthalmologists because steroid use may be needed.
Oral Zoster (oral shingles): When the 2nd and 3rd branches of the trigeminal nerve (lower nose, cheeks, teeth, palate, jaw, lips) are affected, shingles lesions can appear on the oral mucosa, hard palate, maxilla, tongue and mandible. Typically, lesions with an erythematous surround are seen on the mucosa.
Cranial Zoster (cranial shingles): This involves the nerves affecting the head and neck. In cranial zoster, head and neck pain, lymphadenopathy and fluid-filled blisters (vesicles) on an erythematous base may be seen.
Otic Zoster (Ramsay Hunt syndrome): This arises from involvement of the nerves of the external ear canal. Otic zoster usually begins with one-sided ear pain, which may be accompanied by ringing in the ear and dizziness. There may be loss of taste in the front two-thirds of the tongue. Ear pain and facial paralysis may develop.
Hand, Foot and Mouth Disease
Hand, foot and mouth disease is caused by certain types of coxsackievirus. It is more common in children and is highly contagious. It is spread via the respiratory route. After a short, mild prodromal period, the lesions first begin in the mouth, followed by lesions on the hands and feet. The elementary lesion is an oval vesicle on an erythematous base. It occurs on the soles, palms and in the mouth. The vesicles in the mouth burst, leaving erosions, which clinically look like aphthous ulcers. No treatment is needed; it heals on its own without scarring within 7–10 days.
Molluscum Contagiosum: The causative agent is molluscum contagiosum virus (MCV), a DNA virus of the poxvirus group. In this disease, which is common in children, transmission occurs through direct skin contact. In adults, transmission is mostly through sexual contact. It is a benign viral disease of the skin and mucous membranes characterised by papules with a central dimple (umbilication). The face, the area around the eyes, the genital area and the trunk are the most common locations. The lesions begin as papules 3–5 mm in diameter and rarely reach 3 cm (giant lesions). The most important feature of these shiny, light-coloured, dome-shaped, individual papules is their depressed (umbilicated) centre. When the papules are squeezed with forceps, a cheesy core is seen to come out of the centre. Irritated lesions may become secondarily infected with bacteria, and their appearance may change. When located around the eyes, conjunctivitis and keratitis may develop. It spreads through shaving or scratching. The disease does not leave immunity. Lesions tend to regress spontaneously after 6 months. When there are many small lesions, it may be confused with verruca vulgaris, verruca plana juvenilis and lichen planus. With giant lesions, differential diagnosis from keratoacanthoma and basal cell carcinoma should be made.
Treatment: After topical anaesthesia (EMLA), the papules are removed with forceps and iodine solution is applied. Cautery and cryotherapy are other treatment methods. As the incubation period ranges from 2 to 7 weeks, patients should be monitored for new lesions after treatment.
Orf and Milker's Nodule: The causative agents are orf virus and pseudocowpox virus of the parapoxvirus group. Orf, also known as ecthyma contagiosum, is transmitted from sheep and goats infected particularly around the mouth. It is common among people who slaughter these animals. Milker's nodule is a disease transmitted from the udders of cows. The two diseases are quite difficult to distinguish clinically, and both are mostly seen on the hands and fingers. The virus enters through a scratch in the skin, and the first sign appears at the site of entry after about a week. The lesion heals spontaneously within 4–6 weeks with minimal scarring. Each lesion passes through 6 different stages. It starts as an erythematous macule and quickly becomes a papule. Then a papulovesicle with a red centre and a pale surround, described as a target lesion, develops. It quickly takes on a weeping, eroded appearance and the hairs on it fall out. In the repair stage, black dots form on its surface as it dries. Papillomatous structures develop on the nodule. In the final stage the lesion flattens, becomes covered with a crust and heals. Mild swelling, fever and pain accompany both conditions. Lymphadenopathy is present in both, but is more severe in milker's nodule. Treatment is symptomatic.
Gianotti-Crosti Syndrome
Gianotti-Crosti syndrome, also called papular acrodermatitis of childhood, was first described by Gianotti in 1955 and by Gianotti and Crosti in 1956. GCS is characterised by papular or papulovesicular lesions, prominent on the face, buttocks and limbs. Hepatitis B virus was the first to be associated with GCS, but associations with many different viral infections, including EBV, CMV, coxsackievirus, HIV and parainfluenza virus, have since been reported in this syndrome.
Measles Disease
Measles is a contagious childhood disease caused by a specific virus called morbillivirus. Spread through the respiratory route and by direct contact with an infected person, measles is a disease that requires attention because of how contagious it is. Measles, mostly seen in the winter months, occurs in children aged about 3–10 on average. Although it is also seen in adults, it is more common in children. Measles is a contagious disease that can cause considerable disruption to children's school life or adults' working life.
Measles can also trigger certain complications. It can cause diarrhoea, middle ear infection, and inflammation of the lungs and larynx. Measles is dangerous for babies with weak resistance and for pregnant women, and can even cause death. If the necessary vaccination measures are not taken, measles can spread as an epidemic.
Erythema Infectiosum
The causative agent is parvovirus B19. It affects the erythroid precursor cells in the bone marrow. Foetal infections can cause hydrops fetalis. It is most common between the ages of 5 and 15 (it can also be seen in adults). There may be headache (20%), fever (20%), sore throat (15%), itching (15%), runny nose (10%), abdominal pain (10%) and joint pain (10%). The diagnosis is made clinically and by serology. It causes outbreaks in children and is a mild, fever-free erythematous rash. It is characterised by striking redness of the cheeks ("slapped cheek" appearance) and a skin rash that fades and reappears. There may be a widespread lace-like rash. It increases in sunlight and is not fatal.
Oral Hairy Leukoplakia
Hairy leukoplakia, sometimes called oral hairy leukoplakia, results from infection with Epstein-Barr virus (EBV). Once you are infected with EBV, the virus remains in your body for life. Normally the virus is dormant, but if the immune system is weakened by illness or certain medicines, the virus can reactivate, which can lead to conditions such as hairy leukoplakia.
People with HIV/AIDS are particularly likely to develop hairy leukoplakia. Although the use of antiretroviral medicines has reduced the number of cases, hairy leukoplakia still affects a number of HIV-positive people and may be one of the first signs of HIV infection. The appearance of oral hairy leukoplakia may also be a sign that antiretroviral treatment is failing.
HIV Infection
HIV (Human Immunodeficiency Virus) infection is a chronic infectious disease in which the immune system is progressively suppressed by the causative virus.
The causative virus (HIV) is a retrovirus belonging to the lentivirus family. Retroviruses are enveloped viruses containing single-stranded RNA. By means of the enzyme reverse transcriptase, they can convert their genetic material into double-stranded DNA and integrate it into the host chromosome.
On the surface of human lymphocytes there are specific glycoproteins involved in cell activity and function. Lymphocytes carrying the CD4 cell surface antigen are cells that assist immunological reactions. CD4+ lymphocytes are also the primary targets of HIV infection. Over the course of HIV infection the CD4+ T-cell count steadily falls, and as a result the opportunistic infections and cancers characteristic of AIDS appear.
After the virus is acquired, the disease progresses through certain stages.
I. CLINICAL COURSE OF HIV INFECTION
The natural course of HIV infection is studied by dividing it into seven stages.
1. Transmission of the virus
2. Primary HIV infection (acute HIV infection)
3. Seroconversion (antibody formation)
4. Asymptomatic stage
5. Early symptomatic stage
6. Late symptomatic stage (AIDS)
7. Advanced stage