Manifestations in the oral cavity in infectious diseases in children. Tactics dentist
Rubeola (nine-day or red measles)
Measles, a disease recognised for over two thousand years, is a highly contagious, acute infection caused by the rubella virus. It usually occurs in children. It is seen in every country of the world. Before the use of vaccines, epidemics of measles occurred every two to five years. Cough, cold, fever and a skin rash that begins several days before the initial symptoms characterise the illness. Recovery from measles is usual, but serious complications of the respiratory and central nervous system may occur.
· Prodromal symptoms – fever, malaise, dry (occasional croupy) cough, coryza, conjunctivitis c clear d/c, marked photophobia.
· 1-2 days p prodromal symptoms – Koplik spots on the buccal mucosa.
· Koplik spots – tiny, bluish-white dots surrounded by red halos.
· Day 3 or 4 – blotchy, erythematous, blanching, maculopapular exanthem appears.
· Rash begins at the hairline and spreads cephalocaudally and involves palms and soles.
· Rash typically lasts 5 – 6 days.
· Can see desquimation in severe cases.
· Patients can be systemically ill
· Incubation period 9-10 days
· Patients contagious from 4 days prior to the rash until 4 days after the resolution of the rash
· Highly contagious – 90% for susceptible people
· High morbidity and mortality common in children in underdeveloped countries
· Peak season is late winter to early spring
· Potential complications – OM, PNA, obstructive laryngotracheitis, acute encephalitis
· Vaccination is highly effective in preventing disease
Measles virus belongs to the Morbillivirus group of the Paramyxovirus family. Humans are the only natural host for wild measles virus. The virus is easily destroyed but remains in the droplet form in air for several hours, especially under conditions of low relative humidity. It is spread by direct contact with droplets from respiratory secretions of infected persons. It is one of the most communicable of infectious diseases and is most infectious when cough and cold is at its peak. The virus invades the respiratory lining membrane and then enters the blood stream. It causes inflammation of the respiratory tract and may predispose to secondary bacterial pneumonia.
The incubation period is one to two weeks and is often longer in adults. The illness begins with symptoms of malaise, fever, loss of appetite, conjunctivitis, cough and cold lasting several days. This is followed by bluish-grey spots in the oral cavity (Koplik’s spots) and then a diffuse skin rash beginning on the face and proceeding down the body to involve the extremities. The rash lasts for five days and then peeling of the skin occurs. Several days after the appearance of the rash, the fever abates. The most common complications of measles involve the respiratory tract and the nervous systems. Bacterial super-infection can also cause middle ear infection or pneumonia in severe cases. Encephalitis may be acute or chronic, after measles infection. Transient hepatitis can also occur.
Severe measles can occur in persons who are immunocompromised such as those, being treated for malignancy or those with AIDS. Malnourished children in developing countries may also develop severe measles. In pregnant women, however, measles (rubeola) unlike German measles (rubella) does not cause any congenital anomalies.
Classic measles is diagnosed when a child develops along with cough, cold, conjunctivitis, Koplik’s spots and a skin rash. Leucopenia (a low white blood cell count) is common. Virus isolation in the laboratory is technically difficult. A four-fold increase in the measles antibody titre in acute and convalescent serum samples is considered diagnostic.
The disease is usually self-limited, and supportive therapy such as antipyretics and fluids are indicated. Bacterial super-infection should be promptly treated with appropriate antimicrobials. Prophylactic antibiotics are not known to be of value and are not recommended.
Measles can be prevented by administrating a live vaccine long before an anticipated exposure. It is now recommended that all healthy children be administered live measles vaccines at fifteen months of age. A second dose given in childhood, usually as a measles-mumps-rubella (MMR) is now routine. The first vaccine can be given between six and nine months of age in situations where the incidence of measles is high before the age of one year. Transient fever and rash develop about one week after vaccination in 5 – 15 percent of children. Live measles vaccine is contra-indicated in persons with defects in the cell-mediated immunity and in pregnant women.
Passive immunisation with antibodies is recommended for those at high risk of developing severe measles and for those who have been exposed to the infection. For example, children with malignant disease and those with defects in cell-mediated immunity. To be effective, passive immunisation must be given within six days after an exposure.
rubeola (nine-day or red measles)
Rubella (german measles)
Rubella — commonly known as German measles or 3-day measles — is an infection that primarily affects the skin and lymph nodes. It is caused by the rubella virus (not the same virus that causes measles), which is usually transmitted by droplets from the nose or throat that others breathe in. It can also pass through a pregnant woman’s bloodstream to infect her unborn child.
It’s a generally mild disease in children; the primary medical danger of rubella is the infection of pregnant women because it can cause congenital rubella syndrome in developing babies.
Before a vaccine against rubella became available in 1969, rubella epidemics occurred every 6-9 years, most often among kids 5 to 9 years old. Many cases of congenital rubella occurred as well. Thanks to immunization, there are far fewer cases of rubella and congenital rubella.
Most rubella infections today appear in young, non-immunized adults rather than in kids. In fact, experts estimate that 10% of young adults are currently susceptible to rubella, which could pose a danger to children they might have someday.
· Little or no prodrome in children
· In adolescents – 1-5 days of low-grade fever, malaise, headache, adenopathy, sore throat, coryza
· Exanthem – discrete, pinkish red, fine maculopapular eruption – begins on the face and spreads cephalocaudally
· Rash becomes generalized in 24 hours and clears by 72 hours
· Forchheimer spots – small reddish spots on the soft palate – can sometimes be seen on day 1 of the rash
· Arthritis and arthralgias – frequent in adolescents and young women – beginning on day 2 or 3 lasting 5-10 days
· Up to 25% of patients are asymptomatic – serology testing may be necessary to establish the diagnosis
· Important in establishing the diagnosis if the patient is pregnant or has been in contact c a pregnant woman
· Peaks in late winter to early spring
· Contagious from a few days before the rash to a few days after the rash
· Incubation period 14-21 days
· Complications – rare in childhood – arthritis, purpura c or s thrombocytopenia, mild encephalitis
Signs and Symptoms
Rubella infection may begin with 1-2 days of mild fever (99-
The rubella rash can look like many other viral rashes. It appears as either pink or light red spots, which may merge to form evenly colored patches. The rash can itch and lasts up to 3 days. As the rash clears, the affected skin occasionally sheds in very fine flakes.
Other symptoms of rubella (these are more common in teens and adults) can include headache, loss of appetite, mild conjunctivitis(inflammation of the lining of the eyelids and eyeballs), a stuffy or runny nose, swollen lymph nodes in other parts of the body, and pain and swelling in the joints (especially in young women). Many people with rubella have few or no symptoms.
Rubella in a pregnant woman can cause congenital rubella syndrome, with potentially devastating consequences for the developing fetus. Children who are infected with rubella before birth are at risk for growth retardation; mental retardation; malformations of the heart and eyes; deafness; and liver, spleen, and bone marrow problems.
Contagiousness
The rubella virus passes from person to person through tiny drops of fluid from the nose and throat. People who have rubella are most contagious from 1 week before to 1 week after the rash appears. Someone who is infected but has no symptoms can still spread the virus.
Infants who have congenital rubella syndrome can shed the virus in urine and fluid from the nose and throat for a year or more and may pass the virus to people who have not been immunized.
Prevention
Rubella can be prevented by the rubella vaccine. Widespread immunization against rubella is critical to controlling the spread of the disease, thereby preventing birth defects caused by congenital rubella syndrome.
The vaccine is usually given to children at 12-15 months of age as part of the scheduled measles–mumps-rubella (MMR) immunization. A second dose of MMR is generally given at 4-6 years of age. As is the case with all immunization schedules, there are important exceptions and special circumstances. For example, if your child will be traveling outside the
The rubella vaccine should not be given to pregnant women or to a woman who may become pregnant within 1 month of receiving the vaccine. If you are thinking about becoming pregnant, make sure that you’re immune to rubella through a blood test or proof of immunization. If you’re not immune, you should receive the vaccine at least 1 month before you become pregnant.
Pregnant women who are not immune should avoid anyone who has the illness and should be vaccinated after delivery so that they will be immune during any future pregnancies.
Incubation
The incubation period for rubella is 14-23 days, with an average incubation period of 16-18 days. This means that it can take 2-3 weeks for a child to get rubella after they are exposed to someone with the disease.
Duration
The rubella rash usually lasts 3 days. Lymph nodes may remain swollen for a week or more, and joint pain can last for more than 2 weeks. Children who have rubella usually recover within 1 week, but adults may take longer.
Treatment
Rubella cannot be treated with antibiotics because they do not work against viral infections. Unless there are complications, rubella will resolve on its own.
Any pregnant woman who has been exposed to rubella should contact her obstetrician immediately.
Rubella is typically mild in kids, who often can be cared for at home. Monitor your child’s temperature and call the doctor if the fever climbs too high.
To relieve minor discomfort, you can give your child acetaminophen or ibuprofen. Do not give aspirin to a child with a viral illness because such use has been associated with the development of Reye syndrome, which can lead to liver failure and death.
rubella (german Measles)
Varicella (chickenpox)
Caused by the varicella-zoster virus (VZV), chickenpox used to be a common illness among kids in the
Kids can be protected from VZV by getting the chickenpox (varicella) vaccine. The vaccine significantly reduces the chances of getting chickenpox. Vaccinated kids who do get chickenpox tend to have milder cases and quicker recoveries compared to those who contract the virus and aren’t immunized.
· Caused by varicella-zoster virus
· Highly contagious
· Brief prodrome of low-grade fever, URI symptoms, and mild malaise may occur
· Rapid appearance of puritic exanthem
· Lesions appear in crops – typically have 3 crops
· Crops begin in trunk and scalp, then spread peripherally
· Lesions begin as tiny erythematous papules, then become vesicles surrounded by red halos
· Lesions began to dry – umbilicated appearance, then surrounding erythema fades and a scab forms
· Hallmark – lesions in all stages of evolution
· All scabs slough off 10-14 days
· Scarring not typical unless superinfected
· Cluster in areas of previous skin irritation
· Puritic lesions on the skin
· Painful lesions along the oral, rectal, and vaginal mucosa, external auditory canal, tympanic membrane
· Occurs year-round, peaks in late autumn and late winter through early spring
· Incubation period ranges from 10-20 days
· Contagious 1-2 days prior to rash until all lesions are crusted over
· Complications – secondary bacterial skin infections (GAS), pneumonia, hepatitis, encephalitis, Reye syndrome
· Severe in the immunocompromised host – can be fatal
· Can have severe CNS, pulmonary, generalized visceral involvement (often hemorrhagic)
· Need to get varicella-zoster immunogloblin 96 hours post-exposure to possible varicella
Symptoms
Chickenpox often starts with a fever, headache, sore throat, or stomachache. These symptoms may last for a few days, with fever in the 101°-
Chickenpox causes a red, itchy skin rash that usually appears first on the abdomen or back and face, and then spreads to almost everywhere else on the body, including the scalp, mouth, arms, legs, and genitals.
The rash begins as multiple small red bumps that look like pimples or insect bites, usually less than a quarter of an inch wide. They appear in crops over 2 to 4 days and develop into thin-walled blisters filled with fluid. The blister walls break, leaving open sores, which finally crust over to become dry, brown scabs. The rash is very itchy, and cool baths or calamine lotion may help to manage the itching.
A hallmark of chickenpox is that all stages (red bumps, blisters, and scabs) can appear on the body at the same time. The rash may be more extensive or severe in kids who have skin disorders like eczema, or weak immune systems. Young kids tend to have a mild illness with fewer blisters than older children or adults. In rare cases, serious bacterial infections involving the skin, lungs, bones, joints, and the brain can occur.
Risk of Shingles
Anyone who has had chickenpox is at risk for developing a skin condition called shingles (herpes zoster) later in life. That’s because after an infection, VZV remains inactive in nerve cells near the spinal cord and reactivates later as shingles, which can cause tingling, itching, or pain in one area of the body, followed by a rash with red bumps and blisters. Fortunately, this is a rare occurrence in kids and teens who have healthy immune systems.
It’s also uncommon for someone who’s been vaccinated against chickenpox to develop singles later in life. When it does happen, the case of shingles is usually milder and less likely to cause complications than in a person who wasn’t immunized.
Contagiousness
The chickenpox virus spreads both through the air (by coughing and sneezing), and by direct contact with mucus, saliva, or fluid from blisters. Chickenpox is contagious from about 2 days before the rash appears until all the blisters are crusted over. A child with chickenpox should be kept out of school until all blisters have dried, usually about 1 week. If you’re unsure about whether your child is ready to return to school, ask your doctor.
Chickenpox is very contagious — most kids with a sibling who’s been infected will get it as well (if they haven’t already had the disease or the vaccine), showing symptoms about 2 weeks after the first child does. To help keep it from spreading, make sure your kids wash their hands frequently, particularly before eating and after using the bathroom. And keep a child with chickenpox away from unvaccinated siblings as much as possible.
People who haven’t had chickenpox or the vaccine also can catch it from someone with shingles, but they cannot catch shingles itself. That’s because shingles can only develop from a reactivation of VZV in someone who has previously had chickenpox.
High-Risk Groups
Certain groups of people are more at risk for complications from chickenpox, including pregnant women and anyone with immune system problems. These groups should avoid others who have chickenpox.
If a pregnant woman who hasn’t had chickenpox in the past contracts it (especially in the first 20 weeks of pregnancy), the fetus is at risk for birth defects and the mother is at risk for more health complications than if she’d been infected when she wasn’t pregnant. If she develops chickenpox just before or after the child is born, the newborn is at risk for serious health complications. There is no risk to a developing baby if the mother develops shingles during pregnancy.
If a pregnant woman has had chickenpox before the pregnancy, the baby will be protected from infection for the first few months of life, since the mother’s immunity gets passed on to the baby through the placenta and breast milk.
Those at risk for severe disease or serious complications — such as newborns whose mothers had chickenpox at the time of delivery, patients with leukemia or immune deficiencies, and kids receiving drugs that suppress the immune system — may be given a medication after exposure to chickenpox to reduce its severity.
Prevention
The chickenpox vaccine is 99% effective at preventing the VZV infection in kids. Doctors recommend that kids receive the chickenpox vaccine twice — when they’re 12 to 15 months old, with a booster shot at 4 to 6 years old.
People 13 years of age and older who have never had chickenpox or haven’t gotten the vaccine should receive two doses of the vaccine at least 28 days apart to be protected. While few people who’ve been vaccinated actually develop chickenpox, those who do tend to develop very mild cases of the condition and recover quickly.
Healthy kids who have had chickenpox do not need the vaccine — they usually have lifelong protection against the illness.
Treatment
Since a virus causes chickenpox, doctors won’t prescribe antibiotics to treat it. However, antibiotics may be required if the sores become infected by bacteria. This is pretty common among kids because they often scratch and pick at the blisters.
An antiviral medicine might be prescribed for people with chickenpox who are at risk for complications. The decision to use this will depend on a child’s age and health, the extent of the infection, and the timing of the treatment. Your doctor can tell you if the medication is right for your child.
Dealing With Discomfort
To help relieve the itchiness, fever, and discomfort of chickenpox:
· Use cool wet compresses or give baths in cool or lukewarm water every 3 to 4 hours for the first few days. Oatmeal bath products, available at supermarkets and drugstores, can help to relieve itching. (Baths do not spread the rash.)
· Pat (don’t rub) the body dry.
· Put calamine lotion on itchy areas (but don’t use it on the face, especially near the eyes).
· Serve foods that are cold, soft, and bland because chickenpox in the mouth can make drinking or eating difficult. Avoid feeding your child anything highly acidic or especially salty, like orange juice or pretzels.
· Ask your doctor or pharmacist about pain-relieving creams to apply to sores in the genital area.
· Give your child acetaminophen regularly to help relieve pain if your child has mouth blisters.
· Ask the doctor about using over-the-counter medication for itching.
Never use aspirin to reduce pain or fever in kids with chickenpox because aspirin has been associated with the serious disease Reye syndrome, which can lead to liver failure and even death.
As much as possible, discourage kids from scratching. This can be difficult for them, so consider putting mittens or socks on your child’s hands to prevent scratching during sleep. In addition, trim fingernails and keep them clean to help lessen the effects of scratching, including broken blisters and infection.
Adenovirus
Adenoviral infections affect babies and young children much more often than adults. Childcare centers and schools sometimes have multiple cases of respiratory infections and diarrhea caused by adenovirus.
Adenoviral infections can occur at any time of the year, but:
· respiratory tract problems caused by adenovirus are more common in late winter, spring, and early summer
· conjunctivitis (pinkeye) and pharyngoconjunctival fever caused by adenovirus tend to affect older kids, mostly in the summer
Adenoviral infections can affect children of any age, but most occur in the first years of life — and most kids have had at least one before age 10. There are many different types of adenoviruses, so some kids can have repeated adenoviral infections.
· 30 distinct types
· Variety of infections including conjunctivitis, URIs, pharyngitis, croup, bronchitis, bronchiolitis, pneumonia (occ fulminant), gastroenteritis, myocarditis, cystitis, encephalitis
· Can be accompanied by a rash – variable iature
· Typically can see – conjunctivitis, rhinitis, pharyngitis c or s exudate, discrete, blanching, maculopapular rash
· Can see anterior cervical and preauricular LAD, low-grade fever, malaise
· Peak season is late winter through early summer
· Contagious during first few days
· Incubation period 6-9 days
Coxsackie
Coxsackieviruses are part of the enterovirus family of viruses (which also includes polioviruses and hepatitis A virus) that live in the human digestive tract. They can spread from person to person, usually on unwashed hands and surfaces contaminated by feces, where they can live for several days.
In cooler climates, outbreaks of coxsackievirus infections most often occur in the summer and fall, though they cause infections year-round in tropical parts of the world.
In most cases, coxsackieviruses cause mild flu-like symptoms and go away without treatment. But in some cases, they can lead to more serious infections.
o Brief prodome – low-grade fever, malaise, sore mouth, anorexia
o 1-2 days later, rash appears
o Oral lesions – shallow, yellow ulcers surrounded by red halos
o Cutaneous lesions – begin as erythematous macules then evolve to small, thick-walled, grey vesicles on an erythematous base
o Highly contagious
o Incubation period 2-6 days
o Lasts 2-7 days
o Peak season summer through early fall
o If no cutaneous lesions – herpangina
o less painful and less intense than herpes gingivostomatitis
Signs and Symptoms
Coxsackievirus can produce a wide variety of symptoms. About half of all kids infected with coxsackievirus have no symptoms. Others suddenly develop high fever, headache, and muscle aches, and some also develop a sore throat, abdominal discomfort, or nausea. A child with a coxsackievirus infection may simply feel hot but have no other symptoms. In most kids, the fever lasts about 3 days, then disappears.
Coxsackieviruses can also cause several different symptoms that affect different body parts, including:
· Hand, foot, and mouth disease, a type of coxsackievirus syndrome, causes painful red blisters in the throat and on the tongue, gums, hard palate, inside of the cheeks, and the palms of hands and soles of the feet.
·
· Herpangina, an infection of the throat which causes red-ringed blisters and ulcers on the tonsils and soft palate, the fleshy back portion of the roof of the mouth.
· Hemorrhagic conjunctivitis, an infection that affects the whites of the eyes. Hemorrhagic conjunctivitis usually begins as eye pain, followed quickly by red, watery eyes with swelling, light sensitivity, and blurred vision.
Occasionally, coxsackieviruses can cause more serious infections that may need to be treated in a hospital, including:
· viral meningitis, an infection of the meninges (the three membranes that envelop the brain and spinal cord)
· encephalitis, a brain infection
· myocarditis, an infection of the heart muscle
Newborns can be infected from their mothers during or shortly after birth and are more at risk for developing serious infection, including myocarditis, hepatitis, and meningoencephalitis (an inflammation of the brain and meninges). Iewborns, symptoms can develop within 2 weeks after birth.
Contagiousness
Coxsackieviruses are very contagious. They can be passed from person to person on unwashed hands and surfaces contaminated by feces. They also can be spread through droplets of fluid sprayed into the air when someone sneezes or coughs.
When an outbreak affects a community, risk for coxsackievirus infection is highest among infants and kids younger than 5. The virus spreads easily in group settings like schools, childcare centers, and summer camps. People who are infected with a coxsackievirus are most contagious the first week they’re sick.
Prevention
There is no vaccine to prevent coxsackievirus infection. Hand washing is the best protection. Remind everyone in your family to wash their hands frequently, particularly after using the toilet (especially those in public places), after changing a diaper, before meals, and before preparing food. Shared toys in childcare centers should be routinely cleaned with a disinfectant because the virus can live on these objects for days.
Kids who are sick with a coxsackievirus infection should be kept out of school or childcare for a few days to avoid spreading the infection.
The duration of an infection varies widely. For fever without other symptoms, a child’s temperature may return to normal within 24 hours, although the average fever lasts 3 to 4 days. Hand, foot, and mouth disease usually lasts for 2 or 3 days; viral meningitis can take 3 to 7 days to clear up.
Treating Coxsackievirus Infections
Depending on the type of infection and symptoms, the doctor may prescribe medications to make your child feel more comfortable. However, because antibiotics only work against bacteria, they can’t be used to fight a coxsackievirus infection.
Acetaminophen may be given to relieve any minor aches and pains. If the fever lasts for more than 24 hours or if your child has any symptoms of a more serious coxsackievirus infection, call your doctor.
Most kids with a simple coxsackievirus infection recover completely after a few days without needing any treatment. A child who has a fever without any other symptoms should rest in bed or play quietly indoors. Offer plenty of fluids to prevent dehydration.
Erythema infectiosum (fifth disease)
Erythema infectiosum (also known as fifth disease) is usually a benign childhood condition characterized by a classic slapped-cheek appearance and lacy exanthem. It results from infection with human parvovirus (PV) B19, an erythrovirus.
Signs and symptoms
Mild prodromal symptoms begin approximately 1 week after exposure to PV-B19 and last 2-3 days. They include the following:
· Headache
· Fever
· Sore throat
· Pruritus
· Coryza
· Abdominal pain
· Arthralgias
These symptoms precede a symptom-free period of about 7-10 days, after which the infection progresses through the following stages:
· Phase 1 – The exanthem begins with the classic slapped-cheek appearance, which typically fades over 2-4 days
· Phase 2 – This phase occurs 1-4 days later and is characterized by an erythematous maculopapular rash that fades into a classic lacelike reticular pattern as confluent areas clear
· Phase 3 – Frequent clearing and recurrences for weeks or occasionally months may occur due to stimuli such as exercise, irritation, stress, or overheating of the skin from sunlight or bathing in hot water
Diagnosis
The diagnosis of erythema infectiosum usually is based on clinical presentation alone, and a workup for patients with the classic presentation is not necessary. For patients with other signs or symptoms associated with human parvovirus (PV) B19 or for exposure in a woman who is pregnant, confirmation of infection may be helpful and can be accomplished with the following specialized tests[3, 4, 5] :
· IgM assays – Enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA)
· Dot blot hybridization
· Polymerase chain reaction (PCR) assay
· Loop-mediated isothermal amplification
Management
Because erythema infectiosum most often is a benign, self-limited disease, reassuring the parents of children with the condition often is the only interventioecessary.[6] Symptomatic relief of erythema infectiosum may be provided using nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve fever, malaise, headache, and arthralgia, along with topical antipruritics and antihistamines (which also relieve pruritus). Treatment also includes plenty of fluids and rest.
o Caused by Parvovirus B19
o Affects preschool and young school aged children
o Peak incidence in late winter and early spring, but it is seen year round
o Characterized by rash – large, bright red, erythematous patches over both cheeks – warm, but non-tender
o Facial rash fades, then see a symmetrical, macular, lacy, erythematous rash on the extremities
o Resolution occurs within 3-7 days of onset
o Transmitted by respiratory secretions, replicates in the RBC precursors in the bone marrow
o Can cause aplastic crisis in patients with sickle cell disease, other hemogloblinopathies, and other forms in hemolytic anemia
Erythema infectiosum
Roseola infantum (exanthem subitum)
Roseola infantum and baby measles, or three-day fever, is a disease of children, generally under two years old, although it has been known to occur in eighteen-year-olds, whose manifestations are usually limited to a transient rash (“exanthem“) that occurs following a fever of about three day’s duration.
It is caused by two human herpesviruses, HHV-6 (Human herpesvirus 6) and HHV-7, which are sometimes referred to collectively as Roseolovirus. There are two variants of HHV-6 (HHV-6a and HHV-6b) and studies in the
Typically the disease affects a child between six months and two years of age, and begins with a sudden high fever (39–40 °C; 102.2-
The rare adult reactivates with HHV-6 and can show signs of mononucleosis.
There is no specific vaccine against or treatment for exanthema subitum, and most children with the disease are not seriously ill. A child with fever should be given plenty of fluids to drink.Paracetamol/acetaminophen or ibuprofen could be given to reduce their temperature (but never aspirin, due to the risk of Reye’s Syndrome).
A small percent of children acquire HHV-6 “subclinically”; in other words, they show no outward sign of the disease. Exanthema subitum occurs in approximately 30% of children during primary HHV-6 infection. Others may be debilitated enough that a doctor’s opinion is required to confirm the diagnosis, and particularly to rule out other more serious infections, such as meningitis or measles. In case offebrile seizures, medical advice is essential.
For HHV-6 infection, no pharmacological treatments have been approved as of June 2012. Although they may be unnecessary for exanthema subitum, the usage of Cytomegalovirus treatments (valganciclovir, ganciclovir, cidofovir, and foscarnet) have shown some success. These drugs are given with the intent of inhibiting proper DNA polymerization by competing with deoxy triphosphate nucleotides or specifically inactivating viral DNA polymerases.
o Febrile illness affecting children 6-36 months
o Human herpesvirus 6 is causative agent
o Symptoms include:
o fever, usually >39
o anorexia
o irritability
o these symptoms subside in 72 hours
o As fever defervenscences, usually an erythematous, maculopapular rash that appear on the trunk and then spread to the extremities, face, scalp, and neck
o Occurs year-round
o More common in late fall and early spring
o Incubation period thought to be 10-15 days
roseola infantum
Infectious mononucleosis
Infectious mononucleosis is an infectious, widespread viral disease caused by the Epstein–Barr virus (EBV), one type of herpes virus, against which over 90% of adults are likely to have acquired immunity by the age of 40. Occasionally, the symptoms can recur at a later period. Most people are exposed to the virus as children, when the disease produces no noticeable or only flu-like symptoms. In developing countries, people are exposed to the virus in early childhood more often than in developed countries. As a result, the disease in its observable form is more common in developed countries. It is most common among adolescents and young adults.
Especially in adolescents and young adults, the disease is characterized by fever, sore throat and fatigue, along with several other possible signs and symptoms. It is primarily diagnosed by observation of symptoms, but suspicion can be confirmed by several diagnostic tests. It is generally a self-limiting disease, and little treatment is normally required.
In adolescence and young adulthood, the disease presents with a characteristic triad:
· Fever – usually lasting 10–14 days; often mild, especially in the last 5–7 days.
· Sore throat (acute pharyngitis) – usually severe for 3–5 days, before resolving in the next 7–10 days.
· Swollen glands (lymphadenopathy) – mobile; usually located around the back of the neck (posterior cervical lymph nodes) and sometimes throughout the body.
Another major symptom is fatigue.http://en.wikipedia.org/wiki/Infectious_mononucleosis – cite_note-NICE-3 Headaches are common, and abdominal pains with nausea or vomiting sometimes also occur. Symptoms most often disappear after about 2–3 weeks. However, fatigue and a general feeling of being unwell may sometimes last for months. Fatigue lasts more than one month in an estimated 9–22% of cases. In cases where fatigue lingers, it generally passes spontaneously within 2 years. Mild fever, swolleeck glands and body aches may also persist beyond 4 weeks. Most people are able to resume their usual activities within 2–3 months.
The most prominent sign of the disease is often the pharyngitis, which is frequently accompanied by enlarged tonsils with pus—an exudate similar to that seen in cases of strep throat.http://en.wikipedia.org/wiki/Infectious_mononucleosis – cite_note-Harrison-6 In about 50% of cases, small reddish-purple spots called petechiae can be seen on the roof of the mouth. Palatal enanthem can also occur, but is relatively uncommon.
Epstein-Barr virus
About 90% of cases of infectious mononucleosis are caused by Epstein-Barr virus, a member of the Herpesviridae family of DNA viruses. It is one of the most commonly found viruses throughout the world. Contrary to common belief, EBV is not highly contagious. It can only be contracted through direct contact with an infected person’s saliva, such as through kissing or sharing toothbrushes, cups, etc. About 95% of the population has been exposed to this virus by the age of 40, but only 15-20% of teenagers and about 40% of exposed adults actually become infected.
Cytomegalovirus
A minority of cases of infectious mononucleosis are caused by human cytomegalovirus (CMV), another type of herpes virus. This virus is found in body fluids including saliva, urine, blood, and tears. A person becomes infected with this virus by direct contact with infected body fluids. Cytomegalovirus is most commonly transmitted through kissing and sexual intercourse. It can also be transferred from an infected mother to her unborn child. This virus is often “silent” because the signs and symptoms cannot be felt by the person infected. However, it can cause life-threatening illness in infants, HIV patients, transplant recipients, and those with weak immune systems. For those with weak immune systems, cytomegalovirus can cause more serious illnesses such as pneumonia and inflammations of the retina, esophagus, liver, large intestine, and brain. Approximately 90% of the human population has been infected with cytomegalovirus by the time they reach adulthood, but most are unaware of the infection. Once a person becomes infected with cytomegalovirus, the virus stays in his/her body fluids throughout his or her lifetime.
Transmission
Epstein–Barr virus infection is spread via saliva, and has an incubation period of four to seven weeks.http://en.wikipedia.org/wiki/Infectious_mononucleosis – cite_note-pmid8710247-17 The length of time that an individual remains contagious is unclear, but the chances of passing the illness to someone else may be the highest during the first six weeks following infection. Some studies indicate that a person can spread the infection for many months after symptoms are completely gone, with one particular study indicating as long as 18 months.
Pathophysiology
The virus replicates first within epithelial cells in the pharynx (which causes pharyngitis, or sore throat), and later primarily within B cells (which are invaded via their CD21). The host immune response involves cytotoxic (CD8-positive) T cells against infected B lymphocytes, resulting in enlarged, atypical lymphocytes (Downey cells). When the infection is acute (recent onset, instead of chronic), heterophile antibodies are produced.
When symptoms of infectious mononucleosis have been caused by cytomegalovirus, or by adenovirus or Toxoplasma gondii (toxoplasmosis), a heterophile antibody test will test negative.
Mononucleosis is sometimes accompanied by secondary cold agglutinin disease, an autoimmune disease in which abnormal circulating antibodies directed against red blood cells can lead to a form of autoimmune hemolytic anemia. The cold agglutinin detected is of anti-i specificity.
Diagnosis
The most commonly used diagnostic criterion is the presence of 50% lymphocytes with at least 10% atypical lymphocytes (large, irregular nuclei), while the person also has fever, pharyngitis and adenopathy. Furthermore, it should be confirmed by a serological test. The atypical lymphocytes resembled monocytes when they were first discovered, thus the term “mononucleosis” was coined. Diagnostic tests are used to confirm infectious mononucleosis, but the disease should be suspected from symptoms prior to the results fromhematology. These criteria are specific; however, they are not particularly sensitive and are more useful for research than for clinical use. Only half the patients presenting with the symptoms held by mononucleosis and a positive heterophile antibody test (monospot test) meet the entire criteria. One key procedure is to differentiate between infectious mononucleosis and mononucleosis-like symptoms.
A few studies on infectious mononucleosis have been conducted in a primary care environment, the best of which studied 700 patients, of which 15 were found to have mononucleosis upon a heterophile antibody test. More useful in a diagnostic sense are the signs and symptoms themselves. The presence of splenomegaly, and posterior cervical,axillary and inguinal adenopathies are the most useful to suspect a diagnosis of infectious mononucleosis. On the other hand, the absence of cervical adenopathy and fatigue are the most useful to dismiss the idea of infectious mononucleosis as the correct diagnosis. The insensitivity of the physical examination in detecting splenomegaly means it should not be used as evidence against infectious mononucleosis.[10]
In the past, the most common test for diagnosing infectious mononucleosis was the heterophile antibody test, which involves testing heterophile antibodies by agglutination of guinea pig, sheep and horse red blood cells. As with the aforementioned criteria, this test is specific but not particularly sensitive (with a false-negative rate of as high as 25% in the first week, 5–10% in the second and 5% in the third). About 90% of patients have heterophile antibodies by week 3, disappearing in under a year. The antibodies involved in the test do not interact with the Epstein–Barr virus or any of its antigens. More recently, more sensitive tests have been developed, such as the immunoglobulin G (IgG) andimmunoglobulin M (IgM) tests. IgG, when positive, reflects a past infection, whereas IgM reflects a current infection. Wheegative, these tests are more accurate in ruling out infectious mononucleosis. However, when positive, they feature similar sensitivities to the heterophile antibody test. Therefore, these tests are useful for diagnosing infectious mononucleosis in people with highly suggestive symptoms and a negative heterophile antibody test. Another test searches for the Epstein–Barr nuclear antigen, while it is not normally recognizable until several weeks into the disease, and is useful for distinguishing between a recent-onset of infectious mononucleosis and symptoms caused by a previous infection. Elevated hepatic transaminase levels is highly suggestive of infectious mononucleosis, occurring in up to 50% of patients. A fibrin ring granuloma may be present.
Differential diagnosis
About 10% of people who present a clinical picture of infectious mononucleosis do not have an acute Epstein-Barr virus infection. A differential diagnosis of acute infectious mononucleosis needs to take into consideration acute cytomegalovirus infection and Toxoplasma gondii infections. Because their management is much the same, it is not always helpful, or possible, to distinguish between Epstein-Barr virus mononucleosis and cytomegalovirus infection. However, in pregnant women, differentiation of mononucleosis from toxoplasmosis is important, since it is associated with significant consequences for the fetus.
Acute HIV infection can mimic signs similar to those of infectious mononucleosis, and tests should be performed for pregnant women for the same reason as toxoplasmosis.
Patients with infectious mononucleosis are sometimes misdiagnosed with a streptococcal pharyngitis (because of the classical clinical triad of fever, pharyngitis and adenopathy) and are given antibiotics such as ampicillin oramoxicillin as treatment.
Other conditions from which to distinguish infectious mononucleosis include leukemia, tonsillitis, diphtheria, common cold and influenza (flu).
Treatment
Infectious mononucleosis is generally self-limiting, so only symptomatic and/or supportive treatments are used. The need for rest and return to usual activities after the acute phase of the infection may reasonably be based on the person’s general energy levels. In particular, bed rest need not be prescribed, and a return to normal activities is desirable as soon as it is comfortable for them to be resumed (gradually, if necessary). Nevertheless, in an effort to decrease the risk of splenic rupture experts advise avoidance of contact sports and other heavy physical activity, especially when involving increased abdominal pressure or the Valsalva maneuver(as in rowing or weight training), for at least the first 3–4 weeks of illness or until splenomegaly has resolved, as determined by a treating physician.
Medications
In terms of medications, paracetamol or NSAIDs, such as ibuprofen, may be used to reduce fever and pain. Prednisone, a corticosteroid, is commonly used as an anti-inflammatory to reduce symptoms of pharyngeal pain,odynophagia, or enlarged tonsils, although its use remains controversial due to the rather limited benefit and the potential of side effects. Intravenous corticosteroids, usually hydrocortisone or dexamethasone, are not recommended for routine use but may be useful if there is a risk of airway obstruction, severe thrombocytopenia, or hemolytic anemia. There is little evidence to support the use of aciclovir, although it may reduce initial viral shedding.http://en.wikipedia.org/wiki/Infectious_mononucleosis – cite_note-Torre1999-33 However, the antiviral drug valacyclovir has recently been shown to lower or eliminate the presence of the Epstein–Barr virus in subjects afflicted with acute mononucleosis, leading to a significant decrease in the severity of symptoms. Although antivirals are not recommended for patients presenting with simple infectious mononucleosis, they may be useful (in conjunction with steroids) in the management of patients with severe EBV manifestations, such as EBV meningitis, peripheral neuritis, hepatitis, or hematologic complications.
Although antibiotics exert no antiviral action they may be indicated to treat bacterial secondary infections of the throat, such as with streptococcus (strep throat). However, ampicillin and amoxicillin are contraindicated during acute Epstein–Barr virus infection since the vast majority of patients treated with them develop a diffuse non-allergic rash.Opioid analgesics are also relatively contraindicated due to risk of respiratory depression.
Enlargement of the spleen is common in the second and third weeks, although this may not be apparent on physical examination; some enlargement of the liver may also be present.http://en.wikipedia.org/wiki/Infectious_mononucleosis – cite_note-Ebell2004-10 Jaundice occasionally occurs. A small minority of people spontaneously present a rash, usually on the arms or trunk, which can be macular (morbilliform) or papular. Almost all people given amoxicillin or ampicillin eventually develop a generalized, itchy maculopapular rash, which however does not imply that the person will have adverse reactions to penicillins again in the future. Occasional cases of erythema nodosum and erythema multiforme have been reported.
o Acute self-limiting illness of children and young adults
o Caused by EBV
o Transmission by oral contact, sharing eating utensils, transfusion, or transplantation
o Incubation period 30-50 days (shorter, 14-20 days, in transfusion-acquired infection)
o Don’t usually see “classic mono” in young children
o Prodrome – fatigue, malaise, anorexia, HA, sweats, chills lasting 3-5 days
Symptoms
o fever – can have wide daily fluctuations
o pharyngitis c tonsillar and adenoidal enlargement c or s exudate, halitosis, palatal petechiae
o LAD – anterior cervical and posterior cervical – in classic cases, generalized LAD toward end of wk 1
Symptoms cont:
o splenomegaly – develops in 50% of patients in 2nd-3rd wk
o hepatomegaly in 10% of patients
o exanthem – erythematous, maculopapular, rubelliform rash in 5-10% of patients
Complications:
o pneumonia
o hemolytic anemia and thrombocytopenia
o icteric hepatitis
o acute cerebellar ataxia, encephalitis, aseptic meningitis, myletis, Guillain-Barre
o rarely myocarditis and pericarditis
Complications cont:
o upper airway obstruction from tonsillar and adenoidal enlargement
· seen more often in younger patients
· children < 5 yrs of age c obstruction are more likely to have secondary OM, recurrent bouts of OM, tonsillitis, and sinusitis
o splenic rupture
Diagnosis:
o classic finding – lymphocytosis (50% or more) c 10% atypical lymphocytes
o 80% or more of patients c elevated liver enzymes
o Monospot – detects heterophil antibodies – specific, not as sensitive – 85% of adolescents + and fewer younger patients
o specific EBV antibody titers and PCR
Herpes simplex infections
Herpes simplex virus (HSV)-1 infection is widespread and oral lesions are common. Recurrent intraoral HSV outbreaks start as a small crop of vesicles that rupture to produce small, painful ulcerations that may coalesce. Lesions on the lip are fairly easy to recognize. In the mouth, lesions on keratinized, or fixed, tissues, including the hard palate and gums, should prompt suspicion of HSV infection. Herpetic ulcerations are often self-limiting, although the use of an antiviral medication such as acyclovir is sometimes necessary to control the outbreak.
Herpes simplex virus (HSV) can cause infections that affect the mouth, the face, the skin, the buttocks. Many people acquire the virus and have no symptoms. For others, painful blisters appear near the area where the virus entered the body. Typically, the blisters heal completely but reappear at some point in the future when least expected (or desired). In between attacks, the virus resides deep in the roots of the nerves that supply the involved area. When herpes simplex lesions appear in their most common location, around the mouth and lips, people often refer to them as “cold sores” and “fever blisters.”
There are two types of HSV, type I and type II. In general, type I, also known as herpes labialis, causes infections above the waist, most commonly as oral “cold sores.” However, both types of HSVs are capable of infecting the skin at any location on the body. Herpes infections, no matter where they occur first, have a tendency to recur in more or less the same place. Such recurrences may happen often (for example, several times per year) or only occasionally (for example, once or twice a year).
After infection, the virus enters the nerve cells and travels up the nerve until it comes to a place called a ganglion. There, it lays quietly in a stage that is referred to as “dormant” or “latent.” At times, the virus can become active and start replicating again and travel down the nerve to the skin, causing sores and blisters. The exact mechanism behind this is not clear, but it is known that some conditions seem to be associated with recurrences.
Infections caused by HSV are contagious. The virus is spread from person to person by kissing, by close contact with herpetic lesions, or even from contact with apparently normal skin that is shedding the virus. Infected saliva is a common means of virus transmission. People are most contagious when they have active blister-like sores. Once the blisters have dried and crusted over (within a few days), the risk of contagion is significantly lessened. However, a person infected with HSV can pass it on to another person regardless of the presence or absence of symptoms and visible sores or blisters. This is because the virus is sometimes shed in saliva even when sores are not present. Despite popular myth, it is almost impossible to catch herpes (cold sores) from surfaces, towels, or washcloths.
Herpetic gingivostomatitis
o yellowish white debris builds on the mucosal surfaces causing halitosis
o vesiculopustular lesions on perioral surfaces
o anterior cervical and tonsillar LAD
o symptoms last 5-14 days, but virus can be shed for weeks following resolution
Primary herpes simplex infections
Herpetic gingivostomatitis
o high fever, irritability, anorexia, mouth pain, drooling in infants and toddlers
o gingivae becomes intensely erythematous, edematous, friable and tends to bleed
o small yellow ulcerations c red halos seen on buccal and labial mucosa, tongue, gingivae, palate, tonsils
Skin infections
o fever, malaise, localized lesions, regional LAD
o direct inoculation (usually cold sores)
o lesions are deep, thick-walled, painful vesicles on an erythematous base – usually grouped, but may be single
o lesions evolve over several days – pustular, coalesce, ulcerate, then crust over
Eczema herpeticum (kaposi varicelliform eruption)
Etiology
Although the above cases illustrate two different clinical pictures of eczema herpeticum, they both testify to the need for quick diagnosis. Eczema herpeticum, also known as Kaposi’s varicelliform eruption, refers to a herpetic superinfection of a pre-existing skin disease. This infection may be from auto-inoculation or from an infected contact. Either herpes simplex virus type 1 (HSV-1) or herpes simplex virus type 2 (HSV-2) may be involved.
Disruption of the stratum corneum secondary to skin disease is the most common predisposing factor. There have been reports of eczema herpeticum occurring in atopic dermatitis, pemphigus foliaceous, Darier’s disease, pemphigus vulgaris, pityriasis rubra pilaris, Hailey-Hailey disease, irritant contact dermatitis, cutaneous T-cell lymphoma, seborrheic dermatitis, Wiskott-Aldrich syndrome, congenital icthyosiform erythroderma, and Sezary syndrome. Eczema herpeticum may also occur when there has been recent injury to the skin such as second-degree burns, autografted skin, and post dermabrasion. A commonality among all these diseases is disruption of the integrity of the epidermis.
Immunosuppression, most commonly secondary to medication, also serves as a risk factor for increased spread of HSV on the skin. In many of the diseases listed above, immunosuppressive treatment of the patient’s primary disease results in impairment of the patient’s immunity. Diseases themselves can also impair immunity. For example, Fukuzawa, Oguchi, and Saida (2000) presented a patient with multiple myeloma who developed eczema herpeticum superimposed on his tinea corporis. Diagnosis of eczema herpeticum should alert the practitioner to examine the patient’s immune status. Finally, factors that precipitate herpes simplex should be considered. It is commonly known that sunburn precipitates herpes outbreaks. Wolf, Tamir, Winber, Mitrani-Rosenbaum, and Brenner presented a patient whose diffuse sunburn was complicated by eczema herpeticum.
The onset of eczema herpeticum is marked by multiple clusters of vesicles in the areas of pre-existing skin disease involvement. These vesicles spread, becoming hemorrhagic and crusted. Soon, painful punched-out erosions are evident. These will often coalesce to form large bleeding erosions. The majority of patients will have fever and malaise.
Frequently, the patient will deny any prior history of herpetic infection. However, subclinical infection, where the patient is not aware of prior HSV infection, is quite common. Although 90% of adults have antibodies to HSV-1 and 20% of adults have antibodies to HSV-2, far fewer adults manifest the disease.
Any patient with multiple coalescing vesicles and fever should suggest HSV infection. However, consideration must be given to other viruses capable of creating a similar clinical picture -most commonly animal pox viruses. A history of zookeeping or laboratory work should raise suspicion of such viruses. In addition, exacerbation of the primary skin disease must be considered. Blistering disorders, such as pemphigus vulgaris or bullous pemphigoid, may present with a similar appearance, but should not be accompanied by fever.
Punched-out erosions and vesicles accompanied by fever and extreme pain should alert the health care provider to consider eczema herpeticum. The quickest method of diagnosis is the time-honored Tzanck preparation. A 15 surgical blade should be used to open the top of a vesicle, scraping the underside of the vesicle as well as the base. The blade is then wiped across a glass slide, heat-fixed, and stained with toluidine blue.
Direct fluorescent antibody testing enables rapid identification of the virus. A slide is prepared as above but is not stained. It is sent to the laboratory for immunofluorescent examination with antibodies against HSV-1 and HSV-2. Results are available within several hours.
Viral culture from a fresh vesicle is another way of typing the virus. Culture takes at least 48 hours for final results and may be negative if a swab is taken from a crusted site, often seen in older lesions. Due to the risk of co-existent bacterial infection, it is wise to perform bacterial cultures at the time of viral culture.
Routine histology is able to confirm viral infection, but will not aid in typing the virus. Characteristic changes include ballooning degeneration with eosinophilic cytoplasm in cells, multinucleated cells, and reticular degeneration of epidermal cells. These characteristic changes may be helpful in the diagnosis of atypical HSV or VZV skin manifestations when culture, DFA, or Tzanck was not performed due to low index of suspicion. However, due to the expense, nonspecific “viral” findings, and delay in results, biopsy is not recommended for diagnosis. Likewise, serology for IgM and IgG antibodies to herpes simplex are of little diagnostic value.
· Onset of high fever, irritability, and discomfort
· Lesions appear in crops in areas of currently or recently affected skin (for those with atopic eczema or chronic dermatitis)
· Lesions begin as pustules, then rupture and crust over the course of a couple of days
· Lesions can become hemorrhagic
· Multiple crops can appear over 7-10 days (like varicella)
· Can be mild or fulminant, depending (in part) on the underlying dermatitis
· If area of involvement is large, can be lots of fluid loss and potentially fatal
· Treat promptly c acyclovir
· Risk of secondary bacterial infections
Eczema herpeticum, initially described by Kaposi in 1887, is a potentially life-threatening herpetic superinfection of a preexisting skin disease. Despite the availability of antiviral therapies, eczema herpeticum remains a dermatologic emergency today. Two different cases of eczema herpeticum are presented and the major aspects of this disease are reviewed.
A 6-1/2 month old female with a history of atopic dermatitis presented to her primary care physician with a foul-smelling, sore rash on the face. Treatment with oral antibiotics, amoxicillin and cephalexin, was ineffective. She was referred to the dermatology clinic. On presentation, her mother reported a several day history of fever up to 104 degrees F. Past medical history was significant for atopic dermatitis, particularly of the face. There was no history of immunosuppression. Medication included cephalexin. Family history was positive for “cold sores” in the father.
On exam the patient had monomorphic, crusted
Therapy should be instituted without delay, with high suspicion or positive Tzanck preparation. Acyclovir is the usual treatment, and for severe disease in immunocompromised patients, is dosed at 15 mg/kg/day intravenously for a minimum of 5 days. For less-severe disease in adults, oral treatment with acyclovir 400 mg 5 times daily for 5 to 10 days is satisfactory. Pediatric patients may be treated with acyclovir 25 mg/kg/day, divided into 5 equal doses for 5 to 10 days. Acyclovir is activated by viral thymidine kinase and then acts to inhibit a viral DNA polymerase. It has relatively few side effects. A major risk of toxicity occurs when intravenously administered acyclovir precipitates as crystals in the kidneys. This results in renal impairment but is prevented with adequate hydration.
Pain must be addressed, especially in cases with diffuse involvement. Oral pain medications are helpful in the outpatient setting but inpatients with more extensive erosions should be offered intravenous medication.
Bacterial superinfection should be addressed with oral antibiotics. Most commonly, Staphylococcus coverage is required. If there is no evidence of bacterial superinfection, the use of a topical antibiotic cream such as silver sulfadiazine is recommended to prevent infection.
Patients with a history of recurrent HSV-1 or HSV-2 infection and a chronic skin disease which predisposes them to eczema herpeticum should be offered prophylactic antiviral therapy. Alternatives include acyclovir 400 mg orally twice a day or valacyclovir 500 mg to
If left untreated, eczema herpeticum can become life threatening. Eczema herpeticum has resulted in herpes hepatitis, as well as disseminated intravascular coagulation. Indeed, prior to the introduction of antiviral therapies, fatalities were common. Laboratory examination in a systemically ill patient should include complete blood count with platelets and liver function tests. Additionally, if the face has multiple erosions, an ophthalmology consult should be obtained to rule out herpes keratitis.
Although potentially life threatening, if eczema herpeticum is recognized early it is easily and effectively treated. Any patient with pre-existing skin disease and acute “blistering” should be examined for eczema herpeticum.
Herpes zoster (shingles)
· Secondary chickenpox in an adult
Characterized by a unilateral, painful eruption of vesicles along the distribution of a sensory nerve
· Any branch of the trigeminal nerve may be involved if lesions affect the face.
· Vesicles are often preceded by pain, burning, or paresthesia.
· The disease usually lasts for several weeks.
o Neuralgia may take months to resolve.
