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Retinopathy of Prematurity

What is retinopathy of prematurity?
What causes retinopathy of prematurity?
Who gets retinopathy of prematurity?
How does it cause disease?
Common findings
Treatment
What are the complications?
How do you prevent it?
What research is being done?
Links to other information

David W. Johnson, M.D. Assistant Clinical Professor Department of Ophthalmology University of Colorado Health Sciences Center Denver, Colorado

What is retinopathy of prematurity?
Retinopathy of prematurity is a disease of the retinal blood vessels that can occur in extremely premature infants. The retina is the inner lining of the eye that consists of specialized nerve cells necessary for sight. Blood vessels in the retina develop first from the optic nerve area at the very back of the eye, with growth of blood vessels within the retina toward the front of the eye. The normal process of retinal blood vessel growth is sped in premature infants, leading to the formation of abnormal blood vessels and scar tissue.

What causes retinopathy of prematurity?
Researchers have discovered several risk factors for retinopathy of prematurity. One of the most significant risk factors is prematurity (born before 34 weeks of pregnancy). Another risk factor is low birth weight (less than 1500 grams or approximately 3 pounds). In the past, extremely high levels of oxygen therapy necessary for the survival of premature infants were thought to contribute to retinopathy of prematurity. However, with the precision of modern oxygen monitoring techniques now available, it is unlikely that excess oxygen causes this disease. Retinopathy of prematurity also has been reported in infants who receive no supplemental oxygen. In experiments, retinopathy of prematurity has been produced in animals by conditions simulating low-oxygen levels.

Who gets retinopathy of prematurity?
Infants weighing less than 1250 grams have an approximately 50% chance of developing some retinopathy of prematurity. As birth weight decreases, the likelihood of retinopathy of prematurity increases. More than 90% of infants weighing less than 750 grams develop retinopathy of prematurity. The same trend holds true in relation to when an infant is born. Approximately 30% of infants after 32 weeks of pregnancy develop retinopathy of prematurity, and greater than 80% of infants less than 28 weeks of pregnancy develop retinopathy of prematurity.

How does it cause disease?
The growth of normal retinal blood vessels may be sped, with normal vessels only growing to the middle of the retina. Beyond this, the retina has no blood vessels. Most likely, a chemical signal is then sent out that stimulates the remaining retina to grow new blood vessels. The new blood vessels are abnormal and frail, and they can bleed and scar easily. If enough of this scar tissue is present, it can pull on the retinal tissue, causing a traction retinal detachment. If the situation progresses further, a total retinal detachment can occur, leading to vision loss and, possibly, loss of the eye.

Common findings
An ophthalmologist experienced in the examination for this condition can diagnose retinopathy of prematurity. A set of dilating drops is placed in each eye to dilate the pupil. The infant is examined with an instrument to keep the eyelids open (called a lid speculum), and the retina is inspected with an ophthalmoscope. The eyeball may be manipulated to complete the examination.
The area (zone) of retinal involvement and the severity (stage) of the disease define retinopathy of prematurity.
Zone I is a circular area, roughly equivalent to the optic nerve and macular area in the center of the retina. Zone II is a larger circle surrounding this area, roughly equivalent to the middle of the retina. Zone III is the remaining anterior (or front) retina and represents an area of near maturity of the retinal vessels. Severe retinopathy of premature occurs most often in Zones I and II.
Stage I is defined as a line found at the border of the normal retina and the retina without blood vessels. Stage II is defined as a thickening of the line to form what is called a ridge. These stages probably represent growth of immature retinal cells. Stage III involves growth of new abnormal blood vessels, both on the ridge and elevated above the ridge into the vitreous (clear, gelatinous material between the retina and the lens) area. When Stage III blood vessel growth reaches a certain level, it is best treated by laser. Stage IV involves traction and detachment of the retina. This stage is divided into Stage IV-A, or detachment not involving the macula (area near the center of the retina where vision is most clear), and Stage IV-B, or detachment involving the macular or central retina. Stage V is defined as a total tractional retinal detachment for which there is often no effective treatment.
Plus disease is defined by abnormal vessels that are very tortuous, along with the findings listed above, usually indicating a situation that may require immediate treatment. Rush disease indicates unusually fast progression (1- to 2-week period) from no retinopathy of prematurity to disease that requires treatment.
Most retinopathy of prematurity does not require treatment and resolves on its own. The risk of developing disease that requires treatment is highly related to low birth weight and prematurity. In infants weighing less than 750 grams (approximately 1 1/2 pounds), 15% to 20% of infants developing any retinopathy of prematurity do go on to disease that requires treatment. For infants weighing greater than 1250 grams (approximately 2 3/4 pounds), only 2% of infants developing retinopathy of prematurity go on to disease needing treatment. Some retinopathy of prematurity that develops in the remainder of the infants ultimately resolves on its own.

Treatment
Earlier studies found a beneficial effect of cryotherapy (freezing treatment) to the peripheral areas of the retina (areas without blood vessels) in healing retinopathy of prematurity. Now, cryotherapy has been replaced largely by laser treatment. In both treatments, the peripheral areas of the retina are destroyed, leading to a decreased demand for the growth of new blood vessels. The abnormal new blood vessels then are seen to shrink away, leaving no further effect on the retina.
The ophthalmologist delivers the laser treatment through the dilated pupil with an indirect ophthalmoscope system (similar to the setup used for examination). The treatment generally takes 30-45 minutes per eye, and it often is performed in the neonatal intensive care setting. Intravenous (IV) sedation and pain relief commonly are used, and a breathing tube sometimes is necessary.
The infant usually is reexamined at 2-4 weeks. Re-treatments of problem areas occasionally are necessary. Progression of severe retinopathy of prematurity can occur despite successful cryotherapy or laser treatment. A small percentage of eyes continue on to traction retinal detachment despite adequate treatment.

What are the complications?
Continued retinopathy of prematurity with traction retinal detachment and loss of vision is the final outcome in some cases, although this risk is reduced greatly with well-timed treatment. Even if retinopathy of prematurity resolves on its own or if treatment is required, certain outcomes are common, including nearsightedness (difficulty seeing things far away). Other possible complications include amblyopia (weakened vision in one eye) or strabismus (misalignment of the eyes) with an eye deviating in (esotropia) or out (exotropia) when compared to the other eye. A pediatric ophthalmologist can address all these conditions in the follow-up stage.
Complications of laser treatment or cryotherapy include corneal burns or swelling (edema), lens burns or cataract formation, and vitreous hemorrhage or bleeding into the center cavity of the eye. As mentioned above, retinal traction and detachment can occur despite treatment.

How do you prevent it?
No proven treatment exists to prevent the occurrence of retinopathy of prematurity in infants who are at an increased risk. Careful monitoring of oxygenation status and examination of high-risk infants at 6 weeks after birth effectively identifies cases of retinopathy of prematurity that may need additional treatment. No correlation exists between lighting conditions in the nursery and the development of retinopathy of prematurity.

What research is being done?
The effect of supplemental oxygen on infants with Stage III is being studied in the S-ROP (Supplemental Therapeutic Oxygen for Prethreshold Retinopathy of Prematurity) trial. The initial results from this study indicate no firm beneficial effect of increasing oxygenation in Stage III of this condition. The multicenter CRYO-ROP (Cryotherapy for Retinopathy of Prematurity) study continues to observe infants in a phase III long-term follow-up study.

Links to other information
The American Academy of Pediatric Ophthalmology and Strabismus Web site has additional information on retinopathy of prematurity at http://med-aapos.bu.edu.
Informational brochures are available from The American Academy of Ophthalmology Web site at http://www.eyenet.org.

References
The Committee Classification of Retinopathy of Prematurity. An international classification of retinopathy of prematurity. Arch Ophthalmol. 1984 Aug;102(8):1130-1134.
The International Committee for the Classification of the Late Stages of Retinopathy of Prematurity. An international classification of retinopathy of prematurity. II. The classification of retinal detachment. Arch Ophthalmol. 1987 Jul;105(7):906-912.
Cryotherapy for Retinopathy of Prematurity Cooperative Group. Multicenter trial of cryotherapy for retinopathy of prematurity. Preliminary results. Arch Ophthalmol. 1988 Apr;106(4):471-479.
Cryotherapy for Retinopathy of Prematurity Cooperative Group. Multicenter trial of cryotherapy for retinopathy of prematurity. 3 ï¿½-year outcome-structure and function. Arch Ophthalmol. 1993 Mar;111(3):339-344.
About the Author
David W. Johnson, MD, is an ophthalmologist in private practice specializing in vitreoretinal surgery. He currently holds a teaching appointment as Assistant Clinical Professor in the Department of Ophthalmology at the University of Colorado Health Sciences Center in Denver. Dr. Johnson actively participates in the diagnosis and treatment of retinopathy of prematurity at several Denver area hospitals.
Copyright 2012 David W. Johnson, M.D., All Rights Reserved

Rheumatic Fever, Acute

What is acute rheumatic fever?
Common Causes
Who gets rheumatic fever?
How does it cause disease?
How is rheumatic fever diagnosed?
Treatment
Complications
Prevention
Research

by Edward L. Kaplan, M.D. Department of Pediatrics University of Minnesota Medical School Minneapolis, MN

What is acute rheumatic fever?
Acute rheumatic fever is a disease that affects the body’s connective tissue and central nervous system. It results from a throat or tonsil infection that is caused by group A beta hemolytic streptococci, commonly referred to as “strep throat.” Rheumatic fever is a side effect of the strep infection, not part of the infection itself. Rheumatic fever affects the heart; the joints; the skin, i.e., an unusual rash called erythema marginatum, and subcutaneous nodules, which are small, pea-sized nodules under the skin; or the central nervous system, i.e., Sydenham’s chorea, commonly known as St. Vitus dance.

Common Causes
Rheumatic fever is the result of a streptococcal sore throat; therefore, it is important to prevent and/or treat this infection. Usually, antibiotic treatment prevents rheumatic fever. Although the exact way in which rheumatic fever develops is not understood, it is believed that the patient who develops rheumatic fever (about 3% of patients with untreated strep throat) have an abnormal immune response to some part of the group A streptococcus. Most likely, this is because some parts of the bacteria are almost identical to certain parts of the human heart and other human tissues. This is thought to result in the body essentially reacting against itself (called “auto-immunity” or “antigenic mimicry”).

Who gets rheumatic fever?
Group A streptococcal upper respiratory tract infections are very common among children. Most patients who develop rheumatic fever are in the age range between 5 and 15 years. It is rare for very young children (less than three or four years of age), as well as adults, to develop rheumatic fever, even if they have a strep infection. However, young adults are susceptible. While there is a genetic predisposition (i.e., it “runs in families”) to developing rheumatic fever, reasons for this are not completely understood.

How does it cause disease?
The symptoms of a strep infection include a sudden onset of a very sore throat with a high fever. Nausea and abdominal pain may occur in children. However, many patients who develop strep throat do not develop these classic symptoms. An abnormal immune response by the body, following a period of approximately 10 days to 2 weeks after the strep infection, is believed to cause the clinical signs of rheumatic fever.
The signs and symptoms of rheumatic fever depend on which body systems are affected. In approximately half of the patients with rheumatic fever, the heart is involved. Patients may develop the symptoms of heart failure, such as shortness of breath. Leaking (“incompetence”) of one of the heart valves results in a heart murmur, which can be heard by a physician.
The arthritis of rheumatic fever is not chronic arthritis. It usually occurs in 60% to 70% of patients. It usually affects large joints, such as elbows, wrists, shoulders, ankles, and knees. It rarely affects the fingers, the spine, or the hips. It is called a “migratory arthritis” because in the untreated patient, it will affect one joint one day and move on to another joint a day or so later. It is important that the migratory nature of the arthritis be documented before making this diagnosis.
Sydenham’s chorea, or St. Vitus dance, is much less common than arthritis or rheumatic heart disease, occurring in only 10% to 15% of patients. Patients may develop clumsiness. Emotional changes often may occur. Typically, findings in children are first noted either at the dinner table, where they find it difficult to use utensils and frequently spill milk, or by a schoolteacher, who notices emotional changes and a deterioration in handwriting and other fine motor skills.
The rash of rheumatic fever, called erythema marginatum, is uncommon, and it is seen in only about 5% to 8% of patients. The rash occurs mainly on the trunk; is circumscribed, i.e., confined to a limited space; is not painful; and does not itch.
The subcutaneous nodules of rheumatic fever also are very rare, except in those individuals who have severe heart valve involvement. These are small, pea-sized nodules, which are often on the back of the hand over the knuckles and on the outside of the elbow joint.

How is rheumatic fever diagnosed?
Physicians diagnose rheumatic fever based on a clinical examination, since there is not a single laboratory test that can diagnose it. Clinical criteria, called the Jones Criteria, take into account the most common findings of patients with rheumatic fever. Thus, physicians may use the Jones Criteria to diagnose rheumatic fever. However, the Jones Criteria can be difficult to apply; many diseases may appear to fulfill the Jones Criteria, but are not rheumatic fever. There are five major criteria (carditis, arthritis, chorea, erythema marginatum, and subcutaneous nodules). Less specific findings, called minor criteria, include fever, aching (not arthritis) of the joints, and several very non-specific laboratory tests. The presence of two major criteria or one major and two minor criteria, plus a recent strep infection, should lead to a possible diagnosis of rheumatic fever.

Treatment
Initially, the treatment of rheumatic fever focuses on the therapy of the group A streptococcal infection, which still may be present at the time that rheumatic fever develops, and, then, it focuses on the clinical symptoms of the disease. Treatment of the sore throat in patients with rheumatic fever is very important. Most often, penicillin (or sometimes another antibiotic) is used to treat the sore throat. Penicillin may be given either orally or by injection.
The treatment of the heart disease depends on its severity. Often, either corticosteroids or aspirin are used. If a patient shows signs of a failing heart (“congestive heart failure”), drugs that strengthen the contraction of the heart, and drugs that help to eliminate excess fluids from the body (diuretics), may be used. While steroids may help the acute phase of the heart disease, if there is heart failure, they do not prevent the development of heart valve disease.
The arthritis of rheumatic fever, while very painful, can be controlled with aspirin (“salicylates”). In fact, once aspirin is started in patients with rheumatic fever, it is common for the arthritis to completely subside in 12 to 24 hours. It is thought that if the arthritis does not disappear quickly after beginning treatment with aspirin, the diagnosis of rheumatic fever should be questioned. Steroids are almost never used to treat the arthritis of rheumatic fever. In the acute phase, the pain of the arthritis can be controlled by any number of pain medications available to a physician.
The treatment of Sydenham’s chorea is more difficult. Specific medications are available that help to reduce the uncontrollable neurological movements of this disease. However, the signs and symptoms of Sydenham’s chorea may persist as long as several months, even when appropriate medications are used.
Treatment is not needed for either the rash or the small, painless subcutaneous nodules.

Complications
The main complication of rheumatic fever is rheumatic valvular heart disease. Approximately 50% (but in some instances, more) of patients will develop scarring of the heart valves. Usually, it is the mitral valve (between the left atrium and the left ventricle), but, sometimes, it involves the aortic valve (the valve that directs blood to the body). Rarely, the valves on the right side of the heart (those to the lungs) are affected. When the heart valves become so damaged and cause heart failure, surgery is needed. Often, an artificial heart valve is required. The arthritis associated with rheumatic fever disappears, and it is not a chronic complication. Sydenham’s chorea may recur in patients who have rheumatic fever, but it usually is not a continuing problem. The other symptoms do not cause long-term complications.

Prevention
There are two types of prevention for rheumatic fever: primary prevention and secondary prevention.
Primary prevention means the appropriate diagnosis and treatment of strep throat, thereby preventing an initial attack of rheumatic fever. Usually, this treatment is with penicillin or similar antibiotics (e.g., amoxicillin). Other drugs, such as erythromycin or some of the cephalosporins, can be used effectively. Erythromycin is used mainly for those individuals who are allergic to penicillin. Penicillin may be given either orally for 10 days or by injection. Although shorter courses (less than 10 days) of antibiotics are thought to be equally effective, most professional organizations recommend the full 10 days of oral antibiotic therapy.
Secondary prevention means the prevention of a second or third attack of rheumatic fever in an individual who has already had the disease. In contrast to primary prevention, which is given only at the time of a strep infection, secondary prevention is continuous. The duration of secondary prevention depends on numerous factors; however, it is usually for at least five years and, frequently, for longer periods of time. Secondary prevention requires careful consideration by a physician. These patients may be given either oral penicillin on a daily basis or injections of a long-acting form of penicillin, called benzathine penicillin G, on a monthly basis. Studies have shown that the injection, while painful in some cases, is more effective in preventing patients from recurrent rheumatic fever. Oral sulfa drugs also may be used for secondary prevention, but not primary prevention, of rheumatic fever.

Research
Research in rheumatic fever, which still is a major cause of heart disease in many parts of the world, focuses on two objectives. The first objective is to more completely understand how the strep infection starts the reaction that results in rheumatic fever. The mechanisms that cause rheumatic fever remain poorly understood. Since control of any disease process is most effective when the cause of the disease is known, this research is important. Whether rheumatic fever is affected by a particular kind of streptococcus that causes the throat infection or whether there are genetic predispositions to developing rheumatic fever remains to be fully understood.
Another current and important area of research is the use of a vaccine to prevent strep infections. Public health programs that use vaccines (e.g., measles) successfully are very cost effective. Unfortunately, the preparation of a vaccine against group A streptococci is more difficult because some parts of streptococcus are similar to some parts of human tissue, and because there are many different types of group A streptococci. A cost-effective vaccine against many types of streptococci would have important public health implications. Studies to develop test vaccines are in progress.
Research is important to better understand how a strep infection is spread, why this infection most often affects children, and how to best diagnose and treat the infection in a cost-effective manner.

About the Author
Dr. Kaplan has been interested for many years in streptococcal infections and their reguelae. He is a renowned authority on Acute Rheumatic Fever and the associated complications.
Copyright 2012 Edward L. Kaplan, M.D., All Rights Reserved

Ringworm (Tinea)

What is tinea (or a ringworm infection)?
What causes tinea?
Who gets tinea?
How do dermahytes cause disease?
What are the common findings?
How is tinea diagnosed?
How is tinea treated?
What are the complications?
How is tinea prevented?

Leslie Capin, M.D. Aurora/Parker Skin Care Center Aurora, Colorado
What is tinea (or a ringworm infection)?
Tinea, also referred to as ringworm, is a common fungal infection of the skin. Fungi are widespread in the environment. There are thousands of fungal species, but only approximately 200 species regularly infect humans, causing either superficial or deeper infections, and, occasionally, both.
The body area affected by the infection classifies tinea. “Tinea capitis” is a superficial fungal infection involving the scalp, while “tinea corporis” is a superficial fungal infection involving the trunk, limbs, and face. “Tinea manuum,” or ringworm, is an infection of the hands, whereas “tinea pedis” is a fungal infection the feet. “Tinea unguium,” or “onychomycosis,” affects the nails.

What causes tinea?
Dermahytes, a group of fungi, cause superficial fungal infections, also known as fungal dermatosis, dermahytosis, ringworm, or tinea.

Who gets tinea?
A dermahyte infection of the scalp (tinea capitis) and of the general skin surface (tinea corporis) is very common during childhood. Because tinea capitis is no longer reportable to the Health Department, the true incidence is unknown. Probably, the highest incidence of tinea capitis occurs among children who are 1 to 10 years of age.
A dermahyte infection of the hands (tinea manuum) and of the feet (tinea pedis) is more common in adulthood than in childhood. Tinea pedis is probably the most common dermahytosis worldwide; up to 70% of the population has had this infection. Tinea pedis occurs in males and in females, and the incidence of the infection increases with age. Most cases of tinea pedis occur after puberty. Nail infection (tinea unguium) is unusual during the first two decades of life.
Tinea most commonly occurs in warm, humid, tropical climates. Certain risk factors may increase the likelihood of a person developing an infection. These predisposing risk factors include some systemic disorders and certain environmental and occupational sources. Systemic diseases that may predispose individuals to tinea infections include diabetes mellitus and those with compromised immune systems.
Environmental and occupational risk factors include animal contact, especially with kittens, puppies, and horses; contact sports; use of gymnasiums and swimming pools; and outdoor occupations.

How do dermahytes cause disease?
Dermahytes cause infection by invading keratin, which is a protein in the outermost layer of the skin, in the hair, and in the nails. Direct contact with infected animals, soil, or humans causes tinea.

What are the common findings?
Many patients with a mild tinea infection may have no symptoms. Symptoms include itching and burning, especially when the body, hands, or feet are involved. Patients also may complain of tenderness, swelling, and pain in the affected area. The more severe the infection, the worse the symptoms may become.
Tinea capitis appears as a combination of hair breakage and loss, redness, and scaling of the scalp. The extent of scalp redness and scaling varies from person to person. There can be minimal scaling and redness that resembles a mild form of dandruff, or there can be marked redness, swelling, puss formation, and hair loss.
Some patients have a strong reaction in their scalp to the dermahyte, and may develop tenderness, pain, and swelling of the lymph nodes in their neck. Rarely, patients have an elevated white blood cell count. A long-term, severe case of tinea capitis that is not treated adequately may lead to permanent hair loss and scarring.
Tinea corporis is a dermahyte infection of the general body surface. Physical examination reveals individual and grouped round patches of red, scaly skin. These round patches, or “rings,” (hence the term, “ringworm”) progressively enlarge and migrate outwards from the center of the ring to form expanding rings. As the ring expands, the center of the ring often becomes clear. Tinea corporis is similar in its appearance virtually anywhere on the body. Tinea faciei appears on the face, and tinea cruris is an infection that involves the upper thigh and groin area.
A tinea infection of the hands primarily involves the palms, with a dry scale often looking like small circular areas of scale. Occasionally, a tinea infection of the hands can have small blisters on the palms. For unknown reasons, a tinea infection of just one hand, in conjunction with an infection of both feet, is the most common pattern.
Usually, tinea pedis is red and scaly between the toes and on the soles. The skin of the web spaces between the toes can become red, softened, and swollen. The redness and scaling can spread to the side of the foot. Blister formation is more common on the feet than with the other tinea infections.
A tinea infection of the nails (tinea unguium or onychomycosis) invades the nail plate, and causes the nail to lift, thicken, discolor, and become fragile.

How is tinea diagnosed?
An appointment should be made with a primary care provider or a dermatologist for diagnosis and treatment, if an individual experiences the following: hair loss, accompanied by redness and scaling of the scalp; patches of red, circular, scaly skin on the body, hands, or feet; blisters on the palms and soles; or nail changes.
The health care provider will sample a small piece of scale or blister, hair, or nail, and analyze it under the microscope for a fungal organism to establish the diagnosis. This test is called a potassium hydroxide preparation (KOH). Occasionally, the fungal branches and spores characteristic of the infection cannot be seen under the microscope, and a fungal culture will be sent to the laboratory to establish the correct diagnosis. It may take two to four weeks to obtain the fungal culture results.

How is tinea treated?
Tinea infections are treated with ical or systemic oral antifungal medications, and, occasionally, both. Anytime the infection involves the hair or the nails, an oral antifungal medication must be used. When only the skin is involved, a ical antifungal medication is usually sufficient, if the infection does not cover a large body area.
If a large percentage of the body surface is involved, an oral and ical antifungal medication may be prescribed. Antifungal drugs have become increasingly effective in the treatment of tinea infections, especially the newer antifungal drugs on the market. Experience with most of the newer antifungal drugs is limited to patients over 12 years of age.
Griseofulvin was the first significant oral antifungal on the market used to treat tinea infections. It continues to be the preferred drug in the pediatric population because of its long history of effectiveness, its low cost, and its proven safety profile. Griseofulvin is used frequently to treat tinea capitis and tinea corporis in children. It also is used to treat tinea manuum and tinea pedis.
Common side effects of griseofulvin include headaches and gastrointestinal upset. Rarely, allergic rashes from griseofulvin occur. Griseofulvin may make a patient more sensitive to the sun, and the patient is at risk of developing a photosensitive rash or a sunburn.
Many very effective ical antifungal medications are available over the counter, and they can be used one to two times daily to clear infections (except tinea capitis and onychomycosis). Blistering skin eruptions on the palms and soles should be treated with cool compresses, such as Burrow’s solution. Large blisters should be opened and drained for comfort.
The newer antifungal medications on the market, namely Itraconazole and Terbinafine, are very effective for nail infections. Your primary care provider will help you to decide which ical and/or oral antifungal medication is most appropriate for your child.

What are the complications?
Tinea infections may lead to secondary bacterial infections, hair loss, and scarring. Occasionally, patients will have swollen lymph nodes that may persist

How is tinea prevented?
A cool, dry environment, as well as avoiding exposure to infected animals, soil, and humans, may help reduce infections. Good personal hygiene, thorough drying of the hands and feet, absorbent socks, and wearing breathable natural materials may help prevent infection. For patients that experience recurrent tinea pedis infections, light, ventilated footwear or sandals and a medicated foot powder may be helpful. Sprays or powders with antifungal activity applied into footwear also may help prevent reinfection. Treatment is usually permanent, although the infection may recur.

Roseola

What is roseola?
What causes roseola?
Who gets roseola?
How do HHV6 and HHV7 cause disease?
What are the common findings?
How is roseola diagnosed?
How is roseola treated?
What are the complications?
How can roseola be prevented?
What research is being done?

What causes roseola?
Human herpesvirus type 6 (HHV6) and, sometimes, human herpesvirus type 7 (HHV7) cause roseola. Both are members of the herpesvirus family of viruses.

Who gets roseola?
Almost all children are infected during early childhood with HHV6 and HHV7, but only about one-third of children develop signs of roseola. The peak age for developing roseola is 6 to 15 months of age. More than 95% of cases occur in children younger than 3 years of age.

How do HHV6 and HHV7 cause disease?
HHV6 and HHV7 are transmitted from person-to-person by direct contact or by contaminated secretions of the nose and the mouth. These viruses are spread through the blood throughout the body, which causes the rash.

What are the common findings?
The majority of children with roseola develop a characteristic illness with a very high fever (from 100F to 103F) for approximately three days, which is followed by the onset of a rash the day that the fever resolves. In contrast to what is usually expected with such a high fever, most children, during the fever, behave quite normally and continue with their usual play activities. Some infants may become irritable and have a decreased appetite. In classic cases, the rash typically appears within 24 hours after the fever resolves and then fades over one to three days; however, only approximately 25% of infected children may actually develop the rash.

How is roseola diagnosed?
Roseola is diagnosed primarily on the characteristically high fever followed by the development of the rash once the fever resolves. Unfortunately, this makes it very difficult to diagnose roseola during the course of the fever because, typically, there are no other symptoms.
There is a blood test that is available, but, usually, this is not used for diagnosis because either the illness has resolved completely after a few days, or the diagnosis can be made by the physician with some certainty because of the characteristic high fever followed by the rash.

How is roseola treated?
There is no specific treatment for roseola. Antibiotics are not helpful because a virus causes roseola. Viruses cannot be treated with antibiotics. The disease is usually mild with complete recovery. Fever should be treated with acetaminophen or ibuprofen.

What are the complications?
The major complication of roseola in children is the development of febrile seizures. During the time of the high fever, especially early in the infection, children may have seizures that are caused by the very high fever. Febrile seizures occur in 2% to 3% of all children, and usually are a problem between 6 months and 3 to 4 years of age. Many cases of febrile seizures that occur only once in a child are probably due to roseola.

How can roseola be prevented?
A vaccine for roseola is not available. There is very little information on how to prevent roseola; however, outbreaks are uncommon. The spread of roseola can be prevented by minimizing exposure to children who have symptoms of the disease, and by good handwashing after exposure to the disease.

What research is being done?
Research is being conducted on the transmission of human herpesvirus 6 and to characterize how the virus causes roseola.

About the Authors
Hal Jenson, M.D.
Dr. Jenson graduated from George Washington University School of Medicine in Washington, DC,
He also completed a residency in pediatrics at the Rainbow Babies and Children’s Hospital of Case Western Reserve University in Cleveland, Ohio, and a fellowship in pediatric infectious diseases and epidemiology at Yale University School of Medicine.
Dr. Jenson has an active research program on the biology of Epstein-Barr virus and other human and non-human primate herpes viruses.
He is active in the general pediatric and infectious diseases teaching and clinical activities of his Department and Division, is a co-editor of Nelson Textbook of Pediatrics and of Pediatric Infectious Diseases: Principles and Practice, and authors the book Pocket Guide to Vaccination and Prophylaxis.
Charles T. Leach, M.D.
Dr. Leach received his medical degree at the University of Utah School of Medicine and completed his pediatrics residency as well as a fellowship in pediatric infectious diseases at UCLA.
He is currently Associate Professor and Director of Research in the Department of Pediatrics at the University of Texas Health Science Center at San Antonio.
Dr. Leach conducts scientific research in the areas of herpes virus infections, pediatric AIDS, and infectious diseases among residents of the Texas-Mexico border.
Copyright 2012 Hal B. Jenson, M.D., and Charles T. Leach, M.D., All Rights Reserved

Rotavirus

http://www.cdc.gov/rotavirus/index.html

Rubella (German Measles)

What is rubella?
What causes rubella?
Who gets rubella?
How does the rubella virus cause disease?
What are the common findings?
How is rubella diagnosed?
How is rubella treated?
What are the complications?
How can rubella be prevented?
What research is being done?

by Hal B. Jenson, M.D. Chief, Pediatric Infectious Diseases University of Texas Health Science Center San Antonio, TX and by Charles T. Leach, M.D. Associate Professor of Pediatrics University of Texas Health Science Center San Antonio, TX
What is rubella?
Rubella-also commonly known as German measles or, sometimes, three-day measles because of the characteristic duration of the rash-is usually a mild and frequently inapparent infectious disease in children and adults.
A rubella infection during the first trimester of pregnancy can result in miscarriage, stillbirth, or infants with a pattern of birth defects known as “congenital rubella syndrome.” Congenital rubella syndrome can result in many severe symptoms in the newborn, including poor growth, cataracts, deafness, and heart defects.

What causes rubella?
The rubella virus, an RNA virus of the rubellavirus family of viruses, causes rubella.

Who gets rubella?
Rubella was an important disease that occurred in almost all children before the introduction of the rubella vaccine. Rubella is highly contagious, and it has historically caused large outbreaks. The last epidemic of rubella in the United States occurred in 1964, and resulted in more than 20,000 infants being born with congenital rubella syndrome. Rubella is now very uncommon in the United States. Since licensure of the rubella vaccine in 1969, the incidence of rubella has decreased from an average of more than 47,000 reported cases annually to only 345 cases in 1998, with only 5 cases of congenital rubella syndrome.

How does the rubella virus cause disease?
The rubella virus is transmitted from person-to-person by direct contact or by contaminated secretions of the nose and the mouth. The rubella virus infects the lining of the nose and the upper respiratory tract. Then, it is spread through the blood throughout the body, which causes the rash.

What are the common findings?
The symptoms of rubella are variable and usually very mild. Up to one-half of persons have no symptoms at all. The typical symptoms of a rubella infection are a low-grade fever, swollen lymph nodes (“lymphadenopathy”), and a rash. Such symptoms as fatigue and poor appetite usually are not prominent.
Swollen lymph nodes of the neck are a common feature of rubella. Classically, it appears one day before the rash, and is most prominent in the lymph nodes behind the ears and in the back of the neck. After approximately 12 to 24 hours, the rash appears. The rash is a flat rash that appears all over the body and is very subtle. The rash usually disappears within two to three days. It is commonly itchy in adults, but not in children.

How is rubella diagnosed?
Rubella is diagnosed primarily on initial suspicion from the clinical and physical examination findings and confirmation by a laboratory test for rubella antibodies. The appearance of the rash usually is not characteristic. It is very difficult to be certain of the diagnosis of rubella without testing for the antibodies (i.e., IgM antibodies) found early in the illness.

How is rubella treated?
There is no specific treatment for rubella. Antibiotics are not helpful because a virus causes rubella. Viruses cannot be treated with antibiotics. Fortunately, most persons with rubella have either no symptoms or very mild symptoms, and have complete recovery. The fever should be treated with acetaminophen or ibuprofen.

What are the complications?
Complications of rubella are very uncommon in children. Young female adolescents and young women are more likely to develop transient joint aches and pains that typically affect the fingers, knees, wrists, elbows, and ankles. Usually, this lasts for one to four weeks; however, some patients develop chronic arthritis.
Approximately 1 in 3,000 cases of rubella will develop very low platelet counts, which can interfere with blood clotting. Inflammation of the brain (“acute encephalitis”) may occur in approximately 1 out of 5,000 to 24,000 cases.
Progressive rubella panencephalitis is a rare chronic encephalitis associated with a persistent rubella virus infection of the brain. Approximately 20 cases have been reported, all in males who were 8 to 21 years of age at the onset of the symptoms. Most of these patients also had congenital rubella syndrome. No new cases have been described in the United States in recent years due to the routine rubella vaccination.
A major complication of rubella is congenital rubella syndrome, which occurs when a pregnant mother develops rubella and transmits the viral infection to the developing fetus. The fetus may be severely affected with poor intrauterine growth, cataracts, deafness, and heart defects. These and other findings are usually present at birth.

How can rubella be prevented?
A vaccine for roseola is not available. There is very little information on how to prevent Rubella is effectively prevented by the routine administration of the rubella vaccine, usually given as Measles-Mumps-Rubella (MMR) vaccines to all children. This vaccine is recommended beginning at 12 months of age. A single dose of the rubella vaccine results in protection of approximately 95% of children. A second dose of MMR is recommended at four to six years of age. It is not a problem if an additional dose of the rubella vaccine is given in addition to the two recommended doses.
The spread of rubella can be prevented by minimizing exposure to children who have symptoms of the disease, and by good handwashing after exposure to the disease.
Pregnant women should routinely be tested in early pregnancy for antibodies to rubella. If a pregnant woman who does not have antibodies is exposed to rubella in the first trimester, antibodies can be given as soon as possible to try to prevent infection of the fetus and congenital rubella syndrome. Pregnant women who do not have rubella antibodies should be immunized immediately after delivery.

What research is being done?
Because rubella is now extremely uncommon, and because the vaccine is extremely safe and effective in preventing rubella, there is not much research on rubella currently being performed. There is some research being conducted on the role of the rubella virus in causing arthritis that some persons develop, and on the long-term immunity of the rubella vaccine to confirm that it does provide lifelong immunity.

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