I
Immunizations
http://www.cdc.gov/vaccines/pubs/default.htm
Infant of a Diabetic Mother
What are the classifications of maternal diabetes?
Why are the classifications important?
What are the risks to the infant?
What can be done to decrease the risk of complications to the infant?
What special tests may be required for a diabetic mother during pregnancy?
What special tests may be required for the infant after birth?
What special treatments may be required for the infant after birth?
What is the risk of the infant developing insulin-dependant diabetes?
Jan E. Paisley, M.D. Fellow in Neonatal-Perinatal Medicine William W. Hay, Jr., MD Professor of Pediatrics, Director of the Training Program in Neonatal-Perinatal Medicine Director of the Neonatal Clinical Research Center Section of Neonatology, Department of Pediatrics University of Colorado School of Medicine Denver, Colorado
What are the classifications of maternal diabetes?
The classifications of maternal diabetes are outlined in Table 1.
Why are the classifications important?
The classification of diabetes during pregnancy is important because the outcome of both the mother and the baby are related to the severity and the duration (represented by the different classes) of the mother’s diabetic condition.
In mothers with gestational diabetes, there is an increased risk of large (macrosomic) babies and babies with low blood sugars (hypoglycemia) after birth; however, the overall risk of complications is low.
Large babies and babies with low blood sugars also are associated with Classes A, B, C, and D.1 Large (macrosomic) babies increase the need for cesarean section delivery because the baby can be too big to pass through the mother’s pelvis and vaginal canal.
Class F mothers have the highest risk of delivering abnormally small babies with poor growth while inside the mother’s uterus.1 Class F mothers also have an increased risk of anemia, high blood pressure (hypertension), and decreased kidney function.
Class H mothers have an increased risk of a heart attack or heart failure and sudden death, along with an increased risk of producing abnormally small babies.
Class R mothers have an increased risk of worsened retinopathy, bleeding into the eye (vitreous hemorrhage), or detachment of the retina. They also have an increased risk of delivering small babies, most often by cesarean section.
All classes have an increased risk of abnormally large amounts of amniotic fluid (polyhydramnios). Polyhydramnios increases the risk of pre-term labor and delivery, delivery of the baby’s umbilical cord before the baby (cord prolapse), or early separation of the placenta from the uterus (placental abruption). Cord prolapse and placental abruption can dangerously cut off blood supply to the placenta and the baby.
What are the risks to the infant?
Infants of diabetic mothers, or IDMs, have a significantly increased risk of breathing problems (respiratory distress), especially if they are born before 37 weeks, because their lungs are slower to mature.
Approximately 30% to 40% of IDMs have low blood sugar (i.e., glucose is less than 40 mg/dl) after birth. This condition usually occurs early after birth, often by one to two hours of age. Low blood sugar occurs because of excess insulin in the baby. The excess insulin was produced in the baby while inside the mother’s uterus in response to high blood sugars delivered across the placenta from the mother’s blood. Prolonged or severe low blood sugar (i.e., hypoglycemia) can cause seizures and brain damage. Therefore, IDMs will have their blood sugars checked (usually by “heel stick”) shortly after birth and then several times over the next one to two days.
Approximately 20% of IDMs will have low calcium. If a baby is very sick, shaky, or lethargic, or has seizures despite normal blood glucose, a blood calcium measurement should be performed.
An abnormally high red blood cell count (polycythemia) can occur in IDMs, increasing their risk of jaundice (yellow skin color), feeding difficulties, respiratory distress, or lethargy. The risk of jaundice is increased significantly in IDMs even if they are not polycythemic. One study found that 19% of IDMs developed bilirubin levels greater than 16 mg/dl. Bilirubin is the yellow pigment that comes from the red blood cells and produces the yellow skin color. When there is too much bilirubin in a baby’s blood, it can cause brain damage. Fortunately, this problem is treated easily with light treatment (phototherapy).
The incidence of major congenital anomalies (birth defects) is increased from 6% to 9% in IDMs, compared to a rate of 2% in the general population. The frequency of congenital anomalies is not increased in gestational diabetes; however, two-thirds of these anomalies involve the brain, the nervous system, or the heart. Caudal agenesis (failure of formation of the lower vertebrae and sacrum of the spine) more frequently occurs in IDMs whose mothers had poor blood sugar control around the time of conception and during the first few weeks of pregnancy.
A significant decrease in the incidence of congenital anomalies has been reported with rigorous glucose control in the periconception period.2 Congenital anomalies can be reduced even more if the mother takes folate supplements during the early part of pregnancy.
Poor feeding is a common problem that affects up to 37% of IDMs, often prolonging the hospital stay.
Macrosomia (large birth weight, i.e., larger than 4 kilograms, or 8 pounds) occurs in about one-third of IDMs, and it correlates with high blood sugars and serum fat concentrations in the third trimester of pregnancy.3 Usually, macrosomia is not seen in those mothers with more severe and longer-standing diabetes (e.g., Classes F and R).
Poor heart function or myocardial dysfunction is rare, but increased, in IDMs because of the enlargement of the septum or the wall between the ventricles (the two large pumping chambers of the heart). This condition is called ventricular septal hypertrophy, and can cause congestive heart failure, poor cardiac output, and heart enlargement. However, it often has no associated problems. Sometimes, a heart murmur is heard when IDMs have poor heart function.
Even when there are associated problems with the heart, they usually resolve by two weeks, and the hypertrophy resolves by four months. Good diabetic control during pregnancy can reduce the incidence and the severity of this complication.
Renal vein thrombosis or clotting of the vessel draining blood from the kidney, causing the kidney to swell, is rare; however, it can occur before or after birth in IDMs. It is caused by abnormally low blood anticoagulants that may develop in the baby whose mother is poorly controlled for her diabetes during pregnancy.
Small left colon syndrome can occur in IDMs. This syndrome can cause the delayed passage of a stool after birth, resulting in abdominal distention and a delay in normal feeding.
What can be done to decrease the risk of complications to the infant?
Good glucose control and prevention of ketoacidosis prior to conception and in the first two months of pregnancy will decrease the risk of congenital anomalies. Later in the pregnancy, glucose control is important to prevent macrosomia, hypoglycemia (after birth), and ventricular septal hypertrophy of the baby’s heart. It generally is recommended that the mother’s fasting blood glucose should be from 70 to 90 mg/dl, and, two hours after eating, her blood glucose should be less than 120 mg/dl.2
If a pregnant diabetic woman participates in a program of pregnancy management and surveillance from before conception until delivery, she has at least a 95% chance of having a completely healthy child.1
What special tests may be required for a diabetic mother during pregnancy?
Early screening for congenital anomalies usually includes a serum alpha-ferotein level of the mother to screen for open neural tube defects (spina bifida) and a detailed ultrasound at 18 to 20 weeks. Follow-up ultrasounds may be required for polyhydramnios (increased amniotic fluid), abnormal fetal growth, or early separation of the placenta.
Tests of fetal well being, including daily fetal movement counts and biweekly biophysical testing (ultrasound and fetal heart rate monitoring), usually begin at 28 to 32 weeks.
An amniocentesis may be performed prior to delivery if the mother is at less than 38 weeks gestation to document fetal lung maturity.
The mother’s glucose will be monitored closely during labor, and insulin and glucose treatments often will be adjusted.
What special tests may be required for the infant after birth?
The baby will require frequent blood glucose checks after birth, beginning in the first two hours of birth. These check-ups usually are continued every 2 to 4 hours for at least 24 hours.The red blood cell count, or hematocrit, will be checked after birth to ensure that the baby does not have polycythemia. If significant jaundice occurs, bilirubin levels will be checked.If the baby has jitteriness, lethargy, or poor feeding, despite normal glucoses, the calcium level will be checked.A thorough physical examination will be performed to look for any physical abnormalities and to listen to the heart for any evidence of a heart murmur.The baby’s long-term development will be followed; studies have shown a mild decrease in IQs (93 versus 102) of IDMs with a maternal history of ketones in the urine (ketonuria) during pregnancy, as compared to IDMs with no maternal ketonuria.2 However, significant differences in mental development have not been found between IDMs with good sugar control without ketonuria and other normal babies.
What special treatments may be required for the infant after birth?
If the baby is well after birth, he/she should be nursed or given formula in the first hour. The first blood sugar should be checked within two hours of birth or sooner if the baby develops jitteriness, lethargy, or seizures. If the blood sugar is low (less than 40 mg/dl), the baby should be fed immediately, and the blood sugar rechecked within one to two hours. If the blood sugar is extremely low (less than 25 mg/dl), if the baby is sick or unable to eat, or if the blood sugar remains low despite feeding, an IV with glucose water should be started for the baby. The blood sugar will be rechecked frequently until it is normal and stable.
If congenital anomalies exist, they will need to be treated accordingly; some birth defects may require surgery.
If the baby develops significant jaundice, phototherapy may be required for a short period (usually from two to five days) to break down the bilirubin in the skin.
If the lungs are not mature, the baby could require help with breathing using a machine called a respirator. The baby also could benefit from surfactant. Surfactant is a soap suds-like material that is administered to help lubricate and expand the lungs. Surfactant often is deficient in immature lungs, and most commonly occurs in those IDMs born at less than 37 weeks.
If the baby has difficulty feeding, he/she may require intermittent gavage feeds with a feeding tube. Extra time in the hospital may be required for the baby to learn to feed by either the breast or the bottle.
If the baby develops abdominal distention or has difficulty stooling, a gastrointestinal x-ray with gastrograffin may be required to check if a microcolon is present.
What is the risk of the infant developing insulin-dependant diabetes?
In a series of studies from the Joslin Diabetes Center, only 2% to 3% of IDMs developed insulin-dependant diabetes mellitus before 20 years of age. The risk of subsequent diabetes is slightly higher if both the mother and the father have insulin-dependent diabetes. The risks and the complications to the baby outlined herein do not pertain when only the father has insulin-dependant diabetes.
References
Cloherty JP, Stark AR. Manual of neonatal care. Philadelphia, Lippencott-Raven, 1997.
Fanaroff AA, Martin RJ. Metabolic and endocrine disorders. In: Neonatal-perinatal medicine: diseases of the fetus and infant. 6th ed. St. Louis: Mosby-Year Book, Inc.
About the Author
Dr. Paisley is a second year fellow in Neonatal-Perinatal Medicine in the Section of Neonatology, Department of Pediatrics, University of Colorado School of Medicine in Denver, Colorado. Jan trained in Pediatrics at the University of Utah and was honored to receive a highly prestigious Pediatric Scientist Development Program award.
Jan preferred clinical practice, however, and she has been working for the past 7 years as a general Pediatrician in Ft. Collins, Colorado.
She joined the Neonatal-Perinatal Medicine Training Program in 1998 and is working with Dr. Adam Rosenberg and Dr. William Hay on aspects of cerebral glucose metabolism in a fetal animal model and in newborn human infants.
Dr. Hay is a Professor of Pediatrics at the University of Colorado School of Medicine, Denver, Colorado.
He is the Director of the Training Program in Neonatal-Perinatal Medicine, Director of the Neonatal Clinical Research Center (as Associate Director of the National Institutes of Health and Department of Pediatrics sponsored Pediatric Clinical Research Center), and Scientific Director of The Perinatal Research Center at the University of Colorado Health Sciences Center.
Dr. Hay holds three NIH research grants and a NIH Training Grant in Perinatal Medicine and Biology.
His clinical and basic research interests focus on fetal physiology, fetal and neonatal nutrition and metabolism, glucose disorders in preterm infants, small-for-gestational aged infants, and infants of diabetic mothers, and oxygen monitoring.
Dr. Hay is Secretary-Treasurer of the American Pediatric Society and is a member of the NIH Human Embryology and Development Study Section. He travels widely around the United States and internationally as a visiting scientist and professor.
Dr. Hay also is the senior editor for Current Pediatric Diagnosis and Treatment (a Lange Publication) and co-editor of NeoReviews (American Academy of Pediatrics).
Copyright 2012 Jan E. Paisley, M.D., All Rights Reserved
Infectious Mononucleosis
What is infectious mononucleosis?
What causes infectious mononucleosis?
Who gets infectious mononucleosis?
How does EBV cause disease?
What are the common findings?
How is infectious mononucleosis diagnosed?
How is infectious mononucleosis treated?
What are the complications?
How can infectious mononucleosis 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 infectious mononucleosis?
Infectious mononucleosis, also known as “kissing disease,” mononucleosis, or, sometimes, just “mono,” is an illness characterized by many complaints, but primarily by fever, fatigue, tiredness, enlarged lymph nodes (“lymphadenopathy”), and a sore throat. This disease was originally described in the late nineteenth century as “glandular fever,” and it is still known by that name in Europe.
What causes infectious mononucleosis?
The Epstein-Barr Virus (EBV), a DNA virus that is a member of the herpesvirus family of viruses, causes approximately 90% of cases of infectious mononucleosis. Approximately 10% of cases of infectious mononucleosis-like illnesses are caused by primary infection with cytomegalovirus, Toxoplasma gondii, Human Immunodeficiency Virus (HIV), adenovirus, viral hepatitis, and rubella virus.
Who gets infectious mononucleosis?
EBV is found throughout the world and infects more than 98% of the world’s population. In underdeveloped and developing countries, and in socio-economically disadvantaged populations of the United States, up to 100% of children are infected with EBV by 2 to 4 years of age. In more affluent populations in the United States, initial EBV infection also occurs more often in young children, but approximately 50% of infection occurs during adolescence and young adulthood. Because initial EBV infection in young children tends to be without any symptoms, most cases of what is diagnosed as infectious mononucleosis occurs in adolescence and young adulthood, even though EBV infection is more common in young children.
How does EBV cause disease?
EBV and the other causes of infectious mononucleosis are transmitted from person-to-person by direct contact or by contaminated secretions of the nose and the mouth. EBV then causes infection in the throat that results in the symptoms of a sore throat and swollen lymph nodes in the neck. The virus then spreads to the white blood cells in the blood stream and causes enlarged lymph nodes in other places throughout the body. The virus, like all other herpesviruses, establishes lifelong infection in the affected person. However, this lifelong infection generally does not cause any symptoms.
What are the common findings?
six weeks. Initial infection in young children is often without any symptoms, or with only mild symptoms. Primary infection in approximately 50% of adolescents and adults appears as fever, fatigue and tiredness, swollen lymph nodes, a sore throat, and, sometimes, an enlarged spleen and liver. Symptoms typically develop over several days and persist for a variable period of days, with gradual spontaneous resolution. The total duration of the disease usually is two to three weeks without complications.
How is infectious mononucleosis diagnosed?
Initially, infectious mononucleosis can be diagnosed in an adolescent or adult on the basis of the typical symptoms-fever, fatigue and malaise, swollen lymph nodes, and a sore throat. The complete blood count may show an uncommon type of white blood cells (“atypical lymphocytes”), which can suggest infectious mononucleosis. The diagnosis is confirmed by checking for antibodies to the virus. If one of the many other causes of infectious mononucleosis is considered, specific blood tests for those causes are available.
How is infectious mononucleosis treated?
There is no specific treatment for infectious mononucleosis. Antibiotics usually are not helpful because the primary cause, EBV, is a virus. Viruses cannot be treated with antibiotics. Antiviral therapy with acyclovir has been shown to decrease viral growth and shedding of EBV from the mouth, but this treatment does not affect the severity of symptoms, the duration of the clinical course, or the eventual outcome.
Infectious mononucleosis is treated primarily with rest and symptomatic therapy. Fever should be treated with acetaminophen or ibuprofen. Because the spleen may be enlarged and may easily rupture, it is advisable to refrain from participation in any contact sports and strenuous physical activities for the first two to three weeks of illness, or, if an enlarged spleen is present, until it has resolved.
Some patients with infectious mononucleosis have such greatly enlarged tonsils that they have difficulty breathing or swallowing. For these patients, steroids have been shown to have a dramatic effect in shrinking enlarged tonsils within 12 to 24 hours. However, most persons with infectious mononucleosis do not require steroids.
What are the complications?
The great majority of patients with infectious mononucleosis recover uneventfully without complications. Some chronic conditions have been suggested to be associated with infectious mononucleosis, but this has not been proved. At present, there is no evidence to support the association of EBV infection with chronic fatigue syndrome or chronic immune dysfunction.
EBV is a virus that has been associated with several human cancers, including nasopharyngeal carcinoma, Burkitt lymphoma, Hodgkin disease, and lymphomas and smooth muscle tumors (“leiomyosarcomas”) in individuals with decreased ability to ward off other infections.
How can infectious mononucleosis be prevented?
There is no vaccine for EBV or the other causes of infectious mononucleosis. There is very little information on how to prevent it. Outbreaks are uncommon. Minimizing exposure to the oral secretions of infected persons can prevent the spread of infectious mononucleosis. Most healthy adults excrete EBV from the mouth periodically throughout their lives, with approximately 20% of the healthy adult population excreting EBV at any given time.
What research is being done?
There is much research into the molecular events that are important in the control of EBV after the initial infection resolves. There is interest in developing a vaccine because almost everybody is infected with EBV in childhood and because of the association of EBV with several types of cancer.
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., All Rights Reserved
Influenza Immunization
http://www.cdc.gov/vaccines/hcp/vis/vis-statements/flu.html
Influenza-Seasonal
What is influenza?
What causes influenza?
How does it cause disease?
Who gets influenza?
What are the common findings?
How is influenza diagnosed?
How is influenza treated?
What are the complications?
How can influenza be prevented?
Can the influenza vaccine prevent acute otitis media?
What research is being done?
Links to other information
W. Paul Glezen, M.D.
Department of Molecular Virology and Microbiology
Baylor College of Medicine
Houston, Texas
What is influenza?
Influenza, commonly referred to as the “flu,” is an acute, contagious respiratory infection. The first of the human respiratory viruses to be isolated and characterized, influenza viruses have been studied the most extensively and are the best understood. The term itself, “influenza,” may have come from the Latin word influo, meaning “to flow in,” perhaps indicating its airborne transmission, or it may be of Italian origin, relating to an “influence,” such as the weather, or mystical astrologic causes.
What causes influenza?
Influenza is caused by strains of the orthomyxoviruses. The influenza viruses are comprised of three major types-A, B, and C-and multiple subtypes. Influenza A and B are the two types of influenza viruses that most often cause disease in humans. Influenza A and B viruses have been studied more extensively than influenza C viruses.
How does it cause disease?
Influenza is most prevalent in the winter and the spring. It occurs following close contact with a person who has the illness. Spread by discharges from the mouth and nose of an infected person, the virus is then inhaled and multiplies in the newly infected person. Influenza may occur on a sporadic basis, or it may occur as epidemic influenza (i.e., involving a large, regional population) or as pandemic influenza (i.e., involving a worldwide population).
Who gets influenza?
All persons may contract influenza; however, younger children (under 2 years), pregnant women, American Indians, Alaskan Natives and older adults (over 65 years) are the most susceptible to its effects. Persons at high risk for the complications associated with influenza include those with preexisting medical conditions, such as:
Asthma
Neurological and neurodevelopmental conditions
Chronic lung disease
Heart disease
Blood disorders (such as sickle cell disease)
Endocrine disorders (such as diabetes mellitus)
Kidney disorders
Liver disorders
Metabolic disorders (such as inherited metabolic disorders and mitochondrial disorders)
Weakened immune system due to disease or medication (such as people with HIV or AIDS, or cancer, or those on chronic steroids)
People younger than 19 years of age who are receiving long-term aspirin therapy
People who are morbidly obese (Body Mass Index [BMI] of 40 or greater)
What are the common findings?
In young children, the most common findings of type A influenza include its sudden onset and its associated symptoms of high fever, headache, lack of appetite, fatigue, chills, and muscle aches. Common respiratory findings include a cough, a runny nose, and a sore throat. Other symptoms may include abdominal pain, swollen lymph nodes in the neck area, nausea, vomiting, and diarrhea.
In older children and adolescents with type A influenza, the onset of the illness is abrupt, and is associated with high fever, flushed face, chills, headache, muscle aches, and fatigue.
In type B influenza, children often will have typical “flu-like” symptoms with fever; however, adults frequently will have only respiratory tract symptoms without significant fever.
Influenza C viruses cause illnesses similar to type A influenza; however, the severity of the disease is usually less, and the duration of it is shorter.
How is influenza diagnosed?
Infection with the influenza virus is diagnosed more accurately from groups of patients exhibiting the classic symptoms of influenza, rather than an individual patient. Epidemics occur each winter, and usually begin with a sudden increase in its appearance in the primary care facilities of school-age children with febrile (associated with fever) respiratory tract illnesses.
A diagnostic test called a “Rapid Flu Test” is now available in most physician’s offices. Unfortunately, the reliability of these tests is variable and a person with a negative test may still have the flu. Your health care provider will often make the diagnosis of flu based on your symptoms and physical exam. In certain circumstances, your provider may decide to send a nasal swab to a specialized laboratory for a more definitive diagnosis.
How is influenza treated?
For types A and B influenza viruses, the illness usually resolves itself after several days; however, fatigue and persistent coughing can last for two or more weeks. Bed rest, adequate hydration with oral fluids, control of fever and muscle aches with acetaminophen, and maintenance of comfortable breathing with nasal decongestants and humidifiers are the best courses of treatment in uncomplicated cases of influenza. A persistent cough may be treated with cough suppressants.
Preventative administration of antibiotics should be discouraged. For complicated cases of influenza, a physician should evaluate the patient, and may recommend antibiotic treatment for possible secondary bacterial infections.
The neuraminidase inhibitor oseltamivir (Tamiflu) is FDA-approved for the treatment of uncomplicated acute influenza in patients 1 year and older who have been symptomatic for no more than 2 days.
The neuraminidase inhibitor zanamivir formulated for oral inhalation (Relenza) is FDA-approved for the treatment of influenza in patients 7 years of age and older who, similar to approved uses for oseltamivir, have uncomplicated illness and have been symptomatic for no more than 2 days.
What are the complications?
A patient’s recovery from a case of uncomplicated influenza generally is considered to be excellent.
Complications that may occur as a result of influenza include bacterial infections of the respiratory tract (particularly pneumonia), acute otitis media (ear infections), and sinusitis. Acute myositis, (i.e., severe pain and tenderness in the calves of both legs that occurs suddenly, often with a refusal to walk) may also occur.
Reye’s syndrome may occur as a result of influenza, most commonly when aspirin or aspirin-containing compounds are used in children with influenza. Reye’s syndrome is a constellation of symptoms that can result in degeneration of the liver and/or swelling of the brain.
Rare complications of influenza include encephalitis and other neurologic illnesses (e.g., transverse myelitis, Guillain-Barr syndrome, Parkinson disease), cardiac inflammation (e.g., pericarditis, myocarditis), and kidney failure following myositis (acute inflammation of the muscle).
Despite improvements in living standards and the introduction of antibiotics, an average of 30,000 deaths still are attributed to influenza each year. Most deaths occur in those patients with preexisting chronic medical conditions involving the pulmonary or the cardiovascular systems, in very young patients (less than two years of age), or in elderly patients (older than 65 years of age).
How can influenza be prevented?
The influenza vaccine is the primary method for preventing influenza and its more severe complications. To be effective, the vaccine must contain antigens similar to those of the most likely current strain of the virus. In years when a new strain arises and causes widespread outbreaks, the available vaccine may contain a previous strain of the virus, which may give only modest protection from the flu.
During the 2011-12 season, the strains in this year’s vaccine are the same as last season so children under 9 years of age who had a flu vaccine last year will need only one vaccine this year. Individuals over 9 years of age should receive one vaccine regardless of whether they received a flu vaccine last season.
Worth noting, the influenza vaccine does not affect the safety of mothers who are breastfeeding or their infants.
For those previously unvaccinated children who are nine years old or younger, two doses of the vaccine should be administered at least one month apart in order for it to be effective. If possible, the second dose should be given before the month of December. For those children who are older than nine years, only one dose of the vaccine is necessary.
A live, attenuated (weakened) influenza virus vaccine (FluMist”) administered by nasal spray is now available for healthy children over 2 years of age.
Side effects to the vaccine may occur, and they include fever, “flu-like” symptoms of fatigue and muscle aches, and tenderness at the site of the inoculation (if given by injection). The occurrence of febrile convulsions, which have been associated with the vaccine in very young patients, is rare, and studies have shown no association of an increased frequency of Guillain-Barr syndrome and the influenza vaccine.
Can the influenza vaccine prevent acute otitis media?
Acute otitis media (i.e., ear infection) is the most common cause for illness visits to the pediatrician in the United States, most often occurring in children between the ages of 6 months and 3 years, with the highest incidence in the 6- to 12-month age group.
Studies suggest that the influenza vaccine can decrease the incidence of acute otitis media in children, especially those children between the ages of 6 and 30 months, during the influenza season. These same studies also suggest that other vaccines against respiratory viruses may be an effective way to reduce the incidence of acute otitis media in children.
What research is being done?
Whereas the currently available antiviral drugs, oseltamivir and zanamivir, are effective against influenza A and B viruses, recent resistance has been reported. In intravenous medication, panamivir has been approved for administration to severely ill hospitalized patients with influenza.
Links to other information
Information regarding influenza is available through the Centers for Disease Control and Prevention (CDC) Web site at CDC FLU FACTS.
State and local health departments can be contacted for information regarding the availability of the influenza vaccine, access to vaccination programs, and information about state or local influenza activity.
References
Belshe RB, Mendelman PM, Treanor J, King J, et al. The efficacy of live attenuated, cold-adapted, trivalent, intranasal influenza virus vaccine in children. N Engl J Med 1998;338:1405-12.
Buchman CA, Doyle WJ, Skoner DP, Post JC, et al. Influenza A virus-induced acute otitis media. J Infect Dis 1995;172:1348-51.
Clements DA, Langdon L, Bland C, Walter E. Influenza A vaccine decreases the incidence of otitis media in 6- to 30-month-old children in day care. Arch Pediatr Adolesc Med 1995;149:1113-7.
Glezen WP. Emerging infections: pandemic influenza. Epidemiol Rev 1996;18(1):64-76.
Glezen WP. Influenza control-unfinished business. JAMA 1999; 281:994-5.
Glezen WP. Influenza viruses. In: Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. 4th ed. Philadelphia: WB Saunders, 1998:2024-37.
Glezen WP, Taber LH, Frank AL, Gruber WC, et al. Influenza virus infections in infants. Pediatr Infect Dis J 1997;16:1065-8.
Heikkinen T, Ruuskanen O, Waris M, Ziegler T, et al. Influenza vaccination in the prevention of acute otitis media in children. AJDC 1991;145:445-8.
U.S. Department of Health and Human Services/Centers for Disease Control and Prevention (CDC). Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). Mor Mortal Wkly Rep 1999;48(RR-4):1-28.
About the Author
Dr. Glezen is professor of microbiology and pediatrics at Baylor College of Medicine in Houston, Texas. His research has focused on the consequences and the prevention of respiratory viruses in children.
Dr. Glezen has published more than 125 papers and chapters related to his research. His three grandchildren, Claire, Tyler, and Meghan Gahm, have flourished under the pediatric care of Dr. Dan Feiten.
Copyright 2012 W. Paul Glezen, M.D., All Rights Reserved
