What are Some of the Causes of SGA?

Patient Presentation
A 38 1/7 week gestation, newborn girl was delivered by normal spontaneous vaginal delivery, with Apgar scores of 8 at 1 minute and 9 at 5 minutes, to a 27 year old Hispanic mother with 1 previous living child. The past medical history was significant for the mother having close monitoring during the 3rd trimester because of symmetric small-for-gestational age (SGA) in the fetus. The mother’s other child was also SGA with a similar pattern and currently was a small but healthy 33 month old. The family history was positive for the mother’s sister who had an infant die in utero in the first trimester. There was diabetes and obesity in family. The family had a relatively shorter stature. The mother was average size for her family and was 5’1″, and the father was tall for his family and was 5’7″ with mid-parental height at 10-25%.

The pertinent physical exam at birth showed a small, thin infant with a wrinkled face and a lusty cry. Her weight was 2674 grams (5-10%), her length was 47.5 cm (10-25%) and her head circumference was 33 cm (10-25%) using World Health Organization growth charts. There were no obvious congenital abnormalities and she had a 3-vessel umbilical cord. She had thinner skin and smaller amounts of subcutaneous fat and musculature. Her Ballard examination was scored 34 (a score of 35 corresponding to a 38 week infant). The diagnosis of an infant with symmetric SGA was made. It was felt this was due to a constitutionally small infant.

The patient’s clinical course over the next several hours found that she had normal glucose tests when monitored on the neonatal glucose protocol. By discharge on day 2 of life the infant was feeding every 1-3 hours for about 30 minutes. She was having 2-3 wet diapers/day and had lost 113 grams or about a 4% decrease from her birth weight. At followup on day of life 5, she had continued to nurse well along with some formula supplements that had been given when the mother was sleeping. She had lost another 46 grams and had decreased 6% from her birth weight. Her mother felt that her milk had come in the day before. On followup at day 7 of life the infant had gained 33 grams since the previous visit, and at day 15 she was past her birth weight. She continued to be a smaller infant growing around the 10% for the first several months of life. At age 15 months she was around the 10-25% for weight, and 25% for height and head circumference and was growing appropriately.

Intrauterine growth retardation or fetal growth retardation is due to a pathological process that causes decelerated fetal growth velocity. Small-for-gestational age (SGA) is an infant with growth parameters below the normal range for gestational age. More commonly, SGA is defined as a birth weight < 10% for gestational age. This may be due a pathological or non-pathological process (e.g. constitutionally small fetus). Using these standards, remember that 10% of all infants will be < 10% for weight, and they do not necessarily have an underlying problem and infants who are constitutionally small do not have increased perinatal mortality and morbidity. SGA and IUGR are not synonymous. IUGR always refers to a pathological process, whereas SGA may or may not be a pathological process but just a small infant.

SGA infants classically appear small with thin, loose skin, little subcutaneous fat and decreased muscle mass. The umbilical cord is thin. The face has a shrunken or “wizened” appearance often. Therefore, the gestational age at birth is best determined by the neurological assessment than by the physical appearance.

Symmetric SGA usually reflects a fetal problem and usually occurs in the first trimester with overall growth restriction. The long-term prognosis is not as good as asymmetric SGA reflecting an increased risk underlying disease processes such as a genetic abnormality.

Constitutionally small infants usually have symmetric SGA.

Asymmetric SGA usually reflects a placental problem and usually occurs in the 2nd and 3rd trimesters with growth restriction that is discordant. Usually head circumference is preserved, with length somewhat affected, and weight affected the most.

The earliest gestational ultrasound scans are most accurate for recognition of SGA and especially for correct dating of the pregnancy. Special ultrasound growth curves are used which use initial maternal height and weight, ethnic origin, fetal gender and parity. Abdominal circumference is the most accurate ultrasound measurement to determine SGA.

“The recurrence risk for SGA is 29% if a previous pregnancy was affected and 44% if two previous pregnancies were affected.”

Learning Point
Causes of SGA include:

  • Genetic abnormalities
    • 5-20%
    • Can include: Aneuploidy, single gene mutations, genetic imprinting, partial deletions or duplications, uniparental disomy and other variations including multiple syndromes, (e.g. chondroplasias, growth hormone deficiency, Turner syndrome, etc.).
  • Congenital infection
    • 5-10%
    • Cytomegalovirus and toxoplasmosis are most common
    • Herpes, HIV, influenza malaria, parvovirus, rubella, syphilis, varicella, zika are other common infections
  • Structural problems
    • Often seen along with genetic abnormalities
    • Cardiac anomalies
    • Renal anomalies
  • Placental abnormalities
    • Confined placental mosasiacism
    • Placental growth factors
  • Maternal factors
    • Height, weight, age, parity, ethnicity
    • Maternal disease including hypertension, preeclampsia
    • Chronic maternal disease – inflammatory bowel disease, epilepsy
    • Lifestyle – smoking, alcohol or drug use, obesity
    • Social stressors
    • Multiple gestation
    • Incorrect pregnancy dating

SGA complications include:

  • Newborn
    • Asphyxia
    • Hypoglycemia
    • Immune function impairment
    • Polycythemia and hyperviscosity
    • Thermoregulation impairment
    • Mortality
    • Complications of underlying disease such as genetic, structural or infectious disease
  • Long-term
    • Growth problems especially in weight and height (although many infants will improve)
    • Neurodevelopmental problems
    • Adult disease including increased risk of coronary artery disease, hypertension, hyperlipidemia and chronic kidney disease

Questions for Further Discussion
1. What are common treatments given to, or monitored for, in SGA newborns?
2. What could be included in an evaluation for SGA?
3. What are common causes of large for gestational age (LGA) infants?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for this topic: Birth Weight

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Vrachnis N, Botsis D, Iliodromiti Z. The fetus that is small for gestational age. Ann N Y Acad Sci. 2006 Dec;1092:304-9.

Finken MJJ, van der Steen M, Smeets CCJ, Walenkamp MJE, de Bruin C, Hokken-Koelega ACS, Wit JM. Children born small for gestational age: differential diagnosis, molecular-genetic evaluation and implications. Endocr Rev. 2018 Jul 4.

Mandy GT, Infants with fetal (intrauterine) growth restriction. UpToDate. (reviewed 6/29/18, cited 10/2/18).

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

Does She Have SCID?

Patient Presentation
A pediatrician received a late afternoon phone call from the state’s newborn screening program, about a 4-day-old female whose neonatal screening test was presumptively positive for severe-combined immunodefiency (SCID). The parents had already been contacted and were already planning on coming to their first office visit after discharge the next day. The program coordinator had faxed full information about what the pediatrician should do during the visit and also information for the parents. “The most important part is to make sure that the repeat testing is transported right away to our hospital, so we can get the testing done correctly,” the coordinator stated. “The second most important part is to make sure that the infant isn’t around anyone who is sick because they can get sick very quickly,” she also said.

The following day, the staff brought the infant to a room immediately and weighed and measured her. The medical history showed that she was a full-term infant born to a G2P2 mother without problems during pregnancy or delivery. The baby had no problems during hospitalization. Her mother reported that she was breast-feeding about every 2-3 hours with many wet diapers. Her stools had transitioned and her mother was not concerned about jaundice. The family history was negative for any genetic diseases or children who died young or unexpectedly.

The pertinent physical exam showed an alert female with a weight of 3180 g down 6% from birth but only 2% from discharge. Her length and head circumference were 50-75%. She had no rashes, but she had a black-blue nevus over her sacrum. No abnormal physical findings were noted.

The diagnosis of a healthy appearing infant with a positive neonatal screening test was made. The repeat neonatal screening test was sent after the visit and routine care was discussed as well as infectious disease precautions were re-iterated. The next day the program coordinator called to tell the pediatrician that the repeat testing was totally normal. The original testing was a false-positive result. She asked that the pediatrician contact the family with the results and said that no special precautions needed to be followed. She wanted the family to also know that if they had other questions they could always call the program, but that she was happy that the family had a healthy infant.

Severe-combined immunodefiency (SCID) is actually a group of inherited disorders with an absence or dysfunction of T, B and NK cells that results in severe dysfunction of the immune system. SCID is a primary immunodeficiency. SCID was thought to be a rare disorder but with the advent of neonatal screening the incidence in the US general population is estimated at ~1 in 58,000 live births, but with numbers higher or lower depending on the specific population.

Patients often have failure to thrive, oral candidiasis, and diarrhea as infants as well as a variety of infectious diseases. They can also have interstitial lung disease due to Pneumocystis jiroveci or graft-vs-host disease because of maternal lymphocyte engraphment. Without treatment to reconstitute the immune system, patients usually die at < 2 years of age.

Initially SCID was classified by if the patient was T or B cell deficient or normal, with subsets of NK deficiency or not (i.e. TB NK ,TB+ NK +, etc.) Molecular genetics now has identified multiple genes that are associated with different SCID phenotypes. The genes can cause disease by affecting the hematopoietic precursor survival, cause problems with cytokine signaling, allow toxic metabolite accumulation, genetic recombination, and other mechanisms. Most SCID genes have an autosomal recessive inheritance. Thymic abnormalities are often grouped with SCID because of phenotypic and genetic similarities. DiGeorge syndrome (22q11 deletion sequence) includes congenital athymia which causes similar immunological problems because the T-cells do not have a thymus to properly develop within. DiGeorge syndrome also has other problems associated with it and a review can be found here.

Curative treatment is available through allogeneic hematopoietic stem cell transplantation and is considered the preferred treatment. Gene therapy is also potentially curative for 2 different types of SCID (ADA and IL2RG genes). Adenosine deaminase infusions are also an option for ADA deficient SCID but are not curative. Studies have shown > 90% long-term survival after transplantation when infants are < 3.5 months of age, and have a sibling match.

A review of primary immunodeficiencies can be found here.
A review of potential testing to do for a suspected immunodeficiency can be found here.

Learning Point
In the US, the Department of Health and Human Services has an advisory panel that recommends a core panel of congenital disorders that are recommended to be screened for. SCID was added to the core panel in 2010. Screening for SCID is done through TREC testing (T cell receptor excision circles) using the Guthrie blood spot cards. T cell specific confirmatory testing using flow cytometry and other testing needs to be carried out if TREC is positive.

TREC testing does not identify all forms of combined immunodeficiency or atypical SCID. Other types of testing such as KREC (kappa-deleting recombination excision circles) may increase the ability to identify other forms for SCID. Prenatal testing in high risk families is available.

Questions for Further Discussion
1. Who was “David the Bubble Boy” and what is his link to SCID?
2. What are indications for stem cell transplant?
3. What are the differences between stem cell transplant and gene therapy?
4. What disorders does your state or country test for on newborn screening?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for this topic: Immune System Disorders

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Centers for Disease Control. Severe Combined Immunodeficiency (SCID). Available from the Internet at https://www.cdc.gov/newbornscreening/scid.html (rev. 9/17/15, cited 10/2/18).

Gaspar HB, Hammarstrom L, Mahlaoui N, Borte M, Borte S. The case for mandatory newborn screening for severe combined immunodeficiency (SCID). J Clin Immunol. 2014 May;34(4):393-7.

Cirillo E, Giardino G, Gallo V, D’Assante R, Grasso F, Romano R, Di Lillo C, Galasso G, Pignata C. Severe combined immunodeficiency–an update. Ann N Y Acad Sci. 2015 Nov;1356:90-106.

Chinn IK, Shearer WT. Severe Combined Immunodeficiency Disorders. Immunol Allergy Clin North Am. 2015 Nov;35(4):671-94.

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What is Genomic Imprinting?

Patient Presentation
A 17-month-old male came to the emergency room with emesis and diarrhea for 1 day. His older sister had had similar problems 3 days before but after 36 hours improved. He had emesis three times of stomach contents. He had diarrhea multiple times of brown watery stool that leaked out his diaper twice. There was no blood or mucous in either fluid. He was afebrile. He was drinking small amounts of oral rehydration solution but had not had a wet diaper for 6-8 hours. His past medical history was significant for Silver-Russell syndrome that was diagnosed after birth because of being small for gestational age. He had postnatal growth retardation and was followed closely by gastroenterology. He had required a nasogastric feeding tube for a few months but he had stopped it 9 months ago and currently was growing at the 1st percentile. He saw multiple other services for his overall care, and had been hospitalized for dehydration or feeding difficulties twice in the past. The family history was negative for any genetic or neurological diseases. The review of systems was otherwise normal.

The pertinent physical exam showed a very tired-appearing, small, thin male sitting in his mother’s lap. His weight was down 680 grams from a clinic visit earlier in the week. He had triangular face with a prominent forehead and slightly low-set ears. His mucous membranes were slightly tacky and his capillary refill was 3+ seconds. HEENT examination was otherwise normal as were his heart and lungs. His abdomen showed increased bowel sounds without pain or guarding. Extremities showed a short male with thin musculature.

The diagnosis of a patient with gastroenteritis in the setting of Silver-Russell syndrome was made. Fluid resuscitation was given in the emergency room, but the patient refused to drink and continued to have emesis and diarrhea and so he was admitted. The patient’s clinical course revealed that the emesis and diarrhea resolved by day 2, but the patient was refusing to drink enough. Nutritional services, speech therapy and gastroenterology continued to work with the family and by Day 5 of admission he was taking his usual feedings and was discharged.

Silver-Russell syndrome (SRS) is a rare genetic syndrome first characterized by Silver in 1953 and Russell in 1954. Patients with SRS have characteristic growth patterns and clinical findings, although within an individual patient there are phenotypical differences. Patients are born small-for-gestational age (SGA) but have a relative macrocephaly. There is postnatal growth failure and difficulty feeding, with a very low body mass index. Body asymmetry (e.g. hemihypertrophy) and facial features (i.e. protruding forehead, triangular facies, micrognathia, dental anomalies, downturned mouth corners, and ear anomalies) are characteristic features.

Patients need multidisciplinary specialist care. SGA and feeding difficulties make patients often difficult to manage. Patients have lower muscle mass and excess calories quickly go to excess fat mass if patients are overfed. Gastroenterology, nutrition, speech therapy and psychology often manage these problems. Short stature can be marked (< 3 standard deviations below adult height) and recombinant growth hormone is used for treatment. Body asymmetry may need surgical treatment. Facial malformations can lead to dental, speech and otolaryngological problems that need to be addressed. Data on cognitive development is small, but if developmental or intellectual disabilities are identified they also need multimodal treatment.

Learning Point
Genomic imprinting is an epigenetic modification process, which allows a gene to be expressed in a single allelic, parent-of-origin specific manner. The imprinting occurs in gene clusters that are differentially methylated in both DNA and histones. These epigenetic methylated marks “…are acquired during gametogenesis, and normal embryo development is dependent on their maintenance after fertilization and during embryogensis.” This methylation process does not alter the gene sequence and is inherited independent of classic Mendelian inheritance. Imprinted genes control growth, development and metabolism. More than 100 imprinted genes have been identified in mice. About half of these are conserved in humans.

SRS generally is considered a sporadic inheritance, but there are some families where recessive, dominant or X-linked have occurred. Recurrence risk is considered low, but appropriate genetic counseling is important. Imprinting on chromosomes 7, 11, 15 and 17 have been recognized.

Currently known human imprinting disorders include:

  • Angelman syndrome
  • Beckwith-Wiedemann syndrome
  • Kagami-Ogata syndrome
  • Maternal uniparental disomy of chromosome 20 syndrome
  • Precocious puberty syndrome
  • Prader-Willi syndrome
  • Pseudohypoparthyroidism Type Ib
  • Silver-Russell syndrome
  • Transient neonatal Diabetes Mellitis 1
  • Temple syndrome

Imprinting in one area of chromosome 11 appears to cause some cases of SRS if transmitted maternally, but causes some cases of Beckwith-Wiedemann syndrome if transmitted paternally.

Questions for Further Discussion
1. What are indications for genetic counseling?
2. What support organizations for rare disorders are available locally or nationally?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com and the Cochrane Database of Systematic Reviews.
Information prescriptions for patients can be found at MedlinePlus for these topics: Rare Diseases and Genetic Disorders.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Silver HK, Kiyasu W, George J, Deamer WC. Syndrome of congenital hemihypertrophy, shortness of stature, and elevated urinary gonadotropins. Pediatrics. 1953 Oct;12(4):368-76.

Russell A. A syndrome of intra-uterine dwarfism recognizable at birth with cranio-facial dysostosis, disproportionately short arms, and other anomalies (5 examples). Proc R Soc Med. 1954 Dec;47(12):1040-4.

Eggermann T. Russell-Silver syndrome. Am J Med Genet C Semin Med Genet. 2010 Aug 15;154C(3):355-64.

Ishida M. New developments in Silver-Russell syndrome and implications for clinical practice. Epigenomics. 2016 Apr;8(4):563-80.

Giabicani E, Netchine I, Brioude F. New clinical and molecular insights into Silver-Russell syndrome. Curr Opin Pediatr. 2016 Aug;28(4):529-35.

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa

What is the Recurrence Rate for Guillian-Barré Syndrome and Should She Get An Influenza Vaccine?

Patient Presentation
An 18-year-old female came to clinic with bilateral leg soreness that she felt was not increasing over the past 4 days. She was actually improving at presentation. It worsened with walking up stairs, or when moving from a seated or squatted position to an upright position. She denied pain in other muscle groups or in the actual lower extremity joints. She also denied any paresthesia, difficulty with walking, urinating or defecating, or changes in urine color. She denied any fever, chills, nausea, or difficulty breathing, speaking or swallowing. She had upper respiratory symptoms the week before but had greatly improved. The family was concerned because her past medical history was positive for classic Guillian-Barré syndrome (GBS) when she was 9 years old that was not associated with influenza vaccine and no specific infectious disease was identified by culture at the time. She had slowly improved over 5 months and had no residual symptoms since that time. With more questioning, she noted that she had a big weight lifting workout for gym class the same day as she helped a friend move some boxes on the day before the pain began. “I guess that could be the cause. I didn’t really think about that,” she noted. The family history was negative for neurological disease. The review of systems was negative.

The pertinent physical exam showed a healthy female with normal growth parameters and vital signs. HEENT showed some residual minor rhinorrhea. Her neurological examination was normal including normal sensation and brisk lower and upper extremity reflexes. She had normal strength and tone. She endorsed some minor pain with palpation of the bilateral quadriceps muscles.

The diagnosis of muscle overuse was made. “You have a normal neurological examination and all the other things I would be worried about are negative. No problems with sensing things, walking, breathing, etc. I think you overused your muscles and are sore but getting better,” the pediatrician noted. He went on, “Its influenza season and I know that you and your parents haven’t given you a vaccine usually, but I just want to make sure you don’t have some other reason that would make you high risk now and then you should really get it.” After reviewing high risk individuals, he remarked, “We don’t give the vaccine for people with Guillian-Barré syndrome if they got it within 6 weeks of influenza vaccination. Your Guillian-Barre was not within 6 weeks, so you can get the vaccine. Especially if you become high risk then it is recommended to get it. One thing is if you want to go to medical school as you have told me, that would put you at high risk for flu.”

Guillian-Barré syndrome (GBS) is an acquired, acute, inflammatory, demyelinating polyneuropathy. It is the most common cause of acute and subacute flaccid paralysis in children. GBS causes about 0.4-1.3 cases per 100,000 persons/year in children. It can occur in any age group and the incidence increases among all age groups until a peak in the 50s. Both genders are affected and there may be a slight increase in males.

GBS usually occurs 2-4 weeks after a prodromal gastroenteritis or respiratory illness. GBS causes autoantibody production against Schwann cells of the neuron and the axon itself. There is an increase in anti-ganglioside antibodies which can be specifically identified in about 50% of children.

Classically GBS is a symmetric, progressive ascending muscle weakness and/or paralysis usually first occurring in the legs and then ascending to the upper extremities usually over days to weeks. Areflexia or diminished deep tendon reflexes are early signs (usually first week) if the patient comes to attention. Reflexes can be preserved in some patients though. Sensory changes including pain or paraesthesia can be a first sign in up to 50% of children. The pain can be poorly localized or vocalized because of the children’s age and development. Patients can appear to be ataxic but with further examination this is due to muscle weakness and sensory changes, not actual ataxia. Patients are afebrile.

The nadir when symptoms are the worst is usually around 2 weeks after symptoms begin and most patients begin improving after that. Most have significant improvement by 4 months and most have full recovery. Persistent symptoms can occur with fatigue being the most common, but also paresthesia and pain. Some still have problems including fatigue and sensory issues long term. A review of GBS can be found here.

Learning Point
Recurrences of GBS where patients have 2 or more attacks with an acute inflammatory demyelinating neuropathy are rare. The recurrence rate is quoted as 1-6% with asymptomatic periods ranging from a few months to years (2 months – 37 years depending on the study).

Some studies have demonstrated no incidence of recurrent GBS after seasonal influenza vaccination, and that at the minimum the risk is very small. Therefore GBS has a precaution against seasonal influenza vaccine. The Centers for Disease Control state that “A history of Guillain-Barre Syndrome (GBS) within 6 weeks following a previous dose of any type of influenza vaccine is considered a precaution to vaccination…. Persons who are not at higher risk for severe influenza complications…and who are known to have experienced GBS within 6 weeks of a previous influenza vaccination generally should not be vaccinated. As an alternative to vaccination, physicians might consider using influenza antiviral chemoprophylaxis for these persons…. However, the benefits of influenza vaccination might outweigh the risks for certain persons who have a history of GBS and who also are at higher risk for severe complications from influenza.”

Questions for Further Discussion
1. What groups or individuals are considered high risk for influenza?
2. What causes ataxia? Click here for a differential diagnosis.
3. What causes muscle weakness with and without hypotonia? Click here for a differential diagnosis.

Related Cases

    Symptom/Presentation: Pain

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at SearchingPediatrics.com, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for this topic: Guillian-Barre Syndrome


To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Baba M, Matsunaga M, Narita S, Liu H. Recurrent Guillain-Barre syndrome in Japan. Intern Med. 1995 Oct;34(10):1015-8.

Koul R, Chacko A, Ahmed R, Varghese T, Javed H, Al-Lamki Z. Ten-year prospective study (clinical spectrum) of childhood Guillain-Barre syndrome in the Arabian peninsula: comparison of outcome in patients in the pre- and post-intravenous immunoglobulin eras. J Child Neurol. 2003 Nov;18(11):767-71.

Stowe J, Andrews N, Wise L, Miller E. Investigation of the temporal association of Guillain-Barre syndrome with influenza vaccine and influenza like illness using the United Kingdom General Practice Research Database. Am J Epidemiol. 2009 Feb 1;169(3):382-8.

Kuitwaard K, Bos-Eyssen ME, Blomkwist-Markens PH, van Doorn PA. Recurrences, vaccinations and long-term symptoms in GBS and CIDP. J Peripher Nerv Syst. 2009 Dec;14(4):310-5.

Roodbol J, de Wit MC, Aarsen FK, Catsman-Berrevoets CE, Jacobs BC. Long-term outcome of Guillain-Barre syndrome in children. J Peripher Nerv Syst. 2014 Jun;19(2):121-6.

Gunatilake SS, Gamlath R, Wimalaratna H. An unusual case of recurrent Guillain-Barre syndrome with normal cerebrospinal fluid protein levels: a case report. BMC Neurol. 2016 Sep 5;16:161.

Centers for Disease Control. Prevention and Control of Seasonal Influenza with Vaccines: Recommendations of the Advisory Committee on Immunization Practices – United States, 2018-19 Influenza Season. Recommendations and Reports. MMWR. August 24, 2018. 67(3);1-20. Available from the Internet at: https://www.cdc.gov/mmwr/volumes/67/rr/rr6703a1.htm (cited 9/24/18)

Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital