Marfan syndrome is a connective tissue disease with cardiovascular complications such as aortic root dilation and aneurysm. Diagnosis is based on clinical features, family history, and genetic testing. The Ghent criteria are commonly used, with emphasis on cardiac manifestations. Echocardiographic surveillance is required, and prophylactic medications are used to reduce the chance of aortic root dilation. Aortic regurgitation may require surgery. Marfan syndrome is associated with non-cardiac features, and the clinical criteria can be found on the American National Marfan Foundation website.

There are several genetic mutations that can cause developmental abnormalities and disorders. One such mutation is the activation of the fibroblast growth factor 3 (FGF3) receptor, which leads to achondroplasia and stunted bone growth. Another mutation affects the fibrillin-1 gene, causing Marfan’s syndrome and resulting in tall stature, joint hypermobility, and cardiac abnormalities. Mutations in collagen genes can lead to disorders like osteogenesis imperfecta, Ehlers-Danlos syndrome, and Alport disease. Trisomy 18, or Edwards’ syndrome, is caused by an extra copy of chromosome 18 and results in severe developmental abnormalities and organ system dysfunction. Trisomy 21, or Down syndrome, is caused by an extra copy of chromosome 21 and leads to characteristic physical features such as dysplastic ears and a high arched palate, as well as intellectual disability.

When assessing for a pulse in infants, the recommended areas to check are the femoral and brachial arteries. This is because the carotid pulse may be difficult to palpate due to the short neck of infants. Checking for a central pulse is important as peripheral pulses may be weaker and harder to feel, especially in unwell patients with peripheral shutdown. It is important to note that according to BLS guidelines, the carotid pulse may only be used in children over 12 months old, making it an inappropriate option for an 8-month-old infant. Therefore, options including the carotid pulse are incorrect.

Paediatric Basic Life Support Guidelines

Paediatric basic life support guidelines were updated in 2015 by the Resuscitation Council. Lay rescuers should use a compression:ventilation ratio of 30:2 for children under 1 year and between 1 year and puberty, a child is defined. If there are two or more rescuers, a ratio of 15:2 should be used.

The algorithm for paediatric basic life support starts with checking if the child is unresponsive and shouting for help. The airway should be opened, and breathing should be checked by looking, listening, and feeling for breaths. If the child is not breathing, five rescue breaths should be given, and signs of circulation should be checked.

For infants, the brachial or femoral pulse should be used, while children should use the femoral pulse. Chest compressions should be performed at a ratio of 15:2, with a rate of 100-120 compressions per minute for both infants and children. The depth of compressions should be at least one-third of the anterior-posterior dimension of the chest, which is approximately 4 cm for an infant and 5 cm for a child.

In children, the lower half of the sternum should be compressed, while in infants, a two-thumb encircling technique should be used for chest compressions. These guidelines are crucial for anyone who may need to perform basic life support on a child, and it is essential to follow them carefully to ensure the best possible outcome.

In children, S. pneumoniae is the most probable cause of bacterial pneumonia, as indicated by the presentation of raised inflammatory markers and lobar consolidation on chest x-ray. The child is experiencing persistent fever and tachypnea. Other potential causes include Mycoplasma pneumonia or Chlamydia pneumoniae, while RSV is more commonly associated with bronchiolitis in children under 2 years old. Haemophilus influenzae and Bordetella pertussis are less likely to be responsible for pneumonia in immunized and non-immunocompromised children. Legionella pneumophila is an unlikely cause of pneumonia in a child of this age, despite its potential to cause severe pneumonia.

Pneumonia is a common illness in children, with S. pneumoniae being the most likely cause of bacterial pneumonia. The British Thoracic Society has published guidelines for the management of community acquired pneumonia in children. According to these guidelines, amoxicillin is the first-line treatment for all children with pneumonia. Macrolides may be added if there is no response to first-line therapy, or if mycoplasma or chlamydia is suspected. In cases of pneumonia associated with influenzae, co-amoxiclav is recommended. It is important to follow these guidelines to ensure effective treatment and management of pneumonia in children.

Familial Short Stature in Children

Children who have short parents and are otherwise healthy may have familial short stature. This means that their height and weight fall within the expected range based on their parents’ heights, and growth charts can be used to predict their adult height. In the case of a girl with familial short stature, her predicted adult height would be 154 cm, which falls within the mid-parental range of heights. Delayed puberty would cause a failure to gain height at the beginning of puberty and crossing of height centiles, while inadequate nutrition would cause crossing of both height and weight centiles. Low birth weight can also cause short stature in children, but in the absence of any other history, familial short stature is the most likely explanation. Precocious puberty, on the other hand, causes children to be tall for their age at the onset of puberty, not short.

Juvenile idiopathic arthritis, also known as Still’s disease, is identified by the presence of a distinct salmon-pink rash along with joint pain. While joint pain may also be present in Henoch-Schonlein purpura, the rash in this condition is palpable and purpuric. Meningitis, on the other hand, is characterized by a non-blanching purpuric rash but does not cause joint pain.

Understanding Systemic Onset Juvenile Idiopathic Arthritis

Juvenile idiopathic arthritis (JIA) is a condition that affects individuals under the age of 16 and lasts for more than six weeks. It is also known as juvenile chronic arthritis. Systemic onset JIA, also referred to as Still’s disease, is a type of JIA that presents with several symptoms. These symptoms include pyrexia, a salmon-pink rash, lymphadenopathy, arthritis, uveitis, anorexia, and weight loss.

When investigating systemic onset JIA, doctors may find that the antinuclear antibody (ANA) is positive, especially in oligoarticular JIA. However, the rheumatoid factor is usually negative. It is important to note that systemic onset JIA can be challenging to diagnose, as its symptoms can mimic other conditions.

Bronchiolitis can be more severe in individuals with congenital heart disease, particularly those with a ventricular septal defect. Fragile X is not associated with increased severity, but Down’s syndrome has been linked to worse episodes. Formula milk feeding is a risk factor for bronchiolitis, but does not affect the severity of the disease once contracted. While bronchiolitis is most common in infants aged 3-6 months, this age range is not indicative of a more severe episode. However, infants younger than 12 weeks are at higher risk. Being born at term is not a risk factor, but premature birth is associated with more severe episodes.

Bronchiolitis is a condition where the bronchioles become inflamed, and it is most commonly caused by respiratory syncytial virus (RSV). This virus is responsible for 75-80% of cases, with other causes including mycoplasma and adenoviruses. Bronchiolitis is most prevalent in infants under one year old, with 90% of cases occurring in those aged 1-9 months. The condition is more serious in premature babies, those with congenital heart disease or cystic fibrosis. Symptoms include coryzal symptoms, dry cough, increasing breathlessness, and wheezing. Hospital admission is often necessary due to feeding difficulties associated with increasing dyspnoea.

Immediate referral is recommended if the child has apnoea, looks seriously unwell, has severe respiratory distress, central cyanosis, or persistent oxygen saturation of less than 92% when breathing air. Clinicians should consider referral if the child has a respiratory rate of over 60 breaths/minute, difficulty with breastfeeding or inadequate oral fluid intake, or clinical dehydration. Immunofluorescence of nasopharyngeal secretions may show RSV, and management is largely supportive. Humidified oxygen is given via a head box if oxygen saturations are persistently low, and nasogastric feeding may be necessary if children cannot take enough fluid/feed by mouth. Suction may also be used for excessive upper airway secretions. NICE released guidelines on bronchiolitis in 2015 for more information.

The preferred diagnostic test for necrotising enterocolitis is an abdominal x-ray. This condition, which is a leading cause of death among premature infants, presents with symptoms such as abdominal distension, feeding intolerance, bloody stool, and bilious vomiting. An abdominal x-ray can reveal dilated bowel loops, intramural gas, and portal venous gas. Treatment involves total gut rest and total parenteral nutrition, with laparotomy required for babies with perforations.

Intussusception is diagnosed using abdominal ultrasound, but this is unlikely in this case as the child does not have the characteristic symptoms of paroxysmal abdominal colic pain and red currant jelly stool. Laparotomy is used to investigate perforation, but this is unlikely as the child has no fever. Test feed is used to diagnose pyloric stenosis, but this is also unlikely as the child is presenting with multiple gastrointestinal symptoms. An upper gastrointestinal tract contrast study is used to diagnose malrotation, but this is unlikely as the child was born healthy.

Understanding Necrotising Enterocolitis

Necrotising enterocolitis is a serious condition that is responsible for a significant number of premature infant deaths. The condition is characterized by symptoms such as feeding intolerance, abdominal distension, and bloody stools. If left untreated, these symptoms can quickly progress to more severe symptoms such as abdominal discolouration, perforation, and peritonitis.

To diagnose necrotising enterocolitis, doctors often use abdominal x-rays. These x-rays can reveal a number of important indicators of the condition, including dilated bowel loops, bowel wall oedema, and intramural gas. Other signs that may be visible on an x-ray include portal venous gas, pneumoperitoneum resulting from perforation, and air both inside and outside of the bowel wall. In some cases, an x-ray may also reveal air outlining the falciform ligament, which is known as the football sign.

Overall, understanding the symptoms and diagnostic indicators of necrotising enterocolitis is crucial for early detection and treatment of this serious condition. By working closely with healthcare professionals and following recommended screening protocols, parents and caregivers can help ensure the best possible outcomes for premature infants at risk for this condition.

When a baby has difficulty passing stool, it may be a sign of Hirschsprung’s disease, a condition where nerve cells in the colon are missing. This disease is more common in males and can be diagnosed through a biopsy. It is important to note that not all babies with delayed passage have this disease. Hirschsprung’s disease can also present in later childhood, so it is important to ask about the timing of symptoms in children with chronic constipation or obstruction. This disease is associated with MEN 2A/B, not MEN1, and meconium ileus is a common differential. Pyloric stenosis is associated with non-bilious vomiting, while a temperature is not a factor in suggesting Hirschsprung’s disease.

Paediatric Gastrointestinal Disorders

Pyloric stenosis is more common in males and has a 5-10% chance of being inherited from parents. Symptoms include projectile vomiting at 4-6 weeks of life, and diagnosis is made through a test feed or ultrasound. Treatment involves a Ramstedt pyloromyotomy, either open or laparoscopic.

Acute appendicitis is uncommon in children under 3 years old, but when it does occur, it may present atypically. Mesenteric adenitis causes central abdominal pain and URTI, and is treated conservatively.

Intussusception occurs in infants aged 6-9 months and causes colicky pain, diarrhea, vomiting, a sausage-shaped mass, and red jelly stool. Treatment involves reduction with air insufflation.

Intestinal malrotation is characterized by a high caecum at the midline and may be complicated by the development of volvulus. Diagnosis is made through an upper GI contrast study and ultrasound, and treatment involves laparotomy or a Ladd’s procedure.

Hirschsprung’s disease occurs in 1/5000 births and is characterized by delayed passage of meconium and abdominal distension. Treatment involves rectal washouts and an anorectal pull through procedure.

Oesophageal atresia is associated with tracheo-oesophageal fistula and polyhydramnios, and may present with choking and cyanotic spells following aspiration. Meconium ileus is usually associated with cystic fibrosis and requires surgery to remove plugs. Biliary atresia causes jaundice and increased conjugated bilirubin, and requires an urgent Kasai procedure. Necrotising enterocolitis is more common in premature infants and is treated with total gut rest and TPN, with laparotomy required for perforations.

If acute epiglottitis is suspected, do not attempt to examine the throat. Instead, contact the paediatrician on call and arrange for the child to be reviewed and admitted to the hospital on the same day. This condition can be life-threatening and requires urgent assessment and treatment in secondary care. Hospital transfer should be done by a blue light ambulance. Treatment usually involves intravenous antibiotics after securing the airway, which may require intubation. Nebulised adrenaline may also be used to stabilise the airway, and intravenous steroids are often given. It would be clinically unsafe to advise expectant management or prescribe immediate or delayed antibiotics for this condition.

Acute epiglottitis is a rare but serious infection caused by Haemophilus influenzae type B. It is important to recognize and treat it promptly as it can lead to airway obstruction. Although it was once considered a disease of childhood, it is now more common in adults in the UK due to the immunization program. The incidence of epiglottitis has decreased since the introduction of the Hib vaccine. Symptoms include a rapid onset, high temperature, stridor, drooling of saliva, and a tripod position where the patient leans forward and extends their neck to breathe easier. Diagnosis is made by direct visualization, but x-rays may be done to rule out a foreign body.

Immediate senior involvement is necessary, including those who can provide emergency airway support such as anaesthetics or ENT. Endotracheal intubation may be necessary to protect the airway. It is important not to examine the throat if epiglottitis is suspected due to the risk of acute airway obstruction. The diagnosis is made by direct visualization, but only senior staff who are able to intubate if necessary should perform this. Treatment includes oxygen and intravenous antibiotics.

Common Skin Rashes and Infections: Symptoms and Characteristics

Parvovirus Infection: Also known as ‘slapped cheek syndrome’, this mild infection is characterized by a striking appearance. However, it can lead to serious complications in immunocompromised patients or those with sickle-cell anaemia or thalassaemia.

Pityriasis Rosea: This rash starts with an oval patch of scaly skin and is followed by small, scaly patches that spread across the body.

Impetigo: A superficial infection caused by Staphylococcus or Streptococcus bacteria, impetigo results in fluid-filled blisters or sores that burst and leave a yellow crust.

Scarlet Fever: This rash is blotchy and rough to the touch, typically starting on the chest or abdomen. Patients may also experience headache, sore throat, and high temperature.

Urticaria: This itchy, raised rash is caused by histamine release due to an allergic reaction, infection, medications, or temperature changes. It usually settles within a few days.

Slipped Upper Femoral Epiphysis: Symptoms and Risk Factors

Slipped upper femoral epiphysis is a condition that commonly affects obese adolescent boys with a positive family history. It is characterized by the displacement of the femoral head from the femoral neck, which can lead to a range of symptoms.

The most common symptoms of slipped upper femoral epiphysis include an externally rotated hip and antalgic gait, decreased internal rotation, thigh atrophy (depending on the chronicity of symptoms), and hip, thigh, and knee pain.

It is important to note that 25% of cases are bilateral, meaning that both hips may be affected. This condition can be particularly debilitating for young people, as it can limit their mobility and cause significant discomfort.

Overall, it is important for healthcare professionals to be aware of the risk factors and symptoms of slipped upper femoral epiphysis, as early diagnosis and treatment can help to prevent further complications and improve outcomes for patients.

Total Anomalous Pulmonary Venous Connection

Total anomalous pulmonary venous connection (TAPVC) is a condition that causes cyanosis in newborns. It is characterized by an abnormality in blood flow where all four pulmonary veins drain into systemic veins or the right atrium, with or without pulmonary venous obstruction. This results in the mixing of systemic and pulmonary venous blood in the right atrium.

In contrast, conditions such as patent ductus arteriosus (PDA), atrial septal defect (ASD), and ventricular septal defect (VSD) are left to right shunts. Tricuspid atresia is another condition that is typically associated with cyanosis, but mitral regurgitation is not.

It is important to understand the differences between these conditions and their effects on blood flow in order to properly diagnose and treat them. Further reading on TAPVC can be found on Medscape.

Investigation and Management of Meningitis in Children

Meningitis is a serious condition that can affect children. When investigating meningitis, it is important to note any contraindications to lumbar puncture, such as signs of raised intracranial pressure, focal neurological signs, papilloedema, significant bulging of the fontanelle, disseminated intravascular coagulation, or signs of cerebral herniation. For patients with meningococcal septicaemia, a lumbar puncture is contraindicated, and blood cultures and PCR for meningococcal should be obtained instead.

The management of meningitis in children involves administering antibiotics, such as IV amoxicillin (or ampicillin) and IV cefotaxime for children under three months, and IV cefotaxime (or ceftriaxone) for children over three months. Steroids should be considered if the lumbar puncture reveals certain findings, such as purulent cerebrospinal fluid, a high white blood cell count, or bacteria on Gram stain. Fluids should be administered to treat shock, and cerebral monitoring should be conducted, including mechanical ventilation if necessary.

It is also important to notify public health authorities and administer antibiotic prophylaxis to contacts. Ciprofloxacin is now preferred over rifampicin for this purpose. Overall, prompt and appropriate management of meningitis in children is crucial for ensuring the best possible outcomes.

During the first 10 minutes after birth, it is normal for a healthy newborn to have SpO2 readings that are not optimal. It is also common for them to experience temporary cyanosis, which typically resolves on its own and does not require intervention. It is important to evaluate the baby’s appearance and color using the APGAR scoring system at 1 minute after birth, and then again at 5 and 10 minutes.

Cyanosis, a bluish discoloration of the skin, is a common occurrence in newborns. Peripheral cyanosis, which affects the hands and feet, is often seen in the first 24 hours of life and can be caused by crying or illness. Central cyanosis, on the other hand, is a more serious condition that occurs when the concentration of reduced hemoglobin in the blood exceeds 5g/dl. To differentiate between cardiac and non-cardiac causes of central cyanosis, doctors may use the nitrogen washout test, which involves giving the infant 100% oxygen for ten minutes and then measuring arterial blood gases. A pO2 of less than 15 kPa indicates cyanotic congenital heart disease, which can be caused by conditions such as tetralogy of Fallot, transposition of the great arteries, and tricuspid atresia.

If cyanotic congenital heart disease is suspected, initial management involves supportive care and the use of prostaglandin E1, such as alprostadil, to maintain a patent ductus arteriosus in ductal-dependent congenital heart defects. This can serve as a temporary measure until a definitive diagnosis is made and surgical correction is performed.

Acrocyanosis, a type of peripheral cyanosis, is a benign condition that is often seen in healthy newborns. It is characterized by bluish discoloration around the mouth and extremities, such as the hands and feet, and is caused by vasomotor changes that result in peripheral vasoconstriction and increased tissue oxygen extraction. Unlike other causes of peripheral cyanosis that may indicate significant pathology, such as septic shock, acrocyanosis occurs immediately after birth in healthy infants and typically resolves within 24 to 48 hours.

Understanding Autosomal Recessive Inheritance

Autosomal recessive inheritance is a genetic pattern where a disorder is only expressed when an individual inherits two copies of a mutated gene, one from each parent. This means that only homozygotes, individuals with two copies of the mutated gene, are affected. Both males and females are equally likely to be affected, and the disorder may not manifest in every generation, as it can skip a generation.

When two heterozygote parents, carriers of the mutated gene, have children, there is a 25% chance of having an affected (homozygote) child, a 50% chance of having a carrier (heterozygote) child, and a 25% chance of having an unaffected child. On the other hand, if one parent is homozygote for the gene and the other is unaffected, all the children will be carriers.

Autosomal recessive disorders are often metabolic in nature and can be life-threatening compared to autosomal dominant conditions. Understanding the inheritance pattern of autosomal recessive disorders is crucial in genetic counseling and family planning.

Causes of Cyanotic Congenital Heart Disease in Newborns

Cyanotic congenital heart disease is a condition that results in low oxygen levels in the blood, leading to a bluish discoloration of the skin. There are several causes of this condition in newborns, including transposition of the great arteries (TGA), tetralogy of Fallot with severe pulmonary stenosis, hypoplastic left heart syndrome, severe ventricular septal defect, and tricuspid atresia with atrial and ventricular septal defect.

Transposition of the great arteries (TGA) is the most common cause of cyanotic congenital heart disease in newborns. In this condition, the aorta and pulmonary trunk are switched, which is incompatible with life without an associated mixing defect such as atrial septal defect, ventricular septal defect, or patent ductus arteriosus.

Tetralogy of Fallot with severe pulmonary stenosis is another cause of cyanotic congenital heart disease in newborns. This condition results in cyanosis early after birth due to a severely stenotic pulmonary outflow, which maximizes the right-to-left shunt through the ventricular septal defect.

Hypoplastic left heart syndrome is a cyanotic congenital heart disease that is usually associated with pulmonary edema. This condition is caused by dysgenesis of the left ventricle, which leads to mixing of arterial and venous blood and subsequent cyanosis.

Severe ventricular septal defect results in left-to-right shunting of blood, which typically does not result in cyanosis until progressive cardiac decompensation occurs. This makes it an unlikely cause of cyanotic congenital heart disease in newborns who present with cyanosis immediately after birth.

Tricuspid atresia with atrial and ventricular septal defects is another cause of cyanotic congenital heart disease in newborns. This condition results in right-to-left blood shunting without pulmonary edema early after birth, but it is less common than other causes of cyanotic congenital heart disease.

The appropriate treatment for a pediatric patient with intestinal malrotation and volvulus is Ladd’s procedure, which involves the division of Ladd bands and widening of the base of the mesentery. Malrotation occurs when the midgut does not complete its rotation during development, resulting in the cecum being fixed in the right upper quadrant by peritoneal bands known as Ladd bands. This can lead to the formation of a volvulus, which requires untwisting and removal of the Ladd bands, as well as resection of any necrotic bowel and removal of the appendix. The Kasai procedure is used for biliary atresia, Ramstedt pyloromyotomy for pyloric stenosis, and rectal washouts for Hirschsprung’s disease.

Paediatric Gastrointestinal Disorders

Pyloric stenosis is more common in males and has a 5-10% chance of being inherited from parents. Symptoms include projectile vomiting at 4-6 weeks of life, and diagnosis is made through a test feed or ultrasound. Treatment involves a Ramstedt pyloromyotomy, either open or laparoscopic.

Acute appendicitis is uncommon in children under 3 years old, but when it does occur, it may present atypically. Mesenteric adenitis causes central abdominal pain and URTI, and is treated conservatively.

Intussusception occurs in infants aged 6-9 months and causes colicky pain, diarrhea, vomiting, a sausage-shaped mass, and red jelly stool. Treatment involves reduction with air insufflation.

Intestinal malrotation is characterized by a high caecum at the midline and may be complicated by the development of volvulus. Diagnosis is made through an upper GI contrast study and ultrasound, and treatment involves laparotomy or a Ladd’s procedure.

Hirschsprung’s disease occurs in 1/5000 births and is characterized by delayed passage of meconium and abdominal distension. Treatment involves rectal washouts and an anorectal pull through procedure.

Oesophageal atresia is associated with tracheo-oesophageal fistula and polyhydramnios, and may present with choking and cyanotic spells following aspiration. Meconium ileus is usually associated with cystic fibrosis and requires surgery to remove plugs. Biliary atresia causes jaundice and increased conjugated bilirubin, and requires an urgent Kasai procedure. Necrotising enterocolitis is more common in premature infants and is treated with total gut rest and TPN, with laparotomy required for perforations.

Indomethacin is the preferred treatment for patent ductus arteriosus (PDA) in newborns, administered postnatally rather than antenatally to the mother. PDA is a congenital heart condition characterized by a left-right shunt where blood flows from the aorta to the pulmonary vessel through the patent ductus arteriosus. Although newborns with PDA may appear normal, a continuous machine-like murmur can be detected upon auscultation. Premature babies are more likely to have PDA, which may spontaneously close in asymptomatic patients. Symptomatic babies undergo an echocardiogram a few days after birth to determine whether medical or surgical management is necessary. Medical management involves administering indomethacin or ibuprofen to the newborn, while prophylactic treatment immediately after delivery or administering medication to the mother has no role in PDA closure. Prostaglandin analogues can maintain ductus arteriosus patency after birth and are useful in managing certain congenital heart diseases.

Patent ductus arteriosus is a type of congenital heart defect that is typically classified as ‘acyanotic’. However, if left untreated, it can eventually lead to late cyanosis in the lower extremities, which is known as differential cyanosis. This condition is caused by a connection between the pulmonary trunk and descending aorta that fails to close with the first breaths due to increased pulmonary flow that enhances prostaglandins clearance. Patent ductus arteriosus is more common in premature babies, those born at high altitude, or those whose mothers had rubella infection during the first trimester of pregnancy.

The features of patent ductus arteriosus include a left subclavicular thrill, a continuous ‘machinery’ murmur, a large volume, bounding, collapsing pulse, a wide pulse pressure, and a heaving apex beat. To manage this condition, indomethacin or ibuprofen is given to the neonate, which inhibits prostaglandin synthesis and closes the connection in the majority of cases. If patent ductus arteriosus is associated with another congenital heart defect that is amenable to surgery, then prostaglandin E1 is useful to keep the duct open until after surgical repair.

Differential Diagnosis for a Child with Inspiratory Stridor and Barking Cough

Croup is a common respiratory illness in children under 2 years old, characterized by inspiratory stridor and a barking cough. Other symptoms include hoarseness, fever, and dyspnea, which are usually worse at night. The illness can last up to 7 days, with the first 24-48 hours being the most severe.

Asthma, on the other hand, presents differently with wheezing and chest tightness, rather than inspiratory stridor. While shortness of breath, especially at night, is a common symptom, it does not account for the fever.

Simple viral cough is a possible differential, but the absence of other systemic symptoms makes croup more likely.

Whooping cough is not indicated by this history.

Bronchiolitis usually presents less acutely, with difficulty feeding and general malaise during the incubation period, followed by dyspnea and wheezing. Therefore, it is less likely to be the cause of the child’s symptoms.