Brown Pediatrics

Brown's Pediatric Residency Blog

Category: Infectious Disease

Trouble in Paradise



Case: George is a 5 year-old boy presenting to an Emergency Department (ED) complaining of abdominal pain and loose stools following a recent tropical vacation. How should we proceed? Is there any way that we could have prevented this?

What is traveler’s diarrhea?

    1. Classic Definition: ≥ 3 unformed stools in 24 hour period with nausea, vomiting, cramps, fever, blood in stool (Stauffer et al, 1990)
      • For infants and young children, some authors define diarrhea as ≥ 2-fold increase in unformed stool (Ashkenazi et al, 2016)
    2. Moderate diarrhea: 1-2 loose stools per 24 hour period
    3. Mild diarrhea: 1 loose stool per 24 hour period
    4. Duration (CDC, 2016)
      • Viral : 2-3 days
      • Bacterial: 3-7 days
      • Protozoal: weeks to months

Etiology (Ashkenazi et al., 2016)


Electron Microscope Image of E. Coli (Pixabay Image)

    1. Bacterial: E. Coli (ETEC, EHEC, EAEC, etc), Campylobacter jejuni, Salmonella spp., Shigella spp.,  are the most commonly seen, though Aeromonas spp. increasingly noted (CDC, 2016).
      • Of note, E. Coli (O157:H7) [associated with hemolytic uremic syndrome] has not been described in traveling children (Mackell, 2005)
    2. Viral: rotavirus, norovirus, adenovirus
    3. Parasite: Giardia (most common), Cryptosporidium, Cyclospora, entamoeba (uncommon)
    4. Etiologic agent generally identified in less than ⅓ of cases



    1. General incidence: 10-40% of travelers (Pitzinger B et al, 1991), though can affect up to 70% of travelers depending on the location they were traveling in (CDC Yellow Book)
      • Highest risk in Asia, Sub-Saharan Africa, and Latin America (Hagmann et al, 2010)
    2. Young children at the highest risk and manifest most severely (Ashkenazi et al, 2016)
    3. Children visiting family and/or friends are at higher risk as compared to tourists


    1. Microbiologic identification is generally unnecessary
    2. If fever and colitis  think Campylobacter, Shigella, EHEC
    3. Predominance of upper GI symptoms  Giardia, isospora, cyclospora
    4. If recent antimicrobials  -> C. diff
    5. If ill, send cultures for salmonella

Role for Prevention? (Connor, 2015)

  1. Choosing food and beverages wisely while traveling has been the cornerstone of advice
    • Unfortunately, studies do not show benefit to this practice (Steffen et al, 2004)
  2. Hand hygiene very important
  3. For children older than 12 years old, bismuth subsalicylate has been shown to reduce incidence of traveler’s diarrhea by 50%
    • Inconvenient dosing: 2 tabs, four times daily
  4. Prophylactic antibiotics are not generally recommended
    • May be considered in “high-risk hosts” (e.g. immunosuppressed)

His dad asks: how should he treat this?


    1. Maintaining hydration is the most important treatment
      • Use urine output as a guide (if normal urine output, diarrheal illness is mild)
    2. If evidence of dehydration: Preferentially use oral rehydration solution (Desforges, 1990)
      • WHO solution made with: Glucose (20g/L), 3 salts (3.5g/L) [sodium chloride, potassium chloride, and sodium bicarbonate]
      • Rationale for use is intestinal co-transport of glucose and sodium
    3. Role of antibiotics
      • Warranted in severe diarrhea (>4 stools in 24 hr period, fever, blood/pus in stool)
        1. Azithromycin is treatment of choice (Ashkenazi et al., 2016)
        2. Rifaxamin for children ≥ 12 years old
        3. Fluoroquinolones (Note: not FDA approved for children)


      1. Diarrheal illness in children returning from travel is not uncommon
      2. Younger children at higher risk of significant morbidity
      3. Maintaining hydration is essential; utilize oral route
      4. Antibiotics not well studied, beneficial in severe cases
      5. For all traveler’s, utilize CDC’s Website to provide resources and guidance

Online Resources

  • CDC:

Faculty Reviewer: Michael Koster, MD


Ashkenazi S et al. “Travelers’ Diarrhea in Children: What have we learnt?” The Pediatric Infectious Disease Journal. 2016;35(6)698-700.

Connor BA. “Traveler’s Diarrhea.” CDC Health Information for International Travelers 2016. Ed. G. Brunette. Oxford University Press, 2015.  Print and Online

Desforges JF. “Oral therapy for Acute Diarrhea- The Underutilized Simple Solution.” NEJM. 1990; 323:891- 894.

Hagmann S et al. “Illness in Children After International Travel: Analysis From the GeoSentinel Surveillance Network.” Pediatrics. 2010. 125(5)e1072-e1080

Mackell S. “Traveler’s Diarrhea in the Pediatric Population: Etiology and Impact.” Clin Infect Dis. 2005;41(Suppl 8)S547-S552.

Pitzinger B et al. “Incidence and clinical features of traveler’s diarrhea in infants and children.” The Pediatric Infectious Disease Journal. 1991;10(10)

Stauffer WM et al. “Traveling with Infants and Small Children. Part III: Traveler’s Diarrhea.” Journal of Travel Medicine. 2002;9(3):141-50

Steffen R et al. “Epidemiology of Travelers’ Diarrhea: Details of a Global Survey.” J Travel Med. 2004;11(4)231-238.



Image of the Week: 8/3

Created on 8/3/2016 by Vanessa Hand, MD


A 17 year-old male in obvious distress is brought the ED by his sister. She states that  this morning he woke up with a fever and a sore throat. However, over the next few hours his voice has been changing and is now more “hoarse.” She notes that during this time he also developed difficulty breathing. Below is an x-ray obtained upon presentation. What are you most concerned about?


Case courtesy of Dr Maxime St-Amant, From the case rID: 26840

 Radiology Findings: Typical findings of epiglottitis with enlarged epiglottis and aryepiglottic folds.

Diagnosis: Acute Epiglottitis


  • Combination of sore throat, dysphagia, “hot potato” voice and high fevers classically described
  • Difficulty with breathing may be most common chief complaint (Mayo-Smith et al, 1995)
  • Symptoms progress rapidly, usually over hours (Stroud et al, 2001)
  • Physical Exam Shows:
    • Vitals: Febrile, Tachypnea
    • Visibly Distressed Child; “Tripoding” position
    • Muffled or hoarse voice

Epidemiology (Shah at al, 2004)

  • Historically caused by H. Influenza type B, however vaccination has largely shifted etiology to other organisms
  • Rate dropped from 5/100,000 to 0.6-0.8/100,000 (immunized)
  • Increased age of presentation from 3 yo to 6-12 yo 

Causative Organisms

  • H. influenzae, penicillin resistant S. pneumoniae, S. Aureus, β-hemolytic strep


  • Minimize stimuli, stressful procedures
  • Maintain airway, anesthesia/ENT intubate in OR
  • Antibiotics: Ceftriaxone or Ampicillin/Sulbactam; add Vancomycin or Clindamycin if concern for MRSA

Faculty Reviewer: Brian Alverson, MD


Mayo-Smith MF et al. “Acute Epiglottitis. An 18-year experience in Rhode Island.” Chest. 1995;108(6):1640-7

Shah RK et al. “Epiglottitis in the Hemophilus influenzae Type B Vaccine Era: Changing Trends.” The Laryngoscope. 2004;114(3): 557-60

Stroud RH et al. “An update on inflammatory disorders of the pediatric airway: epiglottitis, croup, and tracheitis.” Am J Otolaryngology.  2001;22(4):268-275

Clinical Case: A Limp

A 4 year-old boy presents to the emergency room with a chief complaint of worsening limp. His parents tell you that yesterday he complained of pain in his left leg, and today he refuses to bear weight. On exam, he is febrile to 39º Celsius, tachycardic and appears ill. Exam is significant for exquisite tenderness over the left distal femur. There is no redness or swelling of the left knee. His labs are significant for WBC of 14, CRP of 150, ESR of 90. Blood cultures are drawn. X-ray of the femur reveals non-specific swelling around the femur, but no fracture. MRI shows:


What is the Diagnosis?


Image: Case courtesy of Dr Mohammad A. ElBeialy, From the case rID: 38589

Diagnosis: Acute Hematogenous Osteomyelitis

What is It?

Osteomyelitis is an infection of the bones that occurs either via hematogenous spread (most common in children), bacterial spread from local (contiguous) infections (cellulitis or septic arthritis), or traumatic inoculation. Long bones are more likely to be affected, with the femur being the most commonly affected bone (see below).

NEJM osteo


Skeletal Distribution of Acute Osteomyelitis in Children. From: Peltola H, Pääkkönen M. N Engl J Med 2014;370:352-360.


  1. Who is affected?
    • In developed countries, annual incidence is 8 out of 100,000 children. In developing countries, the incidence is much higher
    • Boys are affected twice as much as girls
  2. Who are the major pathogenic players?
    • Skin organisms predominate!
      • S. aureus is the most common etiologic agent
        • S. aureus possess virulence factors making it especially good at infecting bone
      • S. pyogenes 
    • Other common organisms
      • S. pneumoniae, H. influenza (though less common given vaccination; often affects joints, as compared to bones)
      • Kingella Kingae (most common in children under 4)
    • Sickle Cell disease
      • Consider Salmonella (though staph/strep still more common)
    • Neonatal Osteomyelitis
      • The organisms listed above still cause infections, but can also see: GBS, coag. negative Staph, Enterobacteriaceae

Clinical Presentation and Management

  1. Clinical Presentation 
    • Most common findings in children with osteomyelitis are pain of affected area and loss of function, however 2 distinct clinical syndromes have been described:
      • Children presenting with fever, localized pain, who appear acutely ill (likely septic)
      • A more indolent course, with gradual onset of pain and concurrent loss of function. In this presentation, the child may be afebrile or have low-grade fevers
    • As the lower extremity is more commonly affected, a common presentation is a child with a limp
    • Always consider osteomyelitis when dealing with a fever of unknown origin
    • Neonatal osteomyelitis is more likely to be associated with septic arthritis as well as be multi-focal
  2. Diagnosis
    • Physical Exam: As above, there are two main presentations, but most commonly children will demonstrate:
      • Fever
      • Localized erythema, swelling, inability to bear weight
    • Lab Studies
      • Serum Inflammatory Markers (CRP/ESR)
      • Blood Cultures (large studies show blood cultures positive in 48% [Peltola et al.])
      • CBC (may show mild-moderate leukocytosis, although normal white count does not exclude the diagnosis)
    •  Imaging
      • MRI is the most sensitive modality (Sensitivity: 88-100%, Specificity: 75-100%. [Song et al.])
      • Bone Scintigraphy
      • Plain Radiographs: Early in disease will show soft tissue swelling. (Sensitivity: 43-75%; Specificity: 75-83%)
    •  Microbiologic Data
      • Blood cultures as above
      • Bone biopsy, debridement
      • Abscess drainage, if applicable
  3. Treatment:
    • Choice of antibiotic: Empiric therapy in children should adequately cover S. aureus based on local susceptibility patterns (If suspecting osteomyelitis in a neonate, also need to consider Gram-negative organisms).
      • First Generation Cephalosporin (e.g. cefazolin)
      • Anti-staph Penicillin (nafcillin, oxacillin, etc)
      • Clindamycin (if suspecting MRSA and local resistance to clindamycin is low)
      • Vancomycin
      • Linezolid
    • Choice between IV and PO antibiotics
      • Historically, AHOM treated with long courses of IV antibiotics
      • Recent data suggests that a 2-4 day course of IV antibiotics, followed by oral antibiotics is as efficacious as IV therapy alone in uncomplicated cases (Peltola et al)
    • Duration of therapy
      • Historically, treatment duration ranged from 4-8 weeks
      • Recent data suggests that 3 week courses may be appropriate in carefully selected patients (Peltola et al, Song et al).
  4.  Conclusions
    • In pediatric patients, osteomyelitis is most often a hematogenous infection
    • S. aureus and S. pyogenes are the most common etiologic agents
      1. However, in small children, always consider Kingella spp.
    • Most common presenting complaints are fever and loss of function (lower extremities affected more commonly than upper extremities)
    • MRI is the most sensitive diagnostic modality
    • Initial Treatment is aimed at Staph and Strep, while consulting local susceptibility patterns
    • In uncomplicated cases following initial IV treatment, oral regimens have been shown to be as effective as IV regimens.
Case Presentation Radiographic Findings:
  • Altered marrow signal intensity of the distal left femur with low T1 and hyper intense T2 and PDFS signals. A focal destruction of the posteromedial distal femoral cortex is noted with elevated periosteum and periosteal reaction as well as subperiosteal 3.0 x 1.2 cm. cystic collection is noted with low T1 and hyper intense PDFS signal intensity.
  • Inflammatory changes with oedema signal and mild muscle enlargement are seen within the distal thigh and periarticular musculature with hypointense T1 and hyperintense T2 and PDFS signal.
  • Normal both hip joints with no evidence of significant joint effusion or septic arthritis.
  • The findings are those of distal femoral osteomyelitis with subperiosteal abscess and inflammatory myositis of the distal thigh muscles.


Faculty Reviewer: Michael Koster, MD



  1. Akakpo-Numado GK et al. “Current Bacterial Causes of Osteomyelitis in Children with Sickle Cell Disease” Sante 2008;18(2)67-70
  2. Conrad DA. “Acute Hematogenous Osteomyelitis.” Peds in Review 2010;31(11)
  3. Pääkkönen M, Peltola H. “Antibiotic treatment for acute hematogenous osteomyelitis of childhood: Moving towards shorter courses and oral administration.” International Journal of Antimicrobial Agents 2011;38:273-280
  4. Peltola H, Pääkkönen M, Kallio P, Kallio MJ. Short- versus long-term antimicrobial treatment for acute hematogenous osteomyelitis of childhood: prospective, randomized trial on 131 culture-positive cases. Pediatr Infect Dis J 2010;29:1123-1128
  5. Peltola H, Pääkkönen M. “Acute Osteomyelitis in Children.” N Engl J Med 2014;370:352-360.
  6. Song KM, Sloboda JF. “Acute Hematogenous Osteomyelitis in Children.” J Am Acad Orthop Surg 2001;9(3)166-75

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