1. What is important in the Survival for an organism
    • Balance between host and other
    • Pathogens vs commensal vs symbiote
  2. What is the Estimated # of bacteria on Earth
    • 5,000,000,000,000,000,000,000,000,000,000
    • 5 x 1030
    • five octillion
  3. What is common with the relationship between the host and the organism
    • Some organisms almost always symbiotic / commensal (Lactobacillus)
    • Some organisms are always pathogenic (e.g., Shigella, Bacillus anthracis)
    • In humans, most organisms are neither (e.g., Flavimonas orizahabitans)
    • Some can be either, given the right circumstances
    • e.g., Enterococcus, E coli, Streptococcus agalactiae, etc.
  4. What determines disease?
    The interaction between host and bug determines disease.
  5. Does the same bug cause the same effects in all patient?
    No, The same bug in different patients might have different outcomes.

    • Will antibiotics cure a disease if a patient has a poor immune system?
    • No, A functioning immune system is better than all antibiotics. Antibiotics just assist the body in fighting disease. Antibiotics won’t work if there is no immune system. If you have a compromised immune system, antibiotics may not be able to get the job done.

    • What is important to remember when deciding on medical interventions?
    • Medical interventions can increase risk of infection. Need to think about the risks versus benefits. All interventions are a balance between risk and benefit.

    • What is very important in infectious diseases?
    • Exposure is everything in infectious disease
  6. Why are the risks of term Neonates?
    • Higher risk for infection
    • naïve immune system- lack of memory B & T cells & neutrophils with poor function
    • complement levels low
    • IgG obtained from mother but the specificity may not be against the bugs that they are exposed to
  7. What is extremely important in trying to clear infection?
    Complement system, intact skin and mucosal barriers
  8. What are the risks of Preterm Neonates?
    • Even higher risk for infection
    • complement levels lower than in term infants
    • less IgG transferred from mother
    • in extremely premature infants skin is immature
  9. What does prolonged ROM cause?
    Opens fetus up to infection because they no longer have protection
  10. How does congenital infections affect the fetus
    • Congenital infections can cause defects
    • Some infections can be immunosuppressive
    • If the have one STD they may have another ( remember to consider this)
  11. What is puerperal fever?
    • Fever from Group strep A infection – this is an extremely fast bacteria-can die within hours
    • Not often seen in US
    • From unclean practices
    • NEVER blow off maternal fever – in group A- mother gets fever after birth and is dead within 4 hours
  12. Where does GBS colonize?
    In genital track and rectum
  13. What special problems exist in the Neonatal population?
    • Twins / multiples
    • Prolonged rupture of membranes
    • Maternal illnesses,
    • (Congenital) infections
    • Puerperal fever
    • Maternal flora (e.g., GBS)
    • Birth environment not ideal (toilet delivery, en route delivery, home delivery)
  14. What Problems do hospitalized neonates face?
    • most of the time the infant is premature thus has a longer stay
    • hospital organisms
    • prolonged antibiotic exposure
    • violation of natural barriers (ET tubes, IVs, UAC/UVC, etc.)
  15. Is an infant who has better PNC and from a better “environment” less likely to get infected by a congenital infection
    Infants can have the same bug even though they come from different environments – don’t think that just because an infant has excellent PNC that they won’t have a nasty bug
  16. What are the causes of non infectious diseases in the sick neonate?
    • Respiratory distress syndrome /hyaline membrane disease
    • apnea of prematurity
    • meconium aspiration syndrome
  17. What are the main causes of Infectious disease in neonates?
    Sepsis from bacteremia meningitis, urinary tract infection
  18. What is Neonatal Sepsis
    • Putrifaction
    • severe systemic infection often involving the bloodstream
    • from the Greek σήψις, ultimately from σήπειν (to rot)
  19. Why is it difficult to diagnose Neonatal Sepsis
    • Problematic diagnosis in neonates
    • signs non-specific
    • patient cannot communicate
    • often difficult to determine cause
    • symptoms can result from other processes
  20. What should worry you about temperature and sepsis
    Hypothermia – liver is beginning to shut down due to metabolic processes are slowing down and unable to maintain temp
  21. What will change first heart rate or BP when sick
    Infants will increase heart rate before they change blood pressure when sick
  22. What are the signs of Neonatal Sepsis
    • temperature instability (high/low)
    • respiratory distress
    • tachycardia d/t catecholamine drive and hypotension
    • apnea (prematurity vs infection)
    • lethargy / irritability – never blow off abnormal behavior in a baby
    • jaundice (conjugated often) – because the excretion mechanisms are out of whack- pay attention especially when it won’t go away
    • poor feeding / residuals – one of the first things to shut down is the gut (remember that other things can cause this as well – like opiod)
    • vomiting – this is pretty rare
    • abdominal distension because it is associated with a lot of things like NEC, perforation
    • necrotizing enterocolitis – need to think about systemic infections in these kids
  23. How do you diagnose Neonatal Sepsis?
    • Have to think about a lot of stuff:
    • high clinical suspicion (“rule out”)
    • patient scenario
    • WBC (high or low)
    • I:T ratio > 0.2-0.3 (this is a higher ratio some people say 0.08 but then more kids are on antibiotics- so need to look at other things if you are suspicious)
    • platelet count (high or low) – this is a acute phase reaction, low platelets are present in NEC and in fungal infection (for fungal infections this isn’t always a definite)
    • acute phase reactants (CRP)
  24. How is the I:T ratio important in neonatal sepsis?
    • immature : total
    • bands + myelocytes + metamyelocytes :bands + segs + myelocytes + metamyelocytes
    • Remember if have an infant with high immatures but borderline I:T- most likely septic
  25. What are tests to confirm sepsis?
    • blood cultures!!!!! – a negative blood culture always doesn’t mean that they aren’t septic use one bottle – want to maximize the yield
    • CSF cultures!!!!! – this is VERY important
    • urine cultures – (after first week or so) getting a good urine sample is extremely important, a bagged urine isn’t usually that great in neonates and peds
    • no ET cultures!!!!! – these don’t tell us a lot – can introduce bugs into the trachea- unless there is pus coming out of the tube then don’t need one
  26. What is Neonatal Meningitis
inflammation of the meninges

    • What is meninges
    • plural of meninx
    • any of the three layers covering the brain and spinal cord
  27. What is the meninx
    • derived from the French méninge, ultimately from a corruption of Aristotelian Greek μηνιγξ

    • How was the word meningitis derived
    • meninx + (νόσοσ)ίτης (disease of)
  28. What is the The hallmark of meningitis
    Pain – this is difficult to assess in neonates
  29. In one month old how do you interpret nuchal rigidity
    Meningitis until proven otherwise
  30. What are the signs of meningitis
    • Inflammation of the meninges causes the principle manifestations
    • nuchal rigidity
    • (Kernig’s, Brudzinski’s)
    • headache
    • photophobia
  31. Why is diagnosing meningitis in the neonatal population difficult
    • The problem is that in neonates, these are unreliable:
    • nuchal rigidity, (Kernig’s, Brudzinski’s), headache, photophobia
  32. How do you treat Neonatal Meningitis
    • must dose antibiotics higher
    • continue an aminoglycoside (these don’t usually get into CSF but they do when meninges are inflamed) pending CSF cultures
    • cefotaxime useful for late-onset
    • longer therapy duration – to ensure total elimination of infection
    • no CSF taken must assume – this isn’t good- always get CSF
  33. What antibiotic should be used with meningitis
    • May be region specific – some bugs may be resistant in a particular area
    • Empirical therapy – prior to culture results
    • ampicillin 200-400 mg/kg/d div q6h
    • plus
    • gentamicin 2.5-3.5 mg/kg/d
  34. What should you use to treat Special cases of meningitis
    • vancomycin if foreign bodies or known MRSA in NICU
    • cephalosporins controversial in NICU setting – b/c of fungal infections that may occur
    • antifungal coverage if suspected -
  35. What is early onset sepsis?
    • Early-onset disease (0-7 days)
    • From vaginal / stool flora
    • Remember that babies pick up bugs very quickly
  36. What is Late-onset disease?
    • (>7 days)
    • vaginal / stool flora and environmental exposures
  37. What are the most common causes of early-onset disease
    • • Escherichia coli
    • • Streptococcus agalactiae (GBS)
    • • Listeria monocytogenes
    • • Haemophilus influenzae
  38. What are the most common causes of Late-onset disease
    • • Streptococcus agalactiae (GBS)
    • • Staphylococcus epidermidis – more common in neonates that in other groups
    • • Gram negative rods (incl. E coli)
    • • Staphylococcus aureus
    • • fungus (usually Candida)
  39. What is GBS
    • S agalactiae (GBS)
    • first seen in bovine mastitis
    • rose to prominence in 1970s
    • biphasic disease peak in neonates – Incidence Peaks at birth, then plummets, then rises slightly between 1 week and 3 months;
  40. How often are infants colonized in a GBS positive mother
    S agalactiae (GBS)50% of infants become colonized and of these 50%, 98% are aymptomatic and 2% are early onset
  41. How has GBS prophylaxis changed the incidence of GBS infectionin neonate?
    • Previously #1 in neonatal sepsis
    • was 1-4/1000 live births
    • was 75% of neonatal sepsis
    • now 0.5/1000
  42. What are the Risk factors for getting GBS
    • • prior infant w/ invasive GBS
    • • GBS UTI in pregnancy
    • • preterm delivery
    • • intrapartum fever > 38°C
    • • ROM > 18 hrs
  43. What should you know about Early-onset GBS disease
    • source is mother’s vagina / GI
    • can cause sepsis / bacteremia /pneumonia / meningitis
    • associated with shock /respiratory distress / apnea
    • can occur in treated
  44. What should you know abour Late-onset GBS disease
    • source can be birth but is often postnatal exposure
    • can cause sepsis / bacteremia /pneumonia / meningitis
    • also causes osteomyelitis /septic arthritis / cellulitis ( this is different than early onset)
  45. What is the screening based approach for S agalactiae (GBS)
    • pregnant women at 35-37 wks are screened
    • offer intrapartum prophylaxis
    • if Cx +ve / no other factors
    • give prophylaxis if one or more risk factors
  46. What is the risk factor based approach for S agalactiae (GBS)
    • risk factor based approach – this isn’t very effective
    • no screening performed
    • give prophylaxis if one or more risk factors
  47. What is the typical intrapartum prophylaxis for S agalactiae (GBS)
    • PCN-G IV drug of choice - ampicillin IV acceptable
    • IV clindamycin, erythromycin, 1st generation cephalosporin, if PCN allergy
    • give 4 hrs prior, 2+ doses
  48. What are the Strategies for the exposed infant to S agalactiae (GBS)
    • close observation
    • in preterms, CBC / BCx
    • in terms without prophylaxis: CBC / BCx
    • if sick, workup & antibiotics
  49. What are Strategies for diagnosis of GBS
    • culture from sterile body site
    • A positive blood cx will show GPC pairs / chains and β-hemolytic
    • must look at blood & CSF
    • if mom was pretreated, clinical judgment
  50. What does GBS look like under the microscope?
    GPC in pairs or clusters
  51. What is the treatment for S agalactiae (GBS)
    • Strategies for treatment
    • Empirical - ampicillin & gentamicin
    • targeted- ampicillin & gentamicin
    • bacteremia: Tx 14 d from 1st neg
    • meningitis: Tx 21 d (or more)
  52. What is Escherichia coli
    • Enteric Gram negative rod
    • “gut bug”
    • like GBS, picked up at delivery
    • can be spread nosocomially
  53. What is associated with Escherichia coli infection
    • Galactosemia**
    • other metabolic diseases
    • fetal hypoxia
    • acidosis
    • bladder extrophy /myelomeningocoele any inappropriate open of spinal cord near the anus)
  54. What are the Strategies for diagnosis of e.coli
    • culture from sterile body site- GNR- confirmed by biochemical tests
    • must look at blood & CSF
    • if pretreated, clinical judgment – may need to think about it, just because they were pretreated doesn’t mean that they aren’t there
  55. What does e coli look like under the microscope
  56. What are Strategies for treatment of ecoli
    • E coli can become resistant
    • Empirical ampicillin & gentamicin
    • Targeted - based on sensitivities but cefotaxime good choice
    • double-coverage for duration
    • bacteremia: Tx 14 d from 1st neg
    • meningitis: Tx at least 21 d –
    • **need to do repeat cultures to make sure that the antibiotics are working
  57. What are Other GNR infections
    • • can be vaginal / gut flora
    • • can be nosocomial
    • • frequently more resistant
    • • often associated with longer stay
    • • treatment based on
 identification and sensitivities – this is very important before you start antibiotics
  58. What is Listeria monocytogenes
    • • uncommon
    • • important pathogen in pregnant woman & fetus,infant, immunocompromised
  59. What are key characteristics of Listeria monocytogenes
    • Ubiquitous
    • Aerobic
    • non-spore forming
    • cold-tolerant (5-45°C) – this is very important – it likes the cold- it has a good system for turning genes on and off depending on the temp – allows them to still replicate motile
    • small Gram positive rod
  60. What does listeria look like under the mocroscope
    Small GPR
  61. What are the unique properties of listeria
    • It will put themselves into a vesicle to get inside the cell, then it busts out, it then forms a motility device to move it to the next cell
    • Allows them to cross barriers - placenta, blood-brain barrier
  62. Where is Listeria monocytogenes found?
    • association with raw meat, unpasteurized milk / cheese
    • has been associated with unpasteurized fruit juice / cider
    • can present as granulomas on infant skin / placenta
  63. What are the Strategies for treatment of Listeria monocytogenes
    • Targeted - ampicillin (best drug of choice) + gentamicin
    • They have an inherent resistance to cephalosporins
  64. Would cephalosporins be a good choice for treatment of listeria
    No – listeria has an inherent resistance to cephalosporins
  65. CASE 3-week-old ex-26 wk infantextubated, develops apnea, bradycardia,feeding intolerance, WBC 8,000; no shift, blood cultures obtained - grow GPC clusters - identified as Coagulase Negative Staphylococci (CoNS) What is your treatment?
  66. Vanc plus gent
  67. Is CoNS / S epidermidis the same thing?
    • NO
    • CoNS ≠ S epidermidis
    • used interchangeably
    • large group of similar organisms
  68. What is CoNS / S epidermidis
    • leading cause of late-onset sepsis in NICU
    • symptoms mostly indolent: As + Bs and the “dwindles” – not acting well
    • ubiquitous skin organism
    • often contaminates plastic foreign bodies (Catheters, ET tubes)
    • forms glycoprotein slime antibiotic penetration inhibited
  69. Why is CoNS / S epidermidis resistant to many antobiotics
    • forms glycoprotein slime antibiotic penetration inhibited
  70. Is CoNS / S epidermidis a pathogen or Contaminant?
    • the last organisms killed by povidone-iodine (iodine works by time- so these organism are last to die – if don’t let it dry then the positive BC may be an error)
    • interpretation of a single positive blood cx is problematic because it could just be contamination
    • multiple positives more likely real
  71. What are clues that CoNS / S epidermidis is not just a contaminant?
    • clinical status
    • WBC & Plts
  72. What are the Strategies for therapy CoNS / S epidermidis
    • ≥70% of isolates resistant to nafcillin
    • vancomycin + gentamicin
    • if clinically stable, can often wait to start vancomycin
  73. Is nafcillin a good choice for CoNS/ S epidermidis treatment
    No, ≥70% of isolates resistant to nafcillin
  74. How do you determine if infection from CoNS / S epidermidis is systemic or just in the line
    • comparison of line vs periphery if both are positive then it probably real
    • line can clear on antibiotics
    • pulling line can clear without antibiotics
    • if sick, pull line. Period.
  75. How to you treat CoNS / S epidermidis in VP shunt infections
    pull shunt. Period.
  76. Where do you often find S aureus•
    ubiquitous skin organism• lives in moist areas - axillae, groin, nares, T-zone• dried skin increases colonization – eczema kids have a bigger problem
  77. How do you treat CoNS / S epidermidis in a line infection
    • if not pulled, must culture off antibiotics to document clearance
    • duration of therapy varies
  78. What is S aureus associated with?
    • • usually nosocomial pathogen
    • • associated w/ hospital outbreaks
    • • DUMC MRSA rate 50%
  79. How does S aureus progress
    • starts as bacteremia,sticky bug, disseminates
    • Leads to lung abscess / pneumonia endocarditis osteomyelitis / septic arthritis kidney / liver / spleen abscess CNS abscess / meningitis
  80. What are the Strategies for therapy for S aureus
    • toxic infant, consider vancomycin
    • start with double coverage
    • vancomycin + gentamicin or nafcillin + gentamicin
    • Tx length depends on site
  81. What are the treatment methods for S aureus in line infection
    pull the line. Period - delay associated with dissemination
  82. What are Fungi
    • ubiquitous saprophytes
    • found in soil,
    • environment
    • some normal bowel flora
  83. You have a 26 wk preterm infant critically ill w/ GNR (presumed meningitis)
    • 3 wks cefotaxime + gentamicin good early response, then near the end of therapy
    • As + Bs, “not acting right” WBC 7,000; no shift Plt 35,000 *****What do you think
    • Clues: platelets abnormal, long term antibiotics
    • Fungus
  84. When does the isk of fungal infection increases
with more antibacterials
  85. What is the most common fungal pathogen in NICU
    • Candida
    • C parapsilosis > C albicans
  86. How does candida cause an infection?
    • attaches to epithelia, pseudohyphae penetrate buds, can spread via blood
    • forms abscesses / mycetomas in kidney, spleen, liver, brain, bone, endocarditis
  87. What are the risk factors for Candida
    • extremely low birth weight
    • prolonged antibiotics
    • broad-spectrum antibiotics- 3rd gen cephalosporins
    • IV catheters / prolonged ETT
    • prolonged TPN / lipids – the yeast loves the high sugar content
  88. What are the clinical features of Candida—
    • pustular rash (congenital)
    • thrush / diaper dermatitis /skin-fold infections
    • systemic disease similar to bacterial sepsis
  89. What are Strategies for diagnosis of Candida
    • difficult to diagnose
    • 20-60% BCx positive
    • thrombocytopenia common
    • lesion / abscess culture helpful
    • fungal blood cultures for some
    • Sick kid plus low platelet count – think of this
  90. How do radiographs help with fungal dx
    abdominal ultrasound (kidney, liver, spleen)head ultrasound / CT / MRIplain films / bone scanMay see fungal balls
  91. What are the Strategies for work-ups for fungal infections
    • if cultures positive, you should- radiology, LP with cultures, fundoscopic exam – fungal balls, echocardiogram – fungal balls
    • If the cultures are negative you may consider these things
  92. What are the Strategies for treatment of fungal infections (Candida)
    • amphotericin B is drug of choice
    • liposomal amphotericin B with renal impairment(not renal disease)
    • fluconazole in renal disease
    • echinocandins (micafungin)
  93. What Strategies for treatment of a candida line infection
    • remove lines. Period. – unless they will die without the line
    • duration varies
  94. What is the problem with Line removal
    • Pediatric ID always says pull the line
    • Neonatology gotta keep the line
    • find a compromise position
  95. What are basic rules about pulling the line
    • Always pull. Period.
    • • Candida
    • • S aureus
    • • Multiple positives
    • Maybe can keep line. Maybe.
    • • CoNS, some GNR
  96. What is the Classic presentation of neonatal herpes?
    vesicles on the presenting part – but this isn’t always truefrequently do not see vesicles
  97. 38 wk term infant, AGA, excellent prenatal care, breech delivery, at 48 hrs, fever
    • WBC 7,000; no shift, rash noted What are the clues here
    • Rash at 48 hours and fever
    • This is herpes
  98. What are the Three primary syndromes of herpes
    • Mucocutaneous – peaks at 1 week
    • Disseminated – peaks at 2 weeks
    • neonatal encephalitis- peaks at 3 weeks
  99. When does the presentation of the classic forms of herpes decrease
    Neoantal herpes in the classic forms pluments at 4 weeks

    • What is the problem with mucocutaneous & disseminated
    • often have CNS findings
  100. What clinical test should be completed for Neonatal Herpes
    • LP (HSV culture and PCR)- very important to send the PCR
    • culture of vesicles (and DFA) – unroof the vesicle and get the cells from the base – this is where the virus is
    • surface culture - (eye, ear, mouth, axilla, anus)
    • LFTs – almost always associated with hepatitis
    • cervical culture of mother – almost all primary infections are cervicitis
  101. What used to be the dx test to confirm Neonatal Herpes
    • Once upon a time diagnostic test of choice for encephalitis wasbrain biopsy! And Growth usually within 5 days
    • But PCR is now in house at DUMC BUT sensitivity not 100%
  102. What is the incidence of Neonatal Herpes
    • Est. 1 in 3000 to 1 in 20,000 births
    • NC 2001 → 118,185 births
    • 6 to 40 cases across entire state
  103. What are the Strategies for treatment of neonatal herpes
    • acyclovir 20 mg/kg iv q8h x 21d
    • we follow these kids in ID clinic keep them on ACV for 1-2 years
    • Studies show that there is a decreased chance of herpes encephalitis with prolonged treatment
  104. What is Herpes Encephalitis
    • Very severe disease
    • mortality estimates 25-75% (even with therapy)
    • patients are sick! - not better after 1-2 days
    • Intense inflammation
    • Prefers the temporal lobes
    • usually findings on MRI / CT
  105. WHAT IS a fever without source (FWS)
    • fever of recent onset
    • no adequate explanation based and on history and physical exam
    • fever without source (FWS) ≡ fever without localizing signs
  106. What is a fever of unknown origin (FUO) in pediatrics
    • fever of >7 days duration
    • no diagnosis after initial work-up
  107. What are the characteristics of fever without source (FWS)
    fever of recent onset (<1 week)no adequate explanation based on history and physical exam(should be careful H+P)5-10% (22%) of children with fever lack localizing signspeak incidence in 2nd year of lifeestimated a practicing pediatrician sees this once every 4-5 days
  108. Compare FWS andFUO
    • Differential diagnoses are different
    • FWS needs more immediate evaluation
    • FUO – Can take a more thoughtful approach
  109. What are the symptoms of FWS
    • some are presenting with a new chronic illness
    • some are gravely ill
    • most are not
    • the evaluation is a bit like panning for gold…you must always pay attention!
  110. How is FUO different than FWS?
    • you are out of the acute stage
    • you have already done a work-up
  111. What are the two approaches to further work-up of FUO
    • test for everything at once
    • test in a stepwise fashion – this is preferred
  112. What is the FUO—Epidemiology
    • Different as compared to adults ( inadults FUO is cancer until proven otherwise)
    • most have uncommon presentations of common illnesses
    • case series—only 5 of 418 had rare disorder
    • most series state that 10-20% of cases never get a diagnosis (50%) – important to tell the family this
    • Tell them that - unlike adults, most children get better
  113. Who works together to dx FUO
    • in cases of FUO, three services are routinely consulted
    • Infectious Diseases, Rheumatology, Hematology/Oncology
    • In most cases the diagnoses are
    • infectious >rheumatologic >oncologic
  114. What should you remember when trying to dx FWS & FUO
    • direct your work-up with two principles in mind
    • 1. Look for things that are common (UTI)
    • 2. Look for things that will kill you (Meningitis and bacteremia)
  115. What is the rational for work up in Bacterial disease in FWS in neonates
    • Remember that the most common organisms in neonates (0-3 months) are
    • Streptococcus agalactiae
    • Escherichia coli
    • Listeria monocytogenes
  116. What is the rational for work up in Bacterial disease in FWS in infants/toddlers
    • Remember that the most common organisms in infant / toddler (3 mos to 3 yrs)
    • Haemophilus influenzae type B
    • Streptococcus pneumoniae
    • Neisseria meningitidus
  117. What is the rational for work up in Bacterial disease in FWS in Bacterial disease in children / adolescents (3-19+ yrs)
    • Streptococcus pneumoniae
    • Neisseria meningitidus
  118. What are the Current statistics of causes of FWS
    now, <1% of children with FW have bacteremia and, risk of complications lowerbadness rate <<1%
  119. Why is the a Shift of FWS in 3-36 month olds (the current statistics of FWS)
    we now have excellent vaccine coverage against Haemophilus influenzae type BStreptococcus pneumoniae
  120. What are the historical statistics of bacteremia in FWS in children
    • historically, 3-5% of children with FWS had bacteremia
    • and, 5-10% of those would develop meningitis if not treated
    • 10% would develop a localized infection
    • 30% would have persistence of bacteremia
    • overall badness rate of1.4-2.5%
  121. What should you remember when have a child < 2 months who has FWS
    remember to always work up a child less than 2 months with FWS bc they haven’t received their immunizations
  122. When would you get a CSF for FWS
    • after careful H+PIf child is <3mo,if suspicion if exposed
    • Get a CSF culture, CSF analysis
  123. Who would you get a urine culture on
    after careful H+Pfor girls <2yo, boys <6mo(to 1yo if uncircumcised)
  124. How do you work up FWS—
    • careful H+P
    • everyone gets a blood culture, CBC/D
    • Possible urine culture (all girls < 2 and all boys <6m, 1 yr if uncirc)
    • Possible CWR
  125. When would you start Empirical Tx
    • if work-up is unrevealing
    • unsure of follow up care
    • unsure of reliable information
    • no relationship with family
  126. What is the empirical antibiotic of choice for FWS
    • ceftriaxone and daily follow-up
    • orals in select cases
  127. What did Kevin Watt, Erica Waddle, and Ravi Jhaveri find r/t FWS?
    • They assessed charts of infants < 3m who had a blood cx in the ED for 9 years; Each infant had a fever of 38, and no obvious source of infection
    • They found a serious bacterial infection in 6.5% (97-01) and 17% (02-06)
    • E coli UTI was the most common cause
    • There was a high resistance to ampicillin - Gentamicin often covered these
Gent and cef are best for meningitis
  128. What is the benefits of FUO—
    • patient should have already had
    • blood culture, CBC/D
    • urine culture, U/A
    • CXR
  129. What is the next step of getting a dx in FUO
    • Need to look at the common organisms and the ones that can kill you
    • Involve Rheumatology, Hemoc, and ID
  130. What tests need to be sent for rheumatology
    • send ESR, CRP
    • consider ANA (antinuclear antibodies) if strongly suspect a rhematology disease
    • This is rare in children so these tests are enough in the beginning
  131. What tests need to be sent for Hematology/Oncology
    • repeat CBC + manual differential
    • send chemistries, including Ca and uric acid
    • call H/O, discuss BM
    • bone marrow culture is helpful to hemoc and ID
  132. What tests need to be sent for Infectious Diseases
    • serial blood cultures (endocarditis) – hallmark of endocarditis is continuous positive blood cultures
    • place PPD (tuberculosis) -
    • send viral studies (sinus, pharynx, stool, urine)
    • send complement (CH50) – rare but an easy test
    • consider imaging: bone scan (osteomyelitis), MRI (bones, joints), CT (occult abscesses)
    • consider cardiology (Kawasaki)
    • consider unusual cultures / tests Brucella, MOTT (mtcobacteria other that TB Bartonella, Francisella, HACEK,Mycoplasma, etc.
    • every child getting an FUO w/u should get HIV testing!!!
    • never forget STIs send RPR, culture for GC, and culture for Chlamydia
    • culture any site / fluid / tissue you can
  133. What are the basic functions of the complement
    • Lysis of cells, bacteria and viruses.

    • Opsonization, which promotes phagocytosis of particular antigens
    • Binding to specific complement receptors on the cells of the immune system, triggering specific cell functions, inflammation, and certain immunoregulatory molecules.
    • Immune Clearance, which removes immune complexes from immune system and deposits them in the spleen and liver.
  134. Should you send for every rare test that you can think of
    • don’t send tests for unusual genetic disorders unless the history dictates it
    • These rare test costs of lots of money
  135. What is the empical therapy for FUO
    • in general, NONE WHY
    • we know that: most children will get better, most children have common illnesses
    • and it hasn’t killed them yet!
    • giving antibiotics to a child with FUO, especially after it has been going on for a while, is like shooting a gun into a dark room
  136. When is it a FUO too much or too often?
    • My kid has a cold constantly…(probably daycare)
    • My kid has had three pneumonias this year…(worrisome, asthma?)
    • My kid has had pneumonia and meningitis and a joint infection…(ain’t right) – this isn’t normal
  137. 10 yo ♀ with recurrent fevers to 102°F daily for six weeks►also has generalized malaise►unusual rash on legs►good workup by PMD►family worried THIS was a mycoplasm infection What are the clues
    Fever, rash
  138. What should you remember about Immune Deficiency
    • These are uncommon, but you will see them never forget HIV!!!
    • and consider SCID, CGD, diGeorge, etc.
    • context is everything - daycare? playmates? family history?siblings?underlying disorders? past history?
  139. 8 mo ♂ with third episode of pneumonia
    ►growth reasonable►no FHx of recurrent illnesses►CXR with multifocal infiltrates►PMD worriedChronic granulomas disease What are the Clues
  140. CXR
  141. 5 yo ♀ with daily fevers increasing in height for four weeks
    ►some cervical lymphadenopathy►tired look►initial lab work normal►weight curve has flattenedShe had lymphoma, What are the clues
  142. Flattened weight curve
  143. What are the Goals in infection ID
    • discuss infections that can kill or maim without prompt attention
    • outline presentation,labs needed, interventions needed
  144. You are in the ED on Wednesday, near the end of your shift. You are asked to eyeball an 11 mo male with decreased feeding and urination, fever and lethargy, all with sudden onset. On exam you see a rash on with small, non-blanching, red macules with dark centers
    Your next action for this patient should beA. diagnose a viral illness and dischargeB. obtain a blood cultureC. perform a lumbar punctureD. administer ceftriaxone IM.
  145. This is menigecococcal – this is a characteristic rash – So answer is BCD
  146. A child is dx with meningitis Children in his daycare room should
    A. receive routine careB. receive vaccination against pneumococcusC. receive rifampin prophylaxisD. have lumbar punctures performed.
  147. Answers C- receive rifampin- anyone with close contact
  148. On Thursday, you see a 6yo ♀ with 3 days of fever & sore throat. Her mother reports a red, raised rash. You find HR 120, T 39. Her L leg below the knee is swollen. She is crying and inconsolable.
    Your next action for this patient should beA. LA Bicillin for strep throatB. start oral penicillinC. start IV penicillin and clindamycinD. call for a surgical consult.
  149. This is necrotizing faciitis – choose C & D, the clues are red rash and leg swollen – this is a surgical emergency
  150. On Friday, you see a 20mo ♀ with a 2 day history of fever & fussiness. Her mother notes the child is refusing to walk and is fussy with diaper changes. You see a child with T 38.5 and holding her R leg flexed and externally rotated.
    Your next action for this patient should beA. call for an orthopedic consultB. call radiology for a hip ultrasoundC. start meropenemD. diagnose toxic synovitis and discharge on NSAIDs.
  151. This is septic arthritis of the hip – choose A & B
    The clues are the flexed externally rotated hip
  152. On Sunday, you see a 5yo ♂ with 3-4 days of congestion / rhinorrhea. This morning his mother noted the acute onset of R eye swelling. On exam you see tense edema of the eyelid with proptosis, lateral gaze paralysis, conjunctival injection.
    Your next action for this patient should beA. IVIG infusionB. Call ENT / OphthoC. start 3rd generation cephalosporinD. thyroid studies.
  153. This is orbital cellulitis – the clue is proptosis choose B & C
  154. On Monday, you see a 2yo ♂ whose family are recovering from a “flu-like” illness. He had been recovering until this morning when he developed a distressed look and high fever. On exam he has inspiratory stridor, retractions, and a normal O2 saturation.
    Your next action for this patient should beA. Immediate intubationB. CXRC. Chest CTD. administer nebulized albuterol.
  155. Choose B based on respiratory symptoms
  156. On Monday, you see a 2yo ♂ whose family are recovering from a “flu-like” illness. He had been recovering until this morning when he developed a distressed look and high fever. On exam he has inspiratory stridor, retractions, and a normal O2 saturation. The CXR is shows no foreign body, little parenchymal disease.
    A. Immediate intubationB. start vancomycinC. Chest CTD. administer nebulized albuterol.
  157. This is bacterial trachitis – flu like symtoms is a clue b/c this is a side effect of the flu; choose A & B
  158. In 1985, you see a 3yo ♀ who had mild fever and cough followed by the sudden onset of respiratory distress and irritability. She is hoarse, sitting in mother’s lap, leaning forward, drooling, and has retractions.
    Your next action for this patient should beA. Immediate intubation by the internB. CXRC. immediate intubation by an anesthesiologistD. start an IV for antibiotics.
  159. This is epiglottitis- the clue is the drooling
Card Set
Lecture # 3 management