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Pediatric Infectious disease
2015
Bandith S.
Department of Pediatric
Mahosot hospital
A 4 month-old boy with fever and
seizure
Chief complaint: Uncontrolled seizure, referred
from a provincial hospital.
Present illness:
• Previously has been healthy
• 7 days PTA had high grade fever
• Brought to District hospital and treated as a
bacterial pharyngitis (unknown ATB)without
improvement
• A day later , developed right ptosis and
generalized tonic seizure
Present illness:
• Then was referred to provincial hospital on
23/9/2015 and diagnosed Menigo-encephalitis,
treated with Ceftriaxone and diazepam.
• 2 day after admission still has fever,
generalized non pitting edema and not able to
control seizure, watery stool, no vomiting ,no
rash or petechia
• Therefore, was referred to MSH on Sep 28 2015
Past history of illness
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5th child of family
Normal delivery
No vaccination
Only breast feeding
Grandmother had PTB in 2009 with complete
treatment
• The others are healthy
Physical examination
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T 38.50c , RR 45, SpO2 99%, BW 10kg,
AVPU (on Diazepam)
generalize tonic seizure and generalize none pitting edema
No bulging fontanel, right ptosis
Abdomen: no HSM ,lower abdominal mass 10x 8 cm
Lung : clear, no adventitious sound
Heart : Normal S1,S2, no murmur
Skin: Normal, no rash, no petechia
Ext: warm, CRT<2s,no cyanosis
No BCG scar
• What is your initial diagnosis?
• What are you going to do next?
Initial management
• Control seizure with Midazolam and
phenobarbital
• Continue Ceftriaxone
• Fundus examination but not success
• Fontanel U/S not found ICP
• Laboratory investigations
Investigation
CBC
Biochemical test
WBC
28.17
Creatinine
37.551 mmol/l
Lym
33.9%
BUN
19.2mg/dl
MON
7.3%
CRP
Positive
Gran
58.8%
RBC
3.79
ESR
21
HGB
9.6 g/dl
Hct
27.15%
Microcytic
1+
MCV
72
Hypochromic
1+
MCH
35.3
Target cell
Few
RDWc
14.1%
PLT
783
Morphoogy of RBC
Reticulocyte count
0.4%
Electrolyte
K
4.39
Na
134.2
Cl
99.3
Ca
10.3
Investigation
CSF
Opened pressure
25
Color
Turbid
WBC
670
Polymorphs
88.81
Lymphocytes
11.19
Eosinophil
0
Other
0
Red cells tube 1
0
Red cells tube 3
0
CFS Albumin
55
CSF glucose
65
Blood glucose
77
CSF
Gram stain Negative
Culture
Negative
PCR
Positive for N. meningitidis
Final diagnosis
• Meningococcal meningitis with iron deficiency
Meningococcemia
• Highest rate of colonization(up to 40%) in
adolescents and young adults; colonization rare in
children < 10 years
• Respiratory route of transmission
• Peak of disease in children under 2 year of age and
smaller peak in adolescence
• Risk of disease increased by smoking ;
overcrowding; prior viral RTI;
• Serogroup distribution varies over time and with
geographical ocation: serogroup A in Africa and Asia
Clinical features
• Four presentations:
1. Bacteremia without sepsis
2. Meningococcemia without meningitis
3. Meningitis with or without meningococcemia
4. Meningo-encephalitis
• Other clinical manifestations: Myocardial
dysfunction , arthritis ,pericarditis ,pneumonia
conjunctivitis ,cranial nerve dysfunction
Diagnosis
• Microbiology diagnosis usually is made by
Gram stain of CSF and/or culture of blood or
CSF
• PCR of blood or CSF can yield higher rate of
identification(especially with receipt oa ATB
prior sampling)
Treatment
• Early and appropriate antibiotic treatment
markedly improves the outcomes.
• Ceftriaxone as empiric therapy for suspected
cases
• If the organism is proven to be penicillin
susceptible, can be switched to penicillin,
• Also reasonable to continue Ceftriaxone given
the excellent efficacy, convenient dosing, and
affordability of these agents.
Duration of therapy
• Should be 5-7 days
• Some studies suggest one dose of an
appropriate antibiotic may be sufficient
• Response to therapy usually is rapid
Chemoprophylaxis Regimens for contacts of
patients of Meningococcal disease
Antibiotic
Dose
Rifampin
10 mg/kg/dose(Max. dose 600 mg) PO
every 12 hours for 4 doses ( for
infants< 1 month of age,5mg/kg/dose)
Ceftriaxone
Single injection of 125 mg IM for
children < 15 years; 250 mg IM for
children > 15 years and adults
Ciprofloxacin
Single dose 20 mg/kg PO(max.500mg)
Azithromycin
Single dose 10 mg/kg/dose(Max. 500mg)
Case progression
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Seizure stopped
Fully conscious a day later
Stopped anticonvulsive drugs
Continued Ceftriaxone for 14 day
Discharged without sequelae
No prophylaxis needed for staffs
Vaccine prevention
• Monovalent serogroup C meningococcal
conjugate vaccine
• Quadrivalent meningococcal A,C,Y,W135
conjugate vaccine
References
• Michael A.Neisseria meningitidis.In Mendell,
Douglas, and Benett,s Principles and practice
of infectious disease 7th ed.
• Allan R Tunkel et al.IDSA practical guideline for
the management of bacterial meningitis CID
2004
• American Academiy of Pediatrics.
Meningicoccal infection,In Redbook 2012
Neonatal sepsis
Early-onset
(< 7 days
Late-onset
(> 7 -89days)
Late-onset
(3 – 6 months)
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type III(80%
meningitis),E.coli(70%)Enteric
gram negative bacilli, S.viridans,
MRCoNS(4%),S.aureus(8%),Can
dida spp.(6%),E.coli(5%) Enteric
gram negative
bacilli,(2%),GBS(2% ສ
ີ່ ວນ
MRCoNS,
S.aureus,Candida
spp.,E.coli,Enteric gram
negative bacilli GBS
3-6 ເດ
ື ອນ
Neonatal sepsis
Early-onset
(< 7 days
Late-onset
(> 7 -89days)
Late-onset
(3 – 6 months)
Clinical
manifestation
Pneumonia 35-55%,septicemia 25- Meningitis 30-40%,septicemia
Common: Septicemia
55%,hypotension 25%,meningitis 45-55%,arthritis 5-10%,skin
without source infection
5-10%
infection or lymphadenitis 1-2 % Uncommon: Septicemia
with source infection
Antibiotics
First choice: Ampicilline+
Gentamycin
Alternative:
Ampicilline +Cefotaxim
Duration of
treatment
Septicemia 10-14 days
Meningitis 14 days( E. coli, Enteric gram-negative bacilli 21
Arthritis or osteomyelitis 3-4 weeks days)
Mortality rate
Preterm 5-25%
Term 1-3%
Ampicilline +Gentamycine or
Cefotaxime
2%
Cefotaxime+ Amikacin or
Gentamycine
<5%
References
• American Academy of Pediatrics. Group B
Streptococcal infections. In: Pickering LK, Baker CJ,
Kimberlin DW, Long SS, editors. 2015 Red Book: Report
of the Committee on Infectious Diseases. 30th ed. Elk
Grove Village, IL: American Academy of Pediatrics
2015;745-50.
• Morven SE. Postnatal bacterial infections. In: Richard
JM, Avroy AF, Michele CW, editors. Fanaroff and
Martin’s Neonatal-Perinatal Medicine: Disease of the
Fetus and Infant. 10th ed. Saunders Elsevier 2015:793806.
• Pia SP and Carol JB. Group B Streptococcal infection. In:
Ralph DF, James DC, Gail JD, editors. Feigin and
Cherry’s Textbook of Pediatric Infectious Diseases, 7th
ed. Saunders Elsevier 2014:1239-58.
J Trop Pediatr. 2014 Feb;60(1):10-6. doi:
10.1093/tropej/fmt064. Epub 2013 Jul 31.
Epidemiology of bacteremia in young
hospitalized infants in Vientiane, Laos, 20002011.
Anderson M1, Luangxay K, Sisouk K, Vorlasan L,
Soumphonphakdy B, Sengmouang V,
Chansamouth V, Phommasone K, Van Dyke R,
Chong E, Dance DA, Phetsouvanh R, Newton PN.
Diphtheria outbreak in Laos
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What is diphtheria?
 Diphtheria is an acute, toxin-mediated
disease
 Toxin production occurs when a patient is
infected with a toxin-producing strain of
Corynebacterium diphtheriae (aerobic gram
+ bacillus)
 There are 4 biotypes (gravis, intermedius,
mitis, and belfanti), all of which may
produce the toxin
Total 14 case
Clinical 12
Death :1
Confirm 01
Lab. : pending
Total 01 case
Clinical 01
Lab. : negative
Total 222 cases
Clinical 188(2 deaths)
Confirm 34( 144
specimens , 4 deaths)
Total 10 cases
Clinical 08 no deaths)
Confirm 02( 10
specimens ,( 01 deaths)
Total 192 cases
Clinical 162
Confirm 21( 82
specimens,
2deaths)
 Total: 561
 Confirmed:
67 (273
specimen)
 Pending: 15
 Total death: 9
Total 122 cases
Clinical 113( no deaths)
Confirm 09( 30
specimens ,2 deaths)
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Seroprevalence of diphtheria and tetanus
antibodies according to the number of DTP vaccine
doses (data from children who provided
vaccination records).
Vaccines
listed
Children with
yellow cards N
= 66 (%)
DTP-HepB 9 (13.6)
(1)
DTP-HepB 2 (3.0)
(1+2)
DTP- HepB 55 (83.3)
(1+2+3)
Children with
antidiphtheria
antibodiesN(%)
3 (33.3)
Children with
anti-tetanus
antibodiesN(%)
3 (33.3)
2 (100)
2 (100)
46 (83.6)
51 (92.7)
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Coverage of Penta3 and MR < 1, 2007-2013
100%
90%
80%
70%
60%
Penta3
50%
MR
40%
30%
20%
10%
0%
2007
2008
2009
2010
2011
2012
2013
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Transmission
• Usually spread person-to-person via droplets
• Prolonged, close contact is usually required for
infection
– Close contacts: sleeping in the same house,
kissing/sexual contacts, health-care workers who
have given mouth-to-mouth resuscitation
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Pathogenesis
The diphtheria toxin inhibits cellular protein
synthesis and causes local tissue destruction/
pseudomembrane formation in the pharynx
The toxin is also absorbed into the blood stream
where it may cause systemic effects:
• myocarditis
• neuritis
• thrombocytopenia
• proteinuria
Patient's infected with non-toxin producing strains
may have mild-moderate pharyngitis but do not
develop a pseudomembrane or have systemic effects
Clinical Presentation
 Incubation: range 1-10 days (avg 2-5)
 Classified based on site affected
 May involve many sites (anterior nasal,
pharyngeal, tonsillar, laryngeal,
cutaneous, ocular, genital)
Complications
Most complications are secondary to the toxin
(including death)
Most frequent complications: myocarditis and
neuritis
Myocarditis: may present as cardiac arrhythmias
(either early or weeks after initial presentation)-->may
lead to heart failure. If myocarditis occurs early, it is
often fatal.
Complications
Demyelinating peripheral neuritis: usually effects the
motor nerves. Typically resolves completely.
• Paralysis of soft palate: usually during 3rd
week of illness
• Paralysis of eye muscles, limbs, and
diaphragm: may occur after the 5th week
• Secondary pneumonia/respiratory failure may
result from diaphragmatic paralysis
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Death
• Fatality rate: 5-10%
• Higher fatal rates among children under 5 yrs
and adults greater than 40 yrs old
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Diagnosis
 Clinical manifestations
 Swab and culture pharyngeal areas.
 Toxin detection
Differential diagnosis
• Infectious mononucleosis
• Group A streptococcal tonsillopharyngitis
• Epiglottitis
• Viral pharyngitis
• Vincent’s angina
• Oral candidiasis
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Treatment
• Should begin immediately based on clinical
presentation
– Antitoxin
– Antibiotics
– Supportive care
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Antibiotics
• Three major benefits:
– Kills the organism
– Prevents further toxin from being formed,
slows the spread of local infection,
– Reduces transmission.
• The disease is usually not contagious after 48
hours of antibiotics. Two consecutive
negative cultures should be obtained after
completion of therapy.
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Antibiotics
• Erythromycin (500 mg four times daily for 14
days) or
• Roxithromycine 150 mg every 12 hours for
adult and 2-2.5 mg /kg divided every 12
hours for 14 days
Anti- toxin
• Patients should be first tested for sensitivity
(the anti-toxin is made from horse serum and
may cause severe anaphylaxis).
• The anti-toxin will neutralize unbound toxin
and prevent disease progression.
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Anti- toxin
• The dose of antitoxin depends upon the site
and severity of infection:
• Pharyngeal/laryngeal disease:20,000-400.000
units
• Nasopharyngeal disease: 400,000-600,000
units
• > 3 days of illness or bull neck:80,000-120,000
units
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Prevention
For close contacts (household contacts):
• Diphtheria booster
• 7-10 days of antibiotics (erythromycin or
penicillin)
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