This document provides information about pertussis (whooping cough). It discusses the causative bacteria, Bordetella pertussis, and describes the typical three stages of the disease - catarrhal, paroxysmal, and convalescent. It notes the disease is highly contagious and a major killer of infants. Complications in infants can include pneumonia, seizures, and death. Diagnosis is usually clinical based on symptoms, and confirmed with lab tests. Antibiotics are the treatment of choice and aim to shorten the illness and prevent spread. Immunization provides protection but does not prevent all cases of pertussis.

4. WELCOME
ALL

5. E. P. I. TARGET
DISEASES
(DPT POLIO HIB MR PCV)

6. Why immunisation?
 Measles, polio, DPT, Hib, S pneumoniae, rotavirus, TB, etc.
are killers. HBV and rubella are not U-5 killer
 EPI led to 17,000 fewer U-5 death/d in 2012 than in 1990
 Still: 18,000 U-5 death/d or 6.6 million/y (50% in Sub
Saharan Africa; 30% in S Asia) in 2012
 To stop these deaths. S Asia has strong progress: >50%
reduction since 1990; but in SS Africa it is 45%

7. World Distribn. of Deaths: U-5y: 2012
6.6million death: >50% preventable/Rx with simple, affordable
interventions. 45% deaths linked to Mn.

8. World Disease Burden of Vax.-Preventable U-5 MR
Pertussis
13%
Hib*
13%
Measles
8%
Tetanus
4%
Pneumococca
l diseases*
32%
Rotavirus*
30%
• 17% of global total death
• 1.5million deaths in children
preventable through vaccination
*WHO estimates

9. EPI target Ds in Bangladesh (10)
• TB
• Diphtheria, Pertussis, Tetanus (DPT)
• Poliomyelitis
• HBV
• HIB
• Measles, Rubella (MR)
• S pneumoniae

10. Other vax. available in Bangladesh
• HPV
• HAV
• Varicella-zoster
• Influenza
• Typhoid
• Cholera
• Rota virus
• Yellow fever
• Meningococcus

11. Vaccines in pipeline
• Dengue
• Malaria
• HEV
• Ebola
• HIV
• Improved BCG
• Zica, etc.

12. Intracranial hge
Severe Cough

13. Very tenacious sticky sputum
Broken BV in eyes and face
What is the Dx?

14. • ‘Whooping’ Cough/100
days’ cough
• Highly contagious
• ‘Killer’ in small infants
PERTUSSIS
(persistent intense cough)

15. Pertussis: an ARI c/by B. pertussis, and uncommonly
by a few other MOs, characterized by 3 stages:
catarrhal, paroxysmal, convalescence
Aetiology
• B. pertussis (Classical)
• Others:
– B. parapertussis, B. bronchiseptica
– Adenovirus 1, 2, 3, 5
– M pneumoniae, C trachomatis, C pneumoniae

16. B pertussis
fastidious, Gram-ve, pleomorphic rod
• No growth on ordinary media
(lab to be informed beforehand!)
• Does not survive in environment (P2P spread)

18. B pertussis aka Bordet-Gengou bacillus

19. Epidemiology
70% cases in <1y age. Endemic every 3-5y
• Humans only. P2P: contact, droplets
• Mild/atypical in older  source for children
• Highly contagious in stage- 1 (~100%)
• Immunity is incomplete
• I P: 7-10d. PI varies (-2 +6w of cough):
– Infant: 6w after onset; adult: 2w …
• Severity: immune status, previous pertussis, ABT
IP: incubation period. PI: period of infectivity

20. Pathogenesis
• Basically bronchitis
• Locally invasive; toxin mediated:
– severe inflam.: necrosis, infiltration: debris  sticky
scanty sputum  severe cough
• May cause Br. Pn., bronchiectasis, collapse
• Brain cortical atrophy from IC hge and anoxia
Pertussis toxins: pertactin, lymphocytotic factor, filamentous
hemagglutinin, fimbrial proteins agglutinogens)

21. Bronchiolar plugging and alveolar dilatation in pertussis in an infant

22. Clinical Stages
Catarrhal stage: ~1-2 w. Mimics coryza: LGF, cough, red
watering eyes. Dx usually missed. ABT can abort
Paroxysmal stage: 2-4w/longer
• Forceful cough of  severity; 5-10 bouts /expn.  whoop
and vomiting
• Flushed/cyanosed face, bulging bloody watering eyes
• Protruded tongue, dribbling
• Distended neck veins
• Fever is absent or minimal

23. CF in Infants (paroxysmal stage)
• Paroxysmal cough 100%
• Post-tussive emesis 80%
• Prolonged dyspnoea (neonate) 80%
• Whoop 70%
• Convulsion 25%
• Mortality <4mo age 40%
Atypical presentation
• <6 mo age: apnea, no whoop. Severest in preterm
• Older children and adults: milder-shorter, prolonged
cough ± paroxysms. No whoop in adults

24. S/he is apathetic, loses wt. rapidly
Triggers of paroxysms
– eating, drinking, sneezing, yawing, wind
– laughing, playing, smoke
– suggestion
Physical examination
• Generally uninformative; May be no signs
• Diffuse rales, and ronchi may be noted
• Petechiae may be seen

26. Convalescence stage
• Signs of improvement over weeks-months
• RT can stay irritated for months-years: Paroxysms
may occur with each RTI during this period
Complications
• Respiratory:
• CNS:
• Alimentary system:
• Others:

27. Complications: Respiratory Sys.
• Pneumonia: primary, secondary
• Reactivation of TB
• Bronchiectasis
• Collapse
• Emphysema
• Pneumothorax
• AOM

28. 4w-old: pertussis pn. with air trapping and progressive
collapse. Segmental/lobar atelectasis are not uncommon

29. 4-w neonate died of pertussis pn. (2y S aureus) with air trap. He had SD hge.

30. Pertussis pn in a 7-y.
Obliteration of
cardiac borders is
common

31. Complications: CNS
• Hemorrhage, SD hematoma, brain atrophy
• Seizures (Pertussis encephalopathy: hge+atrophy+seizures)
• SIADH
Complications: Alimentary Sys.
• Frenulum ulceration
• Rectal prolapse, umbilical/inguinal hernia
• Intussusception, melena
• Malnutrition

32. SD hge in pertussis. Previously, 36k died/y in US, most in

36. Melena

37. Complications: Others
• Over exhaustion
• Dehydration
• Tetany
• Hypoglycemia
• Epistaxis, sub-conj. bleeds, purpura
• Diaphragmatic rupture

38. Rupture of diaphragm: A. mimics loculated pneumothorax. B. NGT
shows herniated stomach

39. Prolonged QT

40. Dx: mainly clinical
• High index of suspicion in stage 1: immunity, contact,
neighborhood
• Classical paroxysm is v. suggestive
• Cough >2w with post-tussive emesis is an important clue
Lab.
• CS:
• CBC: absolute lymphocytosis (20-50K) is typical (not in B
parapertussis and immunized). It parallels the severity
• CXR: perihilar infiltrates, Br.Pn., emphysema, etc.
• PCR for rapid Dx

41. CS: should be done in all cases. Takes 10-14d
Negative: after 4thw of illness, immunized, ABT
• NP secretions (aspiration/Dacron/Ca alginate swab)
• Media: Regan-Lowe (transport) and B.G.
• Inform lab* beforehand
DD:
• Other c/of bronchitis
• Foreign body
• Toxic damage to RT by gases
• Lipoid/chemical pneumonia
*Inform lab as these media are not routinely available

42. • Erythromycin x14d is DoC
– Aborts paroxysm in Stage 1
– Shortens duration, reduces spread, prevents relapse
– In Stage 2 ABT has no effect
• Azithromycin and clarithromycin are alternative
• Resistance is rare
Penicillins, cephalosporins ineffective
TREATMENT
(Azithro.10–12mg/kg/d, p.o., x5d; max. 600mg/d
Clarithro. 15–20 mg/kg/d, p.o., in 2 dd; max. 1 g/d x7d)

43. Nursing is v. important
– Avoid triggers, hydration, nutrition
– suction clearance, O2
– Betamethasone, albuterol may  severity
No cough suppressants
Admission: Infants <6 mo
– to manage apnea, hypoxia
– feeding difficulties, dehydration
– other complications
– ICU

44. IMMUNISATION
• 5 doses: 4th at 15-18mo; 5th (DT) at school entry
• Immunity is not absolute/permanent
• It may not prevent infection. Mild illness may not be
recognized and can spread
Prognosis
• Mortality ~40 % in infants <5mo
Death:
• Anoxia, rapid dehydration
• Malnutrition, hypoglycemia
• Over exhaustion, encephalopathy

45. Points to Ponder
• Pertussis is fatal in small babies
• Severe damage to RT cilia  RT is reactive for 1y
• Causes innumerable complications
• Immunity is neither complete/permanent
• Cl. Dx is essential
• No growth on ordinary media
• Rx can abort the disease in coryzal stage
• Can reactivate TB

46. This unvaccinated child has severe
cough and vomiting. Answer the
following:
1.What is the diagnosis?
2. What is the c/of such bleeding in
this child?
3. What are other complications?
OSPE

47. MCQ
Classical pertussis
• causes neutrophilic leukocytosis
• causes leukemoid reaction
• is complicated by apnea in neonates
• immunization confers excellent protection
• causes death by septicemia
• the bacteria grows in common media
• makes blood culture positive

48. ‘Bull neck’: LAP and
edema

49. What is the Dx?

50. DIPHTHERIA
a serious d. c/by C. diphtheriae (only locally invasive):
– fatal local obstructing and
– fatal systemic toxicity
• Spreads P2P. Fate depends on:
– strain (toxic/not), circulation, immunity
• Man only. Both non-/toxigenic cause obstruction
• Only toxigenics cause toxemia
• 50% mortality
• Now rare

51. Common site: URT
• Also skin, eye, ear, genitalia, wound
• Exotoxin: degeneration/necrosis of heart, nerves (paralysis)
kidneys, adrenals. Interval: myocarditis 2w. neuritis 3-7w
• DPT vax.: requires booster/10y
Characteristic pseudomembrane
• Necrosed tissue+exudate+bacteria
• Tough-fibrinous adherent
• Gray to black (~bleed)
• Attempt to remove it causes bleeding

52. Diphtheritic
tracheobronchial
membranes

53. Conjunctival D. Conj. membrane: strep., pneumo., D; chemical,
ligneous conj., adenovirus or HSV

54. Nasal diphtheria

55. Diphtheria in wound

56. Tonsilopharyngeal D
Insidious: LGF, disproportionately toxic, malaise, sore throat,
irritable, dysphagia, bull neck, rapid pulse, ± respiratory
and CV collapse. Very distinctive membrane extends from
pharynx to palate. Palatal palsy: nasal voice +/-
regurgitation. May die in 7–10d
Laryngeal D
Usually extension from pharynx
• Croup, severe chest retraction, hoarseness
• Restless, but soon becomes weak, drowsy
• A grave situation! Urgent tracheostomy/intubation

57. Diagnosis
Clinical Dx is urgent!
• Extended membrane, disproportionately toxic; noisy
breaths, stridor, hoarseness, bull neck, palatal palsy
• Serosanguinous nasal discharge
• Confirmed by CS, FAB staining
• Toxigenicity test by using guinea pigs
IMPORTANT!
• Diphtheria like MO on smear does not establish Dx. CS
essential. But Cl. Dx is enough to start Rx
• Mortality is ~5%. Untreated ~50%

58. White Patch Over Tonsils
 Follicular tonsillitis
 D i p h t h e r i a
 Inf. Mono.
 Agranucytosis
 Leukemias
 Candidiasis
 Herpangina
• Vincent’s angina
• Post tonsillectomy
membrane
• Ac. Toxoplasmosis
• Ac. CMV

59. Herpangina

60. Oral thrush

61. Follicular tonsillitis

62. Inf. mononucleosis

63. Treatment
A. Neutralize toxin
• Equine ADS for blood toxins (not fixed) after
desensitization if sensitive (5-20%)
Dose varies: site, circulation, toxicity, duration, LAP
• Pharyngeal/laryngeal ≤48hr  20-40 th i.u.
• Nasopharyngeal disease  40-60 ,,
• Extensive for 3d/bull neck  80-120 ,,
B. ABT : Penicillin/erythromycin DoC. For 14d.
C. Supportive: life support
ADS: antidiphtheric serum. ABT: antibiotic therapy

64. Complications
Obstruction:
• Hypoxia, CV collapse
• Bull neck, dysphagia
• Pn., hemorrhagic pn.
Toxemia:
Neuritis: paralysis of palate,
pharynx, eye, diaphragm,
ciliary B, GBS
Myocarditis
Gastritis
Hepatitis
Nephritis, ATN

65. MCQ
In diphtheria:
• most strains are toxigenic
• natural infx. does not exclude vaccination
• greatest obstruction occurs with pharyngeal D
• antibiotic alone is curative
• positive Albert Stain is diagnostic
• cardiac failure occurs due to toxic myocarditis
• the pseudomembrane is easily separable

66. WelcomeAll
WelcomeAll

72. POLIOMYELITIS
• Enterovirus: damage AH cells: partial/full paralysis
• Spreads: P2P, mucus/phlegm, feces
• Enters gut and URT, multiplies in throat and gut, spread to
nerve by blood and lymph
• IP: 5-35d. 3 patterns: subclinical (commonest)
nonparalytic, paralytic (1%)
• Massive vax.: practically eradicated it from most countries
except a few Afro-Asian countries
AH: anterior horn

73. CF
• Fever, myalgia, HA, abnormal reflexes, back stiffness, stiff
neck, ANS features
• Tests: cultures from throat, stools, or CSF
Rx
• Only supportive:
– moist heat for muscle pain and spasms
– Analgesic (no narcotics)
– Physiotherapy, orthopedic appliances and surgery
• If severe: lifesaving measures

74. Tripod sign

75. Complications
• Paralysis, aspiration pn., pulmonary edema
• Myocarditis, shock
• Paralytic ileus, disability, deformity, urine retention, UTI
Prognosis
• Depends on the clinical type and area affected
• Most cases recover.
• CNS involvement is a medical emergency
• Disability is more common than death
Prevention: OPV (live) and IPV (inactive). No OPV in HIC
• OPV: herd immunity. Pulse dosing in LICs
HIC: high income countries. LIC:

77. MCQ
• Both OPV and IPV are live vax
• OPV is used globally
• Both polio vax. gives herd immunity
• OPV pulse dosing is used in LICs only
• Most polio cases are subclinical
• Polio paralysis is usually symmetrical
• Bangladesh is polio free

80. What is the Dx?

81. ‘The Severe’
Measles
(rubeola)
David Morley

82. Measles is a killer and
blinding disease
specially for
malnourished children

83. Measles is a viral ID of man. Spreads P2P
• Main sign: an itchy MPR (exanthem) and tiny white spots in
mouth (enanthem). 3 stages:
catarrhal, eruptive, convalescence
• F, cough, rhinitis, conjunctivitis. Rash on 4th day of F
• Severely ill. Serious complications
• Vax. prevents it
• IP: 7-18d. But SSPE: ~10.8y; not contagious
• PI:- -5 +5 d of rash
MPR: maculopapular rash

84. Pathology:
• MPR: starts at hair line, behind ears; eyes, RT and GIT
Spreads downwards. Stays 7–10d: post measles staining
• Rash reaches feet: F goes!
• Rash may bleed (black measles)
• Mouth: Koplik spots; devastating ulcers
• Severe depletion of VA
• RT: Pn., bronchiolitis; bronchitis, bronchiectasis, AOM
• CNS: Encephalitis, SSPE
• GIT: D, malabsorption

85. Pathology …
Immune system
• Immunoparesis (T&B cell)
• Diarrhea
Appendix
• Lymphoid hyperplasia
• Pathognomic Warthin-Finkeldey Giant cell
• Appendicectomy not needed
Eyes: VADX, Keratoconjunctivitis, Keratomalacia
Nutrition: VADX, Enteritis

86. Post measles staining

87. Noma/
cancrum
oris

88. SEQUELAE CAN BE RESTORED with
APPROPIATE TECHNOLOGY

90. DIAGNOSIS
• Mainly clinical. Giant cells in nasal smear
• Culture of virus (urine, blood, nasopharynx)
• Sp. IgM
Rx: No sp. Rx. Only supportive:
Most important: Vitamin A
– 200,000 i.u. day1, day 4 and day 8. It  MM
• FEB, feeding, oral hygiene
• Rx of complications. ABT only for 2y infx.
• Ig may benefit in severe Mn

91. • VADX, blindness
• AOM
• Laryngotracheitis
• Bronchitis
• Bronchiectasis
• Bronchiolitis
• Giant Cell Pn.
• PM enteropathy
• Mouth ulcers
• Myocarditis
• Encephalitis
• SSPE (1/1000)
Complications: by virus itself

92. Eye damage (by virus and VADX)
– Conjunctivitis, keratitis, keratomalacia. Was the
commonest nutritional blindness
Secondary infx
• Unmasking of TB
• Bronchitis, bronchiolitis, bronchiectasis
• ALTB (croup), bacterial pneumonia
• AOM, diarrhea
Pneumoniain measles: viral, giant cell (Hecht),
bacterial, tuberculous

93. Complications: immunoparesis
• Unmasking of TB, depressed CMI (Pseudo-ve MT)
• Low response to vaccines
• Diarrhea, malabsorption, 2y infx. (v. common)
• If fever recurs suspect 2y infx.
Causes of death
• Fulminant course, pn., diarrhea, severe Mn., VADX
• Neurologic complications
Any non-accidental death within 1 mo of measles is
measles related death

94. Subac. Sclerosing Panencephalitis (SSPE)
• A rare, chr., progressive encephalitis in children and young
adults (?mutation of virus)
• There is restricted expression of envelope proteins: no
infectious particles like the M protein produced: no
immune response. No spread!
Progression
• Stage 1: irritable, altered personality, dementia, MR
• .. 2: fit, ataxia, more MR, speech problems, dysphagia
• .. 3: steady decline in body function, blindness. Pt. is
likely to be mute and/or comatose
No cure. Inosine pranobex, ribavirin, IF alpha/beta
Aka Dawson Disease, Dawson E or measles E

95. MRI at presentation (A, B)
and 3 mo later (C, D). A
and C are T1; B and D T2.
A B shows focal
abnormality in the white
matter of L frontal lobe,
consisting of a
hypointense signal on the
T1 and a hyperintense
signal on T2. In the FU
scan, this is less obvious
, but advanced diffuse
cortical atrophy is seen,
(ventriculomegaly ,
markedly enlarged sulci
(arrowheads in C)

98. MCQ
• Measles can deplete VA totally
• MT can be negative after measles
• Vaccines should not be deferred after measles
• Noma is a recognized complication of measles
• 2 doses of measles vaccine are required
• It is the commonest c/of nutritional blindness
• SSPE is a slow virus infection

99. Severe muscular
spasms with
trismus from
contamination of
umbilical stump

100. Risus
sardonicus

101. Opisthotonos: back is bent backward with forward bowing
What is Dx?

102. TETANUS
• Fatal! Neurotoxin from vegetative form anerobic spore
forming G+ve C. tetani. IP: 3d–3w-months (~14d)
• Ubiquitous; soil, dust, dung; grows in deep wound: dead
tissues; no tissue damage nor inflam.
•  contamination  shorter IP  severer disease
• Painful generalized myospasm. Death is usually from
suffocation. Subsides over weeks if recovers
• Brain not affected. Mentally clear
• NT: 5-14 d (8 days disease)
NT: neonatal tetanus

103. LT secondary to parent’s attempt to drain a boil with a contaminated thorn

104. TREATMENT
Medical emergency. Must hospitalize
• Supportive: control spasm, FEB, nutrition
• Control of ANS instability if any:
– ventilator SOS:
• Wound management:
Control of spasms is most important
• Anticonvulsant: Best survival is achieved by flaccid
paralysis and mechanical ventilation
• TIG 3000-6000iu im for all. No local infiltration (cannot
neutralize fixed toxin)
• IVIG can be considered

105. Anticonvulsants
• Diazepam, Midazolam, Chlorpromazine
• Baclofen and other muscle relaxants
ANS instabilities
• Temp. instability, Cardiac arrhythmias
• Unstable BP, Excessive secretions
Temperature instability
HGF in tetanus: Spasms, Sympathetic over-stimulation,
Infection, Dehydration

106. TETANUS PRONE WOUND
• Containing dirt, feces, soil, or saliva
• Has necrotic or gangrenous tissue
Aggressive care is essential: part of prevention
Aim: eradication of the MO
• Remove dead tissue and FB
• No extensive débridement for punctures
• No wide excision of cord stump
WOUND MANAGEMENT

107. Past Doses Clean, Minor Tetanus prone
Td TIG Td TIG
<3 or unknown Y2 N Y Y3
34 No5 No No6 No
2 Children <7 y, DTaP. DT if pertussis is CI. 7 y: Td
3 Equine ATS used when TIG is NA
4 If only 3 doses a 4th is given
5 Yes, if >10 y since last dose
6 Yes, if >5 y since last dose
TT in Wound Management

108. ABT
• Metronidazole is the DoC. Pen. G is alternative
• Duration: 10-14d
TIG
• Give TIG in HIV, regardless of h/of TT
• Child 7y: use Td; <7y: DTaP/DTP/DT
• Separate sites for TT and TIG
• TIG does not preclude immunization
• TIG does not impair immunogenesis
PO/IV metronidazole (30 mg/kg/d/6-h. Pen. G (100 000 U/kg/d/4-6h; max. 12 million U/day) IM

109. COMPLICATIONS
• Aspiration pn.
• Dysphagia
• Dyspnea, apnea
• Secondary infx.
• IC Hge
• Fractures, soft tissue
injury
• Hyperpyrexia
• Hypoglycemia
• Hyperglycemia
CAUSES OF DEATH
•Over-exhaustion, Aspiration pn., Hypoglycemia
• IC Hge, Dehydration

110. Immunization
• TT is toxoid; better as Td. Very stable: months at room
temp. Very effective. May be given with other vax.
• Given as DTP/DTaP, DT, Td ( diphtheria content)
– TT for pregnant and women of CBA
• Children 6w-7 y: x5 TT and diphtheria toxoid
• 5th before school entry. Then each 10y
• For wilderness expeditions: 1 booster if not taken in 5y
HIB conjugate vx. containing TT (PRP-T) are not substitutes for TT vx

111. POINTS TO PONDER
• Non-communicable
• Completely preventable
• Non-inflammatory toxic response
• Disease does not confer immunity
• Spasm control is the mainstay of Rx

112. MCQ
Tetanus
• is commonly focal
• is a communicable disease
• Dx mainly clinically
• The vaccine is highly effective
• is more common in elderly people
• Pt. stays mentally clear
• can cause hyperpyrexia

113. Hemophilus influenzae type b (Hib/HIB)
• Severe sepsis, particularly among infants
• During late 19C was believed to cause flu
• Aerobic Gram-negative, polysaccharide capsule
• 6 different serotypes (a - f)
• 95% of invasive disease is c/by type b (Hib)
• Colonizes nasopharynx: affects local and distant sites
• Antecedent URTI may be a contributing factor

114. Cellulitis
6%
Arthritis
8% Bacteremia
2%
Meningitis
50%
Epiglottitis
17%
Pneumonia
15%
Osteomyelitis
2%
HIB: Clinical Features*
*prevaccination era

115. Hib Meningitis
• 50-65% of meningitis in the prevaccine era
• Deafness or neurologic sequelae in 15-30%
• CFR: 2-5% despite of effective ABT
• Hospitalization required
• Rx: 3G cephalosporin, or chloramphenicol plus ampicillin.
Ampicillin-resistance is now common
• Reservoir: human; asymptomatic carriers. Droplets
• Incidence has fallen 99% since prevaccine era
CFR: case-fatality rate

116. 0
5
10
15
20
25
1990 1992 1994 1996 1998 2000 2002 2004
Incidence
Incidence*of Invasive Hib Disease, 1990-2004
*Rate per 100,000 children <5 years of age
Year

117. 0
20
40
60
80
100
120
140
160
180
200
0-1 12-13 24-25 36-37 48-49 60
Age group (mos)
IncidenceHaemophilus influenzae type b, 1986
Incidence* by Age Group
*Rate per 100,000 population, prevaccine era

118. Polysaccharide Conjugate Vax.
• Enhanced Ab. production. Given with other vax.
• 3 primary from 6w; 2 boosters
• Generally not for >59mo of age
• Consider for high-risk: asplenia, immunodeficiency, HIV,
HSCT: 1 pediatric dose

119. Pneumococcal Disease
• Gram-positive S. pneumoniae (Pasteur in 1881)
• Reservoir: human; spread: droplets
• 90 serotypes. Vaccine in 1977
• Polysaccharide capsule important virulence factor
• Type-specific Ab is protective
Clinical Syn.: Pneumonia, Bacteremia, Meningitis
• 2005: 1.6 million died; (0.7-1million U-5), mostly in LICs
• In HICs, <2y and the elderly carry the major burden of IPD
• Immunodeficiencies greatly increase the risk. Increasing
ABR underlines the urgent need for vax.

120. Pneumococcal Disease in Children
• Sepsis without known site is the commonest presentation
• Leading c/of bacterial meningitis among U-5; highest
among infants. Common c/of AOM (5million)
Pneumonia: Ac. onset: F, Shaking chills, pleuritic chest p.,
productive cough, SoB, tachypnea, hypoxia. 175,000
admn. in USA/y. 36% of adult CAP and 50% of HAP.
Common bacterial complication of flu and measles
CAP: community-acquired pn. HAP: hospital-acquired pn.

121. Pn. Bacteremia
• >50,000/y in the USA
• More among elderly and very young
• CFR: ~20%; 60% among the elderly
Pn. Meningitis
• 3,000 - 6,000/y in the USA
• CFR: ~30%; 80% in the elderly
• Neurologic sequelae common
AOM: acute otitis media

122. Children at more Risk of IPD
• Functional/anatomic asplenia, especially SCD
• Overcrowding, poor clothing, malnutrition
• HIV
• Cochlear implant
• Out-of-home group child care
• USA: Afro-American, Alaskan Native, American Indian in
Alaska, Arizona, or N Mexico
• Navaho children in Colorado and Utah
Outbreaks not common: generally occur in crowding
IPD often has underlying illness and may have high fatality
SCD: sickle cell disease

123. Invasive Pn. D. (IPD): Incidence by Age
0
50
100
150
200
250
<1 1 2 3 4 5-17 18-34 35-49 50-64 65+
Age Group (Yrs)
Rate*
*Rate per 100,000 population
Source: Active Bacterial Core surveillance/EIP Network

124. Pneumococcal Vax.
• Growing ABR underlines urgent need for vax.
• Vax. is most effective for Px
– 3 pneumococcal conjugate vaccines (PCV) covering 7, 10
and 13 serotypes (PCV7, 10, 13)
– 1 unconjugated polysaccharide vax. covering 23 strains
(PPV23)
• WHO recommends PCV
ABR: antibiotic resistance

125. Rubella
• Acute, contagious viral infection that occurs most
often in children and young adults
• Rubella infection in pregnant women may cause fetal
death or congenital defects known as congenital
rubella syndrome (CRS)
• Estimated 110,000 babies are born with CRS annually
• Single dose of vaccine > 95% long-lasting immunity
• Often combined with Measles, Mumps, and/or
Varicella vaccine

129. Next Lec.:
Childhood
Injury
(ACCIDENTS IN CHILDREN)

130. THANK YOU