covering most of EPI covered diseases in Bangladesh

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