WELCOME
ALL
E. P. I. TARGET
DISEASES
(DPT POLIO HIB MR PCV: 8)
Introduction
IMMUNIZATION is a process of making a person immune to
an ID, typically by a vaccine which stimulates the
immune system to protect against that ID
• It is a proven tool for controlling & eliminating (e.g. Small
Pox) life-threatening ID. It can avert 2-3 mln. deaths/y
• It is one of the most cost-effective investments, & can be
made available to even hard-to-reach target groups; &
does not require any major lifestyle change
Why immunisation?
To stop preventable ID
 Measles, polio-, DPT, Hib, S. pneumoniae, rotavirus, TB,
etc. are killers. HBV & rubella are not U-5 killer
• 2015: 16k U-5 death/d (50% in SS Africa; 30% in S. Asia).
>50% are preventable/treatable by simple, measures
Children in SS Africa are >x14 more likely to die
than those in HICs
 S. Asia has done strong progress: >50% reduction since ‘90
Leading c/of U-5 death: preterm, pn., BA, D & malaria. 45%
of all child deaths are linked to malnutrition
SS: sub Saharan. HICs: high income countries.BA: birth asphyxia. D: diarrhoea. Mn: malnutrition
World Distribn. of Deaths: U-5y: 2012
6.6million death: >50% preventable/Rx with simple, affordable
interventions
World Burden of Vax.-Preventable U-5 death
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
EPI target Ds in Bangladesh (10)
• TB
• Diphtheria, Pertussis, Tetanus (DPT)
• Poliomyelitis: OPV, IPV
• HBV
• HIB
• Measles, Rubella (MR)
• S pneumoniae
Other vax. available in Bangladesh
• HPV
• HAV
• Varicella-zoster
• Influenza
• Typhoid
• Cholera
• Rota virus
• Yellow fever
• Meningococcus
• Rabies
Not Available in BD
• Dengue
• Hepatitis E
• Japanese encephalitis
• Malaria
• Tick-borne encephalitis
Vaccines in pipeline
• Malaria
• HEV
• Ebola (effective vax. in pipeline)
• HIV
• Improved BCG, pertussis
• Zica, etc.
• Campylobacter jejuni
• Chagas Disease
• Chikungunya
• Enterotoxigenic E coli
• Enterovirus 71 (EV71)
• Group B Streptococcus
• Herpes Simplex Virus
• Human Hookworm D
• Leishmaniasis
• Nipah Virus
• Nontyphoidal Salmonella D
• Norovirus
• Paratyphoid
• Respiratory Syncytial Virus
• Schistosomiasis D
• Shigella
• S aureus
• S pyrogenes
• Improved TB
• Universal Influenza Vaccine
Intracranial hge
Severe Cough
Post-tussive emesis
Very tenacious sticky sputum
Broken BV in eyes & face
What is the Dx?
‘Whooping’ Cough/100
days’ cough
• Highly contagious
• ‘Killer’ in small infants
PERTUSSIS
(persistent intense cough)
Pertussis: an ARI 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 & - pneumoniae
Epidemiology
Fastidious, Gram-ve, pleomorphic rod. No growth on ordinary
media (lab to be informed beforehand !)
• Does not survive in environment (P2P spread)
• Only human reservoir
70% cases in <1y age. Endemic every 3-5y
• Mild/atypical in adults  source for children
• Highly contagious in stage 1 (~100%)
• Immunity is i n c o m p l e t e
• I P: 7-10d. PI varies (-2 +6w of cough)
IP: incubation period. PI: period of infectivity
B pertussis aka Bordet-Gengou bacillus
Pathogenesis
• Basically b r o n c h i t i s
• Locally invasive; toxin mediated:
– severe inflam.: necrosis, infiltration: debris  sticky
s c a n t y sputum  severe cough
• May cause Br. Pn., bronchiectasis, collapse
• Brain: cortical atrophy from IC hge. & anoxia
Pertussis toxins: pertactin, lymphocytotic factor,
hemagglutinin, fimbrial proteins agglutinogens)
Bronchiolar plugging & alveolar dilatation in pertussis in an infant
Clinical Stages
A. Catarrhal stage: ~1-2w. Mimics coryza: LGF, cough, red
watering eyes. Dx usually missed. ABT can abort it
B. Paroxysmal stage: 2-4w/longer
• Forceful cough of  severity; 5-10 bouts/expn. whoop & vomiting
• Flushed/cyanosed face, bulging bloody watering eyes
• Protruded tongue, dribbling, distended neck veins
• Fever is absent/minimal
Severity: immune status, previous pertussis, ABT
C. Convalescence stage
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 & adults: milder-shorter, prolonged
cough ± paroxysms. No whoop in adults
S/he is apathetic, loses wt. rapidly
Triggers of paroxysms
– eating, drinking
– sneezing, yawing, wind
– laughing, playing,
– smoke
–Suggestion!
PE: generally uninformative; May be no signs
• Diffuse rales, & ronchi may be noted
• Petechiae may be seen
Bilateral subconjunctival hge. in an infant with pertussis
Convalescence stage
• Signs of improvement over weeks-months
• Resp. Tract can stay irritated for months-years:
Paroxysms may occur with each RTI during this time
Complications
• Respiratory:
• CNS:
• Alimentary system:
• Others:
Complications: Respiratory Sys.
• Pneumonia: primary, secondary
• Reactivation of TB
• Bronchiectasis
• Collapse
• Emphysema
• Pneumothorax
• AOM
4w-old: pertussis pn. with air trapping & collapse
(segmental/lobar collapse not uncommon)
4-w. Died of pertussis pn. (2y S. aureus): air trap. He had SD hge.
Pertussis pn. in a
7-y. Obliteration
of cardiac
borders is
common
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
SD hge in pertussis. Past: 36,000 died/y in US, most in first 6 mo of life
Melena
Complications: Others
• Over exhaustion
• Dehydration
• Tetany
• Hypoglycemia
• Epistaxis, sub-conj. bleeds, purpura
• Diaphragmatic rupture
Rupture of diaphragm:
A. mimics loculated pneumothorax. B. NGT in herniated stomach
Prolonged QT
Tetany
Dx: mainly clinical
• High index of suspicion in stage 1: immunity, contact,
neighborhood
• Classical paroxysm is very suggestive
• Cough >2w with post-tussive emesis is an important clue
Lab.
• CS:
• CBC: absolute lymphocytosis (20-50K) is typical (not in B
parapertussis & immunized). It parallels the severity
• CXR: perihilar infiltrates, Br.Pn., emphysema, etc.
• PCR for rapid Dx
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) & 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
• Erythromycin x14d is DoC
– Aborts paroxysm in Stage 1
– Shortens duration, reduces spread, prevents relapse
– In Stage 2 ABT has no effect
• Azithromycin & clarithromycin are alternative
• Resistance is rare
Penicillins, cephalosporins ineffective
TREATMENT
Azithro.10–12mg/kg/d, max. 600mg/d x5d
Clarithro. 15–20 mg/kg/d, in 2 dd; max. 1 g/d x7d
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
IMMUNISATION
• 5 doses: 4th at 15-18mo; 5th at school entry
• Immunity is not absolute/permanent
• It may not prevent infection. Mild illness may not be
recognized & can spread
• DPT vax.: requires booster/10y
Prognosis
• Mortality ~40 % in infants <5mo
Death:
• Anoxia, rapid dehydration
• Malnutrition, hypoglycemia
• Over exhaustion, encephalopathy
Points to Ponder
• Pertussis is fatal in small babies
• Severe damage to RT cilia  RT is reactive for 1year
• It 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
This unvaccinated child has severe
cough & vomiting
1.What is the Dx?
2. What is the c/of such bleeding in
this child?
3. What are other complications?
OSPE
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
• Whoop is characteristic in all ages
‘Bull neck’ (LAP &edema)
What is the Dx?
Pharyngeal D: membranes covering
tonsils &uvula in a 15y F
DIPHTHERIA
a serious d. c/by only locally invasive C. diphtheriae
– fatal: local obstruction and
– fatal: systemic toxicity
• Spreads P2P. Fate depends on:
– strain (toxic/not), circulation, immunity
• Man only
• Both non-/toxigenic strains cause obstruction
• Only toxigenic strain causes toxemia
• 50% mortality. Now rare
P2P: person to person
Common site: URT
• Also skin, eye, ear, genitalia, wound
• Exotoxin: degeneration/necrosis of heart, nerves (paralysis)
kidneys, adrenals
– Interval: myocarditis 2w. neuritis 3-7w
Characteristic pseudomembrane
• Necrosed tissue + exudate + bacteria
• Tough-fibrinous; adherent
• Gray to black (~bleed)
• Attempt to remove it causes bleeding
Diphtheritic
tracheobronchial
membranes
Conjunctival D.: membranous conj.: strep., pneumo., D; chemical,
ligneous conj., adenovirus or HSV
Nasal diphtheria: 5y
Diphtheria in wound
Tonsilopharyngeal D
Insidious: LGF, disproportionately toxic, malaise, sore
throat, irritable, dysphagia, bull neck, rapid pulse, ±
respiratory & CV collapse
Very distinctive membrane: 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
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 is
essential. But Cl. Dx is enough to start Rx
• Mortality is ~5%. Untreated ~50%
Gram-positive C diphtheriae, stained using the methylene blue technique.
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
Follicular tonsillitis
Inf. mononucleosis
Herpangina: coxsackie A16
Oral thrush
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 thousand i.u.
• Nasopharyngeal disease  40-60 ,,
• Extensive for 3d/bull neck  80-120 ,,
B. ABT : Penicillin/erythromycin DoC x14d
C. Supportive: life support
ADS: antidiphtheric serum. ABT: antibiotic therapy
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
MCQ
In diphtheria:
• most strains are toxigenic
• natural inf. 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
WelcomeAll
WelcomeAll
POLIOMYELITIS
• Enterovirus. 3 strains: damage AH cells: partial/full palsy
• Spreads: P2P, mucus/phlegm, feces
• Enters gut & URT, multiplies in throat & gut, spread to
nerve by blood & 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. Bangladesh is free
AH: anterior horn
CF
• Fever, myalgia, HA, abnormal reflexes, back stiffness, stiff
neck, ANS features
• Tests: cultures from throat, stools, or CSF
ANS: autonomic nervous system
Rx
• Only supportive:
– moist heat for muscle pain &spasms
– Analgesic (no narcotics)
– Physiotherapy, orthopedic appliances & surgery
• If severe: lifesaving measures
Tripod sign
Complications
• Paralysis, aspiration pn., pulmonary edema
• Myocarditis, shock
• Paralytic ileus, disability, deformity, urine retention, UTI
Prognosis
• Depends on the clinical type & area affected
• Most cases recover
• CNS involvement is a medical emergency
• Disability is more common than death
Prevention: OPV (live) & IPV (inactive). No OPV in HIC
• OPV: herd immunity. Pulse dosing in LICs
HIC: high income countries. LIC: low income countries
MCQ
• Both OPV & 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 is eradicable
• Polio paralysis is usually symmetrical
• Bangladesh is polio free
• Vaccine polio virus may cause paralysis (VAPP)
• Polio causes ascending type of paralysis
What is the Dx?
‘The Severe’
Measles
(rubeola)
David Morley
Measles is a killer &
blinding d. specially for
malnourished children
Measles is a viral ID of man. Spreads P2P
• Main sign: cough, an itchy MPR (exanthem) & tiny white
spots in mouth (enanthem). 3 stages:
catarrhal, eruptive, convalescence
• HGF, cough, rhinitis, conjunctivitis
• Rash on 4th day of fever
• 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. PI: period of infectivity
Pathology
• MPR: starts at hair line, behind ears; eyes, RT & GIT
Spreads ; stays 7–10d: post measles staining
• Rash reaches feet: Fever goes!
• Rash may bleed (black measles)
• Mouth: Koplik spots; devastating ulcers
• Severe depletion of Vitamin A
• RT: Pn., bronchiolitis; bronchitis, bronchiectasis, AOM
• CNS: Encephalitis, SSPE
• GIT: Diarrhea, malabsorption
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
Post measles staining
Noma/
cancrum
oris
SEQUELAE CAN BE RESTORED with
APPROPIATE TECHNOLOGY
DIAGNOSIS
Mainly clinical. Giant cells in nasal smear
• Culture of virus (urine, blood, nasopharynx)
• Specific IgM in serum
Rx: No sp. Rx. Only supportive:
• Most important: Vitamin A
– 200k i.u. day1, d4 & d8. It decreases MM
• FEB, feeding, oral hygiene
• Rx of complications. ABT only for 2y infx.
• Ig may benefit in severe malnutrition
MM: morbidity & mortality. FEB: fluid & electrolyte balance . ABT: antibiotc therapy
• VADX, blindness
• AOM
• Laryngotracheitis
• Bronchitis
• Bronchiectasis
• Bronchiolitis
• Giant Cell Pn.
Pn: pneumonia. SSPE: subacute sclerosing
panencephalitis
• PM enteropathy
• Mouth ulcers
• Appendicitis
• Myocarditis
• Encephalitis
• SSPE (1/1000)
Complications
by virus itself
Eye damage (by virus & VADX)
– Conjunctivitis, keratitis, keratomalacia. Was the
commonest nutritional blindness in our country
Secondary inf.
• Unmasking of TB
• Bronchitis, bronchiolitis, bronchiectasis
• ALTB (croup), bacterial pneumonia
• AOM, diarrhea
Pneumoniain measles: viral, giant cell (Hecht),
bacterial, tuberculous
Complications: immunoparesis
• Unmasking of TB
• Depressed CMI (Pseudo-ve MT)
• Low response to vaccines
• Diarrhea, malabsorption, 2y inf. (v. common)
• If fever recurs suspect 2y inf.
Causes of death
• Fulminant course, pn., diarrhea, severe Mn., VADX
• Neurologic complications
Any non-accidental death within 1 mo of measles is measles
Subac. Sclerosing Panencephalitis (SSPE)
• A rare, chr., progressive encephalitis in children & 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
SSPE: MRI at Dx (A, B) & 3mo
later (C, D)
A & C are T1; B & D T2
A B: focal abnormality in white
m. of L frontal lobe,
with hypointense signal
on T1 & a hyperintense
signal on T2
FU scan: this is less obvious ,
but advanced diffuse
cortical atrophy is seen,
(ventriculomegaly,
markedly enlarged sulci
(arrowheads in C)
MCQ
• Measles can deplete VA totally
• It is the commonest c/of nutritional blindness
• 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
• SSPE is a slow virus infection
• SSPE is infectious
• Appendicitis in measles usually need operation
• Secondary bacterial infection is common in measles
Severe muscular
spasms with
trismus from
contamination of
umbilical stump
Risus
sardonicus
Opisthotonos: back is bent backward with forward bowing
What is Dx?
TETANUS
• Fatal ! Neurotoxin from vegetative form of 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/inflam
•  contamination  shorter IP  severer disease
• Painful generalized myospasm. Death is usually from
suffocation. Subsides over weeks if recovers
• Brain not affected. Mentally c l e a r !
• NT: 5-14 d (8 days disease)
NT: neonatal tetanus
LT secondary to parent’s attempt to drain a boil with a contaminated thorn
A preschool boy with Localized Tetanus 2y to parent’s attempt to drain
a boil with a contaminated mesquite thorn
TREATMENT
Medical e m e r g e n c y ! M u s t 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 & mechanical ventilation
• TIG 3000-6000iu im for all. No local infiltration (cannot
neutralize fixed toxin)
Anticonvulsants
• Diazepam, Midazolam, Chlorpromazine
• Baclofen & other muscle relaxants
ANS instabilities
• Temp. instability, cardiac arrhythmias
• Unstable BP, excessive secretions
Temperature instability
HGF in tetanus: spasms, sympathetic over-stimulation,
infection, dehydration
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 & FB
• No extensive débridement for punctures
• No wide excision of cord stump
WOUND MANAGEMENT
ABT
• Metronidazole is the DoC. Pen. G is alternative
• Duration: 10-14d
TIG
• Give TIG in HIV, regardless of h/of TT
• TT: child 7y: use Td; <7y: DTaP/DTP/DT
• Separate sites for TT &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
Past Doses Clean, Minor Tetanus prone
Td TIG Td TIG
<3 or unknown Yes2 No Yes Yes3
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
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
Immunization
• TT is toxoid; better as Td
• Very stable & effective. : months at room temp
• May be given with other vax.
• Given as DTP/DTaP, DT, Td ( diphtheria content)
– TT for pregnant & women of CBA
• Children 6w-7 y: x5 TT & 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
POINTS TO PONDER
• Non-communicable
• Completely preventable
• Non-inflammatory toxic response
• Disease does not confer immunity
• Spasm control is the mainstay of Rx
• No herd immunity
MCQ
Tetanus
• is commonly focal
• is a communicable disease
• Dx mainly clinical
• The vaccine is highly effective & stable & very cheap
• Immunisation confers herd immunity
• is more common in elderly people
• Pt. stays mentally clear
• can cause hyperpyrexia
• can cause aspiration pn.
• can cause hypoglycemia
Hemophilus influenzae type b (Hib/HIB)
• Severe sepsis, particularly among infants
• It was believed to cause flu
• Aerobic G-ve. Has polysaccharide capsule
• 6 different serotypes (a - f)
• 95% inf. is c/by type b (Hib)
• Colonizes nasopharynx: affects local & distant sites
• Antecedent URTI may be a contributing factor
Cellulitis
6%
Arthritis
8% Bacteremia
2%
Meningitis
50%
Epiglottitis
17%
Pneumonia
15%
Osteomyelitis
2%
HIB: Clinical Features*
*prevaccination era
Hib Meningitis
• 50-65% of meningitis in the prevaccine era
• Deafness or neurologic sequelae in 15-30%
• CFR: 2-5% despite of effective ABT
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
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
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
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
S. pneumoniae
• Gram-positive S. pneumoniae
• Reservoir: human; spread by droplets
• 90 serotypes
• Polysaccharide capsule is important virulence factor
• Type-specific Ab is protective
Pneumonia, Bacteremia, Meningitis, AOM
• 2005: 1.6 million died; (0.7-1million U-5), mostly in LICs
• In HICs, <2y & the elderly mostly affected
• Immunodeficiencies greatly increase the risk
• Increasing ABR underlines urgent need for vax.
ABR: AB resistance
Pneumococcal Disease in Children
• Sepsis without focus is the commonest presentation
• Leading c/of bacterial meningitis among U-5; highest
among infants
• Most common c/of AOM (5million/y)
Pneumonia: 36% of adult CAP & 50% of HAP
Ac. onset: F, shaking chills, pleuritic chest p., moist
cough, SoB, tachypnea, hypoxia. 175k adm. In
US/y. Common bacterial complication of
flu & measles
CAP: community-acquired pn. HAP: hospital-acquired pn. AOM: acute otitis media
Pn. Sepsis
• >50,000/y in the USA
• More among elderly & very young
• CFR: ~20%; 60% among the elderly
Pn. Meningitis
• 3k-6k/y in the USA
• CFR: ~30%; 80% in the elderly
• Neurologic sequelae common
Children at more Risk of IPD
• Functional/anatomic asplenia, especially SCD
• Overcrowding, poor clothing, malnutrition
• HIV
• Cochlear implant
• Out-of-home group child care
Outbreaks not common: generally occur in crowding
IPD often has underlying illness & may have high fatality
SCD: sickle cell disease
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
Pneumococcal Vax.
• Growing ABR: urgent need for vax.
• Vax. is most effective for Px
– 4 doses of pn. conjugate vax. (PCV) covering 7, 10 & 13
serotypes (PCV7, 10, 13)
– 1 unconjugated polysaccharide vax. covering 23 strains
(PPV23)
• WHO recommends PCV
ABR: antibiotic resistance
Rubella
• Ac., contagious viral inf. that occurs most often in
children & young adults
• Rubella in pregnancy may cause fetal death or cong.
defects known as cong. rubella syn. (CRS: blindness,
deafness, heart defects)
• 1,10,000 babies are born with CRS/y
• Immunization
– Single dose of vax.: >95% immunity; 2nd dose 100%
– Usually combined with Measles, Mumps, and/or Varicella vaccine
MCQ
• Pneumococcus is a capsulated bacteria
• Rubella can cause deafness in adolescents
• Hib is a common c/of epiglottitis
• Pneumococcal vax. covers all strains
• AOM can cause meningitis
Next Lec.:
Childhood
Injury
(ACCIDENTS IN CHILDREN)
THANK YOU

Epi target diseases

  • 5.
  • 6.
    E. P. I.TARGET DISEASES (DPT POLIO HIB MR PCV: 8)
  • 7.
    Introduction IMMUNIZATION is aprocess of making a person immune to an ID, typically by a vaccine which stimulates the immune system to protect against that ID • It is a proven tool for controlling & eliminating (e.g. Small Pox) life-threatening ID. It can avert 2-3 mln. deaths/y • It is one of the most cost-effective investments, & can be made available to even hard-to-reach target groups; & does not require any major lifestyle change
  • 8.
    Why immunisation? To stoppreventable ID  Measles, polio-, DPT, Hib, S. pneumoniae, rotavirus, TB, etc. are killers. HBV & rubella are not U-5 killer • 2015: 16k U-5 death/d (50% in SS Africa; 30% in S. Asia). >50% are preventable/treatable by simple, measures Children in SS Africa are >x14 more likely to die than those in HICs  S. Asia has done strong progress: >50% reduction since ‘90 Leading c/of U-5 death: preterm, pn., BA, D & malaria. 45% of all child deaths are linked to malnutrition SS: sub Saharan. HICs: high income countries.BA: birth asphyxia. D: diarrhoea. Mn: malnutrition
  • 9.
    World Distribn. ofDeaths: U-5y: 2012 6.6million death: >50% preventable/Rx with simple, affordable interventions
  • 10.
    World Burden ofVax.-Preventable U-5 death 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
  • 11.
    EPI target Dsin Bangladesh (10) • TB • Diphtheria, Pertussis, Tetanus (DPT) • Poliomyelitis: OPV, IPV • HBV • HIB • Measles, Rubella (MR) • S pneumoniae
  • 12.
    Other vax. availablein Bangladesh • HPV • HAV • Varicella-zoster • Influenza • Typhoid • Cholera • Rota virus • Yellow fever • Meningococcus • Rabies Not Available in BD • Dengue • Hepatitis E • Japanese encephalitis • Malaria • Tick-borne encephalitis
  • 13.
    Vaccines in pipeline •Malaria • HEV • Ebola (effective vax. in pipeline) • HIV • Improved BCG, pertussis • Zica, etc. • Campylobacter jejuni • Chagas Disease • Chikungunya • Enterotoxigenic E coli • Enterovirus 71 (EV71) • Group B Streptococcus • Herpes Simplex Virus • Human Hookworm D • Leishmaniasis • Nipah Virus • Nontyphoidal Salmonella D • Norovirus • Paratyphoid • Respiratory Syncytial Virus • Schistosomiasis D • Shigella • S aureus • S pyrogenes • Improved TB • Universal Influenza Vaccine
  • 14.
  • 15.
    Post-tussive emesis Very tenacioussticky sputum Broken BV in eyes & face What is the Dx?
  • 16.
    ‘Whooping’ Cough/100 days’ cough •Highly contagious • ‘Killer’ in small infants PERTUSSIS (persistent intense cough)
  • 17.
    Pertussis: an ARIcharacterized by 3 stages: catarrhal, paroxysmal, & convalescence Aetiology • B. pertussis (Classical) • Others: – B. parapertussis, B. bronchiseptica – Adenovirus 1, 2, 3, 5 – M. pneumoniae; C. trachomatis & - pneumoniae
  • 18.
    Epidemiology Fastidious, Gram-ve, pleomorphicrod. No growth on ordinary media (lab to be informed beforehand !) • Does not survive in environment (P2P spread) • Only human reservoir 70% cases in <1y age. Endemic every 3-5y • Mild/atypical in adults  source for children • Highly contagious in stage 1 (~100%) • Immunity is i n c o m p l e t e • I P: 7-10d. PI varies (-2 +6w of cough) IP: incubation period. PI: period of infectivity
  • 20.
    B pertussis akaBordet-Gengou bacillus
  • 21.
    Pathogenesis • Basically br o n c h i t i s • Locally invasive; toxin mediated: – severe inflam.: necrosis, infiltration: debris  sticky s c a n t y sputum  severe cough • May cause Br. Pn., bronchiectasis, collapse • Brain: cortical atrophy from IC hge. & anoxia Pertussis toxins: pertactin, lymphocytotic factor, hemagglutinin, fimbrial proteins agglutinogens)
  • 22.
    Bronchiolar plugging &alveolar dilatation in pertussis in an infant
  • 23.
    Clinical Stages A. Catarrhalstage: ~1-2w. Mimics coryza: LGF, cough, red watering eyes. Dx usually missed. ABT can abort it B. Paroxysmal stage: 2-4w/longer • Forceful cough of  severity; 5-10 bouts/expn. whoop & vomiting • Flushed/cyanosed face, bulging bloody watering eyes • Protruded tongue, dribbling, distended neck veins • Fever is absent/minimal Severity: immune status, previous pertussis, ABT C. Convalescence stage
  • 24.
    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 & adults: milder-shorter, prolonged cough ± paroxysms. No whoop in adults
  • 25.
    S/he is apathetic,loses wt. rapidly Triggers of paroxysms – eating, drinking – sneezing, yawing, wind – laughing, playing, – smoke –Suggestion! PE: generally uninformative; May be no signs • Diffuse rales, & ronchi may be noted • Petechiae may be seen
  • 26.
    Bilateral subconjunctival hge.in an infant with pertussis
  • 27.
    Convalescence stage • Signsof improvement over weeks-months • Resp. Tract can stay irritated for months-years: Paroxysms may occur with each RTI during this time Complications • Respiratory: • CNS: • Alimentary system: • Others:
  • 28.
    Complications: Respiratory Sys. •Pneumonia: primary, secondary • Reactivation of TB • Bronchiectasis • Collapse • Emphysema • Pneumothorax • AOM
  • 29.
    4w-old: pertussis pn.with air trapping & collapse (segmental/lobar collapse not uncommon)
  • 30.
    4-w. Died ofpertussis pn. (2y S. aureus): air trap. He had SD hge.
  • 31.
    Pertussis pn. ina 7-y. Obliteration of cardiac borders is common
  • 32.
    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
  • 33.
    SD hge inpertussis. Past: 36,000 died/y in US, most in first 6 mo of life
  • 37.
  • 38.
    Complications: Others • Overexhaustion • Dehydration • Tetany • Hypoglycemia • Epistaxis, sub-conj. bleeds, purpura • Diaphragmatic rupture
  • 39.
    Rupture of diaphragm: A.mimics loculated pneumothorax. B. NGT in herniated stomach
  • 40.
  • 42.
    Dx: mainly clinical •High index of suspicion in stage 1: immunity, contact, neighborhood • Classical paroxysm is very suggestive • Cough >2w with post-tussive emesis is an important clue Lab. • CS: • CBC: absolute lymphocytosis (20-50K) is typical (not in B parapertussis & immunized). It parallels the severity • CXR: perihilar infiltrates, Br.Pn., emphysema, etc. • PCR for rapid Dx
  • 43.
    CS: should bedone in all cases. Takes 10-14d Negative: after 4thw of illness, immunized, ABT • NP secretions (aspiration/Dacron/Ca alginate swab) • Media: Regan-Lowe (transport) & 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
  • 44.
    • Erythromycin x14dis DoC – Aborts paroxysm in Stage 1 – Shortens duration, reduces spread, prevents relapse – In Stage 2 ABT has no effect • Azithromycin & clarithromycin are alternative • Resistance is rare Penicillins, cephalosporins ineffective TREATMENT Azithro.10–12mg/kg/d, max. 600mg/d x5d Clarithro. 15–20 mg/kg/d, in 2 dd; max. 1 g/d x7d
  • 45.
    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
  • 46.
    IMMUNISATION • 5 doses:4th at 15-18mo; 5th at school entry • Immunity is not absolute/permanent • It may not prevent infection. Mild illness may not be recognized & can spread • DPT vax.: requires booster/10y Prognosis • Mortality ~40 % in infants <5mo Death: • Anoxia, rapid dehydration • Malnutrition, hypoglycemia • Over exhaustion, encephalopathy
  • 47.
    Points to Ponder •Pertussis is fatal in small babies • Severe damage to RT cilia  RT is reactive for 1year • It 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
  • 48.
    This unvaccinated childhas severe cough & vomiting 1.What is the Dx? 2. What is the c/of such bleeding in this child? 3. What are other complications? OSPE
  • 49.
    MCQ Classical pertussis • causesneutrophilic 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 • Whoop is characteristic in all ages
  • 50.
  • 51.
    What is theDx? Pharyngeal D: membranes covering tonsils &uvula in a 15y F
  • 52.
    DIPHTHERIA a serious d.c/by only locally invasive C. diphtheriae – fatal: local obstruction and – fatal: systemic toxicity • Spreads P2P. Fate depends on: – strain (toxic/not), circulation, immunity • Man only • Both non-/toxigenic strains cause obstruction • Only toxigenic strain causes toxemia • 50% mortality. Now rare P2P: person to person
  • 53.
    Common site: URT •Also skin, eye, ear, genitalia, wound • Exotoxin: degeneration/necrosis of heart, nerves (paralysis) kidneys, adrenals – Interval: myocarditis 2w. neuritis 3-7w Characteristic pseudomembrane • Necrosed tissue + exudate + bacteria • Tough-fibrinous; adherent • Gray to black (~bleed) • Attempt to remove it causes bleeding
  • 54.
  • 55.
    Conjunctival D.: membranousconj.: strep., pneumo., D; chemical, ligneous conj., adenovirus or HSV
  • 56.
  • 57.
  • 58.
    Tonsilopharyngeal D Insidious: LGF,disproportionately toxic, malaise, sore throat, irritable, dysphagia, bull neck, rapid pulse, ± respiratory & CV collapse Very distinctive membrane: 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
  • 59.
    Clinical Dx isurgent! • 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 is essential. But Cl. Dx is enough to start Rx • Mortality is ~5%. Untreated ~50%
  • 60.
    Gram-positive C diphtheriae,stained using the methylene blue technique.
  • 62.
    White Patch OverTonsils  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
  • 63.
  • 64.
  • 65.
  • 66.
  • 67.
    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 thousand i.u. • Nasopharyngeal disease  40-60 ,, • Extensive for 3d/bull neck  80-120 ,, B. ABT : Penicillin/erythromycin DoC x14d C. Supportive: life support ADS: antidiphtheric serum. ABT: antibiotic therapy
  • 68.
    Complications Obstruction: • Hypoxia, CVcollapse • Bull neck, dysphagia • Pn., hemorrhagic pn. Toxemia: Neuritis: paralysis of palate, pharynx, eye, diaphragm, ciliary B, GBS Myocarditis Gastritis Hepatitis Nephritis, ATN
  • 69.
    MCQ In diphtheria: • moststrains are toxigenic • natural inf. 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
  • 70.
  • 76.
    POLIOMYELITIS • Enterovirus. 3strains: damage AH cells: partial/full palsy • Spreads: P2P, mucus/phlegm, feces • Enters gut & URT, multiplies in throat & gut, spread to nerve by blood & 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. Bangladesh is free AH: anterior horn
  • 77.
    CF • Fever, myalgia,HA, abnormal reflexes, back stiffness, stiff neck, ANS features • Tests: cultures from throat, stools, or CSF ANS: autonomic nervous system Rx • Only supportive: – moist heat for muscle pain &spasms – Analgesic (no narcotics) – Physiotherapy, orthopedic appliances & surgery • If severe: lifesaving measures
  • 78.
  • 79.
    Complications • Paralysis, aspirationpn., pulmonary edema • Myocarditis, shock • Paralytic ileus, disability, deformity, urine retention, UTI Prognosis • Depends on the clinical type & area affected • Most cases recover • CNS involvement is a medical emergency • Disability is more common than death Prevention: OPV (live) & IPV (inactive). No OPV in HIC • OPV: herd immunity. Pulse dosing in LICs HIC: high income countries. LIC: low income countries
  • 81.
    MCQ • Both OPV& 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 is eradicable • Polio paralysis is usually symmetrical • Bangladesh is polio free • Vaccine polio virus may cause paralysis (VAPP) • Polio causes ascending type of paralysis
  • 84.
  • 85.
  • 86.
    Measles is akiller & blinding d. specially for malnourished children
  • 87.
    Measles is aviral ID of man. Spreads P2P • Main sign: cough, an itchy MPR (exanthem) & tiny white spots in mouth (enanthem). 3 stages: catarrhal, eruptive, convalescence • HGF, cough, rhinitis, conjunctivitis • Rash on 4th day of fever • 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. PI: period of infectivity
  • 88.
    Pathology • MPR: startsat hair line, behind ears; eyes, RT & GIT Spreads ; stays 7–10d: post measles staining • Rash reaches feet: Fever goes! • Rash may bleed (black measles) • Mouth: Koplik spots; devastating ulcers • Severe depletion of Vitamin A • RT: Pn., bronchiolitis; bronchitis, bronchiectasis, AOM • CNS: Encephalitis, SSPE • GIT: Diarrhea, malabsorption
  • 89.
    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
  • 90.
  • 91.
  • 92.
    SEQUELAE CAN BERESTORED with APPROPIATE TECHNOLOGY
  • 94.
    DIAGNOSIS Mainly clinical. Giantcells in nasal smear • Culture of virus (urine, blood, nasopharynx) • Specific IgM in serum Rx: No sp. Rx. Only supportive: • Most important: Vitamin A – 200k i.u. day1, d4 & d8. It decreases MM • FEB, feeding, oral hygiene • Rx of complications. ABT only for 2y infx. • Ig may benefit in severe malnutrition MM: morbidity & mortality. FEB: fluid & electrolyte balance . ABT: antibiotc therapy
  • 95.
    • VADX, blindness •AOM • Laryngotracheitis • Bronchitis • Bronchiectasis • Bronchiolitis • Giant Cell Pn. Pn: pneumonia. SSPE: subacute sclerosing panencephalitis • PM enteropathy • Mouth ulcers • Appendicitis • Myocarditis • Encephalitis • SSPE (1/1000) Complications by virus itself
  • 96.
    Eye damage (byvirus & VADX) – Conjunctivitis, keratitis, keratomalacia. Was the commonest nutritional blindness in our country Secondary inf. • Unmasking of TB • Bronchitis, bronchiolitis, bronchiectasis • ALTB (croup), bacterial pneumonia • AOM, diarrhea Pneumoniain measles: viral, giant cell (Hecht), bacterial, tuberculous
  • 97.
    Complications: immunoparesis • Unmaskingof TB • Depressed CMI (Pseudo-ve MT) • Low response to vaccines • Diarrhea, malabsorption, 2y inf. (v. common) • If fever recurs suspect 2y inf. Causes of death • Fulminant course, pn., diarrhea, severe Mn., VADX • Neurologic complications Any non-accidental death within 1 mo of measles is measles
  • 98.
    Subac. Sclerosing Panencephalitis(SSPE) • A rare, chr., progressive encephalitis in children & 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
  • 99.
    SSPE: MRI atDx (A, B) & 3mo later (C, D) A & C are T1; B & D T2 A B: focal abnormality in white m. of L frontal lobe, with hypointense signal on T1 & a hyperintense signal on T2 FU scan: this is less obvious , but advanced diffuse cortical atrophy is seen, (ventriculomegaly, markedly enlarged sulci (arrowheads in C)
  • 102.
    MCQ • Measles candeplete VA totally • It is the commonest c/of nutritional blindness • 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 • SSPE is a slow virus infection • SSPE is infectious • Appendicitis in measles usually need operation • Secondary bacterial infection is common in measles
  • 103.
    Severe muscular spasms with trismusfrom contamination of umbilical stump
  • 104.
  • 105.
    Opisthotonos: back isbent backward with forward bowing What is Dx?
  • 106.
    TETANUS • Fatal !Neurotoxin from vegetative form of 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/inflam •  contamination  shorter IP  severer disease • Painful generalized myospasm. Death is usually from suffocation. Subsides over weeks if recovers • Brain not affected. Mentally c l e a r ! • NT: 5-14 d (8 days disease) NT: neonatal tetanus
  • 107.
    LT secondary toparent’s attempt to drain a boil with a contaminated thorn A preschool boy with Localized Tetanus 2y to parent’s attempt to drain a boil with a contaminated mesquite thorn
  • 108.
    TREATMENT Medical e me r g e n c y ! M u s t 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 & mechanical ventilation • TIG 3000-6000iu im for all. No local infiltration (cannot neutralize fixed toxin)
  • 109.
    Anticonvulsants • Diazepam, Midazolam,Chlorpromazine • Baclofen & other muscle relaxants ANS instabilities • Temp. instability, cardiac arrhythmias • Unstable BP, excessive secretions Temperature instability HGF in tetanus: spasms, sympathetic over-stimulation, infection, dehydration
  • 110.
    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 & FB • No extensive débridement for punctures • No wide excision of cord stump WOUND MANAGEMENT
  • 111.
    ABT • Metronidazole isthe DoC. Pen. G is alternative • Duration: 10-14d TIG • Give TIG in HIV, regardless of h/of TT • TT: child 7y: use Td; <7y: DTaP/DTP/DT • Separate sites for TT &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
  • 112.
    Past Doses Clean,Minor Tetanus prone Td TIG Td TIG <3 or unknown Yes2 No Yes Yes3 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
  • 113.
    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
  • 114.
    Immunization • TT istoxoid; better as Td • Very stable & effective. : months at room temp • May be given with other vax. • Given as DTP/DTaP, DT, Td ( diphtheria content) – TT for pregnant & women of CBA • Children 6w-7 y: x5 TT & 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
  • 115.
    POINTS TO PONDER •Non-communicable • Completely preventable • Non-inflammatory toxic response • Disease does not confer immunity • Spasm control is the mainstay of Rx • No herd immunity
  • 116.
    MCQ Tetanus • is commonlyfocal • is a communicable disease • Dx mainly clinical • The vaccine is highly effective & stable & very cheap • Immunisation confers herd immunity • is more common in elderly people • Pt. stays mentally clear • can cause hyperpyrexia • can cause aspiration pn. • can cause hypoglycemia
  • 117.
    Hemophilus influenzae typeb (Hib/HIB) • Severe sepsis, particularly among infants • It was believed to cause flu • Aerobic G-ve. Has polysaccharide capsule • 6 different serotypes (a - f) • 95% inf. is c/by type b (Hib) • Colonizes nasopharynx: affects local & distant sites • Antecedent URTI may be a contributing factor
  • 118.
  • 119.
    Hib Meningitis • 50-65%of meningitis in the prevaccine era • Deafness or neurologic sequelae in 15-30% • CFR: 2-5% despite of effective ABT 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
  • 120.
    0 5 10 15 20 25 1990 1992 19941996 1998 2000 2002 2004 Incidence Incidence*of Invasive Hib Disease, 1990-2004 *Rate per 100,000 children <5 years of age Year
  • 121.
    0 20 40 60 80 100 120 140 160 180 200 0-1 12-13 24-2536-37 48-49 60 Age group (mos) IncidenceHaemophilus influenzae type b, 1986 Incidence* by Age Group *Rate per 100,000 population, prevaccine era
  • 122.
    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
  • 123.
    S. pneumoniae • Gram-positiveS. pneumoniae • Reservoir: human; spread by droplets • 90 serotypes • Polysaccharide capsule is important virulence factor • Type-specific Ab is protective Pneumonia, Bacteremia, Meningitis, AOM • 2005: 1.6 million died; (0.7-1million U-5), mostly in LICs • In HICs, <2y & the elderly mostly affected • Immunodeficiencies greatly increase the risk • Increasing ABR underlines urgent need for vax. ABR: AB resistance
  • 124.
    Pneumococcal Disease inChildren • Sepsis without focus is the commonest presentation • Leading c/of bacterial meningitis among U-5; highest among infants • Most common c/of AOM (5million/y) Pneumonia: 36% of adult CAP & 50% of HAP Ac. onset: F, shaking chills, pleuritic chest p., moist cough, SoB, tachypnea, hypoxia. 175k adm. In US/y. Common bacterial complication of flu & measles CAP: community-acquired pn. HAP: hospital-acquired pn. AOM: acute otitis media
  • 125.
    Pn. Sepsis • >50,000/yin the USA • More among elderly & very young • CFR: ~20%; 60% among the elderly Pn. Meningitis • 3k-6k/y in the USA • CFR: ~30%; 80% in the elderly • Neurologic sequelae common
  • 126.
    Children at moreRisk of IPD • Functional/anatomic asplenia, especially SCD • Overcrowding, poor clothing, malnutrition • HIV • Cochlear implant • Out-of-home group child care Outbreaks not common: generally occur in crowding IPD often has underlying illness & may have high fatality SCD: sickle cell disease
  • 127.
    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
  • 128.
    Pneumococcal Vax. • GrowingABR: urgent need for vax. • Vax. is most effective for Px – 4 doses of pn. conjugate vax. (PCV) covering 7, 10 & 13 serotypes (PCV7, 10, 13) – 1 unconjugated polysaccharide vax. covering 23 strains (PPV23) • WHO recommends PCV ABR: antibiotic resistance
  • 129.
    Rubella • Ac., contagiousviral inf. that occurs most often in children & young adults • Rubella in pregnancy may cause fetal death or cong. defects known as cong. rubella syn. (CRS: blindness, deafness, heart defects) • 1,10,000 babies are born with CRS/y • Immunization – Single dose of vax.: >95% immunity; 2nd dose 100% – Usually combined with Measles, Mumps, and/or Varicella vaccine
  • 130.
    MCQ • Pneumococcus isa capsulated bacteria • Rubella can cause deafness in adolescents • Hib is a common c/of epiglottitis • Pneumococcal vax. covers all strains • AOM can cause meningitis
  • 133.
  • 134.