epi target diseases
TRANSCRIPT
WELCOME
ALL
E. P. I. TARGET DISEASES
(DPT POLIO HIB MR PCV)
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%
World Distribn. of Deaths: U-5y: 2012
6.6million death: >50% preventable/Rx with simple, affordable interventions. 45% deaths linked to Mn.
World Disease Burden of Vax.-Preventable U-5 MR
Pertus-sis 13%
Hib* 13%
Measles 8%
Tetanus4%Pneumococcal
diseases*32%
Ro-tavirus*
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• HBV• HIB• Measles, Rubella (MR)• S pneumoniae
Other vax. available in Bangladesh • HPV• HAV• Varicella-zoster• Influenza• Typhoid• Cholera• Rota virus• Yellow fever• Meningococcus
Vaccines in pipeline
• Dengue• Malaria • HEV• Ebola• HIV• Improved BCG• Zica, etc.
Intracranial hge
Severe Cough
Very tenacious sticky sputum
Broken BV in eyes and face
What is the Dx?
• ‘Whooping’ Cough/100 days’ cough
• Highly contagious• ‘Killer’ in small infants
PERTUSSIS (persistent intense cough)
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
B pertussisfastidious, Gram-ve, pleomorphic rod• No growth on ordinary media
(lab to be informed beforehand!)• Does not survive in environment (P2P spread)
B pertussis aka Bordet-Gengou bacillus
Epidemiology70% 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
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)
Bronchiolar plugging and alveolar dilatation in pertussis in an infant
Clinical StagesCatarrhal 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
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
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
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:
Complications: Respiratory Sys.• Pneumonia: primary, secondary• Reactivation of TB• Bronchiectasis• Collapse• Emphysema• Pneumothorax• AOM
4w-old: pertussis pn. with air trapping and progressive collapse. Segmental/lobar atelectasis are not uncommon
4-w neonate died of pertussis pn. (2y S aureus) with 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. Previously, 36k died/y in US, most in first 6 mo of life
Mel
ena
Complications: Others
• Over exhaustion• Dehydration• Tetany• Hypoglycemia • Epistaxis, sub-conj. bleeds, purpura• Diaphragmatic rupture
Rupture of diaphragm: A. mimics loculated pneumothorax. B. NGT shows herniated stomach
Prolonged QT
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
CS: should be done in all cases. Takes 10-14dNegative: 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
• 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 rarePenicillins, cephalosporins ineffective
TREATMENT
(Azithro.10–12mg/kg/d, p.o., x5d; max. 600mg/dClarithro. 15–20 mg/kg/d, p.o., 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 (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
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
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
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
‘Bull neck’: LAP and edema
What is the Dx?
DIPHTHERIAa 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
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
Diphtheritic tracheobronchial
membranes
Conjunctival D. Conj. membrane: strep., pneumo., D; chemical, ligneous conj., adenovirus or HSV
Nasal diphtheria
Diphtheria in wound
Tonsilopharyngeal DInsidious: 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 DUsually extension from pharynx• Croup, severe chest retraction, hoarseness• Restless, but soon becomes weak, drowsy• A grave situation! Urgent tracheostomy/intubation
DiagnosisClinical 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%
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
Herpangina
Oral thrush
Follicular tonsillitis
TreatmentA. 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
Complications
Obstruction: • Hypoxia, CV collapse• Bull neck, dysphagia • Pn., hemorrhagic pn.
Toxemia:Neuritis: paralysis of palate,
pharynx, eye, diaphragm, ciliary B, GBS
Myocarditis GastritisHepatitisNephritis, ATN
MCQIn 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
Wel
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Welcom
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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
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
Tripod sign
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:
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
‘The Severe’ Measles
(rubeola)
David Morley
Measles is a killer and blinding disease
specially for malnourished children
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
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
Pathology …Immune system• Immunoparesis (T&B cell)• DiarrheaAppendix • Lymphoid hyperplasia• Pathognomic Warthin-Finkeldey Giant cell• Appendicectomy not neededEyes: VADX, Keratoconjunctivitis, KeratomalaciaNutrition: 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)• 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
• VADX, blindness• AOM• Laryngotracheitis • Bronchitis• Bronchiectasis • Bronchiolitis• Giant Cell Pn.
• PM enteropathy• Mouth ulcers• Myocarditis• Encephalitis• SSPE (1/1000)
Complications: by virus itself
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
Pneumonia in measles: viral, giant cell (Hecht), bacterial, tuberculous
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
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 comatoseNo cure. Inosine pranobex, ribavirin, IF alpha/betaAka Dawson Disease, Dawson E or measles E
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)
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
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 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
LT secondary to parent’s attempt to drain a boil with a contaminated thorn
TREATMENTMedical 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
Anticonvulsants• Diazepam, Midazolam, Chlorpromazine• Baclofen and other muscle relaxants
ANS instabilities• Temp. instability, Cardiac arrhythmias• Unstable BP, Excessive secretions
Temperature instabilityHGF 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 preventionAim: eradication of the MO• Remove dead tissue and FB• No extensive débridement for punctures• No wide excision of cord stump
WOUND MANAGEMENT
Past Doses Clean, Minor Tetanus prone
Td TIG Td TIG<3 or unknown Y2 N Y Y3
34 No5 No No6 No2 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
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
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: 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
POINTS TO PONDER
• Non-communicable• Completely preventable • Non-inflammatory toxic response• Disease does not confer immunity • Spasm control is the mainstay of Rx
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
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
Cellulitis6%
Arthritis8% Bacteremia
2%
Meningitis50%
Epiglottitis17%
Pneumonia15%
Osteomyelitis2%
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• 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
0
5
10
15
20
25
1990 1992 1994 1996 1998 2000 2002 2004
Inci
denc
eIncidence*of Invasive Hib Disease, 1990-2004
*Rate per 100,000 children <5 years of ageYear
020406080
100120140160180200
0-1 12-13 24-25 36-37 48-49 60Age group (mos)
Inci
denc
eHaemophilus 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
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.
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.
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
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 crowdingIPD often has underlying illness and 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)
Rat
e*
*Rate per 100,000 population Source: Active Bacterial Core surveillance/EIP Network
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
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
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