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MEASLES CASE MANAGEMENT

AND VIT A SUPPLEMENTATION

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WHY MEASLES ?

One of the leading causes of death < 5 years


Highly contagious. Infectivity > 90%

>95% deaths in developing world

Case fatality rate: 35% [1030% in displaced


population]
Severe measles is more likely among
Poorly nourished young children,
Those with insufficient vitamin A,
Poor immune system / HIV/AIDS.

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WHY MEASLES ?

Only occurs in human [does not occur in


animals]
Most potent & effective vaccine

Impact of vaccination
Last Decade: >one billion children aged 9 mo - 14
years vaccinated
23% of the overall decline in under-five deaths
between 1990 and 2008
79% drop in measles deaths between 200015
WHO IS AT RISK?
Unvaccinated young children

Overcrowding

MEASLES RETURNS WHEN WE LET


DOWN OUR GUARD

In USA decreased vaccine coverage resulted


in >55,000 cases and 123 deaths in 1991

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MEASLES BEYOND JUST INFECTION
Measles -Viral Infection : self limiting

But
Decreases Immunity
Malnutrition
Unmasks infection Tuberculosis
Measles complications
It can lead to or exacerbate vitamin- A
deficiency leading to Blindness

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WHO Goal
By the end of 2015
To reduce global measles deaths by at
least 95% compared with 2000 levels.

By the end of 2020

Toachieve Measles and rubella


elimination in at least five WHO
regions
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MEASLES :EPIDEMIOLOGY

Measles virus
RNA virus
Family Paramyxoviridae
Genus Morbillivirus

Season : Spring / winters


Children < 5 years Transmission : droplet infection
Infectivity: 3 days before / 6 days
after rash
Infectivity > 90%
PATHOGENESIS
4 Phases:
Incubation period- lasts 10 days. Entry,
primary viremia, RE cells and sec viremia
Prodromal: Skin and mucus membrane
attachment, viral replication, cell death, giant
cell formation, necrosis of epithelium and viral
shedding starts
Exanthematous: Antibody production begins.
Viral replication and symptoms begin to
subside. Virus also infects CD4 cells and
decreases cell mediated immunity
Recovery: in 2-3 days
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TRANSMISSION
Droplet infection

Portal
of entry- respiratory tract or
conjunctivae

Face to face contact not necessary

Virus is viable in suspended air even 1 hour


after patient leaves the room

Secondary spread can occur from airplanes,


hospitals, clinics
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PATHOLOGY
Necrosis of resp. tract epithelium
Small vessel vasculitis on skin/oral
mucus membrane
Histology of rash/exanthem- large
giant cells with 26 nuclei
Warthin-Finkeldey giant cells
pathognomic of measles upto 100
nuclei

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MEASLES VIRUS
WHERE AND WHEN IN THE BODY

Cl Dis

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MEASLES COURSE OF DISEASE End of RASH but
not end of
Disease

Complications

IP 10 15 days

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CLINICAL FEATURES CONTD..

Characteristic
erythematous (red)
maculopapular (blotchy)
rash appears on the 3rd -
7th day, starting behind the
ears and spreading to rest
of body.

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CHILDREN WITH MEASLES

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CHILDREN WITH MEASLES

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CHILDREN WITH MEASLES

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KOPLIK SPOTS

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CLINICAL MANIFESTATIONS.. TYPES

Typical measles

Sub-clinicalmeasles: Mild with brief


rash and no other symptoms. Seen in
infants, vaccinated, after receiving blood
products. They do not shed virus & not
infective
CLINICAL MANIFESTATIONS.. TYPES

Atypicalmeasles: Seen in children after


vaccination with killed vaccine. Centripital rash,
complicated by pneumonia and pleural effusion.
Due to abnormal immune response to vaccine by
development of immune complexes which
circulate and cause more damage

Hemorrhagic Measles ( Black Measles):


Severe form with oral, skin bleed and bowel
bleeding .

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HEMORRHAGIC MEASLES

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DIAGNOSIS..
Clinical

Koplik spots reddish


spots with bluish white
centre inside cheek at
the level of pre-molars.
over soft / hard palate/
conjunctiva and vagina

Conjunctivitis

Corneal edema

Oral ulcer
DIAGNOSIS

Multinucleated giant cells in smears of


nasal mucosa

Low WBC, relative lymphocytosis

ESR and CRP remains normal if not


complicated by bacterial infection
DIAGNOSIS
IgM antibodies appear 1-2 days after the onset of
rash and persists upto 1 month

Ifnegative in sample collected within 72 hours-


repeat it

Four fold rise in IgG titer ( paired sera in 2-4


weeks

Viral culture from secretions (blood, resp


secretions, urine)

Molecular detection by PCR (polymerase chain


reaction) 23
COMPLICATIONS

Respiratory tract-
-Upper
sinusitis, mastoiditis, croup, tonsillitis,
acute otitis media, retropharyngeal abscess
-Lower-
tracheitis, bronchiolitis, pneumonia
CVS- myocarditis

GIT- GE, appendicitis, nephritis

Eye- conjunctivitis, corneal opacity, scaring

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COMPLICATIONS
Skin- vasculitis, cellulites, TSS

Blood- bacteremia, thrombocytopenia

CNS- encephalitis, SSPE, GBS

Pregnancy- maternal morbidity, still birth,


congenital malformation

Others- flaring of TB, malnutrition

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COMPLICATIONS

Pneumonia most important cause of death

Acute otitis media most common complication

Most common bacterial pathogens-


Streptococcus pneumoneae,
Haemophilus influenzae,
Staphylococcus aureus

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COMPLICATIONS: 510% OF CASES
Respiratory Otitis media, pneumonia

GIT Diarrhoea

CNS Encephalitis, Encephalomyelitis, GBS,


SSPE
CVS Myocarditis

Eye Corneal scarring, blindness

Exacerbate TB
COMPLICATIONS OF MEASLES

Corneal scarring
causing blindness

Encephalitis

Pneumonia &
diarrhea
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BASIC PRINCIPLES OF MANAGEMENT
Anticipate complications
Encourage breast feeding
Provide nutritional support to all
children
Administer vitamin A 2 doses
Give paracetamol if temp > 39C
Give ORS-Zinc for diarrhea
Treat eyes promptly to prevent blindness
Use antibiotics if indicated
Admit severely ill children
Monitor growth regularly
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MEASLES AND VITAMIN A

Low vitamin A levels: ~ higher rates of


complications & deaths
Synergy of measles & vitamin A deficiency have
additive effect on epithelia and immune system
leading to ~ 1 million deaths
Measles itself may lead to severe acute depletion of
vitamin A
Precipitates keratomalacia & blindness

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VITAMIN A SCHEDULE FOR TREATMENT OF
MEASLES

Immediately on
Age Next day
diagnosis

< 6 months 50,000 IU 50,000 IU

6 11 months 1,00,000 IU 1,00,000 IU

> 12 months 2,00,000 IU 2,00,000 IU

2 dose schedule is more effective than single dose schedule


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Thank you

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