Introduction

 Measles is among the leading causes of child

morbidity and mortality worldwide. Despite
remarkable progress in the control of measles,
measles still continues to claim the lives of millions
of children every year around the world.
 The majority of this mortality takes place in the
world’s poorest countries, particularly in sub-
Saharan Africa, where a combination of factors such
as crowding, exposure at a younger age and
malnutrition contribute substantially to the high
case fatality rates.
 In Ethiopia, measles is among the most common
cause for morbidity and mortality in children.
 However, routine measles immunization
coverage has increased from 29% in 1994 to
59.7% in 1999.
 This is still relatively very low.
 Due to this low coverage rate and prevailing poor
living conditions, measles outbreaks frequently
occur in different parts of the country.
 Major outbreaks with large attack rates resulting
in as high as 15 – 20% case fatality rates have
been reported in this country.
 Measles related case fatality rates range
between 3-5% in non-epidemic circumstances
According to the routine reports of health
facilities to the Ministry of Health of Ethiopia
between 1980 and 1990, the measles incidence was
very high in children under 15 years, particularly in
the 1 to 4 years age groups.
Etiology

Measles virus (MV),a negative-sense enveloped

RNA virus, is a member of the Morbillivirus genus in
the Paramyxoviridae family.
It is an RNA virus, which belongs to a group of
myxoviruses.
Measles virus (MV) is an efficient pathogen that
persists when a population is large enough to
support it.
It is able to cause acute infection in any individual
only once in his/her life time
Epidemiology

 Approximately 30 million measles cases are

reported annually to World Health Organization.
 Most reported cases are from Africa.
 Measles epidemics occur every 2-3 years in
population with large susceptible groups.
 Transmission is primarily person-to-person via
droplet spread; direct contact with nasal or
throat secretions of infected persons and less
commonly by particles freshly soiled with nose
and throat secretions.
 Human beings are the only reservoir of the
measles virus.
Transmission

 The portal of entry of measles virus is through

the respiratory tract or conjunctivae following
contact with large droplets or small droplet
aerosols in which the virus is suspended.
 Patients are infectious from 3 days before the
rash up to 4–6 days after its onset.
 Approximately 90% of the exposed susceptible
individuals develop measles.
Pathology

 In lymphoreticular tissue, lymphoid hyperplasia

is prominent.
 Fusion of infected cells results in multinucleated
giant cells, the Warthin-Finkeldey giant cells that
are pathognomonic for measles, with up to 100
nuclei and intracytoplasmic and intranuclear
inclusions
Pathogenesis

Measles consists of 4 phases

Incubation period
Prodromal illness
Exanthematous phase
Recovery
During incubation, measles virus migrates to
regional lymph nodes.
A primary viremia ensues that disseminates the
virus to the reticuloendothelial system.
A secondary viremia spreads virus to body surfaces.
 Face-to-face contact is not necessary because
viable virus may be suspended in air up to 1 hr
after a source case leaves a room.
 Secondary cases have been reported in
physicians' offices and in hospitals by spread of
aerosolized virus
Risk factors

 Young age
 Malnutrition
 Lack of immunization
 Low maternal immunity
Clinical manifestations

 Measles is a serious infection characterized by

high fever, an enanthem, cough, coryza,
conjunctivitis, and a prominent exanthem.
 After an incubation period of 8–12 days, the
prodromal phase begins with a mild fever
followed by the onset of conjunctivitis with
photophobia, coryza, a prominent cough and
increasing fever
The onset of the disease is characterized by
symptoms of the initial catarrhal (prodromal) phase
that usually lasts 3-5 days and is characterized by:
ƒ Low or moderate fever
ƒ Red eyes/lacrimation
ƒ Runny nose/ Coryza
ƒ Cough
 These symptoms nearly always precede the
appearance of koplik Spots
 Koplik spot appear as 1 to 2 mm grayish white
spots, is the pathognomonic sign of measles and
appears 1 to 4 days prior to the onset of the rash
 They appear & disappear rapidly, usually with in
12-18 hours.
 Koplik spots have been reported in 50–70% of
measles cases but probably occur in the great
majority
 Reddish (erythematous), maculopapular rash
typically occurs in cephalocaudal (top-bottom)
progression.
 The skin rash appears by the third day after the
onset of fever, cough & coryza.
 The fever classically rises, often reaching 40oC,with
the appearance of the rash.
 The rash usually starts as faint macules on the upper
lateral parts of the neck, behind the ears, along the
hairline, and on the posterior parts of the neck
 With the onset of the rash, symptoms begin to
subside and the rash fades over about 7 days in
the same progression as it evolved, often leaving
a fine desquamation of skin in its wake.
 Of the major symptoms of measles, the cough
lasts the longest, often up to 10 days.
 In more severe cases, generalized
lymphadenopathy may be present, with cervical
and occipital lymph nodes especially prominent.
Inapparent measles
infection
 In individuals with passively acquired antibody, such
as infants or recipients of blood products, a
subclinical form of measles may occur.
 The rash may be indistinct, brief, or, rarely, entirely
absent.
 Likewise, some individuals who have received
vaccine when exposed to measles may develop a
rash but few other symptoms.
 Persons with Inapparent or subclinical measles do
not shed measles virus and do not transmit infection
to household contacts.
Atypical measles

 Children who had received the original formalin-

inactivated measles vaccine at times developed a
more severe form of disease called atypical
measles.
 Patients had onset of high fever and headache
followed by the appearance of a maculopapular
rash on the extremities that become petechial
and purpuric and progressed in a centripetal
direction.
 The illness was frequently complicated by
pneumonia and pleural effusions.
 It is thought that atypical measles was caused by
development of circulating immune complexes
that formed due to an abnormal immune
response to the vaccine
Laboratory

 The diagnosis of measles is almost always based

on clinical and epidemiologic findings.
 Laboratory findings in the acute phase include
reduction in the total white blood cell count, with
lymphocytes decreased more than neutrophils.
 Absolute neutropenia has been known to occur,
however.
 In measles not complicated by bacterial
infection, the erythrocyte sedimentation rate
and C-reactive protein levels are normal
 In the absence of a recognized measles
outbreak, confirmation of the clinical diagnosis is
often recommended.
 Serologic confirmation is most conveniently
made by identification of immunoglobulin M
(IgM) antibody in serum.
 IgM antibody appears 1–2 days after the onset of
the rash and remains detectable for about 1 mo.
 If a serum specimen is collected <72 hours
following onset of rash and is negative for
measles antibody, a repeat specimen should be
obtained.
 Serologic confirmation may also be made by
demonstration of a 4-fold rise in IgG antibodies
in acute and convalescent specimens taken 2–4
wk later.
 Molecular detection by polymerase chain
reaction is possible but is a research tool
Complications

Approximately 30% of reported measles cases have

one or more complications.
The most common complications that occur are:
Vit A deficiency
Gastroenteritis
ƒPneumonia
ƒOtitis media
ƒEncephalitis
Different infections
 Mouth ulceration
 ƒ Acute glomerulonephritis
 ƒ Acute renal failure
 ƒ Severe Protein energy malnutrition
Subacute Sclerosing
Panencephalitis
 SSPE is a chronic complication of measles with a
delayed onset and an outcome that is nearly always
fatal.
 It appears to result from a persistent infection with
an altered measles virus that is harbored
intracellularly in the CNS for several years.
 After 7–10 yr the virus apparently regains virulence
and attacks the cells in the CNS that offered the
virus protection.
 This “slow virus infection” results in inflammation
and cell death, leading to an inexorable
neurodegenerative process
 Clinical manifestations of SSPE begin insidiously
7–13 yr after primary measles infection.
 Subtle changes in behavior or school
performance appear, including irritability,
reduced attention span, or temper outbursts.
 This initial phase (stage I) may at times be
missed because of brevity or mildness of the
symptoms. Fever, headache, or other signs of
encephalitis are absent.
 The hallmark of the 2nd stage is massive
myoclonus
 This coincides with extension of the
inflammatory process site to deeper structures in
the brain, including the basal ganglia.
 Involuntary movements and repetitive
myoclonic jerks begin in single muscle groups
but give way to massive spasms and jerks
involving both axial and appendicular muscles.
 Consciousness is maintained
 In the 3rd stage, involuntary movements
disappear and are replaced by choreoathetosis,
immobility, dystonia, and lead pipe rigidity that
result from destruction of deeper centers in the
basal ganglia.
 Sensorium deteriorates into dementia, stupor,
then coma
 Stage IV is characterized by loss of critical
centers that support breathing, heart rate, and
blood pressure.
 Death soon ensues.
 Progression through the clinical stages may
follow courses characterized as acute, subacute,
or chronic progressive.
Management

 Properly organized hygienic conditions for the

patient
 ƒCareful nursing care
 ƒ Protection from secondary infection
 ƒ Continuous feeding giving more fluids than
usual
 ƒ Control fever
 ƒ Watching (actively anticipating for)
complications.
Measles cases are hospitalized when:
ƒThey have severe and complicated measles.
ƒUnsatisfactory home condition or not possible to
arrange proper Nursing care.
There is no specific anti viral therapy
Treatment is mainly symptomatic and supportive:
Antipyretics (acetaminophen) for fever
Bed rest
Maintenance of an adequate fluid intake
Keep the room comfortably warm
Vitamin A Prophylaxis:(to be given immediately)
ƒ Less than 6 months: 50,000 IU
ƒ 6 – 12 months: 100,000 IU
ƒ 12 months to 5 years: 200,000 IU given orally
Reduced morbidity and mortality (recent study
showed) in malnourished African children with
severe measles
 Recommendations for Vit A
 Children 6 mo to 2 yr of age hospitalized with measles
and its complications
 Children >6 mo of age with measles who are not already
receiving vitamin A supplementation and who have any
of the following risk factors:
 Immunodeficiency
 Clinical evidence of vitamin A deficiency
 Impaired intestinal absorption
 Moderate to severe malnutrition
 Recent immigration from areas where high mortality
rates attributed to measles have been observed
Prevention

 Patients shed measles virus from 7 days after

exposure to 4–6 days after the onset of rash.
 Exposure of susceptible individuals to measles
patients should be avoided during this period.
 In hospitals, standard and airborne precautions
should be observed for this period.
 Immunocompromised patients with measles will
shed for the duration of the illness, and isolation
should be maintained throughout.
Vaccine
Measles vaccine given at the end of 9mo according
to EPI schedule.
Pertussis

 Pertussis is an acute respiratory tract infection

that was well described initially in the 1500s.
 Sydenham first used the term pertussis, meaning
intense cough, in 1670; it is preferable to
whooping cough because most infected
individuals do not “whoop.”
Introduction

 The classic clinical features of pertussis are readily

recognizable as a prolonged respiratory illness with
paroxysmal coughing often followed by forced
inspiratory effort causing a "whoop."
 However, many children who are infected with
Bordetella pertussis do not have this typical
constellation of symptoms.
 Atypical presentations occur frequently in young
infants and in vaccinated individuals.
 The atypical features vary depending upon age and
length of time since the last vaccination.
 Despite widespread vaccination, the incidence of
pertussis has been rising, particularly among
adolescents and young adults.
 As a result, more young infants are exposed to
infection.
 It is in this young population that significant
morbidity and mortality occur
Etiology

 Bordetella pertussis is the sole cause of epidemic

pertussis and the usual cause of sporadic
pertussis.
 Bordetella parapertussis is an occasional cause of
sporadic pertussis that contributes significantly
to total cases of pertussis in eastern and western
Europe, but accounts for <5% of Bordetella
isolates in the United States.
 B. pertussis and B. parapertussis are exclusive
pathogens of humans and some primates.
Epidemiology

 There are 60 million cases of pertussis each year

worldwide, resulting in >500,000 deaths
 Pertussis is extremely contagious, with attack
rates as high as 100% in susceptible individuals
exposed to aerosol droplets at close range.
 B. pertussis does not survive for prolonged
periods in the environment.
 Chronic carriage by humans is not documented.
 After intense exposure as in households, the rate
of subclinical infection is as high as 80% in fully
immunized or previously infected individuals.
 When carefully sought, however, a symptomatic
source case can be found for most patients.
 Neither natural disease nor vaccination provides
complete or lifelong immunity against
reinfection or disease.
 Protection against typical disease begins to
wane 3–5 yr after vaccination and is
unmeasurable after 12 yr.
 Subclinical reinfection undoubtedly has
contributed significantly to immunity against
disease ascribed previously to both vaccine and
prior infection
 Coughing adolescents and adults (usually not
recognized as having pertussis) currently are the
major reservoir for B. pertussis and are the usual
sources for “index cases” in infants and children.
Pathogenesis

 Bordetella organisms are tiny, fastidious, gram-

negative coccobacilli that only colonize ciliated
epithelium.
 Exact mechanism of disease symptomatology
remains unknown.
 Bordetella species share a high degree of DNA
homology among virulence genes
 Only B. pertussis expresses pertussis toxin (PT), the
major virulence protein.
 PT has numerous proven biologic activities (e.g.,
histamine sensitivity, insulin secretion, leukocyte
dysfunction), some of which may account for
systemic manifestations of disease.
 PT causes lymphocytosis immediately in
experimental animals by rerouting lymphocytes to
remain in the circulating blood pool.
 PT appears to have a central but not a singular role in
pathogenesis
 Tracheal cytotoxin, adenylate cyclase, and PT
appear to inhibit clearance of organisms.
 Tracheal cytotoxin, dermonecrotic factor, and
adenylate cyclase are postulated to be
predominantly responsible for the local epithelial
damage that produces respiratory symptoms
and facilitates absorption of PT
Clinical manifestations

 Classically, pertussis is a prolonged disease,

divided into catarrhal, paroxysmal, and
convalescent stages.
 The catarrhal stage (1–2 wk) begins insidiously
after an incubation period ranging from 3–12
days with no distinctive symptoms of congestion
and rhinorrhea variably accompanied by low-
grade fever, sneezing, lacrimation, and
conjunctival suffusion
 As initial symptoms wane, coughing marks the
onset of the paroxysmal stage (2–6 wk).
 The cough begins as a dry, intermittent, irritative
hack and evolves into the inexorable paroxysms
that are the hallmark of pertussis.
 A well-appearing, playful toddler with
insignificant provocation suddenly expresses an
anxious aura and may clutch a parent or
comforting adult before beginning a machine-
gun burst of uninterrupted coughs, chin and
chest held forward, tongue protruding
maximally, eyes bulging and watering, face
purple, until coughing ceases and a loud whoop
follows as inspired air traverses the still partially
closed airway
 Post-tussive emesis is common, and exhaustion
is universal.
 The number and severity of paroxysms escalate
over days to a week and remain at that plateau
for days to weeks.
 At the peak of the paroxysmal stage, patients
may have more than 1 episode hourly.
 As the paroxysmal stage fades into the
convalescent stage (≥2 wk), the number,
severity, and duration of episodes diminish.
Diagnosis
 Pertussis should be suspected in any individual
who has pure or predominant complaint of
cough, especially if the following are absent:
fever, malaise or myalgia, exanthem or enanthem, sore
throat, hoarseness, tachypnea, wheezes, and rales.

 For sporadic cases, a clinical case definition of

cough of ≥14 days' duration with at least 1
associated symptom of paroxysms, whoop, or
post-tussive vomiting has a sensitivity of 81%
and specificity of 58% for culture confirmation.
 Pertussis should be suspected in older children
whose cough illness is escalating at 7–10 days
and whose coughing episodes are not
continuous.
 Pertussis should be suspected in infants <3 mo of
age with apnea, cyanosis, or an acute life-
threatening event (ALTE).
 B. pertussis is an occasional cause of sudden
infant death.
 Leukocytosis (15,000–100,000 cells/mm3) due to
absolute lymphocytosis is characteristic in the
catarrhal stage

 Adults, partially immune children, and occasionally

young infants have less impressive lymphocytosis

 A severe course and death are correlated with

extreme leukocytosis (median peak white blood cell
count fatal vs nonfatal cases, 94 vs 18 × 109 cells/L)
and thrombocytosis (median peak platelet count
fatal vs nonfatal cases, 782 vs 556 × 109/L)
 The chest x-ray is only mildly abnormal in the
majority of hospitalized infants, showing
perihilar infiltrate or edema (sometimes with a
butterfly appearance) and variable atelectasis.
 Parenchymal consolidation suggests secondary
bacterial infection.
 Pneumothorax, pneumomediastinum, and air in
soft tissues can be seen occasionally
 Culture

 Polymerase chain reaction (PCR) to test

nasopharyngeal wash specimens has a
sensitivity similar to that of culture, averts
difficulties of isolation, but is not
standardized or available universally
Serology
Treatment

Goals
1.Limit paroxysms
2.Observe severity of cough
3.Maintain nutrition ,rest, recovery
Admission

 Infants less than 3 months old

 Children with complications
 Underlying diseases
 Prematurely born babies
Goals of admission

 Assess progression of disease and likelihood of

life-threatening events at peak of disease,
 Prevent or treat complications, and
 Educate parents in the natural history of the
disease and in care that will be given at home.
Typical paroxysms

 Duration <45 sec

 Red but not blue color change
 Tachycardia, bradycardia (not <60 beats/min in
infants)
 oxygen desaturation that spontaneously resolves at
the end of the paroxysm
 whooping or strength for self-rescue at the end of
the paroxysm
 self-expectorated mucus plug
 post-tussive exhaustion but not unresponsiveness
 Infants whose paroxysms repeatedly lead to life-
threatening events despite passive delivery of
oxygen or whose fatigue leads to hypercarbia
require intubation, paralysis, and ventilation
Caveats in Assessment and Care
of Infants
 Infants with fatal
with potentially Pertussis
pertussis may
appear well between episodes.
 A paroxysm must be witnessed before deciding
between hospital and home care.
 Only analysis of carefully compiled cough record
permits assessment of severity and progression
of illness.
 Suctioning of nose, oropharynx, or trachea
should not be performed on a “preventive”
schedule.
 Feeding in the period following a paroxysm may
be more successful than following napping.
 Family support begins at the time of
hospitalization with empathy for the child's and
family's experience to date, transfer of the
burden of responsibility for the child's safety to
the health care team, and delineation of
assessments and treatments to be performed.
 Family education, recruitment as part of the
team, and continued support after discharge are
essential
Antibiotics

 An antimicrobial agent is always given when

pertussis is suspected or confirmed primarily to
limit the spread of infection and secondarily for
possible clinical benefit.
 Macrolides are preferred agents, which have
similar efficacy in vitro
 Resistance has been reported rarely.
 A 7- to 10-fold relative risk for infantile hypertrophic
pyloric stenosis (IHPS) has been reported in neonates
treated with orally administered erythromycin.
 Azithromycin is the preferred agent for use in neonates.
 Limited use in neonates has not signaled increased risk
for IHPS.
 All infants <1 mo of age treated with any macrolide
should be monitored for symptoms of pyloric stenosis.
Isolation

 Patients with suspected pertussis are placed in

respiratory isolation with use of masks by all health
care personnel entering the room.
 Screening for cough should be performed upon
entrance of patients to emergency departments,
offices, and clinics to begin isolation immediately
and until 5 days after initiation of macrolide
therapy.
 Children and staff with pertussis in child-care
facilities or schools should be excluded until
macrolide prophylaxis has been taken for 5 days
Care of contacts

 A macrolide agent should be given promptly to

all household contacts and other close contacts,
such as those in daycare, regardless of age,
history of immunization, or symptoms.
 The same age-related drugs and doses for
prophylaxis are used for treatment.
 Visitation and movement of coughing family
members in the hospital must be assiduously
controlled until erythromycin has been taken for
5 days
Complications
 Infants <6 mo of age have excessive mortality
and morbidity, with infants <2 mo of age having
the highest reported rates of pertussis-
associated hospitalization (82%), pneumonia
(25%), seizures (4%), encephalopathy (1%), and
death (1%).
 Infants <4 mo of age account for 90% of cases of
fatal pertussis. Preterm birth and young
maternal age are significantly associated with
fatal pertussis
 The principal complications of pertussis are
apnea, secondary infections (such as otitis media
and pneumonia), and physical sequelae of
forceful coughing
 Fever, tachypnea or respiratory distress between
paroxysms, and absolute neutrophilia are clues
to pneumonia.
 Expected pathogens include Staphylococcus
aureus, Streptococcus pneumoniae, and bacteria
of oropharyngeal flora.
 Children who have pertussis before the age of 2 yr
may have abnormal pulmonary function into
adulthood.
 Increased intrathoracic and intra-abdominal pressure
during coughing can result in conjunctival and scleral
hemorrhages, petechiae on the upper body, epistaxis,
hemorrhage in the central nervous system (CNS) and
retina, pneumothorax and subcutaneous emphysema,
and umbilical and inguinal hernias.
 Laceration of the lingual frenulum is not uncommon.
 Apnea or bradycardia or both may result from
apparent laryngospasm or vagal stimulation just
before a coughing episode, from obstruction during
an episode, or from hypoxemia following an
episode.
 Lack of associated respiratory signs in some young
infants with apnea raises the possibility of a primary
effect of PT on the CNS.
 Seizures are usually a result of hypoxemia, but
hyponatremia from excessive secretion of
antidiuretic hormone during pneumonia can occur
 The only neuropathology documented in
humans is parenchymal hemorrhage and
ischemic necrosis.
 Particular association of pulmonary hypertension
with pertussis is unexplained
Prevention

 Vaccination