Common childhood infections

TEWODROS H/MARIAM (MD)

Objectives
• Measles
• Mumps
• Rubella
• Polio
• Pertussis
• Diphtheria
Measles
• Measles is highly contagious diseases
• a major cause of morbidity and mortality in
unvaccinated infants and children
▫ especially those living in developing countries
where measles vaccines are not universally
available.
• Etiology
• Measles virus is :
▫ a single-stranded lipid enveloped RNA virus
▫ is inactivated by lipid solvents such as ether and
chloroform;
▫ the virus is also inactivated by heat (>37°C),
ultraviolet light, and extremes in pH (<5 and >10).
▫ Infectious virus can be maintained for long periods
at -70°C.
Etilology Cont…
▫ a member of the Morbillivirus genus of the
Paramyxoviridae family
▫ 6 major structural proteins
 the hemagglutinin (H) protein
 mediates viral attachment to host cells, is essential
for primary infection.
 Neutralizing antibodies confer lifelong immunity to
measles and are primarily directed against the H
protein
 fusion (F) protein
 enhances cell-to-cell spread of the virus
 Matrix (M) protein - important in viral assembly
 polymerase phosphoprotein (P), and large
protein (L)
 important in RNA polymerase activity
 nucleoprotein (NP)-structural nucleocapsid
protein.
EPIDEMIOLOGY.
• Measles virus infects only humans and primates.
• In developing countries, measles currently
accounts for approximately 1 million deaths a
year.
• Patients are infectious from 3 days before the
rash up to 4–6 days after its onset.
• The portal of entry of measles virus is through
the respiratory tract or conjunctivae
Cont…
• Prior to the use of measles vaccine, the peak
incidence was among children 5–10 yr of age
• Epidemics occur irregularly in about 2-4yrs
interval
• A prevalence of greater than 90% immunization
of infants has been shown to produce disease-
free zones.
• Possibility that measles can be
eradicated(biologic similarities with smallpox)
.a distinctive rash as a sentinel marker.
.no animal reservoir.
.no vector
.one serotype
.no transmissible latent virus
.seasonal occurrence with disease free period
.an effective vaccine
Pathology and pathogenesis
• Measles infection causes necrosis of the respiratory
tract epithelium and an accompanying lymphocytic
infiltrate.
• Measles produces a small vessel vasculitis on the
skin and on the oral mucous membranes.
• Fusion of infected cells results in multinucleated
giant cells, the Warthin-Finkeldey giant cells that
are pathognomonic for measles
• The essential lesion of measles is found in the skin,
conjunctivae, and the mucous membranes of the
nasopharynx, bronchi, and intestinal tract
Clinical manifestations
• Measles has three clinical stages:
▫ an incubation stage
 lasts approximately 10–12 days to the first prodromal
symptoms
▫ a prodromal stage
 usually lasts 3–5 days
 is characterized by a low-grade to moderate fever, a dry
cough, coryza, and conjunctivitis.
 Temperature rises abruptly up to 40⁰C and drops within
2 days
 Koplik spots appear
 the pathognomonic sign of measles,
 grayish white dots, usually as small as grains of sand, that
have slight, reddish areolae; occasionally they are
hemorrhagic
 tend to occur opposite the lower molars but may spread
irregularly over the rest of the buccal mucosa.
Cont…..
• Exanthem /Rash phase
▫ 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 cheek.
▫ lesions become increasingly maculopapular as the
rash spreads rapidly over the entire face, neck, upper
arms, upper part of the chest and down to the whole
body.
▫ Start to fade with the same pattern as it appeared
when the rash reaches to the legs after about 48 hours.
▫ Black measles –
▫ If fever lasts more than 4 days - complications
Cont…
• Otitis media, bronchopneumonia, and
gastrointestinal symptoms such as diarrhea and
vomiting are more common in infants and small
children (especially if they are malnourished)
than in older children.
• Atypical measles - in recipients of formalin
inactivated vaccine who later exposed to wild
virus
Diagnosis
• Usually apparent from the clinical picture
• All cases of measles should be reported
• Measles IGM test- detectable up to1 mo after the
illness but may be limited to the first 72 hrs of
the rash.
• Measles virus can be isolated by tissue culture in
human embryonic or rhesus monkey kidney
cells.
• multinucleated giant cells can be demonstrated
in smears of the nasal mucosa.
Differential diagnosis

• rubella
• roseola infantum (human herpes virus 6)
• infections resulting from echovirus,
coxsackievirus, adenovirus; infectious
mononucleosis; toxoplasmosis;
meningococcemia; scarlet fever; rickettsial
diseases; Kawasaki disease; serum sickness; and
drug rashes.
• There is no specific antiviral therapy; treatment
Treatment
is entirely supportive.
• Antipyretics (acetaminophen or ibuprofen) for
fever
• maintenance of an adequate fluid intake and
nutritional support.
• Antibiotics for bacterial complications.
• Vitamin A supplementation
Complications
• attributable to the pathogenic effects of the virus on the respiratory tract and immune
system
• Morbidity and mortality from measles are greatest in patients <5 yr of age (especially <1 yr
of age) and those >20 yr of age.
• Acute otitis media is the most common complication of measles
• Pneumonia is the most common cause of death in measles – due to the virus or bacterial
super infection by S.pneumonia, H.influenzae and S. aureus.
• Croup, tracheitis, and bronchiolitis are common complications in infants and toddlers with
measles
• Mouth ulcers, malnutrition
• Suppress response to PPD test, reactivation of latent Tb
• Diarrhea and vomiting – dehydration
• Encephalitis
• Febrile seizures
• Sub acute sclerosing pan encephalitis
 rare causes chronic encephalitis due to persistent viral infection, occurs after 5-15yr of 1 st
infection
 myoclonic seizure with progressive dementia,most die in 6-9months
Corneal scarring
causing blindness
Vitamin A Deficiency

Encephalitis
Older children, adults
~ 0.1% of cases
Chronic disability
Prevention
• Isolation precautions, especially in hospitals and
other institutions, should be maintained from the
7th day after exposure until 5 days after the rash has
appeared.
• Measles live attenuated vaccine – 85-95% efficacy
• Post- exposure prophylaxis
▫ Passive immunization with immune globulin is
effective for prevention and attenuation of measles
within 6 days of exposure.
• Vaccine within 72 hours of exposure in selected
groups.
Mumps
• Mumps is an acute self-limited infection
characterized by fever, bilateral or unilateral
parotid swelling and tenderness, and the
frequent occurrence of meningoencephalitis and
orchitis.
• it remains endemic in parts of the world with
poor vaccine coverage
Etiology
• Mumps virus is in the family Paramyxoviridae
and the genus Rubulavirus.
• a single-stranded pleomorphic RNA virus
encapsulated in a lipoprotein envelope
• Two surface glycoproteins
▫ HN (hemagglutinin-neuraminidase) and
 mediate absorption of the virus to host cells
▫ F (fusion) - mediates penetration into cells
• Mumps virus exists as a single immunotype, and
humans are the only natural host.
EPIDEMIOLOGY
• Mumps is spread from person to person by
respiratory droplets.
• Virus appears in the saliva from up to 7 days
before to as long as 7 days after onset of parotid
swelling.
• occurs primarily in young children between the
ages of 5 and 9 and in epidemics about every 4
years
• infection occurred more often in the winter and
spring months.
PATHOLOGY AND PATHOGENESIS
• Mumps virus targets the salivary glands, central
nervous system (CNS), pancreas, testes, and, to a
lesser extent, thyroid, ovaries, heart, kidneys,
liver, and joint synovia.
• initial viral replication occurs in the epithelium
of the upper respiratory tract.
• Infection spreads to the adjacent lymph nodes
by the lymphatic drainage, and viremia ensues,
spreading the virus to targeted tissues
• Mumps virus causes necrosis of infected cells
CLINICAL MANIFESTATIONS.
• incubation period for mumps ranges from 12 to 25
days
• Mumps virus infection may result in clinical
presentation ranging from asymptomatic or
nonspecific symptoms to typical illness associated
with parotitis
• case presents with a prodrome lasting 1–2 days
consisting of fever, headache, vomiting, and
achiness.
• Parotitis then appears and may be unilateral initially
but becomes bilateral in about 70% of cases
• The parotid gland is tender
• Ingestion of sour or acidic foods or liquids may
enhance pain in the parotid area.
• As swelling progresses, the angle of the jaw is
obscured and the ear lobe may be lifted upward
and outward
• The parotid swelling peaks in approximately 3
days then gradually subsides over 7 days.
DIAGNOSIS.
• the diagnosis could be made based on history of exposure to mumps
infection,
▫ an appropriate incubation period, and
▫ development of typical clinical findings.
• Parotitis - elevated amylase level.
• isolation of the virus
▫ in cell culture,
▫ detection of viral antigen by direct immunofluorescence, or
▫ identification of nucleic acid by reverse transcriptase polymerase chain
reaction.
• serum mumps immunoglobulin G (IgG) antibody between acute
and convalescent serum specimens by
▫ complement fixation,
▫ neutralization hemagglutination, or
▫ enzyme immunoassay (EIA) tests can also establish the diagnosis
DIFFERENTIAL DIAGNOSIS
• Other viral infections e.g. parainfluenza viruses 1 &3,
influenza A, CMV, EBV, HIV…
• Bacterial parotitis – S. aureus
COMPLICATIONS.
• The most common complications of mumps are:
▫ meningitis, with or without encephalitis, and
▫ gonadal involvement.
• Uncommon complications include :
▫ conjunctivitis, optic neuritis, pneumonia, nephritis, pancreatitis,
▫ thrombocytopenia, arthritis, myocardial involvement.
• Maternal infection with mumps during the 1st trimester of
pregnancy results in increased fetal wastage.
• perinatal mumps disease has been reported in infants born to
mothers who acquired mumps late in gestation.
treatment
• No specific antiviral therapy is available for
mumps.
• Management should be aimed at reducing the
pain associated with meningitis or orchitis and
maintenance of adequate hydration.
• Antipyretics may be given for fever.
PROGNOSIS.
The outcome of mumps is nearly always
excellent, even when complicated by encephalitis
• PREVENTION.
▫ Immunization with the live mumps vaccine is the
primary mode of prevention
▫ Should be avoided in immunocompromised and
pregnants
▫ vaccine effectiveness of 88% for 2 doses of MMR
vaccine compared with 64% for a single dose
Rubella
• Rubella (German measles or 3-day measles) is a
mild, often exanthematous disease of infants and
children
• is typically more severe and associated with
more complications in adults.
• Its major clinical significance is transplacental
infection and fetal damage as part of the
congenital rubella syndrome (CRS).
ETIOLOGY
• Rubella virus is a member of the family Togaviridae
and is the only species of the genus Rubivirus.
• It is a single-stranded RNA virus with a lipid
envelope and 3 structural proteins
▫ a nucleocapsid protein associated with the nucleus and
▫ 2 glycoproteins, E1 and E2, associated with the
envelope.
• The virus is sensitive to heat, ultraviolet light, and
extremes of pH but is relatively stable at cold
temperatures.
• Humans are the only known host.
EPIDEMIOLOGY.
• most common in preschool-aged and school-
aged children.
• Vaccination significantly reduced incidence in
developed countries
• The period of highest communicability is from 5
days before to 6 days following appearance of
the rash.
The viral mechanisms for cell injury and death in rubella are not well
Pathogenesis
understood
for either postnatal or congenital infection
Cont..
• The most important risk factor for severe congenital
defects is the stage of gestation at the time of
infection
• Maternal infection during the 1st 8 wk of gestation
results in the most severe and widespread defects.
• The risk for congenital defects has been estimated
at
▫ 90% for maternal infection before 11 wk of gestation,
▫ 33% at 11–12 wk,
▫ 11% at 13–14 wk, and
▫ 24% at 15–16 wk.
• Defects occurring after 16 wk of gestation are
uncommon, even if fetal infection occurs.
Cont…
• Mechanisms of cellular and tissue
damage in the infected fetus may include:
▫ tissue necrosis due to vascular
insufficiency,
▫ reduced cellular multiplication time,
▫ chromosomal breaks, and
▫ production of a protein inhibitor causing
mitotic arrests in certain cell types.
CLINICAL MANIFESTATIONS
• rubella is a mild disease not easily discernible from other viral
infections
• Following an incubation period of 14–21 days, a prodrome of
low-grade fever, sore throat, red eyes with or without eye pain,
headache, malaise, anorexia, and lymphadenopathy begins.
▫ Suboccipital, postauricular, and anterior cervical lymph nodes are
most prominent.
• Child may have rash, which is variable and not distinctive
▫ begins on the face and neck as small, irregular pink macules that
coalesce, and it spreads centrifugally to involve the torso and
extremities
▫ The rash fades from the face as it extends to the rest of the body
▫ The duration of the rash is generally 3 days
▫ 25–40% of children may not have a rash
• Leukopenia, neutropenia, and mild thrombocytopenia have
been described during postnatal rubella.
DIAGNOSES.
• Specific diagnosis of rubella is important:
▫ for epidemiologic reasons,
▫ for diagnosis of infection in pregnant women and
▫ for confirmation of the diagnosis of congenital
rubella
• The most common diagnostic test is rubella
immunoglobulin M (IgM) enzyme
immunosorbent assay
• reverse transcriptase polymerase chain reaction
test, or viral culture could be performed.
COMPLICATIONS
• Thrombocytopenia
▫ occurs in about 1 : 3,000 cases of rubella
▫ more frequently among children and in
girls
▫ It manifests about 2 wk following the onset
of the rash with petechiae, epistaxis,
gastrointestinal bleeding, and hematuria.
▫ It is usually self-limited
• Arthritis
▫ more commonly among adults
▫ classically involves the small joints of the
hands
▫ self-limited and resolves within weeks
without sequelae
Cont…
• Encephalitis – two forms
▫ Postinfectious encephalitis
 Uncommon
 It appears within 7 days following onset of the rash with
headache, seizures, confusion, coma, focal neurologic signs,
and ataxia
 Most patients recover completely
▫ Progressive rubella panencephalitis
 is an extremely rare complication of either acquired rubella or
CRS
 rubella virus may be isolated from brain tissue
 The clinical findings and course are undistinguishable from
SSPE and other “slow virus” neurodegenerative syndromes
 Death occurs 2–5 yr after onset
• Guillain-Barré syndrome and peripheral neuritis are
rarely reported
• Myocarditis is a rare complication
Congenital Rubella Syndrome
• Result of in utero infection of the fetus during
pregnancy
• The pathologic findings of CRS are often severe and
may involve nearly every organ system
• Nerve deafness is the single most common finding
among infants with CRS
• Unilateral or bilateral cataracts are the most serious
eye finding, occurring in about ⅓ of infants
• Cardiac abnormalities occur in half of the children
infected during the 1st 8 wk of gestation.
▫ Patent ductus arteriosus is the most frequently
reported cardiac defect, followed by lesions of the
pulmonary arteries and valvular disease
Pathologic Findings of Congenital
Rubella Syndrome
Clinical Manifestations of Congenital
Rubella Syndrome
• A variety of late-onset manifestations of
CRS have been recognized including
▫ diabetes mellitus (20%),
▫ thyroid dysfunction (5%), and
▫ glaucoma and visual abnormalities
associated with the retinopathy
• TREATMENT.
▫ There is no specific treatment available for
either acquired rubella or CRS
• SUPPORTIVE CARE
▫ antipyretics and analgesics.
▫ Intravenous immunoglobulin or corticosteroids
can be considered for severe, nonremitting
thrombocytopenia.
▫ Management of children with CRS is more
complex and requires pediatric, cardiac,
audiologic, ophthalmologic, and neurologic
evaluation and follow-up
▫ Hearing screening is of special importance since
early intervention may improve outcomes.
• PROGNOSIS
▫ Postnatal infection with rubella has an excellent
prognosis
▫ Long-term outcomes of CRS are less favorable and
somewhat variable
• PREVENTION
▫ Patients with postnatal infection should be isolated
from susceptible individuals for 7 days after onset of
the rash.
▫ Counseling should be provided about the risks and
benefits of termination of pregnancy
▫ Rubella vaccine -usually administered combined with
measles and mumps (MMR)
Poliomyelitis
• Poliomyelitis is caused by poliovirus
• The polioviruses are
▫ nonenveloped, single-stranded RNA viruses belonging to
the Picornaviridae family, in the genus Enterovirus, and
▫ include 3 antigenically distinct serotypes (types 1, 2, and 3).
• Polioviruses spread from the intestinal tract to the
central nervous system (CNS), where they cause aseptic
meningitis and poliomyelitis, or polio.
• The polioviruses are extremely hardy and can retain
infectivity for several days at room temperature.
 EPIDEMIOLOGY
• 90–95% of infections are inapparent but induce protective
immunity
• Clinically apparent but nonparalytic illness occurs in about
5% of all infections
• paralytic polio occurs in about 1/1,000 infections among
infants to about 1/100 infections among adolescents
• in developing countries with poor sanitation, infection
early in life results in infantile paralysis
• Poor sanitation and crowding have permitted the
continued transmission of poliovirus in certain poor
countries in Africa and Asia
▫ despite massive global efforts to eradicate polio, in some
areas with an average of 12–13 doses of polio vaccine
administered to children in the 1st 5 yr of life
• Humans are the only known reservoir for the
polioviruses, which are spread by the fecal-oral
route.
• Poliovirus has been isolated from feces for >2 wk
before paralysis to several weeks after the onset
of symptoms
Pathology and pathogenesis
• Polioviruses infect cells by adsorbing to
the genetically determined poliovirus
receptor
• wild-type and vaccine strains of
polioviruses gain host entry via the
gastrointestinal tract
• Regional lymph nodes are infected, and
primary viremia occurs after 2–3 days
• The virus seeds multiple sites, including
the reticuloendothelial system, brown fat
deposits, and skeletal muscle
• The exact mechanism of entry into the CNS is not
known.
• Once entry is gained, the virus may traverse
neural pathways, and multiple sites within the
CNS are often affected
• poliovirus primarily infects motor neuron cells in
the spinal cord (the anterior horn cells) and the
medulla oblongata (the cranial nerve nuclei).
• clinical signs of weakness in the limbs develop
when more than 50% of motor neurons are
destroyed
• Other neurons affected are
▫ the nuclei in the roof and vermis of the cerebellum,
▫ the substantia nigra, and occasionally the red
nucleus in the pons;
▫ there may be variable involvement of thalamic,
hypothalamic, and pallidal nuclei and the motor
cortex.
 CLINICAL MANIFESTATIONS
• incubation period of poliovirus is usually considered to be 8–12
days, with a range of 5–35 days
• Poliovirus infections with wild-type virus may follow 1 of several
courses:
▫ inapparent infection,
 occurs in 90–95% of cases and causes no disease and no sequelae;
▫ abortive poliomyelitis;
 In about 5% of patients
 a nonspecific influenza-like syndrome occurs 1–2 wk after infection
 Fever, malaise, anorexia, and headache are prominent features, and
there may be sore throat and abdominal or muscular pain
 illness is short lived, up to 2–3 days
 Recovery is complete, and no neurologic signs or sequelae develop
▫ nonparalytic poliomyelitis; or
 In about 1% of patients infected with wild-type poliovirus
 more intense headache, nausea, and vomiting, as well as soreness and
stiffness of the posterior muscles of the neck, trunk, and limbs.
 Nuchal and spinal rigidity are the basis for the diagnosis of nonparalytic
poliomyelitis during the 2nd phase
 Physical examination reveals nuchal -spinal signs and changes in
superficial and deep reflexes
• paralytic poliomyelitis.
▫ Paralytic poliomyelitis develops in about
0.1% of persons infected with poliovirus
▫ Paralysis, if it occurs, appears 3–8 days
after the initial symptoms.
▫ 3 clinically recognizable syndromes that
represent a continuum of infection
differentiated only by the portions of the
CNS most severely affected.
(1) spinal paralytic poliomyelitis,
(2) bulbar poliomyelitis, and
(3) polioencephalitis.
 Spinal paralytic poliomyelitis
• May follow abortive polio by 2-5 days
• severe headache and fever occur
• Severe muscle pain is present, and sensory and motor phenomena (e.g.,
paresthesia, hyperesthesia, fasciculations, and spasms) may develop.
• On physical examination the distribution of paralysis is characteristically
spotty.
• Single muscles, multiple muscles, or groups of muscles may be involved in
any pattern
• Within 1–2 days, asymmetric flaccid paralysis or paresis occurs
• The proximal areas of the extremities tend to be involved to a greater extent
than the distal areas
• Sensation is intact; sensory disturbances, if present, suggest a disease other
than poliomyelitis
• Paralysis of the lower limbs is often accompanied by bowel and bladder
dysfunction ranging from transient incontinence to paralysis with
constipation and urinary retention.
• Atrophy of the limb, failure of growth, and deformity is common and is
especially evident in the growing child
 Bulbar poliomyelitis
• may occur as a clinical entity without apparent
involvement of the spinal cord
• clinical manifestations by dysfunctions of the cranial
nerves and medullary centers
• Cranial nerve involvement is seldom permanent
• The clinical findings seen with bulbar poliomyelitis are:
▫ respiratory difficulty
▫ paralysis of extraocular, facial, and masticatory muscles
▫ nasal twang to the voice or cry caused by palatal and
pharyngeal weakness
▫ inability to swallow smoothly, resulting in accumulation of
saliva in the pharynx
▫ absence of effective coughing
 ▫ involvement of vital centers in the medulla, which manifest as
 irregularities in rate, depth, and rhythm of respiration;
 cardiovascular alterations, including blood pressure changes
(especially increased blood pressure), alternate flushing and
mottling of the skin, and cardiac arrhythmias; and
 rapid changes in body temperature
▫ paralysis of 1 or both vocal cords, causing hoarseness,
aphonia, and ultimately asphyxia
• Polioencephalitis
▫ a rare form of the disease in which higher centers of the brain
are severely involved
▫ Seizures, coma, and spastic paralysis with increased reflexes
may be observed.
▫ Irritability, disorientation, drowsiness, and coarse tremors
are often present with peripheral or cranial nerve paralysis
 DIAGNOSIS
• Poliomyelitis should be considered in any unimmunized or
incompletely immunized child with paralytic disease
• Clinical - combination of fever, headache, neck and back pain,
asymmetric flaccid paralysis without sensory loss, and
pleocytosis does not regularly occur in any other illness
• Serologic testing demonstrates seroconversion or a 4-fold or
greater increase in antibody titers, when measured during the
acute phase of illness and 3–6 wk later
• CSF
▫ often normal during the minor illness
▫ with CNS involvement demonstrates a pleocytosis of 20–300
cells/mm
 Cells may be polymorphonuclear early during the course of the disease
but shift to mononuclear cells soon afterward
▫ the CSF protein is normal or only slightly elevated at the outset of
CNS disease but usually rises to 50–100 mg/dL by the 2nd week of
illness
• The World Health Organization (WHO) recommends
that the laboratory diagnosis of poliomyelitis be
confirmed by isolation and identification of poliovirus
in the stool, with specific identification of wild-type
and vaccine-type strains.
• In suspected cases of acute flaccid paralysis, 2 stool
specimens should be collected 24–48 hr apart, as soon
as possible after the diagnosis of poliomyelitis is
suspected
• Poliovirus concentrations are high in the stool in the
1st week after the onset of paralysis -80-90% positive
but yield decreases to <20% starting from 3wks.
• a minimum of 8–10 g of stool should be collected
 Differential diagnosis
• West-nile virus,
• Varicella-zoster virus,
• GUILLAIN-BARRÉ SYNDROME
• Acute transverse myelitis
• Epidural abscess
• Spinal cord compression; trauma
• Exotoxin of Corynebacterium diphtheriae
• Toxin of Clostridium botulinum
• Tick bite paralysis
• Myasthenia gravis
• Hypokalemic periodic paralysis
 Treatment
• There is no specific antiviral treatment for poliomyelitis
• management is supportive and aimed at :
▫ limiting progression of disease,
▫ prevention of ensuing skeletal deformities, and
▫ preparation of the child and family for prolonged treatment
required and for permanent disability if this seems likely
• All intramuscular injections and surgical procedures are
contraindicated during the acute phase of the illness
▫ may result in progression of disease
• management of pure bulbar poliomyelitis consists of
maintaining the airway and avoiding all risk of inhalation
of saliva, food, or vomitus
 PROGNOSIS
• outcome of inapparent, abortive poliomyelitis and
aseptic meningitis syndromes is uniformly good
• outcome of paralytic disease varies
▫ In severe bulbar poliomyelitis, the mortality rate may be
as high as 60%
▫ recovery phase lasts usually about 6 mo, beyond which
persisting paralysis is permanent
• Post polio Syndrome - 30–40% of persons who
survived paralytic poliomyelitis in childhood may
experience muscle pain and exacerbation of existing
weakness, or they may develop new weakness or
paralysis
PREVENTION
• Vaccination is the only effective method of
preventing poliomyelitis
• Vaccines – IPV / OPV
• OPV used in our country – at birth, 6wks, 10wks and
14wks
• Polio eradication – planned by WHO by 2000, then
2008
▫ Strategies
 routine immunization,
 National Immunization Days (NIDs),
 acute flaccid paralysis surveillance, and
 mopping up immunization
 Pertussis
• Pertussis = intense cough
• Some times called whooping cough
• ETIOLOGY
▫ Bordetella pertussis – commonest
▫ Bordetella parapertussis - occasional cause
• EPIDEMIOLOGY
• There are 60 million cases of pertussis each year
worldwide, resulting in >500,000 deaths
• extremely contagious, with attack rates as high as
100% in susceptible individuals exposed to aerosol
droplets
• Neither natural disease nor vaccination provides
complete or lifelong immunity against reinfection or
disease
• Protection against typical disease begins to wane with
age
PATHOGENESIS
• B. pertussis expresses pertussis toxin (PT), the
major virulence protein
▫ biologic activities (e.g., histamine sensitivity, insulin
secretion, leukocyte dysfunction
• B. pertussis also produces other biologically active
substances
▫ filamentous hemagglutinin (FHA)
▫ Agglutinogens (fimbrae) – e.g pertactin which is
important for attachment
▫ Tracheal cytotoxin - inhibit clearance of organisms,
responsible for the local epithelial damage that
produces respiratory symptoms and facilitates
absorption of PT
 CLINICAL MANIFESTATIONS
• pertussis is a prolonged disease divided into:
▫ catarrhal - 1–2 wk
 nondistinctive symptoms of congestion and rhinorrhea variably
accompanied by low-grade fever, sneezing, lacrimation, and
conjunctival suffusion
▫ paroxysmal - 2–6 wk
 a dry, intermittent, irritative cough evolving into the inexorable
paroxysms that are the hallmark of pertussis
 loud whoop follows as inspired air traverses the still partially
closed airway
 Post-tussive emesis is common
▫ convalescent stages
 the paroxysmal stage fades into the convalescent stage (≥2 wk),
the number, severity, and duration of episodes diminish
▫ infants <3 mo of age may have apnea, cyanosis, or an acute
life-threatening event
 DIAGNOSIS
• Mainly clinical when patient has classical
manifestations
• Leukocytosis (15,000–100,000 cells/mm3) due to
absolute lymphocytosis is characteristic in the
catarrhal stage
• chest x-ray - may show perihilar infiltrate or edema
(sometimes with a butterfly appearance) and variable
atelectasis
• Isolation of B. pertussis in culture remains the gold
standard for diagnosis
▫ Regan-Lowe charcoal agar
▫ Stainer-Scholte media
 TREATMENT
• Goals of therapy are :
▫ to limit the number of paroxysms,
▫ to observe the severity of the cough,
▫ to provide assistance when necessary, and
▫ to maximize nutrition, rest, and recovery without sequelae
• Admition:
▫ all infants below 6 months
▫ if significant complications occured
▫ children with underlying cardiac, pulmonary, muscular, or
neurologic disorders
• Antibiotics – macrolids are preferred
• Isolation – respiratory isolation
• Care of Household and Other Close Contacts – antibiotics,
vaccination
COMPLICATIONS
• Infants <6 mo of age have excessive
mortality and morbidity
• apnea, secondary infections (such as otitis
media and pneumonia), and physical
sequelae of forceful coughing
• Bronchiectasis
• 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
PREVENTION
• Universal immunization of children with
pertussis vaccine, beginning in infancy with
periodic reinforcing doses, is central to the
control of pertussis
• Vaccines – DTaP / DTP
• In our country – DTP used
• Given at the age of 6wks, 10wks & 14wks
• Adverse effects – rare
▫ high fever, persistent crying of ≥3 hr duration,
hypotonic hyporesponsive episodes, and seizures
▫ May require exemption of subsequent vaccination
 Diphtheria (corynebacterium
diphtheria)
• An acute toxic infection caused by
corynebacterium species
Etiology
-C.diphtheria → most common agent, aerobic,
non encapsulated, non-spore forming, mostly
non motile, pleomorphic, gram +ve bacilli
→ 4 biotypes (mitis, intermedius,
belfanti, gravis)
-C.ulcerans: rarely
 Cont…
Epidemiology
• An exclusive inhabitant of human mucous membranes &
skin
• Spread by airborne respiratory droplets or direct contact
with respiratory secretions exudate from skin lesions
• Asymptomatic respiratory tract carriage is important in
transimission
• Outbreaks are associated with homelessness, crowding,
poverty, alcoholism, poor hygiene, contaminated
fomites, underlying dermatosis, & introduction of new
strains from exogenous sources
 Cont…
Pathogenesis
• Both toxigenic & non toxigenic C.diphtheriae cause skin
& mucosal infection & can rarely cause focal infection
after bacteremia
• The major virulence lies in its ability to produce the
potent 62-kd polypeptide exotoxin, w/c inhibits protien
synthesis & causes local tissue necrosis
• With in the 1st few days of respiratory tract infection, a
dense necroticcoagulum of organisms, epithelial cells,
fibrin leukocytes, & erythrocytes forms, advances &
becomes a gray-brown, leather-like adherent
pseudomembrane (diphtheria – Greek for leather)
 Cont…
• Removal is difficult & reveals a bleeding edematous
submucosa
• Paralysis of the palate & hypopharynx is an early local
effect of the toxin
• Toxin absorption can lead to systemic manifestations:
kidney tubular necrosis, thrombocythopenia,
cardiomyopathy, & /or neuropathy
• b/se the above Cxns can occur 2-10 wks after
mucocutaneous infection, the pathophysiology in some
cases is suspected to be immunologically mediated
 Cont…
C/Ms
Respiratory tract diphtheria
-Primary focus of infection is the tonsils or
pharynx (94%) followed by nose & larynx
-Infection of the anterior nares is more common
among infants & causes serosanguineous,
purulent, erosive rhinitis with membrane
formation. Shallow ulceration of the external
nares & upper lip is characteristic
 Cont…
-In tonsilar & phrangeal diphtheria: sore throat,
fever, dysphagia, hoarsness, malaise, headache
-Underlying soft-tissue edema & enlarged LNs can
cause a bull-neck appearance
 Cont…
Cutaneous diphtheria
-An indolent, non progressive infection cxzed by a
superficial, ecthymic, non healing ulcer with a
gray-brown membrane
-Pain, tenderness, erythema, & exudate are typical
-Local hyperesthesia or hypesthesia is unusual
 Cont…
Infection at other sites
-Uncommon
-Ear (otitis externa), eye (purulent & ulcerative
conjuctivitis) & the genital tract (purulent &
ulcerative vulvovaginitis)
-Endocarditis: clusters among IV drug users, skin
is portal of entry, & almost all strains are
nontoxigenic
 Cont…
Dx
-Culture of the specimens obtained from
mucocutaneous lesion
-G-stain & fluorescent antibody is unreliable
 Cont…
Cxns
-Respiratory tract obstruction by pseudo
membranes
-Toxic cardiomyopathy
-Toxic neuropathy
 Cont…
Rx
-Antitoxin therapy
-Antibiotic therapy: erythromycine or pencillens
for 14 days
-Wound care with soap & water
-Bed rest
 Cont…
Px
-Depends on the virulence of organisms, pt age,
immunization status, site of infection, & speed of
administration of antitoxin
-UAO from respiratory tract diphtheria &
myocarditis account for most death
-10% CFR for respiratory tract diphtheria
 Cont…
Prevention
-Droplet precautions: phrangeal diphtheria
-Contact precautions: cutaneous diphtheria
-Antibiotic prophylaxis for all household contacts
regardless of immunization status
-Vaccination