Lec .

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Pediatrics

Dr. Hasanen
Pertusis and Varicella

Lec. 2
16th April. 2017

Done by: Zainab Abdul Ghany.

2016-2017
‫مكتب آشور لالستنساخ‬
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Pertussis
EPIDEMIOLOGY
 The vast majority of outbreaks of Pertussis are caused by the bacterium Bordetella
pertussis.
 Pertussis syndrome; paroxysmal coughing, can be produced by related bacteria and several
types of adenovirurus.
 Transmission requires close contact with a case.
 healthy carriers are rare but adolescents and adults who have pertussis may have relatively
minor symptoms and be contagious.
 The incubation period is 7 to 10 days.

SYMPTOMS AND SIGNS

 Pertussis is an infection of the respiratory tract that, in the typical case, progresses through
a sequence of symptoms over a period of 4 to 6 weeks.
1- Catarrhal Stage: The initial symptoms are Coryza, mild cough, lacrimation, and low-grade
fever.
 Patients are most contagious at this time.
2- Paroxysmal Stage: The coughing increases in frequency as the young patient works at
trying to keep the tracheobronchial tree open.
 Various stimuli, such as feeding provoke a series of several coughs during a single expiration,
followed by a deep inspiration, often with a characteristic whoop.
 These bouts of coughing gradually increase in severity, requiring hospitalization of infants
and younger children.
 The child may become cyanotic during the struggle to take a breath and clear thick mucus
secretions.
 Vomiting is common at this time.
 Gentle suctioning and positioning will help air exchange.
3- Convalescent Stage: Symptoms gradually diminish over 2 to 4 weeks, and the patient
returns to normal.
 The clinical course is not altered dramatically by the administration of antibiotics or other
medications.

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COMPLICATIONS
 Pneumonia due to the Pertussis organism or, more frequently, to secondary bacterial
invasion is a common complication and a major contributor to the death of infants and
young children who become hypoxic and may have intracranial hemorrhages.
 Other, less serious complications include otitis media, subconjunctival hemorrhage, and
electrolyte abnormalities.

LABORATORY DIAGNOSIS
 Most patients who have Pertussis are diagnosed clinically because of the paroxyms of
cough, especially when accompanied by whoop.
 Diagnosis in the early stage of disease may be made by culturing nasopharyngeal secretions.

TREATMENT
 Infants younger than 6 months of age who have severe paroxysms and difficult feeding or
difficult handling secretions may require hospitalization.
 Antimicrobials given early may moderate symptoms, but they are of little benefit in the
paroxysmal stage except to limit spread of organisms.
 Erythromycin 40 to 50 mg/kg in four divided oral doses is the drug of choice.
 Corticosteroids, and albuterol have been used in the management of pertussis.

PREVENTION
 Protective antibody to pertussis does not cross the placenta. This means that the newborn is
completely vulnerable to infection.
 Pertussis vaccine provides protection against whooping cough. The immunity probably is not
as long-lasting as that following natural disease.
 The immunization of the normal infant begins at the age of 2 months , repeated at 8-week
intervals for a total of three doses with a combined vaccine (DPT).
 Boosters are administered at ages 12 to 18 months and 4 to 6 years.

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CONTROL OF OUTBREAKS
 Close contacts younger than 7 years of age who have not been immunized or who are
immunized inadequately should receive DPT vaccine.
 All household and other close contacts, regardless of vaccination status, should be given
erythromycin 40 to 50 mg/kg per day, orally in four doses (for 14 days).
 Children who have pertussis, if their medical condition permits, may attend school after 5
days of antibiotic treatment.
 Patients not treated with antimicrobials are considered contagious for 3 weeks after onset
of paroxysms.

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Varicella
Name !!!
 The name chickenpox has been around for centuries, it's from the blisters that are seen with
the illness. These red spots were once thought to look like chickpeas (garbanzo beans).
Another theory is that the rash of chickenpox looks like the peck marks caused by a chicken.

DEFINITIONS
 Varicella is a common exanthematous disease that primarily affects children.
 Chickenpox is the clinical syndrome that results from primary infection with varicella zoster
virus.
 Herpes zoster (“shingles” or “zoster”) after reactivation of latent VZV, occur any time after a
primary infection.
 Disseminated zoster in immunocompromised patients consists of severe rash with systemic
findings.
 Congenital varicella syndrome, or varicella embryopathy, is the result of varicella infection in
a woman during the first or second trimester of pregnancy.

EPIDEMIOLOGY
 Varicella infection is more common during the late winter and early spring.
 The mode of transmission is person to person via direct contact with infected mucosa or
airborne particles from respiratory secretions. Trans placental passage of the virus also can
occur.
 Immunity after natural varicella infection is considered lifelong.
 The incubation period is 10 to 21 days.
 Communicability is highest from 2 days prior to rash to 2 days after its onset.
 Susceptible Healthy children may be considered noncontagious after all lesions have crusted
over, although communicability may be prolonged in immunocompromized patients who
have severe infection.
 Children may become infected with varicella after direct contact with active zoster lesions
because these lesions contain infectious virus.

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PATHOGENESIS
 After a person is exposed to VZV, the virus undergoes two phases of replication during the
incubation period.
 Primary replication, 3 to 4 days after exposure, occurs in the oropharynx and regional LN,
followed by a primary viremia.
 A secondary viremia, with intracellular replication within the reticuloendothelial system,
occurs 10 to 21 days after exposure.
 Late in the secondary viremic phase, the virus is delivered to the skin, at which time the
typical cutaneous lesions become evident.
 The virus also is carried to the respiratory mucosa toward the end of the incubation period,
which is the reason for communicability before the onset of rash.
 Following viremia, the virus becomes latent in dorsal root ganglia cells. It remains there until
reactivation, at which time the virus travels back to the skin along the sensory nerve.
 Reactivation likely is due to declining cell-mediated immunity, which explains the increased
incidence in the elderly and in immunocompromised patients.

CLINICAL PRESENTATION
 The rash of varicella often is preceded by a 24 – 48 hrs period of fever, malaise, and other
systemic symptoms.
 The typical exanthem begins as erythematous, pruritic macules that develop into papules
and fluid-filled vesicles.
 The crusting of the vesicles is the final stage of the lesions before resolution, and scarring
occurs rarely.
 One of the most characteristic features of the exanthem is the presence of all stages of
lesions simultaneously.
 The average length of time from the development of the initial lesion to the crusting of all
lesions is approximately 4 to 5 days.
 Neonates born to women who develop primary varicella infection 5 days before to 2 days
after delivery are at increased risk of severe varicella infection, which may be fatal.
 Clinical features of perinatally acquired varicella include severe rash, pneumonia, hepatitis,
and death in 30% of cases.
 Congenital varicella syndrome results when a mother is infected within the first 20 weeks of
gestation. “Zigzag” skin scarring and limb atrophy are characteristic findings of this
embryopathy.
 Brain abnormalities, including hydrocephalus and microcephaly, and eye abnormalities, such
as cataracts and chorioretinitis, also may occur.
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COMPLICATIONS
 The most common complication of varicella is secondary bacterial infection, usually with
Strep pyogenes or Staph aureus.
 Other invasive complications of varicella infection include pneumonitis,
meningoencephalitis, hepatitis, arthritis, and glomerulonephritis.

Herpes Zoster
 Zoster, or “shingles,” is characterized by vesicles clustered in a dermatomal distribution. The
initial presenting symptom frequently is pain at the future site of the lesions, which usually
arise within a few days. Pruritus also may occur.
 The most common sites are those supplied by the trigeminal nerve and the thoracic ganglia.
 New lesions occur over 2 to 3 days, then begin to crust over the next week. Lesions resolve
within 2 weeks.
 The most common complication of herpes zoster is postherpetic neuralgia, which is defined
as pain that lasts longer than 1 month. This is uncommon in children.

DIAGNOSIS
 The clinical appearances of primary varicella and herpes zoster infections are so
characteristic that laboratory testing often is not necessary.
 A Tzanck smear performed on a vesicle scraping shows multinucleated giant cells, but it
does not distinguish between zoster and herpes simplex.
 Viral culture, direct fluorescent antigen and PCR performed on a vesicle scraping are of
diagnostic help.

TREATMENT
 The treatment of primary varicella-zoster infection is supportive, including antipyretics and
antihistamines or oatmeal baths to control fever and itching.
 Because of the risk of Reye syndrome, aspirin is avoided.
 The use of acyclovir is not routinely recommended for healthy children younger than 12
years of age because the disease generally has a benign, self-limited course.
 Oral acyclovir may be considered for those at risk for more severe infection, including
1. Children older than age 12 years,
2. Persons who have chronic disease and
3. Persons who are taking chronic aspirin or corticosteroid therapy.
 Intravenous acyclovir should be used for immunocompromised patients who have varicella-
zoster infection and should be initiated within 24 hours of the onset of the rash.
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POST EXPOSURE PROPHYLAXIS
 Varicella vaccine and varicella-zoster immune globulin (VZIG) are both available for the
prevention of disease in susceptible persons exposed to VZV.
 Significant exposure includes
1. household contacts,
2. close play or
3. hospital contacts,
4. newborns born to mothers who develop varicella 5 days prior to or 2 days after delivery,
and
5. those who have direct contact with active zoster lesions.

ISOLATION
 Airborne and contact precautions should be initiated for hospitalized patients at least 5 days
after the onset of the rash and maintained until all vesicles are crusted.

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Erythema infectiosum
Epidemiology
 The etiologic agent is human parvovirus B 19.
 The fifth disease, is one of the most common childhood exanthems.
 Most often in children ages 4 to 15 years.
 The incubation period of is 4 to 15 days.
 Transmission is via respiratory isolates.

Clinical course
 Headaches, coryza, a low-grade fever, 2 -3 days. The exanthema appears after 7 days.
 The first stage: A bright red rash appears on the cheeks ‘‘slapped cheek appearance’‘.
Circumoral pallor also is common. The child is no longer infectious now.
 The second stage: 1 - 4 days after 1st stage, maculopapular rash on the trunk and
extremities. The rash forms a (lacy reticular pattern), pruritic in up to 15%, usually on the
extensor surfaces, The third stage: 1 - 3 weeks, periodic increases in the intensity of the
rash.

Aplastic crises
 In children who have hemolytic anemia, Parvovirus infects erythrocyte precursor cells
resulting in a severe reticulocytopenia that lasts from 7 to 10 days. Reticulocyte production
returns to normal once the infection has resolved.
 Infections during pregnancy have been implicated in causing hydrops fetalis and
miscarriage. The risk is during 2nd trimester.
 Patients who have aplastic crises may require red blood cell transfusions, but the long term
prognosis also is excellent in these cases.

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Scarlet fever
Epidemiology
 Scarlatina, is a relatively common exanthematous disease caused by group A B-hemolytic
streptococci which produce erythrogenic toxin.
 Commonly associated with pharyngitis.
 Group A B-hemolytic streptococci infections in other sites may also cause scarlet fever.

Clinical course
 After the acute onset of fever, sore throat, and constitutional symptoms, the rash appears
12 to 48 hrs.
 Abdominal pain ± vomiting is a helpful diagnostic sign.
 The enanthem typically consists of enlarged beefy red exudative tonsillitis, palatal
petechiae, and a strawberry-resembling tongue.
 The exanthem is a generalized intense orange-red eruption with a rough, sandpaper
texture.
 Other features: smooth, flushed face with striking perioral pallor, and discrete linear
erythema in skin folds called Pastia’s lines.
 Desquamation begins during 1 to 3 weeks.

Diagnosis and treatment

 The diagnosis of scarlet fever is usually based on its characteristic clinical features.
 It may be confirmed with throat culture and increasing antistreptolysin - O titer.
 Without antibiotic treatment, the exanthem lasts four to five days, leaving a fine scale as it
fades.
 Penicillin is the drug of choice (oral or injectable).

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 THANK YOU
Edited by: Zainab Abdul Ghany.

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