vaccination

Dr. Darawshe mohammad

Live attenuated viral vaccins contraindication in immunodeficiency
and in pregnancy.

Live attenuated bacterial vaccins ( BCG) contraindication in

immunodeficiency. )B CELL (
 Vaccine Rules
• For stimulation of an adequate and persisting antibody response, 2 or
more doses are usually required
• No reduced dose or divided dose should be administered, including to
babies born prematurely or at low birth weight (exception: first dose
hepatitis B).
• Live virus vaccine may have diminished immunogenicity when given
shortly before or during the several months after receipt of
immunoglobulin (Ig) so live vaccine is delayed (3–11 months)- MMR.
 Misconceptions
 The following are not contraindications to immunizations:

• A locale reaction to a previous a vaccine ( redness, soreness,

and swelling).
• A mild, acute illness in an otherwise well child
• Concurrent antimicrobial therapy
• Prematurity—immunize at the chronological age
• A family history of seizures
• A family history of sudden infant death syndrome
 Accepted Precautions and
Contraindications
• Minor illness, with or without a fever, does not contraindicate
immunization.

• Fever, per se, is not a contraindication

• If fever or other problems suggest moderate or serious illness,

the child should not be immunized until recovered.

• Documented egg allergy is not a contraindication to the

MMR.
 Hepatitis B
• First dose should be given soon after birth( minimum neonate
weight 2 kg).
• 3 doses by age 6 months if mother is HBsAg negative.
• If (HBsAg)-positive mother > hepatitis B virus (HBV) plus
hepatitis B Ig at 2 different sites within 12 hours of birth.
• All children and adolescents who have not been immunized
should begin the series during any visit to the physician.
 DTaP
• All DTaP vaccines for United States currently contain acellular
pertussis.
• Total of 5 doses is recommended before school entry, with the
final given at preschool age, 4–6 years
• Pertussis booster (Tdap) vaccine is now recommended during
adolescence, regardless of immunization status; is also
recommended even if one has already had pertussis disease.
 Pneumococcal Vaccines
• Pneumococcal conjugate vaccine PCV13 (Prevnar)
• Purified polysaccharides of 13 serotypes
• Routine administration as a 3-dose series for all children age
12 months.
• 23-valent pneumococcal polysaccharide vaccine (PS23)—
(Pneumovax) given as additional protection to the PCV13 in
some high-risk children (e.g., functional/anatomic asplenia/
immunodeficiency/ cochlear implantation/ csf leak). age >2
years.
 Varicella
• Recommended at age 12 months or older for healthy people
who have not had varicella illness, with second dose at age
4–6 years
• May still have breakthrough varicella; milder than
unimmunized, rarely spreads
• Has been associated with the development of herpes zoster
after immunization (rare)
 Varicella
• Give vaccine to susceptible immunocompetent contacts age
>12 months as soon as possible .

• VZIG:
– All immunocompromised
– Susceptible pregnant women.
– Newborn whose mother had the onset of varicella within 5 days
before delivery to 48 hours after delivery,
– Certain hospitalized premature infants
 Influenza Vaccine
• Inactivated influenza vaccine
– Administered intramusculare
– Given annually during flu season for children greater
than 6 months of age .

• Live influenza vaccine:

– Administered intranasally
– Contraindicated in the immunocompromised,
– Given only to healthy people 2–49 years of age who
are not pregnant and do not have certain health
condition
 Rotavirus Vaccine
• Oral live attenuated vaccine
• Given at ages 2, 4, 6 months
• Essentially no catch-up if behind (no dose after age 8 months)
• Safe, highly effective ( contraindication in patient with history
of intususception).
• Reduce severity of gastroenteritis.
• Measles
Post-exposure HEP. A.
Metabolic disease
 CLASSIC PHENYLKETONURIA
• Deficiency of the enzyme phenylalanine hydroxylase (PAH).
• accumulation of phenylalanine in body fluids and in the brain.
• The affected infant is normal at birth Profound intellectual
disability develops gradually if the infant remains untreated.
• Low IQ- autistic behaviors
• The infants are lighter in their complexion than unaffected
siblings.
• seborrheic or eczematoid rash.
• Neurologic signs include seizures (approximately
• 25%), spasticity, hyperreflexia, and tremors.
• Dx- In infants with positive screening results, diagnosis should
be confirmed by quantitative measurement of plasma
phenylalanine concentration.

• Tx- The mainstay of treatment of PKU is a low–phenylalanine

diet.
 Aspartic Acid (Canavan Disease)
• autosomal recessive disorder and is more prevalent in individuals of
Ashkenazi Jewish descent than in other ethnic groups.
• The deficiency of the enzyme aspartoacylase leads to the
accumulation of N-acetylaspartic acid in the brain, especially in
white matter, and massive urinary excretion of this compound.
• Infants usually appear normal at birth and may
not manifest symptoms of the disease until 3-6
mo of age, when they develop progressive
macrocephaly, severe hypotonia, optic atrophy,
seizures, delayed milestones
• CT scan and MRI reveal diffuse white matter degeneration
• The definitive diagnosis can be established by finding
elevated amounts of N-acetylaspartic acid in the urine/
blood/ csf .
• No specific treatment is available.
• Most patients die in the 1st decade of Life- hypotonia/
seizures.
white matter degeneration- canavan.
 Lysosomal Storage Disorders.
• Tay sachs-
• deficiency of β-hexosaminidase activity’
accumulation in CNS.
• being more frequent in the Ashkenazi Jewish
population.
• Affected infants usually develop normally until 4-
5 month of age when decreased eye contact and
an exaggerated startle response to noise
(hyperacusis) . Macrocephaly, loss of motor
skills,
• macular pallor and retinal cherry-red spots
 death occurring by the age of 4 or 5 yr.
• Dx- clinical . Definitive diagnosis is made by
determination of β-hexosaminidase activities
in peripheral leukocytes.
 GAUCHER disease
• It is one of the most common lysosomal storage diseases and
• the most prevalent genetic defect among Ashkenazi Jews.
• acid β-glucosidase deficiency.
• multisystemic lipidosis characterized by hematologic
Abnormalities -bruising from thrombocytopenia, chronic
fatigue secondary to anemia, hepatomegaly with or without
elevated liver function test. splenomegaly, and bone pain,
organomegaly, and skeletal involvement, pathologic
fractures.
• Treatment of patients with Gaucher disease includes enzyme
replacement therapy.
 FABRY DISEASE
• X-linked
• caused by the absent or markedly deficient activity of α-galactosidase A.
• Clinica- Angiokeratomas (telangiectatic skin lesions), hypohidrosis, corneal
and lenticular
• opacities, acroparesthesias, and with advancing age develop vascular
• disease of the kidney, heart, and/or brain.
• Pain is the most debilitating symptom in childhood and adolescence.
• Fabry crises, lasting from minutes to several days, consist of
• agonizing, burning pain in the hands, feet, and proximal extremities and are
usually associated with exercise, fatigue, fever.
• The major morbid symptoms result from the progressive involvement
• of the vascular system- arrhythmias, left ventricular hypertrophy, angina,
• myocardial ischemia or infarction, TIA . Mitral insufficiency is the most common
valvular lesion.
• Tx- enzyme replacement ( Fabrazyme)
Angiokeratoma-
fabry disease.
 Glycogen Storage Diseases
• Type I GSD- Von Gierke Disease is caused by the
absence or deficiency of glucose-6-phosphatase
• activity in the liver, kidney, and intestinal mucosa.
• AR.
• doll-like faces with fat cheeks, relatively thin extremities,
short stature, and a protuberant abdomen that is a
consequence of massive hepatomegaly; the kidneys are also
enlarged.
• The biochemical hallmarks of the disease are hypoglycemia,
lactic acidosis, hyperuricemia, and hyperlipidemia.
Hypoglycemia and lactic acidosis can develop after a short
fast.
• The diagnosis of type I GSD is suspected on the basis of
clinical presentation and the laboratory findings of
hypoglycemia, lactic acidosis, hyperuricemia, and
hyperlipidemia..

• Treatment is designed to maintain normal blood glucose

levels and is achieved by continuous nasogastric infusion of
glucose or oral administration of uncooked cornstarch( slow
release ).
 Type II Glycogen- pompe disease.
• is caused by a deficiency of acid α-glucosidase (acid
maltase).
• autosomal recessive.
• Affected infants present in the first few weeks to
months of life with hypotonia, a
• generalized muscle weakness with a “floppy infant”
appearance, neuropathic bulbar weakness, feeding
difficulties, macroglossia, hepatomegaly, and a
hypertrophic cardiomyopathy followed by death from
cardiorespiratory failure or respiratory infection usually
by 1 yr of age.
• The confirmatory step for a diagnosis of Pompe disease is
enzyme assay demonstrating deficient acid α-glucosidase or
gene sequencing.
• Tx- Recombinant acid α-glucosidase( enzyme replacement) is
capable of preventing deterioration or reversing abnormal
cardiac and skeletal muscle functions.