The slide is about diseases that can be prevented by providing proper vaccines to childrens

1. Vaccine preventable disease

2. MEASLES

3. Measles
• Highly contagious acute viral disease marked
by
– Prodromal fever, cough coryza , and conjuctivitis
– Pathognomonic enanthem – ‘koptoplik
– Erythenatous maculo – papular rash
• Causative agent – measles virus
– RNA virus
– Morbilli-virus genus
– Paramyxoviridae family
• Infection confers life-long immunity

4. Epidemiology
• ~30 million cases reported annually
• Causes one million deaths, and 15,000-60,000
blindness per year
• Most cases in developing countries
• Mortality – most often due to respiratory and
neurologic complications

5. Epidem…
• Risk factors for infection:
– Unimmunized children
– Immunodeficiency states (HIV/AIDS, leukemia,
steroid therapy, etc), regardless of immunization
status
– Loss of passive (maternal) antibodies prior to age
of routine vaccination

6. Epidem…
• Risk factors for severe measles and its
complication:
– Malnutrition
– Immunodeficiency states
– Pregnancy
– Vitamin A deficiency
• Age specific susceptibility –
– Higher in infants and school-age children
• Complications –
– Common in young children

7. Epidem…
• Eradication possible based on:
– Distinctive rash
– No animal reservoir
– No vector
– Seasonal occurrence with disease free intervals
– No transmissible latent virus
– One serotype and
– An effective vaccine
• Herd immunity achieve when > 90% of infants
are immunized

8. Transmission
• By respiratory route, via droplet spray
• Infected child infectious – 1 week before and 5
days after onset of rash
• Infants protected by passive immunity in the
first 4 – 6 month

9. Pathogenesis
• Initial viral replication – in trachea and
bronchial epithelial cells
• After 2 – 4 days local lymphatic tissue infected
• Followed by viremia before appearance of
RASH
• Essential lesions found in:
• Skin, mucous membrane of naso-pharynx, bronchi, intestinal tract
and conjunctiva

10. Clinical manifestations
• Prodromal stage
– Follows an incubation period of 10-12 days
– Lasts 3-5 days
– Characterized by:
• Fever, cough, coryza, conjuctivitis
• Malaise, myalgia, photo-phobia and peri-orbital edema
• With in 2-3 days koplik’s spots appear in buccal mucosa (disappear
with in 12 – 18 hrs)

11. Clinical…
• Maculo-papular stage
– Characterized by:
• High grade fever
• Rash – begins at the hair line posteriorly and spreads
caudally over the next 3 days with resolution of
prodromal symptoms
• Rash lasts 6 days and fades from head downwards
(desquamations may be present)

12. Clinical…
• Complete recovery – usually within 7-10 days from
the onset of rash
• Complications:
– Infectious
• Broncho-pneumonia
• Otitis media
• Laryngo-tracheo-bronchitis (croup)
• Diarrhea
• Reactivation of TB
– Others
• Blindness (corneal ulceration), hepatitis, encephalitis, sub acute
sclerosing pan encephalitis (SSPE), myocarditis, peri carditis and
thrombocytopenia

13. Laboratory investigation
• Unnecessary, given the classic manifestations

14. Management
• Hydration
• Antipyretics
• Antibiotics (for secondary bacterial infection)
• Vitamin A (therapeutic dose)
• Admission for those with severe complications

15. Prevention
• Isolation – for infectious period
• Routine immunization
• National Immunization Days (NIDs)
• Mop-up Immunization campaigns

16. Chickenpox
• Primary infection caused by varicella-zoster
virus (VZV)
– VZV is a neurotropic human herpesvirus
• Results in establishment of a lifelong latent
infection of sensory ganglion neurons
• Reactivation of the latent infection causes
herpes zoster (shingles).

17. Transmission
• VZV is transmitted in:
– Air born spread of respiratory secretions
– Direct contact with fluid of skin lesions
– Transplacental- neonatal chicken pox
• Period of infectivity - from 24 to 48 hr before the
rash appears and until vesicles are crusted,
usually 3–7 days after onset of rash
• Incubation period -10–21 day
• Infection confers life long immunity

18. PATHOGENESIS
• Inoculation of the virus onto the mucosa of the upper
respiratory tract and tonsillar lymphoid tissue→ virus
replicates in the local lymphoid tissue → subclinical
viremia (1 ry viremia) to reticuloendothelial system→
2nd viremic phase that lasts 3–7 days→ Widespread
cutaneous lesions and organ involvement
• Host immune responses limit viral replication and
facilitate recovery
• The virus establishes latent infection in the sensory
ganglion neurons→ Reactivation→ Herpes zoster

19. Clinical features
• The illness usually begins 14–16 days after
exposure, although the incubation period can
range from 10 to 21 days.
• Prodromal symptoms may be present,
particularly in older children and adults.
– Fever, malaise, anorexia, headache, and occasionally
mild abdominal pain may occur 24–48 hr before the
rash appears.
• fever and other systemic symptoms persist
during the 1st 2–4 days after the onset of the
rash

20. • lesions often appear first on the scalp, face, or
trunk
• Starts as macule → papule → vesicle and pustule
→ crusts
• Pruritic
• Occurs in crops- characteristics
• While the initial lesions are crusting, new crops
form on the trunk and then the extremities;
– the simultaneous presence of lesions in various stages
of evolution is characteristic of varicella
• distribution of the rash is predominantly central
or centripetal
• Subclinical varicella is rare; almost all exposed,
susceptible persons experience a rash

24. Complications
• Secondary skin infection
• Encephalitis, cerebellar ataxia,
• Pneumonia,
• Hepatitis, glomerulonephritis
• Myocarditis, pericarditis,

25. Treatment
• Supportive
• Isolate the diseased until the rash crusts.
• Acyclovir
• Antihistamines may be used to help relieve
the itching.

26. Prognosis
• Good for healthy children
• Poor for immunocompromized, neonates

27. Prevention
• Isolation
• Post exposure prophylaxis
– Vaccine within 3-5 days after exposure
– varicella-zoster immune globulin -administered
intramuscularly within 96 hr of exposure
• Active immunity
• Newborns whose mothers develop varicella 5
days before to 2 days after delivery should
receive 1 vial of VariZIG

28. Mumps

29. • Mumps is an acute self-limited infection
• It is characterized by fever, bilateral or
unilateral parotid swelling and tenderness,
and the frequent occurrence of
meningoencephalitis and orchitis.

30. ETIOLOGY
• Mumps virus is in the family Paramyxoviridae
and the genus Rubulavirus
• Mumps virus exists as a single immunotype,
and
• humans are the only natural host.

31. Transmission
• 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.
– The period of maximum infectiousness is 1–2 days
before to 5 days after parotid swelling.
• Viral shedding before onset of symptoms and in
asymptomatic infected individuals impairs efforts
to contain the infection in susceptible
populations.

32. PATHOGENESIS.
• Following infection, 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 targets the salivary glands,
central nervous system (CNS), pancreas,
testes, and, to a lesser extent, thyroid, ovaries,
heart, kidneys, liver, and joint synovia.

33. CLINICAL MANIFESTATIONS
• The incubation period: ranges from 12 to 25
days, but is usually 16 to 18 days.
• Mumps virus infection may result in clinical
presentation ranging from asymptomatic or
nonspecific symptoms to typical illness
associated with parotitis with or without
complications involving several body systems.
• The typical case presents with a prodrome
lasting 1–2 days consisting of fever, headache,
vomiting, and achiness.

34. • Parotitis then appears and may be unilateral
initially but becomes bilateral in about 70% of
cases
– The parotid gland is tender, and parotitis may be
preceded or accompanied by ear pain on the
ipsilateral side.
– The parotid swelling peaks in approximately 3
days then gradually subsides over 7 days.
– Fever resolves in 3 to 5 days along with the other
systemic symptoms.

37. Diagnosis
• When mumps was highly prevalent, the
diagnosis could be made based on history of
exposure to mumps infection, an appropriate
incubation period, and development of typical
clinical findings

38. • Today, in patients with parotiditis of >2 days of
unknown cause, a specific diagnosis of mumps
should be confirmed or ruled out by virologic or
serologic means. This may be accomplished by
– Isolation of the virus in cell culture, detection of viral
antigen
• Virus can be isolated from upper respiratory tract
secretions, CSF, or urine during the acute illness.
– Serologic testing is usually a more convenient and
available mode of diagnosis.
• A significant increase in serum mumps immunoglobulin G
(IgG) antibody between acute and convalescent serum
specimens

39. Complications
• Orchitis and Oophoritis.
Orchitis
– It begins within days following onset of parotitis in the
majority of cases and
– is associated with moderate to high fever, chills, and
exquisite pain and swelling of the testes.
– In ≤⅓ of cases the orchitis is bilateral.
– Atrophy of the testes may occur, but sterility is rare
even with bilateral involvement.
Oophoritis is uncommon in postpubertal females but
may cause severe pain and when on the right side it
may be confused with appendicitis.

40. Meningitis and Meningoencephalitis.
• Mumps virus is neurotropic and is thought to enter
the CNS via the choroid plexus
• The meningoencephalitis may occur before, along
with, or following the parotitis.
– It most commonly will present 5 days after the parotitis.
• Clinical findings vary with age.
– Infants and young children will have fever, malaise, and
lethargy, while
– Older children, adolescents, and adults will complain of
headache and demonstrate meningeal signs.
• In typical cases, symptoms resolve in 7–10 days.

41. • Pancreatitis
• Cardiac Involvement.
• Arthritis.
– usually occurs within 3 weeks of onset of parotid
swelling.
– It is generally mild and self-limited.
• Thyroiditis.

42. TREATMENT.
• No specific antiviral therapy is available for
mumps.
• Management should be aimed at:
– reducing the pain ,adequate hydration.
– Antipyretics may be given for fever

43. PROGNOSIS.
• The outcome of mumps is nearly always
excellent, even when complicated by
encephalitis, although fatal cases due to CNS
involvement or myocarditis have been
reported.

44. PREVENTION.
• Immunization with the live mumps vaccine is
the primary mode of prevention
• Immunity appears to be long lasting, with
existing serologic and epidemiologic evidence
indicating protection for >25 yr

45. Rubella

46. 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
• Humans are the only known host

47. • Transmission by:
– Respiratory droplets
– Transplacental- result in CRS
• Natural infection confers lifelong immunity

48. PATHOGENESIS
• The viral mechanisms for cell injury and death in
rubella are not well understood for either
postnatal or congenital infection.
• Following infection the virus replicates in the
respiratory epithelium then spreads to regional
lymph nodes
• The period of highest communicability is from 5
days before to 6 days following appearance of the
rash.

49. • 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.
– Defects occurring after 16 wk of gestation are
uncommon, even if fetal infection occurs

50. CLINICAL MANIFESTATIONS
• Postnatal infection with rubella is a mild disease
– 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.
– In children, the 1st manifestation of rubella is
usually the rash, which is variable and not
distinctive
• It begins on the face and neck as small, irregular pink
macules that coalesce, and it spreads centrifugally to
involve the torso and extremities, where it tends to occur
as discrete macules

51. • The rash fades from the face as it extends to
the rest of the body so that the whole body
may not be involved at any 1 time.
• The duration of the rash is generally 3 days,
and it usually resolves without desquamation.
• Subclinical infections are common, and 25–
40% of children may not have a rash.

53. 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

54. DIFFERENTIAL DIAGNOSES
• It is frequently confused with other infections
• In severe cases it may resemble measles.
– The absence of both Koplik spots and a severe
prodrome as well as a shorter course allow for
differentiation from measles.

55. COMPLICATIONS
• Post infectious thrombocytopenia
• Arthritis
• Encephalitis

56. Congenital Rubella Syndrome
• Affects all organ system
• Infant presents with:
– Deafness
– Cataracts
– Congenital Heart disease-PDA-the most common
– Low birthweight
– Mental retardation

57. TREATMENT
• There is no specific treatment available for
either acquired rubella or CRS.
• SUPPORTIVE CARE.
– Antipyretics and analgesics
• PROGNOSIS.
– Postnatal infection with rubella has an excellent
prognosis.
– Long-term outcomes of CRS are less favorable and
somewhat variable.

58. PREVENTION
• Patients with postnatal infection should be
isolated from susceptible individuals for 7 days
after onset of the rash.
• Children with CRS may excrete the virus in
respiratory secretions up to 1 yr of age and
should be maintained in contact precautions until
then unless repeated cultures of urine and
pharyngeal secretions are negative
• Vaccination- MMR

59. Thank You