The document discusses the highly contagious viral diseases, measles and rubella, detailing their causative viruses, clinical presentations, and associated complications. It emphasizes the importance of vaccination to maintain high immunity levels and mitigate outbreaks, while describing the pathophysiology, symptoms like the characteristic rashes, and diagnostic criteria. Additionally, it addresses other conditions like varicella, including their transmission, treatment options, and the significance of supportive care for affected individuals.

2.  An acute viral disease
 Highly contagious
 Measles virus is a single-stranded, lipid-enveloped
RNA virus in the family Paramyxoviridae and
genus Morbillivirus
 Humans are the only host of measles virus
 Maintenance of >90% immunity through vaccination-
NO OUTBREAKS

3.  Necrosis of the respiratory tract epithelium & an
accompanying lymphocytic infiltrate
 Small vessel vasculitis on the skin and on the oral
mucous membranes
 Warthin-Finkeldey giant cells: pathognomonic for
measles, formed by fusion of infected cells, with up
to 100 nuclei and intracytoplasmic and intranuclear
inclusions
 Measles virus also infects CD4+ T cells, resulting in
suppression of the Th1 immune response

4.  4 phases:
Incubation period
Prodromal illness
Exanthematous phase
Recovery

5. Incubation period: measles virus migrates to
regional lymph nodes primary viremia-
disseminates the virus to the
reticuloendothelial system secondary
viremia spreads virus to body surfaces
The prodromal illness begins after the
secondary viremia; associated with epithelial
necrosis, giant cell formation & virus shedding
With onset of the rash, antibody production
begins & viral replication & symptoms begin to
subside

6.  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 3-4 days before to up
to 4-6 days after the onset of rash

7.  High fever, an enanthem, cough, coryza,
conjunctivitis & a prominent exanthem
 Incubation period: 8-12 days
 Prodromal phase: mild fever, conjunctivitis with
photophobia, coryza, a prominent cough and KOPLIK’S
SPOTS
 Koplik spots: enanthem & the pathognomonic sign of
measles
 Appear 1 to 4 days prior to the onset of the rash
 Discrete red lesions with bluish-white spots in the
center on the inner aspects of the cheeks at the level
of the premolars

8.  Koplick’s spots: spread
to involve the lips,
hard palate & gingiva
 They also may occur
in conjunctival folds

9.  Temperature rises abruptly as rash appears & may
reach upto 40OC
 Measles rash: generalized, maculopapular,
erythematous, confluent
 The rash begins on the face around
the hairline & behind the ears
 It then spreads downward
to the neck, trunk, arms, legs
and feet over next 24-48 hours

10.  The rash fades over about 7 days in the same
progression as it evolved
 Leaves a fine, browny, branny desquamation of skin
 Severity of disease: related to the extent and
confluence of rash
 Rash: may be absent in immuno-compromised
children
 Hemorrhagic measles (black measles): bleeding from
mouth, nose or bowels

11.  Diarrhoea: more common in malnourished and small
children
 Severe cases: generalized lymphadenopathy
including cervical & mesenteric lymph nodes
 Mild splenomegaly

12.  Almost always based on clinical and epidemiologic
findings (history of contact)
 Fever of at least 3 days with at least one of three C
(cough, coryza, conjuctivitis)
 Decreased total white blood cell count, with relative
lymphocytosis

13.  IgM antibody in serum: appears 1-2 days after the
onset of the rash & remains detectable for about
1 mo
 Demonstration of a fourfold rise in IgG antibodies in
acute & convalescent specimens collected 2-4 wk
later
 Viral isolation from blood, urine or respiratory
secretions by culture or rt-PCR

14.  Rubella-rashes & fever are less striking
 Roseola infantum (exanthem subitum)- rash appear
as the fever disappears
 Echovirus
 Coxsachie
 Adenovirus
 Infectious mononucleosis
 Scarlet fever-diffuse fleshy papular rash with
“goose flesh” texture

15.  Meningococcemia-rashes are similar but NO
conjuctivitis & cough
 Kawasaki disease- no cough, elevations of
neutrophils and acute-phase reactants; the
characteristic thrombocytosis
 Drug fever

16.  Due to the pathogenic effects of the virus on the
respiratory tract and immune system
Risk factors for complications
 Children <5 years of age & adults >20 years of age
 Severe malnutrition
 Vitamin A deficiency
 Immuno-compromised persons

17.  Pneumonia- giant cell pneumonia (direct viral
infection) or super-imposed bacterial infection
(Streptococcus pneumoniae, Haemophilus
influenzae & Staphylococcus aureus)
 Croup, tracheitis or bronchiolitis
 Acute otitis media
 Sinusitis and mastoiditis
 Retropharyngeal abscess
 Activation of pulmonary tuberculosis

18.  Diarrhea & vomiting
 Appendicitis- obstruction of the appendiceal lumen
by lymphoid hyperplasia
 Febrile seizures
 Encephalitis- 1-3/1,000 cases of measles;
postinfectious, immunologically mediated process,
not due to a direct viral effect

19.  Measles encephalitis in immunocompromised
patients-from direct damage to the brain by the
virus
 Thrombocytopenia
 Myocarditis
 Bacteremia, cellulitis & toxic shock syndrome
 Measles during pregnancy-high maternal morbidity,
fetal wastage & stillbirths & congenital
malformations in 3% of live born infants

20.  Fatal degenerative disease of central nervous
system
 Chronic complication of measles
 Result from a persistent infection with an altered
measles virus that is harbored intracellularly in the
CNS for several years
 Usually after 7-10 year the virus apparently regains
virulence & attacks the cells in the CNS
 Change in personality, gradual onset of mental
deterioration and myoclonus
 Measles vaccination protects against SSPE

21.  SUPPORTIVE
 Maintenance of hydration, oxygenation and comfort
 Antipyretics-comfort and fever control
 Vitamin A supplementation-reduced morbidity and
mortality from measles
 Single dose of 200,000 IU orally for children
≥1 yr of age (100,000 IU for children 6 mo–1 yr
of age and 50,000 IU for infants <6 mo of age)

22.  Isolation- from 7 days after exposure to 4-6 days
after the onset of rash
 Vaccine or immunoglobulin- vaccine is effective in
prevention or modification of measles only if given
within 72 hr of exposure. Immune globulin may be
given up to 6 days after exposure to prevent or modify
infection.
 Immune globulin-for susceptible household contacts
younger than 6 months of age, pregnant women and
immunocompromised persons
 Immunization during an outbreak-immunize infant as
young as 6 months of age; additional dose at 12-15
months of age

23.  Rubella (German measles or 3-day measles)
 Mild exanthematous disease of infants and children
 Major clinical significance- fetal damage as part of
the congenital rubella syndrome
 Etiology: Rubella virus; RNA virus of genus Rubivirus
under family Togaviridae
 Humans are the only known host.

24.  Transmission-through oral droplet or transplacental
route
 Virus is shed in nasopharyngeal secretions 7 days
before exanthem & upto 7-8 days after its
disappearance
 Rubella susceptibility among women of child bearing
age in India- 4%-43%

25.  Infection virus replication in the respiratory
epithelium spreads to regional lymph nodes
viremia viral shedding from the nasopharynx
 Cellular and tissue damage in the infected fetus:
tissue necrosis, reduced cellular multiplication time,
chromosomal breaks & production of a protein
inhibitor causing mitotic arrests
 Most distinctive feature of congenital rubella:
chronicity
 Ongoing tissue damage and reactivation

26.  Risk factor for severe congenital defects: stage of
gestation at the time of infection
 Maternal infection during the 1st 8 wk of gestation:
most severe & widespread defects
 Risk for congenital defects: 90% for maternal
infection before 11 wk of gestation, 33% at 11-
12 wk, 11% at 13-14 wk & 24% at 15-16 wk
 After 16 wk of gestation: defects uncommon

27. POSTNATAL INFECTION
 Incubation period: 14-21 days
 Prodrome: low-grade fever, sore throat, red eyes
with or without eye pain, headache, malaise, anorexia
& lymphadenopathy (suboccipital, postauricular &
anterior cervical lymph nodes)
 Rash: begins on the face & 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

28.  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 & it
resolves without desquamation

29.  About the time of onset of the rash, examination of
the oropharynx- reveal tiny, rose-colored lesions
(Forchheimer spots) or petechial hemorrhages on the
soft palate
 Subclinical infections are common (25-40%)
 Polyarthritis or arthralgia-common in adult females
 Lab findings: Leukopenia, neutropenia & mild
thrombocytopenia

30.  Mild form of measles
 Scarlet fever
 Roseola infantum
 Enteroviral infections
 Drug fever
 Infectoius mononucleosis
 Erythema infectiosum

31.  Supportive history of exposure or consistent clinical
findings
 Rubella specific IgM enzyme immunosorbent assay (4-
72 days)
 Fourfold rise in IgG in sequential sera
 Rubella virus culture from nasopharynx & blood by
tissue culture system or PCR
 WHO definition of PROBABLE infection: fever,
maculopapular rash, lymphadenopathy or
arthralgia/arthritis
 WHO definition of CONFORMED infection: probable
case with IgM positivity within 28 days of onset of rash

32.  Postinfectious thrombocytopenia
 Arthritis- classically involves the small joints of the
hands
 Encephalitis-a postinfectious syndrome following
acute rubella & a rare progressive panencephalitis
manifesting as a neurodegenerative disorder years
following rubella
 Guillain-Barré syndrome, peripheral neuritis
 Myocarditis

33.  Result of in utero fetal infection
 Classical CRS triad: cataract, sensorineural hearing
loss and congenital heart disease
Clinical manifestations:
 Intrauterine growth restriction, postnatal mental and
motor retardation
 Bilateral/unilateral cataract, salt-and-pepper
retinopathy, microphthalmia
 Nerve deafness
 Meningoencephalitis at birth

34.  Patent ductus arteriosus, pulmonary artery stenosis,
VSD & ASD, myocarditis
 Hepatitis
 Dermal erythropoiesis (blueberry muffin lesions)
 Thrombocytopenic purpura
 Anemia
 Hepatosplenomegaly
 Microcephaly
 Interstitial pneumonitis
 Delayed manifestations: Diabetes mellitus (20%),
thyroid dysfunction (5%)

35.  No specific treatment available for either acquired
rubella or CRS
 Supportive treatment- antipyretics and analgesics
 Intravenous immunoglobulin or corticosteroids-for
severe, nonremitting thrombocytopenia
 Hearing screening- important, early intervention
improve outcomes

36. Management of exposed pregnant women
 Rubella antibody status is tested immediately
result positive mother is immune no further
action
 Rubella antibody status negative repeat samples
after 1-2 weeks negative 1st specimen & positive
test result in either the 2nd or 3rd specimen
seroconversion suggesting recent infection
termination of pregnancy

37. Management of congenital rubella syndrome
 Children with CRS may excrete the virus in
respiratory secretions up to 1 yr of age
 Isolation & contact precautions maintained unless
repeated cultures of urine and pharyngeal secretions
have negative results
 Isolation at home my be required for 1 year
 Care of CRS infants require multidisciplinary team
 Prognosis poor
 PREVENTION by IMMUNIZATION

38.  Varicella is an acute febrile rash illness
 Caused by VZV which is a neurotropic human α-
herpesvirus
 Secondary attack rate: 90%
 Transmission: by airborne spread or through direct
contact with skin lesions
 Varicella results from inoculation of the virus onto the
mucosa of the upper respiratory tract and tonsillar
lymphoid tissue

39. Incubation period (10-21 days): replication
in the local lymphoid tissue primary
viremia-disseminates the virus to the
reticuloendothelial system secondary
viremia spreads virus to body surfaces
leading to widespread cutaneous lesions
During the late incubation period-VZV
transported back to the mucosa of the upper
respiratory tract & oropharynx, permitting
spread to susceptible contacts 1-2 days
before the appearance of rash
Host immune responses limit viral replication
and facilitate recovery from infection
Immunocompromised child-continued viral
replication -disseminated infection

40.  Transportation of virus in a retrograde manner
through sensory axons to the dorsal root ganglia
throughout the spinal cord establishment of
virus latent infection in the neurons
subsequent reactivation
herpes zoster, a vesicular rash that usually is
dermatomal in distribution

41.  Prodromal symptoms: fever (moderate), malaise,
anorexia, headache and occasionally mild abdominal
pain, 24-48 hours before the rash appears
 These symptoms resolve within 2-4 days after the
onset of the rash
 Varicella rash often appear first on the scalp, face, or
trunk
 The initial exanthem consists of intensely pruritic
erythematous macules that evolve through the papular
stage to form clear, fluid-filled vesicles
 Clouding & umbilication of the lesions begin in 24-
48 hr

42.  While the initial lesions are crusting, new crops form
on the trunk & then the extremities
 The simultaneous presence of lesions in various
stages of evolution is characteristic of varicella
 The distribution of the rash is predominantly central
or centripetal
Pearl on a rose patel

43.  The average number of varicella lesions is about 300
(10-1500)
 Hypopigmentation or hyperpigmentation of lesion sites
persists for days to weeks in some children
 Severe scarring is unusual unless the lesions were
secondarily infected

44. Vesicular rashes caused by
 Herpes simplex virus
 Enterovirus
 Rickettsial pox
 S. aureus
 Drug reactions
 Contact dermatitis
 Insect bites

45.  CLINICAL
 Leukopenia during the 1st 72 hours after onset of
rash; followed by a relative & absolute lymphocytosis
 Elevated hepatic enzymes
 Specific diagnosis of VZV infection: needed in
immunocompromised children

46.  Mild thrombocytopenia, petechiae (common); purpura,
hemorrhagic vesicles, hematuria & gastrointestinal
bleeding (rare)
 Cerebellar ataxia, encephalitis, Guillian-Barre
syndrome, transverse myelitis
 Pneumonia
 Nephritis, nephrotic syndrome, hemolytic-uremic
syndrome
 Arthritis
 Myocarditis, pericarditis
 Pancreatitis

47.  Orchitis
 Secondary bacterial infections of the skin (group A
streptococci & S. aureus): impetigo, cellulitis,
lymphadenitis & subcutaneous abscesses; varicella
gangrenosa- more invasive skin infections

48.  In infants born to women who have varicella before
20 wk of gestation
Characterized by
 Cicatricial skin scarring in a zoster-like distribution,
limb hypoplasia
 Neurologic abnormalities: microcephaly, cortical
atrophy, seizures & mental retardation
 Eye abnormalities: chorioretinitis, microphthalmia &
cataracts
 Renal abnormalities: hydroureter & hydronephrosis
 Autonomic nervous system abnormalities: neurogenic
bladder, swallowing dysfunction & aspiration pneumonia

49.  If a baby is born <4 days after onset of maternal
varicella or upto 2 days before the onset: high risk
for severe varicella & a high mortality rate

50.  Supportive treatment for fever & itching
Indications for acyclovir in children:
 Malignancies
 BMT
 Chmotherapy or high dose steroid treatment
 HIV infection
 Severe varicella
 Chronic skin disease
 Long term salicylate therapy
 Chlidren >12 years
Treatment should be initiated within 24 hr of the
onset of rash

51.  Foscarnet is the only drug for the treatment of
acyclovir-resistant VZV infections (in children infected
with HIV)