Good lecture

1. Dr Lawrence T. MBUAGBAW,
MBChB(Makerere), FRCP(Edin. & Glasg.),
DTCH(Liverpool), FWACP
Consultant Paediatrician

2. - AETIOLOGY
- Measles virus- single stranded RNA virus of family
Paramyxoviridae and genus Morbillivirus.
Epidemiology
- Wide spread vaccination coverage has led to
decreased endemic transmission ( Note recent
epidemic in the Far North with 20 fatalities and in
other parts of the country).
- Improved healthcare and nutrition have led to a
decrease in morbidity and mortality.Note recent
epidemics in the US and Europe.` `` `-1

3. a) Droplet infection
b) Patients are infectious 3 to 4 days
before the rash and 4 to 6 days after
onset.
C) Portal of entry – respiratory tract or
conjunctivae.
D) 90% of exposed individuals develop
measles.
E) 20% in doctors offices and in hospitals

4. Necrosis of respiratory tract epithelium-
lymphocyte infiltrate plus small vessel
vasculitis of the skin and oral mucous
membrane.
Warthin Finkeldey giant cells are
pathognomic.

5. IP- 8 to 12 days
Prodromal illness
Exanthematous phase
Recovery
Measles virus infects CD4 T cells leading
to immunosuppressive effects.

6.  Measles is characterised by a high fever and
enanthem- cough, coryza, conjunctivitis and a
prominent exanthem.
 IP- 8 to 12days- prodromal stage with mild
fever, conjunctivitis, photophobia, prominent
cough and a high fever.
 Enanthem- Koplik’s spots are pathognomic.
They appear 1 to 4 days before onset of rash
(on the inner aspects of the cheek and may
spread to involve the lips, hard palate and
gingivae. They are present in 50 to 70% of
cases.

7.  2 to 4 days a rash (around the hairline)
behind the ears and on the upper neck as
maculopapular rash to torso then palms and
soles in 50% of the cases. As rash increases,
there is a decrease in symptoms. Rash fades
over 7days as it evolves leading to fine
desquamation.
 Cough last longest up to 10days
 Severe cases- lymphadenopathy especially
cervical and occipital lymph nodes.
 Vaccinated individuals may develop a rash
but few other symptoms.

8. Decreased WBC particularly lymphocytes
Normal ESR and CRP

9. Serologic confirmation- IgM antibody
appears 1-2 days after the onset and
remains detectable for about 1 month after
onset.
4 times increase in IgG Antibodies in
acute and convalescent specimens taken
2 to 4 weeks later.
Viral isolation- blood, urine or respiratory
secretions
PCR- research tool

10. Exanthematous illnesses - rubella,
enterovirus, adenovirus, EBV infection.

11. Related to:
 Overcrowding
 Severe malnutrition
 Low serum retinol levels leading to increased
vitamin A deficiency blindness and mortality
 Giant cell pneumonia caused by direct viral
infection or superimposed bacterial infection- S.
pneumoniae, H. influenzae, S. aureus.
 Bronchitis obliterans
 Croup, tracheitis, bronchiolitis
 Sinusitis and mastoiditis
 Activation of latent TB

12.  GIT plus appendicitis
 Febrile seizures in less than 3% of children
 Encephalitis- lethargy, coma, irritability, coma
and seizures leading to mental retardation,
motor disabilities and deafness.
 Hemorrhagic or black measles- hemorrhagic
skin eruption, keratitis, thrombocytopenia
usually fatal.
 Myocarditis
 Conjunctivitis (bacterial)
 Pregnancy – fetal wastage, stillbirths and
congenital malformation in 3% life born
infants.

13. Chronic complication of measles with
delayed onset and fatal outcome.
Result from infection from altered measles
virus that is harboured intracellularly.
After 7- 10 years the virus regains
virulence and attacks the cells of the CNS
Rare disease
M>F 2:1

14. 7-13 years after measles infection
Subtle changes in behaviour or school
performance- irritability, reduced attention
span or temper outbursts
Fever, myoclonus, involuntary
movements, choreoathetosis, immobility,
dystonia, dementia, stupor, coma and
death

15. Measles antibody in CSF
EEG findings
Isolation of virus or viral antigens in brain
tissue-postmortem or biopsy

16. Supportive
Oral isoprinosine
IV interferon alpha 2b

17. Supportive- hydration, oxygenation,
antipyretics
Vitamin A
Immunocompromised patients- Ribavirin
and/or IV immunoglobulin

18. Dr Lawrence T. Mbuagbaw,
MBChB(Makerere), FRCP(Edinburgh), FRCP(Glasgow),
DTCH(Liverpool), FWACP
Consultant Paediatrician
Senior Lecturer, Faculty of Health Sciences, UB
8/10/2023

19. 8/10/2023
i. Benign communicable exanthematous disease
ii. Caused by the rubella virus, a member of the
togoviridae family
iii. Clinical manifestations and severity vary with age
i. Young children- mild constitutional symptoms ,rash and
sub occipital adenopathy.
ii. Older children, adolescents and adults-complicated by
arthralgia, arthritis and thrombocytopenic purpura
iii. Rarely in children- encephalitis
iv. Teratogenic effects especially when pregnant women
contact the disease in the early weeks of pregnancy =>
transmission through the placenta causes severe
congenital defects, abortions and still births.
v. Successful vaccination with the MMR vaccine has
drastically reduced the number of cases of congenital
rubella syndrome

20. 8/10/2023
A. POST NATAL RUBELLA
i. Droplet infection from the nasopharynx
ii. IP 14-21 days
iii. Prodromal symptoms are unusual in young children
but are common in adolescents and adults 1-5/7
before the rash
a. Eye pain on lateral or upward eye movement
b. Conjunctivitis
c. Sore throat
d. Headache
e. General body aches
f. Low grade fever, chills
g. Anorexia, nausea
h. Tender lymphadenopathy( posterior auricular and sub-
occipital)
i. FORCHEIMER SIGN( exanthem observed in the soft
palate, pinpoint or large petechiae

21. 8/10/2023
a) RASH- rose pink maculopapular rash,
can be pruritic( in adults) starts initially on
the face and neck and spreads to the
trunk and extremities within 24hrs. Begins
to fade and disappears by the 3rd day(3
day measles)
b) Temperature- 38.5 degrees C
c) Lymph nodes
d) Mouth- FORCHEIMER SIGN red papules
on soft palate

22. 8/10/2023
I. SENSORINEURAL HEARING LOSS in
58% of patients, may be unilateral or
bilateral
II. OCULAR ABNORMALITIES: cataract,
infantile glaucoma and pigmentary
retinopathy in 43% of patients. Both eyes
are affected in 80% of patients
III. CONGENITAL HEART DISEASE
I. PDA
II. Pulmonary artery stenosis in 50% of patients.
Cardiac defects and deafness occur in all infants
affected during the first 10/52 of pregnancy.

23. 8/10/2023
Other findings
• Intrauterine growth restriction, prematurity, still
birth and abortion
• CNS abnormalities- mental retardation, behavioral
disorders, hypotonia, meningoencephalitis and
microcephaly
• Hepatosplenomegaly
• Jaundice
• Hepatitis
• Skin and bone lesions
• Endocrine(late)- thyroid disorders and diabetes
mellitus
• Anemia and thrombocytopenic purpura

24. 8/10/2023
i. VIRAL INFECTIONS – Herpes virus 6,
measles, parvovirus B19, CMV,
enterovirus, EBV
ii. Contact dermatitis
iii. Mycoplasma infection
iv. Syphilis
v. Toxoplasmosis

25. 8/10/2023
a. LABORATORY
a. Rubella specific IgM antibodies or
b. > 4 fold rise between acute and convalescent
sera drawn 2-3/52 apart of rubella- specific IgG
c. Others- ELISA, CFT, latex agglutination
d. Rubella viral cultures- urine, CSF, nasopharynx,
blood(buffy coat)
e. FBC, LFT

26. 8/10/2023
i. Supportive
ii. Antihistamine(pruritus)
iii. NSAIDS(arthritis)
iv. IV IG(thrombocytopenia)
v. Multidisciplinary for congenital rubella
syndrome

27. I) Both caused by the same virus (double
stranded DNA virus)
II) Varicella a primary disease of childhood
may affect adults in the tropics( cases in
Nigeria)
III) No known animal reservoir exists
IV) High degree of contagiousness ( 80-90% of
exposed susceptible are infected)
V) Contagious 1-2/7 before rash and 3-7/7
after ( rash encrustation)

28. I) H/o contact 10-20/7 prior to onset.
II) Usually no prodrome but mild febrile
illness with rhinitis 1-3/7 before rash is
occasionally noticed.
III) Transmission – respiratory secretions,
fluids + direct contact

29. a) Abrupt onset of pruritic rash on the scalp, face or
trunk which appears in CROPS. Faint erythema
macules papules  vesicles- thin walled and
located superficially on the skin with a distinct
AREOLA.
b) They rupture easily– rapidly ENCRUST and
frequently become IMPETIGINIZED.
c) Successive crops appear next 2-5/7
PLEOMORPHIC appearance of rash
d) Rash heaviest on the trunk and sparse in the
extremities (CENTRIPETAL)
e) BARRING bacterial infection crusts fall off in 1-3/52
leaving no scars.
f) Systemic symptoms mild to severe (fever)

30. DEVIATION
a) From few vesicles 5 successive crops involving
most of the skin
b) Rarely HAEMORRHAGIC lesions associated with
THROMBOCYTOPENIA
c) ZOSTER-LIKE cluster of lesions
d) BULLOUS AND GANGRENOUS FORMS.
ENANTHEM– shallow mucosal ulceration of posterior
pharynx or oesophagus involved difficult and painful
swallowing.
Differential Diagnosis.
i) Small pox (severe prodrome, centrifugal distribution
hard pearly nodular deep seated rash
ii) Coxsackie
iii) Impetigo
iv) Dermatitis herpetiformis
v) Insect bites
vi) Drug reactions

31. I) Uncommon
II) Secondary bacterial infection if lesions are manipulated–
abscesses, lymphangitis, septicaemia, osteomyelitis etc
III) Pneumonia- rare in children except in severe generalised forms
of the disease neonatal period or malignancy and immune
suppressive drug therapy 1st week of rash and cough,
dyspnoea, tachypnoea, pain, cyanosis, rales, splinting. CXR
diffuse bilateral nodular infiltrate
IV) Newborn mild extensive visceral involvement –use of varicella
zoster immune globulins + vaccination( live attenuated VZV
vaccine) for prophylaxis and prevention
V) Fatal hypoglycaemia
VI) Reye’s syndrome
VII) Hepatitis
VIII) Encephalitis, cerebellar ataxia
IX) Rare complications– transverse myelitis, optic neuritis, orchitis

32. i) SYMPTOMATIC– fluids, antihistamines(
calamine lotion), antipyretics( avoid aspirin
risk of Reye’s syndrome)
ii) Treat infections-local or systemic therapy
VARICELLA IN VACCINATED INDIVIDUALS
MONOVALENT VACCINE
I) Effectiveness is 80%-MMRV or routine 12-
18/12 of age and 4-6yrs
II) Rash is atypical
III) Mild illness
IV) Little or no fever and less contagious

33. a) If mother has varicella 5/7 before and 2/7 after delivery– give
VZV immune globulin
b) Preterm baby < 28/52 gestation give immune globulin above
+ acyclovir 10mg/kg every 8hrs when lesions develop
c) Severe varicella- treat with acyclovir 500mg/m2 tds x7/7
CONGENITAL VARICELLA
I) About 25% of fetuses infected; clinical disease is
uncommon
II) 2% of fetuses whose mothers are infected in the 1st 10/52
of pregnancy  VZV embryopathy  cicatrical skin lesions
hypopigmentation—optic stalk + lens ---encephalitis---
lumbosacral cord damage

34. HERPES ZOSTER(SHINGLES)
* Caused by reactivation of the varicella
zoster virus(VZV) which may remain latent
in the dorsal root and cranial nerve ganglia
for decades.
* Stress and immunosuppression increase
the risk of reactivation.


35.  CLINICAL
i) Mild symptoms -fever,anorexia and lassitude
ii) unilateral dysesthesia 1-3days before rash.
iii)RASH=clusters of grouped papules.Papulo
vesicles,vesicles or eruptions or
 urticarial-like papules in a dermatome ±
secondary infections in elderly patients.
i) Herpes zoster infection remains infectious for
2-3weeks until all the vesicles and pustules
have evolved into crusted plaques.

36.  Diagnosis:
 1.insect bites 2.urticaria 3.herpes simplex virus infections
4.cellulitis
 )Direct fluorescent Antibody(DFA)

 TREATMENT
i) 7 day course of ACYCLOVIR, VARACYCLOVIR or
FAMCICLOVIR.
ii) Anti virals may reduce duration of post herpetic neuralgia
.Treatment- with local lidocaine patches
iii) Anticonvulsants antidepressants and antipsychotic agents.
iv) Antivirals
(a) ophthalmic herpes zoster affects ophthalmic division of Vth
cranial nerve-corneal
 scarring + secondary panophthalmitis ->loss of vision.
 vesicles on the tip of nose and ocular FB sensation.

37.  (b) RAMSAY HUNT SYNDROME.
 -Herpes zoster infection of the geniculate
ganglion leads to ipsilateral facial palsy
 similar to Bell's palsy.
 -vesicles develop in external auditory
meatus ,pinna ,soft palate , and may cause
 DEAFNESS.
 -Painful vesicular rash affecting palate ,
posterior tongue , epiglottis ,tonsillar pillars
 Note;Unilateral presentation
differentiates it from HERPANGINA ,and HSV
INFECTION.


38.  DISSEMINATED HERPES ZOSTER
 -Involves more than 3 dermatomes or has more
secondary lesions outside a dermatome.
 -Affects patients with non-Hodgkins Lymphoma
and HIV.
 -May involve internal organs causing hepatitis,
pneumonia, meningoencephalitis, myelitis or
 motor radiculopathy.
 =Treatment for all above.
 -IV Acyclovir 10mg/kg slowly

39.  HERPES SIMPLEX VIRUS INFECTION(HSV)

* Appear as grouped vesicles on erythematous
base.
* More common in younger people than the elderly.
* HSV1 causes herpetic stomatitis, herpes labialis,
herpetic keratoconjunctivitis and encephalitis.
 HSV2-genital herpes, genital erosions and
systemic infections in immunocompromised patients


40. THANK YOU FOR YOUR
KIND ATTENTION