DEPARTMENT OF MORBID ANATOMY AND HISTOPATHOLOGY

OBAFEMI AWOLOWO COLLEGE OF HEALTH SCIENCES,

OLABISI ONABANJO UNIVERSITY TEACHING HOSPITAL, SAGAMU

BLOCK 1 POSTING SEMINAR DELIVERED BY:

ODUYEMI OYINKANSOLA

DAINI MORAYO

ASORO HENRY

SEMINAR OUTLINE:

INTRODUCTION

ETIOLOGY

EPIDEMIOLOGY

PATHOGENESIS

MORPHOLOGY

CLINICAL FEATURES

INVESTIGATIONS

DIAGNOSIS

MANAGEMENT

COMPLICATIONS

PROGNOSIS

VACCINATION

TREATMENT

SUMMARY

REFERENCES
INTRODUCTION

Measles otherwise known as Rubeola or Morbilli is a highly infectious and one of the most
contagious respiratory disease

It is characterised by fever, respiratory symptoms and a maculopapular rash

It mainly affects children

ETIOLOGY

The cause of measles is the measles virus, a single-stranded, negative-sense enveloped RNA
virus of the genus Morbillivirus within the family Paramyxoviridae.

Humans are the natural hosts of the virus; no animal reservoirs are known to exist.

This highly contagious virus is spread by respiratory droplets released through sneezing or
coughing (which can remain active and contagious either air borne or on surfaces, for up to 2
hours) and inhalation of such

Risk factors for severe measles and its complications include the following:

Malnutrition

Underlying immunodeficiency

Pregnancy

Vitamin A deficiency

EPIDEMIOLOGY

The key epidemiologic features are highlighted below:

The virus is highly contagious; in apparent infection are rare

The prevalence and age incidence are related to population density, economic and
environmental factors and the use of an effective live virus vaccine

Measles is endemic throughout the world and epidemics recurs every 2-3 years

WHO estimated in 2005 that there were 30-40 million measles cases, 530, 000 deaths and
15,000-60,000 cases of blindness caused by measles annually worldwide.

In Nigeria, suspected cases of measles in 2004 and 2005 were about 32,000 and 98,000 and
death attributed were about 600 and 2,500 in both years respectively.
An effective measles vaccine was introduced in 1963.

PATHOGENESIS

The incubation period is typically 8-12 days and may last up to 3 weeks in adults

When infected droplets are inhaled, the virus invades the respiratory epithelial cells, multiply
there, penetrate the mucosa and the basement membrane of the blood vessel. The viruses are
thus released into the bloodstream. [PRIMARY VIREMIA].

It takes about 2-3 days

Primary viremia leads to subsequent infection of this RES

Following further viral replication in regional and distal RES sites, release of virus result in
secondary viremia which occurs 5-7 days after initial infection

This secondary viremia seeds the epithelial surfaces of the body including the skin,
respiratory tract, conjuctiva

Replication occurs in the lymphocyte which aid in dissemination

The viruses attach themselves via the HAEMAGGLUTININ glycoprotein on the viral
surfaces to a COMPLEMENT REGULATORY PROTEIN– CD46 RECEPTOR and fuses
with the cell membrane by the action of FUSION GLYCOPROTEIN(F), this allows the
release of the viral nucleocapsid directly into the cell.

The measles virus inhibits cytokine activity- it inhibits the action of Interferon (produced
within hours in response to viral replication) which inhibits viral replication. At maturation,
the fusion protein is activated and this causes fusion of adjacent cell membrane resulting in
the formation of large syncytia.

Most children, however, develop T-cell mediated immunity to measles virus in some blood
vessels that control the viral infection and produce the measles maculopapular rash, a
hypersensitivity reaction to viral antigens in the skin.

This appears about day 14 and the virus-specific immune response is also detectable when
rash appears

This last for about 1 week after which there is clearance of the virus and fading of the rash.

However, the rash doesn’t occur in patients with deficiencies in cell-mediated immunity

Measles infection causes immunosuppression resulting in secondary infections which are the
major cause of morbidity and mortality
MORPHOLOGY

GROSS

Blotchy, reddish brown rash of measles virus infection on the face, trunk and proximal
extremities produced as a result of

Dilated skin vessels

Edema

Moderate nonspecific mononuclear perivascular infiltrate

Koplik spots - ulcerated mucosal lesions in the oral cavity near the opening of the stensen
ducts (pathognomonic of measles)

HISTOLOGY

Lymphoid organs have:

marked follicular hyperplasia

large germinal centers

randomly distributed multinucleated giant cells – warthin-finkeldey cells which have

eosinophilic nuclear and cytoplasmic inclusion bodies

Koplik spot:

Neutrophil exudate

Necrosis

Neovascularization(abnormal formation of new fragile blood vessels)

Giant cells
CLINICAL FEATURES

Fever as high as 40 degrees

Coryza (running nose)

Cough (brazzy and husky due to laryngeal and trachea involvement)

Conjuctivitis,

Lacrymation

Sneezing

KOPLIK SPOTS

This is a spot present on the mucous membrane in the mouth, it is pathognomic for measles.
The spot appears on the 3rd-4th day of prodromal period. One to two days before the spot,
there is intense buccal hyperemia. This spots appear as a punctuate blue white spot on the
bright red background of the buccal mucosa opposite the lower molar tooth, just near the
stensens duct.

Measles rash (generalized maculopaular erythemathous)

Just at the peak of respiratory symptoms, most especially on the 4th day, measles rash
appears. As the temperature continues to increase, more rash appears. The rash starts on the
face, spreads from the face to the neck, trunk, extremities and in very severe cases ,involve
the soles of the hands and feet.

Maculopapular eruptions begins behind the ears and on the hairline on the forehead, gathers
on the face and trunk but not much on the extremeties.

Severity of the rash depends on the extent of spread and confluence.

Mild rashes are scattered and not confluent, severe rashes are confluent and extends to the
palms and sole of the foot.

As the rashes spreads to the extremities, fever usually drops. Persistent fever even as rashes
spreads to the extremities indicates complications.

Rashes fades in the same order of appearance leaving a desquamation of the skin.

Desquamation is more severe in malnourished children

OTHER CLINICAL FEATURES

Anorexia

Vomiting

Diarrhea

Generalized lymphadenopathy

INVESTIGATIONS

Viral culture- To isolate the virus

Serology – To detect IgM and IgG antibodies to measles

Full blood count- Shows levels of leucopenia and thrombocytopenia

Serum electrolyte, urea, and creatinine- to check for renal status

Chest Xray- To check pneumonia and Tuberculosis

CSF analysis- to check for encephalitis and other cerebral involvement

Surface swabs – For microscopy culture and sensitvity testing.

DIAGNOSIS

Clinical diagnosis

History of fever for at least 3days with one of the 3 (cough, coryza and conjuctivitis)

Observation of koplik spots

Laboratory diagnosis

Presence of positive measles IgM antibodies

Isolation of measles virus in respiratory specimen

MANAGEMENT

Admit patient and ensure adequate bed rest.

Ensure adequate nutrition to maintain calorie intake.

Antipyretics for fever

Anticonvulsant for seizures

Eye toileting and care of mouth sores

Vitamin A administration for babies.

Antiboitics for secondary infections. Prophylactic antiboitics is not indicated for measles

COMPLICATIONS

Respiratory complications are

Bronchopneumonia

Emphysema

Obstructive laryngitis(croup)

Pnuemothorax

Otitis media

Subcutaneous emphysema

Gastrointestinal complications are

Diarrhoea

Stomatitis

Severe anorexia

Cancrum oris

Severe malnutrition

Occular complications are Keratitis,Xerophthalmia,blindness

Cardiac complications are

Myocarditis, Chronic congestive failure, Inversion of T wave, Prolonged PR wave

Hematologic complications are

Thrombocytopenia,Vascular damage

Disseminated intravascular coagulopathy

CNS complications are

Febrile convulsion, Acute encephalitis

Subacute sclerosing panecephalitis

This is a persistent degenerative viral infection of the brain, occurs 7 years after measles
infection and can be seen in 5 out of 10 reported cases of measles. It causes myoclonic
seizures, ataxia and can lead to death.

PROGNOSIS

Measles is a major cause of childhood morbidity and mortality but most children recover.

Prognosis is bad when there is

Malnutrition

Immunosuppression

Overcrowding

VACCINATION

MMRV – Measles – Mumps – Rubella – Varicella

DEVELOPED COUNTRIES

1ST dose – 18months

2nd dose – 4 – 5 years to increase rates of immunity

DEVELOPING COUNTRIES

1ST dose – 6months

2nd dose – 9months to increase rates of immunity

Some cultures refuse immunization and hence have increased number of cases

Vaccination is contraindicated in pregnancy and people with compromised immunity.

TREATMENT

ANTIVIRAL

Rivabarin

SUPPORTIVE CARE

Symptomatic treatment

Fever – acetaminophen, ibuprofen

Itching - calamine lotion

Bacteria superimposition - antibiotics

Seizure – anticonvulsants

SUPPLMENT TREATMENT

VIT A
SUMMARY

Measles is a viral infection, incubation period 10-12 days, it is rare in children under
6months, koplik spot is path gnomonic of the disease, it is one of the most common
childhood diseases. Occurrence has reduced because of success in vaccination. Still common
in the developing countries. Risk factors include malnutrition, vitamin A deficiency e.t.c. No
specific treatment but symptoms can be managed. Complications involves almost all body
systems. Infection with the virus confers lifelong immunity.

REFERENCES

ROBBINS AND COTRAN 9TH EDITION

INFECTIOUS DISEASES BY DR (MRS) M.B. FETUGA

INTERNET