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MEASLES,
COMPLICATIONS AND
POST DEBILITY
Presenter: Dr.Valentina Daniel
Supervising SR: Dr. Esuola
Supervising Consultant: Dr. Ekere
OUTLINE
• 1. Introduction
• 2. Epidemiology
• 3. Pathophysiology
• 4. Clinical Features
• 5. Investigations
• 6. Complications
• 7. Differential Diagnoses
• 8. Treatment
• 9. Post Measles Debility
• 10. Prevention
• 11. References
INTRODUCTION
• Measles is a highly contagious viral disease caused
by Morbillivirus, a member of the Paramyxovirus
family, which is transmitted to a susceptible
individual through aerosol or by direct contact.
• The virus infects the mucous membranes of an
exposed individual and then spreads to other parts
of the body.
• Measles is known to infect only humans with no
known animal reservoir.
• Measles has an incubation period of about 10
days (with a range of 7 to 18 days).
• It is characterized by prodromal fever,
conjunctivitis, coryza, cough and presence of
Koplik spots
• The mortality rate for measles infection in
children is usually 0.2%, but may be up to 10% in
malnourished children.
• In cases with complications, the mortality rate
may rise to 20-30%
EPIDEMIOLOGY
• Measles is an acute and extremely contagious
viral disease that has caused approximately 2.6
million deaths before the introduction of the
vaccine.
• Measles affects up to 20 million people a year
worldwide, most of these infections are seen in
the developing areas of Africa and Asia
Epidemiology
•Globally, measles mortality fell 60% from an
estimated 873,000 deaths in 1999 to 345,000
in 2005
•In Africa, measles remains a leading cause of
death and disability in most countries
•In 2015, theWorld HealthOrganization (WHO)
estimated that of the 134,200 measles deaths
recorded, majority were in sub-Saharan
Africa.
Epidemiology
• The United Nations Office for the Coordination
of Humanitarian Affairs (OCHA) reported
recently that from February to May 2023,
measles outbreaks attributed to the continuous
influx of unvaccinated children from hard-to-
reach and extremely hard-to-reach areas in
north-east Nigeria claimed the lives of more than
50 children.
Epidemiology
•Borno State was the most affected,
recording over 5,000 suspected cases, with
Jere LGA and Maiduguri Metropolitan
Council recording 1,644 and 1,627 cases,
respectively, by the end of May 2023.
•There were 917 suspected cases of measles
inYobe State, with 9 deaths from measles-
related complications, and 66 suspected
cases of measles reported in Adamawa
State
Pathophysiology
•Measles is a systemic infection.
•The primary site of infection is alveolar
macrophages or dendritic cells.
•Two to three days after replication in the
lung, measles virus spreads to regional
lymphoid tissues followed by a systemic
infection.
Pathophysiology
•Following further viral replication in regional
and distal reticuloendothelial sites, a second
viremia occurs 5 to 7 days after initial
infection.
•During this phase, infected lymphocytes and
dendritic cells migrate into the sub-epithelial
cell layer and transmit measles to epithelial
cells.
• Following amplification in the epithelia, the
virus is released into the respiratory tract
Clinical Features
•The clinical picture of measles can be
divided into three stages:
prodromal
eruptive
convalescent
KOPLIK SPOTS
Clinical features
•The primary or prodromal phase lasts 4-6
days and is characterized by the presence
of high fever, malaise, coryza,
conjunctivitis, palpebral edema, and dry
cough.
•Most cases show the characteristic Koplik
spots of the disease, located in the buccal
mucosa at the height of the second molar,
and appear two to three days before the
rash and disappear on the third day.
•The second phase, the eruptive stage, is
characterized by the appearance of a
maculo-papular rash, initially fine that
subsequently becomes confluent.
•The rash begins behind the auricle and
along the hair implantation line, and
extends downward to the face, trunk, and
extremities.
• The third phase or convalescence occurs after
three to four days when the rash begins to
disappear, in the same order in which it
appeared, leaving brown spots and producing a
thin peeling of the skin.The fever disappears two
to three days after the rash begins, as does the
general malaise.
• In atypical measles, the onset is acute, with high
fever, headache, abdominal pain, and myalgia.
• The rash may be minimal in children with
measles modified by the vaccine.
• In addition, they may not have one or more of the
classic triad - cough, coryza, or conjunctivitis.
Unusual manifestations of measles include
pneumonia, otitis media, myocarditis,
pericarditis, and encephalitis.
Investigations
•Serological tests with specific
immunoglobulin G (IgG) and
immunoglobulin M (IgM) measurements,
molecular biologic techniques with reverse
transcription-polymerase chain reaction
application, and viral isolation are available
for diagnostic confirmation.
•The measles specific IgM antibody in
primary infection, which is confirmatory of
disease, are detected from the third day of
the rash and remain positive for 30 to 60
days.
Investigations
•For the evaluation of IgG, there is more than
a four-fold increase in antibodies between
the acute and convalescence phases of the
disease.
•Measles RNA can be detected by a
polymerase chain reaction from pharyngeal
or nasopharyngeal swabs or urine samples.
•This test confirms the disease and allows the
genotyping of the agent.
Complications
•Bacterial super-infection, including
pneumonia
•Acute thrombocytopenic purpura
•Encephalitis
•Transient hepatitis
•Subacute sclerosing panencephalitis
Differential diagnoses
rubella,
scarlet fever,
drug rash,
serum sickness ,
roseola infantum,
infectious mononucleosis,
erythema infectiosum,
Kawasaki disease
Differential diagnoses
• Rubella causes a rash similar to measles with
head to caudal distribution, mild respiratory
symptoms, the absence of conjunctivitis. Still, it
is accompanied by the presence of adenopathies
- which is characteristic of this disease.
• Roseola is characterized by an illness beginning
with a high fever, which subsides after a few
days, accompanied by the appearance of a rash
in the central part of the body, without the
presence of Koplik's points.
Differential diagnoses
• Mononucleosis is a febrile viral disease, a
characteristic course with few symptoms during
childhood, contrary to what happens in more
advanced ages. Mononucleosis manifests itself
by pharyngeal compromise, polyadenopathy,
and hepatosplenomegaly, and the rash can have
different forms of presentation.
• In Kawasaki disease, there is an ocular
compromise with the presence of conjunctivitis
without exudate, and the respiratory
compromise is not part of this pathology.
Differential diagnoses
• Group A Streptococcus (particularly Scarlet
fever) may present with a similar rash (a
coarse, sandpaper-like, blanching,
erythematous) to measles in association with
pharyngitis.
• Drug rash: A rash caused by drug
hypersensitivity often resembles the measles
rash, but a prodrome is absent, there is no
cephalocaudal progression or cough, and
there is usually a history of recent drug
exposure.
TREATMENT
•There is no specific treatment of measles
except supportive care to relieve common
symptoms associated with this condition.
•Supportive measures include antipyretics
for fevers, hydration, and adequate
nutritional support, including the
encouragement of breastfeeding.
•TheWorld Health Organization
recommends the administration of vitamin
A for all children with measles, but
particularly for children who reside in areas
where the case fatality rate is more than
1%, areas with known vitaminA deficiency,
and in severe cases of complicated
measles.
• For infants less than 6 months of age, the doses
are 50,000 IU
• for children between 6 and 12 months, 100,000 IU;
• for children aged 12 months and older, 200,000 IU.
• The measles virus is susceptible to the medication
ribavirin in vitro, but due to a lack of clinical data,
its routine use is not recommended.
• It may be considered for use in certain high-risk
groups.
POST MEASLES DEBILITY
• Subacute sclerosing panencephalitis (SSPE) is a
very rare, but fatal disease of the central nervous
system that results from a measles virus infection
acquired earlier in life.
• SSPE generally develops 7 to 10 years after a
person has measles, even though the person
seems to have fully recovered from the illness.
• The risk of developing SSPE may be higher for a
person who gets measles before they are 2 years
of age.
•Subacute sclerosing panencephalitis is
characterized by progressive cognitive
decline.
•Symptoms typically present about 8 to 11
years of post-measles infection.
•Initially, personality or behavior changes
are present, in addition to poor school
performance and intellectual deterioration.
•There is a steady decline in motor function
with myoclonus in most cases, autonomic
dysfunction, and focal paralysis.
•Some patients have seizures, either focal
or generalized, and about one-third of
patients with SSPE develop epilepsy.
Patients eventually fall into a vegetative
state or akinetic mutism, which is shortly
followed by death
•The course of SSPE has been divided into
stages, each of which describes a certain
phase of the disease.
•Stage I includes many personality or
behavioral changes, such as irritability,
dementia, lethargy, social withdrawal, or
speech regression.
•Stage II is made up of the progressive
decline in motor function, including
myoclonus, dyskinesia, and dystonia.
•Stage III consists of patients who have
progressed to extrapyramidal symptoms,
posturing, and spasticity.
•Stage IV occurs when patients develop
akinetic mutism, autonomic failure, or
enter a vegetative state.
DIAGNOSIS OF SSPE
•Serologic testing
•Electroencephalography (EEG)
•Neuroimaging (CT or MRI)
SSPE is suspected in young patients with
dementia and neuromuscular irritability.
EEG shows periodic complexes with high-
voltage diphasic waves occurring
synchronously throughout the recording.
•CT or MRI may show cortical atrophy or
white matter lesions.
•CSF examination usually reveals normal
pressure, cell count, and total protein
content; however, CSF globulin is almost
always elevated, constituting up to 20 to
60% of CSF protein.
•Serum and CSF contain elevated levels of
measles virus antibodies.
•Anti-measles IgG appears to increase as
the disease progresses.
•If test results are inconclusive, brain biopsy
may be needed.
Treatment of SSPE
•Supportive care
•Anticonvulsants and other supportive
measures are the only accepted treatments.
•Isoprinosine, interferon alfa, and
lamivudine are controversial, and antiviral
medications have generally not proved helpful
Prognosis for SSPE
•The disease is almost invariably fatal within
1 to 3 years (often pneumonia is the
terminal event), although some patients
have a more protracted course.
Prevention
Vaccine
• Vaccination against measles is the most effective and
safe prevention strategy
• Measles vaccine is available as a combined vaccine with
measles-mumps-rubella vaccine
Post-exposure Prophylaxis
• Susceptible individuals exposed tomeasles may be
protected from infection by either vaccine administration
or with Ig
• The vaccine is effective in prevention or modification of
measles if given within 72 hr of exposure
• Ig may be given up to 6 days after exposure to prevent or
modify infection
Prevention strategies
•Primary –
Vaccination. Measles can be prevented
with measles-containing vaccine, which is
primarily administered as the combination
measles-mumps-rubella (MMR) vaccine.
•Secondary :- Secondary prevention
includes steps to isolate cases and treat or
immunize contacts so as to prevent further
cases of meningitis or measles, for
example, in outbreaks.
Tertiary Prevention:
•It is implemented in symptomatic patients
and aims to reduce the severity of the
disease as well as of any associated sequelae.
While secondary prevention seeks to prevent
the onset of illness, tertiary prevention aims
to reduce the effects of the disease once
established in an individual.
Quaternary prevention
• Public health interventions to reduce the
secondary spread of measles are:-
vaccination of susceptible contacts;
human immunoglobulin (Ig) for susceptible
contacts;
quarantine of susceptible contacts;
isolation of active measles cases; and
special vaccination clinics or activities during
outbreaks to increase population immunization
coverage
Conclusion
• Measles is a highly contagious viral infection
spread by air/droplet transmission
• There are several symptoms but it is
characterized by a distinctive rash.
• Measles can be prevented by vaccination, either
singly or in addition to mumps and rubella, all of
which can also have serious complications.
• High vaccination coverage provides a ‘herd
immunity’ effect which also protects those who
are unable to be vaccinated
Thank you for listening
references

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MEASLES, COMPLICATIONS AND POST DEBILITY.pptx

  • 1. MEASLES, COMPLICATIONS AND POST DEBILITY Presenter: Dr.Valentina Daniel Supervising SR: Dr. Esuola Supervising Consultant: Dr. Ekere
  • 2. OUTLINE • 1. Introduction • 2. Epidemiology • 3. Pathophysiology • 4. Clinical Features • 5. Investigations • 6. Complications • 7. Differential Diagnoses • 8. Treatment • 9. Post Measles Debility • 10. Prevention • 11. References
  • 3. INTRODUCTION • Measles is a highly contagious viral disease caused by Morbillivirus, a member of the Paramyxovirus family, which is transmitted to a susceptible individual through aerosol or by direct contact. • The virus infects the mucous membranes of an exposed individual and then spreads to other parts of the body. • Measles is known to infect only humans with no known animal reservoir.
  • 4. • Measles has an incubation period of about 10 days (with a range of 7 to 18 days). • It is characterized by prodromal fever, conjunctivitis, coryza, cough and presence of Koplik spots • The mortality rate for measles infection in children is usually 0.2%, but may be up to 10% in malnourished children. • In cases with complications, the mortality rate may rise to 20-30%
  • 5. EPIDEMIOLOGY • Measles is an acute and extremely contagious viral disease that has caused approximately 2.6 million deaths before the introduction of the vaccine. • Measles affects up to 20 million people a year worldwide, most of these infections are seen in the developing areas of Africa and Asia
  • 6. Epidemiology •Globally, measles mortality fell 60% from an estimated 873,000 deaths in 1999 to 345,000 in 2005 •In Africa, measles remains a leading cause of death and disability in most countries •In 2015, theWorld HealthOrganization (WHO) estimated that of the 134,200 measles deaths recorded, majority were in sub-Saharan Africa.
  • 7. Epidemiology • The United Nations Office for the Coordination of Humanitarian Affairs (OCHA) reported recently that from February to May 2023, measles outbreaks attributed to the continuous influx of unvaccinated children from hard-to- reach and extremely hard-to-reach areas in north-east Nigeria claimed the lives of more than 50 children.
  • 8. Epidemiology •Borno State was the most affected, recording over 5,000 suspected cases, with Jere LGA and Maiduguri Metropolitan Council recording 1,644 and 1,627 cases, respectively, by the end of May 2023. •There were 917 suspected cases of measles inYobe State, with 9 deaths from measles- related complications, and 66 suspected cases of measles reported in Adamawa State
  • 9. Pathophysiology •Measles is a systemic infection. •The primary site of infection is alveolar macrophages or dendritic cells. •Two to three days after replication in the lung, measles virus spreads to regional lymphoid tissues followed by a systemic infection.
  • 10. Pathophysiology •Following further viral replication in regional and distal reticuloendothelial sites, a second viremia occurs 5 to 7 days after initial infection. •During this phase, infected lymphocytes and dendritic cells migrate into the sub-epithelial cell layer and transmit measles to epithelial cells. • Following amplification in the epithelia, the virus is released into the respiratory tract
  • 11. Clinical Features •The clinical picture of measles can be divided into three stages: prodromal eruptive convalescent
  • 13. Clinical features •The primary or prodromal phase lasts 4-6 days and is characterized by the presence of high fever, malaise, coryza, conjunctivitis, palpebral edema, and dry cough. •Most cases show the characteristic Koplik spots of the disease, located in the buccal mucosa at the height of the second molar, and appear two to three days before the rash and disappear on the third day.
  • 14. •The second phase, the eruptive stage, is characterized by the appearance of a maculo-papular rash, initially fine that subsequently becomes confluent. •The rash begins behind the auricle and along the hair implantation line, and extends downward to the face, trunk, and extremities.
  • 15. • The third phase or convalescence occurs after three to four days when the rash begins to disappear, in the same order in which it appeared, leaving brown spots and producing a thin peeling of the skin.The fever disappears two to three days after the rash begins, as does the general malaise.
  • 16. • In atypical measles, the onset is acute, with high fever, headache, abdominal pain, and myalgia. • The rash may be minimal in children with measles modified by the vaccine. • In addition, they may not have one or more of the classic triad - cough, coryza, or conjunctivitis. Unusual manifestations of measles include pneumonia, otitis media, myocarditis, pericarditis, and encephalitis.
  • 17. Investigations •Serological tests with specific immunoglobulin G (IgG) and immunoglobulin M (IgM) measurements, molecular biologic techniques with reverse transcription-polymerase chain reaction application, and viral isolation are available for diagnostic confirmation. •The measles specific IgM antibody in primary infection, which is confirmatory of disease, are detected from the third day of the rash and remain positive for 30 to 60 days.
  • 18. Investigations •For the evaluation of IgG, there is more than a four-fold increase in antibodies between the acute and convalescence phases of the disease. •Measles RNA can be detected by a polymerase chain reaction from pharyngeal or nasopharyngeal swabs or urine samples. •This test confirms the disease and allows the genotyping of the agent.
  • 19. Complications •Bacterial super-infection, including pneumonia •Acute thrombocytopenic purpura •Encephalitis •Transient hepatitis •Subacute sclerosing panencephalitis
  • 20. Differential diagnoses rubella, scarlet fever, drug rash, serum sickness , roseola infantum, infectious mononucleosis, erythema infectiosum, Kawasaki disease
  • 21. Differential diagnoses • Rubella causes a rash similar to measles with head to caudal distribution, mild respiratory symptoms, the absence of conjunctivitis. Still, it is accompanied by the presence of adenopathies - which is characteristic of this disease. • Roseola is characterized by an illness beginning with a high fever, which subsides after a few days, accompanied by the appearance of a rash in the central part of the body, without the presence of Koplik's points.
  • 22. Differential diagnoses • Mononucleosis is a febrile viral disease, a characteristic course with few symptoms during childhood, contrary to what happens in more advanced ages. Mononucleosis manifests itself by pharyngeal compromise, polyadenopathy, and hepatosplenomegaly, and the rash can have different forms of presentation. • In Kawasaki disease, there is an ocular compromise with the presence of conjunctivitis without exudate, and the respiratory compromise is not part of this pathology.
  • 23. Differential diagnoses • Group A Streptococcus (particularly Scarlet fever) may present with a similar rash (a coarse, sandpaper-like, blanching, erythematous) to measles in association with pharyngitis. • Drug rash: A rash caused by drug hypersensitivity often resembles the measles rash, but a prodrome is absent, there is no cephalocaudal progression or cough, and there is usually a history of recent drug exposure.
  • 24. TREATMENT •There is no specific treatment of measles except supportive care to relieve common symptoms associated with this condition. •Supportive measures include antipyretics for fevers, hydration, and adequate nutritional support, including the encouragement of breastfeeding.
  • 25. •TheWorld Health Organization recommends the administration of vitamin A for all children with measles, but particularly for children who reside in areas where the case fatality rate is more than 1%, areas with known vitaminA deficiency, and in severe cases of complicated measles.
  • 26. • For infants less than 6 months of age, the doses are 50,000 IU • for children between 6 and 12 months, 100,000 IU; • for children aged 12 months and older, 200,000 IU. • The measles virus is susceptible to the medication ribavirin in vitro, but due to a lack of clinical data, its routine use is not recommended. • It may be considered for use in certain high-risk groups.
  • 27. POST MEASLES DEBILITY • Subacute sclerosing panencephalitis (SSPE) is a very rare, but fatal disease of the central nervous system that results from a measles virus infection acquired earlier in life. • SSPE generally develops 7 to 10 years after a person has measles, even though the person seems to have fully recovered from the illness. • The risk of developing SSPE may be higher for a person who gets measles before they are 2 years of age.
  • 28. •Subacute sclerosing panencephalitis is characterized by progressive cognitive decline. •Symptoms typically present about 8 to 11 years of post-measles infection. •Initially, personality or behavior changes are present, in addition to poor school performance and intellectual deterioration.
  • 29. •There is a steady decline in motor function with myoclonus in most cases, autonomic dysfunction, and focal paralysis. •Some patients have seizures, either focal or generalized, and about one-third of patients with SSPE develop epilepsy. Patients eventually fall into a vegetative state or akinetic mutism, which is shortly followed by death
  • 30. •The course of SSPE has been divided into stages, each of which describes a certain phase of the disease. •Stage I includes many personality or behavioral changes, such as irritability, dementia, lethargy, social withdrawal, or speech regression. •Stage II is made up of the progressive decline in motor function, including myoclonus, dyskinesia, and dystonia.
  • 31. •Stage III consists of patients who have progressed to extrapyramidal symptoms, posturing, and spasticity. •Stage IV occurs when patients develop akinetic mutism, autonomic failure, or enter a vegetative state.
  • 32. DIAGNOSIS OF SSPE •Serologic testing •Electroencephalography (EEG) •Neuroimaging (CT or MRI) SSPE is suspected in young patients with dementia and neuromuscular irritability. EEG shows periodic complexes with high- voltage diphasic waves occurring synchronously throughout the recording.
  • 33. •CT or MRI may show cortical atrophy or white matter lesions. •CSF examination usually reveals normal pressure, cell count, and total protein content; however, CSF globulin is almost always elevated, constituting up to 20 to 60% of CSF protein. •Serum and CSF contain elevated levels of measles virus antibodies.
  • 34. •Anti-measles IgG appears to increase as the disease progresses. •If test results are inconclusive, brain biopsy may be needed.
  • 35. Treatment of SSPE •Supportive care •Anticonvulsants and other supportive measures are the only accepted treatments. •Isoprinosine, interferon alfa, and lamivudine are controversial, and antiviral medications have generally not proved helpful
  • 36. Prognosis for SSPE •The disease is almost invariably fatal within 1 to 3 years (often pneumonia is the terminal event), although some patients have a more protracted course.
  • 37. Prevention Vaccine • Vaccination against measles is the most effective and safe prevention strategy • Measles vaccine is available as a combined vaccine with measles-mumps-rubella vaccine Post-exposure Prophylaxis • Susceptible individuals exposed tomeasles may be protected from infection by either vaccine administration or with Ig • The vaccine is effective in prevention or modification of measles if given within 72 hr of exposure • Ig may be given up to 6 days after exposure to prevent or modify infection
  • 38. Prevention strategies •Primary – Vaccination. Measles can be prevented with measles-containing vaccine, which is primarily administered as the combination measles-mumps-rubella (MMR) vaccine. •Secondary :- Secondary prevention includes steps to isolate cases and treat or immunize contacts so as to prevent further cases of meningitis or measles, for example, in outbreaks.
  • 39. Tertiary Prevention: •It is implemented in symptomatic patients and aims to reduce the severity of the disease as well as of any associated sequelae. While secondary prevention seeks to prevent the onset of illness, tertiary prevention aims to reduce the effects of the disease once established in an individual.
  • 40. Quaternary prevention • Public health interventions to reduce the secondary spread of measles are:- vaccination of susceptible contacts; human immunoglobulin (Ig) for susceptible contacts; quarantine of susceptible contacts; isolation of active measles cases; and special vaccination clinics or activities during outbreaks to increase population immunization coverage
  • 41. Conclusion • Measles is a highly contagious viral infection spread by air/droplet transmission • There are several symptoms but it is characterized by a distinctive rash. • Measles can be prevented by vaccination, either singly or in addition to mumps and rubella, all of which can also have serious complications. • High vaccination coverage provides a ‘herd immunity’ effect which also protects those who are unable to be vaccinated
  • 42. Thank you for listening