Module Measles Tanpa Answer

8/12/2019 Module Measles Tanpa Answer

1/11

MODULE: MEASLES

I. Contributor : dr. Irene Ratridewi, Sp.A (K). M.Kes

II. Learning objective

At the end of this module, student should be able to know :

1. definition of measles

2. the causes of measles

3. pathogenesis of measles

4. clinical manifestations of measles

5. complication of measles

6. diagnosis of measles

7. management of measles

III. Method

This module is designed for medical students at six semester, and will be processed by

combines lectures and small group discussion.

IV. Overview

A. Introduction

Measles, also known as rubeola, is one of the most contagious infectious

diseases in children, with at least a 90% secondary infection rate in susceptible

domestic contacts. Measles is marked by prodromal fever, cough, coryza,

conjunctivitis, and pathognomonic enanthem (ie, Koplik spots), followed by an

erythematous maculopapular rash on the third to seventh day. Infection confers life-

long immunity. A generalized immunosuppression that follows acute measles

frequently predisposes patients to bacterial otitis media and bronchopneumonia. In

approximately 0.1% of cases, measles causes acute encephalitis. Subacute

sclerosing panencephalitis (SSPE) is a rare chronic degenerative disease that occurs

several years after measles infection.

Several case definitions have been established to standardize the approach

to measles outbreaks :

Suspected case A suspected case is defined as a febrile illness accompanied by

rash.

Clinical case A clinical case is defined as an illness characterized by cough,

coryza, or conjunctivitis, a generalized rash lasting for more than three days, and a

temperature >38.3C (>101F).
http://emedicine.medscape.com/article/994656-overviewhttp://emedicine.medscape.com/article/994656-overview


2/11

Probable case A probable case meets the clinical case definition, but is not linked

epidemiologically to a confirmed case and lacks serologic or virologic proof of

disease.

Confirmed case A confirmed case meets the laboratory criteria for measles

(independent of clinical features) or meets the clinical case definition and isepidemiologically linked to a confirmed case.

B. Epidemiology

The practice of administering 2 doses of live-attenuated measles vaccine to

children to prevent school outbreaks of measles was implemented when the vaccine

was first licensed in 1963. From 2000 through 2007, an average of 63 cases were

reported annually to the US Centers for Disease Control and Prevention (CDC). In

2004, 34 cases were reported; after that all-time low, however, the annual incidence

began to increase, with most cases linked either directly or indirectly to international

travel. Incomplete vaccination rates facilitate the spread once the virus is imported to

the United States. Despite the highest recorded immunization rates in history, young

children who are not appropriately vaccinated may experience more than a 60-fold

increase in risk of disease due to exposure to imported measles cases from countries

that have not yet eliminated the disease.

In developing countries, measles affects 30 million children a year and

causes 1 million deaths. Measles causes 15,000-60,000 cases of blindness per year.

Between 2000 and 2008, the number of worldwide measles cases reported to theWHO and the United Nations Childrens Fund (UNICEF) declined by 67% (from

852,937 to 278,358). During the same 8-year period, global measles mortalitydropped by 78%. However, it is believed that global measles incidence and mortalityremain underreported, with many countries, particularly those with the highest

disease burden, lacking complete, reliable surveillance data. Since 2008, France

has been experiencing an outbreak of measles, which has not yet begun to slacken.Over the same period, outbreaks have also been occurring in the 46 countries of theWHO African Region. Worldwide, most reported cases of measles continue to befrom Africa.

Unvaccinated young children are at the highest risk. Age-specific attack rates

may be highest in susceptible infants younger than 12 months, school-aged children,

or young adults, depending on local immunization practices and incidence of thedisease. Complications such as otitis media, bronchopneumonia,

laryngotracheobronchitis (ie, croup), and diarrhea are more common in young

children. In heavily populated, underdeveloped countries, measles is most common

in children younger than 2 years. Unvaccinated males and females are equally

susceptible to infection by the measles virus. Measles affects people of all races.

The WHO-designated Southeast Asia Region improved measles

vaccine coverage between 2000 to 2008, which was associated with a 46 percent

reduction in measles deaths. Nonetheless this Region had approximately 126,000

measles deaths in 2008, representing the majority of all measles deaths in the world

for that year (approximately 77 percent).


3/11

In 2005, the World Health Assembly adopted the WHO/UNICEF Global

Immunization Vision and Strategy, which includes a goal of 90 percent reduction in

global measles mortality between 2000 and 2010. The WHO identified 47 priority

countries to focus measles mortality reduction efforts; these nations jointly account

for approximately 98 percent of measles deaths. The strategy in these nations

includes the following measures: (1) measles immunization with a goal of >90percent national coverage and >80 percent per-district coverage with two doses of

vaccine; (2) surveillance activities, including case investigation and laboratory testing

in all suspected cases; and (3) clinical management of measles cases, including

administration of vitamin A.

C. Aetiology and Pathonegesis

The cause of measles is the measles virus, a single-stranded, negative-sense

enveloped RNA virus of the genus Morbilliviruswithin 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 coughing and sneezing via close personal

contact or direct contact with secretions.

Risk factors for measles virus infection include the following:

Children with immunodeficiency due to HIV or AIDS, leukemia, alkylating agents, or

corticosteroid therapy, regardless of immunization status

Travel to areas where measles is endemic or contact with travelers to endemic areas

Infants who lose passive antibody before the age of routine immunization

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

Malnutrition

Underlying immunodeficiency

Pregnancy

Vitamin A deficiency

In temperate areas, the peak incidence of infection occurs during late winter

and spring. Infection is transmitted via respiratory droplets, which can remain active

and contagious, either airborne or on surfaces, for up to 2 hours. Initial infection and

viral replication occur locally in tracheal and bronchial epithelial cells. After 2-4 days,

measles virus infects local lymphatic tissues, perhaps carried by pulmonary

macrophages. Following the amplification of measles virus in regional lymph nodes,

a predominantly cell-associated viremia disseminates the virus to various organs

prior to the appearance of rash.

Measles virus infection causes a generalized immunosuppression marked by

decreases in delayed-type hypersensitivity, interleukin (IL)-12 production, and

antigen-specific lymphoproliferative responses that persist for weeks to months after

the acute infection. Immunosuppression may predispose individuals to secondary

opportunistic infections, particularly bronchopneumonia, a major cause of measles-related mortality among younger children. In individuals with deficiencies in cellular
http://emedicine.medscape.com/article/985140-overviewhttp://emedicine.medscape.com/article/985140-overview


4/11

immunity, measles virus causes a progressive and often fatal giant cellpneumonia.

In immunocompetent individuals, wild-type measles virus infection induces an

effective immune response, which clears the virus and results in lifelong immunity

A skin biopsy from a lesion of the morbilliform eruption shows spongiosis and

vesiculation in the epidermis with scattered dyskeratotic keratinocytes. Occasional

lymphoid multinucleated giant cells ( 100 nm in diameter) can be identified in

biopsies of Koplik spots, in dermal or epithelial rashes, in hair follicles and

acrosyringium and in lung or lymphoid tissue. These findings are not specific, but

they are suggestive of a viral exanthem. Brain biopsies of patients with measles

encephalitis can reveal demyelination, vascular cuffing, gliosis, and infiltration of fat-

laden macrophages near blood vessel walls.

D. Clinical Features

Measles virus infection can cause a variety of clinical syndromes, including:

Classic measles infection in immunocompetent patients

Modified measles in patients with preexisting, but incompletely protective, anti-

measles antibody

Atypical measles in patients immunized with the killed virus vaccine

Neurologic syndromes following measles infection, including acute disseminated

encephalomyelitis (ADEM) and subacute sclerosing panencephalitis (SSPE)

Severe measles

Complications of measles including secondary infection, giant cell pneumonia, and

measles inclusion body encephalitis

Classic measles infection can be subdivided into the following clinical stages:

incubation, prodrome, exanthem, and recovery . Onset of measles ranges from 7 to

14 days (average, 10-12 days) after exposure to the virus. The first sign of measles

is usually a high fever (often >104o F [40o C]) that typically lasts 4-7 days. The

prodromal phase is also marked by malaise; anorexia; and the classic triad of

conjunctivitis, cough, and coryza (the 3 Cs). Other possible prodromal

manifestations include photophobia, periorbital edema, and myalgias. Prodromal

phase would be followed by enanthema and eruption of rash

Enanthem

Koplik spotsbluish-gray specks or grains of sand on a red basedevelop on the

buccal mucosa opposite the second molars

Generally appear 1-2 days before the rash and last 3-5 days

Pathognomonic for measles, but not always present

Rash

On average, the rash develops about 14 days after exposure

Mild pruritus may also occur
http://emedicine.medscape.com/article/967822-overviewhttp://emedicine.medscape.com/article/967822-overviewhttp://emedicine.medscape.com/article/967822-overview


5/11

Blanching, erythematous macules and papules begin on the face at the hairline, on

the sides of the neck, and behind the ears

Within 48 hours, the lesions coalesce into patches and plaques that spread

cephalocaudally to the trunk and extremities, including the palms and soles, while

beginning to regress cephalocaudally, starting from the head and neck

Lesion density is greatest above the shoulders, where macular lesions may coalesce The eruption may also be petechial or ecchymotic in nature

Patients appear most ill during the first or second day of the rash

The exanthem lasts for 5-7 days before fading into coppery-brown hyperpigmented

patches, which then desquamate

Immunocompromised patients may not develop a rash

Clinical course

Uncomplicated measles, from late prodrome to resolution of fever and rash, lasts 7-

10 days Cough may be the final symptom to appear

Modified measles

Occurs in individuals who have received serum immunoglobulin after exposure to the

measles virus

The incubation period may be as long as 21 days

Similar but milder symptoms and signs may occur

Atypical measles

Occurs in individuals who were vaccinated with the original killed-virus measles

vaccine between 1963 and 1967 and who have incomplete immunity

A mild or subclinical prodrome of fever, headache, abdominal pain, and myalgias

precedes a rash that begins on the hands and feet and spreads centripetally

The eruption is accentuated in the skin folds and may be macular, vesicular,

petechial, or urticarial

E. Complication

Most complications of measles occur because the measles virus suppresses

the hosts immune responses, resulting in a reactivation of latent infections or

superinfection by a bacterial pathogen. Consequently, pneumonia, whether due to

the measles virus itself, to tuberculosis, to or another bacterial etiology, is the most

frequent complication. Pleural effusion, hilar lymphadenopathy, hepatosplenomegaly,

hyperesthesia, and paresthesia may also be noted.

Complications of measles are more likely to occur in children younger than 5

years, and complication rates are increased in persons with immune deficiency

disorders, malnutrition, vitamin A deficiency, and inadequate vaccination.

Immunocompromised children are at increased risk for severe infections andsuperinfections. Common infectious complications include otitis media, interstitial


6/11

pneumonitis, bronchopneumonia, laryngotracheobronchitis (ie, croup), exacerbation

of tuberculosis, transient loss of hypersensitivity reaction to tuberculin skin test,

encephalomyelitis, diarrhea, sinusitis, stomatitis, subclinical hepatitis, lymphadenitis,

and keratitis, which can lead to blindness. In fact, measles remains a common cause

of blindness in many developing countries.

Rare complications include hemorrhagic measles, purpura fulminans,

hepatitis, disseminated intravascular coagulation (DIC), subacute sclerosing

panencephalitis (SSPE), thrombocytopenia, appendicitis, ileocolitis, pericarditis,

myocarditis, acute pancreatitis, and hypocalcemia. Transient hepatitis may occur

during an acute infection.

Approximately 1 of every 1,000 patients develops acute encephalitis, which

often results in permanent brain damage and is fatal in about 10% of patients. In

children with lymphoid malignant diseases, delayed-acute measles encephalitis may

develop 1-6 months after the acute infection and is generally fatal. An even rarercomplication is SSPE, a degenerative CNS disease that can result from a persistent

measles infection. SSPE is characterized by the onset of behavioral and intellectual

deterioration and seizures years after an acute infection (the mean incubation period

for SSPE is approximately 10.8 years).

SSPE has been divided into the following stages :

Stage I Stage I consists of insidious development of neurologic symptoms such as

personality changes, lethargy, difficulty in school, and strange behavior. Stage I may

last from weeks to years. Stage II Stage II is characterized by myoclonus, worsening dementia and long

tract motor or sensory disease. The patient eventually develops a highly

characteristic form of myoclonus in which massive myoclonic jerks occur

approximately every 5 to 10 seconds. Stage II usually lasts 3 to 12 months.

Stages III and IV Stages III and IV are characterized by further neurologic

deterioration with eventual flaccidity or decorticate rigidity and symptoms and signs of

autonomic dysfunction. Myoclonus is absent. Stage IV is a vegetative state. Death

usually occurs during Stage IV but is possible in any of the stages.The rate of

progression can be variable. Stabilization at one stage for a period of time can occur,

though in general patients tend to progress from one stage to the next. Some

patients have a remitting and relapsing course. Seizures can occur in any of the

stages.

Acute disseminated encephalomyelitis (ADEM) is a demyelinating disease

that presents during the recovery phase of measles infection, typically within two

weeks of the exanthem. ADEM is also known as postinfectious or postvaccination

encephalomyelitis. In contrast, subacute sclerosing panencephalitis (SSPE) presents

years after initial infection. ADEM is thought to be caused by a postinfectious

autoimmune response, rather than active measles infection of the central nervous

system. Consistent with this hypothesis is the observation that measles virus has

only rarely been isolated from the brains of patients with ADEM.
http://www.medscape.com/viewarticle/493855http://emedicine.medscape.com/article/969401-overviewhttp://emedicine.medscape.com/article/969401-overviewhttp://www.medscape.com/viewarticle/493855


7/11

The major manifestations of ADEM include fever, headache, neck stiffness,

seizures, and mental status changes such as confusion, somnolence, or coma. Other

findings may include ataxia, myoclonus, choreoathetosis, and signs of myelitis, such

as paraplegia, quadriplegia, sensory loss, loss of bladder and bowel control, and, in

patients with myelitis, back pain. Analysis of cerebrospinal fluid generally

demonstrates a lymphocytic pleocytosis and elevated protein concentration. ADEM isassociated with a 10 to 20 percent mortality. Survivors frequently have residual

neurologic abnormalities including behavior disorders, mental retardation, and

epilepsy.

The complications of measles in the pregnant mother include pneumonitis,

hepatitis, subacute sclerosing panencephalitis, premature labor, spontaneous

abortion, and preterm birth of the fetus. Perinatal transmission rates are low.

F. Diagnosis

Although the diagnosis of measles is usually determined from theclassic clinical picture, laboratory identification and confirmation of thediagnosis are necessary for public health and outbreak control. Laboratoryconfirmation is achieved by means of the following:

Serologic testing for measles-specific IgM or IgG titers Isolation of the virus Reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation

Measles-specific IgM titers

Obtain blood on the third day of the rash or on any subsequent day up to 1 monthafter onset

The measles serum IgM titer remains positive 30-60 days after the illness in mostindividuals but may become undetectable in some subjects at 4 weeks after rashonset

False-positive results can occur in patients with rheumatologic diseases, parvovirusB19 infection, or infectious mononucleosis

Measles-specific IgG titers

More than a 4-fold rise in IgG antibodies between acute and convalescent seraconfirms measles

Acute specimens should be drawn on the seventh day after rash onset Convalescent specimens should be drawn 10-14 days after that drawn for acute

serum The acute and convalescent sera should be tested simultaneously as paired sera

Viral culture

Throat swabs and nasal swabs can be sent on viral transport medium or a viralculturette swab

Urine specimens can be sent in a sterile container

Viral genotyping in a reference laboratory may determine whether an isolate isendemic or imported


8/11

In immunocompromised patients, isolation of the virus or identification of measlesantigen by immunofluorescence may be the only feasible method of confirming thediagnosis

Polymerase chain reaction

RT-PCR, if available, can rapidly confirm the diagnosis of measles[3]

Blood, throat, nasopharyngeal, or urine specimens can be used Samples should be collected at the first contact with a suspected case of measles

Studies for Suspected Complications

Chest radiography

If bacterial pneumonia is suspected, perform chest radiography. The frequent occurrenceof measles pneumonia, even in uncomplicated cases, limits the predictive value of chestradiography for bacterial bronchopneumonia.

Lumbar puncture

If encephalitis is suspected, perform a lumbar puncture. CSF examination reveals thefollowing:

Increased protein Normal glucose Mild pleocytosis with predominance of lymphocyte

G. Management

Treatment of measles is essentially supportive care with maintenance of good

hydration and replacement of fluids lost through diarrhea or emesis. Intravenous (IV)

rehydration may be necessary if dehydration is severe. Fever management with

standard antipyretics is appropriate.

Airborne precautions are indicated for hospitalized children during the period of

communicability (ie, 3-5 day before the appearance of a rash to 4 days after the rash

develops in healthy children and for the duration of illness in patients who are

immunocompromised). Susceptible health care workers should be excused from work

from the fifth to the 21st day after exposure. Hospitalization also be indicated fortreatment of measles complications (eg, bacterial superinfection, pneumonia,

dehydration, croup). Secondary infections (eg, otitis media or bacterial pneumonia)

should be treated with antibiotics; Patients with severe complicating infections (eg,

encephalomyelitis) should be admitted for observation and antibiotics, as appropriate to

their clinical condition.

Vitamin A supplements have been associated with reductions of approximately50% in morbidity and mortality and appear to help prevent eye damage andblindness.The World Health Organization recommends all children diagnosed withmeasles should receive vitamin A supplementation regardless of their country of

residence, based on their age, as follows:


9/11

Infants younger than 6 months50,000 IU/day PO for 2 doses Age 6-11 months - 100,000 IU/day PO for 2 doses Older than 1 year - 200,000 IU/day PO for 2 doses Children with clinical signs of vitamin A deficiency The first 2 doses as

appropriate for age, then a third age-specific dose given 2-4 weeks later

Postexposure prophylaxis should be considered in unvaccinated contacts; timely

tracing of contacts should be a priority. Prevention or modification of measles in exposed

susceptible individuals involves the administration of measles virus vaccine or human

immunoglobulin (Ig).

In the United States, the measles virus vaccine is routinely administered along

with the mumps and rubella vaccines as the measles-mumps-rubella (MMR) vaccine.

The vaccine is preventive if administered within 3 days of exposure. Contraindications to

the vaccine include immunodeficiency; generalized cancers (eg, leukemia, lymphoma);

active, untreated tuberculosis; and therapy with immunosuppressants. HIV infection isonly a contraindication in the presence of severe immunosuppression (ie, CD4 counts

lower than 15%).

Human Ig prevents or modifies disease in susceptible contacts if administeredwithin 6 days of exposure. Human Ig is given to the following individuals:

Those who are immunocompromised Infants aged 6 months to 1 year (morbidity is high in children younger than 1 year Infants younger than 6 months who are born to mothers without measles immunity Pregnant women

In contacts for whom the vaccine should be deferred (eg, pregnant patients),human Ig 0.25 mL/kg (not to exceed 15 mL) should be administered intramuscularly (IM)immediately after exposure, and the measles vaccine should be given 6 months later.Exposed immunocompromised patients with a contraindication to vaccination shouldreceive human Ig 0.5 mL/kg (not to exceed 15 mL) IM.

Modul Task

Male, 4 years old, suffered from high grade fever for 4 days, accompanied by common coldand red conjunctiva. Then there was erythematous maculopapullar rash came from back ofthe ear that is spreading to all of the body. Last immunization was at 4 months old and the

patient never came again because of fever at the time he was had to be had beenvaccinated.

1. What is the patients diagnosis ?2. How is the management for this patient and the prevention ?


10/11

Suggested Readings

1. American Academy of Pediatrics. Measles. In: Pickering LK, ed. Red Book: Report ofthe Committee on Infectious Disease. Elk Grove, Ill: AAP; 2006:441-52.

2. Barinaga, JL et al. Clinical Presentation and Diagnosis of Measles dalam

file:///H:/UpToDate19.3/contents/mobipreview.htm?23/61/24528 20113. Bar-On S, Ochshorn Y, Halutz O, Aboudy Y, Many A. Detection of measles

virus by reverse-transcriptase polymerase chain reaction in a placenta. J

Matern Fetal Neonatal Med. Aug 2010;23(8):935-7.

4. Bekhor, D. Prevention and treatment of measles dalam

file:///H:/UpToDate19.3/contents/mobipreview.htm?26/62/276162011

5. Benkimoun P. Outbreak of measles in France shows no signs of abating. BMJ. May

20 2011;342:d3161.

6. Centers for Disease Control and Prevention (CDC). Update: measles--United States,

January-July 2008. MMWR Morb Mortal Wkly Rep 2008; 57:893.

7. Chen, SSP. Measles dalamhttp://emedicine.medscape.com/article/966220-overview2014

8. Fusilli G, De Mitri B. Acute pancreatitis associated with the measles virus: case

report and review of literature data. Pancreas. May 2009;38(4):478-80.

9. Garg RK. Subacute sclerosing panencephalitis. J Neurol 2008; 255:1861.

10. Global measles mortality, 2000-2008. MMWR Morb Mortal Wkly Rep. Dec 4

2009;58(47):1321-6.

11. Hosoya M, Shigeta S, Mori S, et al. High-dose intravenous ribavirin therapy for

subacute sclerosing panencephalitis. Antimicrob Agents Chemother. Mar

2001;45(3):943-5.

12. Lowes R. Three-Fold Increase in Measles Warrants Vigilance, CDC Says. Medscape

Medical News. Available athttp://www.medscape.com/viewarticle/815514.Accessed

December 9, 2013.

13. Maldonado. In: Principles and Practice of Pediatric Infectious Diseases, Long, SS,

Picketing, LK, Prober, CG (Eds), 3rd Ed, Churchill Livingstone, 2008. p. 1122.

14. Measles outbreaks and progress toward measles preelimination --- African region,

2009-2010. MMWR Morb Mortal Wkly Rep. Apr 1 2011;60(12):374-8.

15. Papania MJ, Wallace GS, Rota PA, Icenogle JP, Fiebelkorn AP, Armstrong GL, et al.

Elimination of Endemic Measles, Rubella, and Congenital Rubella Syndrome From

the Western Hemisphere: The US Experience. JAMA Pediatr. Dec 5 2013

16. Perry RT, Halsey NA. The clinical significance of measles: a review. J Infect Dis. May

1 2004;189 Suppl 1:S4-16.

17. Schneider-Schaulies S, Schneider-Schaulies J. Measles virus-induced

immunosuppression. Curr Top Microbiol Immunol. 2009;330:243-69.

18. Sugerman DE, Barskey AE, Delea MG, et al. Measles outbreak in a highly

vaccinated population, San Diego, 2008: role of the intentionally undervaccinated.

Pediatrics 2010; 125:747.

19. World Health Organization. Global eradication of measles.

file://apps.who.int/gb/ebwha/pdf_files/WHA63/A63_18-en.pdf .2010

20. WHO-recommended surveillance standard of measles.file://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.

html2010
http://h/UpToDate19.3/contents/mobipreview.htmhttp://h/UpToDate19.3/contents/mobipreview.htmhttp://h/UpToDate19.3/contents/mobipreview.htmhttp://h/UpToDate19.3/contents/mobipreview.htmhttp://f/UpToDate19.3/contents/mobipreview.htmhttp://f/UpToDate19.3/contents/mobipreview.htmhttp://emedicine.medscape.com/article/966220-overview%202014http://emedicine.medscape.com/article/966220-overview%202014http://emedicine.medscape.com/article/966220-overview%202014http://emedicine.medscape.com/article/966220-overview%202014http://f/UpToDate19.3/contents/mobipreview.htmhttp://f/UpToDate19.3/contents/mobipreview.htmhttp://www.medscape.com/viewarticle/815514http://www.medscape.com/viewarticle/815514http://www.medscape.com/viewarticle/815514http://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.htmlhttp://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.htmlhttp://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.htmlhttp://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.htmlhttp://www.who.int/immunization_monitoring/diseases/measles_surveillance/en/index.htmlhttp://www.medscape.com/viewarticle/815514http://f/UpToDate19.3/contents/mobipreview.htmhttp://emedicine.medscape.com/article/966220-overview%202014http://emedicine.medscape.com/article/966220-overview%202014http://f/UpToDate19.3/contents/mobipreview.htmhttp://f/UpToDate19.3/contents/mobipreview.htmhttp://h/UpToDate19.3/contents/mobipreview.htmhttp://h/UpToDate19.3/contents/mobipreview.htm


11/11

21. World Health Organization. Vision and Strategy 2006-2015 www.who.int/vaccines-

documents/DocsPDF05/GIVS_Final_EN.pdf,2011

22. World Health Organization. WHO/UNICEF joint statement -- global plan for reducingmeasles mortality 2006-2010.file://www.who.int/immunization/documents/WHO_IVB_05.11/en/index.html 2010
http://www.who.int/vaccines-documents/DocsPDF05/GIVS_Final_EN.pdfhttp://www.who.int/vaccines-documents/DocsPDF05/GIVS_Final_EN.pdfhttp://www.who.int/vaccines-documents/DocsPDF05/GIVS_Final_EN.pdfhttp://www.who.int/immunization/documents/WHO_IVB_05.11/en/index.htmlhttp://www.who.int/immunization/documents/WHO_IVB_05.11/en/index.htmlhttp://www.who.int/immunization/documents/WHO_IVB_05.11/en/index.htmlhttp://www.who.int/vaccines-documents/DocsPDF05/GIVS_Final_EN.pdfhttp://www.who.int/vaccines-documents/DocsPDF05/GIVS_Final_EN.pdf

Module Measles Tanpa Answer

Documents

Transcript of Module Measles Tanpa Answer