Multidisciplinary Seminar

VECTOR BOURNE DISEASE: DENGUE,

MALARIA & CHIKUNGUNYA

INTRODUCTIONDEFINITION (WHO)

• VECTORS -> Living organisms that can transmit infectious diseases between humans or from animals to humans

• 2 type of VECTORS • Biological = Completes part of its life cycle in the insect host• Mechanical = Transmit physically

• VECTOR-BORNE DISEASES -> Illnesses caused by pathogens and parasites in human

populations

• Vector borne disease account for over 17% of all infectious disease

• Every year, there are more than 1 billion cases & over 1 million death

DENGUE • Caused by DENV 1, DENV 2, DENV 3, DENV 4• Transmitted by Aedes aegypti and Aedes albopictus• Incubation period : 7-10 days• Emerged as a worldwide problem since 1950s• Endemic in at least 100 countries in Asia, the Pacific, the Americas,

Africa, and the Caribbean• Worldwide, around 50 to 100 million people are infected yearly

including 500,000 DHF cases and 22,000 deaths

• Started as a major public health problem in Malaysia from 1973. • Number of reported DF and DHF in Malaysia shows an increasing

trend from 1995 to 2007

• The incidence rate also shows an upward trend from 44.3 cases/100,000 population in 1999 to 181 cases/100,000 population in 2007.

• National target for Incidence rate is 50/100,000 population.• Incidence rate is higher in the age group 15 years and above. (Highest in

working and school going age)

Increase of dengue deaths in the adult population since 2003

DENGUE(Microbiology)

• Caused by dengue virus (mosquito-borne flavivirus ) - transmitted by

mosquitoes (Aedes aegypti & Aedes albopictus).

• Four distinct serotypes DENV-1,2,3 and 4.

• Each episode of infection induces life-long protective immunity to the

homologous serotype but confers only partial and transient protection against

other serotypes.

• Secondary infection - major risk factor for severe dengue due to antibody-

dependent enhancement.

• Other important contributing factors are viral virulence, host genetic

background, T-cell activation, viral load and auto-antibodies.

• Incubation period: 4-7 days (range 3-14).

INTRODUCTION

DENGUE TRANSMISSION• Mosquitoes acquire the virus when they feed on a carrier of

the virus.• Persons with dengue viruses in their blood can transmit the

viruses to the mosquito 1 day before the onset of the febrile period.

• The patient can remain infectious for the next 6-7 days. • The mosquito can transmit dengue virus if it immediately

bites another host. • In addition, transmission occurs after 8-12 days of viral

replication in the mosquito's salivary glands (extrinsic incubation period). The mosquito remains infected for the remainder of its life.

DENGUE TRANSMISSION• Once inoculated into a human host, dengue has an incubation

period of 3-14 days with average 4-7 days(intrinsic incubation period) for viral replication.

• Infection of target cells, primarily those of the reticuloendothelial system, such as hepatocytes and endothelial cells result in the production of immune mediators

INCUBATION PERIOD

PATHOGENESISSecondary infection

– When an individual is infected with heterotypic dengue virus/another serotype of DENV (i.e. secondary infection), they will produces low levels of non-neutralizing antibodies. These antibodies, directed against 1 of 2 surface proteins.

– When bound by macrophage and monocyte Fc receptors, have been proposed to fail to neutralize virus and instead form an antigen-antibody complex.

– This results in increased viral entry into macrophages bearing IgG receptors, allowing unchecked viral replication with increased cytokine production and complement activation, a phenomenon called antibody-dependent enhancement.

– The affected macrophages release vasoactive mediators that increase vascular permeability, leading to vascular leakage, hypovolaemia, and shock

PATHOGENESIS

Patient recovers from classic dengue caused by one of four serotypes

Antibody against that particular serotype is produced (prevents the virus from binding to the macrophages cells)

Second dengue infection by other serotypes

Large amounts of cross reacting antibody to the first types are produced, in contrast to the current / new antibody for the

second dengue infection

more antibodies produced will lead to large entry of DENV into

monocytes & macrophages

Activate complement

Increased vascular permeability large amounts of

cytokines

large amounts of cytokines

Shock & Haemorrhage Shock & Haemorrhage

Immune complexes formation

DENGUE

Internal Medicine Posting

Common Presentation Sx & Relevant PE

Clinical course of dengueThe incubation period for dengue infection is 4-7 days.

Febrile phase (2-7 days) Sudden onset of high grade fever accompanied by facial flushing, skin erythema, generalised body ache, myalgia, arthralgia and headache. Sometimes, nausea and vomiting.

FBC - progressive decrease in total white cell count

Critical phase (3-5days) Duration : 24-48 hours

Rapid drop in temperature may coincide with an increase in capillary permeability in some patients.

Evidence of plasma leakage includes raised HCT (early marker), haemodynamic instability, fluid accumulation in extravascular space (rather late marker) or hypoproteinemia.

Recovery Phase Plasma leakage stops and followed by reabsorption of extravascular fluid.

HCT level stabilises or drops further due to haemodilution following reabsorption of extravascular fluid. The recovery of platelet count is typically preceded by recovery of white cell count.

History• Date of onset of fever/ illness• Oral intake• Assess for the 7 warning signs• Diarrhea• Bleeding• Change in mental state/seizure/dizziness• Urine output (frequency, volume and time of last voiding)• Other important relevant histories:

– Family or neighborhood history of dengue– Jungle trekking and swimming in waterfall (consider leptospirosis, typhus,

malaria)– Recent travel– Recent unprotected sexual or drug use behavior (consider acute HIV

seroconversion illness)– Co-morbidities (consider sepsis particularly in patients with diabetes mellitus)

Physical examinationi. Assess mental state and Glasgow Coma Scale (GCS) scoreii. Assess hydration statusiii. Assess hemodynamic status

- Skin color- Cold/ warm extremities- Capillary filling time (normal <2 seconds)- Pulse rate- Pulse volume- Blood pressure- Pulse pressure

iv. Look out for tachypnea/ acidotic breathing/ pleural effusionv. Check for abdominal tenderness/ hepatomegaly/ ascitesvi. Examine for bleeding manifestationvii. Tourniquet test (repeat if previously negative or if there is no bleeding manifestation)

Pathophysiology of plasma leakage in DHF and DSS

The primary pathophysiological abnormality seen in DHF and DSS is an acute increase in

vascular permeability that leads to leakage of plasma into the extravascular compartment,

resulting in haemoconcentration and hypovolaemia or shock. Hypovolaemia leads to reflex

tachycardia and generalised vasoconstriction due to increased sympathetic output. Clinical

manifestations of vasoconstriction in various systems are as follows:

• a. Skin - coolness, pallor and delayed capillary refill time

• b. CVS - raised diastolic blood pressure and narrowing of pulse pressure

• c. Renal system - reducing urine output

• d. Gastrointestinal system - vomiting and abdominal pain

• e. CNS– lethargy, restlessness, apprehension, reduced level of consciousness

• f. Respiratory system – tachypnoea (respiratory rate >20/min)

INVESTIGATION

Test ExplanationWhite cell count

In the early febrile phase, WCC is usually normal but will decrease rapidly as the disease progresses. This trend of leukopenia should raise the suspicion of possible dengue infection.

Hematocrit A rising HCT is a marker of plasma leakage in dengue infection and helps to differentiate between DF and DHF but it can be masked in patients with concurrent significant bleeding and in those who receive early fluid replacement. Setting the patient’s baseline HCT in the early febrile phase of disease will be very useful in the recognition of a rising HCT level.

A. Disease Monitoring Test

Test Explanation

Platelet Thrombocytopaenia is commonly seen in dengue infection. In the early febrile phase, platelet count is usually within normal range but it will decrease rapidly as the disease progresses to the late febrile phase or at defervescence and it may continue to remain low for the first few days of recovery.

Liver Function Test

Elevated liver enzymes is common and is characterised by greater elevation of the AST as compared to the ALT. The frequency and degree of elevation of the liver enzymes are higher with DHF compared to DF

B. Diagnostic Tests

Test Explanation

Rapid Combo Test (RCT)

Rapid combo tests are assays that can detect the presence of virus as well as antibodies. Can be read within 15-20 minutes. Tests are useful during the early phase of onset when there is viraemia as well as at a later stage when antibodies against dengue begin to rise.

Virus Isolation The most definitive test for dengue infection. It can only be performed in the lab equipped with tissue culture and other virus isolation facilities. It is useful only at the early phase of the illness. Generally, blood should be collected before day 5 of illness; i.e. before the formation of neutralizing antibodies. During the febrile illness, dengue virus can be isolated from serum, plasma and leucocytes. It can also be isolated from post mortem specimens. The monoclonal antibody immunofluorescence test is the method of choice for identification of dengue virus. It may take up to two weeks to complete the test and it is expensive.

Dengue Antigen and Serology Tests by ELISA

To diagnose, we detect for NS1Ag(1-2 days of fever) IgM IgG (showing post infection)

Dengue IgM test

• This antibody titre is significantly higher in primary infections, compared to

secondary infections. Once the IgM is detectable, it rises quickly and peaks at

about 2 weeks after the onset of symptoms, and it undetectable levels by 60

days. Some patient may persist for more than 90 days.

Indirect IgG test

• In primary and secondary dengue infection, dengue IgG was detected in

100% of patients after day 7 of onset of fever. Therefore dengue IgG is

recommended if dengue IgM is still negative after day 7 with the negative IgG

in the initial test sample.

Non-structural protein 1 (NS1 antigen)

• NS1 antigen is a highly conserved glycoprotein that seems to be

essential for virus viability. Secretion of the NS1 protein is a

hallmark of flavivirus infecting mammalian cells and can be found

in dengue infection as well as in yellow fever and West Nile virus

infection. This antigen is present in high concentrations in the sera

of dengue infected patients during the early phase of the disease.

However, the sensitivity of NS1 antigen detection drops from day

4-5 of illness onwards and usually becomes undetectable in the

convalescence phase.

MANAGEMENT

Criteria for admission1. Symptoms :• Alarm signals• Bleeding manifestations• Inability to tolerate oral fluids• Reduced urine output• Seizure2. Signs :• Dehydration• Shock• Bleeding• Any organ failure

3. Special Situations :• Patients with co-morbidity e.g.Diabetes, Hypertension, IschaemicHeart Disease, Coagulopathies, Morbid Obesity, Renal Failure,Chronic Liver disease, COPD,• Elderly (more than 65 years old)• Pregnancy• Social factors that limit follow-up e.g. living far from healthfacility, no transport, patient living alone, etc4. Laboratory Criteria: Rising HCT accompanied by reducing platelet count

Management of dengue + warning signs

• Cases of dengue with warning signs will probably recover with early intravenous rehydration. Some cases will deteriorate to severe dengue.

Management of bleeding• Mild bleeding such as from the gums, per vagina,

epistaxis or petechiae, usually cease spontaneously and do not require blood transfusion.

• Transfusion of blood and blood components in dengue is indicated when there is evidence of significant bleeding.

Discharge criteria

• Afebrile for 48 hours• Improved general condition• Improved appetite• Stable haematocrit• Rising platelet count• No dyspnoea or respiratory distress from pleural effusion or ascites• Resolved bleeding episodes• Resolution/recovery of organ dysfunction

SUMMARY

Case Discussion• Mrs. SK is a 25 years old Malay women with no underlying diseases

presented to Hospital Sg Buloh with complaint of sudden rising fever associated with chills, arthralgia, myalgia, loss of appetite and persistent vomiting for the past 3 days prior to admission. There is no history of travelling, jungle trekking or swimming. She claimed that she lives at kuarters Sungai Buloh which is an endemic dengue area. She also mentioned that there is fogging occurred at her house area recently.

• On examination, the patient looks alert. She is not tachypneic and tachycardic since her respiratory rate is 19 breaths per minute and her pulse rate is 92 beats per minute with normal rhythm and good volume. Her blood pressure is 127/81 which is normal. As for abdominal examination, the abdomen is flat and not distended. On palpation, the abdomen is soft and non-tender and there is no hepatomegaly can be detected. On respiratory and CVS examination, there is no abnormal findings can be seen.

PROVISIONAL DIAGNOSIS? DIFFERENTIAL DIAGNOSIS?

CHIKUNGUNYA

(Public Health)

CHIKUNGUNYA• Caused by an RNA virus that belong to Togaviridae family. • Transmitted by Aedes aegypti and Aedes albopictus• Chikungunya was first identified in Tanzania in the early 1952 and has

caused periodic outbreaks in Asia and Africa since the 1960s.• Outbreaks are often separated by period of 10 years.• Outbreaks usually occur in post monsoon period when vector

densities is very high.

• Between Jan 2006 and Dec 2009, a study was done based on database of a cluster of patients from National Public Health Laboratory with a clinical diagnosis of chikungunya.

• Of the 13,759 patients, only 6,314 patients were laboratory confirmed to have Chikungunya.

• There were 2 small outbreaks within the state of Perak in 2006 and one outbreak in 2008 & 2009 in Johor.

Chikungunya

Microbiology Team

INTRODUCTION• Chikungunya is a disease that is caused by the chikungunya virus

(CHIKV)• Chikungunya is transmitted to human by female mosquito

(Aedes aegypti and Aedes albopictus).• They bite mostly during the daytime.• Chikungunya is classified as an alphavirus belonging to the

Togaviridae family. The virus is single-stranded RNA surrounded by a lipid envelope.

• The viral particles are small (60-70 nanometers in diameter) and spherical.

• Incubation period is 4 to 8 days but can range from 2 to 12 days.-Medical microbiology 4th edition

Pathogenesis• After inoculation through the bite of an infected

mosquito in the skin, there is transient viremia, and arthropods vectors acquire the virus by sucking blood during this period.

• Then viral replication occurs in liver, spleen, muscle, and lymph nodes.

• Virus then enters the bloodstream and is disseminated.• Interferon (IFN) is early activated, but the viruses

developed several mechanisms to inhibit this antiviral response.

-Molecular Mechanisms Involved in the Pathogenesis of Alphavirus-Induced Arthritis

Chikungunya

Internal Medicine Team

A 33 y/o man presents with high grade fever for 2 days associated with chills, rigor, body rash, severe joint

and muscle pain. Otherwise, no nausea, no vomiting, no headache, no

bleeding tendency, no retro-orbital pain, no diarrhea, no history of jungle trekking, no history of swimming, no similar symptoms in the family members and he does

not lives in dengue prone area.

CASE …

Clinical presentations …

• Fever(24h-48h)• Chills& rigor• antipyretic

• Arthralgia• Morning• Polyarthritis + effusion(small

& large joints)

• Backache• Headache

Uncommon • Rash• Stomatitis• Oral ulcers• Hyperpigmentation• Exfoliative dermatitisRare (Adult) sometimes(Child)PhotophobiaRetro-orbital painVomitingDiarrheaMeningeal syndromeAcute encephalopathy

Guideline on management of Chikungunya fever (2008) WHO

FBCLeucopeniaPredominant lymphocyte

ESRC-reactive proteinRheumatoid factor ++

Investigation…

Guideline on management of Chikungunya fever (2008) WHO

Viral isolationPCRDetection of lgMRising titre Ig G antibody

Treat symptomsFever (paracetamol)Joint pain(NSAID) Dehydration(IV fluid )Physiotherapy (Monitor disability)Skin rash (Calamine lotions/ zinc oxide

cream)

Management…

Guideline on management of Chikungunya fever (2008) WHO

MALARIA(Public Health)

MALARIA• Caused by Plasmodium parasite ( P. falciparum, P. vivax, P. malariae

and P. ovale )• Transmitted by

• Anopheles mosquitoes

• According to WHO, in December 2015, there were 214 million cases of malaria and 438 000 deaths.

• Between 2000 and 2015, malaria• Incidence fell by 37% globally • Mortality rates decreased by 60%

• In Malaysia, Malaria cases have been on the decline from 12,705 cases in 2000 to 4,725 cases in 2012.

• For the past decade (2000-2012) :-- Peninsular Malaysia (3,918 cases -> 1,097 cases)- Sarawak ( 3,011 cases -> 1,571 cases)- Sabah ( 5,776 cases -> 2,052 cases)

• Number of malaria deaths is also reduced from 35 in 2000 and to 16 deaths in 2012.

MalariaParasitology Division

OnG PostingBy: Muhammad Helmi

MalariaA disease caused by an Ampicomplexan parasite from the genus

Plasmodium

This organism are vectored by bloodsucking insect

Knowing The Enemy

-Until today there are 5 types of Malarial parasites

• Plasmodium Vivax• Plasmodium Ovale• Plasmodium Malariae• Plasmodium Falciparum• Plasmodium Knowlesi

Harbored by Anopheles mosquito

Life Cycle

SCHIZOGONY(In Human)

SPOROGONY(In Mosquito)

SCHIZOGONY• Begins with an bite of an infected female Anopheles mosquito

• As blood is drawn out saliva & spindle shaped sporozoites is injected

• Sporozoites make their way to the liver and will reside in the parenchymal cell

• Begin asexual development (schizogony)

• Produces Merozoites which burdens the parenchyma

• Rupture of parenchymal cell

• Merozoites enters the circulation

• For Vivax & Ovale, some sporozoites will go into hypnozoites which will lay dormant

EXOERYTHROCYTIC STATE5-16 (Depends)

-Headache

-Myalgia

-GIT Disturbances

• Circulating Merozoite invade RBC & reticulocytes evelops to young throphozoites

• They will feed on the hemoglobin for growth

• The byproduct will form malarial pigment

• Thropozoites begins to enlarge until it’s nucleus divides to form schizont

• Mature schizont undergoes schizogony forming merozoites (Quantity depends on species)

• RBS unable to contain these parasites & lyse

• Merozoites & all the immunogenic by-product is released to the bloodstream

• This causes MALARIAL PAROXYSYM

• After several generations, some of the merozoites undergo sexual differentiation (Gametogenesis)

• The merozoite develop to Macro (F) & Microgametocytes (M)

• Ingested by Anopheles

ERYTHROCYTIC STATE(Shaking Chills & Fever)

SPOROGONY• The gametocytes matures in the

mosquito

• The union of Macro & Microgametocytes produces a zygote which is known as ookinate

• This stage penetrates to the gut wall and grows to oocyst

• Oocyst gives rise to sporozoites which migrates to salivary gland to repeat the cycle

MALARIA(Internal Medicine Posting)

Clinical Manifestations• The typical Prepatent and Incubation periods following sporozoites inoculation vary slightly

according to the species.

• Prepatent period : time between sporozoite inoculation and the appearance of parasites in the blood

• Incubation period : the time between sporozoite inoculation and the on

Days P. Falciparum P. vivax/P. ovale P. MalariePrepatent Period

6-9 8-12 15-18

Incubation Period

6-25 8-27 16-40

P. falciparum• The most virulent species• Attributed to renal failure( autoimmune phenomenon) aka Black

Water FeverInfection massive lysis of erythrocytes( hamoglobiurea, jaundice) Capilarry blockage of CNS paralysis,coma and death( cerebral malaria)

Malarial Paroxysm• The febrile attacks of malaria• May exhibit splenomegaly, hepatomegaly, jaundice and haemolytic

anaemia during the period of malarial paroxysm.No Species Disease Rigor1 P. falciparum Malignant Tertian Malaria 36-48 hr2 P. vivax Benign Tertian Malaria 48 hr3 P. ovale Benign Tertian Malaria 48 hr4 P. malariae Quartan Malaria 72 hr5 P. knowlesi Quartan Malaria 24 hr

Malarial Paroxysm• Consists of three stages ( 4-8 hours)1. Cold stage - Last 15-60 minutes- Sudden onset of chils, despite elevated

temperature

2. Hot stage- Last 2-6 hours.- Feels an intense heat accompanied by

severe headache, fatigue, dizziness, anaeroxia, myalgia, and nause

3. Sweating stage- Last 2-4 hours- Profuse sweating will ensue and fever will

start to decline.- Patient exhausted and weak, usually fall

asleep.

* Upon awakening, the patient usually feels well, other than being tired, and does not exhibit symptoms until onset of next paroxysm.

Diagnosis

• Blood smears

• Quantitative Buffy Coat( QBC) Test

• Rapid Diagnostic Test ( RDT)

Blood smearsThick smear- Good screening test- Positive or negative- Difficult to diagnose species

Thin smears- Good species differentiation- Requires more time to interpret- Low density infections can be

missed

Quantitative Buffy Coat• The buffy coat is the fraction of an anticoagulated

blood sample that contains most of the white blood cells and platelets following density gradient centrifugation of the blood.

• The blood is taken in a QBC capillary tube which is coated with (a fluorescent dye) and centrifuged.

• The fluorescing parasites can then be observed under ultraviolet light at the interface between red blood cells and buffy coat.

Rapid Diagnostic Test• It detects evidence of malaria parasites (antigens) in human blood. • RDT permit a reliable detection of malaria infections even in remote

areas with limited access to good quality microscopy services.• The tests are simple and the procedure can be performed on the spot

in field conditions. • These tests use finger-stick or venous blood, the completed test takes

a total of 15–20 minutes, and a laboratory is not needed.

Antimalarial drugs classificationInfective stage Hepatic stage Erythrocytic stage

Sporozoites Primary Latent Asexual

CLASS 1

Chloroquine - - - +Artemisnin Compounds

- - - +

Quinine - - - +Fansidar - - - +

Tetracycline - - - +CLASS 2

Proguanil - + - +Atovaquone - + - +

CLASS 3

Primaquine - + + -

Goal treatment of malaria• Cure- Clinical Cure- Radical Cure

• Prophylaxis- Suprresive- Causal

Classification

• Schizonticides:Blood : Class I and IITissue : Class III

Treatment• For all Plasmodium infections sensitive- Chloroquine : loading dose followed by repeated dose for 3 days- Primaquine : day 4 to 14 for vivax and ovale• CQ resistant falciparum malaria :- Artemisnin Combination Therapy• Severe falciparum malaria- Quinine/ ACT parentral, followed by oral ACT

Management in Pediatrics

Uncomplicated P. Falciparum Malaria

1st line treatment

Preffered treatment Alternative treatment

Artesunate/ mefloquine (ASMQ) Artemether/ lumefantrine

Weight (kg) Age dose Weight (kg) dose

5-8 6-11 months 1 ASMQ FDC 25/55mg once daily for 3 days

5-14 DI: 1 tab stat then 1 tab again after 8 hours D2-3: 1 tab BD

9-17 1-6 years 2 ASMQ FDC 25/55mg once daily for 3 days

15-24 D1: 2 tabs stat then 2 tabs again after 8 hours D2-3: 2 tablets BD

18-29 7-12 years 1 ASMQ FDC 100/220mg once daily for 3 days

25-35 D1: 3 tabs stat then 3 tabs again after 8 hoursD2-3: 3 tablets BD

.30 > 13 years 2 ASMQ FDC 100/220mgonce daily for 3 days

>35 D1: 4 tabs stat then again 4 tabs after 8 hoursD2-3: 4 tabs BD

SECOND-LINE TREATMENT FOR TREATMENT FAILURE

• An alternative ACT ( if Riamet were used in the first regimen, use ASMQ for treatment failure and vice-versa)

• OR• • (oral) Artesunate 4mg/kg OD plus clindamycin 10mg/kg bd for a total

of 7 days • OR• • Quinine 10mgsalt/kg 8 hourly plus clindamycin 10mg/kg bd for a total

of 7 days.• Add primaquine 0.75mg base/kg single dose OD if gametocyte is present

at any time during treatment. Check G6PD before giving primaquine.

Treatment for P. vivax,knowlesi,malariae

Treatment for Plasmodium vivax Treatment for Plasmodium knowlesi or malariae

Total chloroquine 25mg base/kg divided over 3 daysD1:10 mg base/kg stat then 5 mg base/kg 6 hours later D2: 5 mg base/kg ODD3: 5 mg base/kg OD ANDPrimaquine* 0. 5 mgbase/kg daily for 14 days

Total chloroquine 25mg base/kg divided over 3 daysD1: 10 mg base/kg stat then 5 mg base/kg 6 hours later D2: 5 mg base/kg ODD3: 5 mg base/kg OD

Treatment for complicated P.Falciparum1st line treatmentD1: IV artesunate 2.4 mg/kg on admission, then repeat again at 12hD2-7: IV artesunate 2.4 mg/kg OD or switch to oral ACTParenteral artesunate should be given for a minimum of 24h or until patient is able to take orally and thereafter to complete treatment with a complete course of oral ACT (ASMQor Riamet). Avoid using ASMQ (Artesunate + mefloquine) if patient presented initially with impaired consciousness as increased incidence of neuropsychiatric complications associated with mefloquine following cerebral malaria have been reported. IM artesunate (same dose as IV) can be used in patients with difficult intravenous access.Children with severe malaria should be started should be started on broad-spectrum antibiotic treatment immediately at the same time as antimalarial treatment.

SECOND LINE TREATMENT

D1 : IV Quinine loading 7mg salt/kg over 1 hour followed by infusion quinine 10mg salt/kg over 4 hours then 10mg/kg 8hourly ORLoading 20mg salt/kg over 4 hours then IV 10mg salt/kg 8 hourly (Dilute quinine in 250ml of D5% over 4 hours)D2-7 : IV Quinine 10mg/kg 8 hourly ANDDoxycycline (>8yrs) (3.5 mg/kg OD) OR Clindamycin (<8yrs) (10 mg/kg/dose bd) given for 7 daysQuinine infusion rate should not exceed 5 mg salt/kg body weight per hourChange to oral Quinine if able to tolerate orally. (Max Quinine per dose = 600mg.) Reduce IV quinine dose by one third of total dose if unable to change to Oral quinine after 48 hours or in cases with renal failure or liver impairment.

Some Points from OnG

MalariaAccounts to 10% maternal mortality worldwide…. Due to ______________

Miscarriage, Preterm Birth, IUGR may be a possible sequele of malaria

Treatment is as discussed by Internal Medicine & teratogens should be avoided

ANEMIA

INFECTION PREGNANGY PRETERM LABOUR

PREVENTION OF VECTOR BORNE DISEASE

Dengue, Malaria & Chikungunya Fever

INDIVIDUAL Aerosol insecticideDestroy or prevent potential breeding sitesWindow’s mosquito net

COMMUNITY Gotong-royong

DISTRICTIC HEALTH OFFICER Health promotions & educations by Health Promotion Unit (UPK)Communication for Behavioural Impact (COMBI)

Primary Prevention (vector control)

Secondary Prevention (outbreak control)• Upgrade the effectiveness in lab diagnosis

• Increase usage of new and modern facilities.

• Management of epidemic • Establish epidemic investigation team• Elimination of adult mosquitoes: Fogging(Diesel + Gokilaths/Actelic ) & Ultra Low

Volume Spraying• Larvaciding (Abate)• Ovitrapping• “Gotong-royong”

• Monitor number of infections • 24 hours notification by medical personnel• Monitor the unidentified fever cases.• Self- reporting to nearest local health clinic• Ensure no new cases reported at Day 14

Tertiary Prevention : (prevention of death)

• Provide standard management of dengue infection such as Clinical

Practice Guideline (CPG) for all medical personnel.

• Re-notification by health personnel if the diagnosis has been

changed from DF to DHF or DF to other diagnosis.

• Carry out compulsory education on dengue hemorrhagic fever for

medical personnel on a continuous basis.

National dengue prevention and control program•Dengue Surveillance•National Cleanliness Policy and Integrated Vector Management (IVM)•Management of Dengue Cases•Social Mobilization and Communication for Dengue•Dengue Outbreak Response•Dengue Research•Reduction of Dengue Burden In The Klang

PREVENTION OF MALARIA• Primary prevention

• Health education• Malarial vaccine (being developed)• Proper clothing , usage of bed nets and repellants• Drug prophylaxis• Anti adult mosquito :indoor spraying with residual insecticides(pyrethroids)• Anti larva measures : biological control

• Secondary prevention• Notification and enforcement• Screening to prevent transfusional malaria

• Tertiary prevention• Provide standard management for malarial infection

PREVENTION AND CONTROL OF CHIKUNGUNYAPrimary prevention• Health promotion and education• Reduce breeding site• Wear clothing with less exposure, insecticide-treated mosquito nets ,

and repellants• Mosquito coils and insecticides vaporizers

Secondary prevention• Diagnosis and treatment• no specific antiviral drug treatment for chikungunya.• Treatment is directed primarily for relieving symptoms

Tertiary prevention• Provide standard management for chikungunya infection