Multidisciplinary Seminar on Vector Borne Diseases such as dengue, malaria and chikungunya was discussed. It was introduced that vectors are living organisms that can transmit infectious diseases between humans or from animals to humans. There are two main types of vectors - biological and mechanical. Vector borne diseases account for over 17% of all infectious diseases and cause more than 1 billion cases and over 1 million deaths every year. Dengue, malaria and chikungunya were some of the key vector borne diseases highlighted. Their causative agents, transmission, clinical features and management were explored. Emphasis was placed on prevention and control of their vectors to curb the spread of these diseases.

1. Multidisciplinary Seminar
VECTOR BOURNE DISEASE:
DENGUE, MALARIA &
CHIKUNGUNYA

2. INTRODUCTION
DEFINITION (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

3. • 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

4. 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

7. • 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

8. • 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)

9. Increase of dengue deaths in the adult population since 2003

10. (Microbiology)

11. • 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).

12. • 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.

13. • 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

15. Secondary 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

16. Pa tient rec overs from c la ssic d eng ue c a used b y one of four
serotyp es
Antib od y a g a inst tha t p a rtic ula r serotyp e is p rod uc ed
(p revents the virus from b ind ing to the ma c rop ha g es c ells)
Sec ond d eng ue infec tion b y other
serotyp es
La rg e a mounts of c ross rea c ting a ntib od y to the first typ es a re
p rod uc ed , in c ontra st to the c urrent / new a ntib od y for the
sec ond d engue infec tion
more a ntib od ies p rod uc ed w ill
lea d to la rg e entry of DENV into
m onoc ytes & ma c rop ha g es
Ac tiva te
c omp lement
Inc rea sed va sc ula r
p ermea b ility la rg e a mounts of
c ytokines
la rg e a mounts of
c ytokines
Shoc k & Ha em orrha g eShoc k & Ha em orrha g e
Immune c omp lexes form a tion

17. DENGUE
Internal Medicine Posting

18. Common Presentation
Sx & Relevant PE

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

20. 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.

21. 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)

22. Physical examination
i. Assess mental state and Glasgow Coma Scale (GCS) score
ii. Assess hydration status
iii. 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 effusion
v. Check for abdominal tenderness/ hepatomegaly/ ascites
vi. Examine for bleeding manifestation
vii. Tourniquet test (repeat if previously negative or if there is no
bleeding manifestation)

24. 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)

25. INVESTIGATION

26. Test Explanation
White 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

27. 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

28. 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

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

30. 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.

31. 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.

32. MANAGEMENT

33. Criteria for admission
1. Symptoms :
• Alarm signals
• Bleeding manifestations
• Inability to tolerate oral fluids
• Reduced urine output
• Seizure
2. Signs :
• Dehydration
• Shock
• Bleeding
• Any organ failure
3. Special Situations :
• Patients with co-morbidity
e.g.Diabetes, Hypertension,
Ischaemic
Heart 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 health
facility, no transport, patient living
alone, etc
4. Laboratory Criteria: Rising HCT
accompanied by reducing platelet
count

34. 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.

35. 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.

36. 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

37. SUMMARY

39. 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?

40. CHIKUNGUNYA
(Public Health)

41. 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.

42. • 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.

44. Chikungunya
Microbiology Team

45. 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

46. 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

47. Chikungunya
Internal Medicine Team

48. 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 …

49. Clinical presentations …
• Fever(24h-48h)
• Chills& rigor
• antipyretic
• Arthralgia
• Morning
• Polyarthritis + effusion(small
& large joints)
• Backache
• Headache
Uncommon
• Rash
• Stomatitis
• Oral ulcers
• Hyperpigmentation
• Exfoliative dermatitis
Rare (Adult) sometimes(Child)
Photophobia
Retro-orbital pain
Vomiting
Diarrhea
Meningeal syndrome
Acute encephalopathy
Guideline on management of Chikungunya fever (2008) WHO

50. FBC
Leucopenia
Predominant lymphocyte
ESR
C-reactive protein
Rheumatoid factor ++
Investigation…
Guideline on management of Chikungunya fever (2008) WHO
Viral isolation
PCR
Detection of lgM
Rising titre Ig G antibody

51. Treat symptoms
Fever (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

52. MALARIA
(Public Health)

53. 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%

54. • 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.

57. Malaria
Parasitology Division
OnG Posting
By: Muhammad Helmi

58. Malaria
A disease caused by an Ampicomplexan parasite from the genus
Plasmodium
This organism are vectored by bloodsucking insect

59. 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

60. Life Cycle
SCHIZOGONY
(In Human)
SPOROGONY
(In Mosquito)

61. 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 STATE
5-16 (Depends)
-Headache
-Myalgia
-GIT Disturbances

62. • 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)

63. 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

64. MALARIA
(Internal Medicine Posting)

65. 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. Malarie
Prepatent
Period
6-9 8-12 15-18
Incubation
Period
6-25 8-27 16-40

67. P. falciparum
• The most virulent species
• Attributed to renal failure( autoimmune phenomenon) aka Black
Water Fever
Infection  massive lysis of erythrocytes( hamoglobiurea, jaundice)
 Capilarry blockage of CNS  paralysis,coma and death( cerebral malaria)

68. Malarial Paroxysm
• The febrile attacks of malaria
• May exhibit splenomegaly, hepatomegaly, jaundice and haemolytic
anaemia during the period of malarial paroxysm.
No Species Disease Rigor
1 P. falciparum Malignant Tertian Malaria 36-48 hr
2 P. vivax Benign Tertian Malaria 48 hr
3 P. ovale Benign Tertian Malaria 48 hr
4 P. malariae Quartan Malaria 72 hr
5 P. knowlesi Quartan Malaria 24 hr

69. 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.

70. Diagnosis
• Blood smears
• Quantitative Buffy Coat( QBC) Test
• Rapid Diagnostic Test ( RDT)

71. Blood smears
Thick 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

72. 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.

74. 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.

76. Antimalarial drugs classification
Infective stage Hepatic stage Erythrocytic stage
Sporozoites Primary Latent Asexual
CLASS 1
Chloroquine - - - +
Artemisnin
Compounds
- - - +
Quinine - - - +
Fansidar - - - +
Tetracycline - - - +
CLASS 2
Proguanil - + - +
Atovaquone - + - +
CLASS 3
Primaquine - + + -

77. Goal treatment of malaria
• Cure
- Clinical Cure
- Radical Cure
• Prophylaxis
- Suprresive
- Causal
Classification
• Schizonticides:
Blood : Class I and II
Tissue : Class III

78. 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

79. Management in Pediatrics

80. 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 hours
D2-3: 3 tablets BD
.30 > 13 years 2 ASMQ FDC 100/220mg
once daily for 3 days
>35 D1: 4 tabs stat then again 4 tabs after 8 hours
D2-3: 4 tabs BD

81. 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.

82. Treatment for P. vivax,knowlesi,malariae
Treatment for Plasmodium vivax Treatment for Plasmodium knowlesi or malariae
Total chloroquine 25mg base/kg divided over 3 days
D1:10 mg base/kg stat then 5 mg base/kg 6 hours later
D2: 5 mg base/kg OD
D3: 5 mg base/kg OD
AND
Primaquine* 0. 5 mgbase/kg daily for 14 days
Total chloroquine 25mg base/kg divided over 3 days
D1: 10 mg base/kg stat then 5 mg base/kg 6 hours later
D2: 5 mg base/kg OD
D3: 5 mg base/kg OD

83. Treatment for complicated P.Falciparum
1st line treatment
D1: IV artesunate 2.4 mg/kg on admission, then repeat again at 12h
D2-7: IV artesunate 2.4 mg/kg OD or switch to oral ACT
Parenteral 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
OR
Loading 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
AND
Doxycycline (>8yrs) (3.5 mg/kg OD) OR Clindamycin (<8yrs) (10 mg/kg/dose bd) given for 7 days
Quinine infusion rate should not exceed 5 mg salt/kg body weight per hour
Change 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.

84. Some Points from OnG
Malaria
Accounts 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

85. PREVENTION OF VECTOR
BORNE DISEASE
Dengue, Malaria & Chikungunya Fever

86. INDIVIDUAL Aerosol insecticide
Destroy or prevent potential breeding sites
Window’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)

87. 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

88. 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.

89. 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

90. 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

91. • Tertiary prevention
• Provide standard management for malarial infection

92. PREVENTION AND CONTROL OF
CHIKUNGUNYA
Primary prevention
• Health promotion and education
• Reduce breeding site
• Wear clothing with less exposure, insecticide-treated mosquito nets ,
and repellants
• Mosquito coils and insecticides vaporizers

93. 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