This presentation may help you understand the malarial infection. this includes major points that are necessary to understand it's route of infection and control.

1. MALARIA
SAFI UR REHMAN QAMAR + CHERYL LYNN C. TAN
27 SEPTEMBER 2019

2. INTRODUCTION
• Malaria is a mosquito-borne disease caused by 5 Plasmodium spp.
 P. falciparum
 P. vivax
 P. ovale
 P. malariae
 P. knowlesi
• Malaria is transmitted by female Anopheles mosquitoes

3. MECHANISM OF DISEASE
• P. falciparum have two life stages.
• Human as a host for asexual reproduction.
• Anopheles mosquito for sexual reproduction.
1. Sporozoites Stage
2. Merozoites Stage
3. Trophozoites Stage
4. Schizonts Stage
5. Gametocytes Stage
www.cdc.gov/dpdx/malaria/modules/malaria_LifeCycle

4. MOLECULAR MECHANISM
• Firstly, the invagination of plasma
membrane during parasite attack that
helps in the formation and regulation of
the parasitophorous vacuolar membrane.
• Secondly, the alternation in the
functioning of antigen during the
development of intracellular parasite
(Dvorak et al., 1975).
• MSP-1 is the main protein which
interacts with the glycoprotein band 3 of
RBCs (Healer et al., 2002).

5. PATHOLOGY
• P. falciparum have the ability of cytoadherence.
• Therefore adhere with the vascular endothelial layer of liver, kidney, brain and lung.
• Parasite starts to replicate and attack more non-infected RBCs and activate
the immune system. This process is called sequestration.
This process is coordinated by three main components (Reeder et al., 1999):
1. P. falciparum histidine-rich protein (PFHRP) links with the erythrocyte membrane
protein 1 (EMP 1)
2. ICAM 1 Receptor
3. CD 36

6. HOST DEFENSE
• Sporozoite entry activate T cells,
cytokines and nitic oxide is produced.
• Cell-mediated immunity (CMI) is
activated against merozoite-infected
cells (Good et al., 1998).
• Antibodies block the parasitic invasion
of RBCs during merozoite stage.
• Antibody further block gametocytes to
develop inside the mosquito gut.
http://idmod.org/docs/malaria/_images/Malaria_I
nfection_within_host_parasite_dynamics.png

7. There are 2 commonly used tests to diagnose malaria
infection:
• Microscopic Analysis of Patient's Blood
 Thick Blood Smear - Presence of Plasmodium spp.
 Thin Blood Smear – Identify the specific specie and
parasite density
• Rapid Diagnostic Test
 Antigen present in all Plasmodium spp.
 Antigen specific to P. falciparum
www.who.int/malaria/areas/diagnosis/rapid-diagnostic-
tests/about-rdt/en/
www.clker.com/clipart-273407.html
DIAGNOSIS

8. • 3 groups of antimalarial
drugs:
Adapted from www.cdc.gov/dpdx/malaria/modules/malaria_LifeCycle
TREATMENT

9. • 3 groups of antimalarial
drugs:
Adapted from www.cdc.gov/dpdx/malaria/modules/malaria_LifeCycle
 1st Group – Artemisinin,
Chloroquine, Quinine
TREATMENT
Asexual Blood
Stage

10. • 3 groups of antimalarial
drugs:
Adapted from www.cdc.gov/dpdx/malaria/modules/malaria_LifeCycle
 2nd Group - Atovaquone +
Proguanil
TREATMENT
Primary Liver Stage +
Asexual Blood Stage

11. • 3 groups of antimalarial
drugs:
Adapted from www.cdc.gov/dpdx/malaria/modules/malaria_LifeCycle
 3rd Group – Primaquine,
Tafenoquine
TREATMENT
Primary Liver Stage +
Hypnozoite + Sexual
Blood Stage

12. • Factors to consider when deciding on the treatment:
 Species causing the infection
 + Primaquine for spp. with hypnozoite stage
 Susceptibility of the parasite / presence of resistance
 P. vivax - Chloroquine for chloroquine susceptible strain; ACT for
chloroquine resistant strain
 Clinical status of the patient
 Severe or uncomplicated malaria
TREATMENT

13. • P. falciparum developed resistance to almost all
available antimalarial drugs.
• The only effective treatment for P. falciparum malaria
is Artemisinin-Based Combination Therapy.
• Artemisinin-Resistance has been confirmed in SEA countries.
• Artemisinin-Resistance is due to a mutation in Pfk13 gene
encoding the kelch13 propeller.
• Mutation in Pfk13 is correlated with delayed parasite clearance
time.
ANTIMICROBIAL RESISTANCE

14. Vector Control
PREVENTION
Personal Protective
Measure
Chemoprophylaxis
https://clipground.com/pic/get
https://www.istockphoto.com

15. • Malaria is curable but only when early diagnosis is made, and
treatment is given in a timely manner.
• Resistance to available antimalarial drugs can lead to high mortality
rate.
• Actions must be made to prevent further development of
resistance.
• Treatment of the infection is not the key to malaria
eradication; PREVENTION is.
• Vaccine is a good way to prevent malaria.
PERSONAL COMMENTARY

16. • Dvorak JA, Miller LH, Whitehouse WC, Shiroishi T. Science. 1975;187(4178):748-50.
• Healer J, Crawford S, Ralph S, McFadden G, Cowman AF. Infect Immun. 2002;70(10):5751-8.
• Reeder JC, Cowman AF, Davern KM, Beeson JG, Thompson JK, Rogerson SJ, et al. PNAS.
1999;96(9):5198-202.
• Good MF, Kaslow DC, Miller LH. Annual review of immunology. 1998;16(1):57-87.
• Vinetz JM. Chemotherapy of Malaria. In: Brunton LL, Hilal-Dandan R, Knollmann BC, editors.
Goodman & Gilman's: The Pharmacological Basis of Therapeutics, 13e. New York, NY: McGraw-
Hill Education; 2017.
• Organization WH. World Malaria Report 2018. Luxembourg: World Health Organization; 2018.
• Organization WH. Guidelines for the treatment of malaria: World Health Organization; 2015.
REFERENCES

17. ANOPHELES DISTRIBUTION
Kiszewksi et al., 2004.

18. RAPID DIAGNOSTIC TEST
https://www.who.int/malaria/areas/diagnosis/rapid-diagnostic-tests/about-rdt/en/

19. ANTI-MALARIAL DRUGS