MALARIA INFECTION IN SUBSAHARAN AFRICA .pptx

malaria infection

1. MALARIA INFECTION UNIVERSITY OF ABUJA UNIVERSITY OF ABUJA COLLEGE OF HEALTH SCIENCES DEPARTMENT OF HISTOPATHOLOGY AND FORENSICS 19/203MBB/050 & 18271012

2. OUTLINES Introduction Relevant history Epidemiology Parasitology Etiology Pathogenesis Clinical features Treatment Diagnosis and investigation conclusion

3. INTRODUCTION Malaria is a potentially life threatening vector-borne infectious disease caused by single-celled protozoan parasites of the genus Plasmodium which could be; Plasmodium viviax ( P.vivax ), Plasmodium falciparum ( P.falciparum ), Plasmodium malariae ( P.malariae )and Plasmodium ovale ( P.ovale ). The parasite is spread to humans through the bites of an infected female anopheles mosquito. Man develops disease after 10 to 14 days of being bitten by an infective mosquito

4. BRIEF HISTORY Malaria parasites is believed to be with us since the dawn of time based on fossil record of mosquitoes up to 30 million years old 1880 - Charles Louis Alphose Lavern discovered malarial parasite . 1898 - Italian scientists Amico Bignami , Battista Grassi and Giovanni Bastianelli – Described the life cycle of parasite. 1902 – Ronald Ross was awarded a Nobel Prize for the demonstration of the vector Anopheles mosquito while serving in India.

5. EPIDEMIOLOGY Malaria remains one of the world's most devastating human parasitic infection. Globally, m alaria is said to cause about 250 million cases and over 500,000 deaths in about 85 nations annually. Malaria affected an estimated 219 million people worldwide in 2017 and killed more than 435,000 people . Malaria occurs in every age group and gender, but the burden is most in children and pregnant women. According to WHO, 90 % of deaths from malaria occurs in sub-Saharan Africa where malaria is a leading cause of death in children younger than 5 years of age . Malaria occurs primarily in tropical and some subtropical regions of Africa , Central and South America , Asia and the Oceania’s . In these areas, there is a tremendous variation in the intensity of transmission of infection

6. EPIDEMIOLOGY MALARIA WORLD MAP

7. MALARIA DISTRIBUTION IN NIGERIA

8. ETIOLOGY OF MALARIA Four Species known to infect Human Plasmodium vivax – Benign Tertian Malaria P. ovale - Ovale tertian Malaria P. malariae – Quartan malaria P. falciparum – Falciparum malaria or Malignant Tertian malaria. Falciparum accounts for 90% of deaths due to malaria and vivax is the most widely spread species because it exists in both temperate and tropical climates.

9. PARASITOLOGY Plasmodium spp are species of protozoa that infect the gastrointestinal tract, blood or tissue of man. They replicate intracellularly . They are susceptible to desiccation and their life cycle usually does not have a free environmental stage . Transmission between host ( arthropod vectors ) alternate between two forms; Trophozoite or Cyst forms . They survive in humans by subverting or evading the immune system, they show tropism for certain tissue essential for completing their life cycle . Human beings are intermediate host, while mosquitoes are definite host to Plasmodium spp.

10. PARASITOLOGY Phylum: Apicomplexa Class: Haematozoea Order: Haemosporida Genus: Plasmodium

11. RISK FACTORS OF MALARIA Stagnant water Temperature and humidity  Urbanization Altitude: seasonal variation Proximity to water bodies Environmental management Climate change International travel

12. LIFE CYCLE AND PATHOGENESIS The life cycles of the Plasmodium species are similar, although P. falciparum differs in ways that contribute to its greater virulence. P. vivax , P. ovale , P. knowlesi , and P. malariae cause low levels of parasitemia , mild anemia, and, in very rare instances, splenic rupture and nephrotic syndrome The life cycle of Plasmodium species is simple, as it involves only humans and mosquitoes. When the mosquito takes a blood meal, sporozoites are released into the human’s blood and, within minutes, attach to and invade liver cells by binding to the hepatocyte receptor for the serum protein. Within liver cells, malaria parasites multiply, releasing as many as 30,000 merozoites when each infected hepatocyte ruptures. During P. falciparum infection, rupture usually occurs within 8 to 12 weeks . In contrast, P. vivax and P. ovale form latent hypnozoites in hepatocytes, which cause relapses of malaria weeks to months after initial infection. The infection of the liver and development of merozoites is called the exoerythrocytic stage.

13. LIFE CYCLE AND PATHOGENESIS This stage is asymptomatic. Once released from the liver, Plasmodium merozoites use a lectin-like molecule to bind to sialic acid residues on glycophorin molecules on the surface of red cells and invade by active membrane penetration. Within the red cells ( erythrocytic stage ) the parasites grow in a membrane-bound digestive vacuole which hydrolyzes hemoglobin through secreted enzymes. The trophozoite is the first stage of the parasite in the red cell and is defined by the presence of a single chromatin mass. The next stage, the schizont , has multiple chromatin masses, each of which develops into a merozoite . Upon lysis of the red cell, the new merozoites infect additional red cells. Paroxysmal fever, chills, and rigors characteristic of malaria occur when the merozoites are released into the blood.

14. LIFE CYCLE AND PATHOGENESIS P. falciparum causes infected red cells to clump together (rosette) and to stick to endothelial cells lining small blood vessels (sequestration), which blocks blood flow. Several proteins, including P. falciparum erythrocyte membrane protein 1 (PfEMP1), associate and form knobs on the surface of red cells. PfEMP1 binds to ligands on endothelial cells, including CD36, thrombospondin, VCAM-1, ICAM-1, and E-selectin. Red cell sequestration decreases tissue perfusion and leads to ischemia, which is responsible for the manifestations of cerebral malaria, the major cause of death in children with malaria. In P. falciparum infection, GPI-linked proteins, including merozoite surface antigens, are released from infected red cells and induce cytokine production by host cells.

15. LIFE CYCLE AND PATHOGENESIS These cytokines, including TNF, IFN-γ, and IL-1, suppress production of red blood cells, increase fever, stimulate the production of reactive nitrogen species (leading to tissue damage), and induce expression of endothelial receptors for PfEMP1. Host resistance to Plasmodium can be i ntrinsic or acquired . Intrinsic resistance stems from inherited alterations that reduce the susceptibility of red cells to productive Plasmodium infections. Resistance may also be acquired following repeated or prolonged exposure to Plasmodium species, which stimulates a partially protective immune response.

16. THE MALARIA CYCLE Dr. Y. J. Peter ( BMBCh , MSc, FMCPath

17. CLINICAL FEATURES The clinical presentation of malaria infection is not specific and can mimic several other clinical cases. Plasmodiasis is associated with immune suppression. But typically, it presents in stages: Cold stage which presents as shivering and feeling cold. Hot stage presents as fever, flush, dry skin, headache, nausea and vomiting. Severe stage presents as abdominal colic, abnormal behaviour and/or altered consciousness.

18. CLINICAL FEATURES Fever Chills General feeling of discomfort Headache Nausea and vomiting Diarrhea Abdominal pain Muscle or joint pain Fatigue Rapid breathing Rapid heart rate Cough

19. DIAGNOSIS AND INVESTIGATION The gold standard for the diagnosis of Malaria is microscopy of blood smear. The rapid diagnostic test (RDT) strip for malaria has been recommended by WHO. The principle is based on the detection of Histidine rich protein and pLDH produced by the plasmodium in the serum of the patient. Its limitations are enormous and may not be used for clinical diagnosis of malaria. It is helpful in epidemiological studies. Polymerase chain reaction may also be used for the diagnosis of malaria. It is best for determining mixed plasmodia infection as well as the resistant genes of the parasite. Its clinical application is limited.

20. COMPLICATIONS OF MALARIA Cerebral malaria, commonly caused by Plasmodium falciparum Acute renal failure Hypoglycemia Jaundice Liver failure Hypotension Bleeding disorder Anemia

21. TREATMENT The treatment of Plasmodiasis is with antimalarials and it is dependent on the clinical assessment of the patient such as; Simple Plasmodiasis Resistant or Recurrent Plasmodiasis Plasmodiasis in pregnancy Plasmodiasis in a Child Plasmodiasis with comorbidity Plasmodiasis with haemoglobinopathy Plasmodiasis with G-6-PD deficiency

22. TREATMENT Antimalarials can be classified based on their chemical structure; 4 Aminoquinolones e.g Chloroquine Quinoline methanol e.g Mefloquine Cinchona alkaloids e.g Quinine Biguanide e.g Proguanil Diaminopyrimidine e.g Pyrimethamine 8 Aminoquinolones e.g Primaquine Antibiotics e.g Tetracycline Sesquitapine lactone e.g Artemether

23. PREVENTION AND CONTROL The control of the vector is the primary means of prevention of malaria Regular mass treatment of children is useful. Preventative chemotherapy in pregnant women has been very helpful in reducing the burden of malaria. The use of insecticide treated mosquitoes net is very important There is no vaccine commercially available for the prevention of Plasmodiasis . Use of monoclonal antibodies may help malaria naïve patients

24. CONCLUSION In conclusion, malaria remains a global health challenge but advances in prevention, diagnosis, and treatments offer hope for its control and eventual eradication. Continued efforts in education, vector control and research are crucial to reducing transmission and minimizing the disease’s impact on affected populations worldwide.

25. REFERENCES Kumar, V., Abbas, A. and Aster, J. (2020) Robbins and Cotran Pathologic Basis of Diseases. 10th Edition , Elsevier, Amsterdam Jawetz , Melnick & Adelberg’s Medical Microbiology 27ed. Karen , W. (2015) Lippincott Illustrated Reviews Pharmacology . 6th Edition, Wolters Kluwer, Alphen and den Rijn, 456-457 .