Malaria Quiz on Diagnosis and Complications

Malaria Epidemiology

• 40% of the global population lives in malaria-endemic areas.
• Malaria affects approximately 270 million people annually, with a mortality rate of 1%.
• This results in 1.27 to 2.7 million deaths yearly, predominantly within the 2-30 year age bracket in Africa.
• P. falciparum is prevalent in most African countries, the Pacific Ocean, and Central South America.
• P. vivax is found mainly in northern Africa.

Malaria Geographic Distribution

• A map depicts malaria transmission areas globally.
• Areas with limited malaria transmission or risk are also shown.
• The majority of transmission clusters are shown in Africa.

Malaria Parasite Prevalence

• P. ovale is endemic to West Africa.
• P. malariae is uncommon outside of Africa.
• In Sudan, P. falciparum is common, along with P. vivax and P. malariae, but not P. ovale.

Malaria Etiology

• Malaria is caused by four species of Plasmodium.
• P. falciparum causes malignant tertian malaria.
• P. vivax and P. ovale cause benign tertian malaria.
• P. malariae is associated with quartan malaria.

Malaria Transmission

• Transmission occurs primarily through infected female Anopheles mosquitoes.
• Approximately 45% of these mosquitoes are efficient vectors.
• Key efficiency factors include longevity and biting efficiency.
• Other transmission routes exist.

Malaria Life Cycle

• The sexual cycle of Plasmodium occurs within mosquitoes (8-35 days).
• The asexual cycle begins with the mosquito bite, which introduces sporozoites into the bloodstream.
• Sporozoites infect the liver, releasing merozoites into the circulation.
• Merozoites infect red blood cells (RBCs) initiating the erythrocytic cycle, producing more parasites.
• Some merozoites develop into gametocytes in the RBCs to complete the cycle.
• The cycle from liver to RBCs takes 5 days for P. falciparum, 8 for P. vivax, 9 for P. ovale, and 15 for P. malariae.

Malaria Erythrocytic Cycle

• Infected RBCs release merozoites, initiating asexual cycles, and some mature into gametocytes.
• P. falciparum infects all RBC types, particularly younger cells.
• P. vivax & P. ovale mostly infect new RBCs.

Malaria Immunity

• Natural immunity factors include sickle-cell trait, thalassemia, G6PD deficiency, Duffy antigen negativity, HLA antigen types and spleen versus splenectomy.
• Acquired immunity results from macrophage stimulation by activated T lymphocytes.
• Merozoite generation produces antigens different from previous ones resulting in antigenic variability.

Malaria Pathogenesis

• Parasitized RBCs block vital organs (sequestration) leading to ischemia, hypoperfusion and anaerobic glycolysis.

• Inflammatory cytokines (e.g., TNF, IL-1) release when merozoites rupture causing inhibition of gluconeogenesis and hypoglycemia.

• Brain involvement can cause loss of consciousness due to elevated CSF lactate or neurotransmission interference.

• Additional effects include kidney glomerulus blockage, lung edema, hemolytic anemia, dyserythropoiesis, and metabolic changes, including lactic acidosis.

• Hypoglycemia can be caused by hepatic gluconeogenesis failure.

• Malaria parasites increase glucose demand in patients with fever.

Malaria Clinical Picture

• Incubation periods vary between 10-14 days (P. vivax, P. ovale) and 18 days to 6 weeks (P. falciparum) and up to 30-40 days ( P. malariae).
• Prodromal symptoms include flu-like symptoms.
• Classical malaria stages: cold (vasoconstiction), hot (vasodilation), and sweating stages.
• Additional symptoms like herpes labials (oral herpes), enlarged spleen after day 10, tender liver, relative lymphocytosis, leucopenia.

P. falciparum Malaria Severity

• P. falciparum is more serious due to broader cell infection.
• It produces more parasites and greater tissue and RBC multiplication.
• Severe cases present with ≥5% parasitized RBCs, >10% with multiple rings, and schizonts (parasite forms) in blood.

Malaria Complications

• Cerebral malaria: includes disturbed consciousness, seizures, coma, papilledema, and cranial nerve palsies.
  • 15% in children and 20% in adults
• Convulsions: as a complication.
• Post-malarial neurological syndrome: early symptoms may include hemiplegia and sensory loss; late symptoms may involve psychosis, encephalitis, and cerebellar ataxia.
• GIT (Gastrointestinal) syndrome: heavy infiltration causing bilious remittent fever, dysenteric malaria.
• Black water fever: rapid onset of fever, hemoglobinuria, jaundice, vomiting, and acute renal failure in non-immune individuals treated with quinine or primaquine.
• Acute renal failure: an early symptom in patients with serious complications; renal failure can occur after malaria recovery.
• Metabolic acidosis: a frequent finding.
• Hypoglycemia: due partially to reduced hepatic gluconeogenesis capacity and increased glucose demands by fever and/or the parasites.
• Pulmonary edema (often 80% in severe cases).

Malaria Diagnosis

• Blood films (thin and thick smears) are critical for species identification and parasite density assessment.
• Bone marrow examination can be more sensitive than blood smears.
• Rapid diagnostic tests (RDTs) based on antibodies (antigen-antibody reactions) are also used.
  • HRP-2 is detectable even after treatment.

Malaria Treatment and Prevention

• Malaria management involves vector control, chemoprophylaxis, and treatment.
• Classification of antimalarials is made based on how they affect the parasite's life stages.

Malaria Definition of Severity

• Cerebral malaria, severe anemia, renal failure (including acute tubular necrosis), acute respiratory distress syndrome (ARDS).
• Hypoglycemia, disseminated intravascular coagulation (DIC), and seizures ( ≥2).
• Parasitemia level of 5-10% and potential acidemia
• Jaundice as a symptom of possible severe complications.