Pathology Of Malaria

Question 1

blood borne protozoan that causes malaria

Answer 1

plasmodium spp(FALCIPARUM, VIVAX, OVALE, MALARIAE AND RARELY KNOWLESI)

Question 2

Most severe form is acused by

Answer 2

p.falciparum and vivax

Question 3

Predisposing factors

Answer 3

Malaria is a disease which can be transmitted to people of all ages, bitten by a vector

Young children: children under 5 years do not have well developed antibodies and

pregnant women: due to immunosupression

in high transmission areas are at a large risk.

Question 4

What ages of rbc do they affect?

Answer 4

p. falciparum attack all generations of rbc
p.vivax attack young rbc
p.ovale and p.malariae attack old rbc

Question 5

Phases of Pathogenesis

Answer 5

Hepatic phase
* Sporozoites ( from the saliva of female anopheles mosquito) infect hepatocytes, multiplying asexually (by schizogany) & asymptomatically for a period of 6-15 days.

• Then they differentiate into merozoites → rupture the hepatocytes → escape to blood stream undetected (wrapping itself in the cell membrane of the infected host liver cell (biofilm)).

Erythrocytic phase
* Within the red blood cells the parasites multiply further, again asexually, periodically breaking out of their hosts to invade fresh red blood cells.
* p. vivax and p.ovale do not immediately develop into merozoites
* They develop first to Hypnozoites (dormant form) for 6-12 month leading to long incubation and late relapses

Question 6

Clinical features

Answer 6

Fever
Headache
Malaise
Vomiting
Diarrhoea
Coma
Sweating
Dic
Abdominal swelling

Question 7

Decribe briefly the Protective factors/ mechanisms of host resistance against malaria infections (PQ)

Answer 7

1. Duffy antigen: many West Africans, particularly those with sickle cell anaemia lack this antigen which acts a receptor for p.vivax. Therefore individuals lacking the Duffy antigen (Duffy-negative) have reduced receptor sites, making it harder for p.vivax to invade red blood cells.
2. Sickle cell antigen: due to the short lifespan of rbc’s, plasmodium cannot complete it’s life cycle
3. Haemoglobin F: HbF has high affinity for O2 therefore it deprives the plasmodium from O2 causing hypoxia? HbF is why babies up to 6 months are resistant to malaria but after 6 months they lose most of their HbF
4. G6PD ENZYME: it causes hemolysis therefore doesn’t allow incubation and maturation due to fast cell destruction

Question 8

Organ changes in malaria

Answer 8

• Brain (cerebral oedema, slatey grey color, petechiae heamorrhage in white matter, ball and ring heamorrhages and dark granuloma)
• Liver ( hepatomegaly, slatey gray color
• Spleen (splenomegaly, ague cake is the enlarged hard spleen of chronic malaria and grey color)
• Kidneys
• Lungs (oedema, grey color)

Question 9

Complications of malaria

Answer 9

• Black water fever (black urine due to haemoglobinuria)
• Cerebral malaria (due to sequestration in the brain capillaries leading to hypoxia in the brain and cerebral malaria)
• Hyperpyrexia
• Anaemia
• Pregnancy related complications
• Algid malaria (Algid malaria is a rare and severe form of malaria) characterized by profound hypothermia, typically occurring in patients with Plasmodium falciparum infection
• Pulmonary oedema

Question 10

Diagnosis of malaria

Answer 10

• Light microscopy (thin and thick films using rowanosky stains)
  thin film: identifies plasmodium species
  thick film: diagnoses infection/ locates the parasite
• Rapid diagnostic test kits
• PCR

Question 11

How to treat malaria

Answer 11

USE OF Artemisinin-based combination therapies (ACTs)