Major clinical manifestations of malaria include: 1. Cerebral malaria, which can cause coma, convulsions, and residual neurological deficits. 2. Severe malarial anemia. 3. Low birth weight in newborns whose mothers had malaria during pregnancy. Complications include cerebral malaria, renal impairment, hypoglycemia, acidosis, and noncardiogenic pulmonary edema. Chronic complications include splenomegaly and nephropathy. Malaria can also increase risk of other infections.

1. CLINICAL FEATURES
&
COMPLICATIONS OF MALARIA

2. CLINICAL FEATURES

3. UNCOMPLICATED MALARIA
First symptoms are non specific:
• Headache, Lassitude, Fatigue
• Abdominal discomfort, muscle and joint
aches, diarrhea
• Followed by fever(irregular at
first), chills, rigors, perspiration, anorexia . In some
cases palpable spleen and slight enlargement of liver
are also present
• Nausea,vomiting, & orthostatic hypotension are
common
Signs:
• Anemia, splenomegaly, hepatomegaly

4. SEVERE FALCIPARUM MALARIA
• Unarousable Coma / cerebral malaria, convulsions
• Renal Impairment
• Noncardiogenic pulmonary edema
• Liver Dysfunction
• Hypoglycemia
• Metabolic acidosis/acidemia
• Hematological abnormality like hemoglobinuria,
normocytic anemia, bleeding,DIC
• Other complications like jaundice, extreme
weakness,hyperparasitemia, impaired consciousness
• Hypotension/shock

5. CEREBRAL MALARIA
• Coma is characteristic and ominous feature of
falciparum malaria
• Manifests as diffuse encephalopathy
• No signs of meningeal irritation
• Eyes : divergent, Corneal reflexes :preserved
• Muscle tone : May be Increased/ Decreased
• Tendon reflexes : Variable, Plantars : Equivocal.
Abdominal & cremasteric reflexes are absent
• Fundus : Retinal hemorrhages, discreet spots of
retinal opacification, papilledema, cotton wool
spots

6. • Convulsions :In children, usually
generalised, often repeated
• Covert seizure : manifest as Tonic clonic eye
movement, hyper salivation
• Residual neurological deficit
(Hemiplegia, CP, cortical
blindness, deafness, impaired cognition and
learning) seen in children who survive
cerbral malaria

7. Major Manifestations of Malaria
Anemia
Lennart Nielson (Karolinska Instituteg), Hedvig Perlmann (Stockholm University) Martin Weber
Cerebral
malaria
George Grau Roll Back Malaria Info Sheet
Low
birthweight
Rick Steketee National Human Genome Research Institute

8. • HYPOGLYCAEMIA .Increases the risk of
mortality in children with cerebral malaria;
may present with convulsions or a
deterioration in level of consciousness.
CAUSES
• 1. Increased peripheral requirement of
glucose consequent upon anaerobic glycolysis.
2. Increased metabolic demands of febrile
illness. 3. Obligatory demand of parasites.

9. • ACIDOSIS This may result form renal
failure, but more commonly there is a primary
lactic acidosis . Lactic acidosis results from : 1.
Anaerobic glycolysis due to microvascular
obstruction. 2. Failure of hepatic and renal
lactate clearance. 3. Production of lactate by
the parasite..

10. • NONCARDIOGENIC PULMONARY OEDEMA
This is a grave and usually fatal manifestation
of severe falciparum malaria and occurs
mainly in adults. Hyperparasitaemia, renal
failure and pregnancy are recognised
predisposing factors

11. • RENAL IMPAIRMENT- Tubular abnormalities
consistent with acute tubular necrosis (ATN)
are seen. Sequestration in glomerular
capillaries, mesangial endothelial cell
proliferation, and immunoglobulin deposits
may be seen.
• MALARIA IN PREGNANCY .Common adverse
effects of malaria in pregnancy : Maternal
anaemia Stillbirths Premature delivery and Intra-
Uterine Growth Retardation (IUGR) result in the
delivery of Low Birth weight (LBW) infants

12. Other complications
• Septicemia may complicate severe malaria.
• Liver dysfunction- mild hemolytic jaundice is
common. Severe jaundice is associated with
P.falciparum infections

13. CHRONIC COMPLICATIONS

14. TROPICAL
SPLENOMEGALY(HYPERREACTIVE
MALARIAL SPENOMEGALY)
• Chronic or repeated malarial infections produce
in certain situations splenomegaly
• This is associated with the production of
cytotoxic IgM antibodies. There is uninhibited B
cell production of IgM and the formation of
cryoglobulins.
• This process stimulates reticuloendothelial
hyperplasia and clearance activity and
eventually produces splenomegaly.

15. • Patients with HMS present with an abdominal
mass or a dragging sensation in the abdomen
and occasional sharp abdominal pains
suggesting perisplenitis.
• Anemia and some degree of pancytopenia are
usually evident, and in some cases malarial
parasites cannot be found in peripheral smears
• Vulnerability to respiratory and skin infections
is increased.

16. QUARTAN MALARIAL NEPHROPATHY
• Chronic or repeated infection with P.malariae
may cause soluble immune-complex injury to
the renal glomeruli, resulting in the nephrotic
syndrome.
• The histologic appearance is that of focal or
segmental glomerulonephritis with splitting of
the capillary basement membrane.
subendothelial dense deposits are seen on
electron microscopy, and imunofluorescence
reveals deposits of complement and
immunoglobulins

17. BURKITT'S LYMPHOMA & EPSTEIN-
BARR VIRUS INFECTION
• Malaria related immunosuppression may
provokes infection with lymphoma virus.
• Burkitts lymphoma is strongly associated with
Epstein-barr virus.

18. THANK U