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MD.Kiyumars Karimi
MALARIA CLINICAL FEATURES
CLINICAL FEATURES
 First symptoms are non specific:
 Headache
 Fatigue
 Myalgia and Arthralgia
 Incubation period:
 Depends on species
 8 to 25 days
 Affected by partial immunity
 Signs:
 Non specific
 Anemia
 Hepatolienal syndrome
Clinical
Syndromes
Acute disease
Complicated Uncomplicated
Chronic
disease
Asymptomatic
Acute Malaria Disease
 Malarial paroxysm stages:
1. Cold stage
2. Hot stage
3. Diaphoresis stage
o Cold stage:
 Feeling of intense cold
 Vigorous shivering
 Lasts 15-30 minute
 Accompanied by headache, nausea & myalgia
Paroxysm stages
o Hot stage:
 Intense Heat
 Dry burning skin
 Hypotension
 Lasts 15 minute to several hours
o Sweating stage:
 Profuse sweating
 Declining temperature
 Exhaustion
 Lasts 2-4 hours
Complicated Malaria
 Cerebral Malaria
 Hypoglycemia
 Non Cardiogenic Pulmonary Edema
 Metabolic Acidosis
 Renal Impairment
 Hematological Disorders
 Liver Dysfunctions
 Hyperpyrexia
 Hyperparasitemia
 Hemoglobinuria
Cerebral Malaria
 Ominous feature of P.falciparum
 Sudden or gradual onset
 Diffuse symmetric encephalopathy
 Focal neurological deficit is uncommon
 Divergent eye and pout reflex is common
 Muscle dystonia
 Preserved corneal reflex except indeep coma
 Retinal hemorrhage in 15 % of patients
 Residual neurological defecit
Hypoglycemia
 Important and common complication
 Associated with poor prognosis
 Problematic in children and pregnant women
 Clinical diagnosis maybe difficult
 Causes:
 Hepatic gluconeogenesis failure
 Increase glucose consumption by host and lesser
by parasite
 drug induced hypoglycemia
Acidosis
 Important cause of death
 Results from organic acid accumulation
 Hyperlactatemia coexist with hypoglycemia
 Acidotic breathing is a sign of poor prognosis
 Bicarbonate or lactate are best biochemical
prognosticators
 Causes:
 Anaerobic glycolysis
 Hypovolemia
 Lactate production by the parasites
 Failure of hepatic and renal lactate clearance
Noncardiogenic Pulmonary Edema
 May develops even after antimalarial therapy.
 More common in adults.
 Mortality rate is >80%
 Predisposing factors:
 Renal failure
 Pregnancy
 Hyper parasitemia
 Pathogenesis:
 Exact pathogenesis is unclear.
 Pulmonary microvascular obstruction and increased
TNF α.
 Aggravated by vigorous administration of IV Fluid.
Renal impairment
 More common among adults.
 High mortality (upto 45%)
 May occur with other vital-organ
dysfunction.
 Manifest as Acute tubular necrosis.
 Renal cortical necrosis never develops
 Pathogenesis:
 Exact pathogenesis is unclear.
 May related to microcirculatory obstruction.
Other Complications
 Anemia results from:
 Accelerated RBC removing by spleen
 RBC destruction by schizont
 Ineffective erythropoiesis
Liver Dysfunction
• Hemolytic jaundice is common.
• sever with P.falciparum infection.
• Pathogenesis:
∙ Hemolysis
∙ Hepatocyte injury
∙ Cholestasis
Malaria in Pregnancy
 Pregnant women prone to sever infection.
 Common adverse effect on foetal:
 Stillbirths
 Fetal distress
 LBW
 IUGR
 Prematurity
 Maternal effect:
 Maternal anemia
 Higher mortality from cerebral malaria
 Premature labor
Malaria in Children
 Mortality is more in children.
 May present with labored deep breathing
 Long term neurocognitive & developmental deficit
 Conditions rare in child:
 Deep jaundice
 Acute renal failure
 Acute pulmonary edema

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Malaria Clinical Features

  • 2. CLINICAL FEATURES  First symptoms are non specific:  Headache  Fatigue  Myalgia and Arthralgia  Incubation period:  Depends on species  8 to 25 days  Affected by partial immunity  Signs:  Non specific  Anemia  Hepatolienal syndrome
  • 4. Acute Malaria Disease  Malarial paroxysm stages: 1. Cold stage 2. Hot stage 3. Diaphoresis stage o Cold stage:  Feeling of intense cold  Vigorous shivering  Lasts 15-30 minute  Accompanied by headache, nausea & myalgia
  • 5. Paroxysm stages o Hot stage:  Intense Heat  Dry burning skin  Hypotension  Lasts 15 minute to several hours o Sweating stage:  Profuse sweating  Declining temperature  Exhaustion  Lasts 2-4 hours
  • 6. Complicated Malaria  Cerebral Malaria  Hypoglycemia  Non Cardiogenic Pulmonary Edema  Metabolic Acidosis  Renal Impairment  Hematological Disorders  Liver Dysfunctions  Hyperpyrexia  Hyperparasitemia  Hemoglobinuria
  • 7. Cerebral Malaria  Ominous feature of P.falciparum  Sudden or gradual onset  Diffuse symmetric encephalopathy  Focal neurological deficit is uncommon  Divergent eye and pout reflex is common  Muscle dystonia  Preserved corneal reflex except indeep coma  Retinal hemorrhage in 15 % of patients  Residual neurological defecit
  • 8. Hypoglycemia  Important and common complication  Associated with poor prognosis  Problematic in children and pregnant women  Clinical diagnosis maybe difficult  Causes:  Hepatic gluconeogenesis failure  Increase glucose consumption by host and lesser by parasite  drug induced hypoglycemia
  • 9. Acidosis  Important cause of death  Results from organic acid accumulation  Hyperlactatemia coexist with hypoglycemia  Acidotic breathing is a sign of poor prognosis  Bicarbonate or lactate are best biochemical prognosticators  Causes:  Anaerobic glycolysis  Hypovolemia  Lactate production by the parasites  Failure of hepatic and renal lactate clearance
  • 10. Noncardiogenic Pulmonary Edema  May develops even after antimalarial therapy.  More common in adults.  Mortality rate is >80%  Predisposing factors:  Renal failure  Pregnancy  Hyper parasitemia  Pathogenesis:  Exact pathogenesis is unclear.  Pulmonary microvascular obstruction and increased TNF α.  Aggravated by vigorous administration of IV Fluid.
  • 11. Renal impairment  More common among adults.  High mortality (upto 45%)  May occur with other vital-organ dysfunction.  Manifest as Acute tubular necrosis.  Renal cortical necrosis never develops  Pathogenesis:  Exact pathogenesis is unclear.  May related to microcirculatory obstruction.
  • 12. Other Complications  Anemia results from:  Accelerated RBC removing by spleen  RBC destruction by schizont  Ineffective erythropoiesis Liver Dysfunction • Hemolytic jaundice is common. • sever with P.falciparum infection. • Pathogenesis: ∙ Hemolysis ∙ Hepatocyte injury ∙ Cholestasis
  • 13. Malaria in Pregnancy  Pregnant women prone to sever infection.  Common adverse effect on foetal:  Stillbirths  Fetal distress  LBW  IUGR  Prematurity  Maternal effect:  Maternal anemia  Higher mortality from cerebral malaria  Premature labor
  • 14. Malaria in Children  Mortality is more in children.  May present with labored deep breathing  Long term neurocognitive & developmental deficit  Conditions rare in child:  Deep jaundice  Acute renal failure  Acute pulmonary edema