This document defines malaria and discusses its transmission, pathogenesis, clinical features, complications, diagnosis, and management. Malaria is caused by Plasmodium parasites transmitted via mosquito bites and characterized by periodic fevers. P. falciparum can cause potentially fatal malaria. Complications include tropical splenomegaly syndrome, nephropathy, and anemia. Diagnosis involves blood smears to identify parasites and antigen testing. Management consists of antimalarial drugs like quinine, addressing complications, and specific treatment for children and pregnant women in high-risk areas.

1. MALARIA
P/B :- DR NIYATI PATEL (PT)
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3. DEFINITION
 Acute febrile illness characterised by paroxysms
of fever as a result of asexual reproduction of
plasmodia within the red cells.
 Causes of malaria
 Plasmodium vivax,
 Plasmodium ovale and
 Plasmodium malariae
 Plasmodium falciparum  potentially fatal malaria.
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4. TRANSMISSION
 (a) Presence of suitable anopheline mosquito,
 (B) Reservoir of malaria infection in the area,
 (C) Suitable non-immune or partly immune hosts
 (D) An environmental temperature with suitable
humidity.
 Infection is normally transmitted to
 Man by the bite of a mosquito,
 Rarely occur across the placenta
 A result of blood transfusion
 Syringe-transmitted malaria among drug addicts
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6.  Infection is initiated by sporozoites from the bite of
a female Anopheles mosquito.
 The sporozoites multiply within hepatocytes, giving
rise to thousands of merozoite  invade RBCs.
 The sporozoites Converted merozoite
 In the RBCs the small ring forms grow through the
trophozoite stage to the schizont form, which
ruptures and releases further merozoites
 Tropozoite stage  schizont  merozoite
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8.  This asexual cycle in the blood
 lasts 48 hours in  P. falciparum, P. vivax and P.
ovale infections,
 lasts 72 hours in  P.malariya.
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9. PATHOGENESIS
 Clinical symptoms and signs are caused by the
asexual forms of the parasite
 Invade and destroy RBCs,
 Localise in tissues and organs by binding to
endothelial cells (cytoadherence)
 Induce release of many pro-inflammatory cytokines
[e.G. Tumour necrosis factor-α (tnf-α)].
 Initiating step when merozoites invade RBCs 
trophozoite  schizont stage bind to epithelial
cells in post capillary venules  microvascular
obstruction (cytoadherent) toxins produced 
cytokine release
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10. CLINICAL FEATURES
 ONSET – Lassitude, anorexia, headache, chillness for several
days before actual attack
 PAROXYSM – 3 CLINICAL STAGES
 1. COLD STAGE – Shivers from head to foot , teeth chatter ,
temperature rise  body covers with blanket  stage for
half n hour
 2. HOT STAGE – Shivers absent, feeling of intense heat 
throwing of blanket
 Flushed face, headache, vomiting, dry and burning Skin 
Temperature rises to 40°C or more  stage lasts for 3-4
hours.
 3. SWEATING STAGE - Patient breaks into profuse
perspiration, and the temperature rapidly declines with
feeling of relief.
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12. COMPLICATIONS
 Tropical splenomegaly syndrome (TSS) – is seen in
endemic falciparum malaria  Clinical features: marked
splenomegaly, lesser degree of hepatomegaly, anaemia
and pancytopenia.
 Quartan malarial nephropathy – is associated with P.
malariae infection. Predominantly affects children
between 5-8 years of age  Clinical features : nephrotic
syndrome several weeks after onset of quartan fever 
Disease progresses slowly to end-stage kidney failure in 3-
5 years.
 Anaemia in malaria,  most common complication 
due to accelerated RBC removal by the spleen, RBC
destruction at parasite schizogony and ineffective
haemopoiesis.
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13. DIAGNOSIS
 1. Clinical – Periodic fever with rigour, sweating,
anaemia and perhaps enlarged spleen.
 2. Blood film – Identification of the parasites in thick
and thin blood film  found during a spike of fever.
 Common microscopic characters of falciparum
malaria are – high concentration of parasites 
predominance of thin ring-shaped trophozoites.
 3. Malarial antigen spot test using parasite LDH – P.
falciparum antigens,
 4. Immunofluorescent microscopy and PCR.
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14. MANAGEMENT
 General Management
 Admission to ICU
 Measurement of glucose and if possible lactate and arterial
blood gases
 Fluid balance – because both dehydration and
overhydration
 Treatment of convulsions with diazepam
 Attention to hypoglycemia and hyponatremia
 Parameters for monitoring treatment include twice daily
parasite counts, regular pH and blood gas measurements
and when appropriate, measurement of glucose (during iv
quinine therapy), lactate, CRP & kidney function
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15.  PHARMACOLOGICAL MANAGEMENTS
 Non-severe falciparum (initial treatment): choice of three
regimens  Quinine sulphate , Atovaquone, Artemether &
Arterolane
 2nd agent follow-on treatment: choice of 3 agents 
Doxycycline , Clindamycin, sulfadoxine – pyrimethamine
 Non Falciparum  Chloroquine
 For ovale, vivax ovale & mixed infection  Primaquine
 For severe falciparum & vivax  quinine sulphate /
dihydrochloride
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16. MANAGEMENT OF
SPECIFIC COMPLICATIONS
 Cerebral malaria – Antimalarial drugs + Mannitol in patients
with raised intracranial pressure.
 Hypoglycemia – Dextrose iv
 Acute renal failure – Dialysis + Nonoliguric renal failure
 Acidosis – Adequate fluid replacement + bloodTransfusion ,
Early haemodiafiltration + ventilation may be used.
 Anaemia – is mainly caused by rupture of infected cells and
haemolysis. Transfusion if Hb falls below 7.5 g/dl.
 Bacterial superinfection – Strep. pneumoniae or Salmonella
spp. is common  antimicrobial
 Jaundice – Mild jaundice is mainly caused by haemolysis 
liver involvement  viral hepatitis
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17. MANAGEMENT FOR CHILDREN
(<5YRS) & PREGNANT WOMEN
 Arear where p.falciparum absent 
chloroquine phosphate
 Area where p.falciparum present 
chloroquine phosphate + proguanil
 Area where p.falciparum & p.vivax  high
risk of transmission  Mefloquine /
chloroquine + proguanil/doxycycline
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18. THANK YOU
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