MALARIA
Presented by:
Abirami sureshkumar
Adarsh D Nair
Date:25-4-2024
Discussion points
Malaria – introduction
Case scenario
Etiological agent
Mode of transmission
Pathophysiology
CLINICAL signs and symptoms
Differential diagnosis
Investigations
Complications
Management
prevention
CASE SCENARIO
■ A 24 yr old boy IT student came to the
casualty with complaints of
■ Fever for 9 days
■ Headache for 9 days
■ Altered sensorium for 1 day
No response was found to the received
antibiotica & h/o travel toLucknow as a part of
his study 2 weeks back
O/E disorientation ,pallor ,spleen palpable and
enlarged by 3cm neck stiffness no find,blood
sugar at admission was 56mg/dL
DIAGNOSIS
■ The most probable diagnosis is MALARIA
INTRODUCTION
■ Malaria is an infectious disease caused by the
protozoal parasite plasmodium
■ Transmitted by the bite of female anopheles
mosquito
■ Commonly seen in tropical and subtropical
countries
ETIOLOGICAL AGENT
■ Most common ETIOLOGICAL agents are:
■ Plasmodium falciparum
■ Plasmodium vivax
■ Plasmodium ovale
■ Plasmodium malariae
■ Plasmodium knowleski
PATHOPHYSIOLOGY
PATHOPHYSIOLOGY
■ Mode of transmission : by the bite of an infected
female anopheles mosquito & may also spread
from the transfusion of blood from infected
people or by the use of contaminated needles
■ PATHOLOGY:
■ The life cycle of plasmodia is complex.It occurs in
two different stages:
■ Asexual stage
■ Sexual stage
PATHOPHYSIOLOGY
■ 1.Asexual cycle:
■ Human infection begins when a female anopheles mosquito
inoculates plasmodial sporozoites from its salivary gland
during a blood meal
■ These microscopic motile forms of parasites are carried
rapidly via blood stream to liver, where they invade hepatic
parenchymal cells and begin a period of asexual
reproduction
■ By this amplification process (intrahepatic /pre – erythrocytic
schizogony /merogony),a single sporozoite eventually may
produce 10,000 to >30,0000 daughter merozoites
PATHOPHYSIOLOGY
■ The swollen infected liver cells eventually
bursts,discharging motile merozoites in to the blood.
■ After entry in to the bloodstream ,merozoites rapidly
invade erythrocytes and become trophozoites.
■ During the early stage of intrahepatic cycle ,the small
ring forms appear
■ As the trophozoites enlarge , species specific
characteristics become evident, pigment becomes
visible and the parasite assumes an irregular or
amoeboid shape
PATHOPHYSIOLOGY
By the end of 48 hrs,intraerythrocytic cycle ,the parasite has
consumed all haemoglobin and now called as a schizont
Multiple nuclear divisions take place and RBCs rupture to
release /6-30 daughter merozoites each capable of repeating
the cycle
■ Disease is due to direct effects of RBC invasion and
destruction by the asexual parasite and the host’/s reaction
■ After a series of asexual cycles ,some of the parasites
develop into morphologically distinct, longer lived sexual
forms or gametocytes that can transmit malaria
■ 2.SEXUAL CYCLE:
■ After being ingested the blood meal the male and female
gametocytes form a zygote
■ This matures into ookinete which penetrate and encyats in
the mosquito gut wall
■ Asexual division occurs and it burst into motile sporozoites
which migrate to the salivary gland of mosquito to await
inoculation in to another human at the next feeding
CLINICAL SYMPTOM
For p.vivax and p.ovale infection
Several days of continued fever on alternate days
Common complaints are : fever ,rigorrofuse perspiration, and
gradual fall in temperature splenomegaly and hepatomegaly
seen, anemia
Relapse are frequent in 2 years after leaving malarious area
For p.malariae & p.knowlesi :
Mild symptoms with bouts of fever every third
day ,parasitemias for yrs with occasional recrudescence of
fever
• CLINICAL SYMPTOMS
■ CLINICAL features of severe malaria: develops in
p.falciparum infection over as short as 12-24 hrs & may
lead to death ,if not treated promptly and adequately
severe malaria is characterized by one or more Of the
features:
■ Impaired consciousness/com
■ Repeated generalized convulsions
■ Renal failure(S .cr >3 mg/dl)
■ Jaundice (S.bilirubin >3 mg/dl)
■ Severe anemia(HB<5 g/dl)
■ Pulmonary edema/ ARDS
■ Hyperglycemia,metabolic acidosis , circulatory
collapse,abnormal bleeding, hemoglobinuric,
hyperthermia, hyperparasitemia and splenomegaly
Differential diagnosis
● Enteric fever
● Brucellosis
● Dengue fever
● Babesiosis
Investigations
Peripheral smear examination: Giemsa-stained
thick and thin films should be examined.In thick film
erythrocytes are lysed, releasing all blood stages of
the parasite. This facilitates the diagnosis of low level
parasitaemias.
Immunochromatographic RDTs for malaria antigens,
such as OptiMAL (which detects the Plasmodium LDH of
P.falciparum and vivax) and Parasight-F (which detects
the P falciparum histidine rich protein) are extremely
sensitive and specific for falciparum malaria but less so
for other species.
Bone marrow aspirate: sometimes parasites cannot be
detected in peripheral blood smears. In these
circumstances examination of smears of bone marrow
aspirate reveals parasites or malaria pigment.
Investigations
PCR testing
Molecular diagnosis by PCR amplification of
parasite nucleic acid is more sensitive than
microscopy or rapid diagnostic tests.
Other lab findings:
Blood: normocytic normochromic anemia, thrombocytopenia.
Acute phase protein : ESR, plasma viscosity, and levels of
C- reactive protein are high.
In complicated malaria there may be metabolic acidosis and
low plasma concentrations of glucose, sodium, bicarbonate,
calcium, magnesium and albumin.
Elevated levels of lactate, creatinine, muscle and liver
enzymes.
Complications
● Cerebral malaria
● Algid malaria
● Renal failure
● Convulsions : more common in children
● Residual neurological sequelae
Management
Mild P. falciparum malaria
artemisinin based treatment is recommended.
Co-artemether is given 4 tabs at 0,8,24,36,48 and 60
hrs.
Alternatives are quinine(600mg 3 times daily for 5-7
days), followed by doxycycline or clindamycin.
Complicated P. falciparum malaria
IV artesunate (2.4mg/kg IV at 0,12 and 24hrs, then
daily for 7 days). When the patient has recovered
sufficiently, oral artesunate 2mg/kg once daily is
given instead of infusions to a total cumulative dose
of 17-18 mg/kg.
IV quinine salt is an alternative, with ECG monitoring.
Non-falciparum malaria
P.vivax, P.ovale, P.knowlesi and P.malariae
infections should be treated with oral
chloroquine but some chloroquine resistance
has been reported from Indonesia and all are
sensitive to ACTs. Radical cure is essential in
patients with P.vivax or P.ovale malaria using
a course of primaquine or tafenoquine.
Prevention
Antimalarial tablets Adult prophylactic dose Regimen
Chloroquine resistance high
Mefloquine 250mg weekly Started 2-3 weeks before
travel and continued until 4
weeks after
Or Doxycycline 100mg daily Started 1 week before and
continued until 4 weeks after
travel
Or Atovaquone plus 1 tablet daily From 1-2 days before
proguanil (Malarone) travel until 1 week after
return
Chloroquine
resistance absent
Chloroquine and 300mg base weekly Started 1 week before
proguanil 100-200 mg daily and continued until 4
weeks after travel
Malaria control in endemic areas
Successful programmes combine vector control,
including indoor residual spraying, use of long
lasting insecticide- treated bed nets and intermittent
preventative therapy.
Question of the day
A 19 year old boy fro Jharkand
admitted with fever with chills and
rigors
•Altered sensorium and decreased
urine output
•Hb – 5.5 g/dL
•Platelet -15,000/mm3
•S.Cr- 4.3
•His urine colour
Question of the day
● What is the diagnosis?
● What is the likely complication?
● Likely etiological organism?
References
● Davidsons medicine
● Harrisons medicine
● Archith Boloor medicine
THANK YOU
