Download MBBS MALARIA Seminar Lecture PPT

MALARIA
Malaria is an acute and chronic illness characterized
by paroxysms of fever,chills,sweats,fatigue,anaemia
and splenomegaly.
Causes more than 1 million deaths each year.(most

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malarial deaths occur amoung infants and young
children.)
Physicians in non endemic areas consider diagnosis of
malaria in any febrile child who has returned from
malaria endemic area within previous year.

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ETIOLOGY
Causative organism : Plasmodium
Prior to 2004 : P.falciparum,P.malariae,P.vivax,P.ovale
In 2004: P.knowlesi (Malasia,Indonasia,Singapore and
Phillipines)

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Transmissiion : by female anopheles mosquitoes
blood transfusion,use of contaminated needles and
transplacentally

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P.vivax and P.ovale: benign tertian malaria
P.falciparum: malignant tertian malaria

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P.malariae: benign quartan malaria

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EPIDEMIOLOGY
Principle areas of transmission: Africa,Asia and South
America.
P.falciparum:Africa,Haiti and New Guinea.

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P.vivax:Bangladesh,Central America,India,Pakistan
and Sri Lanka.
P.vivax and P.falciparum:Southeast Asia,South
America and Oceania.
P.ovale:Africa

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Epidemiology in india
In India, wide distribution of nine anopheline
vectors transmitting three Plasmodial species: P.

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falciparum, P. vivax, and P. malariae.
Anopheles culicifacies is widely distributed and is the
principal vector of rural malaria.
An. stephensi is the primary urban vector,

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Distribution of Malaria in

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Different States of India
The annual parasite incidence (API) is a
malariometric index to express malaria cases per
thousand population.
in most of India, the API was < 2

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, whereas 2?5 API was in scattered regions,
and regions with > 5 API were scattered in the states
of Rajasthan, Gujarat, Karnataka, Goa, Southern
Madhya Pradesh, Chhattisgarh, Jharkhand, and
Orissa and in northeastern states

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The proportion of P. vivax and P. falciparum varies in
different parts of India.
Although mostly indo-gangatic plains and northern
hilly states, northwestern India and southern Tamil
Nadu state have < 10% P. falciparum, and the rest

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are P. vivax infections
In the forested areas inhabited by ethnic tribes, the
situation is reversed, and the P. falciparum
proportion is 30?90%, and in the remaining areas, it
is between 10% and 30%.

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LIFE CYCLE
Definitive host and vector: female Anopheles
mosquito.
Intermediiate host: human
Infective form:sporozoites

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HUMAN CYCLE(SCHIZOGONY)
PRE ERYTHROCYTIC
ERYTHROCYTIC
sporozoites(spindle)enters
Receptor (glocophorin)

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liver > become rounded
Merozoites > ring form
Multiply > meront/schizont
Enlarged to trphozoites
Merozoites (ruture of

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Mitosis>mature schizonts
hepatocytes)
Burst to release merozoites
Micro merozoites > RBC
Parasite feeds on Hb >

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Macro merozoites > liver
haemozoin
Merozoite > gametocytes

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SPOROGONIC CYCLE
Mosquito takes gametocytes

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Exflagellated microgametocyte + macrogametocyte
Zygote>ookinate >oocyst
Oocyst contains sporozoites
Enter salivary gland

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EROTHROCYTIC STAGE

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P.falciparum infect RBC of all age
P.vivax ? only young RBC

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LATENT STAGE
In P.vivax and ovale :
2 types of sporozoites present.

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Some infect hepatocytes.
Others in resting form(hypnozoites)>later
activated>CLINICAL RELAPSE
In P.falciparum and malariae:
no hypnozoites only some erythrocytic parasites

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persists in blood and multiply > SHORT TERM
RELAPSE/RECRUDESCENCE.

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PATHOGENESIS
FEVER - due to release of cytokines

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ANEMIA- hemolysis
sequestration of RBC in spleen
bone marrow suppression
IMMUNOPATHOLOGIC EVENTS -
increased production of proinflammatory cytokines

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TISSUE ANOXIA-

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PATHOGENESIS
Due to local/systemic response to parasite.
Brain:congested with multiple punctiform
haemorrhages

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Tissue hypoxia: due to obstruction of blood flow.
Liver: enlarged and congested , fatty degeneration
and centrilobal necrosis.
Spleen:enlarged and congested,hard with thick
capsule.

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Kidney:enlaarged and congested tubules
Aeamia:decreased erythropoetin levels and increased
haemolysis.

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Complicated malaria

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Cytoadherence

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Trophozoites in peripheral circulation
Cell invasion
Formation of knobs(from mature schizonts) and
protruberances on RBC surface ? act as neoantigens

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causing immune stimulation and vascular stickiness
-Block cappilaries > complication
-Agglutinates
Rosseting

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Cytoadherence causes obstruction of blood flow and

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capillary damage
vascular leakage
TISSUE ANOXIA

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Tissue anoxia leads to complications like cerebral
malaria and acute tubular necrosis

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Hypoxia leads to anaerobic metabolism ? increased
lactate production

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CLINICAL FEATURES
SPECIES

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INCUBATION PERION
P.falciparum
9-14
P.vivax
12-17

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P.ovale
16-18
P.malariae
18-40

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Initial phase: asymptomatic
Classical presentation: paroxysms of fever alternating
with periods of fatigue.
Febrile paroxysms characterized by high fever, sweats,
and head ache , myalgia, back pain, abdominal pain,

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nausea, vomiting diarrhea, pallor, and jaundice.

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P.vivax and ovale : paroxysms coincide with ruture of
shizonts that occue every 48 hours > fever spikes
every 2 nd day
P. falciparum : periodicity less apparent

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P.malariae : rupture occurs every 72 hrs>fever spikes
every 3 rd or 4 th day

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Children with malaria lack paroxysms
Non specific symptoms
low grade fever , head ache , anorexia , nausea ,

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vomiting , and diarrhea.
Distinctive physical signs : splenomegaly ,
hepatomegaly , and pallor.

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BENIGN MALARIA
Fever with rigor followed by anaemia and

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spenomegaly
Febrile paroxysms: 3 stages
1.cold stage: 15-60 mins>intense cold with shivering
2.hot stage:2-6 hrs> patient feels intense hot
temp(>or equal to 41 degree celsius)

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3.sweating stage: profuse sweating temperature
drops rapidly.

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P.falciparum : most severe
Complications unique to it
cerebral malaria , acute renal failure , respiratory

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distress , algid malaria , beeding diathesis.
Parasitaemia : high ( infect both mature an immature
RBC)

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MALIGNANT MALARIA
Cerebral malaria:

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occurs in non immune untreated person.
head ache ,hyperpyrexia,paralysis,confusion may b
present.(RBC aggregration)
Algid malaria:
Peripheral circulatory failure,rapid thready pulse,low

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Bp and cold skin

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Septicemic malaria:
High continuous fever with multi organ failure
Black water fever(malarial haemoglobinuria):
bilious vomiting,passage of dark red/blackish urine

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(intravascular hemolysis by anti-erythrocute
antibody)

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WHO Criteria for severe malaria
Impaired conciousness
Prostration

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Respiratory distress
Multiple seizures
Jaundice
Haemoglobinuria
Abnormal bleeding

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Severe anaemia
Circulatory colapse
Pulmonary oedema

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MEROZOITE INDUCED MALARIA
SEEN IN

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Transfusion malaria
Congenital
Renal transplantation
Shared syringes
Shorter incubation period and no relapse.

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Congenital Malaria
Prenatally\pernatally.
In endemic areas important causeof
abortions,miscarriages,stllbirths,premature
births,IUGR and neonatal deaths.

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Even in absense of transmission from mather to baby
ill effects observed.
Signs and symptoms :
fever,restlessness,drowsiness,pallor,jaundice,poor
feeding,vomiting,diahrrea,cyanosis and

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hepatosplenomegaly.

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