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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
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.
ETIOLOGY
Causative organism : Plasmodium
Prior to 2004 : P.falciparum,P.malariae,P.vivax,P.ovale
In 2004: P.knowlesi (Malasia,Indonasia,Singapore and
Phillipines)
Transmissiion : by female anopheles mosquitoes
blood transfusion,use of contaminated needles and
transplacentally
P.vivax and P.ovale: benign tertian malaria
P.falciparum: malignant tertian malaria
P.malariae: benign quartan malaria
EPIDEMIOLOGY
Principle areas of transmission: Africa,Asia and South
America.
P.falciparum:Africa,Haiti and New Guinea.
P.vivax:Bangladesh,Central America,India,Pakistan
and Sri Lanka.
P.vivax and P.falciparum:Southeast Asia,South
America and Oceania.
P.ovale:Africa
Epidemiology in india
In India, wide distribution of nine anopheline
vectors transmitting three Plasmodial species: P.
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,
Distribution of Malaria in
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
, 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
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
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%.
LIFE CYCLE
Definitive host and vector: female Anopheles
mosquito.
Intermediiate host: human
Infective form:sporozoites
HUMAN CYCLE(SCHIZOGONY)
PRE ERYTHROCYTIC
ERYTHROCYTIC
sporozoites(spindle)enters
Receptor (glocophorin)
liver > become rounded
Merozoites > ring form
Multiply > meront/schizont
Enlarged to trphozoites
Merozoites (ruture of
Mitosis>mature schizonts
hepatocytes)
Burst to release merozoites
Micro merozoites > RBC
Parasite feeds on Hb >
Macro merozoites > liver
haemozoin
Merozoite > gametocytes
SPOROGONIC CYCLE
Mosquito takes gametocytes
Exflagellated microgametocyte + macrogametocyte
Zygote>ookinate >oocyst
Oocyst contains sporozoites
Enter salivary gland
EROTHROCYTIC STAGE
P.falciparum infect RBC of all age
P.vivax ? only young RBC
LATENT STAGE
In P.vivax and ovale :
2 types of sporozoites present.
Some infect hepatocytes.
Others in resting form(hypnozoites)>later
activated>CLINICAL RELAPSE
In P.falciparum and malariae:
no hypnozoites only some erythrocytic parasites
persists in blood and multiply > SHORT TERM
RELAPSE/RECRUDESCENCE.
PATHOGENESIS
FEVER - due to release of cytokines
ANEMIA- hemolysis
sequestration of RBC in spleen
bone marrow suppression
IMMUNOPATHOLOGIC EVENTS -
increased production of proinflammatory cytokines
TISSUE ANOXIA-
PATHOGENESIS
Due to local/systemic response to parasite.
Brain:congested with multiple punctiform
haemorrhages
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.
Kidney:enlaarged and congested tubules
Aeamia:decreased erythropoetin levels and increased
haemolysis.
Complicated malaria
Cytoadherence
Trophozoites in peripheral circulation
Cell invasion
Formation of knobs(from mature schizonts) and
protruberances on RBC surface ? act as neoantigens
causing immune stimulation and vascular stickiness
-Block cappilaries > complication
-Agglutinates
Rosseting
Cytoadherence causes obstruction of blood flow and
capillary damage
vascular leakage
TISSUE ANOXIA
Tissue anoxia leads to complications like cerebral
malaria and acute tubular necrosis
Hypoxia leads to anaerobic metabolism ? increased
lactate production
CLINICAL FEATURES
SPECIES
INCUBATION PERION
P.falciparum
9-14
P.vivax
12-17
P.ovale
16-18
P.malariae
18-40
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,
nausea, vomiting diarrhea, pallor, and jaundice.
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
P.malariae : rupture occurs every 72 hrs>fever spikes
every 3 rd or 4 th day
Children with malaria lack paroxysms
Non specific symptoms
low grade fever , head ache , anorexia , nausea ,
vomiting , and diarrhea.
Distinctive physical signs : splenomegaly ,
hepatomegaly , and pallor.
BENIGN MALARIA
Fever with rigor followed by anaemia and
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)
3.sweating stage: profuse sweating temperature
drops rapidly.
P.falciparum : most severe
Complications unique to it
cerebral malaria , acute renal failure , respiratory
distress , algid malaria , beeding diathesis.
Parasitaemia : high ( infect both mature an immature
RBC)
MALIGNANT MALARIA
Cerebral malaria:
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
Bp and cold skin
Septicemic malaria:
High continuous fever with multi organ failure
Black water fever(malarial haemoglobinuria):
bilious vomiting,passage of dark red/blackish urine
(intravascular hemolysis by anti-erythrocute
antibody)
WHO Criteria for severe malaria
Impaired conciousness
Prostration
Respiratory distress
Multiple seizures
Jaundice
Haemoglobinuria
Abnormal bleeding
Severe anaemia
Circulatory colapse
Pulmonary oedema
MEROZOITE INDUCED MALARIA
SEEN IN
Transfusion malaria
Congenital
Renal transplantation
Shared syringes
Shorter incubation period and no relapse.
Congenital Malaria
Prenatally\pernatally.
In endemic areas important causeof
abortions,miscarriages,stllbirths,premature
births,IUGR and neonatal deaths.
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
hepatosplenomegaly.
This post was last modified on 12 August 2021