Plasmodium

Dr. S. K. Saiful Alam
Lecturer, Microbiology
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Name of species Areas of Bangladesh Where
the species are found
Type of Malaria
P. vivax Flat lands Benign tertian malaria
P. falciparum Hilly areas like Chittagong,
Sylhet, Mymensingh,
Jamalpur Sherpur etc.
Malignant tertian
malaria
P. ovale Not found in Bangladesh Tertian malaria
P. malariae Not done in Bangladesh Quartan malaria

Hosts:
Its life cycle passes through two different hosts :
1. Intermediate host (a vertebrate- man or other animals) –
 Asexual multiplication (schizogony) takes place
 Sexual multiplication (gametogony) starts and gives rise
to gametocytes (infective to definitive host).
2. Definitive host (an invertebrate - female Anopheles mosquito)
–
 Sexual multiplication (sporogony) takes place and gives rise
to Sporozoites (infective to intermediate host).
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Pathogenesis of Malaria:
Agent: Plasmodium.
Host: Human.
Name of clinical illness: Malaria.
Vector – Infected female Anopheles mosquito.
Infective form: Usually sporozoites but trophozoites also can
infect.
Reservoir: Infected children. In Africa , monkeys are reservoir of
P. malariae.
Source of infection: Mainly saliva of infected female anopheles
mosquito containing sporozoites. Also infected blood of man
containing trophozoites.
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Mode of transmission:
 By sporozoites: Bite of infected female Anopheles
mosquito containing sporozoites in their salivary glands.
 By trophozoites:
 Transfusion of blood from a person containing
trophozoites.
 Transplacental transmission.
 Using infected needles/syringes among IVDU.
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Sporozoites-induced Malaria Trophozoites-induced
Malaria
Route of entry Mosquito bite Blood transfusion
Pre-erythrocytic schizogony Present Absent
Hepatomegaly Occurs Does not occur
Incubation Period Long Short
Exo-erythrocytic
schizogony
Present Absent
Relapse May occur Do not occur
Schizonticidal drugs No radical cure because of the
presence of E.E. forms.
Can be radically cured; no E.E.
forms

Incubation period:
In P. vivax , P. falciparum & P. ovale – 10-14 days
In P. malariae – 18 days – 6 weeks
Evolution of the disease in human 4 stages occur.
 Pre-Erythrocytic schizogony (in hepatocytes):
o Consists of only 1 cycle which takes 8 days in P. vivax, 6 days in P.
falciparum and 9 days in P. ovale and P. malariae.
o Parasites pass through trophozoites schizonts and merozoites.
o Liberated merozoites are of 2 types, micromerozoites and
macromerozoites.
o Micromerozoites invades RBC while macromerozoites re enter
into hepatocytes.
o Neither any pathological change nor any clinical features are seen
in this stage.
o Person is not infectious for the mosquitoes.
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Erythrocytic schizogony (in RBCs):
o Micromerozoites enter into RBC and pass through trophozoites,
schizont and merozoite.
o Each cycle lasts for 48 hrs in P. vivax, P. ovale, and P. falciparum
whereas it is 72 hrs in P. malariae.
o This phase is responsible development of clinical features of
malaria.
o The liberated merozoites re enter into new RBC and the cycle
continue for several times.
o After several cycles, the liberated merozoites loose their capacity
to re invade RBC and begin gametogenesis.
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Gametogony (in RBCs inside the capillaries of internal organs
– spleen, bone marrow):
o After several cycles in RBC, parasites develops gametocytes capable
of sexual cycle.
o It takes 4 days to form mature gametocytes .
o 2 types of gametocytes are formed – male gametocyte
(microgametocyte) & female gametocyte (macrogametocyte)
o Gametocytes are not responsible for fever.
o The individual who hourbours gametocytes is known as carrier.
Exo -Erythrocytic schizogony (in hepatocytes):
o Occurs only in P. vivax and P. ovale.
o The parasite in this stage is known as hypnozoite.
o Hypnozoite can be transformed into merozoite at any time.
o Erythrocytic parasite can not transformed into hypnozoite.
o Hypnozoite is responsible for relapse of malaria in P. vivax and P.
ovale.
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Persistence of infection:
1.Recrudescence:
Infection persists inside RBC.
Occurs due to incomplete treatment of falciparum malaria
Low level of parasitaemia continues even after clinical infection is
over.
It may occur up to 1 year.
2.Relapse:
Infection (hypnozoites) persists inside the hepatocyte.
Occurs in P. vivax and P. ovale.
No parasite is found in blood.
May occur up to 2 years.
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Life cycle of Plasmodium in mosquito
 To infect a mosquito, human blood must contain at least 12
gametocytes per mm3
of blood.
 A female anopheles mosquito bites a carrier for blood meal and
takes up asexual & sexual forms (micro & macrogametocyte) of
the parasite.
 In the gut of mosquito, the asexual forms die out but the sexual
forms (micro & macrogametocyte) mature to form male
(microgamete) and female (macrogametocyte) gametes.
 In the mid gut of mosquito, one microgametocyte give rise to 5-
8 microgametes and one macrogametocyte to one
macrogamete.
 One microgamete fertilizes one macrogamete and zygote is
formed. In the next 24 hours, zygote converts into Öokinete
which migrates outside the mucosa of midgut and becomes
Öocyst .
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Inside Öocyst, nucleus divides and becomes a sporozoite (100 -
1000).
The Öocyst ruptures and sporozoites are released into the body
fluid of mosquito.
The released sporozoites migrate in various organs (except
ovary) specially to the salivary glands & salivary ducts .
This mosquito is now infective to man & spreads the infection.
The incubation period in mosquitoes is about 8- 16 days.
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P. vivax P. falciparum
Form of
plasmodium
All form of plasmodium is
present
Only ring form of trophozoites and
crescent shaped gametocyte is present.
Site of infection Infects only in immature
RBC(Reticulocyte cell)
Infects RBC of all ages.
Rate of infection Usually infection does not exceed
2% (Reticulocyte count is <2%),
sometimes it may become 5%.
Infections of RBC usually exceeds 20-
30% sometimes even 90%.
Relapse May occur up to 2 years Does not occur
Recrudescence Does not occur May occur up to 1 year
RBC size in
peripheral blood
Enlarged almost double than
normal RBC
RBC size is not enlarged
6.Multuple
infection
Never found. One parasite infects
one RBC
Multiple infection is common. Multiple
parasit infects one RBC
Acculi formation Not present Present
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Clinical Features of Malaria
1. Febrile attack: It’s the periodic attacks of fever occurs due to
release of toxic metabolites of the parasite formed during each
erythrocytic schizogony. Each attacks of fever has 3 stages :
o Cold stage – A period of 20 min to 1 hr when a patient feels cold.
o Hot stage – A period of 1 to 4 hrs when a patient complains of
very high fever .
o Sweating stage – Fever spontaneously comes down over several
hours and the patient sweats profusely .
Types of malarial fever:
Malarial fever usually maintains a specific pattern except in falciparum
malaria. These patterns correlates with release of merozoites from
infected RBC. Malarial fevers are of following patterns –
o Benign tertian malaria:
 Characterized by fever at every third day.
 Caused by P. vivax.
 Considered benign due to very low mortality. 14

oMalignant tertian malaria:
Caused by P. falciparum.
Fever has no specific pattern.
Considered malignant due to high parasitaemia, very high
mortality.
oOvale tertian:
Caused by P. ovale.
Fever appears in every 3rd
day
oQuartan fever:
Caused by P. malariae.
Fever appears in every 4th
day.
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2. Anaemia: Microcytic hypochromic anaemia occurs due to –
Massive breakdown of infected RBC.
Splenic removal of both infected and non infected RBC.
Auto immune breakdown of RBC.
Increased fragility of RBC.
Decreased life span of infected RBC.
Inappropriate incorporation of iron in to haem.
Bone marrow suppression.
3. Splenomegaly: Due to hypertrophy and hyperplasia of RES
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•Complication of malaria
•Cerebral malaria
•Black water fever
•Renal failure.
•Tropical splenomegaly syndrome
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1. Cerebral malaria:
Erythrocytic schizogony occurs within the capillary of internal organs
like brain, kidney, suprarenal gland, spleen etc.
Increased stickiness of the membrane of Infected RBC which adheres to
the capillary of internal organ.
One infected RBC is surrounded by several non infected RBC which
forms rosette pattern
cerebral blood vessel produces anoxia, which stimulates macrophage
and release IL-1, TNF α and other cytokines and produces symptom.
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2. Black Water Fever:
Characterized by –
o Sudden massive intravascular hemolysis followed by
methaemoglobinaemia haemoglobinurea.
o Previously thought that quinine treatment causes this which is now
been proven wrong.
o Urine becomes coca cola colour.
Imported malaria /Airport Malaria / baggage malaria or taxi rank
malaria:
People who live around airport may be affected by malaria though that
area is non-endemic for malaria. There is not such a strong evidence
but a hypothesis that causing airport malaria. The hypothesis is
malaria spread by the airplane which transmit the vector from
endemic area to the airport area.
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Laboratory diagnosis:
1. Direct evidence:
 Microscopic Examination of peripheral blood film after staining by
Leishman stain.
 Specimen is peripheral blood.
 Blood must be collected during rising temperature or when
temperature has reached the peak.
 2 types of peripheral blood films that can be prepared thin film and
thick film.
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Thick film Thin film
More blood (4 drops) is taken Less blood is taken
Can be diagnosed in low
parasitaemia
Can not be diagnosed
Species can not be diagnosed Can be diagnosed

2. Indirect Evidence :
 Detection of antigen.
 Detection of antibody.
 Detection of nucleic acid sequence
Both the antigen and antibody are detected by Immune
Chromatography Test (ICT).
PCR can be done to detect specie.
Immune chromatographic test (ICT) – Routinely done, high sensitivity &
specificity, cheap, rapid, don’t require sophisticated or expensive
equipments or reagents, available in Bangladesh in some cases its
positive even in patients whose PBF don’t reveal any plasmodium.
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There are a number of genetic factors that protect against malaria:
1. Lack of Duffy blood group antigen: Duffy blood group antigen on
RBC is the receptor for P. vivax. So any person lacking Duffy blood
group antigen is simultaneously resistant to P vivax infection. Found
in West Africans.
2. Protected sickle cell individuals: In sickle cell trait very low oxygen
tension causes parasite to die due to little ATPase activity which
causes low energy production
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Chemoprophylaxix
Chloroquine
• Started at least 1 week before going to endemic area
• Once in every week during the time of staying
• After coming back it will be continued for 4-6 weeks
Doxycycline
• Started at 2-4 days before going to endemic area.
• In endemic area 150 mg daily at same time.
• After coming back it will be continued for 4-6 weeks.
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