Medical Parasitology

Medical parasitology deals with parasites which infect Table 54.1: Classification of Parasites
andproduce disease in human beings.
Group Examples
Darasite: A parasite is a living organism which I. Protozoa (Unicellular)
epends on a living host for its survival and derives
nutrition from the host, without giving any benefit to 1. Amoebae Entamoeba histolytica
E. gingivalis
thehost. Giardia lamblia
2. Flagellates
dost: It is defined as arn organism which harbours the Trichomonas vaginalis
parasite. Different types of host are as follows: Leishmania sp.
1 Definitive host: It is the host that harbours the 3. Sporozoa Plasmodium vivax
adult stage of the parasite or where the parasite P. falciparum
replicates sexually. Toxoplasma gondi
Intermediate host: It is the host that harbours the 4. Ciliates Balantidium coli
larval stages of the parasite or where the parasite II. Helminths (Multicellular)
replicates asexually.
3. Reservoir host: is the host that harbours the
1. Trematodes Fasciola sp.
Schistosoma sp.
parasite and acts as an important source of
infection. 2. Cestodes Taenia sp.
Echinococcus sp.
Host-Parasite Relationship 3. Nematodes Roundworm
An association which is formed between host and Hookworm
Threadworm
parasite may be divided into following types:
1. Symbiosis: Both host and parasite are so dependent
upon each other that one cannot live without the I. PROTOZOA
help of the other. None of them suffers any harm A. Entamoeba histolytica
from the association. Entamoeba histolytica is worldwide in distribution but
2. Commensalism: It is an association in which the
more common in tropical and subtropical countries. It
parasite only is deriving benefit without causing lives in the large intestine of man.
any injury to the host. A commensal is capable of
living an independent life. 1. Morphology
3. Parasitism: It is an association in which the parasite The parasite exists in three forms: trophozoite, pre-cystic
derives benefit and the host gets nothing in return stage and cyst (Fig. 54.1).
and always suffers some injury. The parasite canrnot (i) Trophozoite: It measures 18-40 um (average 20-30
live an independent life. um) in diameter. The cytoplasm of the trophozoite
is divided into two portions-a clear outer ectoplasm
Classification of Parasites and a granular endoplasm. Trophozoites are motile
by pseudopodia. Pseudopodia are long finger-like
Parasitesare classified into protozoa and helminths. A
dassification of parasites of medical importance is given projections of ectoplasm into which endoplasm
in Table 54.1. flows.

293
 204 O Unit Vl. l'arasitology
Pseudopodia

Ectoplasm
Endoplasm
-Nucleus
Karyosome
Chomatin granules

Pre-cystic stage
Trophozoite
Cyst wall

Chromatoid bars Nucleus

Glycogen mass.
Quadrinucleate cyst
Binucleate cyst
Uninucleate cyst
of Entamoeba
histolytica
morphological forms
Fig. 54.1 Different
forms. Man acquires the infection by
Nucleus of trophozoite is spherical in shape and water and food containing these cysts.
ingestion
When the of
cyst
varies in size from 4 to6 um. In stained preparation, reaches the caecum or the lower part of the
it shows a small dot like structure, karyosome, excystation occurs. During this process, each; theileum,
by
which is central in position and surroundedand liberates asingle amoeba with four rnuclei, at
mature
cyst
a clear halo. Nuclear membrane is delicate amoeba which eventually produces eight met tetranucleate
lined with a layer of chromatin granules. The space trophozoites by the division of nuclei by binary
between the karyosome and the nuclear membrane
spoke- These metacystic trophozoites ultimately lodoefisiion.
is traversed by linin network which has a submucous tissue of the large intestine, their normal
like radial arrangement.
stage: It is smaller in size and varies
habitat. Here they grow and multiply by binarvfssi
(ii) Pre-cystic
from 10 to 20 umn in diameter. It is round or oval During growth, E. histolytica secretes aproteoltic
similar
with a blunt pseudopodium. Nucleus has enzyme which brings about destruction and necTOSisof
characters as that of trophozoite. tissues leading to flask-shaped ulcers. Alarge number of
and is muer
wtophozoites are excreted along with blood and
(iüi) Cyst: It is round, 10-15 um in diameter
refractile membrane, called
surrounded by a highly in the faeces. This condition is calledamoebic dysenterv
the cyst wall. Nuclear structure similar to that Sometimes the trophozoites enter into deeper layers and
of trophozoite. A mature cyst is a quadrinucleate may gain entry into the radicals of portal vein to be
spherical body. It starts as a uninucleate body but carried away to theliver. In the liver, they multiply and
soon divides by binary fission to form two and produce amoebic hepatitis arnd amoebic liver abscess.
then four nuclei. Uninucleate and binucleate bodies
also possess aglycogen mass and 1-4 chromidial or After sometime, when the effect of the parasite on the
chromatoid bars.Glycogen mass stains brown with host is toned down and there is increase in the toleran
iodine. Chromatoid bars do not stain with iodine of the host, the lesion starts healing. The trophozoites, in
but appear as refractile bars with rounded ends in the lumen of the large intestine, transform into precys
preparations with normal saline. These bars stain and then into mature quadrinucleate cysts. This proes
black with iron-haematoxylin stain. In a mature is known as encystation.
cyst (quadrinucleate),both the glycogen mass and
chromatoid bars disappear. 3. Pathogenesis and Clinical Features (intestinal
E. histolytica causes amoebic dysentery
2. Life Cycle amoebiasis) and extraintestinal amoebiasis.
E. histolytica passes its life cycle in only one host (Fig. (Yntestinal amoebiasis: Incubation period Pit
54.2).The mature quadrinucleate cysts are the infective characteristic
weeks. The amoebae produce
 295
Ch54. Medical Parasitology 0

Quadrinucleate
cyst

Binucleate cyst

Uninucleate
Cyst
Encystation Encystation
Tetranucleate
amoeba
Pre-cyst

Metacystic
RO trophozoites
Metacystic trophozoite

Fig. 54.2 Life cycie of Entamoeba histolytica

ulcerative lesions and a profuse bloody diarrhoea. (i) Intestinal amoebiasis

Thisiscalled as amoebic dysentery. The ulcers may (a) Stool examination: In acute amoebic dysentery,
be generalised or may be localised to the ileo-caecal stool or colonic scrapings from ulcers are examined
or sigmoido-rectal region. by naked eye and microscopic examination.
Normal saline preparation is useful for the
(üExtraintestinal amoebiasis: Some individuals
demonstration of actively motile trophozoites,
with intestinal amoebiasis develop hepatic
amoebiasis. Amoebic liver abscess is formed. while iodine preparation is required for the
study of cysts or dead trophozoites. Excretion of
may occur in any part of the liver but it is cysts in the stool is often intermittent, therefore,
generally confined to posteriosuperior surface of at least three consecutive specimens should be
the right lobe of liver. The pus, of liver abscess, examinedCharcot-Leyden crystals may appear in
has a characteristic red-brown anchovy sauce saline preparation. These are diamond-shaped
appearance. The pus may yield trophozoites of the crystals, clear and refractile. Amoebic dysentery
parasite. From the liver, trophozoites may enter must be differentiated from bacillary dysentery
into the systemic circulation involving other organs (Table 54.2).
Ssuch as lungs, brain, spleen, skin etc. (b) Blood examination: It shows leucocytosis.
(c) Serological tests: In early cases it is always
Laboratory Diagnosis negative. Antibody can be detected in later stages
Lasolytica
boratory indiagnosis
depends on the demonstration of
the material obtained from any particular
of invasive intestinal amoebiasis. Serological
tests used are indirect haemagglutination assay
Sion, such aSStool, pus from hepatic abscess cases (IHA) and enzyme-linked immunosorbent assay
nd spútum. ELISA).
 296 Q Unit VI. Parasitology
Table 54.2: Distinguishing Features of Amocbic
Dysentery and Bacillary Dysentery
VAmoebic dysentery Bacillary dysentery
Macroscopic > 10 motions per day
Number 6-8 motions per day Small
Amount Copious Odourless
Odour Offensive
Bright red
Colour Dark red
Alkaline
Reaction Acidic Blood and mucus but no faeces
Nature Blood and mucus mixed with faeces Adherent to container
Not adherent to container
Consistency
Microscopic Discrete or in rouleaux formation
RBCs In clumps
Numerous
Pus cells Scanty
Scarce
Eosinophils Present
Numerous; many of them contain RBCs.
Macrophages Very few hence mistaken for E. histolytica
Numerous
Ghost cells Absent
Present Absent
Pyknotic bodies
Absent
Charcot-Leyden Present
Crystals
Parasite Trophozoites of E. histolytica present Absent

Bacteria Many motile bacteria Absent

(ii) Hepatic amoebiasis gEntamoeba gingivalis

(a) Diagnostic aspiration: Trophozoites of E. It is asmall amoeba measuring 10 to 20 um in diameter
histolytica may be demonstrated by microscopy and is actively motile by multiple pseudopodia.
of pus aspirated from hepatic abscess. has only the trophozoitestage and there is no qystc
(b) Liver biopsy: Trophozoites may also be phase. The cytoplasm is divided into clear ectoplasm
demonstrated in the liver biopsy from cases of and granular endoplasm. Cytoplasmic inclusions
amoebic hepatitis. consist of bacteria, leucocytes and other substances
but never RBCs. Nucleus is spherical and has acentral
(c) Examination of blood: It shows leucocytosis. karyosome. Nuclear membrane is lined with cosety
(d) Stool examination: In about 15% cases of hepatic
abscess, cysts of E. histolytica may be demonstrated packed chromatin granules.
in the stool. It indicates persistent intestinal E. gingivalis is a parasite of human mouth. I
infection. occurs as a commensal in gingival tissue around t
(e) Serological tests: Antibody detection is of great teeth, particularly in the unhealthy tissues such as n
value in the diagnosis of hepatic amoebiasis. IHA pyorrhoea alveolaris. However, it may also octur
and ELISA are some serological tests used for apparently healthy mouths and dental plates if they
diagnosis. Serum with antibody titre of 1 :128 or are not cleaned properly. It has also been found in
more by IHA is diagnostic of amoebic hepatitis. the crypts and histologic sections of diseased tonsis
It is transmitted by close contact like kissing or tiu
E. histolytica antigen can also be detected in serum
by ELISA. contaminated drinking utensils.
demonstration ot
B.Entamoeba coli
Laboratory diagnosis depends onmaterial removed
trophozoites of E. gingivalis in the denture.
It is world-wide in distribution. It lives in the lumen of from gingival margin ot gums or from
large intestine. It is non-pathogenic. Life cycle of E. coli is
similar to that of E. histolytica. Entamoeba coli also exists D. Giardia lamblia theretore
inthree stages, i.e, trophozoite, pre-cystic stage and cyst. These flagellates inhabit the intestine and arepresentin
Differences between E. histolytica and E. coli are shown named intestinal flagellates. They are man.
in Table 54.3. duodenum and the upper part of jejunum of
 Ch s4 Medical Parasitology J 297
Table 54.3: Differences between E.
histolytica and E. coli
E. histolytica E. coli

20-30 um
20-40 um
Actively motile
Sluggish
0tylasm Clearly demarcated into ectoplasm and Not demarcated
endoplasm
(tplasmic RBCs, leucocytes and tissue debris but no Bacteria and other materials but never RBCs
ncusions bacteria
Not visible in unstained
Viceus
Karyosome Central
preparation Visible in unstained preparation
Eccentric
Nucear membrane Delicate nuclear membrane lined by fine Thick nuclear membrane lined by coarse
chromatin granules chromatin granules

6-15 um indiameter 15-20 um in diameter

Nucleus 1to 4, central karyosome
Ito 8, eccentric karyosome
Chromatoid bars Rounded
Filamentous

LMorplhology The remnants of the flagella and the suckling disc may
iumhlia exists in two phases -trophozoite and cyst be seen inside the cytoplasm.
Be 543). The shape of trophozoite is like that of atennis
hadminton racket. The dorsal surface is convex while 2. Life Cycle
ntral surface is concave having a suckling disc. The The trophozoites of the parasite multiply in the intestine
eof trophozoite is 14 um long and 7 um broad. The
nterior end is rounded and broad while the posterior of man by binary fission. During unfavourable conditions
in the duodenum, encystment occurs, usually in the large
nd is pointed. It is bilaterally symmetrical, i.e., all the
mans of body are paired and hence there are two intestine. Infection of man occurs by ingestion of cysts.
nostyles, twO nucleiand four pairs of flagella. After ingestion, the cyst hatches out two trophozoites
The(cys)is oval in shape and it is 12 um long and which then multiply and colonise in the duodenum. Due
um broad. There are four nuclei. The axostyles lie to high acidity of duodenum Giardia often localises in
diagonally, forming a dividing line within the cyst-wall. the biliary tract.

-Suckling disc

Nucleus
Nucleus

-Axostyle
Axostyle

Flagella

Cyst

Trophozote

Fig. 54.3 Trophozoite and cyst of Giardia lombla

 298 O Unit VI.
Parasitology
Trophozoites in the
intestine of man

Due to high acidity of

duodenum, trophózoites Multiply by
binary fission
localise in biliary tract

Life Cycle
of
Trophozoites and Giardia lamblia During unfavourable
colonise in duodo
conditions, encystment
occurs in large intestine

Each cyst hatches out Infection in man

two trophozoites
occurs byy ingestion
of cysts

3. Pathogenesis 1. Morphology (Fig. 54.4)

It may cause a disturbance of intestinal function, These flagellates exist only in the trophozoite phas
leading to malabsorption of fat. The patient may and there is no cystic phase. They are_ pear shaped
complain of persistent looseness of bowels, and mild and measure 10-12 um in lerngth. The anterior end is
steatorrhoea. The patient may present as silent case
without any symptom, as chronic enteritis and acute round and cleft like depression (cytostome) is present
enterocolitis, or as chronic cholecystopathy. Sometimes at its side. The single ovoid nucleus is present at the
onlygeneral features such as fever, anaemia and allergic anterior end. There are 3 to 5 anterior flagella which are
manifestations are present. free. The posterior end is pointed. A thicker flagellum
passes backwards along the side of the body and fomns
4. Laboratory Diagnosis the undulating membrane which comes out free at the
Microscopic examination posterior end. The undulating membrane is supported
Demonstration of Giardia trophozoites and cysts in at the base by arod like structure named 'costa'. The
freshly passed stool by wet preparation (saline and axostyle runs down the middle of the body and ends
iodine) is useful for diagnosis. Trophozoites may also in the pointed tail like extremity.
be recovered in the bile.

5. Treatment 2. Pathogenesis
Metronidazole is the drug of choice. T. vaginalis is the causative agent of trichomoniasis in
E. Trichomonas females. In case of males, it causes sexually transmited
The Trichomonads are flagellate protozoa with 3 to disease (STD) causing urethritis. The other two
5 anterior flagella. The genus Trichomonas hasbeen trichomonads (T. tenax, T. hominis) are non-pathogen
classified into three species according to their habitats:
())Arichomonas vaginalis (13 um): inhabiting the 3. Laboratory Diagnosis
female genital tract; also found in the urinary tract
of males and females. Microscopic examination examined
(iY Trichomonas tengx: inhabiting the oral cavity. Vaginal or urethral discharge is
characteristic
ii1y Trichomonas hominis (8um): inhabiting the microscopically in a drop of saline for
ileocaecal region. motile trophozoites.
 299
Ch 54. Medical Parasitology O

Flagella

Undulating
membrane
Nucleus

Costa
Axostyle

Trichomonas vaginalis Trichomonas tenax Trichomonas hominis

Fig. 54.4 Trophozoites of different Trichomonas sp.

FLeishmania donovani nucleus. Axoneme extends from the kinetoplast to

s parasite causes visceral leishmaniasis or kala-azar. It the margin of the body. It represents the root of
in many places in India. It is a parasite of the flagellum.
sendemic
airuloendothelial system. (i) Promnastigote stage (Fig. 54.5): It is aflagellar stage
and is present in insect vectors (sandflies) and in
cultures. It is long, slender, spindle-shaped body
LMorphology (15-20 umx 1-2 um). Nucleus is situated centrally.
The parasite exists in two forms: Kinetoplast lies near the anterior end. Flagellum
Amastigote Occurs in nan.
may be of the same length as the body or even
Fromastigote Occurs in gut ofsandfilyjand longer.
artificial culture.
@Amastigote stage (Fig. 54.5): It is aflagellar stage 2. Life Cycle
and is present in the cells of reticuloendothelial The parasite has two stages in its ife cycle, i.e, amastigote
system of vertebrate hosts (man, dog etc.). It is a form and promastigote form. The amastigote form
round or oval body (2 to 4 um). Nucleus is oval multipliesin the cellsof the reticuloendothelium system
or round and is usually situated in the middle tillthe host cell becomes packed with the parasites. The
of the cells. Kinetoplast lies at right angle of the host cell enlarges and eventually ruptures. The parasites

Flagellum

Nucleus

Kinetoplast
Kinetoplast

Nucleus Axoneme
-Axoneme

Amastigote stage Promastigote stage

Fig. 54.5 Amastigote and promastigote forms of Leishmania donovani

300 QUnit VI.
Parasitology
Amastigote
forms in
reticuloendothelial
system of man

Promastigote
forms change into
Host celI
ruptures
amastigote forms

Life Cycle
of
Bite of sandfly Leishmaniadonovani Parasites in
to man circulation

Amastigote form changes Sandfly draws

into promastigote form in amastigote forms
sandfly during blood meal

are liberated into the circulation. The blood-sucking promastigote forms can be demonstrated whe
insect (sandfly) draws these free amastigote forms this material is cultured in N.N.N. medium
during its blood-meal. (d) Splenicpuncture: It is one of the most valuah.
These amastigote forms develop intopromastigote method for diagnosis. The amastigotes are found
forms which again multiply by binary fission producing in stained films and promastigotes in culture. The
a large number of promastigotes. A sandfly species only risk of splenic pncture is that bleeding mat
named Phlebotomus argentipes acts as Indian vector. continue from the puncture wound resulting in
Infection occurs by biteof infected sandfly. Incubation death.
period varies from 3to6 months.
(ii) Indirect evidences
3. Clinical Features (a) Blood count: There is progressive leucopenia
Leishmania donovani produces the disease kala-azar or The proportion of leucocytes to erythrogtes is
visceral leishmanigsis. It is characterised by pyrexia, greatly altered.
splenomegaly. hepatomegaly. Iymphadenopathy and
general features of anaemia.
(b) Haemoglobin estimation: It reveals anaemia.
e Non-specific serological tests
Aldehyde test: This test indicates increased senum
4. Laboratory Diagnosis gamma globulins and thus is non-specific. Is
Laboratory diagnosis of kala-azar depends upon direct positive only when the disease is of at least thr
evidences and indirect evidences. Direct evidences months duration.
demonstrate L. donovani in specimen.
Antimony test: This test also depends upt
(i) Direct evidences increased serum gamma globulin. It is lessreliabk
Peripheral blood smear: Thick blood film than aldehyde test.
(a) Complement fixation test with W.K.K. antigen
examined for demonstration of amastigote detects antibodies in sera of Kala-azar patient
forms. human
The antigen used was prepared from
(b) Blood culture: Blood culture carn be done in tubercle bacillus by Witebsky, Klingenst Theest
N.N.N.(Novy, MacNeal, Nicolle) medium and Kuhn, hence named as W.K.K. antigen.
incubated at 22°-24°C. Promastigote forms can antigenisn
be demonstrated.
is considered non-specific: since the
prepared from L. donovani.
(c) Bone-marrow aspirate: Bone-marrow aspirate Ja) Specific tests: Indirect haemagglutination(LFAD)
is a useful method for diagnosis. Amastigote (IHA), indirect fluorescent antibody test assa
forms canbe demonstrated ina stained film. The IMmun0sorbent
and enzyme linked
 Ch 54. Medical Parasitology O 301
(ELISA) are more specific tests. ELISA using
species specific monoclonal: red blood cells rupture to release the merozoites
probesare very
useful in the antibodies and DNA
direct detection of which attack new red blood cells and continue
Leishmania antigen. thejr erythrocytic schizogony repeating the cycle.
In(P. falciparum infection, erythrocytic schizonts
Plasmodium aggYegate in the capillaries of the brain and other
herearefour species of Genus Plasmodium: P. vivax, internal organs,)so that only ring forms are found
rliparum, P. malariae and P. ovale. They are protozoa, in the peripheral blood. Differential features of
Using malaria in man. These malarial parasites are various plasmodia are shown in Table 54.4.
orldwide in distribution. In India, P. vivax and .GiY Gametogony (Fig. 54.7): Some merozoites of
are very common but P. ovale does erythrocytic schizogony develop into male and
not female gametocytes known as microgametocytes
ur.
and macrogametocytes respectively. They
LLijfeCycle develop in the red blood cells. These are sexual
ThemalarialI parasites pass their life cycle intwo hosts,
forms and are found in the peripheral blood.
L, man (intermediate host) and female anopheles The microgametocytes of all the four species are
(definitive host). Smaller in size, cytoplasm stains light blue and
nOSquito
Asexual development of
in man and sexual
the nucleus is large and diffuse. In contrast, the
parasite OCCUrs
development in macrogametocytes are larger, the cytoplasm stains
MOSquito.
deep blue and the nucleus is small and compact.
Humancycle . y Exoerythrocytic schizogony: The exoerythro
The sporozoite the infective form of the malarial cytic cycle resembles the pre-erythrocytic cycde.
rasite. These sporozoites are present in the salivary Some sporozoites, on entering into liver cells,
dand of female anopheles mosquitoes. Man gets do not undergo asexual multiplication but enter
tion by the bite of infected mosquito and sporozoites into a resting (dormant) phase. The resting
re introduced directly into the blood circulation. Thus, stage of the parasite is known as hypnozoite.
human cycle starts and it comprises of following stages: After some period (usually up to 2 years),
Pre-erythrocytic schizogony hypnozoites reactivate to become schizonts and
release merozoites. These merozoites attack red
Erythrocytic schizogony blood cells and are responsible for rélapse_of
Gametogony
Exo-erythrocytic schizogony Trophozoites Schizonts
Pre-erythrocytic schizogony: Before -Enlarged RBC
starting erythrocytic schizogony in blood, P. vivax
sporozoites undergo a developmental -Merozoite
phase inside theliver cells. This phase of
Ring Form
development is known as pre-erythrocytic
schizogony. The sporozoites (elongated and Schizönt

spindle-shaped) become rounded inside

the liver parenchymal cells. They undergo P. falciparum Normal Size of RBC
multiple nuclear division and develop
into schizont. The size of schizont varies Ring Form Multiple Ring Schizont
in different species and it contains 20,000 Foms
50,000 merozoites. The pre-erythrocytic
cyde lasts for &days in P. vivax, 6 days in P.malaniae
P. falciparum, 13-16 days in P. malariae and
9days in P. ovale. After completion of this
Ring Form
cycle, the liver cells rupture and release Schizont
merozoites into the blood stream.
y trythrocytic schizogony: The merozoites
released from pre-erythrocytic schizogony
penetrate red blood cells. They pass P.ovale
through the stages of trophozoite, schizont
nd merozoite (Fig. 54.6). Depending on Ring Form Schizont
the species of malarial parasite, there may Fig. 54.6 Erythrocytic stages of different species of Plasmodium
De 6-24 merozoites in red blood cell. The
302 O Unit VI.
Parasitology
human host by the formation of
Male Gametocyte Fernale Gametocyte then transferred to mosquito for further gametocytes which are
female anopheles during its bloodImeal
ingests both the asexual andsexual
Only the mature sexual forms are
from the
forms
capable
of
i the mnosquito and rest diee of
developmenttin
developmparenpatat.seitte,,
A

furtheT
Plasmodium vivax In the midgut of the mosquito, one
develop into 4to 8thread like
named microgamnetes. From one micriomgamemdeitaotceylyte.
filamentous structures
one macrogamete is formed.
a microgamete penetrates into a
macrogametocyte
Fertilisation occurs whenonlyThe
fertilised macrogamete is known as zygote. The
lengthens and matures into an ookinete.
macrogamete.zygote
Plasmodium falciparum develops into an o0cyst. As oOOcyst matures, it The ookinete
size andalarge number of sporozoites (a few in increases
to thousands) develop inside The number oft
it.
in the stomach wall varies from a few to oocysts hundreds
hundred. The oocyst ruptures and releases more than
Plasmodium malariae in the body cavity of the mosquito. The sporozoites
sporozoites
are distributed into various organs and
tissues of the
mosquito. However, they have a special predilection for
salivary glands.
Plasmodium ovale The mosquito is now capable of transmitting the
infection to man.
Fig. 54.7 Gametocytes of Plasmodium species
2. Pathogenesis and Clinical Features
malaria. Exo-erythrocytic schizogony is absent in Infection with the Plasmodium causes intermitent
P. falciparum, therefore, relapses do not occur in fever which is named as malaria. IncubatioD period is
malaria caused by P. falciparum. 10-14 days in P. vivax, P. falciparum and P. ovale but it
is 28-30 days in P. malariae. The typical clinical features
Mosquito cycle consist of febrile paroxysm, followed by anaemia and
The sexual cycle of malarial parasite actually starts in the splenomegaly.
Sporozoites enter
in man

Bite of mosquito
Preerythrocytic/
Exoerythrocytic cycle in liver
Sporozoites

Oocyst Merozoites

Ookinete
Life Cycle
of Erythrocytic
cycle in RBCs
Zygote Malarial Parasite
Fertilisation ATrophozoites
Macrogamete Schizont
MicrogametocyteMacrogametocyte Merozoites
Microgamete

Mosquito Release of
Macrogametocyte merozoites

Gametogony

Microgametocyte
 A

Ch 54. Medical Parasitology O 303

Table 54.4: Differential
Features of Different Plasmodia of Man
Feature P. vivax
rmtsinperipheral P. falciparum P. malariae P. ovale
Trophozoites,
schizonts and Ring forms and
bloxd
gametocy tes (crescent Trophozoites, Trophozoites,
schizonts and
gametocytes schizonts and
Earlytrophozoiteor
shaped) gametocytes gametocytes
2.5 ;um in diameter,
1.25-1.5 Hm in diameter. Similar to that of P. Similar to that of
ningform
cytoplasm
the nucleus oppositemultiple
is rings in one vivax P. vivax
thicker red blood cell, form
accole
Thyphozoite Irregular, amoeboid, Compact form, rarely
vacuole present Band shaped, Compact, not
amoeboid, pigments slightly amoeboid, amoeboid,
collect into a single vacuole vacuole
mass
inconspicuous inconspicuous
4Schizont 9 to 10 um in
4.5 to 5.0 um in 6.5 to 7.0 um in 6.2 um in
diameter, almost diameter, fills two diameter, almost diameter, fills
completely ills an thirds of a normal size fills a normal size about three
enlarged erythrocyte erythrocyte erythrocyte quarters of
slightly enlarged
erythrocyte
S, Merozoites 12-24 in number 18 to 24 in number 6-12 in number 6-12 in number
6Gametocyte Spherical, much
larger than a red
Crescentric (sickle Round, size of a Round, size of a
blood cell
shaped), larger than a red blood cell red blood cell
red blood cell
(0) Female gametocyte Spherical, larger
(Macrogametocyte) than male Sickle-shaped, longer,
more slender, cytoplasm
Similar to that of Similar to that
P.vivax but smaller of P. vivax but
gametocyte, stains deep blue, smaller
cytoplasm stains nucleus is compact
deep blue, nucleus is
small and compact.
() Male gametocyte Spherical, smaller Sickle-shaped, broader, Similar to that of Similar to that of
(Microgametocyte) than female shorter, cytoplasm P.vivax but smaller P. vivax but
gametocyte, stains light blue, nucleus Smaller
cytoplasm stains is diffuse
light blue or pale
blue, nucleus is
large and diffuse
1.Malarial pigments Yellowish-brown Dark-brown Dark-brown Dark yellowish
brown
. Infected erythrocyte Size unaltered, Maurer's Normal size & no
Enlarged, pale, Slightly enlarged,
Schuffner's dots dots present dots, Ziemann's oval shaped and
present dots on prolonged James's dots
staining present
9. Age of the
Young All ages (young Old
erythrocytes infected and old) Young
10. Duration of
48 hours <48 hours 72 hours 48 hours
erythrocytic
schizogony
304 Q Unit VI.
Parasitology
(febrile paroxysm: It comprises of three stages- 3. Immunity
cold stage, hot stage and sweating stage. In the Immunity isspecies-specific tage-specific.
immunity is andAr
infectaiionn-as
cold stage, the patient feels intense cold and specific and lasts only tillmalarial parasite
shivering. During hot stage, patient develops remains active. This type of
high fever (40.0-40.6°C), severe headache,
nausea and vomiting. Fever ends and profuse
premunition immunity.
known
sweating occurs in the sweating stage. The febrile 4. Laboratory Diagnosis
paroxysm synchronises with the erythrocytic (i) Microscopicexamination:: Microscopic
schizogony of the malarial parasite. With a
48 hour cycle of erythrocytic schizogony the of a peripheral blood smear is the
diagnostic procedure in malaria. Thick
cexamiimportnatiaontn
most
fever recurs every third day (P. vivax), with a smears of the blood are prepared on the and thin
72 hour cycle the fever recurs every fourth day
or two different slides.
Blood for samne slide
(P. malariae). collected a few hours after smear
the height should be
of
(ii) Anaemia: After a few paroxysms, anaemia of paroxysm because the parasites are most febrile
a microcytic or normocytic hypochromic type during this period. Blood is taken by abundant
develops as a result of destruction of parasitized
red cells during segmentation of parasites.
finger prior to start of antimalarial
take a drop of the blood
pricking
therapy.
a
For
thick smear, on the
(iii) Splenomegaly: After some paroxysms, spleen is and spread it in an area of 1 cm Square. For slide
enlarged and palpable. smear, take a drop of the blood at one cornerat thin
P. falciparum is the most pathogernic of the the slide and spread it with another slide so that
plasmodium species infecting marn. There are no relapses tail formation occurs at another end. Both thisl
in P. falciparum infection but relapses occur in P. vivax and thin peripheral blood smears are stained wit
infection. It invades erythrocytes of all ages (young Leishman stain. These smears are examined und
and old) but P. vivax infect only young erythrocytes. oil immersion lens.

Complications of P. falciparum infections include Malarial parasites may be quickly detected in the
'pernicious malaria' and black water fever. thick smear but species identification is difficult
Thin smear is examined for identifying the species
Pernicious malaria of plasmodium.The parasites are more along the
Pernicious malaria is life threatening complication upper and lower margins of the 'tail' of the thin
that sometimes occur in acute falciparum malaria. It is smear. A minimum of 100 microscopic ields
due to heavy parasitization. Various manifestations of should be examined in each slide.
pernicious malaria are grouped as cerebral malaria, algid All asexual erythrocytic stages (ring forms,
malaria and septicaemic malaria. trophozoites, schizonts), as well as gametocytes
1. Cerebral malaria: It is characterised by hyperpyrexia, can be found in peripheral blood smear in
coma arnd paralysis. Brain is congested. infection with P. vivax P. malariae and P. ovale,
2. Algid malaria: It is characterised by cold clammy but in P falciparum infection, only the ring forms
skin leading to peripheral circulatory failure. and gametocytes (crescent shaped) can be seen.
Multiple rings in an individual red blood cell with
Black water fever ACcole forms is diagnostic of P.falciparum.
It is a manifestation of infection with P. falciparum Schuffner's dots, in the red blood cells, can be
occurring in those persons who have been previously seen in P. vivax and P. ovale infection, whereas
infected and have had inadequate dose of quinine. It Maurer's dots and Ziemann's dots are seen in
is characterised by intravascular haemolysis,fever and the red blood cells in P. falciparum and P. malariae
haemoglobinuria. infection respectively. Red blood cells are enlarged
The exact mechanism of haemolysis is not known in P. vivax but there is no enlargement of RBC in
but an autoimmune mechanism has been suggested. P. falciparum infection.
Parasitized erythrocytes during previous infection act (ii) Serological tests: Indirect immunofluorescence
as antigen against which antibodies are formed. When test, indirect haemagglutination assay (IHA) ana
subsequent infection and treatmernt with quinine occurs, enzyme linked immunosorbent assay (ELISA
there is massive destruction of erythrocytes because of are the serological tests used for the diagnosis of
antigen-antibody reaction. Black water fever has now malaria.
become rare because newer antimalarials have replaced (iüi) DNA probes: These are sensitive and specitc
quinine. diagnostic methods for the diagnosis of malan.
 Treatment
guine along Withprimaquine is used for treatment
vivax malaria. Artemisinin and its
of
newerr drugs used for derivatives
treatment falciparum
of are the
malaria.
II. TREMATODES
hose are leat-shaped unsegmented worms, called
flukes. Each individual worm is
the Schistosomes which are hermaphrodite except
unisexual. Body cavity is
absent. The worm is oviparous (eggs are
are all operculated (except those of liberated). Eggs
Schistosomes) and
(
develop only in water.

Man-harbours adult worm

Eggs liberated and develop in water

Pass through different stages in snail

Cercariae free in Cercariae on vegetables or

water within second intermediate host

Enter in man and develop Ingested and develop into adult

into adult worms worms B. Ta
Com
Different Trematodes tapev
worl
l. Intestinal trematodes e.g.Fasciola busi eatin
<. Hepatic trematodes e.g. Fasciola hepatica in M
3. Lung trematodes
atodes e.g. Paragonimus westermani
4. Blood trematodes e-g Schistosoma haematobium, S. 1. M

mansoni, S. japonicum
Mode of Infection