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Entamoeba Histolytica:
1. Losch (1875) first described Entamoeba histolytica as Amoeba coli.

2. Leidy first established the genus Entamoeba in 1879.

3. Schaudin established the species Entamoeba histolytica in 1903 and differentiated

into pathogenic and nonpathogenic types.

There are 5 species of Entamoeba in human beings of which E. hartmanni and E. coli
are non-pathogenic, and E. histolytica, E. gingivalis and E. polecki are pathogenic.

Geographical Distribution of Entamoeba Histolytica:

The parasite is worldwide in distribution and more common in most countries of trop-
ics and subtropics rather than temperate zones. E. histolytica is scarcely pathogenic
found in human beings of temperate zones.

Habit and Habitat of Entamoeba Histolytica:

Entamoeba histolytica is an endoparasite and the parasite inhabits the mucous and sub-
mucous layers of the large intestine of man. It may also occur in the liver, lungs and
rarely invades brain, spleen, etc. producing ulcers, but the cyst is found in the intestinal
lumen of man.

Entamoeba histolytica has also recorded in orang-utang, gorilla, chimpanzee, gibbon,

baboon, donkey, dog, cat, rat and pig.

Morphology of Entamoeba Histolytica:

(a) Trophic:
The trophozoites vary in size from 15 to 40 micra, the average being 18 to 25 micra.
Dobell (1919) and others have shown that the parasite has got two races, one large and
the other small. The trophozite of Entamoeba histolytica in living condition shows two
distinct portions, ectoplasm and endoplasm. The ectoplasm is clear and translucent
while the endoplasm is granular.

The endoplasm often contains injested red blood corpuscles. The pseudopodia may be
long, finger-like or short and rounded in shape (Fig. 10.23). In freshly passed stool the
parasite is very active and moves rapidly in a straight line with a single clear
pseudopod at the anterior end.

This is known as ‘directional movement’. The movement becomes sluggish when the
faeces cool down and in this condition the amoeba throws out pseudopodia at various
directions and remains stationary.
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The nucleus is indistinct in living condition but when stained with haematoxylene it
shows a small dot-like central karyosome or endosome, a uniform ring of small periph-
eral chromatin granules and at times some chromatin granules in between them.

Sometimes there may be traces of linin network in the form of fine fibrils in between
karyosome and nuclear membrane. The nuclear membrane is very delicate. The size of
the nucleus is about 4 to 6 micra in diameter.

(b) Cystic:
The cysts of both races of Entamoeba histolytica vary in size from 10 to 20 micra
(average 12 micra) in diameter. In haematoxylin stained preparation a matured cyst
looks spherical and quadrinucleate. Its cytoplasm is clear and often contains black rod-
like chromatoid bars or bodies with rounded ends (Fig. 10.23D).

The young cysts are uninucleate or binucleate and their nuclear structure is just like
that of the trophozoites. But it shows a very small central karvosome and a delicate
nuclear membrane.

Presence of chromatoid bodies is the characteristic of the cysts of Entamoeba

histolytica. They occur either singly or in multiples of two or more.

Remark:
About the exact nature of these bodies there is a controversy. Some authorities
consider it as nutrient material of the cyst while others believe them as excess of
chromatin thrown off during nuclear division.:
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The chromatoid bodies occur in the early stages of the cysts but they disappear in the
mature quadrinucleate cyst.

In young cysts glycogen is present in a diffused state and can be demonstrated in

preparation with Lugol’s iodine solution producing a brownish colour.

Life Cycle of Entamoeba Histolytica:

The life cycle of E. histolytica is completed through a single host-man. Hence it is
called monogenetic. Trophozoite and cyst stages of the parasite are concerned with the
life cycle.

Encystment::
Entamoeba histolytica multiplies by binary fission in the trophozoite stage. They have
the capacity to encyst. Unfavourable conditions in the habitat such as lack of nutrients,
temperature deviations from the optimum range, decreased O2 tensions, lowered pH
and accumulation of metabolic wastes may be the causes for encystment.
Precystic form:
Prior to encystment the trophozoite of each parasite loses its pseudopodium, eliminates
food vacuoles and becomes spherical, called a precystic form. The diameter of this
stage varies 10-20 µm and the structure of the nucleus is like the trophozoite stage of
the parasite.

Mature cyst form::

The precystic form secrets a thin, tough and transparent membrane around it, called the
cyst wall. The animal having a cyst is called a cyst. The process of enclosing in a cyst
is called encystment or encystation. At the early stage the cyst contains a single
nucleus. The single nucleus is divided mitotically forming two nuclei. This is called
binucleate cystic stage.

Then the two nuclei are divided by mitosis and four nuclei occur. The nuclear divisions
take place without cytoplasmic division and this tetra-nucleate cyst is called mature
cyst. The whole process of encystment takes a few hours and the mature cyst lives in
the lumen of the intestine of host only two days.

Tolerance of the cyst:

The cysts of E. histolytica can survive about one month in water and about 12 days on
dry land. They can tolerate the temperature up to 50° Celsius and 4 hours in
formaldehyde solution.

Infection:
At the tetranucleate stage the cyst is infective to a new host. The infective cysts pass
out through the host’s faeces and are introduced into the gut lumen of a new host
through the contaminated drink, food and vegetables.
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Excystment:
Then the infective cysts pass into the lower portion of the small intestine (colon) of the
new host. Here the process of excystment occurs. The excystment is the process by
which the cysts are transformed into the trophozoites.

The cyst wall in the colon becomes permeable by the action of intestinal enzymes, the
trypsin of the intestine. The cyst wall ruptures and 4-nucleate amoeba emerges out
from the cyst.

Factors for excystment:

Temperature, pH, chemical composition of the medium and the flora of the bacteria
may be the reasons for excystment.  

Metacystic form:
After the emergence of quadrinucleate amoeba, the division of cytoplasm immediately
ensues and produces four small metacystic trophozoites.

Trophozoites:
Both the nucleus and cytoplasm of each metacystic trophozoite divide and as a result 8
small amoebulae are produced (Fig. 10.24). These are called young uninucleate
trophozoites. They are motile and penetrate the mucous membrane.

The young trophozoites feed on host tissues, blood, bacteria and yeast and gradually
increase in size to attain maturity. Inside the tissues the trophozoites multiply and start
the procystic form of the life cycle.
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The exact nature of the division of the nucleus is controversial but it is believed by
many authors that it is probably a modified type of mitosis. The chromosome number
of Entamoeba histolytica is stated to be six.

Transmission:
Cysts of Entamoeba are transmitted from one individual to another in a variety of
ways:
1. The cysts are generally transmitted with food or drink.

2. House flies and cockroaches may transmit cysts mechanically.

3. Raw vegetable is also another source of infection.

4. In many countries human faeces are used as fertilizer and thus roots and leaves of
plants remain contaminated with viable cysts. Food handlers are also sometimes
responsible for the spread of infection owing to imperfect personal sanitary measures.

Symptoms:
Amoebiasis or amoebic dysentery is caused by the infection of E. histolytica.

Amoebiasis Questions With Answers

Also referred to as amoebic dysentery, amoebiasis is an intestinal ailment known to be
caused by the parasite, Entamoeba histolytica. This parasite harbours in the intestines
and produces eggs that are passed from the body into the stool.
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1. Amoebiasis causes
(a) Headache and cold
(b) Dysentry
(c) Fever
(d) Severe cold
Answer: (b)
2. Amoebiasis is caused by
(a) Toxoplasma gondii
(b) Entamoeba histolytica
(c) Ascaris lumbricoides
(d) None of these
Answer: (b)
3. Entamoeba histolytica can be cultured in
(a) Diamond’s medium
(b) CLED medium
(c) NNN medium
(d) MacConkey agar
Answer: (a)
4. Presence of ingested RBCs is a characteristic feature of
(a) Entamoeba histolytica
(b) Dientamoeba fragilis
(c) Entamoeba coli
(d) Iodamoeba butcheli
Answer: (a)
5. The most common site for amoebiasis is:
(a) Cecum
(b) Sigmoid colon
(c) Transverse colon
(d) Hepatic flexure
Answer: (a)
6. Amoebiasis is transmitted by
(a) Direct contact with dirty hands
(b) Sexual contact
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(c) Faecal contamination of drinking water and food

(d) All of these
Answer: (d)
7. Differentiation between pathogenic and non-pathogenic strains can be done by
(a) Phagocytic activity
(b) Use of genetic markers
(c) Zymodeme analysis
(d) All of these
Answer: (d)

8. In tissues, amoebiasis is treated with

(a) Tinidazole
(b) Nitazoxanide
(c) Metronidazole
(d) Any of these
Answer: (d)
9. The karyosome of Entamoeba histolytica is
(a) liver
(b) progressive
(c) central
(d) even
Answer: (c)
10. Entamoeba histolytica cysts have _________ nuclei
(a) 1-4
(b) 5
(c) 9
(d) 6-8
Answer: (a)
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Plasmodium Vivax
Plasmodium vivax lives as an intracellular parasite in the red blood corpuscles
(R.B.Cs) of man in the form of its mature adult condition, called trophozoite. The
species of Plasmodium are reported from reptiles, birds and various mammals.

However, Plasmodium is widely distributed in tropical and temperate countries of the

world but they are no longer a problem in the colder countries of the world. Countries
like India, Sri Lanka, Bangladesh, Nepal, Pakistan, etc., are worst affected. In our
country, states like Bihar and Uttar Pradesh suffer a greater setback by the infection of
this parasite. In fact, the infection of Plasmodium is a global problem.

Hosts of of Plasmodium Vivax:

Plasmodium vivax has two hosts; man and female Anopheles mosquito. Man is
considered to be the primary host and female Anopheles mosquito, the secondary or
intermediate host. The common species of Anopheles, which transmit malaria parasite
in India, are A. maculatus, A. stephensi, A. fluvialitis and A. culicifacies.

Structure of Plasmodium Vivax:

As referred to, the parasite, in its mature adult condition, is called trophozoite. The
trophozoite is amoeboid, uninucleated having vacuolated and granular cytoplasm.

An ultra structure of the trophozoite is described below:

Ultra structure of trophozoite:
The ultra structure of Plasmodium Vivax (Fig. 19.1) has been revealed by the electron
microscope. According to electron microscopic studies, the Plasmodium in a red blood
corpuscle possesses a double membrane, the plasma lemma closely applied to the
cytoplasm. The cytoplasm of Plasmodium Vivax contains small dense particles
probably containing ribonucleoproteins.

The endoplasmic reticulum is not well developed and appears as vesicles of variable
shapes. The vesicles are either smooth surfaced or rough surfaced and are loosely
scattered in the cytoplasm. The mitochondria possess double membrane and show
peripheral cristae and a structure less central region.

The number of mitochondria varies with the age, the merozoite has only one
mitochondrion, while the trophozoite has several mitochondria. The Golgi apparatus is
composed of small vesicles arranged in rows. A double layered concentric body is also
found in the cytoplasm attached with the plasma lemma of Plasmodium Vivax.

It appears that the concentric body originates from plasma lemma. Rudzinska (1965)
suspect that the concentric bodies serve the function of mitochondria. One or two
double membrane vacuoles with structure less matrix, also occur in the cytoplasm.
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The function of these vacuoles is unknown. The nucleus is large and its nucleoplasm is
composed of granular and fine fibrillar material. The nuclear membrane is double, to
which RNA particles are attached. The nucleolus lies centrally in the nucleus.
Pinocytosis vacuoles are common in the cytoplasm and serve as food vacuoles. The
food vaculoes may also contain hemozoin depending upon the species of Plasmodium.

The mode of nutrition is saprozoic, occurs by osmotrophy. Organ of locomotion,

contractile vacuole, etc., are not found. Respiration takes place anaerobically.
Reproduction occurs both by sexual and asexual methods.

Life Cycle and Plasmodium Vivax:

The life cycle of Plasmodium vivax is digenetic involving two hosts as mentioned
earlier. Its life cycle is completed both by asexual and sexual phases.
Asexual phase of its life cycle is completed in man by schizogony (differentiated into
exoerythrocytic schizogony involving pre- and post-erythrocytic schizogonic cycles,
and erythrocytic schizogony) and sexual phase of its life cycle is completed in female
Anopheles mosquito by gametogony, syngamy and sporogony.
(a) Part of Life-Cycle of P. Vivax in Man (Asexual Cycle):
It is completed in the following way:
Inoculation:
When an infected female Anopheles bites a man to suck his blood, then along with its
saliva it injects the sporozoite stage of Plasmodium into the human blood. The parasite
remains always in the body of one of the two hosts, hence, the sporozoites do not
possess any protective covering.

The sporozoite, infective stage, is minute measuring about 11 to 12 microns in length

and 0.5 to 1 micron in width, sickle-shaped cell with an oval nucleus; mosquito
inoculates sporozoites in thousands.
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The sporozoites are capable of slight gliding movement. In about half an hour the
sporozoites disappear from the blood stream, and they enter the parenchymatous cells
of the liver where they undergo at least two schizogonic cycles.

Ultra Structure of Sporozoite:

The sickle-shaped body of the sporozoite is covered externally by an elastic, firm
pellicle having longitudinally arranged contractile microtubules. These microtubules
help in the gliding movements shown by the sporozoite. Its anterior end bears an apical
cup being made of three or more concentric rings.

A pair of elongated reservoir like secretory organelles, comparable to roptries of the

sporozoite of Monocystis, open into the apical cup.

These organelles are supposed to secrete some secretion which facilitates its
penetration into the liver cells. Nucleus is single and vesicular having a nucleolus in its
centre. There is a single mitochondrion and a large number of convoluted tubules of
unknown function. However, the micropyle represents the cytostome of other
protozoans.

ADVERTISEMENTS:

Schizogony in Liver Cells:

In the liver cells, the sporozoite grows to form a large, round schizont. The schizont
divides by multiple fission to form about one thousand to several thousand small
spindle-shaped cells called merozoites; this multiple fission is called schizogony. The
schizont ruptures and merozoites are liberated into the sinusoids or venous passages of
the liver.

This phase of asexual multiplication is pre-erythrocytic schizogony and the merozoites

produced by it are also called cryptozoites or cyptomerozoites; these cryptozoites are
immune to medicines and the resistance of the host.
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A second phase of asexual multiplication known as an exo-erythrocytic schizogony

occurs in the liver cells in which the cryptozoites enter into new liver cells and grow
into schizonts, the schizont divides to form merozoites; the merozoites of the second
generation are termed metacryptozoites or phanerozoites.

The exo-erythrocytic schizogony may continue in more liver cells to form a reservoir
of merozoites, or some merozoites after at least two cycles of schizogony may re-enter
the blood stream when they invade erythrocytes.

It is supposed that the merozoites of second generation, i.e., metacryptozoites are of

two types; the more numerous and smaller are micro-metacryptozoites, while larger
and less in number are macro-metacryptozoites.

In fact, the micro-metacryptozoites invade the R.B.Cs and start erythrocytic

schizogony, while the macro-metacryptozoites enter fresh liver cells to continue the
exo-erythrocytic schizogony. The merozoites attack only the young and immature
corpuscles, (the merozoites of P. malariae attack only old corpuscles, while those of P.
falciparum attack all kinds of corpuscles indiscriminately).

Pre-patent and Incubation Periods:

The pre-patent period is the duration between the initial sporozoite infection and the
first appearance of parasite in the blood. In case of P. vivax, it is about 8 days on an
average. The incubation period is the time taken from the infection of man by
sporozoites till the appearance of first malarial symptom.

In case of P. vivax, it is about 14 days on an average ranging from 10 to 17 days. Of

course, during the incubation period the host shows no symptoms of malaria.

Schizogony in Erythrocytes:
In the erythrocytes, a third multiplication phase of schizogony occurs which is known
as erythrocytic schizogony. The micro-metacryptozoite feeds on erythrocytes, a
vacuole appears in it, the nucleus is pushed to one side, and the micro-metacryptozoite
is changed into what is called as the ring-shaped trophozoite, the signet ring stage,
which is 1/3 to 1/2 the size of the erythrocyte.

The signet ring stage is not found in P. falciparum. The trophozoite grows to become
rounded and amoeboid, this is the full grown trophozoite and is known as a schizont.
The large schizont makes the erythrocyte to become very large. The schizont shows
yellowish-brown pigment granules of haemozoin derived from the iron of haemoglobin
of erythrocyte; the enlarged erythrocyte acquires granules called Schuffner’s dots.

The schizont now undergoes multiple fission to form 12 to 24 oval-shaped merozoites;

this phase of asexual multiplication is erythrocytic schizogony. The much weakened
erythrocyte bursts and the merozoites are liberated into the plasma from where they
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enter new erythrocytes, then they repeat the erythrocytic schizogony once every 48
hours.

However, the merozoites may again go from the blood to the liver cells and invade
them to undergo another phase of asexual multiplication which is called post-
erythrocytic schizogony.

Formation of Gametocytes:
After many generations of schizogony in the blood, some of the merozoites slowly
grow large producing much haemozoin, these are inside erythrocytes and do not
change in schizonts but they grow and are transformed into two types of gametocytes
called macro gametocytes and microgametocytes.

The condition which brings about the formation of gametocytes is not known.
Gametocytes appear in the peripheral blood at various intervals after the onset of fever,
they remain inactive while in the human blood. The macro gametocytes are female,
they are round with the food laden cytoplasm and a small eccentric nucleus.

The microgametocytes are male, they have a clear cytoplasm and a large central
nucleus. Both gametocytes contain large amounts of haemozoin; they enlarge the
erythrocytes. Gametocytes remain in the human blood for several weeks, but are
unable to develop any further, it is necessary for them to be taken into the body of an
Anopheles’, if this does not happen they degenerate and die.
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(b) Part of Life-Cycle of P. Vivax in Mosquito (Sexual Cycle):

Many species of Anopheles, but not all species, act as intermediate hosts. If the
gametocytes are sucked up along with human blood by a female Anopheles then they
reach the stomach where corpuscles are dissolved and the gametocytes are set free.

Gametogony:
The microgametocytes, after release in the stomach of mosquito, undergo the process
of ex-flagellation. The cold-bloodedness of the mosquito is said to stimulate this
process. However, the nucleus of microgametocytes divides into 6-8 haploid daughter
nuclei.

These nuclei migrate towards the periphery of microgametocyte. The cytoplasm pushes
out forming long flagellum like structures having one daughter nuclei in each. Thus, 6-
8 flagellum like male gametes or microgametes measuring from 20-25 microns in
length are formed. Soon these gametes separate and start moving actively in the
stomach of mosquito.
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On the other hand, the macro gametocytes undergo maturation process, thereby two
polar bodies are pushed out and a female gamete or macrogamete is formed. The
female gamete is non-motile and develops a cytoplasmic or receptive cone.

Fertilisation:
If microgamete happens to reach the macrogamete, then it enters into the female
gamete at the point of cytoplasmic cone and finally complete fusion of nucleus and
cytoplasm of the two gametes occurs. This results in the formation of rounded zygote.

Several microgametes may approach a macrogamete but only one of them enters the
macrogamete and others shed off. The fusion of male and female gametes is called
syngamy. Here, the gametes are dissimilar (anisogametes), hence, their fusion is called
anisogamy.

Ookinete and Encystment:

The zygotes, thus, formed remain rounded and motionless for 24 hours but soon they
elongate to become worm-like having pointed ends and motile. The zygotes are now
called ookinetes or vermicules. An ookinete measures about 15 to 22 microns in length
and 3 microns in width.

The ookinete moves and bores through the wall of the stomach of mosquito and comes
to lie beneath the outer epithelial layer. (The ultrastructure of ookinete shows the
presence of a central, irregular nucleus, dense cytoplasm, brown pigment granules,
many mitochondria and ribosomes in it. It also shows the presence of contractile
fibrils, the microtubules).
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However, here they become spherical and secrete a thin elastic membranous cyst. The
cyst is also partly secreted by the surrounding tissues of the stomach. Thus, the
ookinetes become encysted and in this condition it is referred to as the oocyst. The
oocyst grows in size and sometimes called sporont.

As many as 50 such oocysts can be seen on the stomach of the host mosquito. Howard
(1906) has observed that the ookinetes which do not succeed in boring the stomach
wall pass out from mosquito’s body with faecal matter.

Sporogony:
The nucleus of oocyst first divides by meiosis and then by mitosis several times (Bano,
1959) and its cytoplasm develops vacuoles forming faintly-outlined cells called
sporoblasts. Particles of chromatin arrange themselves around the periphery of each
sporoblast. Then the cytoplasm forms slender spindle-shaped haploid cells known as
sporozoites.

Each oocyst may have ten thousand sporozoites, and group of sporozoites gets
arranged around the vacuoles. This phase of asexual multiplication in which
sporozoites are formed is called sporogony which is completed in 10-20 days from the
time the gametocytes are taken in by the mosquito, the time depending on the
temperature.

The oocyst bursts and sporozoites are liberated into the haemolymph of the mosquito,
from where they reach its salivary glands and enter the duct of the hypopharynx. The
sporozoites will infect a human host when the mosquito bites and the life cycle is
repeated again.
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Protozoans are unicellular eukaryotes with the absence of cell walls. These non-phototrophic entities are
a diverse collection of species with a shared basic set of attributes. These entities have various
intracellular organelles that carry out different functions. There are several protozoans known to cause
diseases in humans and animals. For instance, Malaria is caused by Plasmodium, Trichomonas, causes
diseases that are sexually transmitted.
1. Which of the following parasites is responsible for the cause of African sleeping sickness or
Gambiense fever?
(a) Leishmania
(b) Trypanosoma
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(c) Entamoeba
(d) Trichomonas
Answer: (b)
2. Tse-tse fly is a vector for sleeping sickness. Which of the following parasite transmits the
infective stage?
(a) Wuchereria bancrofti
(b) Leishmania donovani
(c) Plasmodium falciparum
(d) Trypanosoma gambiense
Answer: (d)
3. Schaffner’s dots are related to _______________.
(a) Entamoeba histolytica
(b) Leucocytes of frog
(c) RBC of man
(d) Epithelium of stomach of the mosquito
Answer: (c)
4. “Amoebiasis” or amoebic dysentery is caused by___________.
(a) Trypanosoma histolytica
(b) Entamoeba histolytica
(c) Entamoeba gingivalis
(d) Plasmodium vivax
Answer: (b)
5. Which of the following statement is true about the Malarial parasites? 
(a) Malarial parasites can be best obtained from a patient when the temperature comes to normal
(b) Malarial parasites can be best obtained from a patient, an hour before the rise of temperature
(c) Malarial parasites can be best obtained from a patient, a few hours after the temperature reaches
normal
(d) Malarial parasites can be best obtained from a patient when the temperature rises with rigour
Answer: (c)
6. Which of the following  “Glossina palpalis” is a vector for 
(a) Filariasis
(b) Plague
(c) Dengue
(d) Gambian fever
Answer: (d)
7. An important drug used for the treatment of malaria – Quinine is extracted from
(a) Red ants
(b) Calyx of cinnamon
(c) Brak of tulsi
(d) Brak of Cinchona
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Answer: (d)
8. Entamoeba gingivalis found in the buccal cavity of man causes
(a) No disease
(b) Pyorrhoea
(c) Bronchitis
(d) Amoebic dysentery
Answer: (a)
9. “Trypanosomiasis” is transmitted by or carrier of Trypanosoma in man is
(a) Fruit fly
(b) Tse-tse fly
(c) Housefly
(d) Mayfly
Answer: (b)
10. The malignant tertian malaria is caused by
(a) Plasmodium malariae
(b) Plasmodium ovale
(c) Plasmodium falciparum
(d) Plasmodium vivax
Answer: (c)
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Taenia solium; Pork tape wormK

 Taenia solium commonly known as the pork tapeworm or the armed tapeworm.
  It is a flat-ribbon like tape worms that causes intestinal taeniasis.
 Adult worms are rarely pathogenic but the encysted larval stage (cysticercus
cellulosae) of the worm caused a serious disease in human called Cysticercosis.

Habitat:

 The adult worm inhabits the small intestine (upper jejunum) of human.

Morphology:

Adult worm:

 Adult Taenia solium is a flattened ribbon like tapeworm that is white in color.

 The adult worm measures about 2-3 meters in length.
 The body of parasite can be divided into 3 parts:- Head (Scolex), neck and body
(strobila)

i. Scolex (Head):

 It measures 1 mm in diameter, about the size of a pin head.

 It is globular in shape and has 4 circular suckers.
 The head is provided with a rostellum armed with a double row of alternating
large and small hooklets (130-180mm long).
 The presence of hooklets gave its name armed tape worm.

ii. Neck:

 The neck is short measuring 5-10 mm in length.

iii. Body (Strobila):

 The body or Strobila consists of segments or proglottids.

 The total number of proglottids are about 800-900.
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 The proglottids may be immature, mature or gravid.

 The gravid segment measures 12 X 6 mm in diameter and looks grayish-black
and transparent when fully developed.
 The worm is hermaphrodite and each segment containing both male and female
reproductive organs.
 The common genital pore is marginal, thick-lipped and is situated near the
middle of each segment alternating between the right and left side.
 Testes consists of 150-200 follicles.
 An ovary is two in number which has a third (accessory lobe).
 The ovary is situated in the posterior side of the segment.
 The gravid consists of a median longitudinal stem of uterus having 7-13
branches on each side of the segment.
 Uterus is completely filled with eggs and each gravid consist nearly 30,000-
50,000 eggs. 
 The vaginal opening is not guarded by a muscular sphincter.
 The gravid segment are expelled passively, in chains of 5 to 6 at a time and not
singly.

2. Eggs:

 Eggs are similar to those of Taenia saginata.

 Each egg is round, brown in color, measures 40-50 µm in diameter
 Each egg consists of two shells.
 The outer shell is thin, transparent and represents the remnant of yolk mass.
 The inner shell, also known as embryophore is brown, thick walled and radially
striated. It encloses the embryo.
 The embryo measures 14-20 µm in diameter with hooklets.
 Eggs do not float in saturated solution of common salt (NaCl).
 Eggs are infective to pigs as well as to humans.

3. Cysticercus cellulosae larvae

 Larvae is cysticercus cellulosae and is the Infective form of parasite.

 It is also known as Taenia cyst.
 The larval form develops in the muscle of pigs as well as various organs of the
human.
 A mature cyst is an opalescent ellipsoidal body and measures 8-10 mm width by
15mm in length. It has a fluid filled milky white bladder like structure.
 The long axis of cyst lies parallel with the muscle fiber. The cyst is separated
from the host tissue by a thin collagenous capsule. There is a dense milk white
spot at the side, where the scolex with its hooks and suckers remain invaginated.
 The cavity of cyst is fill with a clear fluid rich in albumin and salts.
 21

 The larvae can live for about 8 months in muscles of pig and can only develop
into adults when ingested by man.

Life cycle of Taenia solium:

 The life cycle is completed in two hosts.

 Definitive host: Human
 Intermediate Hosts: Pig, occasionally human.

 Humans acquire infection by ingestion of inadequately or improperly cooked

pork infected with cysticerci.
 Inside the alimentary canal of man the scolex on coming incontact with bile
exvaginates and anchor to the gut wall with its hooks and suckers.
 The larvae develops into an adult worm by gradual strobilisation.
 The worm grows to sexual maturity in 2-3 months and start producing eggs
which are then passes in the faeces along with the gravid segments.
 The pig gets infection by ingestion of eggs or gravid proglottids passed in
human faeces.
 In the intestine of pig, the oncospheres hatch out of eggs.
 They attach to the intestinal mucosa by hooks, penetrate the gut-wall and gain
entrance into the portal vessels or mesenteric lymphatic, finally reaching the
systematic circulation.
 22

 Usually they travel via the portal vein and successively reach the liver, right side
of heart, lungs, left side of heart, brain or other tissue with high blood flow.
 The naked onchospheres are filtered out from the circulating blood into the
muscular tissue where they ultimately settle down and undergo further
development.
 They lose their hooklets, enlarge, and develops into a fluid-filled cyst within a
period of 9-10 weeks.
 They remain viable for up to 8 weeks in muscle of pig during which they remain
infective for human.
 The new host gets infection by ingestion of the infected meat of pig and the
cycle is repeated.
 Occasionally humans get infection by eating food or drinking water
contaminated with eggs.
 On ingestion, the onchospheres are released from the eggs in the intestine. These
larva invade the intestinal mucosa and are then carried by the circulation to
different tissue where they develops into cysts.
 In human most cysts are produced in the CNS, skeletal muscles, eye and
subcutaneous tissue giving rise to a condition called cysticercosis.

Mode of transmission:

 Ingestion of uncooked pork infected with tape worm

 Ingestion of food and water contaminated by the eggs present in the infective
faeces of a Taenia carrier.
 Endogenous auto infection: Anus-hand-mouth transfer of eggs by contaminated
hands of person with poor personal hygiene.
 Autoinfection: Reverse peristalsis in which eggs produced by T. solium are
thrown back to the duodenum, where they hatch and cause tissue infection

Pathogenesis of Taenia solium:

 Both adult worm and cyst are pathogenic.

The adult worms are less pathogenic. They occasionally cause mild irritation or
inflammation of the intestinal mucosa by their armed scolex.
 The cyst, (Cysticercus cellulosae) are more pathogenic. They cause a serious
disease cysticercosis in human, mostly cyst are produced in the skin, skeletal
muscles, eye and CNS.
 The cyst can remain viable for few years.
 In the brain the cyst survives by overcoming the host defenses. It secretes the
prostaglandins and other substances that inhibit activation of the complement and
production of cytokines. This result in minimal host inflammation around the live
cysticercus. The live cyst is surrounded by a local minimal cellular reaction that
consists of few eosinophiles and macrophages.
 The dead cyst is surrounded by a dense infiltration that consists entire spectrum
of inflammatory cells, including leucocytes and multinucleated giant
 23

macrophages, inflammatory cells and less frequently foreign body giant cells.
Outside this area a zone of fibrosis and chronic inflammatory infiltration are
present.

Clinical diseases caused by Taenia solium infection

1. Intestinal Taeniasis:

 Mostly the infection is asymptomatic.

 In symptomatic cases, the clinical symptoms are nonspecific and mild and
includes- nausea, abdominal discomfort, hunger pain, loss of weight, chronic
indigestion etc.
 Less frequently nausea, vomiting, headache and diarrhea are present in few
cases.

2. Cysticercosis:

 Cysticercosis is the infection with the larval stage of the parasite.

 Human beings acquire infection through faccal oral contamination with T.
solium eggs from tapeworm carriers or by auto infection.
 Clinical manifestation depend on the affected organ; neurocysticercosis and
ophthalmic cysticercosis are associated with substantial morbidity.

i. Extraneural  cysticercosis:

 Subcutaneous cysticercosis present as small, movable, painless modules that are

commonly noticed in the arms or chest.
 After a few months or even years, the modules become swollen, tender and
inflamed and then they gradually disappears.
 Muscular cysticercosis is a causal finding, appearing as dot shaped or ellipsoidal
calcifications.
 In rare cases, very massive parasite burdens enlarge the patient’s limbs
(muscular pseudohypertrophy).
 The heart is another occasional location, infected in about 5% of patient’s
cardiac cysticercosis is asymptomatic.

ii. Ophthalmic cysticercosis:

 This condition is present in 20% of cases.

 Most cysts are found in the vitreous, subretinal space and conjunctiva.
 The condition may present as iritis, ureitis and palpebral conjunctivitis.
 The cyst in subconjunctival or subretinal sites may present as slowly growing
nodules confusing with tumors.
 Occasionally, subretinal eye cyst may lead to blindness due to detachment of
retina.
 24

iii. Neurocysticercosis:

 The parasite commonly infects the CNS, causing neurocysticercosis as a clinical

disorder.
 After entering the CNS, cysticerci are visible and elicit few inflammatory
changes in the surrounding tissue.
 Cysticerci cause symptoms because of mass effect or by blocking the circulation
of cerebrospinal fluid, most symptoms are the direct result of the inflammatory
process that accompanies cyst degeneration.
 Symptoms and signs are varied and nonspecific.
 Epileptic seizures are the commonest presentation and generally represent the
primary or sole manifestation of the disease.
 Seizures occur in 50-80% of cases with parenchymal brain cysts or
calcifications.
 The disease also present with intracranial hypertension, hydrocephalus or both in
20-30% of cases.
 The syndrome is related to the location of parasites in the cerebral ventricles or
basal cisterns blocking circulation of CSF and is caused by several different
mechanisms- the presence of the parasite itself, ependymal inflammation or
residual fibrosis.
 Occasionally a cyst grows larger than the usual and acts in the same way as a
tumor mass (giant cyst).
 These giant cysts compress adjacent cerebral structures, causing localized
deficits and intracranial hypertension. Motor deficits can also arise because of
oedema secondary to cyst degeneration or as a result of stroke complicating the
infection.
 In children and teenagers, an acute encephalitic presentation can happen, more
likely in female than male. Massive non encephalitic forms also occur.
 Compromise of the spine occurs in adult 1% cases, presenting with compressive
manifestation.

Laboratory Diagnosis of Taenia solium:

Specimen:

 Faeces, muscle tissue, blood, csf

1. Macroscopic examination:

 A naked examination of the specimen can be made for segment or proglottids.

 The whitish segment can easily be recognized against the dark yellow mass of
the faeces.

2. Stool Microscopy:
 25

 Demonstration of eggs and less frequently proglottids and scolex in faeces is

used as tool for diagnosis.
 Eggs:  
 Eggs are demonstrated by a thick faecal smear examination.
 The eggs shed irregularly, so 2-3 stool sample should be collected.
 Eggs can be seen in perianal area and can be detected by cellophane swab.
 Since eggs of T. soluim and T. saginata are similar, species diagnosis can be
made by Acid-fast staining. Eggs of T. soluim are non-acid fast whereas T.
saginata is acid fast.
 Proglottids:
 The gravid proglottids are found in faeces or recovered from the under clothings.
 They are washed in clean water and placed between two sides.
 The sides are held by adhesive tape at each end and are examined by hand less
for lateral branches.
 Demonstration can be facilitated by staining them with india ink, injected
through the genital pores.
 Observation:
 Taenia soluim: 7-12 lateral branches on each side of utetine stem
 T. saginata: 10-20 lateral branches on each side of utenine stem.
 Scolex:
 T. soluim – bears a row of hooks
 T. saginata- lacks hooks.
 The scolex is not always recovered following the treatment and the method is
hazardous.

3. Antigen detection:

 This is a very useful for screening the cases of intestinal taeniasis.

 Antigens capture ELISA polyclonal antisera raised against Taenia is employed
to detect antigen in faeces.

4. Serodiagnosis:

 Serological tests are employed to detect anti-cysticercus antibodies in serum or

CSF.
 ELISA (sensitivity 75%, specificity 85%). Antigen can be detected by ELISA
using specific monoclonal antibodies.
 Enzyme-linked immunoelectro transfer blot (EIIB). Sensitivity 90 % specificity
50-70%.
 Detection of antigens in serum or CSF indicates recent or viable infection.

5. Histopathological diagnosis

 Diagnosis of Neurocycticercosis (NCC) is made by demonstrating cysticerci in

the biopsy tissue obtained from brain during post mortem.
 26

 Skeletal cysticercosis can be diagnosed by histological  examination of biopsy.

6. Imaging method:

 X-ray of the soft tissue in arm and thigh, chest and neck may show dead,
calcified or elongated cysts.  
 X-ray of the skull may reveal cerebral calcification and intracranial lesions in the
neurocysticercosis.
 CT scan is best method for detecting dead, calcified and multiple cysts is
pathognomonic of neurocysticercosis.
 MRI shows a mural nodule within the cyst which is pathognomonic for NCC.

7. Other test:

 CSF protein level are elevated in neurocycticercosis.

 CSF may show lymphocytosis- Mononuclear pleocytosis is frequent
 Glucose levels may be mildly to moderate low.
 Cell counts rarely exceed 300/mm3
 Eosinophils in the CSF are common but nonspecific  binding

Treatment of tape worm infection:

i. Praziquantel– drug of choice.

 Dose- oral.
 50 mg/kg body weight
 3 divided doses for 15 days.

ii. Niclosamide:

iii. Albendazole:

 A dose of 400 mg twice daily for 30 days.

iv. Surgery:

 For cysticercosis of ocular, ventricular and spinal cord.

Prevention and control of taeniasis:

 Avoidance of eating raw or insufficiently cooked pork

 Inspection of pork for cysticerci.
 Proper sanitation facilities.
 Treatment of infected persons.
 Avoidance of food contaminated with eggs of T. solium

Epidemiology and geographical distribution

 27

 Taenia solium is found worldwide.

 It is most common in pork-eating countries, usually in low socio-economic and
poor sanitation.
 50 million people are infected worldwide.
 T. solium infections are endemic in central and South America, non- Islamic
countries of South East Asia, South Africa especially among the Bantu
communities.
 Eastern Europe and China areas of highest prevalence include Latin America
and Africa.

Question 1 : An important character of Platyhelminthes is

A) Monoecious

B) Vitelline glands

C) Flat animals

D) Flame cells

Answer : D
Question 2 : Flat worms are
A) Diploblastic

B) Triploblastic

C) Monoblastic

D) None of the above

Answer : B
Question 3 : Coelom in flat worms is
A) Well developed

B) Poorly developed

C) Schizocoel

D) Absent

Answer : D
Question 4 : Animals with self fertilization is
A) Paragonimus
B) Dugesia
C) Taenia solium
D) None of the above

Answer : C
Question 5 : Which is a free living fresh water flat worm?
 28

A) Planaria
B) Schistosoma
C) Fasciola
D) Taenia
Answer : A
Question 6 : Vital system absent in Tapeworm is
A) Nervous system

B) Digestive system

C) Excretory system

D) Reproductive system

Answer : B
Question 7 : In which animal, pharynx can be everted?
A) Dugesia
B) Fascicola
C) Taenia
D) Ascaris
Answer : A
Question 8 : Respiration in Dugesia is
A) Aerobic

B) Anaerobic

C) Both

D) None of the above

Answer : A
Question 9 : In platyhelminthes
A) Nerve cords are present

B) Nerve cords are absent

C) Nerve nets are present

D) Nerve nets are absent

Answer : A
Question 10 : Segments of Tapeworm are called
A) Scolex

B) Cysticercus

C) Proglottides

D) Onchospheres

Answer : C
 29

Question 11 : The tissue in platyhelminthes between viscera and body wall is called
A) Coelom

B) Parenchyma

C) Mesoderm

D) Chaoanoderm

Answer : B
Question 12 : Tapeworm respires
A) Through suckers

B) Through mouth

C) Through lateral pores or sterigmata

D) Anaerobically

Answer : D
Question 13 : Animals belonging to platyhelminthes are also called flat worms because
A) Their head is flat

B) They have dorsoventrally compressed body

C) They creep over the surface

D) The alimentary canal is flattened

Answer : B
Question 14 : Scolex occurs in
A) Hydra
B) Ascaris
C) Taenia
D) Liver Fluke

Answer : C
Question 15 : Incomplete alimentary canal occurs in
A) Fasciola
B)  Ascaris
C) Wuchereria
D) Rhabditis
Answer : A
Question 16 : Which is free swimming stage in the life history of Fasciola ?
A) Miracidium

B) Sporocyst

C) Redia
 30

D) None of the above

Answer : A
Question 17 : Proglottides of Tapeworm proliferate from
A) Scolex

B) Other proglottides

C) Neck

D) Special region in neck

Answer : C
Question 18 : Parasitic adaptation of flatworm is
A) Anaerobic respiration

B) Secretion of antienzymes

C) Resistant covering, cuticle integument

D) All the above

Answer : D
Question 19 : The disease caused by Fasciola is
A) Liver rot

B) Cysticercosis

C) Taeniasis

D) None of the above

Answer : A
Question 20 : Taenia saginata differs from Taenia solium as it lacks
A) Rostellum

B) Suckers

C) Scolex

D) None of the above

Answer : A
Question 21 : Apolysis is
A) Removal of mature proglottides

B) Removal of immature proglottides

C) Removal of gravid segments

D) None of the above

 31

Answer : C
Question 22 : Regeneration is best shown by flat worm
A) Fasciola
B) Planaria/Dugesia
C) Schistosoma
D) Echinococcus
Answer : B
Question 23 : Which one is blood fluke?
A) Schistosoma
B) Echinococcus
C) Fasciola
D) Taenia
Answer : A
Question 24 : Dog Tapeworm is
A) Schistosoma haematobium
B) Opisthorchis sinensis
C) Taenia nana
D) Echinococcus granulosus
Answer : D
Question 25 : The secondary host of Taenia saginata is
A) Cow

B) Sheep

C) Pig

D) Both A and B

Answer : D
Question 26 : The secondary host of Taenia solium is
A) Buffalo

B) Sheep

C) Pig

D) Goat

Answer : C
Question 27 : In Schistosoma
A) Male is longer than female

B) Male is broader than female

C) Male has gynaecophoric canal for holding female

D) Both B and C
Answer : D
Question 28 : The number of proglottides in Taenia solium is about
A) 500
 32

B) 900

C) 300

D) 200

Answer : B
Question 29 : Four suckers present on the scolex of Tapeworm are meant for
A) Attachment

B) Sucking food

C) Crushing food

D) All the above

Answer : A
Question 30 : A cestode with only 3 segments is
A) Taenia solium
B)  Diphyllobothrium latum 
C) Echinococcus
D) Hymenolepis nana
Answer : C
Question 31 : Fasciola hepatica is a
A) Endoparasite

B) Free living

C) Ectoparasite

D) Both B and C
Answer : A
Question 32 : Cysticcercus stage of Taenia solium is found in
A) Man

B) Pig

C) Goat

D) Sheep

Answer : B
Question 33 : Liver Fluke belongs to class
A) Trematoda

B) Turbellaria

C) Cestoda

D) Nematoda
 33

Answer : A
Question 34 : The body of a Tapeworm  consists of
A) Scolex and neck

B) Scolex and proglottides

C) Scolex, neck and proglottides

D) Neck and strobila

Answer : C
Question 35 : Fasciola hepatica occurs in
A) Bile duct of sheep

B) Liver of sheep

C) Liver of man

D) Human bile ducts

Answer : A
Question 36 : Tape worm is
A) Anoxybiotic

B) Oxybiotic

C) Aerobic

D) None of the above

Answer : A
Question 37 : Each segment of Taenia is
A) Monoecious

B) Dioecious

C) Asexual

D) None of the above

Answer : A
Question 38 : Hydatid worm is
A) Schistosoma indicum
B) Ancylostoma duodenale
C) Enterobius vermicularis
D) Echinococcus granulosus
Answer : D
Question 39 : The infective stage of Fasciola hepatica is
A) Sporocyst
 34

B) Redia

C) Cercaria

D)  Metacercaria

Answer : D
Question 40 : Which one of the flatworms has eyes?
A) Fasciola
B) Dugesia
C) Schistosoma
D) Echinococcus
Answer : B
Question 41 : Hexacanth is activated by
A) Bile salts

B) Pancreatic juice

C) Intestinal juice

D) None

Answer : A
Question 42 : Hexacanth reaches
A) Voluntary muscles

B) Involuntary muscles

C) Cardiac muscles

D) None of the above

Answer : A
Question 43 : The disease caused by Taenia is
A) Cysticercosis

B) Liver rot

C) Ascariasis

D) None

Answer : A
Question 44 : Fasciola attaches itself to walls of the bile ducts by means of
A) Anterior sucker

B) Adhesive zone

C) Posterior sucker/acetabulum

D) Spiny cuticle and posterior sucker

 35

Answer : D
Question 45 : Human infection of Taenia solium occurs by taking pork having
A) Cysticerci

B) Onchospheres

C) Hexacanths

D) Adult worm

Answer : A
Question 46 : Pig gets infection of Taenia solium through food contaminated with
A) Onchospheres

B) Cysticerci

C) Hexacanths

D) Adult worm

Answer : A
Question 47 : Scolex of Taenia  solium contains
A) Rostellum

B) Hooks

C) Suckers

D) All the above

Answer : D
Question 48 : Taenia solium attaches itself to the intestinal wall by means of scolex through its
A) Suckers

B) Suckers and hooks

C) Hooks

D) Adhesive glands

Answer : B
Question 49 : Fluke occurring in human beings is
A) Fasciolospsis
B) Fasciola
C)  Dugesin
D) Echinococcus
Answer : A
Question 50 : In case of human beings, hydatid cysts occur over
A) Stomach
 36

B) Liver

C) Lungs

D) Both B and C
Answer : D
 37

Ascaris lumbricoides:
Morphology, life cycle, Pathogenesis, lab diagnosis and Treatment

Ascaris lumbricoides: 

Morphology, life cycle, Pathogenesis, lab diagnosis and Treatment

Ascaris lumbricoides is an intestinal round worm. It is the largest intestinal nematode

to infect Human. The adult worm lives in small intestine and grow to a length of more
than 30 cm. Human is only the natural host and reservoir of infection.

The round worm infection occurs worldwide. The number of infected persons is
estimated to be more than 2 billion. The main epidemic region with prevalence rate of
approx. 10-90% includes countries on South east Asia, Africa and latin America.

Morphology:

Adult:

The round worm resembles to earthworm. It is elongated tapering to both end, anterior
being thinner than posterior. Freshly excreted worm is yellowish pink in color, which
gradually changes to white.

The worm is sexually diamorphic.

 38

 Adult male: 15-30 cm in length, 3-4 mm in diameter, tail curved

 Adult female; 20-40 cm length, 2-6mm diameter, tail straight

Egg:

Ascaris egg is round or oval, 60*40 µm size, thick brown shell and have rough surface.
It is the infective form of parasite.

 i) Un fertilized egg; large, more elongated (38-55*78-105) µm

 ii) fertilized egg; ovoid (35-50*50-70)µm, golden brown color

Life cycle:

The life cycle of Ascaris completes in single host. Human.

 Adult worm lives in small intestine

 Stages in life cycle:

Stage I: Eggs in faeces

 Sexually mature female produces as many as 200,000 eggs per day, which are
shed along with faeces in unembryonated form. They are non infective.

Stage II: Development in soil

 Embryonation occurs in soil as optimum temperature of 20-25C with sufficient

moisture and O2
 39

 Infective larva develops within egg in about 3-6 weeks.

Stage III: Human infection and liberation of larvae

 Human get infection with ingestion of embryonated egg contaminated food and
water
 Within embryonated state inside egg, first stage larvae develops into second
stage larvae. This second stage larvae is known as Rhabtitiform larvae
 Second stage larve is stimulated to hatch out by the presence of alkaline pH in
small intestine and solubilization of its outer layer by bile.

Stage IV: migration of larvae through lungs

 Hatched out larvae penetrates the intestinal wall and carried to liver through
portal circulation
 It then travels via blood to heart and to lungs by pulmonary circulation within 4-
7 days of infection.
 The larvae in lungs molds twice, enlarge and breaks into alveoli.

Stage V: Re-entry to stomach and small intestine

 From alveoli, the Larvae then pass up through bronchi and into trachea and then
swallowed.
 The larvae passes down the oesophagus to the stomach and reached into small
intestine once again.
 Small intestine is the normal habitat of Ascaris and it colonises here.
 Within intestine parasite molds twice and mature into adult worm.
 Sexual maturation occurs with 6-10 weeks and the mature female discharges its
eggs in intestinal lumen and excreted along with faeces, continuing the life cycle.
 The life span of parasite is 12-18 months

Pathogenesis:

1. Mode of transmission:

 faeco-oral route, by contaminated vegetables or water.

2. Pathogenesis:

Infection of A. lumbricoides in man is known as Ascariasis. There are two phase in
ascariasis.

Phase I: migrating larvae

 40

 The migrating larvae causes pathological lesions. The severity of lesions

depends upon the sensitivity of host, nutritional status of host and number of
migrating larvae.
 During migration and molding through lungs, larvae may causes pneumonia
with low grade fever, cough and other allergic symptoms.

Phase II: Adult worm

 Few worm in intestine produce no major symptoms and but some time give
abdominal pain especially in children.
 The adult worm produce trauma in host tissue and the wandering adults may
block the appendical lumen or common bile duct and even small intestine.
 Large number of adult worms affects the nutritional status of host by robbing the
nutrition leading to malnutrition and growth retardation in children.
 The metabolites of living or dead worm are toxic and immunogenic.
 lumbricoides also produces various allergic toxin, which manifests fever,
conjunctivitis and irritation.

Clinical manifestation:

Most of the Ascaris infection is asymptomatic.

1. Symptomatic ascariasis; two types

2. Intestinal Ascariasis
3. Pulmonary Ascariasis

1. Intestinal ascariasis;

 Nausea
 Vomiting
 Colicky abdominal pain
 Abdominal distention
 Weight loss and diarrhea
 Malbasorption of nutrition
 Growth retardation
 Heavy worm in children leads to intussusception and total obstruction
 Complications: Appendicitis, Biliary colic and perforation of bile duct,
Hepatomegaly

2. Pulmonary ascariasis;

 Transient eosinophilic pneumonitis (loeffler’s disease); elevated IgE

 Bronchospasm
 Dyspnea and wheezing
 Fever
 41

 Non-productive cough and chest pain

Lab diagnosis:

1. Specimen: stool, sputum
2. Microscopy: examination of stool by saline emulsion or concentration by
floatation methods employed to unembryonated egg
3. X-ray
4. Serodiagnosis: Indirect haemagglutination test, Immuno-fluorescence assay
5. Ultrasonography and CT scan
6. Other test: blood count  shown peripheral eosinophilia

Treatment and prophylaxis:

 Mebendazole: drug of choice, (100mg twice a day for 3 days)

 Albendazole: 500mg single dose
 Pyrantel pamoate: single dose of 1omg/kg weight
 Piperazine citrate

1. The common name for Ascaris lumbricoides is:

A. Roundworm
B. Hookworm
C. Whipworm
D. Threadworm

2. Ascaris lumbricoides infection are more likely occur in:

A. Tropical climates
B. Pork eating countries
C. Developing countries
D. Western countries

3. What is the infective form of Ascaris lumbricoides?

A. Unembryonated ova
B. Embryonated eggs
C. Larvae
D. All of the above

4. What is the common specimen source required to detect Ascaris lumbricoides?

 42

A. Sputum
B. Faeces
C. Food sample
D. Both a and b are correct

5. Main feature that distinguishes fertilized egg from unfertilized eggs of Ascaris
lumbricoides?
A. Size
B. Colour
C. Shape
D. All of the above

6. Female Ascaris worm releases approximately 200 000 - 2 000 000 eggs per day.
A. True
B. False

7. What sorts of drugs are used in treatment against ascariasis?

A. Albendazole
B. Mebendazole
C. Erythromycin
D. Anthelmintics
E. All a,b and c are correct

8. Ascaris spp are commonly contracted by host via:

A. Faecal-oral route
B. Respiratory route
C. None of the above
 43

Wuchereria Brancofti:
Morphology, Life Cycle and Pathogenicity | Zoology
Habit and Habitat of Wuchereria Bancrofti:
Wuchereria bancrofti is a filaroid nematode, causing a very tragic, horrifying and
debilitating disease known as filariasis. This disease has been known from antiquity
and was the first discovery of insect (culex mosquito) transmission of a human disease.

In general, infection with any of the filarial nematode may be called as filariasis but
traditionally, the term filariasis refers to lymphatic filariasis caused by Wuchereria or
Brugia species. Filaroids are tissue dwelling parasites in all classes of vertebrates
except fish.

The genus Wuchereria was named after Wucherer, a Brazilian physician who reported
the presence of larvae in chylous urine in 1866. The adult female was described by
Bancroft in 1876. Wuchereria bancrofti is distributed widely in tropics and subtropics
of Asia (India, Bangladesh, Myanmar, China), Africa and South America.

Morphology of Wuchereria Bancrofti:

A. Adult:
The adult worms are whitish, translucent, threadlike worms with smooth cuticle and
tapering ends. The head is slightly swollen and bears two circles of well-defined
papillae (Fig. 6.10). The mouth is small and lack buccal capsule. The female worm is
larger (80-100 mm long and 0.24-0.3 mm wide) than the male (40 mm long and 0.1
mm wide) (Fig. 6.10).

The vulva is near the level of the middle of the oesophagus. Males and females remain
coiled together usually in the abdominal and inguinal lymphatics and in the testicular
tissue of human. The adult worms live for many years, probably 10-15 years or more.

B. Juvenile:
 44

Female Wuchereria are ovoviviparous. The juveniles or embryos are released encased
in its elongated egg shell, which persists as a sheath. These embryos are referred to as
microfilariae. The sheath is delicate and close fitting but can be detected where it
projects at the anterior and posterior ends of the microfilaria.

The embryos have colourless, translucent body with a blunt head and pointed tail,
measuring about 250-300 µm in length 6-10 µm in thickness. It is actively motile and
can move forward and backward, within the sheath.

When stained with leishman or other Romanowsky stains, structural details can be
made out. Along the central axis of microfilaria, a column of granules can be seen,
which are called somatic cells or nuclei. At the head end is a clear space devoid of
granules, called the cephalic space. In microfilaria bancrofti, this space is as long as it
is broad.

In the anterior half of the microfilaria is an oblique area devoid of granules, called the
nerve ring. Approximately midway along the length of body is the anterior V-spot
which represents the rudimentary excretory system. The posterior V-spot (tail spot)
represents the cloaca or anal pore. The genital cells (G-cells) are situated anterior to the
anal pore, hi M. bancrofti, the tail tip is devoid of nuclei (Fig. 6.11).

The microfilariae circulate in the blood stream. In most Asian country including India,
they show a nocturnal periodicity in peripheral circulation of human. It is seen in large
numbers in peripheral blood only at night, between 10 pm and 4 am. This correlates
with the night biting habit of the vector (culex mosquitoes).

Periodicity may also be related to the sleeping habits of the hosts. It has been reported
that if the sleeping habits of the hosts are reversed, over a period, the microfilariae
change their periodicity from night to day. They are believed to spend the day time
mainly in capillaries of the lung and kidney or in the heart and great vessels.
 45

Life Cycle of of Wuchereria Bancrofti:

Wuchereria Bancrofti requires two hosts for completion of its life cycle. Man is the
only definitive host and no animal host or reservoir is known for W. bancrofti. The
intermediate host is the female mosquito of the genus Culex. The major vector in India
and most other parts of Asia is Culex fatigans.

A. In Mosquito:
When a vector mosquito feeds on a carrier the microfilariae are taken in with the blood
meal and reach the stomach of the mosquito. Within 2 to 6 hours, they cast off their
sheath (ex-sheathing), penetrate the stomach wall and within 4 to 17 hours migrate to
the thoracic muscles where they undergo further development.

During the next 2 days, they metamorphose into the first-stage larva which is a
sausage-shaped form with a spiky tail, measuring 125-250 × 10-15 µm. Within a week,
it moults once or twice, increases in size and becomes the second-stage larva,
measuring 225-325 × 15-30 µm.

In another week, it develops internal structures and becomes the elongated third-stage
filariform larva (J3), measuring 1,500-2,000 x 15-25 µm. It is actively motile and
infective. It enters the proboscis sheath of the mosquito, awaiting opportunity for
infecting human, the definitive host (Fig. 6.12).
 46

There is no multiplication of the microfilaria in the mosquito and one microfilaria

develops into one infective larva only. The time taken from the entry of the
microfilaria into the mosquito till the development of the infective third-stage larva
located in its proboscis sheath, constitute the extrinsic incubation period.

Its duration varies with environmental factors such as temperature and humidity as
well as with the vector species. Under optimal conditions, its duration is 10 to 20 days.

B. In Human:
When a mosquito with infective larvae in its proboscis feeds on a person, the larvae get
deposited, usually in pairs, on the skin near the puncture site. The larvae then enter
through the puncture wound or penetrate the skin by themselves.

The infective dose for man is not exactly known, but many larvae fail to penetrate the
skin and many more are destroyed in the host tissues by immunological and other
defence mechanisms. However, it is found that a very large number of infected
 47

mosquito bites are required to ensure transmission to man – perhaps as many as 15,000
infective bites per person.

After penetrating the skin, the third-stage larvae enter the lymphatic vessels and are
carried usually to abdominal or inguinal lymph nodes, where they develop into adult
forms. There is no multiplication at this stage, and only one adult develops from one
larva, male or female.

They became sexually mature in about 6 months and mate (Fig. 6.12). The gravid
female worm releases large number of microfilariae, as many as 50,000 per day. They
pass through the thoracic duct and pulmonary capillaries to the peripheral circulation.

In the peripheral blood, the microfilariae do not undergo any further development. It
they are not taken up by a female vector mosquito they die. Their life-span is believed
to be about 2 to 3 months. It is estimated that a microfilaria density of at least 15 per
drop of blood is necessary for infecting mosquitoes. Densities of 20,000 microfilariae
or more per ml. of blood may be seen in some carriers.

Pathogenicity of Wuchereria Bancrofti:

Mode of Transmission:
Filariasis is usually transmitted to man through mosquito biting. The disease can be
accidentally transmitted through blood transfusion, when the donor is infected with
microfilariae.

Incubation Time:
The period from the entry of the infective third-stage larvae into the human host, till
the first appearance of microfilariae in circulation is called the biological incubation
period or the pre-patent period. This is usually about 8 to 12 months.

The period from the entry of the infective larvae, till the development of the earliest
clinical manifestation is called the clinical incubation period. This is very variable, but
is usually 8 to 16 months, though it may often be much longer.

Pathogenesis:
The effects of infection with Wuchereria bancrofti display a wide spectrum from
clinically silent infections, with no apparent inflammation or parasite damage, to mild-
to-intense non-granulomatous chronic lymphatic inflammation, to a variety of
granulomatous obstructive reactions.

Asymptomatic Phase:
Individuals with asymptomatic infections usually have high microfilaremias (a
condition of having microfilariae in the blood). It appears that in such people the TH1
type of immune response is down regulated and TH2 type is stimulated. The cytokine
IL-4, which suppresses activation of TH1 cells, is elevated and IFN-Ƴ is depressed.
 48

Eventually, after a long period (several years), this tolerance or hypo-responsiveness

often breaks down and inflammatory reactions rise.

Thus, two phases of lymphatic filariasis viz:

(1) Hypo-responsiveness, and

(2) Chronic lymphatic disease are initiated by the parasite and immune factors.

A significant proportion of individuals in endemic areas show neither symptoms nor

microfilaremia; these are the “endemic normals”. That many such people are actually
infected with adult worms can be demonstrated by detection of worm antigen in their
blood, although the mechanism of the amicrofilaremia remains unexplained in such
cases.

Inflammatory (Acute) Phase:

Inflammatory responses are due to antigens from adult worms, particularly females but
not caused by microfilariae. It is now clear that much inflammation is due to invasion
by bacteria from the skin surface.

Adult worms in the lymph channels cause dilation of the channels and interfere
with lymph flow, resulting in various symptoms which may be described as
follows:
(i) Lymphangitis:
Here acutely inflammed lymph vessels may be seen as red streaks underneath the skin.
Lymphatics of testis and spermatic cord are frequently involved.

(ii) Lymphadenitis:
This is the repeated episodes of acute inflammation of lymph nodes associated with
fever and chills, tenderness along superficial lymphatics. Inguinal nodes are most often
affected and axillary nodes less commonly.

(iii) Lymphedema:
This follows successive attacks of lymphangitis, and usually starts swelling around the
ankle, spreading to the back of the foot and leg. It may also affect the arms, breast,
scrotum, vulva or any other part of the body. Initially the edema is pitting in nature but
in course of time becomes hard and non-pitting.

(iv) Lymphorrhagia:
Rupture of lymph vessels leading to release of lymph or chyle.

(v) Filarial fever:

High fever of sudden onset often with rigor, lasting for two to three days that occurs
repeatedly at intervals of weeks or months. This fever is accompanied by lymphangitis
and lymphadenitis.
 49

Additional common symptoms in the acute stage of filariasis include orchitis

(inflammation of the testes, usually with sudden enlargement and considerable pain),
hydrocele (forcing of lymph into the tunica vaginalis of the testis or spermatic cord),
and epididymitis (inflammation of the spermatic cord).

In such cases, extensive proliferation of living cells with much inflammatory cell
infiltration occurs. The most prominent cells include lymphocytes, plasma cells and
eosinophils. Abscesses around dead worms may develop with accompanying bacterial
infection.

Obstructive Phase:
The obstructive phase is marked by lymph varies, lymph scrotum, hydrocele, chyluria
and elephantiasis. Lymph varies are “varicose” lymph ducts, caused when lymph
return is obstructed and the lymph “piles up”, greatly dilating the affected duct. This
causes chyuria or lymph in urine, a common symptom of lymphatic filariasis.

A feature of the chronic obstructive phase is progressive infiltration of the affected

areas with fibrous connective tissue or ‘scar’ formation after inflammatory episodes.
However, dead worms are some-times calcified instead of absorbed, usually causing
little further difficulty.

In many cases, repeated attack of acute lymphatic inflammation leads to a condition

known as elephantiasis (Ancient Greek and Roman writers compared and described the
thickened and fissured skin of infected persons to that of the elephant, though it is a
nonsense word, literally meaning “a disease caused by elephant.

But the word is so deeply entrenched, however, that it is not likely ever to be
abandoned). This is a chronic lymphedema with much fibrous infiltration and
thickening of the skin. In men the organs most commonly afflicted are the scrotum,
legs and arms (Fig. 6.13), in women the legs and arms are usually afflicted, with the
vulva and breasts being affected more rarely.
 50

The skin becomes thickened due to accumulation of fibrous connective tissues,

granulomatous tissue and fat. The skin surface becomes coarse, with warty
excrescences; cracles and fissures develop, with secondary bacterial infection.
Microfilariae usually are not present in such thickened organs.

Elephantiasis is thus a result of complex immune responses of long duration. After the
worms die and are absorbed, the symptoms gradually disappear. Repeated super-
infections over many years are usually required for elephantiasis to occur.

Prevention and Control of Disease Caused by of Wuchereria Bancrofti:

The two measures in prevention and control of filariasis are:
(i) Eradication of the vector mosquito, and

(ii) Detection and treatment of carriers.

In endemic areas, insect repellents, mosquito netting and other preventive measures
against the vector mosquito (see mosquito control measures) should be adopted. In
such areas, peoples (suspected to be carriers) should undergo regular diagnosis for
filariasis.

The drug of choice for the past 40 years has been diethylcarbamazine (DEC, Hetrazan)
which eliminates microfilariae from the blood and careful administration usually kills
the adult. The standard treatment has been 6 mg/ kg doses given over a period (7 to 12
days) to a cumulative total of 72 mg/kg, though this dose has some side effects.
 51

In recent years, it was discovered that a good control could be achieved with a single
dose of 6 mg/kg given annually or semiannually; side-effects are fewer and logistics
are much easier.

Edematous limbs are sometimes successfully treated by applying pressure bandages,

which force the lymph out of the swollen area. Any connective tissue proliferation that
might have developed however will not be affected. Surgical removal of elephantoid
tissue is often possible.

Wuchereria bancrofti: Morphology, life cycle and Epidemiology

 Wuchereria bancrofti or Bancroft filarial worm is a parasitic filarial nematode
spread by a mosquito vector.
 It is one of the three parasites that causes lymphatic filariasis (commonly known
as elephantiasis), an infection of the lymphatic system by filarial worms.
 The parasite as named after physician Otto Wucherer and parasitologist Joseph
Bancroft both of whom extensively studied the filarial infections.

Habitat

 Adult worms are found in the lymphatic vessel, especially the lymph nodes.
 The microfilariae are found in the peripheral blood, occasionally they are also
found in chylous urine or in hydrocele fluid.

Morphology of W. bancrofti

1. Adult worms

 W. bancrofti exhibits considerable sexual dimorphism.

 These are minute, long hair like transparent (often creamy in color) nematodes.
 They are filiform in shape with both ends tapering.
 The head end terminating in a slightly round swelling, and surrounded by two
rows of 10 sessile papillae. The posterior end contains anus at its terminal end.
 The male measures 2.5-4 cm in length with 0.1 mm in thickness. The tail end is
curved ventrally and contains two spicules of unequal length.
 The females are longer than males measure 8-10 cm in length with 0.2-0.3 mm
in thickness. Its tail end is narrow and abruptly pointed. The females are
oviparous.
 The adults obtain their nourishment from the lymph of the lymphatic system.
 The life span of the adult worms is long, probably several years (5-10 year or
even more).

2. Microfilariae (Embryos):

 The first stage of larva is called microfilariae.

 52

 They are very active in their habits and can move both with and against the
blood stream, when sustained, they appear as colorless and transparent bodies
with blunt heads and pointed tails.
 The embryo measures about 290 mm in length by 6-7 mm in breadth.
 When dead and stained with Romanowsky’s stains, they show the following
morphological features:
 Hyaline sheath:
 It is a sac like envelope which is much longer (359 mm) than the larval
body represents the chorionic envelop of the eggs.
 It remains as investing membrane around the larva.
 Cuticle:
 It is lined by subcuticular cells and is seen only with vital stains.
 Somatic cells or nuclei:
 Nucleiappear as granules in the central axis of the body and extend from
the head to the tail end, except the terminal 5% of the tip of the tail. This is
the distinguishing feature of the parasite.
 The space at the anterior end devoid of granules is seen called as cephalic
space.
 The granules are broken at definite places serving as the landmarks for
identification of the species.
 They include:
(a) Nerve ring; an oblique space
(b) anterior V-spot represents the rudimentary excretory system
(c) the posterior V spot or tail spot represents the terminal part of the
alimentary canal/anus or cloaca.

3. Third stage of larva (infective form):

 The L3 larva the infective form of the parasite is found only in mosquito.
 They are elongated, filariform, measures 1.4-2 cm in length and 18-23 cm in
breadth.

Life cycle:

 W. bancrofti completes its life cycle in two hosts:

 Definite host: Human
 Intermediate host: mosquito, belonging to genus Culex, Aedes and
Anopheles.
 Life cycle in Human: Entrance in the human and development into adult
worms
 Infection is acquired by the bite of infected mosquito during which L3
larva are deposited on the skin.
 The L3 larva are not directly injected into the blood stream.
 The L3 larva are deposited on the skin near the site of the puncture.
 53

 Later attracted by the warmth of the skin, the larva enters through the
puncture wound or penetrates through the skin on their own.
 The L3 larva after penetrating the skin, reaches the lymphatic channels,
settles down at some spot (inguinal, scrotal or abdominal lymphatics),
metamorphose and becomes sexually mature.
 The male fertilizes the female and the gravid females discharge
microfilariae which usually appear in the peripheral blood in 8-12 month of
infection.
 These micro filariae circulate in the blood for 6 months to 2 years and
then die if not taken by mosquito.
 Life cycle in Mosquito: Stages in the development of micro filaria
 Microfilaria ingested by the mosquito lose their sheath within 2 to 6 hours
of their arrival in the stomach.
 Then they penetrate the gut wall and migrate to the thoracic muscle,
where they rest and begin to grow.
 In the next 2 days, microfilaria become thick, short sausage shaped with a
short spiky tail, measuring 124-200 mm in length 10-17 mm in breadth. This
is the first stage larva L1.
 The larvae possesses a rudimentary digestive tract.
 During 3-7 days of time, the larva grows rapidly, moults once or twice
and measures 225-330 mm in length by 15-30 mm in breadth. This is
the second stage larva L2.
 Metamorphosis completes by 10-11days with distinct features such as the
tail atrophies to a mere stump and the digestive system, body cavity and
genital organs are now fully developed. This is the third stage larva L3.
 These L3 larva are the infective form which enters the proboscis sheath of
the mosquito on or about the 14th day.
 When the mosquito bites a man during the blood meal, the L3 larva are
released from the tip of proboscis of mosquito and the cycle is repeated.
 Development in mosquito takes place within 10-20 days.

Epidemiology of Wuchereria bancrofti

 W. bancrofti is largely confined to tropics and subtropics. They are found in

India, West-Indies, Puerto Rico, Southern China, Japan, Pacific Island, West and
central Africa, South America.
 The disease is endemic in 83 countries with more than 1.2 billion at risk.
 It is estimated that more than 120 million people are infected.
 More than 25 million men suffer from genital symptoms and more than 15
million people suffer from lymphedema or elephantiasis of leg.

Periodicity:

 The microfilariae of oriental countries (India and China) show nocturnal

periodicity.
 54

 They are found periodically in peripheral blood at night especially between

10pm to 4 am.

Helminths or parasitic worms are huge macroparasites. When in adult forms, they are visible to the bare
eyes. Most of these are intestinal worms, transmitted from the soil affecting the gastrointestinal tract.
Some other parasitic worms harbouring the blood vessels are schistosomes. These worms are known to
live and feed in the living host, obtaining nutritional requirements and shields while they in turn disrupt the
ability of the host to absorb nutrients.
1. Dracunculiasis is caused by the ___________ worm and transmitted by the __________ vector
(a) Dracunculus medinensis; freshwater crustacean
(b) Dracunculus medinensis; mollusc
(c) Mycobacterium ulcerans; freshwater crustacean
(d) Mycobacterium ulcerans; mollusc
Answer: (a)
2. Parasite that is also a vector host is
(a) Ascaris
(b) Bug
(c) Fasciola
(d) House fly
Answer: (b)
3. Filarial larva can be collected from man’s
(a) Peripheral blood at midnight
(b) smears of spleen
(c) smears of intestinal contents
(d) biopsy of liver
Answer: (a)
4. This disease is caused by a nematod
(a) Amoebiasis
(b) Leprosy
(c) Filariasis
(d) Poliomyelitis
Answer: (c)
5. This does not accurately describe Lymphatic filariasis
(a) intermediate vector is the mollusc
(b) mainly affects the lower limb
(c) Chyluria is the most common manifestation
(d) is caused by the parasitic worms Wuchereria bancrofti and Brugia malayi
Answer: (a)
6. All of these are symptoms of Dracunculiasis infection except
(a) Septic arthritis
(b) Abscess
 55

(c) Facial redness

(d) Tetanus
Answer: (c)
7. Chenopodium oil is used in
(a) Smallpox
(b) Typhoid
(c) Ascariasis
(d) Tuberculosis
Answer: (c)
8. This insect transmits relapsing fever
(a) Cimex
(b) Apis
(c) Drosophila
(d) Gryllus
Answer: (a)
9. Enterobiasis diseases is caused by
(a) Hookworm
(b) Filarial worm
(c) Roundworm
(d) Pinworm
Answer: (d)
10. Which is a helminth disease
(a) Polio
(b) Filariasis
(c) Filaria
(d) Diphtheria
Answer: (b)
 56

BIOLOGY OF CHORDATES AND NON CHORDATES

Classification of Animal Kingdom
The science of classifying organisms is called taxonomy. Every species discovered so far are classified
into five kingdoms – one among them is Kingdom Animalia or Animal kingdom. The members of kingdom
Animalia are further classified into different Phyla, Class, Order, Family, and Genus based on certain
identifiable characteristic features.

One of the most fundamental forms of classification of animals is the presence or absence of the
notochord. Hence, two major groups exist, namely: Chordates and Non-chordates.

Non-chordates and the Chordates

The notochord is a flexible rod made out of a material similar to cartilage. If an animal has a notochord
during any stage of its life, it is classified as a chordate. Contrary to popular belief, chordates do not
exclusively include vertebrates.
There are invertebrates that possess a notochord during some point in their lives and hence, are
classified as chordates. Thus all vertebrates are chordates but not all chordates are vertebrates.

Non-chordates
Non-chordates are animals without a notochord – the rod-like elastic structure that supports the body.
This phylum consists of a small group of worm-like, marine species with an organ-system level of
organization.
Members of phylum Porifera, Coelenterata, Ctenophora, Platyhelminthes, Aschelminthes, Annelida,
Arthropoda, Mollusca, Echinodermata and Hemichordata fall under Non-chordates.
The general characteristic features of Non-Chordates are:

 They are cylindrical, triploblastic, coelomate, or pseudocoelomate animals.

 Respiration in these animals takes place through gills, trachea or body surface.
 57

 Most of the times, sexes cannot be distinguished among the members.

 Modes of reproduction involve sexual and asexual
 Fertilization is external, though internal fertilization also occurs in some species.
 The body of non-chordates generally includes an open type of circulatory system.

Chordates
Chordates are animals characterized by the presence of notochord at some stage during their
development. Members possess a hollow nerve cord and pharyngeal gill slits. The other general
characteristic features of Chordates are as follows:

 They are bilaterally symmetrical, triploblastic, and coelomate with the organ-system level of
organization.
 They hold a post-anal tail
 The body includes a closed circulatory system.
 In some members of Phylum Chordata, the notochord is present only in the larval tail, and in
some, it is present throughout their life from head to tail region.
 Chordates have many sub-divisions and Protochordates are one of the earliest to evolve.
Phylum Chordata is divided into three subphyla: Urochordata, Cephalochordata, and Vertebrata.

Subphylum – Urochordata
It is also referred to as Tunicata which are marine animals. The body of these animals is surrounded by a
leathery covering (similar to a tunic, hence the name). Larvae are free-swimming, the notochord is
present only in the tail of larvae and after settling on the seabed, they get transformed into sessile adults.
They are generally hermaphrodites.
Examples include – Ascidians, Doliolum, Oikopleura, etc.

Subphylum – Cephalochordata
It mainly consists of small, fish-like marine animals in which the notochord is extended along the entire
body. The animals also have pharynx, which is large with numerous gill- slits. Members of this subphylum
have separate sexes.
Example include – Amphioxus or lancelet.

Subphylum – Vertebrata
In this subphylum, the notochord is present in the embryonic stages and is replaced by a vertebral
column in the adult. They have 2, 3 or 4 chambered heart, paired appendages for locomotion and kidneys
for excretion or osmoregulation.

Vertebrates Classification
The subphylum Vertebrata is divided into five classes of vertebrates. These five classes
of vertebrates comprise of all the species of animals and have developed vertebral column as well as an
internal skeleton.
There are over 66,000 species of vertebrates identified under phylum Chordata till date. The defining
feature of vertebrates is that their bodies are bilaterally symmetrical, coelomic, triploblastic, and with
complex differentiation of body tissues and organs.
Other characteristic features of vertebrates are:

 Presence of a true vertebral column and internal skeleton with muscle attachment points for body
movement.
 A front-side muscular heart with two, three or four chambers.
 Kidneys for excretion and osmoregulation
 A paired appendages which may be fins or limbs.
 Possess notochord during the embryonic stage.
 58

 Vertebrates are the only chordates to possess a brain as a part of the central nervous system.

Classification of Vertebrates
 Pisces
 Amphibia
 Reptilia
 Aves
 Mammalia

Class Pisces (Fishes)

They are aquatic animals, having a streamlined body and a pair of fins which are used for propulsion and
movement. Furthermore, fish are cold-blooded, but the discovery of a new species in 2015 has changed
this perception. The opah or the moon-fish is a fully warm-blooded fish capable of regulating its body
temperature.
Endoskeleton may be cartilaginous or bony and respiration occurs through gills. They do not possess
eyelids because the surface of the eye is to be kept moist all the time.
Examples of Class Pisces includes dogfish and Rohu.
Read More: Pisces

Class Amphibia
They usually comprise those organisms which are cold-blooded and require an aquatic habitat to lay
eggs. These organisms are mainly characterized by the two pairs of limbs, smooth and moist skin for
respiration. They also possess protruding eyes which are protected by usually more than one pair of
eyelids. (Frogs have 3).
Examples of Class Amphibia are frog, toad, and salamander.
Further Reading: Amphibia

Class Reptilia
Class Reptilia comprises those organisms which are ectothermic in nature (cold-blooded). They are
characterized by osteoderms which form scales, bony plates or scutes on the skin.  Reptiles also lack an
external ear and some reptiles such as snakes are actually “deaf” and instead, pick up vibrations through
the ground.  Another amazing sense that only snakes possess is Thermoception. This means that snakes
can see infrared radiation emitted by objects or prey.
Examples of Class Reptilia are Tortoise, Wall lizard, Snake, etc.
Extended Reading: Class Reptilia

Class Aves (Birds)

Most members have a streamlined body specially designed to offer low air resistance during flight. In
such birds, the forelimbs are modified into wings, with the power coming from breast muscles. Feathers
play important roles, from flight, thermal insulation to water-proofing.  All members of this class are warm-
blooded and are able to regulate their body temperature.
Aves have beaks, which are used for various functions such as preening and feeding. Furthermore, birds
are considered to be the living relatives of dinosaurs (evolved from a group of meat-eating dinosaurs
called the theropods).
Examples of Class Aves are Parrot, Pigeon, Duck, etc.
Read More: Aves

Class Mammalia
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These organisms are distinguished by the presence of mammary glands. They have two pairs of limb for
walking, grasping, swimming, flying, etc. Digits are provided with claws, nails or hooves. Skin is covered
by hair and they have an external ear called pinnae. They are warm-blooded animals.