Structure life-cycle pathogenesis and control measure of Eimeria tenella.

E.tenella is the most pathogenic of the coccidian parasites which infect domestic chickens, and related genera belong to subclass coccidia of protozoan subphylum Sporozoa.They are generally intercellular parasites of the epithelial lining of host's alimentary canal. e.tenella is a monogenetic i, the -life cycle involves only in one host.( fowl) The life cycle can be conveniently be described under two phases, asexual cycle or schizogony and sexual cycle or gametogony or sporogony. Most of the life cycle is intercellular.They cause a several disease condition known as coccidiosis in their hosts.

Summary

E.tenella is the most pathogenic of the coccidian parasites which infect domestic chickens, and related genera belong to subclass coccidia of protozoan subphylum Sporozoa.They are generally intercellular parasites of the epithelial lining of host's alimentary canal. e.tenella is a monogenetic i, the -life cycle involves only in one host.( fowl) The life cycle can be conveniently be described under two phases, asexual cycle or schizogony and sexual cycle or gametogony or sporogony. Most of the life cycle is intercellular.They cause a several disease condition known as coccidiosis in their hosts.

Things to Remember

  • Habit, habitat, and morphology of E.tenella.
  • A life cycle of E. tenella related to Asexual and Sexual cycle.
  • Pathogenesis , symptom treatment, and prevention of E. tenella.
  • E. tenella cause a several disease condition known as coccidiosis.

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Subjective Questions

Q1:

Define goiter?


Type: Very_short Difficulty: Easy

Show/Hide Answer
Answer: <p>Goiter is an enlargement of the thyroid gland resulting feom high production of TSH. &nbsp;Goiter may be associated with diminished, normal or increased thyroid function.</p>

Q2:

List down its causes, clinical features and its treatment and prevention?


Type: Short Difficulty: Easy

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Answer: <p><strong>Causes</strong></p>
<p>_ deficiency of iodine in food and water.</p>
<p>_ disease of pituitary gkand and thyroid gland.</p>
<p>&nbsp;</p>
<p><strong>Clinical features</strong></p>
<p>_ delay growth and development of children.</p>
<p>_ sign and symptoms of hypothyroidism eg.weight gain, cold intolerance, dry flaky skin and hair.</p>
<p>_ enlargement of thyroid gland.</p>
<p>_ myxoedema which is most marked in skin of hands, fet and eyelids.</p>
<p>&nbsp;</p>
<p><strong>Treatment</strong></p>
<p>_ Hypothyroidism should be treated with thyroxin hormone.</p>
<p>_ If it is iodine deficiency goiter, supplement of potassium iodidr60mg3 times per day is its treatment.</p>
<p>&nbsp;</p>
<p><strong>Prevention</strong></p>
<p>_ Supply iodized salt in iodine -poor areas.</p>
<p>_ Eat food rich in iodine ,such as sea food,fish, sea, fish,cod liver oil,meat , vegetables etc.</p>
<p>_ nutritional education.</p>

Q3:

What is calcium and write about its deficiency, sign and sympyoms, treatment and prevention?


Type: Long Difficulty: Easy

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Answer: <p><strong>Calcium deficiency</strong></p>
<p>Calcium is a major mineral elements of body. Its constitute 1.5% of the body weight of an adult human. An average adult body contains about 1200 gm of calcium of which over 98% is found in the bones. The amount of calcium in blood is usually about 10mg/dl.</p>
<p>&nbsp;</p>
<p><strong>Function</strong></p>
<p>Ionized calcium in the plasma has many Vital function including;</p>
<p>_ contraction of muscles</p>
<p>_ cardiac action</p>
<p>_ milk production</p>
<p>_ relay of electrical and chemical message that arrive at a cell's surface membrane to the biochemical machinery within the cell.</p>
<p>&nbsp;</p>
<p><strong>Deficiency</strong></p>
<p>No clear cut disease due to calcium deficiency has ever been observed, even under conditions of low intake. It has been established that if the intake of vitamin D is adequate, the problems of rickets do not arise even with low calcium intake. There problems may arise due to calcium deficiency.</p>
<p><strong>Sign and symptoms</strong></p>
<p>_ Tetany characterized by muscle cramps, numbness, tingling in limbs.</p>
<p>_ Osteoporosis</p>
<p>_ Joint pain</p>
<p>_ Heart palpitations</p>
<p>_ Impaired growth</p>
<p>&nbsp;</p>
<p><strong>Treatment</strong></p>
<p>_ 400-500 mg of calcium per day for one month.</p>
<p>&nbsp;</p>
<p><strong>Prevention</strong></p>
<p>_ Nutritional education</p>
<p>_ Eat food rich in calcium such as milk and milk product, eggs ,fish and fruits etc.</p>
<p>_ The physiological requirements are higher in children, expectant and nursing mothers, so calcium supplement to the pregnancy since second trimister to till lactating pwriod as well as for children too.</p>

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Structure life-cycle pathogenesis and  control measure of Eimeria tenella.

Structure life-cycle pathogenesis and control measure of Eimeria tenella.

Habit and Habitat Morphology:

Eimeria tenella is the most pathogenic of the coccidian parasites which infect domestic chickens and has a worldwide distribution. It is a major cause of disease and may be associated with a high rate of mortality, particularly among young chickens. The life cycle of coccidia parasites involves asexual and sexual development in the gut with location depending on the specific species The result of the sexual development is the production of resistant cysts (oocysts) that are secreted with the faeces. In the external environment, the oocysts undergo development (sporulation) to form infectious oocysts, which have a characteristic appearance.

In this case ofEimeria spp, the oocysts contain four sporocysts, each containing to sporozoites (the infectious stage). These oocysts transmit the infection to new susceptible hosts when ingested. This is summarised below. The oocysts is a unique structure in its ability to survive in the external environment for extended periods, making control of infections very difficult. The oocysts are protected by a wall that is resistant to chemical and physical insult. In fact in the laboratory oocyst are stored in 2% sulphuric acid. This wall renders them resistant to routine disinfectants and sterilisation of houses is impossible without gases such as methyl bromide or ammonia. Oocysts are sensitive to heat and desiccation.

Lifecycle of Eimeria tenella:

E. tenella is monogenetic, i,e its life cycle is involve in one host(fowl). Various stage of the complicated life cycle may conveniently be described under two phases, asexual cycle or schizogony and sexual cycle involving gametogony and sporogony. Much of the life cycle is intracellular.

[I] Asexual cycle (schizogony)

There are 2 or sometimes 3) generations of schizonts and merozoites which are morphologically distinguishable.

1. First generation schizogony.

The beginnings of the complex life cycle of E. tenella may be taken to be initiated by the infection of epithelial cells of host caecum by sporozoites.

(a) Infection by sporozoites.

The infected foul passes out oocysts or zygocysts with faecal matter. When these oocysts are swallowed by a new or healthy bird, its digestive juices dissolve the cyst wall and release the sporozoites which enter the gut epithelial cells. Within the epithelial cells, the sporozoites grow in size and multiply by schizogony.

(b) Sporozoite.

It is the earliest intracellular stage of the parasite. It ie elongated, slightly curved, a microscopic unicellular organism with one pointed and another end blunt. The pellicle, forming an external envelope, contains longitudinally arranged contractile microtubules which help in wriggling movements of the organism. Cytoplasm includes a vesicular nucleus, a mitochondrion, Gligibodies, endoplasmic reticulum, ribosomes, lysosomes and vacuoles containing reserve food.

(c) Trophozoite.

The sporozoite soon increases in size and becomes pear-shaped. This stage of the parasite is called trophozoite. The characterised feature of trophozoite is the presence of an eosinophil globule at the blunt end. This globule strains brightly with eosin and black with haematoxylin.

Trophozoite absorbs nourishment through its general surface from the surrounding cytoplasm of the host cell. It grows considerably so that the host cell and its nucleus hypertrophy but are not destroyed.

(d) Schizont.

Eventually, the trophozoite undergoes multiple fission by schizogony . Repeated mitotic nuclear divisions are followed by the formation of cytoplasmic masses. This results in a multinucleated first generation schizont.It is somewhat oval in shape ith vacuolated cytoplasm and numerous small peripherally arranged nuclei.

(e) Merozoites.

Within the schizont, the peripherally arranged nuclei with cytoplasmic masses become perform bodies called merozoites. As many as 900 merozoites may be produced by a single first generation schizont. Each merozoite is very small and inconspicuous body, which is measuring about 2-4 microns in length and 1-1.5 microns in width.Its one end is pointed and contains a terminal granule while the other end is rounded which contain a number of cytoplasmic granules.The host cells containing schizonts are hypertrophied and are finally extruded into the lumen of the caecum. The schizonts burst and the first generation merozoites escape to invade other epithelial cells.

2. Second generation schizogony.

The liberated merozoites set up new infections and schizogony may be repeated several times causing serious damage to the epithelial cell.

(a) Invasion of fresh host cells.

A first generation merozoite invades a fresh epithelial cell and comes to lie within its cytoplasmic soon grow into a trophozoite.

(b) Trophozoite.

The trophozoite resembles its counterpart of the first generation, except that, lacks an eosinophil globule.It feeds upon the host cytoplasm and its nucleus undergoes repeated mitotic divisions forming multinucleated schizont.

(c) Schizont.

The second-generation schizont differs very much from the first generation schizont. It is larger in size and nucleus are scattered throughout its cytoplasm and nucleus consists of distinct nucleolus or karyosome.

(d) Merozoites.

Within the schizont,the cytoplasmic divisions results in the aggregation of cytoplasmic bits around each nucleus and these nucleated cytoplasms metamorphose into second generation merozoites.

The second generation merozoite is also elongated and pyriform with a rounded and a blunt end. They are larger than the first generation merozoites, measuring about 16 microns in length and 2 microns in breadth. Their number in a single schizont is about 250 which is less than in the first generation. When the infected host cells become hypertrophied, the schizonts burst and merozoites escape.

Fig-1. E.tenella. Life-cycle.
Fig-1. E.tenella. Life-cycle.

[II] Sexual cycle (Gametogony and sporogony).

A few second generation merozoites may produce third generation schizonts. These are not common, small and each produces 3 to 30 merozoites. However, most of the second-generation merozoites do not repeat schizogony. They initiate the sexual cycle and develop into gametocytes which produce gametes.

1. Gametogony.

The gametogony are sexually distinguished into two types:

(a) Male or microgametocytes.

After invading the host epithelial cells, some of the merozoites become male gametes or microgametocyte which is small, oval, and measure about 5.5 to 18 microns in length. It shows repeated nuclear divisions and gives rise to numerous small, comma-shaped biflagellated male or microgametes. Each of them bears a nucleus, mitochondria, and 2 flagella.

(b) Female or macrogametocyte.

The female is oval but comparatively larger,measuring 8-25 microns in length.Each macrogametocyte develops into a single female cell or macrogamete.

2. Fertilization.

Detail of the fertilisation is not known.A microgamete fused with a macrogamete and thus fertilisation takes place inside the host cell which resulting fertilised cell or zygote.

3. Oocyst.

The zygote, in the host cell, secretes a thick double-layered cyst wall around itself. It has a thick outer and a delicate inner layer. According to Monne and Honig (1954), the outer layer is quinone-tanned protein, while the inner layer is a lipoprotein layer. The zygote is now referred as an oocyst. It is oval in shape and measures 20-26 microns by 16.5-23 microns.

It does not undergo further development in the host cell. The completed oocysts fall in the cavity of the intestine by the rupture of the host cells. From here they are expelled outside the bird's body in faeces. The passing out of oocysts in enormous number may be seen on the 7 to 8 day of infection. It can survive for a longer time under aerobic conditions.

4. Sporogony.

Within 24 hours the zygote within oocyst divided by meiosis into4 haploid cells called sporoblast or zoitoblasts. Each sporoblast then secrets a tough wall, the sporocyst or zoitocyst around and become a spore. Each spore divides mitotically to produce to sporozoites or zones. Thus, a mature oocyst includes 8 sporozoites, two within each sporocyst. E.tenalla is thus tetraspores and di zoic. Division of the encysted zygote into sporozoites generally takes place outside the host after the oocysts pass out with faecal matter. Under suitable temperature and moisture conditions, each oocyst sporulates in about 21 hours and become infective.

5. Transference of oocysts.

The infective oocysts are easily passed on onto other members of the flock through direct ingestion of droppings (faecal matter) or contaminated food.

6. Liberation of sporozoites.

Into the gut lumen of the new host, the sporozoites liberate out through a pore or micropyle in the oocyst, under the influence of mechanical pressure and set up new infections.

Pathogenesis.

E.tenella causes a fatal diseases chickens called caecal coccidiosis. It is caused due to extensive destruction of the caecal epithelium, with sloughing off the all and severe haemorrhage. The symptoms include bloody droppings, pale feces, and shanks, bloody vent and enlargement of caeca or with yellowish grey cheese-like ceres. In advanced stages, the infected bird shows restlessness, dropping wings, ruffled feathers, and unsteady gait.

Prevention and Treatment.

Infection of young chicken can be prevented through proper hygienic conditions and with range management. Floors of poultry houses, yards and ranges must be cleared periodically by scrubbing them through the hot lye solution.

Coccidiostatic drugs, which mostly include sulpha drugs, are added in prescribed doses in the poultry feed and water for a few days, mostly at the time when infants are being reared, or when coccidiosis is apprehended. These drugs help the birds to develop immunity from the coccidial organism.

The chicken who have caught coccidiosis are treated with sulpha drugs . Sulphamezathene and sulphaquinoxaline, taken at the rate of 0.5% with drinking water for about a week, promise complete relief. because of its low toxicity, sulphaquinoxaline is generally recommended.

Reference:

Jordan E.L. and P. S., Verma. Invertebrate Zoology, New Delhi,: S. Chand and Company Pvt. Ltd., 2011.

Kotpal, R. L.,Modern Text Book of Zoology: Invertebrates, New Delhi, India: Rastogi Publications,2011.

http://parasite.org.au/para-site/text/eimeria-text.html

http://www.worldpoultry.net/PageFiles/29382/001_boerderij-download-WP6572D01.pdf

https://en.wikipedia.org/wiki/Eimeria_tenella

Lesson

Protozoa

Subject

Zoology

Grade

Bachelor of Science

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