Life History
The life history of Ascaris is monogenetic as it involves only one host, i.e., man,
However, the life history of Ascaris can be studied as under :
1. Copulation and fertilisation. Copulation takes place in host's intestine. During Copulation male ascaris moves in such a way that its cloacal aperture faces the vulva of the female and then male thrusts its penial setae to open the vulva of female and they come to lie in the seminal receptacle part of the uteri, wait for eggs to come through the oviduct for fertilisation During fertilisation the entire sperm enters the egg. Soon,after fertilisation the glycogen globules of the egg migrate to the surface to from the fertilisation membrane which soon hardens into a thick, clear inner chitinous shell. Soon, thereafter, the fat globules of the egg from a lipoid layer below the chitinous shell. Now, as the fertilised egg passes down, the uterine wall secretes an outer thick, yellow or brown aluminous (proteinous) coat or outer shell having a characteristic wavy surface or ripplings. These eggs are now known as mammiliated eggs; such eggs are elliptical in shape measuring 60-70 by 40-50.
2. Zygote. So, to say the zygote has a thick, clear inner shell, lipoidal layer and an outer shell which is warty and yellow or brown in colour. The fertilized eggs(zygotes)
Are laid by female Ascaris in the small intestine of the host and they pass out with the
Facece; they are unsegmented when they leave the host. One female may lay from
15,000 to 200,000 eggs. The eggs production of Ascaris is astounding, one mature female may have up to 27 million eggs. The eggs become stained yellowish or brown in the intestine. Eggs fall on the ground and can remain alive for months in the moist soil though complete drying kills them. In order to develop they require oxygen, moisture and a temperature lower than that of the human body, the most favourable temperature is 85F.
They require a period of incubation outside the humane body.
3. Early development(Outside the host). The stages of early embryonic development, say the cleavage or segmentation, etc., start in the soil. The pattern of cleavage is spiral determinate.
The fertilised err undergoes two cleavages to form four cells or blastomeres; in fact the first cleavage results in a dorsal cell AB and a ventral cell P1,The second cleavage causes AB to divide into an anterior cell A and a posterior cell. B, while the ventral cell P1 divides into a dorsal cell EMST and a ventral cell P2. These four cells are at first arranged it the shape of a T in Ascaris, but later they become appaenged in a rhombid shape, as P2 comes to lie posterior to EMTS, which is characteristic of menatodes. However, these four cells are now called A,B,P2 and S2 or EMST. These cells undergo further cleavage to from smaller blastomeres.
However in the next cleavage A and B divide into A1,A1 and B1,B2 cells respectively,P2 divide into P3 and C, while EMST into MST and E.Thereafter,P3 and E dived into P4 and D and E1 and E2 respectively. The P4 further divides into G1 and G2. The fate of the various cells resulted so far is fixed, i. e., the descendants of A and B will,
Pseudocoel cell, and the lining of the stomodaeum, the descendants of E (E1 and E2) give
Rise to the entire endoderm of the intestine, the descendants of P4 (G1 and G2) will
Give rise the germ cells and C and D will together take part in the formation of ectoderm
And mesoderm
Thus, the cleavage of embryonic cells continues giving rise to a blastula at the 16-celled stage which is characterized by having a cavity, the blastocoel. Then gastrula is formed by epiboly or overgrowth of ectodermal cells over the endodermal cells. And by
5. Later development in new host.(Outside the host). They do not develop in the intestine but go on typical wandering tour of 10 days. They bore through the intestine wall and enter the mesenteric circulation and pass through the hepatic portal vein to enter the liver, from where they enter the hepatic vein and through the postcaval vein come to the right side in the heart, from where they are carried several times through the body along with the blood stream, then they go
through pulmonary arteries into the lungs. In the lungs, juveniles rupture the capillaries and enter the
alveoli where they live for some days, here they grow and moult to become 3rd stage larvae which moult again
to become 4th stage larvae. From the alveoli of the lungs, the 4th stage juveniles make their way through the bronchioles and
and bronchus into the trachea and then to the throat from where they are swallowed into the esophagus and reach the
Small intestine for the second time. During this 10-day tour, the juveniles have grown abount ten times and are 2 to
3 mm long. In the intestine the fourth and final moulting takes place, and in 60 to 75 days, they grow into adolt males and females and attin sexual
maturity. The length of the parasite in the host averages only 9 months to a yaer.
However, the life history of Ascaris lumbricoides can be represented as:Adults-->fertilised eggs pass out-->larvae develop in egg shell and moult
twice--> swallowed by man --> intestine where juveniles hatch--> bore through intestine--> mesenteric veins--> hepatic portal vein--> liver--> hepatic vein--> postcaval vein
--> right side of heart--> pulmonary artery--> lungs--> alveoli where third moulting occurs--> bronchioles--> bronchus--> trachea--> glottis--> oesophagus--> intestine where foruth
moulting occurs--> grow into adults.
PATHOGENICITY OR PARASITIC EFFECTS
As many as 500 to 5,000 adult Ascaris may de present ina single host and they may cause abodominal discomforts
and colic pains accompanied with diarrhoea, vominting, and a slight temperature. They may block the intestine and appendix. Because of their habit of wandering in the
gut, they may enter the bile or pancreatic ducts and interfere with digestion, or they may
injure the intestine and cause peritonitis. At times they wander into the nose. They produce toxins which
irritate the mucous membrane of the gut, or prevent digestion of proteins by the host by destroying trypsin, or they may cause general nervousness, delirium or convulsions, In children
where infection is more common they dull the mental capacity and stunt growth. Their juveniles
cause inflammation and haemorrhage in the lungs which results in pneumonia which may prove fatal. The disease caused
by Ascaris is generally referred to as ascariasis.
TREATMENT
A mixture of oil chenopodium and tetrachloroethylene is good; but one gm of hexylresorcinol in a gelatine capsule with fasting for 12 hours before treatment ant 4 hours afterwards,
followed by a purgative removes about 95% of Ascaris infection. Other anti-helminth
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