Friday, March 12, 2010

Parasitic Protozoan Imp topic for Various Life Science Examination 2010

Parasitic Protozoans
[A] Entamoeba dysenteriae (=histolytica)

1. Lambl discovered Entamoeba in 1859. Losch discovered its pathogenic nature in 1875.
2. It is Monogenetic Endoparasite of the large intestine (colon) of man and other mammals.

Pathogenesis:
The adult Trophozite or Magna form secretes histolytic enzymes which dissolve and damage the intestinal wall producing ulcers in it. Blood and mucus comes out of the ulcers and passes out along with the faeces of the patient. This disease is known as amoebic dysentery or Amoebiasis.
Life Cycle:
1. Inside the ulcers, the adult tropozoite divides repeatedly by reproducing by Binary Fission to produce 2 types of individuals: Magna forms (large sized) and Minuta forms or Pre-cystic forms (small-sized).
2. Magna forms remain inside the ulcers and keep on reproducing by binary fission but minuta forms come out of the ulcer and undergo following changes:
(a) Withdraw pseudopodium and become rounded.
(b) Store reserve food in the form of chromotoid bodies.
(c) A cyst is secreted i.e. Entamoeba becomes encysted (Encystment).
(d) Nucleus divides twice by mitosis to form 4 nuclei.
3. These Quadrinucleate cysts pass out along-with the faeces. These are infective stages for new a host.
4. Cysts are spread by houseflies, ants cockroaches etc. which carry them on their appendages or in their intestine and transfer them to the foodstuffs.
5. Man gets the infection by swallowing food and water contaminated by quadrinucleate cysts (Quadrinucelate cysts remain viable for 8-10 days. They die due to desiccation/or at a temperature of 50oC).
6. In man's small intestine the cystwall is digested by Trypsin and the Tetranucleate Metacystic amoeba hatches out (Excystment).
7. Metacystic Amoeba divides by binary fission to produce Eight uninucleate daughters/amoebulae which pass into the large intestine and grow into adult trophozoites.
Therapy:
1. Common drugs are injections of Emetine; Tablets of antibiotics e.g. Fumagilin, Terramycin, Erythromycin and Aureomycin are quite effective. For the complete eradication of infectin when dysentery has been controlled, certain Arsenic compounds (Carbarsone, Milibis) and iodine compounds (Chiniofon, Diodiquin, Vioform) are given in small doses.
2. In Chronic infection of Entamoeba, the trophozoites escape into the general blood circulation of the body causing secondary infection in Liver, Lung, Brain etc. producing abscesses in these organs. For these Extra-Intestinal infections Chloroquine is given.
3. Most significant advancement in the treatment of Amoebiasis has been the use of Metronidazole which has been found to be quite effective in case of both intestinal and extra intestinal infection. Some of the popular Anti-amoebic drugs are Entobex, Diogyl, Amibactin, Dependal, Enteroquinol, Flagyl, Metrogyl, Tridazole etc.


[B] Entamoeba gingivalis

Found in the roots of teeth, gums, pus-pockets of Tonsils of Man & other mammals. Cytoplasm clearly divided into Ectoplasm & Endoplasm; Pseudopodia 2 to 3; Feeds upon Bacteria found in the debris and White Blood Corpuscles; Transmission is direct through saliva & kissing; No cyst formation occurs. It aggravates the already present Pyorrhoea.

[C] Entamoeba coli

Found in the lumen of the human colon; Cytoplasm not clearly divided into Ectoplasm & Endoplasm; Pseudopodium-one; Feeds upon Bacteria and debris; Man is neither benefited nor harmed by its presence (COMMEMSAL); Transmission through Eight Nucleate Cysts; No further nuclear division occurs in the Cyst.

TRYPANOSOMA
(A Flagellate Protozoan)

A saprozoic blood parasite of man & domestic animals causing "Trypanosomiasis". It slowly glides or swims in the plasma by vibratile movements of its Flagellum and undulating membrane. Feeding occurs by diffusion through pellicle and by pinocytosis. Trypanosomes reproduce only asexually by Longitudinal Binary Fisson in both the vertebrate and invertebrate hosts. The reserve food of Trypanosoma consists of Volutin Granules (Glycogen/Protein/Nucleic Acid). Trypanosoma is a Polymorphic Protozoan having Trypanosome (Trypanomastigote); Crithidial (Epimastigote); Leptomonad (Promastigote); and Leishmania (Amastigote) forms in its life-cycle. Crithidial forms are found in the salivary glands of Tse-tse fly.

1. T. gambiense- West & Central Africa2. T. rhodesiense- East Aftrica The primary host is man (Homo) Intermediate or Vector hostTse-Tse fly (Glossina palpalis)Tse-Tse fly (Glossina morsitans)

Sleeping Sickness:
When Tse-Tse fly bites a man for its blood-meal it pours a drop of saliva containing anticoagulant. Alongwith the saliva Tryanosomes are inoculated into the blood of man. For about three months, trypanosomes live in the Blood-plasma and Lymph glands causing fever (Gambian – Fever) & anaemia. The sleeping sickness is caused when parasites invade cerebro-spinal fluid and brain-cells resulting in extensive damage to the C.N.S. The patient wants to sleep constantly, finally passing into a state of COMA. If untreated, it ends in death. Tryparsamide and Antryside are used in the treatment of sleeping sickness.
3. Trypanosoma cruzi = causes CHAGAS' DISEASE:
In Central and South America; being tranmitted by blood-sucking Triatomid Bugs (Kissing Bugs – Triatoma & Rhodnius) which serve as Intermediate hosts. Man gets the infection when its skin (exposed wounds, conjunctiva) comes in contact with faeces of the bug containing Trypanosomes. It is an intracellular parasite of the tissues of heart, voluntary muscles, C.N.S. and glands. Chagas' disease is characterized by fever, anaemia and disturbances of C.N.S. It is more common in infants and children.
4. Trypanosoma evansi causes "SURRA" disease of cattle in Africa, Asia & S. America. Similarly, Trypanosoma brucei causes "NAGANA" disease of cattle in Africa. These are also digenetic parasites being transmitted by blood sucking Dipteran flies. T. lewisi is found in Rats in North America. It is non-pathogenic and is transmitted by Rat-flea.
LEISHMANIA
(A Flagellate Protozoan)

1. Leishmania donovoni:
Causes Kala-azar (Dumdum Fever) or Visceral Leishmaniasis in Man in Africa, India, China, & America. Parasites attack endothelial cells of blood vessels, Lymphatics, Spleen, Liver, Bone-marrow and eventually Leucocytes of blood. Parasites are found both outside and inside the tissue cells but they are less numerous in circulating blood. The symptoms include fever, anaemia, enlargement of spleen and liver. The Intermediate or Vector hosts are blood-sucking Sandiflies (Phlebotomus sp.) in whose proboscis they are stored.
2. Leishmenia tropica:
It causes a human skin-disease known as "Oriental Sore" or Delhi Boil or Cutaneous Leishmaniasis in India, Africa, Russia, Torpical America. Parasites are found in the endothelium of skin capillaries and dermal tissues of sores. Sores cause ulcerating wounds which take several months to heal. The disease is transmitted by the blood-sucking Sandiflies or by direct contact.

3. Leishmania brasiliensis:
Cause "Espundia or Bubos" or Naso-oral Leishmaniasis in Americans. The insect vector is sandfly, in this case too.

Some Other Pathogenic Protozoans

Name of the Parasite Transmission Disease
1. Trichomonas vaginalis(Flagellate) Monogentic, Direct through sexual intercourse. Inflammation of mucous-membrane of vagina in women (vaginitis) and Urethra in men, leading to Leucorrhoea.
2. Trichomonas hominis Monogenetic, Transmission through infective cysts in faeces. Large intestine of man and other mammals, associated with Diarrhoea, and Dysentery.
3. Trichomonas tenax Monogenetic, Transmission direct through kissing T. tenax and E. gingivalis are found in pus pockets formed between teeth and the gum in the disease Pyorrhoea. They probably aggravate the disease.
4. Giardia – (Lamblia) intesinalis (Flagellate) Monogenetic, Transmission through infective cysts in faeces. Small intestine of man, associated with Diarrhoea. (Giardiasis)
5. Balntidium coli (a ciliate) Monogenetic, Transmission through cysts. Large intestine of Man, Monkey, pigs etc. causes ulcerations in colon resulting in Balantidial Dysentery.



MALARIAL PARASITE

IMPORTANT SCIENTISTS :-
1. LANCISI in 17th century first suspected a relationship between Malaria and Mosquito.
2. CHARLESS LAVERAN (1880) discovered that Malaria is caused by a protozoan parasite, Plasmodium. He was the first to have observed various stages of plasmodium in Man’s blood. CELLI (1885) supported Lavern’s observations. GOLGI (1885) made a detailed study of blood cycle.
3. SIR RONALD ROSS(1898) was the first to observe oocysts on the stomach of Anopheles (Nobel Award 1902).
4. GRAASSI (1898), for the first time described the Life-Cycle of Plasmodium in Mosquito
5. SHORTT & GARNHAM (1948) studied Pre-Erthrocytic and Exo-Erthrocytic cycle.

1. P. falciparum : = 9-12 days
2. P. vivax : = 10-14 days
3. P. ovale : = 10-14 days
4. P. Malariae : = 28-30 days

PRODROMAL SYMPTOMS: Symptoms appearing before the actual attacks of malarial fever are Nausea, Loss of appetite, Constipation, Insomnia, Mouth becomes dry, Headache and Bodyache.

PAROXYM (Fits of Fever): The actual attack of Malarial fever whose duration is about 6 hours includes 3 stages:
I. Rigor Stage : Chilling & Shivering
II. Febrile Stage : High fever 1040 to 1050 F
III. Defervescent Stage : Profuse sweating brings down the temperature

TIME REQUIRED FOR THE COMPLETION OF ERYTHROCYTIC CYCLE
1. In P. falciparum, P. vivax and P, ovale the erythrocytic cycle is completed in 48 hours, hence the fever comes every third day.
2. In P. malariae, the erythrocytic cycle is completed in 72 hours hence the fever comes every 4th day.

TYPES OF MALARIA
A. Tertian Malaria: Paraoxym every third day. Tertian malaria is of 2 types:-
(a).Benign Tertian : Mild Malaria caused by P. vivax & P. ovale. Death rates is low because merozoites destroy old and mature RBC’s.
(b). Malignant Tertian: Fatal malaria caused by P. falciparum, death rate is high because infected RBC’s usually clump together and block capillary blood circulation in vital organs like brain, lungs, heart etc. Because of large scale destruction of RBC’s (Pernicious Malaria) haemoglobin is excreted in urine (Black water fever).

B. Quartan Malaria: Paroxysm every 4th day; caused by P.malariae. Large scale destruction of young RBC’s might lead to secondary complications.

C. Quotidian Malaria: Paroxysm irregular or daily, caused by mixed species infection.

1. P.OVALE is the rarest of the four speceies of Malaria parasities. P.ovale is mostly restricted to west Africa P. Vivax is the commonest species being prevalent in both tropical and temperates Parts of the world. P. malariae is also found in both tropical and tempreture climates but it is less common than P.vivax. P. falciparum is very common in tropical countries (Tropical Malaria)

2. P. falciparum causes the most dangerous kind of malaria called Malignant tertian of Aestivo-autumnal malaria Since erythrocytic cycles are completed in 24 to 48 hours this is also knows as Sub-tertian Malaria.
In falciparum infection, RBC’s clump together and prevent proper flow of blood into `the brain & other vital orans. Because of this and the toxic effect of the parasite, the patient suffers from total loss of consciousness (Coma) and sometime sudden death occurs. this Cerebral Malaria “is responsible for thousands of malarial deaths ;

Effects of Malaria on Human being:

1. Anaemia: (Shortage of Haemoglobin) due to large Scale destruction if RBC’s
2. phagocytic cells of Reticulo- endothellal system found in the Spleen and Liver phagocytize and remove the infected RBC’s and merozoites from the blood circulating through them . These organs produce more and more phaocytic cells resulting in their own enlargement. Enlarged spleen probably releases Lysolecithin which further destroys RBC’s Toxic substances & pigments are deposited in the liver, spleen and under the skin.
3. Because of the large scale break down of RBC’s large quantities of Bile pigments (Bilirubin & biliverdin) are produced which gradually accumulate in blood giving the skin, mucous membrances,a yellow colour causing Jaundice.

Therapy/Treatment of Malaria:

Quinine is the oldest drug obtained from the bark of Cinchona tree of family Rubiaceae. it destroy all the stages of the parasite in patients blood .Atebrin (mepacrine) camoquin chloroquine are similar to quinine. Paludrine pentaquine Daraprim and camoprima are other anti malarial drugs which destory both exo-erythrocytic stages of the parasite.
Halofantrine has been found to be quite effective against falciparum infection Artemesin is a new anti –malarial drug, obtained from the plant Artemesia annua, Family compositae (developed by CIMAP,Lucknow). Artemesin is effective against cerebral Malaria,

Control of Malaria

(A) Destruction of Anopheles;

1. Adults can be destroyed by using insecticides like DDT , B.H.C, Pyrethrum etc.Fumigants such as Sulphur,Tarcamphor or derivatives of Naphtha are burnt to produce poisonous fumes that kill the mosquitoes.
2. Destruction of breeding places by maintaining proper drainage and not allowing the stagnation of the water.
3. Destruction of larvae & pupae by spraying oil on the water surface, thus preventing them from carrying out their normal respiration. The Biological Control lies in producing natural enemies of mosquito larvae, pupae into the ponds such as fishes (Gambusia; Lebistes Trouts Minnows; Stickle- Backs) Ducks insectivorous plants like Utricularia Droseraa etc.
4. Introduction of larvicidal Bacillus sphaericus in water bodies (Rajamohan et al, 1992).
5. Introduction of Blue Green Algae like Aulosira & Anabaena in water bodies.
(B) Prevention of infection (Prophylaxis)
1. mosquito can be prevented from biting by using mosquito nets and using mosquito repellents.
2. prophyactic drugs such as quinine and chloroquine if taken daily in small quantities , suppress malaria.

Relapse of malaria:
Exo- erythrocyties cycles may revive after a period of dormancy in case of P.vivax P. malariae and P ovule infection after the disease has been completely cured merozoites produced by these cycles attack RBC’s and may cause a Relapse of malaria.

· in case of P. falciparum infection greenish Maurer’s dots; in the infection of P. malariae Zeimann’s dots and in the infection of P. ovale james dots are formed in the cytoplasm of RBC’s .
· The duration of Mosquito–cycle is 10-17 days in P.vivax ; 16 days in P. ovale 22 days in P. falciparum and about 25-30 days in P. malariae.
· N.M.E.P. (National Malaria Eradication Programme) was started in India in 1953.
· P.berghei is found in rats & P. gallinacum is found in chickens.
· August 20 is celebrated as malaria Day. August 29-Mosquito Day

Plasmodium

1. Malaria is caused by a protozoan parasite, plasmodium and it is transmitted by Female Anopheles mosquito.
2. Life –cycle of Plasmodium is DIGENETIC i.e. two types of hosts are required:-
i).primary or Definitive or principal host is man.
ii).Secondary or intermediate or carrier or vector host is female anopheles mosquito.
Common species of Anopheles spreading malaria in our country are--- A. culicifacies, A. fluviatilis A. stephensi A. maculatus etc. plasmodium can not be transmitted by other species of mosquito because of its host- specificity.
Monkey serves as a Reservoir host for plasmodium. Reservoir host for leprosy
3. Plasmodium is pathogenic to man but ‘non pathogenic ‘to mosquito.




1 Sickle –shaped Sporozoites are infective stages of the Parasite for man. Thousands of sporozoites are inoculated into the man’s blood during mosquito bite.
2. Sporozoites disappear from blood-stream within half an hour or so. They dissolve the capillaries and enter into the liver cells with the help of histolytic enzymes secreted by a pair of secretary organelles.





1. Soon after its entry in the liver-cell, the sporozoite changes into a CRYPTOZOITE which grows to become a schizont. The schizont undergoes schizogony (a type of asexual reproduction by multiple fission) producing large number of CRYPTOMEROZOITES (100 to 1000).

2. Schizont and the liver cell burst releasing cryptomerozoites in blood sinusoids of Liver from where they escape into the blood circulation of the body to start Erythrocytic Cycle.

3. This is the first exo-erythrocytic cycle which is also known as Pre-Erythrocytic cycle. The time required for the completion of Pre-Erythrocytic Cycle is known as Pre-Patent Period (about 8-10 days)
4. Exo-erythrocytic cycle is absent in Plasmodium falciparum.

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1 Some of the cryptomerozoiteis of the pre –erythrocytic cycle reinvade fresh liver –cells and change into Metacyptozoites (or phanerozoites) they are of two types ;
Micrometacryptozoites and macrometacryptozoites producing Micrometacryptomerozoites (about 1000) and Macrometacryptomerozoites (about 64) respectively by Schizogony.

2. Macrometacryptomerozoites reinvade fresh liver cells to continue the exo-erythrocytic cycles but Micrometacryptomerozoites attack RBC’s (just like the cryptomerozoites of the pre- erythrocytic cycle) to participate in the Erythrocytic cycle.




1. This cycle is started by merozoites (first of all by cryptomerozoites and
then by micrometacryptomerozoites)

2. After entering into the RBC the merozoite change into a young Trophozoite it develops a non – contractile vacuole which pushes the nucleus and cytoplasm toward the periphery giving it a ‘SIGENT-RING’ appearance.

3. With the help of its lytic enzymes the trophozoite feeds upon the cytoplasm of RBCs and grows to become AMOEBOID. it breaks haemoglobin to Globin (digestible) and Haematin (undigestible). Heamatin granules get deposited in the cytoplasm of the trophozoites in the form of brownish black toxic pigment called Haemozoin. Meanwhile yellowish orange granules of unknown nature called Schuffner’s Dots appear in the cytoplasm of the host RBC.

4. The Adult Inracellular Trophozoite. of plasmodium is now know as schizont which undergoes schizogony to produce about 24 merozoites or schizozoites.schizont and the host RBC burst . Ruptured RBCs are referred to as ghost cells. merozoites, haemozoin garnules and some other toxic substances are released in the blood plasma. it marks the end of the Erythrocytic schizogony and at this stage; the patient gets the characteristic attack of malarial fever.

Attack of Malarial Fever

5. The interval between the inoculation of sporozoits into the man’s blood and first attack of malarial fever is called INCUBATION PERIOD.
6. Erythrocytic cycle is completed in fixed time of either 48 hrs or 72 hrs., depending upon the species of plamodium. that is why the malaria patient gets the attack of fever each time the erythrocytic cycle is completed.
7. Most of the schizozoties re-enter into the RBC to continue the erythrocyte for increasing the number of schizozoites in the blood .However, some of the schizozoites attack RBC to become Gametocytes or GAMONTS which are of 2 types: Microgamonts and Megagamonts.
8. No further change is possible inside the body of man because he is warm-blooded. Gamonts need low temperature for developmeny hence they come in peripheral circulations of man between 10 pm to 2am When the female mesquites a malarial patient in the night she sucks the gamonts. Thus, Gamonts are ingective for the intermediate host (Mosquito).
9. If gamonts are not transferred into the body of the mosquito within few hours after their formation then they stages and disintegrate in man’s blood.



A. SEXUAL CYCLE OR GAMOGONY
1. Gamonts are resistant, hence they can not be digested inside the stomach of Mosquito. Here they undergo gametogenesis (Sexual-Cycle) to produce gametes.
2. Microgamont produces 6-8 microgametes or sperms by Exflagellation.On the other hand, Megagamont produces only one megagamete produces only one megagamete or ovum by Oogenesis. Ovum develops a cone of reception for receiving the microgamets.
3. Fertilization of a macrogamete by a microgamete results in the formation of a nonmotile spherical ZYGOTE in the lumen of the stomach of mesquite. There is a nuclear as well as cytoplasmic-fusion, hence it is called SYNGAMY. Since the fusing gametes are dissimilar, this syngamy is Anisogamous.
4. Now the Zygote becomes elongated, motile and worm-like to be know as OOKINETE.
5. Ookinete penetrates the stomach wall until it comes on the surface of the stomach. Zygote becomes encysted and now is called Oocyst.
B.SPOROGONY OR SPORE FORMATION:
1. The Oocyst grows to become SPORONT. It's nucleus divides repeatedly to form SPOROBLASTS or ZOITOBLASTS.
2. Sporoblasts then multiply and give rise to sporozoites which get arranged in a spokelike fashion. About ten thousand sporozoites are produced from a single Oocyst. A mosquito may have 50 to 500 Oocysts on its stomach.
3. Sporozoites swim in the haemolymph and then enter into the salivary glands where they are stored to be inoculated into the primary host i.e. man.
Ø Attempts have been made to develop vaccines against vulnerable malarial parasite stages using dead or attenuated parasites, but without success.
Ø One possible reason is that the antigen of the parasite may change over time, so that antibodies against the original antigens fail to recognize the new antigens.
Ø In the 1960 it was demonstrated that resistance to P. falciparum among west Africans was associated with the presence of Hb-s in their RBC
Ø Hb-s differ from normal Hb-A by a single amino acid, Valine in each half of Hb molecule, consequently these RBC responsible for sickle cell disease have a low binding capacity for oxygen. Because the malarial parasite has a very active aerobic metabolism, it can not grow and reproduce within thee RBC.

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