LEISHMANIA DONOVANI

      Leishmania donovani is one of the major protozoan flagellate parasites responsible for causing leishmaniasis. It is also commonly known as kala-azar or dum dum fever. It dwells in the reticulo-endothelisalLeishmania currently affects 12 million people in 88 countries per year. The core terai-region of Nepal is one of the infected places in a country

History

Leishman and Donovon reported this organism simultaneously. Leishman from London in 1903 and Donovan from Madras in the same year.

Distribution

This parasite is endemic in many countries like China, India, Africa, Europe and Russia. The tropical zones are the favorite places for this parasite. It has been also reported from many places of terai region of Nepal.

Morphology

This parasite exists in two stages namely promastigote and Amastigote stages

Amastigote Stage

—  Round or oval, measuring 2-4 micrometer

—  Outer covering is pellicle

—  Nucleas oval or round

—  Kinetoplast, DNA contaning and a mitrochondrial structures

—  Axoneme, the root of the flagellum lies near the kinetoplast.

—  Absence of free flagellum

Promastigote Stage

—  Short and oval but fully developed are slender spindle shaped bodies.]

—  Measures 5-10l*2-3w micrometer

—  Nucleus lies on the centre.

—  Kinetoplast lies near the anterior end

—  Consist of only one flagellum

Life Cycle

 The life cycle of leismania donovani completes in two host. Thus it shows digenetic life cycle. The hosts are

—  Primary Host- Man

—  Secondary or Intermediate host- Sand fly

—  Reservoir host- Man, Dogs

 Life Cycle In Man

When an infected sand fly sucks the blood of man along with its saliva a number of promastigote forms enter the blood stream of man. Here they become amastigote forms by losing their flagella. It attacks the macrophage cell of liver or spleen. It appears to be well adapted to a life inside these cells. They remain unaffected by the proteolytic enzymes of host within the macrophage the Leishmania divides by binary fission once in every 24 hours. These are liberated in blood after the rupture of macrophage.

Life cycle in sand fly

When the female sand fly sucks the blood of man along with blood and macrophages the Leishmania enter the alimentry canal. Within the gut they multiply by binary fission. Their number is increased during 4-5 days of blood meal. Soon the parasites migrate forward and the foregut is occupied by them. It gradually moves into the salivary glands by 7-8 days. Finally if these infected  sandfly bites a healthy person they transmits the parasites of promastigote’s stage to new host. In this way life cycle completes in a sandfly.

Method of Transmission- The transmission of leishmania donovani from one person to another is carried out by a sandfly. During their blood meal they transmit the parasite present in their salivary glands

Incubation Period- 3-6 months and sometimes sympotomps may appear even after a years.

Pathogenesis- It causes a disease known as visceral leishmaniasis or black fever. Its sypmotomps are Black Sickness (Hyperpigmented skin), Hepatosplenomegaly , High fever, Emaciation, Swollen gland, Fatigue, Anemia, Weight Loss etc.

Diagnosis- Through microscopically examination of blood and

Biopsy material taken from bone marrow or spleen of patient.

Treatment- The choice of drugs are antimony compounds and they are,

—  Stibamine

—  Aminostiburea

—  Neostibosan

—  Neostam

—  Sodium Antimony  gluconate

Preventive Measures

•      Control of sand fly populations

•      Providing barriers to protect humans from sand fly bites

•      Elimination of reservoir hosts

•      Treatment of infected individuals

•      Health education and awareness.

Entamoeba Histolytica Video

Life Cycle of Plasmodium vivax

Life Cycle of malaria causing parasite (Plasmodium vivax)


Life cycle of malarial parasites completes in two hosts ie. Man and Female anopheles mosquito. In man the parasites develop asexually whereas in female anopheles mosquito it develops sexually.

Asexual Cycle
Malaria infection in the human host starts when the sporozoites are injected into the blood stream during a blood meal by an infectious mosquito. Although it is assumed than one single
sporozoite is capable of initiating the infection in men, the number of sporozoites injected by a mosquito bite is supposed to vary from dozens to thousands. It is likely that this number strongly affects the clinical picture: the greatest the sporozoite load, the shortest the incubation period and the most serious the symptoms. The sporozoites remain into the circulation for a short period, calculated as 60 minutes at maximum, before they actively enter the liver of the host. The Kuppfer cells in the liver may be invaded but the sporozoites are not able to develop in those cells and die shortly after invasion. Most parasites however invade the hepatocytes (Cells of the liver) and start the asexual exo-erythrocitic schizogonic cycle.
Sporozoites inside the liver cell rapidly grow in size by absorbing nourishment. Nucleus of sporozoites divides into several small pieces and piece is enclosed by cytoplasm. Thus, about 80-1000 merozoites of 1µ are produced. (The schizont formed in liver cell is called by some authors as cryptozoites and its products are called cryptomerozoites, some author call them simply merozoites)
Merozoites are liberated by the bursting of liver cells due to the pressure on liver cells. Merozoites thus liberated reach the fine blood sinusoids of liver from where they reach the general blood circulation. Whereas,some of the merozoites again attack the fresh liver cells. (In the exoerythrocytic cycle, there is no effect of various drugs as the parasite is intracellular.)

Erythrocytic or Schizogonic Cycle
Merozoites penetrate the RBC. It burrows into red blood cells and slowly enters the resting stage. This is the trophozoite stage in which parasite is converted into a rounded body with a single nucleus and grows at the expense of protoplasm of RBC. The trophozoite attains its maximum size. Soon, a vacuole is formed in the middle of cytoplasm, which pushes the nucleus to one side. This trophozoite stage is called a signet ring stage. Soon, the vacuole disappears and parasite changes to amoeboid form. This stage is called ameboid stage. In this stage parasite feeds on the haemoglobin and other contents of RBC.
After feeding, amoeboid form increase in size and becomes round. The stage is called schizont. At the mean time, some small granules called Schuffer’s granules (dots) appear in the RBC cytoplasm. This is the toxic released by parasites and are called haemozoin which are responsible for causing the fever. The nucleus of schizont multiplies by multiple fission to form 12-24 daughter nuclei
At the end of this phase the schizogonic cycle is completed, the erythrocyte ruptures releasing the merozoites into the blood stream and the merozoites discharged into the circulation invade new erythrocytes to repeat the schizogonic cycle. While some merozoites will develop into two types of gametocytes ie. Microgametocytes and megagametocytes. The further development of gametocytes takes place in female Anaopheles mosquito. The life span of gametocytes is only few hours. If these gametocytes are not taken by mosquito, then die soon.

Sporogony or Sexual Cycle
When a female anopheles mosquito bites a malarial patient and sucks the blood having gametocytes for its food by piercing into the skin, further development of the gametocytes is only possible in the stomach of female anopheles and not any other type of mosquito. If mosquito is other type, the gametocytes are destroyed in its stomach.

Maturation of Gametocytes
a) Microgametocytes:- The microgametocytes become very active and their nuclei divide into several small nuclei. A number of six to eight flagella like microgametes are formed. A nucleus move to each flagellum. Flagella start lashing movements and break off from the cytoplasm. These structures are called microgametes, which can be compared to spermatozoa and this process is called exflagellation.
b) Macrogametocytes:- The mega or macrogametocytes develop into female gametes or ova. The megagametocytes show little change. It enlarges in size and develops a reception cone. This structure is called female gamete or ova.

Fertilization and sporozoites formation
Microgametes make active lashing movements and approach megagamete, one of the microgamete reaches to protoplasmic projection of megagamete. The nuclei of mega and microgamete fused resulting in the formataion of zygote after fertilization. Zygote remains inactive for sometime but later on becomes elongated or worm like ookinete or vermicule. It moves into the stomach of the host. There it passes into the epithelium and finally reaches in between the epithelial and subepithelial tissues. Zygote becomes enclosed into a cyst called oocyst. Afterwards, oocyst attains maximum size and the nucleus of the oocyst divides into several nuclei to form hundred of spindle-shaped nuclei. This process is called sporulation.
Cyst brust and sporozoites are liberated into the body cavity or haemocoel of mosquito. Sporozoites are motile and majority of them reach the salivary glands of the mosquito. Eventually, sporozoites enter the salivary duct along with the saliva. When a mosquito in this condition pierces the skin of man, some sporozoites are injected with the saliva into the puncture caused by the mosquito. Sporozoites then reach liver cell and cycle is repeated.


Pathogenesis
The disease caused by plasmodium is malaria. The basic symptom is intermittent fevers with chills and shivering. The general symptom of malaria includes three successive stages. In cold stage which lasts for 15 to 60 minutes, the patient feels intense cold and uncontrolled shivering. It is followed by the hot stage which lasts for 2-6 hours, the patient experiences intently hot. The fever reaches to 41 degree centigrade or higher. Severe headache, vomiting and nausea are common. Afterwards come the sweating stage, when the patient sweats much, then the temperature drops rapidly and patient usually falls into deep sleep. The complete symptom usually begins in early afternoon and lasts for 8-12 hours.

Preventive Measures
Destruction of Vectors
Prevention of infection
Treatment of infected person
Avoid mosquito bites etc

Life Cycle of Giardia Intestinalis

Classifications Phylum: Protozoa Class: Flagellata Order: Diplomonadida Genus: Giardia Species: lamblia

GIARDIA INTESTINALIS

Giardia lamblia is a flagellated protozoan parasite that colonises and reproduces in the small intestine, causing giardiasis. The giardia parasite attaches to the epitheleum by a ventral adhesive disc, and reproduces through binary fission. Giardiasis does not spread through the bloodstream, nor does it spread to other parts of the gastro-intestinal tract, but remains confined to the lumen of the small intestine.

Host: Giardia infects humans, but is also one of the most common parasites infecting cats, dogs and birds. Mammalian hosts also include cows, deer and sheep.

History

1681 AD: Leeunwenhock found this parasite while examining his own stool

1859: Lambl describe it as the parasite for the first time and named as intestinalis

It was named as Giardia lamblia by the Prof. Giard and Prof. Lambl

Distribution:

Worldwide, more prevalent in warm climates, and in children. Since 1988, WHO has estimated that in Africa, Asia and Latin America there are over 280 million G. intestinalis infections yearly…..

Habit and Habitat: It is the most common intestinal protozoan parasite found in the duodenum and the upper part of jejunum of human small intestine.

Morphology

It exists on two stages namely, Trophozoite and Cystic stage

Trophozoite Stage:

Bilaterally Symmetrical

Paired Body Organs

Rounded Anteriorly and Pointed Posteriorly

Looks like longitudinally split pear or tennis racket

Dorsal surface is convex and the ventral concave

Size: 14 µm

Body Organells- Two axostyles, two nuclei, four pairs of flagella, 2 parabasal body and one sucking disc

They are found attached on the epithelial surface of small intestine by the help of sucking disc.

Cystic Stage

Ø Oval in shapes (12 µm long and 7 µm broad)

Ø Four nuclei are presents in cluster

Ø Retracted Cytoplasm

Ø The axostyle lie more or less diagonally seems like a dividing line within the cyst wall.

Ø Flagella are retracted and curved.

Life Cycle:

Giardia infection can occur through ingestion of dormant cysts in contaminated water, food, or by the faecal-oral route (through poor hygiene practices). The Giardia cyst can survive for weeks to months in cold water and therefore can be present in contaminated wells and water systems, especially stagnant water sources such as naturally occurring ponds, storm water storage systems, and even clean-looking mountain streams.

Within 3o minutes of ingestion, the cyst hatches out into trophozoites. The pear-shaped,

flagellated trophozoite inhabits the epithelial border of the upper two-thirds of the small

intestine, where it absorbs nutrients from the intestinal tract and reproduces by binary fission, approximately every five hours.

When the condition in the duodenum is unfavorable, encystment occurs and the cell divides into two within the cyst. The resulting trophozoites and cysts then pass through the digestive system in the feces. While the trophozoites may be found in the feces, only the cysts are capable of surviving outside of the host. Diarrheal stools may contain trophozoites due to rapid intestinal transit that may not allow sufficient time for cysts to form

Mode of Infection:

Mature Cyst is the infective stage. Infection is fecal-oral type. It is brought about by the ingestion of mature cysts through food or drink contaminated with cysts.

Pathogenicity

Ø With the help of the sucking disc, the parasite attaches on the epithelial cells of intestine and may cause disturbance in intestinal function

Ø Steatrrhoea (pale, foul smelling, greasy stools)

Ø Chronic enteritis and acute entero-colitis

Ø Allergy due to toxic effect of parasite

Ø Jaundice, loss of weight, appetite, weakness etc

Diagnosis

Ø Direct microscopic examination of stool specimens for cyst and trophozoites.

Ø Direct Fluorescent Antigen (DFA) test of stool specimens for cysts and trophozoites

Tratment

Metronidazole, Furazolidone (effective for children) and Chloroquine.

Prevention

Ø Washing hands with soap and water after toilet,

Ø Cutting nails regularly;

Ø Using boiled water;

Ø Consume properly washed vegetables,

Ø Protection of foods from possible contamination with flies and

Ø Proper disposal of sewages,

Life Cycle of Entamoeba histolytica

Entamoeba Histolytica

Entamoeba histolytica is a microscopic and endoparasite of human causing a disease known as amoebiasis. It is one of the more serious of the parasitic infections of humans, affecting an estimated 50 million persons worldwide. It is an amoeba, meaning a single cell organism that divides by binary fission and can replicate in the intestinal tract, primarily in the large intestine or colon. In the colon the organisms actually bore their way into the bowel wall, and cause ulcerations, severe bloody diarrhea called dysentery, and abdominal pain.

It is cosmopolitian in distributin (found across the globe). It is abundantly found in the tropical and subtropical region and are mostly common on the place where sanitation is poor.

Morphology

Entamoeba histolytica exists on three forms, namely,

Ø Trophozoite/Magna form (Pathogenic and Active Stage)

Ø Pre-Cystic Stage/ Minuta Stage

Cystic Stage (Infective and resting Stage)

Trophozoite

Pre Cystic Stage

¢ Smaller in size as compared to tropozoite stage.

¢ Encystment occurs by forming cyst wall in intestinal lumen.

¢ Food vacuoles are absent here

¢ Ingested food particles and RBC are seen in endoplasm

Cystic Stage

Ø Dormant/resistant stage

Ø Spherical

Ø 1-4 nuclei, (4 in mature cysts), uninucleate to quadrinucleate (mature cyst)

Ø Bluntly rounded chromatoidal bars

Ø Matured Cyst can sustain 12 days in a cool and moist place and in water 9-30 days

Life Cycle

The life cycle of entamoeba histolytica completes in a single host. viz Man. So it is also called a monogenetic parasites. Human Beings get infecton with this parasite through the consumption of contaminated food and water with quadrinucleate cyst. The gystric juice inside the stomach cannot dissolve the cystic wall due to some kind of resistance on it. As soon as the cyst reaches to the small intestine it will get dissolved through the trypsin enzyme present in duodenal region. From this cyst, now arises a parasite known as metacyst. This process is known as excystation. Now the nucleus of metacyst divides to form eight nucleated metacyst. Finally eight tropozoites will develop from a single metacyst. These tropozoites starts to grow and lodges into the mucosa and submucosa region of large intestine.

Under the commencement of unfavourable condition, a cystic wall starts to develop in each trphozoite. This stage is called Pre-Cystic stage. The single nucleus of the cyst soon undergoes a division to form two and then into four daughter nuclei. This stage of cyst is quadrinucleate. It does not develop further in the large intestine and reaches to outer environment through the faeces. Finally, if these cysts are consumed by next person s/he will get infected again. In this way life cycle of entamoeba histolytica completes in a single host.

Mode of Infection

Ø Oral –faecal type

Ø By ingesting food and water containing quadrinucleate cyst

Ø House fly may act as vector sometimes

Incubation Period- 4-5 days

Pathogenecity

¢ Primary lesions in large intestine at submucosa region

¢ Histolysi, cytolysis, necrosis

¢ Secondary lesion in liver, lungs and brains (Chronical Stage)

Treatment

The choice of drugs are,

Metronidazole, Paramomycin, Diloxanide furoate, Indoquinol, Chloroquine, Schnidazole etc

Prophylaxis (Prevention)

¢ Washing hand with soap and water after toilet

¢ Use toilet

¢ Do not consume under cooked food

¢ Boil water

¢ Wash the vegetables properly

¢ Health Education and awarness

¢ Cover the food stuff.

Monetization of externalities

Nepal is regarded as a third world country. Being a undeveloped countries, we are suffering from many externalities and today i am going to make sense about how we are becoming victim of pollution and climate change and their externalities.

Climate change is simply due to the green house gases. These gases are responsible for the increase of temperature in this heaven like earth. To be continued...........