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Structure and life history of Protozoa


Structure and life history of Protozoa (e.g., Entamoeba histolytica, Plasmodium vivax, Trypanosoma gambiense, Leishmania donovani) :

STRUCTURE AND LIFE HISTORY OF PROTOZOA

Protozoa: Structure and Life History

Protozoa are a diverse group of single-celled eukaryotic microorganisms, many of which are free-living, but some are parasitic and can cause significant diseases in humans and animals. Their remarkable adaptability is reflected in their varied structures and complex life cycles. This section elaborates on the structure and life history of four medically important protozoa: Entamoeba histolyticaPlasmodium vivaxTrypanosoma gambiense, and Leishmania donovani.

ENTAMOEBA HISTOLYTICA: THE CAUSATIVE AGENT OF AMOEBIASIS

Entamoeba histolytica: The Causative Agent of Amoebiasis

Entamoeba histolytica is an anaerobic parasitic amoebozoan that primarily infects humans and other primates, leading to amoebiasis, a disease characterized by intestinal and extraintestinal manifestations.

Structure:
  • Trophozoite Stage: This is the motile, feeding, and multiplying stage of the parasite, typically found in the large intestine. Trophozoites are irregular in shape, ranging from 10 to 60 µm in diameter. They possess a single nucleus with a characteristic small, centrally located nucleolus (karyosome) and finely dispersed chromatin. Their cytoplasm is distinctly divided into a clear, refractile outer ectoplasm and a granular inner endoplasm. The ectoplasm is responsible for the formation of pseudopods, which are used for locomotion and phagocytosis. Ingested red blood cells, a hallmark of pathogenic E. histolytica trophozoites, may be visible within the endoplasm.
  • Cyst Stage: The cyst is the infective and resistant stage, found in the feces of infected individuals. Cysts are spherical or ovoid, ranging from 10 to 20 µm in diameter, and are surrounded by a thick, protective cyst wall, allowing them to survive harsh environmental conditions outside the host. Mature cysts typically contain four nuclei, similar in appearance to the trophozoite nucleus. Chromatoid bodies, which are rod-shaped structures composed of ribosomal RNA, may also be present in immature cysts but usually disappear as the cyst matures.
Life History:
The life cycle of Entamoeba histolytica is relatively simple, involving only one host (humans).
  1. Infection: Humans become infected by ingesting mature quadrinucleated cysts, usually through contaminated food or water (fecal-oral route).
  2. Excystation: Upon reaching the small intestine, the protective cyst wall is weakened by digestive enzymes, leading to excystation. Each quadrinucleated cyst gives rise to a metacystic amoeba, which then undergoes nuclear and cytoplasmic divisions to produce eight small trophozoites.
  3. Colonization: These trophozoites migrate to the large intestine, where they colonize the lumen or invade the intestinal mucosa. They multiply by binary fission.
  4. Pathology: In pathogenic infections, trophozoites adhere to and invade the intestinal epithelium, causing ulcerations and tissue destruction, leading to symptoms like dysentery (bloody diarrhea), abdominal pain, and fever. They can also spread to extraintestinal sites, most commonly the liver, forming amoebic liver abscesses.
  5. Encystation: As the trophozoites are passed down the colon, they begin to dehydrate and transform into cysts. Encystation is triggered by unfavorable conditions in the colon, such as dehydration of feces.
  6. Transmission: Both trophozoites and cysts are passed in the feces. While trophozoites are fragile and do not survive long outside the host, the resistant cysts are immediately infective upon excretion and are responsible for transmission to new hosts.

PLASMODIUM VIVAX: THE MAJOR CAUSE OF BENIGN TERTIAN MALARIA

Plasmodium vivax: The Major Cause of Benign Tertian Malaria

Plasmodium vivax is one of the most widespread human malaria parasites, responsible for benign tertian malaria, characterized by recurrent fevers every 48 hours.

Structure:
  • Sporozoites: The infective stage transmitted by the mosquito, sporozoites are slender, spindle-shaped cells (10-15 µm long) with an apical complex, which aids in host cell invasion.
  • Trophozoites (Ring Form): Early trophozoites in red blood cells appear as delicate, ring-shaped structures with a single vacuole and a chromatin dot.
  • Trophozoites (Amoeboid Form): As the trophozoite matures, it becomes more irregular and amoeboid in shape, filling a significant portion of the red blood cell. Schüffner's dots (fine, red stippling) become visible in the infected erythrocyte, a characteristic feature of P. vivax infection.
  • Schizonts: Mature schizonts contain multiple merozoites (typically 12-24) within the red blood cell, ready to rupture and infect new erythrocytes.
  • Gametocytes: The sexual stages, macrogametocytes (female) and microgametocytes (male), are typically round or oval and larger than ring forms. Macrogametocytes have compact chromatin and a blue cytoplasm, while microgametocytes have diffuse chromatin and a pale pink cytoplasm.
  • Hypnozoites: Dormant liver stages that are unique to P. vivax and P. ovale, responsible for relapses.
Life History:
The life cycle of Plasmodium vivax is complex, involving two hosts: humans (intermediate host) and Anopheles mosquitoes (definitive host).

A. Human Cycle (Asexual Cycle):
  1. Sporozoite Injection: An infected female Anopheles mosquito injects sporozoites into the human bloodstream during a blood meal.
  2. Exoerythrocytic (Liver) Stage: Sporozoites rapidly travel to the liver and invade hepatocytes. Inside liver cells, they develop into schizonts. This stage is known as the exoerythrocytic or pre-erythrocytic schizogony. Some sporozoites can differentiate into dormant forms called hypnozoites, which can remain viable for months or years and are responsible for malarial relapses.
  3. Merozoite Release: Mature liver schizonts rupture, releasing thousands of merozoites into the bloodstream.
  4. Erythrocytic (Red Blood Cell) Stage: Merozoites invade red blood cells, preferentially young erythrocytes and reticulocytes due to the presence of the Duffy antigen receptor.
  5. Trophozoite Development: Inside the red blood cell, the merozoite transforms into a ring-form trophozoite, which then grows into an amoeboid trophozoite.
  6. Schizogony: The trophozoite undergoes asexual multiplication (schizogony), forming a schizont containing multiple merozoites.
  7. Erythrocyte Lysis and Fever: The infected red blood cell ruptures, releasing new merozoites that infect fresh red blood cells, perpetuating the erythrocytic cycle. The synchronous rupture of infected red blood cells and release of parasitic metabolic byproducts trigger the characteristic paroxysms of fever, chills, and sweats associated with malaria.
  8. Gametocyte Formation: Some merozoites, instead of forming schizonts, differentiate into sexual forms called gametocytes (male microgametocytes and female macrogametocytes). These are the infective stages for the mosquito.
B. Mosquito Cycle (Sexual Cycle):
  1. Gametocyte Ingestion: When a female Anopheles mosquito bites an infected human, it ingests gametocytes along with the blood meal.
  2. Gametogenesis: In the mosquito's midgut, the gametocytes mature into male and female gametes. The microgametocytes undergo exflagellation, forming motile microgametes.
  3. Fertilization: A microgamete fuses with a macrogamete to form a diploid zygote.
  4. Ookinete Formation: The zygote develops into a motile, elongated form called an ookinete.
  5. Oocyst Development: The ookinete penetrates the mosquito's midgut wall and encysts on its outer surface, forming an oocyst.
  6. Sporogony: Inside the oocyst, thousands of sporozoites develop through multiple rounds of asexual reproduction (sporogony).
  7. Sporozoite Migration: The mature oocyst ruptures, releasing sporozoites that migrate to the mosquito's salivary glands, ready to infect a new human host during the next blood meal.

TRYPANOSOMA GAMBIENSE: THE CAUSE OF WEST AFRICAN SLEEPING SICKNESS

Trypanosoma gambiense: The Cause of West African Sleeping Sickness

Trypanosoma gambiense is a hemoflagellate parasite that causes chronic West African sleeping sickness (Gambian trypanosomiasis), a severe and often fatal disease affecting the central nervous system. It is transmitted by tsetse flies.

Structure:
  • Trypomastigote Form (in mammals): This is the predominant form found in the bloodstream, lymph, and cerebrospinal fluid of the mammalian host. Trypomastigotes are elongated, spindle-shaped cells (12-35 µm long) with a single flagellum originating from a kinetoplast (a dense granule containing mitochondrial DNA) located near the posterior end. The flagellum runs along the undulating membrane before becoming free at the anterior end.
  • Epimastigote Form (in insect vector): This form is found in the mid

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