Medical Parasitology MCB336 Past Paper PDF 2024

MEDICAL PARASITOLOGY MCB336 PROTOZOA Protozoa of medical Importance: structure, geographical distribution, source of infection/transmission, life cycle, disease. Protozoans are usually single-celled and heterotrophic (using organic carbon as a source of energy), belonging to any of the major linea...

MEDICAL PARASITOLOGY MCB336 PROTOZOA Protozoa of medical Importance: structure, geographical distribution, source of infection/transmission, life cycle, disease. Protozoans are usually single-celled and heterotrophic (using organic carbon as a source of energy), belonging to any of the major lineages of protists and like most protists, typically microscopic. All protozoans are eukaryotes and therefore possess a “true,” or membrane-bound, nucleus. They also are non-filamentous and are confined to moist or aquatic habitats, being ubiquitous in such environments worldwide. Features of protozoans The protozoans are unified by their heterotrophic mode of nutrition, meaning that these organisms acquire carbon in reduced form from their surrounding environment. Many protozoans either perform photosynthesis themselves or benefit from the photosynthetic capabilities of other organisms. Protozoans are motile; nearly all possess flagella, cilia, or pseudopodia that allow them to navigate their aqueous habitats. Protozoans are also strictly non-multicellular and exist as either solitary cells or cell colonies. Protozoa are unicellular eukaryotes that form an entire Kingdom. Protozoa are basically grouped into five based on their means of locomotion and mode of reproduction. They are: Amoeba, Ciliates, Flagellates, Sporozoa and Microspora. AMOEBA (Sarcodina) They are typically amoboid and use pseudopodia to move or protoplasmic flow. The species of human medical importance are Entamoeba, Naegleria and Acanthoamoeba. They have no defined shape and extend one or many lobose pseudopodia. Entamoeba are pseudopod forming tiny protozoan parasite of man and animals in the subphylum Sarcodina. About seven species have been recovered from the gut of man. They are E. histolytica, E. dispar, E. moshkovskii, E. coli, E. polecki and E. hartmanni. E. gingivalis is recovered from the buccal cavity of man. E. histolytica is the only known pathogenic species of the human intestinal amoebae. E. dispar, E. hartmanni, E. coli and E. polecki are commensals found in the large intestine. The large trophozoite and cyst of E. coli can be identified by the splinter-like chromatid bodies in its cytoplasm, and by the fact that its cysts can possess up to eight nuclei. Structure Entamoeba cells are small, with a single nucleus and typically a single lobose pseudopod taking the form of a clear anterior bulge. They have a simple life cycle. The trophozoite (feeding-dividing form) is approximately 10-20μm in diameter and feeds primarily on bacteria. It divides by simple binary fission to form two smaller daughter cells. Almost all species form cysts, the stage involved in transmission (with the exception of Entamoeba gingivalis). Depending on the species, these can have one, four or eight nuclei and are variable in size; which help in species identification. Uni- nucleated trophozoites convert into cysts in a process called encystation. Geographic Distribution Pathogenic Entamoeba species occur worldwide and are frequently recovered from fresh water contaminated with human faeces. The majority of amoebiasis cases occur in developing countries where sanitation and hygiene are poor; places like day-care, prisons and psychiatrics. Risk groups include men who have sex with men, travellers, recent immigrants, immunocompromised persons, and institutionalized populations. Diagram of Trophozoite of Entamoeba histolytica (Two trophozoites have ingested erythrocytes, and all 3 have nuclei with small, centrally located karyosomes). Amoebiasis Amoebiasis is caused by E. histolytica, a protozoan that is found worldwide. Another species of amoeba, E. dispar, has been reported as a potential cause of amoebic liver abscess. The highest prevalence of amoebiasis is in developing countries where barriers between human faeces and food and water supplies are inadequate. Although most cases of amoebiasis are asymptomatic, dysentery and invasive extraintestinal disease can occur. Amoebic liver abscess is the most common manifestation of invasive amoebiasis, but other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites. The National Institute of Allergy and Infectious Diseases (NIAID) has classified E. histolytica as a category B biodefense pathogen because of its low infectious dose, environmental stability, resistance to chlorine, and ease of dissemination through contamination of food and water supplies. Only 1–100 cysts are required to cause amoebic dysentery in animal models, an infectious dose comparable to the notoriously contagious Shigella sp. Transmission E. histolytica is transmitted through the ingestion of the cystic form (infective stage) of the protozoa. Viable in the environment for weeks to months, cysts can be found in faecal contaminated soil, fertilizer, or water or on the contaminated hands of food handlers. Faecal-oral transmission can also occur in the setting of anal sexual practices or direct rectal inoculation through colonic irrigation devices. Life cycle Amoebiasis is the disease caused by E. histolytica and is composed of two main syndromes: dysentry and liver abscesses. Cysts and trophozoites are passed in faeces. Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrhoeal stool. Infection with Entamoeba histolytica (and E. dispar) occurs through ingestion of mature cysts from faecally contaminated food, water, or hands. Exposure to infectious cysts and trophozoites in faecal matter during sexual contact may also occur. Excystation occurs in the terminal ileum or colon or small intestine, resulting in trophozoites (invasive form) which are released, and they migrate to the large intestine. Trophozoites may remain confined to the intestinal lumen (A: noninvasive infection) with individuals continuing to pass cysts in their stool (asymptomatic carriers). The trophozoites can penetrate and invade the colonic mucosal barrier, leading to tissue destruction, secretory bloody diarrhoea, and colitis resembling inflammatory bowel disease (B: intestinal disease), or blood vessels, reaching extraintestinal sites such as the liver, brain, and lungs (C: extraintestinal disease) through the portal circulation. The liver is the most common site of extraintestinal amoebiasis. Trophozoites multiply by binary fission and produce cysts , and both stages are passed in the faeces. The life cycle of the amoeba is completed when trophozoites in the large intestine encyst and are excreted in the faeces of the host. Cysts can survive days to weeks in the external environment and remain infectious in the environment due to the protection conferred by their walls. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to the gastric environment. E. histolytica may be observed with the ingested red blood cells (erythrophagocytosis); E. dispar may occasionally be seen with ingested erythrocytes as well, although its capacity for erythrophagocytosis is much less than that of E. histolytica. Clinical Presentation The majority of infections restricted to the lumen of the intestine (“luminal amoebiasis”) are asymptomatic. Amoebic colitis, or invasive intestinal amoebiasis, occurs when the mucosa is invaded. Symptoms include severe dysentery and associated complications. Severe chronic infections may lead to further complications such as peritonitis, perforations, and the formation of amoebic granulomas (amoeboma). Amoebic liver abscesses are the most common manifestation of extraintestinal amebiasis. Pleuropulmonary abscess, brain abscess, and necrotic lesions on the perianal skin and genitalia have also been observed. Treatment: Metronidazole and tinidazole. Life cycle of Entaemoba histolytica CILIATES (Ciliophora) Ciliate, or ciliophora, are members of the protozoan phylum Ciliophora, with about 8,000 species. Ciliates are single-celled organisms that, at some stage in their life cycle, possess cilia, short hairlike organelles used for locomotion and food gathering. Ciliates have one or more macronuclei and from one to several micronuclei. The macronuclei control metabolic and developmental functions; the micronuclei are necessary for reproduction. Reproduction is typically asexual, although sexual exchange occurs as well. Asexual replication is usually by transverse binary fission or by budding. Sexual phenomena include conjugation (genetic exchange between individuals) and autogamy (nuclear reorganization within an individual). Sexual reproduction does not always result in an immediate increase in numbers; however, conjugation is often followed by binary fission. The only human parasite in this group is Balntidium coli, which is a giant intestinal ciliate of human and pigs. Causal Agents Balantidium coli, a large ciliated protozoan, is the only ciliate known to be capable of infecting humans. It is often associated with swine, the primary reservoir host. Humans can also be reservoirs, and other potential animal hosts include rodents and nonhuman primates. Morphology The organism is surrounded by cilia. B. coli has two developmental stages, a trophozoite stage and a cyst stage. In trophozoites, the two nuclei are visible. The macronucleus is long and sausage-shaped, and the spherical micronucleus is nested next to it, often hidden by the macronucleus. The opening, known as the peristome, at the pointed anterior end leads to the cytostome, or the mouth. The cysts are smaller than the trophozoites and are round and have a tough, heavy cyst wall made of one or two layers. Usually only the macronucleus and sometimes cilia and contractile vacuoles are visible in the cyst, however, both nuclei are present because nuclear multiplication does not occur when the organism is a cyst. Living trophozoites and cysts are yellowish or greenish in color. Morphology of Balantidium coli Balantidiasis Epidemiology B. coli occurs worldwide. Because pigs are the primary reservoir, human infections occur more frequently in areas where pigs are raised, sanitation is inadequate, and especially among those that are in close contact with swine. The disease is considered to be rare and occurs in less than 1% of the human population. The disease poses a problem mostly in developing countries, where water sources may be contaminated with swine or human feces. Transmission Balantidium is the only ciliated protozoan known to infect humans. Balantidiasis is a zoonotic disease and is acquired by humans through the faecal-oral route from the normal host, the domestic pig, where it is asymptomatic. Contaminated water is the most common mechanism of transmission. B. coli life cycle Infection occurs when a host ingests a cyst, which usually happens during the consumption of contaminated water or food. Once the first cyst is ingested, it passes through the host's digestive system. While the cyst receives some protection from degradation by the acidic environment of the stomach through the use of its outer wall, it is likely to be destroyed at a pH lower than 5, allowing it to survive easier in the stomachs of malnourished individuals who have less stomach acid. Once the cyst reaches the small intestine, trophozoites are produced. The trophozoites then colonize the large intestine, where they live in the lumen and feed on the intestinal flora. Some trophozoites invade the wall of the colon using proteolytic enzymes and multiply, causing ulcerative pathology in the colon wall, and some of them return to the lumen of the large intestine and appendix, where they replicate by binary fission, during which conjugation may occur. In the lumen, trophozoites may disintegrate or undergo encystation. Encystation is triggered by dehydration of the intestinal contents and usually occurs in the distal large intestine, but may also occur outside of the host in faeces. The mature cyst forms are released into the environment when faeces are passed, and can go on to infect a new host. It can thrive in the gastrointestinal tract as long as there is a balance between the protozoan and the host without causing dysenteric symptoms. Infection most likely occurs in people with malnutrition due to the low stomach acidity or people with compromised immune systems. In acute disease, explosive diarrhea may occur as often as every twenty minutes. Perforation of the colon may also occur in acute infections which can lead to life-threatening situations. Extraintestinal infection is rare but potentially serious and typically occurs secondary to intestinal infection. Peritonitis and liver abscesses have been noted following intestinal perforation or rupture of fulminant colonic ulcers. Invasion of urogenital tract may be caused by contamination from the anal region or through fistulae caused by severe infection. Clinical Presentation Most cases are asymptomatic. Clinical manifestations, when present, may be acute or chronic with abdominal symptoms. Complications of associated diarrhoea or dysentery can occur in protracted infections. Symptoms may be severe or fatal in debilitated/immunocompromised persons. Life cycle of Balantidium coli Treatment: Metronidazole, tetracycline and iodoquinol. SPOROZOA Sporozoa: Plasmodium species, Babesia microti, Toxoplasma gondii, Cryptosporidium species This group undergo complex sexual and asexual reproductive phases. Human parasites among them include Plasmodium species, Cryptosporidium, Cyclospora and Toxoplasma, which are all intracellular parasites. Plasmodium species Plasmodium is a member of the phylum Apicomplexa, a large group of parasitic eukaryotes. Within Apicomplexa, Plasmodium is in the order Haemosporida and family Plasmodiidae. Over 200 species of Plasmodium have been described. Plasmodium are obligate parasites of vertebrates and insects. The life cycles of Plasmodium species involve development in a blood-feeding insect host which then injects parasites into a vertebrate host during a blood meal. Parasites grow within a vertebrate body tissue (often the liver) before entering the bloodstream to infect red blood cells. The ensuing destruction of host red blood cells can result in malaria. They undergo the asexual replication process of merogony inside host red blood cells and produce the crystalline pigment hemozoin as a byproduct of digesting host hemoglobin. During this infection, some parasites are picked up by a blood-feeding insect to continue the life cycle. Species of Plasmodium are distributed globally wherever suitable hosts are found. Insect hosts are most frequently mosquitoes of the genera Culex and Anopheles. Over the course of the 20th century, many other species were discovered in various hosts and classified, including five species that regularly infect humans: P. vivax, P. falciparum, P. malariae, P. ovale, and P. knowlesi. P. falciparum is by far the most lethal in humans, resulting in hundreds of thousands of deaths per year. Although the parasite can also infect people through blood transfusion, this is very rare, and Plasmodium cannot be spread from person to person. Some of subspecies of Plasmodium are obligate intracellular parasites. Epidemiology Approximately 250 million people suffer from malaria, and between one and two million die annually. The majority of deaths occur in African children and nearly all are caused by P. falciparum. Malaria occurs throughout most of the tropical regions of the world. P. falciparum predominates in Africa, New Guinea, and Haiti while P. vivax is more common in Central America and the Indian subcontinent. The prevalence of these two species is approximately equal in South America, and eastern Asia. P. malariae is found in most endemic areas, especially throughout sub-Saharan Africa, but is much less common than other species mentioned. P. ovale is relatively unusual outside of Africa and where it is found, comprises