Medically Important Protozoa PDF
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Al Rayyan International University College
Dr. Hend Hussein
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This document provides an in-depth look at medically important protozoa, including their classification, life cycle, pathology, and methods for diagnosis and treatment. It focuses on specific protozoan species like Entamoeba histolytica, Giardia lamblia, and Balantidium coli, emphasizing their significance in human health.
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Medically important Protozoa By. Dr. Hend HUSSEIN Associate professor of Medical PARaSITOLOGY Faculty of Medicine Al Rayyan Colleges Objectives: Identify classification of Protozoa. Recognize different species of medically important proto...
Medically important Protozoa By. Dr. Hend HUSSEIN Associate professor of Medical PARaSITOLOGY Faculty of Medicine Al Rayyan Colleges Objectives: Identify classification of Protozoa. Recognize different species of medically important protozoa and point out Pathogenic species. Discuss life cycle of medically important protozoa. Identify morphological characters of different stages of medically important protozoa Discuss Pathology caused by medically important protozoa. Identify clinical picture of medically important protozoa Discuss different ways of diagnosis and regimen of treatment of medically important protozoa Important parasites: Endoparasites Helminths Protozoa Trematodes Cestodes Nematodes Classification of Protozoa Types of protozoa Amoebas (Entamoeba histolytica). Ciliates (Balantidium coli). Flagellates (Giardia lamblia). Sporozoa (Plasmodium malaria). Gastrointestinal Protozoa Large intestinal protozoa: Rhizopoda: Entamoeba histolytica. Ciliophora: Balantidium coli. Small intestinal protozoa: Flagellates: Giardia lamblia Several protozoan species in the genus Entamoeba colonize humans, but not all of them are associated with disease. Entamoeba histolytica is well recognized as a pathogenic species of amoeba. The word histolytic literally means "Tissue destroyer“, it is always associated with intestinal and extraintestinal infections. Non Pathogenic (Harmless commensals)include: 1. Mouth Amoeba: E. gingivalis 2. Intestinal Amoeba: Entamoeba coli, Endolimax nana, Iodamoeba butschlii The other species are important because they may be confused with E. histolytica in diagnostic investigations. Entamoeba histolytica Amoebae Kingdom : Animalia Sub kingdom : protozoa Phylum : Sarcomastigophora Sub phylum : Sarcodina Class : Lobosea Sub class : Gymnamoebia Order : Amoebida Sub order : Tubulina Genus : Entamoeba Species : histolytica LIFE CYCLE OF Genus Entamoeba E. histolytica passes its life cycle in only one host. It is a direct life cycle. E. histolytica shows two different stages. 1. Trophozoite (the growing or feeding=tropho stage). 2. Cystic stage (inactive form). Entamoeba histolytica trophozoite Size: 10-60 approximately 20 μm in diameter. Nucleus with central karyosome and fine peripheral chromatin. Cytoplasm well differentiated into outer clear ectoplasm and inner granular endoplasm. Trophozoites are Irregular in shape due to pseudopodia which are extension of the ectoplasm and used by the parasite for moving. Entamoeba histolytica trophozoites Encystation: This is the process of transformation of trophozoite to cyst and occurs inside the lumen of the intestine of an infected individual in order to protect itself while coming out to the outside environment. During encystation, the parasite becomes rounded and is surrounded by a highly refractile membrane, called the cyst wall. Entamoeba histolytica cyst Size: 12-15 μm in diameter. Rounded with well developed cyst wall. Nuclei: 1-4 identical to that of trophozoite (with central karyosome and fine peripheral chromatin). Cytoplasm: may contain chromatoid body= cigar shaped bodies. Entamoeba histolytica cysts Life cycle of Entamoeba histolytica Infection by Entamoeba histolytica occurs by ingestion of mature cysts ( infecive stage) in contaminated food, water, or hands (mode of infection). Excystation occurs in the small intestine (due to lysis of cyst wall by trypsin in the small intestine) AFTER PASSING THE HCL MEDIA OF THE STOMACH. Trophozoites are released, which migrate to the large intestine. The trophozoites multiply by binary fission. Trophozoites of E. histolytica live in the mucous and submucous layers of the large intestine of man( HABITAT). Cysts are formed to face the unfavorable conditions. Cysts and trophozoites are passed in feces. Cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool. The cysts can survive days to weeks in the external environment Because of the protection conferred by their walls, and are responsible for transmission. Trophozoites passed in the stool are rapidly destroyed once outside the body, and if ingested would not survive exposure to saliva and the gastric environment Pathology According to the immune state of the patient. The trophozoites may fail to attach the intestinal mucosa if the immune system is intact. In Some patients where the immune barrier is disrubted trophozoites attack the intestinal epithelium but remain confined to the intestinal mucosa (intestinal disease), causing flask shaped ulcers and intestinal manifestations. In other cases trophozoites penetrate the mucosa and travel through the bloodstream to cause pathologic manifestations in extra- intestinal sites such as liver (most common site), brain, and lungs (extraintestinal disease). Clinical Presentation A wide spectrum of clinical picture according to virulence of the species and the immunity of the host: luminal amebiasis asymptomatic infection. Invasive intestinal amebiasis(flask ulcers) dysentery, colitis, appendicitis. Invasive extraintestinal amebiasis liver abscess, peritonitis, pleuropulmonary abscess, and cutaneous amebic lesions. Pathology Flask shape ulcer in the large intestine Histopathology AMOEBIC LIVER ABCESS( Extraintestinal Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains evade the complement-mediated lysis in the bloodstream. Trophozoites that reach the liver create unique abscesses with well-circumscribed regions of dead hepatocytes surrounded by few inflammatory cells and trophozoites. Secondary bacterial infection may occur on the lysed tissue inside the cavity with formation of pus. Diagnosis A. Clinical diagnosis: History and clinical picture (symptoms: diarrahea with mucous and blood abdominal pain---Signs; abdominal tenderness maximum at lower abdomen, pallor, tachycardia) B. Laboratory diagnosis: Stool examination: Macroscopic: Stool is bulky offensive with mucous and blood. Microscopic: Identification of cysts and trophozoites in stool specimen is the most specific method for diagnosing E. histolytica. This can be done in the intestinal amebiasis. Immunological diagnosis. It is a diagnostic method that relies on antigen-antibody reaction for detection of the disease, it is either: Indirect Antibody detection it depends on finding antibodies specific to E.histolytica in patient serum. It is most useful in patients with extraintestinal disease (i.e., amebic liver abscess) when organisms are not generally found on stool examination. Direct Antigen detection it depends on finding antigen specific to E.histolytica in patient serum. Treatment Amebic dysentery Metronidazole 500–750 mg three times a day for 5–10 days Amebic liver abscess Metronidazole 750 mg 3 times a day orally for 10 days, was reported to be curative in 90% of patients with amebic liver abscess. patient compliance=The degree of adherence of a Pt to a prescribed drug, according to which his response to this drug will be determined Non compliant patient. Who will not follow the correct dose or course of treatment will be more liable to suffer from recurrence or complication Entamoeba histolytica Disease : intestinal and extraintestinal amoebiasis. Habitat: large intestine Definitive host: Human. Infective stage: cysts….never trophozoites Diagnostic stage: cysts or may be trophozoites. Clinical picture: amoebic dysentery (intestinal amoebiasis) complication--- Extraintestinal manifestation. Diagnosis: Detection of cysts or may be trophozoites in stool samples of patients. sero-diagnosis ( detection of antibody response) is very helpful in extraintestinal amoebiasis since it is a closed lesion in most cases (no cysts or trophozoites in stool). Treatment: Metronidazole is the drug of choice. Balantidium coli Life cycle Life cycle Cysts are the stage responsible for transmission of balantidiasis (infective stage). The host most often acquires the cyst through ingestion of cysts in contaminated food or water(mode of transmission). Following ingestion, excystation occurs in the small intestine, and the trophozoites colonize the large intestine(habitat). The trophozoites reside in the lumen of the large intestine of humans and animals, where they replicate by binary fission. Trophozoites undergo encystation to produce infective cysts in order to withstand unfavourable conditions. According to the immune state of the patient some Trophozoites invade the mucosa of the colon and secrete proteolytic enzymes with the action of the cilia causing extensive destruction of tissues with occurrence of flask shaped ulcer like that of E. histolytica. Mature cysts are passed with stool trophozoites may pass in stool in severe diarrhea. Clinical Presentation Symptoms can be Clinical disease Clinical severe in occurs only when manifestations, debilitated persons Most cases are the resistance of when present, with perforation of asymptomatic and host is lowered by recurrent the intestine and the person is said predisposing factors dysentery, peritonitis but never to be healthy like malnourishment, abdominal extraintestinal carrier concurrent parasitic pain colic, abscesses are or bacterial formed (due to infection. tenesmus and large size of the weight loss. trophozoite) Diagnosis A. Clinical diagnosis: History and clinical picture. B. Laboratory diagnosis: Macroscopic: Stool is bulky offensive with mucous and blood. Microscopic: Identification of cysts and trophozoites Motile trophozoites are found in diarrheal stool and cysts are found in formed stools. The trophozoites can be easily recognized by their large size, kidney shaped macronucleus, and small micronucleus and rapid motility. The cysts can also be recognized in the formed stools by their round shape and presence of their large kidney shaped macronucleus and small micronucleus. Diagnosis A. Clinical diagnosis: History and clinical picture. B. Laboratory diagnosis: Stool examination: Macroscopic: Stool is bulky offensive with mucous and blood. Microscopic: Identification of cysts and trophozoites in stool specimen is the most specific method for diagnosis. Immunological diagnosis. Indirect Antibody detection is most useful in patients with fibrosed ulcers Direct Antigen detection may be useful in addition to microscopic diagnosis in detecting parasites. Treatment Balantideal dysentery Metronidazole 500–750 mg three times a day for 5–10 days Balantidium coli Disease : intestinal balantidiasis. Habitat: large intestine. Clinical picture: Balantidial dysentery. Definitive host: Human. Infective stage: cysts….never trophozoites Diagnostic stage: cysts or may be trophozoites. Diagnosis: Detection of cysts or may be trophozoites in stool samples of patients. Biopsy in closed lesions. Treatment: Metronidazole is the drug of choice. Giardia duodenalis(intestinalis) Giardia duodenalis (G.intestinalis) It is the most common protozoan pathogen and is worldwide in distribution. Giardiasis is the most common cause of water-borne, parasitic diarrhea. Giardiasis is the most common parasitic cause of traveler's diarrhea through contaminated water Giardia lamblia exists in two forms, an active form called TROPHOZOITE, and an inactive form called CYST. The inactive cyst, can exist for prolonged periods outside the body, Cysts are resistant forms and can survive several months in cold water, so it is responsible for spread of infection (infective stage) The trophozoite cannot live long outside of the body, therefore it cannot spread the infection to others. Mode of infection 1. Contaminated water (the cyst stage is resistant to chlorine). 2. Ingestion of improperly washed undercooked vegetables and fruits. 3. Accidental swallowing of water during swimming in contaminated water in pools and spa. 4. Faeco-oral route from asymptomatic carrier. 5. Autoinfection from contaminated hands 6. Mechanical transmission by house fly. Life cycle of Giardia intestinalis Life cycle of Giardia intestinalis Giardiasis Infection occurs by the ingestion of cysts in contaminated water, food, or by the fecal-oral route (contaminated hands)(mode of infection). G. lamblia lives in the duodenum and upper jejunum and is the only protozoan parasite found in the lumen of the human small intestine. In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites). Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk. and is responsible for causing the signs and symptoms of giardiasis. Encystation occurs as the parasites transit toward the colon (unfavourable condition). The cyst is the stage found most commonly in non-diarrheal stool, while trophozoites are found in diarrheal stool in which time is not enough for encystation. Cysts can survive in water, for example in fresh water lakes and streams. As a result, giardiasis is the most common cause of water-borne, parasitic illness. Giardia lamblia trophozoite and cyst Giardia lamblia trophozoites Trophozoite. A. Ventral view; B. Lateral view; C. Quadrinucleate Cyst Pathogenesis Infective dose is 10–100 cysts. G. lamblia is typically seen within the crypts of duodenal and jejunal mucosa. It does not invade the tissue, but remains tightly adhered to intestinal epithelium by means of the sucking disc. The main pathology is damage of the epithelial brush border of intestinal mucosa causing extensive and chronic changes in the villous architecture interfering with their main function which is absorption of all essential nutrients. Mal-absorption of fat, protein, carbohydrates and all fat soluble vitamins. Clinical picture According to the state of immunity clinical picture ranges from asymptomatic, to severe malabsorption syndrome. Asymptomatic infected individuals are considered active carriers who transmit the infection to others with no symptoms. Symptomatic individuals suffer from a wide range of symptoms: 1. Malabsorption of fat leads to fatty diarrhea (steatorrhea), and flatulence(abdominal distention). 2. Malabsorption of protein leads to hypoproteinemia and edema. 3. Signs of vitamin deficiency due to malabsorption of fat soluble vitamins 4. Increase motility leads to dull epigastric or colic. 5. Children may develop chronic diarrhea, malnutrition weight loss and growth retardation. Diagnosis A. Clinical diagnosis: History of traveling and clinical picture. B. Laboratory diagnosis: Stool examination: Stool is offensive odor, pale colored ,fatty, and floats in water(lentil Macroscopic: soap appearance)with no blood. Microscopic: Identification of cysts and trophozoites in stool specimen is the most specific method for diagnosis. Duodenal aspirate examination (string test); if microscopic examination is negative in patient in whom giardiasis is highly suspected Immunological diagnosis. Indirect Antibody detection in serum or stool (detection of copro antigen). Direct Antigen detection may be useful in addition to microscopic diagnosis in detecting parasites. Duodenal aspirate examination (string test); string test involves swallowing a string with a weighted gelatin capsule, to obtain a sample from the upper part of the small intestine. The capsule is swallowed and one end of the string is taped to the side of the patient’s face. The capsule dissolves in the stomach and the string, which is weighted at its distal end, passes into the duodenum. Following a period of approximately 4 hr, the string and any adsorbed gastrointestinal fluid is withdrawn through the mouth. Any bile, blood, or mucus attached to the string is examined under the microscope as a wet preparation for the presence of the trophozoites. Treatment Appropriate fluid and electrolyte balance is critically important and is considered first line of treatment in any diarrheal disease. Metronidazole 250-500 mg three times a day for 5–10 days. Tinidazole as a single oral dose of 1 gm for adults. Different in pathology between Entamoeba histolytica and Giardia intestinalis Entamoeba histolytica pathology Giardia intestinalis pathology