Introduction to Parasites - Bonnie Buxton Ph.D. - PDF

Introduction to Parasites Part 1: The protozoans Bonnie Buxton, Ph.D.  Parasites Covered in This Lecture Protozoans Helminths Amoeba Trematodes Naegleria fowleri Schistosomes Entamoeba...

Introduction to Parasites Part 1: The protozoans Bonnie Buxton, Ph.D.  Parasites Covered in This Lecture Protozoans Helminths Amoeba Trematodes Naegleria fowleri Schistosomes Entamoeba Cestodes histolytica Taenia solium Ciliates Nematodes Not discussed Ascaris sp Flagellates Hookworms Giardia Enterobius Sporozoans vermicularis Plasmodium  Recommended Reading and Learning Objectives https://www.cdc.gov/dpdx/az.html Appropriate chapters in Murray’s Medical Microbiology Learning objectives Be able to define every term used in this ppt Identify the type of parasite (protozoan (which type) or helminth- which type) Describe each step of the life cycle, making sure to understand how humans are infected, how the infectious forms survive in the environment if applicable Identify the infectious and diagnostic forms by name and image Identify the geographic distribution Describe the pathogenesis of the infection- how does the organism cause disease Describe the clinical manifestations of infection Be able to answer all questions posed in the ppt  Whys study parasites? Do parasitic infections occur in the US? Rural areas without sewer systems- rely on septic tanks which must be emptied after several years If septic tanks are not emptied, sewage backs up causing leakage on ground and into homes News story 2017: Hookworm, a disease of extreme poverty, People install pipes to carry is thriving in the US south. sewage 30+ feet away from their Why? house and empty on the ground Studies have shown hookworms, round worms, Strongyloides in such environments America's dirty divide News story 2021 A deadly parasite that burrows into the body through bare feet could be multiplying in this US community  Why study parasites? They do occur in the US, especially associated with poverty They are found in other countries to which US citizens travel for: Work Pleasure Medical or aid missions Military deployment  Generalities about parasites Eucaryotic organisms in a variety of phyla Much more variable group compared to viruses, bacteria or fungi Tremendous size variation Often very complex life cycles Often zoonotic Helminths (worms) often generate eosinophil response, protozoa (single-celled organisms) do not.  Types of Parasites Protozoa Single cell organisms Helminths (worms) Trematodes- flat worms Cestodes- tape worms Nematodes- round worms Arthropods Blood-sucking arthropods – mosquitoes, ticks, lice often discussed in Parasitology.  Parasitic Protozoa Major groups Intracellular Amoebas Extracellular Flagellates Life cycle forms: Ciliates Trophozoites Sporozoa Cysts Sporozoites Merozoites Gametocytes Schizonts Amoebas Causing Human Disease Naegleria fowleri Free-living amoeba Highly fatal infections Entamoeba histolytica True parasite Highly pathogenic, invasive disease Case In August, a 9 year old boy developed fever and a persistent right sided headache. Three days previously, he had been swimming in a farm pond. The following day he became very drowsy and developed a stiff neck. A lumbar puncture done in the emergency room showed evidence of inflammation consistent with meningoencephalitis. Mobile amoebas were seen on a wet mount of the CSF.  Case continued The child became unresponsive after 2 days hospitalization. A CT scan showed a lesion in the right frontal lobe and diffuse cerebral edema. Naegleria fowleri infection was suspected. Despite appropriate anti-microbial therapy, the child died after 4 days. Autopsy revealed N. fowleri trophozoites in brain.  Trophozoites cultured from CSF Naegleria fowleri Amoeba Free living Causes rapidly progressive, highly fatal meningoencephalitis What is the life cycle of this organism? Brain tissue at autopsy- large cluster of N. fowleri trophs with destruction of surrounding tissue Life Cycle of free-living amoeba, Naegleria fowleri  Case A 28-year-old man who had served in the Army for 6 years had a 2 year history of intermittent blood-tinged diarrhea. He had served in Somalia, Panama, Afghanistan and Kuwait. Sigmoidoscopy and barium enema studies revealed pseudopolyps in the colon, consistent with inflammation of the bowel. Fecal exam revealed cysts and trophozoites of the causative agent.  Entamoeba histolytica cys Pathogenic amoeba t Human pathogen- no animal reservoir Worldwide distribution, especially developing countries Associated with intestinal and extra-intestinal disease Diarrhea Toxic megacolon Abscesses in liver, brain, lung Two stages- cyst and trophozoite Cyst is infectious form, stable in the environment Troph is form that replicates, cannot survive in environment trophozo ite  Entamoeba histolytica Trichrome stain of Entamoeba histolytica trophozoites in amebiasis. Two diagnostic characteristics are observed. Two trophozoites have ingested erythrocytes (large black structures), and all 3 have nuclei with small, centrally located karyosomes. Life Cycle of Entamoeba histolytica cys t trophozo ite Global Importance of Entamoeba histolytica Found worldwide, especially in developing countries Causes 50 million cases of diarrhea and >100,000 death/yr globally annually, especially among children Infection does not result in sterilizing immunity-re-infections common and disabling Associated with areas of poor community sanitation, without access to clean water Also associated with overcrowding and poor personal hygiene ie, hospitals for intellectually or developmentally disabled Pathogenesis and Potential Outcomes of Entamoeba histolytica Infection  Summary of Pathogenesis of Symptomatic Entamoeba histolytica Infection Ingestion of cyst in fecal contaminated water or from fecal-contaminated hands Cyst releases trophozoites after stimulation with gastic acid in stomach Most infections are asymptomatic- parasites in lumen of intestine, cysts shed in formed feces; survive in environment for days to weeks In symptomatic infections (~10%), trophozoities invade intestinal wall, replicate, release cytotoxins killing intestinal epithelial cells and inflammatory cells attracted to area; Results in intestinal inflammation and hemorrhage with cramping abdominal pain, bloody diarrhea; histopath –s ee flask-shaped ulcers- see next slide Trophs can invade through intestinal mucosa, travel through blood to other sites and continue to replicate, kill tissue and form abscesses Most common extra-intestinal sites are liver and brain Entamoeba histolytica- be able to recognize these diagnostic forms Cyst with 4 nuclei visible Trophozoites  Protozoa: Parasitic Flagellates Giardia lamblia Intestinal parasite Causes diarrhea, malabsorption Found worldwide including US Trichomonas vaginalis Genital infection, spread sexually Causes genital discharge (urethritis, cervicitis) Worldwide distribution Leishmania sp Several species causing disfiguring skin infection or highly fatal infection of internal organs Transmited by sandflies Found in middle east, Africa, parts of South America  Case A 12 year old boy presents with a 1 week history of malaise, weakness, abdominal cramps and diarrhea. Upon questioning, the boy admits to feeling bloated and having excessive flatulence. The stool is grey or light colored and greasy or fatty in appearance (steatorrhea) and is not visibly bloody.  Case continued Physical exam reveals he has normal vital signs, no evidence of dehydration but does have general abdominal tenderness. History reveals that 2 weeks ago, he returned from a week long boy scout camping trip. He admitted to drinking from a stream during the long hike to the camp site.  Case continued Stool samples were taken for bacterial culture, occult blood and ova and parasites exam (O&P). Stool cultures failed to find any pathogenic bacteria and no visible or occult blood was found in the stool. 3 O&P exams with 3 different stool collected over a two day period were negative, however, the forth revealed actively motile trophozoites in fresh diarrhetic stool (see photograph)  Giardia lamblia Life forms: Trophozoites Found in watery stool Actively replicating form, does not survive in environment Cysts Found in more formed stools Does not replicate Can survive in the environment Infectious form Life Cycle of Giardia  Life Cycle of Giardia Infection occurs by the ingestion of cysts in contaminated water, food, or person-to-person by a fecal-oral route (hands or fomites) Encystation occurs as the parasites transit toward the colon. 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 Both cysts and trophozoites can be found in the feces (both are diagnostic stages) The cysts are hardy and can survive several months in cold water. Cysts are also resistant to cholination in municapal water treatment The cyst is the stage found most commonly in nondiarrheal feces Cysts are resistant forms and are responsible for transmission of giardiasis. While animals are infected with Giardia, their importance as a reservoir is unclear.  Epidemiology of Giardia Transmitted in fecal contaminated water, contaminated fruit or vegetables or fecal-oral route between people In US often associated with fresh water streams Beaver may be a reservoir Crowded conditions, institutions, poor community sanitation Worldwide distribution Cause of traveler’s diarrhea More common in warmer climates Infections more common in children In US associated with day care centers  One traveler’s description: Exploring South America A Long, Bad Day It had been a horrible day. The worst part was that it was not yet over. As I queued for customs and immigration in Caracas, I could feel the turbulence building in my bowels….I was stricken with the most virulent, utterly pungent, long-lasting case of flatulence that I had ever experienced. How ironic that I should suffer from this problem after almost three months of gastrointestinal good fortune in Ecuador, Peru, and Bolivia…. When I exited the plane and saw the lines of people waiting to get their passports inspected and stamped, I panicked…. Dragging a near lethal fart behind me like a heavy duffel bag, ……. http://www.jetcityjimbo.com/samerica/sa13_longbad.shtml  Pathogenesis of Giardiasis Excystation occurs in stomach with exposure to gastric acid Trophs are released in duodenum and jejunum, multiply by binary fission and attach to intestinal villi, causing flattening of the villi Small numbers of parasites may cause asymptomatic infection In heavy infections, parasites can cover mucosal surface of small intestine, lead to malnutrition, inability to absorb fat –soluble vitamins, weight loss Leads to mucosal inflammation without necrosis Malabsorption, especially of fats, secondary to decreases in absorptive area Leads to foul-smelling, watery, fatty stools  Diagnosis of Giardia Cyst in stool sample Fecal O&P- may need to be repeated Trophs intermittently present in diarrheic stool Cysts intermittently present in formed stool Antigen detection tests also available- should not take place of trophozoite O&P exam A PCR test is also available cyst  Case A 42-year-old male aid worker who recently returned from rural Uganda presents to the ED with high fever and confusion. His wife indicates that while in Uganda he took chloroquine to prevent malaria, but she is concerned that he has the disease anyway. A peripheral blood smear confirms that he is infected with Plasmodium falciparum, a cause of malaria. What kind of parasite is Plasmodium sp. How did he become infected? Why did he become infected when taking malaria preventative? Malaria Etiology: Plasmodium sp. Protozoan/Sporozoan Intracellular in hepatocytes and RBCs Species affecting humans P. vivax P. ovale P. malariae P. falciparum Impact of Malaria 300-500 million infections per year worldwide 1-2 million deaths/yr primarily in children 95% of deaths due to P. falciparum Huge humanitarian and socioeconomic impact in affected countries Life Cycle Clinical Manifestations of Malaria Incubation period 1-2 weeks Prodrome of flu-like illness, headache, anorexia, photophobia, headache, malaise Classic signs: high fever (103-106F), chills, rigors- due to host reaction to rupture of RBCs, with release of toxic hemoglobin and other cellular debris, and release of the parasite antigens which lead to host secretion of TNF and IL-1. Chills fever, rigors reappear cyclically in most infections (every 48-72 hours) P. vivax and P. ovale: every 48 hours P. malariae: every 72 hours P. falciparum: merozoites released daily- fever and chills are constant CNS involvement or renal involvement can occur in P. falciparum infections with increased fatality rates  P. vivax, P. ovale and P. malariae infections P. vivax most prevalent, geographically widespread species infecting humans Both P. vivax and P. ovale replicate in young RBCs (newly developed from reticulocytes) P malariae replicates in older RBCs Both P. vivax and P. ovale form hypnozoites (dormant form)- found in liver Hypnozoites can begin to replicate Schizont that emerged from a weeks to years after apparent hypnozoite in the liver recovery, leading to relapse Additional drug (primaquine) is needed for treatment of hypnozoites (see treatment) P. falciparum Most severe infection Many strains are resistant to chloroquine Replicates in erythrocytes of any age More parasite replication and RBC lysis compared to other species  Complications of P. falciparum infection Infection with this species can lead to death due to CNS and kidney damage; particularly lethal to pregnant women and their fetuses Falciparum-infected RBCs express parasite antigen pfEMP-1 on membrane. pfEMP-1 binds to ICAM-1 on endothelial cells leading to RBC blockage of small vessels This blockage blocks blood supply to organs leading to organ damage – explains severe damage in kidneys, CNS and placenta Organ damage also secondary to RBC lysis and accumulation of toxic hemoglobin breakdown products Urine of patient with P. falciparum -related kidney damage. Known as blackwater fever  Diagnosis of Malaria Identification of parasites in Giemsa-stained blood smears Can see: ring forms gametocytes trophozoites schizonts P. falciparium in RBCs Multiple ring forms in a single cell Schizont Banana-shaped gametocyte P. vivax in RBCs Ring forms Schizont Gametocyte (ruptured, releasing merozoites)  Treatment/Control/Prevention of Malaria Treatment and prevention complicated by chloroquine resistance in P. falciparum Many of same drugs are used for treatment and prophylaxis Malaria vaccine just recommended by WHO in 2021 Sporozoite antigen of P. falciparum attached to hepatitis B virus surface antigen (HBsAg) Mosquito Control Insecticides Avoid Mosquito Bites Insect repellents Bed nets- highly effective and inexpensive! Case In January 2006, a 26-year-old Peace Core volunteer in Botswana had onset of urinary frequency. In April 2006 she was evaluated by a Peace Corps medical officer. Although a urinalysis was normal, she was treated with antibiotics for a presumed bacterial cystitis. The patient had been stationed in an arid area of southern Botswana for the past two years and reported no recreational freshwater exposure in that country. However, in December 2005 she had snorkeled during a 7-day period at a lake in Malawi. Case continued Because of progressive symptoms, including incontinence, lower extremity pain, and difficulty walking, in August she was referred to a medical center in South Africa for further evaluation, where an MRI scan revealed a mass in her spinal cord. A tumor was suspected, and she was evacuated to the United States for neurosurgical consultation. Case continued A schistosomiasis FAST-ELISA was positive at CDC, and an immunoblot confirmed the presence of antibody to Shistosoma hematobium. Routine stool and urine examinations, a 24-hour filtered urine examination, and a rectal biopsy specimen were all negative for schistosome eggs. What kind of organisms are schistosomes? How might she have become infected with schistosomes? What kind of diseases are they associated with? Trematodes “Flukes” 1cm size Complex life cycles Snails (usually fresh water) are intermediate hosts Examples of Parasitic Trematodes Fasciola hepatica- liver fluke Chronic, intermittent biliary obstruction and inflammation Schistosoma sp. blood flukes Abdominal pain, hepatosplenomegaly, bloody diarrhea S. haemotobium can result in a transverse myelitis with flaccid paraplegia Paragonimus westermani Oriental lung fluke Chronic cough, hemoptysis Schistosomiasis Schistosoma haematobium Schistosoma mansoni Schistosoma japonicum Schistosoma Life Cycle Schistosoma sp. Geographic Distribution Schistosomiasis-Clinical Manifestations Acute illness Serum sickness-like illness due to immune response to egg production Chronic illness Depends on species Due to immune response to eggs Granulomatous lesions interfere with organ function  Schistosome Granulomas S. mansoni egg in liver S. hematobium eggs in bladder wall Diagnosis Identification of eggs in stool or urine S. heamatobium S. japonicum S. mansoni  Treatment (FYI) Praziquantel Control Education regarding disease acquisition Improved sanitation Bio-control agents (predatory snails) Use of molluscicides Drainage of marsh areas  Cestodes Tape worms strobila Up to 1 meter in length Complex life cycles scolex Morphology of Cestodes scolex proglottids egg Examples of Parasitic Cestodes Taenia saginata- beef tapeworm Taenia solium- pork tapeworm Echinococcus granulosis Echinococcus multilocularis  Case A 4-year-old immigrant boy from Mexico developed a new onset seizure. Imaging of the brain revealed multiple lesions in the parietal region His serum was positive for antibodies to Taenia solium. What kind of organism is this? How might the boy have become infected? What other important organisms belong to this group?  Taenia solium Pork tapeworm Worldwide distribution, especially is pork-producing developing countries Pigs- intermediate hosts Humans-definitive hosts Adult worms in intestine, usually asymptomatic Humans can also become infected with cysticerci (larval form) Cysts can occur in numerous sites CNS invasion= neurocysticercosis Life Cycle of Taenia solium Note- this life cycle is complex and confusing- pay close attention to the details in notes pages- testable! Neurocysticercosis Oncospheres arise from ingested eggs migrate through intestine wall Encyst in tissues throughout body Cysts reach mature size in 3 months (can be several cm in diameter) In CNS, cause: seizures, hydrocephalis, cranial nerve damage, visual impairment  Neurocysticercosis Cysts in parietal region Cyst in 6 yr old boy. Peru. Diagnosis and Treatment of Neurocysticercosis Diagnosis aided by CT and MRI Serologic tests for anti-cysticercal antibodies Treatment (FYI): praziquantel, albendazole Nematodes Round worms Ascaris Macroscopic adults; microscopic eggs and larvae Various species infect intestines, blood, lymphatics and tissues Morphology of Nematodes Adults Eggs (diagnostic) Ascaris sp. Examples of Parasitic Nematodes Ascaris lumbricoides –human roundworm Toxocara canus- dog roundworm Necator americanus- human hookworm Wuchereria bancrofti- filarial worm Dirofilaria immitis- dog heartworm  Case A 5-year-old child from rural Thailand presents with severe abdominal pain. Abdominal obstruction is noted by imaging, and surgery is performed to resect the obstructed bowel. Worms of the species Ascaris lumbricoides were found to be the cause of the obstruction  Ascaris lumbricoides Large roundworm (30cm in length) Most common human parasites worldwide, including US 25% of world’s population (>1 billion people) are infected Prevalent in poor community sanitation, especially areas where Note how big this human waste is used as fertilizer thing is! See also picture on previous Ascaris suis from pigs can also cause slide! You may see this worm in Q bank human infections with identical questions etc symptoms. Life Cycle of Ascaris lumbricoides  Life Cycle Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces. Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed. Upon reaching the small intestine, they develop into adult worms. Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.  Clinical Features During the lung phase of larval migration, pulmonary symptoms can occur (cough, dyspnea, hemoptysis, eosinophilic pneumonitis). Infections may cause stunted growth in children High worm burdens may cause abdominal pain and intestinal obstruction as in this case. Migrating adult worms may cause symptomatic occlusion of the biliary tract. Most commonly, adult worms cause no acute symptoms.  Laboratory Diagnosis Fertilized eggs Microscopic identification of eggs in the stool is the most common method for diagnosing intestinal ascariasis. Note thick, bumpy wall around mature egg containing larva Developing embryo Egg with larva  Case A 2-year-old boy (“Mr. Cranky-Pants”) presents to his pediatrician for a normal well-child visit. His mother reveals that the child has been unusually cranky for several weeks, often waking up at night crying. She is also concerned that his anal area is reddish and irritated although she washes it carefully when changing his diapers. The pediatrician conducts a “scotch-tape test” and finds eggs of the roundworm parasite, Enterobius vermicularis. How common is this infection? How did this child become infected? What other round worms are of medical importance?  Enterobius vermicularis The most common helminthic infection in the United States (an estimated 40 million persons infected). Also called human pinworm. Adult females: 8 to 13 mm, adult male: 2 to 5 mm.) Humans are the only hosts of E. vermicularis. Worldwide distribution Infections more frequent in school- or preschool- children and in crowded conditions. Enterobiasis appears to be more common in temperate than tropical countries. Life Cycle of Enterobius vermicularis Life Cycle of Enterobius vermicularis Eggs are deposited on perianal folds. Self-infection occurs by transferring infective eggs to the mouth with hands that have scratched the perianal area. Person-to-person transmission can also occur. Transmission: May also be acquired through surfaces in the environment that are contaminated with pinworm eggs (e.g., curtains, carpeting, contaminated clothes or bed linens). Following ingestion of infective eggs, the larvae hatch in the small intestine and the adults establish themselves in the colon. The time interval from ingestion of infective eggs to oviposition by the adult females is about one month. The life span of the adults is about two months. Gravid females migrate nocturnally outside the anus and oviposit while crawling on the skin of the perianal area. The larvae contained inside the eggs develop (the eggs become infective) in 4 to 6 hours under optimal conditions  Clinical Features of Enterobiasis Most common in children 5-9 yr, and their parents. Enterobiasis is frequently asymptomatic. The most typical symptom is perianal pruritus, especially at night, which may lead to excoriations and bacterial superinfection/cellulitis. Occasionally, invasion of the female genital tract with vulvovaginitis and pelvic or peritoneal granulomas can occur. Colonoscopy showing worm Other symptoms include anorexia, irritability, and abdominal pain. Laboratory Diagnosis Microscopic identification of eggs collected in the perianal area is the method of choice for diagnosing enterobiasis. Best done in the morning, before defecation and washing, by pressing transparent adhesive tape ("Scotch tape test", cellulose-tape slide test) on the perianal skin and then examining the tape placed on a slide. Alternatively, anal swabs or "Swube tubes" (a paddle coated with adhesive material) can also be used. Eggs can also be found, but less frequently, in the stool, and occasionally are encountered in the urine or vaginal smears. Adult worms are also diagnostic, when found in the perianal area, or during ano-rectal or vaginal examinations.  Case A 2017 study of poor sewage sanitation in rural areas found many homes in Lowndes County, Alabama had no septic systems. Instead sewage from homes was carried by PVC pipes to ditches 30 feet from homes. Several children in Lowndes County, Alabama, were found to be anemic and stunted in their growth due to hookworm infection. The problem of poor community sanitation still exists in many rural, impoverished areas in the US as it does in 3rd world countries. FYI: Case Explained The “black belt” region of Alabama (so named because for the rich, black topsoil) is one of the poorest regions in the US. The population is largely African American and 30-40% of children live in poverty (data from 2019). Lack of sewer systems and high ground water levels lead to poor community sanitation, and helminth infections of children can still be found here.  Necator americanus and Ancylostoma duodenale The human hookworms include two species, Ancylostoma duodenale and Necator americanus. Globally, the second most common human helminthic infection (after ascariasis). Adult males are 7-11mm; females: 9-13 mm Worldwide distribution, mostly in areas with moist, warm climate. Hookworms of animals can penetrate the human skin causing cutaneous larva migrans, but do not develop any further (A. braziliense, A. caninum) Life Cycle of Hookworms  Life Cycle of Hookworms Eggs are passed in the stool , and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil , and after 5 to 10 days (and two molts) they become become filariform (third-stage) larvae that are infective. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the human host, the larvae penetrate the skin and are carried through the veins to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed. The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall with resultant blood loss by the host. Most adult worms are eliminated in 1 to 2 years, but longevity records can reach several years. Some A. duodenale larvae, following penetration of the host skin, can become dormant (in the intestine or muscle). In addition, infection by A. duodenale may probably also occur by the oral and transmammary route. N. americanus, however, requires a transpulmonary migration phase. Clinical Features of Hookworm Infection Iron deficiency anemia due to blood loss is most common symptom Adult worms ingest blood, secrete anti-coagulase, release hyaluronidase and other hydrolytic enzymes, to degrade intestinal mucosa and blood vessels, resulting in blood extravasation. Nausea, vomiting and diarrhea, abdominal pain and nutritional and metabolic symptoms may occur Severe infections can cause delayed growth and poor intellectual development in children Local skin manifestations ("ground itch") can occur during penetration by the filariform (L3) larvae Respiratory symptoms can be observed during pulmonary migration of the larvae.  Diagnosis of Hookworms O&P exam: Microscopic identification of eggs in the stool is the most common method for diagnosing hookworm infection.  Parasites Covered in This Lecture Protozoans Helminths Amoeba Trematodes Naegleria fowleri Schistosomes Entamoeba Cestodes histolytica Taenia solium Ciliates Nematodes Not discussed Ascaris sp Flagellates Hookworms Giardia Enterobius Sporozoans vermicularis Plasmodium