Notes for Exam 2 – Parasitology | BIOL 4105, Study notes of Biology

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Other Flagellates Giardia lamblia and Trichomonas vaginalis  pathogens Chilomastis mesnili, Retortomonas intestinalis, pentatrichomonas hominis, Trichomonas tenax  commensals Usual mode of transmission= fecal contamination of food/water  T. vaginalis obvious exception to this Giardia lamblia  Order= Dipolomonadida; Family= Hexamitidae  Host= humans  Distribution is worldwide  Host niche= small intestine o Only parasitic protozoan of small intestion o Most common flagellated parasite of GI tract  Direct life cycle  Morphology: trophozoite and cyst (infective stage) o Trophozoite= pear-shaped, 2 nuclei (both are transcriptionally active), 8 flagella; adhesion disc on ventral surface o Cyst= 4 nuclei  Encystment occurs in large intestine  Transmission: often water-borne o Cyst must be ingested o Reservoirs= wild and domestic mammals (dogs, cats, beavers, sheep, cattle) o Children most susceptible  problem in day cares Soruces of Giardia Cysts 1. Any water supply (*Chlorination does not kill cysts) 2. Unwashed fruits and veggies 3. Objects: diapers, toys, bathroom fixtures 4. Post bathroom usage (no hand washing) Giardiasis  Inapparent carrier: assymptomatic (cyst passers)  Acute: profuse watery diarrhea o Stomach cramps o Bloating and foul smelling flatulence o Rotten egg taste in mouth  Chronic: prolonged diarrhea episodes o Malabsorption  weight loss o Hypoproteinemia o Fat soluble vitamin deficiency Pathology for Giardia  No tissue invasion  Feed on mucus secretions (doesn’t feed on you)  Physically interferes with nutrient absorption  For chronic giardiasis: flattened villi (malabsportion); steatorrhea (fatty stool)  Hosts develop protective immunity o IgA antibody involved o Can be reinfected Giardiasis Diagnosis  Cysts in fecal samples o May see only trophs in watery diarrhea  ELISA o Antigen capture= tests for antigens; distingues current infection o 1 sample enough o Dual kit: tests for both Giardia and Cryptosporidium  Can also do String test (not used often) Giardiasis Treatment (no alcohol consumption)  Flagyl (metronidazole)= TID for 5 days  Tindamax (tinidazole)= 1 dose  Furazolidone for children  Lots of fluids Prevention  Wash hands  Chlorination or idoniation of water  Filtration (pored with 1 micrometer or less)  Boil water if not potable  Wash fruits and veggies with treated water  Don’t engage in water sports for 2 weeks after diarrhea stops Trichomonads  Axostyle  Sarcocystis spp Schizogony  Multiple fission o Nucleus divides multiple times o Undergoes one cytokinesis o Results in multiple daughter cells from 1 parent  Called: o Merogony (merozoites) o Sporogony (sporozoites) o Gametogony (gametes) 3 Phases in Apicomplexan Life Cycle  Merogony (within host)  Gametogony (within host)  Sporogony (usually outside host)  Sporozoites= infective stage o Contained within sporocyst  New host must ingest sporulated oocyst Eimeria oocyst: 4 sporocysts with 2 sporozoites each Isospora oocyst: 2 sporocysts with 4 sporozoites each Eimeria tenella (affects chickens)  Morbidity (number of people that get sick) and mortality (those who get sick and die)  both are high  Niche= ceca (epithelial cells of lining)  Ingestion of sporulated oocysts in feed or water  Merogony occurs in epithelial cells of cecum  Gametogony in same place  Sporogony outside host  Host defenses o Shed cells o Fecal express o macrophages **Unsporulated oocysts aren’t infective Isospora belli  Only isospora species to infect man  Distribution: tropical (not USA)  Profuse watery diarrhea, abdominal cramping, fever o Immunocompromised individuals o Infants and young children  Least common of intestinal coccidian that infect humans  Niche: small intestine  Diagnosis: oocysts in fecal sample  Treatment: TMP-SMX (Bactrim) Cyclospora cayetanensis (fairly new)  Worldwide  considered emerging pathogen  Niche: jejunum of small intestine  Explosive watery diarrhea o Cramping abdominal pain o Vomiting o Persists several weeks  Self-limiting  Sources: o Contaminated food o Contaminated water  Oocyst= 2 sporocysts with 2 sporozoites each  Very refractile- not easily visualized in unstained fecal sample  Acid-fast stain  see reddish oocyst; quite large  Diagnosis: acid fast stain of fecal smear (look at size bar; very large compared to others)  Treatment: same for isospora Cryptosporiididae Family  Worldwide  Zoonosis (only host specificity is vertebrates)  mammals, birds, reptiles, fish o Not host specific  2 species infect humans o Cryptosporidium parvum  Immunocompromised, infants and elderly at risk  No apicoplast  apicoplast genes still present but they have been moved to the nucleus  Direct life cycle o Sporogony occurs inside  internal sporulation o Don’t go inside cell; created extracytoplasmic “intracellular” environment  Does have host cell membrane around it but can’t be recognized by lysosomes within cell o 2 types of oocysts with no sporocysts  only 4 sporozoites  Thick-walled= go out in feces; very resistant to environment; infective stage  Survive weeks to months in moist envirobnments  Resistant to chlorination  Thin-walled= attach to epithelial cells; rupture in GI tract  autoinfection (never left body)  Re-infection within host o Merogony and gametogony: within fused microvilli of epithelial cells  entire GI tract (host niche) Clinical Cryptosporoidosis  Profuse watery diarrhea, abdominal pain, nausea and vomiting  In immunocompetent host o 1-2 weeks duration o Self-limiting  In immunocompromised host o Becomes chronic and persistent o Can be fatal (includes infants and elderly)  Pathology o Fluid and electrolyte loss  Asymptomatic carriers o No clinical signs o Shed infective oocysts  can infect others  Route of transmission 1) Water-borne: lakes, swimming pools, water parks, contaminated municipal water supply 2) Food-borne: filth flies, poor hygiene of infected handlers 3) Day care centers 4) Lab techs (oocysts in fecal samples infective Diarrhea lasting longer than a week  Giradia lamblia or Cryptosporidium parvum Cryptosporoidosis Diagnosis  Acid fast stain of fecal sample (much smaller size of oocyst)  ELISA kits o Dual kit for both Cryptosporidium and Giardia  Intestinal biopsy o After negative results from less invasive diagnostic techniques Crypto Treatment  Nitazoxanide (Alinia): not effective for immunocompromised (HIV)  Static drug Congenital Toxoplasmosis (mom is not at risk; can’t say that fetus will get parasite if mom is infected)  Tachyzoites can cross placenta o Mom must have acute toxo with parasitemia after she becomes pregnant  Infection in fetus o Varied clinical picture o Gestation period at time of infection o Infective does size  1st trimester= infection rates lowest but parasite damage greatest  3rd trimester= infection rates highest but parasite damage least  Born symptomatic (classic triad of signs) o Hydrocephaly o Intracranial calcification of cysts o Chorioretinitis  Born asymptomatic but problems later o Seizures o Mental retardation o Visual problems  Born asymptomatic  no effects at all Possible Severe Consequences to Fetus (won’t necessarily happen)  Mental retardation  Blindness  Seizure  Hearing loss  Death (stillbirths, abortions) Recrudescent Toxo  Immunocompromised; loss of immunity (bradyzoites  tachyzoites)  Brain  encephailits (cerebral toxo)  Heart  mycocarditis  Eye  chorioretinitis (ocular toxo)  In GI tract, liver, lung, skin possible Toxo Diagnosis  Antibody detection (IgG and IgM)  PCR- detection of o CSF, ocular fluid o Prenatal and neonate: amniotic fluid IgM can’t cross the placental barrier to so detection of IgM means it came from fetus IgM + and IgG-  wait 2 weeks for immune response  IgG+ also indicates individual just got infected  If not positive, then false positive and no infection IgM typically produced only in first contact Ability of T. gondii to evade host cell defesnses:  Intracellular defenses Rx-  Fetal toxoplasmosis o Spiramycin- DOC o Given to mom to cross placenta to the fetus o Antibiotic  Immunocompromised: o Pyramethamine- sulfadiazine o Folic acid antagonists o Cannot give during pregnancy due to the risk of developing spina bifida and other birth defects  Congenitally infected neonate (after birth) o Pyramethamine-sulfadiazine + folinic acid o A preventable disease o Cool all meat: Freezing, salting, smoking, pickling with not reliably kill bradyzoites Wash raw fruits and veggies Pregnant women- wear gloves when gardening  Don’t clean cat litter box  If you have to make sure you do it everyday, because the chances are you are not going to have any sporulated oocysts  If you have cat keep it indoors  Wash hands immediately after stroking cat- that is free roaming o Oocyst can cling to fur Sarcocystis spp  Herbivorous intermediate host  Carnivorous definitive host  Not pathogenic in humans  Humans- definitive host- Sarcocystis hominis  Infective stage for intermediate host o Sporozoites in sporocyst- (definitive host don’t shed oocyts!) o Internal sporulation and ruture of thin walled oocyst in gut o Sporocysts with sprozoites out in feces  Infective stage for definitive host o Bradyzoites in tissue cyst You can see sarcocysts with the naked eye Apicomplexans II- Chapter 9 Organisms that cause malaria and malaria- like diseases Genus- Plasmodium Species- falciparum, vivax (ovale), malariae Genus- Babesia Species- bigemina, microti, divergens, canis Plasmodium spp  One stage must be blood of vertebrate host  Heteroxenous o Cannot use the term definitve host or intermediate host  P. malaria  quartan malaria  P. ovale  mild tertian Paroxysm= sudden onset of recurrent signs of symptoms  Ex: periodic spasms of fever and chills in malaria  Based on what the parasite is doing within RBCs Rigor  Cold stage: paroxysmal chills with high fever and shivering  Hot stage: sense of being very hot with severe headache, dizziness, nausea, etc o Fever has subsided  Profuse swelling Classic Clinical Signs  Cyclic fever (104-106)  Chills  Headache  Myalgia (ache all over- flu like)  Malaise and lethargy  Anemia (parasite killing RBCs) o Intravascular hemolysis o Bone marrow suppression  Enlarged liver and spleen  Nausea, vomiting, diarrhea (small children)  Jaundice Two Major Factors for Pathogenesis 1) RBC destruction 2) Host inflammatory responses Malignant Tertian Malaria  Most prevalent type (over 50%)  Most pathogenic o Highest mortality rate  Especially in children, pregnant women, elderly o High fatality rate in all if untreated  Can recrudesce but not relapse Why is P. falciparum the most pathogenic? a) 40,000 merozoites per sporozoite b) Infects all ages of RBCs (25% RBCs infected is fatal) o Greatest parasitemia levels o Greatest destruction of RBCs  hemolysis of both infected and uninfected RBCs c) Deep vascular schizogony o RBCs sequester in capillaries of major organs d) Drug resistance Deep vascular schizogony  This is why only early ring stages and gametocytes seen in peripheral blood  Infected RBCs sequester in blood vessels of major organs o Capillary beds congested with infected RBCs o Parasite induces protein “knob” on RBC membrane o Helps bind parasite to endothelial cells of capillary o Pregnant woman: sequester in placental vessels Why sequestration?  Parasite defense  prevents premature destruction of infected RBCs by spleen  Allows parasite to continue life cycle development Tertian malaria: merogony is every 48 hours Only forms seen in peripheral blood  Early rings o May be multiple rings in 1 RBC  Banana-shaped gametocytes (which are infective stage for mosquito) o Appear about 10 DPI o Viable for 4 days Organs become black from hemozoin as a result of RBCs being destroyed Falciparum Malaria (Malignant Tertian)  Severe anemia (worst than in all other malarias) o RBC infected and uninfected destroyed o Loss of iron because it’s bound to hemozoin (waste product) o Decreased production of RBCs  Bone marrow suppression  No RBCs being produced  Can’t recycle iron in hemozoin  Decrease in WBC production  Host inflammatory response Possible consequences of falciparum  Severe malaria  means severe parasitic infection  Cerebral malaria (check with Nicole) o Always fatal if untreated (within 24-72 hours) o Doesn’t cause permanent damage o Coma symptoms  unconscious with no response to pain  hyperthermia (up to 108o)  hyperparasitiemia= peripheral parasitemia very high  convulsions/seizures o Coma pathogensis: 2 hypothesis A. Mechanical  hypoxia B. Biochemical  nitric oxide effect  Renal failure Results of Massive Hemolysis of RBCs 1) Severe anemia and leucocytopenia o Very low RBC and WBC numbers o Caused by hemolysis and bone marrow suppression 2) Hemoglobinuria 3) Jaundice o Liver can’t handle overload of hemoglobin breakdown products o Liver can’t metabolize all the bilirubin o Excess bilirubin is deposited into tissues Kidney  Filters soluble substances  only things dissolved in plasma  Can’t filter insoluble or particulate substances o Carriers defective version of hemoglobin  G6PDH deficient individuals  Beta thalassemia Immunity  Acquired (antibody mediated) o Infants: antibodies in breast milk o Weaned children are the most susceptible  Premunition= low level of parasitemia blocks new infection  Complete (sterile) cure  susceptible again Why does CMI not work?  RBCs don’t have HMC1 molecules and can’t be sent to cytotoxic T cells Diagnosis of Malaria  Microscopy: stained peripheral blood smears  ELISA:L antigen capture; optimal o Measures parasite enzyme (positive= active infection)  IFA: antibody detection in patient serum  PCR Any prolonged fever of unknown origin (regardless of travel history)  malaria should be considered Treatment of Malaria  Quinine (no resistant yet) o Not used much because of serious side effects o Reserved for severe cases and/or resistant malaria specied o Selectively cidal  Kills meroizites schizonts  No effect on sporozoites, liver stages or gametocytes o Major side effects  Ringing in ears (tinnitus)  hearing loss  Increase in RBC hemolysis  Increase insulin output by pancreas  hypoglycemic shock  Fetotoxic (causes abortions)  Cardiotoxicity  can cause serious cardiac arrythmias  DOC  cerebral malaria o Severe P. falciparum infection o Rapidly absorbed and distributed in body  Chloroquine o Cidal= kills parasites o Synthetic quinine related drug but without its side effects o P. falciparum resistant worldwide  Mefloquine  Atovaquone + proguanil (Malarone)  Primaquine o Kills hypnozoites meaning the liver stages (no effect on P. falciparum or P. malaria) o No effect on RBCs  Artemisinins (plant derivatives) o Artesunate o For cerebral malaria and can’t take quinine/quinidine Antibiotics in combo with quinine in chloroquin restant falciparum cases  Ex: clindamycin, doaxcycline, tetracycline o Attacks mitochondial DNA  Apicomplexans have apicomplast with its own DNA Recommendations for Malaria Treatment (US)  Assume falciparum malaria until ID’d  Immediate treatment with o Atovaquone-proguanil o mefloquine  If severe: quinine with doxycycline or clindamycin  If not falciparum, can use chloroquin CDC Travel Recommendations 1) Prophylaxis: before, during and after trip  don’t skip doses 2) Sleep under netting 3) Clothing that covers 4) Repellants (DEET) Prevention in Endemic Regions  Vector reduction  Minimize contact with mosquitos  Chemotherapy Babesia spp  Biological vector= tick  Zoonosis  Disease ranges from mild rever to life threatnening  Human medicine  Emerging infections  Veternivary medicine  been around for a while Babesia bigemina  Host: cattle (primarily), humans  Vector: Boophilus annulatus B. microti  Host: humans, rodents  Vector: Ixodes scapularis (deer tick) B. duncani  Host: humans  Vector: unknown B. divergens  Host: cattle, humans (Europe)  Vector: Ixodes ricinus B. canis  Host: dogs  Vector: Rhipicephalus sanguineous (brown dog tick) and Dermacentor variabilis (American dog tick) General Life Cycle: Vertebrate Host  Infective stage= sporozoite  Invade RBCs (no liver cycle)  Feeds on hemoglobin (but no hemozoin)  Binary fission  merozoites  Intrvasuclar hemolysis  Gametogony: gametocytes (in vertebrate host)  ray bodies (gametes) (in tick host)  Freezing, drying are fatal (will kill miracidium) Miracidium  Ciliated and free-swimming  Needs snail host quickly  Mucous trail of snail attracts it  Some species require snail to eat it Sporocyst  Metamorphosis of miracidium in snail  No mouth or digestive system  Germinal sac (asexual reproduction Redia  More advanced germinal sac  has oral sucker  Mouth, pharynx, short gut o Feed on host tissues, sporocysts, other redia  Produce more embryos  daughter redia Cercaria  Juvenile stage  Mouth and digestive e system  Penetration glands at anterior to: o  Can be infective stage for vertebrate hosts Metacercaria  Encysted form of metacercaria o Intermediate host (if 2nd int host) o On aquatic vegetation (if no 2nd int host)  Must be ingested by vertebrate host Value of metacercarial stage  Longer viability  Mans of transmission to definitive host How trematodes infect definitive host  Direct penetration  cercaria  Ingestion on metacercaria (either in intermediate host or on plants) 3 reproductive strategies (all are sexual reproduction and require fusion of sperm and egg) 1) Self-fertilize (ex: Fascioloa hepatica) 2) Cross fertilize (Paragonimus westermani) 3) Separate sexes Schistosomes Intermediate hosts: snail Definitive hosts: humans, other mammals, birds, turtles, fish Mature in vascular system (blood) of host Schistosomiasis  Distribution: Africa, Asia, South America, Caribbean  Chronic, debilitating S. heomatboium, japonicum( far east), mansoni (Caribbean, South America  only one in new world) Dioecious= separate sexes  Pair up in human host  Remain paired for life (in copula)  Dimorphic o Males: larger, shorter  Has gynecophoral groove (where female stays) o Females: smaller and longer Host niche  Schistosoma haemitobium (can never cause liver problems) o Unrivary bladder veins  causes urinary tract disease o No known animal reservoirs  Schistosoma japonicum o Superior mesenteric veins (small intestine)  cause intestine and liver disease o Zoonosis o Major reservoirs: cattle, water buffalo  Schistosoma mansoni o Inferior mesenteric veins (large intestine)  causes intestine and liver disease o No animal reservoirs Schistosome eggs  S. haematobium: ovoid with terminal spine  S. mansoni: ovoid with lateral spine (on the side)  S. japonicum: round with rudimentary spine (small bump)  not always seen Schistosome Life Cycle Egg (requires water)  miricidium(each will give rise to only one sex) sporocyst (2 generations) cercaria  adult  Intermediate host: snail  Definitive host: humans (by cercaria)  3 month cycle from egg to egg Snail hosts (no snails capable of vectors for human schistosome spp)  S. mansoni: Biomphalaria spp  S. japnicum: Oncomelania spp  S. haematobium: Bulinus spp Schistosome Cercaria  Attracted to skin secretions (amino acids and fatty acids)  Process: o Attach to skin o Release chemicals to signal others o Creep to hair follicle o Penetrate skin: loses tail, sheds outer coat insde  30 min to get inside host  Sheds outer coat when it enters host. Why? o Cercaria has to first survive in hypertonic environment Schistosomule (little schistosome)  Capillaries  Heart  lung  heart  Liver  venous plexus  Stay in liver for about a month o Mature and mate (pair up) Host vs. Parasite  Evades host defenses by camouflage  Can cause retrograde UT problems  Possible cancer development Very Severe Chronic Schistosmiasis  Small number infected with S. mansoni or S. japonicum  Liver fibrosis extremely sever o Enlarged liver o Severe portal hypertension (increased resistance to blood flow in liver vessels) o Greatly enlarged spleen  End result= chronic passive congestion of liver o Ascites (fluid accumulation in abdominal cavity) Hepatic portal vein does not become blocked by eggs  Eggs are microscopic and plug up small vessels such as capillaries Resistant to Blood Flow in Liver  Passive congestion of liver  Formation of ascites and major shunting of eggs to spleen  Starting problems in spleen  End result: ascites, hepatomegaly andsplenomegaly S. mansoni  pipe stem fibrosis in liver around blood vessels Impaired Blood Flow and Portal Hypertension  Liver produces collateral circulation  Allows eggs to bypass liver and get to lungs  Loss of functioning lung tissue  Pulmonary hypertension  Heart failure can result Egg production  S. japonicum is most pathogenic and its eggs are more likely to go to (ectopic) abnormal locations (brain lesions)  May have few to none in feces with a chronic infection Squamous cell carcinoma of bladder  caused by S. haematobium Complications by S. Haematobium  Pain on urination  Hematuria= whole blood cells in urine (develops gradually)  Eggs trapped in bladder wall  calcification and fibrosis of bladder wall  loss of bladder elasticity  increased frequency of urination  Polyp formation (granuloma forms around eggs and trapped them)  Common sequelae: bladder cancer (squamous cell carcinoma of bladder) Hydronephros and hydroureter: backup of urine from bladder; causes extreme pressure to cause renal failure Diagnosis of Schistomiasis  Find eggs: urine (haematobium), feces (japonicum and mansoni)  Buildup of chronic fibrous tissue in gut and bladder prevents eggs from passing out so not found in feces or urine o Rectal or bladder biopsy to find trapped eggs  ELISA o Not good for japonicum o Specificity varies according to species o Sensitivity poor  Best time to collect urine sample is around noon  when egg excretion is maximal Transmission Requirements (2)  Fecal/urine contamination of water sources  Snail vector present  Risk factors o Traditions and customs o Human wastes for fertilizer o Streams as human waste disposal sites o Wading, bathing, playing in contaminated water **S. mansoni is the only one found in the new world (South America) Treatment  Praziquantel DOC o Effacicius (1 dose kills all adults) o Low number of side effects o Low cost o Mechanism of action: dual effect 1. Disrupts parasite’s tegument (“unmasks” worm)  causes them to lose protein 2. Disrupts flow of calcium ions in nervous system of worm killing it Immunity= Concomitant  Type of protective immunity  Takes years to develop  No effect on adults  Stops cercaria prevents new infections and an increasing worm burden Removal of adults (sterile cure)= host susceptible to reinfection Prevention/Control  Education  Cure infected individuals  Vector control (difficult and some chemicals not eco-friendly)  Vaccines (not yet achieved) Cercarial dermatitis  Swimmers itch/Swamp itch/nutria itch o Infection w/ cercaria of other schistosomes o Maculopapular rash o No fluid  You can be infected by schistosomes in USA. It isn’t made for humans so you will kill it but it still is annoying humans cannot get schistosomiasis o Infection with cercaria; killed by immune response Trematodes  Hermaphroditic  Most self-fertilize  Intermediate host= aquatic snail Liver flukes  Fasciola hepatica  Fasciolopsis buski (exception: intestinal fluke)  Fasciola gigantic  Fascioloides magna Fasciola hepatica (“liver rot”)  Sheep liver fluke  Worldwide  common in south/west USA  asymptomatic  False positive for infection with Fasciola hepatica  Result of eating infected beef or sheep liver with eggs o Eggs pass on through GI tract o Eggs out in feces  Recheck after liver free diet for 2 weeks Why can you not get infected from meat with eggs?  Not next host for development  Requires snail Prevention  Reservoirs keep pastures infected  Snail control is difficult o Ability of snail host to aestivate in dry conditions  Prevent fecal contamination of water sources o difficult  Best way: don’t eat unwashed fresh veggies Fasciola gigantic  Similar shape to hepatica but much larger  Same life cucle Fascioloides magna Liver fluke  Similar to F. hepatica (life cycle and size) o Except: in liver tissue (not bile ducts)  Doesn’t infect humans  Deer, elk, caribou= normal hosts  Cattle  dead end hosts  In sheep  die  Produces melanin pigments (tracks black in liver) Fasciolopsis buski  Common in orient o Endemic regions: 60% infection rate in people  Found in humans and pigs  Largest fluke to infect humans (can be 3 in. long)  Fecal contamination of water  Ingest metacercaria on aquatic plants o Water chestnuts o Bamboo o Lotus o Water caltrop  Host niche: GI tract (small intestine)  Prolific egg producer Clinical Signs F. buski  Light infection (asymptomatic)  Heavy infection o Abdominal pain o Diarrhea with mucus  Lots of mucus in feces often 1st indication there is a gut irritation from something  could be from a parasite or from something else o Interfere with digestion/nutrient absorption Pathology Caused by F. buski 1) Direct trauma o Feed on SI epithelial cells o Cause ulcers in muscoa o Interfere with digestion and absorption (children  hypoproteinenmia) 2) Gut obstruction o In very heavy infections can block intestine 3) Immunopathologic: allergy to worm products (secreted/excreted o Has caused fatal anaphylaxis in a few individuals Why a persistant high infection rate in endemic regions?  Aquatic vegetation: economically important  Fertilizer used F. buski Diagnosis  Eggs in feces o Indistinguishable from F. hepatica eggs  Gut damage and diarrhea Treatment  Praziquantel o Early and light  success o Chronic and heavy Prevention  Boil veggies for a few seconds before eating  Proper disposal of feces Transmission: human feces in water