Notes for Parasitology Exam I
Notes for Parasitology Exam I Biol 4330
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Parasitology Exam I Tropical disease overview/ Basic principles and concepts Protozoans toxoplasmagondii (gets into the brain of cats). Trypanosomes brucei (blood, African sleeping sickness), cruzi (South America, shagas disease; initial symptoms and then real disease doesn't happen until about ten years later). Malaria plasmodium, high fivers, transmitted by mosquitos Giardia treat water while camping/hiking Trichomonas Leishmania can either be internal and interpreted with macrophages, mucus membranes, Helminths worms cestodes tapeworms Nematodes roundworms, heartworm, pinworm, hookworm, wachereria bancrfti, (elaphantis). Filarial worms, ascaris Ectoparasites fleas, mites, ticks Leech TRematodes Bot fly larvae Tropical disease overview/ Basic principles and concepts Parasitology ● Understanding parasites themselves ● Understanding relationships of parasites with their hosts ● Basic characteristics, what unites them ● What diseases they cause, if they cause disease, how they interact with the host. Symbiosis ● Living together ● Both partners benefit ● Any two organisms living in close association ● Symbionts ● Parasites are the symbionts that benefit, the host usually does not. Type of Symbiosis ● Mutualism ○ Benefits both partners ○ Usually obligatory ○ Termites and their Protozoa in their intestines 1 ● Commensalism ○ Eating at the same table ○ One partner benefits, the host is neither benefited or harmed ○ Facultative or obligatory ○ Sharks and the remoras ● Parasitism ○ One of the participants harms its host or lives in expense of the host ○ Can be ectoparasites or endoparasites ■ Ticks ectoparasites ■ Ascaris endoparasite ○ Trypanosomes live in blood stream and feed on glucose Parasites ● Organisms that grow, feed, and are sheltered on or in a different organism while contributing nothing to the survival of that organism ● Obligatory relationship for the parasite. ○ Without the host, the parasite will not survive ● Can be unicellular or multicellular ● Some reproduce inside their host, some do not. ● Live in highly enriched environments. ● Have deficient metabolic pathways and depend on the host for nutrients. ● Many have complex life cycles ○ Multiple stages within different hosts ○ Plasmodium, takes different forms Types of Hosts ● Definitive ○ Parasite reaches sexual maturity ○ If there is only one host ○ Where the parasite reproduces if there is no sexual reproduction ● Intermediate ○ Required for parasite’s development but parasite does not reach sexual maturity ● Transport ○ No parasite development but it remains ineffective ● Reservoir ○ An animal that harbors an infection that can be transmitted to humans ○ Can be pets, partially domesticated animals ○ Trichanallous is transmitted by wild animals Adaptations to Parasitism ● Ability to invade host ● Ability to evade host immune response ○ Parasite can change what they look like ○ Plasmodium ● Ability to find particular niches within host ● Loss of some metabolic capacities ● Loss of some systems ● Altered energy generation strategies ● Increased specialization of attachment structures 2 ○ Tapeworms, anterior end grasps intestinal wall. ● Increased reproductive potential ○ Ascaris eggs are extremely resilient to environmental change. Parasitology and Human Welfare How many people are affected Where these diseases are found What is being done about it Parasitology and Human Welfare ● Prevalence ○ The number of cases of a disease at a given time ○ Percent of hosts infected ● Incidence ○ The number of new cases of a disease per unit time ● Numbers have not changed much ● Infections in the US ● Emergence of the new disease agents ○ Cyclospora cayetanensis ○ Drug resistance ■ Parasites are incredibly adaptive ● US citizens normally acquire diseases by traveling to other countries ● Financial losses ○ DALE (disease altered life expectancy) ● Improvements sometimes increase parasitic disease ● Parasitologist’s dilemma ○ Cure disease, they die of something else Parasites of Domestic and Wild Animals ● Wild animals usually do not experience massive death due to parasitic infections ● Domestic animal living conditions ○ Coccidiosis ○ Protozoan that infects chickens and can wipe out entire barn within a few weeks ● Zoonosis ○ Transmission to humans of parasites normally found in wild and domestic animals ○ Trichinella spp. ■ Infects pig ■ Eat undercooked pig. ○ Lyme disease ■ Normally infects deer ■ Get bite by deer tick Protozoa Helminths 3 Differences unicellular multicellular Multiply rapidly within the Do not proliferate in the definitive host definitive host Possible Chemotherapeutic metabolism associated with energy metabolism Targets growth and division Nutrient uptake Neuromuscular junction Some anabolic pathways Approaches for the Control of Parasitic Infections ● Immunization ○ Not many, difficult to find ● Chemotherapy ○ Many are also hard on the host ○ Based off of arsenic ● Improvement of sanitation conditions ○ Take away potential of fecal oral contact ● Control of vector populations ○ Insects that transmits them ○ Mosquito nets to prevent malaria ● Elimination of reservoir hosts Rational Chemotherapy ● Exploit differences in neurophysiology between host and parasite ● Interfere with essential energy metabolism ● Affect essential biosynthetic reactions ● Interfere with essential cellular structure Geographical Distribution of Parasites Human African Trypanosomiasis (T. Brucei) South of the Sahara Desert, the Fly Belt Tsetse fly; can't have cattle because they can infect cows. African Sleeping Sickness Chagas’ Disease Reduviid bug, kissing bug South America/Mexico Leishmania Leishmaniasis Kalaazar:enlargement of organs, found in Middle East, sub saharan africa Cutaneous (old world) same area Cutaneous (new world) South America 4 Malaria Primarily Africa (subsaharan), Southeast Asia, South America, Middle East One million deaths per year Hookworm Africa, South America, Asia, Middle East Grows in through foot Onchocerca Falalarial worm Cutaneous tissue, constant itching, cause inflammatory response Brazil, Africa Loa loa distribution Africa Wuchereria Bancrofti Elephantis is Parasitic Protozoa ● Unicellular ● Extremely diverse ● Specialized organelles ● Plasma membrane modifications ● Varying methods of locomotion ● Cause some of the most severe and life threatening of parasitic diseases Form and Function of Protozoa ● Many have multiple nuclei ● Plasma membrane ○ Many more than one as part of the pellicle (part of the cytoskeleton) ○ Alveoli pockets or spaces bound by epithelium ○ Undulating membranes ■ Trypanosomes and trichomonads ○ Glycocalyx ■ Glycoproteins surface coat Organelles ● Mitochondria ● Golgi apparatus (dictysomes) ○ Multiple large parabasal bodies ○ Many be part of the kinetosomes a (basal bodies of the flagellum) ● Microbodies ○ Spherical membrane bound organelles with a dense granular matrix 5 ○ Found in plants and animals, but most have peroxisomes Microbodies ● Peroxisomes ● Hydrogenosomes ○ trichomonads ○ Produce molecular hydrogen ● Glycosomes ○ Unique to kinetoplastida ○ Contain glycolytic enzymes ● Extrusomes ○ Release contents outside organism ○ Found in a variety of organisms ○ A variety of extrusomes Locomotion ● Flagella ○ Axoneme + outer sheath ○ Arises from the kinetosomes ○ Undulating membranes ● Cilia ● Pseudopodia ○ Temporary extensions of the cell membrane ○ Amebas Reproduction ● Asexual ○ Binary fission ○ Multiple fission (schizogony) ■ Some amoebas and apicomplexa ■ The nucleus and other organelles divide repeatedly before cytokinesis ■ Schizonts,meronts, or segmenters ○ Budding ● Sexual ○ Meiosis followed by the Union of two haploid cells (gametes) ■ Gametes can be the same or different ○ Conjugation ■ Only nuclei unite ● Encystment ○ Secrete a resistant covering and enter a resting stage or cyst ○ Provides protection against unfavorable conditions ○ Return to favorable conditions stimulates excystation Feeding and Metabolism ● Feeding ○ Photosynthetic or heterotrophic ■ Usually particle feeders ○ Food vacuoles ■ Digestive organelles that form around any ingested food ■ Pinocytosis and phagocytosis 6 ○ Metabolism ■ Biochemistry varies depending on environment ■ Anaerobic ● No TCA, electron transport but still need to oxidase NADH ● Types of end products; ;active, ethanol, succinctly, acetate, short chain fatty acids Introduction to Kinetoplasta: Chapter Five Kinetoplasta ● Includes the trypansomes and leishmania ○ Cause diseases such as African Sleeping Sickness, Chagas’ diseas and leishmaniasis ● Two Families ○ Bodonidae ■ Free living or parasite of fish and invertebrates ○ Trypanosomatida ■ Human and veterinary pathogens ■ Difficult control problems ■ Dramatic pathological effects Unique Features of Trypanosomes ● Many are heteroxenous ○ Have multiple hosts ● Flagellar pocket ○ Many functions including Endocytosis and exocytosis ○ Flagellum Exits the cytoplasm ○ Involved in immune evasion ● Paraxial Rod ● Undulating membrane some species, characteristic feature of most of them ● Some have a glycocalyx ● Glycosomes ○ Evolved from peroxisomes ○ Organelles where glycolytic reactions take place ○ Processes such as Beta oxidation, lipid biosynthesis ● RNA editing ○ A short piece of RNA is spliced into every mRNA molecule ● Kinetoplast ○ A DNA containing region within the mitochondria ○ Besides the kinetosome at base of the flagellum ○ Contains a network of linked DNA circles ■ 2050 copies of 22kb Maxicircle DNA ● Act like mitochondrial DNA ● Encode for mitochondrial proteins ● Ribosomal RNA ■ 1020,000 1kb Minicircle DNA ● Guide RNA 7 ● Involved in RNA editing process ● Heterogeneous and ever changing ● Cannot function without its transcription ■ During certain life cycle stages, there are different sorts of editing. Family Tropanosomatida ● All have a single nucleus ● Either elongated with a flagellum or rounded with a short flagellum ● Hemoflagellates ○ During one stage they live in blood or fixed tissues of vertebrates ● Have different morphological forms ○ Different in shape and position of the kinetosome and kinetoplast General Structure Mitochondrian is extremely long and extends most of the length of the body. Trypanosome Morphological Stages: Trypomastigote ● definitive stage of the life cycle ● Undulating membrane ● Posterior kinetoplast ● What the bloodstream form of the parasite looks like and the infective stage. 8 Trypanosome Morphological Stages: Promastigote ● Flagellum extends forward ● Anterior kinetoplast ● Found in the insect vector ● Flagellum is relatively short Trypanosome Morphological Stages: Amastigote ● short flagellum 9 ● spheroid body ● Short flagellum ● Tiniest eukaryotic cells ● Definitive stage of leishmania Trypanosome Morphological Stages: Epimastigote ● anterior kinetoplast ● Short, undulating membrane ● Less mobile than trypomastigotes ● Found in insect and mammalian hosts 10 A comparison of the different life cycles Circle arrow indicates asexual reproduction Antigenic Variation ● VSG: variant surface glycoprotein expressed in bloodstream forms; Tryps have ~1000 genes for VSG ● Only 1 VSG is expressed at a time ● Produced/released through the flagellar pocket then covers the surface coat ● Allows the parasite to stay one step ahead of the immune response (also seen in other parasites including Plasmodium and Schistosoma). 11 Genus Trypanosoma ● Salivaria ○ Parasites develop in the anterior portion of the insect gut ○ Includes: Trypanosoma brucei ○ Transmitted by saliva ● Stercoraria ○ Parasites develop in the hindgut of the insect ○ Includes: Trypanosoma cruzi Trypanosoma brucei ● distributed throughout tropical Africa (15N to 25S) ● Area known as Fly Belt ○ Covers 4.5 million square miles ○ 60 million people at risk ● 3 subspecies: ○ T. B. Brucei, Tb. Gambiense, Tb.rhodesiense Trypomastigote in blood smear ● kinetoplast posterior to the nucleus ● Found in all species of Trypanosoma ● Reproduces in the vertebrate host Glossina ● genus for tsetse fly ● 23 species recognized ○ 20 act as vectors 12 ● Typically 714 mm long Epimastigote of Trypanosoma ● kinetoplast is anterior to the nucleus ● Stage that reproduces in the vector gut African Trypanosomiasis (sleeping sickness) ● causative agent: Trypanosoma brucei ● Vector: tsetse fly (Glossina sp.) ● Major disease species: ○ T.b.brucei nagana in cattle/horses ○ T.b.rhodesiense acute form in humans (Eastern Africa) ○ T.b.gambiense chronic form in humans (Western Africa) Trypanosoma brucei rhodesiense ● found in Eastern Africa; acute form (no somnambulism patients die within months) ○ Rapid onset and death within months ● Transmitted by woodland species of tsetse fly (Glossina morsitans). ● Chancre is more obvious than in gambiense (disappears within 12 weeks) ○ Chancre is a swelling of the bite area. ● Reservoir hosts are game animals ● Characterized by high parasitesmia ● Winterbottom’s sign (swollen lymph node at the base of the neck). ● Fevers, generalized pain, cramps, weakness, headaches, rapid weight loss, can have heart involvement and affect ability of muscle to maintain integrity, some nervous system involvement but only if it enters the cerebrospinal fluid and patients usually die before that, lymph nodes. Trypanosoma brucei gambiense ● causes chronic infection (leading to CNS involvement and somnambulism) ● Found in western/central Africa ● TRansmitted by riverine species of tsetse fly (Glossina palpalis). ● Chancre is less obvious than in rhodesiense ● Reservoir hosts are domestic animals (pigs, dogs, cows) as well as antelope ● Do not get diagnosed until they've had the disease for years ○ By the it's too late ● Extreme exhaustion, mental fog, decreased coordination, tongue tremor, paralysis, convulsions. Parasites are everywhere. Person will fall into a coma and die of the symptoms of the disease ● Treatment is not effective. Will die within about three years Trypanosoma brucei brucei ● causes “nagana” in ruminants (cattle/horses/antelope) ● Found in the fly belt of Africa, which has been rendered useless for cattle farming Trypanosoma brucei Group ● Salivarian trypanosomes ● Complex life cycle within 2 hosts: mammal and tsetse fly (Glossina sp.) ● Vertebrate bloodstream forms: 13 ○ Long, slender trypomastigotes ■ Multiply rapidly in bloodstream ■ Anaerobic metabolism ■ Just use fermentation due to the high levels of glucose in the bloodstream. ○ Short stumpy trypomastigotes ■ aerobic metabolism ■ Infective to the tsetse fly ■ Ready for insect gut African Trypanosomiasis Prevalence: 60 million at risk Incidence: 10,000 new cases/year Symptoms: intermittent fever as the parasitesmia cycles Diagnosis: demonstration of parasite in blood, cerebrospinal fluid (late), bone marrow; Winterbottom’s sign Pathology: myxedema, wasting disease, neuropathy Treatment ● 1st stage:Pentamidine (T. b. gambiense) or Suramin (T.b. rhodesiense) ● 2nd stage: melarsoprol an arsenical, Difluoromethylornithine (DFMO), DMFO+nufurtimox ● Control: need to try to remove habitat and prevent contact (problemsreservoir hosts, lots of good vectors and suitable habitats); since tsetse flies are day feeders… Grazing livestock at night? Chagas’ Disease: New World Trypanosomiasis ● Causative Agent: Trypanosoma cruzi ● Vector: reduviid bug (triatoma) ● Resovoir: lots of mammals (dogs/cats...and armadillos!) ● Portion of lifecycle is in blood, untreatable once it enters cells. ● First described in 1909 by Dr. Carlos Chagas in Brazil ● Transmission via dedication of metacyclic trypomastigotes with feces into wounds. ● Invasion of cells (spleen, liver, lymph nodes and all muscle cells). ● Transformation into amastigotes and formation of pseudocysts ● 20 million infected ● 90 million at risk ● 50,000 deaths annually 14 Shigoma: the initial bite of the kissing bug. Parasites prefer skeletal or muscular cells but will infect any type of cell. ● assassin bug/kissing bug/ vinchuchas ● Live in cracks in Adobe huts/thatched roofs ● Bugs tale nightly blood meal ● Find host via receptors on antennae (thermo mechano olfactory (10^3 sensillae) Trypomastigotes of T. cruzi. These forms often have a characteristic C shape Amastigotes (pseudocyst) of T. cruzi. Pathology of T. cruzi Acute Phase ● Chagoma red nodule formed as local inflammation ● Romana’s sign edema of conjunctiva and eyelid (50% of patients) ● Formation of pseudocysts ● Anemia, pain, chills, nervous disorders ● Death can follow within 1 month if heart is involved. Chronic Phase ● ● ● Results from nervous system disorders 1020 years post infection ● Pseudocyst rupture (release of trypomastigotes) ○ Heart failure ○ Megacolon ○ Megaesophagus ○ Death Pathology Summary ● fever, lymphadenopathy, hepatosplenomegaly ● Acute disease usually subsides spontaneously, but can be fatal with involvement ○ Heart: acute myocarditis 15 ○ CNS: meningoencephalitis ● Most common evidence of disease are cardiac and gastrointestinal sequelae many years after infection ○ Ventricular arrhythmias Diagnosis and Treatment Diagnosis: ● xenodiagnosis: triatoma new is allowed to feed on suspected patient; wait 2030 days then look for parasites in the gut ● Serology is poor (low Ab tire during acute phase) ● Blood smear is poor (low parasitaemia) Treatment: none for intracellular stages, so basically incurable ● must be early in infection ● Best mechanism is to prevent the disease ○ Improve housing ○ Pesticides ○ Screening of blood donations Leishmaniasis ● Causative agent: members of genus Leishmania ● Vector: the sandfly ● Prevalence: ~15 million cases ● Incidence: 1 million new cases/year ● More than 350 million people at risk ● Vertebrate is host primarily mammals ○ dogs, humans, primates ○ Zoonosis is commonly the infection for humans ● Widespread disease ● 88 different countries affected ● Foci in Africa, Middle East, Europe, South and Central America Three Major Disease forms: 1. Cutaneous: a. L. tropica (oriental sore) b. L. major c. L. mexicana (Chiclero ulcer) d. Can have potential secondary infection 2. Visceral: a. L. donovani (Kala azar) b. most every organ can be infected c. causes enlargement 3. Mucocutaneous a. L. brasiliensis b. Brazil (Espundia); Peru (Uta); Venezuela/Paraguay (Pian bois) c. rots the skin away 16 Leishmania displays 2 morphological stages: Promastigotes in the sandfly gut midgut/hindgut Transferred by saliva Amastigotes in vertebrate tissues Promastigotes of Leishmania sp. from culture ● grows in the vector ● injected into the human host when the vector feeds. ● promastigotes are approximately 25 micrometers in length Mastigote filled with amastigotes (25 micrometes) Immunology Challenges: 1. Parasites live in macrophages 2. Parasites reside in phagolysosomes that normally function to digest foreign particles 3. species of Leishmania differ from each other 4. Don’t fully understand how the human host contributes to the disease 5. Treatment may result in a new symptom that was not originally seen. How can Leishmania amastigotes live in macrophages without being killed? parasites are taken up into phagolysosomes parasites produce factors that disrupt normal macrophage function parasites down regulate production of reactive oxygen intermediates appear to decrease production of lysosomal enzymes produce specific inhibitors and alter vacuolar pH supress antigen presentation and Tcell activation by macrophages 17 With better understanding of these parasites, could these be genetically engineered to specifically target macrophages that induce the T cells that attact the myelin sheaths in MS? Cutaneous Leishmaniasis Old World (OWL) Caused by: L. tropica and L. major Transmitted by different species of Phlebotomus Other names: oriental sore and Delhi boil Middle east and Africa L. tropica found in densly populated regions in WEst/Central Africa, the Middle East/Mediterranean and India Lesion appears at bite mark (red papule) Ulcer appears (within 2 weeks); it is dry with a high number of amastigotes Ulcer can treat itself L. major similar to L. tropica but found in sparsely populated areas of Africa/Asia/Middle East lesion ulcerates quickly with a few amastigotes Diagnosis LD bodies (amastigotes) from ulcer Can self cure within 2 months to a year Treatment pentavalent antimonials like pentostam/glucantime (i.m. for a week) headache, pain, Miltefosine (hexadecylphosphocholine) cutaneous and visceral 95% cure rate in stage 3 originally developed for cancer patients orally Protective immunity inoculation in an inconspicuous location (esp. female children in ME) Cutaneous Leishmaniasis New World Disease is a zoonosis Causative agent: L. mexicana Transmitted by Lutzomiya Rodents are reservoirs Primarily impacts forest laborers like those working on gum trees (chicle) Chiclero’s uncler Will spontaneously self heal (within months) except on the ear hard to treat, does not respond well to drugs Visceral Leishmaniasis endemic in tropical areas Africa, Europe, South and Central America, Asia 18 droughts and famine, poor sanitation, scattered spread 95% found in Brazil, India, Sudan Kala azar Dumdum fever Causative agent: L. donovani Causes most serious disease: the parasites penetrate all the organs of the reticuloendothelial system: liver spleen bone marrow lymph glands Symptoms: initial fever/chills and malaise initial redness at bite site hyperplasia (compensatory) in spleen/liver… hepatosplenomegaly get decreased RBC production...anemia/wasting death will occur within 23 years without treatment Symtoms can occur within weeks up to a year Usually 23 months Diagnosis LD bodies in tissues/secretions (spleen puncture) Treatment Same as L. tropica plus bed rest and nursing care Relapse or PKDL (post kala azar dermal leishmanoid) can occur with inadequate treatment 12 years after initial treatment Cutaneous condition resulting from incomplete treatmenf of Kala Azar up to 20 years post infection seen in up to 60% of treated cases in the Sudan characterized by hypopigmented macules, papules, or nodules Mucocuaneous Leishmaniasis causative agent: L. brasiliensis Vector: lutzomyia espundia, uta American Leishmaniasis mostly western hemisphere 1st lesion at bite site heals within 615 months 2nd lesion develops in mucocutaneous tissues lips, palate, pharynx leads to gross disfiguration necrosis and secondary bacterial infection are common Same drugs as L. donovani albeit somewhat resistant course of treatment is extremely long tissue damage is irreversible 19 Giardia and Trichamonas Lumenal Protozoa Flagellates Giardia intestinalis (lamblia) Trichomonas vaginalis Amoebae Entamoeba histolytica Naegleria fowlerii (free living, not truly a parasite) Phylum Retortamonada Cosmopolitan in distribution Transmission Sexual Contact Oralfecal contamination Asexual reproduction Diagnosis demonstration of parasites in fecal smears or vaginal metabolism Anaerobic energy metabolism no mitochondria Infections treated with metronidazole 23 day dose at 12 doses/day some resistance Giardia intestinalis most common intestinal protozoan parasite cosmopolitan in distribution (anyone can be infected) Transmitted by swallowing mature cysts in contaminated water supply or food Outbreaks when animals like beavers and muskrats become infected any animal can serve as a reservoir, it just has to contaminate the water supply have an adhesive disk that attaches to intestinal wall. Cyst stage is the infective stage 40 species of giardia TRophozoites are small (12 micrometers to 15) long 2 nuclei; 2 median bodies, 4 pairs of flagella Adhesive dis on ventral surface No mitochondria, golgi, lysosomes or smooth ER. 20 Giardia Life Cycle TRophozoites live in the small intestine attach to host cells can interfere with absorption Can go to a relatively large number rapidly Cysts are found in the colon dehydration pass out with the feces cysts have two nuclei and go through a bit of maturation mature cyst has four nuclei extremely resistant Every cyst produces two trophozoites Trophozoites are not infective. Only cysts. is usually the form found in stool host becomes infected when cysts are injested Giardia metabolism aerotolerant anaerobes no mitochondria therefore no TCA or electron transport primary nutrient is glucose arginine as well B vitamins and our bile salts. store glycogen end products of metabolism are: CO2, ethanol, and acetate. Giardia Pathogenesis symptoms: increased mucus production, diarrhea, dehydration, intestinal pain, flatulence begin 12 weeks after infection heavy infection interferes with absorption of fats and other nutrients massive infections possible, as many as 14 billion cysts in a watery stool Antigenic variation 180 different variations do not lyse the cells they attach to. Usually not deadly. Giardia Epidemiology highly contagious 200 million people may be infected worldwide 21 ½ million new infections each year increased occurrence when wild animals become infected diagnosis: recognition of trophozoites or cysts in fecal smears Treatment metronidazole (flagyl) for one week whole family will be treated. 12 doses a day prevention is the best method sanitation Trichomonads flagellated protozoa of the vagina or urethra of females and the urethra of males transmission primarily by sexual intercourse normal acidity of the vagina inhibits infection parasites decrease the acidity; encourages growth no cysts characterized by: anterior tuft of flagella short undulating membrane axostyle Trichomonads Morphology two different variations Trichomonads Metabolism aerotolerant anaerobes degrade carbohydrates to acetate and lactate and CO2 Produce molecular hydrogen in absence of O2 hydrogenosomes No mitochondria Trichomonads Hydrogenosomes produce molecular hydrogen in absence of oxygen Species of Trichomonads Trichomonas foetus infection in cows and other large ruminants that causes spontaneous abortions Trichomonas tenax commensal that lives in the mouth cavity does not cause serious disease spread by kissing, sharing food/drinks Trichomonas vaginalis lives in the urogenital tracts of men and women. often asyptomatic T. vaginalis: Trichomoniasis one of the most common STDs worldwide distribution that affects 190 million per year USA 2.3 million infected Tropics 1040% of all females 22 Symptoms: females have inflammation with itching and copious white discharge males are asymptomatic; cause of persistent infections in females acute infections can become chronic with a lessening of symptoms 528 days of infection increases susceptibility to HIV and other STDs Diagnosis: identification of parasites in vaginal discharge Treatment: metronidazole for five days both sexual partners some resistance has been documented due to loss of two oxidoreductases Exam: covers all material includes: matching section (column of organisms and multiple answers) 2 large essay questions (one over life cycle, pathogenesis, distribution, treatments) DETAILS. Definitions (give word and you have to write the definitions) Spelling. Underline the names. Life cycle diagram that needs to be labeled, maybe two. Bonus question CDC has the life cycles 23
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