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2014-10-11 02:51:27
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  1. define heteroxenous, give an example
    • Life cycle includes multiple hosts for different stages
    • EX- blood/tissue of vertebrates AND intestines of blood-sucking invertebrates
  2. Why are blood protozoa referred to as hemoflagellates?
    • They require hematin (obtained from blood hemoglobin) for aerobic respiration
    • *NOTE- lab cultures for these organisms must contain blood
  3. What genera are associated with the term "hemoflagellates"?
    • Leishmania
    • Trypanosoma
  4. Give a brief physical description of hemoflagellates (applies to both genera)
    • Elongated with 1 flagellum OR rounded with tiny non-protruding flagellum
    • All forms have one nucleus
    • Kinetoplast: DNA-rich conspicuous part of mitochondria
    • K-B complex: kinetoplast is very near to basal body that flagellum arises from
    • Sexual reproduction is absent
  5. What are the 4 distinct morphological forms that might be seen in the life cycle of hemoflagellates (both genera)?  Which organism might they occur in?  How do they differ morphologically? Be specific.
    • "A. P.E.T."
    • Amastigote (vertebrate host)
    • Promastigote (invertebrate host - flies)
    • Epimastigote (invertebrate host - flies)
    • Trypomastigote (vertebrate host)
    • differ in placement and origin of the flagellum in relation to the nucleus
    • *NOTE- no specific sequence of progression between stages
  6. Describe the amastigote stage of Hemoflagellates in detail (morphological description, location, definitive stage?)
    • Rounded
    • 1 prominant nucleus
    • 1 very short flagellum projecting barely (if at all) beyond cell surface
    • kinetoplast
    • Kinetoplast: aggregation of mDNA in hemoflagellates, easily seen by light microscopy
    • Pellicular microtubules: provide structural support beneath cell membrane (like pellicle)
    • Develops in vertebrate host cells
    • Definitive stage in Leishmania (form taken in vertebrate host)
  7. What locations are L-D bodies likely to infect? Why?  Describe the process of infection of these areas.
    • Macrophages, spleen, and bone-morrow (cells responsible for defense against invasion)
    • After macrophage ingestion they form a parasitophorous vacuole by surrounding the ingested vacuole in host ER (for camoflauge)
    • The parasite lives/reproduces within this protected vacuole
  8. What are the Leishmania reservoirs?  How do they contribute to Leishmania infection?
    • Many mammals are reservoirs (canines and rodents most common) and are not diseased with infection
    • Leishmaniasis is a zoonosis, so it cannot be transferred directly between humans
    • Reservoir hosts cause sandfly infection after taking an infected bloodmeal
  9. Describe the life cycle of Leishmania
    • Female sandfly takes blood meal from infected mammal and ingests amastigotes
    • Amastigotes transform into promastigotes inside sandfly gut
    • Promastigote reproduces by binary fission (1-3 weeks)
    • Insect's anterior gut and pharynx become clogged with promastigotes which use their flagella to attach
    • When sandfly feeds promastigotes become loosened and deposited in skin of mammal
    • Macrophages quickly respond and engulf the promastigotes, which transform back to amastigote form (no need for flagella)
    • Amastigotes fortify themselves in parasitophorous vacuole and reproduce by binary fission
    • Eventually cell ruptures, releasing huge #s of amastigotes and spreading infection
  10. What factors determine the extent of Leishmania infection in a mammalian host?
    • spp of Leishmania
    • temperature
    • immune status of host
  11. What are the 4 species of Leishmania?  How are they categorized/named?
    • L. donovani
    • L. tropica
    • L. major
    • L. braziliensis
    • Categorized based on biochemical differences
    • Named after location
  12. Leishmania donovani- Discovery, disease names, distribution, # cases each year, geographical distribution, disease severity, location within mammals, vector
    • William Leishman & Charles Donovan (1903) discovered in spleen smears of a solider who died of a fever in Dum-Dum, India
    • AKA Dum-Dum fever, kala-azar, and visceral leishmaniasis
    • ~500,000 new cases each year
    • Global distribution (every continent except Australia and Antarctica)
    • >90% in Bangladesh, Brazil, India, Nepal, and Sudan
    • Often fatal (2nd deadliest parasitic disease)
    • Found in liver, spleen, bone marrow, lymph nodes, intestine (VISCERA)
    • vector is Phlebotomus
  13. Leishmania donovani- specific lifecycle events in humans, result of infection, incubation period
    • Phlebotomus injects promastigotes into skin
    • Promastigotes rapidly multiply and are engulfed by macrophage
    • Binary fission continues inside macrophage, causing cell lysis and escape
    • These "escaped" protozoa are again engulfed and the same process occurs
    • Hosts immunity is HEAVILY damaged
    • Incubation period may range from 10 days to 1 year (average 2-4 months)
  14. Leishmania donovani- disease development/symptoms, What less common forms of disease can be caused by Leishmania?
    • Visceral leishmaniasis
    • Develops weeks to months after sandfly bite
    • Initial symptoms are slow (104F fever, vomiting, weakness)
    • Then progress to anemia, protrusion of abdomen from hepatosplenomegaly, weight loss, and even death in untreated cases (1-2 years)
    • *NOTE- death is often caused by secondary pathogens due to incapacitated immunity
    • Infantile kala-azar: affects children
    • Post-kala-azar dermal leishmanoid: (reddish depigmented nodules in skin) develops in some cases after 1-2 years of inadequate treatment.
  15. What are the different forms of Leishmaniasis?  Give symptoms/differences.  How is temperature involved?
    • Visceral (systemic): affects entire body
    • Occurs 2-8 months after sandfly bite (do not remember bite)
    • Can lead to deadly complications
    • Parasites heavily damage immune system by destroying macrophages
    • Cutaneous: affects skin
    • skin sores typically start at site of sandfly bite
    • Mucocutaneous: affects mucous membranes and skin
    • Leishmania that prefer 35C causes cutaneous/mucocutaneous manifestation, while those that prefer 37C cause visceral manifestation
  16. Leishmania donovani- diagnosis, treatment, control
    • Hepatosplenomegaly suggests visceral leishmaniasis
    • Confirmatory tests include demonstration of parasites via biopsy (microscopy or xenodiagnosis)
    • xenodiagnosis: direct innoculation of lab animals with tissue from patient, infection in animal confirms suspected parasite in human
    • Not easily treated, many transfusions are required
    • Chemotherapy requires careful intermuscular injections of antimony (serious side effects if injected in excess, relapse or post-kala-azar dermal leishmanoid if insufficient)
    • Only prevention is protection from Sandfly bites and extermination of infected dogs (reservoirs)
    • *NOTE- sandflies are small enough to fit through mosquito nets
  17. Leishmania tropica- disease name, development/symptoms, geographical location, prevention
    • cutaneous leishmaniasis, Jericho boil, oriental sore, Delhi boil
    • similar life cycle/clinical symptoms to L. donovani
    • Initial sign of infection is appearance of vascularized nodule on skin at bite site (commonly hands, feet, legs, and face)
    • Found primarily in M0 around cutaneous sores/ulcers (unlike L. donovani which is found in M0 in blood)
    • Lesion is dry, filled with amastigotes, persists for months before ulcerating
    • Nodule may erupt and spread forming additional cutaneous lesions
    • Found in densely populated areas of middle east, India, Peru, Bolivia,  Brazil, and Mexico
    • Prevention is to avoid Sandfly bite and destroy canine reservoires
  18. Leishmania major- disease names, development/symptoms, geographical location, prevention
    • cutaneous leishmaniasis, Jericho boil, oriental sore, Delhi boil
    • similar life cycle/clinical symptoms to L. donovani
    • Initial sign of infection is appearance of vascularized nodule on skin at bite site (commonly hands, feet, legs, and face)
    • Found primarily in M0 around cutaneous sores/ulcers (unlike L. donovani which is found in M0 in blood)
    • Lesion is moist, contains few amastigotes, and disappears quickly
    • Nodule may erupt and spread forming additional cutaneous lesions
    • Found in sparsely populated areas of Africa
    • Prevention is to avoid Sandfly bite and destroy canine reservoires
  19. Leishmania braziliensis- disease name, vector, disease development/symptoms, severity, geographical location, diagnosis, treatment
    • American leishmaniasis, chiclero ulcer, espundia, uta, or mucocutaneous leishmaniasis
    • vector is Lutzomyia
    • Primary lesion appears as small red nodule on skin after sandfly bite
    • secondary lesion always appears elsewhere on the body and this site is always distinctive based on geographic location (Mexico/Central America- chiclero ulcer on ear, Brazal- espundia or uta in nasal tissue)
    • Amastigotes are found in macrophages in ulcerations of the skin (similar to L. major/tropica)
    • Severe mucous membrane destruction leads to permanent disfigurement
    • Amastigotes are found in M0 in skin ulcers
    • Found in South and Central America
    • Diagnosed by finding L-D bodies in infected tissue, culturing parasite in vitro if possible
    • Treatment with antimony compound injections, antibiotics for secondary infections
    • *NOTE- relapse is common, but a person has lifelong immunity after elimination of parasite
  20. How does Trypanosoma affect livestock in Africa?
    • Huge numbers of livestock (up to 10,000/day) are killed by Trypanosoma
    • This makes agriculture impossible
  21. What are the two major categories of Trypanosomes with a brief description and the disease they cause?
    • African trypanosomes: found in Africa
    • T. brucei rhodesiense (African sleeping sickness)
    • T. b. gambiense (African sleeping sickness)
    • American trypanosomes: found in the western hemisphere
    • T. cruzi (Chagas disease AKA American trypanosomiasis)
  22. Describe the nomeclature of African Trypanosoma, describe the general similarities/differences between them
    • In early 1900s 3 African spp were named - T. brucei (didn't infect humans), T. rhodesiense (acute disease), and T. gambiense (chronic disease)
    • Later discovered to be closely related and reduced to subspecies of species T. brucei
    • Life cycle is identical
    • Epidemiologically distinct
    • Vector is Tsetse fly of Glossina
  23. Describe the life cycle of African trypanosomes (start with infected blood meal.  Very long)
    • T. b. rhodesiense and T. b. gambiense
    • Tsetse Fly (Glossina) ingests bloodmeal containing short, stumpy trypomastigotes (this is the only form that can infect the fly)
    • *NOTE-Mitochondrion with prominent cristae allow this form of the trypomastigote to live in the anaerobic environment of the insect midgut
    • After ingestion the stumpy trypomastigotes elongate, lose their surface coat, and become procyclic trypomastigotes
    • The procyclic trypomastigotes increase via binary fission and migrate anteriorly
    • Enter fly's midgut ~10th day after ingestion as epimastigotes (metamorphosis during migration)
    • Epimastigotes move to salivary glands/ducts and multiply ~12th day after ingestion
    • Epimastigotes have transformed into metacyclic trypomastigotes by end of 3rd week
    • Tsetse fly (Glossina) injects saliva infected with metacyclic trypomastigote into skin of victim
    • -----
    • Once in the circulatory system metacyclic tryopmastigotes spread rapidly and migrate to the CSF
    • *NOTE- trypomastigotes are polymorphic in the blood and have 3 potential forms (long and slender, short and stumpy, and intermediate)
    • *NOTE- both epimastigote and trypomastigotes are required for life cycle completion
  24. How can you differentiate between metacyclic trypomastigote and trypomastigote of African trypanosomes?
    • Metacyclic trypomastigote mitochondria have few cristae, are blunt shaped, and have short/free flagellum
    • Trypomastigotes have prominant cristae, are elongated (although different forms exist)
  25. Describe the polymorphic forms of African trypanosome trypomastigotes (image answer)
  26. T. b. gambiense- vector, location, disease, progression
    • Tsetse fly (Glossina papalis and Glossina tachinoides)
    • West Africa
    • West African (or Equatorial or Gambian) sleeping sickness
    • Less dangerous (chronic) disease
    • 1-2 weeks after bite a red sore appears at site
    • Weeks to months later fever, headache, swelling near eye/hands, and swollen lymph nodes will occur
    • After infection invades CNS personality changes, loss of concentration, difficulty walking/talking, and sleeping all day with insomnia at night may may occur
    • Fluctuation in parasite #s in blood produces period remission alternating with high parasitic density (caused by variant antigenic types)
    • If left untreated infection worsens until death occurs (months-years after infection)
    • Many African animals (antelopes, buffalo) are reservoirs
  27. T. b. brucei- vector, location, disease
    • Tsetse fly
    • Found exclusively in Africa
    • does not affect humans
    • Causes nagana ("to be in low spirits") in domestic African animals (pigs, camels, goats, sheep)
    • Symptoms include fever, anemia, diarrhea, and often death
  28. T. b. rhodesiense- vector, location, disease, progression
    • Tsetse fly (Glossina morsitans)
    • East Africa
    • East African (or Rhodesian) Sleeping Sickness
    • More deadly form of disease
    • 1-2 weeks after bite a red sore appears at site
    • Weeks to months later fever, headache, swelling near eye/hands, and swollen lymph nodes will occur
    • Patient often dies before any CNS symptoms appear (3-9 months)
    • Wild game and domestic animals serve as reservoir
  29. What are VATs and how do they affect the host? (give all info available)
    • VATs (variant antigenic types) is the name given to the different surface coat chemical compositions that can be employed by Trypanosoma
    • >1000 VATs are possible
    • The ability to change surface antigens is what allows Trypanosoma to persist in the blood in the face of the immune system and causes periodic fluctuation in #s
  30. Describe the symptoms of infection with African trypanosomes (can be discussed together)
    • T. b. gambiense and T. b. rhodesiense
    • Inflammatory response occurs at bite site for 1-2 days (trypanosomal chancre)
    • Chancre includes reddening of skin, swelling of 2-5cm, and enlargement of adjacent lymph nodes
    • After blood and lymph are invaded, headache and fever develop
    • Lymph glands in the neck region swell (Winterbottom's sign)
    • Tremors of the tongue and tongue, mental dullness, and other neurological symptoms appear (loss of appetite, extended sleeping, and paralysis)
    • Rapid weight loss results from anorexia, anemia, drowsiness, coma, and eventually death results
  31. Describe the diagnosis of infection with African trypanosomes (can be discussed together)
    • T. b. gambiense and T. b. rhodesiense
    • Preliminary diagnosis based on clinical and other neurological symptoms
    • Chancre can be used if the patient is seen early enough (1-2 weeks)
    • Winterbottom's sign (swollen cervical glands in neck) is a classic diagnostic tool
    • Examination of blood smears, marrow, or CSF for trypomastigotes is performed after initial assessment
    • Antibody testing may also be available
  32. Describe the treatment of infection with African trypanosomes (can be discussed together)
    • T. b. gambiense and T. b. rhodesiense
    • prior to CNS involvement treatment usually involves suramin which is effective, but can be toxic to some patients
    • After CNS involvement the only treatment is arsenic drug Melarsen Oxide (Mel B)
    • Mel B is highly toxic and must be given under strict supervision, plus it isn't always effective!
  33. Describe the prevention and control of infection with African trypanosomes (can be discussed together)
    • T. b. gambiense and T. b. rhodesiense
    • Avoiding being bitten by Tsetse flies in endemic areas
    • This is difficult due to daytime feeding, persistence, large numbers, and ability to bite through thin clothing
    • Attempted control through vector control (usually unsuccessful)
    • 1) Tsetse flies cover huge landmass in Africa and aerial spraying is expensive
    • 2) Clearing vegetative bush is expensive and ecologically destructive
    • 3) Trapping flies (traps w/ insecticide) is popular in some areas
  34. Describe the abnormal ways that Trypanosoma can be tranismitted
    • Sexual intercourse (fluids)
    • Placenta
    • Mother's milk
    • Milk from infected cattle
    • Consumption of contaminated blood (Masai tribe from Kenya engage in this behavior)
  35. Trypanosoma cruzi- AKA, discovery, disease name
    • American Trypanosome
    • Carlos Chagas (1909) dissected several hemipteran bugs and found hindguts swarming with tryanpanosome epimastigotes
    • Chagas sent the bugs to the Oswaldo Cruz institute where they were allowed to feed on marmosets/guinea pigs
    • Trypanosomes appeared in their blood in 1 month
    • Diseased children inhabiting a small Brazilian village were later found to harbor the same flagellates
    • T. cruzi causes Chagas' Disease
  36. Trypanosoma cruzi- vector (name, information)
    • Panstrongylus megistus "Kissing bug" (bite face and around lips during sleep) and other hemipteran insects
    • BOTH sexes feed on blood
    • Infection occurs when infected fecal material is rubbed into bite/eyes- not directly injected during bite
  37. Trypanosoma cruzi- life cycle (starting with insect bloodmeal)
    • Kissing bug ingests blood containing trypomastigotes
    • Trypomastigotes undergo repeated binary fission during passage through GI tract of insect
    • Metamorph into epimastigotes by the time they reach the midgut
    • Continued replication occurs as the epimastigotes pass into insect hindgut
    • Infective metacyclic trypanosomes appear in rectum ready to be excreted in feces by the 10th day
    • *NOTE- 50-100% of bug population is typically infected, much higher than other trypanosomes
    • Kissing bug bites host and defecates simultaneously
    • Host typically unknowingly rubs feces into bite or eye during sleep
    • Trypomastigotes enter blood stream and invade cells (incl M0) and transform into amastigotes where they reproduce by binary fision
    • NOTE- spleen, liver, lymph glands, and muscles are most vulnerable to infection
    • Infected cells eventually rupture and amastigotes are released into other cells
    • Nervous, reproductive, and digestive systems are also invaded
    • pseudocyst: large amount of amastigotes in cardiac muscle fiber (can also form elsewhere)
    • Some of the released amastigotes revert to trypomastigote form and re-enter the bloodstream
    • *NOTE- unlike other trypanosomes T. cruzi NEVER repr in blood and cannot produce variable antigens (VATs)
    • *NOTE- in chronic cases trypomastigotes are rarely seen in blood because circulating antibodies easily destroy them
  38. How do trypomastigotes of T. cruzi differ from T. b. gambiense and T. b. rhodesiense?
    • Trypomastigotes of T. cruzi are shorter (~20um compared to 40um) and show a caracteristic "U" or "C" shape in blood stains
    • T. cruzi does not have VATs and thus cannot survive in the blood 
    • T. cruzi NEVER reproduces in the blood (likely for this reason)
  39. Trypanosoma cruzi- geographic location, prevalence, risk factors, Brazil vs American
    • Distributed in most of Central and South America
    • Affects 12-20 million people (some surveys have reported ~30% of adults die of T. cruzi infection)
    • Incidence is greatest in rural areas, among the poor (old houses facilitate easy access from Kissing bugs)
    • American trypanosmiasis affects cats, dogs, bats, opossums, armadillos, rodents, and other reservoirs (common in southern states)
    • Few cases of naturally acquired human infections reported (preference of reservoirs for blood meal + defecation occurs AFTER meal)
  40. T. cruzi- symptoms
    • Chagas disease is chronic
    • Infected persons show few (if any) signs of disease
    • Often survive for decades while infected
    • Chagoma: analogous to a chancre, it is the first sign of infection
    • Romana's sign: chagoma involving the eye (extremely swollen) if infection occurred through conjunctiva
    • Acute cases show fever, headache, and weakness 1-3 weeks after infection, but it is never fatal.  Chronic condition resumes afterward.
    • Although signs may not be apparent repeated cycles of intracellular multiplicatio continuously destroy cells (especially neurons)
    • If pseudocysts are concentrated in the GI tract peristalsis may be inhibited and organs may become hugely distended (megaesophagus, megacolon)
    • megaesophagus- victim unable to swallow, may starve
    • megacolon- may lead to rupture and death
    • If pseudocysts aggregate in heart muscle (common) the neuronal and muscle cells are destroyed, weakening the heart wall and potentially causing aneurysm, irreversible damage, and death from heart attack
  41. T. cruzi- diagnosis
    • Exam of fresh blood within the 1st month following infection may reveal T. cruzi trypomastigotes (especially if acute phase is in progress)
    • Xenodiagnosis- uninfected kissing bugs are forced to feed on patient then feces/gut are examined 3-4 weeks later (looking for T. cruzi)
  42. T. cruzi- treatment, prevention, control
    • No effective treatment for Chagas disease
    • Nifurtimox has shown some promise in early cases, but course is long
    • Once the flagellate invades the host cell it is shielded from the action of any drug (chronic phase cannot be treated)
    • Well built and maintained homes are unlikely to harbor bugs
    • Bed or mosquito nets may help to prevent contact between bugs and sleepers
    • *NOTE- in heavily infected homes bugs crawling over nets may still defecate on person
    • Spraying the house interior with insecticide is effective, but expensive
    • In some areas (Brazil) infection via blood transfusion is a serious risk, and blood should be screened