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2- Flagellates1- Trypanosoma spp.2- Leishmania spp.3- Giardia spp.4- Trichomonas spp.
1- Trypanosoma spp. 2- Leishmania spp.Called Hemoflagellates because they have a flagellum and require blood medium to culture them.A.K.A. KinetoplastaFlagellum is attached to an undulating membrane attached to a kinetoplast.There is evidence for sexual reproduction but when it occurs is not known.They can also absorb and use foreign DNA.
Two host life cycleHumans and their domestics are Definitive HostInsect vectors are the Intermediate HostFour life stagesNot all stages occur in all speciesCertain stages are found in specific hostsEpimastigotes and promastigotes in insect IHAmastigoes and trypomastigotes in DH1- Hemoflagellates
1- Trypanosoma spp.1- Trypanosoma gambiensi2- T. rhodesiensi3- T. curzi4- T. lewisi
1- Trypanosoma gambiensi2- T. rhodesiensiDefinitive Host: Humans. Not pathenogenic to any other species. Native ruminates serve as reservoirs for T.b. rhodesiense, but not T.b. gambiense.Intermediate Host: Tsetse fly (Glossina)Mode of transmission: Bite of infected tsetse flyTsetse fly (Glossina)
T. b. gambiense is found in west central and central Africa.
T. b. rhodesiense found in central and east central AfricaGeographic DistributionT. b. gambienseT. b. rhodesiense
Location: Throughout the body in the blood and tissuesPathology: Both subspecies cause African Sleeping Sickness.T.b. gambiense causes chronic, long-term form.T.b. rhodesiense causes an acute form.Starts with a small sore at bite.Trypimastigotes divide rapidly and spread throughout body1- Trypanosoma gambiensi2- T. rhodesiensi
Pathology (cont): Lymph nodes become swollen and congestedParticularly the nodes in neckCalled Winterbottoms signPathology
T.b. gambiense frequently goes to CNSCauses the chronic, sleepiness associated with African Sleeping SicknessApathy, mental dullness, disturbance of coordinationIncrease in sleepiness, finally to coma, and death.Death may also occur from malnutrition, falling, or other infectionsPathology
T.b. rhodiensiense rarely invade the CNS but causes death much faster.Usually due to invasion of heart tissueBoth subspecies produce intermittent periods of fever, particularly in early stages.Due to antigen shifts of the parasite.They can also take antigens from host body and put them on their bodyMuch pathology may be due to heightened immune response killing uninfected body cells.Pathology
Trypomastigotes in the blood smear.Can also be in cerebrospinal fluid Serological test available
3- Trypanosoma curziDefinitive Host: Humans, dogs, cats, opossums, armadillos, and wood rats.Intermediate Host: Reduviid bugs (Kissing bug or assassin bugs).Location in the Definitive Host: Throughout the body. Trypomastigotes in bloodAmastigotes most common in spleen, liver, and muscles, including heartMode of Transmission: Host rubs tryps into bite wound.
Throughout much of central and South America.12-19 million infectedAnnual incidence 561,0002-3 million with chronic symptoms45,000 die from disease every year.A few cases in U.S. in Maryland, Georgia, Florida, Texas, Arizona, New Mexico, California, Alabama, and Louisiana.Geographic Distribution
2- Leishmania spp.Leishmania donovaniL. tropica.
Leishmania donovaniDefinitive Hosts: Humans. Reservoir includes most mammalsIntermediate Hosts: Phlebotomus sand fly.Mode of Transmission: Bite of infected Sand FlyLocation in D.H.: Immune system, including spleen, liver, lymph nodes and bone marrow
Geographic DistributionProbably originated in Old WorldMoved to New World with slave trade
PathologyCauses Visceral LeishmaniasisA.K.A. Kala-azar, Dum-Dum FeverAmastigote is engulfed by macrophage.Macrophage doesnt kill amastigote.Neutrophils and eosinophils will kill amastigotes.Multiplies, breaks out, and each invades another macrophage.Also destroys macrophages in the spleen, liver, and lymph nodesBody starts manufacturing macrophages to replace them.Results in severe wasting and anemia
PathologyMacrophage Infected with amastigotes of Leishmania
PathologyEarly symptoms include malaise, vomiting, low-grade fevers.Followed with chronic wasting, anemia, enlargement of abdomen due to greatly enlarged spleen and liver.Death usually follows in 1-2 years if untreated.
Some people recover spontaneouslyRelated to age and nutritionSome people who were treated later develop Post-Kala-azar dermal leishmanoid Face bumpsRepeat of treatment usually clears up the bumps.
DiagnosisAmastigotes in liver tissue, macrophages, spleen, other organs.IFA, ELISA tests have been developed but cant tell between L. donovani and L. tropica.Need to eliminate possibility of typhoid, paratyphoid, malaria, syphilis, tuberculosis, dyssentery, and relapsing fever which cause similar symptoms.
1- Genital flagellatesTrichomonas spp.
2- Intestinal flagellatesGiardia spp.
Genital flagellatesTrichomonas spp.Trichomonas vaginalisDefinitive Hosts: Humans. Reservoir includes most mammals and birdsIntermediate Hosts: NothingMode of Transmission: during sexual inter course by trophozoite
Geographic DistributionTrichomonas are found in man, monkeys, rodents, fowls, pigeons, doves, termites and slugs. Distributed in all countries
PathologyCauses milky yellowish irritant vaginal discharge in femaleUlceral discharge may occur in male
DiagnosisIn female: Examination of vaqginal discharge for trophozoites and urine sampleIn male: Examination of prostatic fluid and urine sample
Intestinal flagellatesGiardia spp.Definitive Hosts: Humans. Intermediate Hosts: NothingMode of Transmission: quadri-nucleated cyst in contaminated food and drinkFlies and cockroaches play an important role in transmission
Geographic DistributionWorldwide, more prevalent in warm climates
PathologyChildren are affectedMucus production, diarrha, dehydration, intestinal pain, weight loss.
DiagnosisMicroscopic examination of fecal material for identification of trophozoite.PCR analysis for detection of giardia DNA from both trophozoites and cysts