3 1- Hemoflagellates 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.
4 1- Hemoflagellates Two host life cycle Humans 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 DH
5 1- Trypanosoma spp. 1- Trypanosoma gambiensi 2- T. rhodesiensi 3- T. curzi4- T. lewisi
6 1- Trypanosoma gambiensi 2- 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)
7 Geographic Distribution T. b. gambiense is found in west central and central Africa.T. b. rhodesiense found in central and east central AfricaT. b. gambienseT. b. rhodesiense
9 1- Trypanosoma gambiensi 2- T. rhodesiensiLocation: 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 body
10 Pathology Pathology (con’t): Lymph nodes become swollen and congested Particularly the nodes in neckCalled Winterbottom’s sign
11 Pathology T.b. gambiense frequently goes to CNS Causes 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 infections
12 PathologyT.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.
13 Diagnosis Trypomastigotes in the blood smear. Can also be in cerebrospinal fluidSerological test available
14 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.
15 Geographic Distribution 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.
18 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
19 Geographic Distribution Probably originated in Old WorldMoved to New World with slave trade
20 Pathology Causes Visceral Leishmaniasis A.K.A. Kala-azar, Dum-Dum FeverAmastigote is engulfed by macrophage.Macrophage doesn’t 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
21 PathologyMacrophage Infected with amastigotesof Leishmania
22 Pathology Early 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 bumps”Repeat of treatment usually clears up the bumps.
24 DiagnosisAmastigotes in liver tissue, macrophages, spleen, other organs.IFA, ELISA tests have been developed but can’t 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.
26 Trichomonas vaginalis Genital flagellatesTrichomonas spp.Trichomonas vaginalisDefinitive Hosts: Humans. Reservoir includes most mammals and birdsIntermediate Hosts: NothingMode of Transmission: during sexual inter course by trophozoite
27 Geographic Distribution Trichomonas are found in man, monkeys, rodents, fowls, pigeons, doves, termites and slugs.Distributed in all countries
28 Pathology Causes milky yellowish irritant vaginal discharge in female Ulceral discharge may occur in male
30 DiagnosisIn female: Examination of vaqginal discharge for trophozoites and urine sampleIn male: Examination of prostatic fluid and urine sample
31 Intestinal flagellates Giardia 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
32 Geographic Distribution Worldwide, more prevalent in warm climates
33 Pathology Children are affected Mucus production, diarrha, dehydration, intestinal pain, weight loss.
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