Blood and Tissue Flaggelates Notes PDF

PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES BLOOD AND TISSUE FLAGELLATES Diseases caused by these flagellates have not been diagnosed in the Philippines. However, medical technologists should still study about it because the intermediate hosts of these paras...

PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES BLOOD AND TISSUE FLAGELLATES Diseases caused by these flagellates have not been diagnosed in the Philippines. However, medical technologists should still study about it because the intermediate hosts of these parasites can also be found in the Philippines. Thus, infections from migrants may spread in our country. DEVELOPMENTAL STAGES Stage Common Description illustration Name Amastigote Leishmanial No Flagella Form Promastigote Leptomonad Flagella found in Form front of Nucleus Epimastigote Crithidial Form Flagella in center of organism Trypomastigo Trypanosomal Flagella originates at te Form posterior end of organism PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES BLOOD FLAGELLATES: TRYPANOSOMES Trypanosoma cruzi  o Etiologic agent of CHAGAS DISEASE or AMERICAN TRYPANOSOMIASIS o An intracellular parasite o Exhibits all four stages of development. o Intermediate host: TRIATOMINE BUGS/REDUVIID BUG (Triatoma, Rhodnius, Panstrongylus spp.) o At the site of inoculation, a local inflammation is produced: CHAGOMA- a small painful reddish nodule o May also enter conjunctiva of the eye and cause edema of the eyelid: ROMAÑAS SIGN – unilateral periorbital edema in child o It can cross placenta and cause prenatal disease LIFE CYCLE: 1. Triatomine bug takes a blood meal and ingests trypomatigote from an infected human host. 2. Trypomastigotes transform into epimastogtes in the midgut of the bug. 3. Epimastigotes multiply by longitudinal fission and transform into promastigote and later into the infective metacyclic trypomastigotes. 4. These metacyclic trypomastigotes appear in the insect’s rectum and are passed in the feces. 5. Triatomine bug takes another blood meal and introduce the metacyclic trypomastigotes in its feces. It may gain entrance into human host through scratched skin or through mucus membranes that are rubbed with fingers contaminated with the bug’s feces. 6. The metacyclic trypomastigotesare engulfed by macrophages of Reticuloendothelial system (spleen, liver, etc). 7. Inside the cells they transform into amastigotes and multiply by binary fission. 8. Intracellular amastigotes transform into trypomastigotes, then burst out of the cell and enter the bloodstream. 9. Trypomastigotes infect other cells in new infection sites. Clinical manifestations can result from this infective cycle. *In humans: - trypomastigotes (found in the bloodstream) - amastigotes (in tissue cells) *In the triatomine bug: -epimastigote and promastigote (in the midgut) -metacyclic trypomastigote (in hidgut) PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES TRANSMISSION:  o Feces from Triatomine/Reduviid Bug rubbed into bite wound o Placental Transfer o Blood Transfusion DIAGNOSIS: o C, U, or S-shaped trypomastigotes in blood, CSF or lymph nodes o Xenodiagnosis o Serological Tests Treatment: Nifurtimox and Benznidazole Trypanosoma brucei complex o Causative agent of African Sleeping Sickness o Intermediate host: TSETSE FLY (Glossinaspp) o Acute infection: EAST AFRICAN SLEEPING SICKNESS/Rhodesian trypanosomiasis T. brucei rhodesiense found in East and South Africa o Chronic infection: WEST AFRICAN SLEEPING SICKNESS/Gambian trypanosomiasis T. brucei gambiense found in West and Central Africa o Earliest sign in African Trypanosomiasis is the CHANCRE - a local, hard, painful lesion at the site of inoculation o T. gambiense causes coma in 6-12 months o T. rhodesiense causes coma in a month o Both causes elevated IgM in serum and CSF LIFE CYCLE: 1. Tsetse fly takes a blood meal and ingests trypomastigote from an infected person. 2. Trypomastigotes transform into procyclic trypomastigotes in midgut and multiply by binary fission. 3. Procyclic trypomastigote migrate into salivary glands and transform into epimastigotes. 4. Epimastigote multiplies and transform into metacyclic trypomastigote. PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES  5. Tsetse fly takes another blood meal and injects the metacyclic trypomastigote through its saliva into the bloodstream of the human host. 6. Trypomastigotes multiply by longitudinal binary fission in various body fluids such as blood, lymph, and spinal fluid. In chronic diseases, the trypomastigotes invade the CNS. GAMBIAN TRYPANOSOMIASIS o 1ST yr of infection = trypanosomes in blood and lymphatics; manifestation of rice plums consistency of lymph nodes known as WINTERBOTTOM’S SIGN o Beginning of 2nd yr = CNS involvement, inversion of sleep cycle, and hyperesthesia a.k.a KERANDEL’S SIGN Hyperesthesia - An increased sensitivity to touch or painful stimuli. o Patient experience mental dullness and lacks interest in work RHODESIAN TRYPANOSOMIASIS o More rapid and fatal o Clinical features are the same to those of Gambian Trypanosomiasis o However, onset of symptoms occur within a few days after a tsetse bite o Death occurs within weeks to months DIAGNOSIS o Trypomastigotes in blood, lymph, or CSF o Best sample = CSF o Serologic tests PARASITOLOGY NOTES UIC-MT/MLS BLOOD AND TISSUE FLAGELLATES TISSUE FLAGELLATES : LEISHMANIAS The three species of Leishmania differ only in clinical manifestations and geographic distributions. o They are exclusively intracellular parasites. o They are diagnosed by tissue biopsy and serological methods o Intermediate host: SANDLY (Phlebotomus spp.) o May be transmitted congenitally, through blood transfusion, by contamination of bite wounds, or by contact. LIFE CYCLE 1. Sandfly takes a blood meal and ingests the macrophages infected with amastigotes. 2. Amastigotes transform into promastigote stage in midgut. 3. Promastigote multiply and migrate to the proboscis of the sandfly. 4. Sandfly takes another blood meal and inject promastigote in the skin.  5. Promastigotes invade the reticuloendothelial cells and transform into amastigotes. 6. Amastigotes multiply by binary fission until cell ruptures. 7. When the cell ruptures, the amastigotes released will invade new cells: *L. tropica – in lymphoid tissue of skin; L. donovani– in visceral organs; L. braziliensis – in skin and mucous membranes Leishmania tropica o Localized intracellularly in skin macrophages and histiocytes o Causes Oriental sore or Cutaneous leishmaniasis, Oriental boil, or Baghdad or Delhi boil. Leishmania braziliense/ Leishmania braziliensis o Causes Espundia or Mucocutaneous Leishmaniasis o Lesions caused by this parasite resemble those of cutaneous leishmaniasis. Later, however, even after several decades, metastatic spread to the oronasal and pharyngeal mucosa may occur, causing highly disfiguring leprosy-like tissue destruction and swelling known as “Tapir Nose”. Leishmania donovani o Amastigote spreads to viscera, multiplies in macrophages in liver and spleen o Causes Dumdum fever, Kala-azar, or Visceral Leishmaniasis. This is characterized by double spiking chills and fever daily. o Enlargement of spleen and liver occurs References: Philippine Textbook of Medical Parasitology 2nd Edition by Belizario, V., et. al Medical Parasitology Review Outline by Rabor, R., et. al