Species

Morphology

Disease caused

All trypanosomes are heteroxenous or at least are transmitted by vectors. Various species pass through ama blood and tissue fluids, but some occupy intracellular habitats. The majority are transmitted by blood-feeding i hosts. Salivaria: develops in the anterior portions of the digestive tract (anteri

Trypanosoma brucei rhodesiense

Subspecies of Trypanosoma brucei ; morphologically indistinguishable, vary in infectivity for diff. species of hosts, produce somewhat different pathological syndromes, etiological agents of African sleeping sickness; there are physiological differences between subspecies; differ in pathogenesis, growth rate, and biology

causes a more acute type of infection

Trypanosoma brucei gambiense

Causes a chronic form of sleeping sickness (invasion of CNS, multiply, and enter intercellular spaces in brain) ; native game animals serve as reservoirs for Rhodesian trypanosomiasis not Gambian

Trypomastigotes are found in circulating blood. They are slender, and posterior end is pointed. Free flagellum is moderately long, undulating membrane is narrow with only 2-3 undulation at a tie along its length. Trypanosoma cruzi Chagas' disease - manifests acute and chronic phases

Trypanosoma cruzi

Chagas' disease - manifests acute and chronic phases

Kinetoplast is subterminal and is the largest of any trypanosome, sometimes causing the body to bulge out. Commonly dies in a question marke shape (retained in stained smears). Amastigotes develop in muscles and other tissues. They are spheroid and occur in clusters.

Leishmanias are heteroxenous. Part of life cycle is spent in a sand fly gut where they become promastigotes. R found. Cause a complex of diseases called leishmaniasis, which is a zoonosis with a wild animal reservoir. Live clinical manifestations, drug treatment may precipitate a subsequent clinical manifestation quite different from th parasites pass through midgut or hindgut, where they transform into procyclic promastigotes that attach to the g lining and forming plaques (hemidesmosomes) > 8th day: flagellates metamorphose into slender, active, metac differing only in size. Only the nucleus and very large kinetoplast can be seen, and cytoplasm appears vacuolat properties, especially in their membrane components, and in the mechanism by which they survive.

Leishmania donovani

Symptoms

vectors. Various species pass through amastigote, promastigote stages, with other forms developing in the invertebrate host. Parasites of all vertebrate c majority are transmitted by blood-feeding invertebrates. Divided into two broad groups: Salivaria and Stercoraria, based on characteristics of their devel nterior portions of the digestive tract (anterior station development); Stercocaria: develops in vector's hindgut (posterior station development).

Small sore (chancre) often develops at the site where metacyclic trypanosomes are inoculated. This disappears after 1-2 weeks > protozoa gain entry to the blood and lymph channels > reproduce rapidly, producing parasitemia and invading all organs of the body. Intermittent periods of fever at early stages > increase in number of trypanosomes in circulating blood, increase in swelling of lymph nodes, generalized pain, headache, weakness, and cramps

Rarely invade the nervous system.

Acute phase - most common and sever among children. Inoculation of trypanosomes from the bug feces into the wound > Local inflammation > small red nodule (chagoma) with swelling of regional lymph nodes > trypanosomes enter through the conjunctiva of the eye > edema of the eyelid and conjunctiva and swelling of the preauricular lymph node (Romana's sign) > pseudocysts may be found in almost any organ of the body > anemia, loss of strength, nervous disorders, chills, muscle and bone pain, varying degress of heart failure. Heart muscle is usually invaded, with up to 80% ganglion cells lost.

Chronic stage - most often seen in adults. Spectrum of symptoms is primarily the result of CNS and PNS dysfunction. Part of the inefficency in heart function is caused by loss of muscle tone resulting from destroyed nerve ganglia.Heart becomes enlarged and flabby.

y gut where they become promastigotes. Remainder of life cycle is completed in vertebrate (mammal) tissues where only amastigotes (Leishman-Donov a zoonosis with a wild animal reservoir. Live in inside macrophages of vertebrate host, amastigotes in marcophages reside in phagolysosomes, species di clinical manifestation quite different from that of the original infection (post-kala-azar dermal leishmanoid). Sand flies ingest amastigotes from blood of procyclic promastigotes that attach to the gut and replicate by binary fission > 4th or 5th day after feeding: promastigotes move to the esophagus and pha s metamorphose into slender, active, metacyclic promastigotes that are injected into the next blood meal. All amastigotes look similar in vertebrate tissues n be seen, and cytoplasm appears vacuolated in stained preparations. Short axoneme is visible within the cytoplasm. Amastigotes of species differ in their chanism by which they survive.

Pathogenesis

Distribution

ages, with other forms developing in the invertebrate host. Parasites of all vertebrate classes. Most live in o two broad groups: Salivaria and Stercoraria, based on characteristics of their development in the insect Stercocaria: develops in vector's hindgut (posterior station development).

Invade the CNS > chronic, sleeping sickness stage of infection > increase in apathy and mental dullness with accompanied disturbances of coordination > tremor of the tongue, hands, and trunk > paralysis and convulsions > sleepiness> coma > death. Death may be due to malnutrition, pneumonia. Heart failure, and other parasitic infections. Central and East Central Africa Can enter microvascular endothelial cells of the blood-brain barrier. In acute infections of small animals: death occurs rapidly with a high level of parasitemia, mortality results from overall disruption of physiological processes. In humans: neurological involvement results in demyelinating encephalitis, accompanied by dementia, occasional hallucinations, and decreased consciousness.

Causes a more rapid course toward death (lymph nodes in the neck, groin, and legs swell up West Central and [Winterbottom's sign]). Infection causes rapid weight loss and heart involvement, causes no Central Africa somnambulism or other protracted nervous disorders found with T. b. gambiense

Entrance of metacyclic trypanosomes into cells of subcuteanous tissue > acute local inflammatory reaction > 1-2 weeks after: parasites spread to regional lymph nodes and begin to multiply in cells that phagocytose them. Intracellular amastigotes undergo repeated divisions to form large numbers of parasites, producing a pseudocyst > generalized parasitemia > parasite invades almost every type of tissue in the body (show a particular preference for muscle and nerve cells). South and Central America

South and Central America

Reversion to amastigote, pseudocyst formation, retransformation to trypomastigote, and pseudocyst rupture are repeated in newly invaded cells. Rupture of pseudocyst > acute inflammatory response with degeneration and necrosis of nerve cells (especially of ganglion cells). Degeneration is the indirect result of parasitism of supporting cells, such as glial cells and macrophages.

completed in vertebrate (mammal) tissues where only amastigotes (Leishman-Donovan [L-D] bodies) are of vertebrate host, amastigotes in marcophages reside in phagolysosomes, species differ in terms of on (post-kala-azar dermal leishmanoid). Sand flies ingest amastigotes from blood of infected animal > ry fission > 4th or 5th day after feeding: promastigotes move to the esophagus and pharynx, attaching to the are injected into the next blood meal. All amastigotes look similar in vertebrate tissues: spheroid to ovoid, ns. Short axoneme is visible within the cytoplasm. Amastigotes of species differ in their biochemical

Insect Vectors

Form structure

Tend to be pleiomorphic in natural infections (in vertebrate host): from long, relatively slender trypomastigotes with a long free flagellum through intermediate forms to short, stumpy individuals with no free flagellum; small kinetoplast usually near the posterior end; undulating membrane is Glossina morsitans, G. pallidipes, G. conspicuous swynnertomi Long, slender trypomastigotes have a single, simple mitochondrion extending anteriorly from their kinetoplast; cristae are few, short, and tubular

G. palpalis and G. tachinoides

conenosed bugs; reduviid bugs known to defecate on host's skin, feces contain metacyclic tryapansomes; triatomine bugs

Undulating membrane and flagellum disappear soon after parasite enters host. Intermediate forms (promastigotes and epimastigotes) can be seen in the interstitial spaces. Some complete metamorphosis into trypomastigotes and find their way into the blood.

Panstrongylus megistus, Triatoma sordida, T. brasiliensis (Brazil); T. infestans (Chile and Uruguay); Rhodnius prolixus (northern South America); T. dimidiata (Central America); T. barberi (Mexico); Dipetalogaster maxius (southern Baja California)

soon after parasite enters host. Intermediate forms (promastigotes and epimastigotes) can be seen in the interstitial spaces. Some complete metamorphosis into trypomastigotes and find their way into the blood.

Intermediate hosts and vectors are sand flies. Old World: Phlebotomus and Sergentomyia ; New World: Lutzomyia , Brumptomyia , and Warileya

Form function

Locomotor organelles

Reproduction

Flagellum -

Kinetoplast movement away from the posterior end in the midgut trypomastigote and anterior to the nucleus in the epimastigote reflects the elaboration of the posterior section of mitochondrion

Flagellum

Asexual reproduction in fly vector

Mitochondrion "pushes" kinetoplast forward

Flagellum

Trypomastigotes, although abundant in the blood in early infections, do not reproduce until they have entered a cell and have transformed into amatisgotes. Most frequently invaded are cells of the spleen, liver, and lymphatics and cells in cardiac, smooth, and skeletal muslces. Nervous system, skin, gonads, intestinal mucosa, bone marrow, and placenta also are infected.

Flagellum

Trypanosomes can actively penetrate host cells, but they may also enter through phagocytosis by host macrophages. Repeated binary fission produces many amastigotes, killing the cell > lysis > protozoa attack other cells.

Life Cycle

Encystment

Blood meal > locates in posterior section of midgut: multiplies in trypomastigote form (10 days) > migrate to foregut (12th - 20th day) > migrate to esophagus > pharynx > hypopharynx > salivary glands: become epimastigotes, attach to host cells or lie free in lumen > [asexual generations] > become metacyclic trypomastigotes (small, stumpy and lack a free flagellum; infective to vertebrates) {FLY: complete in 15 - 35 days} > in vertebrates: multiply as trypomastigotes in blood and lymph

Do not invade or live within cells but inhabit the connective tissue spaces within various organs and the reticular tissue spaces of the spleen and lymph nodes. Abundant in lymph vessels and Short, stumpy forms are the only ones infective to tsetse flies, and the intermediate intercellular spaces of the brain. forms are transitional from the long, slender noninfective forms. Transition is marked by increasing elaboration of the mitochondrion.

In vertebrate hosts: live in the blood, lymph, spleen, and cerebrospinal fluid.

Triatomine bugs ingest trypomastigotes > trypomastigotes pass through posterior portion of insect's midgut > become short epimastigotes > longitudinal fission > long, slender epimastigotes. 8-10 days after infection: short metacyclic trypomastigotes found in insect rectum.

Pseudocysts - cyst-like pockets of parasites that form in muscle cells.

Triatomine bugs ingest trypomastigotes > trypomastigotes pass through posterior portion of insect's midgut > become short epimastigotes > longitudinal fission > long, slender epimastigotes. 8-10 days after infection: short metacyclic trypomastigotes found in insect rectum.

Pseudocysts - cyst-like pockets of parasites that form in muscle cells.

Recent Studies

Feeding and metabolism

Excretion and osmoregulation

Strain 1: passed by syringe from one vertebrate host to another; becomes monorphic; slender trypomastigotes no longer infective to tsetse fles; cannot be cultivated in vitro , morphology and metabolism correspond to those in natural infections; very active consume substantial amounts of glucose and oxygen

Depend entirely on glycolysis: degrade glucose > pyruvate only; has no tricarboxylic acid cycle or oxidative phosphorylation by way of the classical cytochrome system (requires oxygen, not sensitive to cyanide)

Strain 2: placed in vitro culture systems; morphology and metabolism revert to those found in fly midgut; kinetoplast farther from posterior end and close to nucleus

Blood clot in vector's midgut: complete degradation of glucose through glycolysis, the tricarboxylic acid cycle, and the cyanide-sensitive cytochrome system

Oxygen consumption of blood and intracellular forms is the same as that of culture forms. Bloodstream forms have Krebs cycle and classical cytochrome system.

T. cruzi is a "partial aerobic fermenter". Some of the glucose carbon consumed is degraded completely to carbon dioxide.

Oxygen consumption of blood and intracellular forms is the same as that of culture forms. Bloodstream forms have Krebs cycle and classical cytochrome system.

It excretes a substantial portion as succinate and acetate.

Endosymbionts

Species

Morphology

Disease caused

Symptoms

Pathogenesis

Distribution

Insect Vectors

Form structure

Form function

Locomotor organelles

Reproduction

Life Cycle

Encystment

Recent Studies

Feeding and metabolism

Excretion and osmoregulation

Endosymbionts