Background Information on the

Family- Trypansomatidae

• Two important genera are Trypanosoma and Leishmania
• Are heteroxenous evolved from monoxenous
• Parasitize all vertebrate classes 
• Part of life cycle in invertebrate host
• Hemoflagellates 
• Causes several diseases: most recognizable is sleeping sickness

4 morphological stages of the 

Family- Trypansomatidae

• Amastigote
• Promastigote
• Epimastigote
• Trypomastigote

Represented by round forms, flagella not visible, intracellular parasite

And 

in which genus can this form be found?

Amastigote

Leishmania has amastigotes in its vertebrate host

Amastigote

-Small round, flagella not visible

Represented by flagella anterior to the nucleus, 

And

Where are they found?

Protomastigote

Found in insect vector of Leishmania

Represented by flagella located close to the kinetoplast, emerging from the side of the body to run along a short undulating membrane 

And

Where is it found? 

Mature and final stage of genus Trypanosoma

Kinetoplast lies posterior to the Nucleus

Flagella lies on the side of the body along a long undulating membrane

And

Where can it be found?

Causes live stock disease known as Nagana 

Live in intracellular body fluids 

Are anterior station parasite

Its intermediate host is Glossina sp. - Tsetse fly

Symptoms include: anemia, edema, watery eyes, runny nose, fever, uncoordination, paralysis, death

Control: cut low bushes, eliminate reservoirs, and spray insecticides

Trypanosoma brucei gambiense (T.b. gambiense)

and

Trypansoma brucei rhodesiense (T.b. rhodesiense)

Acute form of African Sleeping Sickness, acute for a few months

Winterbottom's sign

Diagnosis: blood smear for trypomastigote/ serologic test for antibodies

Treatment:multiple courses for IV arsenic, some newer but all difficult

Control:control flies

T.b. rhodesiense

Causing sleeping sickness

T.b. gambiense

Causes sleeping sickness

Morphologically indistinguishable from Typanosoma brucei

Causes dourine in horses and donkeys 

No insect vector

Passed during coitus so that it is a venereal disease

Symptoms: Genital endema and depigmentation

Death due to body-wide paralysis

Morphologically indistinguishable from Typanosoma brucei

Causes dourine in horses and donkeys

No insect vector

Venereal disease

Symptoms: genital edema and depigmentation

Death due to body-wide paralysis

Trypanosoma brucei brucei causes a disease called _______

Trypanosoma brucei brucei

T.b. gambiense

T.b. rhodesiense

Trypanosoma equiperdum

T. cruzi

T. lewisi

Trypanosoma equiperdum

Causes a disease known as dourine and is passed through intercourse

Causes Chagas' disease

Vectors include several bugs of Reduvidae (cone-nosed bug)

Symptoms: Chagoma and or Romana's sign 

Ranges from Mexico through South America

Trypomastigotes picked up from host blood by feeding vector

Become epimastigotes in midgut and reproduces

10 days later they are infective trypomastigotes

Enter vertebrate host as bug feeds 

Usually they are phagocytized by monocytes

If they survive, within monocytes they become amastigotes and multiplying until monocysts burst

Trypomastigotes travel to other areas in the body repeating this scenario to form pseudocysts of amastigotes that will burst

Epimastigote in bug, with in 10 days they will become trypomastigote

bursting of pseudocysts releases toxins and causes immune reactions which lead to necrosis

Small children succumb to heart failure and usually die within 3 weeks

Autonomic nerve tissue degeneration can lead to megaesophagus or megacolon

Person can't even swallow

Diagnosis: blood smear with trypomastigotes since they do not reproduce until they enter host cell

Treatment: Some drugs being tested to kill extra-cellular stages, but amastigotes are safe from them because some goes into other cells after the bursting of the monocytes

Currently there is no cure 

Trypanosome of the genus Rattus

Vector is the rat flea: Nosopsyllus fasciatus

Rat produces ablastin, which is an antibody that inhibits reproduction of trypomastigotes

Rat gets parasite as it is trying to bite the flea off its skin eating flea with the parasite in it. It either picks up the flea or its feces

Not pathogenic to rat because the rat's immune system produces a substance called ablastin in response to parasite. 

Leishmania tropica

Leishmania donovani

Leishmania braziliense

Leishmania mexicana 

Vector: sandfly 

Promastigotes from insect are infective

Promastigotes enter reticuloendothelial tissues of liver and spleen and become amastigotes called Leishman-Donovan (L-D) bodies

Amastigote release and circulate, some enter other cells

Oriental sore, cutaneous leishmaniasis

Found in: parts of Africa, India, and Middle East

Diagnosis: Skin scrapings for amastigotes (L-D)

Treatment: antimony drugs or immune system will conquer it in about a year as the cell burst and release them

Deliberate inoculation with promastigotes

L. donovani kala azar

Happens when you stop taking treatments

L. donovani kala azar

Happens when you stop taking treatments

Can be found in central Mexico to northern Argentina and Panama

Sore will develop within a few weeks to months

Heal within about a year following secondary lesion

Secondard lesion called espundia or uta

Death by secondary infection or respiratory problems

Diagnosis: Check for L-D bodies

Treatment: antimony drugs over a long period of time

Can destroy voice box

Range similar to L. braziliense but more north, even to Texas

Secondary lesion called chiclero ulcer

Diagnosis: Check for L-D bodies

Treatment: antimony drugs over a long period of time

Commensal of colon

Trophs in colon or loose stools

Teardrop shape

Anterior to nucleus and cytostome (cells mouth)

Cysts as feces dry

No cell division as cysts

Host ingest cysts in water

Becomes trophs after it reaches the stomach

4 flagella rises from the kinetosome that we are unable to see

3 are anterior and the 4th lies on the side of the cytostome

Most common intestinal flagellate of humans

Side by side nuclei

Trophs live in small intestine

Four pairs of flagella

Adhesive disc

Cyst form in colon and dry still 4 nuclei

Host ingest cyst

Excysment in duodenum 

Disease: giardiasis

Pathogenesis: More problem for children than adults 

Interferes with fat absorption 

jaundice: bilirubin

Reservoirs: bears, beavers, dogs, cats, sheep

Diagnosis: cysts or trops in stool

Several oral drugs- treat entire family

Inflammation of the vagina and urethra of females and urethra and prostate of males

Passed venerially-intercourse

Sometimes passed on toilet seats or washcloth

No cysts stage, ONLY TROPH STAGE

Release substance that can change the pH level of the vaginal (vaginal acidity)

Diagnosis: troph in discharge

Cure: oral drug by both partners

In men, it is asymptomatic 

Affects chicken and turkey

Causes infectious enterohepatitis or histomoniasis

Several troph stage but NO CYST

One flagellum but 4 kinetosomes

Other anatomy includes pelta, parabasal body, exosyle

Ameboid movement and pseudopodia

Lyse host cells causing peritonitis in cecum and liver necrosis

Blackhead symptom 

Can have numerous body shapes depending on its enviroment

Control: Do not raise chickens and turkey together, several preventive drugs can be added to food

Three ways of transmission for the parasite Histomonas meleagridis

1. Gain entrance with food that raise stomach pH then they can get right pass the stomach
2. In eggs of nematode, Heterakis gallinarum so the worm is a definitive host.
3. Heterakis eggs eaten by earthworms, eggs hatch in earthworm, earthworm eaten by bird, earthworm is paratenic host

Usually commensal of cecum

Considered commensal of human that feeds on bacteria

No flagellum, moved by pseudopodia 

Two nuclei-arrested telophase

NO CYSTS stage

Attached nuclei by spindle

Transmission: trophs destroyed by gastric jusices

Maybe passed in eggs of nematode pinworm, Enterobius vermicularis

Nucleus with endosome (DNA clump together)

Chromatin granules

Chromatiod bars in early cysts

Food vacuoles in trophs

Dysentery

Trophozoites: in intestines and diarrhetic stools 

Food vacuoles within cytoplasm, single nucleus, large, motile

Precysts and cysts-intestine and dry stool

Glycogen vacuole, chromatid bars

Metacysts (older)- nucleus divides to 4 nuclei

Metacystic troph

Can be virulent or non virulent to humans

Can exist in humans as commensal

Have multiple form with endosome located at center

Pathogenesis: intestinal lesions, hepatic amebiasis, pulmonary amebiasis, cutaneous amebiasis

Fecally contaminated water or food

Filth fly- Musca domestica

Diagonsis: trophs or cysts in intestinal or stool smears

Most common intestinal ameba of humans

Commensal

Eccentric endosome

Jagged chromatoid bars

Eight nuclei in metacysts

Commensal of cecum

Half the size of E. histolytica

Large endosome variably placed

Clear around endosome

Up to 4 nuclei in metacysts

Iodamoeba buetschilii

Usually commensal of cecum, but sometimes associated with ectopic lesion

Large endosome, no chromatin

Cysts- single nucleus and glycogen vacuole (rectangular) stained with iodine

Feeds on bacteria

Morphologically variable

Primary amebic meningiocephalitis (PAM)

Cyst, ameba, flagellate form

Normally a soil ameba

Flagellated in contaminated water

Forced in nasal passages, moves up through cribriform plate to brain. 

Common in meal worms- Tenebrio molitor

Gregarina

Eimeria tenella cecum

Toxoplasmosis

Cats are definitive host but many animals including humans can be hosts

Ingest oocysts (or tachyzoites or bradyzoites) which has 2 sprocysts released in small intestine

In cats, they enter small intestine cells and begin sexual reproduction, some become gamete

In others, they travel to other cells, usually macrophages

In host, cell sporozoite divides to tachyzoites and are released

Tachyzoites can enter other cells and divide again

or can be infective if the intermediate is eaten

They prefer brain and nervous system, and skeletal muscle

In time, they become bradyzoites which just multiply more slowly

walls forms around them and they are now zoitiocysts

any of these are infective if host is eaten

sexual reproduction occurs only in cat

Oocyst passed in cat feces

Gut tissue quickly replaces so usually not a problem in adult cats

In brain or retina, can cause irreparable damage, but usually immunity has built up by then

Could lead to encephalitis, paralysis, or blindness

Most human cases are asymptomatic except if on immuno- suppressant drugs or HIV

Congenital: mother contractions T. gondii while pregnant, she is not immune and it crosses the placenta

Birth defects or still birth are common usually they are nerological damage. 

Can be passed by eating undercook beef, pork, or lamb

Flies, sandbozes, transfusions, transplant

Humans pick up parasite by petting cat. Flies can have it on their feet.

Zoitocysts with bradyzoites ingested by carnivore when eating a herbivore. 

Parasitize many herbivores that serve as intermediate host. Carnivores are definitive host.

Humans can be definitive or intermediate

Not as pathogenic is T. gondii

T. gondi zoitocysts

Four species affect humans- more human death and economic loss than any other parasite

Heteroxenous

Invertebrate/ definitive host is Anopheles spp. mosquito 

Hard to control

1 genus that causes malaria- plasmodium

In birds/ reptiles, invertebrate host

First division is meiotic, the mitotic for thousands of haploid  sporozoites

they burst and sporozoites migrate to salivary glands

Injected to verterbrate host while feeding 

Mosquito releases sporozoites into blood as it feeds

Quickly invade internal organs, usually liver

Normally occur an hour after initial inoculation

in liver, become intracellular trophs-extraeythrocytic stage, no longer considered sporozoite, Troph feeding stage

divide asexually by schizogony, cell bursts releasing thousands of merozoites

Sometimes reenter liver cells 

Eventually, merozoites enter RBCs, so now erythocytic stage

Become feeding trophs in RBCs

large vacuoles cause ring stage

eventually divides becoming schizont

Cell bursts and merozoites released

Chills, fevers, fatigue

Gametes released in mosquito gut 

Microgamete divides into6 or 8 by budding

They bud off and each has a flagellum

Joins macrogametes to form ookinete which is the only diploid stage (zygote)

Migrates through the gut wall to hemocoel side, divides and becomes oocysts 

Benign tertian malaria

Counts about 40% of human malaria, mostly Asia

Does well in temperate climates

By 7th day after exposure each sporozoite will have produced some thousands merozoits

Invade RBCs, but also reinvade liver -extraerythocytic stage can go dormant in liver cells for a long period of time

Lead to relapse

Later ring stage have Shuffner's dots

Schizogeny complete in about 48 hours and all infected RBCs then burst.

Troph takes up most of RBCs- 16 merozoites will be formed by schizogeny

As troph enlarge, RBC size increase leading to the burst of the red blood cells. Upon bursting, immune reaction causes chills and fever, loss of RBCs causes weakness

Merozoites reenter other RBCs, some go through schzogeny some become gametocytes

Another 48 hours RBCs burst again, so by third day, so tertian

Gametocytes mature in about 4 days

Macrogametocytes fill nearly entire RBCs

Microgametocytes smaller

Other merozoites only attack young RBCs so limit to the number they can destroy at a time so benign. 

Ring stage takes about 1/3  or 1/4 of blood cells

P. vivax

Malignant tertian malaria

Does best in tropical climate 

50% of all human malaria 

EE stage can be in the liver or the brain

Only one EE stage, so merozoites do not reenter organs

Merozoites cant enter all ages of RBCs so it is malignant

About 5.5 day after exposure EE schizont rupture and release about 30,000 merozoites

They do reenter EE cells

They enter RBCs, divides as schizonts, and release merozoites as RBCs, burst after 48 hours 

Sometimes multiple infections of RBC with more than one troph in it

Maurer's spots

Merozoites can reenter other RBCs such that 65% gets infected with 25% fatal

Some become schizont and others become gametocytes 

Both gametocytes are crescent shap

If you could kill EE merozites, disease is cured

P. falciparum troph ring

Quartan malaria-72 hours

Tropical climates but spotty distribution

About 7% of human malaria

only old rbcs so parasitemia is low

Relapse occur 

Band form in later troph

Found throughout the world and is declining

No Shuffners' nor mauers dots

Both macro and microgametes fill the RBCs

Anemia- red blood cell destruction

fever and chills, headace, delirium (blood vessels dialte)

Jaundice and iron deposition

Blackwater fever-renal failutre

Pernicious malaria