GENUS TRYPANOSOMA Flashcards
Trypanosoma
✓ Flagellate protozoan parasites that live in the blood, lymph and various tissues of their vertebrate hosts
✓ parasites of all vertebrate classes
✓ majority are transmitted by blood-feeding invertebrates, although other transmission mechanisms exist
Genus Trypanosoma under Subgenus NANNOMONAS
T. congolense and T. simiae
Genus Trypanosoma under Subgenus DUTTONELA
T. vivax
Genus Trypanosoma under Subgenus MEGATRYPANUM
T. theileri and T. melophagium
Genus Trypanosoma under Subgenus TRYPANOZOON
T. brucei brucei, T. brucei gambiense, T. brucei rhodesiense, T. equinum, T. evansi and T. equiperdum
2-3um Leishmania amastigote maybe the smallest eukaryotic cells
Amastigote
flagellum is very short, projecting only slightly beyond the flagellar pocket
Amastigote
elongated body with flagellum extending forward as a functional organelle
Promastigote
kinetosome and kinetoplast are located in front of the mucleus, near the anterior end of the body
Promastigote
Kinetoplast and kinetosome are still located between the nucleus and the anterior end, but a short undulating membrane lies along the proximal part of the flagellum
Epimastigote (Crithidial)
Kinetoplast and kinetosome are near to the posterior end of the body
Trypomastigote (trypanosome)
flagellum runs along the surface, usually continuing as a free whip anterior to the body
Trypomastigote (trypanosome)
Two broad groups of Trypanosomes
✓ Hemoflagellates
✓ Mucoflagellates
blood and tissue parasites
Hemoflagellates
live in the mouth and the cecum/colon
Mucoflagellates
Two broad groups of Trypanosomes
✓ Salivaria
✓ Stercoraria
develops at the anterior portions of the digestive tract (anterior station)
Salivaria
Example of Salivaria
T. brucei ssp., T. evansi, T. congolense, T. vivax
develop at the vectors hindgut (posterior station)
Stercoraria
Example of Stercoraria
T. cruzi, T. lewisi, T. theileri, T. melophagium, T. canorini
do not require development in an intermediate host
Trypanosoma equiperdum and T. equinum
Salivarian Trypanosome
Fly takes in the trypanosome by feeding- Develops into infective form in the salivary glands- Infective form transferred to animal by feeding
Stercorarian Trypanosome
Fly takes in the trypanosome by feeding- Trypanosome develops into infective form in the rectum- Infective form transferred to another animal through feces
Modes of Transmission of Trypanosomes
• Cyclical
• Non-cyclical
• Coitus
• Transplacental
• Ingestion of fresg carcasses or organs of animals which died of the infection intrauterine
anterior station development; multiplication and transformation in the gut and proboscis; transmission is by feeding
Salivaria
posterior station development; multiplication in the gut; infective forms migrate to the rectum and passed out in the feces
Stercoraria
mechanical transmission by TABANIDS and STOMOXYS; no cross transmission because trypanosomes die quickly
Noncyclical
arthropod intermediate host (biological)
Cyclical
Pathogenesis of Trypanosomes
✓ Lymphoid enlargement
✓ Hemolysis
✓ Cell degeneration and inflammatory infiltrate
exhaustion of cellular elements
lymphoid enlargement
failure of phagocytic system
Hemolysis
tissue degeneratiom particularly the CNS and the heart muscles
Cell degeneration and inflammatory infiltrate
Determines the spread of Trypanosomiasis
• Distribution of vectors
• Virulence
• Host preference
Trypanosoma brucei consists of 3 subspecies;
✓ Trypanosoma brucei brucei
✓ Trypanosoma brucei gambiense
✓ Trypanosoma brucei rhodesiense
pleomorphic, showing long slender, short stumpy and intermediate forms
Trypanosoma brucei
represents the ancestral form
Trypanosoma brucei
T. b. gambiense and T. b. rhodesiense have evolved from it
All utilize the GLOSSINA FLIES (TSETSE FLIES) as the vector. ID by wing veination “Hatchet cells”
Trypanosoma brucei
Trypanosoma brucei life cycle
° only 2 stages in life cycle
° Epimastigote and the trypomastigote stages
Trypanosoma brucei brucei transmit;
- African Animal Trypanosomiasis
(AAT: tsetse disease, tsetse fly disease, AFRICAN ANIMAL NAGANA)
Trypanosoma brucei brucei affects livestock animals like?
Sheep, goats, oxen, horses, camels, pigs, dogs, donkeys, and mules; non-pathogenic to humans
Lives in the blood, lymph nodes and spleen and CSF
Nagana (Trypanosoma brucei brucei)
Pathogenesis of Nagana (T. b. brucei)
✓ Horse, mules and donkey, dogs- suffer acutely and may die in 15 days
Symptoms of Nagana (T. b. brucei)
Anemia, edema, watery eyes and nose and fever; blindness is common in dogs
are parasitic in the bloodstream of sheep, goats, cattle, horses, pigs and dogs may also be infected but cattle most important
Trypomastigotes
Trypomastigotes
- Cattle become emaciated and uncoordinated
- Cattle die in a few weeks to months
common drug treatment of trypomastigotes
Berenil
Infects humans only causing SLEEPING SICKNESS
Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense
called as sleeping sickness
Human African Trypanosomiasis (HAT)
Vector of T. b. gambiense and T. b. rhodesiense (Sleeping sickness)
Glossina palpalis and G. morsitans
less plentiful. cannot live in lab animals
T. brucei gambiense
Reservoir host of T. b. gambiense
goats, cattle & pigs
T. brucei gambiense transmitted by?
G. palpalis
More plentiful. Can live in lab animals. Nucleus is shifted posteriorly
T. brucei rhodesiense
Reservoir host of T. brucei rhodesiense
wild game animals
T. brucei rhodesiense transmitted by?
G. morsitans
Pathogenesis of HAT
- Chancre
- Swollen and congested lymph nodes at neck, groin and legs
develops where metacyclic trypanosomes are inoculated
Chancre
Swollen and congested lymph nodes at neck, groin and legs
Winterbottom’s sign
rapid weight loss and heart involvement; no somnambulism or other protracted nervous disorders
T. b. rhodesiense
invade the central nervous system, they initiate the chronic, sleeping-sickness stage of infection
T. b. gambiense
Pathogenesis of Sleeping sickness
Chancre- blood- lymphatics- CNS- Death
increase apathy, disinclination to work, mental dullness; tremor of the tongue, hands, paralysis or convulsions usually follow
Sleeping Sickness
Sleeping sickness
- sleeping increases with patient falling asleep even while eating or standing
- finally coma and death ensue (malnutrition, pneumonia, heart failure, severe fall)
Treatment for Sleeping sickness most common used, useful but they have severe side effects
Melarsoprol or Suramin
Trypanosoma congolense
- Causes “Nagana disease”
- fatal in cattle and other domestic animals; wild ruminants
- Africa
- Transmitted by Glossina and biting flies
- Severe anemia with no immature RBC
Trypanosoma vivax
- Causes “Souma”
- Affects the blood of ruminants and other animals; wild game animals are reservoir
- Africa, South and Central America
- Mucosal and serosal hemorrhages in the body, anemia
causes Nagana disease
Trypanosoma congolense
fatal in cattle and other domestic animals; wild ruminants
Trypanosoma congolense
Trypanosoma congolense transmitted by?
Glossina and biting flies
can cause sever anemia with no immature RBC
Trypanosoma congolense
causes Souma
Trypanosoma vivax
Affects the blood of ruminants and other animals; wild game animals are reservoirs
Trypanosoma vivax
can cause mucosal and serosal hemorrhages in the body, anemia
Trypanosoma vivax
Affects blood of large ruminants
Trypanosoma theileri
present in the Philippines (65% prevalence in cattle and carabaos on culture but responds negative to mouse test)
Trypanosoma theileri
Trypanosoma theileri transmitted by?
Biting flies; TABANUS and HAEMATOPOTA
Transmitted by biting flies; Tabanus and Haematopota
Trypanosoma theileri
has been associated with “Turning sickness” in Uganda, abortion and decreased milk yield
Trypanosoma theileri
may interfere with the diagnosis of Surra (larger than T. evansi)
Trypanosoma theileri
Treatment for Trypanosoma Theileri
° Diminazene aceturate (DA)
° Isometamidium chloride (IMC)
° Suramin
° Quinapyramine
most widely used. binding to kinetoplast DNA thereby inducing complete and irreversible loss of kDNA in certain strains of trypanosomes
Diminazene aceturate (DA)
highly toxic because they are DNA intercalating agents. Use in field is not recommended
Isometamidium chloride (IMC)
ureic component, no longer used. Inhibition of enzymes involved with the oxidation of reduced nicotinamide-adenine dinucleotide (NADH)
Suramin