Protozoa III - Trypanosoma Flashcards
What phylum do Trichomonas belong to?
And name at least 2 other familiar parasites to belong to the same higher group.
Excavata
Giardia and Leishmania also belong to Excavata, though they belong to different classes than Trichomonas.
Trichomonas gallinae
Family Trichomonadidae
Avian trichomonosis
Tritrichomonas foetus
Family Trichomonadidae
Bovine and cats tritrichomonosis
Describe Trichomonas gallinae.
A protozoan parasite but NOT a zoonosis!
Alt. names: Pigeon canker, frounce in raptors, “roup” in pigeons.
Firstly discovered in 2005 in Great Britain from finches; 2009 – in the nordics.
Colonizes upper respiratory tract and intestinal tract.
Adult birds are asymptomatic carriers due to acquired immunity.
More common from August to October.
Spreading through migratory birds.
Host range of Trichomonas gallinae.
Mostly a pigeon parasite. Infects other birds (inc. raptors and chickens, turkeys, passerines). Mostly in young birds.
Pathogenesis of protozoan Trichomonas gallinae.
Colonizes upper respiratory tract and intestinal tract so: Necrotic lesions in the crop and oropharynx, liver, air sacs and cranium.
Transmission of Trichomonas gallinae. (3)
by crop milk – adult to offspring
by saliva – in water or feed
by predatory (raptor birds)
Not very resistant in outside.
Symptoms of trichomonas gallinae.
Apathy and emaciation
Digestive disorders – vomiting and green feces.
Head shaking, dirty beak and back side of the body.
High mortality among young pigeons through obstruction of the esophagus or pharynx or due to freezing.
Trichomonosis diagnosis.
Cross lesions
Crop or mouth swabs from unfed animals – microscoping (lens 10x)
- suspended immediately in a phosphate- buffered saline solution on a cover slip
- wriggling flagellar parasite, stays in the field
Autopsy
From mouth, faeces, crop or blood cells in vitro culture.
Molecular methods: PCR
Trichomoniasis treatment.
dimetridazole and metronidazole
- not licensed for food-producing animals
- increasing resistance problem
Vitamin A supplementation
Prophylactic treatment of breeding birds before breeding season!
Trichomoniasis control measures
Sensitive to drying!
- Regular cleaning and drying of bird eating houses.
NB: feeding birds increases the spread!
Host range of TRItrichomonas foetus.
(don’t confus with trichomonas gallinae etc. spp. that only infect birds)
Tritrichomonas foetus has been recovered from cattle, pigs and cats in several parts of the world, and may occur in other mammals.
TRItrichomonas foetus causes
Disease TRItrichomoniasis
- Cattle: reproductive tract - bovine venereal tritrichomoniasis – transmission by mating.
- Early fetal death and temporary infertility - extended calving intervals.
- Cats: large intestine
- Chronic large bowel diarrhea
- Pigs: stomach, nasal passages, cecum, colon.
Notifiable disease!
Potential Zoonosis
Distribution of Tritrichomonas fetus in bovine
Distribution worldwide – in herds with natural mating.
life cycle and reproduction types for tritrichomoniasis
Simple life cycle, reproduction by binary fission. (Trophozoite and pseudocyst)
Transmission of tritrichomoniasis in bovine:
Transmission in bovine:
- Direct contact – natural service/venereal (both directions)
Transmission of tritrichomoniasis in cats:
- Fecal-oral from cat to cat
- Indirect through food or snails?
tritrichomoniasis tissue location in bovine?
in cats?
Tissue location in bovine:
Female: the lumen of the female genital tract.
Male: the crypts of the surface epithelium of the penis and prepuce.
Tissue location in cats: large intestine
Pathogenesis and symptoms of tritrichomoniasis in COWS. (not bulls)
Cows: Parasite replicates in the mucosa of the vagina - vaginitis.
Later after fertilization it migrates through cervix into the uterus - endometritis.
Next: placentitis, chorionitis, foetal pneumonia.
- early abortion before 4th months, occasionally pyometra
- also poss. no abortion – live calves being born
Symptoms: chronic inflammation of the reproductive tract, early abortion, infertility, irregular ostrus cycle, pyometra or endometritis
NB: spontaneous recovery – immunity for one breeding season.
Pathogenesis and symptoms of tritrichomoniasis in BULLS.
Parasites in preputial cavity, urethrae and testes.
No signs in chronically infected bulls, are asymptomatic carriers.
Lifelong infection.
Pathogenesis tritrichomoniasis in CATS.
Inhabits the epithelial surface, crypts of the cecum and colon causing colitis.
Crypt cell hypertrophy, hyperplasia.
Asymptomatic to symptomatic cases.
Signs 2-7 days post infection.
Mainly in young cats and kittens.
Giardia spp. and Tritrichomonas fetus both present in host in 12% of cases together.
Symptoms of tritrichomoniasis in CATS.
Tenesmus, flatulence, anorexia, depression
Chronic diarrhea
Small amounts of liquid, frequent defecation,
often with fresh blood and mucous, yellow-green, bad smelling.
Diagnosis of tritrichomoniasis.
Clinical findings
Note that at least cats will not have No hematological or biochemical abnormalities (not sure about bovine).
Direct fecal smear of fresh feces, then microscopy for finding trophozoites.
Culture (purpose-made InPouch TF culture media kit, pictured)
PCR: extraction of DNA in feces
A bull is considered to be free of tritrichomonas fetus infection if:
- At least 3 preputial washing fluid samples no parasites were detected.
- A bull has mated at least 5 heifers without infecting them.
Protozoan genera Trypanosoma and Leishmania belong to what
phylum
class
order
family
phylum Excavata
class Kinetoplasta
order Trypanosomatida
family Trypanosomatidae
Leishmania spp. morphological forms
Amastigote = a protist cell that does not have visible external flagella or cilia. The term is used mainly to describe an intracellular phase.
Promastigote = the extracellular promastigote develops within the insect vector.
Trypanosoma spp. morphological forms
epimastigote = A stage in unicellular life-cycle, typically trypanosomes, where the flagellum is anterior of the nucleus, and attached the cell body by a short membrane.
trypomastigote = the flagellated stage of trypanosomes found in peripheral blood, are large, extracellular protozoa
Infective form for Leishmania.
promastigote
Infective form for Trypanosoma.
trypomastigote
Describe Genus Trypanosoma I group: salivaria:
Transmitted with the saliva of the vector (tsetse fly, Glossina spp.).
Causes African trypanosomiasis - sleeping sickness, surra, nagana.
Back end rounded;
Kinetoplast small and close to back end.
e.g. T. brucei, T. evansi,
Describe Genus Trypanosoma II group: stercoraria:
Transmitted with the feces of the vector (various insects).
Causes American trypanosomiasis - Chagas disease.
Back end long and pointed;
Kinetoplast large and clearly subterminal.
e.g. T. cruzi T. theileri
II group, Stercoraria are also known as
= “American trypanosomes”
They cause chagas disease.
Spp. to belong to Trypanosoma genus II group, Stercoraria.
T.cruzi (humans and mammals)
T.theileri
T.melophagium
T.lewisi
Describe Trypanosoma cruzi.
Causes chagas disease in people.
Wild animals are main reservoirs
- 150 wild species (foxes, marsupials, etc.).
Domestic animals: dogs, cats, horses.
Transmitted by “kissing bug” vectors that bite you on your face as you sleep.
Life cycle and transmission of Trypanosoma cruzi.
Insect carrying trypansoma bites human (or other mammal that can then act as reservoir).
Trypomastigotes from bug penetrate human cells where they transform into amastigotes and multiply asexually.
Amastigotes mature into trypomastigotes and enter bloodstream.
Trypomastigotes in the bloodstream can be picked up by new bugs during a blood meal.
Life cycle of Trypanosoma cruzi in bugs.
Trypomastigotes in the bloodstream of humans or other mammal can be picked up by new bugs during a blood meal.
Bug ingests trypomastigotes.
The parasite is an epimastigote in the bug midgut (don’t know how) where they multiply.
Then they become trypomastigotes again.
It seems the bug feces contains trypomastigotes which is how they would enter the bite wound.
Transmission of Trypanosoma cruzi
- through vector bite
- through the mucosa of the eye, nose and mouth
- through skin wounds, cuts
- through blood transfusion
- congenital/ transplacental
- organ transplantation
- ingestion of infected vector
- ingestion of blood or tissues with parasites
- predation of infected mammals?
Clinical findings of chagas disease in acute form.
Incubation time weeks to years
Acute form
- young animals
- lesions in myocardium and CNS
- diarrhea, lethargy, seizures, lymphadenopathy
- cardiac arrhythmia
- sudden death
Clinical findings of chagas disease in chronic form.
Chronic form
- up to few years after acute disease
- ventricular arrhythmias
- myocardial dilation, congestive heart failure
- fluid in abdomen, lungs
- lifetime disease
Pathogenesis of Chagas disease
Destruction of muscle tissue by multiplying T.cruzi.
Intracardiac nervous system lesions
Auto–immunity - inflammation
FIBROSIS
organ level pathology found in Chagas disease
ventricles and chambers dilated
hydropericardium
reduction in cardiac muscle
congestive cardiac insufficiency (CCI)
increased right ventricle size
focal myocarditis
hematological & biochemical findings in Chagas disease
Anemia
leukopenia and neutropenia
hypoglycemia
elevated protein values
I group, Salivaria are also known as
“African trypanosomes”
they cause african trypanomiasis
Spp. to belong to Trypanosoma genus I group, Salivaria.
“African trypanosomes”
T.brucei gambiense
T.brucei rhodesiense both affect humans, are transmitted by tsetse flies and cause sleeping sickness.
The others are spp. to affect only animals.
Life cycle and transmission of Trypanosoma brucei.
A tsetse fly bites a human and injects trypomastigotes.
Are carried to other sites via bloodstream. They multiply asexually.
The trypomastigotes circulate in blood during the acute phase and are undetectable in the latent phase.
A tsetse fly can pick up these trypomastigotes from an infected human (or mammal) host.
Life cycle of Trypanosoma brucei in bugs.
A tsetse fly can pick up trypomastigotes from an infected human (or mammal) host.
The trypomastigotes transform in the bug midgut and multiply asexually.
They leave the midgut and transform into epimastigotes which multiply in the bug salivary gland.
They then transform into trypomastigotes again. These are the stage which are injected into a new host during a bite.
VECTORS for African trypanosomiasis
Trypanosoma evansi transmitted by Tabanids (horse fly).
Causative agent of Surra disease.
Trypanosoma brucei, T. vivax, T. congolense transmitted by Tsetse fly (Glossinidae).
Causative agent of Nagana disease.
Trypanosoma evansi causes Surra disease which is characterized by?
Progressive anaemia, weight loss, icterus, lethargy, weakness.
Symptoms in dogs similar to rabies.
Vector: Tabanidae and vampire bats
(Surra means “heavy breathing through nostrils” in marath language)
Clinical symptoms of Dourine disease caused by Trypanosoma brucei equiperdum.
Incubation period 1 week to 6 months!
Three phases:
1. Acute (1-2 months) – edematous swelling of genitals, fever, edema.
- „subacute “ – cutaneous plaques, abortion, emaciation.
- Chronic (many years) – deadly nervous phase, anemia, face paresis.
