Parasites Flashcards
Trypanosoma brucei gambiense - Geographic distribution
Occurs in tropical Africa, its limited on west coast to districts 15N and 18S of the equator
Trypanosoma brucei gambiense - Morphology
In fresh blood: colourless spindle shaped bodies that move rapidly in a spinning motion amongst RBC. a slender, elongated, colourless, sickle-shaped and flattened microscopic body
14-33 micrometers in LENGTH, and 1.5-3.5 micrometers in BREADTH.
Anterior end is more pointed than the blunt posterior end, with both sides tapering.
cytoplasm is granular and stains PALE BLUE while containing DARK-BLUE volutin granules
nucleus is located towards the centre of the cell and it stains a reddish-purple
undulating membrane is pale blue and stretches throughout the trypanosome and then merges with its body towards the anterior end
The kinetoplast is typically dark red while stained while the flagellum is red while stained
Trypanosoma brucei gambiense - Life Cycle
- The tsetse fly feasts on human blood, releasing metacyclic trypomastigotes
- Metacyclic trypomastigotes mature into bloodstream trypomastigotes which are carried further to different sites
- They then multiply via binary fission in bodily fluids such as blood, lymph or spinal fluid
At this stage they are diagnosable, able to return into the tsetse fly when it takes a blood meal.
- When the bloodstream trypomastigotes reach the fly’s midgut, they transform into Procyclic trypomastigotes, which can then reproduce via binary fission
- The Procyclic trypomastigotes then transform into epimastigotes which then multiply in the salivary duct of the fly
- These then transform into metacyclic trypomastigotes and the cycle is ready to repeat
Trypanosoma brucei gambiense - Diagnosis + Pathogenicity
Found in blood during fever, in lymph node aspirations during early illness or in cerebrospinal fluid. Direct smears of fluids may not always be able to show trypanosomes, in which case a direct sample of them may be able to be cultured.
Able to be spread through bodily fluids and the bite of a tsetse fly.
it causes proliferation in the lymph nodes, causing generalized lymphoid hyperplasia
Growth of parasites in the CNS can lead to localized antibody-antigen reactions which can lead to disruption of collagen fibres and destruction of fibroblasts
They may also invade the blood-brain barrier and damage white matter
Anaemia and immunosuppression is noted, which makes the patient more susceptible to secondary infection
It can successfully evade the hosts immune system by switching its glycoproteins at its cell surface making it harder for the immune system to bind and attack it
Hypergammaglobulinemia is also characteristic, it is the overproduction of more than one class of immunoglobulins by plasma cells
Trypanosoma cruzi - Geographical Distribution
Only in the western hemisphere, from the south in the USA, to Argentina southwards
Trypanosoma cruzi - Morphology
Spindle shaped
20 micrometers in length
With giemsas stain, cytoplasm stains blue and the nucleus , kinetoplast and flagellum stain red or violet.
The kinetoplast is seen as a large body protruding out from the cell
Trypansomes have a characteristic c shape in microscopic preparations
The trypomastigote doesn’t divide in the bloodstream and instead only multiplies in the reticuloendothelial and other tissue cells as amastigote forms or promastigote or epimastigote when its about to escape from its intracellular location
The amastigote form is round/ovoid in shape and measures 1.5-4 micrometers in diameter.
Each amastigote has a large nucleus that is ruby-red in color and either rod like, or it has a rod shaped kinetoplast that is similar to the color of iodine (deep violet / black) with giemsas stain
Trypanosoma cruzi - Life Cycle
Primary vectors are the triatomid bugs
The bugs are infected when feeding of an infected animals blood.
Inside the midgut the parasite transforms into epimastigotes where it then migrates to the hind gut, becoming an infective trypomastigote
These infective trypomastigotes are then released via the bugs feces, which may be accidentally rubbed into the abrasion from the bite or a nearby wound.
In mammalian hosts, these organisms enter macrophages immediately and become amastigotes multiply
In humans they can be found in reticuloendothelial cells of the spleen,liver, lymph nodes and lymphatic tissue
Furthermore superarenal gland, testes , ovaries, bone marrow and striated muscle cells may be invaded
Trypanosoma cruzi - Diagnosis + Pathogenicity
Can find trypomastigotes in fever or early infection.
Blood cultures, animal inoculations and xenodiagnosis is also helpful
triggers an inflammatory response where lymphatic spread then carries T Cruzi to lymph nodes.
From there they encounter WBCs, which although often kill them, can sometimes be penetrated and used as a breeding ground for T Cruzi
As an amastigote they can spread the infection throughout the body by travelling in the bloodstream
Within cardiac muscle, amastigotes proliferate to form pseudocysts which cause a loss of muscle function, a diffuse inflamatory exudate and proliferation of intestinal connective tissue.
Within the CNS, the cortex and meninges may be inflamed and small granules form around trypomastigotes/amastigotes in the brain around the small vessels
This may cause a gradual loss of function and create disability, until the patient dies
Plasmodium Spp - Geographical Disribution
P. Ovale
P. Vivux
P. Malariae
P. Falciparum
P. Ovale - primarily occurs in tropical Africa but other endemic areas include new guinea and the west phillipines. It is prevalent in west Africa ie Ethiopia and has been reported in south east asia
P. Vivux - worldwide distribution, found predominately in temperate climates, as well as large areas of tropics. It occurs in north and south of the equator within 15-16 degree summer isotherms.
P. Malariae - common in tropical areas such as Burma and sri lanka, and parts of india. It may also be prominent in certain areas of Malaysia and Indonesia.
P. Falciparum - limited to but very commonly distributed in tropic and subtropics, particularly in Africa and asia.
Plasmodium Spp - Morphology
P. Vivax
Early trophozoite/ ring - large, one prominent chromatin dot, sometimes 2, often 2 rings in one cell
Late trophozoite - large, markedly ameboid, abundant, chromatin, prominent, vacuole, pigment in fine rods
Young schizont or pre-segmnenter - large, kinda ameboid, dividing chromatin masses, numerous pigment in rods
Mature schizont or segmenter - large pigment coalescent
Merozoites - 12-24, usually 12-18
Microgametocytes - spherical compact, no vacuole, undivided chromatin, diffuse coarse pigment, cytoplasm stains light blue
Macrogametocytes - spherical, compact, larger than micro, smaller nucleus, pigment same, cytoplasm stains darker blue
Pigment (excluding mature schizonts) - short, delicate rods, irregular, scattered, doesnt coalesce
Alterations in infected RBC - enlarged, decolourised, Schuffners dots seen
Asexual phase - 48 hrs
Prepatent period min - 8 days
Incubation period - 8-31days avg 14
Interval between parasite patency and gametocyte appearance - 3-5 days
Developmental period in mosquito - 30/ more days at 17.5 C. 16-17 days at 20C. 10 days at 25-30C `
Plasmodium Spp - Morphology
P. Ovale
Early trophozoite/ ring
Late trophozoite
Young schizont or pre-segmnenter
Mature schizont or segmenter
Merozoites
Microgametocytes
Macrogametocytes
Pigment (excluding mature schizonts)
Alterations in infected RBC
Asexual phase
Prepatent period
Incubation period
Interval between parasite patency + gametocyte appearance
Developmental period in mosquito
Plasmodium Spp - Morphology
P. Malariae
Early trophozoite/ ring
Late trophozoite
Young schizont or pre-segmnenter
Mature schizont or segmenter
Merozoites
Microgametocytes
Macrogametocytes
Pigment (excluding mature schizonts)
Alterations in infected RBC
Asexual phase
Prepatent period
Incubation period
Interval between parasite patency + gametocyte appearance
Developmental period in mosquito
Plasmodium Spp - Morphology
P. Falciparum
Late trophozoite
Young schizont or pre-segmnenter
Mature schizont or segmenter
Merozoites
Microgametocytes
Macrogametocytes
Pigment (excluding mature schizonts)
Alterations in infected RBC
Asexual phase
Prepatent period
Incubation period
Interval between parasite patency + gametocyte appearance
Developmental period in mosquito
Plasmodium Spp - Life Cycle
P. Ovale
P. Vivux
P. Malariae
P. Falciparum
Female mosquitoes of the genus anopheles are definitive hosts of plasmodia, when a mosquito bites an infected person, it may draw in male and female gametocytes of the parasite into its stomach.
The male microgametocyte matures to become microgametes which may fertilize a macrogamete that has matured from a macrogametocyte
This forms a zygote called an OOKINETE
The ookinete penetrates the stomach wall of the mosquito and rounds up beneath the outer covering to become an oocyst.
When the oocyst develops and grows, a large number of sporozoites break out and wonder the mosquito’s body and eventually end up into the mosquitoes salivary glands.
This may be inoculated into the next person bitten
These sporozoites injected into the B stream leave the blood vascular system and invade parenchymal cells of the liver.
With all 4 species of plasmodium, they asexually reproduce in the liver. However with P vivax and p Ovale, a portion of these enter a resting stage before undergoing this multiplication.
Said resting state is called a HYPNOZOITE
While in the liver, merozoites are rapidly produced in infected cells. These infected cells soon rupture and release merozoites into the blood stream.
Merozoites can infiltrate and reproduce in a cycle called “schizogony”,and destroy erythrocytes due to the high production of them within the erythrocyte.
Then gametocytes are soon produced, which can be picked up by a female mosquito in order for the cycle to repeat
Plasmodium Spp - Diagnosis
P. Ovale
P. Vivux
P. Malariae
P. Falciparum
Symptoms of vivax and quartan infections, although characteristic, may be unreliable to quantitate. Hence blood smear analysis should always be conducted.
In infections with vivax, ovale and malariae all asexual stages as well as the gametocytes are visible in the peripheral blood
In falciparum however, usually only the rings, young trophozites or gametes are visible; plasmodia may be found in febrile paroxysm in all infections but especially in falciparum. Theyre situated within cappilaries of internal organs, so repeated blood films may be required
Sternal bone marrow biopsy is rarely useful in malaria diagnosis too
When it comes to microscopic diagnosis, thick blood films are better for parasite detection, while thin blood films are better for parasite identification
