Protists

Question 0

What is encystment and what are its purposes?

Answer 0

Encystment is the formation of a cyst around parasitic protists

They protect the organism from adverse environmental conditions

provide shelter for reproductive processes

allow transmission of the parasite from one host to another

Question 1

Define the term protist?

Answer 1

Protists are eukaryotic organisms that are either single-celled or have only simple multicellular structures.

Huge genetic diversity

Found in fresh water, salt water, soil and as symbionts in plants, animals and fungi

Feeding strategies vary. Some can photosynthesise, some are heterotrophs and feed of other organisms

Can reproduce via sexual and asexual means depending on the environmental conditions

Question 2

What is excystment?

Answer 2

The emergence of a vegetive parasitic protist from a cyst. This protist is a trophozoite

The ingestion of a cyst is a common way for humans to become infected. Excystment occurs in the gut

Question 3

What structure is common between the majority of protists?

Answer 3

They have one of more flagella at some point within their life cycle which are used for movement and feeding
They are structurally different to bacterial flagella

Question 4

What is a flagellate?

Answer 4

A protist which has a flagella during the adult stage of their life cycle.

Question 5

What are Protozoa?

Answer 5

Single called animal like cells
Unable to photosynthesise
Contain one or more nuclei

Question 6

Why is antiprotist therapy often unsuccessful?

Answer 6

Protists are eukaryotes, so have the same type of molecules and metabolism as their hosts. Thus it is difficult to achieve selective toxicity.

Two treatments which are successful are folic acid antagonists as the protists are unable to use the hosts folic acid where as the host can obtain what they require from their diet

Melarsopol is a drug based on arsenic which inhibits protist enzyme activity

Question 7

What is Giardiasis?

Answer 7

Diarrhoeal disease causes by the protist Giardia spp - usually Giardia lamblia in humans

Question 8

Describe the Giardia protist and it’s life cycle?

Answer 8

Very ancient protist.
Has no mitochondria - has a mitosome instead which is evolved from mitochondria
Cysts are ingested in contaminated food or water.
Excystment is initiated in the stomach by the high pH but does not occur until the lower pH of the small intestine
The protist has four flagella which is uses to move to the gut epithelium where is attaches via sucker pads and specific receptors.
It prevents fat absorption and cause loose fatty stools
If the protist is moved through the digestive system the decrease in pH triggers encystment where a thick mucous layer forms around the cyst and binary fission occurs to form four nuclei. The cyst allows safe transmission to a new host when excreted.
Cysts can survive in the soil etc for months
When infection occurs metronidazole can be administered but the infection can clear by itself

Question 9

What is Trichomoniasis?

Answer 9

Sexually transmitted disease caused by the protist Trichomonas vaginalis.
It has four flagella and no mitochondria, instead it has a hydrogenosome
No cyst stage - transmitted in trophozoite stage
Attach to the vaginal mucosa via adhesins
Cause irritation and foul discharge
Diagnosis via fluorescent antibodies in urine or vaginal swab and PCR procedure analysing the urine or vaginal swab

Question 10

What is Trypanosomiasis?

Answer 10

Disease caused by the protist trypanosomes
Causes sleeping sickness or human African trypanosomiasis (HAT) in Africa and Chagas’ disease in Central and South America

Has a complex life cycle which involves more than one type of host and an insect vector

Question 11

Describe the four different morphological forms of Trypanosomes?

Answer 11

Typically, the trypomastigote form occurs extracellularly in both the denitive host and the vector (e.g. in humans infected with Trypanosoma
spp.).

The amastigote is an intracellular form occurring in the denitive host

The promastigote and epimastigote are forms found in the insect vectors (Figure 6.2a).

The position of the kinetoplast relative to the nucleus and the origin of the agellum differ in each of the four morphological types.

Question 12

How is trypanosomiasis transmitted?

Answer 12

It is transmitted in its trypomastigote form to the host via the bite of a tsetse fly

Question 13

Once in the blood stream, what two forms do the trypomastigote take?

Answer 13

trypomastigotes develop into two forms:

a long slender form that multiplies by binary fission

a stumpy form that is non-dividing but is the only form that is infective for a biting tsetse fly.

Question 14

What are the differences between the two strains of Trypanosoma species?

Answer 14

Trypanosoma brucei gambiense
Chronic disease 
Kills in three years 
Attacks the CNS and causes lethargy 
Transmitted by the tsetse vector

Trypanosoma brucei rhodesinese
Acute
Kills within a year
Inflammation of lymph nodes and kills small blood vessels supplying the brain and heart
Transmitted by the tsetse fly for a reservoir of wild and domesticated livestock.

Question 15

How are African trypanosomes able to produce prolonged infections in vertebrate hosts?

Answer 15

The prime means of producing prolonged infections relates to the trypanosomes ability to vary a major surface antigen (the variant surface
antigen, VSG) within a single infection, thus progressively evading the immune response of the host.

Question 16

How can the African trypanosome achieve this compared with the situation in the Influenza virus?

Answer 16

The African trypanosomes have an extensive repertoire of genes (perhaps up to 1700) for these VSGs in their genome, of which, in any individual
trypanosome, just a single gene is expressed at any one time, whereas the influenza virus depends on mutation and also recombination between the
genome of different viruses.

Question 17

Outline the genetic mechanism by which variant surface glycoprotein (VSG) antigen change is achieved. (Note: some researchers prefer the
term variant specific glycoprotein. The two terms are interchangeable.)

Answer 17

The expression of a VSG gene is primarily dependent on a recombination process called gene conversion. Here non-expressed versions of a VSG
gene are copied from an internal chromosome site into one of a number of sub-telomeric expression sites.

Question 18

The trypanosome genome contains many VSG pseudogenes

do these pseudogenes play any role?

Answer 18

Early in infection, gene conversion via recombination appears to involve complete VSG genes. However at later stages of infection parts of non-expressed VSG pseudogenes appear able to recombine with VSG genes already in an expression site and produce novel complete genes

Question 19

Why are there no vaccines against African trypanosomes?

Answer 19

The ability to vary their surface antigens is so extensive that it has, so far, completely frustrated any attempt to produce vaccines.

Question 20

What is the transmission route for American trypanosomiasis (Chagas disease)?

Answer 20

The pathogen is a protist called Trypanosoma cruzi which is spread by species of reduviid bug
Also called the kissing bug as it is attracted to exhaled carbon dioxide and therefore tends to bite around the mouth

Question 21

How are the metacyclic trypomastigotes transmitted in American trypanosomiasis?

Answer 21

The vector fly defecates in the wound from where it has just fed and the trypanomastigotes are in the faeces.

Question 22

How are the metacyclic trypomastigotes transmitted in Human African trypanosomiasis?

Answer 22

In the saliva of the tsetse fly

Question 23

Describe the life cycle of the human African trypomastigotes?

Answer 23

The protist enters the blood stream of he host via the saliva of a tsetse fly
At this stage it is a metacyclic trypomastigote (actively dividing)
In the blood the trypomastigote transforms into either short stumpy or long slender form
The stumpy form is taken up by a new tsetse fly which feeds on the infected human
In the fly the short stumpy trypomastigote transforms into a procyclic form in the fly mid gut
It travels to the salivary gland of the fly and changes into the epimastigote form where it multiples
The final transformation is to the metacyclic form which is then infective to the next human that the fly bites.
They are extracellular parasites

Question 24

Describe the life cycle of the American trypanosomiasis trypomastigote?

Answer 24

The trypomastigote enters the host via the faeces of the kissing bug The trypomastigotes enter macrophages and muscle cells Replication by binary fission occur inside the cells - this is the amastigote phase The infected cell eventually bursts and releases the progeny which then form trypomastigotes and the cycle continues When the kissing bites this host it can now take up the trypomastigotes in the blood meal When the trypomastigotes enter the mud gut of the kissing bug they move to their epimastigote stage and then finally to the metacyclic trypomastigote stage where they can then infect a host via infection in bite wounds via the fly faeces

Question 25

What is the main cause of death in chronic American trypanosomiasis?

Answer 25

Heat failure due to the damage caused by the amastigote form of the parasite which enters muscle cells causing them to lyse

Question 26

What are the three forms of Leishmaniasis?

Answer 26

cutaneous, muco-cutaneous visceral infection

Question 27

What causes Leishmaniasis?

Answer 27

Leishmania species of protist 20 species are pathogenic to humans This disease is zoonotic in wild and domesticated animals

Question 28

How is Leishmania transmitted?

Answer 28

By the bite of female sand flys with the family Phlebotominae

Question 29

Describe the life cycle of the Leishmania species?

Answer 29

Infective stage is the promastigote which is transmitted by the bite of the female sand fly Promastigotes enter the macrophages in the blood stream where they change to their amastigote form and multiply by binary fission Macrophages lyse and release many amastigotes Into the blood stream The amastigotes can now be taken up in the blood meal of a biting sandfly where they enter the gut and transform into Promastigotes and migrate to the mouth part of the fly in order to be injected to the next host

Question 30

How do the Leishmania parasites survive in the macrophages?

Answer 30

The parasite is able to survive within macrophages because it overcomes their normal killing mechanism by raising the pH of the normally acidic phagolysosome inside the macrophage, creating an alkaline environment in which the protease enzymes are unable to function.

Question 31

Describe cutaneous leishmaniasis?

Answer 31

Symptoms range from a single sore or ulcer at the bite wound of the sandfly to multiples sores all over the body Heal within the year and the patient is then immune Treated with antimonials

Question 32

Describe Muco-cutaneous leishmaniasis?

Answer 32

This is a chronic disease Ulcers appear months and sometimes years after the initial infection and infect the mouth, nose and skin of the host Treated with antimonials and amphotericin B.

Question 33

Describe Visceral leishmaniasis?

Answer 33

``` Systematic disease 2-3 week incubation Causes dark pigmentation of the skin If left untreated can be fatal Treated with antimonials and amphotericin B Occurs in only six countries worldwide ```

Question 34

What are amoebae?

Answer 34

Animal like, single expelled protists which move and feed by extending cytoplasmic pseudopodia.

Question 35

Describe the life cycle of Entamoeba histolytica?

Answer 35

Infection occurs via faeces infected food and water Excystment occurs in he small intestine and meta cysts are release which subsequently divide to give 8 amoeba which travel to the large intestine where they either live as harmless commensals or attack the mucous membranes causing inflammation, cysts and dysentery Symptoms are profuse bloody diarrhoea The amoebae can spread and cause cysts in the brain, liver and lungs At some stage the amoebae in the intestines encyst and are shed in the faeces Asymptomatic carriers are a major source of infection The amoebae have no mitochondria, instead they have a mitosome Diagnosis is via a stool sample Treated by Metronidazole and tinidazole for amoebic dysentery and patients with liver abscesses. Asymptomatic carriers can be treated with iodoquinol or paromomycin

Question 36

Describe Acanthamoeba spp. amoebiasis?

Answer 36

Common in fresh water and moist soil Can cause a brain infection called primary amoebic meningoencephalitis and eye infections which can cause blindness Diagnosis of eye infection is via eye scraping Diagnosis of nervous system infection is done via analysis of CSF

Question 37

What are apicomplexans?

Answer 37

Belong to the phyla apicomplexia Named after the apical complex which is found at one end of their cell which facilitates penetration into the host cells. Have no flagella Can reproduce sexually and asexually Can have more than once host With asexual reproduction occurring in the intermediate host and sexual production occurring in the definitive host Causes toxoplasmosis, cryptosporidiosis and malaria

Question 38

What is the causative agent on toxoplasmosis?

Answer 38

Toxoplasma gondii This organism can asexually replicate in almost any warm blooded host but only sexual reproduction occurs in the definitive host - the cat

Question 39

Describe the life cycle of toxoplasma gondii?

Answer 39

Sporozoites are formed when the organism reproduces sexually in the cat host, these sporozoites are ingested by an intermediate host in he form of oocytes which then release the sporozoites into the small intestines of the intermediate host. The sporozoites penetrate the host cells and transform into Tachyzoites which divide rapidly and are released when the cell lyses The tachyzoites then infect muscle and neuronal cells as well as macrophages Tachyzoites then transform into Bradyzoites which form cysts Cats become infected by eating animals which have cysts I their tissue or through oocytes shed in cat faeces

Question 40

What effect does toxoplasmosis have in humans?

Answer 40

Common in humans which are often asymptomatic Acute toxoplasmosis involves painful swellings of the lymph nodes and necrosis of the heart, lungs and liver Can cross the placenta causing deformities and still birth After infection in adults lifelong immunity is obtained If an individual becomes immunosuppressed the parasite reproduces rapidly and can be fatal. Those infected can show slower reaction times and behavioural abnormalities such as mice which show no fear of cats!

Question 41

How is toxoplasmosis diagnosed and treated?

Answer 41

Diagnosis is by serological testing for the presence of patient antibodies against the Toxoplasma pathogen, or by PCR detection of parasite DNA. Toxoplasmosis may be treated with a combination of pyrimethamine and sulfadiazine. In pregnancy, spiramycin may be used and clindamycin has been used to treat infections involving the brain.

Question 42

Describe Cryptosporidiosis?

Answer 42

This is a diarrhoeal disease caused by Cryptosporidia Often found in cattle and their oocytes are shed in faeces Speed via water and food contamination Oocytes are very resistant to chlorine and are so small they are unable to be filtered by normal methods

Question 43

Describe the life cycle of Cryptosporidium spp?

Answer 43

Do not use an intermediate host or vector Cryptosporidium parvum is the most common for common Once ingested the oocytes excyst in the small intestine and release haploid sporozoites They invade the epithelial cells of the intestine and divide asexually into merozoites These enter uninfected epithelial cells and continue to divide These then become male or female gamonts which further divide into micro gametes. The male and female gametes then fuse and reproduce sexually forming sporozoites which are contained within an oocyte and released I the faeces Symptoms are profuse watery diarrhoea stomach cramps and fatigue