8.7: Pathogenic Protists - Biology

Human Pathogens

A pathogen is anything that causes disease. Other protist pathogens prey on plants, effecting massive destruction of food crops.

Plasmodium Species

Members of the genus Plasmodium must colonize both a mosquito and a vertebrate to complete their life cycle. In vertebrates, the parasite develops in liver cells and goes on to infect red blood cells, bursting from and destroying the blood cells with each asexual replication cycle (Figure 1).

Of the four Plasmodium species known to infect humans, P. falciparum accounts for 50 percent of all malaria cases and is the primary cause of disease-related fatalities in tropical regions of the world. In 2010, it was estimated that malaria caused between one-half and one million deaths, mostly in African children.

During the course of malaria, P. falciparum can infect and destroy more than one-half of a human’s circulating blood cells, leading to severe anemia. In response to waste products released as the parasites burst from infected blood cells, the host immune system mounts a massive inflammatory response with episodes of delirium-inducing fever as parasites lyse red blood cells, spilling parasite waste into the bloodstream. P. falciparum is transmitted to humans by the African malaria mosquito, Anopheles gambiae. Techniques to kill, sterilize, or avoid exposure to this highly aggressive mosquito species are crucial to malaria control.

This movie depicts the pathogenesis of Plasmodium falciparum, the causative agent of malaria:

A link to an interactive elements can be found at the bottom of this page.


Trypanosoma brucei, the parasite that is responsible for African sleeping sickness, confounds the human immune system by changing its thick layer of surface glycoproteins with each infectious cycle (Figure 2). The glycoproteins are identified by the immune system as foreign antigens, and a specific antibody defense is mounted against the parasite. However, T. brucei has thousands of possible antigens, and with each subsequent generation, the protist switches to a glycoprotein coating with a different molecular structure. In this way, T. brucei is capable of replicating continuously without the immune system ever succeeding in clearing the parasite. Without treatment, T. brucei attacks red blood cells, causing the patient to lapse into a coma and eventually die. During epidemic periods, mortality from the disease can be high. Greater surveillance and control measures lead to a reduction in reported cases; some of the lowest numbers reported in 50 years (fewer than 10,000 cases in all of sub-Saharan Africa) have happened since 2009.

This movie discusses the pathogenesis of Trypanosoma brucei, the causative agent of African sleeping sickness:

A link to an interactive elements can be found at the bottom of this page.

In Latin America, another species, T. cruzi, is responsible for Chagas disease. T. cruzi infections are mainly caused by a blood-sucking bug. The parasite inhabits heart and digestive system tissues in the chronic phase of infection, leading to malnutrition and heart failure due to abnormal heart rhythms. An estimated 10 million people are infected with Chagas disease, and it caused 10,000 deaths in 2008.

Plant Parasites

Protist parasites of terrestrial plants include agents that destroy food crops. The oomycete Plasmopara viticola parasitizes grape plants, causing a disease called downy mildew (Figure 3). Grape plants infected with P. viticola appear stunted and have discolored, withered leaves. The spread of downy mildew nearly collapsed the French wine industry in the nineteenth century.

Phytophthora infestans is an oomycete responsible for potato late blight, which causes potato stalks and stems to decay into black slime (Figure 4). Widespread potato blight caused by P. infestans precipitated the well-known Irish potato famine in the nineteenth century that claimed the lives of approximately 1 million people and led to the emigration of at least 1 million more from Ireland. Late blight continues to plague potato crops in certain parts of the United States and Russia, wiping out as much as 70 percent of crops when no pesticides are applied.

Protists as Plant Pathogens

Many protists act as parasites that prey on plants or as decomposers that feed on dead organisms.

Learning Objective

Describe the ways in which protists act as decomposers and the actions of parasitic protists on plants

Key Points

    • Plasmopara viticola causes downy mildew in grape plants, resulting in stunted growth and withered, discolored leaves.
    • Since downy mildew has a higher incidence in the late summer, planting early in the season can reduce the threat of downy mildew fungicides are also somewhat effective at preventing downy mildew.
    • Phytophthora infestans causes potato late blight (potato stalks and stems decay into black slime) and was responsible for the Irish potato famine in the nineteenth century. saprobes feed on dead organisms, which returns inorganicnutrients to soil and water.


    an organism that lives off of dead or decaying organic material

    fungus-like filamentous unicellular protists the water molds

    plant disease caused by oomycetes causes stunted growth in plants as well as discolored, withered leaves

    Full Text

    Soil protists: a fertile frontier in soil biology research

    Protists include all eukaryotes except plants, fungi and animals. They are an essential, yet often forgotten, component of the soil microbiome. Method developments have now furthered our understanding of the real taxonomic and functional diversity of soil protists. They occupy key roles in microbial foodwebs as consumers of bacteria, fungi and other small eukaryotes. As parasites of plants, animals and even of larger protists, they regulate populations and shape communities. Pathogenic forms play a major role in public health issues as human parasites, or act as agricultural pests. Predatory soil protists release nutrients enhancing plant growth. Soil protists are of key importance for our understanding of eukaryotic evolution and microbial biogeography. Soil protists are also useful in applied research as bioindicators of soil quality, as models in ecotoxicology and as potential biofertilizers and biocontrol agents. In this review, we provide an overview of the enormous morphological, taxonomical and functional diversity of soil protists, and discuss current challenges and opportunities in soil protistology. Research in soil biology would clearly benefit from incorporating more protistology alongside the study of bacteria, fungi and animals.

    Underneath it all: Dishing the dirt on protists

    Protists, a diverse group of eukaryotic microbes, respond to the plant’s influence on the physicochemical and biological properties of the root zone in a similar way as previously observed for bacteria and fungi. Protists interact with other rhizosphere microbes through predation and can be plant pathogens. Credit: Javier A. Ceja-Navarro

    Plants evolved in a world dominated by prokaryotic and eukaryotic microbes. Underneath the surface, plant roots interact with microbes in the soil, also called the rhizosphere microbiome.

    Although bacteria and fungi are well-studied in the rhizosphere (the layer closest to the roots), other components, including viruses and protists, are less well known. A protist is any eukaryotic organism (an organism whose cells contain a nucleus) that is not an animal, plant or fungus. Most protists are unicellular, and many in soil are predators—i.e. they feed on bacteria, fungi, algae—or parasites.

    To better understand the extent to which biological and environmental factors shape protist communities, a Lawrence Livermore National Laboratory (LLNL) researcher and collaborators analyzed protist communities associated with the rhizosphere and surrounding soil of switchgrass plants in different developmental stages. Switchgrass is a prairie grass native to the U.S. that has excellent potential as a bioenergy feedstock and is of significant interest to the Department of Energy (DOE). The team found that the diversity of protists was lower in the rhizosphere than in the bulk soil and that the composition of protist communities changes through the different phenological stages of the plant. The research appears in the journal Microbiome.

    Despite their widespread distribution and ecological importance, protists remain one of the least understood components of the soil and rhizosphere microbiome. Knowledge of the roles that protists play in stimulating organic matter decomposition and shaping microbiome dynamics continues to grow, but it's still unclear what biological and environmental factors mediate protist community assembly and dynamics.

    "Studies focusing on understanding the mechanisms of plant establishment in soil need to consider protists as a key part of the plant microbiome," said lead author Javier Ceja Navarro from Lawrence Berkeley National Laboratory (LBNL). "Including protists in terrestrial ecological studies closes the knowledge gaps in our understanding of the complexity of the soil microbiome and microbial trophic interactions."

    In the new study, the team showed that while the types of abundant protists changed during plant growth stages, some plant pathogenic protists and omnivorous protists reoccurred at many stages of development and protist co-occurrence networks were more complex in the rhizosphere than in the bulk soil.

    "The results demonstrate that, just like their bacterial prey, protists respond to changes in the environment around plants' roots," said LLNL scientist Jennifer Pett-Ridge, a co-author of the paper. "Protists play a key role in mobilizing carbon and soil nutrients as they graze upon bacteria that are plentiful in the rhizosphere. Improving our understanding of patterns in rhizosphere-associated protist communities will help shed light into the root-microbe-soil ecosystem."

    Pett-Ridge heads LLNL's DOE Scientific Focus Area looking at the soil microbiome, aptly called "Microbes Persist," because the team is interested in how microbes affect how much carbon sticks around in soil.

    8.7: Pathogenic Protists - Biology

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    The Tick Microbiome: Why Non-pathogenic Microorganisms Matter in Tick Biology and Pathogen Transmission

    Ticks are among the most important vectors of pathogens affecting humans and other animals worldwide. They do not only carry pathogens however, as a diverse group of commensal and symbiotic microorganisms are also present in ticks. Unlike pathogens, their biology and their effect on ticks remain largely unexplored, and are in fact often neglected. Nonetheless, they can confer multiple detrimental, neutral, or beneficial effects to their tick hosts, and can play various roles in fitness, nutritional adaptation, development, reproduction, defense against environmental stress, and immunity. Non-pathogenic microorganisms may also play a role in driving transmission of tick-borne pathogens (TBP), with many potential implications for both human and animal health. In addition, the genetic proximity of some pathogens to mutualistic symbionts hosted by ticks is evident when studying phylogenies of several bacterial genera. The best examples are found within members of the Rickettsia, Francisella, and Coxiella genera: while in medical and veterinary research these bacteria are traditionally recognized as highly virulent vertebrate pathogens, it is now clear to evolutionary ecologists that many (if not most) Coxiella, Francisella, and Rickettsia bacteria are actually non-pathogenic microorganisms exhibiting alternative lifestyles as mutualistic ticks symbionts. Consequently, ticks represent a compelling yet challenging system in which to study microbiomes and microbial interactions, and to investigate the composition, functional, and ecological implications of bacterial communities. Ultimately, deciphering the relationships between tick microorganisms as well as tick symbiont interactions will garner invaluable information, which may aid in the future development of arthropod pest and vector-borne pathogen transmission control strategies.

    Keywords: microbial interactions microbiome tick tick borne pathogens tick symbionts.


    Origin and acquisition of tick…

    Origin and acquisition of tick microorganisms. Red arrows: vertebrate pathogens acquired from tick…

    Simplified eubacterial phylogeny showing the…

    Simplified eubacterial phylogeny showing the evolutionary relationships between the ten genera containing maternally…

    Evolutionary relationships between pathogenic and…

    Evolutionary relationships between pathogenic and non-pathogenic (symbiotic) forms within the Francisella , Coxiellai…


    Unikont have a genetic structure wherein three genes are fused with each other. The cellular structure is eukaryotic and most of these organisms are either amoeboid without flagella or are organisms having just one protruding flagellum.

    Subcategories of Unikont

    This super category is further divided into the following two subcategories:-

    • Amoebozoa – These are the generic amoeboids whose movements are dependent upon their internal cytoplasmic flow.
    • Choanozoa – These are animal like protists most of which are parasitic.

    Thus a precise overview of the different kinds of protists complete with a three-tier classification is given. Since all protists have a eukaryotic cell structure, they all undergo the typical eukaryotic cell cycle which includes the three stages of resting phase, inter phase and mitosis. Being mostly of microscopic magnitude, a lot of protists have potential pathogenic capabilities. Such protist pathogens may take up animals as well as plants as hosts and, as a result, make the latter diseased.

    The malaria-causing protist, Plasmodium falciparum is a prominent example of pathogenic protists. As we can see from the above varieties of protists, this biological kingdom consists of a vast diversity and each group and subgroup of protists differ from others, sometimes slightly and sometimes significantly, in terms of morphology, characteristics and a lot of other aspects.

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    Algae belong to the kingdom Protista, and are simple photosynthetic organisms. Based on the occurrence of pigments and food reserves, algae are classified into different types, namely blue green algae&hellip

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    Diatoms, Golden Algae, Brown Algae, and Water Molds: The Stramenopiles

    • a yellow-brown pigment (which gives them their color). It is a carotenoid called fucoxanthin.
    • chlorophylls a and c

    All four of them (plus a number of other groups not listed) share genes closely-homologous to those in both green and red algae. This suggests that they are all descended from a heterotrophic eukaryotic ancestor that acquired both a green alga and a red alga by a secondary endosymbiosis. (While the water molds no longer are photosynthetic, they still retain both green and red alga genes.)


    Diatoms are unicellular. Their cell wall or shell is made of two overlapping halves. These are impregnated with silica and often beautifully ornamented. The photo (courtesy of Turtox) is of Arachnoidiscus ehrenbergi magnified some 400 times.

    Diatoms are major producers in aquatic environments that is, they are responsible for as much as 40% of the photosynthesis that occurs in fresh water and in the oceans. They serve as the main base of the food chains in these habitats, supplying calories to heterotrophic protists and small animals. These, in turn, feed larger animals.

    Golden Algae (Chrysophyta)

    • Most are unicellular.
    • Found in fresh water.
    • Important producers in some aquatic food chains.
    • In low light conditions, may lose their chlorophyll and turn heterotrophic feeding on bacteria and/or diatoms.
    • Over 1000 species alive today many more in the fossil record.

    Brown Algae (Phaeophyta)

    • The rockweeds and kelps. Some kelps grow as long as 30 meters.
    • All are multicellular although without much specialization of cell types.
    • Most are found in salt water.
    • Used for food in some coastal areas of the world and harvested in the U. S. for fertilizer and as a source of iodine.

    Water Molds (Oomycetes)

    As their name suggests, water molds were once considered to be fungi. But unlike fungi, the cell wall of water molds is made of cellulose, not chitin. Furthermore, their gene sequences are very different from those of fungi (and most closely related to those of diatoms, golden and brown algae).

    • Some species (e.g., Saprolegnia, Achyla) are parasites of fishes and can be a serious problem in fish hatcheries.
    • Downy mildews damage grapes and other crops.
    • Phytophthora infestans, the cause of the "late blight" of potatoes. In 1845 and again in 1846, it was responsible for the almost total destruction of the potato crop in Ireland. This led to the great Irish famine of 1845&ndash1860. During this period, approximately 1 million people starved to death and many more emigrated to the New World. By the end of the period, death and emigration had reduced the population of Ireland from 9 million to 4 million.
    • Phytophthora ramorum, which is currently killing several species of oaks in California.

    7 Parasitic Forms of Flagellates | Phylum Protozoa

    It is also known as Giardia intestinalis and it lives as parasite in the intestine of man and causes a disease called giardiasis. The distribution is cosmo­politan. Trophozoites measure 9-20 by 6-15 micra. Cytostome is absent. Protoplasm is clear. Ventral side of the body is flat and dorsal side is convex.

    The posterior end is pointed but anterior end is round. A bean- shaped sucking disc is present on the ventral surface. Two elongated nuclei and two parabasal bodies are present.

    There are eight rhizoplasts and flagella in following arrange­ments—right-1, left—1, anterolateral-1, postero-lateral-1, ventral-2 and caudal-2. Cysts measure 8-14 by 6-10 micra and contain 2 to 16 nuclei. Infection occurs through as a trailing or posterior flagellum beyond contaminated drink or food (Fig. 10.7).

    Parasitic Form # 2. Trichomonas Hominis:

    These cosmopoli­tan parasites have trophozoites of 5-20 micra and inhabit the intestine of cattle. It also lives as commensal in the colon of man. The cytostome is distinct and parabasal bodies are absent. The protoplasm contains single nucleus and food vacuoles. Number of free flagella varies from 3-5.

    Two blepharoplasts are situated in front of and anterior to the nucleus. Three to four flagella arise from the blepharoplast close to the nucleus and are directed anteriorly.

    From the other blepharo­plast arises the fixed flagellum, costa and axostyle. The fixed flagellum is accompanied by the undulating membrane throughout the whole length of the body and then continues as a posterior flagellum beyond the body length (Fig. 10.8).

    Parasitic Form # 3. Trichomonas Vaginalis:

    Cosmopolitan in­habits as a parasite in the vagina of women and also found in the urethra of man. Ap­proximately 10-30 micra in length and more or less oval in shape (Fig. 10.9). Nucleus is elongated cytostome is less distinct parabasal body is large undulating membrane is short. No cyst formation does not survive more than 24 hours outside the body of the host. Transmission is direct through males.

    Parasitic Form # 4. Haemoflagellates:

    The Haemoflagellates are a group of flagellates which habitually live in the blood or tissues of man and other vertebrates. The haemoflagellates of man belong to the family Trypanosomatidae.

    The family includes two genera namely, Trypanosoma and Leishmania. These parasites are structurally complex and are of consi­derable pathogenic importance to man. Trypanosomes are uniflagellated blood parasites of man and other vertebrates.

    They occur in variety of forms and all these forms (Fig. 10.10) are represented in the life cycle of Herpetomonas muscarum (a member of the family Trypanosomatidae) which is a parasite in house fly. The life cycle of Trypanosoma revolves round two hosts—one vertebrate and the other invertebrate. The trypanosomes show polymorphism, presenting different morphological forms under different conditions.

    The polymorphic forms are (Fig. 10.10):

    I. Leishmanial form or Amastigote Form:

    The body is round or oval with a nucleus and a kinetoplast but no flagellum is present.

    II. Leptomonad form or Promastigote Form:

    The whole structure is thread-like, nucleus centrally located, blepharoplast is anterior to the nucleus, the rhizoplast arises from the blepharoplast and runs straight up to the anterior extremity and then emerges as a free flagellum twice as long as the body.

    III. Crithidial form or Epimastigote Form:

    The flagellum is not completely free and runs along the surface and up the anterior end. It is in association with the undulating mem­brane which is short. Beyond the anterior end the flagellum is free.

    IV. Trypanosoma form or Trypomastigote Form:

    The blepharoplast is situated behind the nucleus. Flagellum skirts the whole length of the body and remains at­tached to the undulating membrane.

    Leishmanial forms leave the body along with the excreta of the fly. Ingestd Leishmania reaches the oesophagus of vertebrate host and is transformed into leptomonad form.

    The genus Trypanosoma includes the typi­cal blood parasites of man and other verte­brates. They are transmitted by the blood­sucking invertebrates from vertebrate to vertebrate. Trypanosomas occur in all verte­brates, but are pathogenic to man and some domestic mammals.

    The major pathogenic trypanosomes of man are: Trypanosoma gambiense and T. rhodesiense—the causative agents of African sleeping sickness. The pathogenic trypanosomes have a similar life history. The biological account of some trypanosomes will give an account of the group in general.

    Parasitic Form # 5. Trypanosoma Cruzi:

    Causative agent of Schizotrypanosomiasis or Chagas’ disease. Distribution has recorded in Central and South America. Trypanosoma forms occur in the blood stream of man but do not multiply there. They are 20 micra in length and 3-7 micra in breadth. Kinetoplast is big and situ­ated posterior to nucleus. Nucleus is elon­gated. Undulating membrane is narrow, free end of flagellum is not more than half the body length.

    Trypanosoma forms change to leishmanial forms and the change is revers­ible. Leishmanial forms are ovoid and 4 micra in diameter. Presence of distinct nucleus and rod-shaped kinetoplast, short rhizoplast per­pendicular to kinetoplast may be seen. Leishmania forms reproduce by binary fission and take refuge in muscle fibres, neurons, testis, thyroid gland and skin (Fig. 10.11).

    The blood-sucking hemipterous bugs of the family Triatomatidae are the intermediate hosts. Parasites in trypanosoma forms enter the gut of the bugs and transform to crithidial forms several weeks after, the crithidial forms switch over to trypanosoma forms and are then called Metacyclic trypanosoma.

    Man becomes infected by the deposition of excreta of bugs on the bruised skin, con­junctiva of eye and even lips.

    Parasitic Form # 6. Trypanosoma Gambiense:

    Causative agent of west African trypanosomiasis or sleeping sickness. They occur in the lymph glands, in reticular tissue of spleen, blood and at a later stage in the cerebro-spinal fluid in trypano­soma forms only and divide by binary fis­sion. The trypanosoma forms are 15-32 micra in length.

    The undulating membrane is much convoluted, nucleus is posteriorly placed and kinetoplast is round. Cytoplasm bears volutine granules (Fig. 10.12).

    Three types of trypanosoma forms are known:

    The intermediate host is the blood-suck­ing tsetse fly, Glossina palpalis, which infects man in two ways:

    (a) Direct Transmission:

    When a fly bites a man infected with trypanosoma, some trypanosomas stick to the proboscis and when this fly bites another man the trypasnosoma are introduced into him provided the time between the successive bites do not exceed few hours.

    (b) Cyclical Transmission:

    When the fly takes the infecting meal the parasites enter the midgut, remain there for two days and start multiplying. To avoid washing out by the movement of gut, the parasites take refuge in the extraperitrophic space—the space between gut wall and peritrophic membrane (a thin membrane which envel­ops the blood imbibed by the fly) and mul­tiply.

    Then they come out in huge numbers to the proventriculus after ten days and reach the salivary gland on the 12 th day. They become ready for infection after 20 day.

    The fly introduces the trypanosomas in the blood stream of man along its bite (Fig. 10.13).

    Among the other Trypanosomas, the Trypanosoma rhodesiense causes east African sleeping sickness Trypanosoma brucei causes nagana fever of African domestic animals and transmitted by Glossina Trypanosoma evansi causing surra disease of Indian horses, cattle, camels and transmitted by tabanid flies Trypanosoma equiperdum causing dourine dis­ease of horses and mules are transmitted directly during coition.

    The non-pathogenic trypanosomes also occur in man. Trypanosoma primatum of anthropoid apes, Trypanosoma rangeli of man in Venezuela and Columbia and Trypanosoma rotatorium of frogs are some of the typical non-pathogenic trypanosomes.

    Parasitic Form # 7. Leishmanias:

    Members of the genus Leishmania which are parasitic to man and other vertebrates occur in Leishmanial forms (flagellaless forms) and in the intermediate hosts they are seen in leptomonad forms (flagellated forms). Three members of the genus are parasites in man and they offer close resemblance to one another.

    In man the leishmanias (Fig. 10.14) are intracellular parasites of the reticulo­endothelial system namely, the endothelial cells, large mononuclear leucocytes and Kupffer cells of liver. In case of heavy infec­tion they have been found to invade ectoder­mal cells and polynuclear leucocytes.

    Leishmanias are oval in shape and meas­ure 2-4 micra by 1.5-2 micra. The nucleus is elongated with a rod-shaped kinetoplast which is perpendicular to the nucleus. Flagellum is absent. Binary fission is the mode of multiplication. By their successive divi­sions the parasites become overcrowded in the host cell, which is ultimately destroyed.

    The intermediate host is the sand fly be­longing to the genus Phlebotomus. The fly ingests leishmanias along with the blood of the vertebrate host. In the midgut of the fly the parasites increase in size, develop flagella and are metamorphosed into long, slender Leptomonad forms in four days. The leptomonas multiply vigorously by binary fission and reach the proventriculus of the fly.

    Re­peated multiplication inside the proventricu­lus causes complete obstruction of the organ. As a result, when the sand fly tries to ingest blood, the meal goes no further than the oesophagus. This causes a regurgitation of the sucked blood and the leptomonads are introduced in the blood stream along with the regurgitation.

    It resides in the viscera and is the causative agent of visceral leishmaniasis or fatal kala-azar. It is preva­lent in eastern India, China, central Asia, east Africa, South America and Russia.

    Man be­comes infected by becoming associated with a sylvatic or non-domestic reservoir jackal and domestic reservoir dog. Spreading of the disease among human being is caused by the intermediate host Phlebotomus (Indian vec­tor, Phlebotomus argentipes).

    (i) In kala-azar, the parasite attacks the endothelial cells, bone marrow, Kupffer cells of liver, blood vessels of the spleen and lymph glands (lymph nodes).

    (ii) These organs are enlarged and there is a symptom of bloodlessness and high fever.

    The control of sand fly (Phle­botomus sp.) is to control of mosquito of ma­laria.

    (i) If antimony compounds are treated to the patients, proves successful.

    (ii) Urea stibamine, Amino stiburea, Solistibosan, Pentamidine isothionate may be the effective drugs.

    Resides in human skin and is the causative agent of the cuta­neous leishmaniasis or oriental boil and oriental sore. It is most predominant in the old world. Sylvatic reservoir is wild rodents and the domestic reservoir is dog. Transmis­sion is through Phlebotomus (Indian vector, Phlebotomus sergenti).

    Leishmania Brasiliensis:

    It resides in the cutaneous and mucocutaneous parts of human body and is the causative agent of Espundia—a serious disease of buccal and nasal cavities. It is prevalent in the New- world. Sylvatic reservoir is a rodent and opossum and the domestic reservoir is dog. Transmission occurs, through Phlebotomus.

    Watch the video: What Are Pathogens? Health. Biology. FuseSchool (November 2021).