Microbiome/Commensal Protozoa Flashcards - Dr. Mansfield - Exam 1

⭐ Q: How do microbiota, microbiome, and metagenome differ?

A microbiota is the community of microorganisms living in or on a host, whereas the microbiome is the collection of genetic material within that microbial community and can also be called its metagenome.

Microbiota

• the actual microorganisms

• can include bacteria, archaea, protozoa, fungi, viruses, and sometimes helminths

Microbiome

• the genetic material of a microbiota

• associated with a particular niche, such as the gut

Metagenome

• another term used in the lecture for the genetic material of the microbiota

⭐ Q: What groups of microorganisms can make up a mammalian microbiota?

A: A mammalian microbiota can include bacteria, archaea, protozoa, fungi, viruses, and sometimes helminths.

🔎 What this means:
The microbiota is not just bacteria.

Even though much microbiome research focuses heavily on bacteria, the lecture explicitly includes several different types of microorganisms.

For the learning objective, the professor particularly names:

• bacteria

• viruses

• fungi

• protozoa

⭐ Q: How do symbiosis, commensalism, mutualism, and parasitism compare?

Symbiosis broadly describes organisms living together, while commensalism benefits one organism without harming or benefiting the other, mutualism benefits both organisms, and parasitism involves dependence of a parasite on its host.

⭐ Q: How do a pathogen, pathobiont, and opportunistic pathogen differ?

A pathogen can cause disease, a pathobiont normally lives as a symbiont but has disease-causing potential, and an opportunistic pathogen causes infection when an unusual opportunity makes the host more susceptible.

Pathobiont

A potentially disease-causing organism that normally lives as a symbiont.

Opportunistic pathogen

Takes advantage of conditions not normally available, such as:

• weakened immunity

• disrupted microbiota

• breached body barriers

Q: How do zoonosis, anthroponosis, and reservoir differ?

A zoonosis can transfer naturally between vertebrate animals and humans

an anthroponosis is a human disease transmissible to animals

and a reservoir is the normal source in which an infectious agent lives and multiplies.

• can be a person, an animal, a plant, soil and etc

A reservoir does not necessarily have to be clinically sick.

It is simply the ecological source maintaining the infectious agent.

Q: How do disease, pathogenesis, and pathology differ?

Disease is an abnormal condition that impairs normal function, pathogenesis describes how the disease develops, and pathology is the study of the changes, the structural and functional changes, caused by disease.

Q: What does “health” mean in the terminology pre-work?

The pre-work presents health as a concept that can include normality, biological function, homeostasis, physical and psychological well-being, and productivity including reproduction.

Q: Why is culture alone unable to completely characterize a microbial community?

Culture gives an incomplete view of a microbial community because it detects only an unknown fraction of the organisms and many microbes cannot be cultured using standard methods.

If you only grow microorganisms on plates, organisms that won't grow under your chosen laboratory conditions become invisible to you.

⚠ Lower priority Q: Why can 16S rRNA gene sequencing be used to characterize bacterial communities?

16S rRNA gene sequencing can characterize bacterial communities because bacteria possess ribosomal genes with variable regions that can be sequenced and compared with reference databases for identification.

⚠ Lower priority Q: How does shotgun metagenomic sequencing differ from 16S-based community analysis?

Shotgun metagenomics sequences community DNA broadly rather than specifically targeting the 16S rRNA gene, allowing strain-level resolution and functional information such as virulence and antibiotic-resistance content.

🔎 What this means:
16S mainly helps answer:

“Which bacteria are present?”

Shotgun sequencing can additionally help answer:

“What genetic capabilities does this community have?”

such as:

• strain-level resolution

• functional profiling

• antibiotic-resistance genes

• virulence-factor content

⚠ Lower priority Q: How do metagenomics, metatranscriptomics, and metabolomics differ?

Metagenomics studies community DNA, metatranscriptomics studies community RNA, and metabolomics studies the small-molecule metabolic products produced by the community.

⚠ Lower priority: These methods are lecture background rather than explicit learning-objective targets.

⭐ Q: How does the gut microbiota develop over time according to the infant example in the lecture?

The gut bacterial community changes in a predictable sequence over time.

The baby's gut does not start out with the same microbiota it will have later. Different broad groups of bacteria become more common at different stages of development. The slide shows Firmicutes first → then more Proteobacteria → then more Bacteroidetes after solid food → then a more diverse/enriched Bacteroidetes community later.

Gut microbiota develops through microbial succession, with different groups becoming prominent at different developmental stages and dietary transitions.

For example:

Early baby gut:
🦠 lots of certain Firmicutes

Then the baby gets older:

🦠 Firmicutes
🦠🦠 more Proteobacteria

Then solid food starts:

🦠 Firmicutes
🦠 Proteobacteria
🦠🦠🦠 more Bacteroidetes

its not that the bacteria disappear, its that proportions change and the whole community composition changes over time

💡 Think:
The gut microbiota develops like an ecosystem after a new island forms: different populations arrive and change over time.

⭐ Q: How can microbiota be naturally transferred between animals?

Microbiota can be transferred through behaviors such as fecal re-ingestion in herbivores and social/environmental contact, allowing animals to acquire microorganisms from other animals or their surroundings.

Fecal re-ingestion

Occurs especially in herbivorous species, including examples such as:

• rabbits

• rodents

• piglets

• foals

• dogs

• nonhuman primates

It can also allow animals to recover microbial products such as vitamins and amino acids.

• for example in Hyena pasting, a scent-marking behavior, allows Young hyenas to acquire clan-associated bacteria by rubbing their anal glands against grass n stuff

🔎 What this means:
Microbiota aren't permanently isolated within one individual.

Animals continually interact with:

• other animals

• food

• feces

• physical environments

and those interactions can transfer microorganisms.

Q: Why can fecal re-ingestion be physiologically useful to some animals?

Fecal re-ingestion can be useful because it allows animals to recover nutrients supplied by gut microbes and can help compensate for dietary changes.

The lecture notes that rats prevented from re-ingesting feces showed reduced growth rates.

⭐ Q: What are the major roles of indigenous microbiota in mammalian health?

Indigenous microbiota support mammalian health by promoting tissue and immune development, improving nutritional capabilities, supplying nutrients, detoxifying dietary compounds, and preventing colonization by outside pathogens.

In List form:

• development/differentiation of mucosal epithelium

• immune-system development

• nutritional development

• nutrient provision

• detoxification

• colonization resistance

⭐ Q: How can normal microbiota influence intestinal development and function?

Normal microbiota can provide nutrients, promote nutritional capabilities, increase intestinal movement and water absorption, alter the chemical environment, and stimulate intestinal epithelial growth and differentiation.

In list form its:

• ↑ peristalsis

• ↑ large-intestinal water absorption

• detoxification of harmful dietary constituents

• altered stomach pH

• altered large-intestinal redox conditions

• epithelial growth/proliferation/differentiation

• altered intestinal epithelial gene expression

⚠ Lower priority Q: What vitamins can normal intestinal microbiota provide according to the lecture?

Normal intestinal microbiota can contribute to production of vitamin K and several B vitamins.

Examples listed:

• vitamin K

• folic acid/B9

• vitamin B12

• vitamin B2

• biotin/B7

• thiamine/B1

• nicotinic acid/B3

• pyridoxine/B6

⭐ Q: How do the microbiota and innate immune system influence one another?

The innate immune system helps control which microbes live in the body and how abundant they are, while normal microbiota help the immune system develop and function properly.

The microbiota can:

• increase lymphocytes and plasma cells in the gut

• increase the size of some peyer’s patches, lymph nodes, spleen, thymus etc

• increase macrophage movement and phagocytosis

• increase IgG and IgA production

• improve colonization resistance against pathogens

Microbiota → immune system:
Living with normal microbes helps “train” and develop the immune system so it becomes better at responding to pathogens.

⭐ Q: What is colonization resistance, and how does normal microbiota protect the host from pathogens?

Colonization resistance is when the normal (commensal) bacteria already living in the body make it harder for harmful pathogens to move in and establish themselves.

They do this by:

• taking up attachment sites

• using available nutrients

• changing the local environment

• producing substances that inhibit other microbes

🔎 What this means:
The pathogen has to compete with bacteria that are already living there.

⭐ Q: How do microbial food webs form in the gastrointestinal tract?

Microbial food webs form because different microbes interact and use products generated by other members of the community, allowing nutrients to flow through interconnected microbial populations.

🔎 What this means:
One microorganism's waste product can become another microorganism's food.

So the microbiota functions more like an ecosystem than a random pile of independent organisms.

Q: What is the gut-brain axis?

The gut-brain axis is a bidirectional communication system between the gastrointestinal tract and brain that also involves the resident microbiota.

The lecture says this connects emotional/cognitive brain centers with peripheral gut function and its microbial community.

⭐ Q: What can cause loss of normal colonization resistance, and what is the consequence?

Antibiotic treatment or rapid dietary changes can disrupt normal gut microbiota, causing loss of colonization resistance and increased susceptibility to infection.

⭐ Q: Why is microbiome failure especially important in herbivores such as cattle?

Microbiome failure is especially important in herbivores because they depend on symbiotic gut microorganisms to obtain usable energy and nutrients from plant structural material that the host cannot efficiently digest alone.

⭐ Q: What is transfaunation/FMT in cattle, and how can it help restore a failed rumen microbiota?

Transfaunation or fecal microbiota transplantation in this lecture involves orally transferring ruminal fluid from a normal donor animal to provide rumen bacteria, protozoa, and fermentation products to an animal with a disrupted rumen ecosystem.

⭐ Q: What are the general characteristics of protozoa?

Protozoa are single-celled eukaryotic organisms that lack a rigid cell wall, vary widely in form, and are usually motile and heterotrophic.

Characteristics list from the slides:

• eukaryotic

• unicellular

• no rigid cell wall

• highly variable size and structure

• most are motile

• most are heterotrophic

🔎 What this means:
Eukaryotic means their cells contain membrane-bound structures

Heterotrophic means they need to obtain nutrients from other sources because they can’t produce everything themselves

The slides also describe:

• food vacuoles for digestion

• contractile vacuoles for eliminating excess water

• direct uptake of soluble nutrients

• some protozoa living symbiotically with bacteria

⭐ Q: What are the four major protozoal groups in this lecture?

The four protozoal groups are:

1. Ciliates — Ciliophora

2. Flagellates/Hemoflagellates — Mastigophora and Zoomastigophora

3. Amoebae — Sarcodina

4. Apicomplexa — Sporozoa and Hemosporidians

⭐ Q: How do ciliates, flagellates, amoebae, and Apicomplexa differ structurally or in locomotion?

Ciliates use cilia

• they have two types of nuceli

  • a macronucelus and a micronucleus

  • Macronucleus = runs the cell's everyday activities, like metabolism and gene expression.

  • Micronucleus = mainly involved in reproduction/genetic exchange and preserving genetic information.

Flagellates use flagella

• Flagella can be used for:

  • movement

  • capturing/moving food

Amoebae use pseudopodia

• A pseudopodium is a temporary extension of the cell membrane and cytoplasm.

• Amoebae don't have permanent “legs.” They basically change their body shape to crawl.

  
  

Apicomplexa possess specialized apical structures used to enter host cells

• Apical just means “at one end of the cell.”

• its a ring-like, tubular, and filamentous structures at that end

• These structures help the parasite attach to and enter host cells.

⭐ Q: What role do commensal (normal) protozoa play in the rumen?

Rumen protozoa, especially anaerobic ciliates, contribute to feed digestion and fermentation and form an important component of the rumen microbial ecosystem.

These organisms live in an anaerobic environment and help break down plant material such as cellulose.

⭐ Q: How do the commensal ciliates in ruminants, Holotrich and Spirotrich rumen ciliates differ?

Holotrich ciliates primarily convert soluble sugars into starch, whereas Spirotrich ciliates consume starch and cellulose.

⭐ Q: How can rumen protozoa both benefit and sometimes compete with their host?

Rumen protozoa generally benefit the host by digesting plant material and other nutrients and by becoming a nutrient source themselves, but during starvation they can compete with the host for rumen protein.

⭐ Q: What are the major stages, location, and structural characteristics of Balantidium coli?

Balantidium coli is a protozoan that exists in two different forms during its life cycle: a trophozoite and a cyst.

Trophozoite

• the active form inside the host

• lives in the cecum and colon

• moves using cilia

• reproduces

• can invade the large-intestinal mucosa

Cyst

• the tough, protected form

• has a resistant wall

• survives harsh conditions such as stomach acid

• is passed in feces

• helps the organism survive and spread to another host

⭐ Q: What is the life cycle of Balantidium coli?

Balantidium coli is a protozoan that switches between a tough cyst form for survival/transmission and an active trophozoite form that lives and reproduces in the large intestine.

The sequence goes:

• Cyst is ingested and survives GI conditions, stomach acid etc

• Cyst reaches the large intestine → undergoes excystation

  • Excystation = the cyst opens and releases the active trophozoite.

• Trophozoite = active intestinal form

  • the trophozite lives in the large intestine and reproduces by binary fission (where one divides into two) or conjugation (where two organisms exchange nuclear material)

• Some trophozoites can invade the intestinal mucosa

  • some can become invasive and damage host tissue

• Trophozoites turn back into cysts

  • as they reach the rectum they undergo encystation to turn back into cysts

• Finally, Cysts leave the host in feces and the cycle repeats
  
  

⭐ Q: How does Balantidium coli differ in pigs versus humans?

Balantidium coli is generally a commensal/asymptomatic (normal) organism in pigs but can act as a zoonotic pathogen in humans and cause balantidiosis.

Pigs have no clinical signs bc its normal for them to have it. They act as a reservoir for the protozoa

Humans get infected with it, can cause dysentery (severe diarrhea with blood and mucus)

For pigs its a normal gut protozoa, for humans its a pathogen

⭐ Q: what is Tritrichomonas musculis and how does it interact with its mammalian host?

Tritrichomonas musculis is a single-celled commensal flagellated protozoan that lives in the intestines of mice.

It stimulates host antibacterial defenses and colonization resistance without causing direct mucosal injury in the example presented.

• It attaches to small-intestinal epithelium

• promotes inflammatory signaling

• promotes T-helper cell responses

• increases antibacterial defenses

• can protect against Salmonella Typhimurium

This example shows that a protozoan can stimulate the immune system without simply being classified as a disease-causing parasite.

⭐ Q: Why is Tritrichomonas musculis a good example of the complexity of “commensal” organisms?

Tritrichomonas musculis illustrates that a commensal organism can enhance antibacterial protection while also increasing susceptibility to harmful intestinal inflammation and colon cancer under some circumstances.

🔎 General Idea:
“Commensal” doesn't necessarily mean:

“This organism can never contribute to anything harmful.”

The host-microbe relationship depends on context.

⭐ Q: How does Tritrichomonas foetus disease differ in cattle versus cats?

Tritrichomonas foetus is pathogenic in both cattle and cats, but in cattle it primarily causes sexually transmitted reproductive disease, whereas in cats it primarily causes prolonged diarrhea.

In cattle it can cause abortion and even pyometras

In cats its just diarrhea

Main idea is just that in different species, the same protozoan has different effects

⭐ Q: What are the two stages of Giardia, where does it live, and how does each stage function in its life cycle?

Giardia also has two stages named Trophozite and Cyst

Giardia’s trophozoite stage attaches to intestinal epithelium and its tough cyst stage survives outside the host and permits transmission.

Trophozoite

• tear-drop shaped

• has attachment/suction structure

• adheres to intestinal epithelium

• colonizes the duodenum

• reproduces by binary fission

Cyst

• tough oval form

• environmental/transmission stage

• passed in feces

⭐ Q: What is the general Giardia life cycle?

1. Host ingests a cyst

2. Trophozoite develops and attaches to the brush border of the villous epithelium of the intestines

3. it reproduces through binary fission

4. at some point in the intestine encystation happens again

5. cyst leaves host in feces

⭐ Q: What is the epidemiology and transmission pattern of Giardia described in the lecture?

Giardia is commonly found in dogs, cats, and many other animals and is transmitted primarily by the fecal-oral route, often through contaminated water

There are different genetic groups of giardia that infect different species, these genetic families are called assemblages

Assemblage Families:

A and B: Mammals including humans

C and 😩 Dogs

E: Hoofed animals like horses, etc

F: cats

G: Rats

⭐ Q: Why can Giardia be considered a commensal/pathobiont in some animals but a pathogen in others or under some conditions?

Giardia can exist without clinical disease in many infected animals but can also cause giardiasis with gastrointestinal dysfunction, making its host relationship context-dependent.

Most infected animals are asymptomaticm this is called pathobiont, meaning the organism may be present without causing disease but it has the potential to become harmful

🔄 UPDATED Card ⭐ Q: How should Entamoeba histolytica be classified and understood based on the later protozoa lecture?

This protozoa lecture classifies Entamoeba histolytica as a pathobiont of dogs, cats, and humans that is usually asymptomatic but can cause severe intestinal and systemic disease.

The terminology pre-work mentioned E. histolytica while explaining commensalism, but this later organism-specific lecture gives you more detail and explicitly calls it a pathobiont.

⭐ Q: What are the transmission, tissue effects, and disease pattern of Entamoeba histolytica in this lecture?

Entamoeba histolytica is an amoeba that iusually causes an asymptomatic intestinal infection but can cause severe colitis and may spread hematogenously to damage other organs.

So it is a pathobiont

Transmission methods:

• transmitted through fecal contamination, including contaminated water

• can invade the intestine → colitis and bloody diarrhea

• can spread through the bloodstream to other organs

Disease pattern:

intestinal invasion
→ colitis
→ bloody diarrhea

Possible extraintestinal spread (outside the intestines):

organism enters bloodstream
→ hematogenous spread (spread through bloodstream)
→ can cause damage in other organs

Yes we need to know ALL this stuff :,) based on the LOs

⭐ Q: What structural features distinguish Apicomplexa from the other protozoal groups?

Apicomplexa are distinguished by specialized structures at their apical end that help them interact with and penetrate host cells.

Apical = at one end of the organism.

The apical end can include structures like the polar ring, conoid, rhoptries, and micronemes.

⭐ Q: How do coccidia interact with host tissues, and why are they pathogenic?

Coccidia are pathogenic because they replicate inside host cells and damage or kill those cells when new parasites emerge.

Consequences described:

1. Replicates inside host cell
   → replicated parasites exits cell
   → breakout causes host cell to die
   → intestinal barrier is disrupted from cell damage/death
   → greater opportunity for secondary pathogens to infect
   → causes diarrhea, including bloody diarrhea

⭐ Q: What are merogony, gametogony, and sporogony in the generalized coccidian life cycle?

Coccidia use merogony for asexual multiplication, gametogony for production of male and female gametes, and sporogony to produce infectious sporozoites from the zygote/oocyst stage.

In list form:

• Merogony/Schizogony = the asexual reproduction process, they are the same thing

  • Merogony = make LOTS of parasites

    • Merogony/Schizogony clones itself to make merzoites (daughter parasites)

• Gametogony: makes male and female sex cells aka gametes for sexual reproduction

  • Microgamete (male gamete)

  • Macrogamete (female gamete)

  • and thus they create zygotes the fusion baby

• Sporongony: Makes the infectious form, sporozoites, for the next host

  • zygote goes on to become oocyst that develops into sporoziote

⭐ Q: What is the complete generalized coccidian life cycle taught in the lecture?

1. Host ingests oocyst
↓
2. Oocyst excysts (breaks open) in gut
↓
3. Sporozoites penetrate intestinal epithelial cells
↓
4. Sporozoites develop and undergo merogony
↓
5. Merozoites are released and infect new cells
↓
6. Additional merogony occurs
↓
7. Gametogony produces micro- and macrogametes
↓
8. Gametes fuse → zygote
↓
9. Thick-walled oocyst is shed in feces
↓
10. Oocyst sporulates (lets out spores) in the environment
↓
infectious oocyst ready for another host

⭐ Q: How do the protozoa in this lecture illustrate the spectrum from commensalism to pathobiont behavior to pathogenicity?

The lecture presents protozoal relationships as a continuum in which some organisms normally benefit or coexist with the host, some can shift between harmless and harmful behavior, and others directly cause tissue injury and disease.

COMMENSALS

Rumen ciliates

• Holotrichs

• Spirotrichs

• contribute to digestion/fermentation

Tritrichomonas musculis

• can enhance antibacterial defense

PATHOBIONTS

Giardia

• many infections asymptomatic

• can cause giardiasis

Entamoeba histolytica

• usually asymptomatic

• can cause severe disease

Host-dependent/opportunistic example

Balantidium coli

• commensal in pigs

• pathogenic/zoonotic in humans

PATHOGENS

Tritrichomonas foetus

• reproductive disease in cattle

• diarrhea in cats

GI coccidia

• intracellular replication

• epithelial-cell death

• intestinal disease

⭐ Q: How do the major protozoa examples compare in host, location/tissue interaction, and disease relationship?

The protozoal examples differ substantially in where they live, whether they invade tissue, which hosts they infect, and whether they behave primarily as commensals, pathobionts, or pathogens.

Rumen ciliates
→ ruminant rumen
→ participate in fermentation
→ commensal/symbiotic

Balantidium coli
→ cecum/colon
→ pigs commonly asymptomatic; may invade mucosa
→ pig commensal/reservoir, human pathogen

Tritrichomonas musculis
→ intestinal epithelium
→ stimulates immune defenses without mucosal injury in example
→ commensal with potential inflammatory downside

Tritrichomonas foetus
→ cattle reproductive tract / cat GI tract
→ disease
→ pathogen

Giardia
→ duodenum/villous brush border
→ attaches rather than following coccidian intracellular pattern
→ often asymptomatic, but can cause disease

Entamoeba histolytica
→ intestine; may spread through blood
→ asymptomatic or invasive
→ pathobiont

Coccidia
→ inside intestinal epithelial cells
→ host-cell destruction during replication
→ pathogens

• Memorize this table. yes i mean it :,)
  
  

• Learning Objectives:

• recall the scientific/common names of example protozoa mentioned

• describe their general life cycles and host interactions

• describe how they interact with host tissues

• distinguish commensal vs pathobiont vs pathogenic

• compare their epidemiology and host interactions

Organism	What I think you should definitely know
Balantidium coli	Ciliate; cyst + trophozoite; pigs often asymptomatic/reservoir; can cause disease in humans
Tritrichomonas musculis	Flagellate; mouse intestinal commensal; can alter/stimulate immune responses
Tritrichomonas foetus	Flagellate pathogen; cattle = reproductive disease; cats = diarrhea
Giardia	Flagellate; cyst + trophozoite; fecal-oral/water transmission; attaches to intestine
Entamoeba histolytica	Amoeba/pathobiont; usually asymptomatic but can invade intestine → colitis/bloody diarrhea
Coccidia	Apicomplexa; intracellular parasites; damage host cells; generalized merogony → gametogony → sporogony cycle