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Microbiology for Dentists > 22. Parasites > Flashcards

22. Parasites Flashcards

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1
Q

Parasitic protozoa are …

A
  • pathogenic microbial eukaryotes
  • protists
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2
Q

Define ‘symbiosis’

A
  • association between organisms from different species
  • diff types of association can be defined with 3 main categories - mutualism, commensalism and parasitism
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3
Q

Define ‘mutualism’

A
  • both partners benefit from the interaction and they are co-dependent or thriving
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4
Q

Define ‘commensalism’

A
  • one partner benefits from interaction
  • the other is neither harmed nor benefitted
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5
Q

Define ‘parasitism’

A
  • one partner relies on host for nutrients and shelter
  • there is potential cost to the host - potential pathogen causing pathologies
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6
Q

Most parasitic protozoa are … meaning
Some are … - they don’t cause …

A
  • obligate symbionts, they require a host to complete life cycle
  • facultative pathogens - disease all the time - blurs distinction between parasites, commensals and mutualists
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7
Q

Define ‘opportunistic pathogens’

A
  • those that cause pathologies when host is compromised
  • e.g due to immunodeficiency - as in HIV-AIDS due to malnutrition and chemotherapies
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8
Q

The outcomes of a host-parasite interaction depends on …

A
  • characteristics from all interacting partners and environments
  • importance of context of interactions like oral microbiota
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9
Q

Adaptations of parasites to host

A
  • highly adapted to one or more body sites of host to progress through life cycle
  • best adapted parasites are least pathogenic - don’t kill host
  • many parasite-host relationships are long-term, chronic, highly intimate - evidence for commensalic and mutualistic relationships
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10
Q

Explain monoxenous and heteroxenous parasites

A
  • some parasites require a single host for completing life cycle - called monoxenous like Trichomonas tenax
  • ones needing 2 or more are heteroxenous defining intermediate hosts as those needed for development and definite hosts where sexual maturity is reached
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11
Q

What is a promiscuous parasite?

A
  • they are capable of infecting a broad range of hosts
  • e.g Trichomonas tenax
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12
Q

Define ‘zoonoses’

A
  • human diseases caused by animal parasites
  • animal hosts represent resevoirs for human pathogens
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13
Q

Mucosal surfaces mediate simultaneously 2 contradictory functions. What are they?

A
  • protect individual from microbial, chemical and physical insult
  • facilitate exchanges between outside and inside the body
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14
Q

How do microbiota link to mucosal surface function?

A
  • members of microbiota are intimately associated with both of the mucosal surface functions at respiratory, digestive and urogential tracts
  • oral mucosa only mediate protective functions however
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15
Q

Define ‘eubiosis’

A
  • microbiota taxonomic and functional configurations
  • that lead to homeostasis/promote health
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16
Q

Define ‘dysbiosis’

A
  • abnormal microbiota taxonomic and functional configurations
  • lead to pathologies - even in absence of overt pathogens - concept of pathobionts
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17
Q

Define ‘pathobionts’

A
  • members of microbiota that have potential to cause damage/pathologies
  • context dependent
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18
Q

Some mucosal microbial parasites are considered … rather than overt pathogens

A

pathobionts

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19
Q

What archaea involved in oral microbiota?

A
  • methanobrevibacter oralis-like
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20
Q

Bacteria involved in oral microbiota?

A
  • responsible for oral disease
  • for caries, periodontitis, microbial eukaryotes
  • some oral bacteria can infect other body sites
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21
Q

Microbial eukaryotes involved in oral microbiota?

A
  • fungi (occasional infections, Candida spp.)
  • protists-protozoa-microbial parasites - members of microbiota, pathobionts (T. tenax, E. histolytica)
22
Q

Define ‘autochthonous microbiota’

A
  • micro-organisms characteristically found at particularly site
  • adapted to survive and grow at given site
  • two common examples is Trichomonas tenax and Entamoeba gingivalis
23
Q

Define ‘allochthonous microbiota’

A
  • micro-organisms transiently present at given site
  • organisms not specific to site but colonise transiently or if site is compromised in injury/immunodeficiency e.g AIDS
  • Leishmania species for example at oral-skin interface
24
Q

2 fundamental issues in periodontitis

A
  • bacteria undoubtedly principal cause of gingivitis but host response to bacteria dictates disease progress
  • overwhelming evidence demonstrates it’s uncontrolled host inflammatory/immune response that largely drive tissue destruction
25
Q

Key questions about periodontitis

A
  • what drives localised/contained inflammatory response to gingivitis to progressive, destructive periodontitis?
  • is bacterial invasion of tissues an initiator or consequence of disease?
  • is it a spontaneous evolution of maturing biofilms or is it driven by changing environment mediated by host response?
26
Q

Explain cutaneous leishmaniasis

A
  • most common form
  • causes skin legions mainly ulcers
  • life-long scars left and serious disability/stigma
  • over 95% of new CL cases occur in 6 countries - Afghanistan, Algeria, Brazil, Columbia, Iran, Iraq and Syria
  • estimated around 600,00 to 1 million new cases appear worldwide annually
27
Q

Explain visceral leishmaniasis

A
  • aka kala-azar
  • fatal if untreated in over 95% of cases
  • irregular bouts of fever, weight loss, enlargement of spleen and anaemia
  • most cases in Brazil, East Africa and South-East Asia. 50,000 to 90,000 new cases worldwide a year (lots in Sudan, South Sudan, Nepal, Somalia, Brazil, China)
28
Q

Explain mucocutaneous leishmaniasis

A
  • leads to partial or total destruction of mucous membranes of nose, mouth, throat
  • over 90% of mucocutaneous leishmaniasis occur in Bolivia, Brazil, Ethiopia and Peru
29
Q

2 common microbial eukaryotes associated with periodontitis

A
  • Trichomonas tenax
  • Entamoeba gingivalis
30
Q

Roles of Trichomonas vaginalis

A
  • infects humans
  • genitourinary tract
  • associated with HIV, bacterial vaginosis, pelvic inflammatory disease and low birth weight
31
Q

Role of Trichomonas gallinae

A
  • infects birds
  • common in pigeons and columbiform
  • causes epidemics and high mortality rates
32
Q

Role of Trichomonas tenax

A
  • infects humans, dogs and cats
  • oral cavity, upper GI tract and lungs
  • associated with periodontis (35% PP)
  • identified in uretha of MSM
33
Q

Trichomonas species can be isolated in …

A

humans and birds

34
Q

Phylogeny supports a … origin of Trichomonas species

A

zoonotic

35
Q

Explain T. tenax in human patients

A
  • more frequent associated with severe periodontitis
  • 2 genotypes (among 3) were significantly associated with it
  • T. tenax appears to be associated with onset/evolution of periodontal diseases
  • cause or consequence of disease can’t be established
36
Q

What Trichomonads are present in the gut?

A
  • various
  • Dientamoeba fragilis
  • Pentatrichomonas hominis
37
Q

What Trichomonads are present in the lung?

A
  • various
  • AIDS
  • ARDS
  • CF patients
38
Q

What Trichomonads are present in the mouth?

A
  • tenax
  • associated with periodontitis
39
Q

What Trichomonads are present in the UGT?

A
  • Trichomonas vaginalis
40
Q

What Trichomonads are present in the skin?

A

none

41
Q

Pathobiology of Trichomonas vaginalis

A
  • T. vaginalis endosymbionts
  • with TVV - totoviruses
  • incites inflammation in host immunity
42
Q

What is the molecular basis of Trichomonas spp. mucosal life style and pathology?

A
  • cell surface proteins involved in parasite-microbiota/host interactions
  • metabolic enzymes
  • enzymes targeting other microbes
  • shared and transcribed genes among trichomonas spp. are prioritised for functional characterisation
43
Q

What are BspA proteins?

A
  • expressed on cell surface of 2 oral bacterial pathogens (Tannerella forsythensis/bacteroidetes and Treponema denticola/spirochetes)
  • adhesins mediating binding to epithelial cells and ECM proteins and cell-cell interactions between Tannerella and Treponema
  • mediate invasion of epithelial cells and trigger innate immune and antibody responses
44
Q

What could be the function of BspA proteins in Trichomonas tenax?

A
  • induce inflammation (?)
  • binding to human cells/proteins?
  • mediate binding to oral bacteria-phagocytosis?
45
Q

What are candidate peptidoglycan targeting enzymes?

A
  • NlpC/P60, GH19, GH25
  • shared genes across all 3 trichomonas species
  • could target members of microbiota present in various species and mucosa
  • can explain capacity to thrive on various mucosal surfaces (oral, upper digestive tract and urogenital tract) across different species (pigeon, pet animals, human)
  • can contribute at facilitating zoonotic transfers
46
Q

Define peptidoglycan fragments as important inducers of inflammation?

A
  • relative stimulatory potency of pnuemococcal wall components
  • exposed to human peripheral blood mononuclear cells (lymphocytes, monocytes, natural killer cells, dendritic cells)
47
Q

Pathway for peptidoglycan fragments causing inflammation

A
  • PNG fragments stimulate broad specificity inflammatory responses recruiting and activating phagocytes
  • PNG as pathogen-associated molecular patterns (PAMP)
  • PAMP consist of molecules not found in host, including bacterial cell wall components like PGN
  • recognition of PAMPs is mediated by specific proteins called pattern recognition molecules - these activate inflammatory signalling pathways and stimulation of innate immune response
48
Q

Entamoeba … is the loss of cyst form, entamoeba … with cysts

A
  • giginvalis
  • histolytica
49
Q

Virulence regulation of E. histolytica

A
  • pathobiota induces inflammatory cascade, barrier dysfunction and nutrient malabsorption which increase susceptibility to E. histolytica infection
  • alters host microbiota - microbiota controls host nutrient availability and absorption level, integritty of mucins - leptin production, competitive exclusion of pathogens and intestinal barrier function/ion transport
50
Q

What is the causal relationship between E. gingivalis and periodontitis?

A
  • work shows parasites detected by microscope mainly - if not exclusively - belong to species E. gingivalis and presence of parasite correlates with periodontitis
51
Q

Explain the potential causal link between T. tenax and/or E.gingivalis and periodontitis

A
  • could induce and/or worsen the dysbiotic state of microbial community
  • could be accesory pathogens
  • could be keystone pathogens and initiate damaging inflammation or contribute to worsening inflammatory tone
  • could do all of the above
  • could alternatively benefit from dysbiosis or inflammation to thrive - bystanders
52
Q

It is important to understand the spatial and temporal sequence of events in periodontitis and pocket formation because …

A
  • inflammation always precedes periodontal pathogen overgrowth
  • thus seems most probable that host response not microbes that determine eventual outcome of host parasite interactions with periodontal pockets

Microbiology for Dentists (37 decks)

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