Pathogen Relations with Hosts and Environments Flashcards

1
Q

What is an example of a commensal relationship?

A

An animal’s normal flora

commensal: organism lives in/on its host without causing disease

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2
Q

Give examples of how a commensal host-organism relationship can become a parasitic one.

A

If there is certain compromise to the host that changes the relationship, it can become parasitic.
- Staphylococcus aureus may cause mastitis as a result of udder dame
- Streptococcus zooepidemicus is an opportunistic pathogen that causes pneumonia in horses, secondary to conditions that have already compromised the horse’s defense mechanisms (viral infection, strenuous exercise, prolonged transportation)

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3
Q

What are the differences between pathogens of the normal flora versus those in carrier animals?

A
  • Normal flora pathogens = present in most animals; usually do not cause disease, but if commensal-turned-parasitic, cannot be eliminated from the animal population
  • Carrier animal pathogens = only present in few animals; always do cause disease when shed; can be eliminated from the animal population (culling)
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4
Q

Where in the body is normal flora (list 6 specific sites)?

A
  • The skin
  • The conjunctiva (outer layer) of the eye
  • The pinna and external ear canal
  • The mucous membranes of the G.I.T. (mouth, oropharynx, stomach, small and large intestinces, rectum)
  • The upper respiratory tract (cranial to larynx)
  • The lower genitourinary tract (distal urethra, posterior to cervix/vagina)

Sparse microbiome in conjunctiva due to constant flushing by tears/inhibitory action of lysozymes

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5
Q

Where in the body are sterile sites?

A
  • The anterior and posterior chambers of the eye
  • The lower respiratory tract (caudal to the larynx)
  • The upper genitourinary tract (bladder, proximal urethra, anterior to cervix/uterus)
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6
Q

Explain why transitory bacteria rarely induce inflammation in sterile sites.

A

They are cleared rapidly by the host’s defense mechanisms which are adapted to keep bacterium #s very low at these sites.

Transitory bacteria: microorganisms that are usually not found in the body/at a particular body site.

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7
Q

What are obligate (“true”) pathogens?

A

Microorganisms that require a host to fulfill their life cycle

E.g., macroparasites

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8
Q

What are opportunisitc pathogens?

A

Normal flora bacteria (commensal relationship with host) or saphrocytes, both of which only can cause diseases if conditions permit them to invade, especially when host’s defense mechanisms are impaired –> induction of inflammatory repsonse

Cause the maority of bacterial infections

other conditions: tissue damage, transitory bacteria in non-sterile sites

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9
Q

How do endogenous vs exogenous infections occur?

A

Endogenous: when bacteria that live on skin or mm take advantage of impaired host defense mechanisms, and behave as opportunistic pathogens

Exogenous: after direct or indirect transmission from an infected animal or the environment

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10
Q

When is medical treatment aimed at the pathogen itself, versus at increasing the host’s defense mechanisms?

A

Highly virulent pathogens require lower bacterial numbers and little host tissue compromise to cause disease –> tx aimed @ pathogen

Weakly virulent pathogens require several bacteria and much host tissue compromise to cause disease –> tx aimed @ increased host’s defense mechanisms

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11
Q

What are 3 common, highly virulent pathogens?

A

Staphylococcus aureus
Escherichia coli
Streptococcus spp.

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12
Q

What is a common, weakly virulent pathogen?

A

Staphylococcus epidermis

causes mastitis

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13
Q

Which immunity responds first?

A

Innate

Non-specific

First and second lines of defense (physical & chemical barriers, and cellular defense like phagocytes, dendritic and NK cells)

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14
Q

What are examples of external factors that modify a host’s defense mechanisms and make it more susceptible to infection?

A
  • extreme temperatures
  • nutritional deficiencies
  • overcrowding (stress)
  • transportation (stress)
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15
Q

What are examples of internal factors that modify a host’s defense mechanisms and make it more susceptible to infection?

A
  • tissue damage (direct trauma; allergies; ischemia)
  • host responses (endocrine changes; immunosuppressive organisms)
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16
Q

Dogs have a microbiome on their pinna/external ear canals of gram (+), Staphylococcus pseudointermedius bacteria. When their ears get wet, they can develop otitis externa. Why is this bacteria considered a “good pathogen?”

A

S. pseudointermedius does not require much host tissue compromise to produce an infection (and is therefore a highly virulent pathogen)

17
Q

Some animals infected with leptospirosis show no signs, yet still shed the bacteria. This is an example of what?

A

Carrier animal

Infected host shows no clinical signs, yet is still a potential source of infection for other susceptible hosts

18
Q

What are the virulence factors of a “good pathogen”?

A

Good pathogens must have the ability to…
1. attach & colonize
2. invade the host’s body
3. evade any of host’s innate defense mechanisms
4. produce molecules that cause dysfuntion or lysis of the host’s immune system mechanisms

Recall that a pathogen may also vary in virulence based on genetic variation factors

19
Q

Give an example of a bacterial disease transmitted via inhalation

A

kennel cough

inhalation of aerolized bacteria

20
Q

Give an example of a bacterial disease transmitted via ingestion

A

Lepto in dogs

contaminated urine in drinking sources like lakes, creeks, streams

21
Q

What is a bacterial disease transmitted via inocculation?

A

infection through the skin or mm by simple contact, injections (e.g., biting insects, cross-contaminated needle) or wound infections

22
Q

Give an example of a bacterial disease transmitted transplacentally

A

Botulism

via infected milk –> abortion or premature birth

23
Q

What is the advantage of pathogenic bacteria performing Phase Variation?

A

Phase Variation: switching on/off expression of a gene product, particularily one tht is unnecessary or unhelpful at that time in that environment

Saves metabolic energy + reduces chances of host producing an effect immune response to one of the bacteria’s virulence factors that they might need later on for infection

Virulence factors: adhestion, invasion, evasion, toxins, etc.

24
Q

What does Random Phase Variation of virulence factors generate in bacteria?

A

Subpopulations of diverse phenotypes, where the supopulation that prevails in existing conditions is the one that persists in the host.

25
Q

What are some examples of ways the mobile genetic elements (plasmids, phages, pathogenicity islands) of bacteria encode virulence factors?

Pathogenicity Islands: occupy large regions of the bacterial genome

A

Adhesions, toxins, antibiotic-resistance genes

Virulence factors = make a GOOD pathogen

26
Q

What is a clonal population of a gene encoding virulence factors?

A

These genes are only distributed on a specfic strain; the virulence factors which they encode are only present on this strain

E. coli, S. aureus

27
Q

Which bacteria has more diverse strains, clonal or non-clonal bacteria?

A

Clonal - each strain has virulence factors unique to that strain, which also produces virulence variation amongst different strains (some are highly virulent whilst others are weakly virulent)

This is why proper sample collection is imperative!

28
Q

How do pili/fimbriae allow gram (-) bacteria to be good pathogens?

A

They allow the bacteria to attach to specific cell surface receptors on the host for aid in colonization
- Also aid in resisting flushing action by host’s innate immune system

29
Q

How can bacteria passively enter a host?

A

through compromised epithelial surfaces of the skin or mucous membranes

S. aureus

30
Q

How can bacteria actively enter a host’s “leaky” GIT, versus the respiratory and urogenital tracts’ tight junctions?

A

The tight junctions of the intercellular spaces in the GIT are more “leaky”, allowing bacteria to pass through.

The respiratory and urogenital tracts have more tightly closed intercellular junctions, and so bacteria invade here by secreting exotoxins that enzymatically degrade these barriers.

31
Q

How do pathogenic, extracellular bacteria evade being eliminated by phagocytes?

A

By producing anti-phagocytic molecules, such as capsules, slime layers, biofillms, M protein

32
Q

How do pathogenic, intracellular bacteria evade being eliminated?

A

They are able to avoid the host’s defense mechanisms and survive inside a cell – can multiply in phagoctic cells (facultative or obligate intracellular parasites)

evade killing by phagocytes
evade antibodies
evade antibiotics that cannot penetrate into cells (hydrophilic/lipophobic)

33
Q

Intracellular bacteria can sometimes result in chronic infections. How do these bacteria persist for long periods of time?

A

By performing phase variation on the genes allowing for persistence

34
Q

How can pathogenic bacteria directly and indirectly damage host tissue?

A

Directly: by releasing endo or exotoxins

Indirectly: exotoxins released by the bacteria in order to perform lysis on a phagocyte can also affect other cells/tissues

35
Q

Which type of toxin is produced by the LPS of the outer membranes of gram (-) bacteria? How are they released?

A

Endotoxins – are only released when the cell wall breaks apart as a result of cell death

36
Q

Which type of toxin is highly antigenic, and why?

A

Exotoxins – are produced by live gram (+) or gram (-) bacteria, and contain potent toxins

37
Q

Which type of toxin is easily altered (labile) by changes in heat, chemicals and storage?

A

Exotoxins

On the contrary, Endotoxins are very stable to changes in heat, chemicals and storage because they are a part of the structural component of live, gram (-) bacteria