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MicroImmuno Exam 3 > Bailey 4 Clostridia > Flashcards

Bailey 4 Clostridia Flashcards

1
Q

Are Clostridium gram positive or negative? What shape?

A

They are gram positive rods

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2
Q

Are Clostridium aerobic or anaerobic and do they produce endospores?

A

They are strictly anaerobic and do produce endospores. Note that ~30 species are responsible for human infections and many are found in the environment

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3
Q

What about Clostridium causes disease symptoms?

A

the proteinaceous toxins are responsible for disease symptoms

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4
Q

What genus is responsible for tetanus, botulism, cellulitus, and pseudomembranous colitis?

A

Clostridium

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5
Q

Are spores metabolically active or inactive?

A

inactive

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6
Q

Why is C. difficile named the way it is?

A

it is difficult to culture. It causes pseudomembranous colitis (PMC) and is often contracted when people are on antibiotics for a long period of time and causes SEVERE diarrhea

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7
Q

Where is C. difficile often found?

A

in hospitals where spores are quite difficult to erradicate

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8
Q

Why does C. difficile prosper when lots of antibiotics are taken?

A

They are normally out-competed by other bacteria but in their absence, they thrive

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9
Q

Are the toxins of C. difficile invasive?

A

no

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10
Q

Name the two damaging toxins of C. difficile and what they do

A

Toxin A) causes lots of fluid loss

Toxin B) a cytotoxin that causes tissue damage

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11
Q

How to toxins A & B of C. difficile function?

A

they act in the cytoplasm of host cells on GTP-binding proteins and inactivates the GTP proteins, blocking Na+, resulting in fluid loss

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12
Q

Why is the disease caused by C. difficile called pseudomembranous collitis?

A

because as it kills the epithelial cells of the GI tract, it leaves behind a membrane-like top layer of cell material (fake-membrane)

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13
Q

What is the major pathogen of wound infections (gangrene)?

A

C. perfringens (20-30% of war wounds), found in most soil, causes local damage as well as systemic effects

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14
Q

Is C. perfringens (wound bacteria) invasive? If so, why?

A

it is due to the variety of toxins it produces

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15
Q

Why does C. perfringens especially infect large battle wounds rather than small ones?

A

It needs a special environment to replicate. Remember that is anaerobic, needs a compromised blood supply (burn?), the availability of Ca+ ions and the availability of peptides and AAs

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16
Q

Which C. perfingens toxin is primarily responsible for the tissue damage it causes?

A

There are many toxins that it produces, but Alpha-toxin is the on that damages cell membranes and causes gas gangrene. It hydrolyzes phosphodylcholine and sphingomyelin that leads to cell death. In this process, muscle tissue is destroyed and gas/discoloration is prevalent

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17
Q

What is a treatment for C. perfringens?

A

surgical removal of the infected muscle. There are other methods that have been proposed but they are largely ineffective

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18
Q

What can C. perfringens cause besides gangrene?

A

it can also cause food poisoning which is unrelated to gangrene and is relatively common. It produces an enterotoxin that causes 12-24 hours of diarrhea (short-lived). It goes away within 1-3 days

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19
Q

What is the cause of the botulism disease?

A

It is caused by the ingestion of the preformed botulism toxin (not the bacteria)

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20
Q

How is C. botulinum primarily spread?

A

canned foods

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21
Q

Which of the 8 C. botulinum toxins causes disease in humans?

A

A, B, & E. The botulism neurotoxins are the deadliest substances known to man… one capsule could kill entire human population

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22
Q

Which area of the body is the first to be affected by the botulism toxin?

A

It starts with the cranial nerves and progresses down where it will cause respiratory failure

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23
Q

What is the effect of infant botulism?

A

a “floppy” baby due to the intestinal colonization of botulism. Usually has a good outcome

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24
Q

Where can you get an antitoxin for C. botulinum?

A

horses. Should be administered to individuals ASAP

25
Q

Why are antibiotics not needed for C. botulinum?

A

because the mode of action is through the TOXIN, not the bacteria itself

26
Q

Where is C. tetani found?

A

The GI tract of humans and animals, soil

27
Q

What toxin in C. tetani is responsible for disease?

A

tetanospasmin… responsible for all symptoms

28
Q

What neurotransmitter does C. tetani affect? How about C. botulinum?

A

tetani affects GABA, botulinum afects ACh

29
Q

What does GABA do and how does tetani affect it?

A

gaba is a neuroinhibitor and C. tetani interferes with GABA resulting in muscle spasms (lockjaw - masseter)… descends to neck, back, etc. can cause respiratory seizure

30
Q

How can you prevent C. tetani?

A

DPT (diptheria, pertussus, tetanus) vaccine / antitoxin / surgical debridement

31
Q

What are some characteristics of Clamydiae?

A

small, gram negative, no peptidoglycan (murein) in cell wall

32
Q

Where do Chlamydiae grow?

A

They only grow inside a host / live tissue (humans, insects, protozoa, etc). They have very small genomes and are “energy parasites” meaning they depend on the host for ATP. They also have a complex developmental cycle

33
Q

What is the primary 2 Chlamydia species that infects humans?

A

C. trachomatis & C. pneumoniae

34
Q

What is the most notable disease effect of Chlamydiae?

A

leading cause of preventable blindness in the world. It is a common STD and there is speculation that every person has had “walking” pneumonia caused by C. pneumoniae

35
Q

How are chlamydial infections typically contracted?

A

droplet or direct contact, infect mucosal epithelial cells and usually are local (eyes, lungs, genitalia). four Fs (fingers, flies, etc)

36
Q

Do males or females generally show symptoms of C. trachomatis?

A

males. It is typically asymptomatic in females but chronic and/or repeat infections can cause sterility and/or ectopic pregnancy

37
Q

What is unique about carriage of a C. trachomatis infection?

A

asymptomatic carriage leads to the most damage and scarring

38
Q

How does Chlamydiae enter a cell?

A

it disguises itself as a nutrient, growth factor, etc to bind to specific receptors and become internalized via receptor-mediated endocytosis

39
Q

Once the Chlamydiae is within the vesicle, what does it do?

A

it maintains a pH above 6.2 and prevents vesicle from fusion with lysosomes. The vesicle is also modified with glycolipids for camouflage

40
Q

What are elementary bodies and reticular bodies of Chlamydiae?

A

elementary bodies are when the bacteria is within the vesicle, modifying its characteristics and preparing for release. Reticular bodies are metabolically active and are larger, intracellular active organisms

41
Q

How do reticular bodies of Chlamydiae get the nutrients they need?

A

They develop tube-like structures that allow them to feed on the eukaryotic host cell without leaving their inclusion vacuole.

42
Q

What happens after the reticular bodies of Chlamydiae have gained enough nutrients and replicated to their satisfaction?

A

they convert back to elementary bodies and exit the eukaryotic cell as either invasive or non-invasive elementary bodies (top or bottom)

43
Q

What does C. trachomitis cause?

A

inflammation of the conjuctiva, can cause blindness and scarring of the cornea. It s spread by direct contact with the eye, nose, throat, towels, washcloths, etc

44
Q

What is lymphogranuloma venerum

A

“venerial diesase” STD that is in the lymph nodes that drain the genital tract… mostly in developing countries

45
Q

What is the most prevalent chlamydial pathogen in humans?

A

C. pneumoniae… over half of people… can be asymptomatic or acute, might have something to do with asthma and lung cancer

46
Q

What is one main challenge in the antibiotic treatment of Chlamydiae?

A

Since there are reticular bodies that must be destroyed, the antibiotic must penetrate 4 layers of membrane. In addition, they grow slowly so antibiotics must be used over a long period of time

47
Q

Briefly describe Rickettsiae

A

they are small, gram negative rods that don’t stain well and are obligate intracellular bacteria

48
Q

How are Rickettsiae transfered?

A

animals to human transfer (ticks, lice, fleas, rats) (zoonoses)

49
Q

Do Rickettsiae have to steal ATP like Chlamydiae?

A

no, they can make their own and perform independent metabolism. They also have no flagella or endospores

50
Q

Where do Rickettsiae attach (in terms of cell type)

A

vascular endothelial cells in the small blood vessels under the skin, inducing endocytosis. once inside, they lyse the phagosome and enter the cytosol

51
Q

What phenotypic symptoms does Rickettsiae cause?

A

hemorrhagic rash proportional to the size of the infection. it can travel to the heart and brain but 75% of patients will clear infection before treatment is even administered

52
Q

Briefly describe Ehrlichia

A

obligate intracellular bacteria, transmitted by lone star tick, infects monocytes & macrophages

53
Q

What are the two life cycle stages of Ehrlichia?

A

RC (reticulate cells) —–> DC (dense-core)(spread, analogous to reticular bodies)

54
Q

What is unique about Mycoplasma?

A

They are the smallest organisms capable of growth on cell-free media. They require cholesterol and have a fried egg appaerance. They form small colonies and grow slowly

55
Q

Describe Mycoplasma

A

No cell wall therefore not sensitive to penicillin, cell membranes contain sterols, found in other mammals and in birds

56
Q

What is the only reservoir of Mycoplasma pneumoniae?

A

humans

57
Q

What type of pneumonia is associated with Mycoplama?

A

walking pneumonia. infections are mild and moderately contageous, passed thru respiratory droplets

58
Q

What can cause hemolytic anemia?

A

Mycoplasma (at low temperature, the IgM antibodies cause RBCs to stick together (RARE))

59
Q

What is unique about Mycoplasma gentalium?

A

it is a newly emerging human pathogen responsible for urinary/cervical inflammaion

MicroImmuno Exam 3 (5 decks)

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