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Micro/Immuno > Exam 2 - Bacteria > Flashcards

Exam 2 - Bacteria Flashcards

1
Q

Clostridium: G(?)

A

G(+)

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2
Q

Chlamydiae G(?)

A

G(-)

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3
Q

Rickettsiae G(?)

A

G(-)

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4
Q

Ehrlichiae G(?)

A

G(-)

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5
Q

Clostridium: Spores?

A

Yes

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6
Q

Chlamydiae: Spores?

A

No

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7
Q

Rickettsiae: Spores?

A

No

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8
Q

Ehrlichiae: Spores?

A

No

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9
Q

Clostridium: Ob. Int’cell Parasite? Energy Parasite?

A

No ; No

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10
Q

Chlamydiae: Ob. Int’cell Parasite? Energy Parasite?

A

Yes ; Yes

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11
Q

Rickettsiae: Ob. Int’cell Parasite? Energy Parasite?

A

Yes ; No

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12
Q

Mycoplasma: Ob. Int’cell Parasite? Energy Parasite?

A

No (but needs sterols) ; No

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13
Q

Clostridium (in general) cause disease by ______. (invasive? toxin producing?)

A

Producing toxins

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14
Q

Clostridium are ______ (structurally)

A

Rods

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15
Q

Process of spore formation:

A
  • Part of bacterium buds off
  • That part gets engulfed by mother bacterium
  • Engulfed particle develops a thick peptidoglycan layer and thick protein coat
  • mother cell eventually dies and lyses, releasing the spore
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16
Q

Clostridium difficile normally found in the ______ (site)

A

Intestines

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17
Q

Clostridium difficile causes __________?

A

Pseudomembranous colitis (PMC)

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18
Q

Pseudomembranous colitis is characterized by what appearance? Of what is that appearance consisting?

A

Yellow plaques containing fibrin and cellular debris

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19
Q

Clostridium does not invade the intestinal cells, but produces toxins. In this way, it is similar to what 2 bacteria already covered?

A

E. coli and V. cholerae

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20
Q

What causes diarrhea and Pseudomembranous colitis (PMC), respectively?

A

Toxin A –> enterotoxin leads to diarrhea

Toxin B –> cytotoxin leads to damage of epithelial cells of colon.

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21
Q

What is Toxin A (produced by Clostridium difficile)

A

Enterotoxin that cause fluid production and damage to the mucosa of intestines. It cause epithelial cells too absorb Na+ and causes fluid loss from intestines

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22
Q

What is Toxin B (produced by Clostridium difficile)

A

Cytotoxin causes some damage to the clonic epithelial cells and the dead cells begin to accumulate on the surface/lumen on the intestines. This generates the cellular debris part of the pseudomembrane. The other component of the pseudomembrane is fibrin.

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23
Q

Both toxin A and toxin B (produced by Clostridium difficile) act in the _________ (location) by _______ (mechanism)

A

They act in the cytoplasm. They glycosylate GTP-binding proteins (Ex: Rho, Rac)

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24
Q

How is diagnosis of Clostridium difficile is achieved?

A

Perform ELISA for toxin A. This is necessary because you can’t just look for the bacteria since they are endogenous of the gut, but they SHOULD be only spores and should not be producing the toxins.

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25
Q

Clostridium perfringens is usually found ____ (nature) and in the ______ (part of body and creature)

A

Clostridium perfringens is normally found in soil and digestive tract of animals

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26
Q

Is Clostridium perfringens invasive? Toxin producing?

A

Yes ; Yes (most of the disease is caused by toxins)

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27
Q

Explain how Clostridium perfringens is good at infecting war wounds.

A

Spores are in the soil and then when a soldier gets wounded and gets the wound ‘dirty’ the spores can germinate. The Clostridium perfringens is aided by the anaerobic environment created by blood loss and also by the tissue damage making Ca++ and Peptides and amino acids available.

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28
Q

Initially what happens with a Clostridium perfringens infection? Then what happens?

A

Initially it grows and causes a cellulitis and then progresses to gas gangrene (necrotizing process with gas production in muscle) and is associated with systemic signs of shock

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29
Q

Clostridium perfringens can produce 12 toxins. What is alpha-toxin? What does it do? What results locally and systemically?

A

Alpha-toxin is a Lecithinase (attacks lecithin, or basically phosphotidyl choline, which is embedded in cell membranes) and leads to disrupting cell membranes.

Locally it causes cellulitis and if progresses deeper to destroy muscle it causes myonecrosis. This causes a blue-green look and the toxin attacks dead cells and produces gas bubbles characteristic of Gas Gangrene.

Systemically it causes renal failure and has a 100% fatality of untreated.

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30
Q

Clostridium perfringens is treated by ________.

A

Surgical removal of infected tissue and immediately return blood supply if possible. Once bacteria have germinated, must amputate.

A.B.’s and antitoxins have been tried to control infection but still need to amputate.

Some cases of pressurized O2 helps.

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31
Q

In addition to Gas Gangrene, Clostridium perfringens also produces what?

A

Food poisoning but through different strains than those that cause gas gangrene. Usually in ppl who have eaten contaminated food. Within 12-24 hours water loss, 1-3 days duration. Usually not treated

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32
Q

Where are Clostridium botulinum spores found? Why are they significant?

A

Clostridium botulinum has spores found in soils and seawater. They commonly survive the canning process and then sporulate in the anaerobic environment of a sealed can.

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33
Q

Colstirdium botulinum produces 8 neurotoxins, but A, B, and E are the most common. Describe the neurotoxin structure?

A

They are a stable 900kDa protein complex with a 150kDa toxic component and a 750kDa non-toxic component. The non-toxic component helps the toxin bind to the target cell. The toxic component prevents release of ACh.

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34
Q

How does the Clostridium botulinum toxin affect a cell?

A

The Clostridium botulinum neurotoxin binds to ACh containing neurons that release their neurotransmitter via exocytosis. The toxin prevents the vesicles from docking at the membrane so they cannot release the ACh. This causes flaccid paralysis (usually affecting CN’s and working its way down to where it reaches the respiratory tract and causes death (12-36 hrs).

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35
Q

What does the Clostridium botulinum toxin cause in a person? (what do you see?)

A

Flaccid paralysis.

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36
Q

What are the 3 types of toxins produced by Clostridium botulinum (Mechanism of entry/effect)?

A

Food-borne botulism - ingestion of toxin that has been produced in food by bacteria already present and growing

Wound botulism (rare in the USA) - systemic spread of toxin produced by organisms inhabiting wounds. Contracted by trauma, surgery, subcutaneous heroin injection and sinusitis from intranasal cocaine abuse.

Infant botulism: intestinal colonization of organisms in infants younger than 1 year old. Slow onset with favorable outcome but causes a hypotonic floppy state related to flaccid paralysis. (this is why to not give honey to infants).

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37
Q

Food-borne botulism:

A

ingestion of toxin that has been produced in food by bacteria already present and growing

38
Q

Wound botulism

A

systemic spread of toxin produced by organisms inhabiting wounds. Contracted by trauma, surgery, subcutaneous heroin injection and sinusitis from intranasal cocaine abuse.

39
Q

Infant botulism

A

intestinal colonization of organisms in infants younger than 1 year old. Slow onset with favorable outcome but causes a hypotonic floppy state related to flaccid paralysis. (this is why to not give honey to infants).

40
Q

Clostridium botulism exposure prognosis

A

Mortality rate high as 25% because damage is caused by the toxin, not the bacteria. Antitoxin possible if administered immediately, but it also has some allergic reactions.

Some mm. possible permanent paralysis/damage even with recovery.

41
Q

Clostridium tetani is normally found _________.

A

Ubiquitous in the GI of human and animals, and in soil.

42
Q

Clostridium tetani is associated with wounds (T/F)

A

True, but not as traumatic wounds as seen in C. perfringens.

43
Q

What is the major toxin of Clostridium tenani? Describe its structure. How does it function?

A

Tetanospasmin. It has 2 components: a heavy chain and a light chain. Both must be present to have any functional toxin.

attaches to peripheral nerves near wound site and the toxin gets taken up by endocytosis and gets transported up neuron to CNS (to cells with GABA). It blocks these inhibitory neurons and causes spastic paralysis.

44
Q

What are the first symptoms of Clostridium tetani toxin, Tetanospasmin? Then following symptoms?

A

Lockjaw (aka trismus), then mm of the back and ends up causing a permanently arched back posture and then respiratory failure.

45
Q

Is Clostridium tetani preventable?

A

Yes, with DPT vaccine

46
Q

How does Clostridium tetani vaccine work?

A

Tetanus toxoid is formalin inactivated toxin that retains its antigenicity so the result is an antibody response to the toxin.

In some cases you can give human globulin as passive immunization in tetanus-prone wounds to try to neutralize the toxin, but this really is needed to be down very quickly even before symptoms show.

47
Q

Clostridium tetani prognosis:

A

11% mortality rate.

Antibodies not produced due to low amounts of toxin present.

Surgical debridement of the wound to prevent region of bacterial growth and to try to remove any remaining spores.

48
Q

Clostridium difficile toxin?

A

Toxin A (diarrhea) and Toxin B (PMC)

49
Q

Clostridium perfringens toxin?

A

Alpha-Toxin

50
Q

Clostridium tetani toxin?

A

Tetinospasmin (light and heavy chain - both needed)

51
Q

Clostridium botulinum toxin?

A

8 neuro toxins, A, B, E most common.

150 toxic component and 750 binding component

52
Q

Chlamydiae are intercellular pathogens. What determines this?

A

Their genome is too small to support growth outside of a cell (they depend on the cell for things, including energy!)

53
Q

What is Chlamydiae dependent on the host cell for?

A

Energy

Amino acids

54
Q

4 Species of Chlamydiae, 2 of which are human pathogens:

Chlamydiae trachomatis
Chlamydiae pneumoniae
Chlamydiae psittaci
Chlamydiea pecorum

A 
Chlamydiae trachomatis (human)
Chlamydiae pneumoniae (human)
Chlamydiae psittaci (primarily animal)
Chlamydiea pecorum (primarily animal)
55
Q

What is the leading cause of preventable blindness?

A

Chlamydiae

56
Q

What is the most common sexually transmitted bacterial infections? Viral infection?

A

Bacterial - Chlamydiae

Viral - HPV

57
Q

What 2 things we discussed cause “walking pneumonia”

A

Chlamydiae pneumoniae & Micoplasma

58
Q

How does Chlamydiae spread?

A

Fomites, fingers, flies, and fornication.

It stays locally in the mucosal tissues except for 1 exception (Lymphogranuloma vererum (same species of Chlamydia tractomitis causes it but different strain) is the only strain that can cause a systemic invasion/infection apparent in lymph nodes that drain to the genital tract and cause pain in these lymph nodes.)

59
Q

What is Lymphogranuloma vererum?

A

Lymphogranuloma vererum (same species of Chlamydia tractomitis causes it but different strain) is the only strain that can cause a systemic invasion/infection apparent in lymph nodes that drain to the genital tract and cause pain in these lymph nodes.

60
Q

What diseases does Chlamydia trachomatis cause?

A

Genital tract infections. Generally start with urithritis and may progress to inflammation of epidisimis and prostate or cervix.

Can cause Pelvic Inflammatory Disease in women.

Sometimes it does not infect genital tract and will instead inflame the eye with pussy inflammation –> leads to blindness after scarring/chronic inflammation. This is spread then by direct mucosal contact (ex: towels)

61
Q

Is Chlamydia trachomatis symptomatic?

A

No, this is a problem because it causes chronic infections that lead to preterm birth and some eye and lung infections of newborns (from mother) and chronic inflammation can lead to sterility and/or ectopic pregnancy.

62
Q

What is a Chlamydia Elementary body?

A

Chlamydia trachomatis gets passed from one person to the next as Elementary Body.. It attaches to epithelial cell. The bacterium insects some of its protein and convinces the host cell to engulf it and put in vesicle. Bacteria then changes the vesicle to neutralize the pH, change membrane so lysosome can’t attach.

63
Q

How does Chlamydia bacterium change the vesicle once engulfed by host cell?

A

It neutralizes the pH of the vesicle and puts some host glycolipids in the vesicle membrane so that it can avoid the immune system.

If it didn’t do this, the host cell acidified the vesicle and fuses with a lysosome that ultimately results in breakdown of the bacterium.

64
Q

What is a Chlamydia Reticulate Body?

A

It is a more metabolically active state that forms from an Elementary body, and ultimately will form back into an Elementary body. The reticulate body will divide, but slowly (2-3 days per cycle). 200-1000 inclusions form in a host cell before release and spread to neighbor cells.

*Inclusion body is the vesicle. It contains Elementary bodies and Reticulate bodies at the same time.

65
Q

How do Elementary Bodies and Reticulate bodies of Chlamydia get nutrients?

A

Produce tube-like proteins that extend from microbe all the way through the membrane of the inclusion body and all the way to the cytoplasm of the host cell.

66
Q

What does Chlamydia pneumonia cause?

A

Walking pneumonia. It is generally an asymptomatic or acute respiratory response but chronic respiratory infections have been associated with asthma, cystic fibrosis, lung cancer.

67
Q

Why is it hard to treat Chlamydia?

A

There are 4 membranes to cross to get an antibiotic to the metabolically active Reticulate Bodies, and even if they do get there, the replication is very slow, so this requires long term antibiotics.

68
Q

What do Rickettsiae not have?

A

No flagella, and non-spore forming

69
Q

Where are Rickettsiae commonly found?

A

Animals and humans - commonly pass back and forth

70
Q

Rickettsiae are intercellular parasites and are energy parasites. (T/F)?

A

False. They are intercellular parasites, but unlike Chlamydiae, the Rickettsiae are not energy parasites.

71
Q

Describe the mode of transmission for Rickettsiae.

A

Transmitted by ticks by the American dog tick or American wood tick but not found in the rocky mountains (it’s all east and southern). The tick larva become infected with the bacteria and maintain it in their gut as larva until adult and it feeds on a mammal and it can pass the bacteria from the gut into the host/mammal/human blood stream. There they bind to blood endothelial cells and induce them to engulf them into ensodomal vesicles. Usually starts with small capillaries and progresses to larger vessels. Once inside these cells they secrete phospholipase which lyses the phagosome and they enter the cytoplasm. Once in the cytoplasm they then replicate.

72
Q

How does Rickettsiae rickettsii get out of the host cell?

A

Induces actin polymerization at one end of the cell up to the cell membrane to create a finger-like projection and the bacteria eventually poke their way through the cell at the end of the filopodia.

73
Q

How does Rickettsiae tsutsugamushi get out of the host cell?

A

Budding

74
Q

How does Rickettsiae prowazekii get out of the host cell?

A

Weak lysis

75
Q

What disease does Rickettsiae ricketsii cause?

A

Rocky mountain spotted fever. It is spotted because capillaries get damaged by the bacteria and become a little leaky. The number of spots is proportional to the number of intracellular bacteria.

Lysis of the cells results in leakagae of blood leading to a rash called hemorrhagic spots.

Bacteria usually stays local, but can travel to other vessels including heart and brain.

76
Q

What is the prognosis for Rickettsiae ricketsii infection?

A

Good, 75% of people recover within days, even before treatment.

77
Q

What is the prognosis for Rickettsiae ricketsii infection?

A

Good, 75% of people recover within days, even before treatment.

78
Q

What does Rickettsia prowazekii cause?

A

Typhus fever. It is transmitted by lice between humans and flying squirrels.

79
Q

What does Rickettsia type cause?

A

Fever, maurin typhus, transmitted by rats and rat fleas.

80
Q

Ehrlichia has 2 cell stages. What are they called?

A

It infects as reticulate cells and then replicates as reticulate cells before evolving into metabolically active dense-core cells that will be release from vesicles to infect neighboring cells

81
Q

What types of cells does Ehrlichia infect? What is this called?

A

Immune cells:

Monocytes and macrophages called human monocytic ehrlichiosis

Neutrophils called human granulocyte ehrlichiosis

82
Q

What symptoms do Human monocytic ehrlichiosis and human granulocyte ehrlichiosis cause?

A

Basic “sick” behaviors like fever, headache.

83
Q

Why is it hard to diagnose Ehrlichia and Rickettsiae infections?

A

Most often people present with fever symptoms before any rash or spotted fever type symptoms. People may not realize they have been bit by a tick and thus diagnosis requires eukaryotic cell culture or inoculation of animals and the handling is difficult.

You can also look for antibody titers in response to these bacteria but his takes up to a week to get antibody titers at a level high enough to be detected.

84
Q

What is the smallest organism capable of growth on celll-free media?

A

Mycoplasma (not as small as the Chlamydia, and Rickettsia, and Ehrlichia, they all require host cells.

85
Q

What is the smallest organism capable of growth on celll-free media?

A

Mycoplasma (not as small as the Chlamydia, and Rickettsia, they all require host cells. (Ehrlichia requires sterols? not sure the size though?)

86
Q

Is Mycoplasma sensitive to penicillin?

A

No, because no cell wall! They use sterols instead.

87
Q

What is the primary cause of “atypical pneumonia”?

A

Mycoplasma pneumoniae

88
Q

Mycoplasma pneumonia have only human as a reservoir , and they cause a mild symptomatic infection (T/F).

A

True

89
Q

What does walking pneumonia affect?

A

Only affects the bronchioles, not the alveoli, and no tissue damage. But they do disrupt the cilia and therefore prevents the bacteria from being expelled by coughing.

90
Q

What may cause “hemolytic anemia”?

A

Mycoplasma pneumonia. It is where cold hemagglutinin bind the RBCs at low tempueratures like after breathing in a lot of cold air. This rarely causes clinically significant hemolysis.

91
Q

What does Mycoplasma genitalium cause?

A

Inflammation of the urethra, cervix, and endometrium, and Pelvic inflammatory Disease. (newest emerged human pathogen for this. It can be isolated from synovial and respiratory fluids.

Micro/Immuno (2 decks)

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