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Micro1 final > test 4 > Flashcards

test 4 Flashcards

1
Q

What will secrete exotoxin?

A

Gram + and/or gram - bacteria.

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2
Q

Where else will exotoxin come from besides being secreted by gram + and Gram - bacteria?

A

It can leak into the surrounding fluid following lysis of a bacterial cell.

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3
Q

What do bacteria need to do to produce enough exotoxin to be harmful?

A

The bacteria must colonize tissue.

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4
Q

How are exotoxins made with foodborne illnesses?

A

The bacteria multiples in the food and produces exotoxins.

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5
Q

What are most exotoxins made of?

A

Proteins.

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6
Q

How will the immune system respond to exotoxins that are proteins?

A

Make antibodies.

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7
Q

Many exotoxins are so powerful that fatal damage can occur before what happens?

A

An immune response is mounted.

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8
Q

Why are vaccinations against exotoxins so valuable?

A

For those that are so powerful they cause fatal damage before an immune response is mounted the vaccines are invaluable for quick memory response.

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9
Q

What will heat do to exotoxins?

A

Since most of them are proteins heat will kill them.

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10
Q

Exotoxins are released by every major Gram positive genera except what?

A

Listeria.

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11
Q

Many bacteria that release exotoxins also release what?

A

Endotoxin.

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12
Q

Will exotoxins cause a fever or generalized inflammation?

A

Not usually.

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13
Q

What are the 3 specific targets of exotoxins?

A

Neurotoxins, Enterotoxins, Cytotoxins.

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14
Q

What do neurotoxins do?

A

cause paralysis.

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15
Q

What do enterotoxins do?

A

Act of GI tract to cause diarrhea.

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16
Q

What do Cytotoxins do?

A

Damage a variety of cell types by interfering with cell mechanisms or causing cell lysis.

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17
Q

Endotoxins are what?

A

Lipopolysaccharides (LPS).

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18
Q

What are LPS’s composed of?

A

Lipid A, core polysaccharide, O specific polysaccharide.

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19
Q

LPS is a molecule that is part of what?

A

Outer membrane in Gram Negative bacteria.

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20
Q

LPS’s are fundamental parts of what?

A

The cell wall of gram negative bacteria.

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21
Q

The immune response to endotoxins is due to what?

A

Innate immune response, no specific target.

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22
Q

what will heat do to endotoxins?

A

It will not be destoryed.

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23
Q

What will autoclaving do to endotoxins?

A

Not destroy them.

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24
Q

Name the 2 Gram positive Cocci?

A
  1. Staphylococcus. 2. Streptococcus.
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25
Q

Will staphylococcus be part of our normal flora?

A

Yes.

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26
Q

What are the 2 types of Staphylococcus mentioned?

A
  1. S. Aureus. 2. Staphylococcus epidermidis.
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27
Q

What will the S. aureus pigment be like?

A

Golden.

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28
Q

What is the coagulase like for S. aureus?

A

Positive.

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29
Q

What are the virulence factors of S. aureus?

A

Protein A, and Exotoxins.

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30
Q

What is protein A?

A

Extracellular surface protein that binds to IgG’s and prevents organization by coating bacterium with host immunoglobin.

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31
Q

With S. aureus what is the most potent hemolysin?

A

Alpha toxin.

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32
Q

What will cause Toxic shock syndrome toxin?

A

An exotoxin from S. aureus.

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33
Q

What will toxic shock syndrome do?

A

A superantigen causing release of cytokines which cause a drop in blood pressure and kidney damage.

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34
Q

Toxic shock syndrome was initially associated with what?

A

Tamon use.

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35
Q

S. Aureus causes enterotoxin which is what?

A

An exotoxin if present in food will cause nausea and vomiting if consumed.

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36
Q

Since Enterotoxin from S. aureus is an exotoxin will heat kill it?

A

No it is heat stable.

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37
Q

S. aureus causes Exofoliatin which is what?

A

An exotoxin that destories material that binds together the layers of skin.

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38
Q

What are the different pathogenesis of S. aureus?

A

Furuncles (boils)folliculitis, scalded skin syndr, toxic shock syndr, Pneumonia, soteomyelitis, catheter and shunt infections, wound infections, MRSA

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39
Q

What is the coagulase like for staphylococcus epidermidis?

A

Negative.

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40
Q

What is staphylococcus epidermidis like?

A

opportunistic pathogen.

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41
Q

What type of patients get staphylococcus epidermidis?

A

Compromised patients.

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42
Q

What is the treatment like for Staphylococcus?

A

Difficult since almost all strains produce penixillinase (beta-lactamase).

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43
Q

What type of media is needed for streptococcus growth?

A

Rich media. So little or no growth on a traditional media.

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44
Q

All streptococci can be identified in what way?

A

Hemolysis patterns.

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45
Q

What are the 3 different Hemolysis patterns of streptococcus?

A

Alpha-, Beta-, and Gama-hemolysis.

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46
Q

How can you tell you have a alpha-hemolysis?

A

Partial hemolysis with greenish cast around colonies.

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47
Q

How can you tell you have a beta-hemolysis?

A

Complete lysis of blood cells creating clear area around colonies.

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48
Q

How can you tell you have a gama-hemolysis?

A

no lysis of blood cells.

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49
Q

What are Lancefield groups?

A

Ways to catagorize streptoccus bacteria that is not inclusive and used to some degree still.

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50
Q

What groups of Lancefield are used today?

A

Groups A and B.

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51
Q

What is a more inclusive way to classify strep?

A

By dividing into 4 groups.

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52
Q

What are the 4 inclusive groups that streptococcus can be divided into?

A

lactic, fecal, viridans, Beta-hemolytic.

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53
Q

What is the lactic streptococci like?

A

Non pathogenic, no hemolysis.

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54
Q

Where is Lactic streptococci found at?

A

In milk products.

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55
Q

What is lactic streptococci used for?

A

in dairy fermentation, produce lactic acid that gives sour taste to foods.

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56
Q

Fecal streptococci is found in what Lancefield group?

A

D.

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57
Q

Fecal streptococci is normal flora of what?

A

The intestinal tract.

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58
Q

What are the hemolysis patterns of fecal streptococci like?

A

Different patterns than alpha, beta, and gamma.

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59
Q

Fecal streptococci is clinically a cause of what?

A

Urinary infections, sometimes endocarditis.

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60
Q

Fecal streptococci is what type of pathogen?

A

Opportunistic pathogen that causes disease in weakend patients.

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61
Q

What is another name for Fecal streptococci?

A

Enterococci.

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62
Q

What is VRE?

A

Vancomycin resistant enterococci. A type of fecal streptococci that is resistant to vancomyocin.

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63
Q

What type of group is viridans streptococci?

A

Large heterogenous group.

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64
Q

What type of Lancefield antigens will Viridans streptococci have?

A

None.

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65
Q

What type of hemolysis will Viridans streptococci have?

A

Alpha.

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66
Q

Viridans streptococci is normal flora of what?

A

The mouth and respiratory tract.

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67
Q

Viridans strptococci may cause what?

A

Tooth decay, and bacterial endocarditis (patients that have heart damage or heart condition).

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68
Q

Beta-hemolytic streptococci has strains in both the group A and B of the lancefield groups and what will these strains be?

A

Group A- Streptococcus pyogenes. Group B- Streptococcus agalactiae.

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69
Q

What is the major pathogen of streptococcus?

A

Streptococcus pyogenes.

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70
Q

What type of toxin will Streptococcus pyogenes have?

A

Pyrogenic exotoxins.

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71
Q

What are the pyrogenic exotoxins like with Streptococcus pyogenes?

A

M protein, hyaluronic acid capsule.

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72
Q

What are the different pathogenesis of Streptococcus pyogenes?

A

Streptococcal pharyngitis, Streptococcal impetigo, cellulitis, erysinpelas, Scarlet fever, post streptococcal diseases.

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73
Q

What are post streptococcal diseases?

A

Rheumatic fever, Glomerulonephritis.

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74
Q

What is St. Anthony’s fire?

A

Erysipelas which is a pathogenesis of Streptococcus pyogenes.

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75
Q

What are 3 ways to diagnose sterptococcus pyogenes?

A

blood agarplates, Sensitive to bacitracin, ELISA test.

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76
Q

Name 2 other pathogens of streptococcus?

A

S. agalacitiae, and S. Pneumoniae.

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77
Q

Streptococcus agalactiae is normal flora of what?

A

Female geintal tract in 10-30% of females.

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78
Q

Colonization of Streptococcus agalactiae is like what?

A

Transient.

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79
Q

Streptococcus agalactiae is an important cause of what?

A

Neonatal meningitis, pneumonia, sepsis in first week of life= high mortality.

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80
Q

What will the capsule for Streptococcus pneumoniae be like?

A

Polysaccharide.

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81
Q

What is the purpose of the S. pneumoniae polysaccharide capsule?

A

Major virulence factor and antigenic.

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82
Q

What hemolysis group will S. pneumoniae be in?

A

Alpha.

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83
Q

S. pneumoniae is part of the normal flora in what % of people?

A

5-40%.

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84
Q

Infection occurs when with Streptococcus pneumoniae?

A

If invasive strain moves to lower lungs.

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85
Q

Streptococcus pneumoniae is the most common cause of what in adults?

A

Pneumonia, acute onset with chillsm and high fever. And meningitis.

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86
Q

What will the difference between adult and infant meningitis caused by Streptococcus pneumoniae?

A

Adults stiff necks and no stiff necks in infants.

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87
Q

Streptococcus pneumoniae is a common cause of what in children?

A

Otitis media and sinusitis.

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88
Q

How will Streptococcus pneumoniae be diagnosed?

A

Quellung reaction.

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89
Q

What is the quellung reaction?

A

Mix sample with serum containing antibodies to capsular antigens capsules appear to swell.

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90
Q

What is the treatment for Streptococcus pneumoniae?

A

Polyvalent vaccine and conjugate vaccine.

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91
Q

All members of Neisseria are what?

A

Gram negative diplococci and are oxidase positive and fastidious.

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92
Q

What is Fastidious?

A

Picky eaters.

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93
Q

What are the virulence factors for Neisseria gonorrhoeae?

A

Pili, Gram negative cell wall LOS (similar to LPS), secreted protease IgA that destroys immunoglob A, and membrane proteins that adhere to host cell.

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94
Q

How is Neisseria gonorrhoeae acquired?

A

Through unprotected sexual intercourse.

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95
Q

What happens to Males who acquire Neisseria gonorrhoeae?

A

It penet the mucous membrane of the urethra causing inflam, and they frequently experience pain on urination and purulent discharge from urethra.

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96
Q

Will any males with neisseria gonorrhoeae remain asymptomatic?

A

Yes.

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97
Q

What happens to females who acquire neisseria gonorrhoeae?

A

Most remain Asympotomatic and are reservoirs for disease.

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98
Q

Females who are not asymptomatic with neisseria gonorrhoeae will experience what?

A

Painful urination and discharge, It will infect cervix or rectum. Can cause pelivic inflammatory disease.

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99
Q

What part of the female body can not be infected with neisseria gonorrhoeae?

A

The vagina.

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100
Q

How will infants get neisseria gonorrhoeae?

A

Transmitted from mother to infant during childbirth.

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101
Q

What will Neisseria gonorrhoeae do to infants?

A

Damage cornea and lead to blindness.

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102
Q

How will Neisseria gonorrhoeae be diagnosed?

A

Oxidase test.

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103
Q

What is the treatment for Neisseria gonorrhoeae?

A

Penicillin is no longer effective due to PPNG. Tetracyline for concurrent Chlamydia infection, Prophylaxis- to treat eyes of newborns.

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104
Q

What are the virulence factors for Neisseria meningitidis?

A

Polysaccharide capsule, Endotoxin, Secreted protease (IgA protease=cuts up IgA).

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105
Q

What is the host for Neisseria meningitidis?

A

Humans are the only natural hosts.

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106
Q

Who is at high risk for neisseria meningitidis?

A

Kids 6 months to 2 years, and army boot camps 40% carriers.

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107
Q

Can there be healthy carriers of neisseria meningitidis?

A

Yes 5% of people this is in their normal flora.

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108
Q

What is menigococcemia?

A

Neisseria meningitidis bacteria invade bloodstream from nasopharynx and this can result in deadly sepsis.

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109
Q

What is the classic clue of menigococcemia?

A

Appearance of petechial rash called purpura.

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110
Q

What is waterhouse friderichsen syndrome?

A

A septic shock from neisseria meningitidis bacteria causing a systemic immune response that leads to bilateral hemorrhage into adrenal glands.

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111
Q

How is Neisseria meningitidis diagnosed?

A

Culture body fluids, oxidase test.

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112
Q

What is the treatment for neisseria meningitidis?

A

Elimination of carriers, penicillin, vaccine available but not widely used.

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113
Q

What type of bacteria is clostridium?

A

Gram positive endospore forming rods.

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114
Q

What type of metabolism will colstridium have?

A

Anaerobic.

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115
Q

Where will clostridium be found at?

A

Since it has an endospore it is found in soil and water.

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116
Q

What are 2 ways to get clostridium perfringens?

A

Food poisoning, gas gangrene.

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117
Q

What are the 2 types of food poisoning from clostridium perfringens?

A

enterotoxin A- Diarrhea, cramping. Enterotoxin C- hemorrhagic enteritis= tissue damage and bleeding.

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118
Q

What will gas gangrene from clostridium perfringens do?

A

Exotoxin that destroys muscle, and produces gas.

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119
Q

How is clostridium perfringens diagnosed?

A

Egg yolk agar, anaerobic culture.

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120
Q

What is the treatment for clostridium perfringens?

A

Surgical cleansing (debridement), penicillins.

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121
Q

Clostidium botulinum will cause what?

A

Botulism.

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122
Q

What will botulism cause?

A

Flaccid paralysis by blocking cholinergic synapse by 7 neurotoxins.

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123
Q

What types of botulism will clostridium botulinum cause?

A

Adult and infant.

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124
Q

How is clostridium botulinum diagnosed?

A

Inject mice with serum from patient or left over food if toxin is present mice will die rapidly. In infants toxin can be id in bowel content, not serum.

125
Q

How can clostridium botulinum be prevented?

A

Cook food in canned pressure cookers above 212 F or 100 C for 10 minutes.

126
Q

Clostridium tetani causes what?

A

Neurotoxins block inhibitory impulses to muscles and cause muscles to spasm and contraction-tetany.

127
Q

What is opisthotonos?

A

Spasm in back muscles-head is thrown backwards and the back is bowed like an arch from clostridium tetani.

128
Q

How is clostridium tetani prevented?

A

Toxoid (weakend toxin) vaccine, part of DTP.

129
Q

What will clostridium difficile cause?

A

Pseudomembranous colitis.

130
Q

What is pseudomembranous colitis?

A

A severe infection of the colon.

131
Q

Pseudomembranous colitis often occurs when?

A

After normal gut flora is eradicated by the use of antibiotics.

132
Q

How will clostridium difficile react to antibiotics?

A

Most strains are resistant that?s why when antibiotics kill off a lot of normal flora that clostridium difficile flourishes.

133
Q

What is the treatment of Clostridium difficle?

A

Discontinue antibiotics, and treat with metronidazole, 2nd choice vancomycin.

134
Q

Should you give a patient loperamide and bismuth who has clostridium difficel?

A

No because slowing of fecal transit time is thought to result in extended toxin-associated damage.

135
Q

What is Bacillus like?

A

Gram positive endospore forming rods.

136
Q

What is bacillus metabolism like?

A

Aerobic.

137
Q

Bacillus is endospore forming that has what type of pattern?

A

Bamboo-like pattern.

138
Q

What are the 3 types of bacillus anthracis?

A
  1. Cutaneous anthrax. 2. Gastroinetsinal anthrax. 3. Inhalation anthrax.
139
Q

Cutaneous anthrax is aka?

A

Woolsorters disease.

140
Q

How common is cutaneous anthrax and how is it aquired?

A

Common and endospore enters a cut.

141
Q

How common is GI anthrax and how is it aquired?

A

Uncommon and from uncooked or contaminated meat.

142
Q

How is inhalation anthrax aquired?

A

spores inhaled into alceoli, ex-sporulate and release toxins.

143
Q

What are the symptoms of inhalation anthrax?

A

non-specific symptoms.

144
Q

What is the treatment for Bacillus anthracis?

A

After exposure oral ciprofloxacin. Before exposure there is a vaccine.

145
Q

How was the Bacillus anthracis vaccine made?

A

From an attenuated strain of Bacillus anthracis.

146
Q

What will bacillus cereus cause?

A

There are 2 types of enterotxins 1. Diarrheal. 2. Vomiting.

147
Q

Name 2 gram positive non-endospore forming rod bacteria?

A

Corynebacterium diphtheriae, and Listeria monocytogenes.

148
Q

What is the primary reservoir for corynebacterium diphtheriae?

A

Humans.

149
Q

What are the sources of infection of corynebacterium diphtheriae?

A

Carriers who have recovered, New cases not exhibiting symptoms, people with active disease, contaminated articles.

150
Q

Where will Corynebacterium diphtheriae localize at?

A

In throat and cause swelling of the neck.

151
Q

What will corynebacterium diphtheriae do once localized in the throat?

A

Forms a gray membrane composed of clooted blood, epithelial cells and leukocytes.

152
Q

Corynebacterium diphtheriae produces toxins that do what?

A

Cause nerve damage= paralysis of soft palate and eye muscles. Toxin can be absorbed in blood and damage kidneys, heart, and extrem nerve damage.

153
Q

What is the major concern with the gray membrane in the throat?

A

It can become detached and cause suffocation.

154
Q

How is corynebacterium diphtheriae diagnosed?

A

Schick test

155
Q

What is the treatment for corynebacterium diphtheriae?

A

Antitoxin.

156
Q

How is corynebacterium diphtheriae prevented?

A

Immunization DPT.

157
Q

When will Listeria Monocytogenes be motile?

A

at 22-28 degrees C. Not at body temps.

158
Q

Where is Listeria monocytogenes found at commonly and why?

A

Deli meat because it grows well at 4 Degrees C in a refrigerator.

159
Q

Listeria is ____ hemolytic?

A

Beta.

160
Q

What is unique about Listeria monocytogenes?

A

It produces endotoxin and is gram +.

161
Q

How is Listeria monocytogenes aquired?

A

Ingested in contaminated food.

162
Q

Who is at high risk for listeria moncytogenes?

A

Immunocompromised people, and pregnant women and neonates.

163
Q

Why are neonates at risk for listeria monocytogenes?

A

Contact microbe from asymptoma mother during delivery, and Listera can cross the placental barrier result in miscarriage or delivery of crit ill neonate.

164
Q

Name the 7 gram negative bacteria also known as enterics.

A
  1. E. coli. 2. K. Pneumoniae. 3. Enterobacter. 4. Serratia. 5. Proteus. 6. Salmonella. 7. Shigella.
165
Q

How many gram negative bacteria aka enterics are considered coliforms?

A
  1. E. coli, K. Pneumoniae, and enterobacter.
166
Q

What are coliforms?

A

Facultatively anaerobic, gram negative, non-endospore forming, rod shaped bacteria that FERMENT LACTOSE with gas production.

167
Q

Coliforms are normally found where?

A

Human intestines.

168
Q

Where should coliforms not be found?

A

Outside of intestines.

169
Q

Coliforms are used as an indicator of what?

A

Water quality testing.

170
Q

What type of pathogen is escherichia coli?

A

Opportunistic.

171
Q

How can DNA transfer from E. coli?

A

via conjugation, transposons, lysogenic converion.

172
Q

What will E. coli infections cause?

A

Septicemia, UTI, meningitis, Gastroenteritis.

173
Q

Gastroenteritis is caused by what 4 things?

A
  1. Enterotoxin producing E. coli. 2. Enteroinvasive E. coli. 3. Enteropathogenic E. coli. 4. Enterohemorrhagic E. coli.
174
Q

What is enterotoxin producing E. coli?

A

Traveler’s diarrhea.

175
Q

What is Enteroinvasive E. coli?

A

E. coli invades intestinal cells.

176
Q

What is the main virulence factor with Enteroinvasive E. coli?

A

Encoded on plasmid shared by shigella and E. coli.

177
Q

What will enteroinvasice E coli cause?

A

Produces shiga-like toxin which causes gastroenteritis.

178
Q

What will enteropathogenic E. coli do?

A

Will not invade cells, but adheres to them.

179
Q

Once Enteropathogenic E. coli adheres to cells what will it do?

A

Coded on the plasmid once it adheres it causes loss of microvilli where microbe attaches and causes non-bloody diarrhea.

180
Q

Almost all enterohemorrhagic E. coli belong to what group?

A

serotype o157:H7.

181
Q

What will enterohemorrhagic E. coli do?

A

Produce a toxin known as verotoxin.

182
Q

What will verotoxin do?

A

Blocks a cellular protein that normally prevents the cell from entering apoptosis.

183
Q

What disease is associated with Enterohemorrhagic E. coli?

A

E. colio157:H7.

184
Q

What will the gastroenteritis caused by enterohemorrhagic E. coli be like?

A

Severe abdominal pain and diarrhea which initially is watery, but becomes grossly bloody with occaisonal vomiting.

185
Q

Some victims of Enterohemorrhagic E. coli develop hemolytic uremic syndrom (HUS) and this is characterized by what?

A

Renal failure and lysis of RBC’s.

186
Q

What % of hemorrhagic colitis victims develop HUS?

A

0-15%.

187
Q

How is Escherichia coli diagnosed?

A

It produces a green metalic sheen on EMB agar

188
Q

How can Escherichia coli be distingushed from Enterobacter?

A

use IMViC.

189
Q

Klebsiella pneumoniae is a coliform that is classified by what?

A

Capsule antigens.

190
Q

K. pneumoniae effects who and when?

A

The second most common cause of sepsis in hospitilized patients.

191
Q

People with K. pneumoniae get what type of infections?

A

Urinary caused by Foley catheters, and infant septicemia.

192
Q

Enterobacter is a coliform, but what is the most common species among the enterobacter?

A

Enterobacter aeruginosa.

193
Q

What can Enterobacter aeruginosa cause?

A

(UTI) urinary tract infects.

194
Q

Can serraita ferment lactose?

A

No it is not a coliform.

195
Q

Serratia is noted for it’s characteristic what?

A

Red pigment (only 10% of isolates).

196
Q

Serratia is an opportunistic pathogen in hospitilzed patientes that causes what problmes?

A

Pneumonia, bacteriemia, endocarditis.

197
Q

Can proteus ferment lactose?

A

No it is not a coliform.

198
Q

Proteus is an opportunistic pathogen that has what type of unique feature?

A

Swarming on agar.

199
Q

What type of unique enzyme will proteus have and what will it do?

A

Urease and it breaks down urea to produce cherry red color.

200
Q

Will salmonella be part of the normal flora?

A

No.

201
Q

Can Salmonella ferment lactose?

A

No it is not a coliform.

202
Q

What will salmonella cause?

A

Typhoid fever.

203
Q

Typhoid fever is aka?

A

Enteric fever.

204
Q

Typhoid fever is only caused by a few types of salmonellae, but which one is the most important?

A

Salmonella typhi.

205
Q

How can people get typhoid fever?

A

Humans are reservoirs and it is through fecal-oral transmission. Water and food contaminated with feces and/or urine.

206
Q

Will people still be carriers of typhoid or salmonella after they recover from typhoid fever?

A

Yes in the gallbladder.

207
Q

With salmonella will a large or small dose be needed to cause disease?

A

Small.

208
Q

Salmonellosis starts how long after exposure to salmonella?

A

1-3 weeks.

209
Q

What will salmonella do once inside of people?

A

Invades intestinal cells and then moves into lymph nodes.

210
Q

From the lymph nodes bacteria can do what?

A

can infect multiple systems esp. spleen.

211
Q

What happens to salmonella that are phagocytosed by monocytes?

A

They can survive and divide inside the phagocytes.

212
Q

What is it called when bactria can survive inside of phagocytes?

A

Facultative intracellular parasite.

213
Q

What are the symptoms of typhoid fever?

A

Abdominal pain, headache, weakness, high fever, rose colored spots on chest and/or abdomen.

214
Q

How is typhoid fever or salmonella infections diagnosed?

A

Culture blood, urine or feces to determine serotype.

215
Q

What is the treatment for typhoid fever?

A

Chloramphenicol, cipro, ampicillin.

216
Q

Someone with typhoid fever that is being treated with antibiotics should also have what?

A

IV fluids, electrolytes.

217
Q

How can typhoid fever be prevented?

A

There is a vaccination that is recommended for travel outside of the USA, Canada, Northern-Europe, Australia, and New Zealand.

218
Q

What is the most common type of salmonella infection?

A

Gastroenteritis.

219
Q

How can we get gastroenteritis type of salmonella infection?

A

Animals are reservoirs of infection including chickens, domestic animals, reptiles, cows. Commonly associated with undercooked eggs.

220
Q

How will gastroenteritis salmonella infect eggs?

A

Silently infects ovaries of healthy appearing hens and contaminates the eggs before the shells are formed.

221
Q

What type of toxin will gastroenteritis salmonella have?

A

Both endotoxin and enterotoxin.

222
Q

What is the gastroenteritis salmonella enterotoxin like?

A

Cholera-like.

223
Q

What is the treatment for gastroenteritis salmonella?

A

Fluids and electrolytes.

224
Q

Why wont you give antibiotics to gastroenteritis salmonella infections?

A

They don?t shorten the course of disease.

225
Q

How long will diarrhea last with gastroenteritis salmonella last?

A

a week or less.

226
Q

Shigella is an enteric, but is it part of the normal flora and can itferment lactose?

A

It is not part of normal flora and can’t ferment lactose because it is not a coliform.

227
Q

When will shigella be pathogenic?

A

Always.

228
Q

There are 4 species of Shigella, but which one is the most pathogenic?

A

Shigella dysenteriae.

229
Q

What will shigella dysenteriae cause?

A

Bacterial dysentery.

230
Q

How can we get bacteral dysentery from shigella dysenteriae?

A

Humans are the only reservoir for disease and it comes from fecal-oral transmission(food, fingers, feces, and flies).

231
Q

What will stomach acids do to bacterial dysentery caused by shigella?

A

Not easily killed so infectious dose is low.

232
Q

Shigella dysenteriae produce potent enterotoxin called what and what will it do?

A

Shiga toxin and it kills epithelial cells, but rarely invades bloodstream.

233
Q

What will bacterial dysentery cause?

A

Severe inflammatory response causing bloody diarrhea.

234
Q

Shiga toxin can cause what?

A

Hemolytic uremic syndrome which is often fatal.

235
Q

How are shigella infections diagnosed?

A

SS agar (selective and differential).

236
Q

A selective and differential SS agar is done do distinguish Shigella from what?

A

Salmonella.

237
Q

Name 2 pleomorphic gram negative rods with bipolar staining?

A
  1. Yersinia pestis. 2. Yersinia enterocolittica.
238
Q

Yersinia bacteria are motile and are part of what family?

A

Enterobacteriaceae family.

239
Q

Yersinia pestis caused what?

A

Bubonic plague.

240
Q

The bubonic plague caused how many major epidemics?

A

Three.

241
Q

Where wil yersinia pestis come from?

A

It is endemic in rodent populations of all continents besides Australia and is transmitted by rat fleas.

242
Q

What does the word sylvan mean?

A

Pertaining to the woods or wild.

243
Q

The bubonic plague is classified as what type of disease?

A

Zoonosis.

244
Q

What happens to Yersinia pestis after bacteria enter via a flea bite?

A

Engulfed by macrophages where they multiply and are carried to lymph nodes.

245
Q

What happens to lymph nodes with macrophages with yersinia pestis?

A

They become swollen and are called buboes.

246
Q

What happens to lymph nodes once buboes are formed?

A

The lymph nodes become necrotic allowing large numbers of bacteria to enter the blood-septicemic plague.

247
Q

What is septicemic plague?

A

Endotoxin results in shock and disseminated intravascular coagulation.

248
Q

What is the mortality of septicemic plague?

A

75%.

249
Q

What happens in 10-20% of septicemic plagues?

A

Infection of the lungs from bloodstream and this causes Pneumonic plague.

250
Q

What happens to people with the pneumonic plague?

A

Always fatal in just a few days.

251
Q

What is the prevention and control of Yersinia pestis?

A

Control of rat population and antibiotic treatment.

252
Q

How is yersinia enterocolitica transmitted?

A

Fecal-oral. Ingestion of contaminated food or water.

253
Q

What type of toxin will yersinia enterocolitica have?

A

Heat stable enterotoxin that leads to severe gastroenteritis.

254
Q

Name 3 Gram negative rods that are found widely in nature?

A
  1. Vibrio. 2. Campylobacter. 3. Helicobacter.
255
Q

Vibrio cholerae is a _____ gram negative rod.

A

Curved.

256
Q

What type of flagellum will Vibrio cholerae have?

A

Single polar flagellum that appears to vibrate.

257
Q

What will confer serologic specificity of Vibrio cholerae?

A

O lipopolysaccharides.

258
Q

Vibrio cholerase has at least how many O antigen groups?

A

at least 139.

259
Q

Strains of O group 1 and O group 139 cause what?

A

Classic cholera.

260
Q

Within O group 1 how many biotypes have been identified?

A

2 classic and E1 for vibrio cholerae.

261
Q

O1 and E1 biotype for vibrio cholerae is similar to what?

A

Vibrio cholerae 0139.

262
Q

What will stomach acids do to Vibrio cholerae?

A

Kills it so large amounts are needed to be infected.

263
Q

60% of infections of classic biotype of vibrio cholerae are what?

A

Asymptomatic.

264
Q

75% of infections of E1 biotype of vibrio cholerae are what?

A

Asymptomatic.

265
Q

For those who become infected with vibrio cholerae incubation period is how long?

A

1-4 days.

266
Q

What do Vibrio cholerae do once inside?

A

Adhere to mucosa and multiply, but do not invade the cells.

267
Q

What is Choleragen?

A

An enterotoxin produced by vibrio cholerae.

268
Q

Choleragen causes what?

A

Increased production of cAMP.

269
Q

Accumulations of cAMP cause what?

A

It causes intestinal cells to convert them into little pumps that continuously secrete Cl_ ions accompanied by other ions and water.

270
Q

What else will Choleragen do?

A

Inhibits absorption of Na+.

271
Q

How is Vibrio cholerae prevented?

A

Sewage treatment and water purification, good food hygiene.

272
Q

How is Vibrio cholerae treated?

A

Fluid replacement using oral rehydration salts and in severe casees IV’s.

273
Q

What is the shape of campylobacter?

A

Spiral shaped with unipolar/bipolar flagella.

274
Q

Campylobacter is the major cause of what?

A

Gastroenteritis in the USA (among the top 3).

275
Q

What is the treatment for campylobacter?

A

It is self limiting and lasts 5-8 days.

276
Q

What is the shape of helicobacter?

A

Spiral shaped with unipolar sheathed flagella.

277
Q

Helicobacter is the 2nd leading cause of what?

A

Gastric/duodenal ulcers.

278
Q

How can Helicobacter survive the stomach acids?

A

They produce urease which allows them to create an alkaline microenvironment.

279
Q

How is Helicobacter treated?

A

Antibiotic therapy combined with bismuth.

280
Q

Name 2 obligate anaerobic gram negative bacteria?

A
  1. Bacteroides fragilis. 2. Fusobacterium.
281
Q

What is the shape of bacteroides fragilis?

A

Rod shaped.

282
Q

Bacteroides fragilis is a major component of what?

A

normal flora of GI tract (99%).

283
Q

Besides GI tract where will bacteroides fragilis be found at?

A

Mouth and femal genitourinary system.

284
Q

What is cell wall of bacteroides fragilis like?

A

No endotoxin even though gram negative so cell wall is not toxic.

285
Q

Will bacteroides fragilis possess a capsule?

A

no.

286
Q

Can bacteroides fragilis be a pathogen?

A

Yes an opportunistic pathogen.

287
Q

When will bacteroides fragilis be an opportunistic pathogen?

A

If intestine is perforated it will cause abscesses in peritoneum, and in female genitourinary tract.

288
Q

Bacteroides fragilis is implicated in what disease?

A

Periodontal disease.

289
Q

Fusobacterium is similar to what?

A

Bacteroides.

290
Q

What s the morphology of fusibacterium?

A

Long rods with tapered ends.

291
Q

Fusobacterium is part of what?

A

Normal flora.

292
Q

Can fusobacterium be a pathogen?

A

Yes an opportunistic pathogen.

293
Q

Fusobacterium is an opportunistic pathogen that causes many infections, but which one is most notable?

A

Aspiration pneumonia.

294
Q

How is aspiration pneumonia aquired?

A

Result of inhaling bacteria from aspirated vomitus.

295
Q

Name the 1 obligate aerobic gram negative rod in the notes?

A

Pseudomonas aeruginosa.

296
Q

Pseudomonas aeruginosa is the epitome of what?

A

Opportunistic pathogens.

297
Q

Pseudomonas aeruginosa will not effect who?

A

Healthy patients.

298
Q

Psudomonsa aeruginosa infects what type of tissue in weakened patients?

A

Nearly any tissue.

299
Q

Pseudomonsa aeruginosa is a major cause of what?

A

Nosocomial infection.

300
Q

What type of pigment will pseudomonas aeruginosa make?

A

Blue-green that resluts in blue-green pus and smells sweet.

301
Q

How motile will Pseudomonas aeruginosa be?

A

Highly motile.

302
Q

What will the outside of pseudomonas aeruginosa be like?

A

Produces slime layer.

303
Q

Pseudomonsa aeruginosa have pili for what?

A

Exchange of antibiotic resistant plasmids.

304
Q

What type of toxins will pseudomonas aeruginosa have?

A

Endotoxin and exotoxins and Leukocidins.

305
Q

What are Leukocidins?

A

They inhibit immune response by killing white blood cells, notably neutrophils.

306
Q

Pseudomonas aeruginosa is particularly problematic for who?

A

Burn victims, cystic fobrosis patients and any compromised individual (common in AIDS patients).

307
Q

What is the treatment for pseudomonas aeruginosa?

A

Limited due to multiple resistance.

308
Q

Prevention is key in pseudomonsa aeurinosa which is done by what?

A

Cleaning and monitoring of hospital equipment.

Micro1 final (1 decks)

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