Micro Midterm 2 Flashcards

1
Q

How is a diagnosis for M. pneumoniae made?

A

Usually clinically

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2
Q

Can penicillins and cephalosporins be used to treat M. pneumoniae?

A

No, because it has no cell wall

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3
Q

Which antibiotics are used to treat M. pneumoniae?

A

Macrolides and tetracyclines

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4
Q

In an older patient, is Chlamydophila pneumonia more likely to produce a lower or an upper respiratory tract infection?

A

Lower

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5
Q

How many adults in the U.S. get Chlamydophila pneumoniae per year?

A

~100k

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6
Q

How is C. pneumoniae transmitted?

A

Respiratory droplets

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7
Q

Does C. pneumoniae have a cell wall? Does it replicate extracellularly or intracellularly?

A

Intracellularly

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8
Q

What is an “elementary body” of C. pneumoniae?

A

It is a metabolically inactive, infectious form that can survive outside a host cell

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9
Q

What is the intracellular form of C. pneumoniae called?

A

Reticulate body

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10
Q

What genus of bacteria does this diagram illustrate? It is the second-smallest family of prokaryotes known, after Mycoplasma.

A

Chlamydia

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11
Q

Label the following life cycle states for C. pneumoniae.

A

Top: elementary body, bottom: reticulate bodies

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12
Q

Why does C. pneumoniae evade host defenses so well?

A

Replicating intracellularly, it can evade host detection

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13
Q

Is there a higher risk of C. pneumoniae in immunocompromised patients as compared to immunocompetent patients?

A

It is unclear

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14
Q

What is the annoying symptom of C. pneumoniae that persists for weeks?

A

A cough that does not subside

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15
Q

Does C. pneumoniae typically cause a fever?

A

No

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16
Q

Which age group is most likely to get an asymptomatic C. pneumoniae infection?

A

Children

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17
Q

Symptomatic vs. asymptomatic C. pneumoniae might be associated with the host’s inflammatory predisposition, which could be implied by what vascular condition?

A

Atherosclerosis

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18
Q

Do most cases of C. pneumoniae result in a diagnosis?

A

No

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19
Q

Which antibodies can be detected after C. pneumoniae infection that can diagnose its presence?

A

IgM and IgG antibodies

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20
Q

What is the third-most common cause of atypical pneumonia?

A

Legionella pneumophila

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21
Q

Is Legionella spread from person to person?

A

No

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22
Q

Where does L. pneumophila prefer to live?

A

Aqueous habitats, both fresh and saltwater

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23
Q

How does L. pneumophila transfer from a water source to a person’s respiratory tract?

A

Aerosolization of the water by e.g. a shower head

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24
Q

What is the incubation period of L. pneumophila?

A

2-10 days

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25
Q

Why is L. pneumophila an underreported disease?

A

Generalized typical pneumoniae is often treated with azythromycin, which can also be effective against L. pneumophila, so doctors typically do not end up distinguishing between this and typical pneumonia

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26
Q

What is the shape, size, and gram staining of L. pneumophila?

A

Small, gram-negative bacilli

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27
Q

Is L. pneumophila an anaerobe or an aerobe?

A

Obligate aerobe

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28
Q

Which serogroup of L. pneumophila causes 75%-90% of human infections?

A

Group 1

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29
Q

Does Legionella pneumophila grow on typical bacterial culturing media?

A

No, it requires special media

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30
Q

What organism is this, which is growing well on buffered charcoal agar? Is this a medium that a lab would typically include in a culture assay?

A

Legionella; no, this is atypical media

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31
Q

What phagocytoses L. pneumophila when they reach the lungs?

A

Alveolar macrophages

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32
Q

Can L. pneumophila be deadly? Is there a neutrophil response, or a humoral response, or both? What dying cells trigger a severe inflammatory response?

A

Yes; both responses occur; dying macrophages

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33
Q

Of the top three atypical pneumonias, which is the most dangerous?

A

Legionella pneumophila

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34
Q

How can L. pneumophila be diagnosed by lab tests?

A

Culture of respiratory secretions on selective media, and detection of antigen of serogroup 1 (e.g. via direct fluorescence with antibodies)

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35
Q

What are the mainstays of treatment for L. pneumophila?

A

Macrolides (azythromycin), tetracyclines, and quinolones

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36
Q

Does L. pneumophila replicate intracellularly or extracellularly? How does this affect choice of treatment?

A

Intracellularly; antibiotics that reach an effective intracellular concentration must be used

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37
Q

Do clarithromycin and azythromycin require the bacterium to have a cell wall?

A

No, they block protein synthesis (they are both macrolides)

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38
Q

What are the three most frequent toxic effects of macrolides?

A

Diarrhea, nausea, abdominal pain

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39
Q

What is the common suffix for fluroquinolone antibiotics? Do they inhibit DNA, RNA, protein, or cell wall synthesis?

A

-floxacin; inhibit DNA synthesis (topoisomerase and gyrase inhibition)

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40
Q

Can treatment for atypical pneumonia be administered orally?

A

Yes

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41
Q

How might liver function or kidney function affect choice of a fluoroquinolone?

A

Levofloxacin and ciprofloxacin are eliminated by the kidneys, while moxifloxacin is eliminated by the liver in bile

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42
Q

What is the most common clinical symptom for a GI infection?

A

Diarrhea

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43
Q

Do most infections of the GI tract causing diarrhea require hospitalization?

A

No

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44
Q

What are the big four bacterial pathogens for foodborne diarrheal disease?

A

Vibrio, campylobacter, shigella, salmonella

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45
Q

What strain of E. coli is particularly significant for diarrheal disease?

A

E. coli O157

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46
Q

What is the only gram-positive bacterium that causes common diarrheal disease?

A

Listeria

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47
Q

What are the top two identified bacterial pathogens causing GI disease hospitalization in New York?

A

Campylobacter and Salmonella

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48
Q

What are the three mechanisms for enteric infection?

A

Inflammatory (invasion w/ cytotoxin), noninflammatory (adherence w/ cytotoxin), and penetrating

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49
Q

Which bacterial pathogen has the smallest infectious dose? What about the second smallest?

A

Shigella (100); Campylobacter (1000)

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50
Q

What is the order of magnitude difference between an infectious dose of Salmonella as opposed to Campylobacter?

A

103 greater for Salmonella (106 cells typical infectious dose)

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51
Q

What is a typical infectious dose for E. coli or Vibrio cholerae?

A

108 cells

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52
Q

What dangerous symptom does cholera cause via an exotoxin?

A

Dehydration by diarrhea and vomiting of clear fluid

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53
Q

What bacterium causes cholera and has “cholera” in the species name?

A

Vibrio cholerae

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54
Q

When was the last epidemic of cholera in the US?

A

1911

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55
Q

What is the shape of V. cholerae? What is its gram staining? Does it have spores?

A

Curved to straight bacilli; gram negative; no spores

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56
Q

Which serotypes of V. cholerae cause cholera?

A

O1 and O139

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57
Q

What is the natural environmental habitat of cholera?

A

Aquatic environments

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58
Q

What are the non-life-threatening clinical symptoms of cholera, besides diarrhea and vomiting?

A

Muscle cramps, loss of skin turgor

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59
Q

How does death occur for a cholera patient?

A

Hypovolemic shock, metabolic acidosis, and uremia from tubular necrosis

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60
Q

What is the chemical activity of cholera toxin? What receptor does it act upon? What intracellular signaller is upregulated, causing loss of cell nutrients?

A

It is an A-B type ADP-ribosylating toxin; Ganglioside receptor; cAMP

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61
Q

Are antibiotics needed to treat V. cholerae?

A

No, just rehydration

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62
Q

What is this bacterium that causes bloody diarrhea?

A

Shigella

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63
Q

Is Shigella lactose-fermenting?

A

No

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64
Q

Besides bloody diarrhea, what are two other clinical hallmarks of bacillary dystentery?

A

Abdominal cramps and pain, and tenesmus (painful straining to pass stool)

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65
Q

What does tenesmus mean?

A

Painful straining to pass stool

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66
Q

What is the reservoir of infectious Shigella?

A

Humans, it is transmitted person-to-person

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67
Q

What is the pathogenetic mechanism of Shigella infection?

A

It invades enterocytes and causes cell death

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68
Q

What mechanism of bacillary enteric disease is seen here?

A

Inflammatory + invasive, as in Shigella infection

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69
Q

What does subunit A of the Shiga toxin do? What about subunit B?

A

It permanently inactivates ribosomes; it binds to host receptors

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70
Q

Do organisms beside Shigella produce shiga-like toxins?

A

Yes, some strains of E. coli

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71
Q

Is bacteremia a common complication of Shigella?

A

No

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72
Q

What are the two species of Salmonella that cause enteric disease?

A

Salmonella enterica and Salmonella bongori

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73
Q

What is the shape and gram staining of Salmonella? Are they aerobic? Are they motile? Do they form spores?

A

Gram-negative rods; anaerobic; motile; non-spore-forming

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74
Q

Do Salmonella species produce hydrogen sulfide during fermentation?

A

Yes

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75
Q

Can Salmonella cause bacteremia? What complication typified by rose spots and delirium can result from salmonella infection?

A

Yes; typhoid fever

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76
Q

Are there asymptomatic carriers of Salmonella?

A

Yes, including some that had to be forcibly quarantined

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77
Q

How long does it take for symptoms of Salmonella to present after infection?

A

48h

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78
Q

What is the shape of Salmonella incidence in the US from year to year?

A

Spikey because of sporadic outbreaks

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79
Q

What are three common sources of Salmonella infection besides person-to-person contact?

A

Agricultural products, processed food, and domestic animals

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80
Q

What two cell types are invaded by Salmonella during initial stages of infection?

A

M cells and intestinal macrophages

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81
Q

How does Salmonella interact with microvilli on certain enterocytes to facilitate endocytosis? Can it invade non-phagocytic cells?

A

It attracts them, surrounding itself with the cell’s membrane; yes, it can invade many kinds of enterocytes

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82
Q

What areas of the Salmonella genome contribute most to its virulence?

A

Two pathogenicity islands called SPI1 and SPI2

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83
Q

How does Salmonella survive inside the cell after phagocytosis?

A

It secretes toxins that prevent fusion of lysosomes with the endosome and then replicates in the endosome

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84
Q

How does Salmonella release its anti-lysosomal fusion toxins into the cytoplasm despite being trapped in an endosome after endocytosis?

A

Toxins secreted by salmonella (encoded on the pathogenicity island SPI-2) move to the endosomal membrane and allow transport into the cytoplasm of SPI-2 effector molecules

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85
Q

What is this spirally bacterium that causes enteric symptoms, mainly through the handling of chicken?

A

Campylobacter

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86
Q

What is the shape and gram staining of Campylobacter?

A

Helical, gram-negative

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87
Q

What is Guillain-Barré syndrome? What is the most common antecedent infection?

A

An autoimmune disorder that causes peripheral paralysis after foreign antigens cause mistargeting of the immune response toward nerve tissues; Campylobacter

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88
Q

What pathogen is this, causing gastric and duodenal ulcers?

A

H. pylori

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89
Q

The stomach can normally handle acidity with its mucosal lining, but what happens during H. pylori infection that causes ulceration?

A

The bacterium invades intercellularly, using secreting toxins to disrupt cell-to-cell junctions

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90
Q

Are most infections for H. pylori symptomatic?

A

No

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91
Q

What is the most common cause for gastritis, gastric ulcer, and duodenal ulcer?

A

H. pylori infection

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92
Q

What upper gastric infection that commonly causes gastritis or ulceration is linked to gastric adenocarcinoma?

A

H. pylori

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93
Q

Can non-selective stool cultures diagnose H. pylori?

A

No, it is an upper GI infection and it is hard to isolate on non-selective media

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94
Q

What needs to be added to culture to get proper growth of H. pylori from a stool sample?

A

Bile salts

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95
Q

What tests can distinguish between Salmonella and other enterobacteriaceae?

A

Citrate and ornithine decarboxylase

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96
Q

What three antibiotic resistances are common with the top four bacterial causes of GI infection?

A

Amoxicillin (or penicillins), 1st generation cephalosporins, and trimethoprim-sulfamethoxazole

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97
Q

Since GI bacterial infections are resistant to many antibiotics, which ones are actually used for treatment?

A

Fluroquinolones (-floxacins), 3rd generation cephalosporins (ceftriaxone), and macrolides (azithromycin)

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98
Q

Does daptomycin have gram-negative activity? Why or why not?

A

No; it cannot penetrate the outer membrane sufficiently to cause depolarization

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99
Q

What are the most common manifestations of Klebsiella infection?

A

Pneumonia, UTI, and nosocomial infections

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100
Q

How can E. coli be distinguished from K. pneumoniae in the lab, e.g. after a urine sample for a UTI manifestion?

A

E. coli is indole positive, K. pneumoniae is negative

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101
Q

What is the main reservoir of K. pneumoniae?

A

The lower GI tract of humans, and secondarily the skin and female genital tract

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102
Q

What media is used here to demonstrate K. pneumoniae and E. coli by the fermentation of lactose?

A

MacConkey agar, which gives pink colonies

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103
Q

Is K. pneumoniae motile or non-motile? Is it encapsulated?

A

Non-motile; encapsulated

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104
Q

What common cause of UTIs and pneumonia is seen in this slide?

A

K. pneumoniae

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105
Q

What test is being performed here to judge the virulence of a K. pneumoniae strain?

A

The string test, which sees if the isolate is hypermucoviscous (and therefore more resistant to complement-mediated killing)

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106
Q

What kind of intra-abdominal infections are caused by K. pneumoniae?

A

Liver abscesses, peritonitis, and cholangitis

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107
Q

What is the variant of pneumonia caused by K. pneumoniae called? What is the characteristic type of sputum produced?

A

Friedländer’s disease; “currant jelly”

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108
Q

Is K. pneumoniae a common infection for immunocompetent hosts?

A

No

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109
Q

What is the mortality of a K. pneumoniae infection?

A

Up to 50%

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110
Q

Why does the sputum produced in a K. pneumoniae infection look like currant jelly?

A

The infection is hemorrhagic and necrotizing

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111
Q

What feature of this CXR is consistent with the typical qualities of K. pneumoniae infection?

A

Propensity for upper lobes

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112
Q

After E. coli or Streptococcus, what is the next most common bacterium causing acute inflammation of the peritoneum (peritonitis)?

A

K. pneumoniae

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113
Q

After E. coli, what is the next most common organism isolated in UTIs?

A

K. pneumoniae

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114
Q

Features that distinguish complicated UTIs from uncomplicated UTIs include renal […], emphysematous pyelonephritis, and catheter-associated UTIs.

A

Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.

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115
Q

Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous […], and catheter-associated UTIs.

A

Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.

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116
Q

Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and […]-associated UTIs.

A

Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.

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117
Q

Can K. pneumoniae cause skin and skin structure infections?

A

Yes

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118
Q

What antibiotic are K. pneumoniae almost universally resistant to due to a chromosomal gene encoding an enzyme breaking down the antibiotic?

A

Ampicillin (and other penicillins)

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119
Q

Which penicillins are effective against Pseudomonas and Klebsiella? What are they often combined with?

A

Anti-pseudomonal penicillins which include piperacillin, ticarcillin, and carbenicillin; a β-lactamase inhibitor

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120
Q

Which generation(s) of cephalosporins would be used against K. pneumoniae?

A

3rd or 4th generations, usually cefepime (4th generation)

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121
Q

Does cefepime have activity against gram negatives, gram positives, or both?

A

Both

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122
Q

How many β lactamases are there?

A

Thousands

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123
Q

Are ESBL and KPC chromsomal inducible or plasmid-mediated β-lactamases?

A

Plasmid-mediated

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124
Q

Which β-lactams are reserved for the most sick patients, particularly those with infections from ESBL-containing bacteria?

A

Carbapenems

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125
Q

What kind of drug is imipenem-cilastatin?

A

A carbapenem (β-lactam antibiotic)

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126
Q

Which class of β-lactams is shown here?

A

Carbapenems

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127
Q

What is distinctive about this β-lactam structure? What class is it?

A

It lacks a ring; it is a monobactam

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128
Q

What is the one monobactam clinically available in the US? Is it active against gram negatives, gram positives, or both? Is it effective against aerobic or anaerobic organisms?

A

Azteronam; Gram negatives only; Aerobes only

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129
Q

Can monobactams be hydrolyzed by ESBL?

A

Yes

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130
Q

What is ESBL? When was it first spotted?

A

It is “extended spectrum β-lactamase”, which confers resistance against all β-lactams except carbapenems; in the 1980’s

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131
Q

If a K. pneumoniae strain is resistant to ceftriaxone but susceptible to imipenem, what kind of β-lactamase does it most likely have?

A

ESBL

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132
Q

When were variants of K. pneumoniae resistant to carbapenems first discovered? What plasmid-mediated β-lactamase do they typically have?

A

1990’s; KPC (K. pneumoniae carbapenemase)

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133
Q

Are there other known methods of K. pneumoniae resistance to carbapenems besides KPC?

A

Yes

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134
Q

What fraction of hospital-detected K. pneumoniae in New York State is carbapenem-resistant?

A

21%, significantly higher than the rest of the US

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135
Q

Which three other countries are considered endemic or epidemic for carbapenem-resistant K. pneumoniae?

A

Israel, China, and Greece

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136
Q

What treatment options remain for somebody with carbapenem-resistant K. pneumoniae?

A

Polymyxin, tygacil, and gentamicin

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137
Q

What is the mechanism of polymyxins? Are they effective against gram-negatives, gram-positives, or both?

A

They are cationic agents that bind to the outer membrane disrupting its integrity; only gram-negatives

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138
Q

What tissues cannot be penetrated by polymyxins?

A

Lungs and CSF (cannot cross BBB)

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139
Q

What two toxicities are significant with polymyxins?

A

Nephrotoxicity and neurotoxicity

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140
Q

What is the mechanism of tigecycline? What class of bacteria is it indicated for treating?

A

It is similar to tetracyclines, as it inhibits protein synthesis, but resistance to tigecycline is less common than for tetracyclines; effective against gram-negative bacilli like K. pneumoniae

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141
Q

What drug class can be attempted to treat a gram-negative infection in a patient with a severe β-lactam allergy?

A

Monobactams e.g. aztreonam

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142
Q

What structural component of K. pneumoniae is the most important virulence factor?

A

Polysaccharide capsule

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143
Q

Is imipenem a cure-all for multidrug-resistant gram-negative infections?

A

No, carbapenem resistance is on the rise (especially in New York State)

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144
Q

Which species of anaerobic gram positive bacilli is most commonly seen in the hospital?

A

Clostridium difficile

145
Q

What organism is most often linked with antibiotic-associated diarrhea?

A

Clostridium difficile

146
Q

Which Clostridium causes spastic paralysis? Which causes flaccid paralysis?

A
  • C. tetani*: spastic;
  • C. botulinum*: flaccid
147
Q

Are there many anaerobic bacteria that are normal human commensals?

148
Q

When mixed with aerobic organisms, what do anaerobes tend to form?

149
Q

Do anaerobes produce gas when they metabolize food?

150
Q

What is crepitus?

A

When you push on necrotic tissue and you feel bubbles created by an infectious disease

151
Q

What antibiotic can be used against most anaerobic infections?

A

Penicillin, or penicillin with a β-lactamase inhibitor

152
Q

Besides penicillins, what four other antibiotics are used to treat anaerobic bacterial infections?

A

2nd generation cephalosporins, carbapenems, metronidazole, and clindamycin

153
Q

What is the suffix for carbapenem drugs?

154
Q

What is the mechanism of action of metronidazole?

A

DNA damage

155
Q

What dietary modifications are necessary when taking metronidazole?

A

No alcohol

156
Q

What is the mechanism of clindamycin?

A

It inhibits the translocation step of bacterial peptide synthesis

157
Q

A 63 yo woman receives prophylactic cefazolin before surgery for a hip fracture, and develops fever, abdominal pain, and severe diarrhea. Her WBC is elevated and a colonoscopy is performed. What bacterium is most suspect?

A

Clostridium difficile

158
Q

Does C. difficile form spores? What is its shape and gram staining?

A

Yes, it forms spores; it is a gram-positive bacillus

159
Q

What are three lab tests can be used to make a diagnosis of C. difficile?

A

EIA toxin assay, cytotoxicity assay, and PCR

160
Q

What two toxins of Clostridium difficile are detected by PCR?

A

Toxin A and B, the former is an enterotoxin and the latter is a cytotoxin.

161
Q

What characterizes a toxic megacolon? What surgical procedure may be required for it?

A

A massive dilation of the colon and septic shock; it may require a bowel resection

162
Q

What are the standard treatments for C. difficile?

A

Metronidazole and oral vancomycin

163
Q

Why can oral vancomycin treat C. difficile even though it is poorly absorbed by the gut?

A

C. difficile is a GI infection, and oral vancomycin can act locally on the GI tract without being absorbed

164
Q

What could allow for C. difficile to survive a course of antibiotics and reappear during a relapse?

A

Spore formation

165
Q

What mutation has created hypervirulent strains of C. difficile?

A

They have lost the repressor region of a toxin gene

166
Q

What is the average cost of each case of C. difficile-associated disease?

167
Q

Will alcohol-based sanitizers remove C. difficile spores from one’s hands?

168
Q

What problem results from using gram stains to distinguish C. perfringes?

A

It doesn’t always retain the gram stain, so it may not appear positive even though it is gram positive

169
Q

What kind of hemolysis is distinctive for C. perfringens?

A

Double zones, one with complete hemolysis, and one with partial hemolysis

170
Q

What does the India Ink prep reveal about C. perfringens?

A

The capsule

171
Q

What toxin causes the zone of complete hemolysis by C. perfringens? What about the partial hemolysis?

A

Theta toxin: complete hemolysis;

Alpha toxin: partial hemolysis

172
Q

Can C. perfringens cause soft tissue infections? What about bacteremia?

A

Yes to both

173
Q

What is emphysematous cholecystitis? Which Clostridium species can cause it?

A

Infection of the gall bladder; C. perfringens

174
Q

The third leading cause of food poisoning, after Campylobacter and Salmonella, is…?

A

Clostridium perfringens

175
Q

What is the clinical timecourse for C. perfringens GI infection?

A

24-48 hours

176
Q

What are two chief symptoms of C. perfringens infection?

A

Abdominal cramps and watery diarrhea

177
Q

What antibiotic is used to treat C. perfringens enteric infection?

A

Penicillin

178
Q

What toxin does Clostridium tetani release that causes spastic paralysis and this type of lockjaw? What is this lockjaw called?

A

Tetanospasmin; risus sardonicus (sardonic smile)

179
Q

Clostridium**botulinum is associated with what kind of foods?

A

Improperly canned foods

180
Q

What kind of neurologic disorder results from the AB toxin released by C. botulinum?

A

Flaccid paralysis

181
Q

When a gas is present in a CT scan of infected tissues, what class of organisms can be immediately suspected?

A

Anaerobic gram-positive bacilli

182
Q

What forms when commensal flora of the mouth are allowed to enter a normally sterile space? When anaerobic fermentation leads to production of gas, inflating tissues of the neck and compressing the airway, what is this condition called?

A

Abscesses; Ludwig’s angina

183
Q

What organism is suggested by a liver abscess growing an anaerobic Gram-negative bacillus?

A

Bacteroides fragilis

184
Q

What is the shape and gram staining of Bacteroides fragilis? What enzymes allow it to tolerate oxygen?

A

Pleomorphic gram negative rod; Catalase and superoxide dismutase

185
Q

Actinomyces infections can be characterized by what kind of substance that is excreted through the skin?

A

Sulfur granules, which are actual colonies of the organism

186
Q

What is the shape and gram staining of of Actinomyces?

A

Gram positive branching filamentous rod (bacillus)

187
Q

Where are Actinomyces often found throughout the oral cavity?

A

In molar tooth cavities

188
Q

What is the appearance of Nocardia under the gram stain? What stain with a modified pH is used to distinguish it?

A

Beaded filaments (left); acid fast stain (right)

189
Q

Is Nocardia a symptomatic infection in immunocompetent hosts?

190
Q

Which bacterium is this, visualized with an acid fast stain?

191
Q

Which two infectious organisms are both characterized as branching gram positive bacilli? What growth condition can be used to distinguish them? What stain can be used to distinguish them?

A

Actinomyces and Nocardia; Nocardia can grow aerobically, whereas actinomyces cannot; Nocardia can be stained with acid fast, whereas Actinomyces is not

192
Q

What is Nocardia treated with?

A

Trimethoprim-sulfamethoxazole

193
Q

What gram-positive beaded and fast-growing bacillus is identified with surgical wound infections?

A

Mycobacterium fortuitum

194
Q

Does M. fortuitum grow faster or slower than M. tuberculosis?

195
Q

What is the gram staining and shape of M. fortuitum?

A

Gram positive, bacillus

196
Q

How is M. fortuitum infection of a surgical wound treated?

A

Debridement, macrolides and β lactams

197
Q

What gram positive bacillus (preventable with vaccines) can produce an exotoxin that leads to airway constriction and death? What vaccine provides immunity against it?

A

Corynebacterium diphtheriae; DTaP

198
Q

The DTaP vaccine protects against tetanus, pertussis, and what other bacterial infection?

A

Cornyebacterium diphtheriae, causing diphtheria

199
Q

Is diphtheria common in industrialized nations?

A

No, not after widespread vaccination programs

200
Q

How is Corynebacterium diphtheriae treated?

201
Q

What organism can cause fatal gas gangrene?

A

C. perfringes

202
Q

What does “zoonotic” mean with regard to infections?

A

Zoonotic means that the pathogen is primarily transmitted to humans from animals

203
Q

What is the characteristic symptom of diphtheria?

A

A swollen neck

204
Q

What organism, causing petechial rashes and altered mental status, is seen in this slide?

A

N. meningitidis

205
Q

Is N. meningitidis gram-positive or gram-negative? What is its shape?

A

Gram-negative; cocci

206
Q

Why does C. difficile sometimes present in the hospital after prophylactic administration of antibiotics, e.g. cefazolin?

A

The antibiotics kill the normal gut flora, allowing the C. difficile to replicate without competition

207
Q

What commonly eaten food is particularly susceptible to Listeria colonization when stored at improper temperatures?

A

Soft cheeses

208
Q

What is the primary infective route of L. monocytogenes?

A

The intestinal epithelium, via an ingested substance

209
Q

What organism causes spotted fevers (e.g. Rocky Mountain spotted fever) and various types of typhus?

A

Rickettsia species

210
Q

What organism causes human monocytic ehrlichiosis (HME)?

A

Ehrlichia chaffeensis

211
Q

What organism causes anaplasmosis?

A

Anaplasma phagocytophilum

212
Q

What bacterium causes Lyme disease?

A

Borrelia burgdorferi

213
Q

What organism is this, which is shown microscopically and with the characteristic rash from infection?

A

Borrelia burgdorferi

214
Q

What is the typical shape of a rash for Lyme disease?

215
Q

In early and late Lyme disease, what heart condition can manifest?

A

AV block, possibly causing bradycardia

216
Q

What joint conditions present with long-term Lyme disease?

A

Swelling and arthritic-like symptoms

217
Q

What insect is this? What bacterium does this kind of insect spread?

A

Black legged tick; B. burgdorferi

218
Q

Where is Lyme disease most common?

A

Northeastern US and the region around Wisconsin

219
Q

During what time of year is Lyme disease most likely spread from ticks to humans?

220
Q

What animal is the primary host that blacklegged ticks (that carry Lyme disease) feed from?

221
Q

Which stage of life of the blacklegged tick is most likely to spread B. burgdorferi to humans?

A

Nymph, which is after larva and before adult

222
Q

When are most cases of Lyme disease reported throughout the year?

A

In a unimodal distribution centered around July

223
Q

What bacterium is this rash typical of?

A

B. burgdorferi (Lyme disease)

224
Q

What is the medical term for the “bullseye rash” caused by B. burgdorferi?

A

Erythema migrans

225
Q

During which timecourse after infection are Lyme disease symptoms mostly localized to the site of the tick bite?

226
Q

1-4 months after a bite containing B. burgdorferi, what general change in the localization of symptoms occurs?

A

They become more systemic, involving the nervous system, heart, and the rash is disseminated

227
Q

What two nervous system disorders can result 1-4 months after infection with B. burgdorferi?

A

Cranial nerve palsy and lymphocytic meningitis

228
Q

What two signs of cardiac involvement in Lyme disease can occur 1-4 months after the tick bite?

A

Heart block or myocarditis

229
Q

What does this patient have? How long has he had it?

A

Lyme disease (B. burgdorferi); 1-4 months (rash is disseminated)

230
Q

What are chronic symptoms of late Lyme disease? When do they begin?

A

Intermittent arthritis and vague neurological symptoms, like radicular pain, paresthesias, and Lyme encephalopathy; 4 months to years after the bite

231
Q

What is the best way to diagnose Lyme disease? Why?

A

Clinical picture; antibody and PCR lab tests are not yet reliable, and culturing and staining techniques are not able to demonstrate the organism well

232
Q

What kind of lab tests are available for Lyme disease? Are they reliable for diagnosis?

A

IgG and IgM antibody tests and PCR; no, they are not reliable

233
Q

Why is doxycycline not typically given to children under 8?

A

It has the potential to stain the teeth (incorporation into anything that is being calcified)

234
Q

What is the typical course of antibiotics for non-critical manifestations of Lyme disease? What if there is heart block or meningitis?

A

Amoxicillin for non-critical cases; ceftriaxone for hospitalized cases

235
Q

What is this bacterium, found in docs and raccoons and potentially transmitted to humans?

A

Leptospirosis

236
Q

Which organ systems are affected by leptospirosis?

A

Liver, kidney, skin, and brain

237
Q

How does leptospirosis enter the body?

A

Broken skin or mucosa followed by contact with the organism (e.g. from an infected dog or raccoon)

238
Q

How is leptospirosis treated? What does the first phase of symptoms present as? What is the source of infection?

A

Penicillin; flu-like symptoms; animals

239
Q

Are Rickettsia gram positive or gram negative?

A

Gram negative

240
Q

Do Rickettsia species replicate extracellularly or intracellularly?

A

Intracellularly

241
Q

What is the reservoir for Rickettsia?

A

Hard ticks

242
Q

What disease does R. rickettsii cause that has a 23% case fatality rate?

A

Rocky Mountain spotted fever

243
Q

Where is the greatest concentration of the cases of Rocky Mountain spotted fever within the US?

A

The American Southeast

244
Q

What are classic clinical manifestations of Rocky Mountain spotted fever?

A

Fever, headache and rash

245
Q

What tick-borne disease causes this rash?

A

Rocky Mountain Spotted Fever (R. rickettsii)

246
Q

How does Rickettsia induce its own phagocytosis? How does it escape from the phagosome?

A

By triggering actin rearrangement; release of phospholipase

247
Q

What food-borne organism is R. rickettsii similar to in terms of how the cells propel themselves and spread to adjacent cells?

A

L. monocytogenes

248
Q

Is humoral immunity, cell-based immunity, or both required to clear R. rickettsii? Why?

A

Cell-based; the organism is mostly confined intracellularly so antibodies cannot bind it directly

249
Q

What is the shape and gram staining of Ehrlichia and Anaplasma? Do they grow inside or outside of host cells?

A

Both are tiny round gram negative bacteria; they grow intracellularly

250
Q

Do Ehrlichia break out of the phagosome after phagocytosis?

A

No, they tend to stay within the phagosome

251
Q

Which kind of immune cell is targeted by Ehrlichia chafeensis? Which is targeted by Anaplasma phagocytophillum?

A
  • E. chafeensis*: monocytes;
  • A. phagocytophillum*: granulocytes
252
Q

What kind of insect carries E. chafeensis and A. phagocytophilum?

253
Q

Which other tick-borne disease is carried by the same species of tick that is the reservoir for Lyme disease?

A

Anaplasma phagocytophilum

254
Q

Do rickettsia, ehrlichiosis and anaplasmosis patients present reliably with knowledge of a tick bite?

A

No, they do not recall one in 40% of cases

255
Q

Of rickettsia, ehrlichiosis, and anaplasmosis, which is least likely to produce a rash? Which is most likely?

A

Least likely, anaplasmosis; Most likely, rickettsia

256
Q

What are the symptoms common to rickettsia, ehrlichiosis, and anaplasmosis?

A

Fever, headaches, myalgia, and malaise

257
Q

What is the incubation period for rickettsia, ehrlichiosis, and anaplasmosis?

258
Q

What is the treatment for rickettsia, ehrlichiosis, and anaplasmosis? Should confirmation from the lab be obtained before starting treatment?

A

Doxycycline; no

259
Q

What type of lab test can identify rickettsia, ehrlichiosis, and anaplasmosis before the infection runs its course?

A

PCR (on either infected tissue or blood)

260
Q

Following a tick bite, should you cover it with petroleum jelly to make it detach itself?

A

No, you should use tweezers to remove it as soon as possible

261
Q

What bacterium causes “cat-scratch disease”?

A

Bartonella henselae

262
Q

What is the manifestation of cat-scratch disease in a immunocompetent host? What about in an immunocompromised person?

A

Lymphadenopathy in an immunocompetent person; bacillary angiomatosis (rashes) in immunocompromised

263
Q

What is the etiology for this kind of rash following a cat scratch? Is it more likely in immunocompetent or immunocompromised patients?

A


B. henselae infection has caused small tumors in the endothelium of small vessels; immunocompromised patients

264
Q

What is visualized in a biopsy of a B. henselae related lymphadenopathy?

A

Granulomas and possibly the organism

265
Q

What is the shape and gram staining of B. henselae?

A

Gram negative bacilli

266
Q

Is B. henselae associated with older or younger cats?

A

Usually younger cats

267
Q

What organism causes Q Fever?

A

Coxiella burnetii

268
Q

What is the reservoir for C. burnetii?

A

Cattle, sheep, and goats

269
Q

How is C. burnetii transmitted from cattle, sheep, or goats to humans? What cell type is infected?

A

Via inhalation; macrophages

270
Q

Can you culture C. burnetii?

A

No, it is a biohazard

271
Q

How can brucellosis be contracted?

A

Ingestion of dairy products or contaminated hands, or skin abrasion and contact with infected animals

272
Q

What common symptom characterizes exposure to C. burnetii and brucellosis? What is the typical source of these pathogens?

A

Mysterious fevers and myalgia; farm animals like cattle, goats, and sheep

273
Q

What is the best way to diagnostically confirm most tick-borne diseases? Is it practical to do this before starting treatment?

A

Serology; no, because serology takes two weeks and some tick-borne diseases are rapidly fatal

274
Q

What condition are these symptoms immediately indicative of?

A

Scarlet fever

275
Q

How is scarlet fever usually treated? What is the most serious side effect?

A

Penicillin; allergic reaction

276
Q

A patient that is treated for scarlet fever now presents with this rash. What is most likely to have occurred?

A

Allergic reaction to penicillin

277
Q

Which antibiotic has a characteristic adverse effect of bile sludging?

A

Ceftriaxone

278
Q

Which antibiotic has the characteristic adverse effect of ototoxicity?

A

Aminoglycosides

279
Q

Which antibiotics have the characteristic adverse effect of QTc prolongation?

A

Azithromycin, fluoroquinolones

280
Q

Which antibiotic has the characteristic side effect of tendonitis?

A

Fluoroquinolones

281
Q

A 2 yo boy presents with 2 days of refusal to walk and fever of 39.5°C. What is the most likely infectious organism? Is this a serious infection? What antibiotic should be used?

A

S. aureus (most important cause of septic arthritis);
yes;

vancomycin (not nafcillin or ceftriaxone, in case it is MRSA)

282
Q

Which is the only cephalosporin activate against MRSA?

A

Ceftaroline, a 5th generation cephalosporin

283
Q

What outpatient (oral) antibiotics are often active against MRSA?

A

Clindamycin, doxycycline, and trimethoprim-sulfamethoxazole

284
Q

What treatment for MRSA can cause myositis or creatinine phosphokinase elevation?

A

Daptomycin

285
Q

Which treatment for MRSA has 100% bioavailability? What is its drawback?

A

Linezolid; besides side effects like bone marrow suppression or serotonin syndrome, it is costly

286
Q

Which treatment for MRSA can cause Red Man syndrome?

A

Vancomycin

287
Q

When a serious S. aureus infection, should a clinician wait until its susceptibility to methicillin is determined before treating?

A

No, assume it is MRSA and treat accordingly (vancomycin, daptomycin, linezolid, ceftaroline)

288
Q

An infant presents with fever, lethargy, with no immunizations and a stiff neck. WBC count is elevated and mostly neutrofils, with WBCs present in CSF. What is this infection called? What is the initial treatment until the organism is isolated?

A

Meningitis; vancomycin and ceftriaxone

289
Q

From 1 month old throughout adulthood, what are the top three suspects for bacterial meningitis? What is the empirical treatment?

A

Neisseria meningitidis, S. pneumoniae, and H. influenzae type B; ceftriaxone and vancomycin

290
Q

What additional cause of meningitis must be suspected in an immunocompromised patient? What antibiotic should be added to the regimen to combat it?

A

Listeria; ampicillin

291
Q

Until the age of 1 month, what are the typical suspects for a bacterial meningitis?

A

Group B streptococcus, E. coli, and Listeria

292
Q

Which generation of cephalosporins is needed to treat the CNS?

A

Third generation: ceftriaxone, cefotaxime, ceftazidime

293
Q

Which β-lactams can be used against pseudomonas?

A

Cefepime (4th generation cephalosporin), piperacillin-tazobactam (no CNS penetration), carbapenems such as imipenem, azteronam, ceftazidime (3rd generation cephalosporin)

294
Q

Can Pseudomonas be treated with fluroquinolones?

295
Q

What fluoroquinolone is effective against gram negatives and gram positives, including anaerobes?

A

Moxifloxacin

296
Q

What is the empiric treatment for a enterococci infection in a patient with neutropenia due to AML? What drug will be used instead if susceptibility is discovered?

A

Vancomycin, or if resistance is suspected, linezolid and daptomycin; ampicillin

297
Q

What drugs can be used to treat a C. difficile colitis?

A

Metronidazole and secondarily oral vancomycin

298
Q

Are intra-abdominal abscesses going to contain one species, or multiple species? What is the typical pair of antibiotics used?

A

Multiple; cephalosporin + metronidazole

299
Q

What is the difference in treatment between typical (community-acquired, lobar) pneumonia and atypical pnemonia?

A

Typical pneumonia, if treated as an inpatient, uses ceftriaxone and potentially vancomycin if S. aureus is suspected; they are treated similarly as outpatients (azithromycin and levofloxacin)

300
Q

How many cases of sepsis are diagnosed per year? How many of them result in death?

A

750,000; 31%

301
Q

What is the mainstay of treatment for a patient with severe inflammatory response syndrome?

A

Fluids (normal saline bolus)

302
Q

Why is oxygen provided to a patient undergoing sepsis?

A

Oxygen delivery is impaired, e.g., by lack of functional surface area of the alveoli

303
Q

Out of all the bacterial vaccines that are administered in the US, which has been the least successful in terms of % reduction?

A

Pertussis (82% reduction)

304
Q

What federal body sets policy on vaccines?

A

CDC Advisory Committee on Immunization Practices

305
Q

Can children under the age of 2 develop memory immunity in response to a polysaccharide antigen?

306
Q

What is the minimum human lethal dose of tetanospasmin? What bacterium produces it?

A

2.5 ng/kg; Clostridium tetani

307
Q

What is the difference between an adjuvant and a conjugate vaccine?

A

A conjugate is the attachment of a protein antigen to create a T dependent response to a normally T independent antigen like a carbohydrate, creating longer-term immune system memory, whereas an adjuvant simply stimulates a nonspecific immune response concurrent with the vaccine antigen exposure

308
Q

What is the most common route of vaccine administration?

A

Intramuscular (deltoid or anterolateral thigh)

309
Q

What two types of immune response are elicited by a mucosal administration of a vaccine?

A

Systemic and mucosal (IgA) response

310
Q

What are two methods of mucosal administration of a vaccine?

A

Oral or intranasal

311
Q

Are vaccines for the plague and Lyme disease commonly administered today? What about anthrax and tularemia?

A

No, plague and Lyme disease vaccines are discontinued; anthrax and tularemia vaccines are only given to military personnel

312
Q

What can be done over time to increase the magnitude and duration of antibody response to a vaccine?

A

Booster doses

313
Q

The top four presenting bacterial STD’s are […], chlamydia, gonorrhea, and chancroid.

A

The top four presenting bacterial STD’s are syphilis, chlamydia, gonorrhea, and chancroid.

314
Q

The top four presenting bacterial STD’s are syphilis, […], gonorrhea, and chancroid.

A

The top four presenting bacterial STD’s are syphilis, chlamydia, gonorrhea, and chancroid.

315
Q

The top four presenting bacterial STD’s are syphilis, chlamydia, […], and chancroid.

A

The top four presenting bacterial STD’s are syphilis, chlamydia, gonorrhea, and chancroid.

316
Q

The top four presenting bacterial STD’s are syphilis, chlamydia, gonorrhea, and […].

A

The top four presenting bacterial STD’s are syphilis, chlamydia, gonorrhea, and chancroid.

317
Q

Which STDs increase the risk for HIV transmission and why?

A

STDs that create ulcerative lesions (e.g. syphilis, herpes and chancroid) increase the risk of HIV transmission because of greater exposure between partners of blood-accessible fluids

318
Q

What bacterium causes syphilis?

A

Treponema pallidum

319
Q

High risk groups for syphilis are: men who have sex with men, drug users, and […]

A

High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.

320
Q

High risk groups for syphilis are: […], drug users, and those with multiple sexual partners.

A

High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.

321
Q

High risk groups for syphilis are: men who have sex with men, […], and those with multiple sexual partners.

A

High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.

322
Q

What coats the spirochetes of T. pallidum and protects against phagocytosis?

A

Host cell fibronectin

323
Q

Is syphilis a localized or systemic disease? Are most of the symptoms related to toxins released by T. pallidum or the immune response?

A

Secondary syphilis is systemic, because the spirochete disseminates into the bloodstream; the immune response creates most symptoms

324
Q

What is the prototypical lesion of syphilis? What does it look like?

A

The chancre; painless, smooth ulcer with firm borders and clean base.

325
Q

Why might a patient with syphilis not recognize that they have the chancre (lesion) signalling infection?

A

It is painless, heals on its own in 3-6 weeks, and may be in an internal or hard to see (perianal, intravaginal) area.

326
Q

What STD is this lesion prototypical of? What organism causes it? How long does it take for this lesion to heal on its own?

A

Syphilis; T. pallidum; 3-6 weeks

327
Q

What kind of a lesion is this? What organism is suspect?

A

Chancre; T. pallidum (causing syphilis)

328
Q

What is the shape of T. pallidum?

A

Spirochete

329
Q

What are differential diagnoses (related diagnoses that must be ruled out) for a primary chancre that looks like syphilis (T. pallidum)?

A

Chancroid (H. ducreyi), lymphogranuloma venereum, herpes, and trauma

330
Q

During secondary syphilis, what clinical manifestations can occur?

A

Many possible symptoms: rash, fever, malaise, weight loss, diffuse painless lymphadenopathy, pharyngitis, arthralgia, uveitis…

331
Q

Which STD infection has a secondary stage that this rash a classical sign for?

A

Syphilis: palm and sole rash

332
Q

Does the rash of secondary syphilis only occur on the palms and soles?

A

No, it can also appear on the trunk and elsewhere on the skin

333
Q

If a patient is asymptomatic for syphilis but as immunoreactivitity to anti-treponemal antibodies, should an LP be taken check for CNS involvement?

A

This is controversial, so usually it is not done unless the immunoreactivity is very high

334
Q

What are common symptoms of late syphilis?

A

Aortitis, CNS complications, and gumma formation

335
Q

Can T. pallidum be grown on culture? How is it typically visualized?

A

No; it can be visualized on darkfield microscopy from scrapings of chancres, mucus, or condylomata lata

336
Q

Is there a treponemal antibody test?

337
Q

What is the primary treatment for syphilis? Is there any substitute for this drug in the late stages of the disease?

A

Penicillin; no

338
Q

Syndromes of Chlamydia trachomatis that present clinically are: […] infection, infant pneumonia, conjunctivititis, and ocular trachoma.

A

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.

339
Q

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant […], conjunctivititis, and ocular trachoma.

A

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.

340
Q

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, […], and ocular trachoma.

A

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.

341
Q

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular […].

A

Syndromes of Chlamydia trachomatis that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.

342
Q

What is the most common bacterial STD in the US?

A

C. trachomatis

343
Q

What is the most common cause of urethritis and epididymitis in US men, and the most common cause of urethritis, cervicitis, and acute salpingitis in US women?

A

C. trachomatis

344
Q

Does immunity to C. trachomatis confer long term protection against re-infection?

345
Q

How can C. trachomatis be spread? Can it be spread to a birthed infant?

A

Via abrasion of the skin; yes, via direct inoculation into the eyes and respiratory tract

346
Q

What are genital syndromes caused by C. trachomatis?

A

Cervicitis, urethritis, epididymitis, salpingitis, infertility or ectopic pregnancy

347
Q

Can Chlamydia cause infertility?

A

There is a strong relationship, and the pathogenesis is likely via chronic bilateral scarring of the fallopian tubes

348
Q

What is the shape and gram staining of Neisseria gonorrhea?

A

Bean shaped gram-negative diplococci

349
Q

Is N. gonorrhea more likely to spread male to female or the other way around?

A

Male to female but both are possible

350
Q

Is N. gonorrhea more or less likely to be transmitted per episode of sex than HIV?

A

More likely

351
Q

When is infection by N. gonorrhea most common?

A

Adolescents and young adults

352
Q

Besides the genitourinary tract, where else can N. gonorrhea infections manifest?

A

Anorectal canal, pharynx, and around the liver

353
Q

Does pharyngitis caused by N. gonorrhea usually present with symptoms? If so, what are they?

A

No, it is usually asymptomatic

354
Q

What causes pelvic inflammatory disease?

A

Usually, a bacterial super-infection secondary to N. gonorrhea infection

355
Q

What is Fitz Hugh Curtis syndrome?

A

Perihepatitis caused by N. gonorrhea by direct extension of the organism from the fallopian tubes to the liver capsule

356
Q

What kind of agar is used to culture N. gonorrhea?

A

Chocolate agar with antibiotics (Thayer Martin agar)

357
Q

What is the typical first-line treatment for N. gonorrhea?

A

Ceftriaxone, 125mg intramuscular once

358
Q

What is the second line agent of treatment for N. gonorrhea?

A

Azithromycin

359
Q

What organism causes Chancroid? Is it more common in the developing world or the US?

A

H. ducreyi; in the developing world