Micro Midterm 2 Flashcards
(359 cards)
1
Q
How is a diagnosis for M. pneumoniae made?
A
Usually clinically
2
Q
Can penicillins and cephalosporins be used to treat M. pneumoniae?
A
No, because it has no cell wall
3
Q
Which antibiotics are used to treat M. pneumoniae?
A
Macrolides and tetracyclines
4
Q
In an older patient, is Chlamydophila pneumonia more likely to produce a lower or an upper respiratory tract infection?
A
Lower
5
Q
How many adults in the U.S. get Chlamydophila pneumoniae per year?
A
~100k
6
Q
How is C. pneumoniae transmitted?
A
Respiratory droplets
7
Q
Does C. pneumoniae have a cell wall? Does it replicate extracellularly or intracellularly?
A
Intracellularly
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
9
Q
What is the intracellular form of C. pneumoniae called?
A
Reticulate body
10
Q
What genus of bacteria does this diagram illustrate? It is the second-smallest family of prokaryotes known, after Mycoplasma.
A
Chlamydia
11
Q
Label the following life cycle states for C. pneumoniae.
A
Top: elementary body, bottom: reticulate bodies
12
Q
Why does C. pneumoniae evade host defenses so well?
A
Replicating intracellularly, it can evade host detection
13
Q
Is there a higher risk of C. pneumoniae in immunocompromised patients as compared to immunocompetent patients?
A
It is unclear
14
Q
What is the annoying symptom of C. pneumoniae that persists for weeks?
A
A cough that does not subside
15
Q
Does C. pneumoniae typically cause a fever?
A
No
16
Q
Which age group is most likely to get an asymptomatic C. pneumoniae infection?
A
Children
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
18
Q
Do most cases of C. pneumoniae result in a diagnosis?
A
No
19
Q
Which antibodies can be detected after C. pneumoniae infection that can diagnose its presence?
A
IgM and IgG antibodies
20
Q
What is the third-most common cause of atypical pneumonia?
A
Legionella pneumophila
21
Q
Is Legionella spread from person to person?
A
No
22
Q
Where does L. pneumophila prefer to live?
A
Aqueous habitats, both fresh and saltwater
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
24
Q
What is the incubation period of L. pneumophila?
A
2-10 days
25
Why is *L. pneumophila* an underreported disease?
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
26
What is the shape, size, and gram staining of *L. pneumophila*?
Small, gram-negative bacilli
27
Is *L. pneumophila* an anaerobe or an aerobe?
Obligate aerobe
28
Which serogroup of *L. pneumophila* causes 75%-90% of human infections?
Group 1
29
Does *Legionella pneumophila* grow on typical bacterial culturing media?
No, it requires special media
30
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?
*Legionella*; no, this is atypical media
31
What phagocytoses *L. pneumophila* when they reach the lungs?
Alveolar macrophages
32
Can *L. pneumophila* be deadly? Is there a neutrophil response, or a humoral response, or both? What dying cells trigger a severe inflammatory response?
Yes; both responses occur; dying macrophages
33
Of the top three atypical pneumonias, which is the most dangerous?
*Legionella pneumophila*
34
How can *L. pneumophila* be diagnosed by lab tests?
Culture of respiratory secretions on selective media, and detection of antigen of serogroup 1 (e.g. via direct fluorescence with antibodies)
35
What are the mainstays of treatment for *L. pneumophila*?
Macrolides (azythromycin), tetracyclines, and quinolones
36
Does *L. pneumophila* replicate intracellularly or extracellularly? How does this affect choice of treatment?
Intracellularly; antibiotics that reach an effective intracellular concentration must be used
37
Do clarithromycin and azythromycin require the bacterium to have a cell wall?
No, they block protein synthesis (they are both macrolides)
38
What are the three most frequent toxic effects of macrolides?
Diarrhea, nausea, abdominal pain
39
What is the common suffix for fluroquinolone antibiotics? Do they inhibit DNA, RNA, protein, or cell wall synthesis?
-floxacin; inhibit DNA synthesis (topoisomerase and gyrase inhibition)
40
Can treatment for atypical pneumonia be administered orally?
Yes
41
How might liver function or kidney function affect choice of a fluoroquinolone?
Levofloxacin and ciprofloxacin are eliminated by the kidneys, while moxifloxacin is eliminated by the liver in bile
42
What is the most common clinical symptom for a GI infection?
Diarrhea
43
Do most infections of the GI tract causing diarrhea require hospitalization?
No
44
What are the big four bacterial pathogens for foodborne diarrheal disease?
Vibrio, campylobacter, shigella, salmonella
45
What strain of *E. coli* is particularly significant for diarrheal disease?
*E. coli* O157
46
What is the only gram-positive bacterium that causes common diarrheal disease?
*Listeria*
47
What are the top two identified bacterial pathogens causing GI disease hospitalization in New York?
*Campylobacter* and *Salmonella*
48
What are the three mechanisms for enteric infection?
Inflammatory (invasion w/ cytotoxin), noninflammatory (adherence w/ cytotoxin), and penetrating
49
Which bacterial pathogen has the smallest infectious dose? What about the second smallest?
*Shigella* (100); *Campylobacter* (1000)
50
What is the order of magnitude difference between an infectious dose of *Salmonella* as opposed to *Campylobacter*?
103 greater for *Salmonella* (106 cells typical infectious dose)
51
What is a typical infectious dose for *E. coli* or *Vibrio cholerae*?
108 cells
52
What dangerous symptom does cholera cause via an exotoxin?
Dehydration by diarrhea and vomiting of clear fluid
53
What bacterium causes cholera and has "cholera" in the species name?
*Vibrio cholerae*
54
When was the last epidemic of cholera in the US?
1911
55
What is the shape of *V. cholerae*? What is its gram staining? Does it have spores?
Curved to straight bacilli; gram negative; no spores
56
Which serotypes of *V. cholerae* cause cholera?
O1 and O139
57
What is the natural environmental habitat of cholera?
Aquatic environments
58
What are the non-life-threatening clinical symptoms of cholera, besides diarrhea and vomiting?
Muscle cramps, loss of skin turgor
59
How does death occur for a cholera patient?
Hypovolemic shock, metabolic acidosis, and uremia from tubular necrosis
60
What is the chemical activity of cholera toxin? What receptor does it act upon? What intracellular signaller is upregulated, causing loss of cell nutrients?
It is an A-B type ADP-ribosylating toxin; Ganglioside receptor; cAMP
61
Are antibiotics needed to treat *V. cholerae*?
No, just rehydration
62
What is this bacterium that causes bloody diarrhea?
*Shigella*
63
Is *Shigella* lactose-fermenting?
No
64
Besides bloody diarrhea, what are two other clinical hallmarks of bacillary dystentery?
Abdominal cramps and pain, and tenesmus (painful straining to pass stool)
65
What does tenesmus mean?
Painful straining to pass stool
66
What is the reservoir of infectious *Shigella*?
Humans, it is transmitted person-to-person
67
What is the pathogenetic mechanism of *Shigella* infection?
It invades enterocytes and causes cell death
68
What mechanism of bacillary enteric disease is seen here?
Inflammatory + invasive, as in *Shigella* infection
69
What does subunit A of the Shiga toxin do? What about subunit B?
It permanently inactivates ribosomes; it binds to host receptors
70
Do organisms beside *Shigella* produce shiga-like toxins?
Yes, some strains of *E. coli*
71
Is bacteremia a common complication of *Shigella*?
No
72
What are the two species of *Salmonella* that cause enteric disease?
*Salmonella enterica* and *Salmonella bongori*
73
What is the shape and gram staining of *Salmonella*? Are they aerobic? Are they motile? Do they form spores?
Gram-negative rods; anaerobic; motile; non-spore-forming
74
Do *Salmonella* species produce hydrogen sulfide during fermentation?
Yes
75
Can *Salmonella* cause bacteremia? What complication typified by rose spots and delirium can result from salmonella infection?
Yes; typhoid fever
76
Are there asymptomatic carriers of *Salmonella*?
Yes, including some that had to be forcibly quarantined
77
How long does it take for symptoms of *Salmonella* to present after infection?
48h
78
What is the shape of *Salmonella* incidence in the US from year to year?
Spikey because of sporadic outbreaks
79
What are three common sources of *Salmonella* infection besides person-to-person contact?
Agricultural products, processed food, and domestic animals
80
What two cell types are invaded by *Salmonella* during initial stages of infection?
M cells and intestinal macrophages
81
How does *Salmonella* interact with microvilli on certain enterocytes to facilitate endocytosis? Can it invade non-phagocytic cells?
It attracts them, surrounding itself with the cell's membrane; yes, it can invade many kinds of enterocytes
82
What areas of the *Salmonella* genome contribute most to its virulence?
Two pathogenicity islands called SPI1 and SPI2
83
How does *Salmonella* survive inside the cell after phagocytosis?
It secretes toxins that prevent fusion of lysosomes with the endosome and then replicates in the endosome
84
How does *Salmonella* release its anti-lysosomal fusion toxins into the cytoplasm despite being trapped in an endosome after endocytosis?
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
85
What is this spirally bacterium that causes enteric symptoms, mainly through the handling of chicken?
*Campylobacter*
86
What is the shape and gram staining of *Campylobacter*?
Helical, gram-negative
87
What is Guillain-Barré syndrome? What is the most common antecedent infection?
An autoimmune disorder that causes peripheral paralysis after foreign antigens cause mistargeting of the immune response toward nerve tissues; *Campylobacter*
88
What pathogen is this, causing gastric and duodenal ulcers?
*H. pylori*
89
The stomach can normally handle acidity with its mucosal lining, but what happens during *H. pylori* infection that causes ulceration?
The bacterium invades intercellularly, using secreting toxins to disrupt cell-to-cell junctions
90
Are most infections for *H. pylori* symptomatic?
No
91
What is the most common cause for gastritis, gastric ulcer, and duodenal ulcer?
*H. pylori* infection
92
What upper gastric infection that commonly causes gastritis or ulceration is linked to gastric adenocarcinoma?
*H. pylori*
93
Can non-selective stool cultures diagnose *H. pylori*?
No, it is an upper GI infection and it is hard to isolate on non-selective media
94
What needs to be added to culture to get proper growth of *H. pylori* from a stool sample?
Bile salts
95
What tests can distinguish between *Salmonella* and other enterobacteriaceae?
Citrate and ornithine decarboxylase
96
What three antibiotic resistances are common with the top four bacterial causes of GI infection?
Amoxicillin (or penicillins), 1st generation cephalosporins, and trimethoprim-sulfamethoxazole
97
Since GI bacterial infections are resistant to many antibiotics, which ones are actually used for treatment?
Fluroquinolones (-floxacins), 3rd generation cephalosporins (ceftriaxone), and macrolides (azithromycin)
98
Does daptomycin have gram-negative activity? Why or why not?
No; it cannot penetrate the outer membrane sufficiently to cause depolarization
99
What are the most common manifestations of *Klebsiella* infection?
Pneumonia, UTI, and nosocomial infections
100
How can *E. coli* be distinguished from *K. pneumoniae* in the lab, e.g. after a urine sample for a UTI manifestion?
*E. coli* is indole positive, *K. pneumoniae* is negative
101
What is the main reservoir of *K. pneumoniae*?
The lower GI tract of humans, and secondarily the skin and female genital tract
102
What media is used here to demonstrate *K. pneumoniae* and *E. coli* by the fermentation of lactose?
MacConkey agar, which gives pink colonies
103
Is *K. pneumoniae* motile or non-motile? Is it encapsulated?
Non-motile; encapsulated
104
What common cause of UTIs and pneumonia is seen in this slide?
*K. pneumoniae*
105
What test is being performed here to judge the virulence of a *K. pneumoniae* strain?
The string test, which sees if the isolate is hypermucoviscous (and therefore more resistant to complement-mediated killing)
106
What kind of intra-abdominal infections are caused by *K. pneumoniae*?
Liver abscesses, peritonitis, and cholangitis
107
What is the variant of pneumonia caused by *K. pneumoniae* called? What is the characteristic type of sputum produced?
Friedländer's disease; "currant jelly"
108
Is *K. pneumoniae* a common infection for immunocompetent hosts?
No
109
What is the mortality of a *K. pneumoniae* infection?
Up to 50%
110
Why does the sputum produced in a *K. pneumoniae* infection look like currant jelly?
The infection is hemorrhagic and necrotizing
111
What feature of this CXR is consistent with the typical qualities of *K. pneumoniae* infection?
Propensity for upper lobes
112
After *E. coli* or *Streptococcus*, what is the next most common bacterium causing acute inflammation of the peritoneum (peritonitis)?
*K. pneumoniae*
113
After *E. coli*, what is the next most common organism isolated in UTIs?
*K. pneumoniae*
114
Features that distinguish complicated UTIs from uncomplicated UTIs include renal [...], emphysematous pyelonephritis, and catheter-associated UTIs.
Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.
115
Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous [...], and catheter-associated UTIs.
Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.
116
Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and [...]-associated UTIs.
Features that distinguish complicated UTIs from uncomplicated UTIs include renal abscesses, emphysematous pyelonephritis, and catheter-associated UTIs.
117
Can *K. pneumoniae* cause skin and skin structure infections?
Yes
118
What antibiotic are *K. pneumoniae* almost universally resistant to due to a chromosomal gene encoding an enzyme breaking down the antibiotic?
Ampicillin (and other penicillins)
119
Which penicillins are effective against *Pseudomonas* and *Klebsiella*? What are they often combined with?
Anti-pseudomonal penicillins which include piperacillin, ticarcillin, and carbenicillin; a β-lactamase inhibitor
120
Which generation(s) of cephalosporins would be used against *K. pneumoniae*?
3rd or 4th generations, usually cefepime (4th generation)
121
Does cefepime have activity against gram negatives, gram positives, or both?
Both
122
How many β lactamases are there?
Thousands
123
Are ESBL and KPC chromsomal inducible or plasmid-mediated β-lactamases?
Plasmid-mediated
124
Which β-lactams are reserved for the most sick patients, particularly those with infections from ESBL-containing bacteria?
Carbapenems
125
What kind of drug is imipenem-cilastatin?
A carbapenem (β-lactam antibiotic)
126
Which class of β-lactams is shown here?
Carbapenems
127
What is distinctive about this β-lactam structure? What class is it?
It lacks a ring; it is a monobactam
128
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?
Azteronam; Gram negatives only; Aerobes only
129
Can monobactams be hydrolyzed by ESBL?
Yes
130
What is ESBL? When was it first spotted?
It is "extended spectrum β-lactamase", which confers resistance against all β-lactams except carbapenems; in the 1980's
131
If a *K. pneumoniae* strain is resistant to ceftriaxone but susceptible to imipenem, what kind of β-lactamase does it most likely have?
ESBL
132
When were variants of *K. pneumoniae* resistant to carbapenems first discovered? What plasmid-mediated β-lactamase do they typically have?
1990's; KPC (*K. pneumoniae* carbapenemase)
133
Are there other known methods of *K. pneumoniae* resistance to carbapenems besides KPC?
Yes
134
What fraction of hospital-detected *K. pneumoniae* in New York State is carbapenem-resistant?
21%, significantly higher than the rest of the US
135
Which three other countries are considered endemic or epidemic for carbapenem-resistant *K. pneumoniae*?
Israel, China, and Greece
136
What treatment options remain for somebody with carbapenem-resistant *K. pneumoniae*?
Polymyxin, tygacil, and gentamicin
137
What is the mechanism of polymyxins? Are they effective against gram-negatives, gram-positives, or both?
They are cationic agents that bind to the outer membrane disrupting its integrity; only gram-negatives
138
What tissues cannot be penetrated by polymyxins?
Lungs and CSF (cannot cross BBB)
139
What two toxicities are significant with polymyxins?
Nephrotoxicity and neurotoxicity
140
What is the mechanism of tigecycline? What class of bacteria is it indicated for treating?
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
141
What drug class can be attempted to treat a gram-negative infection in a patient with a severe β-lactam allergy?
Monobactams e.g. aztreonam
142
What structural component of *K. pneumoniae* is the most important virulence factor?
Polysaccharide capsule
143
Is imipenem a cure-all for multidrug-resistant gram-negative infections?
No, carbapenem resistance is on the rise (especially in New York State)
144
Which species of anaerobic gram positive bacilli is most commonly seen in the hospital?
*Clostridium difficile*
145
What organism is most often linked with antibiotic-associated diarrhea?
*Clostridium difficile*
146
Which *Clostridium* causes spastic paralysis? Which causes flaccid paralysis?
* C. tetani*: spastic;
* C. botulinum*: flaccid
147
Are there many anaerobic bacteria that are normal human commensals?
Yes
148
When mixed with aerobic organisms, what do anaerobes tend to form?
Abscesses
149
Do anaerobes produce gas when they metabolize food?
Yes
150
What is crepitus?
When you push on necrotic tissue and you feel bubbles created by an infectious disease
151
What antibiotic can be used against most anaerobic infections?
Penicillin, or penicillin with a β-lactamase inhibitor
152
Besides penicillins, what four other antibiotics are used to treat anaerobic bacterial infections?
2nd generation cephalosporins, carbapenems, metronidazole, and clindamycin
153
What is the suffix for carbapenem drugs?
#NAME?
154
What is the mechanism of action of metronidazole?
DNA damage
155
What dietary modifications are necessary when taking metronidazole?
No alcohol
156
What is the mechanism of clindamycin?
It inhibits the translocation step of bacterial peptide synthesis
157
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?
![]()
*Clostridium difficile*
158
Does *C. difficile* form spores? What is its shape and gram staining?
Yes, it forms spores; it is a gram-positive bacillus
159
What are three lab tests can be used to make a diagnosis of *C. difficile*?
EIA toxin assay, cytotoxicity assay, and PCR
160
What two toxins of *Clostridium difficile* are detected by PCR?
Toxin A and B, the former is an enterotoxin and the latter is a cytotoxin.
161
What characterizes a toxic megacolon? What surgical procedure may be required for it?
A massive dilation of the colon and septic shock; it may require a bowel resection
162
What are the standard treatments for *C. difficile*?
Metronidazole and oral vancomycin
163
Why can oral vancomycin treat *C. difficile* even though it is poorly absorbed by the gut?
*C. difficile* is a GI infection, and oral vancomycin can act locally on the GI tract without being absorbed
164
What could allow for *C. difficile* to survive a course of antibiotics and reappear during a relapse?
Spore formation
165
What mutation has created hypervirulent strains of *C. difficile*?
They have lost the repressor region of a toxin gene
166
What is the average cost of each case of *C. difficile*-associated disease?
\>$3.6k
167
Will alcohol-based sanitizers remove *C. difficile* spores from one's hands?
No
168
What problem results from using gram stains to distinguish *C. perfringes*?
It doesn't always retain the gram stain, so it may not appear positive even though it is gram positive
169
What kind of hemolysis is distinctive for *C. perfringens*?
Double zones, one with complete hemolysis, and one with partial hemolysis
170
What does the India Ink prep reveal about *C. perfringens*?
The capsule
171
What toxin causes the zone of complete hemolysis by *C. perfringens*? What about the partial hemolysis?
Theta toxin: complete hemolysis;
Alpha toxin: partial hemolysis
172
Can *C. perfringens* cause soft tissue infections? What about bacteremia?
Yes to both
173
What is emphysematous cholecystitis? Which *Clostridium* species can cause it?
Infection of the gall bladder; *C. perfringens*
174
The third leading cause of food poisoning, after *Campylobacter* and *Salmonella*, is...?
*Clostridium perfringens*
175
What is the clinical timecourse for *C. perfringens* GI infection?
24-48 hours
176
What are two chief symptoms of *C. perfringens* infection?
Abdominal cramps and watery diarrhea
177
What antibiotic is used to treat *C. perfringens* enteric infection?
Penicillin
178
What toxin does *Clostridium tetani* release that causes spastic paralysis and this type of lockjaw? What is this lockjaw called?
Tetanospasmin; risus sardonicus (sardonic smile)
179
*Clostridium**botulinum* is associated with what kind of foods?
Improperly canned foods
180
What kind of neurologic disorder results from the AB toxin released by *C. botulinum*?
Flaccid paralysis
181
When a gas is present in a CT scan of infected tissues, what class of organisms can be immediately suspected?
Anaerobic gram-positive bacilli
182
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?
Abscesses; Ludwig's angina
183
What organism is suggested by a liver abscess growing an anaerobic Gram-negative bacillus?
*Bacteroides fragilis*
184
What is the shape and gram staining of *Bacteroides fragilis*? What enzymes allow it to tolerate oxygen?
Pleomorphic gram negative rod; Catalase and superoxide dismutase
185
*Actinomyces* infections can be characterized by what kind of substance that is excreted through the skin?
Sulfur granules, which are actual colonies of the organism
186
What is the shape and gram staining of of *Actinomyces*?
Gram positive branching filamentous rod (bacillus)
187
Where are *Actinomyces* often found throughout the oral cavity?
In molar tooth cavities
188
What is the appearance of *Nocardia* under the gram stain? What stain with a modified pH is used to distinguish it?
Beaded filaments (left); acid fast stain (right)
189
Is *Nocardia* a symptomatic infection in immunocompetent hosts?
No
190
Which bacterium is this, visualized with an acid fast stain?
*Nocardia*
191
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?
*Actinomyces* and *Nocardia*; *Nocardia* can grow aerobically, whereas actinomyces cannot; *Nocardia* can be stained with acid fast, whereas *Actinomyces* is not
192
What is *Nocardia* treated with?
Trimethoprim-sulfamethoxazole
193
What gram-positive beaded and fast-growing bacillus is identified with surgical wound infections?
*Mycobacterium fortuitum*
194
Does *M. fortuitum* grow faster or slower than *M. tuberculosis*?
Faster
195
What is the gram staining and shape of *M. fortuitum*?
Gram positive, bacillus
196
How is *M. fortuitum* infection of a surgical wound treated?
Debridement, macrolides and β lactams
197
What gram positive bacillus (preventable with vaccines) can produce an exotoxin that leads to airway constriction and death? What vaccine provides immunity against it?
*Corynebacterium diphtheriae*; DTaP
198
The DTaP vaccine protects against tetanus, pertussis, and what other bacterial infection?
*Cornyebacterium diphtheriae*, causing diphtheria
199
Is diphtheria common in industrialized nations?
No, not after widespread vaccination programs
200
How is *Corynebacterium diphtheriae* treated?
Antitoxin
201
What organism can cause fatal gas gangrene?
*C. perfringes*
202
What does "zoonotic" mean with regard to infections?
Zoonotic means that the pathogen is primarily transmitted to humans from animals
203
What is the characteristic symptom of diphtheria?
A swollen neck
204
What organism, causing petechial rashes and altered mental status, is seen in this slide?
*N. meningitidis*
205
Is *N. meningitidis* gram-positive or gram-negative? What is its shape?
Gram-negative; cocci
206
Why does *C. difficile* sometimes present in the hospital after prophylactic administration of antibiotics, e.g. cefazolin?
The antibiotics kill the normal gut flora, allowing the *C. difficile* to replicate without competition
207
What commonly eaten food is particularly susceptible to *Listeria* colonization when stored at improper temperatures?
Soft cheeses
208
What is the primary infective route of *L. monocytogenes*?
The intestinal epithelium, via an ingested substance
209
What organism causes spotted fevers (e.g. Rocky Mountain spotted fever) and various types of typhus?
*Rickettsia* species
210
What organism causes human monocytic ehrlichiosis (HME)?
*Ehrlichia chaffeensis*
211
What organism causes anaplasmosis?
*Anaplasma phagocytophilum*
212
What bacterium causes Lyme disease?
*Borrelia burgdorferi*
213
What organism is this, which is shown microscopically and with the characteristic rash from infection?
 
*Borrelia burgdorferi*
214
What is the typical shape of a rash for Lyme disease?
Bullseye
215
In early and late Lyme disease, what heart condition can manifest?
AV block, possibly causing bradycardia
216
What joint conditions present with long-term Lyme disease?
Swelling and arthritic-like symptoms
217
What insect is this? What bacterium does this kind of insect spread?
Black legged tick; *B. burgdorferi*
218
Where is Lyme disease most common?
Northeastern US and the region around Wisconsin
219
During what time of year is Lyme disease most likely spread from ticks to humans?
The fall
220
What animal is the primary host that blacklegged ticks (that carry Lyme disease) feed from?
Deer
221
Which stage of life of the blacklegged tick is most likely to spread *B. burgdorferi* to humans?
Nymph, which is after larva and before adult
222
When are most cases of Lyme disease reported throughout the year?
In a unimodal distribution centered around July
223
What bacterium is this rash typical of?
*B. burgdorferi* (Lyme disease)
224
What is the medical term for the "bullseye rash" caused by *B. burgdorferi*?
Erythema migrans
225
During which timecourse after infection are Lyme disease symptoms mostly localized to the site of the tick bite?
3-30 days
226
1-4 months after a bite containing *B. burgdorferi*, what general change in the localization of symptoms occurs?
They become more systemic, involving the nervous system, heart, and the rash is disseminated
227
What two nervous system disorders can result 1-4 months after infection with *B. burgdorferi*?
Cranial nerve palsy and lymphocytic meningitis
228
What two signs of cardiac involvement in Lyme disease can occur 1-4 months after the tick bite?
Heart block or myocarditis
229
What does this patient have? How long has he had it?
Lyme disease (*B. burgdorferi*); 1-4 months (rash is disseminated)
230
What are chronic symptoms of late Lyme disease? When do they begin?
Intermittent arthritis and vague neurological symptoms, like radicular pain, paresthesias, and Lyme encephalopathy; 4 months to years after the bite
231
What is the best way to diagnose Lyme disease? Why?
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
What kind of lab tests are available for Lyme disease? Are they reliable for diagnosis?
IgG and IgM antibody tests and PCR; no, they are not reliable
233
Why is doxycycline not typically given to children under 8?
It has the potential to stain the teeth (incorporation into anything that is being calcified)
234
What is the typical course of antibiotics for non-critical manifestations of Lyme disease? What if there is heart block or meningitis?
Amoxicillin for non-critical cases; ceftriaxone for hospitalized cases
235
What is this bacterium, found in docs and raccoons and potentially transmitted to humans?
Leptospirosis
236
Which organ systems are affected by leptospirosis?
Liver, kidney, skin, and brain
237
How does leptospirosis enter the body?
Broken skin or mucosa followed by contact with the organism (e.g. from an infected dog or raccoon)
238
How is leptospirosis treated? What does the first phase of symptoms present as? What is the source of infection?
Penicillin; flu-like symptoms; animals
239
Are *Rickettsia* gram positive or gram negative?
Gram negative
240
Do *Rickettsia* species replicate extracellularly or intracellularly?
Intracellularly
241
What is the reservoir for *Rickettsia*?
Hard ticks
242
What disease does *R. rickettsii* cause that has a 23% case fatality rate?
Rocky Mountain spotted fever
243
Where is the greatest concentration of the cases of Rocky Mountain spotted fever within the US?
The American Southeast
244
What are classic clinical manifestations of Rocky Mountain spotted fever?
Fever, headache and rash
245
What tick-borne disease causes this rash?
Rocky Mountain Spotted Fever (*R. rickettsii*)
246
How does *Rickettsia* induce its own phagocytosis? How does it escape from the phagosome?
By triggering actin rearrangement; release of phospholipase
247
What food-borne organism is *R. rickettsii* similar to in terms of how the cells propel themselves and spread to adjacent cells?
*L. monocytogenes*
248
Is humoral immunity, cell-based immunity, or both required to clear *R. rickettsii*? Why?
Cell-based; the organism is mostly confined intracellularly so antibodies cannot bind it directly
249
What is the shape and gram staining of *Ehrlichia* and *Anaplasma*? Do they grow inside or outside of host cells?
Both are tiny round gram negative bacteria; they grow intracellularly
250
Do *Ehrlichia* break out of the phagosome after phagocytosis?
No, they tend to stay within the phagosome
251
Which kind of immune cell is targeted by *Ehrlichia chafeensis*? Which is targeted by A*naplasma phagocytophillum*?
* E. chafeensis*: monocytes;
* A. phagocytophillum*: granulocytes
252
What kind of insect carries *E. chafeensis* and *A. phagocytophilum*?
Ticks
253
Which other tick-borne disease is carried by the same species of tick that is the reservoir for Lyme disease?
*Anaplasma phagocytophilum*
254
Do rickettsia, ehrlichiosis and anaplasmosis patients present reliably with knowledge of a tick bite?
No, they do not recall one in 40% of cases
255
Of rickettsia, ehrlichiosis, and anaplasmosis, which is least likely to produce a rash? Which is most likely?
Least likely, anaplasmosis; Most likely, rickettsia
256
What are the symptoms common to rickettsia, ehrlichiosis, and anaplasmosis?
Fever, headaches, myalgia, and malaise
257
What is the incubation period for rickettsia, ehrlichiosis, and anaplasmosis?
5-10 days
258
What is the treatment for rickettsia, ehrlichiosis, and anaplasmosis? Should confirmation from the lab be obtained before starting treatment?
Doxycycline; no
259
What type of lab test can identify rickettsia, ehrlichiosis, and anaplasmosis before the infection runs its course?
PCR (on either infected tissue or blood)
260
Following a tick bite, should you cover it with petroleum jelly to make it detach itself?
No, you should use tweezers to remove it as soon as possible
261
What bacterium causes "cat-scratch disease"?
*Bartonella henselae*
262
What is the manifestation of cat-scratch disease in a immunocompetent host? What about in an immunocompromised person?
Lymphadenopathy in an immunocompetent person; bacillary angiomatosis (rashes) in immunocompromised
263
What is the etiology for this kind of rash following a cat scratch? Is it more likely in immunocompetent or immunocompromised patients?
*B. henselae* infection has caused small tumors in the endothelium of small vessels; immunocompromised patients
264
What is visualized in a biopsy of a *B. henselae* related lymphadenopathy?
Granulomas and possibly the organism
265
What is the shape and gram staining of *B. henselae*?
Gram negative bacilli
266
Is *B. henselae* associated with older or younger cats?
Usually younger cats
267
What organism causes Q Fever?
*Coxiella burnetii*
268
What is the reservoir for *C. burnetii*?
Cattle, sheep, and goats
269
How is *C. burnetii* transmitted from cattle, sheep, or goats to humans? What cell type is infected?
Via inhalation; macrophages
270
Can you culture *C. burnetii*?
No, it is a biohazard
271
How can brucellosis be contracted?
Ingestion of dairy products or contaminated hands, or skin abrasion and contact with infected animals
272
What common symptom characterizes exposure to *C. burnetii* and brucellosis? What is the typical source of these pathogens?
Mysterious fevers and myalgia; farm animals like cattle, goats, and sheep
273
What is the best way to diagnostically confirm most tick-borne diseases? Is it practical to do this before starting treatment?
Serology; no, because serology takes two weeks and some tick-borne diseases are rapidly fatal
274
What condition are these symptoms immediately indicative of?
Scarlet fever
275
How is scarlet fever usually treated? What is the most serious side effect?
Penicillin; allergic reaction
276
A patient that is treated for scarlet fever now presents with this rash. What is most likely to have occurred?
Allergic reaction to penicillin
277
Which antibiotic has a characteristic adverse effect of bile sludging?
Ceftriaxone
278
Which antibiotic has the characteristic adverse effect of ototoxicity?
Aminoglycosides
279
Which antibiotics have the characteristic adverse effect of QTc prolongation?
Azithromycin, fluoroquinolones
280
Which antibiotic has the characteristic side effect of tendonitis?
Fluoroquinolones
281
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?
*S. aureus* (most important cause of septic arthritis);
yes;
vancomycin (*not* nafcillin or ceftriaxone, in case it is MRSA)
282
Which is the only cephalosporin activate against MRSA?
Ceftaroline, a 5th generation cephalosporin
283
What outpatient (oral) antibiotics are often active against MRSA?
Clindamycin, doxycycline, and trimethoprim-sulfamethoxazole
284
What treatment for MRSA can cause myositis or creatinine phosphokinase elevation?
Daptomycin
285
Which treatment for MRSA has 100% bioavailability? What is its drawback?
Linezolid; besides side effects like bone marrow suppression or serotonin syndrome, it is costly
286
Which treatment for MRSA can cause Red Man syndrome?
Vancomycin
287
When a serious *S. aureus* infection, should a clinician wait until its susceptibility to methicillin is determined before treating?
No, assume it is MRSA and treat accordingly (vancomycin, daptomycin, linezolid, ceftaroline)
288
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?
Meningitis; vancomycin and ceftriaxone
289
From 1 month old throughout adulthood, what are the top three suspects for bacterial meningitis? What is the empirical treatment?
*Neisseria meningitidis*, *S. pneumoniae*, and *H. influenzae* type B; ceftriaxone and vancomycin
290
What additional cause of meningitis must be suspected in an immunocompromised patient? What antibiotic should be added to the regimen to combat it?
*Listeria*; ampicillin
291
Until the age of 1 month, what are the typical suspects for a bacterial meningitis?
Group B streptococcus, *E. coli*, and *Listeria*
292
Which generation of cephalosporins is needed to treat the CNS?
Third generation: ceftriaxone, cefotaxime, ceftazidime
293
Which β-lactams can be used against pseudomonas?
Cefepime (4th generation cephalosporin), piperacillin-tazobactam (no CNS penetration), carbapenems such as imipenem, azteronam, ceftazidime (3rd generation cephalosporin)
294
Can *Pseudomonas* be treated with fluroquinolones?
Yes
295
What fluoroquinolone is effective against gram negatives and gram positives, including anaerobes?
Moxifloxacin
296
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?
Vancomycin, or if resistance is suspected, linezolid and daptomycin; ampicillin
297
What drugs can be used to treat a *C. difficile* colitis?
Metronidazole and secondarily oral vancomycin
298
Are intra-abdominal abscesses going to contain one species, or multiple species? What is the typical pair of antibiotics used?
Multiple; cephalosporin + metronidazole
299
What is the difference in treatment between typical (community-acquired, lobar) pneumonia and atypical pnemonia?
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
How many cases of sepsis are diagnosed per year? How many of them result in death?
750,000; 31%
301
What is the mainstay of treatment for a patient with severe inflammatory response syndrome?
Fluids (normal saline bolus)
302
Why is oxygen provided to a patient undergoing sepsis?
Oxygen delivery is impaired, e.g., by lack of functional surface area of the alveoli
303
Out of all the bacterial vaccines that are administered in the US, which has been the least successful in terms of % reduction?
Pertussis (82% reduction)
304
What federal body sets policy on vaccines?
CDC Advisory Committee on Immunization Practices
305
Can children under the age of 2 develop memory immunity in response to a polysaccharide antigen?
No
306
What is the minimum human lethal dose of tetanospasmin? What bacterium produces it?
2.5 ng/kg; Clostridium tetani
307
What is the difference between an adjuvant and a conjugate vaccine?
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
What is the most common route of vaccine administration?
Intramuscular (deltoid or anterolateral thigh)
309
What two types of immune response are elicited by a mucosal administration of a vaccine?
Systemic and mucosal (IgA) response
310
What are two methods of mucosal administration of a vaccine?
Oral or intranasal
311
Are vaccines for the plague and Lyme disease commonly administered today? What about anthrax and tularemia?
No, plague and Lyme disease vaccines are discontinued; anthrax and tularemia vaccines are only given to military personnel
312
What can be done over time to increase the magnitude and duration of antibody response to a vaccine?
Booster doses
313
The top four presenting bacterial STD's are [...], chlamydia, gonorrhea, and chancroid.
The top four presenting bacterial STD's are syphilis, chlamydia, gonorrhea, and chancroid.
314
The top four presenting bacterial STD's are syphilis, [...], gonorrhea, and chancroid.
The top four presenting bacterial STD's are syphilis, chlamydia, gonorrhea, and chancroid.
315
The top four presenting bacterial STD's are syphilis, chlamydia, [...], and chancroid.
The top four presenting bacterial STD's are syphilis, chlamydia, gonorrhea, and chancroid.
316
The top four presenting bacterial STD's are syphilis, chlamydia, gonorrhea, and [...].
The top four presenting bacterial STD's are syphilis, chlamydia, gonorrhea, and chancroid.
317
Which STDs increase the risk for HIV transmission and why?
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
What bacterium causes syphilis?
*Treponema pallidum*
319
High risk groups for syphilis are: men who have sex with men, drug users, and [...]
High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.
320
High risk groups for syphilis are: [...], drug users, and those with multiple sexual partners.
High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.
321
High risk groups for syphilis are: men who have sex with men, [...], and those with multiple sexual partners.
High risk groups for syphilis are: men who have sex with men, drug users, and those with multiple sexual partners.
322
What coats the spirochetes of *T. pallidum* and protects against phagocytosis?
Host cell fibronectin
323
Is syphilis a localized or systemic disease? Are most of the symptoms related to toxins released by *T. pallidum* or the immune response?
Secondary syphilis is systemic, because the spirochete disseminates into the bloodstream; the immune response creates most symptoms
324
What is the prototypical lesion of syphilis? What does it look like?
The chancre; painless, smooth ulcer with firm borders and clean base.
325
Why might a patient with syphilis not recognize that they have the chancre (lesion) signalling infection?
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
What STD is this lesion prototypical of? What organism causes it? How long does it take for this lesion to heal on its own?
Syphilis; *T. pallidum*; 3-6 weeks
327
What kind of a lesion is this? What organism is suspect?
Chancre; *T. pallidum* (causing syphilis)
328
What is the shape of *T. pallidum*?
Spirochete
329
What are differential diagnoses (related diagnoses that must be ruled out) for a primary chancre that looks like syphilis (*T. pallidum*)?
Chancroid (*H. ducreyi*), lymphogranuloma venereum, herpes, and trauma
330
During secondary syphilis, what clinical manifestations can occur?
*Many* possible symptoms: rash, fever, malaise, weight loss, diffuse painless lymphadenopathy, pharyngitis, arthralgia, uveitis...
331
Which STD infection has a secondary stage that this rash a classical sign for?
Syphilis: palm and sole rash
332
Does the rash of secondary syphilis only occur on the palms and soles?
No, it can also appear on the trunk and elsewhere on the skin
333
If a patient is asymptomatic for syphilis but as immunoreactivitity to anti-treponemal antibodies, should an LP be taken check for CNS involvement?
This is controversial, so usually it is not done unless the immunoreactivity is very high
334
What are common symptoms of late syphilis?
Aortitis, CNS complications, and gumma formation
335
Can *T. pallidum* be grown on culture? How is it typically visualized?
No; it can be visualized on darkfield microscopy from scrapings of chancres, mucus, or condylomata lata
336
Is there a treponemal antibody test?
Yes
337
What is the primary treatment for syphilis? Is there any substitute for this drug in the late stages of the disease?
Penicillin; no
338
Syndromes of *Chlamydia trachomatis* that present clinically are: [...] infection, infant pneumonia, conjunctivititis, and ocular trachoma.
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.
339
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant [...], conjunctivititis, and ocular trachoma.
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.
340
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, [...], and ocular trachoma.
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.
341
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular [...].
Syndromes of *Chlamydia trachomatis* that present clinically are: genital infection, infant pneumonia, conjunctivititis, and ocular trachoma.
342
What is the most common bacterial STD in the US?
*C. trachomatis*
343
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?
*C. trachomatis*
344
Does immunity to *C. trachomatis* confer long term protection against re-infection?
No
345
How can *C. trachomatis* be spread? Can it be spread to a birthed infant?
Via abrasion of the skin; yes, via direct inoculation into the eyes and respiratory tract
346
What are genital syndromes caused by *C. trachomatis*?
Cervicitis, urethritis, epididymitis, salpingitis, infertility or ectopic pregnancy
347
Can *Chlamydia* cause infertility?
There is a strong relationship, and the pathogenesis is likely via chronic bilateral scarring of the fallopian tubes
348
What is the shape and gram staining of *Neisseria gonorrhea*?
Bean shaped gram-negative diplococci
349
Is *N. gonorrhea* more likely to spread male to female or the other way around?
Male to female but both are possible
350
Is *N. gonorrhea* more or less likely to be transmitted per episode of sex than HIV?
More likely
351
When is infection by *N. gonorrhea* most common?
Adolescents and young adults
352
Besides the genitourinary tract, where else can *N. gonorrhea* infections manifest?
Anorectal canal, pharynx, and around the liver
353
Does pharyngitis caused by *N. gonorrhea* usually present with symptoms? If so, what are they?
No, it is usually asymptomatic
354
What causes pelvic inflammatory disease?
Usually, a bacterial super-infection secondary to *N. gonorrhea* infection
355
What is Fitz Hugh Curtis syndrome?
Perihepatitis caused by *N. gonorrhea* by direct extension of the organism from the fallopian tubes to the liver capsule
356
What kind of agar is used to culture *N. gonorrhea*?
Chocolate agar with antibiotics (Thayer Martin agar)
357
What is the typical first-line treatment for *N. gonorrhea*?
Ceftriaxone, 125mg intramuscular once
358
What is the second line agent of treatment for *N. gonorrhea*?
Azithromycin
359
What organism causes Chancroid? Is it more common in the developing world or the US?
*H. ducreyi*; in the developing world
