Healthcare Associated Infections Cards Flashcards

1
Q

Describe the gram stain and shape of C. difficile

A

Gram positive rod

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2
Q

How is C. difficile transmitted?

A

Spores are ingested by the fecal-oral route

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3
Q

What is NAP1?

A

The hypervirulent strain of C. difficile that emerged in the 2000s

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4
Q

What is a common reservoir for C. difficile?

A

Asymptomatic infection in nursing home and hospitalized patients

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5
Q

How does C. difficile infect the intestine?

A

Exotoxins bind intestinal epithelial cells and disrupt tight junctions/cytoskeleton to break the intestinal barrier.

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6
Q

What are the two C. difficile toxins and their functions?

A

Toxin A - activates neutrophils/causes leukocytosis; Toxin B - potent, causes disease.

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7
Q

What antibiotics predispose to C difficile?

A

Clindamycin, FQs, cephalosporins; sometimes, vancomycin and metronidazole

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8
Q

What non-antibiotic medications predispose to C difficile?

A

Proton pump inhibitors or H2 blockers; they suppress gastric acid which is part of the host normal defense.

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9
Q

What are the three main complications of C. difficile?

A

Fulminant colitis, toxic megacolon, and bowel perforation (leading to shock)

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10
Q

How is C. difficile diagnosed?

A

Stool toxin PCR

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11
Q

What are the findings of C. difficile on colonoscopy?

A

Yellow pseudomembranes, with inflammation, white plaques and ulceration

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12
Q

A patient has a positive stool PCR for C. difficile. Do you treat him/her?

A

Treat symptomatic patients; do not generally treat asymptomatic treatments.

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13
Q

What antibiotics are used to treat C. difficile?

A

Oral metronidazole or oral vancomycin. Oral vancomycin in severe disease.

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14
Q

How may relapsed/refractory C. difficile be treated?

A

Fecal microbiota treatment aka stool transplant. Stool instilled via NG tube, colonoscopy, or enema.

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15
Q

Why is C. difficile challenging to eradicate from the hospital setting?

A

C. difficile spores are persistent and resistant to alcohol gels or disinfectants. Hand hygiene with soap and water plus contact precautions are required.

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16
Q

Name five medically important gram negative rods

A

E. coli (UTI/HAI), Klebsiella (UTI/HAI), Proteus (UTI), Serratia, Pseudomonas (biofilms)

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17
Q

What is LPS and why is it important?

A

LPS is an endotoxin and component of the outer membrane in gram negative bacteria. It is a potent immune stimulator, causing sepsis and shock particularly in bacteremia. Gram positive bacteria do not have LPS.

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18
Q

Which clinically relevant GNR is oxidase +?

A

Pseudomonas

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19
Q

Which GNR are non-lactose fermenting?

A

Proteus, Salmonella, Shigella, Pseudomonas

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20
Q

Which GNR are lactose-fermenting?

A

E. coli, Klebsiella, Enterobacter, Citrobacter

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21
Q

What bacteria can cause hemolytic-uremic syndrome?

A

E. coli (EHEC)

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22
Q

What is the reservoir for pseudomonas?

A

WATER, soil, plants.

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23
Q

What is the appearance of pseudomonas in culture?

A

Blue-green pigemented, and smells like “sweet grape or corn tortilla”

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24
Q

What does pseudomonas Exotoxin A cause?

A

Skin necrosis, especially in IV drug users

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25
What are common types of infections caused by pseudomonas?
Hot tub folliculitis, swimmer's ear/malignant otitis, burn/wound infections, diabetic foot infecitons, ecthyma gangrenosum. Common in ICUs, CF patients and IV drug users.
26
What is the most important anaerobe causing disease below the diaphragm?
Bacteriodes fragilis
27
What is the most important anaerobe causing disease above the diaphragm?
Fusobacterium
28
What are the common Fusobacterium infections?
Deep neck space infections, orodental, pulmonary infections.
29
What is Lemierre's syndrome?
A clot in the jugular vein infected by Fusobacterium; "jugular vein septic thrombophlebitis"
30
What two ways can bacterial infect the kidneys and cause pyelonephritis?
Uropathogens attach to urinary epithelium and ascend to the bladder; additionally, pyelo can result from bacterial seeding of the kidneys during bacteremia.
31
What organism causes pyelonephritis via bacteremia?
S. aureus
32
What are the most common microbes that cause uncomplicated UTI?
Enteric gram negative rods, E. Coli, Proteus mirabilis, Klebsiella pneumonia
33
What factors make a UTI "complicated"?
Male sex, pregnancy, diabetes, anatomic abnormalities, catheter/instrumentation in the urinary tract, immunosuppression
34
What is the most sensitive lab test for UTI diagnosis?
Pyuria - test for white blood cells in the urine. This is sensitive but not specific (other things cause pyuria)
35
What lab test measures an enzyme released by WBCs?
Leukocyte esterase
36
What organism does a nitrite test help identify?
Enterobacteriaceae
37
When is asymptomatic bacteriuria treated?
Pregnancy or in advance of urologic procedures with risk of bleeding
38
What are the three first line antibiotics for UTIs?
Nitrofurantoin (for lower UTI), TMP-SMX (for upper UTI), and Fosfomycin (lower UTI)
39
What is the second line alternative antibiotic to treat pyelonephritis as an outpatient?
Quinolones (oral outpatient pyelonephritis)
40
What antimicrobials have activity against MRSA?
Vancymycin, Linezolid, Daptomycin (except for pneumonia)
41
What antimicrobials are active against Pseudomonas?
Piperacillin/Ticarcillin, Cephalosporins, Carbapenems. Also FQs (not reliable) and aminoglycosides (high toxicity, poor pulmonary penetration).
42
What organism is most associated with catheter-related UTI?
Klebsiella pneumonia
43
What urine test will suggest a Proteus mirabilis UTI?
Urine pH; proteus mirabilis produces urease, which splits urea into NH3 and CO2, alkalinizing urine.
44
What candida species most often causes mucosal candidiasis?
C. albicans
45
What are 5 clinical types of C. albicans infections? (Hint: 3 in immunocompetent hosts, 2 in immunocompromised hosts)
In immunocompetent: oral thrush, vaginitis, and diaper rash. In immunocompromised: esophagitis and disseminated candidiasis.
46
What does C. albicans biofilm look like under microscope?
Mixture of yeast and hyphal-pseudohyphal forms. Hyphal cells lyse/penetrate cells, yeast cells disperse.
47
How is mucosal candidiasis diagnosed?
Scraping of white plaques invading mucosal surfaces (these plaques CAN be scraped away); direct microscopy with KOH stain
48
What is used to treat mucosal candidiasis in immunocompetent patients?
Topical nystatin (thrush or skin infection), Topical azoles or oral fluconazole (vaginal yeast infections)
49
What is the treatment for disseminated candidiasis?
Oral fluconazoel and IV echinocandins
50
What morphology of C. albicans help for rapid species identification?
Germ tube (outgrowth from spores during germination).
51
What is the gram stain, shape, catalase, and coagulase test description of S. aureus?
Gram positive, cocci, Catalase +, coagulase +
52
Describe how the catalase test differentiates staphylocci from streptococci
Staph is catalase + ; Strep is catalase -
53
What element confers methicillin resistance to S. aureus?
PBP2a, an altered penicillin binding protein encoded by the mecA gene on a staphylococcal cassette chromosome
54
What element confers penicillin resistance to S. aureus?
Penicillinase (an enzyme that cleaves penicillin)
55
What are the three clinical diseases caused by S. aureus toxins?
Toxic shock syndrome, S. aureus food poisoning, Scalded skin syndrome
56
What toxin causes S. aureus Toxic shock syndrome?
TSST-1 (toxic shock syndrome toxin 1), a superantigen that results in widespread T cell activation
57
What toxin causes S. aureus food poisoning?
Pre-formed, heat-stable eneterotoxin
58
What toxin causes scalded skin syndrome?
Exfoliative toxin
59
What are common sources of S. aureus bacteremia?
Catheters, skin infections, pulmonary infections
60
What are the criteria for uncomplicated S. aureus bacteremia?
No endocarditis, no prosthesis, blood clutures 2-4 days post initial cultures are negative, fever decreases after 72 hours of antibiotic therapy, and no evidence of disseminated infection
61
What is the most common cause of infective endocarditis in the industrial world? In the developing world?
Industrial: S. aureus. Developing: viridans streptococcus
62
What are the four main risk factors for S. aureus endocarditis?
IV drug use, healthcare contact, intravascular devices, diabetes mellitus
63
What presentation/outcomes are associated with S. aureus infective endocarditis?
Acute presentation, persistent bacteremia, stroke, and higher mortality than other IE
64
Patients with S. aureus bacteremia are at risk for what bone or joint infection?
Native joint septic arthritis
65
What are the common sites for S. aureus osteomyelitis?
Long bones in children; vertebral bones in adults with bacteremia
66
What percent of hospitalized patients acquire a healthcare associated infection?
4%
67
What are the five most common healthcare-aquired infections? (Types of infections, not microbes)
Pneumonia, surgical site infection, C. difficile colitis, UTI, central catheter bloodstream infection
68
What are two ways to prevent HAI pneumonia?
Elevate head of the bed >30 degrees to prevent aspiration; drain subglottic secretions
69
What three organisms mainly cause HAI pneumonia?
MRSA, Pseudomonas, GNRs
70
What two organisms mainly cause HAI surgical site infection?
MRSA, beta-hemolytic strep
71
What are two ways to prevent HAI surgical site infections?
Pre-operative antibiotics, pre-operative skin prep
72
What is the best way to prevent a HAI urinary tract infection?
Remove the Foley catheter ASAP
73
What four pathogens mainly cause HAI central catheter bloodstream infections?
S. aureus, S. epidermidis, Enterococcus, Candida
74
What are the key risk factors for HAI pneumonia?
Intubation, sedation (leads to aspiration)
75
What are the three key risk factors for surgical site infection?
Obesity, diabetes, immunosuppression
76
What are two main risk factors for catheter-related bloodstream infections?
Immunosuppression, burns
77
What bacterial pathogenesis factor causes sepsis?
LPS endotoxin
78
What are the criteria for systemic inflammatory repsonse syndrome?
Temperature dysregulation, tachycardia, tachypnea, abnormal WBC, abnormal CBC (high bands, high cells or very low cells). Need at least 2.
79
What is the difference between sepsis and severe sepsis?
Sepsis = SIRS + suspected or proven source of infection. Severe sepsis = sepsis + evidence of organ dysfunction/hypoperfusion
80
Name signs of organ dysfunction seen in sepsis.
Including but not limited to: hypotension, hypoxemia, oliguria, high creatinine, metabolic acidosis, coagulopathy, low platelets, altered mental status, high lactate, high liver enzymes
81
Define shock
Severe sepsis + hypotension despite fluid resuscitation
82
What are the three main categories of shock and related clinical syndromes?
Hypovolemic shock (hemorrhage, diarrhea), cardiogenic shock (MI), distributive shock (septic shock, anaphylaxis, neurogenic)
83
How does multiple myeloma predispose to infection?
Decreased Ig; tumor invasion of bone marrow cuases neutropenia
84
What strategies are used to prevent infection in patients with hematologic malignancy?
G-CSF to increase neutrophyl count; prophylaxis with antibacterials and antifungals
85
What tissues are most often involved in complications of systemic candidiasis?
Retinas, heart valves, meninges
86
What type of candidiasis do neutropenic patients often develop?
Hepato-splenic candidiasis
87
What are the presenting symptoms of systemic candidiasis?
Fever, sepsis syndrome, end-organ symptoms. NOT pneumonia.
88
What is most frequently prescribed for systemic candidiasis?
Azoles (fluconazole, voriconazole, posaconazole)
89
What is the mechanism of action of azoles?
Azoles block cell membrane ergosterol synthesis by inhibiting cyt P450
90
What is the mechanism of action of Amphotericin B?
Binds and "punches a hole" in ergosterol, a ocmponent of the fungal cell membrane.
91
What is the mechanism of action of echniocandins?
Inibit cell wall synthesis by inhibiting 1,3 D-glucan synthase
92
For what type of fungal infection should you NOT use echinocandins?
UTI (poor activity in urine)
93
When should antifungals be used as prophylaxis?
Neutropenia, febrile neutropenia post-chemotherapy, GI perforation, or any GI surgery
94
What are "Doomstay GNRs" and where are they a huge problem?
Carbapenem-resistant enterobacteriaceae; rising in India