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Microbiology > Healthcare Associated Infections Cards > Flashcards

Healthcare Associated Infections Cards Flashcards

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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
Q

What are common types of infections caused by pseudomonas?

A

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.

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26
Q

What is the most important anaerobe causing disease below the diaphragm?

A

Bacteriodes fragilis

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27
Q

What is the most important anaerobe causing disease above the diaphragm?

A

Fusobacterium

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28
Q

What are the common Fusobacterium infections?

A

Deep neck space infections, orodental, pulmonary infections.

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29
Q

What is Lemierre’s syndrome?

A

A clot in the jugular vein infected by Fusobacterium; “jugular vein septic thrombophlebitis”

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30
Q

What two ways can bacterial infect the kidneys and cause pyelonephritis?

A

Uropathogens attach to urinary epithelium and ascend to the bladder; additionally, pyelo can result from bacterial seeding of the kidneys during bacteremia.

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31
Q

What organism causes pyelonephritis via bacteremia?

A

S. aureus

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32
Q

What are the most common microbes that cause uncomplicated UTI?

A

Enteric gram negative rods, E. Coli, Proteus mirabilis, Klebsiella pneumonia

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33
Q

What factors make a UTI “complicated”?

A

Male sex, pregnancy, diabetes, anatomic abnormalities, catheter/instrumentation in the urinary tract, immunosuppression

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34
Q

What is the most sensitive lab test for UTI diagnosis?

A

Pyuria - test for white blood cells in the urine. This is sensitive but not specific (other things cause pyuria)

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35
Q

What lab test measures an enzyme released by WBCs?

A

Leukocyte esterase

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36
Q

What organism does a nitrite test help identify?

A

Enterobacteriaceae

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37
Q

When is asymptomatic bacteriuria treated?

A

Pregnancy or in advance of urologic procedures with risk of bleeding

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38
Q

What are the three first line antibiotics for UTIs?

A

Nitrofurantoin (for lower UTI), TMP-SMX (for upper UTI), and Fosfomycin (lower UTI)

39
Q

What is the second line alternative antibiotic to treat pyelonephritis as an outpatient?

A

Quinolones (oral outpatient pyelonephritis)

40
Q

What antimicrobials have activity against MRSA?

A

Vancymycin, Linezolid, Daptomycin (except for pneumonia)

41
Q

What antimicrobials are active against Pseudomonas?

A

Piperacillin/Ticarcillin, Cephalosporins, Carbapenems. Also FQs (not reliable) and aminoglycosides (high toxicity, poor pulmonary penetration).

42
Q

What organism is most associated with catheter-related UTI?

A

Klebsiella pneumonia

43
Q

What urine test will suggest a Proteus mirabilis UTI?

A

Urine pH; proteus mirabilis produces urease, which splits urea into NH3 and CO2, alkalinizing urine.

44
Q

What candida species most often causes mucosal candidiasis?

A

C. albicans

45
Q

What are 5 clinical types of C. albicans infections? (Hint: 3 in immunocompetent hosts, 2 in immunocompromised hosts)

A

In immunocompetent: oral thrush, vaginitis, and diaper rash. In immunocompromised: esophagitis and disseminated candidiasis.

46
Q

What does C. albicans biofilm look like under microscope?

A

Mixture of yeast and hyphal-pseudohyphal forms. Hyphal cells lyse/penetrate cells, yeast cells disperse.

47
Q

How is mucosal candidiasis diagnosed?

A

Scraping of white plaques invading mucosal surfaces (these plaques CAN be scraped away); direct microscopy with KOH stain

48
Q

What is used to treat mucosal candidiasis in immunocompetent patients?

A

Topical nystatin (thrush or skin infection), Topical azoles or oral fluconazole (vaginal yeast infections)

49
Q

What is the treatment for disseminated candidiasis?

A

Oral fluconazoel and IV echinocandins

50
Q

What morphology of C. albicans help for rapid species identification?

A

Germ tube (outgrowth from spores during germination).

51
Q

What is the gram stain, shape, catalase, and coagulase test description of S. aureus?

A

Gram positive, cocci, Catalase +, coagulase +

52
Q

Describe how the catalase test differentiates staphylocci from streptococci

A

Staph is catalase + ; Strep is catalase -

53
Q

What element confers methicillin resistance to S. aureus?

A

PBP2a, an altered penicillin binding protein encoded by the mecA gene on a staphylococcal cassette chromosome

54
Q

What element confers penicillin resistance to S. aureus?

A

Penicillinase (an enzyme that cleaves penicillin)

55
Q

What are the three clinical diseases caused by S. aureus toxins?

A

Toxic shock syndrome, S. aureus food poisoning, Scalded skin syndrome

56
Q

What toxin causes S. aureus Toxic shock syndrome?

A

TSST-1 (toxic shock syndrome toxin 1), a superantigen that results in widespread T cell activation

57
Q

What toxin causes S. aureus food poisoning?

A

Pre-formed, heat-stable eneterotoxin

58
Q

What toxin causes scalded skin syndrome?

A

Exfoliative toxin

59
Q

What are common sources of S. aureus bacteremia?

A

Catheters, skin infections, pulmonary infections

60
Q

What are the criteria for uncomplicated S. aureus bacteremia?

A

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
Q

What is the most common cause of infective endocarditis in the industrial world? In the developing world?

A

Industrial: S. aureus. Developing: viridans streptococcus

62
Q

What are the four main risk factors for S. aureus endocarditis?

A

IV drug use, healthcare contact, intravascular devices, diabetes mellitus

63
Q

What presentation/outcomes are associated with S. aureus infective endocarditis?

A

Acute presentation, persistent bacteremia, stroke, and higher mortality than other IE

64
Q

Patients with S. aureus bacteremia are at risk for what bone or joint infection?

A

Native joint septic arthritis

65
Q

What are the common sites for S. aureus osteomyelitis?

A

Long bones in children; vertebral bones in adults with bacteremia

66
Q

What percent of hospitalized patients acquire a healthcare associated infection?

A

4%

67
Q

What are the five most common healthcare-aquired infections? (Types of infections, not microbes)

A

Pneumonia, surgical site infection, C. difficile colitis, UTI, central catheter bloodstream infection

68
Q

What are two ways to prevent HAI pneumonia?

A

Elevate head of the bed >30 degrees to prevent aspiration; drain subglottic secretions

69
Q

What three organisms mainly cause HAI pneumonia?

A

MRSA, Pseudomonas, GNRs

70
Q

What two organisms mainly cause HAI surgical site infection?

A

MRSA, beta-hemolytic strep

71
Q

What are two ways to prevent HAI surgical site infections?

A

Pre-operative antibiotics, pre-operative skin prep

72
Q

What is the best way to prevent a HAI urinary tract infection?

A

Remove the Foley catheter ASAP

73
Q

What four pathogens mainly cause HAI central catheter bloodstream infections?

A

S. aureus, S. epidermidis, Enterococcus, Candida

74
Q

What are the key risk factors for HAI pneumonia?

A

Intubation, sedation (leads to aspiration)

75
Q

What are the three key risk factors for surgical site infection?

A

Obesity, diabetes, immunosuppression

76
Q

What are two main risk factors for catheter-related bloodstream infections?

A

Immunosuppression, burns

77
Q

What bacterial pathogenesis factor causes sepsis?

A

LPS endotoxin

78
Q

What are the criteria for systemic inflammatory repsonse syndrome?

A

Temperature dysregulation, tachycardia, tachypnea, abnormal WBC, abnormal CBC (high bands, high cells or very low cells). Need at least 2.

79
Q

What is the difference between sepsis and severe sepsis?

A

Sepsis = SIRS + suspected or proven source of infection. Severe sepsis = sepsis + evidence of organ dysfunction/hypoperfusion

80
Q

Name signs of organ dysfunction seen in sepsis.

A

Including but not limited to: hypotension, hypoxemia, oliguria, high creatinine, metabolic acidosis, coagulopathy, low platelets, altered mental status, high lactate, high liver enzymes

81
Q

Define shock

A

Severe sepsis + hypotension despite fluid resuscitation

82
Q

What are the three main categories of shock and related clinical syndromes?

A

Hypovolemic shock (hemorrhage, diarrhea), cardiogenic shock (MI), distributive shock (septic shock, anaphylaxis, neurogenic)

83
Q

How does multiple myeloma predispose to infection?

A

Decreased Ig; tumor invasion of bone marrow cuases neutropenia

84
Q

What strategies are used to prevent infection in patients with hematologic malignancy?

A

G-CSF to increase neutrophyl count; prophylaxis with antibacterials and antifungals

85
Q

What tissues are most often involved in complications of systemic candidiasis?

A

Retinas, heart valves, meninges

86
Q

What type of candidiasis do neutropenic patients often develop?

A

Hepato-splenic candidiasis

87
Q

What are the presenting symptoms of systemic candidiasis?

A

Fever, sepsis syndrome, end-organ symptoms. NOT pneumonia.

88
Q

What is most frequently prescribed for systemic candidiasis?

A

Azoles (fluconazole, voriconazole, posaconazole)

89
Q

What is the mechanism of action of azoles?

A

Azoles block cell membrane ergosterol synthesis by inhibiting cyt P450

90
Q

What is the mechanism of action of Amphotericin B?

A

Binds and “punches a hole” in ergosterol, a ocmponent of the fungal cell membrane.

91
Q

What is the mechanism of action of echniocandins?

A

Inibit cell wall synthesis by inhibiting 1,3 D-glucan synthase

92
Q

For what type of fungal infection should you NOT use echinocandins?

A

UTI (poor activity in urine)

93
Q

When should antifungals be used as prophylaxis?

A

Neutropenia, febrile neutropenia post-chemotherapy, GI perforation, or any GI surgery

94
Q

What are “Doomstay GNRs” and where are they a huge problem?

A

Carbapenem-resistant enterobacteriaceae; rising in India

Microbiology (9 decks)

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