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4.2 Medical Microbiology > HCAI - organisms > Flashcards

HCAI - organisms Flashcards

1
Q

What is the prevalence of C. difficile infections (CDI) among HCAIs?

A

2.4% of HCAIs are CDI.

3% of CDI cases result in death.

CDI may be underdiagnosed due to limited testing (e.g., only inpatients).

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2
Q

What environmental and biological factors contribute to CDI?

A

Bile salts in the gut induce spore germination.

CDI involves toxin-producing organisms and sloughing off of dead cells.

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3
Q

What is the epidemiology of C. difficile in neonates and infants?

A

Neonates and infants up to age 2 are often colonized with toxigenic C. difficile but are typically asymptomatic.

Carriage rates vary significantly.

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4
Q

What role do animals play in CDI?

A

Animal reservoirs, such as pigs, carry C. difficile.

Potential zoonotic transmission exists but not through food products.

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5
Q

How is C. difficile transmitted?

A

Symptomatic and asymptomatic patients serve as important reservoirs.

Diarrheal C. difficile is more transmissible than asymptomatic carriers.

Bedpans (hoppers) are significant transmission sources.

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6
Q

What factors increase the risk of CDI?

A

Length and type of antimicrobial treatment, with fluoroquinolones now considered high-risk.

Host factors:

Elderly: Decline in humoral antibody response.

Underlying diseases.

Bacterial factors:

Mutations in toxin genes and regulators increase virulence and persistence.

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7
Q

What is the clinical progression of CDI in recurrent cases?

A

Antibiotic use leads to infection.

Recurrence follows recovery, causing a cycle of CDI.

Severe outcomes include pseudomembranous colitis and toxic megacolon.

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8
Q

What is the pathogenicity locus in C. difficile?

A

Required for toxin production.

Includes:

TcdC: Regulates toxin A and B production (switched off by TcdC).

TcdE: Releases toxins extracellularly.

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9
Q

Describe toxins A and B in C. difficile.

A

Highly similar toxins involved in pathogenicity.

Mutations and deletions in their binding regions (CROPs) can alter function.

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10
Q

How do C. difficile strains differ?

A

Some strains produce only one toxin.

Ribotype 027:

Increased sporulation.

Hyperproduction of toxins A and B.

Fluoroquinolone resistance.

Associated with severe disease and outbreaks in North America and Ireland.

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11
Q

What are the challenges in diagnosing CDI?

A

Testing often limited to inpatients.

Reference labs in Ireland (e.g., Cherry Orchard) operate selectively and lack comprehensive capacity.

Whole-genome sequencing is used for tracking but remains limited.

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12
Q

What advances have been made in C. difficile diagnostics?

A

Ribotyping identifies strains like Ribotype 027.

Whole-genome sequencing provides detailed epidemiology.

Efforts are underway to develop rapid detection methods (e.g., RT-PCR).

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13
Q

What are the primary treatment options for CDI?

A

Antibiotics:

Vancomycin is now preferred over metronidazole.

Concerns about vancomycin-resistant MRSA persist.

Non-antibiotic methods:

Probiotics and fecal transplants.

Intravenous immunoglobulin (IVIG) containing antibodies against C. difficile.

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14
Q

Why are vaccines against CDI challenging?

A

Elderly patients, the primary risk group, have a poor humoral response to toxoid vaccines.

Young individuals respond well, but vaccinating them does not protect the most vulnerable.

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15
Q

What role does microbiome replacement play in CDI treatment?

A

Restores healthy gut flora, preventing C. difficile overgrowth.

Comparable effectiveness to vancomycin for recurrent CDI.

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16
Q

What are advanced treatment methods?

A

Bowel lavage with direct vancomycin administration.

Experimental therapies, such as monoclonal antibodies and microbiome-based interventions.

17
Q

How can CDI recurrence be prevented?

A

Focus on reducing antibiotic exposure and duration.

Emphasize hygiene and sanitation in healthcare settings.

18
Q

What are key environmental factors in CDI prevention?

A

Proper decontamination of rooms and equipment.

Address reservoirs like sinks and plumbing, especially in ICUs.

19
Q

How does air dissemination contribute to CDI?

A

Evidence suggests airborne transmission of spores.

Outbreak strains like Ribotype 027 sporulate more readily.

20
Q

How has CDI epidemiology changed over time?

A

CDI has shifted from being primarily a healthcare-associated infection in elderly patients on antibiotics to include community-acquired cases in younger populations.

Outbreaks in North America and Ireland highlight changing dynamics.

21
Q

What are the implications of hypervirulent C. difficile strains?

A

Increased disease severity and resistance to treatments like fluoroquinolones.

Enhanced persistence and transmission due to sporulation.

22
Q

How has the effectiveness of metronidazole changed?

A

Once a first-line treatment, its efficacy has been questioned in recent years, leading to a shift toward vancomycin and other therapies.

23
Q

What challenges remain in addressing CDI?

A

Underdiagnosis and limited testing capacity.

Lack of comprehensive surveillance and rapid diagnostics.

Need for effective vaccines for elderly populations.

24
Q

What trends in MRSA prevalence have been observed?

A

MRSA prevalence in Ireland has dropped significantly, reaching an all-time low of 9.7% in 2023, down from over 40% in previous years.

Strains like EMRSA 14 and 15 are dominant.

Glycopeptide resistance, though rare, is harder to detect.

25
Q

What is significant about VRE trends and outbreaks?

A

VRE bloodstream infections have sharply increased, especially in liver units.

First outbreak of linezolid-resistant VRE in Ireland.

Environmental contamination and patient colonization are significant factors.

26
Q

What are the characteristics of Acinetobacter baumannii in HCAIs?

A

Highly resistant through mobile genetic elements.

Persists in the environment (biofilms) and resists disinfection.

Associated with BSIs, pneumonia, and UTIs.

Treatment options are extremely limited.

27
Q

What makes carbapenem-resistant Pseudomonas aeruginosa a challenge?

A

Combines intrinsic and acquired resistance mechanisms.

Reservoirs include wet environments and equipment.

ICU colonization studies reveal high endogenous colonization rates.

28
Q

What is hypervirulent Klebsiella pneumoniae, and why is it concerning?

A

Associated with healthy community patients but causes severe infections like liver abscesses.

Hypervirulence linked to enhanced capsules and siderophore production.

Resistance to carbapenems has emerged in hypervirulent strains.

Surveillance is limited, making detection challenging.

29
Q

What is the global distribution of hypervirulent Klebsiella pneumoniae (hyKP)?

A

Found in 43 out of 124 countries.

Two major lineages:

ST23-K1.

ST23-K57.

30
Q

What are the resistance trends for hyKP?

A

Carbapenemase-producing hyKP cases have increased significantly.

Genes detected include blaOXA-48 and blaNDM-1.

31
Q

What has been observed in Ireland regarding hyKP?

A

28 cases of OXA-48-producing hyKP identified over two years.

Associated with hypervirulent ST23 strains.

Cases linked to hospital or long-term care facility stays.

32
Q

What is notable about hypervirulent Klebsiella pneumoniae ST23 in Ireland?

A

14 cases of carbapenemase-producing K1-ST23 lineage detected.

In 2016, 57% of bloodstream infections caused by K. pneumoniae were carbapenemase-producing in China.

Associated with invasive diseases, including liver abscesses and septicemia.

Early identification essential for infection control.

33
Q

What interventions are essential for controlling HCAI and AMR trends?

A

Reinforcement of infection control measures across hospitals.

Ongoing surveillance and improved diagnostic capabilities.

Development of targeted therapies against emerging hypervirulent strains.

34
Q

What future considerations exist for addressing multidrug-resistant organisms?

A

Investments in novel antibiotics and alternative treatments.

Public health initiatives to manage cross-border AMR risks.

Integrated global surveillance systems to track resistance patterns.

4.2 Medical Microbiology (20 decks)

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