Lecture 10-Hospital Acquired Infection & Antimicrobial Resistance

Hospital Acquired Infection (HAI) or Nosocomial Infection

an infection acquired in hospital that was not present or incubating at admission

Why do infections occur in hospitals?

1. Many vulnerable, sick people are treated in close surroundings so spread easily

2. Common procedures increase the risk of infection, eg. catheterisation, surgery, immuno-suppressive drugs, antibiotics

Risk Factors for Nosocomial Infection

• Health Status

  • Advanced age

  • Malnutrition

  • Alcoholism/smoking

  • Diabetes

• Invasive Procedures

  • Endotracheal intubation

  • Bladder catheter

  • Intravenous catheter

• Treatment

  • Immunosuppression

  • Operative procedures

  • Feeding via a drip

  • Length of stay

Entry of Organisms in a Nosocomial Infection

• Colonisation of GI tract

• Breech of barriers – skin

• Ingestion

• Inhalation

• Environmental contact

Sources of Hospital Acquired Infections

• Contaminated Hospital Environment

• Patient Flora

• Medical Personnel

• Invasive Devices (Catheters, ET tubes, etc.)

Majority of HAI are

• Bloodstream infections (BSIs) including IV catheters

• Urinary Tract Infections (UTIs) or Catheter Associated UTIs (CAUTIS)

• Surgical Site Infections (SSIs)

• Pneumonia including Ventilator Associated Pneumonia (VAP)

• Gastroenteritis including C. diff

Bad Bugs

problematic pathogens that “eskape” the activity of antibiotics

ESKAPE

• E nterococcus faecium / VRE

• S taphylococcus aureus / MRSA

• K lebsiella pneumoniae

• A cinetobacter baumannii

• P seudomonas aeruginosa

• E nterobacteriaceae / E. coli

What is inadequate antibiotic therapy associated with?

poor outcome and emergence of bacterial resistance

Antibiotics process

• Appropriate and early treatment improves chance of success.

• However, empirical use is often necessary as lab results take up to 48 hours

• So initial therapy often involves a broad-spectrum drug. These induce resistance rapidly!

• When results come in then specifically tailor treatment to pathogen and resistance profile.

Consequences of Antimicrobial Resistance

• Mortality: resistant infections = more fatal

• Morbidity: prolonged illness, greater chance of resistant organism spread

• Cost: increase cost of care & newer/more expensive drugs

• Limited Solutions: few new drugs being made

MRSA

Methicillin-Resistant Staphylococcus Aureus

Preventing MRSA

• Screening – identify carriers; nasal swabs; staff! Care when colonised people sent back into the community – build up – readmitted and overwhelms.

• Hand washing – scrupulous hygiene; laundry; instruments; equipment.

• Isolation – exclusion until cleared; contact isolation in hospitals.

• Restricting antibiotic usage – some antibiotics are associated with increased risk of colonisation eg. quinolones.

• Decolonisation – remove carriage.

• Agricultural practice – prevent or limit use in farming

Antibiotic Associated Colitis (AAC)/Pseudomembranous Colitis

severe condition of the colon caused by Clostridioides difficile

• Results in local tissue inflammation as a complication of antibiotic therapy

Risk Factors for AAC

• Existing illness

• Antibiotic usage

• Elderly age

• Recent surgery

• History of AAC

Clostridioides

• Large

• Gram positive rods

• Anaerobes

• Spores survive exposure to air

What two toxins does C. Diff release into the colon?

1. Enterotoxin (toxin A)

2. Cytotoxin (toxin B)

C. Diff Enterotoxin

• induces inflammatory response

• Hypersecretion of fluid

• haemorrhagic necrosis

C. Diff Cytotoxin

• causes actin to depolymerise

• destruction of cellular cytoskeleton

When does C. Diff reach cytotoxic levels?

when it is the predominant organism

What happens to the lining of the colon during a C. Diff Infection

• Denudation

• Haemorrhagic

AAC Pathology

• small white/yellow plaques that, with time, enlarge and develop a haemorrhagic border

• epithelium become necrotic and slough off forming a pseudomembrane with inflammatory exudate

AAC Symptoms

• Fever

• diarrhoea

• abdominal distension/pain

AAC Diagnosis

• made on the basis of a history of antibiotic therapy within the past month and on the clinical symptoms

• Colonoscopy revealing the classical pathology (pseudomembrane) can add weight to the diagnosis.

  • The faeces can be tested for the presence of the etiological agent and/or the presence of toxin A.

Transmission of C.Diff

• Faecal oral route

• hands of people who come into contact with infected individuals/surfaces

C. Diff Spores

• produced when C. Diff bacteria encounter unfavorable conditions

• Survive on clothes/surfaces for long periods

• Resistant to hand sanitizer and routine cleaning

Reduction of C.Diff due to

• Raised awareness due to mandatory reporting as of 2004

• Reinforced infection prevention/control measures

• Enhanced surveillance and screening

• More prudent antibiotic use

• Improved diagnostics

• Better epidemiological tracking (including ribotyping)

3 Types of Antibiotic Resistance

1. Natural/Intrinsic

2. Mutational Acquired

3. Extrachromosomal Acquired

Natural/Intrinsic Resistance

Resistance to a drug prior to exposure

• Ex: low permeability of wall/membrane to drugs

Mutational Acquired Drug Resistance

Resistance develops in response to exposure to a drug

Extrachromosomal Acquired Resistance

(Disseminated by plasmids, transposons or other DNA) - Resistance develops in response to exposure to a drug

Aquired Resistance is driven by 2 genetic processes in bacteria

1. Mutation and Selection (Vertical evolution)

2. Exchange of genes between strains and species (horizontal evolution)

Why are antibiotic resistant bacteria “selected for” in nature so rapidly?

Bacteria are small → small volumes = large numbers of bacteria → lots of chances for mutation

Mutation

Any heritable change in the nucleotide sequence of DNA

• Substitutions

• Insertions

• Deletions