Session 4 Flashcards

1
Q

Apply the infection model to a patient presenting with a hospital infection

A

Patient factors:
Extremes of age
Obesity / malnourished
Diabetes
Cancer
Immunosuppression
Smoker
Surgical patient
Emergency admission

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2
Q

What is a healthcare infection?

A
  • Healthcare infections are infections that arise as a consequence of providing healthcare in patients (not just in hospitals – happens whenever and wherever anyone is providing healthcare). But in hospital patients at least:

Neither present nor incubating at time of admission

This means onset is at least 48 hours after admission

  • Also includes infections in hospital workers and healthcare workers (as a consequence of administering healthcare)
  • Frequent; prevalence is ~8% of in-patients
  • Significant Impact on health – can take weeks or months to resolve, delays treatment/cure, can be fatal e.g. Clostridium Difficile
  • Impact on healthcare organisations (financial cost – up to hundreds of thousands of pounds in total e.g. Surgical site infections cos £7600—£22200, ventilator associated pneumonia cost £12600-£16300. Also financial cost to the individual patient – may be out of job for a long period of time, patient’s company loses productivity
  • A large proportion of HCIs are preventable
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3
Q

What are examples of healthcare pathogens?

A

Examples of healthcare infection pathogens:

  • Viruses: blood borne viruses (hepatitis B, C, HIV), norovirus, influenza, chickenpox, Ebola
  • Bacteria: Staph aureus (including MRSA), Clostridium difficile, Escherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, Mycobacterium tuberculosis
  • Fungi: Candida albicans, Aspergillus species
  • People who stay in hospital longer tend to get an infection and people who get a HCI tend to stay in hospital longer (chicken and egg problem)
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4
Q

Why can resistance to antibiotics develop quickly?

A

Bacteria multiple rapidly
Mutations arise regularly
Segments of DNA can transfer by transformation
Genes can be transferred rapidly by bacteriophages, plasmids or other mobile genetic elements

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5
Q

Explain about transformation and conjugation

A
  • Transformation: many bacterial species incorporate naked DNA into their genome e.g. Streptococcus pneumonia and Neisseria gonorrhoeae incorporate small sections of penicillin-binding protein genes from closely related species to produce a penicillin-binding protein that binds penicillin less avidly so becomes more resistant. Such organisms are still able to synthesize peptidoglycan and maintain their cell walls in the presence of penicillin
  • Conjugation: - horizontal gene transfer - bacteria contain plasmids, circular DNA structures that are found in the cytoplasm. Many genes are carried on plasmids including those that encode metabolic enzymes, virulence determinants and antibiotic resistance. Plasmids can pass from one bacterium to another by conjugation allowing ‘resistance genes’ to spread rapidly in populations of bacterial species that share the same environment (e.g. within the intestine). Combined with antibiotic selective pressures (e.g. in hospitals) that favour the survival of organisms with resistance plasmids, multi-resistant populations may develop.
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6
Q

Explain about transposons and integrons

A
  • Transposons and integrons are mobile genetic elements able to encode transposition and move between the chromosome and plasmids, and between bacteria. Many functions, including antibiotic resistance, can be encoded on a transposon. Resistance to methicillin among Staphylococcus aureus and to tetracycline among Neisseria gonorrhoeae probably entered the species by this route. Integrons are important in transmission of multiple-drug resistance in Gram-negative pathogens. Resistance genes can also be mobilized by bacteriophages (viruses that live in bacteria)
  • Multiple resistance can develop on mobile genetic elements because once a gene is established on the element, it can readily acquire resistance to another agent by one of the mechanisms above. Once there is more than one resistance gene, exposure to any of these agents will permit survival of the organism, which increases the risk of further resistance being acquired.
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7
Q

Describe the principles relating to infection control in a hospital setting: The 4 Ps of Infection Prevention and Control

A
  • Patient: general and specific patient risk factors for infections. Interactions with:

Other patients
Healthcare workers
Visitors

  • Pathogen: virulence factors, ecological interactions (with other bacteria and/or antibiotics/disinfectants)
  • Practice: general and specific activities of healthcare workers

Policies and their implementation
Organisational structure and engagement
Regional and national political initiatives
Leadership at all levels from government to the ward

  • Place: healthcare environment e.g. arrangement of rooms, number of beds in bays/wards, carpeting in clinical areas (there should be no carpeting), presence of hand washbasins

Fixed features
Variable features

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8
Q

Explain about patient interventions and halting patient to patient transmission

A

Patient interventions (when commensal normal flora gets into wrong part of the body, this leads to a healthcare associated infection e.g. bacteria from large bowel goes through a perforated appendix into peritoneal cavity): - makes up the majority of HCIs. General (pathogens)

  • Optimise patient’s condition: smoking cessation, optimal nutrition, optimal blood glucose control in diabetics before surgery
  • Antimicrobial prophylaxis (normally given as a single dose in anaesthetic room before surgery)
  • Skin preparation
  • Hand hygiene

Patient interventions: Specific (against a specific pathogen)

  • MRSA screens
  • Mupirocrin nasal ointment
  • Disinfectant body wash

Halting patient to patient transmission

  • Physical barriers: isolation of infected patients (however these patients are often unintentionally seen less often by HCPs), protection of susceptible patients
  • Isolation of infected patients: double door system with a coupling interlocking system
  • Protection of susceptible patients: air filters making air sterile for immunocompromised patients e.g. patient awaiting bone marrow transplant
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9
Q

Explain about healthcare worker interventions

A
  • Healthy: disease free, vaccinated (e.g. flu jab every year)
  • Good practice: good clinical techniques (e.g. sterile non-touch/aseptic non-touch), hand hygiene, personal protective equipment, antimicrobial prescribing
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10
Q

Explain about environmental interventions

A
  • Built environment: space/layout, toilets, wash hand basins
  • Furniture and furnishings
  • Cleaning: disinfectants, steam cleaning (more effective for cleaning of surfaces), hydrogen peroxide vapour (toxic but sterilises room however can’t be done in clinical areas when people are present)
  • Medical devices: single use equipment (normally sterilised by gamma radiation), sterilisation (for re-use, Central Supplies Sterile Department – pressure cooker guarantees sterilisation by destroying spores and reducing bacterial load by a million fold), decontamination. If instrument is going into a sterile site, it needs to be sterilised.
  • Appropriate kitchen and ward food facilities + good food hygiene practice
  • Theatres
  • Positive/negative pressure rooms
  • Immunosuppressed patients
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11
Q

Describe the use of personal protective equipment with regard to infections in a hospital setting

A
  • PPE helps prevent the transmission of infection in the hospital.
  • Don PPE before you have contact with any patient + use carefully – don’t spread any contamination
  • Limit surfaces and items touched
  • Patients, hospital staff and visitors should use PPE when there will be contact with blood or other bodily fluids
  • Gloves
  • Masks – surgical, respiratory (have a tight seal around your nose and mouth and offers protection e.g. from mycobacterium tuberculosis – protects respiratory tract)
  • Eye protection – face shields and goggles
  • Clothing – gowns, aprons, head covering and shoe covers
  • Need to remove and dispose of PPE safely to protect others – immediately use hand hygiene.

Factors influencing PPE selection

  • Type of exposure anticipated (splash / spray versus touch / large volumes of blood or bodily fluids, category of isolation precautions)
  • Durability and appropriateness for the task (e.g. whether a gown needs to be fluid resistant or fluid proof or neither)
  • Fit (Is it right size for individual?)
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12
Q

To appreciate and describe some of the global concerns relating to hospital acquired infections and drug resistance.

A
  • New resistance mechanisms emerge and spread globally threatening our ability to treat common infectious diseases, resulting in death and disability of individuals who until recently could continue a normal course of life
  • Without effective anti-infective treatment, many standard medical treatments will fail or turn into very high risk procedures
  • There are high proportions of antibiotic resistance in bacteria that cause common infections (e.g. UTIs, pneumonia, bloodstream infections) in all regions of the world. A high percentage of hospital-acquired infections are caused by highly resistant bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) or multidrug-resistant Gram-negative bacteria
  • Treatment failures due to resistance to treatments of last resort for gonorrhoea (third-generation cephalosporins) have now been reported from 10 countries. Gonorrhoea may soon become untreatable as no vaccines or new drugs are in development
  • Patients with infections caused by drug-resistant bacteria are generally at increased risk of worse clinical outcomes and death, and consume more healthcare resources than patients infected with the same bacteria that are no resistant.
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13
Q

Describe the characteristics of Clostridium difficile and what antibiotics are associated with it?

A
  • Gram positive, anaerobic, spore forming rods
  • The organism has been linked to a spectrum of intestinal disorders associated with antibiotic treatment, ranging from an asymptomatic carrier state to mild mor moderate watery diarrhoea, to fulminating, life-threating pesuomembranous colitis (PMC – a severe ulcerating disease of the large bowel)
  • It’s harboured in the large intestine of a small % of health humans, where it tends to remain in low numbers.
  • The mode of transmission is via the spore form, which is extremely difficult to eradicate from the environment and is often carried on the hands of healthcare personnel who are caring for multiple patients.
  • Its associated with antibmicrobial drugs. Most symptomatic patients have received an antimicrobial agent in the recent past. Virtually all antimicrobial drugs have been implicated however the most common antimicrobial drugs associated as cephalosporins, ampicillin and clindamycin.
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14
Q

What is the pathogenesis of Clostridium difficile?

A
  • The sequence of events in antibiotic-associated C.difficile diarrhoea begins with suppression of normal flora by the antimicrobial drug, with persistence of the spore form of C. difficile. Clindamycin suppresses the most common type of bacteria in the flora, the anaerobic bacteria; this suppression may explain the strong association of its use with C. difficile diarrhoea. C. difficile is either present already in the flora or is acquired from the hospital environment during antibiotic treatment.
  • At some point during or after antibiotic administration, the spores germinate and the vegetative form of C. difficile grows in large numbers, producing its toxins. When toxin production achieves a critical level in the large bowel, diarrhoea begins. As the disease progresses, PMC may develop
  • The organism produces its toxins in the intestinal lumen and the toxins cause damage to the epithelial lining of the bowel wall. The major toxins are designated A and B. Toxin A causes both fluid production and damage to the mucosa of the large bowel. Toxin B is a cytotoxin that causes rounding up of tissue-culture cells.
  • Toxins A and B are enzymes, which act in the cytoplasm of the host cell to glycosylate small guanosine 5’-triphosphate (GTP)-binding proteins such as Rho and Rac using UDP-glucose as the substrate. Glucosylated Rho and Rac are inactive and the cell loses its cytoskeletal structure and can die as a result.
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15
Q

Describe the treatment for Clostridium difficile

A
  • A mild infection can usually be controlled by withdrawing treatment with the antibiotics causing the infection. More severe cases can be treated using vancomycin and metronidazole.
  • Relapse is common, occurring in around one in four cases and requires further treatment. Life-threatening cases may need surgery to remove a damaged section of the bowel. Severe cases can be fatal, especially when they occur in people who are already very ill. Other treatment may be immunoglobulins (concentrated antibodies) or a new treatment option, faecal transplantation (a sample of faeces from a healthy donor is placed into the colon of a patient using a catheter – limited access to this treatment).
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16
Q

What are the tests for diagnosis of C. difficile? And what kind of prevention can you do?

A

Tests for diagnosis:

  • The standard laboratory diagnosis of the disease detects toxin A in the stool sample of patients using an immunological test called an enzyme-linked immunosorbent assay (ELISA).
  • Blood test measures WBC – a very high level could indicate a more severe form of C. difficile infection. Blood tests can also detect mineral imbalances that can occur as a result of dehydration
  • Colonoscopy/sigmoidoscopy
  • CT scan of colon

Prevention:

  • Healthcare workers: wear gloves and aprons, where possible isolate patients, wash their hands regularly and thoroughly (alcohol gel is not effective against C. difficile spores so regular use of soap and water is essential)
  • Clean and disinfect surfaces that may have come into contact with bacteria or spores such as toilets, loor, bedpans and beds
  • Visitors: follow hand washing advice and avoid healthcare environments if you are feeling unwell or have recently had diarrhoea
17
Q

Describe the characteristics of Staphylococcus aureus and its pathogenesis

A

Asymptomatic carriage of S. aureus is found in up to 40% of healthy people in the nose, skin, axilla or perineum. This is important in healthcare workers especially if they carry an invasive or resistant strain (e.g. MRSA)
Pathogenesis:

  • Coagulase: converts fibrinogen to fibrin which may form a protective barrier
  • Adhesion molecules: binds fibronectin and collagen which assists adherence
  • Lytic enzymes: lipase which breaks down host tissue
  • Protein toxins: Panton-Valentine leucocidin (PVL) toxin => tissue damage, Toxic shock syndrome toxin (TSST) andenterotoxins – lead to shock and toxicity

Can cause infectious syndromes such as impetigo (primary skin infection, transmitted from person to person), secondary skin infections (associated with eczema, surgical wounds, intravenous devices burns), pneumonia (rare but may follow influenza), endocarditis (can be rapid and destructive; associated with intravenous drug isuse or colonization of intravenous devicies), Osteomyelitis, Septic arthritis

18
Q

Explain about MRSA and transmission

A
  • S. aureus can be cultured on most laboratory media. Phenotypic identification depends n demonstrating coagulase, catalase enzymes and typical ‘cluster of grapes’ morphology.
  • Methicillin-resistant S. aureus (MRSA) is caused by possession of the mecA gene which codes for a penicillin-binding protein that binds the drug less well. Glycopeptides such as vancomycin or teicoplanin are required for those strains.
  • Glyopeptide-resistant strains (GRSA) have resistance because of the vanA vanB genes required from enterococci.
  • Other antibiotics that remain effective include linezolid, aminoglycosides, erythromycin, clindamycin, fusidic acid, chloramphenicol and tetracycline
  • In methicillin-sensitive strains, first- and second-generation cephalosporins are effective.
  • S. aureus spreads by airbone transmission and via the hands of healthcare workers. Patients colonized or infected with MRSA or GRSA should be isolated in a side room with wound and enteric precautions (dedicated hand-washing and toilet facilities, disposable aprons and gloves, disinfection, handwashing afterwards etc)
  • Staff may become carriers and disseminate the organism widely in the hospital environment. Carriage may be eradicated by using topical muprocin and chlorhexidine.
19
Q

Describe the characteristics of norovirus

A
  • Single-stranded RNA non-enveloped virus.
  • Faecal-oral transmission, person-to-person contact and via aerosolization of the virus and subsequent contamination of surfaces
  • Highly contagious, affects all ages and most common cause of viral gastroenteritis
  • Incubation period lasts between 12 and 48 hours. Not usually dangerous and no specific treatment available.
20
Q

How would you go about preventing norovirus?

A

Preventing norovirus spreading (patient):

  • Wash hands frequently
  • Don’t share towels and flannels
  • Disinfect surfaces that an infected person has touched (outbreaks are common because the virus can survive for several days on surfaces or objects touched by an infected person). Best to use a bleach-based container.
  • Was any items of clothing or bedding that could have been contaminated. Wash the items separately and on a hot wash to ensure the virus is killed.
  • Flush away any infected faeces or vomit in the toilet, and clean the surrounding area
  • Avoid eating raw, unwashed produce and only eat oysters from a reliable source. Oysters have been known to carry the norovirus
  • Avoid visiting hospitals if you have the symptoms
  • If infected, avoid preparing food and direct contact with others for at least 48 hours after symptoms disappear

Preventing norovirus (HCPs):

  • Follow handwashing techniques carefully
  • Remove and wash contaminated cloting or linens
  • If you have symptom, you should not work
  • Disinfect routinely high touch patient surfaces and equipment
  • Use gowns and gloves when in contact with, or caring for patients who are symptomatic with norovirus
  • Should be isolated or put in rooms with other patients with the same infection
21
Q

List some facts about Streptococcus pneumoniae

A
  • Aerobic Gram positive, seen in pairs – typically alpha-haemolytic but can be variable
  • Has a polysaccharide capsule that protects it from phagocytosis
  • Pathogenesis: pro-inflammatory cell wall components e.g. C-polysaccharide, F-antigen; IgA2 protease; pneumolysin – a cytotoxin that stimulates immune responses; adhesins that bind to cell surface carbohydrates (e.g. choline binding protein A, pneumococcal surface protein A); tissue damaging enzymes (e.g. neuraminidase, hyaluronidase)
  • Carriage is usually asymptomatic – most common in the young or smokers, associated with overcrowding
  • Over 90 highly antigenic capsular serotypes and antibodies to specific types are protective
  • Children under 1 year of age are vulnerable to acute pneumonia.
  • Complement deficiency, HIV infection, smoking, alcoholism and splenectomy predispose to severe infection. The bacteria are able to adhere to pneumocytes and invade the bloodstream by hijacking the platelet-aggregating factor receptor pathway and produce complement-mediated damage to the alveolus through the action of pneumolysin.
  • Acute otitis media, sinusitis and acute pneumonia are the most common infections – cause between 50 and 75% of community-acquired pneumonia, up to 25-30% of which may develop bacteraemia (important complication with a high mortality despite treatment). Direct or haematogenous spread can give rise to meningitis.
  • Significant numbers of S. pneumonia have developed resistance through a genetically modified penicillin-binding protein gene.
  • Susceptible to erythromycin, cephalosporins, tetracycline, rifampicin and chloramphenicol but multiple drug resistance is going. Where high-level penicillin-resistance occurs, a glycopeptide (usually vancomycin) should be added.
22
Q

What should you do next?

A

LOOK OVER WEEK 4 Case Study Lecture AND NOTES!!!