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year 4 CDM 2 > Case 12: Infection general > Flashcards

Case 12: Infection general Flashcards

1
Q

Pathophysiology of a fever

A
  • Pyrogens (Prostaglandin E1) causes raising of thermostatic set point in the Hypothalamus
  • Temperature raising response: Vasoconstriction, shivering, Piloerection, increased metabolism
  • Fever
  • Core body reaches new set point
  • Temperature reducing response: vasodilation, sweating, increased ventilation
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2
Q

Pyrogenic activators

A
  • Infectious factors: Gram- bacteria (Lipopolysaccharide (LPS)/Endotoxin), Gram+ bacteria (Exotoxins/Peptidoglycans), viruses
  • Non-infectious factors: Antigen-antibody complexes, complement, Non-infectious chemical irritants, Drugs (antibiotics, steroids, chemotherapy agents)
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3
Q

Endogenous pyrogens (released from cells within the body)

A
  • Fever inducing cytokines: TNF, IL-1, IL-6, IFN
  • Derived from: mononuclear cells, macrophages, T-lymphocytes, Kupffer cells, endothelial cells, Tumour cells
  • Can be released due to exogenous pyrogens, chemicals or tissue damage
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4
Q

Classical fever patterns: sustained and intermittent

A
  • Sustained: body temperature sustained as high (variation only 0.5 degrees)- seen in parenchymal or interstitial tissue inflammation (pneumonia, UTI, typhoid fever)
  • Intermittent- wider variation of temperature, swings between normal and feverish in <24hr. Assoictated with abscess’s, empyema, intermittent septimaemia
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5
Q

Classical fever patterns: Remittent, Relapsing

A
  • Remittent- significant variation in temperature in rapid fashion, baseline however doesn’t return to normal. Seen in IE
  • Relapsing- Intermittent pattern before resolution of fever and then fever returning. Cycle of fever to non-fever is >24 hours. Seen in malaria and other intracellular infections
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6
Q

Pyrexia of unknown origins

A
  • Sustained or recurrent pyrexias for ≥3 weeks
  • No identified cause after evaluation: in hospital for 3 days, ≥3 outpatient visit
  • Categories: classic, Nosocomial, Immunodeficient, HIV
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7
Q

Causes of classic FUO (fever of unknown origin)

A
  • Infection: abscess, infective endocarditis, tuberculosis, complicated UTI
  • Geography/travel: Meliodosis, visceral leishmaniasis, amoebic abscess
  • Connective tissue young: Still’s/JRA
  • Connective tissue adult: RA, SLE
  • Connective tissue elderly: GCA, PMR
  • > 60: malignancy and CTD are more important
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8
Q

Nosocomal FUO

A
  • Hospitalised for >48 hours
  • No infection present or incubating at admission
  • Diagnosis uncertain after ≥3 days of appropriate evaluation
  • (Microbiological cultures incubated for ≥2 days)
  • Causes: Catheters/devices, Thrombophlebitis, UTI/RTI, Drug fevers, C.Diff (normally secondary to antibiotics), ICU (ventilators, ET tube, NG tube), stroke
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9
Q

FUO immunodeficiency

A
  • Cell-mediated immunodeficiency: Congenital, Biologic/ immunomodulatory therapies
  • Neutropaenia mediated immunodeficiency: Haematological disorders (lymphoma, leukaemia), Chemotherapy, < 500 neutrophils/µl
  • Findings: blunted ‘typical’ inflammatory response (difficult to localise things), there will be a lack of radiological changes
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10
Q

FUO in HIV

A
  • Primary HV infection ‘Seroconversion illness’
  • AID’s: PCP, Myobacterial, Toxoplasmosis, CMV, Lymphoma
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11
Q

Fever/Pyrexia of unknown origin (FUO/PUO)

A
  • Fever for > 3 weeks
  • Adequate routine investigation
  • No diagnosis
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12
Q

FUO: Labratory

A
  • Blood cultures
  • Blood-borne viruses (BBV) – HIV/HBV.HCV
  • Blood films – cells, parasites
  • Serology
  • FBC – differential
  • U+E/LFT/bone chemistry
  • TFTs
  • Inflammatory markers – CRP, ESR, ALP
  • Auto-antibodies – ANA, dsDNA
  • Stool, urine, sputum, swabs
  • Ascitic/pleural/synovial fluid
  • Bone marrow
  • Biopsy
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13
Q

FUO imaging

A
  • CXR
  • US – liver/spleen
  • Cross-sectional CT
  • HRCT
  • CT PET
  • Labelled white cell scan (scintigraphy)
  • Bone scan
  • MRI
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14
Q

Healthcare associated infections (HCAI’s)

A

Develop either as a direct result of healthcare interventions such as medical or surgical treatment, or from being in contact with a healthcare setting. Generally a preventable harm

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15
Q

Preventing HCAI’s

A
  • Appropriate infection control and good hygiene (washing hands)
  • Safe prescribing and antimicrobial stewardship
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16
Q

What’s included in HCAI’s

A
  • As a direct result of treatment in, or contact with, a health or social care setting
  • As a result of healthcare delivered in the community
  • Outside a healthcare setting (for example, in the community) and brought in by patients, staff or visitors and transmitted to others (for example, norovirus).
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17
Q

Risk factors for HCAI’s

A
  • MRSA: Recent hospitalisation, Use of broad-spectrum antibiotics
  • C.difficile: Recent hospitalisation, Use of broad-spectrum antibiotics, Use of PPI (omeprazole)
  • CPE: Recent hospitalisation in a high risk area (Greece)
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18
Q

Examples of HCAI’s

A
  • C.difficile
  • MRSA
  • CAUTI
  • MSSA bacteraemia
  • Indwelling catheter (line) related infections
  • HAP and VAP
  • Surgical site infections
  • GI infections eg. norovirus as part of an outbreak
  • Candida auris
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19
Q

Burden of HCAI’s

A
  • Increased mortality
  • Increased morbidity
  • Increased length of stay
  • Increased risk of antimicrobial resistance
  • Staff sickness (outbreaks, BBVs)
  • Indirect and direct financial costs
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20
Q

Investigations for HCAI

A
  • Blood tests: FBC, U&E, LFT, CRP
  • Microbiology: Blood culture, urine culture, stool culture (C.diff testing), MRSA and CPE screen
  • Abdominal X-ray: for obstruction
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21
Q

General management for MRSA

A
  • Isolation and barrier nursing – contact and enteric precautions
  • MRSA decolonisation – topical skin washes +/- nasal and throat decolonisation
22
Q

Infection control legislation

A
  • Health & Safety at Work Act 1974: covers occupational health
  • COSHH (Law on the Control of Substances Hazardous to Health)
  • Workplace Regulations
  • Building Regulations
  • HTM’s (health technical memoranda): advise about the design and installation of healthcare buildings (ventilation, water)
  • HBN’s (health building note): notes detailing a project from start to finish about infection control
23
Q

Water born infections which can occur in hospitals

A
  • Legionella and Pseudomonas
  • High risk groups: Immunocompromised, children, burns, ICU
  • Areas at risk: type of taps, sinks. Areas with low use (not flushing pipes, taps), Redundant piping
  • Monitored by taking water samples
24
Q

Ventilation principles

A
  • Ventilation is a means of removing and replacing the air in a space- prevents airborne transmission
  • Dilution of contaminants: opening window
  • Clean airflow path: negative pressure rooms (remove more air then is allowed in)- isolate patients with infection. Positive pressure rooms- protect neutropenic patients. Ultra clean ventilation is done for joint replacement
  • Control of Hazards: extraction of fumes and excess moisture
  • Comfort

Airborne spread pathogens: TB, Measles, Chickenpox

25
Q

Critical areas for ventilation

A
  • Surgical Operating departments
  • Aseptic Pharmacies (production)
  • UCV Theatres
  • Burns units
  • Laboratories
  • Obstetrics / Maternity departments
  • Isolation rooms / wards (both +ve & -ve)
  • Laser Surgical units
  • Imaging units (CT, MRI, X- Ray, etc.)
26
Q

MRSA

A
  • Meticillin Resistant Staphylococcus aureus (gram positive)
  • S.aureus which is resistant to Meticillin, flucloxacillin, also resistant to other antibiotics in the Beta-Lacta class (Co-amoxiclav, cephaloxin, tazocin).
  • Can be resistant to other antibiotics
27
Q

MRSA in hospital

A
  • Will have to use different antibiotics, wear PPE, isolate patient, try to decontaminate etc
  • Spreads from person to person and is more common in healthcare settings
  • Antibiotics which are used in MRSA infections: Vancomycin, Teicoplanin
28
Q

MRSA eradication

A
  • If found on nose swab: nasal mupirocin 2% in white soft paraffin
  • If found on skin: Chlorohexidine wash
  • MRSA is cleared after 3 negative tests 1 week apart
29
Q

CPE

A
  • Carbapenemase Producing Enterobacterales (gram negative)
  • Enterobacterales are a group of Gram negative bacteria that live in the gut eg E coli, Klebsiella
  • Resistant to carbapenems and beta-lactam antibiotics and most antibiotics (multi-resistant). Often only 1-2 antibiotics which work
  • Spreads from person to person
  • Areas where CPE is common- London, Manchester, abroad hospitals
30
Q

How is MRSA screening performed

A
  • Charcoal swabs for: Nose (both nostrils), Throat (back of throat), Groin (perineum), Any wounds or device sites, CSU if catheterised
  • Nasal swab most important: done for 5s
  • Swabs are plated on agar and appear green
31
Q

How is CPE screening performed

A
  • Rectal swab or stool sample: Stool is better but harder to collect
  • Red topped swab – for PCR (only the 5 most common resistant genes- specific) and lateral flow (5 genes)
  • Charcoal (black topped) swab – for culture (sensitive)
  • Different hospitals ask for different numbers of swabs spaced apart (often 48 hours)
32
Q

C.difficile

A
  • Clostridioides difficile is an anaerobic, gram positive, spore-forming bacteria. Found in the guts of healthy people
  • Causes infection when there is disruption to the normal microbiological flora i.e. broad spectrum antibiotics
  • Mode of transmission: ingestion of bacteria or spores
33
Q

Risk factors for C.difficile

A
  • Broad-spectrum antibiotic use i.e. cephalosporin, clindamycin, quinolones
  • Acid supressing medications (PPIs)
  • Increasing age
  • Hospitalisation
  • Underlying morbidity particularly immunosuppression
  • Inflammatory bowel disease
  • C.difficile strains associated with severe disease- eg. type 027
  • Exposure to other patients with C.difficile and/or contaminated environment (including the hands of HCWs)
34
Q

C.difficile symptom presentation

A

Symptoms can range from self limiting diarrhoea to pseudomembranous colitis, toxic megacolon, perforation and death. Disease is caused by toxins of C.diff which damage the colon linning

35
Q

Symptoms of C.diff

A
  • Severe gastroenteritis
  • Profuse watery diarrhoea
  • Abdo pain
  • Fever
  • Characterised by raised WCC
36
Q

Indicators of C.diff severity

A
  • WCC >15
  • Acutely rising serum creatinine (AKI)
  • Fever >38.5
  • Evidence of severe colitis (clinical peritonitis, radiological changes)
37
Q

C.diff treatment

A
  • First line: oral vancomycin for 10 days
  • Recurrent: if <12 weeks of symptom resolution then oral Fidaxomicin, if >12weeks oral vancomycin or fidaxomicin
  • Mild-moderate: oral or IV Metronidazole
  • Life threatening: IVIG with combination of IV metronidazole and oral vancomycin +/- surgical management
  • Faecal transplant in recurrent disease
  • Colectomy if toxic megacolon
38
Q

Conservative treatment of C.diff

A
  • Barrier nurse in side room- enteric precautions,
  • deep clean of room after discharge
  • stop any antibiotics that may have caused it
  • review need for PPIs and H2 agonists
  • supportive management e.g. hydration
  • 48hr isolation
  • IV fluids
39
Q

Staging of C.diff

A
  • Mild: normal WCC
  • Moderate: raised WCC (<15), 3-5 loose stools per day
  • Severe: raised WCC (>15), increased creatinine (>50% above baseline), Temp >38.5, severe colitis
  • Life threatening: hypotension, partial or complete ileus, Toxic megacolon, CT evidence of severe disease
40
Q

C.diff complications and prevention

A
  • Complications: Dehydration, AKI, Electrolyte Imbalance, Pseudomembranous colitis, Toxic megacolon, Colonic perforation, Peritonitis
  • Prevention: Antimicrobial stewardship, review of PPI’s/H2 antagonists (particularly if on antibiotics), infection control
41
Q

C.diff diagnosing

A
  • Stool sample: GDH, PCR, toxin
  • U&E’s might show dehydration, electrolyte imbalance, AKI
  • Results: Not detected, C.diff carrier (bacteria but no toxins), C.diff toxin (active disease)
42
Q

Indications for catheter

A
  • Catheters are always colonised with bacteria, doesn’t mean they are infected
  • Urinary retention
  • Bladder outlet obstruction: Enlarged prostate or blood clots
  • Clinically ill: adequate fluid balance
  • End of life
  • Abdo wounds
  • Strict immobilised like pelvic fractures
  • Peri-operatively: short term catheterisation for surgery
43
Q

CAUTI- clinical disease

A
  • Can be difficult to diagnose: the catheter mean there’s no frequency or dysuria
  • New onset or worsening of fever, rigors, altered mental status, malaise, or lethargy
  • Flank/loin pain, pelvic discomfort, costovertebral angle tenderness
  • Acute haematuria
  • Risk of progressing to urosepsis
  • Biofilm forms on catheter which can be a source of infection
44
Q

Purple bag syndrome

A

Where urine in catheter bag appear purple. Due to accumulation of dietary tryptophan due to reduced GI transit i.e. constipation. Caused by Providencia spp, does not indicate UTI but should do a full examination and look for constipation.

45
Q

CAUTI diagnosis

A
  • No dipstick (will always be positive with catheter)
  • Urine cultures: after TWOC/catheterisation or from the catheter port site (not catheter bag)
  • Don’t treat if asymptomatic
  • Blood cultures (if abnormal temperature/systemically unwell): do before starting antibiotics
  • Discuss with Micorbiology about sensitivity
46
Q

CAUTI treatment

A
  • Catheter removal or change. Can do a TWOC if long term catheter
  • Antibiotics (only if you have to keep the catheter in): based on urine culture or local guideline. 7 days course
  • If systemically unwell: IV antibiotics for urosepsis post blood culture
47
Q

CAUTI prevention

A
  • Avoid catheters: collect urine with carboard urine pot
  • Insertion using good aseptic technique
  • Unobstructed flow – no kinks in tubing, keep the bag secured below the level of the bladder to avoid backflow, empty drainage bag when necessary
  • Encourage mobilisation, recognise and treat dehydration, resolve constipation, encourage good hygiene
  • Removal of catheter when no longer required
  • Routine catheter changes for long term catheters
  • Not routinely offered antibiotic prophylaxis for CAUTI unless lots of previous infection. Never offer long term antibiotic prophylaxis
48
Q

Basic bacterial morphology

A
  • Cocci (round) clusters i.e. Staphylococcus
  • Cocci chain or pairs i.e. Streptococci
  • Bacilli (rods): Pseudomonas, Enterobacter, Proteus
  • Coccobacili (rods that are shorter and more curved): i.e. E.Coli
  • Spirochetes i.e. Treponema syphilis, Lyme disease
49
Q

Importance of Gram stain

A

Identifies if its gram negative or positive and the morphology (shape). Can have results 12-36hrs before identification and sensitivities on this basis can prescribe appropriate antibiotics

50
Q

Sensitivity testing

A

What antibiotic at what concentration prevents growth? Is it over the threshold value? E tests will show the MIC (minimum value of antibiotic which works)

51
Q
A

year 4 CDM 2 (39 decks)

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