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Acute Infection Flashcards

1
Q

What would a sustained fever point to?

A
  • interstitial parenchymal infections
  • e.g. pyelonephritis or pneumonia
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2
Q

What would intermittent fever point towards?

A
  • abscesses
  • empyemas
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3
Q

What would a remittent fever point towards?

A
  • there is quite a bit of variation but it never returns to baseline
  • examples include
    • infective endocarditis
    • blood stream infections
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4
Q

What would relapsing fever point towards?

A
  • points towards intracellular infections like malaria, parasitic infections and (? rickettsial diseases)
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5
Q

What are the most common causative agents of viral encephalitis?

A
  • herpes simplex virus 1 (HSV-1) - 19%
    • absence or presence of cold sores does not predict HSV-1 encephalitis
  • VZV (5%)

Other important causes include:

  • imported viral infections e.g. Japanese B encephalitis
  • other infections - TB
  • acute disseminated encephalomyelitis - triggered by infetion or vaccination
  • antibody mediated autoimmune encephalitis e.g. anti-NMDA, anti-VGKC antibodies

(cause not found in 4 in 10 cases)

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6
Q

What are the clinical features that suggest encephalitis?

A
  • classical symptoms
    • fever
    • headache
    • reduced conscious level
    • personality or personality change
    • new onset of seizures
  • BUT - diagnosis is often delayed
    • fever not always present
    • personality change often attributed to delirium/intoxication
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7
Q

Tips for diagnosing encephalitis:

A
  • a high index of clinical suspicion is key
  • in a patient with fever and headache encephalitis is suggested by
    • ​seizure
    • focal neurological signs
    • neuropsychiatric features
  • a reduction in the Glasgow coma scale is a crude marker of confusion
    • need collateral history to establish a baseline and pickk up more subtle symptoms
    • perform full neurological examination including mental state examination
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8
Q

How would you investigate viral encephalitis? (gold standard/key for diagnosing)

A
  • lumbar puncture
    • general findings:
      • white bloods cells up (lymphocytes)
      • protein up
      • glucose equal to serum reading
    • specific tests
      • PCR on CSF for HSV1 and 2, VZV and enteroviruses
    • clinical features allow differentiation from viral meningitis
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9
Q

What other diagostic tests (apart from LP) would you want to do if you have ? viral encephalitis?

A
  • neuro-imaging
    • MRI can show evidence of brain parenchyma inflammation
  • other tests
    • EEG - especially to rule out subtle motor seizures or non-convulsive status epilepticus
    • HIV test - wider investigations are required in immune compromised patients
    • if relevant travel history - serology and PCR for other neurotropic viruses
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10
Q

Does a negative HSV-1 CSF PCR exclude encephalitis?

A
  • approx. 10% of patients have an initial negative lumbar puncture
  • if clinical suspicion remains, consider a repeat LP at 24-48hours
  • HSV can be excluded if:
    • HSV PCR in the CSF is negative on TWO occasions 24-48 hours apart, and MRI is normal
    • HSV PCR in the CSF is negative ONCE >72 hours after neurological symptom onset, with unaltered conciousness, normal MRI (performed >72 hours after symptom onset) and a CSF white cell count <5 cells/mm3
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11
Q

What is the treatment of HSV encephalitis?

A
  • general
    • supervision and reassurance
    • fluid and hydration
    • feeding
    • treat complications e.g. seizures
  • anti-viral therapy
    • do not delay starting treatment if there is clinical suspicion
    • intravenous aciclovir 10mg/kg three times daily
    • 14-21 day course is required
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12
Q

What is the prognosis of HSV encephalitis?

A
  • mortality
    • no treatment ~70% die
    • treatment: 10-20% dies
    • worse outcomes with delayed treatment >24 hours
  • acute complications
    • venous sinus thrombosis
    • status epilepticus
    • stroke
    • aspiration pneumonia
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13
Q

What is the long-term morbidity of HSV encephalitis?

A
  • often life-changing
  • ~60% survivors are left with a permanent neurological disability
  • specialist neuro-rehabilitation may be required
  • problems include:
    • inappropriate behaviour/poor social skills
    • fatigue/sleep disturbance
    • epilepsy
    • hormone problems
    • sexual dysfunction
    • inability to understand
    • personality changes
    • emotional problems
    • physical difficulties
    • memory problems
    • problems with new learning
    • problems with pain and other sensations
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14
Q

Bacterial meningitis:

What different causes need to be considered more specifically in the elderly, neonates and those who are immunocompromised?

A
  • listeria
    • consumption of unpasteurised dairy products
      • listeria monocytogenes should be considered particularly in the elderly and those who are immunosuppressed
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15
Q

What are the common causes of bacterial meningitis?

A
  • streptococcus pneuomiae (pneumococcal meningitis)
  • neiserria meningitidis (meningococcal meningitis)
  • haemphilus influenzae
  • listeria monocytogenes
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16
Q

What are the clinical features of bacterial menigitis?

A
  • classical features include:
    • Headache
    • fever
    • neck stiffness
    • altered mental status
  • BUT absence of these features does not exclude meningitis
    • 2+ of these symtpoms are present in 95% of cases
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17
Q

What are the clinical signs that suggest meningitis?

A
  • neck stiffness test (test in supine patient)
    • Kernig’s
      • flex hip nad extend knee
      • positive = pain in back and legs
    • Brudzinski’s sign
      • passively flex head
      • positive = flexion at hips to life legs
    • Very poot sensitivity but good specificity (s cannot be used to rule out meningitis but presence makes meningitis very likely)
  • Rash
    • non-blanching purpuric rash suggests meningococcal sepsis
    • only present in ~2/3 of cases
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18
Q

What factors suggest a poor prognosis from meningitis?

A
  • disseminated intravascular coagulation
    • rapidly progressive rash
  • severe sepsis/septic shock
    • poor cap refill, oilguria and systolic BP<90
    • resp rate <8 or >30
    • PR <40 or >140
    • Acidosis pH <7.3 or BE worse that -5
    • WBC <4
  • raised ICP
    • marked decrease in conscious level or fluctuating
    • focal neurology
    • persistent seizures
    • bradycardia and hypertension
    • papilloedema

Urgent senior review and critical care assessement required

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19
Q

What are the investigations to confirm meningitis?

A
  • Blood tests
    • FBC, U&Es, LFTs, coag, CRP, lactate and blood cultures
    • consider 16SPCR (s. pneumoniae and N. meningitidis)
  • LP
    • tests to identify the pathogen
      • gram stain and culture
      • PCR - viruses, S.pneumonia, N.meningitidis
  • Brain imagaing is not usually required prior to LP unless signs of ICP
    • new onset or recent seizures
    • papilloedema
    • focal neurological deficit
    • reduced or deteriorating conscious level (GCS<12)
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20
Q

What would you find on LP for viral vs bacterial causes?

A
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21
Q

What is the management of suspected bacterial meningitis?

A
  • A-E assessment and sepsis 6
  • Antibiotic therapy
    • Pre-hospital
      • only in patients with signs of meningococcal sepsis e.g. non-blanching rash
      • IM benzylpenicillin or ceftriaxone
    • Hospital
      • abx given within 1 hour of arrival if meningitis or sepsis suspected
        • ideally immediately after LP and blood cultures
      • standard sepsis abx not used in this scenario as need ones that can cross the blood brain barrier i.e. 3rd gen cephalosporins generally used
        • Cefotaxime/ceftriaxone (or chloramphenicol if penicillin allergy)
        • duration of therapy depends on causative organism
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22
Q

If meningococcal septicaemia suspected in patient with penicillin allergy in GP, would you still give the antibiotics?

A

Yes, only omit this treatment if there is a clear history of anapylaxis. If there is a history of a rash after penicillin, this is not a contraindication.

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23
Q

Is there a role for steroids in treating bacterial meningitis?

A
  • steroids may mitigate the excessive inflammatory response thought to cause adverse events in patients with meningitis
  • evidence
    • cochrane review suggests that steroid treatment is associated with
      • modest reduction in mortality in pneumococcal meningitis
      • reduction in risk of hearing loss
  • Current UK guidelines
    • start dexamethasone ideally shortly before but certainly within 12 hours of the first dose of antibiotics
    • continue for 4 days only in cases where pneumococcal meningitis is confirmed or though probable
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24
Q

Prognosis for bacterial meningitis?

A
  • mortality
    • meningococcal infection
      • 4-8% in children
      • 7% in adults
    • pneumococcal infection
      • 8% in children
      • 20-37% in adults
  • significant morbidity causing problems such as
    • deafness
    • cognitive impairment
    • focal neurological deficits
    • epilepsy
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25
Q

Is there a role for post-exposure prophylaxis?

A
  • only recommened for meningococcal infection
  • aim - to eradicate nasal carriage of N. meningitidis
  • offered to:
    • close contacts - living in same house or sharing kitchen in halls of residence
    • high risk exposure - exposed to airway secretions e.g. intubation or CPR (thereofre some staff may need treatment)
  • recommmended treatment
    • ciprofloxacin oral for a single dose
    • rifampicin oral for 2 days
    • ceftriaxone IM inhection for a single dose
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26
Q

Has vaccination affected the incidence of bacterial meningitis in the UK?

A
  • UK infants are routinely vaccinated against:
    • haem influenzae B - previously one of the leading causes
    • meningitis ACWY
    • meningitis B
    • strep pneumoniae
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27
Q

Viral meningitis:

A
  • viruses are the most common cause of meningitis in the UK
    • enteroviruses > HSV 1&2 > VZV
      • enteroviruses - think of this particularly if viral meningitis develops after vomiting bug
  • difficult to reliably differentiate from bacterial meningitis on the basis of clinical assessment
  • LP is diagnostic
    • lymphocytosis with relatively normal protein and glucose
    • virus detection by PCR on cerebrospinal fluid
  • self-limiting and managed supportively
    • no evidence for benefit of anti-viral treatments
  • causes significant long-term morbidity
    • particularly fatigue, headaches, slowed thinking and mood disturbance
    • effects can last for many months
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28
Q

What are the common and important risks of a lumbar puncture?

A
  • common
    • back pain, shooting pain down legs at time of procedure (occurs if off centre and patients need to notify you if they are experiencing any of these symptoms), localised bleeding
  • rare (<1%)
    • persistent headache (due to persistent leak of CSF), infection, lower limb weakness
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29
Q

How do you counsell a patient getting a lumbar puncture?

A
  • Explain the procedure
    • A ‘spinal tap’ that involves using a needle to obtain a sample of the fluid surrounding the brain and spinal cord from a space between vertebrae in the lower back
  • Describe the likely benefits
    • To aid diagnosis (therapeutic if raised intracranial pressure)
  • List common and important risks
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30
Q

What are the indications for LP?

A
  • diagnostic
    • infection - meningitis (bacterial/viral/fungal) or encephalitis
    • sub arach
    • other - MS, malignancy
  • therapeutic
    • reduce ICP e.g. idiopathic intracranial hypertension
  • spinal epidural
    • pain relief (during labour)
    • anaesthesia (e.g. lower limb surgery)
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31
Q

Cautions and contraindications for lumbar puncture:

A
  • Indications for brain imaging prior to lumbar puncture
    • This is due to the risk of brain herniation through the foramen magnum
      • Focal neurological signs
      • Presence of papilloedema
      • Continuous or uncontrolled seizures
      • Reduced or fluctuating conscious level
  • Bleeding risk
    • Deranged blood clotting or a low platelet count
    • Taking anticoagulation ( e.g. warfarin if INR >1.4)
  • Others
    • Signs of severe sepsis or a rapidly evolving rash (indicating risk of coagulation problem)
    • Infection at the site of the lumbar puncture
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32
Q

Describe the position and technique used for LP:

A
  • US guided technique should be used
  • Positioning allows for the largest possible gap between vertebrae
  • Lying on the side can be difficult to find landmarks so a sitting position can be used, however you cannot measure opening pressure in sitting position as this would be increased by gravity
  • Needle introduced in the L3/4 space, however L2/3 and L4/5 can be used depending on the anatomy of the patient
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33
Q

Bedside assessment of LP samples:

A

Appearance

  • Normal - clear (‘gin-coloured’)
  • Cloudy/purulent – meningitis
  • Blood-stained - subarachnoid haemorrhage, or a traumatic tap

Opening pressure

  • Normal is 8-20cm
  • May be elevated due to infection, inflammation, haemorrhage and idiopathic intracranial hypertension
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34
Q

What is analysed in a LP sample?

A

Cell count

  • Red blood cells
    • Normal – 0-10 cells/ul
    • ↑ traumatic tap, subarachnoid haemorrhage
  • White blood cells
    • Normal – 0-5 cells/ul
    • ↑ neutrophils – bacterial meningitis
    • ↑ lymphocytes – viral & TB meningitis/ encephalitis, (& inflammatory conditions, malignancy)
    • In real life it is often not as clear cut and may be a mixed picture
  • Protein
    • Normal - 0.15-0.45 g/L
    • ↑infection (TB > bacterial > viral), inflammatory conditions, Guillain-Barre syndrome
    • Oligoclonal bands in multiple sclerosis
  • Glucose
    • Paired with blood glucose
    • Normal - 60-80% of serum glucose
    • ↓ (<50%) in infection (esp. bacterial, TB and fungal)
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35
Q

Described the expected gram stain results for meningitis:

A

Gram positive

  • Peptidoglycan wall retains crystal violet stain (dark purple)
  • pneumococcal meningitis
    • Streptococcus pneumoniae is a gram-positive, α-hemolytic, lancet-shaped diplococcus - catalase-negative but produces hydrogen peroxide.

Gram negative

  • Crystal violet not retained by cell wall; counter stained with safranin stain (pink)
  • Meningococcal meningitis
    • gram negative coffee-bean shaped diplococci
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36
Q

Why are some bacteria gram positive and some are gram negative?

A
  • Gram positive bacteria take up the basic dye (crystal violet)
    • Their thick peptidoglycan cell wall allows them to resist alcohol decolourisation and they retain the dark purple colour
  • Gram negative bacteria allow the crystal violet to wash out and so decolourise
    • Their thin cell wall is less stable
    • The decolourisation bacteria can then be counterstained pink with further application of a different dye, safranin
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37
Q

What technique is used for gram staining?

A
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38
Q

Describe what you would see looking at streptococci under the microscope (strep pneumoniae, enterococci, oral (viridans) strep, strep pyogenes):

A

Gram positive cocci

Round or oval shaped

Sometimes you can guess what they might be by their shape and chain formation (but you can’t confirm unless you have colonies on a culture to test) eg:

  1. Strep pneumoniae – tends to form typically lancet shape and like to group in pairs
  2. Enterococci (a subset of Streptococci) – tend to form short chains
  3. Oral (viridans) Streptococci (inhabit oral mucosa) – can form long chains
  4. Strep pyogenes – medium to long chain
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39
Q

Describe what streptococci look like when grown on agar plate:

A
  • grown on agar containing 5% sheep blood incubated in 5-10% CO2
    • greyish white colonies
    • may be shiny or matte depending on type
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40
Q

How do you differentiate streptococci from staphylococci (both look similar and are gram-positive)?

A

Catalyse test:

  • scoop a colony on a small loop and dip into hydrogen peroxide solution
  • staphs contain catalase: H2O2 –> H2O + O2 and bubbles indicate a positive test
  • streps are catalyse negative (no bubbles)
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41
Q

Describe patterns of haemolysis seen in streptococcal bacteria:

A

Streptococci produce extracellular enzymes that lyse the red blood cells in the agar. This can result in complete or partial clearing seen around colonies.

The type of haemolysis present helps differentiate between possible species of streptococcus and can guide further identification steps.

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42
Q

What further identification can be carried out to identify species of streptococcus? What would the indications be to do this?

A

Sometimes specific species do not need to be known as they will not affect management, however there are certaiin circumstances where it does need to be known:

  • in infections such as endocarditis, we need to know the species eg Streptococcus gallolyticus and specific antibiotic susceptibility profile in order to give optimal, evidence based, tailored treatment

Further tests include:

  • mass spectrometry
  • panel of biochemical reactions
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43
Q

Describe the two methods of susceptibility testing:

A

Standard method in the lab:

  • Discs of filter paper impregnated with specific concentrations of antibiotics placed on agar plate which has been evenly spread with the bacteria and diluted in water
  • Antibiotic concentrates in agar around disc
  • Zones of inhibition of bacterial growth around discs suggests the particular antibiotic kills the bacteria
  • The bacteria is reported as susceptible to the antibiotic

E tests

  • MIC = minimum inhibitory concentration. More specific than disc testing
  • MICs may be useful in deciding which antibiotic to use for planning long courses for deep infections
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44
Q

Explain how fevers arise:

A
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45
Q

What criteria have to be fulfilled to define a fever as ‘pyrexia of unknown origin’?

A
  • Sustained or recurrent pyrexias for ≥3 weeks
  • No identified cause after sufficient evaluation:
    • in hospital for 3 days
    • ≥3 outpatient visits
  • No diagnosis
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46
Q

What are the types of PUO?

A
  • ‘Classic’
  • nosocomial
  • immunodeficient
  • HIV
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47
Q

What are important causes of classic PUO?

A

Infection

  • Abscess
  • Infective endocarditis
  • Tuberculosis
  • Complicated UTI
  • Geography/travel
    • Melioidosis
    • Visceral leishmaniasis
    • Amoebic abscess

Connective tissue

  • Young
    • Still’s/JRA
  • Adult
    • Rheumatoid arthritis
    • SLE
  • Elderly
    • giant cell arteritis
    • polymyalgia rheumatica

As population age increases, cancer is more likely as cause of PUO.

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48
Q

What is nosocomial FUO?

A
  • hospitalised for >48 hours
  • no infection present or incubating at admission
  • diagnosis uncertain after >3days of appropriate evaluation
  • (microbiology cultures incubated for >2 days)
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49
Q

What are the causes of nosocomial PUO?

A
  • catheters/devices
  • thrombophlebitis
  • UTI/RTI
  • drug fevers
  • C. diff
  • ICU - ventilator, ET tubes, NG tubes
  • stroke
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50
Q

What needs to be considered with PUO in immunodeficiency?

A
  • Cell-mediated immunodeficiency
    • Congenital
    • Biologic/immunomodulatory therapies
  • Neutropenia
    • Haematological disorders
    • Chemotherapy
    • <500 neutrophils/ul
  • N.B blunted ‘typical’ inflammatory responses
  • N.B lack of radiological changes
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51
Q

What can cause PUO in HIV?

A
  • primary HIV infection ‘seroconversion illness’ –> AIDS
  • PCP
  • mycobacterial
  • toxoplasmosis
  • CMV
  • lymphoma
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52
Q

What kinds of investigations would you consider with PUO?

A

Laboratory

  • 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

Imaging

  • CXR
  • US – liver/spleen
  • Cross-sectional CT
  • HRCT
  • CT PET
  • Labelled white cell scan (scintigraphy)
  • Bone scan
  • MRI
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53
Q

What are the incubation periods of important travel-related infections? (do not learn the whole table, only those relevant)

A
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54
Q

Describe broadly the assessment needed for a travel related infection:

A
  • Symptoms/signs
    • Fever: important to define pattern
    • Rash
    • Arthralgia
    • GI symptoms
      • Abdo pain, diarrhoea, constipation, blood
    • Full systems review
      • Including neuro and GU
  • Investigations
    • Full blood count
    • U&Es
    • LFTs
    • Coagulation
    • Blood gas
    • Blood culture
    • Throat/sputum/stool/urine/CSF as appropriate
  • Special tests
    • Malaria films
    • Serology
      • E.g Rickettsiae, Dengue, HIV, Viral hepatitis, Syphillis
    • PCR
      • E.e Dengue (blood), Herpes + enteroviruses (CSF), TB
    • Special stains – ZN/auramine (TB), Grockott (fungi)
    • Special cultures – mycobacterial, fungal
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55
Q

What areas is dengue fever endemic to?

A

South East Asia and South America

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56
Q

What type of mosquito transmit dengue?

A
  • aedes aegyptii and aedes albopictus
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57
Q

What is the WHO criteria regarding dengue?

A
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58
Q

What is the course of illness of dengue?

A
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59
Q

What is the clinical manifestation of scrub typhus?

A
  • Incubation period is 4~21 days
  • Sudden onset with a fever
  • 1st week, systemic toxic symptoms
  • 2nd week, get worse, complication
  • 3th week, convalesce (if prompt diagnosis and treatment)
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60
Q

What happens during the febrile phase of dengue?

A
  • fever
  • normally normal WCC
  • fairly normal PLTs
  • HCT may be normal
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61
Q

What happens during the critical phase of dengue?

A
  • normally after about day 4
  • Manifests with shock and bleeding as capillaries tend to start to leak, therefore plasma starts to leak out into extravascular compartment
  • As a result, there is marked drop in the WCC and PLTs, as a result HCT increases
    • Intravascular compartment becomes depleted
    • Need to recognise this because it is key to management of patient, and also important as when the patient begins to recover, they begin to reabsorb the fluid and so you must be careful not to fluid overload them at this point.
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62
Q

What is the ELISA test?

A

During the febrile phase, there is high viral load and so PCR can be used to detect the virus (dengue antigen capture ELISA can be used to rapidly diagnose within 30 minutes). However, at the end of the febrile phase IgM/IgG antibodies start to climb and so these are used for diagnosis during the critical and recovery phase.

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63
Q

How is dengue diagnosed in symptomatic patients?

A

5 days or less post onset of fever:

  • Detection of viral RNA (RT-PCR)
  • Detection of viral antigen (NS1)

5 days of more post onset of fever:

  • Detection of IgM antibodies host response as host response to infection (IgM antibodies can last up to 6 months; a positive IgM test is only suggestive of recent infection)
  • Detection of IgG antibodies (IgG antibodies persist for life; a positive IgG test result proves evidence of post infection)

Use of RT-PCR + IgM or NS1 + IgM tests can extend the window of detection of acute dengue to 10 days post onset of fever.

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64
Q

What is the management of dengue?

A
  • treatment is mainly supportive
  • in the febrile phase
    • prevent dehydration
  • in the critical phase
    • correct dehydration
    • replace ongoing losses
  • in the recovery phase
    • prevent fluid overload
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65
Q
A
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66
Q

What area is scrub typhus endemic to?

A

Tsutsugamushi triangle

  • North - northern Japan and far-eastern Russia
  • South - northern australia
  • West - to pakistan and afghanistan
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67
Q

What are the specific features of scrub typhus?

A

Eschar

  • Probability: higher than 60%
  • Location: axillary fossa, inguinal region, perianal region, scrotum, buttocks and the thigh
  • Appearance: an ulcer surrounded by a red areola, is often covered by a dark scab
  • This is the most specific manifestation of scrub typhus

Maculopapuplar rash

  • Onset: appear at the end of the 1st week, lasts 3~7d
  • Location: chest, abdomen, whole trunk, or upper and lower limbs. Rarely involves the face, palms and soles

Lymphadenopathy

  • Regional lymphadenopathy:
    • Occur at the end of the 1st week
    • Localise: the draining lymph node around the primary eschar
    • Characterised by tenderness and enlargement
  • Generalised lymphadenopathy: appears 2-3 days later
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68
Q

What is found on investigation for scrub typhus?

A
  • Haematology:
    • Leukopenia
    • Normal total WBC
    • May be elevation if patient has presented with some complications
  • Biochemical:
    • Injury of liver function, CRP

Serological examinations

  • Weil-felix: can be positive as early as 4th day after onset – used in poorer healthcare infrastructures
    • >1:160 or increase 4 times during the course
    • Easy for operation (easily accessibility) but poor for specialisation (poor specification and sensitivity)
  • Gold standard for diagnosis: indirect fluorescent antibody)
    • positive at end of first week
  • IIP (indirect immunoperoxidase test): comparable to those from IFA. More available

Pathology

  • Early course: perivascular lymphohistiocytic and extravasated erythrocytes and dermal oedema
  • Advanced lesion – shows dermal and epidermal necrosis
  • Immunohistochemical – positive staining for R. rickettsie
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69
Q

How do you diagnose scrub typhus?

A
  • Epidemiology data: visit the endemic area during the past 3 weeks. Working, camping or sitting on grass
  • Clinical manifestation: Eschar, regional lymphadenopathy, fever, maculopapular rask, leukopenia, failed therapy with common antibiotic drug
  • Laboratory examination: Weil-felix reaction with titers beyond 1:160 or fourfold rise during the course of the disease
  • (PCR for Orientia tsutsugamushi from blood of feverish patient)
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70
Q

What are important differential diagnoses of scrub typhus and how do you differentiate between these?

A
  • Epidemic typhus: occurs in winter and spring, bite by louse, Weil-felix with OX19 is positive
  • Typhus: slow onset, persistent high fever, confusion, bradycardia, digestive symptoms, rose rash, no eschar, widal test positive. Blood culture to typhus bacillus is positive
  • Leptospirosis: tenderness of calf muscle, microscopic haematuria
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71
Q

What is the treatment of scrub typhus?

A
  • Sensitive antibiotics decrease fatality from as high as 30% (untreated) to 2%
  • General treatment
    • Supportive IV fluids
    • Intensive nursing care and prevent complication
  • Pathogen treatment
    • Chloramphenicol: 2g per day for adult, 25mg/kg of bw per day for children
    • Doxycycline: 0.2g per day for adult (tetracycline alternative)
    • Azithromycin 500mg daily
    • Roxithromycin: 0.6g per day for adult, 2~3mg/kg/d for child
  • Strains resistant to doxycycline and chloramphenicol
  • Combination therapy with doxycycline and rifampicin should be used if resistance suspected
  • Azithromycin – shown to be promising against strains that are resistant from
72
Q

How is malaria spread?

A
73
Q

Describe the 5 plasmodial species that are known to cause malaria in humans:

A
  • Plasmodium falciparum (Malignant tertian)
  • Plasmodium vivax (Benign tertian)
  • Plasmodium ovale ( “ “ )
    • Vivax and ovale are also important to know about as they cause debilitating disease however they are rarely fatal
    • These species are known to have a dormant liver stage which can lead to relapsing episodes of clinical malaria
  • Plasmodium malariae (Quartan)
    • Can cause low levels of disease with periods of recrudescence that may go on for many years or even decades but it is currently less important than it has been in the past in terms of global burden of incidence
  • (plasmodium knowlesii infrequent. Probably zoonosis)
    • Infrequently diagnosed in humans, probably zoonosis that effects monkeys much more
74
Q

What is the pattern of fever in malaria and why?

A
  • When the erythrocytic stage is initiated, a periodicity sets in and cycles of red cell ruptures starts happening roughly every 48 hours (this is what earns the tertian periodicity fever which is classical of falciparum malaria – fever spikes every 48 hours)
75
Q

What happens to red blood cells in malaria (particularly falciparum malaria) and what clinical effect does this have?

A
  • Sequestration: Falciparum malaria itself gives rise to malignant disease itself – the shape of the red cell becomes distorted and the surface of the red cell becomes covered in little lumps (which are clumps of parasitic protein which are electrically charged).
  • Altered rheology – alters flexibility of red cells
  • Electrical charge
  • Intra-cellular adhesion (likely to adhere to each other, to other cells and the intima of vasculature)

(Again, this mainly happens in falciparum malaria). Red cells therefore become sequestrated in microvasculature, some tissues being more susceptible than others (brain, kidneys, eventually tissues such as bowel mesentery, pulmonary bed and digital extremities). Clinically can cause:

  • Cerebral malaria – reduced GCS and seizures
  • Renal failure – either biochemical changes or oliguria leading to anuria
  • ARDS - people with falciparum are particularly susceptible to pulmonary oedema and an ARDS picture
  • Tissue acidosis – direct result of sequestration as this can cause an infarct in capillary beds leading to tissue hypoxia and acidosis
  • Coagulopathy – accumulating tissue damage exacerbates any coagulopathy present
76
Q

What allows vivax and ovale to become dormant in humans?

A

Vivax and ovale species will not only produce merozoites in schizonts in the liver, but also hypnozoites which remain dormant in the liver – this allows the parasite to survive in the human host during cooler parts of the year in more temperate environments and will re-emerge when the mosquito vectors are feeding more actively

77
Q

What causes jaundice in malaria?

A

Jaundice and haemolytic anaemia can occur when large numbers of red cells are infected and then all rupture.

78
Q

What happens to the blood glucose level in patients with malaria?

A

When trophozoites are readily feeding on glucose in the blood, this will cause levels to decrease in the blood. This is also partly explained by increased basal metabolic rate in infected cells.

79
Q

What are the symptoms to malaria?

A

Anyone returning from a malaria endemic area with:

  • Fever (or a history of fever)

Other features (not always present):

  • Rigors
  • Headache +/- confusion
  • Myalgia, arthralgia
  • Nausea, vomiting, diarrhoea
  • Dark urine

Fever + travel history = think of malaria and do a blood film!!

80
Q

What associated signs may or may not be seen in patients with malaria?

A
  • Fever
  • Jaundice
  • Pallor
  • Splenomegaly
  • Hepatomegaly
  • Altered consciousness
  • Focal neurological signs
  • Coma
81
Q

What are the complications of malaria/indications for IV treatment?

A
  • Cerebral involvement – reduced GCS/seizures
  • Anaemia – Hb < 8g/dL
  • Lactic acidosis – pH<7.3 (i.e. need to do ABG or VBG to monitor lactate)
  • Renal failure
    • Oliguria < 0.4ml/kg/hr
    • Creatinine > 265
  • Pulmonary oedema/ARDS
  • Hypoglycaemia – BM <2.2mmol/L
  • Shock – BP <90/60
  • Bleeding/DIC
  • Haemoglobinuria
82
Q

What are the appearance of trophozoites on blood film?

A
  • characteristic double chromatin dots
  • usually only one in each cell
    • a cell is said to be hyper-parasitised when there are two trophozoites in the same cell
83
Q

What is the appearance of a shizont on a blood film?

A
  • contains many merozoites
  • if we see schizonts on the film, then we know the current parasitaemia may increase by 10-fold in the near future when it ruptures
84
Q

How do you classify malaria and how does this impact management?

A

Uncomplicated: ALL of the following – these patients would be suitable for oral treatment if there were no further issues, as long as they are not vomiting are able to take oral medications

  • Parasitaemia <2%
  • No schizonts
  • No clinical complications

Potentially severe: ANY of the following – IV treatment

  • Parasitaemia >2%
  • Parasitaemia <2% with schizonts
  • Parasitaemia <2% with complications

Severe – IV treatment

  • Complications present, regardless of parasitaemia
85
Q

Describe the clinical pictures seen in benign malaria:

A
  • P. vivax: Asia, South America
  • P. ovale: West & Central Africa
    • Both vivax and ovale are usually associated with lower rates of parasitaemia (<2%) and due to not causing sequestration of RBCs we don’t see cerebral malaria, renal failures and capillary bed ischaemia with these species
    • Hypnozoites (get in both vivax and ovale) – if these are not eradicated along with the active infection then you will get relapse in the future
      • Dormant liver stage
      • Relapsing malaria
  • P. malariae:
    • Least common
    • Never causes severe disease
    • May persist for decades
    • Rare cause pf nephrotic syndrome
86
Q

What drugs are used to treat severe malaria?

A

Quinine

  • Cardiac toxicity (due to sodium channel blockade) – ECG monitoring required (prolonged QT intervals and wide QRS complexes)
  • Cinchonism – tinnitus vertigo, vomiting, headache, nausea, abdominal pains and occasionally visual disturbance (sometimes temporary blindness)
    • Rarely an indication to stop treatment
  • When patient is ready to switch to oral treatment, continuation with oral therapy must be with a second agent (doxycycline or clindamycin)

Artesunate

  • Standard of care globally is currently IV artesunate as first-line for severe malaria, however not currently licenced in the UK so sometimes there is a problem with supply – this is improving
  • Minimum 24 hours therapy, however if after this the patient is improving then a switch can be made to oral treatment
  • Delayed post-treatment haemolysis at about 70 days so patients need to be warned about this
87
Q

What drugs are used as oral therapy for malaria? (in uncomplicated, non-severe disease)

A
  • Artemether-lumefantrine: 4 tablets then 4 tablets at 8, 24, 36, 58 and 60h
    • First-line in the UK
  • Atovaquone/proguanil (Malarone): 4 ‘standard’ tablets daily for 3 days
  • Quinine sulfate 600mg 8 hourly for 5-7 days plus doxycycline 200mg daily (clindamycin 450mg 8 hourly for pregnant women) for 7 days
88
Q

What is used to eradicate hynozoites (to prevent relapse in vivax and ovale)?

A
  • Primaquine 2 weeks, oral
  • G6PD enzyme activity must be measured before taking this drug
    • G6PD deficiency – at risk of haemolysis due to oxidative stress imposed by metabolising this drug
      • These patients may need to be treated at a lower dose for a longer time, but expert advice should always be sought
89
Q

What types of drugs are used for chemoprophylaxis of malaria?

A

Causal

  • Directed against hepatic stage (i.e. schizonts, not hypnozoites)
  • Prevents progression to erythrocyte stage
  • Continue for 7 days following last possible exposure
  • Examples: atovaquone/proguanil (malarone)

Suppressive

  • Directed against erythrocytic stages
  • Continue for 4 weeks post-exposure
  • Examples – chloroquine (rarely used for falciparum prophylaxis these days due to widespread resistance), doxycycline (very fair-skinned individuals need to be warned about hypersensitivity to sun and frequently causes GI upset), mefloquine (once weekly – should not be to patients with strong history of severe depression or psychological history due to side effects)
90
Q

Where is malaria endemic to?

A
  • P. falciparum: Widespread, but primarily in tropics and subtropics
  • P. vivax: Widespread in tropical and subtropical areas and extends into temperate areas. Relatively uncommon in Africa
  • P Malariae: Broad but patchy geographical distribution
  • P. ovale: Primarily tropical Africa and west pacific islands. Sporadic distribution in SE Asia. NOT found in S America or Indian subcontinent but, there have been a small number of cases reported in Bangladesh.
  • P knowlesi: Confined to SE Asia
91
Q

What routine malarial investigations are used in Newcastle?

  • FBC
  • Thick and thin films
  • Carestart Combo Rapid Test (pan pLDH/falcip HRP-2)
A
  • FBC
  • Thick and thin films
  • Carestart Combo Rapid Test (pan pLDH/falcip HRP-2)

A negative malaria film does not exclude a diagnosis of malaria. If there is a strong suspicion of malaria but the initial films are negative, then repeat films should be requested 12-24hrs and 48hrs.

92
Q

What is seen on FBC in a patient with malaria?

A
  • Particular note should be taken of the patient’s platelet and WBC counts
  • Malaria can often be associated with reduced leukocyte/neutrophil numbers
  • Platelet numbers are moderately or markedly reduced in approx. 80% of patients with malaria
  • Malaria parasites DNA/RNA can show as fluorescent populations on haematology FBC analysers that utilise flow cytometry
93
Q

What is quantitative buffy coat screening (QBC)?

A
  • blood is centrifuged in a capillary tube coated with acridine orange
  • the parasites separate into their own level
  • the acridine orange stains nucleic acid which then fluoresces when excited with blue light when examined under a fluorescent microscope (i.e. you can see the malaria)
94
Q

Explain thick and thin films:

A
  • The gold standard for malaria screening
  • Thin films are fixed in methanol and stained with a MGG stain pH 6.8
  • Additional diagnostic information can be gained by examining Giemsa-stained thin films pH 7.2
  • Thick films are stained unfixed with Fields stain pH 7.2 (screening)
95
Q

What are rapid malaria diagnostic tests (e.g. carestart malaria HRP2/pLDH combo test)?

A
  • strip pre-coated with two different monoclonal antibodies
  • two different capture lines
  • one test line (i.e. monoclonal antibody) is specific to falciparum and one is specific to vivax, malariae and ovale
  • there are relatively high rates of false positive and false negatives therefore these tests should never be used in isolation and thick and thin films must be examined
96
Q

What is the benefit of PCR in malaria?

A
  • Parasite nucleic acids are detected using polymerase chain reaction (PCR).
  • Although this technique may be slightly more sensitive than smear microscopy, it is of limited utility for the diagnosis of acutely ill patients in the standard healthcare setting (slow)
  • PCR results are often not available quickly enough to be of value in establishing the diagnosis of malaria infection.
  • PCR is most useful for confirming the species of malarial parasite after the diagnosis has been established by either smear microscopy or RDT.
97
Q

What about malarial antibodies? Are they useful in the acute setting?

A
  • Antibodies to malaria can be detected using enzymatic immunoassays or immunofluorescence techniques.
  • The antibodies to the asexual blood stages appear days to weeks after the infection and may persist for months.
  • Although useful in survey work or for screening blood donors and reducing wastage, they are of little value in the “acute” malaria situation.
98
Q

Describe different routes of infection of bone:

A
  • Haematogenous spread
    • Associated with staph aureus
    • Children are at risk of salmonella and so can get hematogenous infection of native bone by salmonella
    • TB can be spread hematogenously to bones
  • Direct inoculation
    • People who have had metal plates inserted are at risk of direct inoculation (coagulase negative staphylococci)
      • These often form biofilms of the surface of the metal – these types of infections are very difficult to eradicate with antibiotics alone
  • Contiguous spread
    • for example diabetic ulcers (or any type of ulcer) can cause polymicrobial infections of the bone (which can then spread via haematogenous route)
99
Q

What is a biofilm and why are they important in osteomyelitis?

A
  • a structured community of microorganisms adhering to a surface and producing an extracellular matrix of polysaccharides”
    • (i.e. another community of bacteria in a blob of extracellular matrix that adheres to a surface – behaves very differently than other bacteria floating free)
  • very associated with device related infections but you do not need prosthetic material in your body to have a biofilm
    • chronic osteomyelitis is often assciated with biofilms
  • sessile (refers to bacteria in biofilms) ve planktonic (free bacteria)
    • sessile bacteria are relatively resistant to immune defences and antibiotics
100
Q

Presentation of bone & joint infections:

A
  • Clinical presentation is highly variable
    • Septic arthritis tends to present with rapid onset of pain, swelling and redness in a single joint
    • Prosthetic joint infection may present with joint pain & evidence of inflammation at the surgical site
    • Vertebral osteomyelitis presents with back pain & may progress to cause neurological signs
    • Chronic osteomyelitis often causes a sinus which does not heal (sinus is a break in the skin that does not heal and often discharges bits of dead bone)
101
Q

What investigations do you need to order for a suspected joint/bone infection?

A
  • Bedside tests
    • Fever is often absent
  • Blood tests
    • RBC, U&Es, CRP, blood cultures
  • Microbiology tests
    • Joint aspiration, bone biopsy, tissue biopsy, sonication of excised prosthetic material
  • Radiology
    • Plain X-rays, CT scans, MRI scans
102
Q

How do you manage bone/joint infection?

A
  • “Medical” v. “Surgical” management (debridement many be the most important component of treatment)
  • Antibiotic therapy needs to be directed at the organism isolated or empirical therapy is necessary (I think flucloxicillin can be used empirically - see BNF treatment summary)
  • Antibiotics which penetrate bone well are preferred
  • Courses of antibiotics need to be relatively prolonged
    • Four weeks for septic arthritis
    • At least 6 weeks for vertebral osteomyelitis & prosthetic joint infections
  • Prolonged courses of IV therapy may be delivered via ‘OPAT’ clinics
  • Oral therapy may be as effective as IV therapy in many cases
103
Q
A
104
Q

How does disseminated gonococcal infection present?

A
  • Purulent monoarthritis and/or
  • Triad of tenosynovitis, dermatitis (papules, pustules, necrotic lesions) and asymmetric migratory polyarthralgia
  • May occur several days to weeks following initial infection
105
Q

What are the risk factors for disseminated gonococcal infection?

A
  • Female sex
  • HIV infection
  • Menses
  • Low socioeconomic or educational status
  • Pregnancy
  • Multiple sexual partners
  • SLE
  • Complement deficiency
106
Q

How do you diagnose disseminated gonococcal infection?

A
  • Blood culture (may be negative)
  • Synovial fluid analysis (joint aspirate)
  • Gram stain will show inflammatory effusion with neutrophil predominance plus or minus gram-negative diplococci
    • ​neisseria gonorrheae is oxidase positive and catalase positive
  • Culture & sensitivity testing
  • NAAT PCR (if available and validated for synovial fluids)
107
Q

What is the appearance of neisseria gonorrheae on blood smear? (disseminated gonococcal infection)

A
108
Q

What is the treatment of disseminated gonococcal infection?

A
  • IV ceftriaxone 2 weeks with appropriate oral switch for further 4 weeks (e.g. oral cipro)
  • Joint drainage for purulent arthritis (may need to be repeated several times)
109
Q

What is the characteristic arthritis presentation of parvovirus B19?

A
  • symmetrical polyarthralgia
    • similar to rheumatoid
  • arthritis is transient
  • other symptoms of parvovirus include:
    • prodromal illness that consists of fever, malaise, headache, myalgia, nausea and rhinorrea
  • risk factors include exposure to children (i.e. teachers at risk)
110
Q

How does acute septic arthritis of native joint present?

A

Definition: the infection of 1 or more joints cause by pathogenic inoculation of microbes.

Presentation

  • painful joint
  • hot joint
  • swollen joint
  • restricted joint
111
Q

How do you diagnose septic arthritis?

A
  • clinical
  • joint aspiration for urgent gram stain, culture and sensitivity
112
Q

What is the management of septic arthritis?

A
  • Empirical antibiotic therapy should be commenced once appropriate cultures have been taken
  • according to NICE:
    • flucloxicillin
    • if penicillin allergic
      • clindmycin
    • if MRSA suspected
      • vancomycin (or teicoplanin)
    • if gonococcal arthritis or Gram-negative infection suspected, cefotaxime (or ceftriaxone)
  • other management
    • Depending on result of Gram stain likely require joint washout / orthopaedic intervention for definitive treatment
    • Rationalise antibiotics according to positive cultures
    • If haematogenous spread, ensure full systemic enquiry and appropriate investigations to ensure no seeding elsewhere
113
Q

What do you need to remember about staph aureus in the post-op setting?

A

Staphylococcus aureus highly pathogenic and very likely a causative organism for either post-operative wound infection or early prosthetic joint infection.

Remember on gram stain:

  • appear as gram positive cocci in clusters
114
Q

When someone presents with post-op infection post any joint surgery, what broad spec antibiotics would be used (pre-culture results)?

A
  • if MRSA suspected cover with e.g. teicoplanin, vancomycin, linezolid
  • broad spec agent that covers gram negative bacteria - piperacillin/tazobactam (Tazocin)
115
Q

What is a common causative agent of early onset prosthetic joint infection?

A

The most likely diagnosis is early onset prosthetic joint infection secondary to Staphylococcus aureus:

  • Gram positive cocci in clusters, catalase positive, coagulase positive organism

Antibiotics alone will not be able to treat this. Prompt surgical action must be taken to optimise the changes of salvaging the prosthesis.

116
Q

What common pathogens have to be considered in joint infections:

A
117
Q

Chronic vs acute periprothestic joint presentation and management:

A
118
Q

What regulations and legislation is in place to ensure good practice is followed to prevent HCAIs?

A
  • Health & Safety at Work Act 1974
  • COSHH (Law on the Control of Substances Hazardous to Health)
  • Workplace Regulations
  • Building Regulations
  • HTM’s (health technical memoranda) & HBN’s (health building note)
    • Comprehensive advice and guidance on the design, installation and operation of specialised building and engineering technology used in the delivery of healthcare
119
Q

Who is in charge of ensuring safe water in the hospital?

A
  • Team of specialities that creates, implements and maintains a Water Safety Plan (WSP)
  • WSP – designed to ensure that the water used in hospitals and similar healthcare settings is safe to use by patients, staff and visitors, and poses minimal risk of infection from waterborne pathogens
120
Q

What water-borne pathgoens are associated with hospital outbreaks?

A
  • Pseudomonas
  • Legionella

Need to consider high risk groups:

  • immunocompromised
  • children
  • burns
  • ICU
121
Q

What areas of plumbing are at risk of being colonised with water-borne pathogens?

A
  • types of taps/sinks
  • areas with los use (not flushing pipes/taps)
  • redundant piping
122
Q

What are the principles of ventilation?

A

Ventilation is a means of remvoing and replacing the air in a space:

  • dilution of contaminants
  • clean airflow path
  • control of hazards
  • comfort
123
Q

When are negative pressure rooms used?

A
  • infected patient in isolation:
    • air from anteroom flows into patient’s room
124
Q

When are positive pressure rooms used?

A
  • when a patient needs protected from infection e.g. neutropenic
    • air flows from patient room into anteroom
125
Q

When are ultracelan ventilation rooms used?

A
  • joint replacement/orthopaedic operations
126
Q

What is airborne transmission and what infections are airborne?

A

Airborne transmission

Spread of an infectious agent caused by the dissemination of droplet nuclei/aerosols (<5u) that remain infectious when suspended in air over long distances and time (vs droplet transmission >5-10u)

  • TB, measles and chickenpox
  • n.b.
    • viruses - 0.1u
    • M. TB - 2-4u
    • bacteria - 10-16u
    • fungi and spores - 3-10u
  • It is important to have appropriate ventilation to prevent airborne infection
127
Q

What areas is ventilation critical?

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.)
  • Pathology departments
  • Mortuaries
  • Steriliser / packaging units (CSSD’s)
  • Hydrotherapy units
  • Infectious diseases units
  • Intensive Treatment / Therapy units
128
Q

What is MRSA?

A
  • Methicillin Resistant Staphylococcus aureus
  • Staph aureus is a Gram-positive bacterium that causes infections such as cellulitis, pneumonia, endocarditis and device-related infections
  • It can also colonise the skin and nasopharynx of healthy people without causing infection
  • MRSA is resistant to methicillin – and hence also flucloxacillin
  • It is often resistant to other antibiotics too (multi-resistant)
129
Q

Why screen for MRSA?

A
  • Knowing that a person is colonised with MRSA means that if they develop an infection which might be caused by Staph aureus, they might need different antibiotics to treat it
  • MRSA can be spread from person to person, so identifying carriage helps us put measures in place to prevent spread
  • MRSA carriage is more common in those who have recently been in a healthcare facility eg hospital
130
Q

What is CPE?

A
  • Carbapenemase Producing Enterobacterales
  • Enterobacterales are a group of Gram-negative bacteria that live in the gut eg E coli, Klebsiella
  • Carbapenems are very broad-spectrum antibiotics that can resist most of the enzymes that bacteria produce to break down antibiotics
  • CPE produce a carbapenemase enzyme that breaks down the carbapenem
  • They are resistant not just to carbapenems but to most antibiotics (multi-resistant)
131
Q

Why screen for CPE?

A
  • Knowing that a person is colonised with CPE means that if they develop an infection which might be caused by Gram negative organisms, they might need different antibiotics to treat it
  • CPE can be spread from person to person, so identifying carriage helps us put measures in place to prevent spread
  • CPE carriage is more common in those who have recently been in a healthcare facility in a place where CPE is common – in some other countries and in some parts of the UK (London, Manchester)
132
Q

How is MRSA screening performed?

A
  • Charcoal swab (black top)
  • Separate swabs for
    • Nose (both nostrils)
    • Throat (back of throat)
    • Groin (perineum)
    • Any wounds or device sites
    • CSU if catheterised
  • Different hospitals use different combinations
  • Swabs are plated onto MRSA selective agar and incubated
  • This agar contains an indicator dye so staph aureus colonies are green (other skin organisms will be white)
  • It also contains antibiotics so selective organisms will be killed and not able to grow
133
Q

How is CPE screening performed?

A
  • Rectal swab or stool sample
    • Stool is better but harder to collect
  • Red topped swab – for PCR
  • Charcoal (black topped) swab – for culture
  • Different hospitals ask for different numbers of swabs spaced apart (often 48 hours)
  • This can be performed using selective agar for CPE, or by testing the sample directly using PCR or lateral flow
  • PCR and lateral flow only look for the 5 most common genes which confer resistance
  • There are many more
134
Q

What is Clostridioides difficile?

A
  • anaerobic, gram positive, spore-forming bacteria which is found in the the guts of healthy people (33%) where it does not cause any symptoms
  • problem arises when the person becomes unwell or takes broad spec bacteria (wipes out ‘good’ bacteria)
    • therefore c.diff is not kept in check and can produce high levles of toxin, which cause clinical disease when in high enough concentrations
  • ingestion of spores is route of transmission (although recent evidence suggests can also be airborne?)
  • the spores can remain viable in the environement for long periods of time
135
Q

What are the risk factors for acquisition and disease severity of c. diff?

A
  • Broad-spectrum antibiotic use
    • Some more implicated than others- fluoroquinolones, cephalosporins, clindamycin
  • Acid supressing medications (PPIs)
  • Increasing age
  • Hospitalisation
  • Underlying morbidity particularly immunosuppression
  • Inflammatory bowel disease
  • Certain C.difficile strains more associated with severe disease- eg. type 027
  • Exposure to other patients with C.difficile and/or contaminated environment (including the hands of HCWs!)
136
Q

What is the clinical picture of c. diff?

A
  • Symptoms can range from mild self-limiting diarrhoea to pseudomembranous colitis, toxic megacolon, perforation and death
    • Disease is caused by the toxins produced by C.difficile damaging the lining of the colon
  • Indicators of disease severity:
    • WCC >15
    • Acutely rising serum creatinine (AKI)
    • Fever >38.5
    • Evidence of severe colitis (clinical peritonitis, radiological changes)
137
Q

What are the treatment options of c. diff?

A
  • Antibiotics:
    • Metronidazole (PO or IV) – mild-moderate disease
    • Vancomycin (PO ONLY) – severe or recurrent disease
    • Fidaxomicin (PO) – non life-threatening recurrent disease
  • IVIG with combination of IV metronidazole and oral vancomycin +/- surgical management in life-threatening disease
  • Faecal transplant in recurrent disease
138
Q

What are the complications of c. diff?

A
  • Dehydration
  • AKI
  • Electrolyte Imbalance
  • Pseudomembranous colitis
  • Toxic megacolon
  • Requirement for colectomy
  • Colonic perforation
  • Peritonitis
  • Death
139
Q

How do you diagnose c.diff?

A
  • Stool sample!
    • GDH
    • PCR
    • Toxin
  • Interpreting the results:
    • Not detected
    • C.difficile CARRIER
    • C.difficile TOXIN DETECTED
140
Q

How do you prevent c. diff?

A
  • Address the risk factors!
    • Antimicrobial stewardship
    • Review of PPIs/H2-antagonists
    • Infection control
  • Not all risk factors are modifiable- age, hospitalisation, need for specific antibiotics
141
Q

Does colonisation of a urinary tract catheter = infection?

A

No, catheters quickly become colonised by bacteria but that does not result in clinical infection

142
Q

What are the risk factors of CAUTI?

A
  • Presence of urinary tract catheter!
  • Manipulation of catheter, trauma
  • Negates one of the body’s main defences against UTI: the direction of flow of urine down the urethra which helps wash out bacteria
  • Biofilm formation on prosthetic material: microbial cells embedded in a sticky extracellular matrix that adheres to a surface. This acts as a source of infection, and can’t be eradicated due to poor penetration of antibiotics

No catheter  no CAUTI

143
Q

How do you diagnose CAUTI?

A
  • No urine dipsticks!!!
    • Chronic bacterial colonisation of a catheter will result in permanently positive dipstick results. This means that the dipstick results will not help with any decision-making process
  • Urine culture, taken following TWOC/re-catheterisation, or from the catheter port site (NOT the catheter bag)
    • NB asymptomatic bacteriuria is not diagnostic – don’t treat a positive urine result in an asymptomatic patient
  • Blood cultures (if abnormal temperature/systemically unwell)
144
Q

What is the process for sending a urine sample when testing for CAUTI?

A
  • You send a catheter sample of urine (CSU) from the catheter port, and send it to the Microbiology laboratory for culture
  • On the request form, you include the specimen type, symptoms, and any other relevant clinical details
    • E.g. recent C.difficile infection, any antibiotic allergies (for example giving antibiotics to someone who has had recent c. diff puts them at high risk for reoccurrence so weight risk verses benefit)
  • Next day, the culture shows >100,000 colony forming units of Klebsiella pneumoniae
  • No sensitivity results are given on the report, so you call the Microbiology department for advice
145
Q

What are the treatment options for CAUTI?

A
  • Catheter removal or catheter change
  • Antibiotics, if required:
    • Look back at previous urine cultures to see if the patient has previous results that help inform the decision
    • Otherwise, the treat according to local antibiotic guidelines for UTI
      • 7 days for ‘complicated UTI’
    • If systemically unwell: IV antibiotics for urosepsis, rationalise according to culture results
146
Q

Are there any measures to prevent CAUTI?

A
  • Avoidance of urinary tract catheters
  • Insertion by properly trained personnel, 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
    • Antibiotic prophylaxis not routinely required unless significant previous infection associated with catheter manipulations
  • Long term antibiotic prophylaxis/methenamine Hippurate – NOT ROUTINELY ADVISED
147
Q

How is gram staining carried out?

A
  1. Fixation of specimen to slide (heat or methanol)
  2. Application of primary stain (Crystal Violet) then rinse
  3. Application of mordant (binds stain more tightly- Iodine) then rinse
  4. Decolourisation (acetone or ethanol) then rinse
  5. Application of counter-stain (Safranin or Carbolfuschin) then rinse
  6. Blot dry
148
Q

What do some common organisms appear like on gram stain?

A
  • Gram positive cocci in clusters
    • Staph aureus (including MSSA and MRSA)
  • Gram positive cocci in pairs
    • Streptococcus pneumoniae
  • Gram positive cocci in chains
    • Enterococci
    • Other streptococci (eg. Group A Strep)
  • Gram positive rods:
    • Clostridium perfringens
  • Gram negative cocci:
    • Neisseria gonorrhoea
    • Neisseria meningitidis
  • Gram negative rods:
    • Pseudomonas aeruginosa
    • E.Coli
    • Klebsiella pneumoniae
    • Salmonella sp.
    • Enterobacter sp.
149
Q

What is the pathogenesis of endocarditis?

A
  • Endocarditis = Infection and inflammation of the endothelial surface of the heart by a micro-organism.
  • Turbulent blood flow can cause damage to smooth surfaces leading to the accumulation of platelets / fibrin / leucocytes which can then become infected by any circulating microorganisms and form a vegetation
150
Q

What is the most common presentation of endocarditis?

A
  • Vegetations
151
Q

How can IE present?

A
152
Q

What are the risk factors of infective endocarditis?

A
  • Almost any type of structural heart disease can predispose to IE. Rheumatic heart disease was the most frequent underlying lesion in the past, and the mitral valve was the most commonly involved site
  • Prosthetic valves and cardiac devices (such as permanent pacemakers and cardioverter defibrillators)
  • Congenital heart disease
  • Injection drug use (IVDU)
  • Human Immunodeficiency Virus infection (particularly if accompanied by immunocompromise)
  • Extensive health care system contacts
153
Q

What are the most common causative organisms of IE?

A
  • strep and staph collectively account for 80% of all cases
    • The emergence of health care-associated IE has been accompanied by an increase in the prevalence of Staphylococcus aureus and coagulase-negative staphylococci, whereas the proportion of IE due to viridans group streptococci (VGS) has declined.
  • enterococci are the third leading cause of IE and are increasingly linked to healthcare
  • infections that involve gram-negative and fungal pathogens in IE are rare
154
Q

What happens if a blood culture comes back negative in suspected IE?

A
  • In approximately 10% of cases of IE, blood cultures are negative
    • Most commonly due to patient receipt of antibiotics before the diagnostic work-up.
    • ‘True’ culture-negative IE is caused by fastidious microorganisms that are difficult to isolate with conventional microbiological techniques.
      • Causes include
        • Coxiella burnetii (the causative agent of Q fever, associated with abattoirs / livestock)
        • Bartonella spp (associated with alcoholism or homelessness)
        • Brucella spp (associated with contact with livestock or abattoirs)
        • Tropheryma whipplei
        • Brucella spp (travel to the Middle East or the Mediterranean or consumption of unpasteurized dairy products)
        • Bartonella henselae (contact with cats)
        • Aspergillus spp. (extensive health care contact in a patient with a prosthetic valve)
155
Q

What clinical features suggest a diagnosis of endocarditis?

A
156
Q

What are the end organ manifestations of IE?

A
  • Embolic manifestations include (figure):
    • Portions of the fibrin–platelet matrix of the vegetation may dislodge from the infected heart valve and travel with arterial blood until lodging in a vascular bed downstream from the heart. (left sided heart disease will result in systemic emboli) (right sided heart disease will cause septic emboli in lungs)
  • Immunological manifestations include:
    • Skin: findings such as Osler’s nodes consist of arteriolar intimal proliferation with extension to venules and capillaries and may be accompanied by thrombosis and necrosis. Immune complexes may be found within the lesions.
    • Renal: immune complex deposition glomerulonephritis
    • Systemic: Rheumatoid factor may be raised
157
Q

How do you investigate suspected IE?

A
  • Basic initial investigations on presentation as follows:
  • Bloods
    • Inflammatory markers may be raised: CRP, ESR, WCC, Plts
    • Look for end organ damage/comorbidities: U&E, LFTs
  • Blood Cultures
    • Ideally 3 sets with a period of time between each (1-6 hrs)
    • 2 sets within 1 hr if septic and starting antibiotics
    • Do not wait for temperature spike – bacteraemia is constant in IE regardless of temperature
  • ECHO
    • TTE (transthoracic) or TOE (transoesophageal) (should be low threshold for transoesophageal if TTE is negative due to it being more sensitive)
158
Q

What are the investigations for surgery in IE?

A
159
Q

What is the prognosis for patients with IE?

A
  • Mortality
    • No treatment 100%
    • Treatment – 20-25% die
160
Q

What are indicators of poor outcome in patients with IE?

A
161
Q

What are the modified duke criteria?

A

Predisposing heart conditions include valvular heart disease, valve replacement, structural congenital heart disease, previous endocarditis or hypertrophic cardiomyopathy.

162
Q

How do you use the modified duke criteria to diagnose infective endocarditis?

A
163
Q

What did the POET study show?

A

Efficacy and safety of shifting to oral antibiotic treatment was non inferior to continues IV treatment, in the case of:

  • In stabilised patients with left-sided endocarditis caused by Streptococcus spp, Enterococcus faecalis, Staphylococcus aureus, or coagulase-negative staphylococci
  • Across co-morbidities, native vs prosthetic valve and surgically vs conservatively treatment

Oral antibiotics may safely be administered during approximately half of the recommended antibiotic treatment period

  • Potentially as outpatient treatment
  • More than 50% of patients with endocarditis may be candidates for partial oral antibiotic treatment
164
Q

What are the requirements when taking blood to test for IE?

A
  • If chronic/subacute presentation: 3 optimally filled sets to be taken from peripheral sites with 6 or more hours in between them prior to antibiotics
  • If septic shock: 2 optimally filled sets at different times within 1 hour prior to antibiotics
165
Q

What should be routinely tested for in culture negative IE?

A
  • Coxiella burnetti (Q fever)
  • Bartonella spp

Considered if these two are negative:

  • Chlamydia, legionella, mycoplasma

Brucella if risk of exposure

166
Q

Decribe empiral treatment for both NVE and PVE:

A

Risk factors for enterobacteriaceae, pseudomonas:

  • IVDU, elderly, diabetic
167
Q

What antibiotics are indicated in staphylococcal endocarditis?

A

Guidelines suggest antibiotics therapy for at least 4 weeks in NVE, and 6 weeks PVE or patients with secondary lung abscesses and osteomyelitis.

168
Q

What antibiotics are indicated in streptococcal endocarditis?

A

In the treatment of streptococcal endocarditis, the minimum concentration of penicillin to inhibit growth of bacteria is required. Those with high MIC of over 0.5mg/L should be treated as per enterococcal guidelines.

169
Q

What antibiotics are indicated for enterococcal endocarditis?The BSAC guidelines suggest that first line therapy for susceptible enterococci is amoxicillin or high dose penicillin combined with gentamicin.

A

The BSAC guidelines suggest that first line therapy for susceptible enterococci is amoxicillin or high dose penicillin combined with gentamicin.

Glycopeptides such as vancomycin and teicoplanin, in combination with gentamicin are second line for susceptible enterococci.

170
Q

What treatment should be initiated if a fungal cause of IE is suspected?

A

Fungal endocarditis is common in patients with prosthetic valves but also can occur in IVDU, neonates and immunocompromised patients.

  • Candida infections: usually HCAI, first line is amphotericin
  • Aspergillus infections: surgical valve replacement is mandatory for survival, variconazole is first line with confirmation of susceptibility to variconazole and therapeutic drug level monitoring, (amphotericin B can be an alternative but some species are resistant).
171
Q

What are the HACEK group of organisms?

A
  • Fastidious extracellular Gram-negative bacteria, including:
    • Haemophilus species
    • Aggregatibacter actinomycetemcomitans
    • Cardiobacterium hominis
    • Eikenella corrodens
    • Kingella kingae
  • 3% of cases
172
Q

How do you treat HACEK IE?

A
  • Beta lactamases stable cephalosporin or amoxicillin (if isolate is susceptible)
  • Gentamycin for first 2 weeks of therapy
  • Ciprofloxacin can be considered an alternative agent
173
Q

Tell me about coxiella burnetti:

A
  • most common cause of culture negative IE
  • treatment:
    • at least 18 months
    • combination of doxycycline and hydroxychloroquine
174
Q

Tell me about bartonella species and IE:

A
  • gram negative, causes up to 3% of all IE
  • transmitted by body louse
    • RFs include homelessness and alcoholism (quintana)
  • cat scratch fever
    • rare cause of endocarditis (henselae)
  • treatment:
    • gentamicin in combination with a beta lactam or doxycycline, minimum four weeks
175
Q

What is dengue shock syndrome?

A

The pathogenesis of DSS is not fully understood, but may be due to immune priming by prior exposure to a different serovar. DSS is a significant problem in endemic areas where people are repeatedly exposed, particularly affecting young children and elderly, but is less common in travellers. These features raise the question of whether his febrile illness in Sri Lanka the year before was also an episode of Dengue Fever.

176
Q

What acronym can be used to remember the signs and symptoms associated with IE?

A
  • Fever
  • Roth’s spots
  • Osler’s nodes
  • Murmur
  • Janeway lesion
  • Anaemia
  • Nail haemorrhage
  • Emboli
177
Q

What is the significance of Strep. gallolyticus (formerly known as Strep. bovis) in IE?

A

There have been several studies showing a close association between S. gallolyticus (formerly known as strep bovis) endocarditis and colon cancer, with incidence between 18% and 62%. It has been standard of care to screen the patients with S. gallolyticus endocarditis for colon cancer (eg colonoscopy and/or CT scan).

CDM (7 decks)

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