W07 - Clinical 2 - S Aureus; Sepsis; Influenza; Zoonoses Flashcards

1
Q

Spectrum of S. aureus infections and source of bacteraemia

A
  • staphylococci = gram+ = grape-like clusters
  • highly virulent = HAI causes
  • colonisation sites act as resevoir for future infection

*S. aureus commonly identified agent for skin and soft tissue infections
=> local complications or distant septic mets
- bones and joints (esp w/ prosthetics)
- epidural space and intervertebral discs
- native and prosthetic cardiac valves
- visceral abscesses in spleen, kidney, lungs

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2
Q

Investigations of S.aureus bacteraemia

A

Microscopy + culture before commending Abx Rx

Repeat cultures after commencing AbxRx

Biopsy (bone)

XR, CT, MRI, Radionuclide imaging

  • lung abscess
  • septic lung emboli? = CT pulmonary angiogram

Transthoracic echo.= TOE

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3
Q

Management of S. aureus bacteraemia​

A

> FLUCLOX: uncomplicated S. aureus for 14d
(Vancomycin for allergies)

> TEICOPLANIN: single daily dosing adv.

> LINEZOLID: bacteriostatic, good bone penetration and oral bioavailability

> DAPTOMYCIN: well tolerated. daily dosing.

> VANCOMYCIN: poor penetration, slow bactericidal activity, inconvenient administration

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4
Q

Define sepsis and septic shock using the Sepsis -3 guidelines

A

life-threatening organ dysfunction caused by dysregulated host response to infection
+ SOFA >2

sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation

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5
Q

Be able to use qSOFA to determine whether a patient is more likely to require intensive care

A
  • HypoT, systolic <100
  • Altered mental
  • Tachy, RR >22/min

≥2 suggest greater risk of poor outcome

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6
Q

Understand the pathophysiology of sepsis, including the reasons why some infections present differently under different circumstances

A
• breach of host barriers, resulting in infection reaching bloodstream
=
*uncontrolled inflamm response
* features of imm suppr
- delayed hypersensitivity 
- Inability to clear infection
- Predisposition to nosocomial infection

1) Release of bacterial toxins
LPS (gram -ve); MAMP (gram +ve); SuperAg TSST or exotoxins (gram +ve)

2) Release of mediators
LPS requie binding proteins to bind to macrophages whereas LTA (MAMP) do not
= pro-inflamm mediators
or
= anti-inflamm mediators (to compensate)

3) Effects of specific excessive mediators
= dysbalance between mediator forces

anti-inflamm = septic shock w/ organ failure and death

pro-inflamm = Immunoparalysis with uncontrolled infection and multiorgan failure

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7
Q

Describe the clinical presentation of sepsis and septic shock

A

Altered mental

Tachypnoea

Jaundice; ⇧LiverEnz. ⇧PT ⇩Albumin

Oliguria/Anuria ⇧Creatinine

Tachycardia, HypoT

⇧PT ⇧D-Dimer ⇩Platelets ⇩Protein C

Fever/Hypothermia

Hyperglc. >8mmol/l in absence of DM

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8
Q

Outline the principles of clinical management of sepsis using Sepsis 6

A

take:
blood cultures, blood lactate, urine output

give:
O2 sats 94-98
IV abx
IV fluid challenge (30ml/kg)

2As
Air + Abx

2Bs
Blood culture + Blood gas with lactate (lactate marker of generalised hypoperfusion/severity + mitochondrial toxins, alcohol, malignancy)

2Cs
Crystalloid Bolus
Catheter

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9
Q

Appreciate importance of the individual components of Sepsis 6.

A

a

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10
Q

Understand the importance of empiric antimicrobial therapy in patients presenting with sepsis and in whom there is no positive microbiology

A

a

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11
Q

Outline the classification and typing of influenza viruses, including the importance of antigenic shift and drift.

A

(human only)
INFLUENZA B

INFLUENZA C

Haemagglutinin (H) Antigen (attachment and entry into cell)

Neuraminidase (N) Antigen (enables new virion to bereleased from host cell)

Ag Drift = genetic variation point mut. for Ab-binding sites = imm system cannot combat properly and produces vaccine mismatch

Ag Shift = abrupt major change in virus resulting new H/N combos = species jump, or creation of new subtype + genetic reassortment

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12
Q

Outline the epidemiology of seasonal, epidemic and pandemic influenza

A

Pandemic affects more of the population, more complications, sporadic timing, affects greater age range

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13
Q

Outline the laboratory diagnosis of influenza

A

a

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14
Q

Describe the presentation of influenza in the community and of severe disease (including possible complications) in a hospital setting

A

Incubation = 2-4d

Abrupt fever
\+cough
\+sore throat
\+ myalgia
\+headache
\+malaise

systemic
viral swabs; PCR
* CXR
* blood culture

=> acute bronchitis;
2º bacterial pneumonia - CURB65

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15
Q

Describe the role of antiviral agents in the treatment of influenza

A

within 48hr of symptom onset and risk of complication development

NEURAMINIDASE INHIBITORS
> OSELTAMIVIR (oral) - uncomplcated
n/v, abdo pain, diarrhoea

> ZANAMIVIR (inhaled/IV)
rare adverse effects

Prego
> Oseltamivir (oral)

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16
Q

Describe the role of immunisation in preventing outbreaks of influenza

A

Seasonal flu vaccine contains 3 viral dna = most likely circulating
0.5ml intramuscular injection

*sore arm adverse effect

UNIVERSAL VAX:
only contains the HA stem = less likely to change unlike the HA head.

17
Q

CURB65

A
Confusion
Urea >7mmol/l
Respiratory rate >30mm
Blood Pressure (diastolic <60 or systolic <90)
>65 years of age
18
Q

When does an individual become non-infectious?

A

IMMUNOCOMPETENT ADULTS

24hrs after last ‘flu symptoms (fever & cough)
Or when anti-viral therapy completed
Which ever is longer

19
Q

Define the term zoonosis.

A

Infectious diseases transmitted naturally between humans and animals wild or domestic​

Enzoonotic - animal resevors > humans but little onward transmission

20
Q

Appreciate the epidemiology of these diseases.

A

SPILLOVER = moving from different zoonotic pools to humans

21
Q

Recognise the common clinical features of the most important zoonoses - brucellosis, Lyme disease, toxoplasmosis, leptospirosis, Q-fever, psittacosis

A

BRUCELLOSIS

LYME DISEASE (Borrelia burgdorferi)

  • tick, lxodes ricinus
  • summer months
  • NEUROBORRELIOSIS: facial nerve palsy, radicular pain (worse at night), lymphocytic meningitis

*erythema mgrans OR ELISA then IMMUNOBLOT

> DOXYCYCLINE; AMOXICILLIN
CEFTRIAXONE

TOXOPLASMOSIS

LEPTOSPIROSIS (Spirochete - L. icterohaemorrhagica, L. hardjo)

  • contaminated water
  • Undifferented fever; myalgia, headaches & abdominal pain
  • severe disease is low probability = jaundice, AKI, bleeding; or pulmonary haemorrhage

*IgM & IgG / microscopic agglutination test

> DOXYCYCLINE
(2) AMOXICILLIN
CEFTRIAXONE (severe)

Q-FEVER (Coxiella Burnetti)
- farm animals

*prego, imm compr., heart valve disease

PSITTACOSIS (Chlamydia psittaci)

  • birds
  • respiratory symptoms

RABIES (LYSSAVIRUS)
- virus ascends spinal cord > encephalitis

  • hydrophobia, insomnia, confusion
  • ascending flaccid paralysis; fever; confusion; coma
  • PCR skin biopsy, saliva

> Milwaukee protocol
Antibody

22
Q

Describe the long-term sequelae of Lyme disease

A

higher proportions of sequelae reported from exposed patients were: neck pain, myalgia, arthralgia, paresthesia, sleep disorder, poor appetite, and concentration difficulties.

23
Q

Understand how to approach the diagnosis and treatment of common zoonoses.

A

a