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Year 5 - Pathology > MICRO: Infection CPC > Flashcards

MICRO: Infection CPC Flashcards

1
Q

What is shown on this CXR?

A
  • Bilateral shadowing
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2
Q

If you suspect atypical CAP but treatment does not work, patient is hypoxic and significantly desaturates on exercise,CT scan shows ground-glass opacity in both lungs, what should you suspect?

A

PCP pneumonia (pneumocystis jirovecii)

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3
Q

What is the treatment for PCP?

A

1st line: Co-trimoxazole 960mg BD

2nd line:Clindamycin + Primiquine (G6PD norm), IV methylprednisolone

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4
Q

What CD4 count should prompt you to start prophylaxis for PCP?

A

<200 cells/mm3

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5
Q

The arrow is pointing to a PCP cyst. What stain has been used here?

A

Methenamine silver stain (Grocott-Gomori)

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6
Q

At what time point is the viraemic peak in HIV infection?

A

4 weeks post-infection –> viraemic peak

Seroconversion –> symptoms (e.g. fever, rash)

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7
Q

Which type of lymphoid tissue does HIV tend to target?

A

gut-associated lymphoid tissue (GALT)

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8
Q

What is the major determinant of immune damage and short term outlook in HIV?

A

CD4 count

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9
Q

List some HIV-associated infections and the CD4 count at which they would be seen.

A
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10
Q

Describe the differences that may be seen in infections in the immunodeficient compared to non-immunodeficient patients.

A

Infectious agents may vary in type or frequency:

  • Common agents common (e.g. pneumococcus)
  • Uncommon infectious agents arise (often not problematic in immunocompetent)
    • Atypical mycobacteria
    • Fungal
    • Viral (CMV, HSV [i.e. reactivation])
  • Other (e.g. toxoplasmosis)

Speed of progression may also be different

Presentation may be different

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11
Q

List 5 causes of immunodeficiency.

A
  • Inherited
  • Acquired
    • Iatrogenic
      • Immunosuppressive agents
      • Steroids
      • Chemotherapy
      • Radiotherapy
    • HIV
    • Chronic illness (diabetes, cancer)
    • Malnutrition
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12
Q

Name an infection associated with…

  1. T cell defects
  2. B cell defects
  3. Neutrophil defects
  4. Complement defects
A
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13
Q

Which types of infections are alcohol-dependent patients at risk of?

A
  • Encapsulated organisms
  • Indolent/slow growing organisms e.g. Actinomyces
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14
Q

What is actinomyces? What are the complications of actinomyces infection?

A

Actinomyces:

  • Gram-positive rod that branches
  • Closely related to Nocardia (another gram +ve rod)

Complications:

  • Causes lung and brain abscesses in immunocompromised patients
  • Difficult to treat
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15
Q

If you suspect Actinomyces, what must you tell the lab?

A

Notify the histopathologist and microbiologist that you are worried about actinomyces so they can start growing ASAP.

May need to keep on culture for longer and histopathologists can look for typical features

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16
Q

What are the histopathological features of actinomyces?

A

Basophilic granules or ‘sulfur granules’

17
Q

What are the microbiological features of actinomyces?

A
  • Gram +ve rods which form branches
  • Grocott stain is used
18
Q

What is the most important principle of management of osteomyelitis?

A
  • Removal of devitalised tissues and prevention of extension of infection with adequate drainage is important
  • Antibiotics play a secondary role
19
Q

What feature shown here in osteomyelitis, can make it difficult for antibiotics to reach the source of infection?

A

Fibrous capsule - impenetrable so antibiotics cannot enter (created as it keeps the infectin ‘out of sight’ from the immune system).

This would cause treatment failure, even if the correct antibiotic was being used.

20
Q
A
21
Q

What are faecal cultures routinely tested for?

A
  • Salmonella
  • Shigella
  • E. coli O157
  • Campylobacter
  • C. difficile toxin – only tested for in those <65 years, need to ask otherwise
22
Q

What actions need to be taken in suspected C difficile?

A
  1. Isolate in single room – 1g = 1 billion spores so very transmissible
  2. Assess severity
  3. Stop offending ABx if possible
  4. Wash hands with soap and water before and after each patient contact and use gloves and apron – C diff forms spores
  5. Commence C. difficile care pathway, fluid balance chart and Bristol stool chart
23
Q

How transmissible is C difficile?

A

1g faeces = 1 billion spores so very transmissible

24
Q

How do you assess the severity of C. difficile i.e. what factors are/are not considered?

A

Imperial C. difficile guidelines

  • T>38.5ºC
  • HR>90
  • WCC>15
  • Rising Creatinine
  • Clinical or radiological signs of severe colitis
  • Failure to respond to therapy at 72h

Severe = 1 or more of the following –> early surgical and gastroenterology review

DIARRHOEA is not part of the criteria

25
Q

Why is diarrhoea not part of the scoring system for C difficile severity?

A

With very severe cases you may get an ileus and megacolon which is a surgical emergency. With this you do not pass any diarrhoea at all.

26
Q

What is the management of non-severe C difficile?

A

1st line:

  • Metronidazole 400mg PO TDS 10-14 days

If not responding after 72 hours:

  • Consider changing to: Vancomycin 125mg PO QDS 10-14 days
27
Q

What is the management of severe C difficile infection?

A
  1. Vancomycin 125mg PO QDS 14 days + consider adding metronidazole 500mg IV TDS
    • discuss with ID: higher doses of vancomycin may be appropriate in severely ill patients

Fidaxomycin is a new drug associated with fewer relapses so may be increasingly used

28
Q

What is the management of severe C difficile with colonic dilatation?

A
  1. Vancomycin 125-250mg PO QDS + metronidazole 500mg IV TDS 14 days
    • liaise with ID/micro, gastroenterologists/surgeons as they may get an ileus/megacolon requiring emergency surgery
29
Q

What is the management of severe C difficile with ileus/vomiting?

A
  1. Consider intracolonic vancomycin
    • liaise with ID and gastroenterologist surgeons
30
Q

What are the characteristics of C difficile Ribotype 027? What toxins does it produce?

A

This is a superbug type of C difficile associated with a severe outbreak in June 2005.

  • Increased severity of disease
  • Increased mortality
  • Produces:
    • 16 x more toxin A
    • 23 x more toxin B
31
Q
A

All of them

Overuse of any antibiotic can cause C. difficile (although metronidazole is used to treat in some cases)

32
Q

How does C difficile spread?

A

Faecal-oral route through spores

33
Q

What are the risk factors for C. difficile infection?

A
  • Antibiotics use
  • 65+ years (many children colonised but do not get problems)
  • Duration of hospital stay (after 4 weeks, half of patients become positive)
  • Severe underlying diseases
  • Almost always associated with a recent history of antibiotic use (clindamycin, cephalosporin, ciprofloxacin)
34
Q

Name 3 antibiotcs whose recent use is associated with C. difficile infection.

A

clindamycin, cephalosporin, ciprofloxacin

35
Q

What other iatrogenic causes can precipitate C difficile?

A
  • Cytotoxic drugs
  • Antacids/PPIs – the higher the pH the more GI pathogens and more spores survive to travel to the colon where they germinate
  • Non-surgical GI procedures (e.g. NG tubes)
36
Q

Describe the onset of C difficile.

A

Onset is usually abrupt, with explosive, water, foul-smelling diarrhoea

37
Q

What is the pathophysiology of C difficile?

A

The organism produces two toxins:

  • One toxin damages the epithelial cells (cytotoxin) –> neutrophil infiltration of tissues
  • The other disrupts the tight junctions –> loss of fluid within the bowels

–> pseudomembranous colitis = fibrous plaques and damaged mucosa which looks like membranes

NOTE: high WCC + low CRP is common in C. difficile infection

38
Q

Is CRP always high in C difficile?

A

No, high WCC + low CRP is common in C. difficile infection

39
Q

List some measures used for prevention of C difficile infections.

A

Cleanliness and hygiene

  • Hand hygiene with soap and water
  • Isolation
  • Use of PPE
  • Enhanced environmental cleaning (with chlorine)

Restrictive approach to antibiotic prescription

  • Only use narrow-spectrum where possible

Year 5 - Pathology (89 decks)

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