Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

4 - Y5 a Path lectures 2021/22 > Microbiology 3S: Infection CPC > Flashcards

Microbiology 3S: Infection CPC Flashcards

1
Q

Diagnosis?

A

Community Acquired Pneumonia → Infective exacerbation of COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tx of Community Acquired Pneumonia?

A

co-amoxiclav + clarithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe this CT chest. What does it show?

A
  • patchy consolidation + ground-glass opacity in both lungs;
  • predominant in upper and mid-zones in distribution
  • = PCP (pneumocystitis pneumonia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What should be conducted after ground glass opacities are seen on CT chest?

A
  • sputum induction,
    • expectorated sputum has poor sensitivity, should not be used
    • → direct fluorescent-antigen testing → +tive for Pneumocystis

if sputum negative:

  • → bronchoscopy + bronchoalveolar lavage
    • → stained with Grocott-Gomori methenamine-silver stain → +tive for Pneumocystis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the typical clinical picture of PCP?

A
  • SoB ON EXERTION (reduced exercise tolerance)
  • low O2 sats
    • SpO2 tends to drop on exertion more
  • CXR = fairly normal,
  • CT = ground-glass shadowing (widespread, bilateral)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Algorithm for PCP diagnosis if clinically suspected?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Causative organism of PCP?

A

Pneumocystis jirovecii pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Tx for PCP? Risks?

A
  • 1st line: co-trimoxazole 960mg BD
    risk: widespread erythematous rash → co-trimoxazole stopped → OD prednisolone
  • 2nd line: Clindamycin + Primiquine (G6PD norm) + IV methylprednisolone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diagnosis?

A

PCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnosis?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does this show (bronchoalveolar lavage from bronchoscopy)?

What stain has been used?

A
  • The arrow is pointing at one of the cysts (PCP)
  • Visualised using a methenamine silver stain (Grocott-Gomori)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Epidemiology of PCP?

A
  • AIDS defining illness of lung
  • commonly found in HIV +tive patients or those who are immunosuppressed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the natural history of HIV-1 infection?

A
  • Seroconversion (development of specific antibodies in the blood serum as a result of infection or immunisation) → symptoms
    • (e.g. fever, rash)
  • Eventually, viral load falls & CD4 count recovers
  • Then asymptomatic, which can last for years
  • Eventually, viral load rises & CD4 count falls
  • Then, immunocompromised and at risk of AIDS-defining conditions e.g. PJP/PCP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which parameter is a major major determinant of immune damage in HIV?

A

CD4 count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which conditions can develop as CD4 count falls in the later months/years of HIV infection?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the infection agents in HIV?

A
  • Common agents (e.g. pneumococcus)
  • Uncommon agents (often ubiquitous but cause no problem in immunocompetent patients)
    • Atypical mycobacteria
    • Viral (CMV, HSV [i.e. reactivation])
    • Fungal
    • Other(e.g.toxoplasmosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the presentation of infections vary in HIV +tive patients vs HIV -tive?

A
  • Normally, the symptoms of an illness are due to the immune response rather than the pathogen itself
  • So, the presentation in HIV can be quite abnormal (due to immune compromise)
    • I.E. may present with miliary TB or TB meningitis
  • Speed of progression may also be different
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes of immunodeficiency?

A
  • Inherited
  • Acquired
    • Iatrogenic
      • Immunosuppressive agents e.g. Steroids
      • Chemotherapy
      • Radiotherapy
    • HIV
    • Chronic illness (diabetes, cancer)
    • Malnutrition
19
Q

What are the infectious agents & general features of infection in:

  • B cell defect
  • T cell defect
  • neutrophil defect
  • complement defect
A
20
Q

Diagnosis?

A

meningoencephalitis (following lung transplant - immunocompromised)

21
Q

Brain. Diagnosis?

A

cryptococcus fungal meningoencephalitis

(following lung transplant - immunocompromised)

22
Q

What infection can alcoholics get?

A

~ be immunodeficient

can have infections from:

  • common organisms e.g. pneumococcus
  • uncommon organisms e.g. Actinomyces
23
Q

What is Actinomyces?

What can it cause clinically?

A

Gram-positive rod that branches

Causes lung abscesses in immunocompromised patients

24
Q

Describe the course of Actinomyces

A
  • indolent/slow-growing
    • slow growing HENCE = hard to grow in labs, notify histopathologists that you’re worried about Actinomyces infection so they can start growing ASAP
  • go on for a long time,
  • very difficult to treat
25
Q

Lung. Diagnosis?

A

Actinomyces lung abscess

  • right picture: basophilic/sulfur granules
26
Q

What stains are used on culture of pus/histology of lung tissue for ?actinomyces

A
  • Gram stain (microbiology lab)
    • gram +tive
    • branched!
  • Grocott stain (histopathology lab)
27
Q

What is the 1st line Tx for Osteomyelitis?

A

IV flucloxacillin (staph aureus cover)

28
Q

What should be done if initial Tx for osteomyelitis is insufficient?

A
  • Washout and debridement – deep infection therefore metal work removed
    • Required as organisms that grow on prosthetics often form biofilms which ABx cannot penetrate
  • → culture organism in lab
29
Q

Which Abx has good penetration & biofilm-disrupting activity?

(useful for osteomyelitis in cases where there is metalwork present)

A
  • rifampacin
30
Q

What are the general Mx principles of osteomyelitis?

A
  • Antimicrobial therapy alone is NOT curative in most cases of osteomyelitis
  • Continuous drug over a long period of time will lessen the amount of discharge, but it will not cure the disease because it cannot sterilise dead bone or cavities with necrotic content and rigid walls
  • Removal of devitalised tissues and prevention of extension of infection with adequate drainage is important
    • i.e. (removal of prosthesis) + aggressive surgical debridement
  • Fibrous capsules can form which makes it impenetrable to ABx and it becomes a chronic source of infection
31
Q

Principles of prosthetic joint infection?

A

Removal of prosthesis and adequate debridement is the MOST IMPORTANT part of treatment

  • Antibiotics play a secondary role (NOTE: in this case, the organisms remained sensitive to antibiotics for months, however, treatment failed due to the presence of infected prosthetic material and inadequate debridement)
  • However, the consequences of aggressive debridement must be considered (it carries significant morbidity)
  • Consider other sources of infection:
    • Intravascular lines (e.g. venflons, central lines, PICC lines)
    • Prosthetic heart valves (ends of the valves are poorly vascularised so it is difficult to treat infection)
    • Prosthetic implants (e.g. cosmetic or reconstructive)
32
Q

Initial Tx of chronic leg ulcers (erythematous, painful and has fevers)?

A
  • IV ceftriaxone + metronidazole
    • metronidazole = strep and staph cover
  • IV vancomycin
    • MRSA cover

immediate → leg ulcer swab

33
Q

If leg ulcer swab grew Pseudomonas aeruginosa, what is the Tx?

A
  • IV piperacillin/tazobactam OR
  • PO clindamycin + ciprofloxacin + gentamicin
34
Q

What organisms are cultured for in a faeces sample as routine?

A
  • Salmonella
  • Shigella
  • E. coli O157

Must be asked for:

  • Campylobacter
  • C. difficile toxin (automatically done if >65yrs)
35
Q

Summarise C difficile infection

A
  • Clostridium difficile-associated disease usually presents with:
    • diarrhoea - explosive, watery, foul-smelling
  • abdominal pain,
  • leukocytosis,
  • Hx of recent ABx use,
  • fever,
  • abdominal tenderness, and distension.
  • Testing should be limited to patients with unexplained, new-onset diarrhoea (defined as 3 or more unformed stools in 24 hours)
  • Tx:
    • discontinue the inciting antimicrobial agent
      • start therapy with oral fidaxomicin / vancomycin
36
Q

What bloods are commonly seen in C difficile infection?

A

high WCC + low CRP

37
Q

What is the aetiology of C difficile infection?

A
  • Broad-spectrum ABx disrupt the normal bowel flora,
    • most commonly ampicillin, cephalosporins, clindamycin, carbapenems, and fluoroquinolones
  • → Clostridium difficile colonisation occurs after this disruption to bowel flora by ingestion of heat-resistant spores (foeco-oral)
  • → spores convert to vegetative forms in colon
  • → Pseudomembranous colitis
    • you are left with fibrous plaques and damaged material which looks like membranes

Can also be precipitated by:

  • cytotoxic drugs,
  • antacids/PPIs,
    • NOTE: PPIs are a risk factor because they raise the pH of the stomach, meaning that more GI flora and C. difficile spores can survive the stomach and travel down to the colon
  • non-surgical GI procedures (e.g. NG tubes)
38
Q

What toxins does C difficile produce?

A

One toxin damages the epithelial cells (cytotoxin) → neutrophil infiltration of tissues

The other disrupts the tight junctions → loss of fluid within the bowels

39
Q

What must be done once patient tests positive for C Difficile?

A
  • Isolate in single room
  • Assess severity
  • Stop offending ABx if possible
  • Wash hands with soap and water before and after each patient contact and use gloves and apron
  • Commence C. difficile care pathway, fluid balance chart and Bristol stool chart
40
Q

How is C difficile infection classified/stratified according to severity in Imperial guidelines?

A
41
Q

What are the Imperial C difficile guidelines?

A
42
Q

What is the superbug type of C. difficile? Summarise

A
  • C. difficile Ribotype 027
  • Associated with a severe outbreak in June 2005
  • Associated with increased severity of disease
  • Produces:
    • 16x more toxin A
    • 23x more toxin B
43
Q

Colon. What does it show?

A

pseudomembranous colitis

44
Q

Colon. What does it show?

A

Pseudomembranous colitis

4 - Y5 a Path lectures 2021/22 (37 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions