31 Infections in the compromised host Flashcards

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1
Q

What are primary and secondary defects of innate immune system?

Primary is more common in paediatric population
Secondary more common in adults

A

Primary -

  • complement deficiency
  • phagocyte cell deficiencies - e.g chronic granulomatous disease

Secondary -

  • burns
  • trauma
  • surgery
  • catheter
  • foreign body e.g joint/ shunt
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2
Q

What are defects of adaptive immune system?

Primary

A

Primary (T/ B cell defects) -
- B cells - Burton-type agammaglobulinaemia due to lymphocyte production error in bone marrow

  • T cells - DiGeorge. Thymus problem means lymphocytes cannot mature
  • SCID (severe combined immunodeficiency) which is genetic defect in which antibodies cannot be fully formed by B cells, and T cells cannot produce antigen recognition receptors
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3
Q

What are defects of adaptive immune system?

Secondary

A

Secondary -

  • malnutrition
  • infectious disease
  • neoplasia
  • radiation
  • chemotherapy
  • splenectomy
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4
Q

Which infections cause immunosuppression?

A
Measles
Mumps
Rubella
EBV
CMV
HIV
HTLV

Mycobacterium tuberculosis/ leprae
Brucella

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5
Q

Burn wound become colonised within few hours of injury. What are most common pathogens?

A
Pseudomonas
Staph aureus
Staph pyogenes 
enterococci
Candida

Once skin invaded, can easily invade lymphatics/ blood

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6
Q

Staph epidermidis in blood culture is often contaminant.

In which clinical situations should we be concerned?

A

IE

Prosthetic joint septic arthritis

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7
Q

Haematological malignancy - why are they risk of infection?

A

Significant neutrophil deficiency

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8
Q

What are examples of opportunistic pathogens?
Any opportunistic pathogen infection should mean we consider testing patient for HIV

Viruses

A
HBV
HCV
HIV
Polyomaviruses - BK, JC
Adenovirus
Herpes - HSV, VZV, EBV, CMV, HHV6, HHV7, HHV8
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9
Q

What are examples of opportunistic pathogens?
Any opportunistic pathogen infection should mean we consider testing patient for HIV

Fungi

A
Candida
Aspergillus
Cryptococcus
Histoplasma
PCP
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10
Q

What are examples of opportunistic pathogens?
Any opportunistic pathogen infection should mean we consider testing patient for HIV

Parasites

A

Toxoplasma

Strongyloides

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11
Q

What are examples of opportunistic pathogens?

Gram-positive

A
Staph aureus
Coagulase-negative staph
Streptococci
Listeria
Nocardia
Mycobacterium TB/ MAC
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12
Q

What are examples of opportunistic pathogens?

Gram negative

A

Enterobacteraceae

Pseudomonas

Legionella

Bacteroides

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13
Q

How do glucocorticoids cause immunosuppression?

A
  • induce the apoptosis of lymphocytes
  • alter leukocyte migration and redistribution
  • inhibition of cytokine gene expression, resulting in a decreased release of interleukins (IL), interferons (IFN) and tumor necrosis factor (TNF), such as IL-2, IL-6, IFN-γ and TNF-α,
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14
Q

Histoplasmosis lives in soil, transmitted airborne. Causes mild infection in immunocompetent. Can cause infection in immunocompromised years after exposure

Which countries have histoplasmosis?

A

Have low threshold for investigation if have ever visited these areas -

USA
SA
Sub-Saharan Africa (African histoplasmosis)
Asia

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15
Q

Histoplasma can spread from alveoli, via lymphatics, and cause disseminated disease many years later.

How to diagnose histoplasma infection?

A

Culture of blood, sputum, BAL may yield organism

May need bone marrow/ lymph node biopsy

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16
Q

What is treatment of histoplasma infection?

A

Amphotericin

Itraconazole can be given after for long term prophylaxis

17
Q

Aspergillus has worldwide distribution. Lives in soil, transmitted airborne. Causes mild infection in immunocompetent.

Invasive aspergillosis has high mortality rate

What are treatment options for invasive aspergillus?

What is prophylaxis?

A

Treatment -

  • Amphotericin B IV
  • reduction in steroids/ immunosuppression may be required

Prophylaxis - capsofungin, posaconazole, voriconazole

18
Q

How to diagnose PCP infection?

A

BAL sample required

PCR - NNUH

19
Q

What is treatment of PCP?

A

Moderate-severe PCP (PaO2 <9.3kPa) -

  • co-trimoxazole high dose, 21 days
  • plus corticosteroids 40mg BD 5 days, 40mg OD 5 days, 20mg OD 11 days

Mild PCP
- co-trimoxazole oral 21 days

Pentamidine/ dapsone/ primaquine alternatives

20
Q

Actinomycetes are gram positive rods, closely related to mycobacterium. Different in that they form branching filaments.

Primarily infect lungs or skin, but can spread to kidney/ CNS. Ubiquitous in soil

What are main species of Actinomycetes?

A

Actinomyces

Nocardia asteroides

21
Q

Actinomycetes (actinomyces/ nocardia) are slow growing, and easily overgrown by commensals. Therefore need special culture media

What is treatment?

A

Co-trimoxazole
Sulphonamides
Aminoglycosides

Antibiotics for 6-12 months

22
Q

MAC affects those who are immunocompromised. Ubiquitous in water

How does it present?

A

Usually pulmonary involvement

Can affect any system - CNS, liver, bone marrow/ GI

23
Q

How does MAC treatment differ to M. TB?

A

MAC is resistant to conventional antituberculosis drugs

High dose azithromycin/ clarithromycin with rifampicin and ethambutol

Continue for 1 year after culture negative

24
Q

Diagnosis of MAC is important.

How to diagnose?

A

Culture/ stain on sputum/ blood/ stool depending on symptoms

Often cases of MAC mis-diagnosed as TB

25
Q

HIV/ HTLV are associated with strongyloides activation and can cause life threatening disseminated infections. Lungs/ brain/ liver most commonly infected

Which countries have strongyloides?

A

NA
SA
Africa
Asia

26
Q

What is epidemiology spread of HTLV?

A

SA
Africa
Asia

NA/ UK/ Australia to lesser extent

27
Q

Complement deficiency/ asplenia increases risk of infection.

Which organisms?

A

Encapsulated organisms

Neisseria meningitidis
Neisseria gonorrhoea
Streptococcus pneumoniae
Hameophilus influenzae

28
Q

Patient presents with candidaemia. What other investigations are required?

A

Investigate source e.g cannula

Investigate immunodeficiency - HIV test

ECHO

Ophthalmology

29
Q

27 year old Carribbean woman with SLE, treated with rituximab. Presents with diarrhoea.

What is most likely cause of symptoms?

Cryptosporidium
Cyclospora
Giardia
Isospora
Strongyloides
A

Giardia

Rituximab is monoclonal antibody to CD20, expressed on all mature B cells (except plasma cells) and can cause hypogammaglobulinaemia

No travel history definitely given, so giardia is most likely. Although others (except strongyloides) can be acquired in UK

30
Q

Renal patient about to receive transplant. She is CMV IgG negative. Potential living donor is CMV IgG positive

What is next step?

Do not go ahead with transplant
Give IVIG post-operatively
Give valganciclovir prophylaxis for 90 days
Transplant and monitor CMV DNA monthly
Transplant with no prophylaxis/ monitoring

A

Give valganciclovir prophylaxis for 90 days as high risk of primary infection

31
Q

57 year old with RA about to commence rituximab. HBV serology

HBsAg neg
HBcAb pos
HBsAb 10 MIU/ml
HB DNA <20 IU/ ml

What is next step?

  • Do nothing - is now immune to HBV after past exposure
  • Monitor HBV DNA/ LFTs weekly
  • Offer booster HBV vaccine prior to rituximab
  • Start entecavir prophylaxis until end of rituximab
  • Start prophylaxis lamivudine before rituximab
A

Start prophylaxis lamivudine before rituximab and continue for 18 months after cessation of rituximab.

Tenofovir/ entecavir are newer drugs, which may be offered

All B-cell depleting therapies with anti-HBc positive should be on prophylaxis

If HBsAg and anti-HBc positive - should be on full HBV treatment