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Microbiology > Infections of Immunocompromised host > Flashcards

Infections of Immunocompromised host Flashcards

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1
Q

What is primary immunodeficiency?

A

Inherited (so quite rare)

- due to exposure in utero to environmental factors

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2
Q

What is secondary immunodeficiency?

A

An underlying disease state or treatment for a disease that inhibits/wipes out part of the immune system
- common

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3
Q

Why are numbers of immunocompromised patients increasing?

A

Improved survival at the extremes of life
Improved cancer treatment
Developments in transplant techniques
Developments in intensive care
Management of chronic inflammatory conditions
- immunomodulatory agents including steriods

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4
Q

What is the most common cause of morbidity and mortality in the immunocompromised host?

A

Infections - a specific deficiency increases susceptibility to pathogens normally eradicated by that defense mechanism

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5
Q

A specific deficiency increases susceptibility to pathogens

normally eradicated by that defense mechanism, but why is it not always that straightforward?

A

Basic patterns are recognisable, but organisms are unpredictable
Isolated deficiencies are rare as there is a complex interplay of pathways
- malfunction of one part often influences another
Underlying diseases and their treatment affect a range of mechanisms

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6
Q

Which parts of the immune system do cytotoxic drugs, irradiation and steroids affect?

A

Neutrophil function

  • Chemotaxis
  • Phagocytic activity
  • Intracellular killing
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7
Q

If netrophil function is affected, which pathogens are most likely to infect a patient?

A 
Gram positive cocci
- staph aureus 
- coagulase negative staph
- viridans strep
- enterococci
Anaerobes
- bacteriodes
- clostridia 
Gram negative bacilli
- E.coli
- pseudomonas aeruginosa 
- klebisella pneumoniae
- enterobacter 
Fungi
- cadida
- aspergillus
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8
Q

Describe chronic granulomatous disease.

A

An X-linked inherited disorder (most common inherited)
Defect in gene coding for NADPH oxidase
- deficient production of oxygen radicals
- defective intracellular killing
Recurrent bacterial and fungal infections
- abscesses in the lungs, lymph nodes and skin
- inflammatory responses; widespread granuloma formation

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9
Q

What are the most common pulmonary infections in chronic granulomatous disease?

A

Aspergillus
Staph aureus
Nocardia

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10
Q

What conditions/drugs suppress cellular immunity?

A

DiGeorge syndrome - failure of T-cell proliferation
Malignant lymphoma
Cytotoxic chemotherapy
Extensive irradiation
Immunosuppressive drugs
Allogenic stem cell transplantation, especially in GvHD
- because of high dose steriod treatment
Infections - HIV, mycobacterial infections, measles, EBV and CMV

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11
Q

Which kinds of immunosuppresive drugs cause suppression of cellular immunity?

A

Corticosteriods
Cyclosporin - immunosuppressant used to prevent organ rejection
Tacrolimus - more potent than cyclosporin
Alemtuzumab - anti-CD52 monoclonal
Rituximab - anti-CD20 monoclonal used in rheumatoid arthritis
Purine analogues (fludarabine) - causes profound lymphopaenia used in cytotoxic chemotherapy

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12
Q

What are some causes of humoral immunity suppression?

A 
Bruton agammaglobinaemia (primary, rare)
Lymphoproliferative disorders cause decreased antibody production
- CLL, multiple myeloma
- preserved in acute leukemia
Intensive radio/chemotherapy
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13
Q

What happens if someone doesn’t have a spleen, or it is under active?

A

Splenic macrophages eliminate non-opsonised microbes (encapsulated bacteria) with a specific opsonising antibody required for phagocytosis of encapsulated bacteria
- lack of this impairs activity of all phagocytic cells

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14
Q

What bacteria/viruses are most likely to affect someone with humoral deficiency, splenectomy or hyposplenism?

A

Strep pneumoniae
Haemophilus influenzae type B
Neisseria meningitidis

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15
Q

What are the physical barriers against microbial invasion?

A 
Skin
Conjunctivae 
Mucous membranes
- gut
- respiratory tract
- GU tract
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16
Q

How do we protect out mucosal surfaces from colonisation?

A

Colonisation resistance occurs due to our normal flora

- they coat our mucous surfaces and stop colonisation of pathogenic organisms (e.g. C.diff)

17
Q

How is our skin effective at preventing pathogenic invasion?

A

Desquamates - high turnover physically removes organisms from the skin surface
Dry
Slightly acidic pH
Temperature 5C cooler than the body, so the organisms can’t live
Secretory IgA in sweat

18
Q

What impairs the integrity of the skin?

A 
Chemotherapy/irradiation
Cuts
Abrasions 
Sclerosis 
Burns
Surgical incisions - cellulitis common
Lines/needles
19
Q

Why are lines and needles important methods of infection in an immunocompromised host in a hospital environment?

A

Hickman lines - chemotherapy administration
Venflons
- used and wiggled too often
- organisms can travel up the venflon or sit in the port and wait for it to be opened
- S.aureus
- cellulitis due to disseminated S.aureus

20
Q

How can organisms be introduced into the body and enter through mucosal surfaces?

A

Ventialtion - direct lines of access into respiratory tract

21
Q

How can chemotherapy and irradiation impair the integrity of the GI tract?

A

High mitotic index and inflammatory response in the lymphoid tissue.
This causes mucositis -> pain, dysphagia, xerostomia and ulceration
- if the pH is affected, the organisms may be able to survive the stomach
This impairs GI function and its permeability
Nutritional status is altered

22
Q

How does impaired nutritional status cause immunodeficiency?

A

Compromise integrity of the host defences
- Anorexia
- Nausea and vomiting
- Mucositis
- Metabolic derangements
Iron deficiency reduces microbial capacity of neutrophils and T-cell function

23
Q

What is the clinical definition of severe nutritional deficiency?

A

less than 75% ideal body weight
or
rapid weight loss and hypoalbuminaemia

24
Q

How can organ dysfunction lead to increased susceptibility for infection

A

Obstruction - build up of secretions increases susceptibility
CNS tumors/spinal cord compression
- loss of cough/swallow reflex
- incomplete bladder emptying
Diabetes mellitus - reduced opsonisation, chemotaxis
Stress - reduced T-cell function

25
Q

Why are premature babies more at risk of immunosuppression?

A

Intubation risks
- no surfactant means they can’t breath properly
Can’t develop normal gut flora like most babies do when they go home with their families
- hospital flora, which are very resistant
Chronic lung disease and infection are biggest risks

26
Q

What is the greatest risks to remember when thinking about infection in solid organ transplantation?

A

Normal signs and symptoms of infection are diminished/not present due to the immunosuppressive drugs the patient is on
- no antibody response

27
Q

How should infection in solid organ transplantation be managed?

A

Prophylactic therapy is most important
- bacterial
- fungal
- viral
Empirical therapy is the only option for treatment
- choice is complicated due to drug interactions/toxicities
- resistance is common

28
Q

What infections are most common less than one month after a transplant?

A

Donor associated infections
- latent (TB, syphilis, HIV)
- active at time of procurement (staph, E.Coli)
Pathogens in patient at the time of transplant

29
Q

What infections are most common 2-6 months after a transplant?

A

Opportunistic infections

  • community acquired
  • aspergillus
  • pneumocystis
30
Q

How can pneumocytis jerovecii be identified?

A

Respiratory infection
- cough, dyspnoea, wheeze, shortness of breath
Fine mottled appearance on lung fields

31
Q

What is the most concerning feature of aspergillus infections?

A

This spore producing fungus that erodes into large blood vessels and causes hemorrhage

  • can disseminate widely
  • stroke
32
Q

If an immunocompromised patient comes in with neutropaenic fever, what is the diagnosis?

A

Infection until proven otherwise

33
Q

What is septic shock?

A

Sepsis induced hypotension requiring inotropic support
OR
Hypotension that is unresponsive to adequate fluid resuscitation

34
Q

What is the definition of febrile neutropenia?

A

A neutrophil count of less than 0.5 (or less than one is they have recent chemotherapy
PLUS
Fever/hypothermia or SIRS or SEPSIS/SEPTIC SHOCK

35
Q

What is the immediate clinical management of neutropenic sepsis (fibrile netropenia)?

A 
SEPSIS 6
Deliver high flow oxygen
IV fluid resuscitation
Blood cultures before antibiotics
IV antibiotics as per risk category 
Serum lactate and PBC
Urine output and consider catheter
36
Q

When assessing someone for neutropenic sepsis, what things must you remember?

A

Don’t wait for confirmation of neutropenia in patients who are haemodynamically compromised
Assess with 15 mins of presentation
Assess sepsis severity with NEWS
Institute SEPSIS 6 withing one hour

37
Q

What antibiotics are given in cases of neutropenic sepsis?

A

IV Piperacillin/tazobactam (Tazocin)
or
IV Vancomycin and ciprofloxacin or azteronam
- consider gentamicin

38
Q

What antibiotics are given in cases of neutropenic sepsis with septic shock or a NEWS greater than 5?

A

IV Piperacillin/tazobactam (tazocin) and gentamicin
or if allergic
IV Vancomycin, gentamicin and ciprofloxacin or azternam

39
Q

What antibiotics are used for known ESBL carriers, acute leukemia or an AlloSTC?

A

IV meropenem (for intoropic support)
And
an aminoglycoside

Microbiology (21 decks)

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