infection in the immunocompromised Flashcards

1
Q

what is the background of infections in an immunocompromised host?

A

there is a problem with some part of the immune system and disruption of specific defence or an organ or system which could be cellular or humoral. You can often predict the infection if you know the underlying disease and will generally be low pathogenicity or opportunistic infections

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2
Q

how can you get a immunodeficiency?

A

congenitally or acquired

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3
Q

what is the innate defence?

A

it is non specific - everyone has the same

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4
Q

what is the adaptive immune system?

A

it is specific - everyone has different depending on what they are exposed and adapted to - humoral or cellular

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5
Q

what are the innate defences?

A

proteins, lungs, skin, commensal flora in gut, mucous membranes

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6
Q

what comprises the proteins in innate immunity?

A

interferons, acute phase proteins, lysozymes and complement

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7
Q

what is an example of a disruption to the lungs and what does it comprise?

A

in the lungs there are goblet cells and the muco-ciliary escalator. This is involved in CF

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8
Q

what is in the skin?

A

flora, sebum and acts as a barrier - burns can disrupt

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9
Q

what alters the normal commensal gut flora?

A

antibiotic treatment - immunosupressed - candida and C difficile as opportunistic infections

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10
Q

what comprises mucus membranes?

A

tears, phagocytes and urine

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11
Q

when are you more likely to pick up an infection?

A

extremes of age, pregnancy and malnutrition

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12
Q

what are the presenting characteristics or oral thrush?

A

white plaques and candidiasis

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13
Q

how do burns affect the immune system?

A

extensive burns make hosts more susceptible to organisms such as staph aureus, psuedomonas and strep

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14
Q

what is the neutrophil important for?

A

the initial breach of the innate defences

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15
Q

how can you classify neutrophil deficiency?

A

quantitatively - less are present - neutropenic

qualitatively - lose ability to kill or chemotaxis

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16
Q

what is involved in qualitative loss of neutrophils?

A

rare and congenital - lose ability to signal - chemotaxis

the killing power is inherited such as in CGD - risk of staph aureus infection

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17
Q

what is involved in the quantitative neutrophil deficiency?

A

it may be from cancer treatment, bone marrow malignancy or aplastic anaemia. It is especially important if there are fewer than 0.5x10^9 for prolonged time, 50% will develop infection with high mortality and over 50% of those with pseudomonal infections will die within 24 hours if not treated. It can be weeks long with bacterial or fungal risk

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18
Q

what is the risk of a neutropenic patient?

A

viral infection, bacterial infection - if having chemotherapy then can cause ulcers or bacteriaemia so normal flora can enter and cause infection and fungal infections such as candida in the blood stream which is rare and causes illness. Aspergillus goes into the alveoli via inhalation of hyphal spore - if have cancer as well it is exacerbated

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19
Q

how would you treat neutropenia?

A

use the empirical therapy concept and a broad spectrum treatment. Antipseudomonal penicillin (+gentamicin) and then if doesnt work add second line therapy on such as carbapenem. Granulocyte stimulating factors are less common and are used to correct immunodeficiency

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20
Q

how can T cell deficiencies be caused?

A

they can be acquired through drugs such as steroids or ciclosporin after transplantation or congenital which is rare and results in T cell dysfunction (+hypogammaglobulinaemia)

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21
Q

where may opportunistic infections be found?

A

intracellularly

22
Q

what are examples of opportunistic a)bacteria, b)fungi and c)viruses?

A

a) listerial monocytogenes, mycobacteria
b) candida, pneumocytis or cryptococcus
c) HSV, CMV or VZV - treat with serological testing and acyclovir or ganciclovir

23
Q

how will a new patient with HIV often present?

A

cryptococcal meningitis

24
Q

what is the risk of VZV in the immunodeficient?

A

shingles

25
Q

what is cryptosporidium parvum?

A

it is a parasite that is shed in the oocytes of cattle or humans and transmitted through the fecal oral route. Most patients will recover after a prolonged illness of up to 3 weeks and will present as an adult as weight loss and as a child failure to thrive. It will take far longer when T cell deficient and the treatment is symptomatic or occasionally antibiotics

26
Q

what is the TORCH organism that affects pregnant ladies and is a risk in cat litter?

A

toxoplasma gondii

27
Q

what is hypogammaglobulinaemia?

A

it is problems with antibodies and is treated with immunoglobulin therapy to replace?

28
Q

what is a rare congenital hypogammaglobulinaemia?

A

X linked agammaglobulinaemia

29
Q

what is an acquired hypogammaglobulinaemia?

A

it is multiple myeloma or burns

30
Q

what organism can result in hypogammaglobulinaemia?

A

encapsulated bacteria such as s.pneumoniae, parasitic such as giardia lamblia

31
Q

how does giardia lamblia present?

A

diarrhoea, fatty stools and under microscope it looks like it has a face and a tail

32
Q

what bacteria are present in menigitis?

A

gram negative cocci usually

33
Q

how prevalent is complement deficiency?

A

rare - hereditary

34
Q

what is an important pathogen in complement deficiency?

A

encapsulated bacteria - need complement to help kill these - if C5-C8 are deficient then neisseria meningitidis is important as gives meningitis and then recurrent S pneumoniae infections and poor quality opsonisation

35
Q

what is the function of the spleen?

A

source of complement proteins and antibody producing B cells - remove the opsonised bacteria from the blood

36
Q

what is the risk of splenectomy?

A

high mortality - vaccination, prophylactic penicillin and education - seek help if unwell

37
Q

what is the process of sickle cell in the spleen?

A

patient has already deteriorated and in process has damaged spleen and it’s function

38
Q

what are the causes of injury to spleen?

A

surgical, traumatic or functional

39
Q

what organisms can cause injury to the spleen?

A

N. meningitidis, S. pneumoniae, H. influenzae B, malaria

40
Q

what are biologics?

A

they are antibodies or other peptides that inhibit the inflammatory cytokine cycle to prevent depletion of B cells, TNF and inhibit T cell activation

41
Q

what are biologics used in?

A

severe RA

42
Q

what is the risk of biologics?

A

risk of TB, HZV, listeria monocytogenes and legionella pneumophilia

43
Q

what is a solid organ transplant?

A

it is a whole organ such as a liver after a paracetamol overdose

44
Q

what is a stem cell transplant used in?

A

haematological malignancies

45
Q

what is antirejection medication used in?

A

supress cell mediated immunity to stop the effect of cytotoxic and natural killer cells - degree of immunosupression varies on how closely the donor and recipient are matched and the organ involved

46
Q

what is the process of organ transplantation infection?

A

initial infection, surgery and hospital admissions, organ received, opportunistic infections during initial immunosupression and then later opportunistic infections

47
Q

how would you manage the infections in the immunodeficient?

A

prevention is most important through hand washing, you need to remove catheters and lines, reverse the defect or stop immunosupression and treat the known infection using empirical concept and taking specimen samples from the likely site of infection

48
Q

what are the clinical examinations done in the immunodeficient?

A

history and examination, urgent diagnosis and treatment, blood cultures, respiratory samples and other system samples and radiology and histopathology

49
Q

what is the main management in a febrile neutropenic?

A

give broad spectrum antibiotics immediately after blood cultures

50
Q

what do you avoid in T cell deficient hosts?

A

live vaccines

51
Q

where is candida albicans found and what is the risk of this?

A

around plastic and lines - bloodstream infections

52
Q

what is the management for candida albicans infection?

A

line out and antifungal therapy for two weeks after - liposomal amphotericin B then fluconazole