Steriods, azathiprine, mycophenalate, tacrolimus, methotrexate, cyclosporin, TNF inhibitors (the mabs).
Critical illness
Immune changes
Loss of lymphoid tissue
Drugs - sedatives, inotropes, opioids.
Overproduction of anti-inflam cytokines. Correct balance of pro and anti-inflam response needed for normal immunity.
Neuroendocrine, metabolic and hormonal facrtors
Heamatological malignancy

Increased from encapsulated bacteria (Neisseria, Strep, Haemophilus).
Mechanism poorly understood.
Immunisations and penicillin prophylaxis.
Blood transfusion
Reduced risk with leukodepleted blood.
Total body irradiation

Temporary loss of immunoglobulin. No difference in infection between IG and plasmapheresis for GB.
Results in immunosuppression as fetus has foreign antigens which mother must not attack.

White cell scans can be used to look for abscesses such as psoas (not of use in neutropenia) and gallium scans detect cancer, sarcoid and infection.

Solid organ transplant
Recipients are high risk for viral infection. Monitor CMV by PCR.
!st month post transplant

  • Wound infection, pneumonia, UTI, CRBSI.
  • Bacteria and candida.
1-6 months
  • Opportunistic infections from immunosuppression.
  • Viral (CMV most common - up to 50%. Also EBV, Hep B and C)
  • Fungal (PCP aspergillus)
  • TB
>6 months
  • Most free from infection as on low level immunosuppression.
  • Those on higher levels at same risk as 1-6 months
Antigen testing
  • CMV
  • Cryptococcus
  • Galactomannan (cell wall constituent of aspergillus)
rtPCR for RNA
  • HIV
Urinary antigen
  • Legionella, pneumococcus
Bacteria, fungi, viruses

Absolute neutrophil count (ANC) <1 x 106 increases susceptibility to infection.
Most cytotoxic drugs cause immunosuppression.
Add antifungal if fever persists for 72h.
Aspergillus most common.
Consider PCP and viruses.

Low in AIDS, marrow suppression, immunosuppressants (steroids, azathioprine, mycophenalate), Guillan Barre
T helper cell (CD4 count) assesses risk of opportunistic infections (HIV)

Biochemical markers

>25% predicts infection 1 day before WBC or pyrexia.
from previous day has a PPV of 97% for resolution of sepsis.

More sensitive and specific than CRP or IL6

TREM-1 (triggering receptor on myeloid cells) expressed in response to bacteria and fungi.

Innate (non-specific)

Physical - resists 99% orgs
Skin barrier
Antimicrobial secretions of sweat and tears
Mucous of GI tract and upper airway
Stomach acid
GI tract populated with commensals to prevent overgrowth of hostile species

- resists 1%
Do not recognise substance to be attacked
Activated immediately in response to potential threats
Comprises inflammatory response induced by cytokines, complement cascade and phagocytosis by myeloid derived WBCs (neutrophils, monocytes (macrophages), eosinophils, basophils (mast cells) and natural killer cells (kind of T lymphocyte)
Macrophages (monocytes which have migrated to tissues) phagocytose, release toxic chemicals and secrete cytokines which regulate the immune response.
Toll-like receptors on neutrophils bind LPS on cell walls of gram -ve bacteria and stimulates nuclear factor KB to ‘turn on’ cytokine induced inflammatory response.

Acute phase response
Haemopoietic system and liver switch from albumin production to acute phase proteins such as CRP and fibrinogen.
Many limit inflammation

Adaptive (specific) - resists 0.1%

Lymphoid derived B and T lymphocytes.
Presentation in lymphoid tissues (lymph nodes and spleen).
B cells synthesise and secrete antibody in response to antigen.
T cells - helper (cytokines) and killer cells (cytotoxic).
T helper cells (CD4). Type 1 proinflammatory - interferon and IL2. Type 2 and anti-inflam - IL4, 5 and 13. Both needed for immunity/healing.
  • Immunoglobulins - Ig A, D, E, G, M.
  • Bind specifically to antigens.
  • Ig and complement opsonise (tag) bacteria for phagocytosis.
  • An enzyme system of β-globulin plasma proteins.
  • Opsonises and destroys cell membranes.
  • Activated by specific Ig (classical) or drugs/toxins in the absence of antibody (alternative).