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The immunocompromise patient1. AIDS.2. Other form of immunocompromise:

a. Neutropenia. b. Reduced cell-mediated immunity.c. Reduced humoral immunity.d. Incompetence of cellular element.e. Nonspecific reduction in host resistance.

1. AIDS- Pyogenic pneumonia- Mycobacterial infection

o Tuberculosiso Nontuberculous (atypical) mycobacterial infection.

- Fungal infectiono PCPo Candida albicanso Cryptococcus neoformanso Coccidiodes immitiso Histoplasmosiso Aspergilus

- Protozoal infectiono Toxoplasmao Cryptosporidium

- Human Herpesvirus infections- AIDS associated airway disease.- Thoracic neoplasm and non infectious complication

o AIDS-related lymphoma, kaposi sarcoma, lymphocytic interstitial pneumonia, persistent generalized lymphadenopathy and bronchogenic carcinoma

2. Other form of immunocompromise

- Neutropenia ; defense againts microorganism. Neutropenia may be featureof disease itself or due to drug or radiation. Neutropenia= PMN count> reducecirculating antibody i.e.; thymic aplasia, asplenia or splenectomy. Lead tomarked susceptibility to infection with encapsulated organism such asStreptococcus spp.

- Incompetence of cellular element ; enzymatic defect of neutrophils>>

chronic granulomatous disease or silicosis lung may not adequate responseto pulmonary tuberculosis .- Nonspecific reduction in host resistance ; advanced age, alcoholism, DM,

, malneutrition or cancer.

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Radiologic evaluation and diffential diagnosis of pulmonary opacities inimmunocompromise host.

Impared cell Nature of immunocompromise

Cause of immunocompromise Common infection organism

Granulocyte Alteredinflammatoryresponse

- Acute and chronicmyelocytic leukemiaSteroid- Chemotherapeutic agentsIrradiation- Chronic granulomatousdisease

Bacteria Escherichia coliStaphylococcus aureusSerratia marcescens

Pseudomonas aeruginosa Klebsiella pneumonia Enterobacter spp Proteus spp Legionella pneumophila Nocardia asteroidsFungi

Aspergillus sppMucor spp

T lymphocyte Reduced cell-mediatedimmunity

- Lymphoma- AIDS- Steroid- Chemotherapeutic agent- Irradiation- Renal insufficiency- Solid organ transplant

Bacteria Legionella micdadeiSalmonella spp

N. asteroidsTbVirusesCytomegalovirusVaricella-zoster virus

Herpes simplexRespiratory syncytial virusFungi

Aspergillus sppCryptococcus neoforman

Histoplasma capsulatumCoccidiodes immitis

Pneumocytis jeroveciParasiteToxoplasma gondii

HelminthStrongiloides stercolaris

B lymphocyte Reduce antibodyformation

- Lymphoma- Acute and chroniclymphocytic leukemia- Multiple myeloma- Hypogammaglobulinemia- Steroid- Chemotheraputic agent

Bacteria E. coli P. aeruginosa K. pneumoniaStreptococcus pneuoniae

Haemphilus influenzaVirusesCytomegaluvirusRespiratory syncytial virusFungi

P.jiroveciMacrophage Impair

granulomatousresponse

- Silica BacteriaM. tuberculosisFungi

Blastomyces dermatitidis

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H. capsulatum

Bone marrow transplantationPulmonary complication are seen in 40-60% of BMT recipients and manycomplications have significant motality

Intravenous hematopoietic element into a patient whose bone marrow has beenablate by high dose CMT and total body irradiation.

A 2-3 weeks period of profound bone marrow dysfunction before graft engufment iscommon. Neutropenic render the patient susceptible to bacterial and fungal infection.Process of severe neutropenia usually last only approximately 4 weeks.

Lymphocyte is the most sensitive cellular element in the body. After the first month,there is a continuous recovery of immune function that usually complete at 1 year.

Autologous (patient own marrow) recipient have much lower incidence of CMV,fungal infection and idiopathic pneumonia syndrome. Further more they are notsubject to graft-versus-host or obliterative bronchiolitis.

Complication within first monthMost common infection are caused by bacterial, Aspergillus or Candida spp.

Bacterial sepsis occurs in up to 50% particularly in the first 2 weeks. Gram-negativeorganism is common due to venous catheter. Radiographically evidence of bacterial

pneumonia is uncommon in this period, presumably due to prophylactic antibiotic.But when it occurs radiographic manifestations are nonspecific; focal or multifocalconsolidation, rapid progression to more diffused opacification. Aspergillus or Candida spp. Infection are most common fungal in this period.Airway-invasive or angioinvasive form encountered during this period.

Viral infections are uncommon.

Common noninfectious complications include pulmonary edema, hemorrhageand drug toxicity.

Engraftment syndrome is characterized by fever, skin rash and capillaryleak. It occurs in one third to half of effected patient.

Diffused alveolar hemorrhage occurs in up to 21% of transplant patient and hashigh motality rate, between 50-80%. It not associated with coagulation disorder. Mayrepresents a complication of leukostasis caused by neutrophil suddent influx into the

lungs. Chest radiograph show diffused consolidation, but one third show diffusedreticular opacity. CT can show scatter or diffused ground glass opacity. These findingcan not be distinguishable from other complication especially pulmonary edema.However the two conditions can usually be distinguished by clinical.

Drug toxicity should always be considers in the form of diffused alveolar damage.

Early phase complications (30-100 day after transplantation)Depressed cellular and humoral immunityTwo most important pulmonary complications are CMV pneumonia and the

idiopathic pneumonia. CMV pneumonia is the most important infection in BM

transplant patient. More than 70% of all recipients develop clinical or subclinicalinfection of CMV. The clinical manifestations are extremely varies include retinitis,encephalitis, esophagitis, enterocolitis, hepatitis and nephritis. Pneumonia is the most

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serious manifestations with incidence of 10-40% in allogenic transplantation; 85%mortality rate has been report.

Other viural pneumonia is higher incidence such as herpes simplex virus,adenovirus.

Pneumonia occurs for 40% of transplantation related death. Approximatelyhalf of patients are noninfectious. This condition is calledIdiopathic pneumoniasyndrome (IPS). Mortality is high (>70%). IPS is manifested as diffuse alveolar damage. Chest radiograph show scatter or diffused opacities which may progress toconsolidation. CT show ground-glass opacities in the early stage, later stage mayshow more linear opacities with evidence of architectural distortion

Clark criteria for diagnosis include (1) sign and symptoms of pneumonia; (2)chest radiograph show multilobar opacity; (3) abnormal pulmonary physiologyincrease A-a gradient and restrictive pulmonary function test abnormality (4) rigorousexclusion of infection pathology by bronchoalveolar larvage.

Acute graft versus host (GVHD) is also occurs in this period (20-100days).GVHD; result from transplantation of immunocompetent donor lymphocytes thatattack recipient host. The GVHD effect predominately extrapulmonary; exforiativedermatitis, diarrhea and liver dysfunction. However GVHD may potentiate the effectof more common pulmonary complication such as infection.

Late phase complication(>100 days)The major late phase complication is chronic GVHD occurs in one third or one half of patient surviving in first 100 days. Clinical manifestation are similar tothose autoimmune disease; scleroderma, primary biliary cirrhosis and sicca syndrome.50% of late complication had NSIP or diffuse alveolar damage. Which obliterated

bronchiolitis and obliterate pneumonia may occur.Varicellar zoster infection also occur in this time frame. Most case

manifestations are cutaneous.