and Pallav Gupta2
(1)
Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India
(2)
Department of Histopathology, Sir Ganga Ram Hospital, New Delhi, India
Bacterial organisms even of low virulence may cause local or disseminated infections in immunocompromised patients. In these patients the inflammatory response is impaired with masking of signs and symptoms. Various immunocompromised states leading to enhanced vulnerability to bacterial infections are:
- 1.
Defective cell-mediated immunity: These patients are prone to infections with intracellular organisms, e.g., mycobacteria, nocardia, and salmonella.
- 2.
Defective humoral immunity: These patients are prone to infections with encapsulated bacteria, e.g., S. pneumoniae and H. influenzae.
- 3.
Granulocytopenia: These patients are prone to infections with Gram-negative bacilli, e.g., E. coli, Klebsiella, and P. aeruginosa.
Some of the bacterial infections elicit distinct morphological alterations and can be diagnosed on histopathological or cytopathological evaluation. However, majority of bacterial infections do not induce specific tissue reaction; therefore the “gold standard” for the diagnosis of these infections continues to be bacterial culture. The specimen for bacterial culture should be obtained prior to antibiotic therapy.
Mycobacterium Tuberculosis:
Two species of mycobacteria, M. tuberculosis and M. bovis, cause tuberculosis in man. M. tuberculosis is usually transmitted through airborne droplets; however both M. tuberculosis and M. bovis may also be transmitted through contaminated milk. In primary infection the organisms cause localized pulmonary disease. In immunocompromised host, the primary infection may progress to cavitation, pneumonia, or disseminated infection. A defective immune response leads to ill-formed granulomas with large areas of necrosis harboring abundant tubercle bacilli. Characteristic clinical manifestations are often occult; tuberculin test is not useful in these patients; however on Ziehl-Neelsen staining, sputum samples often reveal heavy positivity for acid-fast bacilli. Besides culture, PCR helps in rapid identification.
Besides M. tuberculosis, the immunocompromised individuals are also susceptible to infection with certain opportunistic mycobacteria. Two closely related species of mycobacteria, M. avium and M. intracellulare, together form Mycobacterium avium complex (MAC). MAC complex causes lymphadenitis, skin lesions, lung involvement, and disseminated disease in immunocompromised host. Profound diarrhea may be seen in patients with gastrointestinal involvement. MAC infection is usually resistant to most of the antimycobacterial agents.
In these patients, the lesions may not show characteristic well-formed epithelioid granulomas on histological or cytopathological evaluation; rather ill-formed epithelioid granulomas against necrotic background may be seen. However, these lesions are often heavily positive for acid-fast bacilli on Ziehl-Neelsen stain.
FNA-Tubercular Lymphadenitis in a Renal Allograft Recipient
Fig. 2.1
(a, b) A 30-year-old male patient receiving live-related renal allograft 10 years back otherwise having stable renal function presented with mild pain in the abdomen and low-grade fever for the past 1 year. USG abdomen revealed enlargement of para-aortic lymph nodes; guided FNA showed degenerate leukocytes intermixed with few histiocytes, ill-defined collections of epithelioid cells, and foamy macrophages against necrotic background (a MGG ×400). Ziehl-Neelsen stain showed plenty of acid-fast bacilli (b ZN stain ×1000) (Contributor – Prof. Manoj Jain, Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India)
Tubercular Lymphadenitis in a Renal Allograft Recipient
Fig. 2.2
(a, b) A 35-year-old male patient who received live-related renal allograft 15 months back and was being maintained on triple-drug immunosuppression presented with low-grade fever and left cervical lymphadenopathy for 2 months. The lymph node biopsy showed well-formed multiple coalescing epithelioid granulomas along with multiple Langhans giant cells and central caseation (a HE ×100). Ziehl-Neelsen stain showed few acid-fast bacilli at the periphery of necrotic areas (b ZN ×1000). Histological diagnosis of tubercular lymphadenitis was offered
Tubercular Lymphadenitis in a HIV-Positive Patient
Fig. 2.3
(a–c) A 36-year-old HIV-positive male patient presented with fever associated with evening rise of temperature since 2 months with h/o weight loss and loss of appetite. On examination he was found to have bilateral cervical and axillary lymphadenopathy. There was no hepatosplenomegaly. The X-ray chest (PA) was WNL. Routine hematological workup revealed Hb content of 10.1 g/dl, total WBC count 9200/cu mm with neutrophils 40, lymphocytes 52, eosinophils 3, and monocytes 5 %, respectively. ESR was 58 mm. CD4 count was 85/cu mm. Excisional axillary lymph node biopsy showed ill-defined epithelioid granulomas against necrotic background along with inflammatory infiltrate (a, b HE ×200). Ziehl-Neelsen stain showed fair number of acid-fast bacilli in the necrotic areas (c ZN ×1000)
FNA-Tubercular Lymphadenitis in a HIV-Positive Patient
Fig. 2.4
(a, b) A 28-year-old male taxi driver by profession presented with PUO, weight loss, generalized weakness, and persistent generalized lymphadenopathy for 3 months. FNAC from the cervical lymph node revealed mixed inflammatory infiltrate against a necrotic background (a MGG ×200). Ziehl-Neelsen stain revealed the presence of large number of acid-fast bacilli (b ZN ×1000). Subsequent investigations revealed that the patient was HIV positive with CD4 counts of 120/cu mm
Tuberculosis Liver in an Immunocompromised Patient
