Reactive Lymphadenitis Any immune response against foreign antigens- lymph node enlargement (lymphadenopathy ) Infections and nonmicrobial inflammatory stimuli involve the lymph nodes, which act as defensive barriers Infections that cause lymphadenitis - acute or chronic. In most instances, the histologic appearance of the nodes is entirely nonspecific.
ACUTE CONDITIONS: Cat-scratch disease Lymphogranuloma venereum Mesenteric lymphadenitis Staphylococcal infection CHRONIC CONDITIONS: With eosinophilic predominance Kimura’s Disease Langerhan’s Cell Histiocytosis Castleman’s disease Granulomatous Tuberculosis Atypical Mycobacteriosis Syphilis Lymphogranuloma venereum Sarcoidosis Brucellosis Non specific/Non granulomatous Leprosy Whipples Fungal Infection- Histoplasmosis Parasitic- Toxoplasmosis Viral- AIDS Related Lymphadenopathy Infectious Mononucleosis Viral Lymphadenitis Necrotizing features seen in Acute Conditions : Kikuchi necrotising lymphadenitis Tularemia Fungal infections (early lesions of histoplasmosis ) Miscellaneous- Bubonic plague Anthrax Melioidosis
Acute Nonspecific Lymphadenitis confined to a local group of nodes draining a focal infection, or generalized in systemic bacterial or viral infections.
Morphology Macroscopically, inflamed nodes- swollen, gray-red, and engorged . M/E- large germinal centers with numerous mitotic figures Macrophages often contain particulate debris of bacterial origin or derived from necrotic cells.
Acute suppurative lymphadenitis Cause is a pyogenic organism, a neutrophilic infiltrate -seen about the follicles and within the lymphoid sinuses With severe infections, centers of follicles undergo necrosis - abscess
Affected nodes - tender,firm If abscess extensive - fluctuant and soft Overlying skin red, and penetration of the infection to the skin - draining sinuses With control of the infection, the lymph nodes can revert to their normal appearance or , if damaged by the immune response, undergo scarring
Chronic Nonspecific Lymphadenitis Three morphological patterns , depending on the causative agent : follicular hyperplasia, paracortical hyperplasia, or sinus histiocytosis
Follicular Hyperplasia Cause – any stimuli that activate B-cell immune response. Large oblong germinal centres (Secondary follicle light zone) surrounded by collar of mantle zone(resting naïve B-cells- dark zone). Normal germinal centres : - Polarised
Follicular Hyperplasia Tingible body macrophages: - Macrophages pred. found in germinal centres . Interspersed b/w germinal centers Contain immunoblast nuclear debris. immunoblasts undergo apoptosis- if fail to produce Ab with high affinity to Ag.
Causes of follicular hyperplasia Non-specific reactive follicular hyperplasia rheumatoid arthritis, toxoplasmosis , and the early stages of HIV infection Kimura disease
Architectural Features Follicular Hyperplasia 1)Preservation of nodal architecture. 2)Follicles-more prominent in cortical portion. 3 ) Size & shape of follicles- marked variation(elongated, angulated, dumb-bell forms). 4)Reaction centre- sharply demarcated Follicular lymphoma 1)Complete effacement of normal architecture 2)Evenly distributed throughout cortex and medulla. 3)Size & shape of follicles- moderate variation. 4)Fading of follicles
Follicular Hyperplasia Vs Follicular Lymphoma
Follicular hyperplasia Follicular lymphoma
Paracortical Hyperplasia characterized by reactive changes within the T-cell regions of the lymph node . On immune activation, parafollicular T cells transform into large proliferating immunoblasts that can efface the B-cell follicles. Eg : viral infections ( EBV), following certain vaccinations (e.g., smallpox), immune reactions induced by certain drugs ( eg: phenytoin ).
Sinus Histiocytosis distention and prominence of the lymphatic sinusoids, due to marked hypertrophy of lining endothelial cells and an infiltrate of macrophages ( histiocytes ). Seen in lymph nodes draining cancers and may represent an immune response to the tumor or its products . Rosai Dorfman Disease.(sinus histiocytosis with massive lymphadenopathy.)