Page 442 - Robbins Basic Pathology by Vinay Kumar, Abul K. Abbas, Jon C. Aster

428 C H A P T E R 11 Hematopoietic and Lymphoid Systems
antigens can lead to lymph node enlargement (lymphade-
nopathy). The infections causing lymphadenitis are varied
and numerous, and may be acute or chronic. In most
instances the histologic appearance of the lymph node
reaction is nonspecific. A somewhat distinctive form of
lymphadenitis that occurs with cat-scratch disease is
described separately later.
Acute Nonspecific Lymphadenitis
This form of lymphadenitis may be isolated to a group of
nodes draining a local infection, or be generalized, as in
systemic infectious and inflammatory conditions.
MORPHOLOGY
Inflamed nodes in acute nonspecific lymphadenitis are
swollen, gray-red, and engorged. Histologically, there are
large germinal centers containing numerous mitotic
figures. When the cause is a pyogenic organism, a neutrophilic
infiltrate is seen around the follicles and within the lymphoid inflammatory nodule, vesicle, or eschar is sometimes
sinuses. With severe infections, the centers of follicles can
undergo necrosis, leading to the formation of an abscess.
Affected nodes are tender and may become fluctuant if
abscess formation is extensive. The overlying skin is fre-
quently red and may develop draining sinuses. With control
of the infection the lymph nodes may revert to a normal
“resting” appearance or if damaged undergo scarring.
Chronic Nonspecific Lymphadenitis
Depending on the causative agent, chronic nonspecific
lymphadenitis can assume one of three patterns:
follicular hyperplasia, paracortical hyperplasia, or sinus
histiocytosis.
MORPHOLOGY
Follicular Hyperplasia. This pattern occurs with infec-
tions or inflammatory processes that activate B cells, which
migrate into B cell follicles and create the follicular (or
germinal center) reaction. The reactive follicles contain
numerous activated B cells, scattered T cells, and phagocytic
macrophages containing nuclear debris (tingible body
macrophages), and a meshwork of antigen-presenting follicu-
lar dendritic cells. Causes of follicular hyperplasia include
rheumatoid arthritis, toxoplasmosis, and early HIV
infection. This form of lymphadenitis can be confused mor-
phologically with follicular lymphoma (discussed later). Find-
ings that favor follicular hyperplasia are (1) the preservation
of the lymph node architecture; (2) variation in the shape and
size of the germinal centers; (3) the presence of a mixture
of germinal center lymphocytes of varying shape and size;
and (4) prominent phagocytic and mitotic activity in germinal
centers.
Paracortical Hyperplasia. This pattern is caused by
immune reactions involving the T cell regions of the lymph
node. When activated, parafollicular T cells transform into
large proliferating immunoblasts that can efface the B cell
follicles. Paracortical hyperplasia is encountered in viral
infections (such as EBV), after certain vaccinations (e.g.,
smallpox), and in immune reactions induced by drugs (espe-
cially phenytoin).
Sinus Histiocytosis. This reactive pattern is characterized
by distention and prominence of the lymphatic sinusoids,
owing to a marked hypertrophy of lining endothelial
cells and an infiltrate of macrophages (histiocytes). It
often is encountered in lymph nodes draining cancers and
may represent an immune response to the tumor or its
products.
Cat-Scratch Disease
Cat-scratch disease is a self-limited lymphadenitis caused
by the bacterium Bartonella henselae. It is primarily a disease
of childhood; 90% of the patients are younger than 18 years
of age. It manifests with regional lymphadenopathy, most
frequently in the axilla and the neck. The nodal enlarge-
ment appears approximately 2 weeks after a feline scratch
or, less commonly, after a splinter or thorn injury. An
visible at the site of the skin injury. In most patients the
lymph node enlargement regresses over a period of 2 to 4
months. Encephalitis, osteomyelitis, or thrombocytopenia
may develop in rare patients.
MORPHOLOGY
The nodal changes in cat-scratch disease are quite character-
istic. Initially sarcoid-like granulomas form, but these then
undergo central necrosis associated with an infiltrate of neu-
trophils. These irregular stellate necrotizing granulo-
mas are similar in appearance to those seen in a limited
number of other infections, such as lymphogranuloma vene-
reum. The microbe is extracellular and can be visualized with
silver stains. The diagnosis is based on a history of exposure
to cats, the characteristic clinical findings, a positive result on
serologic testing for antibodies to Bartonella, and the distinc-
tive morphologic changes in the lymph nodes.
NEOPLASTIC PROLIFERATIONS
OF WHITE CELLS
Tumors are the most important disorders of white cells.
They can be divided into three broad categories based on
the origin of the tumor cells:
• Lymphoid neoplasms, which include non-Hodgkin lym-
phomas (NHLs), Hodgkin lymphomas, lymphocytic
leukemias, and plasma cell neoplasms and related dis-
orders. In many instances tumors are composed of cells
resembling some normal stage of lymphocyte differen-
tiation, a feature that serves as one of the bases for their
classification.
• Myeloid neoplasms arise from progenitor cells that give
rise to the formed elements of the blood: granulocytes,
red cells, and platelets. The myeloid neoplasms fall into
three fairly distinct subcategories: acute myeloid leuke-
mias, in which immature progenitor cells accumulate in
the bone marrow; myeloproliferative disorders, in which an
inappropriate increase in the production of formed