Lymph nodes & spleen, nonlymphoma

Lymph nodes-infectious / parasitic disorders

Toxoplasmosis



Last author update: 21 February 2022
Last staff update: 21 February 2022

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PubMed Search: Toxoplasmosis[TI] lymph nodes[TIAB] pathology

Tayler A. van den Akker, M.D.
Julie Feldstein, M.D.
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Cite this page: van den Akker TA, Feldstein J. Toxoplasmosis. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/lymphnodestoxoplasma.html. Accessed December 9th, 2022.
Definition / general
  • Lymphadenitis caused by infection with the protozoan Toxoplasma gondii
Essential features
Terminology
  • Toxoplasma lymphadenitis
  • Glandular toxoplasmosis
  • Piringer-Kuchinka lymphadenopathy
ICD coding
  • ICD-10:
    • B58.8 - toxoplasmosis with other organ involvement
    • B58.89 - toxoplasmosis with other organ involvement
Epidemiology
Sites
  • Toxoplasma gondii is a protozoan which can invade many cell types (Ioachim: Ioachim’s Lymph Node Pathology, 4th Edition, 2008)
    • Lymph nodes are commonly affected: unilateral posterior cervical node is characteristic
    • Other lymph nodes can often be involved
    • Generalized lymphadenopathy or hepatosplenomegaly unusually occurs
  • In the human host, the parasites form tissue cysts in skeletal muscle, myocardium, brain and eyes; these cysts may remain throughout the life of the host
Pathophysiology
  • Cats are the only known definitive host for sexual stage of reproduction (Centers for Disease Control DPDx: Toxoplasmosis [Accessed 6 January 2022])
  • Cats become infected after consuming intermediate hosts harboring tissue cysts or by ingestion of sporulated oocysts
  • Trophozoites multiply in intestine and produce oocytes
  • Unsporulated oocysts are shed in the cat's feces
    • Oocysts are usually shed for 1 - 3 weeks and in large numbers, up to several million (Lancet 2004;363:1965)
    • Oocysts take 1 - 5 days to sporulate in the environment and become infective
  • Intermediate hosts in nature (including humans, birds and rodents) become infected after ingesting soil, water or plant material contaminated with oocysts
    • Through ingestion of contaminated soil or water
    • Ingestion of infected, undercooked meat
  • Oocysts are degraded by digestive enzymes and transform into trophozoites
    • Tachyzoites are the crescentic / oval shaped, rapidly multiplying stage of the parasite (Lancet 2004;363:1965)
    • Tachyzoites are released into the intestine
    • Enter all nucleated cells, form cytoplasmic vacuoles, replicate, where finally host cells are disrupted, releasing tachyzoites (Lancet 2004;363:1965)
    • Carried by macrophages and spread by lymphatics and blood vessels to infect tissues
    • Tachyzoite form leads to the strong inflammatory response and tissue destruction, causing the clinical manifestations of the infection (Lancet 2004;363:1965)
    • Tachyzoites are transformed into bradyzoites under the pressure of the immune response to form cysts (thousands of bradyzoites per cyst) and survive the lifetime of the host
Etiology
  • Toxoplasmosis gondii infection
Diagrams / tables

Images hosted on other servers:
Life cycle

Life cycle

Clinical features
  • Immunocompetent individuals:
  • Immunocompromised patients (Centers for Disease Control DPDx: Toxoplasmosis [Accessed 6 January 2022]):
    • Caused by reactivation of chronic infection
    • Often have central nervous system (CNS) disease
    • Systemic disease occurs in severe immunodeficiency
      • Myocarditis, pneumonitis, chorioretinitis, encephalitis
      • In AIDS, toxoplasmic encephalitis is the most common cause of intracerebral mass lesions
  • Congenital toxoplasmosis:
    • In the U.S., the age adjusted seroprevalence among women of childbearing age (15 - 44 years) was 9% in 2009 to 2010 (Am J Trop Med Hyg 2014;90:1135)
    • Third trimester has the highest risk of transmission
    • First trimester poses greatest damage to fetus
    • Neonatal clinical manifestations vary widely:
      • Hydrocephalus, microcephaly, intracranial calcifications, chorioretinitis, strabismus, blindness, epilepsy, psychomotor or mental retardation, petechia due to thrombocytopenia and anemia (Lancet 2004;363:1965)
    • In congenital infection, patients are often asymptomatic until the second or third decade of life, when lesions develop in the eye
  • Rarely, ocular infection may lead to visual loss
  • Ocular Toxoplasma infection, an important cause of retinochoroiditis in the U.S., can be the result of congenital infection or infection after birth
Diagnosis
Laboratory
Prognostic factors
  • Immunocompetent individuals (Lancet 2004;363:1965):
    • Self limiting infection
  • Immunodeficient patients:
    • Risk of disseminating infection
    • Almost always due to reactivation of chronic infection (Lancet 2004;363:1965)
      • Encephalitis, chorioretinitis, pneumonia, multiple organ involvement or death
Case reports
Treatment
Microscopic (histologic) description
  • Lymph node
    • Preserved architecture
    • Capsule / pericapsule: with minimal involvement
    • Sinuses with distended monocytoid B cells
      • Large cells with sharp cell boarders, clear cytoplasm and darkly stained nuclei
    • Follicles with florid reactive follicular hyperplasia
      • Numerous tingible body macrophages
      • Germinal centers with ragged, indistinct margins
    • Interfollicular and paracortical areas with epithelioid histiocytes
      • Invade germinal centers
      • Form collections of < 25 histiocytes (microgranuloma)
    • Medullary cords with plasma cells and immunoblasts
    • Toxoplasma cysts and bradyzoites are rare (1% of cases)
  • References: Ioachim: Ioachim’s Lymph Node Pathology, 4th Edition, 2008, Medeiros: Diagnostic Pathology - Lymph Nodes and Extranodal Lymphomas, 2nd Edition, 2017
Microscopic (histologic) images

Contributed by Tayler A. van den Akker, M.D.
Histologic triad

Histologic triad

Follicular hyperplasia

Follicular hyperplasia

Reactive follicles, monocytoid cells

Reactive follicles, monocytoid cells

Epithelioid histiocytes

Epithelioid histiocytes

Epithelioid histiocytes, monocytoid B cells

Epithelioid histiocytes, monocytoid B cells

Toxoplasma special stain

Toxoplasma special stain


AFIP images
Toxoplasmic lymphadenitis

Toxoplasmic lymphadenitis

Monocytoid B cells

Monocytoid B cells

Virtual slides

Images hosted on other servers:
Brain, toxoplasmosis

Brain, toxoplasmosis

Cytology description
Cytology images

Contributed by Bobbi Pritt, M.D.
Tachyzoites of <i>Toxoplasma gondii</i>

Tachyzoites of Toxoplasma gondii

Positive stains
  • Anti-T. gondii antibodies can detect parasites in tissue
Negative stains
Electron microscopy description
Electron microscopy images

Images hosted on other servers:
Toxoplasma tissue cyst within an intact neurone

Toxoplasma tissue cyst within an intact neurone

Molecular / cytogenetics description
  • Polymerase chain reaction (PCR)
    • Toxoplasma genomes are detected by conventional and nested PCR
Videos

Classic histomorphology of toxoplasma lymphadenitis

Great teaching case of cerebral toxoplasmosis

Sample pathology report
  • Lymph node, right inguinal, excisional biopsy:
    • Reactive lymphoid follicular hyperplasia, monocytoid B cell hyperplasia and aggregates of epithelioid histiocytes, suggestive of toxoplasma lymphadenitis (see comment)
    • Comment: The classic triad present in this case (follicular hyperplasia, intrafollicular clusters of epithelioid cells and aggregates of monocytes) is reported to have a 91% specificity for toxoplasma lymphadenitis. There is no evidence of lymphoma. The morphologic findings are very suggestive of toxoplasmosis. Serologic studies are recommended to confirm the diagnosis.
    • Microscopic description:
      • Right cervical lymph node: The lymph node is enlarged and has a preserved architecture with a thin capsule and open sinuses. There is evidence of reactive lymphoid follicular hyperplasia. In addition, numerous small, well defined aggregates of epithelioid histiocytes are noted, including within the germinal centers. Focally, monocytoid B cell hyperplasia is present. There is no morphologic evidence of lymphoma.
      • Special stains for AFB and GMS are negative for microorganisms.
      • Immunohistochemical staining performed on block A1 shows that the CD20+ B cells are confined to the germinal centers, while the CD3+ T cells are interfollicular. Monocytoid B cells also express CD20. Immunohistochemical stain for toxoplasma is positive. There is no staining for cytomegalovirus. In situ hybridization for EBV encoded RNA (EBER) is negative.
      • Note: Control slides show appropriate reactivity.
      • Left inguinal lymph node for flow cytometry:
        • The following analytes were tested: Kappa, Lambda, CD5, CD23, CD10, CD20, CD19, CD45, sCD3, CD57, CD4, CD7, CD8, CD2 (total of 14)
    • Flow cytometry interpretation:
      • Cytospin: Morphologic evaluation of Diff-Quik stained cytospin shows no increase in atypical lymphocytes.
      • Flow cytometry: Analysis was performed with the above antigens. The T cells show no loss of pan T cell antigens. The B cells are polytypic. The findings provide no evidence of a non-Hodgkin lymphoma.
Differential diagnosis
Board review style question #1

The classic histologic pattern seen in toxoplasmosis lymphadenitis includes

  1. Fibrosis with necrosis
  2. Florid follicular hyperplasia, perifollicular epithelioid histiocytes and patches of monocytoid B cells
  3. Necrosis without neutrophils
  4. Reactive follicular hyperplasia, T cells and a lack of histiocytes
  5. Well formed granulomas with multinucleated giant cells
Board review style answer #1
B. The histologic triad of toxoplasma lymphadenitis includes reactive follicular hyperplasia, perifollicular / interfollicular epithelioid histiocytes and aggregates of monocytoid B cells.

Comment Here

Reference: Toxoplasmosis
Board review style question #2
Which of the following statements is correct regarding the life cycle of Toxoplasma gondii?

  1. Although prevalent worldwide, T. gondii is relatively uncommon in the U.S.
  2. Cysts containing tachyzoites localize in tissues (skeletal muscle, brain and eyes)
  3. Oocysts are shed, unsporulated, in the feces of cats and sporulate in the environment to become infective
  4. Rodents, cats and birds are definitive hosts, while humans are intermediate hosts
Board review style answer #2
C. Oocysts are shed, unsporulated, in the feces of cats and sporulate in the environment to become infective. Cats are the only definitive host, while birds, rodents and humans are intermediate hosts. T. gondii is the most common parasite in the U.S. Oocysts transform into tachyzoites after ingestion. Tachyzoites localize in tissues and develop into tissue cysts containing bradyzoites.

Comment Here

Reference: Toxoplasmosis
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