Synonym

• Toxoplasmosis serology
• Toxoplasmosis titer

Tubes

The specimens may consist of:

• Blood sample
• Red or tiger top tube
• 7 mL of venous blood or cord blood
• Other body fluids
• Amniotic Fluid
• Bronchoalveolar lavage fluid (BAL)
• Cerebrospinal fluid (CSF)
• Vitreous and aqueous humor
• Tissue biopsy samples of brain, lymph node etc.

Additional information

• Paired sera (one collected within 1 week of illness and another 2-3 weeks later) or serial testing preferred
• Handle blood sample gently to prevent hemolysis
• Send specimens to lab immediately

Info

• Toxoplasmosis is caused by the coccidian protozoan, Toxoplasma gondii. This obligate intracellular parasite causes infection in humans and other mammals. Immunocompromised individuals and developing fetuses are most severely affected by this infection.
• Toxoplasmosis testing involves a group of tests to detect the presence of the protozoan T gondii or its antigen and antibodies
• The group of tests to detect Toxoplasma gondii infection include:
• Serologic tests
• Toxoplasma culture
• Histopathologic examination
• Polymerase chain reaction (PCR)

Clinical

• The clinical utility of toxoplasmosis testing include:
• Aids in the diagnosis of toxoplasmosis
• As a screening test and serial serology testing in seronegative pregnant women
• To detect congenital toxoplasmosis in utero and infants born to infected mothers
• For serial testing in infants until congenital infection is definitely excluded
• Aids in the detection of latent toxoplasma infection (IgG) in HIV infected or immunocompromised persons
• To differentiate CNS toxoplasmosis from infectious mononucleosis (IM) and CNS lymphoma
• Document past exposure or immunity in the community or population
• The cat is the definitive host that becomes infected by eating contaminated raw meat, wild birds, or mice. The protozoan passes through three stages in its life cycle i.e., tachyzoite, bradyzoite, and sporozoite (oocysts). These oocysts are passed in the cat's feces and sporulate in the envoirnment
• Transmission to humans occurs primarily through acquired and congenital routes
• Acquired transmission may result from:
• Ingestion of tissue cysts from contaminated raw or undercooked beef, lamb, pork, or wild game (50% of cases in US)
• Contaminated knives, utensils, cutting boards or food that has had contact with raw meat
• Ingestion of oocysts from soil, milk, water, or vegetables
• Inhalation of oocysts or handling contaminated matter including cat litter
• Contaminated blood transfusions, organ transplants, and accidental inoculation acquired in the laboratory
• Vertical transmission occurs transplacentally especially in the first trimester (10-25% transmission) and second trimester (60-90% transmission)
• Toxoplasmosis can be clinically classified as follows:
• Congenital toxoplasmosis
• Acquired toxoplasmosis
• Toxoplasmosis in immunocompromised host
• Ocular toxoplasmosis
• Congenital toxoplasmosis:
• Infants born to infected mothers usually do not have any symptoms at birth (80%), but may develop symptoms later in life that can be fatal
• Chronic maternal infection is not associated with congenital disease
• Congenital Toxoplasmosis presents with the triad of:
• Chorioretinitis (61%)
• Cerebral calcifications (72%)
• Hydrocephalus (44%)
• Other general findings include:
• CSF abnormalities (>50%)
• Fever
• Hepatomegaly (50%)
• Hypoglycemia (19%)
• Jaundice (64%)
• Microcephaly
• Motor abnormalities (58%)
• Psychomotor retardation
• Rash
• Seizures (17%)
• Splenomegaly (56%)
• Thrombocytopenia (39%)
• When maternal infection occurs in the third trimester, the fetal infection rate is high (72% at 36 weeks), but the disease in the newborn is mild or subclinical. When the maternal infection occurs in the first trimester, fetal infection rate is lower (6% at 13 weeks), but these infants typically manifest severe forms of infection
• Infected infants are treated, whether or not they are symptomatic, to avoid late complications and sequelae
• Acquired toxoplasmosis:
• An average incubation period is 10-23 days after ingestion of under-cooked meat or 5-20 days after ingestion of infected cat feces
• Toxoplasma infection is subclinical and asymptomatic in 80-90% of cases. It is benign and self-limited in non-preganant immunocompetent individuals
• It may be clinically seen as:
• Fever
• Sore throat
• Malaise and myalgia
• Maculopapular skin rash that spares the palms and the soles
• Lymphadenopathy
• Hepatosplenomegaly
• In acute primary infection antibodies develop in the following patterns:
• IgM antibodies develop 1-2 weeks after the onset of illness, peak by 6-8 weeks, and decline by 3-4 months
• IgG antibodies appear at about three weeks, peak in two months, and persist for life
• Toxoplasmosis in immunocompromised patients:
• Immunocompromised persons (CD4 T-cell counts <100/µL) such as AIDs patients, patients on chemotherapy or medications after an organ transplant, usually present with severe fatal infection and complications, usually due to reactivation of latent infection (rarely due to primary infection)
• Brain, heart, lung, and skeletal muscles are the primary sites of infection
• 20-30% of immunodeficient persons develop Toxoplasma encephalitis (of which ~20% do not develop anti-toxoplasma antibodies)
• It may be clinically seen as:
• Fever
• Headache/Encephalitis
• Confusion
• Pneumonia
• Chorioretinitis
• Disseminated disease (typically fatal)
• Myocarditis
• Focal neurologic deficit such as:
• Aphasia
• Ataxia
• Cranial nerve palsies
• Hemiparesis
• Tremor
• Visual field defects
• Toxoplasma prophylaxis should be given based on seropositivity or seronegativity and CD4+ T-lymphocyte count (typically with TMP/SMZ or pyrimethamine)
• Ocular toxoplasmosis:
• Recent studies have indicated that that ocular manifestations are more common in acquired than congenital toxoplasmosis
• This condition primarily causes retinitis and uveitis (iris and choroid), the hallmark of the disease being necrotizing retinochoroiditis, which may be primary or recurrent
• It also affects the optic nerve resulting in optic neuritis and papillitis associated with edema known as Jensen disease
• It may clinically present as:
• Blurring of vision
• Floaters
• Red eye
• Metamorphosia
• Photophobia
• Complication of this condition include:
• Retinal vasculitis
• Posterior vitreous detachment
• Vitreous precipitates
• Anterior uveitis
• Keratic precipitates (KP)
• Toxoplasmosis in pregnant women may cause spontaneous abortion

Additional information

• Lab diagnosis of toxoplasmosis include:
• Serology tests:
• It is the routine method of diagnosis most often from serum and cerebrospinal fluid (CSF), and less frequently from vitreous fluid
• ~50-60% of adults in the U.S. have antibodies against T gondii
• Various methods to detect the antitoxoplasma antibodies include:
• Enzyme-linked immunosorbent assay (ELISA)
• Indirect fluorescent antibody test (IFA)
• Indirect hemagglutination test
• Complement fixation (CF)
• Sabin-Feldman dye test (gold standard)
• Clinical evaluation of antitoxoplasma antibodies IgM include:
• The presence of IgM antibodies indicate acute infection or active disease (IgM titer >1:16)
• IgM antibodies are present in ~75% of infants with congenital toxoplasmosis
• Newborns and immunodeficient patients may not demonstrate an IgM antibody response and IgM antibodies if formed, may persist for more than a year
• IgA antibody testing is more sensitive and specific method of diagnosing congenital and acute toxoplasmosis
• Clinical evaluation of antitoxoplasma antibodies IgG include:
• The presence of IgG antibodies indicate current infection (serial rising titers) or past infection (low titers not rising)
• A positive IgG test in early pregnancy indicates that the client was exposed to toxoplasmosis in the past but is now immune
• Titer of ³1:256 indicates recent exposure or current/active infection
• Titer of ³1:1024 is significant for active disease
• Titers of >1:128 is suspicious of infection
• Titers of 1:16-1:64 occurs with ocular toxoplasmosis or may represent past exposure
• Culture:
• Culture is especially useful in ocular toxoplasmosis and in immunodeficient persons
• Isolation of parasites can be done from body fluids (blood, CSF, BAL, vitreous, or amniotic fluid) or tissue biopsy in the appropriate clinical setting
• The disadvantage of culture is the 6 weeks it takes to obtain a result and limited availability of this test
• Histopathologic examination:
• This is useful in immunocompromised patients with suspected encephalitis or other brain involvement
• Detection of the parasites by hematoxylin and eosin, eosin/methylene blue fast staining, Wright-Giemsa staining or immunohistochemistry of the following specimens
• CSF
• Bronchoalveolar lavage fluid (BAL)
• Touch preparations
• Tissue biopsy specimens (brain, lymph node)
• Polymerase chain reaction (PCR):
• Detection of parasitic DNA by PCR is especially useful in detecting congenital infections in utero from amniotic fluid
• PCR in CSF has a sensitivity of 50-60% and a specificity of 100%
• It is also detected from bronchoalveolar lavage fluid, vitreous, and aqueous humor of HIV-infected patients with toxoplasmosis
• PCR from brain tissue does not indicate active infection because tissue cysts persist in the brain long after acute infection
• PCR from blood samples has a low sensitivity for diagnosis of toxoplasmic encephalitis in AIDS patients
• Toxoplasma serology is part of the TORCH (toxoplasmosis, rubella, cytomegalovirus, and herpes simplex type 2) panel routinely performed on pregnant women
• False positive test results may be due to:
• Antinuclear antibodies (ANA)
• Rheumatoid factor (RF)
• HIV infection
• Other infections in newborns
• False negative test results may be due to presence of excessive IgG when using the indirect immunofluorescence assay (IFA) for IgM
• Related laboratory tests include:
• Alanine Aminotransferase
• Bilirubin
• Complete blood count (CBC)
• Creatinine
• CSF testing
• Fetal fibronectin
• HIV testing
• TORCH panel
• Urinalysis

Nl Result

Consult your laboratory for their normal ranges as these may vary somewhat from the ones listed below.

• Serology tests: Negative
• IgG: <1:16
• IgM Adult: <1:8
• IgM Infant: <1:2
• Culture: No isolation of Toxoplasma gondii
• Histopathologic examination: Not detected
• Polymerase chain reaction: Negative / T gondii DNA not detected

Interpretation of Serologic testing:

High Result

A positive result depending upon the test will indicate either previous or current infection. As with all tests, there may be a false positive rate depending upon the test.

Interpretation of Serologic testing:

Low Result

Negative testing is consistent with no T. gondii infection. However, early in the course of disease or in immunocompromise, results may be negative despite presence of infection.

References

• ARUP Laboratories®. Toxoplasma gondii Antibodies, IgG & IgM. [Homepage on the internet]©2006. Last updated in September 2006. Last accessed on January 30, 2007. Available at URL: http://www.aruplab.com/guides/ug/tests/0050521.jsp
• Bahar IH et al. [The importance and validity of anti-Toxoplasma gondii IgG, IgM, IgA antibodies and IgG avidity tests in the diagnosis of Toxoplasmosis infection during pregnancy.] [Article in Turkish]. Turkiye Parazitol Derg. 2005;29(2):76-79.
• Centers for Disease Control: Toxoplasmosis. [Homepage on the Internet]. Last reviewed on September 20, 2004. Last accessed on January 23, 2007. Available at URL: http://www.cdc.gov/NCIDOD/dpd/parasites/toxoplasmosis/factsht_toxoplasmosis.htm
• Chandramukhi A et al. Diagnosis of neurotoxoplasmosis by antibody detection in cerebrospinal (CSF) fluid using Latex Agglutination Test and ELISA. J Commun Dis. 2004 Sep;36(3):153-8.
• eMedicine from WebMD®. Toxoplasmosis. [Homepage on the Internet] ©1996-2006. Last updated on September 26, 2006. Last accessed on January 23, 2007. Available at URL: http://www.emedicine.com/oph/topic707.htm
• Gaddi PJ et al. Cytokine regulation of immunopathology in toxoplasmosis. Immunol Cell Biol. 2007 Jan 16; [Epub ahead of print].
• Guillaume MP et al. Hemophagocytic syndrome associated with extracerebral toxoplasmosis in an HIV-infected patient. Eur J Intern Med. 2006 Nov;17(7):503-4.
• HIV InSite®. Toxoplasmosis and HIV. [Homepage on the Internet]©2006. Last updated in March 2006. Last accessed on January 23, 2007. Available at URL: http://hivinsite.ucsf.edu/InSite?page=kb-05-04-03
• Holland GN. Ocular toxoplasmosis: a global reassessment. Part II: disease manifestations and management. Am J Ophthalmol. 2004 Jan;137(1):1-17.
• Jones J et al. Congenital toxoplasmosis. Am Fam Physician. 2003 May 15;67(10):2131-8. Available at URL: http://www.aafp.org/afp/20030515/2131.html
• Laboratory Corporation of America. Toxoplasma gondii Antibodies, IgG. [Homepage on the internet]© 2001. Last updated on September 26, 2006. Last accessed on January 23, 2007. Available at URL: http://www.labcorp.com/datasets/labcorp/html/chapter/mono/se024100.htm
• SahasrabudheNS et al.Pathology of Toxoplasma myocarditis in acquired immunodeficiency syndrome. Indian J Pathol Microbiol. 2003 Oct;46(4):649-51.
• Siahanidou T et al. Neuroendocrine abnormalities in a neonate with congenital toxoplasmosis. J Pediatr Endocrinol Metab. 2006 Nov;19(11):1363-6.
• UTMB Laboratory Survival Guide®. TOXOPLASMA GONDII ANTIBODY IgG. [Homepage on the Internet]© 2006. Last reviewed on October 1, 2004. Last accessed on January 23, 2007. Available at URL: http://www.utmb.edu/lsg/LabSurvivalGuide/micro/TOXOPLASMA%20GONDII%20ANTIBODY%20IgG.html
• UTMB Laboratory Survival Guide®. TOXOPLASMA GONDII ANTIBODY IgM. [Homepage on the Internet]© 2006. Last reviewed on October 1, 2004. Last accessed on January 23, 2007. Available at URL: http://www.utmb.edu/lsg/LabSurvivalGuide/micro/TOXOPLASMA%20GONDII%20ANTIBODY%20IgM.html