Clinical Lab Handbook

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The LIAISON® Lyme Total Antibody Plus assay uses chemiluminescent immunoassay (CLIA) technology for the qualitative determination of lgG and IgM antibodies of Borrelia burgdorferi in human serum and plasma (K2-EDTA, Li-heparin) samples. This assay is intended for use on samples from patients with signs and symptoms that are consistent with Lyme disease.

Positive or equivocal results with the LIAISON® Lyme Total Antibody Plus should be confirmed with additional testing by one of the following methodologies:

a). Standard two-tier test (STTT) methodology using an IgG and/or IgM Western blot test for Borrelia burgdorferi

or -

b). Modified two-tier test (MTTT) methodology using one or more of the following LIAISON® assays:

LIAISON® Lyme IgM and/or LIAISON® Lyme IgG

Lyme disease is caused by the tickborne spirochete Borrelia burgdorferi and is the most common vector-borne disease in the United States. The CDC initiated surveillance for Lyme disease in 1982, and since 1991 Lyme disease has been a nationally reportable disease. In the United States, the disease is primarily localized to states in the northeast, mid-Atlantic, upper north-central regions and northwestern California. The bacterium, Borrelia burgdorferi is the etiologic agent of Lyme borreliosis, a disease which is transmitted by different tick species of the genus Ixodes.

Lyme borreliosis is a multisystemic disorder that can affect several organs, such as skin, nervous system, large joints and cardiovascular system. Even though Lyme disease spirochetes elicit a vigorous immune response, Borrelia bacteria may survive and persist in the circulation of infected patients. Similar to syphilis, Lyme borreliosis generally progresses through several different stages, from early to late infection:

1. Stage 1 – Localized infection: After an incubation period, a slowly expanding skin lesion, erythema migraines (EM), forms at the site of the tick bite in 70-80% of the cases. General flu-like symptoms including malaise, fatigue, headache, arthralgia, myalgia and fever may accompany the skin lesion.
2. Stage 2 – Disseminated infection: B. burgdorferi often disseminates within days to weeks after disease onset. Possible clinical manifestations include secondary skin lesions, acute lymphocytic meningitis and musculoskeletal pain in joints, tendon, muscle or bone.
3. Stage 3 – Persistent infection: After weeks of disseminated infection, the Lyme disease agents may still survive in localized niches and may persist up to several years. Months after onset of illness, about 60% of untreated patients with this infection experience intermittent attacks of arthritis.

Differential diagnosis of Lyme disease is difficult as clinical manifestations associated with different stages of the disease are variable and diagnosis of persistent infection is challenging in that the IgM/IgG anti-Borrelia antibody response can remain positive for months or even years after antibiotic therapy(4,5,6). Diagnosis of Lyme disease is based upon a physician’s review of clinical symptoms, patient’s exposure to an endemic area, and laboratory test results. In ambiguous cases, there may be a greater reliance on laboratory data to confirm the diagnosis.

86618; Positive/Indeterminate testing reflexes to: (86617 x 2)

Equivocal and Positive tests will be sent to reference lab for confirmatory testing via modified 2-tier testing algorithm