Clinical Education Center
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- ABL Kinase Domain Mutation in CML, Cell-based
- ABO Group and Rh Type
- Acid-Fast Bacillus (AFB) Identification, Sequencing and Stain, Paraffin Block
- ADAMTS13 Activity with Reflex to ADAMTS13 Inhibitor
- Alcohol Metabolites, Quantitative, Urine
- Alpha-Globin Common Mutation Analysis
- Alpha-Globin Gene Deletion or Duplication
- Alpha-Globin Gene Sequencing
- Anti-Müllerian Hormone AssessR™
- Anti-PF4 and Serotonin Release Assay (SRA) for Diagnosing Heparin-induced Thrombocytopenia/Thrombosis (HIT/HITT)
- Antiphospholipid Antibodies
- ASCVD Risk Panel with Score
- Autoimmune Epilepsy Evaluation
- Autoimmune Diseases, Tests for
- B-cell and T-cell Clonality Assays by PCR
- B-Type Natriuretic Peptide (BNP)
- BCR-ABL1 Gene Rearrangement, Quantitative PCR
- Beta-Globin Complete
- BRCAvantage®, Ashkenazi Jewish Screen
- BRCAvantage®, Rearrangements
- BRCAvantage™, Comprehensive
- BRCAvantage™, Single Site
- CDH1 Sequencing and Deletion/Duplication
- Clostridium difficile Diagnostic Testing
- C1 Inhibitor, Protein and Functional Tests
- Calreticulin (CALR) Mutation Analysis
- Carbapenem Resistant Enterobacteriaceae Culture Screen
- Cardio IQ Lipoprotein Fractionation, Ion Mobility
- Cervical Cancer, TERC, FISH
- CFvantage® Cystic Fibrosis Expanded Screen
- Chlamydia trachomatis, TMA
- Chlamydia trachomatis/Neisseria gonorrhoeae RNA, TMA
- Chromosomal Microarray, POC, ClariSure®, Oligo-SNP
- Chromosomal Microarray, Postnatal, ClariSure® Oligo-SNP
- Chromosome Analysis and AFP with Reflex to AChE, Fetal Hgb, Amniotic Fluid
- Chromosome Analysis, Amniotic Fluid
- Chromosome Analysis, Blood
- Chromosome Analysis, Blood with Reflex to Postnatal, ClariSure® Oligo-SNP Array
- Chromosome Analysis, Chorionic Villus Sample
- Chromosome Analysis, High Resolution
- Chromosome Analysis, High Resolution with Reflex to Postnatal, ClariSure® Oligo-SNP Array
- Chromosome Analysis, Mosaicism
- Chromosome Analysis, Neonatal Blood
- Chromosome Analysis, Sister Chromatid Exchange
- Chromosome Analysis, Tissue
- Chromosome DEB Assay for Fanconi anemia
- Chronic Lymphocytic Leukemia (CLL) - Diagnostic and Prognostic Testing
- Culture, Fungus
- Culture, Urine, Routine
- Cystic Fibrosis Screen
- Cytomegalovirus (CMV) and Epstein Barr Virus (EBV) PCR
- D-Dimer, Quantitative
- Dementia, Secondary Causes
- Dengue Virus Testing
- Diabetes Risk Panel with Score and Cardio IQ® Diabetes Risk Panel with Score
- Drug Testing, General Toxicology (Blood, Urine, or Serum)
- Drug Toxicology Alcohol Metab, QN, Oral Fluid
- Drug Toxicology Monitoring, Oral Fluid Testing
- Factor V (Leiden) Mutation Analysis
- Familial Mediterranean Fever Mutation Analysis
- First Trimester Screen, hCG
- First Trimester Screen, Hyperglycosylated hCG (h-hCG)
- FISH, Angelman
- FISH, MET Amplification
- FISH, Myeloma, 17p-, rea 14q32 with Reflexes
- FISH, Prader-Willi
- FISH, Prenatal Screen
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- HCV Genotyping
- Helicobacter pylori (H pylori) Antibody Discontinuation
- Heparin, Anti-Xa
- Hepatitis B Surface Antibody, Quantitative
- Hepatitis C Antibody with Reflex to HCV RNA, PCR with Reflex to Genotype
- Hepatitis C Viral RNA Genotype 1 NS5A Drug-resistance
- Hepatitis C Viral RNA Genotype 3 NS5A Drug Resistance
- Hepatitis C Viral RNA NS3 Drug Resistance
- Hepatitis C, RNA, Quantitative, PCR
- Hereditary Cancer Panels: MYvantageTM Hereditary Comprehensive Cancer Panel and GIvantageTM Hereditary Colorectal Cancer Panel
- Hereditary Hemochromatosis DNA Mutation Analysis
- Herpes Simplex Virus (HSV) Type-Specific IgG Antibodies
- Herpes Simplex Virus Type 2 (HSV-2) IgG Inhibition, ELISA
- HIV-1 Coreceptor Tropism, Proviral DNA
- HIV-1 Coreceptor Tropism, Ultradeep Sequencing
- HIV-1 Integrase Genotype
- HIV-1/2 Antigen and Antibodies, Fourth Generation, with Reflexes
- HPV mRNA E6/E7
- Influenza A and B Antigen, Immunoassay
- Influenza Type A and B Antibodies
- Insulin, Intact, LC/MS/MS
- Integrated Screen, Part 1
- Integrated Screen, Part 2
- Intrinsic Factor Blocking Antibody
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- Maternal Serum AFP
- Melanoma, BRAF V600E and V600K Mutation Analysis, THxID®
- Metanephrines, Fractionated, Free, LC/MS/MS, Plasma
- Methylenetetrahydrofolate Reductase (MTHFR), DNA Analysis
- Microalbumin (Urinary Albumin Excretion)
- Pain Management and CYP2D6/CYP2C19
- Pain Management, Naltrexone, Quantitative, Urine
- Partial Thromboplastin Time, Activated (aPTT)
- Penta Screen
- PIK3CA Mutation Analysis
- Platelet Antibody Screen (Indirect)
- PNH with FLAER (High Sensitivity)
- Prothrombin Time with INR
- PTH, Intact and Calcium
- Streptococcus pneumoniae (Pneumococcal) Antibody Tests
- Saccharomyces cerevisiae Antibodies (ASCA) (IgG, IgA)
- Sequential Integrated Screen, Part 1
- Sequential Integrated Screen, Part 2
- Serum Integrated Screen, Part 1
- Serum Integrated Screen, Part 2
- Serum Pregnancy Tests
- Sickle Cell Screen
- Stepwise, Part 1
- Stepwise, Part 2
- SureSwab® Trichomonas vaginalis RNA, Qualitative TMA
- SureSwab®, Candidiasis, PCR
- TP53 Sequencing and Deletion/Duplication
- T4, Free
- Tamoxifen and Metabolites, LC-MS/MS
- Testosterone Testing
- Total Testosterone, LC/MS/MS
- Triple Screen
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SureSwab® Trichomonas vaginalis RNA, Qualitative TMATest code(s) 19550, 90521, 90801, 15509, 16491, 16492, 17333, 91448, 91437
Question 1. What is Trichomonas vaginalis?
T vaginalisis a single celled, pathogenic, protozoan parasite with only a trophozoite phase and no cyst stage. This organism is pear shaped with a characteristic undulating membrane and is highly motile. Since there is no cyst stage, T vaginalis does not survive long outside the host.
Question 2. What diseases does T vaginalis cause?
This organism is considered one of the most common curable, sexually transmitted infections (STI) in the United States. Some studies suggest that T vaginalis is more prevalent than Chlamydia trachomatis. Over seven million cases of T vaginalis are estimated to occur annually in both males and females. The actual number of cases may be underestimated since 1) infection with T vaginalis is not a reportable disease in the U.S.; 2) a significant number of cases are asymptomatic (10 to 50%); and 3) most tests (excluding transcription mediated amplification [TMA]) are not sensitive enough to detect the presence of this parasite.
Trichomonad infections are harbored in the urogenital tract in females and may result in vaginitis, cervicitis, and urethritis. A significant number of infected females will have copious urogenital discharge along with small hemorrhagic lesions. Complications in pregnant women include premature labor, low-birth-weight offspring, premature rupture of membranes, and post-abortion or post-hysterectomy infections. Asymptomatic infections can also occur in females.
Infections in men are predominately asymptomatic. These asymptomatic male carriers serve as a reservoir for transmission to women during sexual intercourse. The most common symptom of a trichomonad infection in men is dysuria and discharge. Infection with this organism may result in chronic prostatitis and may contribute to infertility. Trichomonad infections have also been implicated as being a cofactor for HIV transmission.
Trichomonad infections such as neonatal pneumonia are known complications. This organism may infect the newborn via contaminated secretions during the birthing process.
Question 3. What is the T vaginalis TMA test?
The T vaginalis TMA assay (manufactured by Hologic®) is an alternative to other T vaginalis tests such as culture, wet-mount, or direct probe testing (Affirm™ Bacterial Vaginosis/Vaginitis Panel). The T vaginalis test is FDA cleared and combines the technologies of target capture, TMA, and hybridization.
After the specimen is collected for TMA testing, it is placed into a special transport solution that releases the trichomonad target rRNA and protects it from degradation. During the initial phase of testing, the target rRNA is separated by washing from the remainder of the sample. This is performed by capturing the target rRNA through the use of a specific oligomer and magnetic microparticles.
After the wash cycle has been completed, the target rRNA is ready for amplification. The target amplification assay is based upon the ability of complementary oligonucleotide primers to specifically anneal and allow enzymatic amplification of the target nucleic acid strands. The TMA process amplifies a specific portion of the target 16S rRNA from T vaginalis through various DNA and RNA intermediates; ultimately RNA amplicon molecules are generated.
The detection of the final RNA amplicon product is achieved through the use of nucleic acid hybridization. A labeled chemiluminescent DNA probe, complementary to a region on the amplicon product, binds the RNA to form stable RNA: DNA hybrids. A selection reagent is able to differentiate hybridized from unhybridized probes, based on chemiluminescence.
Question 4. How accurate is the T vaginalis TMA test?
The T vaginalis TMA test is the most sensitive and specific assay available for detecting T vaginalis in clinical samples. The sensitivity of this assay approaches 100% when using vaginal and endocervical swabs and is slightly less sensitive (90% to 95%) when using urine samples. Since TMA detects rRNA targets (up to one million targets per T vaginalis trophozoite), this assay can easily detect down to one organism per sample. Specificity of the T vaginalis TMA assay approaches 100%.
Other T vaginalis assays are less sensitive. One of the most common assays used in clinical practice to detect trichomonads is the microscopic examination of a wet mount. The test is inexpensive, but does require an experienced microscopist to detect the presence or absence of the motile trophozoites. Though highly specific, the test is much less sensitive (50% to 60%) as compared to TMA. Trichomonad culture is more sensitive (up to 75%) than direct microscopy, but requires several days for the organisms to grow before being detected by microscopic exam of the specific trichomonad culture broth. The direct probe for T vaginalis (Affirm™) was shown to be statistically less sensitive (63%) than TMA for detecting this organism. Papanicolaousmears are considered to have a sensitivity of less than 10% for trichomonads (see references 1 and 2).
Question 5. How does one treat T vaginalis infections?
The drugs of choice for treating trichomonad infections are either metronidazole or tinidazole. All sexual partners of infected patients should be treated. Treatment failures are most commonly due to lack of compliance in taking the drugs. True metronidazole resistance has been described and may be increasing. Patients should always discuss specific treatment options with their doctors.
Andrea SB, Chapin KC. Comparison of Aptima Trichomonas vaginalis transcription-mediated amplification assay and BD Affirm VPIII for detection of T vaginalis in symptomatic women: performance parameters and epidemiological implications. J Clin Microbiol.2011;49:866–869.
Nye MB, Schwebke JR, Body BA. Comparison of APTIMA Trichomonas vaginalis transcription-mediated amplification to wet mount, microscopy, culture, and polymerase chain reaction for diagnosis of trichomoniasis in men and women. Am J Obstet Gynecol. 2009; 200:188.e1-188.e7.
Soper D. Trichomoniasis: under control or under controlled? Am J Obstet Gynecol. 2004;190:281-290.
Weinstock H, Berman S, Cates W, Jr. Sexually transmitted diseases among American youth: incidence and prevalence estimates. Perspect Sex Reprod Health. 2004;36:6-10.
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