Blood testing for chlamydia

Blood testing for chlamydia

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I am working with the bacterium Chlamydia trachomatis.

The main test for this species is the naat test, which is based on amplification. But I would like to know how the bacteria affects the blood composition, and if there is a method of diagnosing it from the blood.

Blood antibody tests for Chlamydia trachomatis can be done, but they are far less reliable than amplification:

According to our results, serologic testing for Chlamydia can exclude active infection of the lower genital tract with a high reliability (> or = 95%). However, detection of C. trachomatis can only be reliably achieved by nucleic acid amplification assays.

Low correlation of serology with detection of Chlamydia trachomatis by ligase chain reaction and antigen EIA

Well, I checked your question about chlamydia and there is a way to check if someone has chlamydia from his blood. They take some blood and after they check if there is the Chlamydia bacteria. If they are not sure they simple do a NAAT test. The NAAT test will sure sow if there is chlamydia or something else.

The microimmunofluorescence test for Chlamydia pneumoniae infection: technique and interpretation

A brief description of current procedures for the Chlamydia microimmunofluorescence (MIF) test is presented. To date, use of MIF serology with Chlamydia pneumoniae (TWAR) antigen has provided the most sensitive and specific method for diagnosis of acute TWAR infection. In primary infections, the TWAR IgM antibody response is longer lasting and IgG antibody is slower to develop compared with Chlamydia trachomatis infection. Unlike other Chlamydia species, only a single serovar for C. pneumoniae has been recognized in the MIF system and cross-reaction with other species is negligible. While IgM antibody response is an important marker for serodiagnosis of acute infection, rheumatoid factor often causes false-positive reactions. Persistent TWAR IgG antibody has been useful for seroepidemiologic studies and an association of TWAR IgG antibody and atherosclerotic diseases has been observed. IgA antibody may not be a useful marker for chronic TWAR infection or for acute infection.

Specimen Collection, Transport, Storage And Processing

Chlamydiae are labile bacteria, and viability can be maintained by keeping specimens cold and minimizing the time between specimen collection and processing in the laboratory. A variety of swab types can be used, but toxicity related to materials in swabs can be problematic. It is useful, therefore, to test swab types for toxicity in cell cultures or interference in nonculture assays when proprietary swabs are not provided by the manufacturer. As a general rule, swabs with wooden shafts should not be used. Cotton, Dacron and calcium alginate swabs may all be used, although toxicity has been noted with specific lots of each (6). The cytobrush has also been used to collect endocervical specimens. It appears to collect more cells than swabs and has been associated in some investigators' experiences with higher recovery rates of chlamydiae and higher rates of antigen detection by direct fluorescent antibody (DFA). Regardless of whether a cytobrush or swab is used, clinicians and other health care providers should be trained to collect adequate specimens for chlamydia detection. Table ​ Table1 1 summarizes recommendations for matching specimen type to diagnostic methods. For successful culture of chlamydiae, swabs, scrapings and small tissue samples should be forwarded to the laboratory in a special chlamydial transport medium such as 2SP (0.2 M sucrose-phosphate transport medium containing 10 µg of gentamicin/mL, 25 µg of vancomycin/mL and 25 U of nystatin/mL). Broad-spectrum antibiotics such as tetracyclines, macrolides or penicillin cannot be used in the transport media because they have activity against chlamydiae. Chlamydial specimens should be refrigerated on receipt in the laboratory if specimens cannot be processed within 24 h after collection, they should be frozen at -70ଌ. Currently, culture is the only assay that provides acceptable results for C trachomatis in legal abuse cases, but collection of specimens for nucleic acid amplification (NAA) tests at the same time may enhance an investigation.


Recommended diagnostic methods according to specimen type for Chlamydia trachomatis

Diagnostic method
SpecimenMicroscopyCultureAD * NAH * NAA †
Cervical– ‡ ++++
Rectal++ § +
Urine +
Bubo pus+ +
Semen + ¶

When specimens are collected for DFA, enzyme immunoassay (EIA), nucleic acid hybridization (NAH) or NAA procedures, the descriptions and procedural instructions given in the product's package insert should be followed. This includes the use of swabs or transport media specified by the manufacturers because the use of other materials may impair the sensitivity and/or specificity of the test.

For cytology, isolation in culture or antigen detection methods, epithelial cell specimens should be collected by vigorous swabbing or scraping of the involved sites. Purulent discharges that lack infected epithelial cells are inappropriate and should be cleaned from the site before the sample is collected. Appropriate sites include the conjunctiva for trachoma or inclusion conjunctivitis, the male anterior urethra (several centimetres into the urethra) and the female cervix (within the endocervical canal) or urethra. Because C trachomatis infects columnar or squamocolumnar cells, cervical specimens must be collected at the transitional zone or within the opening of the cervix. The organism also infects the female urethra, and recovery rates may be improved by collecting a specimen from the urethra and the cervix and sending both to the laboratory. Vaginal swabs are inappropriate for these non-NAA detection methods (Table ​ (Table1). 1 ). It should be remembered that the squamocolumnar transitional zone in prepubertal females is ahead of the cervix, in the vaginal area. Also, culture should be the assay of choice in such patients because of the possibility of medicolegal proceedings.

In women with salpingitis, samples may be collected by needle aspiration of the involved fallopian tube. Endometrial specimens have also yielded chlamydiae. In other clinical situations, the rectal mucosa, nasopharynx and throat may be swabbed. For infants with pneumonia, swabs may be collected from the posterior nasopharynx or the throat however, nasopharyngeal or tracheobronchial aspirates collected by intubation are better specimens. For LGV strains, bubo pus, rectal or urethral swabbing, or biopsy samples should be collected.

First-void urine (FVU) specimens from men and women, and vaginal, introital or vulvar swabs from women are excellent specimens for the detection of C trachomatis by NAA tests (7-10) (Table ​ (Table1). 1 ). FVU is the first 10 mL to 30 mL of urine, and specimens should be obtained ideally between 2 h and 6 h after the last micturition. It is not necessary and may not be advantageous to obtain the first urine specimen passed in the morning. Processing of urine specimens should follow the manufacturer's instructions.

Serum specimens are not recommended for the diagnosis of acute C trachomatis infections because the immune responses detected for these mucous membrane infections are often short lived or due to past infections (11). The two exceptions where serology may be helpful include chlamydial neonatal pneumonia (high immunoglobulin [Ig] M) or chlamydial tubal factor infertility (high IgG). A clotted specimen should be submitted.

General guidelines for processing specimens are listed below. Fresh samples are preferred, but frozen material (-70ଌ) is acceptable. Commercial tests should be used only for approved specimens (as listed in the product package insert). C trachomatis is a biocontainment level 2 agent and is not considered to be a particularly dangerous pathogen to handle in the laboratory. However, a number of laboratory-acquired infections, usually manifested as follicular conjunctivitis, have occurred. The LGV biovar is a more invasive organism, and severe cases of pneumonia or lymphadenitis have occurred when researchers were exposed to aerosols created by laboratory procedures such as sonication or centrifugation.

The following is a condensation of a slightly longer post which can be found at this link.

Dr. Charles Stratton's Current Thinking on How Chlamydia Pneumoniae (Cpn) Infection Causes Specific Diseases

Dr. Stratton has been observing the emerging literature and research on Cpn, as well as the clinical trials of new anti-chlamydial agents (see footnotes at bottom of this page). His unique and expert microbiological perspective on Cpn helps to shed some light on how such a singular organism can engender such multiple and varied clinical diseases.

These observations inform Dr. Stratton’s current thinking about the course and pattern of Cpn infection. I’ve attempted to diagram this below to give the reader a feel for the sequence and locus of Cpn in the body, as well as the resulting disease picture. WHile these should be termed theoretical speculations, his theoretical speculations are based on his considerable research, his expertise in microbiology, and his varied clinical experience in treating numerous Cpn infections in a variety of diseases. The picture he describes makes much clearer the multiple pathways and illnesses caused by Cpn, as well as the challenges in treating it.

Initial Infectious Entry-

The initial entry into the body for Cpn infection is through the respiratory system. Studies have demonstrated that Cpn crosses from the lungs into the blood stream via infecting macrophages, the first response immune cells which are trying to combat the respiratory infection.

These circulating infected macrophages both produce EB’s, the infectious spores of Cpn, directly into the blood stream where they attach to and are carried by red blood cells throughout the body (see the picture on our home page), and are taken up by the natural filter organs of the body where they infect those organs with Cpn.

The Inflammatory Trigger:

Stage is now set for focal diseases: any source of inflammation attracts infected macrophages and white cells as well as EB carrying red cells as part of the body’s natural repair process. Cpn then transfers from damaged macrophages via EB’s and sets up shop in inflamed areas.

At this point in the infection cycle, the type and locus of the Cpn infection then determines which disease will result and manifest symptomatically (the following is meant for example only, and is not intended to be a complete or exhaustive list):

Where specialists, and patients, tend to look at a particular disease as the problem, the microbiological perspective Dr. Stratton brings sees the problem as one of a systemically based infection.

Dr. Stratton now posits that the primary infection in Cpn is of the immune system: immune cells & bone marrow.

  • It is this which, in part, causes such difficulty in getting rid of Cpn.
  • It also causes continuous reinfection if the full spectrum of Cpn infection is untreated.
  • It also lowers the body’s ability to cope with other bacterial and viral infections.
  • This, in turn, fosters further sources of inflammation, and even has the potential (through immuno-incompetence) to compromise the body’s ability to fight cancer and other diseases.

It also answers some common questions that arise in Cpn Combined Antibiotic Protocol (CAP) treatment.

Why do viruses and cold sores “surface” during CAP treatment?

This could be due to apoptosis (cell death) of infected immune cells and resulting neutropenia which temporarily lowers your immune response until these cells are replaced. Hence latent but suppressed viruses and fungi emerge as immune cells, which previously held them in check, die.

Why is aggressive or rapid treatment of Cpn potentially dangerous?

In addition to the misery of massive endotoxin release from killing Cpn, and related cytokine (inflammatory) responses of pain and brain fog, massive kill of Cpn infected cells in the body could potentially cause crashing white counts and potential organ dysfunction or even organ failure (E.G.. liver failure) as large scale apoptosis of infected immune and organ cells occurs. As there is no quantitative measure of infectious load, and no way other than symptoms to know which organs are significantly infected, it behooves physicians treating Cpn to start gradually until some measure of the patient’s response indicates how quickly one can “ramp up” to full treatment. This also suggests that highly potent anti-chlamydial agents such as Rifabutin are not the best first-line treatment, even though they appear to be more effective at killing Cpn more quickly. Once the load has been brought down through gradual introduction of the regular CAP, then a cautious trial of such other agents can be considered.

Dr. Stratton has been paying close attention to reports of drug trials of Rifabutin, a very potent new anti-chlamydial. Even healthy young volunteers showed lowered white cells and liver problems during the Pfizer trials.

Given that Dr. Lee Stewart’s findings that 20-25% of young, healthy blood donors were found to be flow cytometry positive for Cpn, Dr. Stratton believes that these effects could be not so much side effects of Rifabutin, as it has been currently viewed, but rather a main effect of the drug, that of killing Cpn and resulting death of previously infected cells.

In other words, since Cpn infection is ubiquitous and often sub-clinical, and “side” effects from potent antichlamydial agents in so-called “healthy” volunteers are actually main effects--- the subjects were not healthy after all, just not clinically ill.

Multi-year treatment process-

Treating Cpn is a multi-year treatment process because of it’s potential to be widespread throughout in body organs, the vascular system, and immune system, as well as it’s toxicity in treatment (from endotoxins, porphyrins, inflammatory and cellular apoptosis). The more body systems involved, the longer and more difficult it is to treat, both in terms of tolerance of treatment from endotoxins, porphyria and apoptosis, as well as being able to get to all the tissues involved, which have differentials in terms of how antibiotics may concentrate in them. Cpn cells also have active pumps which try to lower concentrations of noxious substances (like antibiotics) which also have to be overcome.

How long treatment will take depends, of course, on the degree of infection, amount of bacterial load, severity of infection and number of organs involved, and so on. We don’t have any quantitative measures of infection currently. A good clinician, knowledgeable about the conditions which Cpn can cause, may be able to make an educated guess as to how many organ systems are involved on the basis of history and symptoms. Dr. Stratton sees the degree of reaction to NAC as a useful rough indicator of EB load—the more you react to it the more EB’s you have built up. He also sees the length of time one has been infected (when symptoms may have started) as a rough indicator of the length of treatment (note: one can only guess at this, as we may have initiated Cpn infection from what seemed a mild respiratory infection many years ago, and did not demonstrate serious problems such as MS until years later).

Dr. Stratton’s rule is “Go as fast as you can but no faster,” i.e. as rapidly as your own particular condition can tolerate given the above factors.

He sees that towards the latter phase of treatment, when one is no longer responding with significant reactions to metronidazole pulses, doing a course of 2 weeks on Flagyl and 2 weeks off while continuing with dual antibiotics, is a useful process to clear remaining tissues. When this is tolerated without significant side effects, a cautious trial of Zithromax and Rifabutin as a final test of Cpn clearance could be tried under careful supervision (watching for plummeting white cells and liver toxicity). At this point one should have cleared organs sufficiently that any apoptosis from the potency of Rifabutin would likely be easily tolerated.

Footnotes: Specific observations

Dr. Stratton has paid particular attention to findings by Dr. Stewart that supposedly young, healthy blood donors are showing positive cultures and flow cytometry for Cpn. Her study showed a number of very important findings with implications for our understanding of Cpn transmission and proliferation in the body.

The first is that approximately 25% of buffy coat samples (a buffy coat is the WBC— white blood cell— portion of spun blood) were culture positive for Cpn. This is not an antigen test, but means that Cpn could actually be cultured or grown in the lab from 25% of white blood cell samples. This means infectious Elementary Bodies are circulating in the blood stream.

The second significant finding in Dr. Stewart’s study, was that approximately 25% of WBC’s were seen by Flow Cytometry to have intracellular Cpn. The work of Yamaguchi, demonstrating messenger RNA from peripheral blood mononuclear cells, suggests that these intracellular Cpn found by Stewart are viable. Thus, we know that viable Cpn in WBCs and infectious Cpn elementary bodies circulate in the blood stream and can go anywhere blood goes and can infect any tissue. I will go into why Dr. Stratton sees this finding as so important in a bit.

Dr. Stratton also notes that, in her study, this 25% of donors infected with viable Cpn, both intracellular and free EB’s, occurred in so-called “young healthy blood donors.” That is, while they were culture-positive for Cpn, they have no disease symptoms and were considered to be a “normal” control sample. Dr. Stratton links this finding to reports from the Pfizer drug trials for Rifabutin, a highly potent anti-chlamydial. In the drug trials for Rifabutin there were some cases of liver failure and also of plummeting white blood cell counts in “healthy” volunteer subjects. This has been interpreted in some places as a potential side effect of the medication.

From Dr. Stratton’s perspective on the biology of Cpn, and utilizing the evidence from Stewart, Yamaguchi and others, if 25% of “healthy” volunteers are in fact infected with Cpn, including potentially liver and immune system (white cells) cells as important sites of infection (see explanation below), then a highly potent anti-chlamydial agent will kill many Cpn in parasitized cells. This could initiate large-scale apoptosis (natural cell death) of those body cells that have been inhibited from apoptosis by the Cpn which previously infected them.

Let me say that again, a little differently. We know that Cpn inhibits apoptosis of its host cell so that the host cell stays alive and the infecting Cpn survives. If you kill the Cpn invader, the host cell is no longer being prevented from it’s natural death and replacement cycle. And If you kill a bunch of Cpn all at once, you have a bunch of your body or organ cells dying all at once, and it takes time for them to be cleared by the immune system and then replaced by the natural cell replacement process. It is this, on a more gradual scale, which David Wheldon has noted makes for continuing die-off like symptoms after a Flagyl pulse has been completed.

So, if a whole bunch of liver cells undergo apoptosis at once then liver failure or liver problems could occur. Similarly, if a whole bunch of immune cells undergo apoptosis then, then macrophages and white cells die and severe neutropenia (lowered white count) could occur. From Dr. Stratton’s perspective, these reports may not be a side effect of the Rifabutin, i.e. an unintended effect of a medication, but rather could be due to it’s main effect—killing Cpn.

Related References-

Prevalence of viable Chlamydia pneumoniae in peripheral blood mononuclear cells of healthy blood donors.

Yamaguchi H, Yamada M, Uruma T, Kanamori M, Goto H, Yamamoto Y, Kamiya S.

Transfusion. 2004 Jul44(7):1072-8.

Department of Infectious Disease, Division of Microbiology, and the Department of 1st Internal Medicine, Kyorin University School of Medicine, Tokyo, Japan.

BACKGROUND: Demonstration of viable Chlamydia (Chlamydophila) pneumoniae in peripheral blood mononuclear cells (PBMNCs) is essential to understand the involvement of C. pneumoniae in atherosclerosis. Nevertheless, the prevalence of viable C. pneumoniae in the blood of healthy donors has not yet been studied. STUDY DESIGN AND METHODS: The presence of C. pneumoniae transcript in PBMNCs from blood of healthy human donors was assessed by real-time reverse transcription-polymerase chain reaction (RT-PCR) with primers for C. pneumoniae 16S rRNA, which is more sensitive than genomic-DNA-based analysis, and by the use of staining with fluorescein isothiocyanate-conjugated chlamydia monoclonal antibody (MoAb). RESULTS: Thirteen of 70 donors (18.5%) showed the presence of bacterial transcript in cultured PBMNCs. The prevalence of bacterial detection and bacterial numbers was significantly increased in PBMNC cultures incubated with cycloheximide. Immunostaining of PBMNCs with antichlamydial MoAb also revealed the presence of bacterial antigen in the PBMNCs judged as positive. Nevertheless, cultivation of C. pneumoniae from all PCR-positive donors was unsuccessful. There was no signifi-cant correlation between the presence of chlamydia and either sex or current smoking habits. A possible age variation, however, in the presence of chlamydia in blood of healthy donors was suggested by the results obtained. CONCLUSION: The bacterial transcripts in PBMNCs obtained from healthy donors were detected by the RT-PCR method. Viable C. pneumoniae may be present in healthy human PBMNCs.

Detection of Chlamydia in the peripheral blood cells of normal donors using in vitro culture, immunofluorescence microscopy and flow cytometry techniques

BMC Infectious Diseases 2006, 6:23 doi:10.1186/1471-2334-6-23

Frances Cirino ([email protected])

Nancy L. Croteau ([email protected])

Chester Andrzejewski Jr. ([email protected])

Elizabeth S. Stuart ([email protected])

Eur J Haematol. 2005 Jan74(1):77-83.

Detection of Chlamydophila pneumoniae in the bone marrow of two patients with unexplained chronic anaemia.

Central Laboratory, University Hospital Mannheim, Mannheim, Germany. [email protected]

Anaemia of chronic disease (ACD) is a common finding involving iron deficiency and signs of inflammation. Here, we report on two patients with ACD where a persistent infection with Chlamydophila (Chlamydia) pneumoniae (CP) was detected in bone marrow (BM) biopsies. Infection was suspected by routine cytology and confirmed by immunofluorescence, electron microscopy, polymerase chain reaction (PCR) including different primer sets and laboratories and sequencing of the PCR product. This is a first report of chlamydial presence in the BM of anaemic patients. The cases are presented because persistent chlamydial infection may contribute more frequently to chronic refractory anaemia than previously suspected.

Tolerance and Pharmacokinetic Interactions of Rifabutin


0066-4804/01/$04.000 DOI: 10.1128/AAC.45.5.1572–1577.2001May 2001, p. 1572–1577 Vol. 45, No. 5

Copyright © 2001, American Society for Microbiology. All Rights Reserved.




This multicenter study evaluated the tolerance and potential pharmacokinetic interactions between azithromycin and rifabutin in volunteers with or without human immunodeficiency virus infection. Daily dosing with the combination of azithromycin and rifabutin was poorly tolerated, primarily because of gastrointestinal symptoms and neutropenia. No significant pharmacokinetic interactions were found between these drugs.

Severe neutropenia among healthy volunteers

given rifabutin in clinical trials


The Ohio State University

College of Medicine and Public Health


Letters to the Editor DECEMBER 2003, p. 592

Comparison of azithromycin and clarithromycin in their interactions with rifabutin in healthy volunteers.

Department of Pharmacology, The Ohio State University College of Medicine, Columbus 43210-1239, USA.

A 14-day, randomized, open, phase I clinical trial was designed to examine possible pharmacokinetic interactions between rifabutin and two other antibiotics, azithromycin and clarithromycin, used in the treatment of Mycobacterium avium complex infections. Thirty healthy male and female volunteers were divided into five groups of six participants each: 18 received 300 mg/day of rifabutin, 12 in combination with therapeutic doses of either azithromycin or clarithromycin the remaining 12 received azithromycin or clarithromycin alone. On day 10 the study was terminated because of adverse events, including severe neutropenia. Fourteen participants who received rifabutin developed neutropenia, including all 12 participants who received azithromycin or clarithromycin concomitantly. Analyses of serum revealed no apparent pharmacokinetic interaction between azithromycin and rifabutin. However, the mean concentrations of rifabutin and 25-O-desacetyl-rifabutin (an active metabolite) in participants who received clarithromycin and rifabutin concomitantly were more than 400% and 3,700%, respectively, of concentrations in those who received rifabutin alone. Physicians should be aware that recommended prophylactic doses of rifabutin may be associated with severe neutropenia within 2 weeks after initiation of therapy, and all patients receiving rifabutin, especially with clarithromycin, should be monitored carefully for neutropenia.


Active genital tract infections with C. trachomatis can be diagnosed by direct detection of the micro‐organism from the infected site. After the acute episode however, the organism may not be detectable any longer, and chlamydia antibodies in serum may be the only indication of previous chlamydia involvement. The aim of screening subfertile women by CAT is to identify patients with previous C. trachomatis infections, who are at increased risk for tubal pathology. It has become evident, however, that not all women develop C. trachomatis antibodies after chlamydia infection ( Schachter et al., 1979), and that not all women with antibodies have tubal pathology. Although the immunopathology underlying chlamydia infection is still poorly understood, antibody tests have been developed for clinical application. The information provided by the manufacturers about the antigenic epitopes used in their tests is very limited, and is restricted to statements that the test contains ‘a’ or ‘some’ specific peptides. Furthermore, manufacturers modify the epitopes used in their tests, which may remain unnoticed by the customers who therefore cannot anticipate changes in test performance. The present study is a clinical comparison of five commercially available chlamydia antibody tests in their ability to predict tubal pathology in subfertile women. Four of these tests had not been evaluated as screening tests for tubal factor subfertility before. We are aware that the results of the study show the diagnostic performances of the tests at a given moment in time only.

In the present study, CAT results were compared with the findings at laparoscopy, and therefore only women who had undergone a laparoscopy were included. Patients with low chlamydia antibody titres are less likely to have tubal pathology and were less likely to be included in the study, since many will have conceived before laparoscopy can be done. This verification bias ( Mol et al., 1999) will influence predictive values of CAT, which are dependent on the prevalence of disease. Verification and selection bias is hard to prevent in clinical studies, however, unless one is prepared to perform the complete fertility investigation of a patient on a single day. Although the bias will result in overestimation of the LR, the overestimation will be similar for all tests investigated.

In comparing the five CAT tests, considerable variation was found in the number of patients with a positive test (Table I). An IgG titre ≥32 was found in 132 women using MIF Biomerieux and in 52 using MIF Labsystems, 53 had a positive test by ELISA Labsystems, 62 by pELISA Medac and 87 by ELISA Savyon. The tests with the highest number of positive test results had the lowest PPV, indicating the highest rates of false positive test results. False positive CAT results (i.e. positive CAT tests in patients without tubal pathology at laparoscopy) may be explained by cross‐reactivity with C. pneumoniae antibodies, which can be found in ∼70% of subfertile women ( Gijsen et al., 2001). In this study a significant correlation was found between C. pneumoniae antibody titres and CAT results in four tests, in particular in MIF Biomerieux (P < 0.00001). This confirms the findings of our previous study using a C. pneumoniae IgG ELISA, in which we found cross‐reactivity to occur between C. pneumoniae and C. trachomatis antibodies in MIF Biomerieux. Since the only CAT test (pELISA Medac) in which no significant correlation with the distribution of C. pneumoniae titres was found did not have the highest PPV, cross‐reactivity with C. pneumoniae antibodies does not seem to be the only explanation for the high rates of false positive test results obtained in the CAT tests. Since not all women with chlamydia antibodies have tubal pathology at laparoscopy, it has been suggested that genetic factors in the host may also play a role, by modulating immune defence mechanisms and the development of late sequelae ( Kinnunen et al., 2002).

Comparing MIF and ELISA, the results (Table I) suggest that ELISA tests tend to have lower sensitivity and NPV, i.e. more false negative test results. In ELISA tests chosen for this study, specific synthetic peptides are used which are considered analogous to the serotype‐specific antigenic determinants of MOMP of C. trachomatis ( Närvänen et al., 1997). These serotype‐specific determinants differ between tests, and may explain the differences found in test performances between ELISA tests of different manufacturers. Furthermore, tests based on highly specific peptides may be so specific that they are not able to detect all relevant antigens ( Bas et al., 2001). Variants of serotypes have been identified in urogenital isolates ( Morré et al., 1998) and mutations have been shown to occur in positions within MOMP ( Dean et al., 2000). Consequently, highly specific tests may not be able to identify all serotypes involved in chlamydia infection, and cause false negative CAT results (i.e. negative CAT tests in patients with tubal pathology at laparoscopy).

There are a few reports in the literature on the diagnostic accuracies of different antibody tests for C. trachomatis, in which the tests evaluated in our study have been included. In these studies either tubal pathology, or the direct demonstration of the micro‐organism in the genital tract, have been used as reference standards for the serological tests. Each reference standard has its limitations, however. Since tubal pathology can be caused by other micro‐organisms in addition to C. trachomatis, it is obvious that tests based on chlamydia antibodies will be imperfect in predicting all tubal pathology. Studies in which the direct detection of the micro‐organism is used as a reference have also limited diagnostic accuracy ( Chernesky et al., 1998 Bas et al., 2001), since superficial infections may provide a poor stimulus for antibody formation. Paukku et al. (1998) did not find a significant difference between the presence of IgG antibodies in 78 patients with tubal factor subfertility, using a modified MIF test and ELISA Labsystems. In a serological follow‐up study of 16 women with C. trachomatis positive cervical swabs, ELISA Labsystems, ELISA Savyon and a MIF test have been used ( Clad et al., 2000). ELISA Labsystems was found to be the most sensitive test, and it was concluded that ELISA Savyon did not cover all chlamydia serotypes. Morré et al. (2002) studied the IgG prevalences in 43 women with PCR positive cervical swabs and 106 PCR negative women. Results obtained by two in‐house MIF tests were compared with results by ELISA Labsystems, pELISA Medac and ELISA Savyon. The authors concluded that the ELISA tests performed as well as the MIF tests.

In the present study the likelihood of tubal factor subfertility improved as the number of positive CAT tests in a patient increased (Table II). Compared with one positive CAT test, the LR improved significantly in patients in whom three, four or five positive tests were found. But from a clinical point of view, performing more than two CAT tests in patients is impractical and expensive. Therefore, we evaluated whether two serially performed tests could be of any benefit in predicting tubal factor subfertility. First, from a stepwise logistic regression analysis it was concluded that the diagnostic performance of the best single CAT test (i.e. MIF Labsystems) could not be improved by adding a second CAT test. Second, we evaluated the performance of a serial set of tests from a laboratory perspective, by constructing a model in which pELISA Medac was performed as the first test and MIF Labsystems as the second test. Although pELISA Medac was found to have a significantly lower OR (8.2) compared with MIF Labsystems (15.7), ELISA tests have the advantage over MIF tests of being less laborious. From our results it can be concluded that if pELISA Medac is performed as the first test on all samples, and all samples with positive test results (i.e. 20% of all samples) are retested with MIF Labsystems, the predictive value of the set (OR 14.2) is comparable to the predictive value of MIF Labsystems as a single test (OR 15.7). Cost‐effectiveness analysis has to demonstrate which strategy is to be preferred: MIF Labsystems as a single test on all samples, or pELISA Medac on all samples and retesting of the positive ones with MIF Labsystems. Third, we hypothesized that two tests with poor agreement (low κ) might have different antigenic properties, and might react with a greater number of serotypes and therefore complement each other. From the results presented in Table III it can be concluded that the low κ set of tests (ELISA Labsystems and MIF Biomerieux) did not improve the predictive value of CAT significantly, compared with the predictive values of the single tests of which the set was composed. Therefore the hypothesis of complementary testing with the set of tests with low κ had to be rejected.

The results of the present study show that there still is no excellent screening test for tubal pathology in subfertile women. In order to develop more accurate tests for the prediction of chlamydia‐associated tubal pathology, future research should focus on the immunopathology of chlamydia infections. Evidence exists that patients with chronic, persisting chlamydia infections are particularly at risk for developing late sequelae. Although IgG antibodies are markers of a previous infection, they do not reflect an ongoing chronic inflammation properly. Candidates to be introduced into screening for tubal factor subfertility, in addition to specific C. trachomatis IgG antibodies, are anti‐HSP60 and anti‐LPS antibodies. HSP60 has been shown to play a prominent role in chronic inflammation and scarring ( Claman et al., 1997), and anti‐LPS antibodies might be indicators of ongoing chlamydia infection ( Tuuminen et al., 2000).

In conclusion, although ELISA tests have been claimed to be highly sensitive and specific, in the present study they were not superior in predicting tubal factor subfertility. Of the five CAT tests evaluated, MIF Labsystems had the best diagnostic performance, and among the three ELISA tests, pELISA Medac performed best. MIF Biomerieux had the largest number of false positive test results, probably due to cross‐reactivity with C. pneumoniae antibodies. Combining two different CAT tests did not improve the predictive value for tubal factor subfertility. Health care evaluation from an economic perspective has to prove whether serial testing with the automated pELISA Medac as a first test, and retesting of all positive serum samples with the more laborious MIF Labsystems, is to be preferred to testing of all samples with MIF Labsystems only.

Systematic review: noninvasive testing for Chlamydia trachomatis and Neisseria gonorrhoeae

Background: Testing of urine samples is noninvasive and could overcome several barriers to screening for chlamydial and gonococcal infections, but most test samples are obtained directly from the cervix or urethra.

Purpose: To systematically review studies that assessed the sensitivity and specificity of nucleic acid amplification tests for Chlamydia trachomatis and Neisseria gonorrhoeae in urine specimens and to compare test characteristics according to type of assay, site of sample collection, presence of symptoms, disease prevalence, and characteristics of the reference standard.

Data sources: Relevant studies in all languages were identified by searching the MEDLINE database (January 1991 to December 2004) and by hand-searching the references of identified articles and relevant journals.

Study selection: Studies were selected that evaluated 1 of 3 commercially available nucleic acid amplification tests, included data from tests of both a urine sample and a traditional sample (obtained from the cervix or urethra), and used an appropriate reference standard.

Data extraction: From 29 eligible studies, 2 investigators independently abstracted data on sample characteristics, reference standard, sensitivity, and specificity.

Data synthesis: Articles were assessed qualitatively and quantitatively. Summary estimates for men and women were calculated separately for chlamydial and gonococcal infections and were stratified by assay and presence of symptoms. The pooled study specificities of each of the 3 assays exceeded 97% when urine samples were tested, for both chlamydial infection and gonorrhea and in both men and women. The pooled study sensitivities for the polymerase chain reaction, transcription-mediated amplification, and strand displacement amplification assays, respectively, were 83.3%, 92.5%, and 79.9% for chlamydial infections in women 84.0%, 87.7%, and 93.1% for chlamydial infections in men and 55.6%, 91.3%, and 84.9% for gonococcal infections in women. The pooled specificity of polymerase chain reaction to gonococcal infections in men was 90.4%. In subgroup analyses, the sensitivity did not vary according to the prevalence of infection or the presence of symptoms but did vary according to the reference standard used.

Limitations: Few published studies present data on the transcription-mediated amplification or strand displacement amplification assays, and few studies report data from asymptomatic patients or low-prevalence groups.

Conclusions: Results of nucleic acid amplification tests for C. trachomatis on urine samples are nearly identical to those obtained on samples collected directly from the cervix or urethra. Although all 3 assays can also be used to test for N. gonorrhoeae, the sensitivity of the polymerase chain reaction assay in women is too low to recommend its routine use to test for gonorrhea in urine specimens.

Chlamydia Complications

If you don’t get treated for chlamydia, you run the risk of several health problems:

  • Women. If left untreated, a chlamydia infection can cause pelvic inflammatory disease, which can damage your fallopian tubes (the tubes that connect your ovaries to your uterus). It can even cause infertility (the inability to have children). An untreated chlamydia infection could also increase your risk of ectopic pregnancy (when the fertilized egg implants and develops outside your uterus). And chlamydia may cause premature births (giving birth too early). If mothers pass the infection to their children during childbirth, the newborn could have eye infections, blindness, or pneumonia.
  • Men. Chlamydia can cause an infection of the epididymis (the tube that carries sperm away from the testes) or proctitis -- inflammation of the rectum.
  • Both. Men and women can get a condition called nongonococcal urethritis (NGU) -- an infection of the urethra.

How to prepare for the test?

  • Women should avoid using vaginal creams or douches 24 hours (one day) before the test.
  • Do not take antibiotics 24 hours before chlamydia testing. (7)

Interpreting results

The sample will be thoroughly checked by a medical technologist or a pathologist. If they found out that your result for chlamydia test is positive, your doctor will start you with a course of antibiotics. It is important to address the infection right away before the infection will reach its advanced stage.

Make sure you finish the course of antibiotics and take it as prescribed by your doctor. It is important to inform your sexual partner about your condition so that he/she can get tested too and be treated the soonest time possible. (7, 8, and 9)

STI Testing Event

*Students only utilizing the STI testing event do not have to pay a bridge fee.

Items to Bring

Personal Identification (only one needed):

Event Forms: SHS recommends that you fill out the appropriate paperwork prior to utilizing the event in order to minimize your wait time. The forms will also be available at the event if you are unable to fill them out in advance.

  • Patient Consent Form (REQUIRED for all participants)
  • HIV/Syphilis Testing Form (blood draw fill out all highlighted sections)
  • Chlamydia/Gonorrhea Testing Form (urine sample fill out all highlighted sections)
  • Chlamydia/Gonorrhea Swab Testing Consent Forms (swab tests)
    • Fill out the appropriate section(s) for your desired swab test area. If you choose to receive both swab tests, please fill out both sections of the form in their entirety.

    What to Expect Day-Of

    Please note: If you are experiencing common STI symptoms (such as: burning during urination, abnormal discharge, sores around genital areas), please schedule an appointment with a clinician. Make an appointment online at or call the SHS Appointment line at (979) 458-8310.

    Arrival: When you arrive at SHS, enter the health center through the main entrance. Look for the STI Testing signage to lead you down to the basement level. Signage will be near the main entrance, as well as when you arrive on the basement level. Check-in for the event will be hosted in the basement conference room.

    Check-In: You will first be asked to show a form of personal identification.

    • Forms: If you have not filled out the event forms prior to arriving at the event, you will be provided copies of the appropriate testing forms when you arrive. Once the forms are completed, please give them to the SHS staff member(s) assisting with check-in.

    Testing Administration:

    • HIV/Syphilis Testing: This is a blood test students are encouraged to have a snack/drink prior to arriving this testing will take place in the basement conference room.
    • Chlamydia/Gonorrhea Urine Testing: Students are encouraged to not urinate for at least one hour prior to collection supplies will be provided for participants. Due to the nature of this testing, students will not need to use a towelette for collection.
    • Chlamydia/Gonorrhea Swab Testing: Testing includes a rectal/anal swab and/or throat swab staff are available to assist, if needed.

    Post-Testing: Once you have completed your requested tests, you are welcome to exit the building. You do not have to check-out after utilizing the event.

    There is no charge for any of the below tests available during this event:

    Blood testing for chlamydia - Biology

    Handling editor Nicola Low

    Contributors The study was designed by all authors. LMC, LJN, BH, AT and SGB were responsible for data collection. SNT, DMW and DJS were responsible for reference and further laboratory testing results. LMC, RJG and HW were responsible for data analysis. All authors contributed to the interpretation of results and findings. LMC drafted the first full manuscript with input to the final version from all other authors. All authors contributed to the interpretation and writing of the manuscript.

    Funding This work was supported by the Australian National Health and Medical Council awards (NHMRC Project Grant Application No 1009902 and Program Grant Application No 1071269). Cepheid (Sunnyvale, CA) supplied the GenXpert devices and cartridges at reduced price.

    Disclaimer The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

    Competing interests None declared.

    Ethics approval West Australian Aboriginal Health Ethics Research Committee (HREC 396) Kimberley Aboriginal Health Planning Forum (HREC 2012-003) West Australian Community Health Board Research Ethics Committee (HREC 2012/16) Townsville (HREC/12/QTHS/133)/Cairns and Hinterland Hospital and Health Service (HREC 12/QCH/89-810) Aboriginal Health Council South Australia (HREC 04-13-500).

    Provenance and peer review Not commissioned externally peer reviewed.

    Data sharing statement As per the approved study protocol, access to these data is limited to select named investigators and remains the property of the participating health services. Access to these data may be considered by contacting the corresponding author of this manuscript.