Chlamydia doesn’t always cause symptoms, but when it does, these are some of the most common.
Chlamydia is a sexually-transmitted bacterial infection in which the bacteria are passed to a new victim during sexual intercourse. It caused few or no symptoms to begin with - usually nothing worse than mild itching - but if left untreated it can cause infertility and sometimes cancer. Fortunately, it can be treated successfully with antibiotics.
However, it is not unusual for people who have been successfully treated to develop a new infection with exactly the same strain as the previous infection, suggesting that the bacteria had somehow survived the antibiotic treatment although symptoms had disappeared, and traces of the bacteria had gone.
Researchers have now shown that chlamydia can take up residence in the gut where it can survive for some considerable time and develop increasing resistance to antibiotics with each course of treatment. The mechanism of this increasing resistance is a classic example of evolution as the antibiotic acts as an environmental selector which removes the non-resistant bacteria from the population gene pool, leaving the resistant form to become dominant in the gene pool.
Tell me all about chlamydia and its pathology. Overview of ChlamydiaThis discovery by a group of researchers at the Julius-Maximilians-Universität (JMU), Würzburg, Bavaria, Germany, is the subject of an open access paper in PLOS Pathogens and a news release from Universität Würzburg:
Chlamydia is a common sexually transmitted infection (STI) caused by the bacterium Chlamydia trachomatis. It's one of the most prevalent STIs worldwide and often goes undiagnosed because it can be asymptomatic, especially in women. Despite being easily treatable with antibiotics, if left untreated, chlamydia can lead to serious health complications.
Types of Chlamydia
Chlamydia trachomatis is the bacterium responsible for causing different types of infections, including:
Pathology of Chlamydia
- Genital Chlamydia: The most common form, affecting the genital areas of both men and women.
- Chlamydia Conjunctivitis (Trachoma): Affects the eyes and is a leading cause of preventable blindness worldwide.
- Lymphogranuloma Venereum (LGV): A more invasive form that can cause severe inflammation of the lymph nodes.
Epidemiology
- Transmission
- Chlamydia is primarily transmitted through sexual contact, including vaginal, anal, and oral sex. It can also be passed from an infected mother to her baby during childbirth, leading to neonatal infections like conjunctivitis or pneumonia.
- Infection Mechanism
- Entry: C. trachomatis infects the epithelial cells of the mucous membranes in the genital tract, urethra, rectum, or eyes.
- Developmental Cycle: The bacterium has a unique biphasic lifecycle:
- Elementary Body (EB): This is the infectious form of the bacterium, which is metabolically inactive. It attaches to and enters the host cell.
- Reticulate Body (RB): Inside the host cell, the EB transforms into the RB, which is metabolically active and replicates by binary fission.
- Host Cell Destruction: After replication, RBs revert to EBs, which are released when the host cell bursts, infecting nearby cells.
- Pathological Effects
- Inflammation: The presence of C. trachomatis triggers an immune response, leading to inflammation at the infection site. This inflammation is the source of symptoms like pain, discharge, and burning during urination.
- Chronic Infection: If untreated, the ongoing infection can lead to chronic inflammation, causing scarring and damage to the reproductive organs.
- Complications:
- Women: Untreated chlamydia can lead to pelvic inflammatory disease (PID), which may cause chronic pelvic pain, ectopic pregnancy, and infertility due to scarring of the fallopian tubes.
- Men: In men, complications can include epididymitis (inflammation of the epididymis), which can also lead to infertility.
- Reactive Arthritis: Chlamydia can also cause reactive arthritis (Reiter's syndrome), a form of inflammatory arthritis that affects the joints, eyes, and urethra.
- Symptoms
- In Women:
- Often asymptomatic (about 70-80%)
- Abnormal vaginal discharge
- Painful urination
- Pain during intercourse
- Bleeding between periods or after sex
- Lower abdominal pain
- In Men:
- Painful urination
- Penile discharge
- Pain and swelling in one or both testicles (less common)
- Rectal pain, discharge, or bleeding (in cases of rectal infection)
- Diagnosis
- Nucleic Acid Amplification Tests (NAATs): The most sensitive and specific tests for detecting C. trachomatis in urine samples or swabs from the cervix, urethra, rectum, or throat.
- Culture: Less commonly used due to lower sensitivity and complexity.
- Direct Fluorescent Antibody (DFA) Test: Uses antibodies tagged with a fluorescent dye to detect chlamydia in samples.
- Treatment
- Antibiotics: The standard treatment involves antibiotics such as azithromycin (single dose) or doxycycline (usually taken over a week). Other options include erythromycin or levofloxacin.
- Partner Treatment: It’s crucial that sexual partners are also treated to prevent reinfection and further spread of the disease.
- Re-testing: Due to the risk of reinfection, especially among young women, retesting is recommended about three months after treatment.
- Prevention
- Condom Use: Consistent and correct use of condoms reduces the risk of transmission.
- Regular Screening: Routine screening is recommended for sexually active individuals, particularly women under 25 and those with multiple sexual partners.
- Abstinence or Monogamy: Reducing the number of sexual partners or practicing monogamy with an uninfected partner also lowers the risk.
- Chlamydia is the most reported bacterial STI in many countries, particularly affecting young people aged 15-24.
- The incidence of chlamydia has been steadily increasing, partly due to improved screening and detection efforts.
Public Health Implications
- Due to its high prevalence and potential for serious complications, chlamydia is a significant public health concern.
- Public health strategies focus on promoting regular screening, particularly in high-risk groups, and ensuring timely and effective treatment to reduce transmission and prevent complications.
Chlamydia Can Settle in the Intestine
Chlamydiae are sexually transmitted pathogens that can apparently survive in the human gut for a long time. Researchers from Würzburg and Berlin report this in the journal PLOS Pathogens.
People who are infected with chlamydia can transmit these bacteria to other people during unprotected sex. The pathogens usually cause no or only mild symptoms at first, such as itching in the vagina, penis or anus. If the infection is noticed, it can be easily treated with antibiotics. If this does not happen, the bacteria can cause serious problems, including infertility and cancer.
A phenomenon is known from everyday clinical practice that can occur after successful antibiotic treatment: when people who have already been treated come to the doctor with a new chlamydia infection, they are often infected with exactly the same strains of bacteria as the previous infection.
It is therefore reasonable to assume that the bacteria find a niche in the body where they are not yet vulnerable, that they form a permanent reservoir there and can become active again later.
Professor Thomas Rudel, corresponding author
Head of the Chair of Microbiology
Biocentre
Julius-Maximilians-Universität (JMU) Würzburg in Bavaria, Germany.
This phenomenon is known as persistence. It is problematic because the chlamydia that persist in the body become increasingly resistant to antibiotics over time.
Intestinal Organoids Experimentally Infected with Chlamydia
In which niche do the bacteria persist? Experiments on mouse models have shown that chlamydia can persist in the intestines of animals. And in humans, too, the bacteria seem to make themselves at home in precisely this place. This is reported by the research groups of Thomas Rudel and Sina Bartfeld in the journal PLOS Pathogens. Professor Bartfeld worked at JMU until 2021; she now heads the Department of Medical Biotechnology at Technische Universität Berlin.
The researchers identified the intestine as a niche with the help of artificial organs in miniature format, so-called organoids. These are structures produced in the laboratory from human intestinal cells that are very similar in structure and function to the model organ.
The teams from Würzburg and Berlin tried to infect the intestinal organoids with chlamydia. They discovered that the inner cell layer of the organoids is very resistant to the bacteria: the pathogens could only penetrate there if the cell epithelium was damaged. From the blood side, however, the chlamydia were able to infect very efficiently.
In this case, we repeatedly found the persistent forms of the bacteria, which can be clearly identified with their typical shape under the electron microscope.
Pargev Hovhannisyan, first author
Chair of Microbiology,
University of Würzburg, Würzburg, Germany.
Clinical Studies and Further Experiments Must Follow
Transferred to the human organism, this would mean that chlamydia infection with subsequent persistence can only occur with difficulty via the inner side of the intestine, but very easily via the blood. However, whether this actually happens in the human body has yet to be confirmed in clinical studies, says Thomas Rudel.
The next step for Thomas Rudel and Sina Bartfeld is to find out whether the chlamydia select certain cell types for their persistence – no easy task, as the intestine consists of hundreds of different cell types. But perhaps it is also factors from the surrounding tissue that trigger persistence. These and other details are now to be investigated.
AbstractBecause the ability to take refuge in the gut and reemerge later with a degree of antibiotic resistance is advantageous to the bacteria, creationists can't logically use the traditional but biologically nonsensical, excuse of 'devolution' caused by 'genetic entropy', and since they insist that all organisms were designed by their putative intelligent [sic] designer, they have no option but to conclude that this ability must have been deliberately designed.
Several reports suggest that intestinal tissue may be a natural niche for Chlamydia trachomatis infection and a reservoir for persistent infections in the human body. Due to the human specificity of the pathogen and the lack of suitable host models, there is limited knowledge on this topic. In our study, we modelled the course of the chlamydial infection in human primary gastrointestinal (GI) epithelial cells originating from patient-derived organoids. We show that GI cells are resistant to apical infection and C. trachomatis needs access to the basolateral membrane to establish an infection. Transmission electron microscopy analysis reveals the presence of both normal as well as aberrant chlamydial developmental forms in the infected cells, suggesting a possible cell-type specific nature of the infection. Furthermore, we show that the plasmid-encoded Pgp3 is an important virulence factor for the infection of human GI cells. This is the first report of C. trachomatis infection in human primary intestinal epithelial cells supporting a possible niche for chlamydial infection in the human intestinal tissue.
Author summary
Chlamydial infection has a high global prevalence and is a major health concern. Untreated infections may cause complications and lead to serious health problems, especially in women. Although the infection is usually localized to the genital tract, experiments performed in a mouse infection model as well as the accumulating clinical data suggest that the human gastrointestinal (GI) tract might represent a hidden infection niche and a source of reinfections. In our study, we used the advantages of the organoid technology to model the chlamydial infection in patient-derived primary GI epithelial cells. We were able to show that these cells are resistant to the infection, however, Chlamydia could utilize a basolateral entry route for efficient infection. Chlamydia form either normal or persistent-like developmental forms in these GI epithelial cells. We also showed the importance of the plasmid-mediated virulence in the infection of human GI cells. The results obtained in the GI infection model replicated phenotypes predicted and expected for Chlamydia human intestinal infection, and therefore support a role of the human GI tract as a potential niche for chlamydial infection.
Introduction
Chlamydia trachomatis is a human-specific pathogen, which causes the most common bacterial sexually transmitted infections worldwide [1]. Different serovars of C. trachomatis have specific tissue tropism and cause diseases at different anatomical sites: serovars A-C cause eye infections, genital infections are usually associated with the serovars D-K and the more invasive serovars L1-L3 infect the lymphatic system [2,3].
Chlamydia are obligate intracellular bacteria with a unique biphasic developmental cycle, during which they alternate between two morphologically and functionally different forms–elementary bodies (EBs) and reticulate bodies (RBs). Chlamydia possess complex and redundant mechanisms for host cell attachment and entry, which explains their ability to infect a wide range of cell types [4]. Several host cell receptors, including human integrin β1 receptor [5], epidermal growth factor receptor 6], fibroblast growth factor receptor [7] and Ephrin A2 receptor (EphA2) [8], have been found to be used by C. trachomatis to enter the host cell. EBs, the infectious forms of the organism, are adapted to survive in extracellular space 9]. Upon contact with the host cell, they induce their internalization and develop in a membrane bound compartment called inclusion, where they differentiate into RBs. After several rounds of replication, RBs re-differentiate into EBs, which are released from the cell to infect neighboring cells [9,10]. Under stress conditions, RBs can enter a non-replicative but viable state called persistence, in order to survive the unfavorable conditions. They can re-enter the developmental cycle after the physiological conditions have normalized [1,10].
The obligate intracellular lifestyle and human specificity of C. trachomatis limit the availability of relevant physiological host models to study the infection. Most of the knowledge about the interactions of C. trachomatis with the host is derived from in vitro experiments, which are mainly based on the use of transformed cell line models and which not always recapitulate the in vivo situation [11]. Since it is possible to infect mice with human C. trachomatis serovars under certain conditions, murine models have been widely used to study the immunopathogenesis. However, these do not always reflect the pathology of the disease observed in humans [12,13]. In recent years, the advances in stem cell biology allowed the establishment of complex human primary cell-based host models, such as organoids, which are currently being actively used in the field of infection biology [14,15]. Chlamydial infection has been recently successfully modelled and studied in both human and murine organoids derived from female genital tract tissues, such as human fallopian tube organoids [16], murine endometrial organoids [17] and human cervical organoids [18]. These studies have profoundly improved our understanding of chlamydial infection.
The majority of studies on C. trachomatis-host interactions focuses on the genital tract. There is only a limited number of studies addressing the infection at extra-genital sites. It is well known that C. trachomatis can infect the epithelium of the human rectum and pharynx, with a high prevalence in men who have sex with men [19]. There have also been reported cases of C. trachomatis DNA and antigens being detected in appendix and intestinal biopsies from patients [20,21].
Besides human-specific pathogens, the genus Chlamydia contains species, which infect wild or domesticated animals [22]. Interestingly, gastrointestinal (GI) infection occurs in most animal hosts and the GI tract is a natural site of Chlamydia infection [23]. Some authors have proposed that C. trachomatis could have evolved as a commensal of the human GI tract [24] and that the human GI tract can be a site of persistent chlamydial infections and a possible reservoir of infections in the genital tract [23,25]. Studies in mice demonstrated that following oral inoculation, the murine chlamydial pathogen C. muridarum crosses multiple GI barriers and establishes a long lasting non-pathological colonization in the large intestine [26]. It was also reported that Pgp3, a chlamydial plasmid-encoded virulence factor, is important for the colonization of the GI tract of mice as it helps Chlamydia to reach the large intestine by providing resistance against gastric acid in stomach and CD4+ T lymphocyte-mediated immunity in the small intestine [26].
In the present work, we investigated C. trachomatis infection in primary epithelial cells derived from different regions of the human GI tract using organoid-based host models. We show that C. trachomatis is able to infect the human GI cells from the basolateral, but not apical surface. Moreover, we demonstrate that in some cells chlamydial development is restricted and leads to the formation of aberrant bodies, hallmarks of persistent infection. We also reveal that the chlamydial plasmid and plasmid-encoded Pgp3 are important virulence factors for the infection of human GI cells as their absence leads to growth defects.
This just another example of how nothing from the world of parasitology can be seen as anything but the design of a malevolent intelligence, if you fall for the intelligent [sic] design hoax, because intentional design inevitably carries a moral dimension which is entirely absent from a mindless, natural process proceeding without a plan. Hence the abundant evidence of merciless cruelty to be found in nature when you look beneath the superficial appearance of design. Evolution is a design process devoid of any moral dimension; not so, intelligent design.
The Malevolent Designer: Why Nature's God is Not Good
This book presents the reader with multiple examples of why, even if we accept Creationism's putative intelligent designer, any such entity can only be regarded as malevolent, designing ever-more ingenious ways to make life difficult for living things, including humans, for no other reason than the sheer pleasure of doing so. This putative creator has also given other creatures much better things like immune systems, eyesight and ability to regenerate limbs that it could have given to all its creation, including humans, but chose not to. This book will leave creationists with the dilemma of explaining why evolution by natural selection is the only plausible explanation for so many nasty little parasites that doesn't leave their creator looking like an ingenious, sadistic, misanthropic, malevolence finding ever more ways to increase pain and suffering in the world, and not the omnibenevolent, maximally good god that Creationists of all Abrahamic religions believe created everything. As with a previous book by this author, "The Unintelligent Designer: Refuting the Intelligent Design Hoax", this book comprehensively refutes any notion of intelligent design by anything resembling a loving, intelligent and maximally good god. Such evil could not exist in a universe created by such a god. Evil exists, therefore a maximally good, all-knowing, all-loving god does not.
Illustrated by Catherine Webber-Hounslow.
Available in Hardcover, Paperback or ebook for Kindle
Illustrated by Catherine Webber-Hounslow.
The Unintelligent Designer: Refuting The Intelligent Design Hoax
ID is not a problem for science; rather science is a problem for ID. This book shows why. It exposes the fallacy of Intelligent Design by showing that, when examined in detail, biological systems are anything but intelligently designed. They show no signs of a plan and are quite ludicrously complex for whatever can be described as a purpose. The Intelligent Design movement relies on almost total ignorance of biological science and seemingly limitless credulity in its target marks. Its only real appeal appears to be to those who find science too difficult or too much trouble to learn yet want their opinions to be regarded as at least as important as those of scientists and experts in their fields.
Available in Hardcover, Paperback or ebook for Kindle
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