Chlamydial Diseases Research Articles

Chlamydiosis in Animals

The Chlamydiaceae family consists of Gram-negative, obligate intracellular bacteria that replicate within the cells of a diverse range of hosts. These hosts include domesticated animals such as cats, dogs, and livestock, as well as wildlife like koalas and birds, exotic species such as reptiles and amphibians, and humans. Chlamydial infection can result in various clinical signs, including respiratory diseases, reproductive failures, ocular pathologies, and enteritis, though the infected organism may remain asymptomatic. In recent years, chlamydial nomenclature has undergone several revisions due to the wide range of hosts, the frequent discovery of novel strains, and the reclassification of existing ones. Given this and the clinical significance of these infections, ranging from asymptomatic to fatal, an updated review is essential. This article outlines key characteristics of Chlamydia species and provides an updated overview of their nomenclature, offering a concise reference for future research on chlamydial diseases.

The MraY Inhibitor Muraymycin D2 and Its Derivatives Induce Enlarged Cells in Obligate Intracellular Chlamydia and Wolbachia and Break the Persistence Phenotype in Chlamydia.

Chlamydial infections and diseases caused by filarial nematodes are global health concerns. However, treatment presents challenges due to treatment failures potentially caused by persisting Chlamydia and long regimens against filarial infections accompanied by low compliance. A new treatment strategy could be the targeting of the reduced peptidoglycan structures involved in cell division in the obligate intracellular bacteria Chlamydia and Wolbachia, the latter being obligate endosymbionts supporting filarial development, growth, and survival. Here, cell culture experiments with C. trachomatis and Wolbachia showed that the nucleoside antibiotics muraymycin and carbacaprazamycin interfere with bacterial cell division and induce enlarged, aberrant cells resembling the penicillin-induced persistence phenotype in Chlamydia. Enzymatic inhibition experiments with purified C. pneumoniae MraY revealed that muraymycin derivatives abolish the synthesis of the peptidoglycan precursor lipid I. Comparative in silico analyses of chlamydial and wolbachial MraY with the corresponding well-characterized enzyme in Aquifex aeolicus revealed a high degree of conservation, providing evidence for a similar mode of inhibition. Muraymycin D2 treatment eradicated persisting non-dividing C. trachomatis cells from an established penicillin-induced persistent infection. This finding indicates that nucleoside antibiotics may have additional properties that can break bacterial persistence.

Molecular Evidence for Subclinical Infection of Chlamydia pecorum in Captive Koalas (Phascolarctos Cinereus) of Japanese Zoos

Chlamydial infections pose a significant threat to the health and long-term survival of koalas. However, the pathogenesis of this disease is not well understood. Chlamydia pecorum (C. pecorum) is an important pathogen affecting wild koalas’ health and their survival. However, the infection status of C. pecorum remains largely unknown in captive koalas across Japanese zoos. Therefore, in this study, we aimed to determine the infection status of C. pecorum in koalas from seven Japanese zoos. We tested swab samples obtained from koalas of these zoos for C. pecorum using qPCR and conventional PCR. We found a 21.74% overall prevalence of C. pecorum in these koalas. Female koalas showed a higher prevalence (24.24%) than male koalas (15.38%). However, no direct association was observed between koala health and C. pecorum loads. Notably, among C. pecorum positive koalas, some showed higher chlamydial loads without any classic signs associated with the progression of chlamydial diseases, such as ocular inflammation and wet bottom. We found higher C. pecorum load in adult koala than other groups. These results shed light on the subclinical infection of C. pecorum in captive koalas, and also may act as a guide for future control measures.

Pathology of Infectious Diseases

Part 1 General principles: changing spectrum of human infectious diseases host-parasite interplay role of pathology in diagnosis of infections types of tissue responses to infection microscopic detection of pathogenic organisms. Part 2 Viral infections: viral pathogenesis viral diseases of the digestive system viral skin rashes systemic and hematopoietic viral disorders adult immunodeficiency syndrome (AIDS) arboviral and zoonotic viral fevers viral encephalitis and myelitis viral myocarditis viral skin growths. Part 3 Chlamydial infections: chlamydial pathogenesis chlamydial diseases. Part 4 Rickettsial infections: rickettsial pathogenesis rickettsial diseases. Part 5 Mycoplasma infections: mycoplasma pathogenesis diseases caused by mycoplasmas. Part 6 Bacterial infections: bacterial pathogenesis diseases caused by pyogenic cocci diseases caused by common gram-negative bacteria bacterial diseases of childhood enteric bacterial diseases clostridial diseases zoonotic bacterial diseases rare gram-negative infections treponemal diseases mycobacterial diseases diseases caused by streptomycetales. Part 7 Fungal and algal infections: fungal pathogenesis superficial mycoses opportunistic mycoses endemic fungal diseases diseases caused by algae (protothecosis). Part 8 Protozoal infections: protozoal pathogenesis diseases caused by luminal protozoa diseases caused by bloodstream protozoa diseases caused by intracellular protozoa. Part 9 Helminthic infections: helminthic pathogenesis diseases caused by tissue nematodes filarial diseases diseases caused by cestodes diseases caused by trematodes. Part 10 Patients at special risk of infection: general risk categories residents and travellers in endemic areas pregnant women and neonates infants and elderly persons the poor, homeless, the addicted patients genetically predisposed immunosuppressed and leukopenic patients AIDS patients. Epilogue: the sience and art of infectious disease medicine.

Epidemiological aspects associated with Chlamydia trachomatis infection

The widespread bacteria causing sexually transmitted infection (STI) worldwide is Chlamydia trachomatis. The prevalence of chlamydial diseases that are spread via sexual contact is relatively high throughout the world. Urethritis and cervicitis are often caused by C. trachomatis, and its aftereffects include ectopic pregnancy, reactive arthritis, epididymitis, tubal factor infertility, proctitis, and pelvic inflammatory disease (PID). In addition, chlamydial infections may cause severe ocular or reproductive illness, resulting in infertility or blindness, depending on the bacterial strain. There have been many ways to calculate transmission probability, but each has drawbacks. It is linked to a broad spectrum of short- and long-term health repercussions and sequelae. In low- and middle-income nations like India, where the majority of the burden goes unreported and where there is a lack of systematic data to assess the situation, improved urogenital C. trachomatis infection management is especially crucial. This study's goal was to highlight the current state of the significant epidemiological factors related to chlamydial infections.

Bortezomib Eliminates Persistent Chlamydia trachomatis Infection through Rapid and Specific Host Cell Apoptosis.

Chlamydia trachomatis, a parasitic intracellular bacterium, is a major human pathogen that causes millions of trachoma, sexually transmitted infections, and pneumonia cases worldwide. Previously, peptidomimetic inhibitors consisting of a hydrophobic dipeptide derivative exhibited significant inhibitory effects against chlamydial growth. Based on this finding, this study showed that both bortezomib (BTZ) and ixazomib (IXA), anticancer drugs characterized by proteasome inhibitors, have intensive inhibitory activity against Chlamydia. Both BTZ and IXA consisted of hydrophobic dipeptide derivatives and strongly restricted the growth of Chlamydia (BTZ, IC50 = 24 nM). In contrast, no growth inhibitory effect was observed for other nonintracellular parasitic bacteria, such as Escherichia coli. BTZ and IXA appeared to inhibit chlamydial growth bacteriostatically via electron microscopy. Surprisingly, Chlamydia-infected cells that induced a persistent infection state were selectively eliminated by BTZ treatment, whereas uninfected cells survived. These results strongly suggested the potential of boron compounds based on hydrophobic dipeptides for treating chlamydial infections, including persistent infections, which may be useful for future therapeutic use in chlamydial infectious diseases.

Cellular Basis for the Enhanced Efficacy of the Fms-Like Tyrosine Kinase 3 Ligand (FL) Adjuvanted VCG-Based Chlamydia abortus Vaccine.

Efficacious vaccines are needed to control genital chlamydial diseases in humans and the veterinary industry. We previously reported a C. abortus (Cab) vaccine comprising recombinant Vibrio cholerae ghosts (rVCG) expressing the conserved and immunogenic N-terminal region of the Cab polymorphic membrane protein D (rVCG-Pmp18.1) protein that protected mice against intravaginal challenge. In this study, we investigated the immunomodulatory effect of the hematopoietic progenitor activator cytokine, Fms-like tyrosine kinase 3-ligand (FL) when co-administered with the rVCG-Pmp18.1 vaccine as a strategy to enhance the protective efficacy and the potential mechanism of immunomodulation. Groups of female C57BL/6J mice were immunized and boosted twice intranasally (IN) with rVCG-PmpD18.1 with and without FL or purified rPmp18.1 or rVCG-gD2 (antigen control) or PBS (medium) per mouse. The results revealed that co-administration of the vaccine with FL enhanced antigen-specific cellular and humoral immune responses and protected against live Cab genital infection. Comparative analysis of immune cell phenotypes infiltrating mucosal and systemic immune inductive tissue sites following immunization revealed that co-administration of rVCG-Pmp18.1 with FL significantly enhanced the number of macrophages, dendritic and NK cells, γδ and NK T cells in the spleen (systemic) and iliac lymph nodes (ILN) draining the genital tract (mucosal) tissues compared to rVCG-Pmp18.1 alone. Furthermore, FL enhanced monocyte infiltration in the ILN, while CD19+ B cells and CD4+ T cells were enhanced in the spleen. These results indicate that the immunomodulatory effect of FL is associated with its ability to mobilize innate immune cells and subsequent activation of robust antigen-specific immune effectors in mucosal and systemic lymphoid tissues.

Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced by Chlamydia muridarum and Its Major Outer Membrane Protein (MOMP) in Mouse J774 Macrophages.

The immunopathology of chlamydial diseases is exacerbated by a broad-spectrum of inflammatory mediators, which we reported are inhibited by IL-10 in macrophages. However, the chlamydial protein moiety that induces the inflammatory mediators and the mechanisms by which IL-10 inhibits them are unknown. We hypothesized that Chlamydia major outer membrane protein (MOMP) mediates its disease pathogenesis, and the suppressor of cytokine signaling (SOCS)1 and SOCS3 proteins are mediators of the IL-10 inhibitory actions. Our hypothesis was tested by exposing mouse J774 macrophages to chlamydial stimulants (live Chlamydia muridarum and MOMP) with and without IL-10. MOMP significantly induced several inflammatory mediators (IL-6, IL-12p40, CCL5, CXCL10), which were dose-dependently inhibited by IL-10. Chlamydial stimulants induced the mRNA gene transcripts and protein expression of SOCS1 and SOCS3, with more SOCS3 expression. Notably, IL-10 reciprocally regulated their expression by reducing SOCS1 and increasing SOCS3. Specific inhibitions of MAPK pathways revealed that p38, JNK, and MEK1/2 are required for inducing inflammatory mediators as well as SOCS1 and SOCS3. Chlamydial stimulants triggered an M1 pro-inflammatory phenotype evidently by an enhanced nos2 (M1 marker) expression, which was skewed by IL-10 towards a more M2 anti-inflammatory phenotype by the increased expression of mrc1 and arg1 (M2 markers) and the reduced SOCS1/SOCS3 ratios. Neutralization of endogenously produced IL-10 augmented the secretion of inflammatory mediators, reduced SOCS3 expression, and skewed the chlamydial M1 to an M2 phenotype. Inhibition of proteasome degradation increased TNF but decreased IL-10, CCL5, and CXCL10 secretion by suppressing SOCS1 and SOCS3 expressions and dysregulating their STAT1 and STAT3 transcription factors. Our data show that SOCS1 and SOCS3 are regulators of IL-10 inhibitory actions, and underscore SOCS proteins as therapeutic targets for IL-10 control of inflammation for Chlamydia and other bacterial inflammatory diseases.

Prolonged Release and Functionality of Interleukin-10 Encapsulated within PLA-PEG Nanoparticles.

Inflammation, as induced by the presence of cytokines and chemokines, is an integral part of chlamydial infections. The anti-inflammatory cytokine, interleukin (IL)-10, has been reported to efficiently suppress the secretion of inflammatory cytokines triggered by Chlamydia in mouse macrophages. Though IL-10 is employed in clinical applications, its therapeutic usage is limited due to its short half-life. Here, we document the successful encapsulation of IL-10 within the biodegradable polymeric nanoparticles of PLA-PEG (Poly (lactic acid)-Poly (ethylene glycol), to prolong its half-life. Our results show the encapsulated-IL-10 size (~238 nm), zeta potential (−14.2 mV), polydispersity index (0.256), encapsulation efficiency (~77%), and a prolonged slow release pattern up to 60 days. Temperature stability of encapsulated-IL-10 was favorable, demonstrating a heat capacity of up to 89 °C as shown by differential scanning calorimetry analysis. Encapsulated-IL-10 modulated the release of IL-6 and IL-12p40 in stimulated macrophages in a time- and concentration-dependent fashion, and differentially induced SOCS1 and SOCS3 as induced by chlamydial stimulants in macrophages. Our finding offers the tremendous potential for encapsulated-IL-10 not only for chlamydial inflammatory diseases but also biomedical therapeutic applications.

Pathway-Wide Genetic Risks in Chlamydial Infections Overlap between Tissue Tropisms: A Genome-Wide Association Scan

Chlamydia trachomatis is the most commonly diagnosed bacterial sexually transmitted infection and can lead to tubal factor infertility, a disease characterised by fibrosis of the fallopian tubes. Genetic polymorphisms in molecular pathways involving G protein-coupled receptor signalling, the Akt/PI3K cascade, the mitotic cell cycle, and immune response have been identified in association with the development of trachomatous scarring, an ocular form of chlamydia-related fibrotic pathology. In this case-control study, we performed genome-wide association and pathways-based analysis in a sample of 71 Dutch women who attended an STI clinic who were seropositive for Chlamydia trachomatis antibodies and 169 high-risk Dutch women who sought similar health services but who were seronegative. We identified two regions of within-gene SNP association with Chlamydia trachomatis serological response and found that GPCR signalling and cell cycle pathways were also associated with the trait. These pathway-level associations appear to be common to immunological sequelae of chlamydial infections in both ocular and urogenital tropisms. These pathways may be central mediators of human refractoriness to chlamydial diseases.

Current Research of Chlamydial Infection Diseases in China

Current Research of Chlamydial Infection Diseases in China

A Review on Chlamydial Diseases in Animals: Still a Challenge for Pathologists?

Chlamydiae have a worldwide distribution causing a wide range of diseases in human hosts, livestock, and companion animals as well as in wildlife and exotic species. Moreover, they can persist in their hosts as asymptomatic infections for extended periods of time. The introduction of molecular techniques has revolutionized the Chlamydia field by expanding the host range of known chlamydial species but also by discovering new species and even new families of bacteria in the broader order Chlamydiales. The wide range of hosts, diseases, and tissues affected by chlamydiae complicate the diagnosis such that standard diagnostic approaches for these bacteria are rare. Bacteria of the Chlamydiales order are small and their inclusions are difficult to detect by standard microscopy. With the exception of avian and ovine chlamydiosis, macroscopic and/or histologic changes might not be pathognomic or indicative for a chlamydial infection or even not present at all. Moreover, detection of chlamydial DNA in specimens in the absence of other methods or related pathological lesions questions the significance of such findings. The pathogenic potential of the majority of recently identified Chlamydia-related bacteria remains largely unknown and awaits investigation through experimental or natural infection models including histomorphological characterization of associated lesions. This review aims to summarize the historical background and the most important developments in the field of animal chlamydial research in the past 5 years with a special focus on pathology. It will summarize the current nomenclature, present critical thoughts about diagnostics, and give an update on chlamydial infections in domesticated animals such as livestock, companion animals and birds, as well as free-ranging and captive wild animals such as reptiles, fish, and marsupials.

Modulation of Inflammation Induced by Recombinant MOMP of Chlamydia in Mouse Macrophages by IL-10 is Mediated by Skewing M1 to an M2 Polarizing Macrophage Phenotype

Abstract The major outer membrane protein (MOMP) of Chlamydia trachomatis (CT) is a very desirable vaccine candidate against CT because it stimulates robust T- and B-cell protective responses. Conversely, we showed that MOMP contributes to CT inflammation by stimulating macrophages to secrete pro-inflammatory cytokines that play pivotal roles in the pathogenesis of chlamydial diseases, and whose secretion levels are modulated by IL-10. We also showed that MOMP induced marked expression of the Socs3 gene in macrophages, correlating with its induction of pro-inflammatory cytokines, and its triggering of an M1 macrophage phenotype. Our goal in this study is to understand the inflammatory nature of MOMP by focusing on key chemokines (CCL5 and CXCL10), NO and Nod1/2 receptors, which are implicated in CT inflammation. We also evaluated their inhibition by IL-10 and its effect on M1 and M2 macrophage phenotypes. Mouse J774 macrophages were stimulated with recombinant MOMP (0.01–10 ug/mL) with/without exogenously added IL-10 (10 ng/mL); supernatants and RNA were collected for cytokine ELISAs, NO production and TaqMan gene expression analyses. Our results showed that rMOMP induced expression of CCL5, CXCL10, NO and Nod1/2 receptors that recognize and activate key inflammatory pathways, which were all modulated by IL-10. Characterization of macrophages revealed that rMOMP increased Nos2 expression, an M1 phenotypic marker, which was modulated by IL-10, suggesting skewing of the M1 phenotype whereas IL-10 upregulated M2 markers including, Arg 1 (and its isoform Arg 2) and Mrc1. Overall, our data helps in understanding the inflammatory nature of MOMP and the potential role played by M1 and M2 phenotypes in mediating IL-10 regulation of CT inflammation.

Chlamydial Lipoproteins Stimulate Toll-Like Receptors 1/2 Mediated Inflammatory Responses through MyD88-Dependent Pathway.

Chlamydiae are very important pathogens which could cause several types of diseases in human, but little is known about its pathogenic mechanism. In order to elucidate host inflammatory response and the signal pathway induced by Chlamydial lipoproteins, the predicted lipoproteins of Chlamydia trachomatis were tested for their ability to induce the release of proinflammatory cytokines by mouse macrophages or human TLR (Toll-Like Receptor) expressing cell lines. The results showed that recombinant proteins of C. trachomatis D381, D541, D067, and D775 displayed a strong ability to induce the release of IL-8 in TLR expressing cell line. The signal pathways involved TLR1/2 and TLR2/CD14 but not TLR4. Moreover, except D067, the proinflammatory cytokine induction by D381, D541, and D775 required the thioacylation site (cysteine) for lipid modification and the induction was through MyD88-mediated pathway. Our data supported that lipoproteins played a vital role in pathogenesis of C. trachomatis-induced inflammatory responses via TLR pathway. It was the first study to characterize other chlamydial lipoproteins after identifying the role of MIP (D541) on pathogenesis of Chlamydial diseases.

Dynamics of NKT-Cell Responses to Chlamydial Infection.

Natural killer T (NKT) cells have gained great attention owing to their critical functional roles in immunity to various pathogens. In this review, we provide an overview of the current knowledge on the role of NKT cells in host defense against and pathogenesis due to Chlamydia, which is an intracellular bacterial pathogen that poses a threat to the public health worldwide. Accumulating evidence has demonstrated that NKT cells, particularly invariant NKT (iNKT) cells, play a crucial role in host defense against chlamydial infections, especially in C. pneumoniae infection. iNKT cells can promote type-1 protective responses to C. pneumoniae by inducing enhanced production of IL-12 by dendritic cells (DCs), in particular CD8α+ DCs, which promote the differentiation of naive T cells into protective IFN-γ-producing Th1/Tc1 type CD4+/CD8+ T cells. This iNKT-cell-mediated modulation of DC function is largely dependent upon CD40–CD40L interaction, IFN-γ production, and cell-to-cell contact. In addition, iNKT cells modulate the function of natural killer cells. NKT cells may be also involved in the pathogenesis of some chlamydial diseases by inducing different patterns of cytokine production. A better understanding of NKT-cell biology will enable us to rationally design prophylactic and therapeutic tools to combat infectious diseases.

Chronic Chlamydial Diseases: From Atherosclerosis to Urogenital Infections

Chlamydiae cause a wide range of diseases in human and animal hosts. Chlamydia pneumoniae and Chlamydia trachomatis are important human pathogens with worldwide distribution that produce significant morbidity. Acute infections with C. pneumoniae cause respiratory tract infections, while chronic infection has been linked to chronic bronchitis, asthma and atherosclerosis. Ocular serovars of C. trachomatis induce trachoma, the leading cause of infectious blindness worldwide. C. trachomatis is the most common bacterial cause of sexually transmitted diseases (STDs) worldwide. Acute infections with genital serovars of C. trachomatis remain clinically silent in most women, but can progress to upper genital tract infection leading to pelvic inflammatory disease (PID), infertility and ectopic pregnancy. Chlamydia-induced, reactive arthritis can develop as a late-term condition after genital C. trachomatis or respiratory C. pneumoniae infection. In this review, we address recent information on pathogenesis, immune response, diagnosis and treatment of chronic diseases induced by C. trachomatis and C. pneumoniae.

Structure-function characterisation of Chlamydophila pneumoniae MOMP

The major outer membrane protein (MOMP) from Chlamydophila pneumoniae is a promising candidate antigen for chlamydophila vaccine development. MOMP is a 40kDa protein, encoded by the gene omp1, accountable for 60% of the total outer membrane mass of Chlamydophila pneumoniae. 2-3% of all Gram negative genomes encode for this particular protein class (porins), emphasising its importance and fueling intensive research into MOMPs structure and function. Our particular interest is in the established link between human infection, by micro-organisms such as Chlamydophila pneumoniae, and atherosclerosis – a multifactorial killer disease in developed nations. Evidence suggests a role for purified MOMP and corresponding MOMP-derived peptides in immune-modulation, leading to a reduced atherosclerotic phenotype in apoE–/– mice through dampening of MHC class II activity. We have used bioinformatics, SRCD and FTIR spectroscopies, and electrophysiology to reveal details of the structure, stability and function of MOMP. Our research to date demonstrates MOMP as a beta-barrel membrane protein containing putative 'hatch' and 'plug' domain helices, which may have implications in its function as a porin. Additionally, we show that MOMP exhibits significant increased thermal stability in the presence of fatty acids, highlighting a role for key 'NPA' and 'NPS' signature motifs present in MOMP in the transport of solutes. Our results proffer solutions to the long standing bottleneck in recombinant production of Chlamydophila MOMPs and their functional characterisation. This work has promising implications for structure-driven vaccine design against Chlamydial related diseases.

Diseases Due to Chlamydiaceae

The Chlamydiaceae are obligate intracellular bacteria that produce a wide variety of infections in many mammalian and avian species. Three species belonging to two genera of Chlamydiaceae infect humans: Chlamydia trachomatis, Chlamydophila psittaci, and Chlamydophila pneumoniae. C. trachomatis is exclusively a human pathogen and is transmitted from person to person via sexual contact, perinatal transmission, or close contact in households. C. psittaci, in contrast, is more widely distributed in nature, producing genital, conjunctival, intestinal, or respiratory infections in many avian and mammalian species. C. pneumoniae is a fastidious organism that produces upper respiratory tract infection and pneumonitis in both children and adults. This chapter details the epidemiology, pathogenesis, diagnosis, and treatment of chlamydial diseases. Sexually transmitted diseases, perinatal infections, adult inclusion conjunctivitis, trachoma, and psittacosis are covered. The chapter also includes tables outlining comparative features of the three species and treatment of sexually transmitted diseases caused by C. trachomatis, as well as a figure illustrating the life cycle of Chlamydiaceae. This review contains 1 highly rendered figure, 2 tables, and 87 references.

Molecular characterisation and expression analysis of Interferon gamma in response to natural Chlamydia infection in the koala, Phascolarctos cinereus

Interferon gamma (IFNγ) is a key Th1 cytokine, with a principal role in the immune response against intracellular organisms such as Chlamydia. Along with being responsible for significant morbidity in human populations, Chlamydia is also responsible for wide spread infection and disease in many animal hosts, with reports that many Australian koala subpopulations are endemically infected. An understanding of the role played by IFNγ in koala chlamydial diseases is important for the establishment of better prophylactic and therapeutic approaches against chlamydial infection in this host. A limited number of IFNγ sequences have been published from marsupials and no immune reagents to measure expression have been developed. Through preliminary analysis of the koala transcriptome, we have identified the full coding sequence of the koala IFNγ gene. Transcripts were identified in spleen and lymph node tissue samples. Phylogenetic analysis demonstrated that koala IFNγ is closely related to other marsupial IFNγ sequences and more distantly related to eutherian mammals. To begin to characterise the role of this important cytokine in the koala's response to chlamydial infection, we developed a quantitative real time PCR assay and applied it to a small cohort of koalas with and without active chlamydial disease, revealing significant differences in expression patterns between the groups. Description of the IFNγ sequence from the koala will not only assist in understanding this species' response to its most important pathogen but will also provide further insight into the evolution of the marsupial immune system.

New Insights into Chlamydiae Persistence: An Energy Metabolism Strategy?

Chlamydiaceae is a family of obligate intracellular bacteria generally considered energy parasites. Several studies have suggested that Chlamydiae are capable of independently producing energy and, more importantly, several genes involved in the energy metabolism are up-regulated during the persistent state. Thus, it has been suggested that chlamydial persistence could be a complex and flexible metabolic strategy designed to favor a lengthy survival in the host cell by evading the immune response. In conclusion, more detailed studies on the shift in the chlamydial energy metabolism, from the active to the persistent form, may be helpful in future to determine whether chlamydial persistence observed in vitro does occur in vivo and whether chronic sequelae of chlamydial diseases may be related to the persistence.