Chlamydia and Coxiella

Chlamydia and Coxiella

Martina Jelocnik Wilhelmina M. Huston and Hayley J. Newton


Despite belonging to distinct classes, Coxiella burnetii, a Gammaproteobacteria, and Chlamydia species, of the class Chlamydiae, are important zoonotic pathogens with broad host range and the capacity to significantly impact both agricultural industries and public health. Animal infection with these organisms can have a range of health implications, including impacting reproductive potential, making these pathogens particularly problematic within agricultural settings and for endangered animals.

An additional key similarity is that both are obligate intracellular bacterial pathogens that require a eukaryotic host to replicate. This trait makes them fascinating organisms to study in the context of the host–pathogen arms race, as they have adapted key strategies for survival within their host. However, identifying and characterizing the role of important virulence factors has been significantly hampered by the challenge of genetically manipulating obligate intracellular organisms (McClure et al. 2017). In recent years, this technical challenge has been overcome for both pathogens, using distinctly different strategies. In 2009, axenic culture conditions for C. burnetii were first described, which facilitated development of a range of genetic manipulation tools (Omsland et al. 2009). While axenic cultivation of Chlamydia species has not been achieved, the development of a transformation protocol and shuttle vectors based on an endogenous plasmid has facilitated genetic manipulation of some Chlamydia species. This has initiated a new wave of molecular pathogenesis discovery.


Chlamydiae are obligate intracellular bacteria that are globally distributed organisms, infecting an unmatched range of hosts, including humans. Members of the family Chlamydiaceae are globally recognized important veterinary and human pathogens (Table 20.1).

Characteristics of the Organism

Chlamydial Lifecycle

The hallmark feature of Chlamydiae is their unique and highly conserved biphasic developmental cycle alternating between the elementary body, the infectious form, and the reticulate body, the replicating form (Figure 20.1). The cycle begins with attachment and entry of the non‐replicative, environmentally persistent, extracellular infectious elementary bodies (0.3 μm in diameter) into the host cell (typically mucosal cells). Once inside the cell, the elementary bodies reside in a membrane‐enclosed vacuole, termed an inclusion, in which they differentiate to larger, metabolically active reticulate bodies (0.5–1.6 μm in diameter), which replicate by binary fission every two to three hours. As the inclusion expands, the reticulate bodies asynchronously begin to differentiate back into elementary bodies (around 20–44 hours). Either through extrusion or host cell lysis (circa 48–70 hours), elementary bodies are released to spread and infect neighboring epithelial cells, perpetuating the infectious process (Elwell et al. 2016; Hayward et al. 2019). Chlamydiae express a type III secretion system (T3SS), a conserved membrane‐spanning needle‐like apparatus, which translocates effector proteins directly into host cells, where they subvert cellular processes to promote bacterial entry, survival, and replication (Figure 20.1).

Table 20.1 Pathogenic Chlamydia species and their host ranges.

Chlamydial species Traditional hosts
Common clinical signs
C. abortus a) Livestock Schematic illustration of animals. Abortion
C. pecorum Livestock Schematic illustration of animals. Polyarthritis, pneumonia, conjunctivitis, abortion, encephalomyelitis
Koala Conjunctivitis, urogenital tract infections
C. suis a) Porcine Schematic illustration of a pig. Conjunctivitis, diarrhea, respiratory and reproductive disorders
C. psittaci a) Birds Schematic illustration of animals and birds. Emaciation, conjunctivitis, respiratory disease
Livestock Respiratory disease, abortion
C. felis a) Feline Schematic illustration of a cat. Conjunctivitis, rhinitis, upper respiratory tract infection
C. caviae a) Rodents Schematic illustration of rats. Conjunctivitis, urogenital infection, rhinitis
C. muridarum Pneumonia, urogenital infection
C. pneumoniae Human Schematic illustration of a man, a turtle, a snake, rat, and a frog. Pneumonia
C. corallus Reptiles Schematic illustration of a crocodile, a snake, and a turtle. Undetermined
C. poikilothermis
C. sanzinia
C. serpentis
Ca. Chlamydia testudinis
Chlamydia crocodili Conjunctivitis, pharyngitis, anorexia, ascites
C. avium Birds Schematic illustration of the birds. Undetermined
C. buteonis
C. gallinaceae
Ca. Chlamydia ibidis

a) Chlamydial species with documented zoonotic transmission to humans.

Schematic illustration of the chlamydial cell cycle.

Figure 20.1 The chlamydial cell cycle. Chlamydial biphasic developmental cycle, where elementary bodies (EB) attach to the surface of host cells (1). Upon entry, the chlamydial inclusion vacuole is formed (2). Elementary bodies differentiate into reticulate bodies (RB), which replicate by binary fission (3, 5). At the end of the cycle the reticulate bodies re‐differentiate into elementary bodies and are released from host cell (6). Under stress, Chlamydiae can develop into aberrant bodies (AB), a non‐replicating, persistent form (4b). T3SS, type III secretion system.

When exposed to stress‐inducing conditions (such as antibiotics, the host immune response, or nutrient depletion) both in vivo and in vitro, reticulate bodies can enter into an alternative state known as chlamydial persistence, transforming into viable but non‐proliferative aberrant bodies (Figure 20.1). Once conditions are optimal and the stressors are removed, Chlamydiae may resume development. Chlamydial persistence allows these bacteria to survive for long periods in the presence of unfavorable growth conditions (Elwell et al. 2016; Chen et al. 2019b). The survival, replication, and continuation of the chlamydial lifecycle depends on the ability of the pathogen to establish an intracellular niche, subvert host cellular processes, acquire host‐derived nutrients and evade the host immune response. When successful, the pathogen can establish an asymptomatic and potentially persistent infection (Chen et al. 2019b; Gitsels et al. 2019).

Pathogenic Species

Almost all members of the family Chlamydiaceae (except the strictly human Chlamydia trachomatis and human C. pneumoniae strains) are globally recognized as major veterinary pathogens, with several of these spilling over to humans (Table 20.1). Recent years have seen expansion of the known members of the family Chlamydiaceae. Currently, the genus Chlamydia contains 15 characterized species: C. abortus, C. suis, C. pecorum, C. psittaci, C. gallinacea, C. avium, C. buteonis, C. caviae, C. felis, C. muridarum, C. pneumoniae, C. poikilothermis, C. serpentis, C. crocodili, C. trachomatis, in addition to four Candidatus (Ca.) species: Ca. Chlamydia corallus, Ca. Chlamydia ibidis, Ca. Chlamydia sanzinia and Ca. Chlamydia testudinis (Cheong et al. 2019).

Source of Infection: Ecology, Evolution and Epidemiology

A common feature of chlamydial infections is their preference for, and persistence in, the gastrointestinal tract of their hosts (Rank and Yeruva 2014), characterized by continuous fecal shedding. Thereby, the main transmission route is considered to be via the fecal–oral route, although chlamydia can be also shed in ocular and respiratory secretions, urine and genital secretions (mucus and sperm), amniotic fluid, and placentae of symptomatic or asymptomatic animals (Borel et al. 2018). The strain virulence, site of infection, and shedding load all impact the likelihood of transmission. Most veterinary species can infect a wide range of animal hosts, with the potential also to cause zoonotic infections in humans (Cheong et al. 2019).

Types of Disease and Pathologic Changes

Disease manifestations in chlamydial infections include: conjunctivitis ranging from mild to blindness, rhinitis, pneumonia, mastitis, arthritis/polyarthritis, pericarditis, polyserositis, encephalomyelitis, placentitis leading to abortion, stillbirth or weak neonates, endometritis/metritis, orchitis/epididymitis/urethritis, infertility, enteritis, and more (Borel et al. 2018). Chlamydial infections generally cause pathology by inducing tissue damage as a result of host inflammatory response rather than by direct cellular toxicity (Elwell et al. 2016).

Livestock Infections

Chlamydia abortus, C. pecorum, C. suis, and C. psittaci cause economically significant infections in livestock globally (Table 20.1).

Chlamydia abortus

C. abortus is responsible for enzootic abortion of ewes, also known as ovine enzootic abortions, an economically important disease of sheep occurring globally in ruminant‐rearing regions, with the exception of Australia and New Zealand (Rodolakis and Laroucau 2015; Jelocnik 2019). Ewes and goats experience late term abortions, stillbirths, or delivery of weak, non‐thriving offspring. C. abortus is thought to be transmitted via the oronasal route by contamination of the environment from abortigenic material and fetuses, vaginal discharges from aborting ewes and fecal shedding, although sexual transmission is also plausible (Wattegedera et al. 2020). When a non‐pregnant ewe or a ewe lamb is exposed to the pathogen, the C. abortus infection can remain latent and asymptomatic. However, when the ewe becomes pregnant, the organism invades the placenta and begins to proliferate, eventually causing abortion in the last two to three weeks of gestation (Gutierrez et al. 2011; Wattegedera et al. 2020). This increased incidence of abortion cases can persist until a large proportion of ewes in the flock have aborted. After aborting, the ewes and goats develop protective immunity to C. abortus but may continue to shed the organism. The disease takes on a cyclic nature that may result in “storms of abortion” when new introductions or primiparous ewes enter the flock (Gutierrez et al. 2011; Rodolakis and Laroucau 2015).

Chlamydial placentitis develops late in gestation, evidenced by placental lesions from days 90–100 of gestation onwards, and from then on gradually progresses to a diffuse inflammatory response, with thrombotic vasculitis and tissue necrosis. Grossly, the C. abortus infected placenta reveals edema, thickening, hemorrhage, necrosis, and purulent exudate. Histopathological examination often shows a purulent to necrotizing placentitis with vasculitis, mixed inflammatory infiltration with predominantly polymorphonuclear neutrophils and intratrophoblastic basophilic chlamydial inclusions can be observed (Livingstone et al. 2017). Fetal infection is secondary to placentitis and can result in focal necrosis in liver, lung, spleen, and less frequently in lymph nodes and brain (Borel et al. 2018).

C. abortus infections also occur in cattle, pigs, yaks, deer, horses, a variety of birds and farmed fur animals, associated with epididymitis, pneumonia, arthritis, and conjunctivitis in ruminants and asymptomatic fecal shedding (Rodolakis and Laroucau 2015; Borel et al. 2018). C. abortus presents a documented zoonotic risk to humans, particularly to pregnant women, and those actively working with small ruminants, including veterinarians and production workers (Pichon et al. 2020). The route of transmission to humans for C. abortus is uncertain, but both direct and indirect contact with infected placenta and infective secretions are likely routes. In humans, clinical manifestation of C. abortus infection can range from mild flu‐like symptoms or pneumonia to severe illness and abortion (Pichon et al. 2020).

Chlamydia pecorum

C. pecorum is a well‐recognized pathogen of domesticated livestock and wildlife, infecting a broad range of hosts, including sheep, cattle, goats, pigs, free‐range ruminants such as ibex and deer, birds, koalas, and other marsupials. In livestock, C. pecorum infections have been associated with sporadic cases of encephalomyelitis, abortions, polyarthritis, conjunctivitis, enteritis, mastitis, pneumonia, reproductive disorders, and asymptomatic fecal shedding. The infection is thought to be endemic in livestock with most infections being clinically inapparent. However, subclinical C. pecorum infections may impact herd performance, leading to chronic pathological changes associated with reduced growth rates in calves (Reinhold et al. 2011).

Ovine C. pecorum polyarthritis (often accompanied by keratoconjunctivitis) is an economically important disease affecting one or more joints, and resulting in swollen joints, palpable synovial joint effusions, lameness, stiffness, anorexia, and weight loss in young sheep (Walker et al. 2018; Ostfeld et al. 2020). Ovine arthritis is characterized by an inflammatory and proliferative response in synovial membranes possibly progressing to chronic changes with articular erosions and fibrotic thickening (Ostfeld et al. 2020). In ruminants, C. pecorum keratoconjunctivitis, characterized by conjunctival reddening, discharge, and blepharospasm, can lead to prominent conjunctival follicular formation, corneal neovascularization and scarring, leading to blindness (Walker et al. 2018; Jelocnik et al. 2019b). Infected cattle can exhibit a range of clinical disease such as sporadic bovine encephalomyelitis (SBE), pneumonia, enteritis, reproductive pathologies (abortions, vaginitis, endometritis) and mastitis (Reinhold et al. 2011). In young cattle, C. pecorum infection can cause fatal SBE, characterized with encephalomyelitis, systemic infection, and fibrinous polyserositis, including pericarditis, pleuritis, peritonitis, and arthritis (Jelocnik et al. 2014). C. pecorum can also cause sporadic abortions in small ruminants and cattle (Struthers et al. 2021; Westermann et al. 2021). Pathological observations may show marked diffuse necrosuppurative placentitis with vasculitis, thrombosis and inflammatory cell infiltration (Westermann et al. 2021), similar to that observed in ovine C. abortus abortion. Furthermore, fetal brain, liver and lung lesions with enteritis and cryptitis can be present (Westermann et al. 2021). In cattle, aborted fetuses, multifocal random suppurative or mononuclear meningoencephalitis with vasculitis can be observed (Struthers et al. 2021).

Chlamydia suis

C. suis is an economically important pig pathogen associated with a range of diseases, such as conjunctivitis, enteritis, pneumonia, pericarditis, polyarthritis, and polyserositis in piglets, and reproductive problems, including vaginal discharge, return to estrus, abortion, increased perinatal and neonatal mortality, epididymitis, and urethritis in adult pigs (Schautteet and Vanrompay 2011). The pathogenicity of C. suis remains unclear, as it is also commonly found in the gastrointestinal tract of pigs as an endemic and generally asymptomatic infection (Hoffmann et al. 2015), although some studies have demonstrated an impact of infections on health and production. C. suis is the only chlamydial species known to have naturally acquired a tetracycline class C (tetC) gene that encodes tetracycline resistance, causing concerns that this resistance will become widespread under selective pressure of tetracycline treatment of fattening pig herds (Wanninger et al. 2016; Unterweger et al. 2020). The zoonotic transmission of C. suis from pigs to humans has been documented, although only with extensive contact (De Puysseleyr et al. 2017).

Chlamydia psittaci

C. psittaci is primarily considered an avian pathogen; however, this species also causes infections in cattle, horses, sheep, and pigs, with growing evidence of transmission from birds to livestock (Cheong et al. 2019). Although C. psittaci infections in livestock are mostly subclinical, they are associated with reduced performance (such as retarded growth of calves, reduced fertility, and decreased milk yield) and respiratory disease (acute bronchopneumonia) in cattle (Ostermann et al. 2013). In both sheep and cattle, C. psittaci infection is also associated with infectious keratoconjunctivitis (Osman et al. 2013).

Globally, sporadic reports of equine C. psittaci infections that may result in reproductive loss and/or abortions are well described. However, this pathogen may also cause equine abortion epizootics (Jelocnik 2019). The mechanism of equine chlamydial abortion remains unknown; however, histopathology studies reveal mild, diffuse, interstitial placentitis, deep chorionitis and allantoitis, amnionitis, and funisitis. In the fetus, acute non‐suppurative interstitial pneumonia with vasculitis and multifocal hepatitis was observed (Jenkins et al. 2018). This pathogen was also described in cases of acute respiratory distress in live neonatal foals. Molecular epidemiology indicated that these equine abortions could result from C. psittaci spillover from birds. Additionally, equine chlamydiosis was associated with apparent zoonotic transmission of C. psittaci from equine placental membranes to humans, a previously unrecognized route of transmission (Jelocnik 2019).

Avian Infections

Avian chlamydial infections and disease (psittacosis and/or ornithosis) were thought to be mainly due to C. psittaci; however, pathogenic potential of other avian species has been described (C. gallinacea and C. avium). Avian chlamydiosis is an economic risk to the poultry industry.

Chlamydia psittaci

C. psittaci is disseminated globally with a broad avian host range, infecting over 500 avian species with highest prevalence in pigeons and psittacine birds (Knittler et al. 2014; Radomski et al. 2016). In avian hosts, C. psittaci infections may vary from subclinical with persistent organism shedding to severe acute disease. Disease presentations in affected birds include wasting, lethargy, air sacculitis, hepatitis, pericarditis, conjunctivitis, and respiratory symptoms including nasal mucopurulent discharge, and pneumonia (Radomski et al. 2016). Between birds, C. psittaci transmission typically occurs by inhalation of the respiratory exudate, but the bacteria can also be excreted in fecal and nasal discharges and feather dust (Knittler et al. 2014).

The zoonotic potential of veterinary chlamydial species is best demonstrated by human C. psittaci infections. Humans can become infected through inhalation of aerosolized bacteria, and through the handling of contaminated feathers, feces, or carcasses (Hulin et al. 2015). In humans, C. psittaci predominantly causes respiratory infections with highly variable clinical symptoms, ranging from asymptomatic to mild or severe pneumonia, and even including often‐fatal systemic disease with involvement of different organs (Radomski et al. 2016). As such, zoonotically acquired C. psittaci infections are an occupational hazard for animal workers, veterinarians, and healthcare workers (Hogerwerf et al. 2020).

Chlamydia gallinacea and Chlamydia avium

The globally distributed avian species C. gallinacea is endemic in chickens but can also infect other poultry and wild birds (Cheong et al. 2019). C. gallinacea‐infected chickens may remain asymptomatic but show significant body weight reduction impacting production (Guo et al. 2016). C. avium has been detected in pigeons and captive psittacids and is likely to cause respiratory disease in parrots and fatal disease in pigeons (Kik et al. 2020; Popelin‐Wedlarski et al. 2020). The pathogenic and zoonotic potential has yet to be elucidated for C. gallinacea and C. avium, as well as other recently described avian species (C. buteonis, Ca. Chasiempis ibidis).

Domesticated Pet Infections: Chlamydia felis, Chlamydia caviae and Chlamydia muridarum

C. felis is an important pathogen causing acute to chronic unilateral or bilateral conjunctivitis, rhinitis, and respiratory disease in cats. Bacterial transmission between cats typically occurs by direct contact of infectious materials, particularly ocular and oronasal secretions (Gonsales et al. 2016). C. felis primarily infects the conjunctival epithelium and causes acute to chronic or recurrent mucoid/mucopurulent to follicular conjunctivitis and rhinitis. Cats with chlamydial upper respiratory tract disease present with sneezing and coughing (Litster et al. 2015). Infected cats can remain persistently infected for long periods, acting as asymptomatic carriers (Gruffydd‐Jones et al. 2009). C. caviae is the most common cause of conjunctivitis in its natural hosts, guinea pigs, although urogenital and respiratory infections are also observed (Cheong et al. 2019). C. caviae can be transmitted to humans following close contact. Human infection may present as community‐acquired pneumonia or as mild conjunctivitis (Ramakers et al. 2017). C. muridarum is a predominantly rodent pathogen, typically causing infection within the respiratory and urogenital tract of mice; however, it is more commonly used as a representative model in chlamydial studies due to pathology reflective of the human pathogen C. trachomatis (Cheong et al. 2019).

Wildlife Infections

Chlamydial Infections in the Koala (Phascolarctos cinereus)

Chlamydial infections in the iconic Australian marsupial the koala are one of the most researched chlamydial infections of wildlife. Both C. pecorum and genetically distinct animal C. pneumoniae strains can infect the koala; however, C. pecorum is the most prevalent pathogen. C. pecorum infections and associated disease pose a very serious threat to the long‐term survival and conservation of this unique Australian native animal (Quigley and Timms 2020).

Almost all Australian mainland koala populations are infected with C. pecorum, with prevalence of infection of 21–88%. The pathogen can be readily detected shedding at the ocular, nasal, urogenital, and rectal sites. Sexual contact, direct contact with infectious discharges from the eyes and/or urogenital tract of infected koalas, and dam to joey transmission are considered routes of transmission for this infection (Jelocnik et al. 2019a; Quigley and Timms 2020). In koalas, C. pecorum infection can manifest as asymptomatic through to severe ocular, urogenital and respiratory disease.

In the eyes, C. pecorum infects the conjunctiva and can lead to keratoconjunctivitis, corneal scarring, and eventual blindness. Acute conjunctivitis is often characterized by serous discharge, blepharospasm, and hyperemia of the conjunctiva and sclera, while in a chronic active conjunctivitis, purulent discharge, conjunctival hyperplasia, chronic active neutrophilic and lymphocytic keratitis with corneal neovascularization and fibrosis can be observed. If left untreated, a chronic inactive keratoconjunctivitis characterized by extensive conjunctival hyperplasia, minimal erythema and mature scarring develops, eventually causing blindness (Gonzalez‐Astudillo et al. 2019).

The urogenital C. pecorum infections (including the urethra, ureters, bladder, and kidneys, upper reproductive tract in females, and prostate, epididymis, and testes in males), can develop into urethritis, cystitis, and/or pyelonephritis. Acute cystitis is characterized by thickening of the bladder wall, with or without pyuria, in both males and females, and fibrosis and ovarian bursal cysts in females. Both can cause severe pain, polyuria and/or urinary incontinence, leading to characteristic “wet‐bottom” (urine staining of the rump fur). Renal complications include hydronephrosis, pyelonephritis, and renal crystal precipitation (e.g. struvite and calcium oxalate). If infection establishes in the reproductive tract, inflammation in both females (e.g. salpingitis, endometritis, vaginitis) and males (e.g. epididymitis, orchitis, urethritis) can lead to infertility (Gonzalez‐Astudillo et al. 2019).

Other less common chlamydial disease can present as a syndrome of rhinitis/pneumonia with coughing, and copious oronasal mucopurulent exudate caused by both C. pneumoniae and C. pecorum. Chlamydial infections in koalas are often accompanied by other comorbidities such as neoplasia, wasting, other infectious diseases, and trauma (Jelocnik et al. 2019a). Chlamydial infections have been described in other Australian native marsupials (e.g., gliders, possums, quolls and bandicoots), but the impact in these hosts remains unknown (Jelocnik 2019).

Other Animal Infections

Chlamydial infections in amphibians and reptiles are common. In amphibians, C. pneumoniae strains are the most common causative agent of disease, often resulting in mortality (Eisenberg et al. 2020). In crocodiles, chlamydial infections can manifest as asymptomatic, or a range of diseases such as kyphoscoliosis in juveniles, conjunctivitis, pharyngitis, ascites, depression, anorexia, and death, with C. crocodili being recently described in these hosts (Chaiwattanarungruengpaisan et al. 2021). Several novel chlamydial species (C. poikilothermis, C. serpentis, Ca. Chlamydia corallus, Ca. Chlamydia sanzinia and Ca. Chlamydia testudinis) have been described in snakes and tortoises, but data documenting pathology are limited.

Virulence Factors and Pathogenomics

Advances in the field of Chlamydia genomics, including both culture‐independent sequencing methods and analytical approaches, have led to deeper understanding of their biology, epidemiology, and pathogenesis. Chlamydia rely on a suite of T3SS effector proteins, which are exported across the bacterial and inclusion membranes into the host cell where they modulate host cell functions. Some of these are believed to be essential to the replication of the organism while others are predicted to confer pathogenic advantage.

Similar to many other intracellular bacteria, members of the genus Chlamydia have conserved reduced genomes of up to 1.5 Mb, with 850–1050 coding sequences (Sigalova et al. 2019). Systematic analyses of whole genome sequences from across the Chlamydia genus has demonstrated that about 75% of genes are universally conserved throughout the genus, likely representing core functions for all, and 382 unique coding sequences were present only in particular genomes, likely important for host‐ or tissue‐specific functions (Sigalova et al. 2019). Almost all Chlamydia, except C. abortus and rare plasmid‐free C. trachomatis isolates, contain a small, highly conserved, non‐conjugative or integrative virulence plasmid containing eight coding sequences and no antibiotic resistance genes (Sigar et al. 2014; Zhong 2017). C. pecorum comparative genomics revealed that the plasmid was common in strains infecting livestock and koalas, but not all C. pecorum strains carry the plasmid (Jelocnik et al. 2015). In C. muridarum, the plasmid was important for chlamydial colonization in the gastrointestinal and urogenital tracts (Ma et al. 2020). Finally, in contrast to many other bacteria, the Chlamydia spp. display no evidence of antibiotic resistance, with the only exception being the tetracycline resistance gene tetA(C), which is found on the genomic Tet‐island in C. suis and encodes a tetracycline efflux system (Marti et al. 2017; Seth‐Smith et al. 2017).

Pathogenomics research has revealed that there are certain loci that are subject to expansion in particular species or strains, suggesting that these are factors for host specificity. A subset of known virulence factors is described here in more detail, including the major outer‐membrane protein (MOMP), the polymorphic membrane proteins (Pmps), T3SS effectors including inclusion membrane proteins (Incs), the chlamydial plasmid, and some metabolic factors.

The chlamydial MOMP (encoded by ompA) is a membrane‐associated protein, with immunodominant hypervariable domains exposed on the outside of chlamydial elementary body. These outer surface regions have multiple T‐ and B‐cell epitopes that induce T‐cell immunity and neutralizing antibodies (Hepler et al. 2018).

The Pmp family of proteins are membrane‐bound, surface‐exposed autotransporters known or expected to have a variety of functions related to host–pathogen interactions, including host cell adhesion and virulence. All Chlamydia species have genes encoding Pmps, which may constitute up to 13% of their genome coding capacity; however, the number of copies varies widely across the species (Vasilevsky et al. 2016). One subset of pmp genes is likely to undergo phase variation, that is the random, high‐frequency, reversible switching of gene expression from on to off. This trait is conferred by homopolymeric polyG tracts in C. pneumoniae and C. abortus that can cause replication‐coupled frameshifting (Sigalova et al. 2019).


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