Chlamydia felis is a Gram-negative, obligate intracellular bacterial pathogen that infects cats. It is endemic among domestic cats worldwide, primarily causing inflammation of feline conjunctiva, rhinitis and respiratory problems. C. felis can be recovered from the stomach and reproductive tract. Zoonotic infection of humans with C. felis has been reported. Strains FP Pring and FP Cello have an extrachromosomal plasmid, whereas the FP Baker strain does not. FP Cello produces lethal disease in mice, whereas the FP Baker does not. An attenuated FP Baker strain, and an attenuated 905 strain, are used as live vaccines for cats.

The genus Chlamydia contains the species C. trachomatis, C. psittaci, C. abortus, C. felis, C. muridarum, C. suis, C. caviae, C. pecorum, and C. pneumoniae. However, there is some dispute that some of these species, including C. felis, should be classified in a separate genus, Chlamydophila, but this has not been widely accepted. C. felis is closely related to C. pneumoniae (causes pneumonia in humans), C. trachomatis (causes Chlamydia in humans), and C. muridarum (causes pneumonia in mice). C. pneumoniae shares 879 orthologs, genes that come from a common ancestor, with C. felis while C. trachomatis and C. muridarium both share 841 orthologs with C.felis. All Chlamydia species are Gram-negative, obligate intracellular pathogens with two distinct life stages (see Characterization) that are able to infect a wide range of mammals and birds around the world.

In 1942, James A. Baker described a pathogen that causes atypical pneumonia in cats, mice, and apparently humans. Back then it was not known that Chlamydia are bacteria, and indeed Baker did not even use the term Chlamydia. Baker started researching this pathogen due to the number of atypical pneumonia cases observed in cats and later discovered that the atypical human pneumonia cases coincided with feline cases. Cats infected with this atypical pneumonia were recognized by their symptoms of sneezing, coughing, and ocular and nasal discharge. The disease was characterized by its highly infectious nature and long infection time. To determine what the causative agent was, Baker made a suspension of the infected cat lungs and used the suspension to infect mice via their nasal passage. The infected specimens died 2–5 days after initial infection. After autopsy of the deceased specimens, Baker confirmed that they died from the same disease from the condition of the lungs of the mice. He could not culture the pathogen using the available culturing methods of the time, so for a while thought that the causative agent might be a virus. Baker did find the causative agent when he spun the infected mouse lungs in a centrifuge. He found the elementary bodies (see § Characterization) of the pathogen that had been separated from the mouse lungs, confirming that they were the causative agent of the disease.

Possibly the same organism was called Miyagawanella felis in the 7th edition of Bergey's Manual (1957), Rickettsiaformis felis in Zhdanov 1953, and Chlamydozoon felis in Ryzhkov 1950. When the combination name Chlamydia psittaci was first published in 1968, all these were considered synonyms and thus subsumed into C. psittaci.

In 1969 the pathogen was again reported to be zoonotic.

In 1999, Everett et al. split out Chlamydophila felis from C. psittaci. This is the first time for this pathogen to be an independent species since the nomenclatural starting-point of the Prokaryotic Code in 1980.

C. felis is a Gram negative (also known as diderm), microaerophilic bacterium, whose cell wall seems to lack peptidoglycan. Its morphology is that of a coccobacillus. C. felis is also an obligate intracellular pathogen that infects eukaryotic cells, specifically cats, but has zoonotic potential. The bacterium like many in its phylum, has evolved to have two distinct life stages: the elementary body (EB) and the reticulate body (RB). The EB is the infectious phase of the pathogen and is characterized by reduced metabolic activity and the inability to replicate. The exact morphology of the EB varies among species within the Chlamydiota phylum. The RB is the replicative phase of the pathogen's life cycle and has a higher metabolic activity compared to the EB. When the extracellular phase (EB) infects the host eukaryotic cell via endocytosis the bacteria transforms into the replicative phase (RB) while remaining in a membrane-bound vesicle called an inclusion. Within the inclusion the RB cells will avoid the host cell's defenses, such as lysosomes, grow, and divide by binary fission. This method of infection and replication is common among the Chlamydia genus. It is currently unknown how the bacteria receive their nutrients from the host while residing in the inclusion.

Many metabolic processes and genes are highly conserved among Chlamydia. Due to C. felis's, and Chlamydia in general, small genome, it is missing the genes for several essential enzymes for metabolic pathways, such as glycolysis and the citric acid cycle. It cannot synthesize nucleotides, nor many cofactors or amino acids. However, the bacteria's ability to synthesize and/or scavenge amino acids and nucleotides varies from species-to-species and from strain-to-strain, as shown by C. felis's ability to synthesize the tryptophan. In order to survive, C. felis will take various metabolites, such as phosphorylated sugars, and other essential molecules from the host cell. It is currently unknown exactly how the bacteria receive these molecules while residing in the inclusion. It is thought that the bacteria receive host lipids by intercepting vesicles departing from the Golgi apparatus and by stealing lipid droplets and host lipid transfer proteins. With the nutrients gathered from the host cell, the bacteria can perform glycolysis and the citric acid cycle. The bacteria also have a fully functional electron transport chain (ETC), which includes a Na⁺ translocating NADH dehydrogenase, cytochrome bd oxidase, and a V-type ATPase. C. felis uses oxygen as its terminal electron acceptor, in which the cytochrome bd oxidase is necessary. The presence of a Na⁺ translocating NADH dehydrogenase suggests that instead of a proton-motive force, the bacteria uses a sodium-motive force for creating an electrochemical gradient across the plasma membrane. C. felis has also been shown to have a complete pentose phosphate pathway (PPP) and gluconeogenesis pathway, as well as being capable of both creating and degrading glycogen.