S. negevensis was first discovered in 1993 as a contaminant of human and simian cell cultures of unknown origin in an Israeli laboratory by Kahane and colleagues, who originally characterized it as a Chlamydia-like microorganism called ‘Z’ (1).
Characteristics & Growth
Simkania negevensis is an obligate intracellular gram-negative bacterium with a host range that includes humans, animals and protozoans, such as amoeba, but excludes slime molds (1,2). Similar to the Chalmydiales, its growth cycle includes two distinct phases, the elementary and reticulate bodies. The larger reticulate bodies (RBs), which are somewhat pleiomorphic in shape, replicate through binary fission and are usually not infectious in most Chamydiales (3). Unlike C. trachomatis, the RBs of S. negevensis may be infectious. The elementary bodies (EBs) do not replicate and are specialized for transmitting infection to other cells upon host cell lysis, so their electron-dense forms appear later during infection, after about 3 days (3). Mature EBs of S. negevensis are distinguishable from other Chlamydiales by their quadrangular or dumbbell shapes (2,3).
After infection, S. negevensis undergoes rapid growth for 2-3 days, during which time reticulate bodies become abundant, and then enters a stationary phase for about 8 days (3). This cycle is much longer than most Chlamydiales, which typically lyse their host cells 2 to 3 days after infection.
The intracellular lifestyle of S. negevensis is supported by four nucleotide transport proteins that allow it to exploit the host cell’s energy and nucleotide pools by importing ATP, GDP, GTP, and RNA nucleotides (4). Since S. negevensis seems unable to make its own nucleotides from scratch, these proteins are vital to the biosynthesis of RNA and DNA.
The full-length 16S and 23S rRNA sequences are 80-87% identical with Chlamydiaceae, and the genome length is 1.7 Mbp, which is 2-3 times larger than the genome of Chlamydiaceae (5). The G + C content of S. negevensis and other Chlamydiae is about 40% despite the smaller genome size of the latter (5,6). Simkania contains a 132-kb conjugative plasmid that is ten times larger than that found in Chlamydiaceae and encodes for proteins involved in metabolic processes, the maintenance and propagation of the plasmid, and virulence (6).
Infants with bronchiolitis and adults with community-acquired pneumonia (CAP) or chronic obstructive pulmonary disease (COPD) have been linked to infection with S. negevensis (7,8). Evidence of S. negevensis infection has been supported with culture, serological tests, and PCR. Despite a lack of reports concerning widespread infection in humans, a high seroprevalence (46-80%) of S. negevensis antibodies has been identified in healthy adults from all over the world (8). The bacteria’s ability to survive and replicate within amoeba provides supports for this broad distribution of S. negevensis, particularly through aquatic environments (2).
Similar to Chlamydia-infected cells, S. negevensis-infected cells display anti-apoptotic mechanisms to ensure host cell survival, allowing the bacteria to continue replication. The apoptotic resistance of cells infected with S. negevensis reaches a peak during the rapid growth phase (2-3 days), and the cells become slightly more susceptible to apoptosis after this phase (6).
Patients with CAP made quick recoveries after treatment with erythromycin (8). S. negevensis is sensitive to tetracyclines and macrolides, but its growth is unaffected by sulfadiazine (1,5,9). S. negevensis is distinguished from Chlamydiaceae by its resistance to ampicillin, penicillin G, and cyclosporine (1).
Because S. negevensis is able to thrive in both amoeba and human host cells and contains a conjugative plasmid, it has considerable potential as a model organism (2,6).
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9. Donati M, Di Paolo M, Avanzi S, Di Francesco A, Fiani N, Favaroni A, et al. Detection of Simkania negevensis in cell culture by using a monoclonal antibody. New Microbiol. 2013 Jan;36(1):85–8.