Simkania negevensis
Classification
Domain: Bacteria Kingdom: Bacteria Phylum: Chlamydiae Class: Chlamydiae Order: Chlamydiales Family: Simkaniaceae Genus: Simkania Species: negevensis
Discovery
S. negevensis was first discovered in 1993 as a contaminant of Vero cell cultures in an Israeli laboratory (Kahane). It was originally characterized as “the chlamydia-like micro-organism Z” (Kahane).
Characteristics & Growth
Simkania negevensis is an obligate intracellular gram-negative bacterium that has been implicated in various respiratory diseases. Its growth cycle includes two distinct phases, the elementary and reticulate bodies, which are typical of the Chlamydiales. The main function of reticulate bodies is to replicate through binary fission and are usually not infectious. Unlike C. trachomatis, the replicative form of S. negevensis may also be infectious. The elementary bodies 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. After infection, S. negevensis undergoes rapid growth for 2-3 days, during which time reticulate bodies appear, and then enters a stationary phase for about 8 days. 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. Since S. negevensis seems unable to make its own nucleotides from scratch, these proteins are vital to the biosynthesis of RNA and DNA.
Genome
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. The G + C content of S. negevensis and other Chlamydiae is about 40% despite the smaller genome size of Chlamydia (Collingro). Simkania contains a 132-kb plasmid that is ten times larger than the plasmid found in Chlamydiaceae and may code for proteins important in pathogenicity and host cell interaction.
Pathology
Infants with bronchiolitis and adults with community-acquired pneumonia (CAP) or chronic obstructive pulmonary disease (COPD) have been linked to infection with S. negevensis. Evidence of S. negevensis infection has been supported with culture, serological tests, and PCR. Despite a lack of reports concerning widespread S. negevensis infection in humans, a high seroprevalence of S. negevensis antibodies has been identified in healthy adults from all over the world. This may be due to the bacteria’s ability to use amoeba for survival and replication that could enable the widespreadedness through aquatic environments.
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.
Patients with CAP made quick recoveries after treatment with erythromycin. S. negevensis is sensitive to tetracyclines and macrolides, but its growth is unaffected by sulfadiazine. S. negevensis is distinguished from Chlamydiaceae by its resistance to ampicillin, penicillin G, and cyclosporine.
Because S. negevensis is able to thrive in both amoeba and human host cells, it has great potential for being a model organism of Chlamydia infection in humans.
