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initially in a waterfowl epidemic in 1904, Providenciae rettgeri is is a species of gram-negative bacteria that is closely related to members of both the Proteus and Morganella genera (O'Hara et al., 2000). It is a faculative anerobe, and is fairly ubiquitous across a wide range of environments. P. rettgeri is known mainly for its association in the gut microbiome with humans and insects, and can potentially be the cause of oppurtunistic infections among these species. In humans, P. rettgeri has been implicated in urinary tract infection, traveler's diarrhea and a variety of noscomial infection-related disesases.
Provdeincia rettgeri has been known to interact with a
variety of organisms, including loggerhead sea turtles, humans, insects (Galac
et al., 2011), nematodes (Jackson et al., 1995), and frogs (Penner et al.,
1979). Depending on context, it can
either function as a pathogen or a non-pathogenic symbiont.
Isolates of P. rettgeri have been prepared from a variety of
insect types, such as the oil fly Helaeomyia
petrolei (Kadavy et al., 2000), the waxmoth Galleria mellonella (Jackson et al., 1995), and Drosophila melanogaster. Of these,
its association with the latter has been the best characterized. P. rettgeri is a natural pathogen of D. melanogaster,
and is capable, under laboratory conditions, of killing a moderate amount
(around 40% 3 days post infection) of a given D. melanogaster population. This infection is mediated by the fly host’s
immune system. However, the mechanism of
this infection is unknown, as ingestion of the bacterial isolates did not
induce virulence. It has been suggested
that pinpricks due to mite wounds might be the sites for bacterial
colonization, leading to the presence of P. rettgeri isolates in wild flies
(Galac et al., 2011).
In other insect types, however, P. rettgeri may play a non-pathogenic
role, such as in Australian tropical fruit flies Bactrocera cacuminata and B.
tryoni (Thaochan et al., 2010). In these flies, P. rettgeri were found to
occupy the midgut region of the digestive system, along with a variety of other
bacteria. While the role of each member
within this system is unknown, it is possible that in this context, P. rettgeri
might play a mutualistic role.
The endosymbiotic bacterium Wolbachia pipientis has been shown to confer numerous advantages to
insect hosts. Interaction between Wolbachia and P. rettgeri has been investigated
on two occasions. The first showed the
presence of contigs identified as P. rettgeri within a sequenced array of Wolbachia genes isolated from the
parasitoid wasp Nasonia vitripennis (Kent et al., 2011). This suggests the existence of horizontal
gene transfer of some sort between the endosymbiont and the pathogen, but in
which context is still unclear. The
second was an attempt to demonstrate Wolbachia’s
ability to defend D. melanogaster against a P. rettgeri infection. The ability to confer immunity against
viruses is innate to Wolbachia’s
symbiotic relationship to D. melanogaster, but the study found no such effect
on P. rettgeri’s virulence (Rottschaefer
et al., 2012).
In humans, P.
rettgeri has been most often characterized as an opportunistic infectious
bacterium (see Diseases.) However, P. rettgeri is one of the more
notable bacterium isolated from the human gut and stool samples. The bacteria’s ability to degrade oxalate may
play, along with other oxalate-degrading species, a secondary role in
preventing the buildup of calcium oxalate stones (Hokama et al., 2005). Interestingly, a P. rettgeri strain cultured in
agar for two weeks lost the ability to regulate oxalate, suggesting a mechanism
by which bacterial levels in the gut may be regulated according to fluctuating levels of this substrate.
Individuals of this species are motile (Penner et al., 1975). A mechanism for this motility has not yet been reported. Members of the Providencia genus display a swarming motility that is inhibited by sodium salicyclate (Kunin et al., 1995).
Like many other members of Providencia, P. rettgeri has been implicated in numerous nocosomal infections worldwide. Complications involving a P. rettgeri infection can arise from multiple routine procedures. In two instances, a P. rettgeri-contaminated blood transfusion led to sepsis and death (Sica et al., 1999). In another case, an implantable cardioverter defibrilator pocket was found to host a relatively mild P. rettgeri infection (Marull & De Benedetti, 2009). Interestingly, cultures of P. rettgeri were recently obtained from a range of ocular infections. It may be very well possible that P. rettgei could be a cause of keratits, dacyocystitis, or conjuntivitus (Koreishi et al., 2006).
Complicating matters is that prior antibiotic therapy is a predisposing factor for these infections, suggesting that P. rettgeri may be highly resistant to commonly used antibiotics (Kaslow et al., 1976). As with many resistant infectious bacteria, P. rettgeri posseses plasmids with genes coding for extended spectrum beta lacatamases (ESBLs), enzymes that degrade various antibiotics. Two specific types of ESBLs have been discovered in P. rettgeri. Resistant P. rettgeri strains harboring 180 kb plasmids containing the TEM-24 beta-lacatamase gene were purified from the respiratory tract of a French hospital patient. Beta lacatamases from the TEM family have been shown to degrade penicillins and cephalosporins; TEM-24 is a known ceftazidimase (Marchandin et al., 1999). Second, imipenem resistant P. rettgeri strains isolated from patients in Japanese hospitals were found to house the metallo-beta-lactamase IMP-1. In addition to its beta lactamase activity, IMP-1 is a carbapenemase and degrades carbapenem antibiotics like imipenem (Shiroto, 2005). Plasmids containing the qnrD gene, which confers resistance to quinolones, have been found within P. rettgeri strains as well (Guillard et al., 2012).
Finally, P. rettgeri has been strongly associated with travelers’ diarrhoea, specifically with tourists from Japan (Yoh et al., 2005). DNA finger printing of affected travelers revealed a high incidence of P. rettgeri in these travelers' feces. However, the lack of a clear mechanism behind this association renders a characterization of P. rettgeri as a enteropathogen difficult.
The taxonomic history of Providencia rettgeri is rife with
many reclassifications and disputes, largely stemming from the difficulty in
characterizing closely related bacteria.
In 1904, Leo Rettger isolated a novel organism from an outbreak of
waterfowl cholera. Hadley et al. finally
described this organism as Bacterium
rettgerei in 1918, naming it after its discoverer (Hadley et al.,
1918). The organism was assigned to the
genus Shigella in 1927, but dropped
from this assignment by consensus after it was discovered that the organism produced
indole, and was, in fact, motile (O’Hara et al., 2000). The organism was assigned to then novel genus
Proteus in 1943, due to its ability to hydrolyze urea. Here it stayed as Proteus rettgeri even as
the Providence group was created out of the old Proteus genus. Finally, in 1978, Proteus rettgeri was moved
into the Providencia group, where is still categorized today.
Defining characteristics for P. rettgeri include phenylalanine
deamination, urea hydrolysis, indole production, growth on Simmons' citrate,
and acid production from meso-inositol. In addition, P. rettgeri is negative for
ornithine decarboxylation and acid production from lactose, maltose, D-xylose,
and L-arabinose (Penner et al., 1975).
has been isolated from both terrestrial and marine environments, yet the study
of this bacterium as an environmental isolate is limited in the literature. Of note is the isolation of P. rettgeri from wastewater and solid
waste compost in Tunisia, a strain of which tolerated high levels of copper,
chromium, and other heavy metals (Hassen
et al., 1998).
In the same region, P.
rettgeri isolates were obtained from loggerhead sea turtles, as described
earlier. It has been speculated that
these isolates’ strong resistance to antimicrobial therapies are due to a
migration of the bacteria throughout the marine environment. Consistent with its confirmed presence in
wastewater, these resistant P. rettgeri
might originate in polluted effluents (Foti et al., 2009).
It can be assumed, despite the lack of an explicit
characterization of P. rettgeri's natural range, that this range must mirror
that of one of its most widespread host.
The fruit fly D. melanogaster
thrives in temperate areas that have been settled by humans, except areas of
extreme cold—these areas comprise much the earth’s landmass. It has recently found that the microbial
diversity within D. melanogaster is relatively constant across geographically
distinct populations (Corby-Harris et al., 2007), which implies that P. rettgeri is likely widespread as
The sequencing of P. rettgeri is in progress; data is available via the National Center for Biotechnology Information
P. rettgeri has only been sequenced at the scaffold/contig level; it is one of many members of the human gut flora under an ongoing sequencing-based investigation at the Genome Institue at Washington University. Alternatively, a strain of P. rettgeri dervied from Drosophila melangaster samples (Dmel1) has been listed for sequencing analysis as well.
Providencia rettgeri are short, non-motile rod-shaped cells 0.5 to 0.8μm in length (Hadley et al., 1918). P. rettgeri forms colonies typical of the genus Providencia, producing glossy, white colonies on agar around 2-3 mm in diameter.
Numerous physiological distinctions between P. rettgeri and
other members of the Providencia
genus have been documented in the pursuit of phylogenetic classification. P.
rettgeri distinguishes itself in its capability to produce acid from
D-Adonitol, D-Arabitol, Erythritol, and other metabolic precursors. Like all members of Providencia, it can reduce nitrate to nitrite.
A well-documented physiological trait which P. rettgeri shares with the likes of E. coli and B. megaterium is the ability to hydrolyze penicillin G to
phenylacetic acid and 6-aminopenicillanic acid (6-APA, Sevo et al., 2002). 6-APA is a key synthetic precursor in the production of many semisynthetic penicillins (see Uses.)
While their metabolism may be inhibited by heavy metals (Amor
et al., 2001), P. rettgeri displays natural
resistance to heavy metal toxicity (Hassen et al., 1998) and can even perform
bioabsorbtion of certain metals (see Uses).
P. rettgeri is susceptible to a number of antibiotic treatments. It is resistant to tetracylines, but is normally susceptible to aminoglycosides, quinolones, fosformycin, and β-lactam
based antibiotics (Stock & Wiedemann, 1998). However, strains have been found harboring various plasmids containing genes known to confer drug resistance to both β-lactam based antibiotics and quinolones, suggesting non-uniform susceptibility due to lateral gene transfer (see Diseases, Genetics.)
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