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Mycoplasma suis, a member of the hemotrophic mycoplasma (HM) group, parasitize erythrocytes of pigs. Increasing evidence suggests that M. suis is also a zoonotic agent. Highly pathogenic strains of M. suis (e.g., M. suis KI3806) have been demonstrated to invade erythrocytes. This complete sequenced and manually annotated genome of M. suis KI3806 is the first available from this species and from the HM group. The DNA was isolated from blood samples of experimentally infected pigs due to the lack of an in vitro cultivation system. The small circular chromosome of 709,270 bp, encoding an unexpectedly high number of hypothetical proteins and limited transport and metabolic capacities, could reflect the unique lifestyle of HM on the surface of erythrocytes.Hemotrophic mycoplasmas (HM) are epierythrocytic, wallless bacteria that comprise a single phylogenetic cluster within the genus Mycoplasma (5). HM infections are found in a wide range of animals (e.g., Mycoplasma suis in pigs), causing infectious anemia (3, 4). The unique life cycle of M. suis and other HM on erythrocytes implies special features allowing HM to adhere to erythrocytes or to perform metabolic exchanges. Moreover, M. suis can invade erythrocytes, leading to high virulence and resistance to antibiotics (2). So far, HM cultivation in cell-free medium has failed, indicating that HM have a special metabolism and/or a high adaption to their hosts.We determined the genome of M. suis strain KI3806, a highly pathogenic and invasive strain. DNA was isolated from experimentally infected piglets using pulsed-field gel electrophoresis and sequenced (EurofinsMedigenomix; Germany) (1, 2).The circular chromosome of M. suis KI3806 is composed of 709,270 bp with a 31%-GC content. The genome includes 32 tRNAs and a single-copy 16S rRNA which is separated from the 23S and 5S rRNA by ϳ165 kb and encoded on the opposite strand. The predicted 809 open reading frames (ORFs) comprise a density of 1.119 genes per kilobase. The average protein size is 259 amino acids, with a coding percentage of 87%. The low number of estimated paralogs (36 coding determining regions [CDS]; 70% identity) corresponds to only one putative transposase. The genome differs from other mycoplasma genomes in the high portion of predicted proteins without functional assignment (64.6%; 523/809), which may reflect the adaptation of M. suis to a special environment but could also be a result of large integration events due to the unit-like organization of these proteins (RG1_33888.0.50303 [region_position], RG2_77345.0.182976, RG3_214881.0.233523, RG4_416009.0.454949, RG5_ 456815.0.523918, and RG6_581193.0.614049). These six regions encode 19 proteins of unknown function per unit at least and sum up to ϳ280 kb, which does not include housekeeping genes but does include sequences for 413 unassigned proteins. A similar scenario is known for the integrative conjugative elements (ICEs) from Mycoplasma agalactiae (6), but ICEs show different genetic content. In M. suis some phage-related proteins, i.e., an in...

Background: We hypothesized that one single episode of acute kidney injury (AKI) reduces long-term survival compared with no acute kidney injury (No AKI) following recovery from critical illness. Materials and methods: A prospective cohort of 2,010 patients admitted to the ICU between 2000 and 2009 at a provincial referral hospital was followed to determine whether AKI influences long-term survival. Results: Of the 1,844 eligible patients, 18.4% had AKI stage 1, 12.1% had stage 2, 26.5% had stage 3, and 43.0% had No AKI, using the KDIGO classification. The mean and median follow-up time was 8.1 and 8.7 years. The 28-day, 1-year, 5-year and 10-year survival rates were 59.6%, 44.9%, 37.4%, and 33.4%, in patients with any AKI (stage 1, stage 2, stage 3), which was significantly worse compared with the critically ill patients with no AKI at any time (P < 0.01). The adjusted 10-year mortality risk associated with AKI was 1.44 (95% CI = 1.2 to 1.7) among 28-day survivors. Patients who had mild AKI (stage 1) had significantly worse survival at 28 days, 1 year, 3 years, 5 years and 10 years compared with No AKI (P < 0.01) (Figure 1A). Patients with sepsis and AKI who survived 28 days had significantly poorer 5-year and 10-year survival compared with nonseptic AKI (P < 0.01) (Figure 1B). Conclusions: Patients with one episode of mild (stage 1) AKI have significantly lower survival rates over 10 years than critically ill patients without AKI. The causes and mechanisms of this association warrant further careful study. Close medical follow-up of these patients may be warranted and mechanistic research required understanding how AKI influences distant events.