A 70-year-old man with a history of polycystic kidney disease, presented to the Urology outpatient clinic with symptoms of chronic urinary obstruction. He was diagnosed with benign prostate hyperplasia and he was treated with photovaporization. Few hours after the procedure he presented with septic shock. Treatment with antibiotics (meropenem, linezolid and daptomycin) and vasoactive drugs was initiated with significant improvement after 72h. Streptococcus pneumoniae was tentatively identified in one of two blood cultures. Urine antigen of S. pneumoniae (BinaxNOW, Abbott) and HIV serology were negative. There were no signs of lung consolidation in the chest radiography.
The presumptive identification of S. pneumoniae in the microbiology laboratory was performed by optochin disc diffusion test incubated in CO2 and in ambient air (susceptible in both atmospheres), and mass spectrometry (MALDI-TOF, Bruker). Susceptibility testing was performed with disc diffusion according to EUCAST (v13.1) (www.eucast.org). The isolate was susceptible to cefotaxime, clindamycin and vancomycin, and susceptible with increased exposure to penicillin and levofloxacin. Treatment was deescalated to ceftriaxone with good clinical progress.
As part of a surveillance programme at the Madrid Autonomous Community, all isolates of S. pneumoniae are analyzed at the Regional Public Health Laboratory for characterization. These results showed that this particular isolate was non typable, and soluble in bile. The capsular polysaccharide biosynthesis A (cpsA) and autolysin (lytA) genes were not detected, while the amplification of the pneumolysin gene (ply) was positive. Given this variety in our findings, whole genome sequencing (WGS) was performed with MinION (Oxford Nanopore) leading to identification of Streptococcus pseudopneumoniae.
S. pseudopneumoniae is a bacterial species closely related to S. pneumoniae, first identified in 2004 as part of the Streptococcus mitis group.1 It is considered an opportunistic pathogen associated with septicaemia and meningitis,2,3 particularly in patients with haematologic disease.
Phenotypic characteristics can provide some clues for its identification, but these may not be definitive, as they can overlap with other streptococcal species. S. pseudopneumoniae colonies have a similar appearance to S. pneumoniae in blood agar plates with alpha-hemolytic activity, but unlike the latter, S. pseudopneumoniae lacks capsule, is often resistant to optochin (inhibition zones <14mm) when incubated with CO2 but susceptible to optochin (inhibition zones >14mm) when incubated in ambient atmosphere, and not soluble in bile.1,4 However, there are exceptions and a variable proportion of S. pneumoniae strains do not have a specific agglutination in the Quellung reaction due to lack of capsule (non-typeable), can be optochin resistant and bile insoluble.5,6 Additionally, a proportion of S. pseudopneumoniae has also been reported as optochin susceptible when incubated in CO2 (16.4%), or bile soluble (36.1%)6 like in our case, although this does not represent the majority of the isolates. Moreover, commercial tests (such as antigen detection or DNA hybridization probes), might not easily discriminate between both species.1,7
The lytA and the cpsA genes are harbored by S. pneumoniae (although the latter may be absent in non-typeable strains), however none of these genes are present in S. pseudopneumoniae, hence being useful for discrimination between both species.6,8 Nevertheless, there are some rare S. pneumoniae strains that show some molecular peculiarities of the lytA gene that confer an atypical bile insoluble phenotype.9
In contrast to the lytA and the cpsA genes absent in S. pseudopneumoniae, some isolates can carry the ply gene.6,10
Our isolate was non-typeable, optochin susceptible when incubated both in CO2 and in ambient air, and bile soluble. The PCR was positive for ply, while negative for lytA.
Resistance rates are often higher in S. pseudopneumoniae, particularly for penicillin (60.7%) and erythromycin (42.6%),6 therefore the correct identification could affect empiric treatment.
In our patient, who presented with an invasive disease (bacteraemia), the urinary tract seemed the most likely focus, although urine culture was sterile. Nevertheless, routine culture media used for urine are not suitable for Streptococcus spp. and culture in enriched media was not performed. To our knowledge, no cases of urinary tract infection caused by S. pseudopneumoniae have been described previously.
In conclusion, it is important to note that relying solely on phenotypic characteristics for the identification of S. pseudopneumoniae can be inconclusive and may lead to misidentification. Molecular methods, such as WGS, might be needed for accurate identification.
