A 48-year-old female was diagnosed with CLD in her early childhood. She was on a lifelong oral substitution of sodium and potassium chloride and otherwise healthy. Suddenly one evening she felt feverish, had stomach cramps, vomited 10 times and experienced extensive watery diarrhoea. She was tachycardic, but not hypotensive. She had no respiratory symptoms, and her oxygen saturation was normal. She was transferred to the ward, where her liquid and salt homeostasis was balanced. She had no prior antibiotic treatment, nor received any toxic substances, nor had a history of travel abroad. She was not an intravenous drug abuser. None of her family members had similar symptoms. Her C-reactive protein increased slightly from normal to 51 mg/l, and she had leucocytosis 11,2-22,6 × 10E9/l. Her secondary hypopotassemia (2,8 mmol/l) and lactic acidosis (3,40 mmol/l) were corrected, and plasma creatinine and alanine aminotransferase values returned to normal (from 126 to 72 micromol/l and from 592 to 17 U/l, respectively). Serum alkaline phosphates, γ-glutamyltransferase and bilirubin were normal. At admission she was hyperglycemic, but not during the follow-up. The abdominal ultrasound examination and thyroidal functions were normal. Faecal pathogens and Clostridium difficile were not recovered. Tests for viral enteritis or specific hepatitis pathogens were not done because her clinical presentation was septicaemia, and because Hepatitis A is not endemic in this region. From one anaerobic blood culture bottle gram-positive anaerobic coccae were recovered. The isolate was identified in a reference laboratory (Huslab, Helsinki, Finland) by sequencing a 528bp fragment of 16S rDNA gene as described . The primers for amplification were (5'->3') AGAGTTTGATCMTGGCTCAG (position 8-27) and GTATTACCGCGGCTGCTG (position 536-519). The sequence had 100% similarity with Sarcina ventriculi strains with accession numbers AM902707.1; AF110272.1; NR_026146.1; D14151.1 when compared to NCBI data base using BLAST analysis.
The patient was treated with oral amoxicillin for 5 days. Since this episode she has been asymptomatic. In the absence of invasive sources (e.g. catheterisation, dialysis, and intravenous drug abuse) it seems reasonable to consider that the gastrointestinal tract may have been the source of entry of this organism into the blood stream. The patient’s symptoms were caused by Sarcinae blood-borne infection because she responded quickly to antimicrobial therapy.
The information on Sarcinae is very scarce in veterinary and human clinical microbiology textbooks with the exception of a few reports [5–8]. Colonisation of Sarcinae in human intestine and the influence of diet on the colonization human intestines by Sarcinae was investigated, and it was found that viable Sarcinae were detected in more than 50% of vegetarians, whereas the bacteria were not found in those with mixed diets . Recently, an interesting report on five cases with Sarcina-like organisms identified in the upper gastrointestinal endoscopic biopsies was presented . This report raised an intriguing question whether Sarcinae can cause disease in humans or whether it is a bystander with the stomach as their natural habitat. The authors  noted that Sarcinae have a peculiar tetrad packeting architecture. Micrococcus species can also occur in tetrads, however these species can be easily distinguished from Sarcinae: Micrococcus is regular size coccae and aerobic while Sarcinae are strict anaerobic, and the size of the cell is as big as of yeasts.