Candida auris is an emerging, multidrug-resistant fungal pathogen that has become a public health threat with an increasing incidence of infections worldwide. Candida auris spreads easily among patients within and between hospitals. Infections and outbreaks caused by C. auris have been reported in the Middle East region including Oman, Kuwait, Saudi Arabia, and Qatar; however, the origin of these isolates is largely unknown. Pathogen whole genome sequencing (WGS) was used to determine the epidemiology and drug resistance mutations of C. auris in Qatar. Forty-four samples isolated from patients in three hospitals and the hospital environment were sequenced by Illumina NextSeq. Core genome single nucleotide polymorphisms (SNPs) revealed that all isolates belonged to the South Asian lineage with genetic heterogeneity that suggests previous acquisition from foreign healthcare. The genetic variability among the outbreak isolates in the two hospitals (A and B) was low. Four environmental isolates clustered with the related clinical isolates, and epidemiologically linked isolates clustered together, suggesting that the ongoing transmission of C. auris could be linked to infected/colonized patients and the hospital environment. Prominent mutations Y132F and K143R in ERG11 linked to increased fluconazole resistance were detected.

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Tigecycline resistance was rare in isolates causing clinically significant infections in the UK and was overestimated ∼2-fold by the BSAC disc method. Adjustment of the breakpoints might overcome this problem but at the risk of increasing the false susceptibility rate. The best advice is to perform dilution tests, e.g. by gradient strip test on isolates with borderline results, especially in severe infection and when tigecycline use is intended.

This study compared specific phenotypic and potential virulence characteristics of StaphyZococcus aureus isolates from invasive infections and nasal carriers. Three hundred and sixty isolates were studied; 154 from septicaemia (69 line associated, 85 non-line), 79 from continuous ambulatory peritoneal dialysis (CAPD) peritonitis, 64 from bone/joint infections and 64 from healthy nasal carriers. The isolates were tested for production of enterotoxins (SE) A, B, C or E, toxic shock syndrome toxin-1 (TSST-1) protein A, and also for lipolytic, proteolytic, fibrinolytic and haemolytic activities. In addition phage typing, crystal violet reaction, urease and galactose breakdown were studied. Seventy-one percent of isolates were enterotoxigenic. Production of SEA was significantly lower amongst the bone/joint isolates. Production of SEB, was lower among the control group compared with CAPD, bone/joint, and non-line septicaemia isolates. SEE production was higher among the bone/joint isolates compared with the CAPD and non-line septicaemias and production of TSST-1 was significantly higher among nasal isolates compared with isolates causing infection. Almost all of the isolates were lipolytic, with highest activity amongst nasal and bone/ joint isolates. Fibrinolytic activity was similar in the five groups of isolates. Proteolytic activity ranged from 35 to 62% of isolates with the lowest frequency among septicaemia isolates. In all, 80-90% of isolates were haemolytic, although CAPD isolates were less likely to be haemolytic. Isolates from the control and CAPD group more frequently belonged to phage group I. TSST-1 does not appear to be an important requirement for invasive infections, but SEB may be. Proteolysis and intensity of lipolysis appear to be less important in septicaemia, and haemolysis may not be important in CAPD pertonitis.

suMMARY A lady with recurrent urinary infection associated with sexual intercourse with her husband is described. The source of the infection was from the husband's chronically infected prostate.Sexual intercourse is a known predisposing factor in causing urinary infections in women.' It is believed that the bacteria colonising the female's urethra are mechanically pushed up to the bladder. There have also been some reported cases of males acquiring urinary infection from their female sexual partners. 23 We report here a case of recurrently sexually acquired urinary infection in a female, derived from her husband who had a source of infection in the form of chronic prostatitis. Report of a caseA 41 year old woman was referred to the Urinary Infection Clinic, Royal Free Hospital, complaining of recurring urgency, frequency, urethral soreness and suprapubic discomfort. Her symptoms started 3 years previously, coinciding with her second marriage. During the last 2 years the attacks became worse, and in the last 12 months she had had more than 10 episodes. Her symptomatic episodes usually occurred 48 hours after intercourse.When seen, the patient was very tense and had a butterfly rash on her face which appeared only when she was subjected to stressful situations. The rash was not acne rosacea and systemic lupus erythematosis was excluded by the appropriate immunological investigations by the Rheumatology Department. She had no renal tenderness or enlargement but had mild suprapubic tenderness. An The patient was treated with pivampicillin 500 mg b.d. for 5 days, which cured the urinary infection.The patient also mentioned that her husband, aged 59 years, had had two "bad" attacks of prostatitis 4 years and 15 years previously. He had been treated with long courses of antibiotics, following which he recovered clinically.Four weeks after the patient had attended the clinic her husband developed another attack of prostatitis, in the form of shivering, fever, an uncomfortable sensation ofheat in the perineal region and thighs, and very painful terminal dysuria. He was seen by his general practitioner who referred him to another hospital. An MSU showed growth of E. coli with the same antibiogram as that isolated from his wife. He was treated with cephradine 500 mg t.d.s. for 6 weeks. A rectal examination and CT performed on him in another hospital showed enlargement of the prostate consistent with prostatitis. (CT was done to exclude malignancy). One week after finishing the antibiotic course he presented to the Urinary Infection Clinic with painful dysuria and suprapubic pain. On examination he was not febrile, with mild suprapubic tenderness. Appropriate urine specimens were taken sequentially (urethral washout, MSU, prostatic secretion, urethral washout)4 which showed high numbers of white cells, which were much higher in the prostatic secretion. Culture demonstrated significant growth of E. coli from both bladder urine and prostatic secretion. This strain was compared with the one isolated from his wife, and was...