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Abstract
A new pattern of disease caused by Panton–Valentine leukocidin (PVL)-positive strains of Staphylococcus aureus is emerging in the UK and worldwide. Community-associated methicillin-resistant S aureus (MRSA) is more likely to produce PVL, a pore-forming cytotoxin inducing leucocyte lysis, which often infects young healthy individuals. The worldwide emergence and continually increasing prevalence of community-acquired PVL–MRSA have recently attracted high-profile media attention and prompted concern regarding the transmissibility and virulence. This paper reports a case of genitourinary tract infection associated with PVL-positive community-associated MRSA in an immunocompetent young man.
- AIDS
- antenatal HIV
- antibiotic resistance
- antiretroviral therapy
- bacterial infection
- epididymitis
- Panton–Valentine leukocidin
- staphylococcus
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- AIDS
- antenatal HIV
- antibiotic resistance
- antiretroviral therapy
- bacterial infection
- epididymitis
- Panton–Valentine leukocidin
- staphylococcus
An 18-year-old British Asian man accompanied by his mother presented to a sexual health clinic having felt unwell following his return from a holiday in south India. He presented with a 4-day history of yellow urethral discharge, dysuria and scrotal pain. He had been prescribed a 4-week course of diethylcarbamazine once a day in India for scrotal pain with a presumptive diagnosis of filariasis. The scrotal ultrasound scan was reported as normal in India. He was not known to have any previous medical illness. He denied the use of intravenous and recreational drugs and any sexual exposure in India.
On genital examination he had tender ulceration of the glans penis, copious yellowish urethral discharge behind a partly retractable prepuce. Multiple superficial folliculitis was present on the bilateral thighs. The rest of the physical examinations were unremarkable.
Urethral swabs for gonococcal culture, urine for Chlamydia trachomatis by nucleic acid amplification, urine for culture and sensitivity, and swabs from ulceration on the glans for herpes simplex virus by PCR were sent for testing. HIV antibody and serological tests for syphilis were sent to the laboratory.
A presumptive diagnosis of herpes simplex virus infection was made and he was treated with aciclovir 200 mg five times a day for 5 days.
He presented 3 days later with his mother with an improvement in the genital ulceration and discharge, but worsening multiple superficial abscesses on the scrotum, lower abdomen and both legs. Blood was taken for a full blood count, and random glucose and swabs were taken for culture and sensitivity from the abscesses. He was started on flucloxacillin 500 mg four times a day for 7 days.
All laboratory results were negative except full blood counts and urinalysis, which showed neutrophilia and elevated white blood cells, respectively. The midstream urine culture was positive for coagulase-negative Staphylococcus. He was prescribed nitrofurantoin 100 mg four times a day for 1 week.
Subsequently, the culture from the abscess yielded a heavy growth of methicillin-resistant Staphylococcus aureus (MRSA) resistant to gentamicin. Further reports identified the PVL gene detected by PCR at the Health Promotion Agency (HPA), Colindale, reference laboratory. A later report from HPA confirmed Bengal Bay clone-like complex on pulsed field gel electrophoresis (PFGE).
All treatment was discontinued immediately and he was started on rifampicin 300 mg and doxycycline 100 mg twice a day for 10 days. Decolonisation treatment and infection control measures were started simultaneously by the local infection control team. The patient made an uneventful recovery.
Scrotal ultrasound performed a few weeks later revealed thickened epididymii on both sides consistent with epididymitis.
Discussion
S aureus is commonly found on human skin and mucosa and is considered to be a commensal flora but potentially pathogenic. In the UK, less than 2% of clinical isolates of S aureus, in both methicillin-sensitive S aureus and MRSA, carry the PVL toxin.1
Community-associated MRSA predominantly causes skin and soft tissue infections, but also other fatal infections such as necrotising pneumonia,2 necrotising haemorrhagic pneumonia and necrotising fasciitis.3
USA300 (ST8) is currently the most prevalent community-associated MRSA clone in the USA, but there are also other predominant strains in different regions of the world, for example, ST80 among European countries.4 The sequence type (ST) corresponds to each group of related PFGE pattern.
Recent studies have shown six genetically distinct lineages of multiple antibiotic-resistant PVL–MRSA, which have been identified in the UK.5 They are β-lactam resistant but are susceptible to most antimicrobial agents; ciprofloxacin in particular is used as a PVL–MRSA marker.1
In our patient, folliculitis and superficial abscesses appeared together with his presentation of genital and urinary tract infection. This is different to previous reported cases as it involves co-infection of the coagulase-negative Staphylococcus and multiresistant Bengal Bay clone (ST772) detected by PFGE. However, HPA has currently replaced PFGE with spa typing as a frontline tool for S aureus typing because it is cheaper, quicker and easier to perform while offering higher throughput for anticipated increased workload with implementation of the enhanced surveillance of MRSA.6
The ST772 clone was first reported in Bangladesh, then India, where common travel to and from Bangladesh was noted.5 A recent study has shown that the ST772 PVL–MRSA cases detected in England were often linked to India and Bangladesh, and has shown a trend of increasing prevalence.5 The high potential transmissibility of ST772 has been further suggested due to a consistently high level of multidrug resistance.5 In addition, the emergence of ciprofloxacin resistance in multiple community-acquired PVL–MRSA lineages has highlighted the diminishing utility of ciprofloxacin susceptibility as a putative marker for PVL–MRSA.5
This case recognised the increasing incidence of PVL–MRSA and alerts all physicians regarding the emergence of drug-resistant lineages in the UK. It highlights the importance of travel history preceding such presentations in an immunocompetent patient.
This case reflects the increasing incidence and morbidity associated with PVL–MRSA. This report draws attention to the potential of PVL S aureus to cause urethritis and epididymitis.
Footnotes
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.