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Prostatitis is the inflammation and infection of the
prostate. The bacterial pathogens involved are similar to those involved in
other urologic infections. Although Escherichia coli is
the most common causative pathogen, other etiologies include Pseudomonas aeruginosa, Klebsiella spp.,
Enterococcus spp., Enterobacter spp., Proteus spp., and Serratia spp. In sexually active
men, Neisseria gonorrhoeae and Chlamydia trachomatis should also
be considered.1 Treatment of prostatitis can be difficult, as many
antimicrobials cannot penetrate into the prostate. Current oral treatment
options include fluoroquinolones, tetracyclines, and sulfamethoxazole/trimethoprim.
However, adverse reactions and increasing resistance against these
antimicrobials warrant alternative options for oral therapy.
Fosfomycin is an attractive potential option because it does not cross-react
with other antimicrobials, making it a good choice in patients with extensive
drug allergies. It retains activity against many of the implicated organisms,
including multidrug-resistant strains such as extended-spectrum beta-lactamase
(ESBL)-producing Enterobacteriales and
vancomycin-resistant enterococci. It is also available in an oral dosage form.
However, aside from a few case reports, there are limited data regarding the
dosing, duration, and efficacy of fosfomycin for the treatment of prostatitis.2,3
Karaiskos and colleagues conducted a prospective observation study that set out
to identify the effectiveness and safety of oral fosfomycin in the treatment of
chronic prostatitis.⁴ Patients were enrolled if they had more than 3 months of
symptoms consistent with prostatitis, positive urine/prostatic secretion
cultures, a negative polymerase chain reaction for sexually transmitted
infections, imaging suggesting prostatic inflammation and did not have other
orally available antimicrobial options (eg, were resistant, had allergies or
adverse reactions). Patients provided consent to participate. Fosfomycin was
dosed at 3 g orally daily for 1 week, then 3 g orally every 48 hours for the
remainder of therapy. Patients were treated for either 6 weeks or 12 weeks, if
they had evidence of prostatic calcifications. Minimum inhibitory concentrations
(MICs) were evaluated via Etest (bioMérieux). Primary outcomes included cure at
end of therapy, defined as resolution or improvement of all signs of
infection, and relapse rates, defined as isolation of the same causative
pathogen during treatment or follow-up, at 3 and 6 months of follow-up.
Forty-four male patients were enrolled, ranging in age from 28 to 82 years
(median 54). Most patients had experienced 2 episodes of chronic bacterial
prostatitis. E coli was the most common
causative pathogen (66%), followed by Klebsiella (14%),
and Enterococcus faecalis (14%). Most
isolates were multidrug-resistant (59%), with 23% displaying evidence of ESBL.
The median fosfomycin MIC was 1.5 mcg/ mL (range, 0.125-32 mcg/ mL) for
gram-negatives and 8 mcg/mL (range 4-24 mcg/ mL) for E faecalis.
Cure was achieved in 82% (36/44 patients) of participants at end of therapy,
with a similar breakdown between the 6- and 12-week groups (Table).
Cure at the 3- and 6-month follow-ups were 80% and 73%, respectively. Fosfomycin
resistance emerged in 5 patients, 2 were in the 6-week group and 3 in the
12-week group. Overall, fosfomycin was well tolerated. Eight patients (18%)
reported diarrhea, which resolved in 4 patients by extending the dosing
interval from every 48 hours to every 72 hours. One patient discontinued
treatment due to diarrhea. No patients tested positive for Clostridioides difficile.
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