Bartonella bacilliformis, endemic pathogen of the Andean region, is intrinsically resistant to quinolones

Abstract

B. bacilliformis presents a constitutive resistance to quinolones, which may be related to the presence of Ala at position 91 of GyrA and 85 of ParC. These results advise against the current clinical guidelines recommending the use of ciprofloxacin to treat bartonellosis in some countries of the Andean area.

Antibiotic resistance in Bartonella bacilliformis clinical isolates from an endemic area of Peru

“…Carrión's disease has two different clinical presentations; an initial febrile and haemolytic anaemia phase, known as Oroya fever, which has a mortality rate ranging from 44% to 88% in untreated patients; and a second phase characterised by the development of dermal eruptions known as Peruvian wart [1,2]. The recommended treatment schedule for the acute phase includes ciprofloxacin as firstline therapy in adults or children aged >14 years, whilst chloramphenicol, trimethoprim/sulfamethoxazole, amoxicillin/clavulanic acid and ceftriaxone are used second-line or in children and pregnant women.…”

“…The recommended treatment schedule for the acute phase includes ciprofloxacin as firstline therapy in adults or children aged >14 years, whilst chloramphenicol, trimethoprim/sulfamethoxazole, amoxicillin/clavulanic acid and ceftriaxone are used second-line or in children and pregnant women. Meanwhile, rifampicin, streptomycin or ciprofloxacin are used in the treatment of Peruvian warts [2]. Despite antibiotic treatment usually resulting in fever reduction and clearance of blood microorganisms within 24 h of starting treatment, both treatment failures and persistent asymptomatic bacteraemia have been reported.…”

“…bacilliformis is intrinsically resistant to nalidixic acid owing to the presence of Ala in positions 91 and 85 of GyrA and ParC, respectively [2].…”

“…The antimicrobial agents tested were amoxicillin/clavulanic acid (20/10 g), ceftazidime Science, Mannheim, Germany), a 233-bp fragment of the gyrA gene and a 349-bp fragment of the parC gene were amplified as described previously [2].…”

“…However, in vitro studies have shown the possibility of the selection of amino acid changes in GyrA that result in high levels of fluoroquinolone resistance [2]. Moreover, selection of isolates exhibiting resistance to others antibiotics has been achieved in vitro, highlighting the risk of in vivo selection and the spread of antibiotic-resistant isolates.…”