Bartonella species are facultative intracellular Gram-negative bacteria which can infect humans and a wide range of animal species. Cat-scratch disease (CSD) is probably the most common Bartonella infection in the northern hemisphere [1, 2]. The hallmark of CSD is enlargement and tenderness of lymph nodes draining the site of inoculation of the microorganism . Regional lymphadenopathy usually develops 2 to 3 weeks after exposure and normally resolves spontaneously after several months . Thirty percent of the patients report low-grade fever and a skin or mucous membrane lesion may be observed at the site of inoculation for 25% to >90% of patients [3, 5]. Extranodal clinical manifestations, such as encephalopathy, neuroretinitis, arthritis, and lytic bone lesions, occur in approximately 10% of patients [3, 5–8]. Furthermore, Bartonella spp. are an important cause for blood-culture negative endocarditis [9–11]. Disease symptoms depend on the immune status of the host; in immuno-compromised hosts, the bacteria are often present in blood and involved in angioproliferative disorders such as bacillary angiomatosis and peliosis hepatis . The domestic cat is the major reservoir of Bartonella henselae, with a confirmed link to disease in humans [13, 14]. Infected cats are usually asymptomatic and develop relapsing bacteraemia for long periods . In a Dutch study, half of the cats were serological positive, and 22% were found to have a B. henselae bacteremia . Bites or scratches from infected cats are associated with development of CSD. Cat fleas, Ctenocephalides felis, are involved in transmission between cats and may be also able to transmit B. henselae to humans: Approximately 30% of patients with CSD do not recall traumatic cat contact [17–19]. Solid evidence to support transmission via cat fleas is lacking. Other Bartonella species, including Bartonella clarridgeiae and Bartonella grahamii, have also been linked to human disease. However, there are only few reports of disease cases linked to these species [20–23].
The number of cases with tick-borne diseases in the Netherlands is on the rise : This is illustrated by the fourfold increase in reported cases of erythema migrans since 1994, up to 22,000 patients in 2009. The most straightforward explanation is the reported increase in the incidence of tick bites . The same tick species transmitting the etiologic agents of Lyme disease may also serve as vector of the causative agent of CSD and maybe also other Bartonella species [25–27]. Several PCR-based studies have demonstrated B. henselae DNA in various Ixodid tick species [26, 28–32]. A recent study demonstrated that B. henselae can be transmitted across the developmental stages of Ixodes ricinus. Altogether, these studies imply that CSD can be acquired from ticks, but studies contradicting this conclusion have also been published . One of the aims of this study is to investigate whether Bartonellaceae, particularly B. henselae, are present in I. ricinus ticks in the Netherlands and form a risk to public health.
Another class of pathogens that can be transmitted by both Ixodid ticks and cat fleas is Rickettsiae. They are fastidious, mostly obligate intracellular alpha-proteobacteria. Hard ticks (Ixodidae) have been identified as vectors of the spotted fever syndrome in humans, which is caused by at least 15 different Rickettsia species . Two infamous members of this group are Rickettsia rickettsii, the causative agent of Rocky Mountain spotted fever, and Rickettsia conorii, the causative agent of Mediterranean spotted fever . Rickettsia helvetica is the most prevalent rickettsial species found in I. ricinus ticks in the Netherlands [37, 38]. To date, the pathogenic potential of R. helvetica is unclear but infection with R. helvetica has been suspected in acute perimyocarditis, unexplained febrile illness, sarcoidosis and recently also meningitis [39–47]. Laboratory diagnosis of rickettsioses is predominantly based on serology. Currently, micro-immunofluorescence is considered as a reference serological assay, but most commercially available tests offer a very limited set of antigens, mostly R. rickettsii and/or R. conorii, and serological cross-reaction with other rickettsial pathogens are common. Notably, some patients suspected to have (suffered from) a (mild) rickettsiosis do not recall a tick bite. In these cases, other potential sources of infection, for example cat fleas, might be involved. Cat fleas may maintain and transmit Rickettsia felis which is the causative agent of flea-borne spotted fever, also called cat flea typhus or summer flu . Clinical signs are similar to those of murine typhus and other febrile illnesses . Patients usually have fever, fatigue, headache, myalgia, rash and elevation of liver enzymes, although these clinical manifestations do not occur in all patients. They can also present abdominal pain, pleuric chest pain, diarrhea, nausea, vomiting, conjunctivitis, and neurological symptoms [50–54]. R. felis appears to have a global distribution , and it is not unlikely that R. felis is also present in the Netherlands. Nevertheless, evidence for the presence of R. felis in Dutch cat fleas is lacking and no autochthonous clinical cases of flea-borne rickettsisos have been reported. In this study, we investigated whether R. felis is present in Dutch cat fleas.