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The New Zealand Medical Journal

 Journal of the New Zealand Medical Association, 28-January-2005, Vol 118 No 1208

A review of emerging flea-borne bacterial pathogens in New Zealand
Patrick Kelly, Sally Roberts, Pierre-Edouard Fournier
Abstract
Recent studies have shown that Rickettsia typhi, R. felis, Bartonella henselae, and B. clarridgeiae occur in New Zealand. To raise awareness of these emerging and re-emerging flea-borne bacterial pathogens among New Zealand health workers, we review the clinical features, diagnosis, and treatment of infections, and the biology of the major flea vectors.

Fleas are the vectors of emerging and re-emerging bacterial pathogens. Four such pathogens are known to occur in New Zealand; Rickettsia typhi, R. felis, Bartonella henselae, and B. clarridgeiae. To raise awareness of these emerging pathogens among New Zealand health workers, in this review we describe the clinical features, diagnosis and treatment of infections and the biology of the major flea vectors.

Flea-borne bacterial pathogens

Rickettsia typhi

This is an obligate intracellular Gram-negative bacterium that is the agent of murine or endemic typhus. The disease occurs world-wide and is increasingly being recognised in travellers, and in people in Australia, parts of the United States and more recently in New Zealand.1–3 The major vector of R. typhi is the oriental rat flea, Xenopsylla cheopis, in which the organism multiplies in the midgut and is excreted in the faeces where it remains viable for years.4 Although X. cheopis can transmit R. typhi by biting,5 infections usually result from inhalation or ingestion of infected flea faeces or inoculation of faeces into pruritic flea bite lesions. Rattus rats are the main reservoir hosts and animals of all ages are highly susceptible to infections, which persist for 2 to 3 weeks but cause no ill-effects.
Clinical manifestations—Rickettsiae multiply in the vascular endothelium and induce vascular injury, which accounts for most of the clinicopathologic findings. Patients with murine typhus have non-specific signs including fever, headache, myalgia, and a non-specific maculopapular rash.6 The disease is seen more commonly in adults but also occurs in children. Laboratory abnormalities include elevated liver enzymes, thrombocytopenia, and mild leucopenia.
Diagnosis—The majority of cases of murine typhus go undiagnosed (as clinical signs are non-specific).6 Definitive diagnosis of infections depends on a high level of suspicion of the disease by physicians and confirmatory laboratory tests. Serological testing for rickettsial infection using an immunofluorescence assay is performed at LabPlus, Auckland District Health Board. Cross-reactivity can occur with other bacteria and this may lead to difficulties with interpreting results.7,8 Nucleic acid amplification testing on whole blood by PCR using primers for the 17 kDa protein and citrate synthase gene is also available. Culture is not routinely performed.
Treatment—Patients respond rapidly to treatment with tetracycline, doxycycline or a fluoroquinolone. Untreated patients show signs for two to three weeks and a significant number are hospitalised, with up to 10% requiring intensive care.

Rickettsia felis

Previously known as the ELB agent, this is a recently described Gram-negative obligate intracellular bacteria which is a member of the spotted fever group (SFG) rickettsiae.9 Although only recognised for a short time, R. felis has already been found in the USA,1 Brazil, Germany, Spain, France, Ethiopia, United Kingdom, Thailand and, most recently, New Zealand.10
While ticks are the principal reservoirs and vectors of the SFG rickettsiae, R. felis is maintained in nature by the cat flea, Ctenocephalides felis. Up to 93% of commercial cat fleas are infected,1 but the prevalence is lower in wild-caught fleas and is 10% in New Zealand.10 R. felis is transmitted transovarially by C. felis which can maintain infections for at least 12 generations without feeding on an infected host.11 R. felis seems to be transmitted by flea bites12 but flea faeces contain viable organisms and transmission might occur with faecal inoculation into pruritic flea bites.
Clinical manifestations—While infections in cats appear to be subclinical, people infected with R. felis may develop severe signs, presumably as organisms multiply in the vascular endothelium. The first case of “flea-borne spotted fever” occurred in Texas in 1994 but patients have now been described in Mexico (3), Brazil (2), Germany (2), France (2), and Thailand (1).13 Mostly, there is no history of recent contact with fleas and clinical signs are non-specific, most commonly including fever, headache and rash. Other signs include marked fatigue, myalgia, photophobia, conjunctivitis, abdominal pain, vomiting, and diarrhoea—as well as solitary, black crusted skin lesions surrounded by a livid halo. Laboratory abnormalities are similar to those seen with murine typhus.
Diagnosis—Diagnoses of infections have been made by PCR and sequencing of DNA extracted from blood or skin biopsy samples using primers for the 17 kDa protein14,15, citrate synthase15,16 and PS 120 protein17 genes found in rickettsiae Recently, R. felis has been established in tissue culture (XTC-2 and Vero cells) and this has enabled serological testing which appears to be reliable and has been used to diagnose infections.16 Serology and PCR for R. felis is available at LabPlus, Auckland District Health Board.
Treatment—Patients have been successfully treated with doxycycline.17 In vitro studies have shown R. felis is sensitive to doxycycline, rifampin, thiamphenicol, and fluoroquinolones—but not to gentamicin, erythromycin, amoxicillin, or cotrimoxazole.

Bartonella henselae

This Gram-negative bacillus was first described in 1993. The domestic cat is the major reservoir of infection and around 10% to 40% of cats have chronic bacteremia,18 which may persist for years. Most infected cats appear healthy but can infect people through scratches, bites, and licks of open wounds. The cat flea, C. felis, also transmits infections, by feeding or when infected flea faeces are inoculated into skin wounds caused by pruritic fleabites. There is some evidence that B. henselae is transmitted by ticks but we have not found organisms in ticks in New Zealand (Kelly P, unpublished data, 2004).
Although B. henselae was first recognised as an agent of bacillary angiomatosis in AIDS patients, the organism is now known to cause a wide variety of other disease syndromes. The nature and severity of the conditions correlate with the immune status of the patient—those with intact or only immature immune systems develop more localised infections, while immunocompromised patients (e.g. AIDS patients) often develop systemic infections which may be fatal.
Clinical manifestations—Bartonelloses are suspected to be the most common bacterial zoonoses acquired from companion animals.
  • Cat scratch disease (CSD)
B. henselae is the major etiological agent of CSD which is probably the most common cause of chronic, benign, lymphadenopathy in children and young adults in developed countries.19 The initial lesion consists of a papule, pustule or vesicle that develops 2 to 3 weeks after a cat bite or scratch, usually on the arms.20 Although the initial lesion heals uneventfully, regional lymphadenopathy (the hallmark of the disease) develops 1 week later and persists for 2 weeks to 3 months before resolving spontaneously. In 75% of patients the adenopathy occurs with mild systemic symptoms including fever, malaise, fatigue, headache, anorexia, weight loss, and emesis that usually resolve within 2 weeks. Enlarged lymph nodes can be tender, and up to 20% of these nodes suppurate. Most cases are self-limiting with the adenopathy resolving spontaneously in 2 to 4 months.
Atypical manifestations of CSD occur in about 15% of patients. The most common is Parinaud’s occuloglandular syndrome where there is unilateral conjunctivitis with pre-auricular lymphadenopathy that probably results from inoculation into the conjunctiva rather than the skin. In some patients, dissemination of the organism can occur to cause granulomas or abscesses in the liver, spleen, bone, or mesenteric lymph nodes. Systemic manifestations of CSD include hepatosplenomegaly, glomerulonephritis, and pleural effusion.19 Various neurological syndromes have been reported with CSD including generalised seizures, transverse myelitis, encephalopathy, neuroretinitis, facial nerve paresis, and peripheral neuritis.21,22
  • Bacillary angiomatosis-peliosis
Bacillary angiomatosis is a potentially fatal pseudoneoplastic vascular proliferative disease that occurs principally in immunocompromised patients, particularly those in the later stages of HIV infection.23 There is considerable evidence that infections result from contact with cats.
Although the skin is most commonly affected, there may be osseous, gastrointestinal, respiratory, lymph node, central nervous system, and bone marrow bacillary angiomatosis (with or without accompanying skin lesions). In the skin, bacillary angiomatosis usually presents clinically as erythematous papules and nodules that may be localised or diffuse and bleed profusely when punctured. They may mimic Kaposi's sarcoma in appearance. In the disseminated forms of bacillary angiomatosis there may be fever, weight loss, and enlargement of the affected organs.
Bacillary peliosis is a very rare condition caused by B. henselae infection of parenchymal vasculature which results in development of cystic, blood-filled spaces in the liver, spleen, or lymph nodes.24 The disease is associated with immunosuppression and traumatic exposure to cats.
  • Bacteremia
Recent studies have shown B. henselae is a cause of fever in HIV-infected people that might not be associated with lymphadenopathy or hepatosplenic involvement.25 In a recent report from South Africa, 10% of people attending an HIV clinic were found to be PCR positive for B. henselae.26 In HIV-uninfected patients (regardless of whether they are immunocompetent or pharmacologically immunosuppressed), B. henselae may cause an acute onset of febrile illness with arthralgia, myalgia, and headaches which may persist or become relapsing. In some patients, B. henselae infections result in long-term asymptomatic persistent bacteraemia. Contact with cats is a major risk factor for B. henselae bacteraemia.25
  • Endocarditis
Endocarditis due to B. henselae occurs most often in patients with pre-existing valvulopathies who have contact with cats and their fleas.27 The mortality rate is high (25%) and most patients require valve replacement surgery.
Diagnosis—There are no pathognomonic clinical features of B. henselae infections, and definitive diagnoses can only be made using laboratory testing. Histology of biopsy samples may provide a presumptive diagnosis, particularly if organisms are demonstrated within characteristic lesions with Warthin-Starry silver impregnation staining. Immunocytochemical techniques are used to detect B. henselae in tissue sections and cytological specimens in specialised laboratories.28
B. henselae can be cultured on most blood-enriched media, but primary isolates are usually only observed after 12 to 14 days of culture, sometimes as long as 45 days.29 Lysis-centrifugation or freeze-thawing of blood samples greatly increases the recovery of organisms. Cultures from immunocompetent people and those previously treated with antibiotics are often negative. Identification of isolates is difficult using standard bacteriological methods and is best accomplished using molecular methods which are also sensitive and specific tests for detecting organisms in tissues and blood.29 A variety of primers have been used in PCR analyses, including those against regions of the 16SrRNA, 17-kDa antigen, and citrate synthase (gltA) genes and the 16S/23S intragenic spacer region.30,31
Serology is a cheap, sensitive, and safe means of supporting clinical diagnoses of Bartonella infections, in particular endocarditis27 and CSD.28 Serological cross-reactivity occurs between Bartonella spp. and tests should be performed against all species known to occur in an area before an etiological diagnosis is made. Generally, highest titres are against the species causing the infection. Immunocompromised patients might not mount significant antibody responses. Culture, PCR, and serology for B. henselae are available in New Zealand.
Treatment—In vitro, B. henselae is susceptible to most antibiotics although only aminoglycosides are bactericidal.32 Most typical cases of CSD, however, respond very poorly to antimicrobial therapy and the disease generally resolves spontaneously within 4 months.33 Although treatment with azithromycin has been suggested for patients with pronounced lymphadenopathy, no therapeutic advantage has been demonstrated.34 There is debate as to whether patients with complicated CSD benefit from antibiotics.35 In immunocompromised patients with CSD or immunocompetent patients with central nervous system involvement, a combination of doxycycline and rifampin has been suggested but there is little data to support the recommendation.35 In patients with suppurative lymph nodes, needle aspiration is an appropriate treatment.
The currently recommended treatment for bacillary angiomatosis and peliosis hepatis is oral erythromycin. Most HIV positive patients with bacillary angiomatosis respond well to antibiotics with complete remissions in 65% of patients within 30 days of treatment.23 Relapses may occur when short (<15 days) courses of treatment are given.
Successful therapy for bartonella endocarditis usually entails replacement of the extensively damaged valve. The optimum antibiotic treatment is not known, but the use of gentamicin with a beta-lactam has been recommended.36

Bartonella clarridgeiae

This organism was first described in 199637 after it was isolated from the cat of an HIV-positive patient with CSD due to B. henselae. The cat is the reservoir of the organism and up to 12% of cats might have concurrent B. henselae infections. The vectors of B. clarridgeiae are unknown, but cat fleas infected with the organism have been found in France, the Netherlands, the Philippines, Indonesia, and now New Zealand.10 Fleas containing DNA of both R. felis and B. clarridgeiae have been found in France.
Clinical manifestations—Serological testing has indicated B. clarridgeiae might be an agent of CSD in people.38 In dogs, the organism has been implicated as an agent of hepatitis and endocarditis.
Diagnosis—The organism can be cultured on solid media and detected by PCR and sequencing.39
Treatment—There is no reliable data on appropriate treatment.

Fleas

Fleas are insects in the order Siphonaptera that have a number of developmental stages in their life cycle. The adults live permanently on the host and feed on its blood. The immature stages develop in the environment and feed on organic debris. The cat flea, C. felis, is the most important ectoparasite of domestic cats and dogs in New Zealand and world-wide. It has a wide host range—readily feeding on people, pets, domestic animals, wild mammals, and rodents.40 Adults can reproduce for up to 3 months and females lay up to 50 eggs per day, which hatch in the environment and develop to pupae in as little as 10 days. Adult fleas may remain in the cocoon for many months before emerging in response to vibration and/or heat. The adults are non-selective feeders and are attracted to their hosts by visual and thermal cues. People are mainly bitten by newly emerging adults; direct transfer of fleas between hosts is uncommon.
The main host of the oriental rat flea, X. cheopis, are Rattus rats but sometimes they occur on the house mouse, Mus musculus. The number of eggs laid per day varies with the species of the host but is less than with C. felis. As with the cat flea, pupae can survive many months of starvation while awaiting a host.

Current information on flea-borne bacterial pathogens in New Zealand

To date, only infections with R. typhi and B. henselae have been diagnosed in people in New Zealand. Locally acquired murine typhus due to R. typhi was first reported in 1991.3 Subsequently, 20 patients from the greater Auckland region have been diagnosed with the disease (unpublished data, S Roberts). The majority of patients lived in northwest Auckland around the Kaipara Harbour, but three cases have occurred in the Coromandel Peninsula region. It is highly likely that it is present in other regions throughout New Zealand, especially those close to current or historic ports. R. typhi DNA has been detected by PCR in rats captured on the properties of two patients but not in fleas obtained from rats or domestic animals.2,10
Two patients infected with B. henselae have been reported in New Zealand; both had neuroretinitis22 and one also had encephalopathy.21 DNA of B. henselae has been identified in the lymph nodes of 3 patients with suspected CSD (unpublished data, S Roberts). Also, the organism has been isolated from 17% of cats in Auckland, and has been identified in 3% of cat fleas collected from dogs and cats presenting to the Veterinary Teaching Hospital of Massey University in Palmerston North.10
In nearby Australia, there have also been relatively few reports of clinical cases of B. henselae infections, although 5% of blood donors are seropositive and 35% of cats from Sydney are bacteremic.41 While infections may be under-reported, recent genotyping studies have shown there is a high level of diversity amongst strains of B. henselae and those isolated from people are more genotypically homogeneous than those associated with feline reservoirs.18 There might, then, be specific genotypes that are more likely to cause clinical infections in people and further studies are indicated to determine the types present in New Zealand.
R. felis and B. clarridgeiae have only recently been reported to occur in their vectors in New Zealand,10 and there have been no reports of human infections.

Prevention of infections

Prevention of infections with flea-borne bacterial pathogens is best achieved by minimising contact with the vectors and reservoirs of the organisms. In the case of R. typh, steps should be taken to eliminate rodents in the household. Rodent fleas (particularly X. cheopis) must be controlled simultaneously, otherwise outbreaks of murine typhus will occur after the rats die and their fleas seek alternative hosts.
Prevention of infections with B. henselae, B. clarridgeiae, and R. felis is best achieved by control of their cat flea vector. Veterinary advice should be sought on the variety of highly effective products, which can eliminate cat fleas from the household and are readily available in New Zealand. Bacteremic cats may also be a source of infection with direct transmission resulting from bites and scratches. Although these cats can be identified by blood cultures, no single antibiotic or combination of antibiotics can reliably eliminate infections from cats. While infected animals can be removed from a household, cats play an important role in improving the quality of life of their owners, particularly children and immunosuppressed people.
Therefore, rather than families being deprived of their cats, the risk of infection can be greatly decreased by instituting effective flea-control strategies and preventing situations where scratches or bites are likely to occur, such as with rough play or during teasing.
A vaccine against B. henselae for cats has been reported but subsequent studies have shown lack of protection following infection and challenge with the different strains of the organism.42

Conclusions

The development of new culture and molecular biology techniques has facilitated the investigation of flea-borne bacterial diseases of people. Application of these techniques in New Zealand has shown that R. typhi and pathogenic Bartonella species are present in the country and that infections occur in people. Also, the pathogenic flea-borne SFG rickettsia, R. felis, has been shown to occur in relatively high proportions of cat fleas. Health workers in New Zealand should, then, be aware of the possibility of infections with these organisms in their patients and diagnostic laboratories in the region should provide appropriate diagnostic tests.
Author information: Patrick Kelly, Professor, Ross University School of Veterinary Medicine, Basseterre, St Kitts, West Indies; Sally Roberts, Senior Microbiologist, Department of Microbiology, Auckland District Health Board, Auckland; Pierre-Edouard Fournier, Physician, Unité des Rickettsies, Faculté de Médecine, Marseille, France
Correspondence: Patrick Kelly, Ross University School of Veterinary Medicine, PO Box 334, Basseterre, St Kitts, West Indies. Fax: +869 465 1203; email: pkelly@rossvet.edu.kn
References:
  1. Boostrom A, Beier MS, Macaluso JA, et al. Geographic association of Rickettsia felis-infected opossums with human murine typhus, Texas. Emerg Infect Dis. 2002;8:549–54.
  2. Roberts S, Ellis-Pegler R. Murine typhus in New Zealand. N Z Public Health Rep. 2001;8:73–5.
  3. Roberts S, Hill P, Croxson M, et al. The evidence for rickettsial disease arising in New Zealand. N Z Med J. 2001;114:372–4.
  4. Traub R, Wisseman CL. The ecology of murine typhus–a critical review. Trop Dis Bull. 1978;75:237–317.
  5. Azad AF, Traub R. Experimental transmission of murine typhus by Xenopsylla cheopis flea bites. Med Vet Entomol. 1989;3:429–33.
  6. Dumler JS, Taylor JP, Walker DH. Clinical and Laboratory Features of Murine Typhus in South Texas, 1980 through 1987. JAMA. 1991;266:1365–70.
  7. Sompolinsky D, Boldur I, Goldwasser RA, et al. Serological cross-reactions between Rickettsia typhi, Proteus vulgaris OX19, and Legionella bozemanii in a series of febrile patients. Isr J Med Sci. 1986;22:745–52.
  8. Raoult D, Dasch GA. Immunoblot cross-reactions among Rickettsia, Proteus spp. and Legionella spp. in patients with Mediterranean spotted fever. FEMS Immunol Med Microbiol. 1995;11:13–18.
  9. La Scola B, Meconi S, Fenollar F, et al. Emended description of Rickettsia felis (Bouyer et al. 2001), a temperature–dependent cultured bacterium. Int J Syst Evol Microbiol. 2002;52:2035–41.
  10. Kelly PJ, Meads N, Theobald A, et al. Rickettsia felis, Bartonella henselae, and B. clarridgeiae, New Zealand. Emerg Infect Dis. 2004;10:967–8.
  11. Wedincamp J, Jr., Foil LD. Vertical transmission of Rickettsia felis in the cat flea (Ctenocephalides felis Bouche). J Vector Ecol. 2002;27:96–101.
  12. Wedincamp J, Jr., Foil LD. Infection and seroconversion of cats exposed to cat fleas (Ctenocephalides felis Bouche) infected with Rickettsia felis. J Vector Ecol. 2000;25:123–6.
  13. Parola P, Sanogo OY, Lerdthusnee K, et al. Identification of Rickettsia spp. and Bartonella spp. in from the Thai-Myanmar border. Ann N Y Acad Sci. 2003;990:173–81.
  14. Zavala-Velazquez JE, Zavala-Castro JE, Vado-Solis I, et al. Identification of Ctenocephalides felis fleas as a host of Rickettsia felis, the agent of a spotted fever rickettsiosis in Yucatan, Mexico. Vector Borne Zoonotic Dis. 2002;2:69–75.
  15. Schriefer ME SJJ, Dumler JS, Bullen MG, Azad AF. Identification of a novel rickettsial infection in a patient diagnosed with murine typhus. J Clin Microbiol. 1994;32:949–54.
  16. Raoult D, La Scola B, Enea M, et al. A flea-associated Rickettsia pathogenic for humans. Emerg Infect Dis. 2001;7:73–81.
  17. Richter J, Fournier PE, Petridou J, et al. Rickettsia felis infection acquired in Europe and documented by polymerase chain reaction. Emerg Infect Dis. 2002;8:207–8.
  18. Iredell J, Blanckenberg D, Arvand M, et al. Characterization of the natural population of Bartonella henselae by multilocus sequence typing. J Clin Microbiol. 2003;41:5071–9.
  19. Windsor JJ. Cat-scratch disease: epidemiology, aetiology and treatment. Br J Biomed Sci. 2001;58:101–10.
  20. Moriarty RA, Margileth AM. Cat scratch disease. Infect Dis Clin North Am. 1987;1:575–90.
  21. McGrath N, Wallis W, Ellis-Pegler R, et al. Neuroretinitis and encephalopathy due to Bartonella henselae infection. Aust N Z J Med. 1997;27:454.
  22. Dai S, Best S, St John M Bartonella henselae neuroretinitis in cat scratch disease. N Z Med J. 2001;114:360–1.
  23. Plettenberg A, Lorenzen T, Burtsche BT, et al. Bacillary angiomatosis in HIV-infected patients—an epidemiological and clinical study. Dermatology. 2000;201:326–31.
  24. Tappero JW, Mohle-Boetani J, Koehler JE, et al. The epidemiology of bacillary angiomatosis and bacillary peliosis. JAMA. 1993;269:770–5.
  25. Koehler JE, Sanchez MA, Tye S, et al. Prevalence of Bartonella infection among human immunodeficiency virus-infected patients with fever. Clin Infect Dis. 2003;37:559–66.
  26. Frean J, Arndt S, Spencer D. High rate of Bartonella henselae infection in HIV-positive outpatients in Johannesburg, South Africa. Trans R Soc Trop Med Hygiene. 2002;96:549–50.
  27. Fournier PE, Lelievre H, Eykyn SJ, et al. Epidemiologic and clinical characteristics of Bartonella quintana and Bartonella henselae endocarditis: a study of 48 patients. Medicine (Baltimore). 2001;80:245–51.
  28. Rolain JM, Gouriet F, Enea M, et al. Detection by immunofluorescence assay of Bartonella henselae in lymph nodes from patients with cat scratch disease. Clin Diagn Lab Immunol. 2003;10:686–91.
  29. La Scola B, Raoult D. Culture of Bartonella quintana and Bartonella henselae from human samples: a 5-year experience (1993 to 1998). J Clin Microbiol. 1999;37:1899–905.
  30. Houpikian P, Raoult D. 16S/23S rRNA intergenic spacer regions for phylogenetic analysis, identification, and subtyping of Bartonella species. J Clin Microbiol. 2001;39:2768–78.
  31. Houpikian P, Raoult D. Molecular phylogeny of the genus Bartonella: what is the current knowledge? FEMS Microbiol Lett. 2001;200:1–7.
  32. Ives TJ, Marston EL, Regnery RL, Butts JD. In vitro susceptibilities of Bartonella and Rickettsia spp. to fluoroquinolone antibiotics as determined by immunofluorescent antibody analysis of infected Vero cell monolayers. Int J Antimicrob Agents. 2001;18:217–22.
  33. Margileth AM. Antibiotic therapy for cat-scratch disease: clinical study of therapeutic outcome in 268 patients and a review of the literature. Pediatr Infect Dis J. 1992;11:474–8.
  34. Bass JW, Freitas BC, Freitas AD, et al. Prospective randomized double blind placebo-controlled evaluation of azithromycin for treatment of cat-scratch disease. Pediatr Infect Dis J. 1998;17:447–52.
  35. Koehler J, Relman D. Bartonella species. In: Raoult D, ed. Antimicrobial therapy and vaccine. 2nd ed. New York: Apple Trees Productions; 2002, pp925–31.
  36. Raoult D, Fournier PE, Vandenesch F, et al. Outcome and treatment of Bartonella endocarditis. Arch Intern Med. 2003;163:226–30.
  37. Lawson P, Collins M. Description of Bartonella clarridgeiae sp. nov. isolated from the cat of a patient with Bartonella henselae septicemia. Med Microbiol Lett. 1996;5:64–73.
  38. Sander A, Zagrosek A, Bredt W, et al. Characterization of Bartonella clarridgeiae flagellin (FlaA) and detection of antiflagellin antibodies in patients with lymphadenopathy. J Clin Microbiol. 2000;38:2943–8.
  39. Rolain JM, Franc M, Davoust B, Raoult D. Molecular detection of Bartonella quintana, B. koehlerae, B. henselae, B. clarridgeiae, Rickettsia felis, and Wolbachia pipientis in cat fleas, France. Emerg Infect Dis. 2003;9:338–42.
  40. Rust MK, Dryden MW The biology, ecology, and management of the cat flea. Ann Rev Entomol. 1997;42:451–73.
  41. Branley J, Wolfson C, Waters P, et al. Prevalence of Bartonella henselae bacteremia, the causative agent of cat scratch disease, in an Australian cat population. Pathology. 1996;28:262–5.
  42. Yamamoto K, Chomel BB, Kasten RW, et al. Homologous protection but lack of heterologous-protection by various species and types of Bartonella in specific pathogen-free cats. Vet Immunol Immunopathol. 1998;65:191–204.
     
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