Updated: Oct 13, 2008
Bartonellosis comprises infections caused by newly emerging pathogens in the genus Bartonella. In 1909, A. L. Barton described organisms that adhered to RBCs. The name Bartonia, later Bartonella bacilliformis, was used for the only member of the group identified before 1993. Rochalimaea (named for Rocha-Lima), a similar group, were recently combined with Bartonella. Although these organisms were originally thought to be rickettsiae, Bartonella bacteria can be grown on artificial media, unlike rickettsiae.
At least a dozen species belong to the genus Bartonella. Three Bartonella species are currently considered important causes of human disease, but other significant human pathogens in this genus will undoubtedly be found in the future. In one study, serum specimens from 114 patients hospitalized with a febrile illness were tested with an indirect immunofluorescence assay (IFA) using rodent and human Bartonella pathogens; 5 patients had high-titer seroconversion to rodent-associated Bartonella.1
B bacilliformis causes Oroya fever and verruga peruana. Bartonella henselae causes catscratch disease (CSD) and peliosis of the liver (often called bacillary peliosis). Bartonella quintana causes trench fever. Both B henselae and B quintana may cause bacillary angiomatosis, infections in homeless populations, and infections in patients infected with HIV.
New Bartonella species that may cause human disease include Bartonella vinsonii, Bartonella clarridgeiae, Bartonella tamiae, Bartonella rochalimae, and Bartonella elizabethae. Several of these other species are found in animals.
For additional information on emerging and reemerging infectious diseases, see Medscape’s Emerging and Reemerging Infectious Diseases Resource Center.
B bacilliformis, which uses a polar flagellum for motility, adheres to and invades RBCs. After entry, the organism replicates in vacuoles. This species also makes an endothelial cell–stimulating factor that causes proliferation of both endothelial cells and blood vessels.
B henselae and B quintana do not bind to intact human erythrocytes in the same way that B bacilliformis does; however, these organisms make a protein binder that adheres to feline RBC membranes, and they penetrate into endothelial cells. Both species also initiate production of an endothelial cell–stimulating factor. Because lysis-centrifugation blood cultures show enhanced isolation of B henselae and B quintana, intracellular forms are most likely present in humans. Erythrocytes may serve as a reservoir for Bartonella species.
B quintana also invades endothelial cells and forms bacterial aggregates that are taken internally by the invasome, a unique phagosomal structure.2 These proliferate and make intracellular blebs.
Catscratch disease caused by B henselae infection occurs in approximately 1 per 10,000 persons.
B quintana is found worldwide and causes febrile outbreaks. Poor sanitation and lack of personal hygiene strongly correlate with transmission by the body louse Pediculus humanus. B quintana is emerging as a recognized cause of disease among homeless persons and persons with AIDS. Trench fever syndrome is found among people with alcoholism and those who are homeless. Persons who are indigent in inner-city Seattle were evaluated for antibodies to B quintana. Approximately 20% of these people had antibody titers of 1:64 or greater; in comparison, this titer was found in only 2% of blood donors.3
B bacilliformis transmission is limited to the Andes Mountains at elevations of 1000-3000 meters because of the habitat of the sand fly Phlebotomus, now called Lutzomyia. Outbreaks of B bacilliformis infection occur only in the Andes. Cases elsewhere in the world are found in travelers.
B henselae is found throughout the world in association with both domestic and feral cats. It has recently been reported in cats in Germany. The cat flea Ctenocephalides felis is an arthropod vector. B henselae has been isolated from ticks, but their competence in disease transmission is unclear.4,5
B quintana infection has been reported in 16% of homeless hospitalized patients in France.
Other species, such as B clarridgeiae, may be a cause of asymptomatic infection in cats.
Catscratch disease usually causes self-limited regional adenopathy. Acute hemiplegia has been reported in an 11-year-old boy.6 Encephalopathy is the most common neurologic complication but is rare.
B henselae is a common cause of culture-negative endocarditis. Valve replacement is required in approximately 80% of cases, but overall prognosis is good, with survival rates in excess of 80%.7 In a 2003 article in Medicine by Houpikian and Raoult, Bartonella endocarditis was associated with B quintana in 75% of cases and with B henselae in 25% of cases. They reported a mortality rate of 7% among 99 patients with Bartonella endocarditis.8
Trench fever is a self-limited relapsing febrile illness. Affected persons regularly recover, even without treatment. Liver abscesses and spleen abscesses in the absence of endocarditis in an immunocompetent host have been described.9
Disseminated forms of bartonellosis develop in patients infected with HIV. Bacillary angiomatosis and culture-negative endocarditis are caused by B henselae and B quintana. Peliosis hepatis is caused by B henselae.
Carrión disease commonly affects the pediatric population in Peru and Ecuador. Mortality and morbidity of the acute phase vary because of superimposed infections and other complications. Mortality rates associated with the eruptive phase, known as Peruvian wart, are extremely low.10
Currently, Bartonella species cause several clinical syndromes, including catscratch disease (with enlarged nodes and other organ involvement), bacteremia, endocarditis, bacillary angiomatosis, peliosis hepatis, Oroya fever, and verruga peruana. The inability to mount an immune response contributes to manifestations observed in immunosuppressed individuals with advanced AIDS and other diseases.
Bacillary Angiomatosis
Catscratch Disease
Catscratch disease: Consider other causes of enlarged lymph nodes, such as localized infections with regional node swelling and systemic diseases. Examples include lymphoma, leukemia, other neoplasms, fungal infection, tularemia, tuberculosis, plague, lymphogranuloma venereum (LGV), AIDS, and syphilis.
Bacteremia and systemic illnesses: Culture-negative endocarditis is always difficult to diagnose. Consider this diagnosis when the Duke criteria for endocarditis are present with negative findings on routine blood cultures. If bartonellosis is suspected, obtain antibody titers for B henselae and B quintana. Other causes of culture-negative endocarditis that merit consideration include legionellosis, Q fever, HACEK group infections (Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae), and fastidious or slowly growing streptococci.
Bacillary angiomatosis: These lesions are often dark purple and resemble Kaposi sarcoma, pyogenic granuloma, or verruga peruana.
Oroya fever and verruga peruana: Febrile patients who have returned from travel to a developing country mandate consideration of a rather large number of possible illnesses depending on the itinerary, activities, and potential for exposures. Serious illnesses to consider include Dengue fever, malaria, tuberculosis, and babesiosis.
Catscratch disease: Lymph node biopsy demonstrates granulomas with stellate necrosis, which are characteristic of catscratch disease. Silver stains, such as Dieterle or Warthin-Starry, may show bacilli.
Bacillary angiomatosis and peliosis hepatitis: Both of these disorders show blood vessel proliferation. Bacillary angiomatosis refers to vascular tumors that readily bleed when cut. The microscopic appearance of neovascular proliferation is diagnostic. Silver stains may demonstrate clusters of Bartonella bacilli. Peliosis refers to blood-filled cystic lesions that may be microscopic or up to a few millimeters in diameter. These lesions are characteristically found in the liver but are occasionally found in the spleen. Bacilli may be visible on electron microscopy.
In an editorial entitled "Bartonellosis: light and shadows in diagnostic and therapeutic issues" in Clinical Microbiology and Infection (2005), Manfredi et al wrote, "The role of surgical debridement and the unpredictable activity of antimicrobial agents warrant further investigation." The authors go on to point out that "The need for, selection and duration of antimicrobial therapy for CSD remain contentious. Suppurative nodes that become tense and painful should be drained, but incision of non-suppurative lesions should be avoided, as chronic draining fistulae or compromised healing may result."25
Bartonellosis is generally treated with macrolides, tetracyclines, aminoglycosides, or chloramphenicol. Chloramphenicol is not usually used to treat either B henselae or B quintana infection, although it has been used to treat B bacilliformis infection. Chloramphenicol has been primarily used to treat Oroya fever.
Duration of therapy is commonly at least 3 weeks. Patients should be monitored for evidence of response and drug toxicity. Because these infections often fail to respond to therapy or patients experience relapse later, switching to antibiotics from other classes (eg, erythromycin, clarithromycin, azithromycin, trimethoprim and sulfamethoxazole, or ciprofloxacin) may be needed. Gentamicin may also be effective.
Longer duration of therapy, from 3 weeks to 2 months, may be required for patients who have peliosis hepatis or disseminated disease, including bacteremia.
A culture-negative endocarditis treatment regimen should include an aminoglycoside (gentamicin) for 2 weeks and ceftriaxone with or without doxycycline for 6 weeks.
If bartonellosis is proven, the guidelines recommend using a regimen consisting of doxycycline for 6 weeks plus gentamicin (1 mg/kg IV q8h for 14 d).
Valve replacement is required in approximately 80% of cases, but overall prognosis is good, with survival rates of 80%.
Patients in the acute phase of Carrión disease should receive ciprofloxacin and, alternatively, chloramphenicol plus penicillin G. Patients in the eruptive phase of the disease should receive rifampin and, alternatively, azithromycin or erythromycin.
Therapy must be comprehensive and cover all likely pathogens in the context of the clinical setting.
Inhibits protein synthesis and bacterial growth by binding to 30S, and possibly 50S, ribosomal subunits of susceptible bacteria. For B quintana infection, bacillary angiomatosis, peliosis hepatitis, and AIDS.
Asymptomatic B quintana bacteremia: 100-200 mg PO qd for 15 d; longer duration of therapy may be needed
<8 years: Not recommended
>8 years: Not established
Bioavailability decreases minimally with antacids that contain aluminum, calcium, magnesium, iron, or bismuth subsalicylate; tetracyclines can increase hypoprothrombinemic effects of anticoagulants; tetracyclines can decrease effects of PO contraceptives; half-life decreases with coadministration of barbiturates, phenytoin, carbamazepine, rifampin, and ethanol; increases cyclosporine concentration
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity occurs in rare cases; reduce dose in renal impairment; use during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
Erythromycin base or equivalent: 250 mg PO qid
Erythromycin ethyl succinate: 400 mg PO qid
Erythromycin ethyl succinate: 30-50 mg/kg/d PO qid
Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis
Documented hypersensitivity; hepatic impairment
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer doses pc); discontinue use if nausea, vomiting, malaise, diarrhea, or abdominal colic occur
Treats mild-to-moderate microbial infections.
Day 1: 500 mg PO
Days 2-5: 250 mg PO qd; may need to repeat if symptoms do not resolve
Day 1: 10 mg/kg PO once; not to exceed 500 mg/d
Days 2-5: 5 mg/kg PO qd; not to exceed 250 mg/d
May increase toxicity of theophylline, warfarin, and digoxin; effects are reduced with coadministration of aluminum or magnesium antacids; nephrotoxicity and neurotoxicity may occur when coadministered with cyclosporine
Documented hypersensitivity; hepatic impairment; coadministration with pimozide
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Bacterial or fungal overgrowth may result with prolonged antibiotic use; may increase hepatic enzymes and cholestatic jaundice; caution in patients with impaired hepatic function; may prolong QT interval; caution in hospitalized, geriatric, or debilitated patients
Inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.
IR: 250-500 mg PO bid
ER: 500-1000 mg PO qd
IR: 7.5 mg/kg PO bid
Toxicity increases with coadministration of fluconazole, astemizole, and pimozide; effects decrease and GI adverse effects may increase with coadministration of rifabutin or rifampin; may increase toxicity of anticoagulants, cyclosporine, tacrolimus, digoxin, omeprazole, carbamazepine, ergot alkaloids, triazolam, and HMG CoA-reductase inhibitors; cardiac arrhythmia may occur with coadministration of cisapride; plasma levels of certain benzodiazepines may increase, prolonging CNS depression; arrhythmia and increase in QTc intervals occur with disopyramide; coadministration with omeprazole may increase plasma levels of both agents
Documented hypersensitivity; coadministration with pimozide or cisapride
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Coadministration with ranitidine or bismuth citrate is not recommended with CrCl <25 mL/min; superinfections may occur with prolonged or repeated antibiotic therapies
Fluoroquinolone with activity against Pseudomonas species, streptococci, MRSA, Staphylococcus epidermidis, and most gram-negative organisms but no activity against anaerobes. Inhibits bacterial DNA synthesis and, consequently, growth.
500-750 mg PO bid
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.
160 mg TMP/800 mg SMZ 1 SS tab PO bid
<2 months: Do not administer
>2 months: 5 mL/kg susp PO bid
May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration of diuretics increases incidence of thrombocytopenia purpura in elderly patients; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine
Documented hypersensitivity; megaloblastic anemia due to folate deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholics, elderly patients, those receiving anticonvulsant therapy, those with malabsorption syndrome); hemolysis may occur in individuals with G-6-PD deficiency; patients with AIDS may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation
Binds to 50S ribosomal subunits and inhibits bacterial growth by hindering protein synthesis. Effective against gram-negative and gram-positive bacteria.
50 mg/kg/d PO/IV divided q6h
Administer as in adults
Coadministration with barbiturates may cause chloramphenicol serum levels to decrease, while barbiturate levels may increase and cause toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum chloramphenicol levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately every 3 d while in therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, or anemia; caution in pregnancy at term or during labor because of potential toxic effects on fetus (ie, gray syndrome)
Aminoglycoside antibiotic for gram-negative coverage. Used in combination with both an agent against gram-positive organisms and another agent that covers anaerobes.
1-2 mg/kg IV/IM q24h; usually reserved for very ill patients or for those who have not responded to initial therapy or have relapsed
Administer as in adults
Coadministration with other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, possibly prolonging respiratory depression; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly) with prolonged very high serum levels
Documented hypersensitivity; non–dialysis-dependent renal insufficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (patient not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
Iralu J, Bai Y, Crook L, et al. Rodent-associated Bartonella febrile illness, Southwestern United States. Emerg Infect Dis. Jul 2006;12(7):1081-6. [Medline].
Dehio C, Meyer M, Berger J, et al. Interaction of Bartonella henselae with endothelial cells results in bacterial aggregation on the cell surface and the subsequent engulfment and internalisation of the bacterial aggregate by a unique structure, the invasome. J Cell Sci. Sep 1997;110 (Pt 18):2141-54. [Medline].
Jackson LA, Spach DH, Kippen DA, et al. Seroprevalence to Bartonella quintana among patients at a community clinic in downtown Seattle. J Infect Dis. Apr 1996;173(4):1023-6. [Medline].
Holden K, Boothby JT, Kasten RW, et al. Co-detection of Bartonella henselae, Borrelia burgdorferi, and Anaplasma phagocytophilum in Ixodes pacificus ticks from California, USA. Vector Borne Zoonotic Dis. Spring 2006;6(1):99-102. [Medline].
Podsiadly E, Chmielewski T, Sochon E, et al. Bartonella henselae in Ixodes ricinus ticks removed from dogs. Vector Borne Zoonotic Dis. Summer 2007;7(2):189-92. [Medline].
Rocha JL, Pellegrino LN, Riella LV, et al. Acute hemiplegia associated with cat-scratch disease. Braz J Infect Dis. Jun 2004;8(3):263-6. [Medline].
Albrich WC, Kraft C, Fisk T, et al. A mechanic with a bad valve: blood-culture-negative endocarditis. Lancet Infect Dis. Dec 2004;4(12):777-84. [Medline].
Houpikian P, Raoult D. Western immunoblotting for Bartonella endocarditis. Clin Diagn Lab Immunol. Jan 2003;10(1):95-102. [Medline].
Durupt F, Seve P, Roure C, et al. Liver and spleen abscesses without endocarditis due to Bartonella quintana in an immunocompetent host. Eur J Clin Microbiol Infect Dis. Oct 2004;23(10):790-1. [Medline].
Huarcaya E, Maguina C, Torres R, et al. Bartonelosis (Carrion's Disease) in the pediatric population of Peru: an overview and update. Braz J Infect Dis. Oct 2004;8(5):331-9. [Medline].
Arvand M, Schad SG. Isolation of Bartonella henselae DNA from the peripheral blood of a patient with cat scratch disease up to 4 months after the cat scratch injury. J Clin Microbiol. Jun 2006;44(6):2288-90. [Medline].
Mantadakis E, Spanaki AM, Psaroulaki A, et al. Encephalopathy complicated by Guillain-Barre syndrome and hydrocephalus and associated with acute Bartonella quintana infection. Pediatr Infect Dis J. Sep 2007;26(9):860-2. [Medline].
Tsuneoka H, Tsukahara M. Analysis of data in 30 patients with cat scratch disease without lymphadenopathy. J Infect Chemother. Aug 2006;12(4):224-6. [Medline].
Albini TA, Lakhanpal RR, Foroozan R, et al. Macular hole in cat scratch disease. Am J Ophthalmol. Jul 2005;140(1):149-51. [Medline].
Patel SJ, Petrarca R, Shah SM, et al. Atypical Bartonella hensalae chorioretinitis in an immunocompromised patient. Ocul Immunol Inflamm. Jan-Feb 2008;16(1):45-9. [Medline].
Baylor P, Garoufi A, Karpathios T, et al. Transverse myelitis in 2 patients with Bartonella henselae infection (cat scratch disease). Clin Infect Dis. Aug 15 2007;45(4):e42-5. [Medline].
Stockmeyer B, Schoerner C, Frangou P, et al. Chronic vasculitis and polyneuropathy due to infection with Bartonella henselae. Infection. Apr 2007;35(2):107-9. [Medline].
Maman E, Bickels J, Ephros M, et al. Musculoskeletal manifestations of cat scratch disease. Clin Infect Dis. Dec 15 2007;45(12):1535-40. [Medline].
Raoult D, Roblot F, Rolain JM, Besnier JM, Loulergue J, Bastides F. First isolation of Bartonella alsatica from a valve of a patient with endocarditis. J Clin Microbiol. Jan 2006;44(1):278-9. [Medline].
Vikram HR, Bacani AK, DeValeria PA, et al. Bivalvular Bartonella henselae prosthetic valve endocarditis. J Clin Microbiol. Dec 2007;45(12):4081-4. [Medline].
Maggi RG, Duncan AW, Breitschwerdt EB. Novel chemically modified liquid medium that will support the growth of seven bartonella species. J Clin Microbiol. Jun 2005;43(6):2651-5. [Medline].
La Scola B, Raoult D. Serological cross-reactions between Bartonella quintana, Bartonella henselae, and Coxiella burnetii. J Clin Microbiol. Sep 1996;34(9):2270-4. [Medline].
Fournier PE, Mainardi JL, Raoult D. Value of microimmunofluorescence for diagnosis and follow-up of Bartonella endocarditis. Clin Diagn Lab Immunol. Jul 2002;9(4):795-801. [Medline].
Raoult D. From Cat scratch disease to Bartonella henselae infection. Clin Infect Dis. Dec 15 2007;45(12):1541-2. [Medline].
Manfredi R, Sabbatani S, Chiodo F. Bartonellosis: light and shadows in diagnostic and therapeutic issues. Clin Microbiol Infect. Mar 2005;11(3):167-9. [Medline].
Raoult D, Fournier PE, Drancourt M, et al. Diagnosis of 22 new cases of Bartonella endocarditis. Ann Intern Med. Oct 15 1996;125(8):646-52. [Medline].
Anderson BE, Neuman MA. Bartonella spp. as emerging human pathogens. Clin Microbiol Rev. Apr 1997;10(2):203-19. [Medline].
Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. Jun 14 2005;111(23):e394-434. [Medline].
Badiaga S, Brouqui P, Raoult D. Autochthonous epidemic typhus associated with Bartonella quintana bacteremia in a homeless person. Am J Trop Med Hyg. May 2005;72(5):638-9. [Medline].
Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: I. Bartonellosis and trench fever. Pediatr Infect Dis J. Jan 1997;16(1):2-10. [Medline].
Bass JW, Vincent JM, Person DA. The expanding spectrum of Bartonella infections: II. Cat-scratch disease. Pediatr Infect Dis J. Feb 1997;16(2):163-79. [Medline].
Batts S, Demers DM. Spectrum and treatment of cat-scratch disease. Pediatr Infect Dis J. Dec 2004;23(12):1161-2. [Medline].
Breathnach AS, Hoare JM, Eykyn SJ. Culture-negative endocarditis: contribution of bartonella infections. Heart. May 1997;77(5):474-6. [Medline].
Brouqui P, Lascola B, Roux V, et al. Chronic Bartonella quintana bacteremia in homeless patients. N Engl J Med. Jan 21 1999;340(3):184-9. [Medline].
Centers for Disease Control and Prevention. Encephalitis associated with cat scratch disease--Broward and Palm Beach counties, Florida, 1994. JAMA. Feb 22 1995;273(8):614. [Medline].
Cheuk W, Chan AK, Wong MC, et al. Confirmation of diagnosis of cat scratch disease by immunohistochemistry. Am J Surg Pathol. Feb 2006;30(2):274-5. [Medline].
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). Jul 2001;80(4):245-51. [Medline].
Gottlieb T, Atkins BL, Robson JM. Cat scratch disease diagnosed by polymerase chain reaction in a patient with suspected tuberculous lymphadenitis. Med J Aust. Feb 15 1999;170(4):168-70. [Medline].
Gouriet F, Lepidi H, Habib G, et al. From cat scratch disease to endocarditis, the possible natural history of Bartonella henselae infection. BMC Infect Dis. Apr 18 2007;7:30. [Medline].
Hipp SJ, O'Shields A, Fordham LA, et al. Multifocal bone marrow involvement in cat-scratch disease. Pediatr Infect Dis J. May 2005;24(5):472-4. [Medline].
Houpikian P, Raoult D. Blood culture-negative endocarditis in a reference center: etiologic diagnosis of 348 cases. Medicine (Baltimore). May 2005;84(3):162-73. [Medline].
James EA, Hill J, Uppal R, et al. Bartonella infection: a significant cause of native valve endocarditis necessitating surgical management. J Thorac Cardiovasc Surg. Jan 2000;119(1):171-2. [Medline].
Kahr A, Kerbl R, Gschwandtner K, et al. Visceral manifestation of cat scratch disease in children. A consequence of altered immunological state?. Infection. Mar-Apr 2000;28(2):116-8. [Medline].
Kim CM, Kim JY, Yi YH, et al. Detection of Bartonella species from ticks, mites and small mammals in Korea. J Vet Sci. Dec 2005;6(4):327-34. [Medline].
Lamps LW, Scott MA. Cat-scratch disease: historic, clinical, and pathologic perspectives. Am J Clin Pathol. Jun 2004;121 Suppl:S71-80. [Medline].
Loutit JS. Bartonella infections: diverse and elusive. Hosp Pract (Minneap). Dec 15 1998;33(12):37-8, 41-4, 49. [Medline].
Maguiña C, Gotuzzo E. Bartonellosis. New and old. Infect Dis Clin North Am. Mar 2000;14(1):1-22, vii. [Medline].
Massei F, Gori L, Macchia P, et al. The expanded spectrum of bartonellosis in children. Infect Dis Clin North Am. Sep 2005;19(3):691-711. [Medline].
Maurin M, Raoult D. Bartonella (Rochalimaea) quintana infections. Clin Microbiol Rev. Jul 1996;9(3):273-92. [Medline].
Maurin M, Raoult D. Isolation in endothelial cell cultures of chlamydia trachomatis LGV (Serovar L2) from a lymph node of a patient with suspected cat scratch disease. J Clin Microbiol. Jun 2000;38(6):2062-4. [Medline].
Moriarty RA, Margileth AM. Cat scratch disease. Infect Dis Clin North Am. Sep 1987;1(3):575-90. [Medline].
Nayler SJ, Allard U, Taylor L, et al. HHV-8 (KSHV) is not associated with bacillary angiomatosis. Mol Pathol. Dec 1999;52(6):345-8. [Medline].
Raoult D, Drancourt M, Carta A, et al. Bartonella (Rochalimaea) quintana isolation in patient with chronic adenopathy, lymphopenia, and a cat. Lancet. Apr 16 1994;343(8903):977. [Medline].
Raoult D, Ndihokubwayo JB, Tissot-Dupont H, et al. Outbreak of epidemic typhus associated with trench fever in Burundi. Lancet. Aug 1 1998;352(9125):353-8. [Medline].
Rolain JM, Brouqui P, Koehler JE, et al. Recommendations for treatment of human infections caused by Bartonella species. Antimicrob Agents Chemother. Jun 2004;48(6):1921-33. [Medline].
Schwartzman W. Bartonella (Rochalimaea) infections: beyond cat scratch. Annu Rev Med. 1996;47:355-64. [Medline].
Slater LN, Coody DW, Woolridge LK, et al. Murine antibody responses distinguish Rochalimaea henselae from Rochalimaea quintana. J Clin Microbiol. Jul 1992;30(7):1722-7. [Medline].
Spach DH, Koehler JE. Bartonella-associated infections. Infect Dis Clin North Am. Mar 1998;12(1):137-55. [Medline].
Gilbert D, Moellering R, Sande M, eds. The Sanford Guide to Antimicrobial Therapy 2000. 30th ed. Hyde Park, Vt: Antimicrobial Therapy Inc; 2000.
Tompkins LS. Bartonella species infections, including cat-scratch disease, trench fever, and bacillary angiomatosis--what molecular techniques have revealed. West J Med. Jan 1996;164(1):39-41. [Medline].
Tsukahara M, Tsuneoka H, Iino H, et al. Bartonella henselae infection from a dog. Lancet. Nov 21 1998;352(9141):1682. [Medline].
Yeh SH, Zangwill KM, Hall B, et al. Parapharyngeal abscess due to cat-scratch disease. Clin Infect Dis. Mar 2000;30(3):599-601. [Medline].
bartonellosis, Bartonella infection, catscratch disease, cat scratch disease, CSD, catscratch fever, cat scratch fever, trench fever, urban trench fever, bacillary angiomatosis, bacillary peliosis, peliosis hepatis, Parinaud oculoglandular syndrome, Parinaud's oculoglandular syndrome, Oroya fever, Carrión disease, Carrión’s disease, verruga peruana, Bartonella bacilliformis, B bacilliformis, Bartonella henselae, B henselae, Bartonella quintana, B quintana, Bartonella vinsonii, B vinsonii, Bartonella clarridgeiae, B clarridgeiae, Bartonella elizabethae, B elizabethae, Bartonella tamiae, B tamiae, Bartonella rochalimae, B rochalimae, Bartonella alsatica, B alsatica, Pediculus humanus, P humanus, Phlebotomus, Lutzomyia, Ctenocephalides felis, C felis, Bartonella endocarditis, Peruvian wart
Kassem A Hammoud, MD, Fellow, Department of Internal Medicine, Division of Infectious Diseases, University of Kansas Medical Center
Kassem A Hammoud, MD is a member of the following medical societies: American College of Physicians, American Medical Association, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Daniel Hinthorn, MD, Director, Division of Infectious Diseases, Professor, Departments of Internal Medicine, Pediatrics and Family Medicine, University of Kansas
Daniel Hinthorn, MD is a member of the following medical societies: American Academy of Family Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Brian Edwards, MD, Consulting Staff, Department of Infectious Diseases, Cotton O'Neil Clinic
Disclosure: Nothing to disclose.
Larry I Lutwick, MD, Professor of Medicine, State University of New York, Downstate Medical School; Director, Infectious Diseases, Veterans Affairs New York Harbor Health Care System, Brooklyn Campus
Larry I Lutwick, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
Joseph F John Jr, MD, FACP, FIDSA, FSHEA, Clinical Professor of Medicine, Molecular Genetics and Microbiology, Medical University of South Carolina; Associate Chief of Staff for Education, Ralph H Johnson Veterans Affairs Medical Center
Disclosure: BioMerieux Honoraria Review panel membership; Cubist Honoraria Review panel membership; Pfizer Honoraria Speaking and teaching; Merck Stock dividends stock holdings
Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.
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