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This continuing education activity addresses the diagnosis, differential diagnosis, treatment, prevention, and interprofessional management of bartonellosis, including cat-scratch disease, trench fever, Oroya fever, verruga peruana, endocarditis, neuroretinitis, bacillary angiomatosis, and other atypical manifestations. Although Bartonella infections can range from self-limited illness to severe disseminated disease, diagnosis is often delayed because the clinical presentations are diverse, exposure histories may be overlooked, and diagnostic testing requires careful interpretation. This activity addresses the practice gap by reviewing the major Bartonella species, reservoir and vector patterns, syndrome-based evaluation, appropriate use of serological, molecular, histopathological, and culture-based testing, and evidence-based treatment strategies. Participants are expected to gain improved diagnostic accuracy, stronger clinical reasoning for syndrome-based evaluation, more appropriate selection of antimicrobial therapy, greater awareness of complications, and enhanced interprofessional coordination to support timely, patient-centered care. Objectives: Identify the major Bartonella species associated with human disease and correlate each species with its reservoirs, vectors, and principal clinical syndromes. Differentiate typical cat-scratch disease from atypical or disseminated bartonellosis on the basis of exposure history, clinical presentation, and risk factors. Select evidence-based treatment strategies for Bartonella infections according to the infecting species, clinical syndrome, patient age, disease severity, and risk of complications. Implement effective collaboration and communication among interprofessional team members to improve outcomes and treatment efficacy for patients with bartonellosis and prevent cases of bartonellosis. Access free multiple choice questions on this topic.

Bartonella spp are intracellular, facultative, gram-negative bacteria that cause a variety of zoonotic and arthropod-borne infections in humans globally. This section focuses on the 3 species most associated with bartonellosis in humans: Bartonella henselae, Bartonella quintana, and Bartonella bacilliformis. B henselae commonly causes cat-scratch disease and may also cause fever of unknown origin, neurologic disease, ocular disease, hepatosplenic disease, including peliosis hepatis, bacillary angiomatosis, and endocarditis, among other syndromes.[1] B quintana is the louse-borne causative agent of trench fever and is also associated with lymphadenopathy, endocarditis, bacteremia, and bacillary angiomatosis.[2][3] B bacilliformis is endemic to the South American Andean valleys, is transmitted by sandflies, and causes Carrion disease with its 2 distinct clinical phases: Oroya fever and verruga peruana.[4]

Bartonella species are an emerging and expanding genus, currently with 42 validly published species and additional candidate species.[5] Of these, 12 to 20 species and subspecies have been associated with human infection.[6][7] Many Bartonella species are maintained in animal reservoirs. Bartonella henselae is found in domestic cats, but Bartonella quintana and Bartonella bacilliformis appear to have humans as their reservoir. Other Bartonella species associated with human infection include Bartonella alsatica, Bartonella clarridgeiae, Bartonella doshiae, Bartonella elizabethae, Bartonella grahamii, Bartonella koehlerae, Candidatus Bartonella melophagi, Bartonella rattimassiliensis, Bartonella rochalimae, Bartonella tamiae, Bartonella tribocorum, Bartonella vinsonii (subspecies arupensis and berkhoffii), and Candidatus Bartonella washoensis.[8][9]

Bartonella species infect a wide range of mammalian hosts and are increasingly recognized as causative agents of human disease. Transmission of Bartonella species often occurs through arthropod vectors, such as fleas, lice, and sandflies. Over time, multiple species have been identified, each exhibiting host specificity for different mammalian reservoirs and relying on distinct arthropod vectors for transmission.[8] Bartonella infections are often persistent and asymptomatic in their natural reservoir hosts.[10] Table. Bartonella Species: Main Clinical Syndrome, Vector, and Reservoir briefly summarizes the known clinical syndromes, vectors, and reservoirs for Bartonella species associated with human infection.[4][8][9][11][12][13][14][15][16][17][18][19] The diversity of newly discovered Bartonella species, combined with the large number of animal reservoir hosts and vectors, raises significant public health concerns about the genus. Table Table. Bartonella Species: Main Clinical Syndrome, Vector, and Reservoir. B henselae Cats and the cat flea, Ctenocephalides felis, act as vectors for transmission of cat scratch disease. Study results have confirmed that the flea transmits the pathogen, which is critical for sustaining the circulation of B henselae within the feline population.[20] Within the flea, B henselae replicates in the intestinal tract and is continuously shed in the feces over the insect's approximately 12-day lifespan.[21] Transmission to humans occurs when flea feces containing the bacteria contaminate cat saliva or claws, allowing transmission via bites, scratches, or contaminated wounds.[1] Results from a recent study have shown that other arthropod vectors, including ticks, could possibly be implicated in transmission to humans.[14] Many cats harbor Bartonella infections without overt clinical signs, although they may experience intermittent bacteremia that persists for prolonged periods. Concurrent infection with multiple Bartonella species is frequently observed.[10] Bartonella species infection in cats has been reported as endemic in many countries, with seroprevalence ranging from 1% to 24%.

Many cats harbor Bartonella infections without overt clinical signs, although they may experience intermittent bacteremia that persists for prolonged periods. Concurrent infection with multiple Bartonella species is frequently observed.[10] Bartonella species infection in cats has been reported as endemic in many countries, with seroprevalence ranging from 1% to 24%. Results from human studies have reported seroprevalence rates ranging from 8.7% to 24%.[22] In the United States, the average annual incidence of cat-scratch disease was reported to be 4.5 cases per 100,000 persons. In adults, the highest incidence rate is in the Southern United States (6.4 cases per 100,000), but the highest overall incidence is among children aged 5 to 9 years (9.4 cases per 100,000). Incidence also peaks in late summer and fall.[23] Patients with cat-scratch disease are more likely than matched controls to own a kitten or to have a history of cat scratches or bites. Kittens are more strongly associated with human cases of cat scratch disease than older cats.[24] B quintana B quintana is a bacterium restricted to human hosts and louse vectors. Epidemics and sporadic outbreaks of trench fever have been reported globally since the early 20th century, with the most significant epidemics occurring during World Wars I and II. Trench fever, the earliest recognized disease caused by B quintana, is estimated to have affected more than 1 million individuals during World War I.[2] The human body louse, Pediculus humanus humanus, is the predominant vector of trench fever; as many as 33% of body lice and 25% of head lice may be infected with B quintana.[25] Bed bugs have also been implicated in transmission.[26] Bartonellosis caused by B quintana is now a reemerging infection, transmitted by the human body louse in conditions of poverty, overcrowding, and in persons who experience homelessness.[2] Transmission of B quintana has also been reported through organ transplant from harvested organs, mostly from high-risk populations.[27] B bacilliformis

Bed bugs have also been implicated in transmission.[26] Bartonellosis caused by B quintana is now a reemerging infection, transmitted by the human body louse in conditions of poverty, overcrowding, and in persons who experience homelessness.[2] Transmission of B quintana has also been reported through organ transplant from harvested organs, mostly from high-risk populations.[27] B bacilliformis B bacilliformis is predominantly endemic to Peru, Colombia, and Ecuador. Sporadic cases have been reported in Chile, Guatemala, and Bolivia, with unconfirmed reports from Thailand in the 1960s. Transmission of B bacilliformis occurs via the bite of the female sandfly from the genus Lutzomyia, most commonly Lutzomyia verrucarum. Traditionally, infection has been associated with inter-Andean valleys at 90° angles to the prevailing winds, at altitudes of 500 to 3200 m above sea level, due to the habitat of the primary vector. Infections appear to be more frequent during El Niño weather patterns.[4]

Inside the host, Bartonella species have been found to infect multiple cell types, but vascular endothelial cells are the primary blood-seeding niche. From there, Bartonella bacteria adhere to erythrocytes through a type IV secretion system, damage erythrocyte membranes with deformin, and then invade erythrocytes through an invasion-associated locus B protein. This process results in the long-lasting erythrocyte bacteremia associated with bartonellosis. Following this establishment, the later stages of pathogenesis are mediated in some species by virulence factors that promote angiogenesis and granulomatous disease.[1][28]

Histopathologic evaluation plays an important supportive role in the diagnosis of bartonellosis, although findings are often variable and not entirely specific. Tissue for examination is typically obtained as paraffin-embedded biopsy material from affected organs. On routine staining, organisms are difficult to visualize because they stain poorly with the Gram stain; therefore, special staining techniques are required.[1] The most commonly used method is the Warthin–Starry silver stain, which highlights the organisms as small, dark-staining bacilli arranged in clumps or chains against a golden-yellow background. While a positive Warthin–Starry stain result strongly suggests active infection, it is not definitive because other organisms, such as spirochetes and certain small bacilli, may also be detected.[1] The histopathologic features of bartonellosis vary with the clinical syndrome and disease stage. In cat-scratch disease, findings vary by tissue and disease progression, whereas other manifestations exhibit more distinctive patterns. For example, in verruga peruana caused by Bartonella bacilliformis, there is prominent dermal vascular proliferation involving both small and large vessels, reflecting a marked angiogenic response. The associated inflammatory infiltrate is mixed, composed predominantly of neutrophils and proliferating endothelial cells, with variable contributions from histiocytes, plasma cells, lymphocytes, and mast cells. Epidermal changes, including hyperkeratosis, parakeratosis, and mild acanthosis, may also be present.[29]

A comprehensive personal, travel, and social history should be obtained, and a physical examination should be performed in any patient seeking medical attention. The differential diagnosis for each syndrome can be extensive, and diagnosis may be delayed because clinicians may need to perform a comprehensive workup and may not initially consider Bartonella infection. Bartonella henselae Cat scratch disease is transmitted by a bite, scratch, or lick from an infected cat that breaks the skin and is the most common presentation of B henselae infection. Cutaneous manifestations typically begin within 3 to 10 days of exposure and progress through vesicular, erythematous, and papular phases. Regional lymphadenopathy typically appears 1 to 3 weeks after inoculation, most commonly in the axillary or epitrochlear nodes, although other sites of inoculation are possible. Lymph nodes may suppurate, requiring drainage in approximately 10% of patients. About two-thirds of patients have a fever. Cat scratch disease is usually benign and self-limited, although simultaneous presentation with other syndromes is possible.[1] Fever of unknown origin: B henselae is an increasingly recognized cause of prolonged fever and fever of unknown origin, especially in children, accounting for up to 5% of cases.[1] Ocular manifestations: After the lymphatic system, the eye is the most frequently affected organ; 5% to 10% of patients with cat scratch disease have ocular manifestations. Parinaud oculoglandular syndrome is the most common ocular manifestation and is characterized by tender lymphadenopathy of the preauricular, submandibular, and cervical lymph nodes with conjunctival, eyelid, and adjacent skin surface infections.[1][30] Ocular involvement can be subclinical, and visual symptoms may not be the presenting symptom. Neuroretinitis is an optic neuropathy classically characterized by optic disc swelling in the presence of a partial or complete macular star and occurs in 1% to 2% of patients.[17] Neurological manifestations: Patients with B henselae infection rarely have neurological manifestations other than neuroretinitis, but reported findings include encephalopathy, neuropathies, nerve palsies, transverse myelitis, and cerebral vasculitis.[1][7]

Ocular manifestations: After the lymphatic system, the eye is the most frequently affected organ; 5% to 10% of patients with cat scratch disease have ocular manifestations. Parinaud oculoglandular syndrome is the most common ocular manifestation and is characterized by tender lymphadenopathy of the preauricular, submandibular, and cervical lymph nodes with conjunctival, eyelid, and adjacent skin surface infections.[1][30] Ocular involvement can be subclinical, and visual symptoms may not be the presenting symptom. Neuroretinitis is an optic neuropathy classically characterized by optic disc swelling in the presence of a partial or complete macular star and occurs in 1% to 2% of patients.[17] Neurological manifestations: Patients with B henselae infection rarely have neurological manifestations other than neuroretinitis, but reported findings include encephalopathy, neuropathies, nerve palsies, transverse myelitis, and cerebral vasculitis.[1][7] Hepatosplenic manifestations: More than half of patients with B henselae infection may present with hepatomegaly, splenomegaly, or hepatosplenomegaly. Patients may also present with abdominal pain, and both granulomatous disease and microabscesses have been described in the abdominal organs.[1] Bacillary peliosis hepatis is a vascular proliferation of sinusoidal hepatic capillaries that results in blood-filled spaces in the liver and presents in patients with immunocompromise with B henselae infection, including those infected with human immunodeficiency virus and, more rarely, solid organ transplant recipients.[31] Culture-negative endocarditis: Although several Bartonella species have been implicated in endocarditis, B henselae and B quintana account for approximately 96% of cases caused by Bartonella endocarditis.[16] Bacillary angiomatosis: Bacillary angiomatosis is a vascular proliferative disorder caused by B henselae or B quintana that affects immunocompromised individuals, especially patients with human immunodeficiency virus and acquired immune deficiency syndrome. Bacillary angiomatosis most commonly presents with reddish-brown papules, epithelioid hemangiomas, and pyogenic granulomas.[1] The condition may also cause subcutaneous, splenic, hepatic, bone, or brain lesions and is characterized by cutaneous lesions, subcutaneous masses, and splenic, hepatic, and bone lesions.[32]

Bacillary angiomatosis: Bacillary angiomatosis is a vascular proliferative disorder caused by B henselae or B quintana that affects immunocompromised individuals, especially patients with human immunodeficiency virus and acquired immune deficiency syndrome. Bacillary angiomatosis most commonly presents with reddish-brown papules, epithelioid hemangiomas, and pyogenic granulomas.[1] The condition may also cause subcutaneous, splenic, hepatic, bone, or brain lesions and is characterized by cutaneous lesions, subcutaneous masses, and splenic, hepatic, and bone lesions.[32] Orthopedic manifestations: In addition to osseous involvement seen with bacillary angiomatosis, B henselae may rarely cause osteomyelitis.[33] Bartonella quintana Trench fever, caused by B quintana, is characterized by episodes of fever with headache, shin pain, and dizziness lasting 1 to 3 days and recurring every 4 to 6 days. The incubation period is 15 to 25 days following inoculation. Following acute trench fever, some patients develop chronic bacteremia. B quintana may also cause endocarditis and bacillary angiomatosis.[2] Bartonella bacilliformis The clinical disease caused by B bacilliformis is Carrion disease, which has 2 phases. The acute phase of Carrion disease, Oroya fever, is characterized by bacteremia about 60 days after inoculation. This phase is accompanied by severe hemolytic anemia and may be associated with fever, malaise, myalgias, headache, jaundice, tachycardia, and hepatomegaly. The chronic phase, verruga peruana, is characterized by endothelial cell-derived, blood-filled nodules erupting on the skin, which appear approximately 4 to 8 weeks after the acute phase resolves. These lesions may appear as multiple red papules, blood-filled cutaneous nodules, or subdermal nodules. Eruptions of verruga peruana may be associated with fever, malaise, lymphadenopathy, bone and joint pain, and headache.[4][34]

The diagnosis of cat scratch disease and other bartonelloses requires a multifaceted approach that integrates clinical presentation with molecular, serological, and histopathological findings. Serology Serology is the most cost-effective initial diagnostic test. Indirect fluorescent antibody testing or enzyme-linked immunosorbent assays can detect antibodies against Bartonella henselae and Bartonella quintana.[1][2] The positive predictive value of serology is variable, especially during the early stages of the disease, and ranges from 10% to 100% for immunoglobulin G (IgG) antibodies and 2% to 85% for IgM antibodies in cat-scratch disease. An elevated IgM titer is consistent with acute disease, generally within 3 months, but IgM positivity is often missed in practice. When cat-scratch disease is strongly suspected, repeat serology at a later date may help detect recent infection before antibodies have formed. Negative serology results alone should not be used to rule out cat-scratch disease. Similarly, positive IgG antibody results may indicate past infection, limiting their specificity for diagnosing acute illness.[1] An indirect fluorescent antibody IgG titer greater than 1:800 is strongly suggestive of recent or active infection and may be used as a major criterion in the diagnosis of endocarditis.[35] A drawback of serological testing is that cross-reactions occur among antibodies to B henselae and B quintana, as well as to Chlamydia species and Coxiella burnetii, which may limit interpretation.[1][2] Culture The culture of Bartonella species provides a definitive diagnosis of active infection, but it is time-consuming, expensive, and technically challenging. Bartonella species are slow-growing and fastidious. Primary isolation takes 2 to 6 weeks of incubation but is often unsuccessful. Even after primary isolation is complete, identification is complicated by slow growth, which limits colony visualization.[1][2][34] Due to these limitations, culture is not routinely recommended in clinical practice. Visualization by Special Stains

The culture of Bartonella species provides a definitive diagnosis of active infection, but it is time-consuming, expensive, and technically challenging. Bartonella species are slow-growing and fastidious. Primary isolation takes 2 to 6 weeks of incubation but is often unsuccessful. Even after primary isolation is complete, identification is complicated by slow growth, which limits colony visualization.[1][2][34] Due to these limitations, culture is not routinely recommended in clinical practice. Visualization by Special Stains Histopathological examination of the affected tissue may reveal neutrophilic and lymphocytic infiltration, suppurating granulomas, or microabscesses. Warthin-Starry silver staining can reveal small, darkly staining bacteria, and immunohistochemical staining has been used to increase histopathologic sensitivity.[1][2][36] For verruga peruana, Giemsa staining highlights cytoplasmic inclusions in endothelial cells known as Rocha-Lima inclusions.[29] Polymerase Chain Reaction Polymerase chain reaction assays can detect Bartonella species DNA in tissue samples, such as lymph nodes or blood. Polymerase chain reaction offers high specificity and rapid identification; however, its sensitivity varies, ranging from 25% to 76% depending on the sample type, species, and disease stage.[1][2][34]

Bartonella species are susceptible to numerous antibiotics in culture, including penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, rifampin, fluoroquinolones, and trimethoprim-sulfamethoxazole. Nonetheless, in vitro activity does not reliably predict in vivo effectiveness. For instance, despite exhibiting a very low minimum inhibitory concentration in vitro, penicillin has proven ineffective in clinical settings.[1] Patients with typical cat-scratch disease will usually resolve without treatment, and most studies of antibiotic therapy have failed to show benefit.[1] However, results from the only randomized controlled trial of antibiotic therapy in typical cat-scratch disease showed a significant reduction in lymphadenopathy within 30 days among patients treated with azithromycin compared with placebo.[37] Generally, patients who present with mild symptoms, such as single regional lymphadenopathy and fever, are offered supportive care, whereas those with more extensive disease are offered antibiotic therapy. Depending on the disease and pathogen, antibiotics can be used in various combinations and for different durations of therapy: Bartonella henselae in patients with cat-scratch disease and extensive lymphadenopathy: Azithromycin 500 mg on day 1 and 250 mg on days 2 to 5 [38] Alternative considerations include rifampin for 2 to 3 weeks, doxycycline plus rifampin, ciprofloxacin for 2 to 3 weeks, and trimethoprim-sulfamethoxazole for 7 to 10 days [1][38] In children, azithromycin dosing is 10mg/kg with a maximum of 500 mg on day 1 and 5 mg/kg with a maximum of 250 mg/kg on days 2 to 5 [1] Bartonella henselae neuroretinitis: Oral doxycycline 100 mg twice daily for 4 to 6 weeks and oral rifampin 300 mg twice daily for 4 to 6 weeks (shorter durations, including 2 weeks, have also been used, and some authors advocate that antibiotic treatment is not necessary) [1][38] Bartonella quintana  for trench fever or chronic bacteremia Oral doxycycline at 200 mg once daily for 4 weeks plus intravenous gentamicin 3 mg/kg for 2 weeks [2][38] Bacillary angiomatosis In children, oral erythromycin 10mg/kg (max dose 500 mg) 4 times daily for 3 months [38] Oral erythromycin 500 mg 4 times daily, or doxycycline 100 mg twice daily for 3 months [2][38] Bacillary peliosis hepatis In children, oral erythromycin 10 mg/kg (max dose 500 mg) 4 times daily for 4 months [38]

Oral doxycycline at 200 mg once daily for 4 weeks plus intravenous gentamicin 3 mg/kg for 2 weeks [2][38] Bacillary angiomatosis In children, oral erythromycin 10mg/kg (max dose 500 mg) 4 times daily for 3 months [38] Oral erythromycin 500 mg 4 times daily, or doxycycline 100 mg twice daily for 3 months [2][38] Bacillary peliosis hepatis In children, oral erythromycin 10 mg/kg (max dose 500 mg) 4 times daily for 4 months [38] Oral erythromycin 500 mg 4 times daily, or doxycycline 100 mg twice daily for 4 months Bartonella endocarditis Doxycycline 100 mg twice daily for 6 weeks, combined with an additional antibiotic Traditionally, this was gentamicin 3 mg/kg/d, but success has been reported with ceftriaxone and rifampin as second-line agents.[2][3][38] Surgery when necessary [3] In culture-negative endocarditis, coverage may also be needed for other possible etiologies [38] Oroya fever In children, chloramphenicol 50 to 75 mg/kg/d divided in 4 doses combined with a ß-lactam for 14 days, or oral ciprofloxacin 250 mg twice daily for 10 days in children ages 7 to 12 [38] Oral or intravenous chloramphenicol 500 mg 4 times daily combined with a ß-lactam antibiotic for 14 days, or oral ciprofloxacin 500 mg twice daily for 10 days [34][38] The rapid development of resistance to ciprofloxacin may occur [34] Verruga peruana In children, oral rifampin 10 mg/kg/day (maximum daily dose of 600 mg) for 14 days [38] Oral rifampin 10 mg/kg/day for 14 days, or streptomycin 15 to 20 mg/kg/day intramuscular for 10 days [34][38]

The differential diagnosis of bartonellosis depends on the clinical syndrome. The differential diagnosis of cat scratch disease includes: Mycobacterial infections (tuberculous or nontuberculosis mycobacteria) Toxoplasmosis Viral lymphadenitis (Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus) Bacterial lymphadenitis Tularemia Lymphoma or leukemia Coccidioidomycosis Leishmaniosis Lymphogranuloma venereum Nocardiosis Sarcoidosis Sporotrichosis Syphilis Toxoplasmosis The differential diagnosis of trench fever and relapsing bacteremia: Tick and louse-borne relapsing fevers Malaria Typhus group rickettsioses Brucellosis Typhoid/paratyphoid fever Viral infections (Epstein-Barr virus, cytomegalovirus, human immunodeficiency virus, acute retroviral syndrome, influenza, adenovirus) Q fever The differential diagnosis of culture-negative endocarditis includes: Coxiella burnetii Brucellosis Tropheryma whipplei Noninfectious endocarditis (Libman-Sacks, marantic endocarditis) The differential diagnosis of oroya fever includes: Autoimmune hemolytic anemia Glucose-6-phosphate dehydrogenase deficiency Dengue hemorrhagic fever Malaria Yellow fever The differential diagnosis of verruga peruana includes: Kaposi sarcoma Bacillary angiomatosis Angiosarcoma Hemangiomas and vascular malformations Verruca vulgaris

The prognosis for cat-scratch disease is generally good, and it usually resolves without treatment within 2 to 6 months.[1] Trench fever is associated with significant morbidity but a low mortality rate.[2] Oroya fever can be fatal in 44% to 88% of patients if untreated and 9% to 11% of patients if treated, making Oroya fever associated with the highest reported fatality rate among bartonelloses. Verruga peruana can cause chronic disability but is rarely fatal.[34] Other disseminated and chronic bartonelloses, especially in patients who are immunocompromised, are associated with significant morbidity and mortality.

Most complications from Bartonella henselae infection are direct effects of the atypical manifestations of illness. Several chronic pain and neuropsychiatric disorders have also been reported in patients with positive Bartonella testing results. However, the direct effect of Bartonella infection on these conditions is less clear.[7] Secondary infections are common in Oroya fever and contribute substantially to its mortality.[34]

In certain presentations of bartonellosis, referral to subspecialists may be warranted based on disease severity and clinical complexity: Infectious disease specialist: Consider for severe, atypical, or disseminated infection, particularly in immunocompromised patients or when diagnosis and management are uncertain Surgeon: May be required for drainage or biopsy of skin or lymph nodes for diagnostic purposes Hematologist/oncologist: Indicated for evaluation and management of severe hemolytic anemia, particularly during the acute phase of Oroya fever Dermatologist: Useful in cases with cutaneous manifestations, such as verruga peruana, to assist with the diagnosis and management of skin lesions

Prevention of Bartonella infections involves simple measures tailored to the specific mode of transmission: Cat scratch disease: Reducing transmission from cats can be achieved by avoiding contact with stray cats, treating flea infestations, and avoiding cat scratches or bites. Trench fever: Preventing infection requires minimizing exposure to human body lice and promptly treating infestations if they occur.[2] Carrion disease: Prevention includes controlling sandfly vectors and preventing bites from infected sandflies. Insect repellents may help prevent bites in areas where B bacilliiformis is endemic.[39] Insecticide-treated bed nets and curtains may help with vector control but are less likely to prevent sandfly bites directly.[34]

Effective patient-centered care for bartonellosis requires interprofessional collaboration among advanced clinicians, nurses, pharmacists, and other health professionals. Clinicians play a critical role in diagnosing and treating complex cases by using serological, molecular, and histopathological tools. Nurses ensure patient education, monitor symptoms, and provide supportive care, while pharmacists optimize antibiotic regimens tailored to the specific Bartonella species and clinical syndrome. Public health professionals play an essential role in vector control and One Health approaches to these zoonoses. Interprofessional communication is critical for coordinating care, especially in cases requiring long-term antibiotic therapy or surgical intervention, such as endocarditis. By fostering teamwork and leveraging each professional's expertise, healthcare teams can enhance patient safety, improve outcomes, and ensure comprehensive care for individuals affected by Bartonella infections.