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Basic biology of Bartonella species

Basic biology of Bartonella species
Literature review current through: Jan 2024.
This topic last updated: Oct 04, 2022.

INTRODUCTION — Bartonella species are fastidious, gram-negative bacteria that cause a range of manifestations, including cat scratch disease (CSD), bacillary angiomatosis (BA), other infections in persons with human immunodeficiency virus (HIV), and South American bartonellosis (Oroya fever and verruga peruana). Bartonella has also emerged as one of the leading causes of culture-negative endocarditis [1,2]. The organisms proved difficult to isolate and characterize. Analysis of Bartonella 16S ribosomal RNA was instrumental in identifying and classifying this species [3]. Although Bartonella species are frequently described as emerging pathogens, Bartonella infection was likely an ancient bacterial disease in humans, as suggested by the detection of Bartonella quintana in the dental pulp of a human that died more than 4000 years ago [4].

The microbiology and pathogenesis of Bartonella infections will be reviewed here. CSD, manifestations in persons with HIV, Bartonella endocarditis, and South American Bartonellosis are discussed separately. (See "Microbiology, epidemiology, clinical manifestations, and diagnosis of cat scratch disease" and "Treatment of cat scratch disease" and "Bartonella infections in people with HIV" and "Endocarditis caused by Bartonella" and "Bartonella quintana infections: Clinical features, diagnosis, and treatment" and "South American bartonellosis: Oroya fever and verruga peruana".)

BACKGROUND — Bartonella species belong to the alpha-2 subgroup of the Proteobacteria based on 16S ribosomal RNA testing and are closely related to the genera Brucella and Agrobacterium. Prior to 1993, the only member of the Bartonella genus that had been identified was Bartonella bacilliformis. In 1993, DNA hybridization data led Brenner and coworkers to propose to unite the genera Bartonella and Rochalimaea, retaining the genus name Bartonella [5]. In 1995, members of the genus Grahamella were merged with the Bartonella genus, but Grahamella species are not known to cause human disease.

The three most important Bartonella species known to cause human disease are B. bacilliformis, B. quintana, and Bartonella henselae. Other Bartonella species reported to have caused disease in humans, but whose role is less well defined, are Bartonella elizabethae [6], Bartonella vinsonii [7,8], Bartonella clarridgeiae [9,10], Bartonella grahamii [11], Bartonella koehlerae [12], Bartonella alsatica [13], and Bartonella rochalimae [14]. Infection with B. elizabethae may be more common than previously appreciated. As an example, investigators performed Bartonella serologic testing on samples collected in 1997 and 1998 from 204 persons who inject drugs in New York City and found 46 percent had positive serologic reactions to B. elizabethae [15]. In addition, one group of investigators used 16S RNA gene sequencing to identify a new serogroup of B. henselae, termed serogroup "Marseille" [16].

Although analysis of 16S ribosomal DNA sequences have characteristically been used to differentiate Bartonella species, investigators have determined that nucleotide base sequence data for a 940-bp fragment of the citrate synthase-encoding gene (gltA) appears more useful than the 16S ribosomal DNA sequence data for investigating the evolutionary relationships of Bartonella species [17]. Phylogenetic studies have determined that the highly virulent pathogen, B. bacilliformis, is the sole representative of an ancestral lineage, and other Bartonella species that cause human disease have evolved in a separate lineage; the evolution of the newer species has correlated with their adaptation to distinct mammalian reservoirs [18,19].

MICROBIOLOGY — Bartonella species are gram-negative, pleomorphic bacteria that stain very poorly in tissues using Gram stain but will stain black with silver-impregnated stains, such as the Warthin-Starry stain. The organisms are slow growing and regardless of which special techniques are used, typically require at least seven days before growth can be detected [20]. Routine culture procedures have low yield, unless the cultures are held for an extended period. Growth of Bartonella species is optimized when specimens are incubated in fresh media at 35 to 37ºC with 5 to 10 percent CO2 concentrations and greater than 40 percent humidity; some of the Bartonella species, such as B. bacilliformis, may grow better at lower temperatures (25 to 30ºC). The preferred medium is freshly prepared rabbit-heart infusion agar, but the organism can grow on various forms of chocolate or blood agar [21].

Bartonella typically does not trigger automated CO2 detection systems. Bartonella has been identified by using acridine orange staining of blood culture broth after seven days of incubation [22]. One group has described a chemically defined, cell-free, extract-free, liquid medium that supports the growth of Bartonella species, including growth from clinical specimens [23]. Another report used a novel, chemically-modified, insect-based liquid culture medium that allowed the growth of at least seven Bartonella species, including B. henselae and B. quintana [24]. Growth of Bartonella from biopsy specimens has also been successful using tissue homogenates co-cultivated with endothelial cell monolayers, but microbiology laboratories do not routinely perform these techniques [25].

NATURAL RESERVOIRS — Bartonella are found globally in a wide range of mammalian species [26,27]. Most Bartonella species that cause human disease are associated with well-defined mammalian reservoirs, including humans, domestic animals, rodents, and wild animals. More recently, the identified range of natural reservoirs for Bartonella species has expanded to include bats and marine animals [27-29]. These mammalian reservoirs can have prolonged infection with Bartonella species [30].

Cats — Epidemiologic evidence suggests that cats serve as the major reservoir for B. henselae human infections [31]. One study in northern California documented B. henselae bacteremia in 56 percent of cats less than one year of age and 34 percent of those at least one year of age [32]. Moreover, 90 percent of the cats less than one year of age and 77 percent one year of age or older had a positive B. henselae serology test. One report found that Bartonella bacteremia was more common in cats owned by patients with CSD compared with control cats (17 of 19 [89 percent] versus 7 of 25 [28 percent], p<0.001) [33]. Thirteen of the 19 bacteremic cats remained culture positive during the ensuing 12-month period. Among the Bartonella isolates from these cats, 23 were identified as B. henselae and one isolate appeared to be a new Bartonella species. In a follow-up study, investigators examined the role of cat contacts as the source of human infection and found four of five B. henselae isolates from human-cat pairs had closely related pulsed field gel electrophoresis patterns, thus further strengthening the proposed role of cats in transmitting this organism to humans [34].

Cats infrequently display clinical signs of B. henselae infection, even when they are persistently infected [33]. However, autopsy findings on these cats often show abnormal histopathology, including peripheral lymph node hyperplasia, splenic follicular hyperplasia, lymphocytic cholangitis/pericholangitis, lymphocytic hepatitis, lymphoplasmacytic myocarditis, and interstitial lymphocytic nephritis [35]. There may be strain differences in the ability to cause overt infection in cats. Among nine cats inoculated with a virulent strain of B. henselae (LSU16), for example, all developed an inoculation papule, a febrile illness, bacteremia by day 14, a peak in bacteremia at 14 to 28 days postinfection, and strong antibody responses to B. henselae, as determined by Western blot analysis and enzyme-linked immunosorbent assay [36].

In France, B. clarridgeiae was detected in the blood of 15 of 94 stray cats (16 percent) [37]. In the San Francisco area, two new species of Bartonella, including B. koehlerae, were characterized from 25 isolates recovered from cats [38]. Expanded information regarding the frequency and natural history of B. koehlerae infection in cats will require further investigation. (See "Microbiology, epidemiology, clinical manifestations, and diagnosis of cat scratch disease".)

Humans — Multiple lines of evidence suggest that humans are the primary reservoir for B. quintana and B. bacilliformis [39,40]. Both of these organisms can establish prolonged infection in humans, and invasion and persistent infection of red blood cells play a major role in Bartonella establishing chronic infection in humans. In addition, the persistence of organisms in red blood cells enables transmission via blood-sucking arthropods [41].

Rats, mice, and dogs — In an extensive analysis of rats from 13 sites in the United States and Portugal, Bartonella species were isolated from the blood of 63 of 325 Rattus norvegicus (19 percent) and 11 of 92 Rattus (12 percent) [42]. The Bartonella species isolated from these rats were most similar to B. elizabethae. B. elizabethae has also been isolated from a rat in Peru [43]. In a subsequent study, multiple Bartonella species were isolated from R. norvegicus and R. rattus that were captured in New Orleans and New York City, and flea infestation predicted isolation of Bartonella in R. norvegicus in both cities [44]. B. vinsonii appears to have both mice and dogs as reservoirs [45]. These pathogens, however, do not play a major role in human disease.

ARTHROPOD VECTORS

Fleas — The cat flea, Ctenocephalides felis, serves as the major vector for cat-to-cat transmission of B. henselae [27,46]. Several studies conducted in the United States have shown that Bartonella species are found in a significant number of cat fleas [30,47-49]. For example, in a study involving sampling of fleas from free-roaming domestic cats in southeastern Georgia, investigators identified Bartonella species in 35 percent of flea pools tested; all fleas in this study were C. felis [49].

Cats that harbor fleas infested with B. henselae can become infectious to humans after they scratch or bite the fleas, a process whereby the cat inoculates its claws or saliva with flea feces that are rich with B. henselae organisms. Subsequently, these cats can infect humans with B. henselae through a scratch, bite, or lick. Cat-to-human transmission most often occurs through cat scratches that result in intradermal inoculation of the contaminated flea feces. Some data suggest fleas may directly transmit B. henselae to humans, but this remains unproven.

Lice — Human-to-human transmission of B. quintana occurs via contact with the human body louse (Pediculus humanus corporis) or head louse (Pediculus humanus capitis) [50], specifically as a result of cutaneous inoculation of lice feces on the skin through scratching [51]. In one study, investigators found a higher viability of B. quintana in body lice feces compared with head lice feces, and this finding correlated with a relatively weakened gastrointestinal tract immune response to B. quintana in the body lice [52]. This study provides a pathogenic mechanism to explain the greater role body lice have relative to head lice in the transmission of B. quintana.

Sandflies — The Lutzomyia verrucarum sandfly has clearly been identified as the vector for B. bacilliformis. In one study, blood was surveyed from 50 animals living in the homes of 11 families whose children had recent bartonellosis in an endemic region of Peru [43]. Bartonella-like bacteria were recovered from four of nine small rodents, but none of the strains was classified as B. bacilliformis using serologic and genotypic methods. Five of these isolates probably represented three previously unrecognized Bartonella species, and one was a likely strain of B. elizabethae.

Ticks — It is unclear if ticks transmit Bartonella to humans. Although several reports have suggested possible tick transmission of Bartonella species to humans, subsequent studies have reported conflicting results [53-55].

PATHOGENESIS — Details of the complex pathogenesis of Bartonella infection in humans has expanded, with an improved understanding of how Bartonella causes a persistent, intracellular infection that escapes both innate and acquired immune responses [56-59]. Most existing data have found that Bartonella primarily infects erythrocytes and vascular endothelial cells [18,56].

Experts have generated a model for the life cycle of Bartonella infection that begins with the inoculation of Bartonella into either a mammalian or human reservoir host [60]. Following cutaneous inoculation, the Bartonella organisms (which are not capable of immediately infecting erythrocytes) appear to establish early dermal infection in migratory cells that transport the Bartonella organisms to vascular endothelial cells, and perhaps other cell types [60,61]. The Bartonella organisms then adhere to and invade endothelial cells [56]. Subsequently, the organisms spill into and seed the bloodstream where intraerythrocytic infection occurs [60].

The propensity to parasitize erythrocytes stems from Bartonella’s requirement for heme, due to an inherent inability to synthesize heme or protoporphyrin IX. Heme is the nonprotein component of hemoglobin that consists of the iron in the ferrous state (Fe2+) bound in the center of protoporphyrin.

Interaction with erythrocytes — The entry of Bartonella into erythrocytes involves adhesion, deformation, and invasion [60]. Flagella play a major role in the organism's search for potential host cells and may also assist in binding to erythrocytes [62]. Cell binding involves attachment to a red blood cell glycolipid receptor and the release of deformin, a compound that induces extensive indentations in erythrocyte membranes [63]. Cell entry appears to involve several processes, including flagellum-induced entry into the invaginations created by deformin and a process not clearly elucidated that involves the invasion associated locus proteins A and B (known as ialA and ialB); these proteins are synthesized from the invasion-associated locus gene region known as ialAB [62].

The Bartonella organisms enter the cell either free within the cytosol or within a vacuole, and subsequently replicate primarily in the erythrocytic vacuole [64]. Eventually, the organism can escape from the cell and, in some instances, causes cell lysis; the cell lysis correlates with the anemia frequently associated with clinical B. bacilliformis infection. Individuals with alcohol use disorders may have more bacteria per erythrocyte than healthy blood donors [65].

Interaction with endothelial cells — B. quintana, B. henselae, and B. bacilliformis all interact with endothelial cells and all can induce angiogenesis. Bartonella have outer membrane proteins, referred to as trimeric autotransporter adhesins, that play a central role in the adhesion to endothelial cells [56]. Three mechanisms have been proposed to explain Bartonella-associated vascular proliferation [66]:

Enhanced endothelial cell proliferation

Inhibition of apoptosis of endothelial cells

Increased secretion of vasculoproliferative cytokines

B. quintana adheres to endothelial cells, is engulfed by the cells, and appears within the cell as a cluster of organisms within a vacuole, similar to the morulae formed by Ehrlichiae or Chlamydiae species [67]. In addition, B. quintana appeared to be intracellular when heart valves from patients with B. quintana endocarditis were examined microscopically [67].

Several studies have also shown that B. bacilliformis induces vasoproliferation and angiogenesis by producing Bartonella angiogenic factor A (BafA), an extracellular autotransporter [68,69]. The BafA protein exerts its activity by binding to and stimulating the signaling pathway of vascular endothelial growth factor receptor 2 [68,69].

B. henselae aggregates on the surface of endothelial cells and is engulfed and internalized in either Bartonella-containing vacuoles (containing one or small clusters of organisms) or a unique host cellular structure termed the invasome (containing a large cluster of organisms) [64,70]. Infection of endothelial cells in vitro with B. henselae leads to activation of hypoxia-inducible factor-1 (HIF-1), the key transcription factor involved in angiogenesis [71]. HIF-1 subsequently triggers the production of vascular endothelial growth factor (VEGF) that leads to proliferation of endothelial cells. These stimulated cells, in turn, enhance the growth of B. henselae in a positive feedback loop [72]. The activation of HIF-1 depends on the expression of Bartonella adhesin A (formerly known as "type IV pili"), a very large protein that mediates binding of B. henselae to extracellular matrix proteins and to endothelial cells [66].

In an in vitro model using human umbilical vein cells and extracellular matrix protein, B. henselae induced long-term endothelial survival and angiogenesis [73]. The organism produced more angiogenesis than did treatment with VEGF itself. These findings could explain how B. henselae causes vasoproliferative disorders, such as bacillary angiomatosis and peliosis hepatis. (See "Bartonella infections in people with HIV".)

Bartonella species appear to increase the production of NF kappa-beta by endothelial cells, a process that recruits monocytes and macrophages, thereby expanding the bacterial cell habitat [74].

Immune response — The immune response to Bartonella infections has become an active subject of investigation. The type and severity of the infection typically correlates with the host’s immune function [75]. One study of the immune response to B. henselae infections in immunocompetent mice found infection with this organism induced a cell-mediated immune response with a Th1 phenotype [76]. In particular, after B. henselae was inoculated into the peritoneum of mice, the animals developed cellular proliferative responses, mainly from CD4 cells, that peaked eight weeks after infection.

In response to the infection, the animals increased production of interferon (IFN)-gamma, but not interleukin (IL)-4. In another study, investigators from Italy examined the interaction of B. henselae and macrophages in a mouse model [77]. Using a mouse macrophage cell line, they found entry of B. henselae into macrophages occurred within 30 minutes and peaked at approximately 160 minutes. Treating the cells with IFN-gamma significantly decreased the number of intracellular B. henselae and the IFN-gamma was associated with nitric oxide release. The investigators concluded that IFN-gamma activation of macrophages likely plays a major role in clearing B. henselae infection, and this microbial activity of IFN-gamma is mediated largely by nitric oxide production.

Studies involving mouse models with Bartonella taylori have shown that neutralizing antibody responses play a critical role in generating an effective immune response [78]. In this study, investigators identified that protective antibody responses target a key Bartonella autotransporter, the bacterial surface determinant CAMP-like factor autotransporter (CFA) [78]. In addition, this study proposed that Bartonella's ability to escape the host immune response may result, at least in part, from CFA antigenic variation [78].

Bartonella species have additional adaptive strategies to evade the host immune response, including use of a multiprotein type IV secretion system, which is embedded in the Bartonella cell envelope [58,59]. In some species of bacteria, the type IV secretion system functions to deliver bacterial proteins into host cells [79]. Several Bartonella species utilize the VirB/VirD4 type IV system to translocate Bartonella effector proteins across the Bartonella cell membrane into host cells [59]. The type IV secretion system also appears to play a significant role in erythrocyte binding and in subversion of multiple host endothelial cell functions that are critical for establishing chronic infection [18].

One study that involved humans found increased IL-10 production among homeless persons with Bartonella bacteremia [80]. The overproduction of IL-10 correlated with an attenuated inflammatory response and, therefore, may play a role in persistent infection in homeless persons. The escape from the immune response is also thought to result from the prolonged antagonism of the host Toll-like 4 (TLR4) receptors by the Bartonella outer membrane lipooligosaccharides, an effect that blunts the normal host production of proinflammatory cytokines, chemokines, and adhesion molecules [81,82].

SUMMARY

Bartonella species are fastidious, gram-negative bacteria, which cause a range of manifestations including cat scratch disease, bacillary angiomatosis and other infections in patients with HIV infection, as well as culture-negative endocarditis. (See 'Introduction' above.)

The three most important Bartonella species known to cause human disease are Bartonella bacilliformis, Bartonella quintana, and Bartonella henselae. (See 'Background' above.)

Bartonella species are gram-negative, pleomorphic bacteria that stain very poorly in tissues using Gram stain but will stain black with silver-impregnated stains, such as the Warthin-Starry stain. The organisms are slow growing and regardless of which special techniques are used, typically require at least seven days before growth can be detected. Routine culture procedures have low yield, unless the cultures are held for an extended period. (See 'Microbiology' above.)

Most Bartonella species that cause human disease are associated with well-defined reservoirs, usually domestic and wild animals. Cats serve as the major reservoir for B. henselae human infections, but infrequently display clinical signs of B. henselae infection. Humans serve as the reservoir for B. quintana and B. bacilliformis. Vectors (fleas, lice, and sandflies) also play an important role in Bartonella infection in humans. (See 'Natural reservoirs' above.)

The pathogenesis of Bartonella infection in humans is not completely understood. Most existing data have focused on Bartonella infection of erythrocytes and vascular endothelial cells. Flagella play a major role in the organism's search for potential host cells and may also assist in binding to erythrocytes. B. quintana, B. henselae, and B. bacilliformis all interact with endothelial cells and all can induce angiogenesis. (See 'Pathogenesis' above.)

The type and severity of the infection typically correlates with the host’s immune function. One study of the immune response to B. henselae infections in immunocompetent mice found infection with this organism induced a cell-mediated immune response with a Th1 phenotype. (See 'Immune response' above.)

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Topic 5519 Version 19.0

References

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