1. Bartonella henselae General: *Aerobic, oxidase-negative, and slow growing gram-negative rod, slightly curved *No flagella to facilitate its movement; however, there is evidence of twitching motility (video) *causative agent of Cat Scratch Disease *Peliosis hepatis caused by B. henselae creates GI symptoms, fever, chills, and an enlarged liver and spleen containing blood filled cavities (seen in HIV patients and as a co-infection to Lyme disease) Requires: *Fastidious conditions; 37 degrees Celsius; highly dependent on the quantity of heme available; requires pH range of 6.8-7.2. *Isolation requires chocolate agar plates and carbon dioxide; slow colony growth (2-6 weeks to form) Genomics/Virulence Factors: *Circular genome of 1.9 Mbp and origin of replication has excess guanine and thymine nucleotides on the leading strand *Uses chromosomal genes for virulence *Potential plasmid has been discovered; however more research is needed *Adherence factors include BadA/Vomp, which functions to mediate bacterial auto aggregation and adhere to extracellular matrix proteins, resulting in cell adhesion and induction of paracrine proangiogenic response *Has Type IV secretion systems, which transport substrate molecules to target cells. The pili participate in attachment to target cells *Cannot use glucose to derive energy due to it's incomplete glycolysis pathway; it uses amino acid catabolism to generate energy. N. Pappe F2013 Modified by DYH

2. Bartonella henselae Mechanisms 1.) Invasome-mediated uptake *Elicits a massive rearrangement of actin cytoskeleton, causing aggregation. *Bacterium is engulfed by host cell membranes to enter the endothelial cells. *Infection elicits a inflammatory response to activate NF-kB (transcription factor to regulate the innate immune response) *Invasome causes a revolving locomotion of cell bodies, which stimulates twisting forces to contribute to the evenly rounded structure of the cell. *Once the cell responds to inflammation, it elicits a response to promote inflammation and cause swelling in the patient. 2.) Adhesion to endothelial cells by the bacterium with HUVECs *Infection by the bacterium drives HUVEC into the cell and vasoproliferative lesions caused by the species are surrounded by neutrophils, which contribute to inflammatory response and involved endothelial cell activation. *Invasion mechanism into the erythrocytes are not yet known *Successful at invading because it inhibits cell death of endothelial cells by controlling caspase activation and DNA fragmentation in apoptosis. *Translocation of BepA also inhibits the cell death– relies on raising the cAMP carried out by the plasma membrane Detection/Treatment/Resistance *Detected by PCR or culture *Susceptible to rifampin, ciprofloxacin, gentamicin, trimethoprim, and sulfamethoxazole; most bacteria are susceptible to chlorine, 70% ethanol, and phenolics.; in immuno-compromised patients, erythromycin, doxycycline, and isoniazid are effective *Resistant to pencillins, cephalosporins, tetracycline, and erthromycin have little effect; resistance to macrolides and to fluoroquinolones has been observed N. Pappe F2013 Modified by DYH