Transcript Bartonella henselae

Bartonella henselae
N. Pappe F2013
Modified by DYH
•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.
Bartonella henselae
N. Pappe F2013
Modified by DYH
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