Bacillary angiomatosis (BA) is the vascular proliferative form of Bartonella infection. Bacillary angiomatosis was first described in 1983 in a patient infected with HIV.1 The disease has since been described in patients following organ transplants and in immunocompromised persons. It is occasionally reported in immunocompetent patients. Initially, bacillary angiomatosis was called epithelioid angiomatosis because of its histologic appearance.
In 1990, Relman et al identified a visible but uncultivable bacillus from affected tissues of patients with bacillary angiomatosis using molecular methods.2 They concluded that the unique 16S gene sequence associated with epithelioid angiomatosis belonged to a previously uncharacterized microorganism, most closely related to Rochalimaea quintana. Later, the same organism was recovered in specialized culture media. The gram-negative organism was later named Rochalimaea henselae, and, in 1993, Rochalimaea was reclassified under the genus Bartonella. Bartonella henselae and Bartonella quintana each have been cultured from and detected in bacillary angiomatosis tissues. Bacillary angiomatosis is the second-most-common angiomatous skin lesion in persons infected with HIV.
B henselae and B quintana are small gram-negative rods in the family Bartonellaceae. Bartonella, Rickettsia, Ehrlichia, and Afipia species all are part of the alpha-2 subgroup of the Alphaproteobacteria.
Bacillary angiomatosis can affect almost any organ system, although it most commonly affects skin and subcutaneous tissue. Subcutaneous lesions may erode into underlying bones (ie, osseous bacillary angiomatosis), especially the tibia, fibula, and radius. Involvement of ribs and vertebrae has been described. Rarely, skeletal muscles may be involved, resulting in pyomyositis. Mucous membranes of the conjunctiva and upper airway and perineum (anus and penis) may be affected. Bacillary angiomatosis may be accompanied by disseminated visceral disease (peliosis), mainly in the liver (peliosis hepatis), spleen, and lymph nodes.
Other internal organs that may be involved include the brain, bone marrow, heart, lungs, pleura, larynx, oropharynx, tongue, esophagus, stomach, duodenum, colon, peritoneum, diaphragm, kidneys, adrenal glands, pancreas, uterine cervix, and vulva. Extrinsic compression of the common bile duct by enlarged peripancreatic, celiac, and portohepatic nodes has been reported.
The pathogenesis of bacillary angiomatosis includes early blood-borne dissemination of organisms. Bartonella organisms readily attach to and may enter erythrocytes. They avoid opsonization and host phagocytosis by unknown mechanisms and become persistent within the intravascular compartment. An angiogenic factor may be responsible for the vascular proliferation observed in patients with bacillary angiomatosis because a similar factor mediates vasoproliferation in verruca peruana, the second stage of Bartonella bacilliformis infection.
Cutaneous lesions result almost equally from B henselae and B quintana infections. However, subcutaneous and osseous lesions are usually caused by B quintana infection. Visceral involvement is almost exclusively caused by B henselae infection. Neurological disorders are associated more frequently with B quintana infection than with B henselae.
Domestic cats (Felis domesticus) are the reservoirs of B henselae, which may be transmitted via cat bites or scratches or, potentially, by bites from cat fleas (Ctenocephalides felis). Kittens are more frequently associated with transmission of B henselae than older cats. Humans appear to be the only reservoir of B quintana; the human body louse, Pediculus humanus, is the transmission vector