What Is Bacillary Angiomatosis?

Bacillary angiomatosis is a bacterial infection that causes abnormal blood vessel growth, producing reddish skin lesions and sometimes damaging internal organs. It is caused by two species of Bartonella bacteria and overwhelmingly affects people with weakened immune systems, particularly those living with advanced HIV. Though it can look alarming and even mimic cancer, bacillary angiomatosis is treatable with common antibiotics, which makes recognizing it early genuinely life-changing for the people most at risk.

The Two Bacteria Responsible

Two closely related species cause bacillary angiomatosis: Bartonella henselae and Bartonella quintana. Both are small, gram-negative bacteria, but they reach people through different routes and tend to cause somewhat different patterns of disease. In a molecular study of 49 patients with bacillary angiomatosis or the related liver condition peliosis hepatis, roughly half were infected with each species. Patients with B. henselae were linked to cat and flea exposure, while those with B. quintana were more likely to be homeless, have low income, and report exposure to body lice.¹

B. henselae is the same bacterium that causes cat scratch disease in people with healthy immune systems. In those individuals, it usually produces a self-limited swollen lymph node near a scratch or bite. But in someone whose immune system is severely suppressed, the same organism behaves very differently, triggering the runaway blood vessel growth that defines bacillary angiomatosis.²

B. quintana has its own historical baggage. It is the same organism responsible for trench fever, a disease that plagued soldiers in World War I. It is transmitted by the human body louse, which is why outbreaks of B. quintana-related bacillary angiomatosis cluster among people living in crowded, unsanitary conditions. That same molecular study found that B. quintana infections were more strongly tied to subcutaneous masses and destructive bone lesions, while B. henselae was the exclusive cause of peliosis hepatis, a condition involving blood-filled cavities in the liver.³

How Bartonella Hijacks Blood Vessel Growth

The defining feature of bacillary angiomatosis is the proliferation of new, disorganized blood vessels in the skin and other tissues. Bartonella does not simply damage tissue the way most bacterial infections do. Instead, it actively tricks the body into building new blood vessels that the bacteria can inhabit and use to sustain themselves.

Researchers have identified a protein on the surface of B. henselae called BafA that functions almost like a counterfeit version of vascular endothelial growth factor, the body’s own signal for sprouting new blood vessels. BafA binds to the same receptor that the real growth factor uses and switches on the downstream signaling cascade, promoting cell proliferation, the formation of tube-like vessel structures, and sprouting of tiny new blood vessels. A closely related version of BafA exists in B. quintana as well.⁴

The process appears to involve cooperation between the infected blood vessel lining and the overlying skin. Studies of a related Bartonella infection found that infected endothelial cells produce one angiogenic signal while the epidermis above them ramps up production of another, essentially creating a two-pronged push for new vessel growth.⁵ The result is the characteristic lesion: a mass of tangled, fragile capillaries packed into a nodule that bleeds easily when bumped.

Who Is at Risk

Bacillary angiomatosis is fundamentally a disease of immune suppression. The vast majority of cases have been reported in people with HIV, and typically in those whose disease is far advanced. A case-control study of 42 HIV-positive patients with bacillary angiomatosis found the median CD4 count was just 21 cells per cubic millimeter, far below the 200-cell threshold that already signals severe immune compromise.⁶ In that study, having a CD4 count below 200 was associated with roughly tenfold increased odds of developing the disease.

Since the widespread availability of antiretroviral therapy, bacillary angiomatosis has become far less common. Most people living with HIV in high-income countries maintain CD4 counts well above the danger zone. But the condition has not disappeared. It still occurs in people who are diagnosed late, who do not have access to treatment, or whose antiretroviral regimen is failing. It also appears in parts of the world where HIV treatment access remains inconsistent.

Beyond HIV, organ transplant recipients are an increasingly recognized risk group. A review of solid organ transplant recipients who developed B. henselae infections found that about two-thirds had received kidney transplants, and the majority presented with disseminated rather than localized disease.⁷ People on chemotherapy for cancer and others taking immunosuppressive drugs can also develop it, though cases remain rare. In immunocompetent people, bacillary angiomatosis is exceedingly uncommon but has been documented in isolated case reports.⁸

What the Skin Lesions Look Like

The cutaneous lesions of bacillary angiomatosis present across a wide spectrum. They can appear as small red or purple papules, larger nodules, or fleshy tumor-like masses. Some sit on the skin surface while others form deeper subcutaneous lumps. The lesions range in color from bright red to deep violet and tend to bleed easily when traumatized. They can appear anywhere on the body and may number from a single lesion to hundreds.⁹

The clinical look-alikes are part of what makes bacillary angiomatosis tricky. The lesions can closely resemble Kaposi’s sarcoma, which is also common in people with advanced HIV, as well as pyogenic granuloma and even melanoma. Because Kaposi’s sarcoma requires a completely different treatment approach, the distinction matters enormously.

Beyond the Skin

Bacillary angiomatosis is not confined to the skin. The infection can involve the liver, spleen, bone, lymph nodes, and other organs, sometimes without any skin lesions at all. One of the best-characterized visceral manifestations is peliosis hepatis, in which blood-filled cystic spaces form throughout the liver. Early descriptions of this condition in HIV-positive patients identified clumps of bacteria in the liver tissue that were identical to those found in skin lesions, and the condition responded to antibiotic therapy.¹⁰ Peliosis can also occur in the spleen; one early case report documented bacillary angiomatosis involving the liver, spleen, and a lymph node simultaneously in an immunosuppressed transplant recipient.¹¹

Bone involvement is another important pattern. Destructive bone lesions, visible on X-rays as punched-out areas, occur in a significant minority of patients. In one imaging study, more than a third of HIV-positive patients with cutaneous bacillary angiomatosis had symptomatic bone lesions that improved with antibiotics.¹² The presence of bone destruction is actually a useful diagnostic clue, since Kaposi’s sarcoma does not cause bone lesions. Case reports have documented dramatic examples, including destruction of a finger’s distal bone in a patient with a CD4 count of just 9.¹³

In the case-control study noted earlier, fever was present in 93% of patients, and roughly a quarter had abdominal symptoms. The combination of elevated liver enzymes, anemia, and a very low CD4 count were the strongest laboratory predictors of the disease.¹⁴ Diagnosis without skin involvement can be substantially delayed, sometimes by months, because the symptoms are nonspecific and mimic many other infections in immunocompromised patients.

Why It Gets Mistaken for Kaposi’s Sarcoma

The confusion between bacillary angiomatosis and Kaposi’s sarcoma is not just cosmetic. Both conditions produce vascular-looking purple or red lesions in the same patient population, and even under the microscope they can share a superficial resemblance. Both may show a nodular architecture built from thin-walled vessels. But the tissue-level details differ in ways a pathologist can spot. Bacillary angiomatosis lesions contain well-formed capillaries surrounded by inflamed tissue rich in neutrophils, along with clusters of bacteria visible on special stains. Kaposi’s sarcoma, by contrast, has slit-like vascular spaces, prominent spindle-shaped cells, scattered red blood cells outside of vessels, and a plasma-cell-dominant inflammatory infiltrate.¹⁵

The practical significance is immense. Kaposi’s sarcoma is a cancer driven by a herpesvirus and treated with chemotherapy or antiretrovirals. Bacillary angiomatosis is a bacterial infection that clears with a course of antibiotics. Mistaking one for the other means either giving unnecessary chemotherapy or withholding antibiotics from someone who desperately needs them. This is especially relevant in resource-limited settings, where advanced diagnostic tools may not be available and the two conditions can be difficult to separate on clinical appearance alone.

Diagnosis

Getting to a definitive diagnosis typically requires a tissue biopsy. Under the microscope, the characteristic finding is a proliferation of small blood vessels surrounded by an inflammatory infiltrate with prominent neutrophils. Using the Warthin-Starry silver stain, pathologists can often see clumps of dark-staining bacilli in the tissue, which is a strong pointer toward the diagnosis.

Blood tests for Bartonella antibodies are available, using indirect immunofluorescence, but they have limitations. They can detect antibodies at the genus level but cannot reliably distinguish between species, and they are known to cross-react with unrelated bacteria.¹⁶ Because many of the affected patients have severely weakened immune systems, their antibody responses may be blunted, making serology even less dependable. In one kidney transplant recipient, serology alone was unreliable and the diagnosis required combining histopathology with molecular testing.¹⁷

PCR-based testing, which detects Bartonella DNA directly from tissue or blood samples, has become an increasingly valuable tool. It can confirm the species involved and does not depend on the patient mounting an adequate immune response. In practice, the most reliable diagnostic approach combines histopathology with molecular testing, rather than relying on any single method.

One consistently reported problem is diagnostic delay. In the case-control study of HIV-positive patients, the median time between the initial medical evaluation and diagnosis was four weeks, but the range stretched from a single day to two full years.¹⁸ When the disease involves only internal organs, the delay tends to be even longer. A transplant recipient with bacillary angiomatosis involving the pancreatic region, liver, and spleen but no skin lesions went through extensive imaging and multiple biopsies before a celiac lymph node biopsy finally provided the diagnosis.¹⁹

Treatment

The good news is that bacillary angiomatosis responds well to antibiotics. Erythromycin is generally considered the first-line treatment, with doxycycline and clarithromycin as established alternatives.²⁰ These are inexpensive, widely available drugs, which makes bacillary angiomatosis one of the more treatable opportunistic infections in the HIV world.

The duration of treatment depends on the extent of disease. For cutaneous bacillary angiomatosis, a systematic review found that a median course of about six weeks was effective for single lesions, while multiple lesions typically required around three months of treatment.²¹ For patients with severe or disseminated disease, many clinicians add rifampin or gentamicin to the regimen, though the optimal combination has not been formally established in randomized trials.²²

Relapse after completing therapy is a recognized problem, particularly in patients who remain immunosuppressed. Some transplant recipients and people with persistently low CD4 counts may need long-term suppressive therapy to prevent recurrence.²³ For people with HIV, restoring immune function through effective antiretroviral therapy is the most important step in preventing relapse. Occasionally, starting antiretrovirals can itself trigger a temporary flare of bacillary angiomatosis lesions as the recovering immune system mounts an inflammatory response, a phenomenon called immune reconstitution inflammatory syndrome. One report described a patient who experienced both this inflammatory flare and a Jarisch-Herxheimer reaction (a short-lived worsening caused by the die-off of bacteria) during treatment; the case resolved with supportive care and continuation of both antibiotics and antiretrovirals.²⁴

The Cat Connection and How to Reduce Risk

Cats are the primary reservoir for B. henselae. The bacteria circulate in the bloodstream of infected cats, often without causing them any visible illness. The cat flea transmits the organism between cats, and infected flea feces on a cat’s claws or teeth are the likely route to humans. An epidemiological study found that traumatic contact with a cat, specifically a bite or scratch, was the exposure most strongly associated with developing bacillary angiomatosis and peliosis. Owning a cat roughly tripled the odds, and a cat bite or scratch nearly quadrupled them.²⁵

B. henselae bacteremia is common in cat populations. A study of cats in Sydney found that about 35% were carrying the bacteria in their bloodstream, with the rate reaching 40% among feral cats compared to 16% among domestic pets.²⁶ Younger cats and strays are more likely to be infected, probably because they have had more flea exposure and less veterinary care.

For immunocompromised individuals who own cats, the practical advice is straightforward: keep cats on a regular flea-control program, avoid rough play that could lead to scratches or bites, and clean any wounds from a cat promptly.²⁷ Getting rid of the cat is not usually necessary. What matters is managing fleas, since the flea is the link that keeps B. henselae circulating between cats and ultimately reaching people.

B. quintana follows a completely different transmission pathway. It spreads through the human body louse, with no animal reservoir required. Prevention centers on controlling lice through hygiene measures and access to clean clothing, which is a public health challenge rather than a personal pet-care decision.

Bacillary Angiomatosis in Transplant Recipients

As organ transplantation has become more common and HIV-related cases have declined, transplant recipients have emerged as a distinct and growing group of bacillary angiomatosis patients. These cases carry their own set of challenges. Transplant patients are often on multiple immunosuppressive drugs that cannot be simply stopped, and the clinical presentation can differ from the classic HIV-associated picture.

In a review of solid organ transplant recipients with B. henselae infections, the majority had disseminated disease rather than the localized cat scratch disease that a healthy person would develop. Fever was nearly universal, present in 93% of cases, and skin lesions were actually a minority finding, appearing in only about a quarter of patients.²⁸ This is a critical point: clinicians accustomed to looking for the telltale skin lesions may not suspect bacillary angiomatosis when only fever and internal organ involvement are present.

The diagnostic difficulty in transplant recipients is compounded by the fact that standard blood cultures do not grow Bartonella, and serological tests can return falsely negative results in patients whose immune systems have been pharmacologically suppressed. A case involving a 75-year-old kidney transplant recipient on belatacept-based immunosuppression illustrated the problem: serologies were negative, blood cultures were negative, and imaging showed suspicious masses in the pancreatic region with multiple liver and spleen lesions. It took a celiac lymph node biopsy to finally confirm bacillary angiomatosis.²⁹ Cases like this underscore that a high index of suspicion and willingness to pursue tissue diagnosis are essential when a transplant patient presents with unexplained fever and organ lesions, especially if they have had contact with cats.