Cat Scratch Disease (Bartonellosis): Symptoms, Causes, Risks, and Treatment

What is Cat Scratch Disease (Bartonellosis)?

Bartonellosis is an infectious disease caused by bacteria of the genus Bartonella. These are small, fastidious, Gram-negative intracellular organisms that can infect red blood cells, endothelial cells, and macrophages. While the genus Bartonella includes many species capable of causing various human diseases, such as trench fever and Carrión’s disease, the species most frequently seen in clinical practice is the one commonly referred to as cat scratch disease (CSD).

Cat scratch disease is most commonly caused by Bartonella henselae type II, a bacterium first definitively identified as the causative agent of the condition in the 1990s. As the name of the disease suggests, it is a zoonosis, an infectious disease transmitted from animals to humans, with the domestic cat serving as the primary animal reservoir.

The Cat as Reservoir

Cats are the principal natural reservoir host of Bartonella henselae. The infection is extremely widespread in the cat population worldwide: epidemiological studies have found prevalence rates of feline B. henselae bacteraemia (the presence of the bacterium in the blood) varies considerably between geographic regions and cat populations. Prevalence can be very high, especially in stray or feral cats; in these groups, the risk of infection is approximately double that of owned domestic cats.

Crucially, cats infected with B. Bartonella henselae infections are almost always asymptomatic. In other words, they show no signs of illness and appear entirely healthy. However, those infected can still carry and transmit the bacterium for prolonged periods, ranging from months to years. This silent carriage, despite the development of an immune response by the animal, makes it impossible to identify infected cats by clinical observation alone. Occasional mild and transient symptoms, such as a brief fever and mild lymph node swelling, have been reported in some infected cats. However, overt illness remains rare.

How Cats Become Infected: The Role of Fleas

The primary mechanism of B. henselae transmission between cats is through the cat flea (Ctenocephalides felis). Fleas become infected by feeding on bacteraemic cats (cats with B. henselae circulating in the bloodstream). The bacterium multiplies in the flea’s midgut and is shed in large quantities in flea faeces (flea dirt). When infected fleas defecate on a cat’s skin and coat, the flea feces can contaminate the cat’s claws. This happens as the cat scratches itself. The feces can also enter the cat’s oral cavity when the cat grooms itself or licks its companions.

Bartonella henselae can remain viable in dried flea faeces for up to 9 days, meaning that flea dirt deposited on a cat’s coat or environment can represent a persistent reservoir of infection.

A research has also demonstrated that certain tick species can harbor Bartonella bacteria. These ticks may transmit the bacteria to mammalian hosts, including humans, during a blood meal. However, the role of tick-borne Bartonella transmission in the epidemiology of human cat scratch disease is still being studied.

How Cats Transmit the Infection to Humans

Transmission of B. henselae from cats to humans occurs through:

1. Scratches: When a cat scratches a person, its claws can cause infection because they may carry Bartonella henselae bacteria. This happens when flea feces, deposited on the skin during a flea infestation, enter the wound and introduce the bacterium directly into the skin. Even superficial scratches that break the skin are sufficient.

2. Bites: Cats’ mouths can be directly contaminated with *B. henselae both through gingival bleeding associated with dental and gingival disease and indirectly through the cat licking its own contaminated skin and claws. A cat bite that breaks the skin can therefore inoculate the bacterium subcutaneously.

3. Licking of broken skin: If an infected cat licks an open wound, abrasion, or mucous membrane on a human, transmission can theoretically occur, although this route is less well established than scratches and bites.

4. Autoinoculation: If a person touches a cat (particularly handling its fur, which may be contaminated with flea dirt) and then touches their eyes without washing their hands, B. henselae can be inoculated onto the conjunctival mucosa, leading to the ocular form of the disease.

Importantly, person-to-person transmission of cat scratch disease does not occur. The infection cannot be passed from one human to another.

Who Is Most Commonly Affected?

Children and adolescents under the age of 15 are statistically the most commonly affected group. This reflects their typically close and frequent physical contact with domestic cats, including play that involves handling, carrying, and interacting with kittens. Kittens have higher rates of feline bacteraemia than adult cats. Additionally, this age group tends to practice hand hygiene less consistently after cat contact. However, cat scratch disease can affect individuals of any age.

Immunocompromised individuals, such as those with HIV infection, organ transplant recipients, and patients receiving chemotherapy, face a significantly higher risk of developing severe and atypical forms of bartonellosis (see the Complications section).

Overview of Clinical Presentation

In immunocompetent individuals (those with a fully functional immune system), cat scratch disease typically runs a benign, self-limiting course. The classical presentation includes:

• Development of a small papule (skin bump) at the site of inoculation, appearing approximately 5 days (range: 3–21 days) after the scratch or bite.
• Swelling of the regional lymph nodes (lymphadenopathy) draining the site of inoculation, developing 2–4 weeks after the initial inoculation.
• Fever, present in a proportion of cases, sometimes accompanied by joint pain and reduced appetite.

The majority of immunocompetent patients recover completely without specific treatment, though the lymphadenopathy may persist for weeks to months.

---

The Infection in Animals and Humans

Bartonella henselae and related species primarily infect cats and humans, though Bartonella strains have been isolated from a broader range of animal species, including:

• Dogs: B. vinsonii subsp. berkhoffii, B. henselae, and other species have been identified in dogs, occasionally causing clinical illness.
• Rabbits: Specific Bartonella species have been identified in rabbit populations.
• Rodents: Various wild and domestic rodent species may serve as reservoirs for different Bartonella species.
• Ruminants: Cattle and other ruminants harbour Bartonella species, some of which may have zoonotic potential.

Infection in Cats

As emphasised above, the vast majority of cats infected with B. henselae often remain entirely asymptomatic, maintaining a persistent bacteraemia (where bacteria circulate in the blood) that can last for months or even years. This occurs despite the presence of an immune response. This long-lasting, asymptomatic bacteraemia is the biological basis for cats’ effectiveness as reservoirs and sources of infection for humans.

When clinical signs do occur in cats (which is uncommon), they may include:

• Transient fever
• Mild lymph node enlargement (lymphadenopathy)
• Occasionally, more significant illness in immunocompromised cats (e.g., those co-infected with feline immunodeficiency virus, FIV, or feline leukaemia virus, FeLV)

Epidemiology

Cat scratch disease is found worldwide wherever domestic cats are kept. Its epidemiology closely mirrors the distribution of flea infestation in cat populations. Geographic regions with year-round warm climates, where fleas flourish, tend to have higher rates of feline B. henselae infection and, correspondingly, higher rates of human cat scratch disease. In temperate climates, CSD follows a seasonal pattern. Incidence is higher in the autumn and winter months, which may reflect the increased time people spend indoors with cats. This trend also aligns with seasonal peaks in flea activity.

The annual incidence of cat scratch disease in the United States is estimated at approximately 9–10 cases per 100,000 population, with higher rates among children and in warmer geographic regions. In Europe, similar patterns are observed, though comprehensive epidemiological data vary between countries.

---

Symptoms

The Classical (Typical) Form

The classical presentation of cat scratch disease, which accounts for most cases and primarily affects children and young adolescents, follows a characteristic clinical progression.

1. Primary Inoculation Lesion (3–21 Days After Scratch or Bite)

The first clinical sign of cat scratch disease is the development of a primary inoculation lesion at the site of the scratch, bite, or skin contact through which B. henselae entered the body. This appears:

• 3–10 days after the initial inoculation (occasionally up to 21 days).
• As a small papule (solid skin bump) or vesicle (fluid-filled blister), typically 3–5 mm in diameter.
• Surrounded by mild redness (erythema) and sometimes covered by a small crust.
• The lesion may evolve into a pustule (a pus-filled bump) before resolving spontaneously over days to a few weeks.
• Pain is often present at the inoculation site.

In most cases, the inoculation lesion appears on the skin of the hands, forearms, or arms. These are the areas most often scratched or bitten by cats. However, in approximately 6% of cases, the primary lesion occurs on the conjunctival mucosa of the eye. This happens because of autoinoculation, when the patient touches their eye with fingers contaminated by cat contact. This ocular primary lesion is typically the first manifestation of the Parinaud oculoglandular syndrome (see Complications section).

2. Regional Lymphadenopathy (2–4 Weeks After Inoculation)

The hallmark of cat scratch disease and its most diagnostically characteristic feature is the development of swollen and often tender lymph nodes (lymphadenopathy) in the lymph node region draining the site of inoculation. This typically occurs 2–4 weeks after the initial scratch or bite.

• The incubation period from scratch to lymphadenopathy is typically 3–21 days, with a mean of approximately 12 days.
• Initially, the enlarged lymph nodes are firm, tender, and fixed to the surrounding tissue.
• Over subsequent weeks, they may become soft and fluctuant (fluid-filled). This change indicates suppuration, or abscess formation within the node. It occurs in approximately 15–20% of cases.
• In advanced suppurative cases, the node may spontaneously drain through the overlying skin, forming a fistulous tract (a channel through which pus drains externally).
• In most patients, the lymphadenopathy resolves spontaneously within 2–6 months, though this resolution may be protracted and distressing for patients and parents.

The lymph node stations most commonly affected are, in order of frequency:

1. Axillary (armpit): Most common, reflecting the predominance of scratches on the hands and arms.
2. Lateral cervical (neck)
3. Submandibular (beneath the jaw)
4. Inguinal (groin)
5. Femoral (upper thigh)
6. Pre-auricular (in front of the ear): Characteristically associated with ocular inoculation.
7. Supraclavicular (above the collar bone)

In approximately 40% of cases, more than one lymph node station is involved simultaneously. Generalised lymphadenopathy (involvement of multiple, widely distributed lymph node groups) is less common and should prompt consideration of alternative diagnoses or of disseminated bartonellosis.

3. Systemic Symptoms

Systemic symptoms, if present, are generally mild in immunocompetent patients. These symptoms include:

• Fever: Present in a variable proportion of patients (estimates range from 30 to 60% across different series), typically low-grade, though occasionally higher.
• General malaise and fatigue: A non-specific sense of feeling unwell.
• Headache
• Joint pain (arthralgia): Affecting one or more joints, typically transient.
• Sore throat
• Loss of appetite (anorexia)

These systemic symptoms are generally self-limiting and resolve spontaneously as the immune response effectively contains the infection.

Systemic (Disseminated) Forms

In approximately 5 to 14% of all cases of cat scratch disease, the infection takes a more widespread, systemic course. This often involves granulomatous changes in visceral organs, particularly the liver, spleen, and mediastinal lymph nodes, which are the lymph nodes located in the space between the heart and lungs. This disseminated, granulomatous form is particularly important in immunocompromised patients (see below) and may also occur in otherwise healthy individuals, though it is less common and generally follows a more benign course in the immunocompetent.

---

Complications

In the vast majority of immunocompetent patients, cat scratch disease runs a benign, self-limiting course with complete recovery and no lasting harm. However, in a small proportion of cases, particularly among immunocompromised individuals, Bartonella henselae may lead to severe, life-threatening, or permanently disabling complications.

Severe Neurological Involvement

Neurological complications of cat scratch disease occur in approximately 2% of cases and can be serious. Manifestations include:

• Encephalopathy: Diffuse brain dysfunction, potentially causing altered consciousness, confusion, and behavioural changes. Cat scratch disease encephalopathy typically presents acutely and dramatically, often resolving without permanent sequelae in immunocompetent patients, though severe cases can cause death or permanent neurological damage.
• Seizures (convulsions): May occur in the context of encephalopathy or as a more isolated manifestation.
• Neuroretinitis: Inflammation of the optic nerve and retina, causing visual disturbance and potentially progressive visual loss. One of the more characteristic neurological manifestations of cat scratch disease.
• Myelitis (spinal cord inflammation) and paraplegia
• Cerebral arteritis (inflammation of cerebral blood vessels)
• Aseptic meningitis: Inflammation of the meninges (the membranes surrounding the brain and spinal cord) without bacterial growth on standard culture.

Bacillary Angiomatosis

Bacillary angiomatosis is a severe, systemic manifestation of Bartonella infection. It occurs almost exclusively in severely immunocompromised patients, particularly those with advanced HIV infection/AIDS. It is characterised by the abnormal proliferation of blood vessels driven by Bartonella infection, resulting in:

• Vascular lesions of the skin: Multiple, reddish-purple, dome-shaped papules or nodules that may resemble Kaposi’s sarcoma clinically and must be distinguished from it histologically.
• Involvement of internal organs, bones, and lymph nodes.
• Systemic illness with fever, weight loss, and malaise.

Without treatment, bacillary angiomatosis is progressive and potentially fatal. With appropriate antibiotic therapy (typically prolonged courses of erythromycin, azithromycin, or doxycycline), it responds well, though relapses are common and long-term secondary prophylaxis may be required in patients who remain immunocompromised.

Peliosis Hepatis

Peliosis hepatis is a rare hepatic manifestation of Bartonella infection (again predominantly in immunocompromised patients) characterised by the development of multiple, blood-filled cystic cavities within the liver parenchyma. The spleen may also be affected (peliosis splenica). Peliosis can cause hepatosplenomegaly, abdominal pain, and abnormal liver function tests, and carries a risk of spontaneous haemorrhage into the peritoneal cavity.

Hepatosplenic Granulomatous Disease

Multifocal granulomatous lesions of the liver and spleen occur in less than 1% of all cat scratch disease cases but represent an important manifestation of more severe, disseminated bartonellosis. Patients typically present with fever, hepatosplenomegaly, and abdominal pain.

Parinaud Oculoglandular Syndrome

The Parinaud oculoglandular syndrome, which occurs in approximately 6% of cat scratch disease cases, is the characteristic presentation of B. henselae infection when the primary inoculation site is the conjunctival mucosa of the eye. It consists of:

• Granulomatous conjunctivitis: Inflammatory lesions (granulomas) on the palpebral or bulbar conjunctiva, producing redness, discharge, and ocular irritation.
• Pre-auricular lymphadenopathy: Prominent, palpable swelling of the pre-auricular lymph nodes (in front of the ear) on the same side as the affected eye.

The syndrome is named after Joseph Jules Parinaud, a French ophthalmologist who first described this clinical constellation. Despite its dramatic appearance, it typically resolves spontaneously in immunocompetent patients, though it may take several months.

Endocarditis

Bartonella henselae (and B. quintana) are recognized causes of culture-negative endocarditis, an infection of the heart valves, and are being identified more frequently. This is a serious, life-threatening complication most commonly occurring in patients with pre-existing valvular heart disease (who already have structurally abnormal valves predisposed to bacterial colonisation). Bartonella endocarditis tends to be subacute, with a slow and insidious onset, and is characteristically difficult to diagnose because Bartonella does not grow on standard blood culture media. Diagnosis requires specific serological testing or molecular techniques. Treatment involves prolonged antibiotic therapy, and valve replacement may ultimately be necessary.

Bacteraemia

Symptomatic B. henselae bacteraemia (bacteria circulating in the bloodstream) is uncommon in immunocompetent individuals but occurs more frequently and with greater severity in immunocompromised patients, particularly those with AIDS, in whom it can manifest as a chronic, relapsing febrile illness.

Disseminated Disease in AIDS

In patients with advanced AIDS, particularly those with very low CD4 lymphocyte counts, B. henselae infection can cause severe, life-threatening disseminated disease, encompassing bacteraemia, bacillary angiomatosis, peliosis hepatis, and involvement of multiple organ systems. This represents one of the most serious opportunistic infectious complications of advanced HIV infection.

Aseptic Meningitis

Inflammation of the meninges without a detectable bacterial pathogen on standard culture, known as aseptic meningitis, has been described as a rare manifestation of cat scratch disease, particularly in children.

---

Diagnosis

The diagnosis of cat scratch disease in humans rests on a combination of clinical suspicion (based on the characteristic history and presentation), serological confirmation, and in selected cases more invasive investigations.

Clinical Assessment

The diagnosis of cat scratch disease should be actively considered in any patient, particularly a child or adolescent, who presents with the following symptoms:

• A history of recent cat contact (scratch, bite, or licking of broken skin), especially with a kitten or a stray/feral cat
• Development of a small, self-limiting skin lesion (papule, vesicle, or pustule) at the site of contact
• Regional lymphadenopathy appearing 2–4 weeks later, in the lymph node region draining the inoculation site
• Associated mild systemic symptoms (fever, malaise, headache)

Recent contact with cats, particularly in endemic areas or during certain seasons, is an essential part of the epidemiological context for clinical assessment. In some settings, a careful clinical and epidemiological assessment is sufficient to diagnose typical cases of cat scratch disease without further investigation.

Serological Testing

Serological testing, which detects specific anti-Bartonella antibodies in the patient’s serum, remains the most widely used and practically accessible diagnostic method for cat scratch disease. It is the preferred initial confirmatory investigation in most hospital and clinical laboratory settings.

The most commonly used serological methods are:

• Indirect fluorescent antibody (IFA) assay: Measures IgG and IgM antibodies against B. henselae antigens. IgM antibodies appear early in infection and decline over weeks to months; IgG antibodies persist for months to years. A significantly elevated IgG titre (typically ≥ 1:256) or a fourfold rise between acute and convalescent sera is considered diagnostic.
• Enzyme-linked immunosorbent assay (ELISA): An alternative format with good sensitivity, used in some laboratories.

Testing paired serum samples is recommended for the most reliable serological diagnosis. One sample should be collected during the acute phase of illness, while a second should be collected 6 weeks later, during the convalescent phase. A rising antibody titre between the two samples provides the strongest serological evidence of recent infection. Cross-reactivity between B. henselae and B. quintana can complicate interpretation.

Culture

Bacterial culture, which involves growing the organism from clinical specimens, serves as the definitive microbiological method. However, it is rarely used in routine clinical practice for cat scratch disease for several reasons:

• Bartonella henselae is a fastidious, slow-growing organism requiring specialised culture media (such as blood agar under 5% CO₂) and prolonged incubation (up to 6 weeks) for optimal isolation.
• Bacterial loads in human specimens (lymph node aspirates or biopsies, pus) are often extremely low, making culture insensitive.
• Many patients have received empirical antibiotic therapy before specialist referral, further reducing the likelihood of a positive culture.

Culture remains the gold standard for definitive species identification when required (e.g., in research settings or atypical presentations).

Blood Culture (Haemoculture)

While blood culture remains the preferred method for diagnosing Bartonella bacteraemia in cats, as bacterial loads in the blood are high and bacteraemia is prolonged, it provides limited diagnostic utility in human cat scratch disease. The exception is severely immunocompromised patients, such as those with AIDS, who may develop sustained, high-grade bacteraemia. In immunocompetent patients with typical CSD, bacteraemia is usually transient and of very low magnitude when it occurs. This level is typically below the threshold of detection by standard blood culture methods.

Biopsy and Histopathology / Molecular Testing

Tissue biopsy, most commonly of an enlarged lymph node, involves histopathological examination and molecular (PCR) testing. This approach is used in selected cases:

• When the diagnosis is uncertain and alternative diagnoses (including lymphoma, tuberculosis, or other granulomatous diseases) must be excluded.
• In chronic or atypical presentations not meeting the serological criteria for diagnosis.
• When the patient has been on antibiotics prior to presentation, making serology less reliable.
• In immunocompromised patients with severe or disseminated disease.

Histopathological findings on lymph node biopsy in cat scratch disease are characteristic but not pathognomonic: they show granuloma formation (collections of macrophages and epithelioid cells) with central stellate necrosis, surrounded by lymphocytes and plasma cells. The Warthin-Starry silver stain may demonstrate pleomorphic bacilli in the tissue, but this is neither sensitive nor specific.

PCR (polymerase chain reaction) testing on biopsy specimens can detect Bartonella DNA, even when the organisms are non-viable or only tiny amounts of bacterial material are present. It can also identify the specific Bartonella species involved. PCR has emerged as a valuable adjunctive diagnostic tool, particularly in culture-negative and serologically equivocal cases.

Laboratory Abnormalities

Non-specific laboratory abnormalities that may accompany cat scratch disease include:

• Elevated white blood cell count (leucocytosis, predominantly neutrophilic)
• Eosinophilia (elevated eosinophil count) in some cases Elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), both markers of systemic inflammation, are present
• Elevated serum globulins

These findings support a diagnosis of bacterial infection but are non-specific and do not confirm cat scratch disease.

---

Treatment

Management in Immunocompetent Patients

In otherwise healthy, immunocompetent individuals with the typical, uncomplicated form of cat scratch disease, antibiotic therapy is generally not mandatory. This is because the disease is self-limiting and resolves spontaneously in the vast majority of cases. Additionally, antibiotic treatment has not been convincingly shown to shorten the natural course of the typical presentation.

Conservative, supportive management is therefore appropriate for most immunocompetent patients:

• Local application of heat: Warm compresses applied to enlarged, tender lymph nodes can provide symptomatic relief.
• Analgesics (pain relief): Over-the-counter analgesics (such as paracetamol or ibuprofen) are appropriate for pain management.
• Non-steroidal anti-inflammatory drugs (NSAIDs): Can be used to reduce pain and inflammation.
• Aspiration of fluctuant nodes: When lymph nodes become fluctuant, meaning they are filled with pus and indicate suppuration, the preferred intervention is needle aspiration. This procedure involves drawing out the pus using a syringe and needle. Aspiration relieves pain, reduces the risk of spontaneous rupture and fistula formation, and can provide specimens for microbiological analysis. Incision and drainage (I&D) is generally avoided, as it can promote fistula formation and delay healing.
• Avoidance of corticosteroids: Corticosteroids (cortisone) should not be used in cat scratch disease. While they suppress inflammation, they also suppress the immune response needed to contain the infection, and their use has been associated with an increased rate of fistula formation and other complications. This is an important clinical principle.

Antibiotic Therapy: When It Is Indicated

Antibiotic treatment is indicated in the following situations:

1. Severe or extensive lymphadenopathy causing significant morbidity.
2. Systemic (disseminated) forms of cat scratch disease with visceral involvement (hepatic, splenic, mediastinal granulomatosis).
3. Immunocompromised patients: In patients with compromised immune function, antibiotic treatment is essential to prevent and manage the severe and life-threatening manifestations described above.
4. Specific severe complications: Including encephalopathy, neuroretinitis, endocarditis, peliosis hepatis, and bacillary angiomatosis.
5. At the clinician’s discretion in immunocompetent patients with significant symptoms or prolonged course.

Antibiotic Choices

Bartonella henselae is sensitive in vitro (in laboratory conditions) to a broad range of antibiotic classes:

• Macrolides: Azithromycin and erythromycin, which are generally considered the antibiotics of first choice for typical CSD requiring treatment. This preference stems from their good in vitro activity, favorable pharmacokinetics, and strong tolerability.
• Amoxicillin and beta-lactam antibiotics (including third-generation cephalosporins)
• Fluoroquinolones: Including ciprofloxacin and levofloxacin
• Aminoglycosides: Including gentamicin
• Rifampicin: Particularly valued in combination regimens for severe or immunocompromised cases
• Trimethoprim-sulfamethoxazole (co-trimoxazole)
• Doxycycline: Particularly important for endocarditis and bacillary angiomatosis

Despite this broad susceptibility profile in vitro, clinical responses to antibiotics in typical cat scratch disease are sometimes inconsistent. This variability stems from the intracellular survival strategy of Bartonella, which offers protection against antibiotics that cannot effectively penetrate cells.

Duration of Treatment

The recommended duration of antibiotic treatment varies according to the severity and clinical form of the disease:

In immunocompromised patients, particularly those with HIV/AIDS, antibiotic therapy must be continued for a minimum of 6 weeks for the initial treatment episode. If relapse occurs after completing treatment, secondary prophylaxis (long-term suppressive antibiotic therapy, typically with doxycycline or erythromycin) must be maintained indefinitely, or until the underlying immunocompromising condition is resolved (e.g., until CD4 counts rise sufficiently on antiretroviral therapy in HIV-positive patients).

Combination Antibiotic Therapy

For severe or life-threatening forms of bartonellosis, such as endocarditis, severe bacillary angiomatosis, and disseminated disease in immunocompromised patients, combination antibiotic therapy is recommended. This approach involves using two or more antibiotics with complementary mechanisms of action to maximize bactericidal activity and reduce the risk of treatment failure or relapse. Typical combinations include doxycycline with rifampicin, or doxycycline with a beta-lactam or aminoglycoside, depending on the clinical scenario.

Preventing Infection: Practical Advice

While cat scratch disease is rarely preventable by avoiding all contact with cats, the following practical measures can meaningfully reduce the risk:

• Avoid rough play with cats that provokes scratching or biting, particularly with kittens (which have higher rates of B. henselae bacteraemia).
• Wash hands thoroughly with soap and water immediately after handling cats or cleaning litter trays.
• Promptly clean and disinfect any cat scratch or bite wound. First, wash the area thoroughly with soap and water. Then, apply an antiseptic and cover it with a clean dressing.
• Avoid touching your eyes, nose, or mouth after handling cats until hands have been washed.
• Maintain regular flea control on all owned cats (and dogs) using veterinarian-recommended flea preventative products. Reducing the flea burden on cats reduces flea faeces contamination of claws and fur, thereby reducing the risk of B. henselae transmission to humans.
• Immunocompromised individuals, including those with HIV/AIDS, organ transplant recipients, and those on immunosuppressive therapy, should exercise particular caution when handling cats. Ideally, they should consult their physician about the risks of cat ownership in their specific situation.

---

Sources and Bibliography

• Florin TA, Zaoutis TE, Zaoutis LB. Beyond cat scratch disease: widening spectrum of Bartonella henselae infection. Pediatrics. 2008;121(5):e1413-e1425. PubMed
• Klotz SA, Ianas V, Elliott SP. Cat-scratch Disease. StatPearls. Treasure Island (FL): StatPearls Publishing; 2023. NCBI/NBK
• Centers for Disease Control and Prevention (CDC). Bartonella henselae: Transmission. CDC
• Rolain JM, Brouqui P, Koehler JE, Maguina C, Dolan MJ, Raoult D. Recommendations for treatment of human infections caused by Bartonella species. Antimicrobial Agents and Chemotherapy. 2004;48(6):1921-1933.
• Angelakis E, Raoult D. Bartonella infections in cat scratch disease. PLOS Neglected Tropical Diseases. 2014;8(5):e2869.
• Maguina C, Garcia PJ, Gotuzzo E, Cordero L, Spach DH. Bartonellosis (Carrión’s disease) in the modern era. Clinical Infectious Diseases. 2001;33(6):772-779.
• Berghoff W. Chronic Lyme disease and co-infections: differential diagnosis. Open Neurology Journal. 2012;6:158-178. PMC reference for tick-borne Bartonella
• European Centre for Disease Prevention and Control (ECDC): Bartonellosis. https://www.ecdc.europa.eu
• British Infection Association (BIA): Guidelines on cat scratch disease. https://www.britishinfection.org
• Spach DH, Koehler JE. Bartonella-associated infections. Infectious Disease Clinics of North America. 1998;12(1):137-155.