eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Catscratch Disease

Author: Stephen J Nervi, MD, Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey School of Medicine
Coauthor(s): Rajendra Kapila, MD, MBBS, Associate Professor, Department of Medicine, UMDNJ, New Jersey Medical School; Roseanne A Ressner, DO, Fellow, Department of Infectious Diseases, Brooke Army Medical Center; Lynn L Horvath, MD, Clinical Assistant Professor of Medicine/Infectious Disease, University of Texas Health Science Center; Consulting Staff, Department of Infectious Disease, Brooke Army Medical Center; Joyce R Drayton, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Disease, Morehouse School of Medicine
Contributor Information and Disclosures

Updated: Jan 26, 2009

Introduction

Background

Catscratch disease (CSD) is a bacterial infection caused by Bartonella henselae, a gram-negative rod. It is associated with a self-limited subacute solitary or regional lymphadenopathy. Patients with catscratch disease usually have a history of sustaining a scratch or bite from a cat or kitten.

Pathophysiology

The hallmark of catscratch disease is regional adenopathy proximal to the site of inoculation.

In immunocompetent patients, Bartonella infection causes a granulomatous and suppurative response. In immunocompromised patients, the response can be vasculoproliferative with neovascularization.

Bartonella is able to promote angioproliferation through adhesion A, which is observed in bacillary angiomatosis, peliosis, and verruga peruana.

Nine outer membrane proteins (OMP) of B henselae have been identified. The 43-kD OMP is a major protein capable of binding endothelial cells; further investigation is needed to clarify its role in the pathogenesis of catscratch disease.

Frequency

United States

An estimated 9.3 cases of catscratch disease per 100,000 population occur each year, with 22,000 cases annually and approximately 2,000 hospitalizations per year in the United States. The median age among individuals who develop catscratch disease is 15 years.

Most cases of catscratch disease occur in the fall and winter.

International

Catscratch disease has been reported worldwide; however, the international incidence is unknown. The disease is more prevalent in areas with warm humid climates.

Mortality/Morbidity

Catscratch disease is typically benign and self-limited in immunocompetent people. Symptoms usually resolve within 2-4 months.

Of affected patients, 5-25% experience a course complicated by involvement of sites other than regional lymph nodes. Patients may also present with constitutional symptoms.

Reynolds et al found that the catscratch disease–associated hospitalization rate in the United States was 0.60 per 100,000 patients younger than 18 years (95% CI, 0.49-0.72) and 0.86 per 100,000 patients younger than 5 years.1

Patients older than 60 years are more likely to present with atypical features of catscratch disease.

Immunocompromised hosts may develop more serious forms of infection with B henselae or Bartonella quintana, such as bacillary angiomatosis, bacillary peliosis, or bacteremia.

Race

Catscratch disease is reported more commonly in whites.

Sex

Catscratch disease is reported more commonly in males, who account for approximately 60% of all cases.

Age

In a database analysis by Jackson et al, 55% of patients with catscratch disease were aged 18 years or younger.2 More adults may develop catscratch disease than previously recognized, as most studies on the disease have focused primarily on pediatric populations. For additional information on pediatric catscratch disease, see the article Catscratch Disease in eMedicine’s Pediatrics: General Medicine volume.

Clinical

History

  • Most patients with catscratch disease (CSD) report a history of exposure to cats (eg, recent cat scratch, bite, lick).
  • Most persons with catscratch disease develop one or more 3- to 5-mm red-brown nontender papules the site of inoculation 3-10 days after the bacteria are introduced.
  • Within 1-3 weeks, lymphadenopathy develops in the nodal group, draining the inoculum site. Lymphadenopathy often consists of a single node and can be moderately tender, with erythema and increased warmth of the overlying skin. Lymphadenopathy should resolve within 2-4 months but lasts up to 6-12 months in rare cases.
  • Up to 10% of nodes may suppurate, requiring needle aspiration.
  • Other symptoms of catscratch disease might include the following:
    • Malaise/fatigue (29.4%)
    • Fever (28%)
    • Anorexia (14.5%)
    • Headache (13%)
    • Sore throat (7%)
    • Arthralgia (2.5%)

Physical

  • Fever may be present. In one series of 1200 cases of catscratch disease, only 9% of patients had a fever higher than 39°C.
  • In 1-3 weeks, the inoculum-site lesions evolve through erythematous, vesicular, and papular-crusted changes.
  • When patients present with painful adenopathy, the original site of inoculation may not be apparent.
  • Nodes draining the site of inoculation enlarge within 1-3 weeks of contact with the kitten or cat. The upper extremities are the most common location (46% axillary and epitrochlear nodes), followed by the neck and jaw region (26% cervical and submandibular nodes), the groin (17.5% femoral and inguinal), preauricular region (7%), and clavicular region (2%). In 10-20% of cases, more than one region is affected. Node size is typically 1-5 cm but may enlarge to 8-10 cm.
  • The following are forms of atypical catscratch disease, accounting for 5-25% of cases:
    • Parinaud oculoglandular syndrome: This syndrome affects 5-10% of patients with catscratch disease and is the most common form of atypical catscratch disease. Parinaud syndrome is characterized by ipsilateral preauricular lymphadenopathy and unilateral granulomatous conjunctivitis. Although this syndrome can be caused by other infections, B henselae is the most common etiologic agent.
    • Neuroretinitis: Unilateral painless vision loss occurs with central scotoma, optic disc swelling, or a macular star referred to as Leber neuroretinitis or idiopathic stellate neuroretinitis. The patient’s vision usually recovers completely within 1-3 months.
    • Acute encephalopathy: The predominant symptom is rapid progression of headache to lethargy and coma. Seizures and even status epilepticus can occur in these patients. The CSF may be normal or may have a lymphocytic pleocytosis. CT scanning and MRI findings are usually normal, and the course is generally self-limited without neurologic sequelae. However, persistent cognitive impairment and death have been reported in some cases. Myelitis, radiculitis, compression neuropathy, and cerebellar ataxia have been reported.
    • Bartonella endocarditis: This condition should be considered in patients with manifestations of endocarditis and negative blood culture results who have regular contact with cats. Possible risk factors include alcoholism, homelessness, and body louse infestation. Patients with Bartonella endocarditis often require valve replacement.
    • Visceral involvement: This usually entails systemic symptoms combined with multiple hypoechogenic-hypodense hepatic or splenic lesions. The liver is described as having a nutmeg appearance with stellate necrotizing granulomata on the histologic examination. This syndrome may develop in the absence of lymphadenopathy.
    • Bone and joint involvement: Osteolytic lesions may develop at various sites, and vertebral osteomyelitis with epidural abscess may occur in these cases. Catscratch disease–associated arthropathy may also occur.
    • Skin: Various skin manifestations occur in approximately 5% of patients with catscratch disease. These manifestations include nonspecific rashes, erythema nodosum, and leukocytoclastic vasculitis. For additional information on cutaneous manifestations of catscratch disease, see the article Catscratch Disease in eMedicine’s Dermatology volume.
  • Immunocompromised patients (eg, those with cancer, persons who have undergone transplantation, and persons with HIV infection) may develop bacillary angiomatosis, bacillary peliosis, or persistent or relapsing fever with bacteremia.
    • Bacillary angiomatosis: This vasculoproliferative disease mostly involves the skin but can involve the other organs. It manifests as numerous brown to violaceous tumors of the skin and subcutaneous tissues. Without antibiotic therapy, the disease progresses with dissemination. The lesions are very similar to verruga peruana, the chronic form of Carrión disease (Oroya fever) from Bartonella bacilliformis infection.
    • Bacillary peliosis: This condition involves the solid internal organs with reticuloendothelial elements (usually the liver, but the spleen, abdominal lymph nodes, and bone marrow may also be involved). Vasculoproliferation of sinusoidal hepatic capillaries may result in blood-filled spaces in the liver.
    • Persistent or relapsing fever with bacteremia: This is another distinct clinical syndrome in immunocompromised individuals.

Causes

  • Catscratch disease is usually caused by B henselae, formerly known as Rochalimaea henselae. In the genus Bartonella, B bacilliformis, B quintana, Bartonella elizabethae, Bartonella vinsonii, and Bartonella koehlerae are also responsible for human disease.
  • In 1993, Dolan et al isolated B henselae from lymph nodes of patients with catscratch disease. Bartonella species are small pleomorphic, fastidious, facultative, gram-negative, and intracellular bacilli. Infection appears to confer lifelong immunity, as reports of recurrences of clinical catscratch disease are rare.3
  • Domestic cats are the natural reservoir and vectors of B henselae. In cats, B henselae infection is asymptomatic. Fleas are believed to transmit the bacteria between cats, and seroprevalence in cats is highest in warm or humid climates, where prevalence of flea infestation among cats is higher.
  • The transmission of B henselae from cats to humans occurs via a scratch or bite when the bacterium is present on the cat’s claws or oral cavity. Kittens younger than 12 months are 15 times more likely to transmit the disease than adult cats. Kittens are more likely to be bacteremic with B henselae and are more likely to scratch. Individuals who have been scratched or bitten by a kitten are 27 times more likely to become infected, and people who have at least one kitten with fleas are 29 times more likely to become infected than people whose animals were free of fleas.
  • Human-to-human transmission has not been reported, and no data support transmission from fleas to humans.

More on Catscratch Disease

Overview: Catscratch Disease
Differential Diagnoses & Workup: Catscratch Disease
Treatment & Medication: Catscratch Disease
Follow-up: Catscratch Disease
References

References

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  2. Jackson LA, Perkins BA, Wenger JD. Cat scratch disease in the United States: an analysis of three national databases. Am J Public Health. Dec 1993;83(12):1707-11. [Medline].

  3. Dolan MJ, Wong MT, Regnery RL, Jorgensen JH, Garcia M, Peters J. Syndrome of Rochalimaea henselae adenitis suggesting cat scratch disease. Ann Intern Med. Mar 1 1993;118(5):331-6. [Medline].

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Further Reading

Keywords

catscratch disease, cat scratch disease, CSD, cat scratch fever, catscratch fever, Bartonella henselae infection, B henselae infection, Bartonella infection, bacillary angiomatosis, peliosis, verruga peruana, Parinaud's oculoglandular syndrome, Parinaud oculoglandular syndrome, Parinaud syndrome, neuroretinitis, acute encephalopathy, endocarditis, Bartonella endocarditis, subacute regional lymphadenitis, bartonellosis, catscratch antigen, CSA, atypical catscratch disease, atypical cat scratch disease, Rochalimaea henselae, R henselae

Contributor Information and Disclosures

Author

Stephen J Nervi, MD, Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey, New Jersey School of Medicine
Stephen J Nervi, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

Rajendra Kapila, MD, MBBS, Associate Professor, Department of Medicine, UMDNJ, New Jersey Medical School
Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, and Infectious Diseases Society of New Jersey
Disclosure: Nothing to disclose.

Roseanne A Ressner, DO, Fellow, Department of Infectious Diseases, Brooke Army Medical Center
Roseanne A Ressner, DO is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Lynn L Horvath, MD, Clinical Assistant Professor of Medicine/Infectious Disease, University of Texas Health Science Center; Consulting Staff, Department of Infectious Disease, Brooke Army Medical Center
Lynn L Horvath, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Armed Forces Infectious Diseases Society, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Joyce R Drayton, MD, Assistant Professor, Department of Internal Medicine, Division of Infectious Disease, Morehouse School of Medicine
Joyce R Drayton, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Preventive Medicine, American Holistic Medical Association, Infectious Diseases Society of America, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Medical Editor

John M Leedom, MD, Professor of Medicine, Keck School of Medicine, University of Southern California; Chief, Division of Infectious Diseases, Department of Internal Medicine, Los Angeles County, University of Southern California Medical Center
John M Leedom, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

John W King, MD, Professor of Medicine, Section of Infectious Diseases, Louisiana State University Health Sciences Center; Director, Viral Therapeutics Clinics for Hepatitis; Consulting Staff, Department of Infectious Diseases, Overton Brook Veterans Affairs Medical Center
John W King, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Association of Subspecialty Professors, Infectious Diseases Society of America, and Sigma Xi
Disclosure: emedicine $50.00 author of chapter

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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