eMedicine Specialties > Otolaryngology and Facial Plastic Surgery > Infectious Diseases

Catscratch Disease

Author: Gauri Mankekar, MBBS, MS, PhD, DNB, Consulting Surgeon, Department of Otolaryngology, PD Hinduja National Hospital, India
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Updated: Jul 22, 2009

Introduction

Background

Catscratch disease (CSD) is a common cause of infectious subacute regional lymphadenitis affecting those lymph nodes that drain the sites of inoculation. Bartonella henselae is considered the principal etiologic agent.^1,2 CSD is one of the most common causes of chronic lymphadenopathy in children and adolescents.

The disease develops following a cat scratch or bite. The initial symptom is formation of a papule at the inoculation site, followed by regional lymphadenopathy within 1-2 weeks. In most patients, the disease resolves spontaneously within 2-4 months. 

In some cases, patients may develop severe systemic disease or may have other atypical manifestations like oculoglandular syndrome, encephalitis, neuroretinitis, pneumonia, osteomyelitis, erythema nodosum, arthralgia, arthritis, and thrombocytopenic purpura.^{3,4,5,6,7,8,9,10}

It is necessary to diagnose CSD in a patient with lymphadenopathy to differentiate a benign process from a neoplastic process.¹¹ However this can be difficult because of limitations to the currently available confirmatory diagnostic tests.¹²

Pathophysiology

Many organ systems are affected by catscratch disease (CSD), including the lymph nodes, CNS, eyes (neuroretinitis), skin (bacillary angiomatosis, erythema nodosum, erythema multiforme), lungs, and bones (arthritis and osteomyelitis).

Lymph nodes

In general, lymph nodes become enlarged in the 1-2 weeks after exposure. They are often tender and occasionally become fluctuant.

Lymphoid hyperplasia with arteriolar proliferation and reticular cell hyperplasia is seen early in the disease. As the disease progresses, granulomas appear, with central necrosis and multinucleated giant cells. Finally, stellate microabscesses form, and nodes can become fluctuant.

Central nervous system

Encephalopathy is the most common neurologic manifestation, occurring in 2-3% of patients. This complication may be more common in adults than in children. The onset is usually abrupt and occurs 1-6 weeks after the lymphadenopathy becomes apparent.

Patients can become confused and disoriented, and their condition can deteriorate to coma. About 50% of patients have a fever. Focal findings of hemiparesis and reflex abnormalities may be noted. Seizures, which occur in as many as 80% of patients with neurologic sequelae, are often prolonged and recurrent.

The pathogenesis of encephalopathy is unknown, but it is not likely due to direct infection, because CSF is usually normal and recovery is rapid, often without antibiotic therapy. CT scans are often normal, and CSF examination shows mononuclear pleocytosis in 20-30% of patients. Electroencephalographs (EEGs) show nonspecific slowing. Recovery is usually complete in a 1 week or longer, but persistent neurologic deficits have been reported.

Neuroretinitis

Patients with neuroretinitis generally present with painless, unilateral visual loss. Examination reveals decreased visual acuity, decreased color vision, and centrocecal scotoma. The optic disc appears edematous, and exudates frequently surround the macula.

Neuroretinitis is possibly due to a subretinal angiomatous nodule similar to that seen in bacillary angiomatosis.

Bacillary angiomatosis

Bacillary angiomatosis almost exclusively occurs in patients who are immunocompromised. Skin lesions consisting of numerous brown to violaceous or colorless vascular tumors of the skin and the subcutaneous tissue are the most common manifestation. Disseminated disease may involve bone, liver, spleen, lymph nodes, the gastrointestinal and respiratory tracts, and bone marrow.

B henselae and Bartonella quintana have been isolated from samples of cutaneous and osseous bacillary angiomatosis lesions. Histologic examination with Warthin-Starry staining reveals vascular proliferation with numerous bacillary organisms.

Pulmonary

Six cases of catscratch disease with pneumonia and 8 cases with pleural thickening and/or effusion have been reported. In these cases, pulmonary features developed 1-5 weeks after lymphadenopathy occurred. Systemic signs of infection, including fever, were present in 85%. One case in which a massive abscess involved the chest wall has been reported.

Vertebral osteomyelitis and splenic abscess

Rolain et al have described vertebral osteomyelitis with splenic abscess in a patient with catscratch disease.¹³ Their diagnosis was made on the basis of molecular detection of Bartonella henselae either on lymph node biopsies or on bone biopsy, histology of the lymph node, serology using in-house microimmunofluorescence assay a. Immunofluorescent detection was also performed directly on slide appositions using a monoclonal antibody.

Frequency

United States

Catscratch disease (CSD) is seen in all regions of the United States. Approximately 22,000 cases are diagnosed each year. Seroprevalence among cats is highest in the southeastern states, coastal California, Hawaii, and the Pacific Northwest. In temperate climates, rates of catscratch disease seem to peak between September and March (75% of cases). In warmer climates, cases are seen between July and August.

The incidence among inpatients is estimated to be 6.6 cases per 100,000 population. However, this estimate likely is low, given that most patients are not admitted to the hospital.

Only 1 genotype of B henselae has been reported in North America.

International

Catscratch disease occurs worldwide. At least 2 genotypes of B henselae have been isolated from cats in Europe. B henselae is endemic in Europe, Africa, Australia, and Japan. In Germany, B henselae was the causative agent of head and neck lymphadenopathy in 61 (13.4%) of 454 patients¹⁴ and the most common cause of lymphadenopathy in adults and children.^14,11

Mortality/Morbidity

No deaths due to catscratch disease (CSD) in immunocompetent patients have been reported. Most patients with typical catscratch disease remain afebrile and do not have constitutional symptoms.

• Lymphadenopathy occurs in the nodal regions draining the inoculation site. These include the upper extremities (46%) and the cervical and submandibular (26%), inguinal (17%), preauricular (6%), and clavicular (2%) regions.
• Patients with atypical catscratch disease can present with prolonged fever, malaise, fatigue, myalgia, weight loss, and hepatosplenomegaly. Patients presenting with disseminated catscratch disease involving the liver and spleen without associated lymphadenitis have been reported.

Race

No racial predilection exists.

Sex

Catscratch disease occurs more frequently in males than in females, with a ratio of 3:2.

Age

• More than 80% of cases occur in persons younger than 21 years.
• Only 10-20% of cases occur in adults. However, catscratch disease (CSD) can occur concurrently with neoplasm and mycobacteriosis especially in adults older than 49 years of age.¹¹

Clinical

History

• History of exposure to cats is a key feature in making the diagnosis.
• Patients often present with chronic (>2-wk) history of tender regional lymphadenopathy. The location of enlarged nodes depends on the site of inoculation, which is usually in the extremities.

Physical

• Physical examination reveals tender lymphadenopathy, often with overlying erythema. About 80% of patients present with tender lymphadenopathy within 1-2 weeks of their exposure.
  • The inoculation site can be identified in up to 65% of patients on careful examination of the skin. The site appears as a macule, papule, or vesicle. The lesion can appear 3-10 days after inoculation and lasts for several days to months.
  • More than 80% of involved lymph nodes occur in the head and neck region, arms, and axillae. In 44-85% of patients, a solitary enlarged node may be present. In 20% of patients, multiple nodes in a single region are involved.
  • Approximately 30% of patients have involved nodes at multiple sites. Examine these patients for multiple inoculation sites. The involved lymph nodes are 1-5 cm, with some nodes as large as 8-10 cm.
  • Suppuration of the involved nodes occurs in 8.5-30% of patients, and the risk of suppuration is proportionate to the size of the lymphadenopathy. In general, lymphadenopathy diminishes over 2-6 weeks, but it can persist for as long as 2 years.
• Fever is present in only 30-50% of patients and generally lasts for 1-7 days. About 32% of patients have prolonged fever, or one lasting up to 3 weeks. Such fever suggests progression to suppurative lymphadenitis.
• Malaise, fatigue, and other constitutional symptoms occur in up to 30% of patients.
• Headache, sore throat, and anorexia are noted in approximately 13% of patients.
• Less common symptoms are splenomegaly (11%), exanthems (4.5%), conjunctivitis (4.3%), and parotid swelling (1.4%). Although erythema nodosum, erythema marginatum, erythema multiforme, and erythema annulare have been associated with catscratch disease, exanthems consist of a truncal maculopapular rash.
• Atypical findings occur in 10-14% of patients. Parinaud oculoglandular syndrome, found in 2-17% of patients, consists of conjunctival granuloma at the inoculation site and preauricular adenopathy.
• Submandibular and cervical adenopathy also may occur. Etiology of this syndrome probably involves rubbing of the eyes after contact with a cat.
• Other atypical manifestations are thrombocytopenic purpura; osteitis resembling bacterial osteomyelitis; hepatosplenomegaly; and CNS involvement, including transverse myelitis, radiculitis, cerebral arteritis, polyneuritis, and meningitis.
• Patients with AIDS have an increased risk of catscratch disease.
  • The inoculation sites may be difficult to distinguish from Kaposi sarcoma.
  • The normally benign course of catscratch disease may be life threatening to an immunocompromised host.

Causes

• B henselae and B quintana most often are implicated in catscratch disease.
• Other possible causes are Bartonella clarridgeiae and Afipia felis.
• More than 90% of patients with catscratch disease report an exposure to cats.
  • About 75% of these patients give a history of cat scratch or bite.
  • B henselae has been isolated from fleas from infected cats.
  • Cats that transmit the illness do not show signs of the disease.
• Cases occurring after scratches from thorns, wood splinters, and crab claws have occurred. However, in each of these cases, the patient recalled that a cat licked the abrasion.
• Dogs have been implicated in 5% of cases.
• Familial outbreaks have been documented and have usually involved siblings, or in rare instances parents.
  • Symptoms among siblings often appear within 3 weeks of the index case.
  • In approximately 1% of diagnosed cases, no animal scratch is implicated.
• Person-to-person transmission has not been documented.
  • The infectious agent is transmitted only from cat to human for a period of 3 weeks.
  • The mode of transmission is direct contact from a scratch, bite, or lick of an infected animal.

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