Version May 2024
INTRODUCTION — Cat scratch disease (CSD) is an infectious disease that is typically characterized by self-limited regional lymphadenopathy. The manifestations of CSD, however, can include visceral organ, neurologic, and ocular involvement [1,2].
The microbiology, epidemiology, clinical features, and diagnosis of CSD will be reviewed here. The treatment of CSD, as well as the evaluation and management of cat bites, are discussed separately. (See "Treatment of cat scratch disease" and "Animal bites (dogs, cats, and other mammals): Evaluation and management".)
MICROBIOLOGY — Although clinical descriptions of CSD existed for more than 50 years, the first convincing evidence of an infectious cause of CSD came in 1983 when investigators at the Armed Forces Institute of Pathology, using a Warthin-Starry stain, demonstrated small, pleomorphic organisms in the lymph nodes of 29 of 34 patients with CSD [3]. Available serologic and culture data provide convincing evidence that Bartonella henselae is the etiologic agent in most cases of CSD [4-6]. In humans and cats, two main B. henselae genotypic groups have been identified based on molecular analysis: the Houston-1 serotype and Marseille serotype [7]. One report also described a case of CSD caused by Bartonella clarridgeiae [8]. In addition, scattered, uncommon cases of CSD may result from Afipia felis, B. clarridgeiae, and perhaps other, as yet unidentified, fastidious organisms [9].
Among persons with HIV (and less commonly other immunocompromised individuals), B. henselae can cause bacillary angiomatosis (BA), peliosis hepatis, and splenitis (see "Bartonella infections in people with HIV"). Rare reports have also documented BA among immunocompetent individuals [10].
PATHOGENESIS — The pathogenesis of CSD remains poorly understood. Disease manifestations result from either local infection, such as lymphadenopathy, or from bloodborne disseminated infection, such as occurs with neuroretinitis or visceral organ involvement. Cats serve as the natural reservoir for B. henselae, and the organism causes intraerythrocytic bacteremia that can persist for a year or longer in some cats [11]. Following inoculation of B. henselae into humans, the organism typically causes a local infection that manifests as regional lymphadenopathy. Within the human host, B. henselae invades endothelial cells causing an acute inflammatory reaction associated with activation of a proinflammatory cascade [12]. It remains unknown why some persons with CSD have infection that remains localized whereas others develop disseminated disease. Some evidence suggests that the presence of the major histocompatibility human leukocyte antigen (HLA) B27 may predispose patients with B. henselae infection to develop uveitis [13].
EPIDEMIOLOGY — CSD generally occurs in immunocompetent individuals and infrequently causes serious illness [14]. Although most commonly a disease of children and young adults, a surveillance study conducted in Israel found that 52 of 846 (6 percent) immunocompetent patients with CSD were ≥60 years of age [15]. Systemic CSD has been described in patients following solid organ transplantation and hematopoietic cell transplantation [16-19]. (See 'Clinical manifestations' below.)
Epidemiologic studies from the United States, Europe, Israel, Australia, and Japan, suggest that CSD has a worldwide distribution [20]. In a study from Germany, CSD was identified in 61 of 454 patients (13 percent) with primary head and neck masses [21]. In the United States, a retrospective study of patients younger than 65 years of age identified 13,273 patients with a diagnosis of CSD from 2005 to 2013 [22]. In this study, approximately 12,000 cases of CSD were diagnosed annually in the outpatient setting and 500 persons with CSD were hospitalized each year. The cases had a seasonal distribution with a peak in January and late summer and fall. In this analysis, the incidence of CSD was highest among those who lived in the southeastern United States (6.4 cases/100,000 population) and in children 5 to 9 years of age (9.4 cases/100,000 population). The incidence of atypical CSD (involving the eye, heart, liver, spleen, etc) in the United States was estimated to be 0.7 cases/100,000 and occurred most commonly in individuals 15 to 49 years of age [23].
TRANSMISSION — Available data suggest that CSD can result from a scratch or bite from a cat infected with B. henselae, as well as from exposure to cat fleas infected with B. henselae. Transmission to humans can also occur via contact of cat saliva with broken skin or mucosal surfaces (eg, mouth and eyes). Although cats are the main reservoir for B. henselae [24], rare cases of CSD have occurred after exposure to dogs, presumably resulting from flea bites. Rarely, CSD occurs in family clusters with more than one child in the family presenting simultaneously with clinical disease [25].
Multiple lines of evidence have directly linked CSD to exposure to cats, especially young cats and cats with fleas [1,5,26]. The cat flea, Ctenocephalides felis, plays a critical role in the horizontal cat-to-cat transmission of B. henselae [27]. In one study of 205 cats in northern California, B. henselae bacteremia was documented in 56 percent of cats less than one year of age and in 34 percent of cats over one year of age [28]. Moreover, 90 percent of cats younger than one year of age and 77 percent one year of age or older had a positive B. henselae serologic test. Most cats infected with B. henselae do not show clinical signs of infection [29].
Fleas have also been implicated in transmission of CSD. In one study of 60 persons with CSD (cases) and 56 age-matched controls, exposure to kittens (odds ratio [OR] 15), a scratch or bite by a kitten (OR 27), and having a kitten with fleas (OR 29) were more common among cases than controls [5]. In a study of B. henselae antibodies in catteries, flea infestation was the risk factor most associated with high seroprevalence [30]. Topical treatments that prevent flea infestations may have a role in preventing transmission of B. henselae from fleas to cats [31-33]. As an example, one study evaluated the use of topical selamectin (a commercially available parasiticide) to prevent transmission of B. henselae in 12 cats who were exposed to B. henselae-positive fleas [31]. Six of the cats were treated with topical 6% selamectin three days prior to and one day after being exposed to the fleas, and six cats received no treatment. None of the treated cats developed B. henselae infection; however, all of the untreated cats developed B. henselae bacteremia.
CLINICAL MANIFESTATIONS — CSD presents in 85 to 90 percent of children as a localized cutaneous and lymph node disorder near the site of organism inoculation. However, in some individuals, the organisms disseminate and infect the liver, spleen, eye, or central nervous system. Patients with localized disease generally have a self-limited illness, whereas those with disseminated disease can have life-threatening complications.
Older patients with CSD are more likely to present with atypical features. In the surveillance study in Israel mentioned above, clinical data for patients with CSD aged ≥60 years (older group) were compared with patients with CSD aged <60 years (younger group) [15]. Lymphadenitis, the hallmark of typical CSD, was less common in the older group compared with those <60 years of age (77 versus 94 percent). By contrast, the older group was more likely to have general malaise (71 versus 51 percent) and atypical manifestation (33 versus 14 percent), including endocarditis (odds ratio [OR] 61.6, 95% CI 12.4-305.1), encephalitis (OR 6.3, 95% CI 1.2-33.3), and fever of unknown origin (FUO; OR 7.3, 95% CI 2.2-24.5). For these reasons, the time from onset of symptoms to diagnosis of CSD in older persons was delayed by >6 weeks when compared with the younger patients (30 versus 13 percent in the younger group).
Cutaneous manifestations — CSD often begins with a cutaneous lesion at the site of inoculation, the so-called primary inoculation lesion. This lesion usually develops 3 to 10 days after the introduction of the organism into the skin and generally evolves through vesicular, erythematous, and papular phases [34,35] (picture 1). Less commonly, the primary inoculation lesion can be pustular or nodular. One report described a patient who developed a paronychia (painful periungual inflammation) caused by B. henselae as a manifestation of an inoculation site lesion [36]. The primary inoculation lesion typically persists for one to three weeks (range several days to several months).
Careful examination of the interdigital spaces, skin creases, and scalp increases the chance of finding the primary inoculation lesion. Inoculation sites other than the skin occur in about 5 to 10 percent of cases and include the eye (nonsuppurative conjunctivitis, ocular granuloma) and mucous membranes (oral ulcer) [34]. The inoculation lesions usually cause minimal symptoms and heal without scarring.
Other uncommon cutaneous manifestations of CSD include a transient macular and papular eruption, erythema multiforme, erythema nodosum, and thrombocytopenic purpura [34].
Lymphadenopathy — Regional lymphadenopathy is the hallmark of CSD. Enlarged lymph nodes appear proximal to the inoculation site, about two weeks (range, 7 to 60 days) after the organism is inoculated into the skin (picture 2). The location of the lymphadenopathy typically correlates with the inoculation site. The most common locations are the axillary, epitrochlear, cervical, supraclavicular, and submandibular lymph nodes, although lymphadenopathy at other sites has also been reported [37-39].
The nodes are almost always tender, often have erythema of the overlying skin, and occasionally suppurate (10 to 15 percent). Node size typically ranges from 1 to 5 cm, but may enlarge to 8 to 10 cm. Lymphadenopathy associated with CSD usually resolves in one to four months, but reports have described persistence of enlarged nodes for one to three years.
In one study, solitary lymphadenopathy occurred in approximately 85 percent of persons with CSD [35]. Less commonly, patients presented with several enlarged nodes in the same anatomic region. In another study, regional adenopathy (single or multiple nodes) occurred in approximately two-thirds of cases, with the remaining one-third of patients having enlarged nodes in several anatomic sites [34]. Generalized lymphadenopathy is rare.
Visceral organ involvement — Visceral organ involvement is an unusual, but important, manifestation of CSD, particularly in children [40-42]; visceral organ CSD can involve the liver, spleen, or both. Patients may have persistent FUO, abdominal pain, and/or weight loss [43]. About half of children with visceral organ involvement have hepatomegaly or splenomegaly evident on physical examination [43]; the liver may be tender to palpation. Many of the patients with visceral involvement have no accompanying peripheral adenopathy. In one review, 100 of 832 patients (12 percent) with CSD had splenomegaly, but these were not patients in whom granulomatous splenitis was documented [44].
An abdominal computed tomography (CT) scan will typically show scattered, multiple defects in the liver and/or spleen that if biopsied, shows necrotizing granulomas (image 1). Biopsies are now rarely performed because the clinical and imaging findings are so characteristic for disseminated CSD. These are manifested as hypoechoic areas on ultrasound.
The erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) is typically elevated and liver function tests may be mildly abnormal.
Fever of unknown origin — B. henselae infection should be considered in the initial evaluation of fever of unknown origin (FUO) and prolonged fever, particularly in children [37,45,46]. A prospective analysis of 146 children with FUO and prolonged fever found that B. henselae was the third most common infectious disease diagnosis [47]. Although some of these children presented with signs and symptoms consistent with typical CSD or hepatosplenic involvement, three of seven patients with confirmed B. henselae infection presented with FUO and no clinical or radiographic manifestations of typical or hepatosplenic CSD. However, B. henselae infection has been described as a cause of FUO in adults. In a series of 66 patients with prolonged fever due to B. henselae from Israel, almost 80 percent were adults [48]; about half the patients presented with a prolonged continuous fever, while a prolonged relapsing fever pattern occurred in the other half of the patients. (See "Fever of unknown origin in children: Etiology", section on 'Cat scratch disease'.)
Ocular manifestations — Ocular manifestations of CSD include Parinaud oculoglandular syndrome, neuroretinitis, papillitis, optic neuritis, and focal retinochoroiditis [49-52].
Parinaud oculoglandular syndrome — Parinaud oculoglandular syndrome is an atypical form of CSD, which is reported in 2 to 8 percent of patients with CSD. Parinaud oculoglandular syndrome is characterized by tender regional lymphadenopathy of the preauricular, submandibular, or cervical lymph nodes associated with infection of the conjunctiva, eyelid, or adjacent skin surface. Usual complaints include unilateral red eye, a foreign body sensation in the eye, and excessive watering of the eyes. Discharge may be serous or purulent and copious in some patients [53,54]. The inoculation of the organism occurs via a cat bite or lick near (or in) the eye, as well as by self-inoculation from another infected site. Serious ocular, orbital, or retinal complications almost never develop as a result of local extension of Parinaud oculoglandular syndrome.
Neuroretinitis — Among all patients with CSD, neuroretinitis develops in about 1 to 2 percent. Neuroretinitis is a syndrome of acute visual loss from optic nerve edema associated with macular exudates; B. henselae is believed to be one of the most common infectious causes of neuroretinitis [55]. The high frequency of CSD as a cause of neuroretinitis is illustrated by a serologic study of patients with neuroretinitis that found 9 of 14 (64 percent) had either elevated IgM or IgG B. henselae titers [56].
Patients with neuroretinitis typically present with fever, malaise, and unilateral blurred vision [57]. On examination:
●Patients usually have unilateral involvement, with decreased visual acuity, often associated with an afferent pupillary defect. (See "The detailed neurologic examination in adults" and "Detailed neurologic assessment of infants and children", section on 'Cranial nerves'.)
●Retinal findings may include hemorrhages, cotton wool spots, and multiple discrete lesions in the deep retina [57].
●Some patients develop a stellate macular exudate (known as a "macular star") (picture 3). Macular stars are due to vascular leakage from the optic nerve head, and can be seen on fluorescein angiography or optical coherence tomography angiography. Patients with B. henselae-induced neuroretinitis may not develop a macular star until one to four weeks after initial presentation, and the exudate may persist for months, despite resolution of the neuroretinitis [49].
Most patients with neuroretinitis appear to have a good long-term prognosis [49,57], although patients with macular exudates may have residual defects that include optic disk pallor, diminished contrast sensitivity, and altered color vision [49]. Other complications with neuroretinitis have been reported, including macular hole with posterior vitreous detachment [58].
Neurologic manifestations — A wide range of neurologic manifestations has been described in patients with CSD, including [58-60]:
●Encephalopathy (most common)
●Transverse myelitis
●Radiculitis
●Cerebellar ataxia
Patients with encephalopathy typically develop abrupt confusion and disorientation, which may progress to coma, approximately one to six weeks after initially presenting with adenopathy. Most of these patients will develop seizures and some develop focal neurologic findings such as hemiparesis as a result of cerebral vasculitis [59].
Among patients with CSD encephalopathy, findings include [58]:
●A normal CT scan of the brain – Most patients
●Mild mononuclear pleocytosis in the cerebrospinal fluid (CSF; usually <50 cells/microL) – 20 to 30 percent of patients
●An abnormal electroencephalogram – Most patients
Although patients typically recover from CSD encephalopathy within several weeks, some will have residual neurologic defects.
Musculoskeletal manifestations — Severe and often disabling musculoskeletal manifestations may occur in patients with CSD [61-65]. In a surveillance study of 913 patients with CSD in Israel, 96 (10.5 percent) had musculoskeletal manifestations [61]. These included myalgia (6 percent), arthritis or arthralgia (5.5 percent), and less commonly tendinitis, osteomyelitis, and neuralgia.
The knee, ankle, wrist, hand, and elbow joints were the most frequently affected. Although joint symptoms usually resolve, five patients developed chronic arthropathy [61,62]. Multivariate analysis identified the following characteristics significantly associated with arthropathy (arthritis or arthralgia):
●Female sex (relative risk [RR], 1.89; 95% CI 1.01-3.52)
●Age greater than 20 years (RR, 11.0; 95% CI 4.3-28.2)
●Erythema nodosum (RR, 4.07; 95% CI 1.38-12.02)
A review of bone infection associated with CSD, published prior to the above study, found 47 cases reported in the literature [63]. The median age was nine years. Bone pain and fever were the predominant clinical manifestations and the most commonly affected sites were the vertebral column and pelvic girdle.
Other atypical manifestations — Scattered reports have documented rare manifestations of CSD, including deep neck space infection [66], scalp eschar with neck lymphadenopathy [67], pneumonia, pleural effusion, pulmonary nodules [68], septic shock, thrombocytopenic purpura (TTP), and hypercalcemia. The hypercalcemia is associated with overproduction of calcitriol, the most active form of vitamin D, and appears to be related to granuloma formation [69]. (See "Hypercalcemia in granulomatous diseases".)
Individuals with solid-organ transplants may have atypical manifestations including TTP, hemophagocytosis, and visceral disease that can resemble post-transplant lymphoproliferative disorder [19,70]. (See "Treatment and prevention of post-transplant lymphoproliferative disorders".)
Infection with B. henselae can also result in culture-negative endocarditis. Such patients have clinical manifestations similar to other patients with subacute bacterial endocarditis. A discussion of Bartonella endocarditis is presented separately. (See "Endocarditis caused by Bartonella".)
APPROACH TO DIAGNOSIS — Most patients with CSD present with typical clinical features, such as regional tender lymphadenopathy, with or without a preceding primary inoculation papular lesion. Atypical clinical findings include visceral organ involvement and ocular or neurologic manifestations.
A probable diagnosis is made based upon the characteristic clinical features and a history of recent cat or flea contact. (See 'Clinical manifestations' above and 'Epidemiology' above.)
Serologic testing with an enzyme immunoassay (EIA) or indirect fluorescence assay (IFA) should be performed in an attempt to support the clinical impression [24,71]. (See 'Serology' below.)
However, serologic testing has serious shortcomings, and a negative serologic test does not rule out CSD in a patient with characteristic epidemiologic and clinical features. Thus, empiric therapy should be initiated in persons with a presumed diagnosis. (See "Treatment of cat scratch disease".)
A lymph node or tissue biopsy is not routinely required for most patients who present with characteristic signs and symptoms of CSD, although it may be warranted in certain circumstances, such as a delayed resolution of systemic symptoms (eg, greater than five to seven days), or if an alternative diagnosis (eg, lymphoma or tuberculosis) is suspected.
If a biopsy sample is obtained, testing should include histology, B. henselae polymerase chain reaction (PCR) test, and Warthin-Starry staining. A positive B. henselae PCR test confirms the diagnosis, and a positive tissue Warthin-Starry stain provides strong support for the diagnosis of CSD (see 'Diagnostic tests' below). Testing to investigate for other disorders should also be performed. In an analysis of 786 lymph node specimens from patients with suspected CSD, infectious agents were identified in 391 of 786 (50 percent) of tissue samples [72]. Although the most commonly identified organism was B. henselae (245 patients, 31 percent), mycobacterial infection was diagnosed in 54 patients (7 percent). Malignancy was diagnosed in 47 of 181 patients in whom specimens suitable for histologic analysis were available (26 percent of those analyzed, 6 percent of total), and disease concurrent with CSD was diagnosed in 13 patients; no diagnosis was obtained in 350 patients (45 percent). The differential diagnosis of CSD is discussed below. (See 'Differential diagnosis' below.)
DIAGNOSTIC TESTS
Serology — Several reference labs perform serologic testing for Bartonella. Two serologic methods, the indirect fluorescence assay (IFA) and enzyme immunosorbent assay (EIA), have been evaluated for diagnosis of CSD, but the commercially available assays use the IFA test. In general:
●IFA IgG titers <1:64 suggest the patient does not have a current Bartonella infection; a low positive titer may represent past infection.
Titers of 1:64 or 1:128 represent possible Bartonella infection, and repeat testing should be performed in 10 to 14 days. Titers ≥1:256 strongly suggest active or recent infection.
●A positive IgM test strongly suggests acute disease (or very recent infection), but the production of IgM is usually brief. Thus, the serologic diagnosis of acute infection can be elusive.
However, a negative serologic test should not rule out CSD if there is a high clinical suspicion for disease. Although one study found that a higher proportion of patients with presumed CSD had an indirect IFA B. henselae IgG titer of ≥1:64 compared with healthy controls (88 versus 3 percent) [4], four subsequent studies from Europe reported problems with B. henselae IFA tests, including poor sensitivity [73,74] and specificity [75,76]. In a study of 156 children with suspected B. henselae infection, an alternative diagnosis was found among those with a B. henselae IgG titer of 1:128 or 1:256 in 34 and 24 percent, respectively [77].
The reported problems with the B. henselae IFA serology tests include:
●Significant cross-reactivity at the species level between B. henselae and B. quintana, especially for IgG assays.
●Sensitivity of the test does not appear to be optimal, especially with IgG assays.
●Prevalence of positive Bartonella serology in the general population is 4 to 6 percent, which creates false-positive test results.
Culture — B. henselae is a fastidious, slow-growing, gram-negative bacterium that requires specific laboratory conditions for optimal growth. It is important to proactively communicate with the microbiology laboratory; by informing them that Bartonella is a potential diagnosis, the laboratory can optimize culture techniques and can extend the incubation period for a minimum of 21 days. As an example, blood culture samples should be collected in pediatric or adult isolator tubes (Wampole, Cranbury, NJ) or in blood tubes containing ethylenediaminetetraacetic acid (EDTA) to increase the probability of isolating B. henselae.
Plating samples onto either chocolate agar or heart infusion agar supplemented with 5 percent rabbit blood enhances isolation of organisms from subcultures. Optimally, the microbiology lab should use fresh agar plates and incubate them in 5 percent CO2 at 35 to 37ºC for a minimum of 21 days. Even employing optimal techniques, most patients with CSD do not have B. henselae isolated from blood cultures.
Isolation of B. henselae from tissue samples remains very difficult, but successful isolation in patients with HIV has been reported by directly plating tissue homogenates onto agar and cocultivating with a bovine endothelial cell monolayer [78]. (See 'Diagnostic tests' above.)
Histopathology — Histopathologic examination of the primary inoculation lesion site reveals acellular areas of necrosis in the dermis. Histiocytes and epithelioid cells surround the areas of necrosis in multiple layers, with the innermost layer often showing a palisading arrangement. A zone of lymphocytes surrounds the histiocytes; multinucleated giant cells are variably present. Although these findings support a diagnosis of CSD, they should not be considered definitive.
The histopathologic findings in involved lymph nodes are nonspecific and depend upon the stage of the disease. Lymphoid hyperplasia is present initially, followed by the development of stellate granulomas. The lymph node centers are acellular and necrotic; histiocytes and peripheral lymphocytes surround these areas, similar to findings in skin samples. Microabscesses often develop and may become confluent at a later stage.
Warthin-Starry stain may demonstrate delicate pleomorphic B. henselae bacilli in chains, clumps, or filaments within areas of necrosis of involved lymph nodes and in the primary inoculation site of the skin. Although a positive Warthin-Starry stain does not provide a definitive diagnosis of CSD, it would strongly suggest a diagnosis of CSD if observed in conjunction with compatible clinical findings.
Polymerase chain reaction — Polymerase chain reaction (PCR) based tests for Bartonella on tissue or blood are available commercially. Intraocular fluid may be tested by PCR to confirm the diagnosis of Bartonella neuroretinitis. (See 'Neuroretinitis' above.)
The different PCR tests have utilized amplification of several distinct Bartonella gene regions [24,79,80]. Although these PCR tests have high specificity and can distinguish among the different Bartonella species, the sensitivity has not been optimal, with an estimated range of 40 to 76 percent.
When PCR is performed on tissue specimens, the timing of the biopsy may influence the results. As an example, one study found that PCR testing is more likely to be positive if it is performed during the first six weeks of infection [21]. In this study of 61 patients with CSD (defined as a compatible clinical presentation and serologic evidence of B. henselae infection), PCR was positive in only 10 of the 212 lymph node specimens on which this test was performed; 9 of the 10 patients with a positive result had a duration of illness of less than six weeks.
PCR testing of blood should not be used for routine evaluation of patients with suspected CSD. In one report, the sensitivity of PCR testing of serum samples in patients with CSD lymphadenitis was <20 percent [81]. Although it is reasonable to perform PCR testing of blood in persons with atypical manifestations of CSD or in those with a serious systemic illness, the sensitivity is still low. As an example, in a study of patients with Bartonella endocarditis, PCR was positive in 25 of 70 (33 percent) serum samples, compared with 48 of 52 (92 percent) of PCR tests performed on valve tissue [82]. (See "Endocarditis caused by Bartonella".)
Skin testing — The CSD skin test, which was one of the tests incorporated into the original diagnostic criteria for CSD, is no longer used since other more specific and sensitive diagnostic tools are preferred [1,2,6]. In addition, the skin test antigen is not widely available, is not standardized, and is not approved by the US Food and Drug Administration (FDA) [1].
DIFFERENTIAL DIAGNOSIS
Fever and lymphadenopathy — When evaluating a patient with lymphadenopathy and fever, it is important to consider alternative and/or concurrent diagnoses, including infectious and noninfectious disorders. Topic reviews that discuss the evaluation of patients with lymphadenopathy are found elsewhere. (See "Cervical lymphadenitis in children: Etiology and clinical manifestations" and "Evaluation of peripheral lymphadenopathy in adults" and "Peripheral lymphadenopathy in children: Etiology", section on 'Localized lymphadenopathy'.)
The presence of tender lymph nodes suggests an infectious cause. The differential diagnosis depends, in part, on the individual's symptoms, where they have traveled or resided, and if they have had close contact with animals or someone who is ill [34,83]. As examples:
●Bacterial adenitis – Bacterial adenitis is typically caused by Staphylococcus aureus or group A Streptococcus. CSD should be considered if a patient fails to respond to an initial antimicrobial regimen directed against these common bacterial pathogens, especially if the patient has epidemiologic risk factors for CSD (eg, exposure to kittens or cats). (See "Group A streptococcal tonsillopharyngitis in children and adolescents: Clinical features and diagnosis" and "Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum", section on 'SSTI'.)
●Mycobacterial infections – Mycobacterial infections (both M. tuberculosis and nontuberculous mycobacteria) can cause lymphadenopathy. Although it is difficult to differentiate tuberculosis from other causes of lymphadenitis on clinical grounds, tuberculosis should be suspected in patients from endemic regions. The diagnosis of mycobacterial lymphadenitis is established by histopathologic examination along with acid-fast bacilli smear and culture of lymph node material. (See "Tuberculous lymphadenitis" and "Nontuberculous mycobacterial lymphadenitis in children".)
●Viral-associated lymphadenopathy – Viral-associated lymphadenopathy is often associated with infection due to Epstein-Barr virus, cytomegalovirus, or HIV. Such patients typically present with diffuse lymphadenopathy, whereas lymphadenopathy associated with CSD is usually limited to the node(s) near the site of inoculation. In addition, patients with viral-associated lymphadenopathy may have epidemiologic risk factors for a specific viral infection, such as a sick contact or a high-risk exposure. (See "Clinical manifestations and treatment of Epstein-Barr virus infection", section on 'Primary infection' and "Epidemiology, clinical manifestations, and treatment of cytomegalovirus infection in immunocompetent adults", section on 'CMV mononucleosis' and "Acute and early HIV infection: Clinical manifestations and diagnosis", section on 'Clinical features'.)
●Toxoplasmosis – Both toxoplasmosis and CSD are associated with adenopathy and cat exposure. However, in contrast to toxoplasmosis, the lymph nodes in patients with CSD are usually tender, often have erythema of the overlying skin, and occasionally suppurate. Serologic testing or biopsy can help differentiate between these two conditions. (See 'Lymphadenopathy' above and "Toxoplasmosis: Acute systemic disease".)
●Other pathogens – Lymphadenopathy accompanied by a cutaneous inoculation lesion can be caused by Nocardia species, Francisella tularensis, Erysipelothrix rhusiopathiae, Bacillus anthracis, or Yersinia pestis. Other rare infectious causes of lymphadenopathy include histoplasmosis and sporotrichosis. Evaluation for a specific pathogen should be guided by the patient's exposure history (eg, fleas, ticks, water) and the location of the primary lesion. (See "Tularemia: Clinical manifestations, diagnosis, treatment, and prevention", section on 'Clinical syndromes' and "Erysipelothrix infection" and "Clinical manifestations, diagnosis, and treatment of plague (Yersinia pestis infection)" and "Clinical manifestations, diagnosis, and treatment of plague (Yersinia pestis infection)", section on 'Clinical manifestations' and "Pathogenesis and clinical manifestations of disseminated histoplasmosis", section on 'Clinical manifestations' and "Clinical features and diagnosis of sporotrichosis", section on 'Clinical presentation and differential diagnosis' and "Nocardia infections: Epidemiology, clinical manifestations, and diagnosis", section on 'Skin'.)
Malignancies may be confused with CSD, including lymphoma, breast cancer, and sarcoma [84]. Other noninfectious causes include congenital and acquired cysts, Kawasaki disease, Kikuchi disease, and sarcoidosis. (See "Clinical presentation and initial evaluation of non-Hodgkin lymphoma" and "Kawasaki disease: Clinical features and diagnosis" and "Kikuchi disease" and "Overview of extrapulmonary manifestations of sarcoidosis".)
Neuroretinitis — For patients with neuroretinitis, etiologies other than CSD that should be considered include sarcoid papillitis, syphilitic perineuritis, tuberculosis, Lyme disease, and rarely toxoplasmosis, toxocariasis, and leptospirosis. Pseudotumor cerebri can also mimic the much less frequent bilateral CSD. (See "Clinical manifestations of Lyme disease in adults", section on 'Ocular manifestations' and "Syphilis: Epidemiology, pathophysiology, and clinical manifestations in patients without HIV", section on 'Neurologic findings' and "Idiopathic intracranial hypertension (pseudotumor cerebri): Clinical features and diagnosis" and "Toxoplasmosis: Ocular disease".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Cat scratch disease (The Basics)")
●Beyond the Basics topic (see "Patient education: Animal and human bites (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Microbiology – Cat scratch disease (CSD) is an infectious disease that is typically characterized by self-limited regional lymphadenopathy. Bartonella henselae is the etiologic agent in most cases of CSD. (See 'Introduction' above and 'Microbiology' above.)
●Transmission – Multiple lines of evidence have directly linked CSD to exposure to cats, especially young cats and cats with fleas. CSD can result from a cat scratch or bite, as well as from a flea bite. It can also be spread via contact with cat saliva with a person's broken skin or mucosal surfaces (eg, mouth and eyes). (See 'Epidemiology' above.)
●Clinical manifestations – In most children (85 to 90 percent), CSD manifests as a localized cutaneous and lymph node disorder, located near the site of organism inoculation. However, in some individuals, the organisms disseminate and infect the liver, spleen, eye, bone, or central nervous system. Patients with localized disease generally have a self-limited illness, whereas those with disseminated disease can have severe, or even life-threatening complications. (See 'Clinical manifestations' above.)
●Approach to diagnosis – For patients with CSD, a probable diagnosis is based upon a combination of clinical findings and a reported exposure to kittens, cats, or fleas. In such patients, the diagnosis is often supported by a positive serologic test for B. henselae. However, a negative serologic test should not rule out the diagnosis, and it is reasonable to initiate empiric therapy based upon a presumptive diagnosis. (See 'Approach to diagnosis' above and 'Serology' above.)
●Role of biopsy – A lymph node or tissue biopsy is not routinely required for most patients who present with characteristic signs and symptoms of CSD, although it may be warranted in certain circumstances, such as a delayed resolution of systemic symptoms (eg, greater than five to seven days), or if an alternative diagnosis (eg, lymphoma or tuberculosis) is suspected. If a biopsy sample is obtained, testing should include histology, Warthin-Starry staining, and a B. henselae polymerase chain reaction (PCR) test, as well as testing to investigate for other disorders. (See 'Approach to diagnosis' above and 'Diagnostic tests' above and 'Differential diagnosis' above.)
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