AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

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• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Background

Catscratch disease (CSD), also known as catscratch fever or subacute regional lymphadenitis, is caused by infection with the gram-negative bacillus Bartonella henselae. Typically a benign and self-limited disease in patients who are immunocompetent, only a small percentage of patients have complications involving the skin, lymph nodes, eyes, liver, spleen, or nervous system. Infection of immunocompromised patients with the same organism leads to a very different disease, bacillary angiomatosis-peliosis, which is characterized by angioproliferative lesions resembling those of Kaposi sarcoma in the skin, liver, spleen, bone, and other organs.

Henri Parinaud¹ sometimes is given credit for the first description of CSD in 1889. However, his oculoglandular syndrome of conjunctivitis with an enlarged preauricular lymph node ultimately was shown to be only a small subset of the possible clinical presentations of CSD, the result of inoculation of the CSD agent into the conjunctivae. Parinaud did not make the association with cat exposure; thus, his contribution is of limited scope.

The history of CSD has been reviewed comprehensively by Carithers² in 1970 and by Margileth³ in 1987 and is summarized here.

Debre and a colleague, Semelaigne, observed an unusual case of suppurating epitrochlear adenitis in a 10-year-old boy at the University of Paris and noted a number of cat scratches on the affected side. These were believed to be portals of entry for tubercle bacilli. When the tuberculin skin test results turned out to be negative, the investigators pursued an infectious cause of feline origin. While bacteriologic investigations yielded no clues, the physicians continued to observe similar cases of spontaneously remitting regional lymphadenitis associated with cat scratches in their pediatric population. Debre postulated tularemia, pasteurellosis, infectious mononucleosis, or tuberculosis as possible etiologic agents, but with no convincing proof.

Foshay, a microbiologist at the University of Cincinnati, suspected CSD to be a possible manifestation of tularemia. On meeting Debre in 1947, the 2 investigators compared notes on "catscratch disease" (Debre) and "cat fever" (Foshay). Foshay had produced an antigen from the pus of affected patients and achieved what was believed to be a diagnostic reaction after intradermal injection. Debre and his colleagues subsequently developed a similar antigen and demonstrated reactions in both old and new cases of CSD. These results⁴ were presented and published in 1950. These investigators also recorded failure of transmission of CSD to 15 different species of animals and possible human-to-human transmission in 1 of 4 cases.

In 1951, Greer and Keefer⁵ published the first report of CSD in American literature, in which they described a broader spectrum of CSD manifestations. In the late 1950s, William Warwick of the University of Minnesota collaborated with Robert Good, MD, in an attempt to transmit CSD to "every variety of lab animal from the monkey to the mouse." Their only positive result was the development of cutaneous lymphadenopathy in a monkey given intracerebral injections of ground lymph nodes and pus. The first thorough review of the world's literature, published in 1967, included 567 references and detailed the manifold clinical presentations. The landmark publication⁶ of a series of 1200 cases evaluated by one observer put the varied clinical presentations into perspective and provided the first realistic analysis of the spectrum of disease.

Discovery and classification of the etiologic agent for CSD is one of the triumphs of modern microbiology. The elegance and power of molecular taxonomy applied to the CSD agent revealed unexpected connections with other well-recognized infectious diseases and a deeper understanding of the pathogenesis of CSD.

Both viruses and Chlamydia had been proposed as possible etiologic agents for CSD, until a small gram-negative motile coccobacillus was observed in infected lymphatic tissue using a Warthin-Starry stain and Brown-Hopp tissue Gram stain in 1983 at the Armed Forces Institute of Pathology.⁷ In 1984, Margileth et al,⁸ using the same staining technique, demonstrated identical organisms in biopsy specimens taken from CSD inoculation papules. The first successful isolation and culture of the CSD organism was performed by English et al⁹ in 1988. Their further studies fulfilled Koch's postulates, and the organism was determined to be the cause of CSD.

One of the isolates from the study by English et al was investigated at the US Centers for Disease Control and Prevention, along with additional specimens from Tripler Army Medical Center in Honolulu. From these specimens, the CSD organism was determined to be a new entity and given the name Afipia (from Armed Forces Institute of Pathology) felis.

Reports associating another agent (Rochalimaea henselae) with CSD began appearing in 1992. Although they are not closely related, R henselae and A felis are members of the alpha-2 subclass of Proteobacteria and share a similar microscopic appearance and affinity for the Warthin-Starry stain. R henselae already had been implicated in the pathogenesis of bacillary angiomatosis, an angioproliferative condition observed in patients who are immunocompromised. Reports of R henselae–associated CSD appeared, and new immunological data subsequently supported a major role for R henselae as the etiologic agent in CSD. Although R henselae now is believed to be the principal pathogen in CSD, both organisms have been reported in some patients with CSD.¹⁰

When the sequences of 16S bacterial rRNA from R henselae and Bartonella were compared, these organisms were determined to be so clearly closely related that they belonged in the same genus. Because Bartonella had historical precedence, R henselae was renamed Bartonella henselae.

A Medscape General Medicine article that may be of interest is "Do Bartonella Infections Cause Agitation, Panic Disorder, and Treatment-Resistant Depression?" 

Pathophysiology

Feline infection with B henselae is common and asymptomatic. In the United States, 28% of surveyed cats had antibodies against the organism. In California, blood cultures were positive in 56% of domestic cats younger than 1 year and in 34% of cats older than 1 year. More than three fourths of all cats in California had antibodies to B henselae as evidence of prior infection; however, only 21% of pet cats were bacteremic, compared with 61% of stray cats.

A similar survey of cats in the Baltimore area found seropositivity in 12-14% of domestic cats versus 44% of feral animals. Cats can be asymptomatically bacteremic for months, even while antibody titers are developing. The organism has been isolated from fleas residing on infected cats. Studies have shown that flea-vectored transmission of infection among cats occurs with high efficiency and that in the absence of fleas, infected cats do not transmit the infection to uninfected cats. Although flea-vectored transmission to humans has not been documented, it could explain some cases in which the patient has no history of exposure to cats. Treatment of cats with doxycycline is associated with a reduction of bacteremia, but whether such treatment prevents relapse or reinfection is unknown.

Familial and household clustering of cases of CSD have been reported. However, only one member of a family in contact with an infected cat usually is affected. Zangwill et al¹¹ found an 18% prevalence rate of seropositivity to B henselae among family members of patients with CSD. Upon further questioning, 43% of these individuals reported symptoms consistent with CSD during the previous 2 months. In the same study, matched control subjects not exposed to cats exhibited a 3.6% seropositivity rate. Carithers⁶ found similar results in a series of 1200 patients; 18.5% of asymptomatic family members had positive CSD antigen skin test results.

Frequency

United States

CSD is not a reportable infection. Seroprevalence rates vary greatly throughout the world, ranging from 0.6-37%. Approximately 22,000 cases occur annually in the United States. The prevalence is estimated to be 9.3 cases per 100,000 population. Cases of CSD occur throughout the United States. The incidence is greater in regions with higher temperatures and humidity (eg, Hawaii, Pacific Northwest, southeastern states, coastal California), while Alaska, the Rocky Mountains, and midwestern states have a prevalence lower than the median. Incidence peaks in the fall and winter months. These trends parallel the feline flea population density. The number of pediatric hospitalizations in the United States for CSD complications was estimated at 437 cases in 2000 children (0.60 in 100,000 children younger than 18 y and 0.86 in 100,000 children younger than 5 y).

Mortality/Morbidity

CSD generally is a self-limited infection, manifesting as a subacute regional lymphadenitis persisting for 3 weeks or more. Very few deaths (2 reported^{12, 13}) from CSD have occurred in immunocompetent patients. However, significant morbidity occurs in 5-10% of cases, usually because of involvement of the central or peripheral nervous system or because of multisystem disseminated disease.

Race

CSD has no documented racial predisposition.

Sex

In some case series, a slightly higher incidence of CSD appears to occur in male patients, while others show equal rates between males and females. One hypothesis to explain a greater incidence among males is the tendency toward rougher play with kittens and cats.

Age

CSD affects persons in all age groups, but most patients are younger than 21 years. The younger age of individuals most likely to acquire CSD reflects their likelihood of exposure to the major risk factor (ie, kittens). A bias may exist in the literature because pediatricians have collected many of the large case series. Adults are more likely to manifest atypical features of CSD.

CLINICAL

Section 3 of 10  

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• Clinical
• Differentials
• Workup
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• Follow-up
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History

Margileth et al studied a series of 1312 patients referred for chronic lymphadenopathy. The diagnosis of CSD was confirmed in 1174 patients via catscratch antigen (CSA) testing, similar to the tuberculosis purified protein derivative (PPD) test. Of this cohort, 88% exhibited a typical course characterized by lymphadenopathy lasting an average of 3 months.  

• Fever and malaise/fatigue were described in approximately one third of patients, none of whom was symptomatic for longer than 1 month.
• An unusual presentation was experienced by 11.6% of the cohort. Of these, Parinaud oculoglandular syndrome (POS) was found in half the patients, followed in decreasing order of frequency by encephalopathy (2.3%), systemic disease (2%), erythema nodosum (0.6%), atypical pneumonia (0.2%), breast tumor (0.2%), and thrombocytopenic purpura (0.1%).
• A subset of patients with severe systemic disease was observed for 7 years.
• Differences between the group with severe disease and those patients with typical CSD included more frequent primary skin or mucous membrane lesions, fewer animal contacts and cat scratches, greater frequency and duration of fevers, and other constitutional symptoms.
• Skin eruptions (eg, urticaria, vesiculopapular lesions, erythema nodosum) occurred 4 times more often in the severe CSD group compared with the typical CSD group. Demographics of the severe disease group included a greater percentage of adult males, who tended to have larger and multiple affected lymph nodes. Fortunately, all patients fully recovered. The greatest period of recuperation was 4.5 years.
• Another interesting finding from this series was evidence of recurrent CSD. Three of the patients in the severe disease category experienced recurrences at 4- to 20-month intervals. One patient presented with recurrent cervical lymphadenitis, whereas the other 2 patients experienced systemic symptoms with periodic fever, malaise, headache, and weight loss. In one patient, the episodes lasted 1-3 months, with a 20-month interval, while the second patient experienced similar episodes with a 10-month interval.

The incubation period ranges from 3-30 days. Patients may remember a self-healing lesion resembling an insect bite on the hand, arm, face, or neck. The most common presenting symptom of patients seeking medical care is tender regional lymphadenopathy, typically cervical, axillary, or epitrochlear nodes. Approximately 50% of patients experience systemic symptoms (eg, fever, headache, malaise, myalgias, arthralgias, exanthemas).

When questioned, patients may recall being scratched, licked, or bitten by a cat in the previous 2-8 weeks. The scratch is not mandatory because transmission can occur by petting alone with subsequent self-inoculation via a mucous membrane, skin break, or conjunctiva. Chronic fluctuant lymphadenitis develops in approximately 1 month and usually occurs in a single node or group of regional nodes draining the inoculation site. More than 65% of cases involve the nodes in the axillae or anterior or posterior triangles of the neck. Lymphadenopathy at multiple sites occurs in 37% of cases. Lymphadenopathy remains regional and regresses over a period of 2-4 months. Rarely, it may persist for a year or more. Approximately 10-15% of nodes suppurate.

Other problems (ie, atypical CSD) occur in approximately 10% of cases. The following are considered atypical manifestations of CSD:  

• POS is the most common atypical presentation of CSD and is characterized by unilateral conjunctivitis with adjacent preauricular lymphadenopathy. Examination of the palpebral conjunctiva on the involved side reveals either a characteristic granulomatous lesion 2-4 mm in diameter or a frank scratch. While POS has been associated with other infections (eg, tuberculosis, tularemia, lymphogranuloma venereum), it most commonly is associated with CSD. Prognosis is identical to that of typical CSD.
• Central nervous system involvement can include encephalopathy, transverse myelitis, cranial or peripheral nerve involvement, and neuroretinitis.
• • Encephalopathy is a complication of CSD described in up to 5% of patients, occurring 1-6 weeks after typical CSD.^{15, 16, 17, 18} Most patients are young, in parallel to the spectrum of patients diagnosed with CSD. Symptoms usually begin with confusion or combative behavior and rapidly progress within hours to seizures and coma. Seizures occur in one half to three fourths of patients and may be self-limited or progress to status epilepticus. Coma complicated by respiratory depression requiring intubation and ventilatory assistance often is reported. Laboratory findings from examination of cerebrospinal fluid (CSF) often are normal. However, when CSF results are abnormal, no consistent patterns emerge. Abnormal findings from EEG, when observed, are nonspecific and transient. Recovery is usually complete in 2-10 days, with no sequelae. CT tomographic or MRI study findings of the brain are usually normal or reveal transient abnormalities.
  • Transverse myelitis presenting as Brown-Sequard syndrome has occurred in a 44-year-old man.¹⁹ The patient experienced rapid resolution of symptoms in a few days and was asymptomatic within 3 months.
  • Cranial or peripheral nerve involvement may occur. Two children with oculoglandular CSD were reported to have developed transient facial nerve paresis. Three adult women reportedly developed peripheral neuritis lasting 1-4 months associated with the onset of lymphadenitis due to CSD.
  • Neuroretinitis (Leber stellate neuroretinitis, Leber idiopathic stellate retinopathy,²⁰ Leber idiopathic stellate maculopathy) was first described in 1916. Patients present with painless, unilateral (rarely bilateral) decreased vision associated with central scotomata. Funduscopic examination reveals optic disc swelling and macular star formation. Permanent loss of vision is not reported, although recovery may take 1-3 months.
• Hepatosplenic CSD is a rare form of atypical CSD found in patients who are immunocompetent. Individuals present with daily fevers up to 104°F (40°C) and no identifiable cause. Physical examination findings are usually normal, with occasional detection of well-healed cutaneous scars secondary to cat scratches. Abdominal discomfort, without focal findings, is commonly reported.  Lymphadenopathy is present in approximately half the cases. Hepatosplenomegaly, jaundice, and elevated transaminase levels are not associated with this condition. The diagnosis is based on characteristic filling defects in the liver, spleen, or both as detected by ultrasonography, CT scanning, and a positive B henselae titer result. Intravenous administration of aminoglycoside antibiotics has been reported to be helpful. Most patients become afebrile within 48 hours of initiating treatment; however, in a few cases, fever has persisted for up to a month, even with antibiotic therapy.
• Blood culture–negative endocarditis has been reported.²¹ Bartonella species account for approximately 3% of all cases of endocarditis, and, now, many cases of blood culture–negative endocarditis are believed to be the result of infection with Bartonella species. Some cases diagnosed as Chlamydia endocarditis also are likely to be caused by Bartonella species because of the high prevalence of cross-reacting antibodies. Of 22 patients proven to have Bartonella endocarditis, 4 were infected with B henselae. Contact with cats was a significant risk factor in this group.
• Osteomyelitis secondary to B henselae, while still rare, is being reported with increased frequency. Hajjaji et al²² reviewed the literature and found 47 cases that met criteria and had sufficient data. They noted the vertebral column and pelvic girdle were the most commonly affected locations. MRI, scintigraphy, and CT scanning can all be used to demonstrate bone involvement. Immunosuppression was not a risk factor. Affected patients responded well to therapy without significant long-term effects. In a case report, a child with osteomyelitis and epidural extension confirmed by polymerase chain reaction responded to intravenous clindamycin and gentamicin.²³

Physical

Careful examination may reveal an inoculation papule in up to 90% of patients. Given the tendency to hold cats against one's chest, the lesion is found most often on the head or upper extremities. Include the scalp, finger web spaces, eyelids, and conjunctiva in a thorough inspection. Multiple sites may be infected.

The initial lesion evolves from a small, 2- to 5-mm reddish-brown macule or vesicle to a papule or pustule over the course of several days. Often, it is mistaken for an insect bite. Lesions typically are nonpruritic and heal in days to months without scarring.

Conjunctival CSD may manifest as nonsuppurative conjunctivitis or ocular granuloma.

Lymphadenitis involving 1 or more nodes in the proximal drainage area of regional lymphatics occurs in all CSD cases approximately 2 weeks (range 5-50 d) after initial inoculation. Nodes are tender and range from 1-5 cm, occasionally exceeding 10 cm. The overlying skin may be erythematous, but only rarely is an associated cellulitis present. The most commonly involved nodes are in the cervical, axillary, inguinal, femoral, preauricular, supraclavicular, and epitrochlear areas. Lymphadenopathy involving multiple sites occurs in approximately one third of patients. Lymphadenitis resolves over 2-4 months, rarely persisting longer than a year.

Other dermatologic manifestations occur in approximately 5% of patients and are more likely to occur in patients with more severe or atypical disease. These manifestations include macular, maculopapular, morbilliform, and petechial rashes. They typically are nonpruritic and resolve in days to weeks. Cases of erythema multiforme, erythema nodosum, erythema annulare, and ecchymoses associated with thrombocytopenia have been reported in patients with CSD, but these are rare.

Causes

B henselae, the etiologic agent for CSD, is a small, fastidious, slow-growing, gram-negative, aerobic, nonmotile, pleomorphic bacillus. Although domestic cats are the principal reservoir for this bacterium, occasional cases of infection associated with dog and monkey bites have been reported. Another species, Bartonella clarridgeiae, has rarely been associated with cases of CSD.

Risk factors for acquiring CSD include ownership of a cat younger than 12 months, having been bitten or scratched by a kitten, and owning at least 1 kitten with fleas. More than 90% of patients with CSD have a history of exposure to cats, and 75% of patients have a history of a cat scratch or bite, usually from a healthy kitten.

DIFFERENTIALS

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Other Problems to be Considered

Consider all causes of subacute and chronic lymphadenopathy and include the following:

• Typical and atypical mycobacterial infection (see Atypical Mycobacterial Infections)
• Nonspecific bacterial lymphadenitis
• Lymphogranuloma venereum
• Tularemia
• Brucellosis
• Infectious Mononucleosis
• Syphilis
• Toxoplasmosis
• Systemic mycoses
• Sarcoidosis
• Nodular lymphomas
• Drug reactions (see Drug Eruptions) 

Consider the following additional diagnoses with the presence of persistent skin papules and regional lymphadenopathy:

• Leishmaniasis
• Nocardiosis
• Fungal infections (eg, coccidioidomycosis, sporotrichosis, histoplasmosis).

Because the clinical manifestations of infection with B henselae are different in patients who are immunocompromised, an entirely different differential diagnosis is appropriate. Bartonella infection leads to vasculoproliferative lesions, namely bacillary angiomatosis (B henselae, Bartonella quintana) and peliosis (B henselae only). The clinical differential diagnosis includes malignant neoplasms (eg, Kaposi sarcoma, angiosarcoma) and benign reactive conditions (eg, pyogenic granuloma, angiolymphoid hyperplasia with eosinophilia).

WORKUP

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Lab Studies

No specific guidelines are available for the diagnosis of CSD. The combination of clinical presentation and a history of exposure to a cat usually leads to the diagnosis. Studies can be used to support the diagnosis. Positive laboratory serology findings can confirm the diagnosis, but a negative result does not rule out disease. A biopsy of skin or lymph node with characteristic histopathology is also helpful when the diagnosis is in question. B henselae isolation from tissue has low yield.

Typically, the diagnosis is based on the presence of 3 of the 4 following criteria:  

• Contact with a cat in association with a scratch or lesion of the dermis, eye, or mucous membrane
• Positive skin test result for CSD
• Regional lymphadenopathy in the absence of other causes as ascertained by PPD testing, serologic studies, and cultures of lymph node aspirates
• Characteristic histopathology in a biopsy specimen of skin or lymph node

CSA skin testing, which uses a preparation derived from infected lymph node tissue of other infected humans, is similar to the intradermal tuberculin PPD procedure. The antigen test is no longer widely available because of concern for the potential transmission of hepatitis viruses, HIV, and prions.

Skin testing is no longer warranted and largely has been replaced by antibody titer testing using indirect immunofluorescent antibody, hemagglutination, and enzyme-linked immunosorbent assay techniques. Of patients suspected of having CSD, 88% have detectable antibody, versus 3% of healthy controls. The timing of immunoglobulin G and immunoglobulin M response is variable, and cross-reactivity between different Bartonella species may occur. In one study, 25% of patients remained immunoglobulin G seropositive for longer than 1 year. Antibody kinetics do not reliably predict severity or duration of disease. The prevalence of seropositivity in cats living in the same house as a human with CSD is 81%, versus 14-44% in unselected households.

Lymph node biopsy generally is not indicated in typical cases of CSD, given the associated morbidity and expense. Node aspiration in patients suspected of having CSD traditionally has been discouraged for fear of fistula formation.

Immunofluorescence testing on both serum and lymph node smears improves the sensitivity and specificity of CSD diagnosis to 97% (based on at least one positive test result). Additionally, consider performing a biopsy of skin or affected lymph node in cases of possible malignancy or in an unclear presentation in an immunocompromised host.

Finally, findings from the CBC count are usually normal, although a mild leukocytosis or eosinophilia may be present. The erythrocyte sedimentation rate may be mildly or moderately elevated. The PPD test should be nonreactive.

Imaging Studies

Imaging procedures are not diagnostic in patients with CSD but may be helpful for excluding other conditions in the differential diagnosis. Atypical CSD may exhibit hepatic or splenic lesions, usually round or oval, ranging from 3-30 mm. They are hypodense on noncontrast CT scans. Injection of contrast material may yield hypodense, isodense, or marginally enhanced lesions when compared with normal parenchyma. These lesions have been observed to spontaneously resolve or calcify over weeks to months.

MRI has been used to diagnose multifocal bone marrow involvement in CSD that has shown negative results based on plain radiography findings, radionucleotide scintigraphy, and CT scanning. MRI is also considered more reliable for the assessment of soft tissue involvement and follow-up of boney lesions than plain radiography.

Procedures

Skin biopsy of the inoculation papule may be diagnostic. Additionally, biopsy of affected nodes is indicated only when attempting to establish a diagnosis other than CSD.

Aspiration of suppurating nodes is both a diagnostic and therapeutic procedure. Treat recurrence of suppuration by incision and drainage. The risk of fistulous sinus tract formation is small. This has been reported only in cases of atypical mycobacterial lymphadenopathy mistaken for CSD.

Histologic Findings

Skin

The dermis contains variously shaped (round, triangular, stellate) areas of necrosis or necrobiosis surrounded by an inner zone of palisading epithelioid histiocytes with a few multinucleated giant cells and an outer zone of lymphocytes. Organisms (visualized with the Warthin-Starry stain or the Brown-Hopp modification of the Gram stain) appear in the necrotic areas singly, in chains, or in clusters.

Lymph nodes

Focal areas of necrosis with neutrophilic infiltration occur near the germinal centers of lymph nodes. Organisms line the vascular sinuses. When necrosis is present, organisms may be seen within histiocytes as well as extracellularly in the necrotic areas and in the lumina of thrombosed blood vessels. Organisms are fewer in number in necrotic areas extensively infiltrated with neutrophils. With disease progression, granulomas may appear with central necrosis and multinucleated giant cells. Late findings include stellate microabscesses, which may fuse within suppurating nodes.

Liver

Hepatic parenchyma may be replaced by zones of organizing granulation tissue containing focal areas of granulomatous inflammation with stellate areas of central necrosis. The necrotic areas are infiltrated with neutrophils and are surrounded by palisading fibroblasts.

TREATMENT

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Medical Care

Controlled studies on treatment options for CSD are lacking; thus, treatment recommendations are based on case reports, reviews, a single controlled trial, and anecdotal data. For most patients with mild or moderate CSD, only conservative symptomatic treatment is recommended because the disease is self-limited.

Margileth et al²⁴ reported the results of therapy for catscratch antigen–proven CSD with 18 different antimicrobials in 268 adult and pediatric patients. They concluded that the following 4 antibiotics were the most effective for patients with severe CSD:

• Rifampin - Efficacy of 87%
• Ciprofloxacin - Efficacy of 84%
• Gentamicin intramuscularly - Efficacy of 73%
• Trimethoprim/sulfamethoxazole (TMP-SMZ) - Efficacy of 58%

These agents were considered moderately to highly effective. They defined effective as 3 days or more of antibiotic treatment and patient improvement (reduced or resolved lymphadenopathy, declining erythrocyte sedimentation rate, and decreased inflammatory and constitutional symptoms) within 3-10 days. Severe disease was defined as persistent high fever (>103.1°F [>39.5˚C]) with severe systemic signs (eg, malaise, fatigue, blindness, headache) and lymphadenitis. Moderate disease included patients with fever (100.9-103.1°F [38.3-39.5˚C]) and fewer systemic symptoms, and mild disease was those with low-grade fever and few or no systemic signs.

The general recommendation is that immunocompromised patients with CSD receive antibiotic treatment, with the choice of antibiotic being the same as their immunocompetent counterparts. Somewhat paradoxically, patients with AIDS and bacillary angiomatosis-peliosis frequently respond to a variety of commonly used antibiotics. Response to erythromycin, isoniazid, rifampin, doxycycline, and ethambutol is reported by Koehler et al.^{25, 26} If an immunocompromised patient has treatment relapse, then prolonged treatment (4-6 mo) is recommended, although this is based on anecdotal data.

Importantly, because of the potential risk of arthropathy, caution should be used if considering the use of fluoroquinolones in patients younger than 18 years.

Supportive treatment includes hydration and analgesics. Warm moist compresses may be applied to tender nodes. Avoid unnecessary manipulation.

Surgical Care

Perform aspiration of suppurative nodes, as detailed in Procedures.

Activity

Neither bed rest nor isolation is indicated.

MEDICATION

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Margileth et al²⁴ reported the results of antibiotic therapy with 18 different antimicrobials for catscratch antigen–proven CSD in 268 adult and pediatric patients. See Treatment for reported efficacy and precautions.

Drug Category: Antibiotics

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting. Antibiotic selection should be guided by blood culture sensitivity whenever feasible.

FOLLOW-UP

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Deterrence/Prevention

• Pet quarantine, disposal, or euthanasia is unnecessary.
• Although doxycycline treatment of cats is associated with decreased B henselae bacteremia, this treatment has not been shown to reduce the risk of cat-to-human transmission.
• Feline B henselae bacteremia has been reported to last from weeks to months, with 100-fold fluctuations in bacteremic levels and intermittent negative cultures.
• The natural history of feline infection and infectivity remains unknown.
• Given the established link between flea infection and B henselae transmission, common sense measures seem prudent (eg, avoiding stray cats, keeping pets free of fleas).

MULTIMEDIA

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Media file 1:  Papulopustular lesions of a primary inoculation site on the hand of a 16-year-old patient. These lesions had been present for approximately 3 weeks. A catscratch antigen skin test was positive with 15-mm induration. No treatment was administered, and her condition resolved spontaneously in 2.5 months. Courtesy of Andrew Margileth, MD.
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Media file 2:  A crusted primary inoculation papule on the neck of a 4-year-old child. Note the adjacent lymphadenitis. This patient had contact with cats and had multiple scratches. Courtesy of Andrew Margileth, MD.
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Media file 3:  This 10-year-old child had contact with dogs but not cats. The impressive lymphadenitis had been present for 5 weeks and was not tender. Pathologic examination of a biopsy specimen of the lymph node revealed nonspecific changes. She had a positive catscratch disease skin test result and negative purified protein derivative skin test results. Treatment with cephalexin was administered with a good response. Complete resolution occurred in 4.5 months. Courtesy of Andrew Margileth, MD.
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Media file 4:  This 13-year-old girl developed fatigue and malaise after being licked and scratched by a cat. The typical conjunctival granuloma was accompanied by a parotid mass and intraparotid adenitis. No treatment was administered, and all her signs and symptoms resolved in 3 months. Courtesy of Andrew Margileth, MD.
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Media file 5:  This 9-year-old boy developed catscratch disease (CSD) encephalitis and a papular pruritic dermatitis after sustaining cat scratches and developing regional lymphadenitis. He was in a coma for 4 days but experienced a complete and rapid recovery within 3 weeks. Biopsy of the skin rash revealed nonspecific changes. The CSD antigen skin test result was positive. Courtesy of Andrew Margileth, MD.
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Media file 6:  This 2.5-year-old boy was recovering from catscratch disease acquired 10 months before when he developed this neck abscess over a period of 3 weeks. Biopsy revealed caseating granulomas; acid-fast bacillus and Warthin-Starry stain results were negative. Courtesy of Andrew Margileth, MD.
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Media file 7:  This 22-year-old man complained of blindness in his right eye beginning 11 days after an illness characterized by fever, malaise, chills, nausea, and tender left femoral lymphadenopathy. He had a history of cat scratches and had 2 inoculation papules on his thigh. The image of the retina shows papilledema and stellate retinitis. His vision returned to baseline in 3 months. He had no reoccurrence in 3 years of follow-up care. Courtesy of Andrew Margileth, MD.
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Media file 8:  Light micrograph of lymph node tissue showing follicular hyperplasia and focal areas of necrosis. Courtesy of Andrew Margileth, MD.
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Media file 9:  Warthin-Starry stained sections of lymph node showing chains and clusters of organisms. Courtesy of Andrew Margileth, MD.
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REFERENCES

Section 10 of 10

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• Differentials
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• Medication
• Follow-up
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