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Cat scratch disease

McGraw, Mark BSN, RN, CCRN, CEN, CTRN

doi: 10.1097/01.NURSE.0000423960.45625.e3
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Although associated with cats, this infection can be carried by many other creatures, including dogs, horses, and certain ticks and flies. Here's the lowdown on how to recognize cat scratch disease and what to teach patients about it.

Mark McGraw is a direct care nurse at Christiana Care Health System in Newark, Del.

The author has disclosed that he has no financial relationships related to this article.

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Figure

EIGHT-YEAR-OLD HD presents to triage with her mother, who reports that HD has been “sick” for the past 2 weeks. She was seen by her pediatrician the previous week after she was scratched by a feral cat. HD was given cephalexin. HD's mother reports increased listlessness, fever, and enlarged, tender axillary masses that have gradually increased in size over the past 3 days. HD begins to cry and says she wants to go home and check on “Molly and her babies.” HD's mother says Molly is one of several stray cats that have been living in a wooded area behind their house.

HD's mother says she had similar signs and symptoms a few weeks earlier but they spontaneously resolved without medical intervention. After an extensive workup to rule out malignancy and life-threatening infections, HD is diagnosed with cat scratch disease, also known as cat scratch fever.

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Not just cats

Cat scratch disease (CSD) is caused by infection with the Bartonella henselae bacterium. B. henselae is a Gram-negative, slow-growing, aerobic bacillus that invades humans when cat saliva that contains the bacteria comes in contact with broken skin. Cats shed the bacteria through their saliva and leave live bacteria on their claws as they clean themselves. B. henselae causes infection similar to other arthropod-borne illnesses such as Lyme disease.1

B. henselae is a benign condition in cats, and the infected animal doesn't display any signs of illness. Cats don't spread the infection to other cats by biting or scratching; it's spread from cat to cat by the cat flea, Ctenocephalides felis. Humans can't transmit CSD to other humans regardless of contact.2

Felis domesticus, or the common house cat, is the primary reservoir for B. henselae as well as the primary vector responsible for transmission of CSD disease to humans.2 But despite the name “cat scratch,” it's important to understand that felines aren't the only reservoir for this disease, nor are they the only species that can transmit the infection to humans. Canines, coyotes, horses, porpoises, sheep ticks, western black-legged ticks, stable flies, and deer flies have all been documented as reservoirs for the bacteria and can transmit the disease to humans.1 Approximately 5% of CSD cases have a canine source.3

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Epidemiology of CSD

An estimated 22,000 CSD infections occur each year in the United States, most of them between August and January.2 The highest incidences of CSD have been reported in southern, warmer, more humid locations whereas western, drier states have the lowest number of reported cases.2 Warm temperatures coupled with higher humidity is the ideal climate for cat flea reproduction.

CSD tends to peak in late fall to early winter, corresponding with feline reproductive cycles and peaks in flea activity.2 Kittens have been implicated more often in the transmission of CSD because they're more inclined to bite and scratch with playful activity. Some statistics report that younger cats are 15 times more likely to transmit B. henselae, and individuals scratched or bitten by a kitten are 27 times more likely to become infected.3

Most individuals with CSD are under age 21.3 Young boys are more likely to become infected than girls of the same age because boys are more inclined to roughhouse with cats and kittens and be bitten or scratched.3,4

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Pathogenesis and pathophysiology

CSD develops from direct cutaneous inoculation of the B. henselae bacteria by contaminated saliva introduced via scratch or bite. Once inoculation has occurred in an immunocompetent person, macrophages and other first-line immune cells in the tissue attack the bacteria and initiate the inflammatory and immune responses. Macrophages and other antigen-presenting cells migrate into the lymphatic system to elicit a more specific immune response.

Bacteria not destroyed by the primary immune defenses may migrate into the endothelial cells that line blood vessels, where they can survive and replicate.5 But bacteria that infect cells aren't safe from the immune response. The bacteria, while replicating intracellularly, will eventually cause changes and mutations in cellular surface proteins. The immune system recognizes the mutated and abnormal proteins as foreign and attacks these cells through humoral and cell-mediated immunity.

Either way, the presence of the foreign bacterial proteins leads to an immune response that's primarily helper T-cell mediated.2 The response by the helper T-cells facilitates and coordinates the rest of the immune response necessary to rid the body of B. henselae.

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Recognizing CSD

Figure

Figure

The typical presentation of CSD is more likely seen in people under age 60. The earliest sign of infection is the development of a pigmented papule at the site of inoculation (see Seeing the sign). Within 1 to 2 weeks, several small papules develop, but they may be missed because of their small size, an inconsistent presence, or their location in a place not readily visible during physical assessment. The lesions may develop into a vesicular, pustular, or nodular presentation, but this is rare.6

Skin lesions, when present, usually precede the development of regional lymphadenopathy by 1 to 2 weeks.2,6,7 The resolution of the cutaneous papules often coincides with the appearance of enlarged lymph nodes (see Lymph node enlargement). This process is one of the hallmark signs of CSD.3 The lymph nodes that drain the site of inoculation become visibly enlarged and may be painful on palpation.4

This unilateral lymphadenopathy is a classic sign of infection with B. henselae. The most common sites for lymphadenopathy are the axillary, epitrochlear, cervical, supraclavicular, and submandibular lymph nodes.7,8 The overlying skin may be erythematous without evidence of cellulitis.9 They can reach several centimeters in diameter and usually persist for 2 to 4 months, but in rare cases they may remain enlarged for up to a year.9

The most common signs and symptoms of CSD include a prolonged fever of unknown origin, hence the nickname “cat scratch fever.”2 Infection with B. henselae is the third most common cause of a fever of unknown origin in adults and children. Other signs and symptoms include headache, fatigue, generalized malaise, arthralgia, anorexia, and pharyngitis. Adults over age 60 are more likely to present with atypical symptoms such as anorexia, pharyngitis, and weight loss.2,3 Typically, CSD spontaneously resolves within a few weeks to months.

The most common atypical infection, occurring in only a small percentage of individuals with CSD, is Parinaud oculoglandular syndrome.9 This is characterized by conjunctival granuloma, conjunctivitis, and adjacent preauricular lymphadenopathy. It develops from direct inoculation with B. henselae when people rub their eyes or touch their face after being licked, bitten, or scratched by a cat with B. henselae, or by a bite or lick near or in the eye.7 Signs and symptoms are consistent with conjunctivitis. This condition usually isn't painful and produces little to no discharge, but the conjunctiva and sclera can become erythematous and edematous.6,10

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Assessment considerations

A CSD diagnosis is based on findings from the detailed history and physical assessment. Ask patients about recent exposures to cats and other animals. Do they have pets, work with animals, volunteer at an animal shelter, or feed stray or feral cats around their homes?

Assess the skin for the primary inoculation lesion by completely exposing limbs and inspecting all ventral and dorsal surfaces. Include the interdigital spaces and scalp, as well as the skin folds to identify any breaks in the dermis. When assessing the lymph nodes, be sure to fully assess all nodes distal and proximal to the area of inoculation.

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Confirming the diagnosis

Although CSD may be suspected from the patient's history and physical assessment, lab testing is needed to confirm the diagnosis. CSD is usually diagnosed on the basis of a positive serologic test.7

A complete blood cell count is usually within normal limits, although the white cell count may be slightly elevated. An elevated erythrocyte sedimentation rate and C-reactive protein are the most commonly reported lab abnormalities, but neither is specific for CSD.2,4 Elevated liver function tests may indicate systemic disease.4

A diagnosis of CSD is confirmed when three of the four following criteria are present along with regional unilateral lymphadenopathy:9

  • feline or flea fecal material contact, with or without scratch marks or a noticeable inoculation site
  • negative lab screening for oncologic, hematologic, or infectious causes of lymphadenopathy such as tuberculosis and leukemia
  • positive immunoassay or antibody testing for B. henselae with a titer greater than or equal to 1:64
  • biopsy of lymph node, skin, organ, bones, or eye granuloma showing granulomatous inflammation consistent with CSD or a positive Warthin-Starry silver stain.7

Like B. henselae, rabies is also transmitted through the saliva of the infected animal. Inquire about the animal's vaccine status, if known, and contact animal control if the animal's vaccination status is in question.

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Beyond CSD

Complications of CSD include involvement of the liver, spleen, or both. Signs and symptoms include dull episodic periumbilical or upper abdominal pain, organomegaly, and elevated liver function tests in the presence of infection with CSD.8 Neuroretinitis often presents with painless, unilateral visual loss with optic nerve edema and macular exudate.8

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Figure

The most severe neurologic complication associated with CSD is B. henselae encephalopathy, which is characterized by abrupt disorientation or confusion. This may progress to coma 1 to 6 weeks after the patient presents with adenopathy. The patient will likely develop seizures and may develop focal neurologic findings, such as hemiparesis from cerebral vasculitis.6,7,9 Cat scratch encephalopathy should be included in the differential diagnosis of any school-age child with a new onset of seizures.3

Cardiac manifestations of CSD have been documented only in patients with a history of valvular heart disease. Signs and symptoms are consistent with heart failure.8 Cat scratch-induced glomerulonephritis presents similar to immunoglobulin A nephritis: hematuria, proteinuria, and cola-colored urine.8

The rarest complication associated with CSD is B. henselae osteomyelitis, usually found at a site distant from the enlarged lymph nodes, suggesting the bacteria's capability to spread beyond infected lymph nodes.8

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Treatment options

The most effective antibiotic for treating CSD is azithromycin.1,57 Patients who can tolerate azithromycin have a faster rate of decrease in lymph node volume over the first few weeks following treatment.8

For patients allergic to or unable to tolerate azithromycin, alternatives include clarithromycin, trimethoprim/sulfamethoxazole (TMP-SMX), rifampin, doxycycline (for those over age 8), ciprofloxacin, amoxicillin-clavulanate, erythromycin, cephalexin, ceftriaxone, or gentamycin.5 Recommendations for patients with hepatosplenic or other disseminated forms of CSD include rifampin and gentamycin administered for up to 14 days.10 In situations where gentamycin is contraindicated and disseminated disease is confirmed, azithromycin is the acceptable alternative.11

Treatment for patients with neurologic manifestations lasts less than 2 weeks but may continue for up to 6 weeks for patients diagnosed or suspected of having neuroretinitis. Treatment recommendations include doxycycline and rifampin. Doxycycline isn't used in children under age 8; azithromycin or TMP-SMX should be used in its place.

Care for patients with CSD is aimed at symptomatic management. Acetaminophen and ibuprofen are usually adequate for most symptoms including fever, headaches, and myalgias. Dosages for children should be weight-based. Application of heating pads, warm showers, and warm compresses to enlarged, painful lymph nodes may facilitate drainage and alleviate pain.

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Education is key

The most important intervention is the teaching of prevention strategies. According to the CDC, at least 40% of cats are infected with B. henselae at some point in their lives.10 Educate patients, especially children, about the dangers of approaching stray or feral animals. Remind them that infected animals may not appear sick, so they can't tell if an animal is capable of transmitting disease. Hand hygiene following even minimal contact with animals will help rinse away any contaminants or flea residue that may have been picked up with contact.

Prompt intervention and assessment of signs and symptoms, along with teaching preventive measures, can help patients avoid the possible complications of CSD and future infections.

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REFERENCES

1. Mosbacher M, Elliott SP, Shehab Z, Pinnas JL, Klotz JH, Klotz SA. Cat scratch disease and arthropod vectors: more to it than a scratch? J Am Board Fam Med. 2010;23(5):685–686.
2. Schutze GE, Jacobs RF. Bartonella species (cat-scratch disease). In: Long SS, ed. Principles and Practice of Pediatric Infectious Diseases. 3rd ed. Philadelphia, PA: Elsevier; 2008.
3. Nervi SJ. Catscratch disease. Medscape Reference: Drugs, Disease and Procedures. 2011. http://emedicine.medscape.com/article/214100-overview.
4. Shandro JR, Jenkins JG. Wilderness acquired zoonoses: cat-scratch disease. In: Auerbach PS, ed. Wilderness Medicine. 6th ed. Philadelphia, PA: Elsevier, 2012; 1148–1150.
5. Lamps LW, Scott MA. Cat-scratch disease: historic, clinical, and pathogenic perspectives. Am J Clin Pathol. 2004;121(suppl):S71-S80.
6. Florin TA, Zaoutis TE, Zaoutis LB. Beyond cat scratch disease: widening the spectrum of Bartonella henselae infection. Pediatrics. 2008;121(5):e1413-e1425.
7. Spach DH, Kaplan SL. Microbiology, epidemiology, clinical manifestations, and diagnosis of cat scratch disease. UpToDate. 2012. http://www.uptodate.com.
8. Stechenberg BW. Cat-scratch disease (bartonella henselae). In: Kliegman RM, Stanton BF, St. Geme JW, Schor NF, eds. Nelson Textbook of Pediatrics. 19th ed. Philadelphia, PA: Saunders; 2011:983–987.
9. Margileth AM. Recent advances in diagnosis and treatment of cat scratch disease. Curr Infect Dis Rep. 2000;2(2):141–146.
10. Centers for Disease Control and Prevention. Cat scratch disease (Bartonella henselae infection). 2011. http://www.cdc.gov/healthypets/diseases/catscratch.htm.
11. Spach DH, Kaplan SL. Treatment of cat scratch disease. UpToDate. 2007. http://www.uptodate.com.
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