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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
By Mark McGraw, BSN, RN, CCRN, CEN, CTRN

EIGHT-YEAR-OLD HD presents to causes infection similar to other southern, warmer, more humid loca-
triage with her mother, who reports that arthropod-borne illnesses such as tions whereas western, drier states
HD has been “sick” for the past 2 weeks. Lyme disease.1 have the lowest number of reported
She was seen by her pediatrician the B. henselae is a benign condition cases.2 Warm temperatures coupled
previous week after she was scratched in cats, and the infected animal with higher humidity is the ideal
by a feral cat. HD was given cepha- doesn’t display any signs of illness. climate for cat flea reproduction.
lexin. HD’s mother reports increased Cats don’t spread the infection to CSD tends to peak in late fall to
listlessness, fever, and enlarged, tender other cats by biting or scratching; early winter, corresponding with
axillary masses that have gradually it’s spread from cat to cat by the cat feline reproductive cycles and peaks
increased in size over the past 3 days. flea, Ctenocephalides felis. Humans in flea activity.2 Kittens have been
HD begins to cry and says she wants to can’t transmit CSD to other humans implicated more often in the trans-
go home and check on “Molly and her regardless of contact.2 mission of CSD because they’re more
babies.” HD’s mother says Molly is one Felis domesticus, or the common inclined to bite and scratch with
of several stray cats that have been liv- house cat, is the primary reservoir playful activity. Some statistics report
ing in a wooded area behind their house. for B. henselae as well as the primary that younger cats are 15 times more
HD’s mother says she had similar vector responsible for transmission of likely to transmit B. henselae, and
signs and symptoms a few weeks earlier CSD disease to humans.2 But despite individuals scratched or bitten by
but they spontaneously resolved without the name “cat scratch,” it’s important a kitten are 27 times more likely to
medical intervention. After an extensive to understand that felines aren’t the become infected.3
workup to rule out malignancy and life- only reservoir for this disease, nor Most individuals with CSD are
threatening infections, HD is diagnosed are they the only species that can under age 21.3 Young boys are more
with cat scratch disease, also known as transmit the infection to humans. likely to become infected than girls
cat scratch fever. Canines, coyotes, horses, porpoises, of the same age because boys are
sheep ticks, western black-legged more inclined to roughhouse with
Not just cats ticks, stable flies, and deer flies have cats and kittens and be bitten or
Cat scratch disease (CSD) is caused all been documented as reservoirs for scratched.3,4
by infection with the Bartonella the bacteria and can transmit the dis-
henselae bacterium. B. henselae is ease to humans.1 Approximately 5% Pathogenesis and
a Gram-negative, slow-growing, of CSD cases have a canine source.3 pathophysiology
aerobic bacillus that invades CSD develops from direct cutaneous
humans when cat saliva that con- Epidemiology of CSD inoculation of the B. henselae bacteria

tains the bacteria comes in contact An estimated 22,000 CSD infections by contaminated saliva introduced
with broken skin. Cats shed the occur each year in the United States, via scratch or bite. Once inoculation
bacteria through their saliva and most of them between August and has occurred in an immunocom-
leave live bacteria on their claws as January.2 The highest incidences petent person, macrophages and
they clean themselves. B. henselae of CSD have been reported in other first-line immune cells in the

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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
tissue attack the bacteria and initi- a vesicular, pustular, or nodular
ate the inflammatory and immune presentation, but this is rare.6
responses. Macrophages and other Skin lesions, when present,
antigen-presenting cells migrate into usually precede the development of
the lymphatic system to elicit a more regional lymphadenopathy by 1 to
specific immune response. 2 weeks.2,6,7 The resolution of the
Bacteria not destroyed by the pri- cutaneous papules often coincides
mary immune defenses may migrate with the appearance of enlarged
into the endothelial cells that line lymph nodes (see Lymph node
blood vessels, where they can survive enlargement). This process is one
and replicate.5 But bacteria that in- of the hallmark signs of CSD.3 The
fect cells aren’t safe from the immune lymph nodes that drain the site of
response. The bacteria, while repli- inoculation become visibly enlarged
cating intracellularly, will eventually and may be painful on palpation.4
cause changes and mutations in cel- This unilateral lymphadenopathy
lular surface proteins. The immune is a classic sign of infection with B.
system recognizes the mutated and henselae. The most common sites
abnormal proteins as foreign and Felines aren’t the only for lymphadenopathy are the axil-
attacks these cells through humoral reservoir for this disease, lary, epitrochlear, cervical, supracla-
and cell-mediated immunity. nor are they the only vicular, and submandibular lymph
Either way, the presence of the species that can transmit nodes.7,8 The overlying skin may be
foreign bacterial proteins leads to the infection to humans. erythematous without evidence of
an immune response that’s primar- cellulitis.9 They can reach several
ily helper T-cell mediated.2 The centimeters in diameter and usually
response by the helper T-cells facili- is the development of a pigmented persist for 2 to 4 months, but in rare
tates and coordinates the rest of the papule at the site of inoculation (see cases they may remain enlarged for
immune response necessary to rid Seeing the sign). Within 1 to 2 weeks, up to a year.9
the body of B. henselae. several small papules develop, but The most common signs and
they may be missed because of their symptoms of CSD include a
Recognizing CSD small size, an inconsistent presence, prolonged fever of unknown origin,
The typical presentation of CSD is or their location in a place not read- hence the nickname “cat scratch
more likely seen in people under ily visible during physical assess- fever.”2 Infection with B. henselae is
age 60. The earliest sign of infection ment. The lesions may develop into the third most common cause of a
fever of unknown origin in adults
and children. Other signs and
Seeing the sign symptoms include headache, fatigue,
A cat scratch inoculation site. generalized malaise, arthralgia,
anorexia, and pharyngitis. Adults
over age 60 are more likely to pres-
ent with atypical symptoms such as
anorexia, pharyngitis, and weight
loss.2,3 Typically, CSD spontane-
ously resolves within a few weeks to
The most common atypical infec-
tion, occurring in only a small per-
centage of individuals with CSD, is
Parinaud oculoglandular syndrome.9
This is characterized by conjunctival
granuloma, conjunctivitis, and adja-
cent 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

52 l Nursing2013 l February www.Nursing2013.com

Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
or lick near or in the eye.7 Signs • positive immunoassay or antibody
and symptoms are consistent with testing for B. henselae with a titer Lymph node enlargement
conjunctivitis. This condition usually greater than or equal to 1:64 An enlarged, nontender, nonery-
thematous axillary lymph node in a
isn’t painful and produces little to no • biopsy of lymph node, skin, organ,
boy with CSD.
discharge, but the conjunctiva and bones, or eye granuloma show-
sclera can become erythematous and ing granulomatous inflammation
edematous.6,10 consistent with CSD or a positive
Warthin-Starry silver stain.7
Assessment considerations Like B. henselae, rabies is also
A CSD diagnosis is based on find- transmitted through the saliva of the
ings from the detailed history and infected animal. Inquire about the
physical assessment. Ask patients animal’s vaccine status, if known,
about recent exposures to cats and and contact animal control if the
other animals. Do they have pets, animal’s vaccination status is in
work with animals, volunteer at an question.
animal shelter, or feed stray or feral
cats around their homes? Beyond CSD
Assess the skin for the primary Complications of CSD include
inoculation lesion by completely involvement of the liver, spleen, or
exposing limbs and inspecting all both. Signs and symptoms include
ventral and dorsal surfaces. Include dull episodic periumbilical or upper
the interdigital spaces and scalp, as abdominal pain, organomegaly, and
well as the skin folds to identify any elevated liver function tests in the
breaks in the dermis. When assess- presence of infection with CSD.8 ing the bacteria’s capability to spread
ing the lymph nodes, be sure to fully Neuroretinitis often presents with beyond infected lymph nodes.8
assess all nodes distal and proximal painless, unilateral visual loss with
to the area of inoculation. optic nerve edema and macular Treatment options
exudate.8 The most effective antibiotic for
Confirming the diagnosis The most severe neurologic com- treating CSD is azithromycin.1,5-7
Although CSD may be suspected plication associated with CSD is B. Patients who can tolerate azithro-
from the patient’s history and henselae encephalopathy, which is mycin have a faster rate of decrease
physical assessment, lab testing is characterized by abrupt disorienta- in lymph node volume over the first
needed to confirm the diagnosis. tion or confusion. This may progress few weeks following treatment.8
CSD is usually diagnosed on the to coma 1 to 6 weeks after the pa- For patients allergic to or unable
basis of a positive serologic test.7 tient presents with adenopathy. The to tolerate azithromycin, alter-
A complete blood cell count is patient will likely develop seizures natives include clarithromycin,
usually within normal limits, al- and may develop focal neurologic trimethoprim/sulfamethoxazole
though the white cell count may findings, such as hemiparesis from (TMP-SMX), rifampin, doxycycline
be slightly elevated. An elevated cerebral vasculitis.6,7,9 Cat scratch (for those over age 8), ciprofloxacin,
erythrocyte sedimentation rate and encephalopathy should be included amoxicillin-clavulanate, erythro-
C-reactive protein are the most in the differential diagnosis of any mycin, cephalexin, ceftriaxone, or
commonly reported lab abnormali- school-age child with a new onset gentamycin.5 Recommendations
ties, but neither is specific for CSD.2,4 of seizures.3 for patients with hepatosplenic or
Elevated liver function tests may Cardiac manifestations of CSD other disseminated forms of CSD
indicate systemic disease.4 have been documented only in include rifampin and gentamycin
A diagnosis of CSD is confirmed patients with a history of valvular administered for up to 14 days.10
when three of the four following cri- heart disease. Signs and symptoms In situations where gentamycin is
teria are present along with regional are consistent with heart failure.8 Cat contraindicated and disseminated
unilateral lymphadenopathy:9 scratch-induced glomerulonephritis disease is confirmed, azithromycin is
• feline or flea fecal material contact, presents similar to immunoglobulin the acceptable alternative.11
with or without scratch marks or a A nephritis: hematuria, proteinuria, Treatment for patients with
noticeable inoculation site and cola-colored urine.8 neurologic manifestations lasts less
• negative lab screening for onco- The rarest complication associated than 2 weeks but may continue for
logic, hematologic, or infectious with CSD is B. henselae osteomyelitis, up to 6 weeks for patients diagnosed
causes of lymphadenopathy such as usually found at a site distant from or suspected of having neuroretinitis.
tuberculosis and leukemia the enlarged lymph nodes, suggest- Treatment recommendations include

www.Nursing2013.com February l Nursing2013 l 53

Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
doxycycline and rifampin. Doxycy- sick, so they can’t tell if an animal Wilderness Medicine. 6th ed. Philadelphia, PA:
Elsevier, 2012; 1148-1150.
cline isn’t used in children under age is capable of transmitting disease.
5. Lamps LW, Scott MA. Cat-scratch disease:
8; azithromycin or TMP-SMX should Hand hygiene following even mini- historic, clinical, and pathogenic perspectives.
be used in its place. mal contact with animals will help Am J Clin Pathol. 2004;121(suppl):S71-S80.
Care for patients with CSD is rinse away any contaminants or flea 6. Florin TA, Zaoutis TE, Zaoutis LB. Beyond
cat scratch disease: widening the spectrum
aimed at symptomatic management. residue that may have been picked of Bartonella henselae infection. Pediatrics.
Acetaminophen and ibuprofen are up with contact. 2008;121(5):e1413-e1425.
usually adequate for most symptoms Prompt intervention and assess- 7. Spach DH, Kaplan SL. Microbiology,
epidemiology, clinical manifestations, and
including fever, headaches, and ment of signs and symptoms, along diagnosis of cat scratch disease. UpToDate. 2012.
myalgias. Dosages for children with teaching preventive measures, http://www.uptodate.com.
should be weight-based. Applica- can help patients avoid the possible 8. Stechenberg BW. Cat-scratch disease
(bartonella henselae). In: Kliegman RM, Stanton
tion of heating pads, warm showers, complications of CSD and future BF, St. Geme JW, Schor NF, eds. Nelson Textbook
and warm compresses to enlarged, infections. ■ of Pediatrics. 19th ed. Philadelphia, PA: Saunders;
painful lymph nodes may facilitate
9. Margileth AM. Recent advances in diagnosis and
drainage and alleviate pain. REFERENCES treatment of cat scratch disease. Curr Infect Dis Rep.
1. Mosbacher M, Elliott SP, Shehab Z, Pinnas
Education is key JL, Klotz JH, Klotz SA. Cat scratch disease and 10. Centers for Disease Control and Prevention.
arthropod vectors: more to it than a scratch? J Am Cat scratch disease (Bartonella henselae infection).
The most important intervention is Board Fam Med. 2010;23(5):685-686. 2011. http://www.cdc.gov/healthypets/diseases/
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Mark McGraw is a direct care nurse at Christiana Care
Health System in Newark, Del.
cate patients, especially children, Reference: Drugs, Disease and Procedures. 2011.
about the dangers of approaching overview.
The author has disclosed that he has no financial
relationships related to this article.
stray or feral animals. Remind them 4. Shandro JR, Jenkins JG. Wilderness acquired
that infected animals may not appear zoonoses: cat-scratch disease. In: Auerbach PS, ed. DOI-10.1097/01.NURSE.0000423960.45625.e3

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Copyright © 2013 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.