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BRIEF REPORT

Asymptomatic Nasal Carriage


of Mupirocin-Resistant, MethicillinResistant Staphylococcus aureus (MRSA)
in a Pet Dog Associated with MRSA
Infection in Household Contacts
Farrin A. Manian
Division of Infectious Diseases, St. Johns Mercy Medical Center,
St. Louis, Missouri

Methicillin-resistant Staphylococcus aureus (MRSA) is an important cause of nosocomialand, increasingly, communityacquiredinfection [1]. Person-to-person spread of MRSA in
the household setting has been reported previously [24]. Eradication of MRSA colonization from nares has been complicated
by the emergence of mupirocin resistance [5]. I report the
isolation of mupirocin-resistant MRSA from the nares of an
apparently healthy dog belonging to a patient who, along with
the patients wife, repeatedly had bouts of soft-tissue MRSA
infections. The relatedness of the MRSA isolates from the dog
and household contacts was demonstrated by PFGE of chromosomal DNA.
Case report. A 48-year-old man with diabetes mellitus and
chronic renal insufficiency was hospitalized on 30 January 2001
for treatment of a right leg-stump infection. Previously, on 1
December 2000, the patient had been admitted for right belowknee amputation because of a nonhealing wound, and readReceived 29 May 2002; accepted 5 August 2002; electronically published 6 January 2003.
Reprints or correspondence: Dr. Farrin A. Manian, Division of Infectious Diseases, St. Johns
Mercy Medical Center, 621 S. New Ballas Rd., St. Louis, MO 63141 (manianfa@aol.com).
Clinical Infectious Diseases 2003; 36:e268
 2003 by the Infectious Diseases Society of America. All rights reserved.
1058-4838/2003/3602-00E3$15.00

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Recurrent methicillin-resistant Staphylococcus aureus (MRSA)


infection in a patient with diabetes and in his wife is described. Culture of nares samples from the family dog grew
mupirocin-resistant (minimum inhibitory concentration
11024 mg/mL) MRSA that had a pulsed-field gel electrophoresis chromosomal pattern identical to the MRSA isolated
from the patients nares and his wifes wound. Further recurrence of MRSA infection and nasal colonization in the
couple was prevented only after successful eradication of
MRSA from the family dogs nares.

mitted on 8 December 2000 for a culture-negative surgical-site


infection; for the latter, he was treated with intravenous vancomycin. On 25 January 2001, a culture of stump drainage
fluid grew MRSA that was resistant in vitro to most antibiotics tested (including trimethoprim-sulfamethoxazole, erythromycin, gentamicin, clindamycin, and tetracycline) but was
susceptible to vancomycin and rifampin; culture of nares samples also grew MRSA with an identical susceptibility pattern.
The patient was treated with intravenous vancomycin, a 10day course of daily chlorhexidine baths, and topical mupirocin
ointment applied twice per day to the nares. Despite resolution
of cellulitis and completion of decolonization therapy, cultures
indicated the presence of MRSA in the patients nares on 26
April, 18 May, and 11 June 2001. Attempts at decolonization
with a 2-week course of oral rifampin and topical mupirocin
in May 2001 were again unsuccessful, despite in vitro susceptibility of the isolate to rifampin. On 12 April and 27 July 2001,
the patients wife, a kidney transplant recipient with diabetes,
had MRSA cellulitis diagnosed (on the basis of wound cultures
and clinical exam) after biopsies of seemingly minor skin
lesions. In both instances, the antibiogram of the isolates was
identical to that of the patients, and nares cultures failed to
grow MRSA.
On 4 August 2001, because of concern over an unidentified
source of MRSA within the household, nares culture was performed for the only other household member, a healthy 18month-old female Dalmatian. The culture grew MRSA with a
susceptibility pattern identical to that of the previous isolates
from the patient and his wife. A second culture of samples from
the dogs nares obtained 9 days later confirmed the presence
of MRSA. A previous MRSA isolate from the patients nares
and the original isolate from the dogs nares were both tested
against mupirocin by Etest (AB Biodisk) and found to be highly
resistant to this drug (MIC 11024 mg/mL)[5]. Genomic DNA
typing by PFGE of chromosomal DNA of the same isolates
from the patient and the dog, as well as an isolate from the
wifes earlier wound cultures, revealed indistinguishable profiles; another previous isolate from the patients wound was
closely related (2-band differences) to these 3 isolates (figure
1). On further questioning, the couple reported that the dog
routinely slept in their bed and frequently licked their faces.
Application of vancomycin ointment (5%) to the nares 2 times/
day for 10 days was prescribed for the patient, his wife, and
the dog. For the dog, a cotton swab laden with the ointment
was inserted 12 cm into each nostril and twirled several times.
Avoidance of intimate contact with the dog was also urged. On

11 September 2001 (2 weeks after completion of decolonization


therapy), culture of samples from the nares of the patient failed
to grow MRSA from the nares of the patient, but the dogs
nares remained culture-positive. Concurrent culture of nares
samples from the patients wife grew MRSA for the first time.
Another course of vancomycin ointment to the nares, similar
to the previous regimen, was prescribed for all 3 household
members. On 11 October 2001, nares cultures for the patient
and the dog grew MRSA, but the result of nares culture for
the patients wife was negative. The 10-day vancomycin ointment regimen was repeated for all household members.
On 30 October 2001, a few days after the completion of
decolonization therapy, the patient developed another bout of
MRSA infection in his leg stump, despite a negative nares culture result; his wife had no open wounds or evidence of skin
infection at that time. Another course of vancomycin ointment,
similar to the prior regimen but for a longer duration (2 weeks),
was prescribed for the patient, his wife, and the dog. Cultures
of nares samples from the couple and the dog obtained 2 weeks
after completion of therapy were negative for MRSA.
On 6 February 2002, the patient presented to the infectious
disease clinic with a new pressure ulcer above the right leg
stump. Although there was no evidence of infection around
the ulcer, a wound swab was obtained; it showed no evidence
of MRSA. Four months after decolonization therapy of the
entire family ended, the patient and his wife remained free of
MRSA infection. The dog remained asymptomatic.
Discussion. To the best of my knowledge, this is the first

BRIEF REPORT CID 2003:36 (15 January) e27

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Figure 1. PFGE patterns of methicillin-resistant Staphylococcus aureus


isolates from the nares and wound of the patient (lanes 3 and 4, respectively), the dogs nares (lane 5), and the wifes wound (lane 6). Lanes
1 and 2, l Standard and internal control isolates, respectively.

reported case of isolation of mupirocin-resistant MRSA from


an animal, a finding with potentially significant ramifications,
given the frequent use of mupirocin as the first-line treatment
for nasal colonization in humans. It is also the first report of
MRSA isolation from an animal in which the relatedness of
the isolate to that of its human contacts was proved by PFGE.
There has been only one other report of MRSA isolation from
a dog, but that case differs from the present one in that the
dog had apparently been symptomatic (it had an eye infection),
mupirocin susceptibility testing was not performed on the isolate, and only phage typing was done to prove the isolates
relatedness to the isolates from the household contacts [6].
Compared with PFGE, phage typing has been shown to have
inferior discriminatory capability in distinguishing MRSA isolates from different sources [7].
The carriage of MRSA by the dog might have played an important epidemiological role in the recurrent infections and colonizations in the patient and his wife. There are several reasons
to suspect this. First, the antibiogram and PFGE patterns of the
MRSA isolate from the dog were identical to those of the isolates
from the patients nares samples and from the patients wifes
wound; they were also closely related to those of the isolate from
the patients wound, on the basis of its PFGE pattern. Second,
despite the apparent eradication of MRSA from the patients
nares, samples from his wifes nares became culture positive,
attendant with the persistence of MRSA in the dogs nares (in
September 2001). Third, despite the eradication of MRSA from
the nares of the patient and a recent negative nares culture result
for his wife, he acquired another MRSA leg-stump infection
(October 2001). Last, termination of the infection and colonization cycle from the patient and his wife was only possible
after the successful eradication of MRSA from the dogs nares.
It is likely that the dog (which had not been ill or hospitalized
or received antibiotics previously) initially became colonized
by MRSA through contact (often intimate) with the patient,
who had previously been hospitalized. In turn, the dog likely
served as a source of reinfection or recolonization for both the
patient and his wife. Direct person-to-person transmission of
MRSA between the patient and his wife might have also occurred, but this possibility would have been less likely in October 2001, when the patient experienced another bout of
wound infection in the absence of MRSA in the couples nares.
In 1959, Mann [8, pp. 46970] reported the isolation of S.
aureus from the nostrils of 23 of 100 dogs and proposed that
the common house pet can serve as an important reservoir
or carrier of staphylococci infective for man. Subsequent studies reported that, compared with many other animals, dogs
seem to be particularly susceptible to nasal carriage of S. aureus
[912], with some studies reporting up to a 70%88% carriage
rate in the canine population [10, 11]. In 1961, Live and Nichols
[13] reported a high rate of nasal carriage of antibiotic-resistant,

e28 CID 2003:36 (15 January) BRIEF REPORT

in household settings. Any investigation aimed at identifying


hidden carriers of MRSA among close patient contacts should
not overlook mans best friend.

References
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3. Hollis RJ, Barr JL, Doebbeling BN, Pfaller MA, Wentzel RP. Familial
carriage of methicillin-resistant Staphylococcus aureus and subsequent
infection in a premature neonate. Clin Infect Dis 1995; 21:32832.
4. Reboli AC, John JF Jr, Platt CG, Cantey JR. Methicillin-resistant Staphylococcus aureus outbreak at a Veterans Affairs Medical Center: importance
of carriage of the organism by hospital personnel. Infect Control Hosp
Epidemiol 1990; 11:2916.
5. Eltringham I. Mupirocin resistance and methicillin-resistant Staphylococcus aureus (MRSA). J Hosp Infect 1997; 35:18.
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Staphylococcus aureus linked with pet dog. Lancet 1994; 344:53940.
7. Bannerman TL, Hancock GA, Tenover FC, Miller JM. Pulsed-field gel
electrophoresis as a replacement for bacteriophage typing of Staphylococcus aureus. J Clin Microbiol 1995; 33:5515.
8. Mann PH. Antibiotic sensitivity testing and bacteriophage typing of
staphylococci found in the nostrils of dogs and cats. J Am Vet Med
Assoc 1959; 134:46970.
9. Abramson AL, Isenberg HD, McDermott LM. Microbiology of the
canine nasal cavities. Rhinology 1980; 18:14350.
10. Courter RD, Galton MM. Animal staphylococcal infections and their
public health significance. Am J Pub Health 1962; 52:1827.
11. Adekeye JD. Studies on possible cross transmission of mercuric chloride
resistant Staphylococcus aureus between dogs and kennel attendants.
Int J Zoon 1981; 8:726.
12. Moeller RW, Smith IM, Shoemaker AC, Tjalma RA. Transfer of hospital staphylococci from man to farm animals. J Am Vet Med Assoc
1963; 142:6137.
13. Live I, Nichols AC. The animal hospital as a source of antibiotic resistant staphylococci. J Infect Dis 1961; 111:195204.
14. Waldvogel FA. Staphylococcus aureus (including staphylococcal toxic
shock). In: Mandell GL, Bennett JE, Dolin R, eds. Principles and practice of infectious diseases. Philadelphia: Churchill Livingstone, 2000:
207192.
15. Melish ME, Campbell. Coagulase-positive staphylococcal infections. In:
Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases.
Philadelphia: W. B. Saunders, 1998:103966.
16. Sheagran JN, Schaberg DR. Staphylococci. In: Gorbach SL, Bartlett JG,
Blacklow NR, eds. Infectious diseases. Philadelphia: W. B. Saunders,
1998:1697703.
17. Ruben FL, Muder RR. Staphylococcal infections. In: Evans AS, Brachman PS, eds. Bacterial infections of humans-epidemiology and control.
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18. Kluytmans J, van Belkum A, Verbrugh H. Nasal carriage of Staphylococcus aureus: epidemiology, underlying mechanisms, and associated
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19. Brodie SJ, Biley FC. An exploration of the potential benefits of petfacilitated therapy. J Clin Nurs 1999; 8:32937.
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coagulase-positive staphylococci among fourth-year veterinary


students, many of whom also had skin infections caused by
the same organism. The high prevalence of antibiotic-resistant
staphylococci among hospitalized dogs, who often received
antibiotics as prophylaxis and therapy, was thought to have
contributed to colonization and disease in these students. The
authors concluded that antibiotic-resistant staphylococci have
become established in veterinary hospitals, which may act as a
source of the organisms for human beings associated with them
as well as for hospitalized animals [13, p. 203]. Experimental
cross-transmission of S. aureus from dogs to kennel attendants
has also been demonstrated [11].
Despite these published reports, the potential for dogs to
serve as a source of S. aureus infections in humans has gone
relatively unnoticed. Indeed, none of the 4 commonly referenced textbooks of infectious diseases even mention the possibility of S. aureus carriage in pet animals serving as a source
of infection in humans [1417]. One possible explanation of
the general disregard for the findings of the aforementioned
studies may be that the relatedness of canine isolates to isolates
from the human contacts was never definitively demonstrated,
because of the inadequate discriminatory abilities of antibiogram and phage typing for distinguishing different strains of
S. aureus, compared with PFGE. With the increasing prevalence
of MRSA in the population and its attendant higher rate of
infection following colonization, as compared with methicillinsensitive S. aureus [18], investigation into asymptomatic MRSA
carriage in canine household members may need serious consideration for patients with recurrent community-acquired
MRSA infections. Furthermore, the increasing popularity of pet
therapy, particularly in health-care facilities [19, 20], where
MRSA may be endemic, also raises questions about the possibility of asymptomatic canine acquisition and the subsequent
spread of MRSA in such settings; further studies are needed to
explore this possibility. Although the treatment of MRSA carriage by the application of topical antimicrobial agents to dog
nares has not been studied systematically, my experience with
the case described here suggests that it may be more difficult
to eradicate MRSA carriage from dog nares than from human
nares, given that several attempts were required before decolonization was successful. Last, although topical vancomycin
therapy was used because of the mupirocin resistance of the
MRSA isolates from the dog and the patient, this treatment
cannot be routinely recommended because of increasing resistance to vancomycin among S. aureus isolates [21].
In conclusion, until further studies are performed, the evaluation of patients with recurrent MRSA colonization or infection that does not have an obvious source should prompt queries regarding any regular contact with pet dogs, particularly

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