Methicillin Resistant Staphylococcus aureus (MRSA) was first described in the human health care setting in the 1960's. Infections
were first described in otherwise healthy people in the 1980's. Disease severity in humans ranges from asymptomatic colonization
of the upper respiratory tract and skin, to clinical disease with varying severity. Disease ranges from mild to severe and
invasive infections. Examples of mild disease include furunculosis and dermatitis which can progress to soft tissue abscessation.
MRSA can cause life-threatening illness, including necrotizing pneumonia, sepsis syndrome, pyomyositis, osteomyelitis, and
necrotizing fasciitis. Purpura fulminans is a shock state with cutaneous hemorrhage and necrosis; systemic signs are present,
including hypotension and coagulopathies, such as disseminated intravascular coagulation (DIC).
Several veterinary species are susceptible to MRSA, including horses, dogs, cats, cattle, and pigs. MRSA isolates are resistant
to all beta-lactam antimicrobials, including penicillins. MRSA isolates are also variably resistant to many other antimicrobial
classes including macrolides and azalides, fluoroquinolones, tetracyclines, clindamycin, among others. This resistance is
genetically coded with the presence of mecA gene. This gene encodes for a penicillin-binding protein, PBP2a. This gene confers
resistance to methicillin and oxacillin, providing the name 'methicillin resistant'.
There are two forms of MRSA affecting humans, hospital- and community-acquired (HA and CA-MRSA). Initially these were discrete,
but over time they have become blended. Hospital acquired MRSA is infection that develops ≥ 48 h after hospitalization or
within a year of hospitalization, surgery, dialysis, or residence in a long-term care facility. Community acquired-MRSA is
infection with onset in the community rather than hospital. Such patients do not have typical risk factors; they are usually
young, and are often athletes, military personnel, students or prisoners. Community acquired MRSA is easily spread with physical
contact and through abrasions or wounds. Shared equipment, including towels, razors, or sports equipment can serve as a means
of spread. The community acquired strains of MRSA possess unique virulence and transmissibility factors, including a Panton-Valentine
Leukocidin (PVL) toxin in > 95 % of isolates. Community acquired strains, despite being methicillin resistant, are often susceptible
to fluoroquinolones, aminoglycosides, macrolides and clindamycin.
Hospital acquired MRSA (HA-MRSA) are most common in immunocompromised, elderly or premature patients, and affected patients
are usually hospital residents. Risk factors for infection with HA-MRSA include indwelling catheters, hemodialysis, and long
term antimicrobial administration. Transmission is usually through person-to-person contact, with hands or fomites such as
hospital equipment. The HA-MRSA strains have a low prevalence of the PVL gene (< 5 %). These strains also differ from community
acquired strains by their resistance MIC patterns- they are not susceptible to other commonly antimicrobials. Initially distinct,
now there is considerable overlap in terms of genotype and antimicrobial susceptibility patterns among CA-MRSA and HA-MRSA.
The clinical syndrome in horses is somewhat similar to that in humans. They can be colonized subclinically in the nares and
gastrointestinal tract. Infections can vary and range from superficial to deep infections. Superficial infections include
dermatitis, wound or incisional infections, joint or tendon sheath infections, and phlebitis. Deep infections include pneumonia,
metritis, umbilical abscesses, scirrhous cord, sinusitis, osteomyelitis, mastitis and septicemia. Horses are most commonly
colonized or infected with USA 500, which is a minor or uncommon human strain that lacks PVL genes.
Treatment of subclinical colonization is isolation of affected horses until they test negative on cultures of nasal swabs.
Otherwise there is no specific recommended treatment for subclinical carriers. Superficial skin infections can be treated
topically with silver sulfadiazine, chlorhexidine, povidone iodine, mupirocin or fusidic acid. More serious superficial infections
such as joint infections and deep infections should be treated with systemic antimicrobials. Selection of antimicrobials should
be based on culture and susceptibility testing, as the susceptibility patterns vary widely among isolates. Chloramphenicol
and amikacin appear to be effective in most isolates seen at our hospital. It should be noted that despite a high percentage
of enrofloxacin-susceptible isolates, these results must be interpreted with caution as in vivo resistance to fluoroquinolones
may develop rapidly.
One study in the equine literature showed that 10 % of equine veterinarians and technicians were colonized asymptomatically.
Another study showed that 16 % of large animal ACVIM diplomates were nasally colonized. The majority of these isolates were
USA500, which is an uncommon human strain. Hand washing between infectious horses and between farms was protective against
being asymptomatically colonized in that study.