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News and Reports |
Source of MRSA in animals
The question of where MRSA in animals came from was examined by Dr Andrew Waller of the Animal Health Trust (AHT), who noted that, although its incidence in animals was relatively low compared with the human situation, MRSA could cause serious disease and had been identified in a wide range of species, including poultry, dogs, cats, horses and cattle.
He believed that it was most likely that methicillin resistance had spread
from humans to animals, particularly considering the close contact companion
animals had with humans. One would therefore expect to see the same strains
circulating in humans and in
animals.
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A number of studies using pulsedfield gel electrophoresis (PFGE) had demonstrated that the same strain of MRSA in an animal could be identified in in-contact humans. One such study described two dog owners suffering from persistent MRSA infection, who relapsed every time they returned home from hospital. Further investigation revealed that their dog was carrying the same strain of MRSA ( F. A. Manian, 2003, Clinical Infectious Diseases, vol36 , pp26 -28 ). He pointed out, however, that these types of studies did not resolve the `chicken or egg situation': did the dog initially acquire the infection from the humans or was it the other way around?
Other studies had shown that many strains of MRSA found in animals were identical to those in the human population, namely UK epidemic MRSA clone 15 (EMRSA-15) and clone 16 (EMRSA-16). In the UK these were the predominant epidemic clones and caused 96 per cent of serious MRSA infections in humans in hospitals. Preliminary data from a collaborative study between the AHT and the Royal Veterinary College (RVC), funded by the Petplan Charitable Trust, to sequence-type canine strains in the UK, had backed up these findings. The researchers used multilocus sequence typing (MLST) to identify specific MRSA strains in dogs. Of the 14 they had analysed to date, 13 were EMRSA-15 and one was EMRSA-16. It appeared that canine strains were generally similar to human strains, implying the transmission of human MRSA strains to animals.
MRSA in the horse
MRSA in horses was explored by Professor Peter Clegg and Dr Nicola Williams from Liverpool veterinary school. Professor Clegg noted that MRSA was first reported in the horse in 1997 and was associated with wound infections. However, since then, MRSA infections had been reported as a cause of pneumonia, osteomyelitis, catheter site infections, metritis and dermatitis.
He said that MRSA was `not a major problem' at the Philip Leverhulme Equine Hospital in Liverpool. It was one of the biggest equine hospitals in the UK and, of 2000 cases seen per year, it had identified five cases of MRSA over the past three-and-a-half years. Three cases arose from joint wounds and joint wound infections, another from pastern dermatitis and one case was isolated from a horse with chronic pleuropneumonia.
In a study conducted between late autumn 2003 and spring 2004, samples were taken from 67 horses at the Liverpool hospital and from 41 other horses that were privately owned and from riding schools. At the hospital, 11 horses were found to be carriers of MRSA; staff were screened but none was found to be positive. All the horses sampled outside the hospital were negative for MRSA. (Details of this study are to be published in Emerging Infectious Diseases; the paper is available online at www.cdc.gov/ncidod/EID/vol11no12/05-0241.htm.)
Dr Williams said that three of the clinical cases and all of the carriers identified from the equine hospital were subjected to PFGE and MLST, which showed five distinct strains, the most common being EMRSA-10. None was related to EMRSA-15 or EMRSA-16, which differed markedly from the findings at the small animal hospital at Liverpool where all the isolates that had so far been identified were EMRSA-15.
Describing the uncertainty surrounding how these strains entered hospitals, she noted that many were resistant to gentamicin, an antimicrobial widely used in equine medicine. She suggested that these particular strains were being selected for; in contrast, the EMRSA strains seen generally in small animals were resistant only to ciprofloxacin as well as methicillin.
MRSA in small animals
How a small animal referral hospital coped with MRSA infection was considered by Professor David Lloyd, from the Queen Mother Hospital for Animals at the RVC. The RVC had begun to recognise cases of MRSA in 1997/98 and, after that, had started to see a substantial increase in the number of MRSA infections in referred cases.
So how did the hospital treat MRSA cases? A diverse range of clinical presentations were referred to the hospital, treatments were tailored to individual patients and encompassed medical, financial and ethical concerns. It did not use certain antibiotics, for example, vancomycin, which it believed should be left for use in human medicine. Simply removing implants, such as external fixators, could result in survival and recovery. If antimicrobials were indicated, oxytetracycline or co-trimoxazole could be effective. As well as this, decolonisation procedures were used in most cases, which involved administration of fusidic acid into mucosal sites, and application of chlorhexidine shampoo to the skin.
Professor Lloyd recommended carrying out swab or tissue sampling for culture and antimicrobial susceptibility testing in all non-responsive infections, non-healing wounds, or if MRSA was suspected for any other reason; for example, if the owner had a healthcare-related job or had just been in hospital.
He also noted that people should be alerted if laboratory testing revealed a resistance pattern for an isolate that was unusual or just not believable. One finding that raised suspicions at the hospital was the identification of cefalexin-resistant Staphylococcus intermedius. S intermedius was very rarely resistant to cefalexin, so it was important to ensure that the organism had been identified correctly.
A survey conducted at the hospital, which had been published recently in the Journal of Antimicrobial Therapy (A. Loeffler and others, 2005, vol 56, vol 56, pp 692-697), aimed to provide more accurate information on its MRSA status. On one day in February 2004, all staff present, all animals (with the owners' consent) and environmental surfaces were sampled for MRSA. The study identified MRSA carriage in 17·9 per cent of veterinary staff, 9 per cent of dogs, and 10 per cent of environmental sites. Most survey isolates were indistinguishable from (56 per cent) or closely related to (26 per cent) EMRSA-15. None was related to EMRSA-16.
Professor Lloyd highlighted the hospital's hygiene and surveillance procedures. It no longer allowed animals with recurring infections to enter the hospital unless they had been tested for MRSA. In emergency cases, they were isolated until they were tested. If the animals required intensive care treatment, `barrier nursing' was implemented, which used very strict hygiene procedures. Alcoholic hand scrubs had also been attached to cages in the intensive care unit.
Human experience
Dr Angela Kearns, from the Health Protection Agency, described the difference between `community-acquired' and `hospital-acquired' MRSA infections in humans. The community-acquired form tended to be unrelated to the hospital-acquired form and was notably more virulent and transmissible. It tended to occur in previously healthy individuals in the community, with no known risk factors for acquiring MRSA.
A particularly virulent form of MRSA was discussed by Dr Marina Morgan, from the Royal Devon & Exeter Foundation NHS Trust. She described the key clinical features of infections caused by an S aureus that produced an exotoxin called Panton-Valentin leukocidin (PVL). PVL exhibited strong cytotoxic activity towards human leucocytes and had the ability to cause severe inflammation and tissue necrosis. All S aureus strains, not just MRSA, could be infected by PVL-producing phages, and the toxin greatly increased the bacterium's virulence. Most PVL-related infections caused recurrent furunculosis and severe recurrent abscesses, but if the S aureus was carried in the nose and throat, it could descend into the lungs causing necrotising pneumonia. Despite aggressive management, including massive doses of antibiotics, this pneumonia had a mortality rate of more than 75 per cent in young, fit people.
She noted that although only 2 per cent of S aureus produced this exotoxin, the more people looked for the strain, the more they found it; she suggested that PVL positivity in strains isolated from recurring skin infections was as high as 8 per cent, and that probably all the strains that caused necrotising pneumonia produced PVL.
The relationship between cleanliness in hospitals and MRSA infection was explored by Dr Stephanie Dancer, from the Southern General Hospital in Glasgow. She noted there was no way to assess the risk of acquiring MRSA from the clinical environment because there was no way of measuring the effect of cleaning. However, just because there was no direct evidence linking surface hygiene and MRSA acquisition, did not mean there was no link. She suggested that it might be time to introduce microbiological standards for surface hygiene levels in hospitals. This would not only allay concerns over the grading of hygiene by visual assessment, but could help convert cleaning to an evidence-based discipline.
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