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Microsoft word - background information on mrsa.doc
Background Information on Meticillin-Resistant Staphylococcus Aureus (MRSA)
How did MRSA develop?
Staphylococcus aureus was the commonest cause of wound infection and sepsis until the
introduction of penicillin in 1940, but epidemic penicillin-resistant strains soon emerged and
throughout the 1950s resistance to streptomycin, tetracycline, chloramphenicol and
Penicillinase-resistant penicillins, such as meticillin, were introduced in 1960 but resistance
to these developed within a year when the first case of MRSA was documented. Initially
infections were severe, requiring treatment with vancomycin, but prevalence decreased in
the 1970s; the reason for this is unclear.
During the 1980s and 90s, epidemic strains of MRSA spread worldwide and MRSA became
endemic in many UK hospitals. Considerable effort and focus - with reduction targets and
national infection control initiatives - have helped to significantly reduce levels of infection in
hospitals over the last ten or so years.
What does MRSA cause?
Staphylococcus aureus (including those that are MRSA) causes anything from
asymptomatic colonisation (where the bacteria are doing no harm but still capable of
causing clinical infection) to a range of infections such as boils, carbuncles, infected
wounds, deep abscesses and blood stream infections, which can be fatal.
What do we mean by colonisation?
About 30% of the general population are colonised by S. aureus. In hospitals, S. aureus
carriage is more likely to be MRSA, because antibiotic-resistant bacteria are selected out by
the use of antibiotics to treat infection. Carriage sites are most commonly the nose and the
skin, especially the axilla or groin. A carrier can be a source of infection for themselves if
they have a wound. In high risk situations (e.g. patients for major surgery like a hip
replacement or heart surgery) if pre-screening shows MRSA carriage, decontamination with
skin and nose treatment is recommended before they are operated on.
S. aureus / MRSA is the commonest cause of wound infection - either after accidental injury
or surgery. This shows as a red, inflamed wound with yellow pus seeping from it. The
wound may break open or fail to heal and a wound abscess could develop.
Pressure ulcers, varicose ulcers and diabetic ulcers (all due to poor blood supply and
superficial skin damage) are often sites of MRSA infection.
Intravenous line infections
MRSA may infect the entry site of an intravenous line causing local inflammation with pus
from which the MRSA can enter the blood to cause a blood stream infection.
If MRSA spreads from a local site into the blood stream it can lodge at various sites in the
body (e.g. lungs, kidneys, bones, liver, spleen) and cause deep abscesses distant from the
original site. These can be painful, with high fever and signs of inflammation near the
infection. The patient will be very unwell and may have rigors (shivers), low blood pressure
(shock) and possibly organ failure. This is usually linked with an associated septicaemia.
MRSA is a rare cause of lung infection except in Intensive Care Units where ventilators
bypass the defences of the nose and throat. MRSA can gain entry to the lungs via the tube
Bacteraemia / septicaemia
MRSA can enter the normally sterile blood stream either from a local site of infection
(wound, ulcer, abscess) or via an intravenous catheter. Bacteraemia describes the
presence of MRSA in the blood. Septicaemia can follow and is the clinical term for a severe
illness caused by the bacteria in the blood stream. The symptoms are not specific to MRSA
and can be the same for other bacteria that cause septicaemia. Typically symptoms can
include high fever, raised white cell count, rigors, disturbance of blood clotting with a
tendency to bleed and failure of vital organs. This is the kind of MRSA infection that has the
Clinical Outcome Measures in Spinal Muscular Atrophy Jacqueline Montes, Andrew M. Gordon, Shree Pandya, Darryl C. De Vivo and Petra Kaufmann 2009; 24; 968 originally published online Jun 9, 2009; The online version of this article can be found at:http://jcn.sagepub.com/cgi/content/abstract/24/8/968 can be found at: Journal of Child Neurology Additional services and information f
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