Blistering Purpura
Transcript of Blistering Purpura
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P 062
STAPHYLOCOCCUS AUREUS: THE ENEMY WITHIN
Dave Bella 1, Patel Mitulkumar 2, Bodasing Neena 1,Cadwgan Anthony M 1
1 Dept of Clinical Infection, University Hospital of NorthStaffordshire, City General Hospital, Newcastle Road,Stoke-on-Trent, Staffordshire ST4 6QG2 Dept of Microbiology, University Hospital of NorthStaffordshire, City General Hospital, Newcastle Road,Stoke-on-Trent, Staffordshire ST4 6QG
We report two cases of severe community acquiredinfections due to staphylococcus aureus.
Case 1 A 51-year-old man presented with a severe ne-crotising and cavitating pneumonia following a trip to Chinaand Malaysia. White cell count was 18 and sputum cultureda Methicillin Sensitive Staphylococcus Aureus (MSSA). Heimproved with IV antibiotics, which was changed to orals af-ter two weeks. However, a large lung cavity persisted de-spite chest drain insertion. Therefore a flutter bag wasinserted, he was discharged and the cavity was reducingon follow-up.
Case 2 A previously well 31-year-old woman was admit-ted with a serious, recurrent axillary abcess and staphylo-coccal toxaemia. White cell count was 16.1 and she wastreated with IV antibiotics and incision and drainage ofthe abcess. She improved with this treatment and was dis-charged. Material from the axillary abcess also culturedMSSA and was positive for TSST.
What is the connection between the two?In both of these cases the infection was caused by
a Panton-Valentine Leukocidin (PVL)-producing strain ofMSSA. PVL, a pore-forming toxin that causes leukocytolysisand tissue necrosis, has been associated with severecommunity-acquired pneumonia in immunocompetent pa-tients and necrotising cutaneous infections.
These cases are unusual as although similar cases ofpneumonia and cutaneous infections have been reported,in contrast to the literature, neither of the cases we reporthad an associated leucopenia. This may be a good prog-nostic feature in PVL cases.
The current incidence of PVL positive staphylococcus au-reus is reported as <2%. In our hospital we do not routinelysend samples of staphylococcus aureus for PVL typing. How-ever, the two incidents of PVL associated infections withinthis five-week time frame highlights the need to regularlyscreen patients with severe or recurrent staphylococcal in-fections, irrespective of leukocytosis.
We also acknowledge and thank Angela Kearns for heradvice.
P 064
CLINICAL AND MICROBIOLOGICALCHARACTERISTICS OF STAPHYLOCOCCAL TOXICSHOCK SYNDROME PRESENTING TO A PAEDIATRICINTENSIVE CARE UNIT
O’Dell E 1, Davies F 2, Kearns AM 3, Festa M 1,Klein JL 2
1 Paediatric Intensive Care Unit, Health Protection Agency(HPA), London2 Dept of Infection, Health Protection Agency (HPA),London3 Guy’s and St. Thomas’ NHS Foundation Trust, London andCentre for Infections, Health Protection Agency (HPA),London
Background: Staphylococcal toxic shock syndrome(STSS) is a toxin-mediated disease which presents with
Abstracts e73
P 063
BLISTERING PURPURA
Hussain A 1, Robinson G 2, Malkin J 1, Duthie M 2,Perera N 1
1 Clinical Microbiology, University Hospitals of Leicester2 Child Health, University Hospitals of Leicester
We present a case of pupura fulminans (PF) secondary tomethicillin-sensitive Stapylococcus aureus (MSSA) infec-tion. The child was admitted in septic shock with bilaterallower limb purpura (fig. 1) complicated by multiple lung ab-scesses and cavitation (fig. 2). MSSA was isolated fromblood, skin and pulmonary tissue and was later confirmedto be expressing the PVL genes but lacked any other toxingenes. The clinical course culminated in surgery.
PF is an acute illness commonly associated with Neisse-ria meningitidis (and to a lesser extent streptococcal infec-tions, malaria and chickenpox). It is characterised bydisseminated intravascular coagulopathy and purpuric skinlesions due to disruption of the protein C anticoagulantpathway. PVL genes are expressed in both MSSA andMRSA. Its association with toxigenic staphylococcal infec-tions is rare and is confined to a few reported cases glob-ally. The true incidence of PVL-positive S. aureus (PPSA)infections is unknown as PF is not notifiable and not all S.aureus isolates are tested for PVL genes. Patients with PFare best managed in an intensive care setting with broad-spectrum antimicrobials, including an anti-MRSA agent.There is some evidence for adding in linezolid or clindamy-cin in confirmed PPSA infections due to their antitoxin prop-erties. The interim guidelines produced by the HealthProtection Agency recommends the use of intravenous im-muoglobulin (IVIG) for its antitoxin properties (2 g/kg/day). There may also be a role for activated protein C inadults as an immunomodulator and anticoagulant. Thereis evidence of spread of PPSA via skin-to-skin contact andfomites. The guidelines recommend that patients and theirclose contacts should be screened for S. aureus carriage.Surgical masks should be worn during intubation and phys-iotherapy in patients with respiratory infections. In conclu-sion, clinicians should be aware that PF is not synonymouswith meningococcaemia and this should be reflected intheir empirical antimicrobial choice, especially if blisteringis a presenting feature.