Health Care associated infection/pathology of the Central Nervous System

Professor Mary CafferkeyAssociate Professor of Clinical Microbiology, RCSI

Which infections?

Acute infection• Encephalitis• Meningitis• Meningoencephalitis• Abscess

Chronic infectionPost-infectious and post-immunisation

complicationsTransmissable spongioform

encephalopathies

• Procedure-Related • Other Intervention related

– Medicinal substance– Transfusion of Blood or Blood products– Transplantation– Immunisation

• Exposure to infection in a Health Care setting

Scope

Procedure-related

• Lumbar puncture/Epidural anaesthesia

• CNS electrodes• Procedures involving the Central

Nervous System– Craniotomy– CSF Shunt placement/removal/revision– Operative procedures

•Exploration/lobectomy/abscess drainage/excision of tumour etc

Lumbar puncture/epidural anaesthesia etc.• Risk• Organism• Prevention• Diagnosis and management

Lumbar Puncture

With aseptic technique, negligible risk of meningitis following lumbar puncture

Theoretical risk in patient with bacteraemia at the time of the procedure

Image: Anaesthesiauk

Short-term – for several daysSubcutaneously tunnelled may be left in place for longer (months)

Very low risk of infection with careful aseptic technique; ? Risk with BacteraemiaCase reports and small series in the literature

Images: Wikipedia.org

Epidural Anaesthesia

Very low risk of infection with careful aseptic technique

? Risk with bacteremia

Case reports & small series in the literature

Spinal anaesthesia

CNS electrodes

• Spinal cord, brain

• Very low risk with careful aseptic technique

• The literature in the last 10+ years has concentrated on the risk of transmissable spongioform encephalopathies (TSEs)

Surgical Procedures involving the CNS

– Craniotomy– CSF Shunt

placement/removal/revision– Operative procedures

•Exploration/lobectomy/abscess drainage/excision of tumour etc

CSF Shunt placed:

• Treatment of hydrocephalus• To relieve pressure in PTC/IIH

Shunt or access device:• To administer cytotoxic agents or,

rarely, painkillers (morphine)

Ventriculoperitoneal (VP) and ventroculoatrial (VA) shunts

Ommaya Reservoir

Instillation of agent into Ommaya Reservoir

Indications for shunt placement:Paediatrics• Hydrocephalus

– Congenital• Aqueductal stenosis, Chiari

malformations, Cysts, vascular malformations

– Acquired• Postmeningitic or post-inflammatory,

IVH, Tumour

• Hydraencephaly

Conen et al., Clin Infect Dis 2008:47:73-82

Indications for shunt placement:Adults

Pople I. J Neurol Neurosurg Psychiatry 2002;73:i17-22

CNS Shunt complications

• Infection• Obstruction

– Proximal end, protein accumulation

– [Distal end, protein accumulation]

– Valve obstruction or malfunction

– Catheter disconnection, kinking or migration

• Overdrainage– Extra-axial fluid collection and brain compression– Subdural haematoma– Chiara 1 malformation

• Slit Ventricle• Intraventricual haemorrhage

•

CNS Shunt Complications

Substantial morbidity and risk of mortality

Long term complications• Cognitive defects• Neurological problems

• Death

Criteria for nosocomial Shunt Infection (modified CDC)

• Growth of a pathogen in the CSF, from the shunt tip, or in wounds overlying the implanted material OR

• Fever (>38oC), headache, neck stiffness, cranial nerve signs or irritability without another recognised cause, physician initiation of antimicrobial therapy, and CSF leukocyte count >5 x106/L, CSF protein >0.45g/L, CSF:Blood glucose ratio <0.5, organisms seen on CSF Gram stain, or organisms isolated from blood culture

CNS Shunt Infection

Occurs in up to c.20% • Most common in the first 6

months after surgery• Most common in those

shunted at <6 months• Risk may vary with cause

of hydrocephalus• Incidence decreases with

increasing age• The risk of infection is

greater with a VA than with a VP shunt

Independent risk factors

• Previous shunt infection

• Shunt dysfunction• Post-operative

leakage of CSF• Experience of the

neurosurgeon• Duration of the

operative procedure

Ferguson SD et al, Observations Regarding Failure of Cerebrospinal Fluid Shunts Early After Implantation Neurosurg Focus 2007;22:E7University of Chicago Children’s Hospital

• Retrospective review of 396 shunt placement procedures during an 8-year period

• Data collected on patient age, race, indication for shunting, origin of hydrocephalus, shunt type, date of shunt revision or removal, and number of subsequent revisions

• For failure due to shunt malfunction – data was obtained on the cause of failure (obstruction of valve, proximal catheter or distal catheter)

• For cases of infection, the identity of the causative organism was recorded

Ferguson SD et al, Observations Regarding Failure of Cerebrospinal Fluid Shunts Early After Implantation Neurosurg Focus 2007;22:E7University of Chicago Children’s Hospital

• 396 shunt procedures• 116 shunts failed (90

patients)• M:59%, non-white

54.3%• Shunts were placed

for hydrocephalus 87.9%, PTC 12.1%

• Mean survival time of newly placed shunts - 6.3 +/- 11.8 months

• Shunt failures – Malfunction 83

(71.5%)– Infection 33 (28.5%)

• Pathogens– Staph epi 54%– MSSA 25%– MRSA 12%– Ps aeruginosa 3%– Others inc Serratia

& Corynebacterium 6%

Ferguson SD et al, Observations Regarding Failure of Cerebrospinal Fluid Shunts Early After Implantation Neurosurg Focus 2007;22:E7University of Chicago Children’s Hospital

• 116 shunts failed• Mean survival time of

newly placed shunts - 6.3 +/- 11.8 months– Malfunction 7.1+/- 12.2– Infection 4.3 +/- 10.7

• Shunt failures – Malfunction 83 (71.5%)– Infection 33 (28.5%)

• The origins of hydrocephalus were similar in the 2 groups

• Shunts for Hydrocephalus longer survival than for PTC (p = 0.051)

• Shunts placed age 0-6 mo shorter survival than those after age 6 mo (p = 0.067)

• Shunts with malfunction almost x2 as likely to last longer than 6 months than with infection (p<0.05)

• Mean shunt survival period almost 7 times greater in white than non-white, 20.4 vs 3.1 mo, ANOVA p <0.05

Clin Infect Dis 2008:47:73-82

Findings

• 48 (62%) of infections within 1 month of surgery

• 61 (78%) had fever• 35 (45%) had neck stiffness• 38 (49%) had local signs of inflammation• 80% had CSF leukocyte count >5 x106/L• 81% had elevated CSF lactate• 52% had CSF:blood glucose ratio <0.5• 58% had CSF protein >0.45g/L

Conen et al., Clin Infect Dis 2008:47:73-82

Conen et al., Clin Infect Dis 2008:47:73-82

Conen et al., Clin Infect Dis 2008:47:73-82

• Retrospective review • Pediatric patients age range 1-16 years who

underwent shunt insertion for hydrocephalus over a 3 year period

• Patient FU 12 mo after surgery.• N = 211 patients had 353 shunting procedures;• M:F 195:158, 55%:45%• Shunt type

– VP 326 (92%), VPL 17 (5%), VA 10 (3%)

• The AIS cohort were younger, more frequently premature, had a greater incidence of ICH and more frequently had programmable valves

Sciubba DM et al, Factors contributing to the Medical Costs of Cerebrospinal Fluid Shunt Infection Treatment in Pediatric Patients with Standard Shunt Components Compared with Antibiotic-impregnated Components Neurosurg Focus 2007;22:E9 Johns Hopkins

Sciubba DM et al, Factors contributing to the Medical Costs of Cerebrospinal Fluid Shunt Infection Treatment in Pediatric Patients with Standard Shunt Components Compared with Antibioticimpregnated Components Neurosurg Focus 2007;22:E9

211 patients had 353 shunting procedures;208 standard shunts, 145 AISs (if full system, clindamycin and rifampicin)

After adjusting for intercohort differences, on multivariate analysis, AIS catheters were independently associated with a 2.4-fold decreased likelihoood of shunt infection (relative risk = 0,041, 95% CI 0.32-0.52, p<0.01

Tuan TJ et al. Treatment and Microbiology of Repeated Cerebrospinal Fluid Shunt Infections in Children Ped Inf Dis J 2011;30 731-735University of California at San Francisco

• n = 31 with second shunt infections (SI-2)• Age <6 mo at initial shunt placement 81%• Male 77%• VP shunt 71% • 18 developed SI-3 (60%) and 8, SI-4 (47%)• The median time to SI-3 was 477 days (range 2-828

days) and SI-4 was 2137 days (range 9-2137 days)

• Gram positive organisms predominated (SI-2 93%, SI-3 94%)

“Children with SI-2 experience high subsequent reinfection rates with a long time to reinfection”

Prevention of CNS shunt infections

• Surgical site preparation

• Prophylactic antibiotics

• “Care bundle”

• Antimicrobial impregnanted catheters

• Antimicrobial impregnanted sutures

Surgical prophylaxis Neurosurgery• Prophylaxis is not effective in reducing infection

rates with intracranial pressure monitors – retrospective analysis n = 215, J Neurol Neurosurg Psych 2000;69:381

Recommended for • Clean non-implant surgery (e.g.,

craniotomy)• Clean, contaminated surgery (through

sinuses or oro/nasopharynx)• Insertion of CSF shunt

Clean, non-implant

Infection in Neurosurgery Working Party of the British Society for Antimicrobial Chemotherapy, Antimicrobial prophylaxis in neurosurgery and after head injury

Lancet 1994;344:1547-51

cefazolin 1-2G iv single dosealternative vancomycin 1 g iv single dose

Clean, contaminated

• Clean, contaminated (through sinuses or oro/nasopharynx)

• clindamycin 900mg iv single dose, or amoxicillin-clavulinic acid 1.2g single dose or cefuroxime 1.5g iv single dose plus metrondidazole 500mg iv single dose

CSF Shunt Insertion

• Meta-analysis suggests benefit of prophylaxis (Cochrane Database 3:CD005365, 2006)

• Cefazolin 1-2g iv single dose, alternative vancomycin 1g iv single dose

• In a hospital with a high prevalence of MRSA infection, vancomycin was more effective (J Hosp Infect 2008;69:337

Quality Improvement/”Care Bundle”

Management of Infection

Causes of HCA meningitis/encephalitis/ encephalopathy

The Patient

• Exposure/Cross-infection• Varicella-zoster, influenza virus, measles

virus, Mycobacterium tuberculosis, (N. meningitidis)

• Transfusion/Transplantation– Cytomegalovirus, Epstein-Barr Virus, West

Nile Virus, Tick-borne encephalitis, rabies, T. pallidum, R. rickettsiae, C. neoformans, Coccidioides spp, H. capsulatum,Toxoplasma gondii, human parvovirus (parvovirus B19), CJD, vCJD

Black : N. Europe

Transplant Recipients HCA Infections that may involve the CNS Recipients of: Haemopoietic cell

transplantation – HCT Solid Organ transplant – SOT

• Cytomegalovirus – SOT and HCT• Toxoplasma gondii - HCTWell established and evidence based

prophylaxis regimens

West Nile Virus• A flavivirus transmitted by mosquitos, blood

transfusions, transplanted organs and breast feeding” (Sanford Guide Antimicrobial Therapy 2011)– recipients of kidney or pancreas transplants, and

hematopoietic stem cell transplants – In one cluster (4 organ recipients), blood

transfusion was the probable source of WNV viremia in the donor

• Blood is now tested in the USA due to increased serum lipase in 11/17 cases

TSEs

• TSEs are fatal degenerative brain diseases occurring in humans and in some animal species

• The causative agent is an altered form of a naturally occurring prion protein (PrP). The altered prion protein is referred to as the scrapie agent or PrPsc and accumulates in the brain producing the characteristic pathology.

• PrPsc are resistant to inactivation by chemicals, heat and other standard inactivation methods

CJD and vCJD• The most common human form of TSE, Creutzfeld

–Jakob Disease (CJD), occurs worldwide - incidence of 0.5-1 case/1,000,000 population pre annum

• Variant CJD (vCJD), was described in the UK in 1995, linked to bovine spongioform encephalopathy. In vCJD, the clinical characteristics are different from those of CJD and the altered PrP is more widely distributed in tissues, particularly in the lymphoreticular system.

Transmission of TSEs• No Person-to-person transmission • Iatrogenic transmission of CJD has

occurred via – contaminated dura mater grafts (c. 110 cases) – corneal surgery (1 case, in 1974)– use of cadaver-derived human growth hormone (c.130

cases, appear to be related to HGH therapy before 1985) – contaminated medical devices (2 definite cases, possibly

5 others; no case since 1976)

• There are 4 reported cases of transmission of CJD via blood transfusion

Variant CJD and blood www.hpa.org.uk

• In the UK there have been 4 cases of vCJD infection associated with blood transfusion, 3 of the 4 developed symptoms of vCJD

• All 4 cases had received transfusions of non-leucodepleted red blood cells between 1996 and 1999.

• From 5th April 2004 individuals who received a blood transfusion in the UK since 1980 are no longer accepted as blood donors

Variant CJD and blood products www.hpa.org.uk 17 Feb 2009

• “Evidence of infection with the agent (abnormal prion protein) that causes variant Creutzfeldt-Jakob Disease (vCJD) has been found at post mortem in the spleen of a person with haemophilia”.

• >70 years, no CNS symptoms; recipient of UK sourced clotting factors before 1999 including one batch of factor VIII from a donor who went on to develop vCJD symptoms 6 months after donation

Control and Prevention of CJD and other Transmissable Spongioform Encephalopathies (TSEs) in Irish Healthcare settings

Draft for Consultation June 2011www.hpsc.ie

vCJD transmission in the healthcare setting

• Infectivity is concentrated in the CNS • The transmission risk results from

parenteral exposure to the much lower concentrations of infectivity found in tissues outside the nervous system. Four human cases of transmission of vCJD through blood transfusion have been documented, despite the very low concentration of TSE infectivity in blood,

• If TSE infectivity were excreted, human urine, which is a source of injectable fertility hormones and other drugs could also pose a risk for transmission

• Intracerebral inoculation of urine from infected animals has not transmitted the condition in experiments to date

TSE infectivity

Gregori Luisa, Kovacs Gabor G, Alexeeva Irina, Budka Herbert, Rohwer Robert G

Excretion of transmissable spongioform encephalopathy infectivity in urine

Emerg Inf Dis 2008;14:1406-12

Hamster scrapie – infectivity in urine at v high level

Prevention of transfusion-related CNS disease: Haemovigilance• Donor Selection• Screening• Leucodepletion• CMV negative blood for specific

groups

Vaccine-preventable infection and Immunisation

Some Bacterial Agents of CNS Disease

Disease CNS Disease Use of Vaccine

Invasive Meningococcal Disease

Meningitis,Meningoencephalitis (rare)

Varies worldwide

Invasive Pneumococcal Disease

Meningitis Conjugate vaccines in routine schedule of childhood immunisation in many countries

Targeted/selective immunisation (PS)

Diphtheria Palatal and facial paralysis, generalised peripheral neuropathy (rare)

Routine immunisation worldwide

Some Viral Agents of CNS Disease

Infection CNS Disease Use of vaccine

Influenza Encephalopathy TIV (LAIV in USA)

Measles Encephalitis, cerebellitis, aseptic meningitis,Subacute sclerosing panencephalitis

Routine immunisation worldwide

Mumps Encephalitis, asepticmeningitis, cerebellitis,

Routine immunisation worldwide

Rubella Post-infectious encephalitis, Progressive rubella panencephalitis, Congenital rubella syndrome

Routine immunisation worldwide

Polio Aseptic meningitis, anterior myelitis leading to acute flaccid paralysis (AFP)

Routine immunisation worldwide

Varicella zoster Cerebellitis, encephalitis Routine immunisation US, AUS, NZ.Targeted immunisation other countries

Incidence of CNS Disease following infection

Infection CNS Disease Incidence

Influenza Encephalopathy Rare

Measles Encephalitis, cerebellitis, aseptic meningitis,SSPE

Encephalitis in 0.1% of reported casesSSPE in 5-10/1,000,000

Mumps Encephalitis, asepticmeningitis, cerebellitis,

Asymptomatic Aseptic meningitis in 50-60%; symptomatic in 15% encephalitis in <2/100,000 M>F

Rubella Post-infectious encephalitis, Progressive rubella panencephalitis,Congenital rubella syndrome

1/6,000 encephalitis

PRE Rare

Polio Aseptic meningitis, anterior myelitis leading to acute flaccid paralysis (AFP)

1-2% aseptic meningitis

1:50 to 1:1,000 AFP

Varicella zoster Cerebellitis, encephalitis ?

Immunisation

Possible mechanisms of CNS adverse events after immunisation• Direct neurotoxic effects• Molecular mimicry – antibodies or

stimulated T cells cross-reacting with host antigens

• Immune complex formation - vasculitis• Loss of self tolerance• Host factors may predispose to

neurological illness following immunisation in some individualsRef: James J Sejvar Vaccine and Neurologic Disease

Semin Neurol 2011;31:338-355

Vaccines and specific neuroloigical events

• Mumps Urabe vaccine strain - aseptic meningitis association

• Guillain Barre Syndrome in recipients of the 1976 swine flu vaccine; attributable risk of <1 additional case /100,000 vaccine recipients

• There has been no evidence of an increased risk with subsequent influenza vaccines

Vaccines and specific neuroloigical events

• Increased incidence of narcolepsy with one of the pandemic influenza A H1N1 vaccines; all cases <20 years; most cases in Finland with initial suggestion of genetic predisposition. Cases notified in Ireland are under investigation

• There has been no evidence of an increased risk with other pandemic influenza vaccines or subsequent A H1N1 containing TIV seasonal influenza vaccines

Vaccines and specific neurological events

• Multiple Sclerosis association with hepatitis B vaccine has been repeatedly hypothesised

• The overwhelming evidence is that there is no association

Vaccines and Encephalopathy• Acute encephalopathy with ongoing

sequelae following whole cell pertussis vaccine – UK study 1976 to 1979; based on 35/1,000 acute encephalopathy cases the estimated relative risk within 7 days of wcP vaccine was 2.4. However the diagnoses among many of the cases were subsequently open to question

• Subsequent studies have failed to demonstrate an association

Immunisation and encephalitisPahud BA et al. Lack of association between

childhood immunizations and encephalitis in California, 1998-2008 Vaccine. 2011 Nov 12. [Epub ahead of print]

The immunization records of 246 pediatric encephalitis cases were reviewed; 110 cases were immunised in the year before the onset of encephalitis

There was no increased risk of encephalitis following pertussis-containing or measles--containing vaccines or any number of vaccines administered in a single immunisation episode

Neuropathology of vaccination• Rorke-Adams LB et al. Neuropathology of

Vaccination in infants and children. Vaccine . 2011 Nov 3;29(47):8754-9. Epub 2011 Aug 18.

• 5545 claims were filed under the National Vaccine Injury Compensation Programme, 1990-1999. CNS tissue was available for evaluation by a neuropathologist in 37 cases (33 fatal, 4 had a biopsy or lobectomy)

The most commonly implicated vaccines were DPT/DTaP, MMR and IPV/OPV, but almost all vaccines in current schedule were alleged to be responsible.

• No lesions – 5• Acute anoxic encephalopathy - 14• Inflammation – 5 Vascular anomalies - 4• Developmental anomalies – 4• Cerebral oedema - 2 Degeneration - 2• Heavy metal exposure - 1

• There was no obvious relationship between type of vaccine, time to onset of symptoms or the lesions found

Vaccines and Acute Disseminated Encephalomyelitis (ADEM)• A primary inflammatory demyelinating

disorder of the CNS, no biological marker – a clinical diagnosis; Relatively rapid onset. Progression and remission of the illness with “characteristic” pattern of CNS lesions on MRI

• Temporally associated with viral infection or immunisation, limited evidence, mainly case reports

• The evidence is strongest for the Semple rabies vaccine, some early smallpox vaccines and early mouse-brain derived JEV

Aetiology of encephalitis

• Granerod et al. UK Health Protection Agency (HPA) Aetiology of Encephalitis Study Group. Causes of encephalitis and difference in their clinical presentations in England: a multicentre, population-based prospective study, Lancet Infect Dis 2010;10:835-44. Epub 2010 Oct 15

• 2 year prospective study 24 hospitals• Infectious causes, non-infectious causes and

autoimmunity• n = 203, median age 30 years (0-87)

Aetiology of encephalitis

• 86 Infectious causes– 38 HSV, 10 VZV and 10 MTB

• 75 unknown• 42 acute immune-mediated

– 16 autoimmunity– 26 ADEM

The Healthcare worker and HCA CNS infection/disease

The HealthCare Worker Infections that may involve the CNS• Physicians and workers with direct

patient contact – Varicella-zoster, HIV, influenza virus,

measles virus, Mycobacterium tuberculosis, N. meningitidis

• Laboratory workers– Mycobacterium tuberculosis, C.

diphtheriae, N. meningitidis, HIV, West Nile Virus, C. burnetii, Coccidioides spp

The HealthCare Worker

Exposure to infection in the healthcare setting – Protective measures

• Standard Precautions• Transmission-Based Precautions• Patient Isolation

• Immunisation• Antimicrobial Chemoprophylaxis

HCW - risk perception

Dinelli MI, Moreira TN, Paulino ER, da Rocha MC, Graciani FB, de-Moraes-Pinto MI

Immune status and risk perception of acquisition of vaccine preventable diseases among health care workers

Am J Infect Control 2009;37:858-60

São Paulo, Brazil, n = 187 HCW

Risk perception• Hepatitis B - 94.1%• Influenza - 92.5%• Meningococcal

Disease - 90.3%• Tuberculosis - 85%• Varicella - 72.7%

Previous disease or immunisation

• Hepatitis B – 82.4%• Tetanus - 87.7%• Diphtheria – 81.8%• Measles - 86.6%• Mumps - 85.6%• Rubella – 85%• Varicella - 82.9%• Influenza – 35.8%

Immunisation for HCW – uptodate with routine immunisations plusThose involved on

direct patient care

• BCG, hepatitis B, varicella, influenza

Non-clinical staff in healthcare settings

• hepatitis B, varicella, influenza

Laboratory & Pathology Staff

• BCG, hepatitis B• Others for those

handling specific organisms e.g, meningococcal ACW135Y, hepatitis A

HCW protection; Pollard and Begg

Risk of IMD to HCWs with direct clinical contact: Limited evidenceRetrospective study E and W 1982-1996• 3 pairs of a primary case and HCW with

secondary infection were identified; transmission probably occurred from exposure to respiratory droplets around the time of admission

• Estimated Attack Rate: 0.8/100,000 HCWs at risk, x25 times that in the general population (p = 0.003)

“The excess risk is small and inappropriate use of prophylactic antibiotics should be avoided” Gilmore A, Stuart J, Andrews N. Lancet 2000;356:1654-1655

HCW – Invasive meningococcal disease• Wear face masks and eye protection

when there is a risk of secretions splashing into face and eyes, when working within three feet of patients known, or suspected, to be infected with micro-organisms transmitted by large-particle droplets (>5 micrometers diameter) that can be generated during coughing, sneezing, talking or the performance of clinical procedures.

CDC

CDC

Invasive meningococcal diseaseHealthcare workers seldom require

chemoprophylaxis, and only if they: • have given mouth to mouth resuscitation to the

case since they became ill, or during the seven previous days

• or their mouth or nose has been directly contaminated (clearly felt) with respiratory droplets/secretions from a probable or definite case around the time of admission

• or they develop conjunctivitis within 10 days of contact with a confirmed or probable case.

www.hpa.org.uk

Laboratory-Acquired Meningococcal Disease

• Following 2 cases in the US - Information request on e-mail discussion groups of Infectious Diseases, Microbiology and Infection Control professional organisations

• Probable case: “An illness meeting the case definition for meningococcal disease in a laboratorian who had occupational exposure to an N. meningitidis isolate within 14 days of illness onset”

CDC Sejvar et al J Clin Micro 2005;43:4811-4

Laboratory-acquired meningococcal disease

• 16 cases worldwide 1985 – 2001, including 6 US cases between 1996 and 2000; 14/16 previously unreported. All 16 were clinical microbiologists. 9 were serogroup B, 7 serogroup C. Eight cases were fatal.

• Estimate: an average of x3 microbiologists are exposed to meningococcal isolates annually in the US – calculated attack rate for the period 1996-2001 was 13/100.000 microbiologists, compared to 0.2/100,000 among US adults in general

Laboratory-acquired meningococcal disease

• In 15 cases, isolate manipulation occurred without respiratory protection; specific risk factors likely associated with exposure to droplets or aerosols

• Prevention – use of Class 1 biological safety cabinets or additional respiratory protection during manipulation of suspected meningococcal isolates

Immunisation for HCW - uptodate with routine immunisations plusThose involved on

direct patient care

• BCG, hepatitis B, varicella, influenza

Non-clinical staff in healthcare settings

• hepatitis B, varicella, influenza

Laboratory & Pathology Staff

• BCG, hepatitis B• Others for those

handling specific organisms e.g, meningococcal ACW135Y, hepatitis A

CLINICAL AND VACCINE IMMUNOLOGY 2011;18:483–486Immunogenicity and Safety of a Multicomponent Meningococcal

Serogroup B Vaccine and a Quadrivalent Meningococcal CRM Conjugate Vaccine against Serogroups A, C, W-135, and Y in Adults Who Are at Increased Risk for Occupational Exposure to Meningococcal Isolates

Alan Kimura,* Daniela Toneatto, Annett Kleinschmidt, Huajun Wang, and Peter Dull Novartis Vaccines

“Sequential administration of 4CMenB and MenACWY-CRM provided robust evidence of an immune response against serogroups A, B, C, W-135, and Y in laboratory workers routinely exposed to meningococcal isolates.”

Summary 1• Lumbar puncture, epidural/spinal anaesthesia and

Clean operative procedures on the CNS are associated with a very low risk of infection

• Diagnosis of CNS shunt infection is challenging• CSF shunt infection is more common in those

undergoing shunting in the first 6 months of life and in the first 6 months after shunting

• Infection after reshunting is more common in those who have a new shunt inserted because of infection

• Quality improvements will serve to reduce the incidence of infections following CNS shunt insertion/revision

Summary 2

• Increasing numbers of infections that may involve the CNS are being recognised, many of which may be transmitted via blood transfusion and transplantation

• The risk of CNS disease associated with many acute viral infections is poorly recognised; typically, complications are more common in infection occurring in adults

• Ongoing vigilance is required to minimise exposure of patients to communicable infections

Summary 3

• In general, the risk of CNS pathology following immunisation is very low

• There is poor perception among HCWs of their risk of HCA CNS disease with the exception of a perceived risk of invasive meningococcal disease

• More widespread screening of HCW for vaccine-preventable infection with immunisation of those who are non-immune will minimise the risk of HCA CNS disease

Summary 4

• Influenza immunisation must be strongly encouraged for HCW

• Appropriate precautions are required to minimise the risk of transmission of infection in the laboratory setting

• The availability of new meningococcal vaccines will raise the possibility of protecting HCWs against their small risk of acquiring invasive meningococcal disease