Lecture 52 - Part 1 Clinical Infections - Vascular and CNS Flashcards
Bacteraemia
not a diagnosis - bacteria have been detected in the blood
what indicates a blood stream infection
bacteraemia + symptoms/signs of infection
eg. intravascular catheter-related bloodstream infection
Types of bacteraemia
Transient
Intermittent
Continuous
Types of intermittent bacteraemia
pneumonia, pyelonephritis, abcess, meningitis, CRBSI
Types of continuous bacteraemia
endocarditis, mycotic aneurysm, pacing lead infection, infected DVT
Infective endocarditis
infection of the endocardium or devices within the heart
Presentation of Infective endocarditis
- non-specific illness (lethargy, malaise, night sweats, anorexia, weight loss)
- Heart failure (SOB, orthopnea, PND)
- Results of extra-cardiac foci of infection (back pain from HVO, stroke, abdominal pain from splenic infarct
Particularly if known heart valve disease, pacemaker, prosthetic valve, congenital heart disease
Clinical examination of infective endocarditis
fevers more than 38 splinter haemorrhages oslers nodes janeway lesions roth spots conjunctival haemorrhages splenomegaly new murmur
Aetiology of infective endocarditis
Staphylococci and Streptococci, enterococci, pseudomonads, enterobacteriaceae
Diagnosis of infective endocarditis
ECG (transthoracic and transoesophageal) and blood cultures ( 3 sets taken at different times) - 2 in severe sepsis
Non-antimicrobial management of infective endocarditis
IE requires antimicrobial therapy - ideally directed towards pathogens identified by blood cultures
in addition, surgery may be required to:
Replace or repair damaged valves
Remove infection when antimicrobials don’t work
Remove infected devices e.g. pacemaker
Prevent complications like stroke
Drain purulent collections e.g. in spleen or spine
Mycotic aneurysm
Definition: aneurysm resulting from, or secondarily infected by microorganisms
Pathogenesis of mycotic aneurysm
Haematogenous seeding (e.g. secondary to IE)
trauma to arterial wall + direct contamination (e.g. IVDU)
extension from a contiguous infected focus
secondary to septic microemboli (e.g. secondary to IE)
Presentation of mycotic aneurysm
usually systemic symptoms of infection and variable symptoms from aneurysm depending on location
- no localising symptoms
- painless swelling
- painful swelling
- symptoms caused by rupture (e.g. intracerebral haemorrhage, collapse.
Aetiology of mycotic aneurysm
Salmonella spp., Staphylococcus aureus, Streptococcus spp., Pseudomonas aeruginosa, Escherichia coli.
Diagnosis of mycotic aneurysm
Imaging (e.g. USS) and detection of bacteria within tissue.
Management of myctoic aneurysm
surgical removal, stenting or coiling (depending on location) with antibiotics
infected DVT
DVTs can be seeded with bacteria during bacteraemia or directly e.g. IVDU injecting into femoral vein, seeds femoral DVT
presentation of INFECTED DVT
symptoms/signs of DVT and systemic infection and/or respiratory symptoms (when infected thrombus breaks from DVT travels via the venous system to the lungs – infected pulmonary emboli)
Aetiology of infected DVT
Depends on mechanism but commonly S. aureus, streptococci and anaerobes in IVDU
diagnosis of Infected dvt
Multiple (3) blood cultures, confirmation of DVT plus exclusion of other causes e.g. IE
Management of infected DVT
Antibiotics plus anticoagulation
What are the different types of primary infection of the central nervous system (CNS)
Meningitis
Encephalitis
Brain Abscess
Subdural Empyema
How infectious agents can enter CNS
Haematogenous spread:
- most common
- usually via arterial route
- can be retrograde (veins)
Direct implantation
- most often is traumatic
- iatrogenic (rare)
- congenital (meningomyelocele)
Local extension (secondary to establish infections): most often from mastoid, frontal sinuses, infected tooth, etc.
Along peripheral nerves: usually viruses: Rabies, Herpes zoster
What is meningitis
Meningitis refers to an inflammatory process of leptomeninges and CSF (Meningoencephalitis refers to inflammation to meninges and brain parenchyma)
classification of meningitis
Acute pyogenic: usually bacterial meningitis
Aseptic : usually viral meningitis
Chronic: Mycobacterium tuberculosis (TBM), spirochetes (neurosyphilis), Cryptococcus
Clinical features which suggest meningitis
Headache irritable neck stiffness photophobia fever vomiting varying levels of consciousness rash
groups below may have non-specific presentation
- neonates
- elderly
- immunosuppressed
Common bacterial pathogens in 0-4 wks
Streptococcus, agalactiae, Escherichia coli, Listeria monocytogenes, Klebsiella pneumoniae, Enterococcus spp, Salmonella spp
Common bacterial pathogens in 4-12 wks
S, agalactiae, E coli, L. monocytogenes, Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitidis
Common bacterial pathogens in 3 months to 18 yrs
H influenzae, N meningitidis, S pneumoniae
Common bacterial pathogens in 18-50 yrs
S pneumoniae, N. meningitidis
Common bacterial pathogens in over 50 yrs
S pneumoniae, N meningitidis, L. monocytogenes, aerobic gram-negative bacilli
Laboratory diagnosis for meningitis
Blood cultures
Lumbar puncture: CSF for microscopy, Gram stain, culture & Biochemistry
EDTA blood for PCR
CSF Abnormalities in Meningitis
Normal
- Clear colourless, 0-5 lymphocytes,
Bacterial
- Cloudy turbid, 100-2000 polymorphs, orgs, high protein, low glucose
Viral (aseptic) - clear, slightly cloudy, 10-500 lymphocytes, protein normal, glucose normal
TB (chronic)
- Clear, slighlty cloudy, 10-500 lymphocytes protein high and glucose low
cryptococcal
-clear, 10-200 lymphocytes, protein slightly elevated, glucose slightly reduced
Viral meningitis
primarily affects children and young adults
milder signs and symptoms
May start as respiratory or intestinal infection then viraemia
CSF shows raised lymphocyte count (50-200/cu/mm); protein and sugar usually normal
full recovery expected
Causes of viral meningitis
Enteroviruses: Echo, coxsackie A,B, polio
Paramyxovirus: mumps
Herpes simples, VZV
Adenoviruses
Other: arboviruses, lymphocytic choriomeningitis, HIV
Tuberculous meningitis
Higher incidence in immigrant populations who come from countries with high TB incidence
Insidious onset
High frequency of complications, cranial nerve palsies
Delayed diagnosis makes complications more likely
CSF shows predominantly lymphocytic response but polymorphs also present
High protein, low/absent sugar
-Remember increasing MDR TB
Encephalitis
- Acute inflammatory process affecting the brain parenchyma
- Viral infection is the most common and important cause, with over 100 viruses implicated worldwide
Symptoms
- fever
- headache
- behavioural changes
- altered level of consciousness
- focal ner
Causes of viral encephalitis
Herpes virus - HSV-1, HSV-2, Varicella Zoster virus,
cytomegalovirus, Epstein-barr virus, human herpes virus 6
-adenoviruses
-influenza A
- Enteroviruses, Poliovirus
-Measles, mumps and rubella viruses
-Rabies
-Arboviruses: Japanese encephalitis; St. Louis encephalitis virus, West Nile encephalitis virus
Herpes encephalitis
Most common cause of sporadic encephalitis in previously healthy
May be evidence of herpes infection of skin, mucosae
Causes severe haemorrhagic encephalitis affecting temporal lobe
Focal signs and epilepsy features
2-4 cases/million people/year
Acute infection or more commonly reactivation of latent infection (trigeminal nerve ganglion)
30% mortality with treatment
70% mortality without treatment
High mortality so treatment urgently needed with
Aciclovir
treatment for herpes encephalitis
Aciclovir
Recurrent meningitis symptoms
> 2 episodes meningitis
Symptom-free intervals
Normal CSF between episodes
Must be differentiated from chronic meningitis
Rabies
Acute, progressive viral encephalitis
Highest case fatality of any infectious disease
One of the most ancient diseases described
Model zoonosis
Pathogenesis of rabies
Virus enters through bite, grows at trauma site for a week and multiplies, then enters nerve endings and advances toward the ganglia, spinal cord and brain.
Infection cycle completed when virus replicates in the salivary glands
Clinical phases of rabies
Prodromal phase – fever, nausea, vomiting, headache, fatigue; some experience pain, burning, tingling sensations at site of wound
Furious phase – agitation, disorientation, seizures, twitching, hydrophobia
Dumb phase – paralyzed, disoriented, stuporous
Progress to coma phase, resulting in death
Brain abscess
A brain abscess is a focal suppurative process within the brain parenchyma (pus in the substance of the brain)
how do brain abscesses occur
Direct spread from “contiguous” suppurative focus (e.g. from ear 40%, sinuses, teeth)
Haematogenous spread from a distant focus e.g. endocarditis, bronchiectasis (often multiple abscesses)
Trauma (e.g., open cranial fracture, post-neurosurgery)
Cryptogenic (no focus is recognised ~15-20 per cent of cases).
Causes of brain abscesses
bacteria depend on the pathogenic mechanism involved
Brain abscesses are often mixed (polymicrobial)
Streptococci (60-70 %) e.g. Streptococcus “milleri”
Staphylococcus aureus (10-15 percent) most common pathogen in abscesses after trauma/surgery
Anaerobes e.g. Bacteroides spp.
Gram negative enteric bacteria (E.coli, Pseudomonas spp.)
Others e.g. fungi, Mycobacterium tuberculosis, Toxoplasma gondii
Clinical presentation of brain abscesses
Headache Focal neurological deficit (30-50%) fever (<50%) Nausea, vomiting seizures neck stiffness papilloedema
Management of brain abscesses
Drainage is treatment of choice (N.B small abscesses can be treated with antibiotics alone)
to urgently reduce intracranial pressure
to confirm diagnosis
to obtain pus for microbiological investigation
to enhance efficacy of antibiotics
to avoid spread of infection into the ventricles
Principles in antibiotic treatment of CNS infections
Physiological properties of blood-brain barrier and blood CSF-barrier are distinct
Penetration of drugs into CSF and brain tissue differ
Ampicillin, Penicillin, Cefotaxime, Ceftazidime, and Metronidazole achieve therapeutic concentrations in intracranial pus
Steroids used for CNS infections
Dexamethasone
10mg IV 15 minutes prior to antibiotics
Shown to decrease morbidity & mortality in S. pneumoniae but NOT N. meningitidis
What is neurosyphilis
Central nervous system invasion occurs early in infection in 30-40% of patients
Asymptomatic neurosyphilis can occur at any stage of syphilis
Early symptomatic forms (months to a few years)
Acute meningitis
Meningovascular (stuttering stroke)
Late symptomatic forms (> 2 years)
General paresis
Tabes dorsalis
Diagnosis by blood & CSF serology
