Infectious diseases Flashcards
Bacterial meningitis
Inflammation of the meninges caused by a bacterial infection
Most common causes: Neisseria meningitidis and streptococcus pneumoniae
Neonates – group B streptococcus (usually contracted during birth from the GBS bacteria that can often live harmlessly in the mothers vagina)
Bacterial meningitis presentation
Fever, neck stiffness, vomiting, headache, photophobia, altered consciousness & seizures
Meningococcal septicaemia: children can present with a non-blanching rash
Kernig’s test & Brudzinski’s test
Kernig’s – patient lying on their back, flexing one hip and knee to 90 degrees & slowly straightening the knee whilst keeping the hip flexed at 90 degrees
- Causes slight stretch in meninges and where is meningitis will produce spinal pain or resistance to this movement
Brudzinski’s test – patient lying on their back & gently use your hands to lift their head & neck off the bed and flex their chin to their chest
- Positive test = patient involuntary flexes hip & knees
Bacterial meningitis investigations
Blood cultures & lumbar puncture (ideally before abx)
Send blood tests for meningococcal PCR
Bacterial meningitis management
Medical emergencies & should be treated immediately
Community – children seen in primary care & a patient with a non-blanching rash should receive an urgent stat injection (IM/IV) of benzylpenicillin prior to hospital transfer
Hospital - < 3 months: cefotaxime & amoxicillin, > 3 months: ceftriaxone
- Vancomycin added if there is risk of penicillin resistant infection
- Dexamethasone if LP suggestive of bacterial meningitis
- Notifiable disease – inform PHE
Post exposure prophylaxis of meningitis
Single dose of ciprofloxacin
Should be given as soon as possible & ideally within 24 hours of the initial diagnosis
Viral meningitis
Herpes simplex virus, enterovirus & VZV
Sample of CSF should be sent for viral PCR testing
Tends to be milder than bacterial & often only requires supportive treatment
- Aciclovir can be used to treat suspected or confirmed HSV meningitis
Bacterial vs viral lumbar puncture
Appearance – cloudy vs clear
Protein – high vs mildly raised/normal
Glucose – low vs normal
WCC – high (neutrophils) vs high (lymphocytes)
Culture – bacteria vs negative
Meningitis complications
Hearing loss
Seizures & epilepsy
Cognitive impairment & learning disability
Memory loss
Focal neurological deficits – limb weakness/spasticity
UTIs
Involve infection in the bladder causing cystitis -> can spread up to the kidneys & cause pyelonephritis
Far more common in women – urethra is much shorter making it easy for bacteria to get into the bladder
Main source of bacteria for UTIs – E.coli can easily make the short journey to the urethral opening from the anus
Cystitis presentation
Dysuria
Suprapubic pain/discomfort
Frequency
Urgency
Incontinence
Confusion
Pyelonephritis presentation
Fever
Loin, suprapubic or back pain
Looking and feeling generally unwell
Vomiting
Loss of appetite
Haematuria
Renal angle tenderness on examination
UTIs investigations
Urine dipstick
Midstream urine sample to the microbiology lab to be cultured & have sensitivity testing
UTIs common organism
Escherichia coli
Klebsiella pneumoniae
Enterococcus
Pseudomonas aeruginosa
Staphylococcus saprophyticus
Candida albicans
Cystitis management
Trimethoprim/nitrofurantoin
- 3 days: simple lower urinary tract infection in women
- 5-10 days: antibiotics for women that are immunosuppressed, abnormal anatomy or impaired kidney function
- 7 days: men, pregnant women or catheter-related
UTIs management in pregnancy
UTIs in pregnancy increase the risk of pyelonephritis, premature rupture of membranes & pre-term labour
7 days of abx (first line = nitrofurantoin, second line = cefalexin or amoxicillin)
- Nitrofurantoin is avoided in 3rd trimester (linked with haemolytic anaemia in the newborn)
- Trimethoprim is avoided in the 1st trimester/if they are on another medication that affects folic acid due to anti-folate effects
Urine for culture and sensitivities
Pyelonephritis management
Refer to hospital if features of sepsis
In community, following abx are recommended for 7-10 days:
- Cefalexin
- Co-amoxiclav
- Trimethoprim
- Ciprofloxacin
Encephalitis
Inflammation of the brain parenchyma
Encephalitis aetiology
HSV – common cause of sporadic encephalitis that can be targeted with treatment
Other viruses: arboviruses, VZV, EBV, HIV
Bacteria – mycoplasma, tuberculosis, rickettsial infections
Fungi – histoplasmosis
Parasites – echinococcus
HSV encephalitis
May be either due to type 1 or type 2 – HSV1 is most commonly seen outside of the neonatal periods
- Rapid onset of fever, headache, altered mental status, new-onset seizures and/or neurological deficits
Can cause infection of the CNS by direct invasion via the trigeminal nerve or olfactory tract following primary oropharyngeal infection OR
Invasion into the CNS may occur due to reactivation of the virus that is able to lay dormant within the neuronal ganglia after a primary infection that may have been subclinical
Encephalitis clinical features
Highly variable depending on underlying cause & area of brain that has been affect
Classic triad – new-onset fever, headache & altered mental status
Seizures, behavioural changes, brainstem dysfunction, memory problems, focal neurological deficits
Encephalitis vs meningitis
Difficult to differentiate
Brain function should be preserved in meningitis
Some cases -> patients may have features of both meningitis and encephalitis (meningoencephalitis)
Encephalitis investigations
Bedsides – obs, urinalysis, ECG, sputum cultures
Bloods – FBC, U&Es, bone profile, LFTs, CRP, blood cultures, coagulation
Imaging – CXR, CT head
EEG
CSF analysis – rise in protein, viral PCR, M,C&S, glucose & serology
HSV encephalitis treatment
Aciclovir -> works by competitively inhibiting the viral DNA polymerase, which prevents replication
IV aciclovir should be started empirically in anyone with suspected encephalitis as high mortality
Full course of treatment is given over 14-21 days
C. difficile
Gram positive bacillus – both spore-forming and toxin-producing
Two important strains:
1) Toxigenic – produce and release two exotoxins, central to pathogenicity
2) Nontoxigenic – cannot produce exotoxins & colonises colon without causing disease
C. difficile pathophysiology
CD can release spores from asymptomatic or symptomatic carriers into the environment
Abx disrupt the normal colonic microbiota -> allows toxigenic strains of CD to multiply & release toxins
- Both toxins promote colonic inflammation, intestinal fluid secretion, mucosal injury, neutrophil chemotaxis & activation
- Toxin B approx.. 10x the virulence of toxin A
C. difficile risk factors
Antibiotic use
Age - >65 years
Hospitalisation
Severe underlying co-morbidities
Others: gastric acid suppression, enteral feeding, obesity, GI surgery & chemotherapy
C. difficile clinical features
Diarrhoea – watery but a small amount of blood may be seen
Abdominal pain
Anorexia
Nausea
Fever
More severe disease – haemodynamic instability (tachycardia and hypotension) & severe systemic symptoms (low GCS, poor urine output, peritonitis)
C. difficile stool tests
Stool testing is required to demonstrate CD toxin or the toxigenic strain of CD
- NAAT (PCR-based testing) – detects one or more genes specific to the toxigenic strain
- EIA (C. difficile enzyme glutamate dehydrogenase) – detects enzyme produced by all strains, quick, unable to distinguish between toxigenic & nontoxigenic strains
- EIA (C. difficile toxin A&B) – detects toxin produced by toxigenic strains
NAAT – inability to distinguish between asymptomatic carriage of a toxigenic strain and active CDI
C. difficile investigations
Bedside – observations, stool samples, blood glucose
Bloods – FBC, U&Es, LFTs, bone profile, lipase, blood cultures, VBG (lactate)
Imaging – AXR, CT abdomen & pelvis (more complicated cases)
Flexible sigmoidoscopy – avoided if typical clinical presentation, confirmed CDI on stool testing and/or response to treatment