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
C. difficile management
All patients – correct fluids, VTE prophylaxis, nutritional support, stop laxatives, stop abx, review need for PPI, stop anti-motility drugs & consider other causes of diarrhoea
Mild to moderate – oral metronidazole/oral vancomycin
Severe – oral vancomycin/fidaxomicin if high-risk of recurrence, consider switching to fidaxomicin or adding metronidazole IV if worsening/no improvement at 7 days
Fulminant – oral vancomycin, metronidazole IV, urgent surgical & critical care review
Faecal microbiota transplantation may be indicated in patients with refractory/recurrent CDI – process of transferring a solution of faecal matter containing bacteria from a highly selected donor into the intestinal tract of a receipt
C. difficile complications
Fulminant colitis – hypotension, ileus and/or toxic megacolon
- May lead to multi-organ failure from profound shock/bowel perforation
TMC – defined as marked colonic dilatation & may be complicated by bowel perforation & haemodynamic collapse
Urgent surgical review for consideration of colectomy
Necrotising fasciitis
Life-threatening rapidly-progressing infection that spreads along the fascial planes and subcutaneous tissue
Two microbial types:
1) Type I - polymicrobial infection, primarily caused by a mixture of anaerobes & aerobes – more common, especially in elderly or co-morbid patients
2) Type II – monomicrobial infection, primarily caused by strep pyogenes & more common is healthy individuals with a history of trauma
Necrotising fasciitis risk factors
Diabetes mellitus
CKD
Alcohol excess
Advanced age or frailty
Malnutrition
Metastatic cancer
Immunocompromised
Necrotising fasciitis clinical features
Progress rapidly
Severe pain, often out of keeping with the overt clinical signs
Patients will often by haemodynamically unstable & may show signs of multi-organ dysfunction
Examination – variable, progression can reveal skin erythema, oedema & signs of skin ischaemia, late signs = skin crepitus, vesicles/bullae & obvious skin necrosis
Necrotising fasciitis investigations
Bloods tests – significantly raised WCC & CRP
Blood gas will likely show a raised lactate +/- metabolic acidosis
May also be signs of worsening renal function, hyponatraemia, impaired liver function, raised glucose & coagulopathy, blood cultures should also be taken
Imaging does not have a routine role
Necrotising fasciitis management
Surgical emergency & needs immediate resuscitation and debridement if this is deemed appropriate
Urgent broad spectrum abx
Resus IV fluids & patient catheterised
Area of redness/discolouration needs to be marked & time denoted
Definitive management – urgent surgical debridement (any necrotic tissue should be excised), all cases should be packed following debridement & undergo a relook in 24-48 hours to check for infection/further necrosis
Reconstructive surgery might be needed after initial debridement
Fever in the returning traveller history
Detailed geography of travel, including setting, time of onset of symptoms, duration of symptoms
Ask about activities & events – bites, diet, fresh-water exposure, dust exposure, sexual activity, game parks, farms, caves, unwell contacts
Enteric fever – typhoid & paratyphoid
Typically imported from India, Pakistan and Bangladesh
Caused by related, gram-negative strains of ‘typhoidal’ salmonella spp:
1) Typhoid – salmonella typhi
2) Paratyphoid (less severe) – salmonella paratyphi
Transmission if faecal-oral from contaminated water/food
Enteric fever symptoms
Fatigue, headache, anorexia
Marked fever, abdominal pain, relative bradycardia, cough, constipation, rose spots
Diarrhoea & hepato-splenomegaly in 2nd week
Enteric fever diagnosis & treatment
Isolation of S. typhi from: blood (cultures in first 10d have increased sensitivity), bone marrow, intestinal secretions, stool (increased sensitivity after first week)
Serology, LFT, PCR
Treatment – azithromycin +/- IV ceftriaxone, antipyretics, fluid management, nutrition
Malaria
Infectious disease caused by Plasmodium species
Plasmodium falciparum is most severe & dangerous member
Spread through bites from the female Anopheles mosquitoes
Malaria life cycle
Infected blood is sucked up by feeding mosquito, malaria in the blood reproduces in the gut of the mosquito producing thousands of sporozoites (malaria spores)
When that mosquito bites another human/animal the sporozoites are injected -> travel to the liver & can lie dormant as hypnozoites for severe years in P. vivax and P. ovale
Mature in the liver into merozoites which enter the blood & infect RBCs -> merozoites reproduce over 48 hours, after which the RBCs rupture releasing loads more merozoites into the blood -> haemolytic anaemia
This is why people with malaria have high fever spikes every 48 hours
Malaria clinical features
Non-specific symptoms – fever, sweats, rigors, malaise, myalgia, headache, vomiting
Signs – pallor (anaemia), hepatosplenomegaly, jaundice (bilirubin is released during the rupture of RBCs)
Malaria investigations
Three thick and thin blood films should be completed within a 36 hour period as a minimum to exclude malaria (12-24 hours apart between tests)
Rapid diagnostic tests – utilises antibodies mounted on a testing strip (must be combined with blood films as rare cases of false negatives)
Malaria management
All patients with falciparum malaria should be admitted for treatment as they can deteriorate quite quickly
Oral option in uncomplicated malaria:
1) Riamet (artemether with lumefantrine)
2) Malarone (proguanil and atovaquone)
3) Quinine sulphate
4) Doxycycline
IV options in severe/complicated malaria:
1) Artesunate
2) Quinine dihydrochloride
Falciparum complications
Cerebral malaria
Seizures
AKI
Pulmonary oedema
DIC
Severe haemolytic anaemia
Multi-organ failure & death
HIV
RNA retrovirus
HIV-1 is the most common type
Virus enters & destroys the CD4 T helper cells
Initial seroconversion flu-like illness occurs within a few weeks of infection, then infection is asymptomatic
HIV transmission
Unprotected anal, vaginal or oral sexual activity
Mother to child at any stage of pregnancy, birth or breastfeeding -> referred to as vertical transmission
Mucous membrane, blood or open wound exposure to infected blood or bodily fluids -> sharing needles, needle-stick injuries/blood splashed in an eye
AIDS-defining illnesses examples
Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia
Cytomegalovirus infection
Candidiasis (oesophageal or bronchial)
Lymphomas
Tuberculosis
HIV testing & monitoring
Antibody blood test – hospital to screen for HIV
Testing for the p24 antigen – checking directly for this specific HIV antigen in the blood -> can give a positive result earlier in the infection compared with the antibody test
PCR testing for the HIV RNA -> tests directly for the quantity of the HIV virus in the blood & gives a viral load
Monitoring – CD4 and viral load
- CD4 count: under 200 cells/mm3 is considered end stage HIV/AIDS and puts the patient at high risk of opportunistic infections
- Viral load: numbers of copies of HIV RNA per ml of blood
HIV treatment
Anti-retroviral therapy – 2 NRTIs (eg. tenofovir & emtricitabine) & a third agent (eg. integrase inhibitor, non-nucleoside reverse transcriptase inhibitor)
- Aim to achieve a normal CD4 count & undetectable viral load
Prophylactic co-trimoxazole is given to patients with a CD4 < 200 cells/mm3, close monitoring of cardiovascular risk factors, blood lipids & appropriate treatment, yearly cervical smears for women, vaccinations should be up to date (avoid live vaccines)
Pyrexia of unknown origin
Pyrexia > 3 weeks with no identified cause after evaluation in hospital for 3 days or > 3 out-patient visits
Mostly are due to common diseases with atypical presentations
Pyrexia of unknown origin investigations
Blood tests – FBC, U&Es, LFT, CRP< ESR, electrophoresis, LDH, CK, ANA, ANCA, RF, HIV test, malaria smear, IGRA for TB
Microscopy and culture – blood x3, urine, sputum, stool, CSF
Imaging – CXR, abdominal/pelvis USS, venous doppler
Other – hepatitis serology, CMV, EBV, autoimmune screen
Pneumonia common organisms
Streptococcus pneumoniae, haemophilus influenzae (gram negative coccobacillus)
Pneumonia atypical organisms
Don’t respond to penicillins - treated with macrolides (clarithromycin), fluoroquinolones (levofloxacin) or tetracyclines (doxycyclines)
Legionella pneumophila - typically caused by infected water supplies or air conditioning units, can cause hyponatraemia by causing SIADH
Mycoplasma pneumoniae - causes a milder pneumonia & can cause a rash called erythema multiforme (target lesions forming by pink rings with pale centres)
-Can cause neurological symptoms in young patient
Chlamydophila - might be a school aged child with a mild to moderate chronic pneumonia and wheeze
Coxiella burnetii (Q fever) - linked to exposure to animals and their bodily (eg. farmer with a flu like illness)
Chlamydia psittaci - typically contracted from contact with infected birds (eg. parrot owner)
Pneumonia other organisms (can be cultured)
Moraxella catarrhalis - immunocompromised patients/those with chronic pulmonary disease
Pseudomonas aeruginosa - patients with cystic fibrosis or bronchiectasis
Staphylococcus aureus - patients with cystic fibrosis
Fungal pneumonia
Pneumocystis jiroveci (PCP) - patients are immunocompromised
Particularly important in patients with poorly controlled/new HIV with a low CD4 count
Dry cough without sputum, SoB on exertion & night sweats
Treatment is with co-trimoxazole
Pneumonia symptoms
Fever
Malaise
Cough (purulent sputum)
Dyspnoea
Pleuritic pain
Pneumonia signs
Dull percussion note
Reduced breath sounds
Bronchial breathing
Coarse crepitations
Increased vocal fremitus
Tachycardia
Hypotension
Confusion
Cyanosis
Pneumonia investigations
CXR
FBC (raised WCCs)
U&Es (for urea)
CRP (raised in inflammation and infection)
Sputum cultures
Blood cultures
Legionella and pneumococcal urinary antigens
Pneumonia diagnostic criteria
CURB-65 to assess whether patient needs to be admitted to hospital
Confusion
Urea > 7
Respiratory rate > 30
Blood pressure < 90 systolic or < 60 diastolic
Age > 65
Score 0/1: consider treatment at home, score > 2 consider hospital admission, score > 3 consider intensive care assessment
Pneumonia management
Mild CAP: 5 day course of oral antibiotics (amoxicillin or macrolide)
Moderate to severe CAP: 7-10 course of dual antibiotics (amoxicillin & macrolide)
Pneumonia complications
Pulmonary complications:
-Parapneumonic effusion
-Pneumothorax
-Abscess
-Empyema
Extrapulmonary complications:
-Sepsis
-AF
Infective endocarditis
Any infection of the endocardial (inner lining of the heart) surface of the heart
Infective endocarditis risk factors
Age: > 60 years old
Male
IV drug use
Dentition: poor dental hygiene, dental infections & certain dental procedures
Structural heart disease
Valvular heart disease
Congenital heart disease
Prosthetic heart valves
Previous IE
Intravascular devices
Immunosuppression
Haemodialysis
Infective endocarditis pathophysiology
Bacteria enter the bloodstream and deposit onto the endocardial surface of the heart
Damaged endocardium promotes platelet and fibrin deposition
This allows organisms to adhere and grow, leading to an infected vegetation
The vegetation may increase in size and cause local destruction of valves -> lead to congestive cardiac failure
Infective endocarditis symptoms
Fever
Malaise, lethargy
Anorexia
Weight loss
Abdominal pain (splenic abscess)
Haematuria (renal embolic phenomenon)
Cardiac symptoms
Infective endocarditis signs
Cardiac murmur - pansystolic murmur of MR/early diastolic murmur of AR
Features of HF
Splinter haemorrhages
Petechiae
Janeway lesions
Osler nodes
Roth spots
Splenomegaly
Infective endocarditis investigations
(GOLD STANDARD: pathological examination of resected valvular tissue/embolic fragments)
Blood cultures
-At least 3 sets of blood cultures should be taken at 30 minute intervals with a good volume of blood per bottle
-Strict aseptic technique & should be taken before initiation of systemic abx
Echo
Transthoracic/transoesophageal (TTE is first choice)
Findings:
-Vegetation
-Abscess formation
-Pseudoaneurysm
-Valve perforation
-New dehiscence of a prosthetic valve
Bedside: urine dip
ECG
Bloods: FBC, U&E, CRP/ESR, LFT, venous blood gas
Thorax and abdominal imaging
Cerebral imaging
Duke’s criteria major criteria
Microbiological criteria
-Typical microorganisms from two separate blood cultures OR
-Microorganisms consistent with IE from persistently positive blood cultures
–>/= 2 positive cultures from samples >/= 12 hours apart
–3 or a majority of >/= 4 separate samples taken at least an hour apart
Evidence of endocardial involvement
-Echo evidence of IE OR
-New valvular regurgitation
Duke’s criteria minor criteria
Predisposing heart condition or IVDU
Fever > 38
Vascular phenomenon - arterial emboli, infectious aneurysm, intracranial haemorrhage, Janeway lesion, conjunctival haemorrhage
Immunological phenomenon - glomerulonephritis, Osler nodes, Roth spots, RF +ve
Microbiological evidence - positive cultures not meeting major criteria
Duke’s criteria results
Definite (clinical) - 2 major criteria OR 1 major & 3 minor criteria OR 5 minor criteria
Possible - 1 major and 1 minor criteria OR 3 minor criteria
Infective endocarditis management
Flucloxacillin
Surgery
Indications:
-Heart failure
-Uncontrolled infection
-Prevention of embolisation
Infective endocarditis prevention
Prophylactic abx
High-risk patients undergoing high-risk procedures
Sub-group of high-risk patients:
Prosthetic heart valves
Previous IE
Congenital heart disease
Infective endocarditis complications
Cardiac - heart failure, perivalvular abscess, pericarditis, cardiac tamponade
Neurological - stroke, abscess, meningitis, encephalitis, haemorrhage, seizures
Metastatic infection - mycotic aneurysm, embolisation, abscess formation
Embolisation sequelae - stroke, blindness, ischaemic limb, splenic/renal infarct, PE, MI
