Infection & Immunology Flashcards
Define an abscess.
A mass of necrotic tissue, with dead and viable neutrophils suspended in tissue breakdown products (pus), surrounded by a layer of inflammatory exudate.
Explain the aetiology / risk factors of an abscess.
The disruption of a tissue barrier through a penetrating injury, local infection or the migration of normal flora to the sterile areas of the body becomes walled off in an attempt to limit further spread of the infection.
Common Bacteria:
- Staphyloccocus
- Streptococci
- Enteric organisms - e.g. E.coli
- Coliforms and anaerobes - e.g. Bacteroides spp.
TB - cold abscesses.
Risk factors:
- Local - tissue necrosis, an under-perfused space or foreign body that provides a focus for infection - e.g. a tooth or root fragment, splinters, mesh of hernia repair or embedded hair
- Systemic - diabetes, immunosuppression (although may interfere with pus formation)
PATHOLOGY
- Bacteria incidte intense acute inflammatory response
- Formation of pus - collection of cellular debris and bacteria
- Becomes surrounded by fibrinous exudate and granulation tissue - macrophages and fibroblasts
- Collagen deposition and walling off
= Abscess
Cold Abscess
- Collections of caseating necrosis
- Conatining myobacterium
- Cold = not associated acute inflammatory response
Summarise the epidemiology of an abscess.
Common in all ages.
Recognise the presenting symptoms of an abscess.
Local effects:
- Pain
- Swelling
- Heat
- Redness
- Impaired function of the area
- Dolor
- Tumour
- Calor
- Rubor
- Functionalaesa
- Celsian features of acute inflammation
Systemic:
- Fever
- Feeling unwell
Recognise the signs of an abscess on physical examination.
Within an organ
- No localizing signs
- Swinging pyrexia - caused by periodic release of microbes or inflammatory mediators into the systemic circulation
Old Adage
= If pus is somewhere and the pus is nowhere, then pus is under the diaphragm
= SUBPHRENIC ABSCESS
Identify appropriate investigations for an abscess and interpret the results.
Bloods
- FBC - high neutrophils
- Imaging - US, CT or MRI
- Imaging - 67-Ga white cell scanning to search for site
- Aspiration - low in glucose, acidic
- Culture of pus for organisms and sensitivity to antibiotics
Generate a management plan for an abscess.
PREVENTION
- Prophylactic antibiotics - e.g. operations
- Given early during an infection
- Often not effective once abscess has formed
GENERAL
- Drainage of pus
- Removal of necrotic and foreign material
- Anti-microbial cover
- Correction of predisposing cause
SURGERY
- Drainage of pus by incision and drainage
- Debridement of cavity
- Free drainage by packing of cavity (if superficial) or by drains (if deep)
IR
- US or CT guidance to localise and aspirate contents
Identify the possible complications of an abscess and its management.
- Cellulitis - skin
- Bacteraemia
- Systemic sepsis
- Chronic abscess
- DIscharging sinus
- Fistula
- Sterile collection
- Antibioma
- Pressure necrosis of surrounding tissues
- Destruction of normal functioning tissue
Summarise the prognosis for patients with an abscess.
Good if adequately drained and predisposing factor removed.
If left untreated, abscesses tend to point to the nearest epithelial surface and may spontaneously discharge their contents.
Depp abscesses may become chronic, undergoing dystrophic calcification.
Define candidiasis.
Infection with candida, especially as causing oral or vaginal thrush.
Explain the aetiology / risk factors of candidiasis.
Dimorphic fungus (yeast) colonizes approx. 30% individuals.
- Colonization begins shortly after birth and persists throughout life
- Found in respiratory, GI, genitourinary tracts and the skin and mucous membranes
- Exists in both yeast (blastospore) phase and hyphal (mycelial) phase, depending on surrounding conditions
- Immunocompetent individuals provide effective immune surveillance against Candida
- Any immune defect can lead to infection and visible disease
Risk factors:
- Antibiotics
- Corticosteroids
- Dental prostheses
- Chemotherapy
- Radiation treatment
- HIV
Summarise the epidemiology of candidiasis.
Rise in Candida infections - due to diabetes, malignancy, chemotherapy, human immunodeficiency virus
200 species - most common C. albicans.
Recognise the presenting symptoms of candidiasis.
- Areas of heat and humidity and maceration
- Burning
- Itching
- Irritation
- Redness and swelling
- Pain and soreness
- Rash
Recognise the signs of candidiasis on physical examination.
Cutaneous
- Under breasts
- In gluteal and inguinal folds
- Diaper area
- Under pannus
- Armpit
- Erythema with satellite papules
- Overlying white plaques - intertrigo
Oral
- Thrush
- Infants and elderly
Identify appropriate investigations for candidiasis and interpret the results.
- Superficial scraping
- Add saline - see pseudohyphae and yeast under microscope
- KOH added to nail or skin specimens to help dissolve the keratin and visualise the yeast
- Calcolfluor white - rapid diagnosis with a fluorescent microscope
- Culture and sensitivities
Skin biopsy with periodic acid-Schiff (PAS) staining
Define cellulitis and erysipelas.
Cellulitis - an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue, characterised by redness, swelling, heat and tenderness and usually occurs in an extremity.
Erysipelas - a distinct form of superficial cellulitis with notable lymphatic involvement, that is raised and sharply demarcated from uninvolved skin.
Explain the aetiology / risk factors of cellulitis and erysipelas.
Often results from penetrating injury (e.g. IV cannulation), local lesions (e.g. insect bites, sebaceous cysts, surgery) or fissuring (e.g. in anal fissured, toe web spaces), which allows pathogenic bacteria to enter the skin.
In rare cases of septicaemia, it can arise spontaneously from blood-borne sources.
Most common organisms: Streptococcus pyogenes, Staphylococcus aureus. (MRSA not uncommon)
If occuring in orbit, Haemophilus influenzae is most common cause, arising from adjacent sinuses.
Risk Factors:
- Diabetes
- Venous insufficiency
- Eczema
- Oedema
- Lymphoedema
Summarise the epidemiology of cellulitis and erysipelas.
Very common.
Main risk factors - skin break poor hygiene, poor vascularization of tissue (e.g. DM)
Recognise the presenting symptoms of cellulitis and erysipelas.
History of cut, scratch or injury.
Periorbital:
- Painful swollen red skin around eye
Orbital cellulitis:
- Painful or limited eye movements
- Visual impairment
Recognize the signs of cellulitis and erysipelas on physical examination.
Cellulitis - acute onset of red, painful, hot, swollen skin
Erysipelas - well-demarcated, bright-red raised skin
Lesion:
- Erythema
- Oedema
- Warm tender indistinct margins
- Pyrexia (may indicate systemic spread)
- Orange-peel appearance
- Bistering & bleeding
Exclude Abscess:
- Test for fluid thrill or fluctuation
- Aspirate if pus suspected
Periorbital:
- Swollen eyelids
- Conjunctival injection
Orbital Cellulitis:
- Proptsis - protrusion of the eyeball
- Impaired acuity and eye movement
- Test for relative afferent pupillary defect, visual acuity and colour vision (to monitor optic nerve function)
Identify appropriate investigations for cellulitis and erysipelas and interpret the results.
Bloods
- WCC / CRP / ESR
- U&E
- Blood culture
Discharge
- Culture & sensitivity
- Skin swab and biopsy
Aspiration
- Often non-purulent, not usually necessary
CT/MRI Scan
- When orbital cellulitis is suspected - to assess the posterior spread of infection
Generate a management plan for cellulitis and erysipelas.
Medical:
- Oral penicillins - e.g. flucloxacillin, benzylpenicillin, coamoxiclav (community)
- Tetracyclines (community)
- Hospital - treat empirically using local microbiological guidelines but change depending on sensitivity of any cultured organisms
- IV use may be necessary
Surgical
- Orbital decompression if orbital cellulitis (emergency)
Abscess
- Can be aspirated, incised and drained or excised completely
Identify the possible complications of cellulitis and erysipelas and its management.
- Sloughing of overlying skin
- Localised tissue damage
- Orbital cellulitis - permanent vision loss, spread to brain, abscess formation, meningitis, carvenous sinus thrombosis
Summarise the prognosis for patients with cellulitis and erysipelas.
Good with treatment
Define Behcet’s disease.
A systemic vasculitis.
Can cause skin and mucosal lesions, uveitis, major arterial and venous vessel disease, and gastrointestinal and neurological manifestations.
Identify appropriate investigations for Behcet’s disease and interpret the results.
1st Line:
- Pathergy testing - induration with or without formation of a pustule within 48 hours
- Rheumatoid factor - negative
- Anti-nuclear antibodies - negative
- Anti-neutrophil cytoplasmic antibodies - negative
- HLA-B51 - present
- Lumbar puncture - hypercellularity, lymphocytosis, polymorphonuclear cells or pleocytosis
- MRI - white matter changes involving midbrain, brainstem and basal ganglia
- Colonoscopy - inflammation and apthous-type ulcers, vasculitis on biopsy
- Upper GI endoscopy - inflammation and apthous-type ulcers, vasculitis on biopsy
- CT chest - haemorrhage, pulmonary aneurysm
- CT chest angiography - haemorrhage, pulmonary aneurysm
- CTPA - pulmonary aneurysm
Emerging:
- Anti-Saccharomyces cervisiae antibodies - may be elevated when GI symptoms are present
Recognise the signs of Behcet’s disease on phyiscal examination.
Common:
- Increased predisposition in certain ethnic / geographic groups
- Oral ulcers
- Genital ulcers
- Uveitis
- Acne lesions
- Erythema nodosum
- Limitated duration of symptoms
- Superficial thrombophlebitis
- Hypopyon - inflammatory cells in the anterior chamber of eye
Uncommon:
- Stroke
- Eye pain, blurry vision, photophobia or photosensitivity
- Memory loss
- Headache, confusion or fever
- Haemoptysis, cough, shortness of breath or chest pain
- Eye redness or tearing
- Impaired speech, balance or movement
- Cramping abdominal pain, diarrhoea or GI ulceration
Recognise the presenting symptoms of Behcet’s disease.
Common:
- Increased predisposition in certain ethnic / geographic groups
- Oral ulcers
- Genital ulcers
- Uveitis
- Acne lesions
- Erythema nodosum
- Limitated duration of symptoms
- Superficial thrombophlebitis
- Hypopyon - inflammatory cells in the anterior chamber of eye
Uncommon:
- Stroke
- Eye pain, blurry vision, photophobia or photosensitivity
- Memory loss
- Headache, confusion or fever
- Haemoptysis, cough, shortness of breath or chest pain
- Eye redness or tearing
- Impaired speech, balance or movement
- Cramping abdominal pain, diarrhoea or GI ulceration
Summarise the epidemiology of Behcet’s disease.
Most commonly seen in Turkey, Israel, the Mediterranean basin and eastern Asia - where Japan and South Korea report the most cases.
Most commonly seen in young people aged 20-30 years.
More active and severe in males.
Explain the aetiology / risk factors of Behcet’s disease.
In many patients, disease activity decreases with time and this natural course can affect treatment decisions about the type and duration of medical therapy.
Presents in various combinations and sequences in patients over time.
Risk factors:
- Age 20-40 years
- Family history
- Genetic predisposition - evidence for genetic anticipation
Define anaphylaxis.
A severe, generalized or systemic hypersensitivity reaction, characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes.
Explain the aetiology / risk factors of anaphylaxis.
A systemic response is caused by the release of immune and inflammatory mediators from basophils and mast cells.
Most frequently caused by allergies to food, medication and venoms.
Non-immunological anaphylaxis - similar symptoms (anaphylactoid reaction).
Risk factors:
- <30 years old - food associated, exercise induced
- Atopy / asthma
- History of anaphylaxis
- Exposure to a common sensitiser - e.g. latex
- Adult age - food, insect venom, medicine related
- Female sex
Summarise the epidemiology of anaphylaxis.
The lifetime prevalence of anaphylaxis is currently estimated at 0.05-2 % in the USA and ~3 % in Europe. Several population-specific studies have noted a rise in the incidence, particularly in the hospitalizations and ER visits due to anaphylaxis.
Recognise the presenting symptoms of anaphylaxis.
- Acute onset
- Shortness of breath
- Confusion or disorientation
- Hives (urticaria)
- Nausea
- Vomiting
- Diarrhoea
- Incontinence
- Abdominal cramps and pain
- Agitation
- Anxiety
- Sense of impending doom = angor animi
Recognise the signs of anaphylaxis on phyiscal examination.
- Airway swelling - angio-oedema
- Inspiratory stridor
- Hoarse voice
- Chest hyperinflation
- Wheezing
- Accessory muscle use
- Cyanosis
- Respiratory arrest
- Pale clammy skin
- Hypotension
- Tachycardia or bradycardia
- Cardiac arrest
- Erythema
- Pruritus
- Rhinits
- Bilateral conjunctivitis
Identify appropriate investigations for anaphylaxis and interpret the results.
1st Line:
- Mast cell tryptase - may be elevated, normally undetectable
- 12-lead ECG - myocardial ischaemia, non-specific ST ECG changes post-adrenaline and with anaphylaxis
- U&E - normal in initial phase of anaphylaxis unless comorbidity present
- ABG - elevated lactate, metabolic acidosis
Consider:
- CXR - may show hyperinflation if bronchoconstriction, interstitial fluid
(After time-critical interventions have been administered)
Generate a management plan for anaphylaxis.
IN CARDIORESPIRATORY ARREST
- CPR and ALS
- Do not give IM adrenaline after cardiac arrest has occurred as circulation to the muscle is inadequate
NOT IN CARDIORESPIRATORY ARREST
- ABCDE
- Position patient and remove trigger
- Adrenaline - IM 150ug adrenaline into anterolateral aspect of middle third of thigh, repeat if no improvement after 5 minutes
- Establish airway plus high-flow oxygen - 94-96% target sats
- IV fluids - rapid IV fluid challenge (500-1000mL, kids 20mL/kg) over <15 mins with crystalloid that has sodium concentration 130-154 mmol/L to counteract fluid shifts associated with vasodilation and/or capillaries
- Serial CR assessments - pulse oximeter, ECG monitor, non-invasive blood pressure monitor
- Nebulised adrenaline
- Nebulised short-acting beta-2-agonist - e.g. salbutamol 5mg every 20-30 mins (adult)
- IV atropine
- IV glucagon
AFTER TREATMENT
- Antihistamine - e.g. chlorphenamine - 10mg IM/IV single dose, may be repeated up to 4 doses per day
- Corticosteroid - e.g. hydrocortisone sodium succinate 200mg IM/IV
- Monitor for biphasic reactions (incidence 1-20%)
- Review by a senior clinician and observation
POST-ANAPHYLAXIS
- Adrenaline autoinjector
- Antihistamine - e.g. chlorphenamine 4mg orally every 4-6 hours, max 24mg / day
- Corticosteroid - e.g. prednisolone
NB:
Length of needle
- 25 mm (blue 23G or orange 25G) needle is best and suitable for all ages
- 16 mm (orange 25G) needle is appropriate for preterm or small infants
- 38 mm (green 21G) needle may be needed in some adults.
Injection technique
- Stretch the skin and give the injection with the needle at a 90° angle to the skin.
Identify the possible complications of anaphylaxis and its management.
- Brain damage
- Kidney failure
- Cardiogenic shock
- Arrhythmias
- Heart attacks
- Death
Summarise the prognosis for patients with anaphylaxis.
With prompt treatment, the overall prognosis of anaphylaxis is good, with a case fatality ratio of less than 1% reported in most population-based studies [Resuscitation Council (UK), 2012].
Define infective endocarditis.
Infection of intracardiac endocardial structures - mainly heart valves.
Explain the aetiology / risk factors of infective endocarditis.
Vegetations form as a result of lodging of the organisms on the heart valves during a period of bacteraemia.
- Made of platelets, fibrin, infective organisms
- Poorly penetrated by immune system
- Destroy valve leaflets
- Invade myocardium
- Invade aortic wall
- Abscess cavities form
- Activation of immune system also causes formation of immune complexes –> cutaneous vasculitis, glomerulonephritis, arthritis
Endocardium can be colonized by virtually any organism, but most common are:
1) Streptococci (40%) - mainly alpha-haemolytic Streptococcus viridans or bovis
2) Staphylococci (35%) - aureus or epidermidis (IVDU)
3) Enterococci (20%) - faecalis
4) Others - e.g. Coxiella burnetti, histoplasma, HACEK - Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
Risk Factors:
- Abnormal valves - e.g. congenital, post-rheumatic, calcification, degeneration
- Prosthetic heart valves
- Turbulant flow - e.g. patent ductus arteriosus or VSD
- Recent dental work
- Bacteraemia
- S.bovis –> GI Malignancy
Summarise the epidemiology of infective endocarditis.
16-22 per million per year (UK)
Recognise the presenting symptoms of infective endocarditis.
- Fever
- Sweats
- Chills
- Malaise
- Arthralgia
- Myalgia
- Confusion
- Skin lesions
- Ask about recent dental surgery or IV drug use
Recognise the signs of infective endocarditis on physical examination.
- Pyrexia
- Tachycardia
- Signs of anaemia
- Clubbing - if long-standing
- New regurgitant murmur
- Muffled heart sounds
- Splenomegay
NB: Right-sided lesions may imply IV drug use.
Frequency:
Mitral > Aortic > Tricuspid > Pulmonary
Vasculitic Lesions:
- Roth’s spots - petechiae on retina
- Petechiae (especially on pharyngeal and conjunctival mucosa)
- Janeway lesions - painless palmar macules that blanch on pressure
- Osler’s nodes - tender nodules on finger / toe pads
- Splinter haemorrhages - nail-bed haemorrhage
Identify appropriate investigations for infective endocarditis and interpret the results.
1) Bloods
2) Urinalysis
3) Blood culture
4) Echocardiography
5) Others
Bloods
- FBC - high neutrophils, normocytic anaemia
- High ESR and CRP
- U&E
- Rheumatoid factor positive
Urinalysis
- Microscopic haematuria
- Proteinuria
Blood Culture
- 3 sets 1 hour apart
- Culture and sensitivity vital but start empirical treatment first
- Culture negative 2-5%
Echocardiography (Transthoracic)
- Transoesophageal echocardiography more sensitive for endocarditis
- Useful for detection of vegetations, valve abscess, diagnosis of prosthetic valve endocarditis, assessment of embolic risk
Others:
- ECG - conduction changes
- CXR - septic pulmonary emboli : focal lung infiltrates, central cavitation - e.g. tricuspid valve endocarditis
Duke’s Classification (2 major, 1 major + 3 minor, all minor):
- MAJOR - positive blood culture in 2 separate samples, positive echocardiogram
- MINOR - high grade pyrexia >38 degrees, risk factors, positive blood culture (no major criteria), positive echocardiogram (not major), vascular signs
+ve echocardiogram = vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation
Risk factors:
- Abnormal valves
- IV drug use
- Dental surgery
Generate a management plan for infective endocarditis.
Antibiotics for 4-6 weeks (at least 6 weeks for prosthetic valve endocarditis).
On clinical suspicion:
- Benzylpenicillin + Gentamycin
- Gentamycin - dose adjusted for peak serum level of 3-4ug/ml, trough <1ug/ml
STREPTOCOCCI
- Continue Benzylpenicillin + Gentamycin
- Alt - Ceftriaxone, Vancomycin
STAPHYLOCOCCI
- Flucloxacillin / Vancomycin + Gentamycin
- Prosthetic - Vancomycin + Gentamicin + Rifampin
ENTEROCOCCI
- Ampicillin + Gentamycin
HACEK
- Ampicillin or Ceftriaxone + Gentamycin
Culture Negative
- Vancomycin + Gentamycin
Surgery
- If poor response or deterioration = urgent valve replacement
- Replacement of prosthees
- Kissing mitral valve vegetations - may be able to salvage
Prophylaxis
- If history of infective endocarditis + undergoing high risk procedures
- High risk procedures - e.g. dental, incision or biopsy of respiratory mucosa, procedures in patients with GI/GU tract infection, procedures on infected skin or musculoskeletal tissue, prosthetic heart valve placement
- Dental - 2g oral amoxicillin 30-60 mins before procedure
Identify the possible complications of infective endocarditis and its management.
- Valve incompetence
- Intracardiac fistulae or abscesses
- Aneurysm formation
- Heart failure
- Renal failure
- Glomerulonephritis
- Arterial emboli from vegetations (brain, kidney, lungs, spleen)
Summarise the prognosis for patients with infective endocarditis.
Fatal if untreated.
When treated, 15-30% mortality.
Define infectious mononucleosis.
A clinical syndrome most commonly caused by Epstein-Barr virus (EBV) infection in 80-90% of cases.
Mononucleosis syndrome used when the syndrome is caused by a non-EBV aetiology.
Explain the aetiology / risk factors of infectious mononucleosis.
Risk factors:
- Kissing
- Sexual behaviour
Summarise the epidemiology of infectious mononucleosis.
More than 90 percent of adults worldwide show serologic evidence of Epstein Barr virus infection.
Most common time to develop clinical infectious mononucleosis: Freshman year in college.
Incubation period: 4-8 weeks.
Recognise the presenting symptoms of infectious mononucleosis.
- Adolescents and young adults
- Febrile illness
- Sore throat
- Enlarged lymph nodes
- Malaise
Recognise the signs of infectious mononucleosis on physical examination.
TRIAD: Fever, Pharyngitis & Lymphadenopathy
+ atypical lymphocytosis
+ positive heterophile antibodies test
+ positive serological test for antibodies against EBV
Other Rarer Signs:
- Splenomegaly
- Rash
- Signs of hepatitis - hepatomegaly, jaundice
- Myalgia
Identify appropriate investigations for infectious mononucleosis and interpret the results.
TRIAD: Fever, Pharyngitis & Lymphadenopathy
+ atypical lymphocytosis
+ positive heterophile antibodies test
+ positive serological test for antibodies against EBV
1st Line:
- FBC - lymphocytosis, atypical lymphocytosis
- Heterophile antibodies - positive
- EBV-specific antibodies - positive for VCA-IgM, VCA-IgG, EA, EBV, EBNA
- LFTs - elevated transaminases (transient, mild)
2nd Line:
- Real-time PCR - EBV DNA detection
- Abdominal US Scan - Splenomegaly
- CT Abdo - Splenic rupture (haemodynamically stable patient when rupture is suspected)
Generate a management plan for infectious mononucleosis.
- Supportive care - paracetamol, ibuprofen, hydration, anti-pyretics, analgesics
- Add Corticosteroid if upper airway obstruction or haemolytic anaemia - Prednisolone
Identify the possible complications of infectious mononucleosis and its management.
- Upper airway obstruction
- Splenic rupture
- Fulminant hepatitis
- Encephalitis
- Severe thrombocytopaenia
- Haemolytic anaemia
- Long-term fatigue & lethargy
Summarise the prognosis for patients with infectious mononucleosis.
Most people with mono recover completely with no long-term problems. The fatigue associated with the condition may persist for a few months after the fever and other symptoms have resolved. Severe complications as described above are very rare.
Define gastroenteritis and infectious colitis.
Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
Explain the aetiology / risk factors of gastroenteritis and infectious colitis.
Caused by viruses, bacteria, protozoa or toxins in contaminated food or water.
Virus - e.g. rotavirus, adenovirus, astrovirus, calcivirus, Norwalk virus, small round structured viruses
Bacteria - e.g. Campylobacter jejuni, E.coli 0157, Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica
Protozoal - e.g. Entamoeba histolytica, Cryptosporidium parvum, Giardia lamblia
Toxins - e.g. from Staphylococcus aureus, Cryptosporidium parvum, Giardia lamblia
Commonly contaminated foods - Improperly cooked meat - e.g. S.aureus, C.perfringens - Old rice - e.g. B.cereus, S.aureus - Eggs & poultry - e.g. Salmonella - Milk and cheeses - e.g. Listeria, Campylobacter - Canned food - e.g. botulism
Non-inflammatory mechanisms - e.g. V. cholerae, enterotoxigenic E.coli (enterotoxins causing enterocytes to release water and electrolytes)
Inflammatory mechanisms - e.g. Shigella, enteroinvasive E.coli (release cytokines, invade, damage epithelium), Salmonella typhi (greater invasion and bacteraemia)
Summarise the epidemiology of gastroenteritis and infectious colitis.
Common
Under-reported
Morbidity & mortality in developing world
Recognise the presenting symptoms of gastroenteritis and infectious colitis.
- Sudden onset nausea
- Vomiting
- Anorexia
- Diarrhoea - bloody or watery
- Abdominal pain / discomfort
- Fever
- Malaise
NB: Enquire about recent travel, antibiotic use and recent food intake - how cooked, source, anyone else ill.
Time of onset:
- Toxins - early, 1-24h
- Bacterial/Viral/Protozoal - 12h or later
Effect of toxin:
- Botulinum - paralysis
- Mushrooms - fits, renal or liver failure
Recognise the signs of gastroenteritis and infectious colitis on physical examination.
- Diffuse abdominal tenderness
- Abdominal distension
- Increased bowel sounds
Severe:
- Pyrexia
- Dehydration
- Hypotension
- Peripheral shutdown
Identify appropriate investigations for gastroenteritis and infectious colitis and interpret the results.
- Blood
- Stool
- AXR or US
- Sigmoidoscopy
Blood
- FBC, blood culture (bacteraemia), U&Es (dehydration)
Stool
- Faecal microscopy for polymorphs, parasites, oocytes, culture, EM (viraL)
- Analyse for toxins, pseudomembranous colitis - e.g. Clostridium difficile toxin
AXR or US
- Exclude other causes of abdominal pain
Sigmoidoscopy
- IBD exclusion
Generate a management plan for gastroenteritis and infectious colitis.
- Bed rest
- Fluids
- Electrolyte replacement
- Oral rehydration solution - glucose, salt
- IV rehydration if severe vomiting
- Antibiotic treatment if severe or infective agent identified - e.g. ciprofloxacin against Salmonella, Shigella, Campylobacter
- Educate on basic hygiene and cooking
NB: Botulism - Botulinum anti-toxin IM and manage in ITU
Identify the possible complications of gastroenteritis and infectious colitis and its management.
- Dehydration
- Electrolyte imbalance
- Pre-renal failure
- Secondary lactose intolerance (infants)
- Sepsis & shock (Salmonella, Shigella)
- Haemolytic uraemic syndrome (E.coli 0157)
- Guillian-Barré syndrome in weeks after Campylobacter gastroenteritis
Botulism - respiratory muscle weakness, paralysis
Summarise the prognosis for patients with gastroenteritis and infectious colitis.
Majority of cases self-limiting
Define conjunctivitis.
The inflammation of the lining of the eyelids and eyeball caused by bacteria, viruses, allergic or immunological reactins, mechanical irritation, or medicines.
Explain the aetiology / risk factors of conjunctivitis.
Risk Factors:
- Exposure to infected person
- Infection in one eye
- Environmental irritants
- Allergen exposure
- Camps, swimming pools, military bases
- Asian or Mediterranean young male
- Atopy
- Contact lens use
- Ocular prosthesis
- Mechanical irritation
Summarise the epidemiology of conjunctivitis.
The incidence of bacterial conjunctivitis was estimated to be 135 in 10 000 in one study.
Recognise the signs of conjunctivitis on physical examination.
- Watery discharge
- Ropy, mucoid discharge
- Purulent discharge
- Itching predominant symptom
- Eyelids stuck together in morning
- Tender, pre-auricular lymphadenopathy
- Conjunctival follicles
- Superficial punctate keratopathy
- Unilateral disease
- Corneal subepithelial infiltrates
- Corneal pannus
- Vesicular skin rash
Identify appropriate investigations for conjunctivitis and interpret the results.
- Rapid adenovirus immunoassay
- Cell culture
- Gram stain
- Polymerase chain reaction
- Ocular pH
Define encephalitis.
Inflammation of the brain parenchyma.
Explain the aetiology / risk factors of encephalitis.
Causes:
- VIRAL - e.g. HSV, herpes zoster, mumps, adenovirus, coxsackie, echovirus, enteroviruses, measles, EBV, HIV, rabies (Asia), Nipah (Malasia), arboviruses transmitted by mosquitos (Jap B encephalitis - Asia, St Louis and West Nile encephalitis - USA)
- NON-VIRAL - e.g. syphillis, Staphylococcus aureus
- IMMUNOCOMPROMISED - e.g. CMV, toxoplasmosis, Listeria
- AUTOIMMUNE OR PARANEOPLASTIC - associated with antibodies - e.g. anti-NMDA or anti-VGKC
Summarise the epidemiology of encephalitis.
7.4 in 100,000 in UK
Recognise the presenting symptoms of encephalitis.
- Can be mild and self-limiting
- Subacute onset (hours to days)
- Headache
- Fever
- Vomiting
- Neck stiffness
- Photophobia - i.e. symptoms of meningism (meningoencephalitis)
- Behavioural changes
- Drowsiness
- Confusion
- History of seizures
- Focal neurological symptoms - e.g. dysphagia, hemiplegia
- DETAILED TRAVEL HISTORY
Recognise the signs of encephalitis on physical examination.
- Reduced level of consciousness with deteriorating GCS
- Seizures
- Pyrexia
- Neck stiffness
- Photophobia
- Kernig’s test positive
- Hypertension
- Bradycardia
- Papilloedema
- Focal neurological signs - e.g. dysphagia, hemiplegia
- Minimental examination may reveal cognitive or psychiatric disturbances
NB: Raised intracranial signs and meningism signs.
Identify appropriate investigations for encephalitis and interpret the results.
- Bloods
- MRI / CT
- Lumbar Puncture
- EEG
- Brain Biopsy
Bloods
- FBC - high lymphocytes
- U&E - SIADH may occur
- Glucose - compare with CSF glucose
- Viral serology
- ABG
MRI / CT
- Excludes mass lesion
- HSV produces characteristic oedema of the temporal lobe on MRI
Lumbar Puncture
- High lymphocytes
- High monocytes
- High protein
- Glucose usually normal
- CSF culture difficult
- Viral PCR now first line
EEG
- Epileptiform activity
- E.g. spiking activity in temporal lobes
Brain Biopsy
- Rarely performed
Define herpes simplex virus.
Includes HSV1 and HSV2.
Explain the aetiology / risk factors of herpes simplex virus.
Alpha-herpes virus with double-stranded deoxyribonucleic acid (dsDNA). Transmitted via close contact with an individual shedding the virus (e.g. kissing, sexual intercourse).
Multiply in epithelial cells of mucosal surface.
Produces vesicles or ulcers.
Lifelong latent infection when virus enters sensory neurons at infection site.
Can then reactivate, replicate and infect surrounding tissue - occurs in response to physical, emotional stresses or immunosuppression.
Summarise the epidemiology of herpes simplex virus.
HSV1 - infection in 2/3 of world’s population (approx 3.7 billion <50 years)
HSV2 - infection in 11% of world’s population ( approx 400 million)
90% adults seropositive for HSV1 by 30 years.
35% adults >60 years seropositive for HSV2.
1/3rd population recurrent HSV infections.
Recognise the presenting symptoms of herpes simplex virus.
HSV1 Primary Infection:
- Asymptomatic
- Pharyngitis
- Gingivostomatitis - may make eating very painful
- Herpetic whitlow - inoculation of virus into a finger
Recurrent infection / reactivation:
- Prodrome (6h) peri-oral tingling and burning
- Vesicles appear (48h), ulcerate and crust over
- Complete healing 8-10 days
HSV2
- Very painful blisters and rash in genital, perigenital and anal area
- Dysuria
- Fever
- Malaise
HSV Keratoconjunctivitis:
- Epiphoria - watering eyes
- Photophobia
Recognise the signs of herpes simplex virus on physical examination.
Primary Infection:
- Subclinical or sensory nerve prodrome (tingling)
- Vesicles
- Shallow ulcers
Systemic Symptoms:
- Fever
- Malaise
- Tender cervical lymphadenopathy
- Heals 8-12 days
Reactivation:
- Usually less severe unless immunosuppressed
Herpes Labialis:
- Cold sore lesion at lip border, predominantly HSV1
Genital Herpes:
- Predominantly HSV2
Gingivostomatitis:
- Fever
- Sore throat
- Tender oropharyngeal vesicles
- Yellow slough filled ulcers
Keratoconjunctivitis:
- Corneal dendritic ulcers
- Avoid steroids
Herpetic Whitlow:
- Painful vesicles on distal phalanx due to inoculation through a break in the skin
Herpes Encephalitis:
- Most common treatable viral encephalitis
- Transfer of virus from peripheral site to brain via neuronal transmission
- Prodrome - fever, malaise, headache, nausea
- Encephalopathy - general/ focal signs of cerebral dysfunction including psychiatric symptoms, seizure, focal neurology (temporal involvement in 60%), memory loss (HSV1 in immunocompetent patients)
Identify appropriate investigations for herpes simplex virus and interpret the results.
- Clinical diagnosis
- Confirmation required in encephalitis, keratoconjunctivitis or immunosuppression
- Viral PCR of CSF, swab or vesicle scraping
- Culture
- Immunofluorescence
- Serology
Define incision and drainage of an abscess.
A time-honored method of draining abscesses to relieve pain and speed healing. Routine cultures and antibiotics are usually unnecessary if an abscess is properly drained.
Summarise the indications for incision and drainage of an abscess.
- Palpable fluctuant abscess
- An abscess that does not resolve despite conservative measures
- Large abscess >5mm
Identify the possible complications of incision and drainage of an abscess.
- Inadequate anaesthesia
- Pain during and after the procedure
- Bleeding
- Reoccurrence of abscess formation
- Septic thrombophlebitis
- Necrotizing fasciitis
- Fistula formation
- Damage to nerves and vessels
- Scarring
Define epididymitis and orchitis.
Epididymitis - inflammation of the epididymis
Orchitis - inflammation of one or both testicles
Acute epididymitis - inflammation of the epididymis characterized by scrotal pain and swelling of less than 6 weeks’ duration.
Acute Epididymo-orchitis - if concurrent inflammation of the testis is present.
Explain the aetiology / risk factors of epididymitis and orchitis.
Sexually active men - most commonly caused by:
- Chlamydia trachomatis
- Neisseria gonorrhoea
- Mycoplasma genitalium
Older men - most commonly caused by enteric pathogens:
- Bladder outlet obstruction
- Recent instrumentation of the urinary tract
- Systemic illness
RISK FACTORS:
- Unprotected sexual intercourse
- Bladder outflow obstruction
- Instrumentation of urinary tract
- Immunosuppression
- Vasculitis
- Amiodarone
- Mumps
- Exposure to TB
Summarise the epidemiology of epididymitis and orchitis.
Usually unilateral.
Recognise the presenting symptoms of epididymitis and orchitis.
- Irritative lower urinary tract symptoms
- Urethral discharge (purulent)
- Fever
Common
- Presence of risk factors
- Age >19 years
- Gradual onset
- Symptoms <6 weeks’ duration
- Frequent and painful micturition
Recognise the signs of epididymitis and orchitis on physical examination.
Common
- Unilateral scrotal pain
- Tenderness
- Hot
- Erythematous
- Swollen hemiscrotum
Uncommon
- Pyrexia
- Fluctuant swelling or induration of scrotal tissue
- Enlarged or tender prostate
Identify appropriate investigations for epididymitis and orchitis and interpret the results.
1st line:
- Gram stain of urethral secretions - >5 WBC per oil immersion field, intracellular gram-negative diplococci
- Urine dipstick test - positive leukocyte esterase tests shown as colour change on the reagent strip
- Urine microscopy - >10 WBC per high-power field
- Urine culture - Isolate of causative organism
- NAAT (nucleic acid amplification test) of urethral secretions or first-void urine - Chalmydia trachomatis, Neisseria gonorrhoea, Mycoplasma genitalium DNA / RNA detected
- Culture of urethral secretions - positive culture for N.gonorrhoea
Consider:
- Colour duplex US - epididymis is enlarged, hyperaemic, low-resistance monophasic arterial waveform pattern, good for localising areas of inflammation
- Surgical exploration - oedematous epididymis with vascular congestion and evidence of surrounding inflammatory reaction, with no evidence of testicular torsion
- 3 early morning urine samples for acid-fast bacilli staining, culture and NAAT - may be positive
- HIV test - may be positive
- Syphilis test - may be positive
Generate a mangement plan for epididymitis and orchitis.
BACTERIAL INFECTION
- Abx
- Supportive measures - paracetamol or naproxen or ibuprofen
NB: Abx
Gonorrhoea / Chlamydia suspected - ceftriaxone and doxycycline
Gonorrhoea / Chlamydia suspected, Gonorrhoea likely - ceftriaxone, doxycycline and azithromycin
Gonorrhoea / Chlamydia / Enteric organisms suspected - ceftriaxone, ofloxacin / levofloxacin
Enteric organisms suspected - ofloxacin or levofloxacin
M Genitalium suspected - moxifloxacin
AMIODARONE-INDUCED
- Discontinuation or dose reduction
- Supportive measures - paracetamol or naproxen or ibuprofen
UNDERLYING VASCULITIS
- Specialist referral to rheumatologist - can be due to Behcet’s Syndrome or Henoch-Schonlein purpura
- Supportive measures - paracetamol or naproxen or ibuprofen
IDIOPATHIC OR VIRAL
- Supportive measures - paracetamol or naproxen or ibuprofen
TB
- Anti-TB antibiotics - guidelines!
- Specialist referral
- Supportive measures - paracetamol or naproxen or ibuprofen
Identify the possible complications of epididymitis and orchitis and its management.
- Scrotal abscess and pyocele
- Testicular infarction
- Fertility problems
- Testicular atrophy
- Cutaneous fistulization from rupture of abscess through tunica vaginalis
- Recurrence, chronic epididymitis and orchialgia
Summarise the prognosis for patients with epididymitis and orchitis.
Most epididymitis cases clear up within 3 months. However, more invasive treatment may be needed in some cases. If an abscess has formed on the testicles, your doctor can drain the pus using a needle or with surgery. Surgery is another option if no other treatments have been successful.
Define HIV.
A pandemic infectious disease whose impact on societies is without precedent.
AIDS - develops over 10-15 years.
Explain the aetiology / risk factors of HIV.
Caused by a retrovirus that infects and replicates in human lymphocytes and macrophages, eroding the integrity of the human immune system over a number of years, culminating in immune deficiency and a susceptibility to a series of opportunistic and other infections as well as the development of malignancies.
Most people are infected through sexual contact, before birth or during delivery, during breastfeeding, or when sharing contaminated needles and syringes.
Risk Factors:
- Needle sharing with IV drug use
- Unprotected receptive anal intercourse
- Unprotected receptive penile-vaginal sexual intercourse
- Percutaneous needle stick injury
- High maternal viral load - mother to child transmission
- Use of progestin-only injectable contraceptives
- HSV-2 infection
Summarise the epidemiology of HIV.
1.7 million people were newly infected in 2018.
Recognise the presenting symptoms of HIV.
- Presence of risk factors
- Fevers
- Night sweats
- Weight loss
- Skin rashes
- Post-inflammatory scars
- Oral ulcers
- Angular cheilitis
- Oral thrush
- Oral hairy leukoplakia
- Diarrhoea
- Wasting syndrome
- Changes in mental status or neuropsychiatric function
- Recent hospital admissions
- TB
- Medical comorbidities
- Sexual activity
- Generalised lymphadenopathy
- Kaposi’s sarcoma
- Genital STIs
- Chronic vaginal candidiasis
- Shingles
- Headaches
- Periodontal disease
- Retinal lesions on fundoscopy
- SOB
- Cyanosis
- Dry cough
- Silent chest
- Peripheral neuropathy
- Hepatomegaly or splenomegaly
- Meningeal signs (bacterial or viral meningitis)
Recognise the signs of HIV on physical examination.
- Presence of risk factors
- Fevers
- Night sweats
- Weight loss
- Skin rashes
- Post-inflammatory scars
- Oral ulcers
- Angular cheilitis
- Oral thrush
- Oral hairy leukoplakia
- Diarrhoea
- Wasting syndrome
- Changes in mental status or neuropsychiatric function
- Recent hospital admissions
- TB
- Medical comorbidities
- Sexual activity
- Generalised lymphadenopathy
- Kaposi’s sarcoma
- Genital STIs
- Chronic vaginal candidiasis
- Shingles
- Headaches
- Periodontal disease
- Retinal lesions on fundoscopy
- SOB
- Cyanosis
- Dry cough
- Silent chest
- Peripheral neuropathy
- Hepatomegaly or splenomegaly
- Meningeal signs (bacterial or viral meningitis)
Identify appropriate investigations for HIV and interpret the results.
1st Line:
- Serum HIV ELISA
- Serum HIV rapid test
- HIV non-invasive tests
- Serum Western blot
- Serum p24 antigen
- Serum HIV DNA PCR
- CD4 count - CD4 count of >500 cells/mL: patients are usually asymptomatic; CD4 count of <350 cells/mL: implies substantial immune suppression; CD4 count <200 cells/microlitre: defines AIDS and places the patient at high risk of most opportunistic infections
- Serum viral load (HIV RNA)
- Drug resistance testing
- Pregnancy test
- Serum hep B serology
- Serum hep C serology
- Serum venereal disease research lab test - positive if syphilis infection
- Treponema pallidum haemagglutination test - positive if syphilis infection
- Rapid plasma reagin - positive if syphilis infection
- Tuberculin skin test
- FBC with differential - anaemia, thrombocytopenia
- Serum electrolytes
- Serum creatinine
- Urinalysis - proteinuria (renal disease), leukocytes and nitriles (UTI)
Consider:
- CXR - Pneumocystis jirovecii pneumonia: interstitial to extensive alveolar shadowing; TB: many abnormalities possible including apical fibrosis/scarring, pleural effusion, hilar adenopathy, miliary pattern, lobar or patchy opacification; bacterial pneumonia: lobar or patchy opacification
- LFTs
- Random of fasting lipid profile - ART high levels
- Random or fasting plasma glucose - ART high levels
- Hep A serology (IgG)
- Toxoplasma serology (IgG)
- Gonorrhoea and Chalmydia testing
- HLA-B*5701 testing
Define mastitis / breast abscesses.
Localised infection with pus collection in breast tissue.
2 main forms - puerperal (lactational) and non-puerperal.
Explain the aetiology / risk factors of mastitis / breast abscesses.
Lactational:
- Milk stasis associated with infection
- Most commonly with Staphylococcus aureus, coagulase-negative staphylococci
Non-Puerperal:
- Staphylococcus aureus and anaerobes
- Enterococci or Bacteroides spp.
- TB and actinomycosis - more rare
- Smoking, mammary duct ectasia / periductal mastitis, associated inflammatory breast cancer excluded
- Associated with wound infections after breast surgery, diabetes and steroid therapy
Summarise the epidemiology of mastitis / breast abscesses.
Lactational breast abscesses are common and tend to occur soon after starting breast-feeding and on weaning, when incomplete emptying of the breast results in stasis and engorgement. Non-lactational abscesses are more common in those aged 30-60 years and in smokers.
Recognise the presenting symptoms of mastitis / breast abscesses.
The patient complains of discomfort and development of a painful swelling in an area of the breast. She may complain of feeling unwell and feverish.
Women with a non-puerperal abscess often have a history of previous infections, systemic upset is often less pronounced.
Recognise the signs of mastitis / breast abscesses on physical examination.
Local
- Area of breast is swollen, warm and tender
- Overlying skin inflammation
- Cracks or fissures in nipple
- Non-puerperal cases - evidence of scars or tissue distortion, or signs of duct ectasia (e.g. nipple retraction)
Systemic
- Pyrexia
- Tachycardia
Identify appropriate investigations for mastitis / breast abscesses and interpret the results.
- USS
- Aspiration for microscopy, culture and sensitivity of pus samples
Generate a management plan for mastitis / breast abscesses.
Medical
- Early, cellulitic phase treated with antibiotics - flucloxacillin for lactational, +metronidazole in non-puerperal
- Breast drainage regularly to prevent milk stasis
Surgical
Lactational
- Daily needle aspiration with antibiotic cover
- Formal incision and drainage for >5cm
- Cosmetically acceptable and ensures full drainage
- Loculi explored and broken down
- Wound may be packed lightly and left open, with daily packing, or primary closure performed
- Breastfeeding should continue from the non-affected breast and the affected side emptied either manually or with a breast pump
- Advice on avoided cracked nipples
Non-puerperal
- Open drainage should be avoided
- Carried out through small incision
- Definitive treatment carried out once infection has settles by the excision of the involved duct system
Identfiy the possible complications of mastitis / breast abscesses and its management.
- Slow wound healing
- Difficulties in breastfeeding
- Poor cosmetic outcome
- Mammary fistula formation
- Overlying skin undergoes necrosis
Summarise the prognosis for patients with mastitis / breast abscesses.
- Untreated, it will eventually point and spontaneously discharge onto the skin surface
- Non-puerperal abscesses tend to recur
Define neutropenic sepsis.
It is defined as a temperature of greater than 38°C or any symptoms and/or signs of sepsis, in a person with an absolute neutrophil count of 0.5 x 10^9/L or lower.
Explain the aetiology / risk factors of neutropenic sepsis.
Causes:
- Cytotoxic chemotherapy - temporary reduction in production of blood cells (5-10 days after chemotherapy neutrophils are at their lowest, recover 5 days later)
- Drugs - azathioprine, methotrexate, sulfasalazine, adalimumab, infliximab
- Stem cell transplantation
- Infections
- Bone marrow disorders such as aplastic anaemia and myelodysplastic syndromes
- Nutritional deficiencies
- Autoimmune
Risk factors:
- People receiving high-intensity chemotherapy regimens
- People undergoing haematopoietic stem cell transplantations
- Age - >60yrs
- Chemotherapy
- Corticosteroids
- Antibiotics
- Advanced maliganncy
- History of previous febrile neutropenia
- Prolonged hospital admission
- Previous surgery
- DM
- Liver disease
- Renal disease
- Poor nutritional status
- CV access device
- TPN - risk of invasive fungal infection
Summarise the epidemiology of neutropenic sepsis.
Rate of increase of deaths is higher for 15-24 year old age group, lower for >80 age group.
Recognise the presenting symptoms of neutropenic sepsis.
- Neutrophil count <0.5 x 10^9/L
- Temperature >38 degrees
- Chills and shvering
- Tachycardia
- Tachypnoea
- Clammy
- Cold
- Pale or mottled skin
- Dizziness
- Confusion
- Disorientation
- Slurred speech
- Diarrhoea
- N&V
