Infection & Immunology Flashcards
Learning objectives
Answer
Define abscess
• A painful collection of pus, usually caused by bacterial infection.
Explain the aetiology/risk factors of abscesses
• They can develop anywhere in the body
• There are TWO main types of abscess:
o Skin abscess
o Internal abscess
• Bacterial infection leads to activation of an immune response and recruitment of neutrophils to the site of infection
• As the white cells attack the bacteria, surrounding tissue is damaged creating a cavity which fills with pus to form an abscess
• Pus = mixture of dead tissue + white cells + bacteria
Summarise the epidemiology of abscesses
- Skin abscesses are relatively common
- IV drug use is a major risk factor for skin abscesses
- Internal abscesses are less common
Recognise the presenting symptoms and signs of abscesses
• Swollen, pus-filled lump under the surface of the skin with associated fever and chills
• Internal abscesses are not visible but are characterised by:
o Pain in the affected area (or referred pain)
o Swinging fevers
o Malaise
Identify appropriate investigations for abscesses
• Ultrasound - can be useful in visualising an abscess
Generate a management plan for abscesses
• Some small skin abscesses may disappear by themselves
• Incision and Drainage
o Before doing this, check to see whether a foreign object is causing the abscess (e.g. needle fragments in IV drug users)
o The abscess is cut open and drained of pus
• Antibiotics
o Can be used alongside incision and drainage
Identify possible complications of abscesses
• Recurrence
Summarise the prognosis for patients with abscesses
• GOOD with treatment
Define anaphylaxis
Acute life-threatening multisystem syndrome caused by sudden release of mast cell and basophil-derived mediators into the circulation
Explain the aetiology / risk factors of anaphylaxis
Immunogenic - IgE-mediated or immune complex/complement-mediated
Non-Immunogenic - mast cell or basophil degranulation WITHOUT the involvement of antibodies (e.g. reactions caused by vancomycin, codeine, ACE inhibitors)
Pathophysiology
o Inflammatory mediators such as histamine are released leading to bronchospasm, increased capillary permeability and reduce vascular tone
o This leads to tissue oedema
Common Allergens
o Drugs (e.g. penicillin)
o Latex
o Peanuts
o Shellfish
o NOTE: anaphylaxis can be caused by the repeat administration of blood products in a patient with selective IgA deficiency (due to the formation of anti-IgA antibodies)
Summarise the epidemiology of anaphylaxis
COMMON
Recognise the presenting symptoms of anaphylaxis
Wheeze
Shortness of breath and a sense of choking
Swelling of lips and face
Pruritus
Rash
NOTE: patients may have a history of other hypersensitivity reactions (e.g. asthma, allergic rhinitis)
Recognise the signs of anaphylaxis on physical examination
Tachypnoea Wheeze Cyanosis Swollen upper airways and eyes Rhinitis Conjunctival infection Urticarial rash Hypotension Tachycardia
Identify appropriate investigations for anaphylaxis and interpret the results
CLINICAL diagnosis
• Serum tryptase, histamine levels or urinary metabolites of histamine may help support the clinical diagnosis
Following an attack
o Allergen skin testing - identifies allergen
o IgE immunoassays - identifies food-specific IgE in the serum
Generate a management plan for anaphylaxis
ABCDE High flow oxygen IM Adrenaline Chlorpheniramine (antihistamine) Hydrocortisone If continued respiratory deterioration, may require bronchodilator therapy Monitor pulse oximetry, ECG and BP
Identify the possible complications of anaphylaxis and its management
SHOCK
Organ damage can result from shock
Summarise the prognosis for patients with anaphylaxis
Good with prompt treatment
Define Behcet’s disease
• An inflammatory multisystem disease that often presents with orogenital ulceration and uveitis
Explain the aetiology/risk factors of Behcet’s disease
- UNKNOWN cause
* Associated with HLA-B51
Summarise the epidemiology of Behcet’s disease
• More common in Turkey, Greece and Central Asia
Recognise the presenting symptoms and signs of Behcet’s disease
- Recurrent ORAL and GENITAL ulceration
- Uveitis
- Skin lesions (e.g. erythema nodosum)
- Arthritis
- Thrombophlebitis
- Vasculitis
- Myo/pericarditis
- CNS symptoms
- Colitis
Identify appropriate investigations for Behcet’s disease
- Diagnosis is very CLINICAL
- Pathergy Test - a needle prick becomes inflamed and a sterile pustule develops within 48 hours
- You may measure complement levels and check for a positive family history
Define candidiasis
• Infection caused by Candida.
Explain the aetiology/risk factors of candidiasis
• Caused by 15 different Candida species • Candida albicans is the MOST COMMON cause of candidiasis in humans • Main types of candidiasis: o Oral candidiasis o Oesophageal candidiasis o Candidal vulvovaginitis o Candidal skin infections o Invasive candidal infections • Risk Factors o Broad-spectrum antibiotics o Immunocompromise (e.g. HIV, corticosteroids) o Central venous lines o Cushing's disease o Diabetes mellitus o GI tract surgery
Summarise the epidemiology of candidiasis
- 60% of the healthy adult population are carriers
- Candidiasis occurs in over 80% of people with HIV
- Candida is one of the most common causes of invasive fungal infections in the Western world
Recognise the presenting symptoms and signs of candidiasis
• Oral Candidiasis
o Oral Thrush (pseudomembranous oral candidiasis) - curd-like white patches in the mouth, which can be removed easily revealing an underlying red base. Most common in neonates
o There are lots of subtypes of oral candidiasis with slightly different features but the main features are: redness of the tongue and mouth, white plaques
• Oesophageal Candidiasis
o Dysphagia
o Pain on swallowing food or fluids
o It is an AIDS-defining illness
• Candidal Skin Infections
o Soreness and itching
o Skin appearance can be variable
o Red, moist skin area with ragged, peeling edge and possibly papules and pustules
Identify appropriate investigations for candidiasis
- Oral Candidiasis - swabs and cultures are not particularly useful because a lot of normal people have candida in their mouth
- Swabs may be relevant to check for drug-resistance
- Therapeutic trials of antifungal (e.g. fluconazole) can help with diagnosis
- Oesophageal Candidiasis: definitive diagnosis is by endoscopy
- Invasive Candidiasis: blood cultures required if candidaemia is possible
Define cellulitis
• Acute non-purulent spreading infection of the subcutaneous tissue, causing overlying skin inflammation
Erysipelas is a superficial infection, affecting the upper layers of the skin, while cellulitis affects the deeper tissues. They can overlap, so it is not always possible to make a definite diagnosis between the two.
Explain the aetiology/risk factors of cellulitis
• Often results from: o Penetrating injury o Local lesions (e.g. insect bits) o Fissuring (e.g. anal fissures) • These allow pathogenic bacteria to enter the skin • Most common organisms o Streptococcus pyogenes o Staphylococcus aureus o NOTE: beware of MRSA • Cellulitis of the orbit (orbital cellulitis) is usually caused by Haemophilus influenzae • Risk Factors o Skin break o Poor hygiene o Poor vascularisation of tissue (e.g. due to diabetes mellitus)
Summarise the epidemiology of cellulitis
• VERY COMMON
Recognise the presenting symptoms of cellulitis
- History of cut, scratch or injury
- Periorbital Cellulitis - painful swollen red skin around the eye
• Orbital Cellulitis - painful or limited eye movements, visual impairment
Recognise the signs of cellulitis on physical examination
• Lesion o Erythema o Oedema o Warm tender indistinct margins o Pyrexia - may suggest systemic spread • NOTE: exclude the presence of an abscess (aspirate if pus suspected) • Periorbital o Swollen eye lids o Conjunctival infection • Orbital Cellulitis o Proptosis o Impaired visual acuity and eye movements o Test for RAPD , visual acuity and colour vision
Identify appropriate investigations for cellulitis
- Bloods - WCC, blood culture
- Discharge - sample and send for MC&S
- Aspiration (if pus is suspected)
- CT/MRI - if orbital cellulitis is suspected (helps assess posterior spread of infection)
Generate a management plan for cellulitis
• Medical
o Oral penicillins (e.g. flucloxacillin) or tetracyclines are effective
o If hospital-acquired - treat empirically based on local guidelines and change depending on the sensitivity of cultured organisms
• Surgical
o Orbital decompression may be needed in orbital cellulitis (EMERGENCY)
• Abscess
o Aspirate
o Incision and drainage
o Excised completely
Identify possible complications of cellulitis
- Sloughing of overlying skin
- Orbital cellulitis - may cause permanent loss of vision, spread to the brain, abscess formation, meningitis, cavernous sinus thrombosis
The severity can range from mild to severe. This will depend on how large the red area is, which part of the body is affected (erysipelas of the face is more serious) and if there are any other health problems such as an impaired immune system or poorly controlled diabetes. Cellulitis and erysipelas can also lead to complications:
Septicaemia, also known as blood poisoning or sepsis (bacteria spreading through the blood, making the person very ill)
Abscess (a collection of pus in the affected area)
Infection spreading to deeper tissues, like the muscle or bone
Long-term swelling of the affected site due to lymphatic vessel damage
Increased likelihood of further cellulitis or erysipelas at the same site
Kidney damage following streptococcal infection
Meningitis following facial erysipelas
Summarise the prognosis for patients with cellulitis
• Good prognosis
Define Conjuctivitis
Conjunctivitis is a common condition that causes redness and inflammation of the thin layer of tissue that covers the front of the eye (the conjunctiva).
Explain the aetiology / risk factors of conjunctivitis
Causes Viruses Bacteria Allergies A chemical splash in the eye A foreign object in the eye In newborns, a blocked tear duct
Risk factors:
Exposure to something for which you have an allergy (allergic conjunctivitis)
Exposure to someone infected with the viral or bacterial form of conjunctivitis
Using contact lenses, especially extended-wear lenses
Summarise the epidemiology of conjunctivitis
Affects 2% annually. Viral is most common
Recognise the presenting symptoms of conjunctivitis
Infective conjunctivitis
If you have infective conjunctivitis, you may also have:
a burning sensation in your eyes
a feeling of grit in your eyes
a sticky coating on the eyelashes – usually when you first wake up in the morning
an enlarged lymph node (gland) in front of the ear
Allergic conjunctivitis
You may have itchy eyes if you have allergic conjunctivitis.
The pattern of symptoms for allergic conjunctivitis depends on the substance you’re allergic to.
Allergies to pollen (hay fever) occur during certain parts of the year. You can have an allergy to:
tree pollen, released during spring
grass pollen, released during the end of spring and beginning of summer
weed pollen, released any time from early spring to late autumn
Recognise the signs of conjunctivitis on physical examination
When symptoms are mild, a diagnosis of viral conjunctivitis can often be made without seeing a doctor, and the condition can be treated at home.
Identify appropriate investigations for conjunctivitis and interpret the results
Based on symptoms, microbial culture
Define encephalitis
• Inflammation of the brain parenchyma
Explain the aetiology / risk factors of encephalitis
Most commonly due to VIRAL INFECTION Viral Causes o Herpes Simplex Virus - MOST COMMON in the UK o VZV o Mumps o Adenovirus o Coxsackie o EBV o HIV o Japanese encephalitis Non-Viral (RARE) o Syphilis o Staphylococcus aureus In immunocompromised patients o CMV o Toxoplasmosis o Listeria Autoimmune or Paraneoplastic o Associated with certain antibodies (e.g. anti-NMDA, anti-VGKC)
Summarise the epidemiology of encephalitis
• UK incidence: 7.4/100,000
Recognise the presenting symptoms of encephalitis
- In most cases, encephalitis is self-limiting and mild
- Subacute onset (hours to days)
- Headache
- Fever
- Vomiting
- Neck stiffness
- Photophobia
- Behavioural changes
- Drowsiness
- Confusion
- History of seizures
- Focal neurological symptoms (e.g. dysphagia, hemiplegia)
- Obtain a detailed TRAVEL HISTORY
Recognise the signs of encephalitis on physical examination
- Reduce consciousness
- Deteriorating GCS
- Seizures
- Pyrexia
Signs of Meningism:
o Neck stiffness
o Photophobia
o Kernig’s test positive
Signs of raised ICP:
o Cushing’s Response: hypertension + bradycardia + irregular breathing
o Papilloedema
Focal neurological signs
MMSE may reveal cognitive/psychiatric disturbance
Identify appropriate investigations for encephalitis and interpret the results
Bloods o FBC - high lymphocytes (indicates viral cause) o U&Es - SIADH may occur as a result of encephalitis o Glucose o Viral serology o ABG MRI/CT o Exclude mass lesion o HSV causes oedema of the temporal lobe on MRI Lumbar Puncture o High lymphocytes o High monocytes o High protein o Glucose is usually normal o Viral PCR EEG - may show epileptiform activity Brain biopsy (rarely needed)
Define epididymitis and orchitis
• Inflammation of the epididymis or testes
o 60% of epididymitis is associated with orchitis
o Most cases of orchitis are associated with epididymitis
Explain the aetiology/risk factors of epididymitis and orchitis
• Most cases are INFECTIVE in origin • Bacterial o If < 35 yrs: Chlamydia and Gonococcus o If > 35 yrs: mainly coliforms (e.g. Enterobacter, Klebsiella) o RARE: TB, syphilis • Viral o Mumps • Fungal o Candida if immunocompromised • 1/3 are IDIOPATHIC • Risk Factors o Diabetes o Rare: vasculitis (e.g. Henoch-Schonlein purpura)
Summarise the epidemiology of epididmytis and orchitis
- COMMON
- Affects all age groups
- Most commonly: 20-30 yrs
Recognise the presenting symptoms of epididymitis and orchitis
- Painful, swollen and tender testis or epididymis
- NOTE: less acute onset than testicular torsion
- Penile discharge
- IMPORTANT: ask about sexual history
Recognise the signs of epididymitis and orchitis on physical examination
- Swollen and tender epididymis or testis
- Scrotum may be erythematous and oedematous
- Pyrexia
- Walking will be painful
- Eliciting a cremasteric reflex may be painful
Identify appropriate investigations for epididymitis and orchitis
• Urine o Dipstick o Early morning urine collections for MC&S • Bloods o FBC - high WCC o High CRP o U&Es • Imaging o Increased blood flow on duplex examination
Generate a management plan for epididymitis and orchitis
• Medical o Antibiotics • Surgical o Exploration of testicles if testicular torsion cannot be excluded clinically o Required if an abscess develops
Identify possible complications of epididymitis and orchitis
- Pain
- Abscess
- Fournier’s gangrene (if the infection is left untreated and spreads)
- Mumps orchitis could cause testicular atrophy and fertility issues
Summarise the prognosis for patients with epididymitis and orchitis
- GOOD if treated
* May take up to 2 months for the swelling to resolve
Define gastroenteritis
• Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort.
Explain the aetiology/risk factors of gastroenteritis
• Caused by viruses, bacteria, protozoa or toxins contained in contaminated food or water (faecal-oral route) • Viral: o Rotavirus o Adenovirus o Astrovirus o Calcivirus o Norwalk virus o Small round structures viruses • Bacterial: o Campylobacter jejuni o Escherichia coli (particularly O157) o Salmonella o Shigella o Vibrio cholerae o Listeria o Yersinia enterocolitica • Protozoal: o Entamoeba histolytica o Cryptosporidium parvum o Giardia lamblia • Toxins from: o Staphylococcus aureus o Clostridium botulinum o Clostridium perfringens o Bacillus cereus o Mushrooms o Heavy metals o Seafood • Commonly contaminated foods: o Improperly cooked meat o Old rice o Eggs and poultry o Milk and cheeses o Canned food
Summarise the epidemiology of gastroenteritis
- COMMON
* Serious cause of morbidity and mortality in the developing world
Recognise the presenting symptoms of gastroenteritis
• Sudden onset nausea, vomiting, anorexia
• DIARRHOEA (bloody or watery)
• Abdominal pain or discomfort
• Fever and malaise
• IMPORTANT: enquire about recent travel, antibiotic use and recent food intake (how the food was cooked, sourced and whether anyone else is ill)
• Time of Onset:
o Toxins = early (1-24 hours)
o Bacterial/viral/protozoal = 12+ hours
• Pay attention to the other effects of toxins:
o Botulinum causes paralysis
o Mushrooms can cause fits, renal or liver failure
Recognise the signs of gastroenteritis on physical
- Diffuse abdominal tenderness
- Abdominal distension
- Bowel sounds are often INCREASED
- In SEVERE gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown
IMPORTANT: ANY DIARRHOEAL CONDITION CAN LEAD TO DEHYDRATION so assess and address the patient’s hydration status immediately
Identify appropriate investigations for gastroenteritis
- Bloods: FBC, blood culture (identify bacteraemia), U&Es (dehydration)
- Stool: faecal microscopy and analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin)
- AXR or ultrasound: exclude other causes of abdominal pain (e.g. bowel perforation)
- Sigmoidoscopy: usually unnecessary unless inflammatory bowel disease needs to be excluded
Generate a management plan for gastroenteritis
- Bed rest
- Fluid and electrolyte replacement with oral rehydration solution (contains glucose and salt)
- IV rehydration may be necessary in those with severe vomiting
- Most infections are self-limiting (so will go away with time)
- Antibiotic treatment is only used if severe or if infective agent has been identified
- NOTE: if botulism is present (due to Clostridium botulinum) treat with botulinum antitoxin (IM) and manage in ITU
- NOTE: this is often a notifiable disease and is an important public health issue
Identify the possible complications of gastroenteritis
- Dehydration
- Electrolyte imbalance
- Prerenal failure (due to dehydration)
- Secondary lactose intolerance (particularly in infants)
- Sepsis and shock
- Haemolytic uraemic syndrome (associated with toxins from E. coli O157)
- Guillain-Barre Syndrome may occur weeks after recovery from Campylobacter gastroenteritis
- NOTE: botulism can lead to respiratory muscle weakness or paralysis
Summarise the prognosis for patients with gastroenteritis
• Good prognosis because most cases are self-limiting
Define infectious colitis
• Inflammation of the colon due to bacteria, parasites or viruses
Explain the aetiology/risk factors of infectious colitis
• Infection leads to inflammation of the colon • Risk Factors o Lack of sanitation o Drinking contaminated water o Antibiotic use
Summarise the epidemiology of infectious colitis
• Quite COMMON
Recognise the presenting symptoms & signs of infectious colitis
- Diarrhoea
- Blood and mucus in the stools
- Lower abdominal pain
- Malaise
- Low-grade fever
Identify appropriate investigations for infectious colitis
- Diagnosis is largely CLINICAL
* Stool culture may be used to identify the causative organism
Define herpes simplex
• Disease resulting from HSV1 or HSV2 infection
Explain the aetiology/risk factors of herpes simplex
• Transmitted via close contact (e.g. kissing, sexual intercourse) with an individual that is shedding the virus
• Pathophysiology
o After primary infection, the virus will become dormant (within nerve ganglia)
o Reactivation may occur in response to physical and emotional stresses or immunosuppression
o The virus causes cytolysis of infected epithelial cells leading to vesicle formation
Summarise the epidemiology of herpes simplex
- 90% of adults are seropositive for HSV1 by 30 yrs
- 35% of adults > 60 yrs are seropositive for HSV2
- More than 1/3 of the world population have recurrent HSV infections
Recognise the presenting symptoms of herpes simplex
• HSV1 - primary infection is often asymptomatic
• Possible symptoms of primary HSV1 infection:
o Pharyngitis
o Gingivostomatitis (eating might be painful)
o Herpetic whitlow (abscess at the end of the finger caused by infection with HSV - it is very painful)
• Symptoms of reactivation of HSV1:
o Prodrome of perioral tingling and burning
o Vesicles appear - they will ulcerate and crust over
o Complete healing within 8-10 days
• Symptoms of HSV2:
o Painful blisters and rash in the genital, perigenital and anal area
o Dysuria
o Fever
o Malaise
• Symptoms of HSV encephalitis:
o Usually caused by HSV1 so causes HSV1 type symptoms
• Symptoms of HSV keratoconjunctivitis
o Watering eyes
o Photophobia
Recognise the signs of herpes simplex on physical examination
• HSV1 Primary Infection
o Tender cervical lymphadenopathy
o Erythematous, oedematous pharynx
o Oral ulcers filled with yellow slough (gingivostomatitis)
o Herpetic whitlow • Herpes Labialis (reactivation affecting the mouth) o Perioral vesicles/ulcers/crusting • HSV2 o Maculopapular rash o Vesicles o Ulcers o All of these are found on the external genitalia, anal margin and upper thighs o Others: inguinal lymphadenopathy, pyrexia • HSV2 Encephalitis o Signs of encephalitis • HSV Keratoconjunctivitis
o Dendritic ulcer on the iris (better visualised with fluorescein)
Identify appropriate investigations for herpes simplex
- Diagnosis is usually CLINICAL
* Vesicle fluid can be sampled and sent for electron microscopy, PCR
Define HIV
• Infection with the human immunodeficiency virus (HIV)
Explain the aetiology/risk factors of HIV
• HIV is transmitted by:
o Sexual intercourse
• Heterosexual intercourse is the MOST COMMON mode of transmission
• Homosexuals are at greater risk in the West
o Blood (and other bodily fluids)
• Mother to child (intrauterine, childbirth, breastfeeding)
• Needles
• Blood transfusions
• Organ transplantation
• Pathophysiology
o HIV enters CD4+ lymphocytes by binding to their gp120 receptors
o Reverse transcriptase allows the incorporation of HIV genetic material into the host genome
o This leads to dissemination of HIV, cell death and eventual T-cell depletion
Summarise the epidemiology of HIV
• Increasing in incidence in Africa and Asia
Recognise the signs and presenting symptoms of HIV
• There are THREE phases of HIV:
o Seroconversion
• Self-limiting
• Fever
• Night sweats
• Generalised lymphadenopathy
• Sore throat
• Others: oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea
o Early/Asymptomatic
• Apparently well
• Some may have persistent lymphadenopathy
• Progressive minor symptoms (e.g. rash, oral thrush, weight loss)
o AIDS
• Syndrome of secondary diseases resulting from immunodeficiency
• Direct Effects of HIV Infection
o Neurological: polyneuropathy, dementia
o Lung: lymphocytic interstitial pneumonitis
o Heart: cardiomyopathy, myocarditis
o Haematological: anaemia, thrombocytopaenia
o GI: anorexia, wasting
o Eyes: cotton wool spots
• Secondary effects resulting from immunodeficiency
o Bacterial Infection: TB, skin infections, pneumococcal infections
o Viral: CMV, HSV, VZV, HPV, EBV
o Fungal: pneumocystic jirovecii pneumonia, Cryptococcus, candidiasis, invasive aspergillosis
o Protozoal: toxoplasmosis, cryptosporidia
o Tumours: Kaposi sarcoma, SCC, non-Hogkin’s lymphoma, Hodgkin’s lymphoma
Identify appropriate investigations for HIV
• HIV testing - HIV antibodies, PCR for viral RNA, CD4 count, viral load
• Others
o Pneumocystic pneumonia - CXR
o Cryptococcal meningitis - brain CT or MRI, LP
o CMV (colitis) - colonoscopy and biopsy
o Toxoplasmosis - brain CT or MRI
o Cryptosporidia - stool microscopy
Define infectious mononucleosis
• Clinical syndrome caused by primary EBV infection
o AKA glandular fever
Explain the aetiology/risk factors of infectious mononucleosis
- EBV is a gamma-Herpes virus (dsDNA)
- It is found in the pharyngeal secretions of infected individuals and is transmitted by close contact (e.g. kissing, sharing eating utensils)
- EBV infection of the epithelial cells of the oropharynx leads to B cell infection
- The infected B cells disseminate EBV across the body leading to a humoral and cellular immune response
- Atypical lymphocytes in the peripheral blood are a classic feature of infectious mononucleosis
- EBV remains latent in lymphocytes
- Reactivation may occur following stress or immunosuppression
Summarise the epidemiology of infectious mononucleosis
• COMMON
• TWO age peaks:
o 1-6 yrs
o 14-20 yrs
Recognise the presenting symptoms of infectious mononucleosis
• Incubation period: 4-8 weeks • Abrupt onset of symptoms: o Sore throat o Fever o Fatigue o Headache o Malaise o Anorexia o Sweating o Abdominal pain
Recognise the signs of infectious mononucleosis on physical examination
- PYREXIA
- Oedema and erythema of the pharynx
- White/creamy exudate on the tonsils
- Palatal petechiae
- Cervical/generalised lymphadenopathy
- Splenomegaly
- Hepatomegaly
- Jaundice (5-10%)
- Widespread maculopapular rash (in patients who have received ampicillin)
Identify appropriate investigations for infectious mononucleosis
• Bloods
o FBC - leucocytosis
o LFTs - high AST/ALT
• Blood Film - lymphocytosis with atypical lymphocytes
• Heterophil Antibody Test (aka Monospot Test, Paul Bunnell Test)
o Based on EBV antigens being similar to antigens on RBCs of many animals but NOT humans
o Mixing blood of an EBV-positive human with animal blood will make the animal’s red cells aggregate and precipitate out of solution
o May give false-negatives in the early stages of infection before antibodies are generated
• Throat swabs - exclude streptococcal tonsillitis
• IgM or IgG to EBV viral capsid antigen
• IgG against Epstein-Barr nuclear antigen (EBNA)
Generate a management plan for infectious mononucleosis
- Bed rest
- Paracetamol and NSAIDs - helps with fever, malaise
- Corticosteroids in SEVERE cases
- IMPORTANT: do NOT give AMPICILLIN or AMOXICILLIN if infectious mononucleosis is suspected - nearly 100% of patients with glandular fever develop a maculopapular rash
- Advice - avoid contact sports for 2 weeks (because of risk of rupturing your spleen)
Identify possible complications of infectious mononucleosis
- Lethargy for several months
- Respiratory - airway obstruction from oedematous pharynx, secondary bacterial throat infection, pneumonitis
- Haematological - haemolytic or aplastic anaemia, thrombocytopenia
- GI/Renal - splenic rupture, fulminant hepatitis, pancreatitis, mesenteric adenitis, renal failure
- CNS - Guillain-Barre syndrome, encephalitis, viral meningitis
- EBV-associated malignancy - Burkitt’s lymphoma (in sub-Saharan Africa), nasopharyngeal cancer, Hodgkin’s lymphoma
Summarise the prognosis for patients with infectious mononucleosis
- Most make uncomplicated recovery (within 3 weeks)
* Immunodeficiency and death are VERY RARE
Define infective endocarditis
• Infection of intracardiac endocardial structures (mainly heart valves)
Explain the aetiology / risk factors of infective endocarditis
• Most common organisms causing infective endocarditis:
o Streptococci (40%) - mainly a-haemolytic S. viridans and S. bovis
o Staphylococci (35%) - S. aureus and S. epidermidis
o Enterococci (20%) - usually E. faecalis
o Other organisms:
• Haemophilus
• Actinobacillus
• Cardiobacterium
• Coxiella burnetii
• Histoplasma (fungal)
• Pathophysiology
o Vegetations form when organisms deposit on the heart valves during a period of bacteraemia
o The vegetations are made up of platelets, fibrin and infective organisms
o They destroy valve leaflets, invade the myocardium or aortic wall leading to abscess cavities
o Activation of the immune system can lead to the formation of immune complexes –> vasculitis, glomerulonephritis, arthritis
• Risk Factors
o Abnormal valves (e.g. congenital, calcification, rheumatic heart disease)
o Prosthetic heart valves
o Turbulent blood flow (e.g. patent ductus arteriosus)
o Recent dental work/poor dental hygiene (source of S. viridans)
Summarise the epidemiology of infective endocarditis
• UK Incidence: 16-22/1 million per year
Recognise the presenting symptoms of infective endocarditis
• Fever with sweats/chills/rigors o NOTE: this might be relapsing and remitting • 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 • New regurgitant murmur or muffled heart sounds • Frequency of heart murmurs: o Mitral > Aortic > Tricuspid > Pulmonary • Splenomegaly • Vasculitic Lesions o Roth spots on retina
o Petechiae on pharyngeal and conjunctival mucosa
o Janeway lesions (painless macules on the palms which blanch on pressure)
o Osler’s nodes (tender nodules on finger/toe pads)
o Splinter haemorrhages
Identify appropriate investigations for infective endocarditis and interpret the results
• Bloods
o FBC - high neutrophils, normocytic anaemia
o High ESR/CRP
o U&Es
o NOTE: a lot of patients with infective endocarditis tend to be rheumatoid factor positive
• Urinalysis
o Microscopic haematuria
o Proteinuria
• Blood Culture
o Do microscopy and sensitivities as well
• Echocardiography
o Transthoracic or transoesophageal (produces better image)
• Duke’s Classification - a method of diagnosing infective endocarditis based on the findings of the investigations and the symptoms/signs
Generate a management plan for infective endocarditis
• Antibiotics for 4-6 weeks • On clinical suspicion = EMPIRICAL TREATMENT o Benzylpenicillin o Gentamicin • Streptococci - continue the same as above • Staphylococci o Flucloxacillin/vancomycin o Gentamicin • Enterococci o Ampicillin o Gentamicin • Culture Negative o Vancomycin o Gentamicin • SURGERY - urgent valve replacement may be needed if there is a poor response to antibiotics
Identify the possible complications of infective endocarditis and its management
- Valve incompetence
- Intracardiac fistulae or abscesses
- Aneurysm
- Heart failure
- Renal failure
- Glomerulonephritis
- Arterial emboli from the vegetations shooting to the brain, kidneys, lungs and spleen
Summarise the prognosis for patients with infective endocarditis
- FATAL if untreated
* 15-30% mortality even WITH treatment
Define malaria
• Infection with protozoan Plasmodium • FIVE types of Plasmodium: o Plasmodium falciparum - MOST SERIOUS o Plasmodium vivax o Plasmodium ovale o Plasmodium malariae o Plasmodium knowlesi
Explain the aetiology/risk factors of malaria
- Transmitted by the bite of the female Anopheles mosquito
- The protozoa grow in red blood cells
- Life Cycle
o Injection of sporozoites into the blood stream by mosquito
o Invasion and replication in hepatocytes
o Parasites reinvade the blood and enter red blood cells
o They replicate within red blood cells and develop ring forms
o Red blood cells rupture and release merozoites, which reinfect other red blood cells
o Gametocytes are taken up when another mosquito feeds, and develop into sporozoites in the gut of the mosquito
o They then move to the salivary gland of the mosquito to be transmitted with the next bite
• Some populations have innate immunity to malaria:
o Sickle cell trait
o G6PD deficiency
o Pyruvate kinase deficiency
o Thalassemia
Summarise the epidemiology of malaria
- Endemic in the tropics
* 250 million people worldwide
Recognise the presenting symptoms of malaria
• Feverish traveller (incubation period can be up to 1 year) • Symptoms are CYCLICAL: o High fever o Flu-like symptoms o Severe sweating o Shivering cold/rigors • NOTE: the interval between cycles of symptoms are slightly different in different types of malaria • Cerebral Malaria Symptoms: o Headache o Disorientation o Coma
Recognise the signs of malaria on physical examination
- Pyrexia
- Anaemia (haemolytic)
- Hepatosplenomegaly
Identify appropriate investigations for malaria
• Thick/Thin Blood Films
o Thick for quantifying
o Thin for identifying type of malaria
• Bloods o FBC - haemolytic picture o U&Es o LFTs o ABG • Urinalysis -check for blood or protein
Define mastitis/breast abscesses
Define breast abscess • Abscess formation in breast tissues. o TWO main forms: • Lactational • Non-Lactational
Explain the aetiology / risk factors of mastitis/breast abscesses
• Caused by INFECTION • Causative organisms defer based on whether the abscess is: o Lactational • Staphylococcus aureus o Non-Lactational • Staphylococcus aureus • Anaerobes • Risk Factors o Lactation o SMOKING o Mammary duct ectasia o Periductal mastitis o Wound infections (e.g. from breast surgery)
Summarise the epidemiology of mastitis/breast abscesses
- Lactational breast abscess are COMMON and tend to occur soon after starting breast feeding or weaning
- Non-lactational breast abscesses are more common in 30-60 yo smokers