Infection and immunology Flashcards
Define varicella zoster
Where does it lie dormant
Primary infection is called varicella (chickenpox).
Reactivation of the dormant virus in the dorsal root ganglia, causes zoster (shingles).
Confusingly also known as herpes zoster in some texts.
Explain the aetiology / risk factors of varicella zoster
Pathogenesis:
Where is the infection, where does virus replicate, where does it remain latent
VZV is an herpes ds-DNA virus. Highly contagious, transmission is by aerosol inhalation or direct contact with the vesicular secretions
Viral inhalation and infection of upper respiratory tract. Viral replication in regional lymph nodes, liver and spleen. By week 2– 3 infection spreads to skin producing rash then leading to clinical resolution. Virus remains latent in dorsal root ganglia (lifelong). Reactivation causes virus to travel down sensory axon to produce dermatomal shingles rash..
Summarise the epidemiology of varicella zoster
Chickenpox peak incidence occurs at 4– 10 years. Shingles peak incidence occurs at > 50 years. About 90% of adults are VZV IgG positive (previously infected).
Recognise the presenting symptoms of varicella zoster
Incubation period (=period between exposure to an infection and the appearance of the first symptoms) 14-21 days
Chickenpox: prodromal (=relating to or denoting the period between the appearance of initial symptoms and the full development of a rash or fever) malaise, mild pyrexia, sudden appearance of intensely itchy spreading rash affecting face and trunk more than extremities, the oropharynx, conjunctivae and genitourinary tract. As vesicles weep and crust over, new vesicles appear.
Shingles: May occur after a period of stress. Tingling/hyperaesthesia in a dermatomal distribution, followed by painful skin lesions. Recovery in 10– 14 days.
Recognise the signs of varicella zoster on physical examination
Chicken pox: Maculopapular rash evolving into crops of vesicles with areas of weeping (exudate) and crusting (vesicles, macules, papules and crusts may all be present at one time), skin excoriation (from scratching), mild pyrexia.
Shingles: Vesicular macular papular rash, in a dermatomal distribution skin excoriation
Identify appropriate investigations for varicella zoster and interpret the results
Both chickenpox and shingles are usually clinical diagnoses.
Vesicle fluid: Electron microscopy, direct immunofluorescence, cell culture, viral PCR (all rarely necessary).
Chickenpox: Consider HIV testing especially in adults with prior history of varicella infection.
Generate a management plan for varicella zoster:
- Varicella? Children vs adults
- Shingles
- Prevention?
Chicken pox (primary infection):
- Children: symptomatic (calamine lotion (=anti-itch), analgesia, antihistamine if severe)
- If >13years old, immuno-suppressed, or have been on long term aspirin (if they’re under the age of 19, due to risk of Reye’s), they need antiviral agent- acyclovir
- Pain relief (aspirin and NSAIDs contraindicated, use paracetemol)
Shingles (reactivation):
-Start antiviral therapy within 72hrs to reduce risk of post-herpetic neuralgia.
IMMUNOCOMPETENT: valaciclovir OR famciclovir, are both better than aciclovir
IMMUNOCOMPROMISED: aciclovit
-Pain relief (NSAIDs are fine here) & calamine lotion
VZIG may be indicated in the immunosuppressed and in pregnant women exposed to varicella zoster. Chickenpox vaccine is licensed in the United Kingdom, but no guidelines available for appropriate use.
Identify the possible complications of varicella zoster and its management
Chickenpox: Secondary infection, scarring, pneumonia, encephalitis, cerebellar syndrome, congenital varicella syndrome.
Shingles:
Postherpetic neuralgia,
zoster opthalmicus (rash involves opthalmic division of trigeminal nerve),
Ramsay Hunt ‘s syndrome (Ramsay Hunt syndrome (herpes zoster oticus) occurs when a shingles outbreak affects the facial nerve near one of your ears. In addition to the painful shingles rash, Ramsay Hunt syndrome can cause facial paralysis and hearing loss in the affected ear),
sacral zoster may lead to urinary retention,
motor zoster (muscle weakness of myotome at similar level as involved dermatome).
Summarise the prognosis for patients with varicella zoster
Depends on the complications. Worse in pregnancy, the elderly and immunocompromised.
When is chickenpox contagious from and until
Contagious from 48 h before the rash and until all the vesicles have crusted over (within 7– 10 days).
Define osteomyelitis
Osteomyelitis is an inflammatory condition of bone caused by an infecting organism, most commonly Staphylococcus aureus.
Affects bone or bone marrow
It usually involves a single bone but may rarely affect multiple sites.
In actue osteomyelitis, dendritic cells and macrophages are trying to wipe out the infection (over a course of weeks). Usually this is successful, but sometimes it turns into chronic osteomyelitis lasting months to years.
Chronic osteomyelitis:
- Affected bone can become necrotic and separate from the healthy bone, known as a sequestrum.
- Healthy bone may then grow around the necrotic area, known as an involucrum
Explain the aetiology / risk factors of osteomyelitis
Aetiology:
1. Haematogenous spread (most common)
Haematogenous osteomyelitis usually involves the metaphysis of long bones in children or the vertebral bodies in adults (vertebral osteomyelitis). In acute haematogenous osteomyelitis, the joint is usually spared, unless the metaphysis is intracapsular, as is found at the proximal radius, humerus, or femur.
- Direct inoculation of micro-organisms into bone (trauma, surgery)
- From contiguous focus of infection
The rising number of patients living longer with multiple comorbidities and the increasing incidence of bone and joint surgery have led to a higher proportion of contiguous focus infection, with haematogenous infections becoming less frequent, except in the immunocompromised host.
Despite these different causes all forms of acute osteomyelitis may evolve and become chronic, sharing a final common pathophysiology, with a compromised soft-tissue envelope surrounding dead, infected, and reactive new bone.
Risk factors: Penetrating injuries surgical contamination intravenous drug misuse diabetes mellitus periodontitis
Summarise the epidemiology of osteomyelitis
The annual incidence was higher for men than for women and increased with age
incidence growing in older adults driven by secular increase in diabetes related cases.
Recognise the presenting symptoms of osteomyelitis
Acute osteomyelitis:
- Non-specific pain at site of infection
- Fever
- Depending on location, may affect use of bone
Chronic:
- Prolonged fevers
- Weight loss (due to chronic inflammatory state)
Recognise the signs of osteomyelitis on physical examination
Local inflammation, erythema or swelling
Low-grade fever
Reduced range of movement
Reduced sensation in diabetic foot ulcer
Identify appropriate investigations for osteomyelitis and interpret the results
Bloods: WBC (usually raised in acute disease, normal in chronic), ESR (usually raised, can be used to monitor treatment), CRP (usually raised, may be more helpful than ESR as it normalises more rapidly after successful treatment)
Imaging: plain x-rays of affected area, bone scan or MRI, and bone biopsy
Complication of osteomyelitis
Septic arthritis of an adjacent joint may be an early complication of acute osteomyelitis in children.
In both acute and chronic osteomyelitis the inflammation can involve the periosteum. An abscess can form between the bone and the periosteum, which can track up the bone
Infection can spread to:
- nearby joint
- overlying muscle
- skin
- blood vessels (leading to thrombophlebitis)
Commonest organism causing osteomyelitis
Staphylococcus aureus most common, which is responsible for one third of all acute osteomyelitis and up to half of all vertebral osteomyelitis.
The next most common organisms implicated in acute osteomyelitis are streptococci, Enterobacteriaceae, and anaerobic bacteria.
Most infections in orthopaedics, including osteomyelitis, are caused by biofilm-forming bacteria
NOTE THAT SALMONELLA particularly affects individuals with sickle cell disease, so they are at risk for staph aureus and salmonella infections
Pastuerella multocida usually spreads form the skin to the bone from a scratch from a cat or dog
What might an x-ray show in osteomyelitis
What about bone scan/MRI
What about bone biopsy
X-ray:
Thickening of the cortical bone and periosteum
Elevation of the periosteum (abscess)
Loss of normal architechture, especially tabecular architecture
Osteopenia (loss of bone mass), which becomes evident when >half bone matrix destroyed
Bone scan:
Confirm
Identify abscess
Bone biopsy:
Identify pathogen and confirm diagnosis
What are vasculitides?
A heterogenous group of autoimmune disorders characterized by inflammation of blood vessels (vasculitis) and subsequent ischemia and damage to the organs supplied by these vessels.
How can vascultides be classified and give some examples of each classification
Based on the size of the vessel affected, it can be classified into small-vessel, medium-vessel, or large-vessel vasculitis
There is overlap.
Large: GCA, Takayasu
Medium: Polyarteritis nodosa
Small:
Microscopic polyangiitis affects mall arteries, arterioles, capillaries and venules (but not veins)
Eosinophilic granulomatosis with polyangiitis (EGPA), also known as allergic granulomatosis or churg strauss, causes inflammation of small and medium-sized blood vessels (vasculitis)
Granulomatosis with polyangitis affects small arteries, arterioles, capillaries, venules and veins
Vignette: woman >50, experiencing visual impairment, with a new-onet headache. What is the treatment
This is consistent with giant cell arteritis.
Mx: high dose glucocorticoids to prevent permanent vision loss. Aspirin to prevent ischaemic events
See MSK for all the boxes
Vignette:
Asian female 35. Attended A&E with syncope and chest pain. Disparity of BP between the two arms. What is the management?
Takayasu arteritis
Asian females, typically < 40 years
Disparity in blood pressure between arms → “pulseless disease” (I can’t TAKA YA pulse)
Bruit over subclavian artery or abdominal aorta
Syncope and angina pectoris
Mx: glucocorticoids
Takayasu arteritis:
Definition
Aetiology and risk factors
Differentiating from other vasculitides in the same classification?
Granulomatous inflammation of the aorta and its major branches, resulting in stenosis of involved blood vessels and subsequent vascular symptoms
Epidemiology of takayasu arteritis
Peak incidence: 15–45 years of age
Asian heritage
♀ > ♂ (3:1)
ASIAN WOMEN
YOUNGER THAN GCA (histologically the same)
Clinical features of takayasu arteritis
Symptoms: Fever, malaise, arthralgia Impaired vision Movement-induced muscular pain in one or more limbs Fainting and angina pectoris
Signs: Reduced bilateral brachial AND radial pulse--> PULSELESS DISEASE Raynauds phenomenon Bilateral carotid bruits HTN
Skin manifestations
Erythema nodosum
Urticaria
Investigations for takayasu
Treatment?
Raised ESR (but ESR is raised even more in giant cell)
GOLD STANDARD: angiography to look for vascular stenosis
Biopsy of affected vessel: granulomatous thickening of aortic arch; plasma cells and lymphocytes in media and adventitia; vascular fibrosis
Treat:
With corticosteroids. Surgical intervention (e.g. bypass) may be required if critical stenosis of aortic arch of branches occurs.
Antihypertensive treatment
Vignette: male with fever and malaise and abdominal , muscle and joint pain. Rash and ulcers and nodules.
Polyarteritis nodosa
Definition of polyarteritis nodosa
Granulomatous?
all and medium-sized vessels, which leads to tissue ischemia; most commonly involving skin, peripheral nerves, muscles, joints, gastrointestinal tract, and kidneys
It’s not granulomatous, is NECROTISING
Epidemiology of polyarteritis nodosa
Assocation?
Important because more common in males than females which is unusual.
Peak incidence 45-65
Associated with hep B and hep C infection
Clinical features of polyarteritis nodosa
Are lungs affected?
Nonspecific symptoms: fever, abdominal, muscle, and joint pain
Renal involvement: hypertension, renal impairment (due to renal artery stenosis)
Coronary artery involvement; increased risk of myocardial infarction
Skin involvement: rash, ulcerations, nodules
Neurological involvement: polyneuropathy (mononeuritis multiplex), stroke
GI involvement: abdominal pain, melena, nausea, vomiting
Usually spares the lungs
Consider in young people who have had a stroke
Which investigations would you want to perform if you suspected polyarteritis nodosa, what would you expect to see
Hep B and C serology as often associated with these infections
A very raised ESR.
Anaemia, leukocytosis
ANCA-negative
Haematuria, proteinuria
Muscle biopsy: transmural inflammation of the arterial wall with leukocytic infiltration and fibrinoid necrosis
Angiography (if tissue cannot be biopsied) : umerous small aneurysms and stenosis of small and medium-sized vessels of the involved organs (pulmonary arteries not usually affected)
Differentiate investigations for Takayasu with that of polyarteritis nodosum
With takayasu angiography is gold standard to assess vascular stenosis
With PAN, muscle biopsy (in the tender muscle group) is gold standard, with angiography if that muscle if not easily accessible
Mnemonic for polyarteritis nodosum
In PAN, the Pulmonary Artery is Not involved, PANmural inflammation of the arterial wall is present, and PAN is often associated with hePANitis B!
Please note that PAN should be considered in young adults presenting with stroke or myocardial infarction! The diagnosis may be confirmed with a biopsy of involved tissue.
Granulomatosis with polyangitis (=Wegener granulomatosis) important features?
The C disease:
Curvy nose (saddle nose deformity), chronic sinusitis, cough, conjuncitivtis and corneal ulceration, cardiac arrhythmias, nonCaseating granulomas, cANCA, corticosteroids and cyclophosphamide as treatment
Somebody attends clinic having repeated sinus infections, as well as ear infections. Now she has a cough, dyspnea and is coughing up blood. There are red cell casts in the urine.
Granulomatosis with polyangiitis (Wegener)
Definition of granulomatosis with polyangiitis
Clinica features
Vasculitis affecting small vessels.
See above for the Cs.
Nasopharyngeal involvement: chronic sinusitis/rhinitis, saddle nose deformity
Chronic otitis media and mastoiditis
Treatment-resistant, pneumonia-like symptoms with cough, dyspnea, hemoptysis
Rapid progressive glomerulonephritis
(URT, LRT and renal feautures)
Investigations for granulomatosis with polyangiitis
PR3-ANCA/cANCA-associated
Biopsy shows granulomatous, necrotizing inflammation of vessels, kidneys, and the lungs.
Chest x-ray/CT: multiple bilateral cavitating nodular lesions
Definition of eosinophilic granulomatosis with polyangiitis (=churg-strauss syndrome)
a multisystem disease characterized by necrotizing granulomatous vasculitis with eosinophilia, which most commonly involves the lungs and the skin but can also affect the renal, cardiovascular, gastrointestinal, central, and peripheral nervous systems.
Potential trigger for eosinophilic granulomatosis with polyangiitis (=churg-strauss syndrome)
Montelukast
Clinical features of eosinophilic granulomatosis with polyangiitis (=churg-strauss syndrome)
Chief complaint is severe allergic asthma attacks
Allergic rhinitis/sinusitis
Skin nodules, palpable purpura
Pericarditis
Gastrointestinal involvement: bleeding, ischemia, perforation
Pauci-immune glomerulonephritis
CNS: impaired mental status, mononeuritis multiplex (loss of motor and sensory function)
Most helpful diagnostic tool?
Most helpful is:
Biopsy (confirmatory test): tissue eosinophilia and necrotizing granuloma. Biopsy anywhere affected.
Peripheral blood eosinophilia
↑ IgE level
Cirulating MPO-ANCA, pANCA
Overall statement for eosinophilic granulomatosis with polyangiitis (churg strauss)
Treatment
Churg-Strauss syndrome = pANCA and polyneuropathy (foot or wrist drop), allergic rhinitis/sinusitis/asthma, vasculitis, eosinophilia, and skin nodules
Treatment same as Wegener: Glucocorticoids, cyclophosphamide
Definition of microscopic polyangiitis
necrotizing vasculitis of small vessels, typically with renal, skin, and pulmonary involvement; however, multiple organ systems may be affected
Clinical features of microscopic polyangiitis. How can it be differentiated from other small vessel vasculitides?
Clinical features:
Renal: pauci-immune glomerulonephritis with hypertension (–> poor prog)
Lungs: pulmonary vasculitis with hemoptysis
Skin: palpable purpura, nodules, necrosis
Diagnostic features of microscopic polyangiitis
Biopsy of involved organ: fibrinoid necrosis with infiltration of neutrophils; no granulomas
Laboratory findings: MPO-ANCA/pANCA (∼ 70% of cases)
Similar to granulomatosis with polyangiitis but spares the nasopharynx!
Define cellulitis & erysipelas
Cellulitis is an acute spreading infection of the skin with visually indistinct borders that principally involves the dermis and subcutaneous tissue.
Erysipelas is a distinct form of superficial cellulitis with notable lymphatic involvement and is raised, sharply demarcating it from uninvolved skin. Non purulent
Cellulitis does not have sharp, well-defined borders, unlike an erysipelas infection, which does.
Explain the aetiology / risk factors of cellulitis & erysipelas
2 most common causative organisms for cellulitis
What is the most likely cause of cellulitis if the infection is non-purulent
What is the most common organism for erysipelas
Common risk factors of cellulitis include
2 common organisms for cellulitis: Staphylococcus aureus or beta-haemolytic streptococci (e.g. GAS which is strep pyogenes).
Consider MRSA(!!)
However, a number of others also can cause it.
Non-purulent cellulitis is most commonly due to beta-haemolytic streptococci (Meeran told us that!). Cellulitis in association with a purulent focus, or recent furunculosis, should prompt consideration of Staphylococcus aureus, including MRSA, as a possible aetiology.
Erysipelas is almost always caused by group A streptococcus (i.e. non purulent, but demarcated!)
In many instances, tinea pedis may cause a disruption in the cutaneous barrier and allow entry to offending bacterial organisms (e.g. in the toes like the homeless patient- tinea pedis interdigitalis)
Risk factors:
- Recent surgery, trauma, or animal bite (cat, dog, insect).
- Prior episodes of cellulitis, pre-existing lymphoedema or venous insufficiency, and tinea pedis interditialis can all predispose to this condition
- Poor hygeine
- Poor vascularisation of tissue (e.g diabetes mellitus)
Recognise the presenting symptoms of cellulitis & erysipelas
Signs and symptoms include an area of redness which increases in size over a couple of days.
A swollen, red, tender, inflamed area of skin with poorly-defined borders is characteristic of cellulitis
Raised erythema with clear demarcations is a hallmark of erysipelas, a superficial form of cellulitis.
Recognise the signs of cellulitis & erysipelas on physical examination
Specifically erysipelas?
If it’s with abscess
If periorbital vs if orbital cellulitis
Macular erythema with indistinct borders, warmth, tenderness, and oedema.
Bullous changes can occur in some cases.
Identify any tinea pedis/disruption of cutaneous barrier
Erysipelas: Raised intense erythema and oedema as well as borders that are pointedly demarcated from uninvolved skin
Abscess: test for fluid thrill or fluctuation. Aspirate if pus suspected
Periorbital: swollen eyelids and conjunctival infection
Orbital cellulitis: proptosis, impaired acuity and eye movement. Test for RAPD, visual acuity and colour vision (to monitor optic nerve function)
Identify appropriate investigations for cellulitis & erysipelas and interpret the results
If query osteomyelitis?
If with abscess?
If NF suspected?
If orbital cellulitis suspected?
1st investigations:
FBC- raised WCC (non-specific, but normal results make it less likely)
Purulent focus culture- may help to identify the presence of resistant pathogens such as MRSA and guide antibiotic selection.
To consider:
Interdigital space culture- lower extremity cellulitis with ipsilateral tinea pedis interdigitalis should do this investigaiton. Can be of use in confirming the organism
Skin biopsy- In cases where the diagnosis is in doubt, skin biopsy is recommended. In addition, in immunocompromised patients who are unresponsive to initial therapy, it can help to identify an unusual pathogen.
Blood culture- usually poor yield in cellulitis so routine use not recommended. Only if constitutional symptoms that might indicate bacteraemia OR if immunocompromised.
Plain radiographs not generally useful unless subjacent osteomyelitis
If an abscess is suspected, an ultrasound may be useful for confirmation
MRI may be helpful if necrotising fasciitis (NF) is suspected. It should not delay surgical consultation if NF is a consideration
CT/MRI if orbital cellulitis suspected, to assess the posterior spread of infection
Generate a management plan for cellulitis & erysipelas
Which antibiotic for each causative organism?
What if there is no abscess
Medical: Oral penicillins (e.g. fluclox, benzylpenicillin, coamox) or tetracyclins effective in most community acquired cases. First generation cephalosporins also mentioned.
Surgical:
Orbital decompression may be required in orbital cellulitis. This is an emergency
Abscess:
Can be aspirated, incised and drained, or excised completely.
Treatment of erysipelas should follow the same principles as that for cellulitis
Identify the possible complications of cellulitis & erysipelas and its management
Sloughing of overlying skin. Localised tissue damage.
Orbital cellulitis: permanent vision loss, spread to brain, abscess formation, meningitis, cavernous sinus thrombosis
Summarise the prognosis for patients with cellulitis & erysipelas
Good with treatment
Which type of cellulitis is an emergency.
What is the most common causative organism
Investigations?
What is the management
In cases of orbital and preseptal (periorbital) cellulitis, differentiating between the two is important, as orbital cellulitis is an emergency and may require surgical intervention in addition to antimicrobial therapy.
Haemophilus influenzae is most common cause. Infection often arises in adjacent sinuses.
Proptosis and pain or limitation with eye movement suggest orbital disease.
A computed tomography scan is useful in discriminating between orbital and preseptal (periorbital) cellulitis and should be ordered if these diagnoses are being considered.
Define infectious mononucleosis
What is the cause, and what type of pathogen is it
Clinical syndrome caused by primary EBV infection. Also known as glandular fever.
EBV is a gamma herpes dsDNA virus. EBV infects oropharyngeal epithelial cells, leading to B cell infection with incorporation of the viral DNA into host DNA
Humoral and cellular immune response and production of IL2 and IFN-g.
The atypical lympocytes (known as Downey cells) are mostly CD8+ T cells.
Lytic phase controlled by immune response, but EBV remains latent in lymphocytes
Explain the aetiology / risk factors of infectious mononucleosis
Transmission
Present in pharyngeal secretions of infected individuals and is transmitted by close contact, e.g. kissing or sharing eating utensils.
Summarise the epidemiology of infectious mononucleosis
1– 6 years (usually asymptomatic!!) and 14– 20 years; > 90% of adult population are EBV immunoglobulin (Ig) G positive.
Recognise the presenting symptoms of infectious mononucleosis
Incubation period?
4-8 weeks incubation
Abrupt onset: sore throat, fever, fatigue, headache, malaise, anorexia, sweating abdo pain
Recognise the signs of infectious mononucleosis on physical examination
Pyrexia
Oedema and erythema of pharynx, fauces and soft palate, with white/creamy exudate on the tonsils which becomes confluent within 1– 2 days, palatal petechiae.
Cervical/generalized lymphadenopathy, splenomegaly (50– 60%), hepatomegaly (10– 20%). Jaundice (5– 10%)
Identify appropriate investigations for infectious mononucleosis and interpret the results
What are heterophile antibodies
Blood: FBC (leukocytosis), LFT (raised aminotransferases)
Blood film: lymphocytosis (>20% atypical lymphocytes, most of which are CD8 +ve T cells)
Paul-Bonnell/Monospot test: detects heterophile antibodies. These are antibodies produced in response to EBV but are not actually against EBV antigents. NOTE: 15% are heterophile Ab negative, especially if patient <14yo!
Throat swaps to exclude streptococcal tonsilitis
IgM/IgG yo EBV viral capsid antigen (VCA): usually present at onset of illness. Only in patients with compatible syndrome AND negative monospot test
IgG against EBNA (epstein barr nuclear antigen: Appears 6-12 weeks after symtpom onset. Presence of IgG EBNA, OR absence of IgG and IgM VCA, excludes acute primary EBV infection, and should prompt consideraton of CMV, HIV and toxoplasmosis
Generate a management plan for infectious mononucleosis
What advice
Bed rest, paracetamol or non-steroidal anti-inflammatory drugs (NSAIDs) for fever, throat discomfort and malaise.
Corticosteroids may be indicated for severe cases (e.g. haemolytic anaemia, severe tonsilar swelling, obstructive pharyngitis).
Advise against contact sports for 2 weeks, as increased risk of splenic rupture
Identify the possible complications of infectious mononucleosis and its management
Despite humoral and T cell immune responses, which control the initial lytic infection, EBV remains latent in lymphocytes. Reactivation may occur following stress or immunosuppression
Resp: Airway obstruction by oedematous pharynx, secondary bacterial throat infection or pneumonitis
Haematological: haemolytic or aplastic anaemia, thrombocytopaenia
GI/renal: splenic rupture, fulminant hepatitis, pancreatitis, mesenteric adenitis, renal failure
CNS: GBS, encephalitis, viral meningitis, brachial plexitis
EBV ass. malignancy: Burkitt’s lymphoma (SS Africa), nasopharyngeal carcinoma (China), post-transplant lymphoma, hodgkin’s lymphoma
Summarise the prognosis for patients with infectious mononucleosis
Most make an uncomplicated recovery in 3– 21 days. Immunodeficiency and death can occur very rarely.
Giving someone with glandular fever certain Abx will result in a skin manifestation.
Which Abx and which skin manifestation
Widespread maculopapular rash in glandular fever patients who have received ampicillin/amoxicillin.
Nearly 100% of patients with infectious mono will develop this!
Note that the Abx aren’t given for the infection! Because its a gamma herpes ds-DNA so abx won’t work
Which of these is NOT an indication for CS use in patients with infectious mononucleosis?
haemolytic anaemia,
severe tonsilar swelling,
confluent white/creamy exudate on tonsils,
obstructive pharyngitis,
confluent white/creamy exudate on tonsils
The other 3 are indications for CS use
What can cause false positives to the monospot test?
pregnancy, autoimmune disease, lymphoma/leukaemia
Give examples of live attenuated viruses.
What is an absolute contraindication for these
The live attenuated vaccines are - MMR, Varicella + Zoster, Sabin polio (not salk is killed), Influenza, Rotavirus and Yellow Fever.
Live vaccines are absolutely contraindicated in immunosuppressed individuals such as those who are taking two immunosuppressant drugs to prevent graft rejection. The intramuscular vaccine is preferred for patients in this situation
Although the intranasal influenza vaccine is a live virus, the intramuscular influenza vaccine is an inactivated (killed) vaccine that cannot cause the flu. So this would be preferred in immunosuppressed people
Which conditions are the following antibodies associated with:
Anti-Saccaromyces cerevisiae antibody
Antimitochondrial antibody
Antismooth muscle antibody
Cytoplasmic antineutrophil cytoplasmic antibody
Perinuclear antineutrophil cytoplasmicantibody
Anti-Saccharomyces cerevisiae antibodies (ASCA) can often be seen in Crohn disease patients.
Antimitochondrial antibody (AMA) is correlated with primary biliary cirrhosis (PBC). PBC involves the destruction of the intrahepatic bile ducts and is not usually characterized by radiological abnormalities
Antismooth muscle antibodies (ASMA) are found in 20-50% of primary sclerosing cholangitis cases. They are highly specific in the diagnosis of autoimmune hepatitis.
C-ANCA is associated with granulomatosis with polyangiitis (GPA), previously known as Wegener disease. GPA is generally characterized by symptoms involving the ears, nose, and throat (sinusitis, otitis media), lungs (hoarseness, cough, dyspnea), or kidneys (hematuria, proteinuria).
In 80% of cases of PSC (and UC), there is an increase in perinuclear antineutrophil cytoplasmic antibodies (p-ANCA), although it is not specific for PSC (it is also found in microscopic polyangiitis and Churg-Strauss syndrome among others).
Treatment of neisseria gonorrhoea infection
Treatment is with a third generation cephalosporin, such as ceftriaxone administered as a single intramuscular (IM) dose.
Current recommendations include coverage for presumed co-infection of Chlamydia trachomatis with azithromycin or doxycycline.
Clinical triad for chlamydia?
What is interesting about chlamydia’s cell wall
Reactive arthritis, conjunctivits and urethritis.
C. trachomatis has a cell wall that lacks muramic acid and unusually, also lacks peptidoglycan.
What is interesting about gonorrhoeae cell wall
Neisseria gonorrhoeae has an unusual cell wall for a gram negative organism in that it lacks lipopolysaccharide and instead has lipooligosaccharide.
What is interesting about the structure of haemophilus influenza
Haemophilus influenza has a polyribosylribitol phosphate component in its capsule, and the vaccine against this organism has this polysaccharide conjugated to a protein to enhance immunogenicity.
Positive culture on chocolate agar?
Chocolate agar is a medium enriched with lysed blood cells (giving it its color), which provides necessary nutrients for the fastidious Neisseria gonorrhea.
How do you distinguish streptococcus pyogenes from streptococcus agalactiae
GBS is beta-hemolytic and bacitracin-resistant.
Group A Streptococcus (strep pyogenes), which is gram-positive, beta-hemolytic, and bacitracin-sensitive
The infections they cause are also different.
Streptococcal pharyngitis is the most common form of pharyngitis and caused by group A Streptococcus (GAS)
Group B Streptococcus (GBS), or Streptococcus agalactiae, can cause meningitis, pneumonia, and sepsis in neonates or young infants
What does alpha, beta and gamma haemolysis look like on plate
Alpha-hemolysis manifests as a green clearing due to incomplete hemolysis yielding biliverdin.
Beta-hemolytic, meaning that growth on sheep blood agar plates will show a golden clearning around each colony due to complete breakdown of heme.
Gamma-hemolysis refers to the absence of hemolysis.
What can be used to diagnose candidate albicans
A potassium hydroxide preparation of the scrapings can be used to diagnose candidiasis.
What disease does group A beta haemolytic streptococcus cause
Aka strep pyogenes.
Pharyngitis (infection of the throat).
Can cause scarlett fever, rheumatic fever, acute glomerulonephritis, sydenham chorea
What is the cause of glomerulonephriits resulting from pharyngeal/skin infections due to group A beta haemolytic streptococcus?
How does it present
Poststreptococcal glomerulonephritis is an immune-complex disorder whose antigen-antibody interaction is not yet well-defined.
Patients would usually present with dark urine and periorbital edema.
Edema is a result of a defect in renal excretion of salt and water. The severity of edema is often disproportionate to the degree of renal impairment.
Haemolytic uraemic syndrome is usually a complication of which infections
Hemolytic-uremic syndrome is a complication of a variety of enteric bacteria, including E. coli, S. dysenteriae, S. typhi, and C. jejuni. It can also be caused by some viruses and some fungi.
Subacute sclerosing panencephalitis is associated with which infection
Subacute sclerosing panencephalitis is a deadly encephalitis caused by persistent rubeola (measles) infection. It primarily affects children and young adults, and there is no cure currently.
AIDs definiting illnesses
include candidiasis
(of the oesophagus, trachea, bronchi or lungs), cervical cancer, Burkitt’s lymphoma,
cytomegalovirus retinitis, mycobacterium avium complex, Pneumocystis jiroveci
pneumonia and toxoplasmosis.
HSV1 is a dsDNA virus.
Primary infection can cause which manifestations
Primary infection is
mostly asymptomatic, but may cause pharyngitis, gingivostomatitis and herpetic
whitlow (digital blisters/pustules).
What happens following primary infection with HSV1
Following primary infection, HSV1 becomes
dormant, classically in the trigeminal ganglia.
Reactivation may occur due to physical
or emotional stress or immunosuppression, and presents as herpes labialis (cold
sores).
What does infection with HSV2 cause
HSV2 is almost exclusively sexually transmitted and it causes genital herpes
(presenting with genital or anal blisters, often with dysuria, fever and malaise).
Define viral hepatitis A & E
Type of virus
Hep A is only Acute hepatitis (hep A=Acute!)
HAV is a non-enveloped RNA picornavirus,
Hep E is usually acute, but can become chronic in immunosuppressed people only.
HEV is a non-enveloped RNA calicivirus
Explain the aetiology / risk factors of viral hepatitis A & E
Route of transmission
What causes the damage
BOTH transmit via the faecal-oral route. HEV also can pass from mother to child during birth
DAMAGE: liver hepatocyte necrosis and liver inflammation caused by the immune response. CD8+ T cells and NK cells target infected cells.
Summarise the epidemiology of viral hepatitis A & E
HAV endemic in developing world, infection often subclinical. Better sanitation in developed world means that seroprevalence is lower.
HEV endemic in Asia, African and Central America
Contaminated food and water - often affects travellers
Recognise the presenting symptoms of viral hepatitis A & E
Incubation period for HAV and HEV is 3-6 weeks
Prodromal: malaise, anorexia (DISTASTE FOR CIGARETTES IN SMOKERS), fever, nausea, vomiting
Hepatitis: prodrome followed by dark urine, pale stools and jaundice lasting ~3 weeks. May last up to several weeks in HAV because of cholestatic hepatitis
Recognise the signs of viral hepatitis on physical examination A & E
Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%).
Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently.
