Infections and Immunology Flashcards

1
Q

Define Behcet’s disease

A

An autoimmune systemic vasculitis affecting all sized vessels, leading to recurrent oral and genital ulcers and uveitis. It can cause skin and mucosal lesions, uveitis, major arterial and venous vessel disease, and GI and neurological manifestations.

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2
Q

Summarise the aetiology of Behcet’s disease

A

Underlying aetiology is unknown
Autoimmune or autoinflammatory
Associated with HLA-B51
Innate and active immune system involved

Risk factors:
Age 20-40 years
Family history of Behcet’s syndrome
Genetic predisposition.

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3
Q

Summarise the epidemiology of Behcet’s disease

A

Most common in those 20-40 years old
More severe symptoms in men
Most common in Turkey, Mediterranean, Israel, East Asia

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4
Q

What are the presenting symptoms and signs on physical examination of Behcet’s disease?

A
Recurrent oral and genital ulcers which are painful, slow healing and large
Anterior uveitis - painful, red eye with decreased vision and sterile pus
Posterior uveitis - painless eye with decreased vision and floaters
Skin lesions - erythema nodosum
Joint stiffness
Abdominal pain
Meningitis - headache, confusion, fever
Arthritis
Thrombophlebitis
Vasculitis
Myocarditis/pericarditis
CNS symptoms
Colitis
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5
Q

What are appropriate investigations for Behcet’s disease?

A

Mostly a clinical diagnosis
Pathergy test - pin prick does not heal normally, becomes inflamed and forms ulcer or lesion (sterile pustule) at that site within 48 hours
Rheumatoid factor to rule out RA (negative)

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6
Q

Define malaria

A

A parasitic infection caused by plasmodium species which is transmitted to humans through a bite from an infected female anopheles mosquito.

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7
Q

Summarise the aetiology of malaria

A
There are 5 types of protozoa which can cause malaria in humans:
Plasmodium falciparum 
Plasmodium malariae
Plasmodium vivax
Plasmodium ovale
Plasmodium knowlesi

P. falciparum causes malaria most often and most severe malaria
Malaria is spread by the bite of an infected female Anopheles mosquito

Sickle cell disease, thalassemia and 6PD deficiency are protective against malaria

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8
Q

Summarise the epidemiology of malaria

A

Endemic in the tropics

In endemic countries it is most common in children <5 years old and pregnant women

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9
Q

What are the presenting symptoms of malaria?

A
Feverish traveller
Cyclic fevers
Headaches
Myalgia
Arthralgia
Fatigue
Rigors
Weakness
Anorexia
Flu-like symptoms
Sweating
Vomiting

Cerebral Malaria Symptoms: headache, disorientation, coma, confusion

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10
Q

What are the signs on physical examination of malaria?

A
Pyrexia 
Anaemia (haemolytic) 
Hepatosplenomegaly 
Tachycardia 
Jaundice
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11
Q

What are the appropriate investigations for malaria?

A

FBC - normocytic anaemia, thrombocytopenia

Giemsa-stained thick blood smear - identify the presence of parasite within RBC
Thin blood smear - identify the specific plasmodium
Rapid diagnostic tests
Serum LFTs: may show elevated BR/aminotransferases
Clotting profile - may have prolonged prothrombin time

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12
Q

Define Sjogren’s syndrome

A

Autoimmune destruction and lymphocytic infiltration of exocrine glands, particularly the lacrimal and salivary glands, resulting in dry eye and dry mouth.

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13
Q

Summarise the aetiology of Sjogren’s syndrome

A

Primary Sjogren’s syndrome - sicca syndrome when it occurs on its own
Secondary Sjogren’s syndrome - Sjogren’s occuring with another autoimmune disorder

Aetiology unknown
Associated with HLA-B8 and HLA-DR3
Associated with infection of exocrine glands

Can be associated with:
Rheumatoid arthritis
SLE
Scleroderma
Polymyositis
Organ-specific autoimmune diseases (e.g. PBC, autoimmune hepatitis, myasthenia gravis)
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14
Q

Summarise the epidemiology of Sjogren’s syndrome

A

The most common of all systemic auto-immune rheumatic diseases
More common in women
Middle aged women - 50-60 years old
60% have the disease secondary to rheumatoid arthritis, SLE, or systemic sclerosis

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15
Q

What are the presenting signs and symptoms of Sjogren’s syndrome?

A
Keratoconjunctivitis:
Blurred vision
Red eye
Itchy eye
Dry eye
Burning eye

Xerosterma:
Dry mouth
Difficulty tasting and swallow
Cracks and fissures in mouth

Crusting and bleeding of nasal septum
Dry skin
Dry vagina - causes dyspareuria
Pain
Lymphadenopathy
Fever
Weight loss
Fatigue
Dry upper airways: leads to a dry cough and recurrent sinusitis 
Dry skin or hair
Dry upper airways: leads to a dry cough and recurrent sinusitis - Dry skin or hai
Dental caries
Myalgia
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16
Q

What are the appropriate investigations for Sjogren’s syndrome?

A
ESR - elevated
Amylase - elevated if salivary gland involvement
Anti-SSA and anti-SSB - positive
Rheumatoid factor positive
ANA 

Schirmer’s Test:
A strip of filter paper is placed under the eyelid
Positive for Sjogren’s syndrome if < 10 mm of the strip is wet after 5 mins

Fluorescein/Rose Bengal Stains: May show punctate or filamentary keratitis

Reduced parotid salivary flow rate
Reduced uptake or clearance on isotope scan

Biopsy salivary or labial glands - shows lymphocytic infiltration

Sialometry - decreased saliva outflow

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17
Q

Define systemic lupus erythematosus

A

A chronic multi-system autoimmune condition which mainly affects women of reproductive age and is characterised by the presence of anti-nuclear antibodies.

4 out of the 11 features must be present for diagnosis:
RASH OR PAIN

Rash - malar or discoid
Arhritis
Serositis - pleuritis, pericarditis
Haemological disorders - haemolytic anaemia, thrombocytopenia, leukopenia
Oral/nasopharyngeal ulcers
Renal disease - proteinuria, red cell casts
Photosensitivity
Anti-nuclear antibodies
Immunological disorder (anti-dsDNA, anti-smith, antiphospholipid)
Neurological disorder - seizures, coma

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18
Q

Summarise the aetiology of systemic lupus erythematosus

A

Autoimmune disorder
Environmental risk factors cause cell apoptosis, leading to release of nuclear components
Genetic susceptibility increases likelihood of these nuclear components being recognised as non-self antigens and decreases clearance
Antigen-antibody complexes form and deposit

19
Q

Summarise the epidemiology of systemic lupus erythematosus

A

Most common in females of reproductive age
Most frequently 15-45 years old
More common and severe in those of Asian and African descent

20
Q

What are the presenting symptoms and signs on physical examination of systemic lupus erythematosus?

A

Fever, weight loss, malaise, lymphadenopathy, splenomegaly
Malar rash - gets worse after sun exposure
Discoid rash
Arthritis - pain in >2 joints
Raynaud’s phenomenon
Oral ulcers
Atypical rashes (e.g. photosensitivity, vasculitis, urticaria, purpura)

Systemic Involvement:
Musculoskeletal: arthritis, tendonitis, myopathy
Heart: pericarditis, myocarditis, arrhythmias, Libman-Sacks endocarditis
Lung: pleurisy, pleural effusion, basal atelectasis, restrictive lung defects
Neurological: headache, stroke, cranial nerve palsies, confusion, chorea
Psychiatric: depression, psychosis
Renal: glomerulonephritis, nephritic syndrome

21
Q

What are the appropriate investigations of systemic lupus erythematosus?

A

FBC - may have haemolytic anaemia, thrombocytopenia, leukopenia
U&Es - urea and creatinine elevated if renal involvement
ESR - elevated
Normal CRP

Anti nuclear antibodies
Anti-smith antibodies
Anti-dsDNA antibodies
Anti-phospholipid antibodies
Rheumatoid factor (30-50%) 
Anti-ENA 
Anti-RNP
Anti-SM
Anti-Ro
Anti-La 
Anti-histone 
Anti-cardiolipin

Urinalysis - red cell casts, proteinuria
Heart and Lungs: CXR, ECG, echocardiogram, CT
Kidneys: renal biopsy (if glomerulonephritis suspected)

22
Q

Define systemic sclerosis

A

An idiopathic, autoimmune condition characterised by functional and structural abnormalities of small blood vessels, fibrosis of skin and internal organs, and production of auto-antibodies.

Diffuse cutaneous systemic scleroderma:
Sclerodactyl
Skin thickening
Pulmonary fibrosis
Raynaud’s phenomenon followed by skin changes with truncal involvement
Tendon friction, joint contracture, heart, GI and renal disease

Limited cutaneous systemic scleroderma/CREST syndrome:
5 main symptoms - calcinosis cutis, raynaud’s phenomenon, eosophageal dysfunction, sclerodactyly, telangiectasis

Scleroderma sine scleroderma: internal organ disease with no skin involvement

23
Q

Describe the aetiology of systemic sclerosis

A

Aetiology unknown
Genetic predisposition with environmental triggers - EBV, parvovirus B19, cocaine
Autoimmune

Diffuse associated with anti-Scl70 and anti-RNA polymerase III antibodies
Localised associated with anti-centromere antibodies

24
Q

Summarise the epidemiology of systemic sclerosis

A

Women three times more commonly affected than men

Onset 30-60 years old

25
Q

What are the presenting symptoms and signs on physical examination of systemic sclerosis?

A

Raynaud’s phenomenon - in cold, fingers turn white, then blue, then red due to vasospasm
Sclerodactyly - initially hands swollen and puffy, develop to tight, thick, shiny skin with no markings
Changes in pigmentation of hands
Digital ulcers
Calcified deposits in fingers
Oesophageal dysmotility - dyshpagia, GORD
Telangiectasia on skin and face
Microstomia (puckering of the skin around the mouth)
Pulmonary fibrosis - cough, restrictive lung pattern
Pulmonary hypertension
Heart: pericarditis or pericardial effusion, myocardial fibrosis, heart failure, arrhythmias
Kidneys: hypertensive renal crisis, chronic renal failure
Neuromuscular: trigeminal neuralgia, muscular wasting, weakness
Beaked nose
Joints - pain, stiffness, restricted movement

Diffuse: symptoms rapidly developing, across whole body, organ involvement early on
Limited: slower development, no organ development, restricted to face and distal limbs

26
Q

What are the appropriate investigations for systemic scleroderma?

A

Autoantibodies:
Anti-centromere - limited
Anti-RNA polymerase III - diffuse
Anti-topoisomerase II/Anti-Scl70 - 30% of diffuse

Pulmonary function tests - show restrictive pattern in diffuse
Lungs: CXR (check for fibrosis), CT scan
Heart: ECG, echocardiography (look for R ventricular hypertrophy secondary to pulmonary fibrosis)
GI: endoscopy, barium studies to check for oesophageal dysfunction
Kidneys: U&Es, creatinine clearance
Neuromuscular: electromyography, biopsy
Joints: radiography
Skin: biopsy (rarely needed)

27
Q

Define vasculitides

A

Group of inflammatory diseases affecting large, medium and small vessels, caused by immunological processes and triggered by infection. Classified based on the vessels size:
Large artery vasculitis - giant cell arteritis, Takayasu’s arteritis
Medium artery vasculitis - polyarteritis nodosa
Small artery vasculitis - granulomatosis with polyangiitis, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis

28
Q

Summarise the aetiology of vasculitides

A

Unknown
Potentially autoimmune condition
Immune complex deposition in the walls of blood vessels leads to inflammation

Risk factors:
Hepatitis B - Polyarteritis nodosa
Age >50 - GCA
Asian female <40 - Takayasu
c-ANCA - granulomatosis with polyangiitis
p-ANCA - microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis

29
Q

Summarise the epidemiology of vasaculitides

A

RARE
Takayasu’s arteritis is most common in JAPANESE FEMALES <40 years old
Giant cell arteritis - females >50y/o
Polyarteritis nodosa - middle aged men, hep B infection

30
Q

What are the presenting symptoms and signs on physical examination of vasculitides?

A
Non-specific symptoms:
Fever
Myalgia
Weight loss
Fatigue
Arthritis
Night sweats

Giant cell arteritis - unilateral headache, jaw claudication, pain on brushing hair, visual disturbance, visual inflammed temporal artery

Takayasu arteritis - carotid bruit, weak or no upper extremity pulses, visual disturbances, neurological signs, difference in blood pressure between two arms

Polyarteritis nodosa - microaneurysms, thrombosis, infarctions, hypertension, testicular pain

Granulomatosis with polyangiitis - haemoptysis, saddle nose deformity, dyspnoea, haematuria, granulomatous vasculitis of upper and lower respiratory tract, nasal discharge, ulceration and deformity, sinusitis, glomerulonephritis

Eosinophilic granulomatosis with polyangiitis - adult onset asthma

31
Q

What are the appropriate investigations of vasculitides?

A

Bloods:
FBC - normocytic anaemia, high platelets, high neutrophils
ESR/CRP - elevated

Autoantibodies:
cANCA - granulomatosis with polyangiitis
pANCA - microscopic polyangiiitis, eosinophilic granulomatosis with polyangiitis

Urinalysis: haematuria, proteinuria, red cell casts (if glomerulonephritis)

CXR: diffuse, nodular or flitting shadows (granulomatosis with polyangiitis, microscopic polyangiitis)

Biopsy: renal, lung, temporal artery (in GCA)

Angiography: to identify aneurysms - string of beads sign in polyarteritis nodosa

32
Q

Define abscess

A

A painful collection of pus (dead cells and tissue, pathogens and immune cells) in a walled off area usually caused by bacterial infection.

33
Q

Summarise the aetiology of abscess

A

They can develop anywhere in the body
There are TWO main types of abscess: skin abscess and internal abscess
Skin abscess often caused by staphylococcus aureus

Bacterial infection leads to activation of an immune response and recruitment of neutrophils.
As the white cells attack the bacteria, surrounding tissue is damaged creating a cavity which fills with pus to form an abscess.

34
Q

Summarise the epidemiology of abscess

A

Skin abscesses are relatively common
IV drug use is a major risk factor for skin abscesses
Internal abscesses are less common

35
Q

What are the presenting symptoms of abscess

A
Swollen pus-filled lump under the surface of the skin
Pain
Redness
Warmth
Swelling
Inflammed skin

If weakened immune system and unable to wall off abscess:
Fever
Vomiting
Nausea

Internal abscesses:
Not visible
Pain in the affected area (or referred pain)
Swinging fevers
Malaise
36
Q

What are the signs on physical examination of abscess?

A

Swollen, pus-filled lump under the surface of the skin which comes to a head
Fever

37
Q

What are the appropriate investigations for abscess?

A

Mainly clinical diagnosis and examination - will be fluctuant
USS visualisation of abscess
Pus analysis

38
Q

What is the management of abscesses

A

Small abscesses may heal by themselves
Incision and drainage (surgical or using long needle if deep abscess)
If large abscess, to prevent reinfection of empty cavity, fill with gauze
Antibiotics if needed

39
Q

What are the possible complications of abscesses?

A
Recurrence
Sepsis
Spread of the infection to brain or spinal cord
Endocarditis
Gangrene
Osteomyelitis
40
Q

Define HIV

A

Infection by the Human Immunodeficiency Virus which targets immune cells, leading to a decreased immune system strength

41
Q

Summarise the aetiology of HIV

A
Transmitted by:
Sexual intercourse
Mother-to-child - intrauterine, breastfeeding, childbirth
Blood transfusion
IVDU
Needlestick
Organ transplant
42
Q

Summarise the epidemiology of HIV

A

Increasing incidence in Asia and Africa

43
Q

What are the presenting symptoms and signs on physical examination of HIV?

A

There are THREE phases of HIV:

  1. Seroconversion: Self-limiting, fever, night sweats, generalised lymphadenopathy, sore throat, oral ulcers, rash, myalgia, headache, encephalitis, diarrhoea
  2. Early/Asymptomatic: Apparently well but some may have persistent lymphadenopathy. Progressive minor symptoms (e.g. rash, oral thrush, weight loss)
  3. AIDS: Syndrome of secondary diseases resulting from immunodeficiency

Direct Effects of HIV Infection:
Neurological: polyneuropathy, dementia
Lung: lymphocytic interstitial pneumonitis
Heart: cardiomyopathy, myocarditis
Haematological: anaemia, thrombocytopaenia
GI: anorexia, wasting
Eyes: cotton wool spots

Secondary effects resulting from immunodeficiency:
Bacterial Infection: TB, skin infections, pneumococcal infections
Viral: CMV, HSV, VZV, HPV, EBV
Fungal: pneumocystic jirovecii pneumonia, Cryptococcus, candidiasis, invasive aspergillosis
Protozoal: toxoplasmosis, cryptosporidia
Tumours: Kaposi sarcoma, SCC, non-Hogkin’s lymphoma, Hodgkin’s lymphoma

44
Q

What are the appropriate investigations of HIV?

A

HIV antibodies
PCR for viral RNA
CD4 count
Viral load

Pneumocystic pneumonia - CXR
Cryptococcal meningitis - brain CT or MRI, LP
CMV (colitis) - colonoscopy and biopsy
Toxoplasmosis - brain CT or MRI
Cryptosporidia - stool microscopy