GP Infectious Disease Flashcards

1
Q

What virus causes infectious mononucleosis (glandular fever)?

A

Epstein Barr Virus (EBV)

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2
Q

How is EBV spread?

A

Kissing, sharing cups, toothbrushes etc
(EBV = found in the saliva)
(Saliva transmission)

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3
Q

When is someone infectious with EBV?

A

Several weeks before the illness begins and intermittently for remainder of patient’s life

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4
Q

At what age do people normally get EBV and when is it more symptomatic?

A
  • Childern → very few symptoms (most common)
  • Teenagers + young adults → more severe symptoms
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5
Q

When is someone classed as having infectious mononucleosis?

A

When the have: EBV + symptomatic

Symptoms = sore throat, fever, fatigue

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6
Q

An adolescent has a sore throat and was given amoxicillin, she comes out in an intensely itchy maculopapular rash. What is the possible diagnosis?

A

Infectious mononucleosis

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7
Q

What happens if a patient with infectious mononucleosis takes amoxicillin or cefalosporins?

A

Patient develops an intensely itchy maculopapular rash

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8
Q

What are the signs and symptoms of infectious mononucleosis?

A

Symptoms:
* Sore throat
* Fatigue

Signs:
* Fever
* Lymphadenopathy
* Splenomegaly (splenic rupture in rare cases)
* Tonsillar enlargement

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9
Q

A teenage presents feeling tired and a sore throat. On examination she has lymphadenopathy, splenomegaly, tonsillar enlargement, and is warm to touch. Possible diagnosis?

A

Infectious mononucleosis

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10
Q

What antibodies do you produce in infectious mononucleousis?

A

Heterophile antibodies
(Multipurpose antibodies that are non-specific to EBV antigens)

Takes up to 6 weeks for these antibodies to be produced

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11
Q

What are the two tests for heterophile antibodies?

A
  • Monospot test (patientts RBC to horses RBCs → heterophile Abx present → reaction to horse RBC → +ve result)
  • Paul-Bunnell test (similar to monospot but sheep RBCs
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12
Q

What is the specificty and sensitivity of the monospot and Paul-Bunnell test for heterophile antibodies in reponse to EBV infection?

A
  • 100% specificity
  • 70-80% sensivity (not everyone who has IM produces heterophile antibodies - can take up to 6 weeks to produce them)
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13
Q

What are the specific antibody tests for EBV?

A
  • The IgM antibody rises early → suggests acute infection
  • The IgG antibody persists after the condition → suggests immunity

These antibodies target something called viral capsid antigen (VCA)

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14
Q

What is the management for infectious mononucleosis?

A
  • Usually self-limiting (acute illness 2-3 weeks, fatigue can last several months after infection cleared)
  • Avoid alcohol (EBV impacts the liver’s ability to process alcohol)
  • Avoid contact sports (splenic rupture risk)
  • Splenic rupture → emergency surgery
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15
Q

Name two complications of infectious mononucleosis

A
  • Splenic rupture
  • Glomerulonephritis
  • Haemolytic anaemia
  • Thrombocytopenia
  • Chronic fatigue

EBV infection is associated with certain cancers, notable Burkitt’s lymphoma

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16
Q

What is Lyme disease?

A

Lyme disease = an infectious disease transmitted to humans through the bites of infected ticks

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17
Q

What is Lyme disease caused by?

A

Lyme disease = is a zoonotic infection caused by a spirochete of genus Borrelia
(transmitted to humans by ticks)

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18
Q

A 57-year old man presents to his GP with a new rash on his leg. He has recently been out walking and thinks he was ‘bitten’. He is systemically well. On examination, there is evidence of a bull’s eye rash on his right calf. Possible diagnosis?

A

Lyme disease

19
Q

Clinical features of Lyme disease

A

Symptoms of Lyme disease depend on the stage of the disease

Early localised disease:
* Expanding ‘bull’s eye’ rash (Known as erythema migrans, which occurs at the site of the tick bite)

Early disseminated disease:
* Multiple ‘bull’s eye’ rashes (due to multiple sites of erythema migrans)
* Weakness of the muscles of the face (due to facial nerve palsy (CN VII))

Late disease:
* Arthritis (usually oligoarthritis with evidence of synovitis)
* Unilateral violet discolouration of the extensor surfaces (known as acrodermatitis chronica atrophicans)

Non-specific symptoms:
* Fever
* Lymphadenopathy
* Headache

20
Q

What is the key sign of Lyme disease?

A

Expanding ‘bull’s eye’ rash

21
Q

Investigations for Lyme disease

A

Clinical diagnosis (in people presenting with erythema migrans)

For patients with suspected Lyme disease without erythema migrans:
First-line: Enzyme-Linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi

22
Q

Management for Lyme disease

A
  • First-line: Doxycycline BD for 21 days (amoxicillin = alternative)
  • Second-line: 2nd course of antibiotics (if symptoms still persist)
23
Q

Complications of Lyme disease

A
  • Jarisch-Herxheimer reaction: following initiation of antibiotic therapy, patients may experience fever, rash and tachycardia due to the release of bacterial endotoxins and microbial antigens following the destruction of microorganisms
  • Neurological symptoms: such as facial nerve paralysis, meningitis and peripheral neuropathy
  • Cardiovascular: complications such as 1st-degree heart block or myocarditis can occur
  • Acrodermatitis chronica atrophicans: violet discolouration of the extensor surfaces which accompanies chronic Borrelia infection
  • Lyme arthritis: a chronic, relapsing, oligoarthritis
24
Q

A 23-year-old woman presents to her GP with a lesion on her lip. On examination, she has evidence of a vesicle that has burst and is healing over. Possible diagnosis?

A

Herpes simplex virus (HSV)

25
Q

What are the two strains of HSV?

A

HSV-1 + HSV-2

Oral herpes simplex (AKA herpes simplex labialis)
* Infection of mouth area + lips → often presenting as cold sores
* HSV-1 (= most causes, 90%)

Genital herpes simplex
* = STI → resulting in genital ulcers
* Can be either HSV-1 or HSV-2

26
Q

Detailed pathophysiology of herpes simplex virus

A

HSV-1: detailed pathophysiology
* HSV-1 infection is typically spread via saliva or other infected bodily secretions
* Once caught, HSV-1 replicates at the site of infection and travels down nerves to the dorsal root ganglion where it can remain dormant
* As such, HSV-1 can be reactivated, with recurrences reported typically 2-3 times per year

HSV-2: detailed pathophysiology
* HSV-2 is spread primarily via sexual contact
* Similarly to HSV-1, HSV-2 lays dormant in the sheath of sensory nerves following initial infection, explaining why it can reactivate and symptoms can return later in life
* Under the microscope, smear samples can show the 3Ms of HSV infection: M ultinucleation, M argination of the chromatin, and M olding of the nuclei

27
Q

How does oral HSV (herpes simplex labialis) present?

A

Signs:
* Presence of vesicles on mucocutaneous surfaces which have ruptured which crust over and heal
* Submandibular lymphadenopathy

Symptoms:
* Lip ulceration: ‘cold sores’
* Malaise/fever
* Sore throat
* Paraesthesia/pain: these precede the lesion by 6-48 hours

28
Q
A
29
Q

How does genital HSV present?

A

Signs:
* Presence of multiple painful blisters which burst and leave erosions/ulcers
* Tender inguinal lymphadenopathy

Symptoms:
* Painful ulceration
* Vaginal/urethra discharge
* Malaise/fever
* Groin pain
* Neuropathic pain in the genital area

30
Q

How does gingivostomatitis HSV present?

A

Signs:
* Cervical + submandibular lymphadenopathy
* Crops of painful vesicles on a red swollen base that often rupture and form ulcers on the pharyngeal and oral mucosa

Symptoms:
* Sore throat
* Malaise/fever
* Excessive salivation or drooling (especially in children)
* Painful ulcers in the mouth

31
Q

Investigations for HSV (herpes simplex virus)

A
  • Oral herpes → clinical diagnosis
  • Genital herpes → requires investigation
  • HSV swabs for NAAT (nucleic acid amplification tests)

Consider STI screen

32
Q

Management of oral herpes

A
  • Simple analgesia: paracetamol or ibuprofen
  • Self-care advice: avoid kissing and oral sex until lesions have fully healed and to avoid touching the lesions
  • Do not prescribe topical anaesthetic or analgesic preparations, mouthwash, or lip barrier preparations
  • Antiviral treatment: for patients who are immunocompromised or in individuals with a severe oral herpes simplex infection

Topical preparations and mouthwash : can be considered as over the counter treatments but are not recommended as a prescribed medication

33
Q

Management of genital herpes simplex

A
  • Antiviral treatment: Aciclovir (within the first 5 days of he start of the genital HSV infection or while new lesions are forming; consider further antiviral treatment in recurrent infection)
  • Self-care advice: avoid sexual intercourse until lesions have cleared
34
Q

What is recommended if a pregnant woman in her third trimester develops her first episode of genital herpes?

A

Caesarean section
(particularly those developing symptoms within 6 weeks of the expected delivery)

35
Q

What is the management of recurrent herpes in a woman that is pregnancy

A

Suppressive therapy
(e.g. daily suppressive aciclovir 400 mg TDS should be considered from 36 weeks of gestation)

36
Q

What type of virus is influenza?

A

RNA virus
(Type A, B, C = affect humans)
Type A + B = most common

37
Q

Info: Influenza

A
  • Type A has different H and N subtypes.

Examples of A strains are:
* H1N1 (which caused the Spanish flu pandemic of 1918 + swine flu pandemic of 2009)
* H5N1 (which causes bird flu).
* Outbreaks of flu typically occur during the winter.

38
Q

Who are given the flu vaccine by the NHS?

A

The flu vaccine is free on the NHS to people at higher risk of developing flu or flu-related complications:

  • Aged 65 and over
  • Young children
  • Pregnant women
  • Chronic health conditions, such as asthma, COPD, heart failure and diabetes
  • Healthcare workers and carers
39
Q

Clinical presentation of influenza

A

The delay between exposure and symptoms is usually around 2 days. Typical presenting features include:

  • Fever
  • Lethargy and fatigue
  • Anorexia (loss of appetite)
  • Muscle and joint aches
  • Headache
  • Dry cough
  • Sore throat
  • Coryzal symptoms
40
Q

Clinical features that differentiate between the common flu and influenza

A

Common cold vs influenza:
* Influenza → abrupt onset
* Common cold → gradual onset

  • Influenza → fever = typical
  • Common cold → fever = rare
  • Influenza → ‘wiped out’ with muscle aches + lethargy
  • Common cold → continue many activities
41
Q

Investigations for influenza

A
  • Point-of-care tests → detect viral antigens (give rapid result) → not sensitive as formal labs
  • Viral nasal or throat swabspolymerase chain reaction (PCR)
42
Q

Management for influenza

A

Heathly patient → not risk of complications → supportive (fluid intake + rest)

Patients at risk of complications:
* Oral oseltamivir (twice daily for 5 days)
* Inhaled zanamivir (twice daily for 5 days)

Treatment needs to be started within 48 hours of the onset of symptoms to be effective.

Post-exposure prophylaxis may be given where patients meet specific criteria:

  • It is started within 48 hours of close contact with influenza
  • Increased risk (e.g., chronic disease or immunosuppression)
  • Not protected by vaccination (e.g., it has been less than 14 days since they were vaccinated)

Options for post-exposure prophylaxis are:
* Oral oseltamivir 75mg once daily for 10 days
* Inhaled zanamivir 10mg once daily for 10 days

43
Q

Complications for influenza

A
  • Otitis media, sinusitis and bronchitis
  • Viral pneumonia
  • Secondary bacteria pneumonia
  • Worsening chronic health conditions, such as COPD and heart failure
  • Febrile convulsions (young children)
  • Encephalitis