Infectious diseases Flashcards

1
Q

What are gram +ve cocci?

A

staphylococci + streptococci (including enterococci)

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2
Q

What are 3 gram -ve cocci?

A

Neisseria meningitidis + Neisseria gonorrhoeae, also Moraxella catarrhalis

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3
Q

Name 5 gram postive rods

A

ABCD L

Actinomyces
Bacillus anthracis (anthrax)
Clostridium
Diphtheria: Corynebacterium diphtheriae
Listeria monocytogenes
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4
Q

Name 6 gram -ve rods

A

Escherichia coli
Haemophilus influenzae
Pseudomonas aeruginosa
Salmonella sp.
Shigella sp.
Campylobacter jejuni

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5
Q

What 5 agents can cause CAP?
What is seen in alcoholics?

A

Streptococcus pneumoniae (accounts for around 80% of cases)
Haemophilus influenzae
Staphylococcus aureus: commonly after influenza infection
atypical pneumonias (e.g. Due to Mycoplasma pneumoniae)
viruses

Klebsiella is seen in alcoholics

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6
Q

What is the most common cause of CAP?

A

Streptococcus pneumoniae (pneumococcus) is the most common cause of community-acquired pneumonia

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7
Q

Give 4 characteristic features of pneumococcal pneumonia?

A

Characteristic features of pneumococcal pneumonia

rapid onset
high fever
pleuritic chest pain
herpes labialis (cold sores)
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8
Q

What are the two types of pnuemococcal vaccine currently in use?

A

There are two type of pneumococcal vaccine currently in use:

pneumococcal conjugate vaccine (PCV)
pneumococcal polysaccharide vaccine (PPV)
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9
Q

Who is routinely offered the pneumococcal vaccine?

A

The PCV is given to children as part of their routine immunisations (at 3 and 12-13 months).

The PPV is offered to all adults over the age of 65 years, to patients with chronic conditions such as COPD and to those who have had a splenectomy (see below).

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10
Q

What 9 groups of people should be given the pneumococcal vaccine?

A

Groups who should be vaccinated:

asplenia or splenic dysfunction

chronic respiratory disease: COPD, bronchiectasis, cystic fibrosis, interstitial lung disease. Asthma is only included if ‘it requires the use of oral steroids at a dose sufficient to act as a significant immunosuppressant’

chronic heart disease: ischaemic heart disease if requiring medication or follow-up, heart failure, congenital heart disease. Controlled hypertension is not an indication for vaccination

chronic kidney disease

chronic liver disease: including cirrhosis and chronic hepatitis

diabetes mellitus if requiring medication

immunosuppression (either due to disease or treatment). This includes patients with any stage of HIV infection

cochlear implants

patients with cerebrospinal fluid leaks

Adults usually require just one dose but those with asplenia, splenic dysfunction or chronic kidney disease need a booster every 5 years.

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11
Q

How is influenza vaccine given to children? when is this given? is this a live vaccine?

A

it is given intranasally
the first dose is given at 2-3 years, then annually after that
it is a live vaccine (cf. injectable vaccine below)

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12
Q

Why would a child be given an injectable influenza vaccine? is this effective?

A

children who were traditionally offered the flu vaccine (e.g. asthmatics) will now be given intranasal vaccine unless this is inappropriate, for example if they are immunosuppressed. In this situation the inactivated, injectable vaccine should be given
only children aged 2-9 years who have not received an influenza vaccine before need 2 doses
it is less effective than the intranasal vaccine

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13
Q

What are 7 contraindications of influenza vaccine in children?

A

Contraindications

immunocompromised
aged < 2 years
current febrile illness or blocked nose/rhinorrhoea
current wheeze (e.g. ongoing viral-induced wheeze/asthma) or history of severe asthma (BTS step 4)
egg allergy
pregnancy/breastfeeding
if the child is taking aspirin (e.g. for Kawasaki disease) due to a risk of Reye's syndrome
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14
Q

What are 4 side effects of the influenza vaccine?

A

Side-effects

blocked-nose/rhinorrhoea
headache
anorexia
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15
Q

What groups of adults get the flu vaccine due to personal health?

A

The Department of Health recommends annual influenza vaccination for all people older than 65 years, and those older than 6 months if they have:

chronic respiratory disease (including asthmatics who use inhaled steroids)
chronic heart disease (heart failure, ischaemic heart disease, including hypertension if associated with cardiac complications)
chronic kidney disease
chronic liver disease: cirrhosis, biliary atresia, chronic hepatitis
chronic neurological disease: (e.g. Stroke/TIAs)
diabetes mellitus (including diet controlled)
immunosuppression due to disease or treatment (e.g. HIV)
asplenia or splenic dysfunction
pregnant women
adults with a body mass index >= 40 kg/m²
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16
Q

What groups of people get the flu vaccine due to personal circumstance i.e. occupationally

A

Other at risk individuals include:

health and social care staff directly involved in patient care (e.g. NHS staff)
those living in long-stay residential care homes
carers of the elderly or disabled person whose welfare may be at risk if the carer becomes ill (at the GP's discretion)
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17
Q

The influenza vaccine
-is this live?
-How should this be stored?
-What is a contraindication?
-is this effective?>
-How long does this take to work?

A

The influenza vaccine

it is an inactivated vaccine, so cannot cause influenza. A minority of patients however develop fever and malaise which may last 1-2 days
should be stored between +2 and +8ºC and shielded from light
contraindications include hypersensitivity to egg protein.
in adults the vaccination is around 75% effective, although this figure decreases in the elderly
it takes around 10-14 days after immunisation before antibody levels are at protective levels
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18
Q

What treatment is used for Exacerbations of chronic bronchitis

A

Amoxicillin or tetracycline or clarithromycin

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19
Q

What treatment is used for Uncomplicated community-acquired pneumonia

A

Amoxicillin (Doxycycline or clarithromycin in penicillin allergic, add flucloxacillin if staphylococci suspected e.g. In influenza)

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20
Q

What treatment is added if you are considering atypical pneumonia?

A

Clarithromycin

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21
Q

What treatment is used for HAP?

A

Within 5 days of admission: co-amoxiclav or cefuroxime
More than 5 days after admission: piperacillin with tazobactam OR a broad-spectrum cephalosporin (e.g. ceftazidime) OR a quinolone (e.g. ciprofloxacin)

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22
Q

Describe the primary infection of TB

A

A non-immune host who is exposed to M. tuberculosis may develop a primary infection of the lungs. A small lung lesion known as a Ghon focus develops. The Ghon focus is composed of tubercle-laden macrophages. The combination of a Ghon focus and hilar lymph nodes is known as a Ghon complex

In immunocompetent people, the initial lesion usually heals by fibrosis. Those who are immunocompromised may develop disseminated disease (miliary tuberculosis).

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23
Q

Describe the secondary infection of TB? what can lead to this?

A

If the host becomes immunocompromised the initial infection may become reactivated. Reactivation generally occurs in the apex of the lungs and may spread locally or to more distant sites. Possible causes of immunocompromise include:

immunosuppressive drugs including steroids
HIV
malnutrition
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24
Q

Where can secondary infection of TB occur?

A

The lungs remain the most common site for secondary tuberculosis. Extra-pulmonary infection may occur in the following areas:

central nervous system (tuberculous meningitis - the most serious complication)
vertebral bodies (Pott's disease)
cervical lymph nodes (scrofuloderma)
renal
gastrointestinal tract
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25
Q

Describe the standard treatment of TB

A

The standard therapy for treating active tuberculosis is:

Initial phase - first 2 months (RIPE)

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol (the 2006 NICE guidelines now recommend giving a 'fourth drug' such as ethambutol routinely - previously this was only added if drug-resistant tuberculosis was suspected)

Continuation phase - next 4 months

Rifampicin
Isoniazid
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26
Q

What is the treatment of latent TB?

A

The treatment for latent tuberculosis is 3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine)

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27
Q

What is the treatment for meningeal TB?

A

Patients with meningeal tuberculosis are treated for a prolonged period (at least 12 months) with the addition of steroids

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28
Q

Who would warrant directly observed therapy for TB?

A

Directly observed therapy with a three times a week dosing regimen may be
indicated in certain groups, including:

homeless people with active tuberculosis
patients who are likely to have poor concordance
all prisoners with active or latent tuberculosis
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29
Q

What is immune reconstitution disease in the treatment of TB?

A

Immune reconstitution disease

occurs typically 3-6 weeks after starting treatment
often presents with enlarging lymph nodes
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30
Q

Which drug side effects?
potent liver enzyme inducer
hepatitis, orange secretions
flu-like symptoms

A

Rifampicin

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31
Q

Which drug side effects?
peripheral neuropathy: prevent with pyridoxine (Vitamin B6)
hepatitis, agranulocytosis
liver enzyme inhibitor

A

isoniazid

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32
Q

Which drug side effects?
hyperuricaemia causing gout
arthralgia, myalgia
hepatitis

A

Pyrazinamide

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33
Q

What has to be checked before starting ethambutol?

A

optic neuritis: check visual acuity before and during treatment

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34
Q

What 8 groups of people get a BCG

A

all infants (aged 0 to 12 months) living in areas of the UK where the annual incidence of TB is 40/100,000 or greater

all infants (aged 0 to 12 months) with a parent or grandparent who was born in a country where the annual incidence of TB is 40/100,000 or greater. The same applies to older children but if they are 6 years old or older they require a tuberculin skin test first

previously unvaccinated tuberculin-negative contacts of cases of respiratory TB

previously unvaccinated, tuberculin-negative new entrants under 16 years of age who were born in or who have lived for a prolonged period (at least three months) in a country with an annual TB incidence of 40/100,000 or greater

healthcare workers

prison staff

staff of care home for the elderly

those who work with homeless people

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35
Q

What does the BCG vaccine contain? What else does this offer protection against?

A

The vaccine contains live attenuated Mycobacterium bovis. It also offers limited protection against leprosy.

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36
Q

Describe the administration of the BCG vaccine

A

any person being considered for the BCG vaccine must first be given a tuberculin skin test. The only exceptions are children < 6 years old who have had no contact with tuberculosis
given intradermally, normally to the lateral aspect of the left upper arm
BCG can be given at the same time as other live vaccines, but if not administered simultaneously there should be a 4 week interval

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37
Q

What are 5 contraindications to the BCG vaccine? what age is this not given to?

A

Contraindications

previous BCG vaccination
a past history of tuberculosis
HIV
pregnancy
positive tuberculin test (Heaf or Mantoux)

The BCG vaccine is not given to anyone over the age of 35, as there is no evidence that it works for people of this age group.

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38
Q

Mycoplasma pneumonia:
-what is this a cause of?
-what is this assoc. with?
-Is this common?

A

Mycoplasma pneumoniae is a cause of atypical pneumonia which often affects younger patients. It is associated with a number of characteristic complications such as erythema multiforme and cold autoimmune haemolytic anaemia. Epidemics of Mycoplasma pneumoniae classically occur every 4 years. It is important to recognise atypical pneumonia as it may not respond to penicillins or cephalosporins due to it lacking a peptidoglycan cell wall.

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39
Q

What are 3 features of mycoplasma pneumoniae?

A

Features

the disease typically has a prolonged and gradual onset
flu-like symptoms classically precede a dry cough
bilateral consolidation on x-ray
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40
Q

What are 7 complications of mycoplasma pneumoniae?

A

cold agglutins (IgM): may cause an haemolytic anaemia, thrombocytopenia

erythema multiforme, erythema nodosum

meningoencephalitis, Guillain-Barre syndrome and other immune-mediated neurological diseases

bullous myringitis: painful vesicles on the tympanic membrane

pericarditis/myocarditis

gastrointestinal: hepatitis, pancreatitis

renal: acute glomerulonephritis

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41
Q

What investigations are used for mycoplasma pneumoniae?

A

Investigations

diagnosis is generally by Mycoplasma serology
positive cold agglutination test → peripheral blood smear may show red blood cell agglutination
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42
Q

What is the management of mycoplasma pneumoniae?

A

Management

doxycycline or a macrolide (e.g. erythromycin/clarithromycin)
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43
Q

What is legionnaires disease caused by? where does this typically colonise? can you get person-person transmission?

A

Legionnaire’s disease is caused by the intracellular bacterium Legionella pneumophilia. It typically colonizes water tanks and hence questions may hint at air-conditioning systems or foreign holidays. Person-to-person transmission is not seen

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44
Q

Give 8 features of legionnaires disease?

A

Features

flu-like symptoms including fever (present in > 95% of patients)
dry cough
relative bradycardia
confusion
lymphopaenia
hyponatraemia
deranged liver function tests
pleural effusion: seen in around 30% of patients
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45
Q

What is the diagnostic testof choice for legionnaireS? what is seen on CXR?

A

Investigations

diagnositic test of choice:urinary antigen
chest x-ray findings are non-specific but may include:
    a mid-to-lower zone predominance of patchy consolidation
    pleural effusions in around 30%
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46
Q

What is the management of legionnaires disease?

A

Management

treat with erythromycin/clarithromycin
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47
Q

What is the treatment for Throat infections

A

Phenoxymethylpenicillin (erythromycin alone if penicillin-allergic)

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48
Q

What is infectious mononucleosis? what is this caused by?

A

Infectious mononucleosis (glandular fever) is caused by the Epstein-Barr virus (EBV, also known as human herpesvirus 4, HHV-4) in 90% of cases. Less frequent causes include cytomegalovirus and HHV-6. It is most common in adolescents and young adults.

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49
Q

What is the classic triad of infectious mononucleosis?

A

The classic triad of sore throat, pyrexia and lymphadenopathy is seen in around 98% of patients:

sore throat
lymphadenopathy: may be present in the anterior and posterior triangles of the neck, in contrast to tonsillitis which typically only results in the upper anterior cervical chain being enlarged
pyrexia
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50
Q

What are 6 features outwith the triad that are seen in glandular fevers?

A

Other features include:

malaise, anorexia, headache
palatal petechiae
splenomegaly - occurs in around 50% of patients and may rarely predispose to splenic rupture
hepatitis, transient rise in ALT
lymphocytosis: presence of 50% lymphocytes with at least 10% atypical lymphocytes
haemolytic anaemia secondary to cold agglutins (IgM)
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51
Q

What happens if you treat glandular fevers with amoxicillin?

A

a maculopapular, pruritic rash develops in around 99% of patients who take ampicillin/amoxicillin whilst they have infectious mononucleosis

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52
Q

How long do symptoms last for in glandular fever?

A

Symptoms typically resolve after 2-4 weeks.

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53
Q

What is the diagnosis of glandular fever?

A

Diagnosis

heterophil antibody test (Monospot test)
    NICE guidelines suggest FBC and Monospot in the 2nd week of the illness to confirm a diagnosis of glandular fever.
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54
Q

What is the management of glandular fever?

A

Management is supportive and includes:

rest during the early stages, drink plenty of fluid, avoid alcohol
simple analgesia for any aches or pains
consensus guidance in the UK is to avoid playing contact sports for 4 weeks after having glandular fever to reduce the risk of splenic rupture
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55
Q

What is mumps caused by?

A

Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring

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56
Q

Describe the spread and the pathophysiology of mumps? what is the incubation period?

A

Spread

by droplets
respiratory tract epithelial cells → parotid glands → other tissues
infective 7 days before and 9 days after parotid swelling starts
incubation period = 14-21 days
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57
Q

What are 3 features of mumps?

A

Clinical features

fever
malaise, muscular pain
parotitis ('earache', 'pain on eating'): unilateral initially then becomes bilateral in 70%
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58
Q

What is the prevention of mumps?

A

Prevention

MMR vaccine: the efficacy is around 80%
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59
Q

What is the management of mumps?

A

Management

rest
paracetamol for high fever/discomfort
notifiable disease
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60
Q

What are 4 complications of mumps?

A

Complications

orchitis - uncommon in pre-pubertal males but occurs in around 25-35% of post-pubertal males. Typically occurs four or five days after the start of parotitis
hearing loss - usually unilateral and transient
meningoencephalitis
pancreatitis
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61
Q

What does Respiratory syncytial virus cause?

A

bronchiolitis

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62
Q

What does Parainfluenza virus cause?

A

croup

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63
Q

What does Rhinovirus cause?

A

common cold

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64
Q

what does Haemophilus influenzae cause?

A

COPD exac, Community-acquired pneumonia
Most common cause of bronchiectasis exacerbations
Acute epiglottitis

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65
Q

What does staph., aureus cause in the respiratory tract?

A

Pneumonia, particularly following influenza

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66
Q

What is given for sinusitis?

A

Phenoxymethylpenicillin

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67
Q

What is given for otitis media?

A

Amoxicillin (erythromycin if penicillin-allergic)

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68
Q

What is given for otitis externa?

A

Flucloxacillin (erythromycin if penicillin-allergic)

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69
Q

What is given for Periapical or periodontal abscess

A

Amoxicillin

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70
Q

What is given for Gingivitis: acute necrotising ulcerative

A

metronidazole

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71
Q

What is given for impetigo?

A

Topical hydrogen peroxide, oral flucloxacillin or erythromycin if widespread

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72
Q

What is cellulitis most commonly caused by?

A

Cellulitis is most commonly caused by infection with Streptococcus pyogenes or less commonly Staphylcoccus aureus. The majority of cases resolve with oral antibiotics.

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73
Q

How is cellulitis diagnosed?

A

The diagnosis of cellulitis is clinical. No further investigations are required in primary care. Bloods and blood cultures may be requested if the patient is admitted and septicaemia is suspected.

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74
Q

What classification system is used to guide how cellulitis is managed?

A

Eron classification
Class Features
I There are no signs of systemic toxicity and the person has no uncontrolled co-morbidities
II The person is either systemically unwell or systemically well but with a co-morbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection
III The person has significant systemic upset such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable co-morbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize
IV The person has sepsis syndrome or a severe life-threatening infection such as necrotizing fasciitis

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75
Q

Who should be admitted for IV antibiotics to treat cellulitis? 6

A

They recommend the following that we admit for intravenous antibiotics the following patients: CKS

Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
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76
Q

What is the management of eron class 1 cellulitis?

A

Eron Class I

oral antibiotics NICE
oral flucloxacillin as first-line treatment for mild/moderate cellulitis
oral clarithromycin, erythromycin (in pregnancy) or doxycycline is recommended in patients allergic to penicillin
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77
Q

what is the treatment of eron class III-IV cellulitis?

A

Eron Class III-IV

admit
NICE recommend: oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
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78
Q

What is the management of animal bites?

A

The majority of bites seen in everyday practice involve dogs and cats. These are generally polymicrobial but the most common isolated organism is Pasteurella multocida.

Management

cleanse wound. Puncture wounds should not be sutured closed unless cosmesis is at risk
current BNF recommendation is co-amoxiclav
if penicillin-allergic then doxycycline + metronidazole is recommended
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79
Q

What are the common bacteria found in human bites? what is the treatment?

A

Human bites commonly cause multimicrobial infection, including both aerobic and anaerobic bacteria.

Common organisms include:

Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella

Co-amoxiclav is recommended, as for animal bites.

The risk of viral infections such as HIV and hepatitis C should also be considered.

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80
Q

what is cat scratch disease caused by? what are 4 features?

A

Cat scratch disease is generally caused by the Gram negative rod Bartonella henselae

Features

fever
history of a cat scratch
regional lymphadenopathy
headache, malaise
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81
Q

What is the treatment of Cellulitis (near the eyes or nose)

A

Co-amoxiclav (clarithromycin, + metronidazole if penicillin-allergic)

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82
Q

What is the treatment of Erysipelas?

A

Flucloxacillin* (clarithromycin, erythromycin or doxycycline if penicillin-allergic)

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83
Q

Who would benefit from post-exposure prophylaxis to chicken pox? what is given?

A

The following criteria should be met to determine who would benefit from active post-exposure prophylaxis:

1. significant exposure to chickenpox or herpes zoster
    e.g. exposure to limited, covered-up shingles may not warrant post-exposure prophylaxis
2. a clinical condition that increases the risk of severe varicella; this includes immunosuppressed patients, neonates and pregnant women
    e.g. long-term steroids, methotrexate and other common immunosuppressants
3. no antibodies to the varicella virus
    ideally all at-risk exposed patients should have a blood test for varicella antibodies
    this should not, however, delay post-exposure prophylaxis past 7 days after initial contact

Patients who fulfill the above criteria should be given varicella-zoster immunoglobulin (VZIG).

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84
Q

Bed bugs
-What is this caused by?
-How is this managed?
-How can this be controlled/prevented?

A

Bed bugs describes a variety of clinical problems including itchy skin rashes, bites and allergic symptoms secondary to infestation with Cimex hemipteru.

Bedbug infestation seems to be an increasingly common presentation within UK general practice. Bedbugs thrive in mattresses or fabrics, and can be extremely difficult to eradicate. Topical hydrocortisone is suitable to control itch, but definitive management is through a pest management company and fumigation of the house.

Bed bug numbers may be controlled by hot-washing bed linen and using mattress covers.

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85
Q

What is lyme disease caused by?

A

Lyme disease is caused by the spirochaete Borrelia burgdorferi and is spread by ticks.

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86
Q

Describe erythema migrans seen in lyme disease? what other systemic features occur within 30 days?

A

Early features (within 30 days)

erythema migrans
    'bulls-eye' rash is typically at the site of the tick bite
    typically develops 1-4 weeks after the initial bite but may present sooner
    usually painless, more than 5 cm in diameter and slowlly increases in size
    present in around 80% of patients.

systemic features
headache
lethargy
fever
arthralgia

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87
Q

What are 5 later features of lyme disease? (after 30 days)

A

Later features (after 30 days)

cardiovascular
    heart block
    peri/myocarditis

neurological
facial nerve palsy
radicular pain
meningitis

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88
Q

What investigations are recommended for lyme disease?

A

Investigation

NICE recommend that Lyme disease can be diagnosed clinically if erythema migrans is present
    erythema migrans is therefore an indication to start antibiotics

enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
if negative and Lyme disease is still suspected in people tested within 4 weeks from symptom onset, repeat the ELISA 4-6 weeks after the first ELISA test. If still suspected in people who have had symptoms for 12 weeks or more then an immunoblot test should be done
if positive or equivocal then an immunoblot test for Lyme disease should be done

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89
Q

What is the management of asymptomatic tick bites?

A

Management of asymptomatic tick bites

tick bites can be a relatively common presentation to GP practices, and can cause significant anxiety
if the tick is still present, the best way to remove it is using fine-tipped tweezers, grasping the tick as close to the skin as possible and pulling upwards firmly. The area should be washed following.
NICE guidance does not recommend routine antibiotic treatment to patients who've suffered a tick bite
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90
Q

What is the manageemnt of suspected/confirmed lyme disease? What reaction can be seen after initiating therapy?

A

Management of suspected/confirmed Lyme disease

doxycycline if early disease. Amoxicillin is an alternative if doxycycline is contraindicated (e.g. pregnancy)
    people with erythema migrans should be commenced on antibiotic without the need for further tests
ceftriaxone if disseminated disease

Jarisch-Herxheimer reaction is sometimes seen after initiating therapy: fever, rash, tachycardia after first dose of antibiotic (more commonly seen in syphilis, another spirochaetal disease)

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91
Q

What is given to treat lower UTI?

A

Trimethoprim or nitrofurantoin. Alternative: amoxicillin or cephalosporin

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92
Q

When is urine culture sent in UTI

A

send a urine culture if:

aged > 65 years
visible or non-visible haematuria
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93
Q

How is UTI managed in a symptomatic pregnant lady?
-what is first line?
-what is second line?

A

if the pregnant woman is symptomatic:

a urine culture should be sent in all cases
should be treated with an antibiotic for
first-line: nitrofurantoin (should be avoided near term)
second-line: amoxicillin or cefalexin
trimethoprim is teratogenic in the first trimester and should be avoided during pregnancy
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94
Q

How is asymptomatic bacteruria treated in pregnant women?

A

asymptomatic bacteriuria in pregnant women:

a urine culture should be performed routinely at the first antenatal visit
Clinical Knowledge Summaries recommend an immediate antibiotic prescription of either nitrofurantoin (should be avoided near term), amoxicillin or cefalexin. This should be a 7-day course
the rationale of treating asymptomatic bacteriuria is the significant risk of progression to acute pyelonephritis
a further urine culture should be sent following completion of treatment as a test of cure
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95
Q

How is UTI treated in men?

A

Men

an immediate antibiotic prescription should be offered for 7 days
as with non-pregnant women, trimethoprim or nitrofurantoin should be offered first-line unless prostatitis is suspected
a urine culture should be sent in all cases before antibiotics are started
NICE Clinical Knowledge Summaries state: 'Referral to urology is not routinely required for men who have had one uncomplicated lower urinary tract infection (UTI).'
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96
Q

What is given to treat acute pyelonephritis>

A

Broad-spectrum cephalosporin or quinolone

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97
Q

What is given to treat prostatitis?

A

Quinolone or trimethoprim

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98
Q

What is the treatment of gonorrhoea?

A

IM ceftriaxone

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99
Q

What is gonorrhoea caused by? what is the incubation period?

A

Gonorrhoea is caused by the Gram-negative diplococcus Neisseria gonorrhoeae. Acute infection can occur on any mucous membrane surface, typically genitourinary but also rectum and pharynx. The incubation period of gonorrhoea is 2-5 days

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100
Q

What are the features of gonorrhoea in males? in females?

A

Features

males: urethral discharge, dysuria
females: cervicitis e.g. leading to vaginal discharge
rectal and pharyngeal infection is usually asymptomatic
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101
Q

Describe the management of gonorrhoea?
-first line
-if sensitivities are known
-if the partient has refused first line treatment

A

Management

ciprofloxacin used to be the treatment of choice. However, there is increased resistance to ciprofloxacin (around 36% in the UK) and therefore cephalosporins are now more widely used
there was a change in the 2019 British Society for Sexual Health and HIV (BASHH) guidelines. Previously the first-line treatment was IM ceftriaxone + oral azithromycin. The new first-line treatment is a single dose of IM ceftriaxone 1g (i.e. no longer add azithromycin). If sensitivities are known (and the organism is sensitive to ciprofloxacin) then a single dose of oral ciprofloxacin 500mg should be given
if ceftriaxone is refused (e.g. needle-phobic) then oral cefixime 400mg (single dose) + oral azithromycin 2g (single dose) should be used
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102
Q

What are the complications of gonorrhoea?
-what is the triad of symptoms?
-What are later complications?

A

Disseminated gonococcal infection (DGI) and gonococcal arthritis may also occur, with gonococcal infection being the most common cause of septic arthritis in young adults. The pathophysiology of DGI is not fully understood but is thought to be due to haematogenous spread from mucosal infection (e.g. Asymptomatic genital infection). Initially there may be a classic triad of symptoms: tenosynovitis, migratory polyarthritis and dermatitis. Later complications include septic arthritis, endocarditis and perihepatitis (Fitz-Hugh-Curtis syndrome)

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103
Q

What are three key features of disseminated gonococcal infection

A

Key features of disseminated gonococcal infection

tenosynovitis
migratory polyarthritis
dermatitis (lesions can be maculopapular or vesicular)
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104
Q

What is the treatment of chlamydia?

A

Doxycycline or azithromycin

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105
Q

what causes chlamydia?
-is this common?
-what is the incubation period?

A

Chlamydia is the most prevalent sexually transmitted infection in the UK and is caused by Chlamydia trachomatis, an obligate intracellular pathogen. Approximately 1 in 10 young women in the UK have Chlamydia. The incubation period is around 7-21 days, although it should be remembered a large percentage of cases are asymptomatic

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106
Q

What is LGV? how is this treated?

A

Lymphogranuloma venereum (LGV) is caused by Chlamydia trachomatis. Typically infection comprises of three stages

stage 1: small painless pustule which later forms an ulcer
stage 2: painful inguinal lymphadenopathy
stage 3: proctocolitis

LGV is treated using doxycycline.

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107
Q

What are the features of gonorrhoea is women? in men?

A

Features

asymptomatic in around 70% of women and 50% of men
women: cervicitis (discharge, bleeding), dysuria
men: urethral discharge, dysuria
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108
Q

What are 7 potential complications of chlamydia?

A

Potential complications

epididymitis
pelvic inflammatory disease
endometritis
increased incidence of ectopic pregnancies
infertility
reactive arthritis
perihepatitis (Fitz-Hugh-Curtis syndrome)
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109
Q

Describe the investigations for chlamydia? what is first line investigation for women vs men? when should chlamydia testing be carried out?

A

Investigation

traditional cell culture is no longer widely used
nuclear acid amplification tests (NAATs) are now the investigation of choice
urine (first void urine sample), vulvovaginal swab or cervical swab may be tested using the NAAT technique
for women: the vulvovaginal swab is first-line
for men: the urine test is first-line
Chlamydiatesting should be carried out two weeks after a possible exposure
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110
Q

Describe the screening for chlamydia

A

Screening

in England the National Chlamydia Screening Programme is open to all men and women aged 15-24 years
the 2009 SIGN guidelines support this approach, suggesting screening all sexually active patients aged 15-24 years
relies heavily on opportunistic testing
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111
Q

What is the first line treatment of chlamydia?

A

doxycycline (7 day course) if first-line

this is now preferred to azithromycin due to concerns about Mycoplasma genitalium. This infection is often coexistant in patients with Chlamydia and there is evidence of rising levels of macrolide resistance, hence why doxycycline is preferred
if doxycycline is contraindicated / not tolerated then either azithromycin (1g od for one day, then 500mg od for two days) should be used
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112
Q

What is the treatment of chlamydia if pregnant?

A

if pregnant then azithromycin, erythromycin or amoxicillin may be used. The SIGN guidelines suggest azithromycin 1g stat is the drug of choice ‘following discussion of the balance of benefits and risks with the patient’

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113
Q

who should be offered a choice of provider for initial partner notification for chlamydia? who should be contacted?

A

patients diagnosed with Chlamydia should be offered a choice of provider for initial partner notification - either trained practice nurses with support from GUM, or referral to GUM
for men with urethral symptoms: all contacts since, and in the four weeks prior to, the onset of symptoms
for women and asymptomatic men all partners from the last six months or the most recent sexual partner should be contacted
contacts of confirmed Chlamydia cases should be offered treatment prior to the results of their investigations being known (treat then test)

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114
Q

What is the treatment for PID?

A

Oral ofloxacin + oral metronidazole or intramuscular ceftriaxone + oral doxycycline + oral metronidazole

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115
Q

What is the treatment for syphilis?

A

Benzathine benzylpenicillin or doxycycline or erythromycin

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116
Q

What is syphilis caused by? how many stages of infection can occur? what is the incubation period?

A

Syphilis is a sexually transmitted infection caused by the spirochaete Treponema pallidum. Infection is characterised by primary, secondary and tertiary stages. The incubation period is between 9-90 days

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117
Q

Describe the primary features of syphilis?

A

Primary features

chancre - painless ulcer at the site of sexual contact
local non-tender lymphadenopathy
often not seen in women (the lesion may be on the cervix)
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118
Q

What are the secondary features of syphilis? when does this occur?

A

Secondary features - occurs 6-10 weeks after primary infection

systemic symptoms: fevers, lymphadenopathy
rash on trunk, palms and soles
buccal 'snail track' ulcers (30%)
condylomata lata (painless, warty lesions on the genitalia )
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119
Q

What are the tertiary features of syphilis?

A

Tertiary features

gummas (granulomatous lesions of the skin and bones)
ascending aortic aneurysms
general paralysis of the insane
tabes dorsalis
Argyll-Robertson pupil
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120
Q

what are 5 features of congenital syphilis?

A

Features of congenital syphilis

blunted upper incisor teeth (Hutchinson's teeth), 'mulberry' molars
rhagades (linear scars at the angle of the mouth)
keratitis
saber shins
saddle nose
deafness
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121
Q

What is the treatment of BV?

A

Oral or topical metronidazole or topical clindamycin

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122
Q

What is BV? what happens to vaginal pH?

A

Bacterial vaginosis (BV) describes an overgrowth of predominately anaerobic organisms such as Gardnerella vaginalis. This leads to a consequent fall in lactic acid producing aerobic lactobacilli resulting in a raised vaginal pH.

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123
Q

What is the criteria used for diagnosis of BV? how many points should be present for diganosis?

A

Amsel’s criteria for diagnosis of BV - 3 of the following 4 points should be present

thin, white homogenous discharge
clue cells on microscopy: stippled vaginal epithelial cells
vaginal pH > 4.5
positive whiff test (addition of potassium hydroxide results in fishy odour)
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124
Q

What is the management of BV in an asymptomatic woman?

A

Management

if the woman is asymptomatic, treatment is not usually required CKS
    e.g. picked up on a swab done for different reasons
    exceptions include if a woman is undergoing a termination of pregnancy
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125
Q

What is the management of BV in a symptomatic woman? what is the cure rate? what is the relapse rate?

A

if symptomatic: oral metronidazole for 5-7 days CKS

70-80% initial cure rate
relapse rate > 50% within 3 months
a single oral dose of metronidazole 2g may be used if adherence may be an issue
the BNF suggests topical metronidazole or topical clindamycin as alternatives
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126
Q

What is the management of BV in pregnancy?

A

if pregnant CKS

results in an increased risk of preterm labour, low birth weight and chorioamnionitis, late miscarriage
it was previously taught that oral metronidazole should be avoided in the first trimester and topical clindamycin used instead. Recent guidelines however recommend that oral metronidazole is used throughout pregnancy
if asymptomatic: discuss with the woman's obstetrician if treatment is indicated
if symptomatic: either oral metronidazole for 5-7 days or topical treatment. The higher, stat dose of metronidazole mentioned above is not recommended
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127
Q

What is trichomonas vaginalis?

A

Trichomonas vaginalis is a highly motile, flagellated protozoan parasite. Trichomoniasis is a sexually transmitted infection (STI).

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128
Q

What are the 5 features of trichomonas?

A

Features

vaginal discharge: offensive, yellow/green, frothy
vulvovaginitis
strawberry cervix
pH > 4.5
in men is usually asymptomatic but may cause urethritis
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129
Q

What is done in the investigation of trichomonas?

A

Investigation

microscopy of a wet mount shows motile trophozoites
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130
Q

What is the management of trichomonas?

A

Management

oral metronidazole for 5-7 days, although the BNF also supports the use of a one-off dose of 2g metronidazole
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131
Q

What is non-gonococcal urethritis? describe a typical case?

A

Non-gonococcal urethritis (NGU, sometimes referred to as non-specific urethritis) is a term used to describe the presence of urethritis when a gonococcal bacteria are not identifiable or the initial swab. A typical case would be a male who presented to a GUM clinic with a purulent urethral discharge and dysuria. A swab would be taken in clinic, microscopy performed which showed neutrophils but no Gram-negative diplococci (i.e. no evidence of gonorrhoea). Clearly, this patient requires immediate treatment prior to waiting for the Chlamydia test to come back and hence an initial diagnosis of NGU is made.

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132
Q

What can cause non-gonococcal urethritis?

A

No cause is found in around half of cases. Possible causative organisms include:

Chlamydia trachomatis
    most common cause
Mycoplasma genitalium
    thought to cause more symptoms than Chlamydia
less common causes
    Ureaplasma urealyticum
    Trichomonas vaginalis
    Escherichia coli
133
Q

What is the management of non-gonococcal urethritis?

A

Management

contact tracing
the BNF and British Association for Sexual Health and HIV (BASHH) both recommend either oral azithromycin or doxycycline
134
Q

What is chancroid? what does this cause?

A

Chancroid is a tropical disease caused by Haemophilus ducreyi. It causes painful genital ulcers associated with unilateral, painful inguinal lymph node enlargement. The ulcers typically have a sharply defined, ragged, undermined border.

135
Q

How many strains of HSV exist? what do these cause?

A

There are two strains of the herpes simplex virus (HSV) in humans: HSV-1 and HSV-2. Whilst it was previously thought HSV-1 accounted for oral lesions (cold sores) and HSV-2 for genital herpes it is now known there is considerable overlap

136
Q

What are three features of HSV?

A

Features

primary infection: may present with a severe gingivostomatitis
cold sores
painful genital ulceration
137
Q

What is the management of HSV:
-gingivostomatitis
-cold sores
-genital

A

Management

gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
cold sores: topical aciclovir although the evidence base for this is modest
genital herpes: oral aciclovir. Some patients with frequent exacerbations may benefit from longer term aciclovir
138
Q

What is the management of HSV in pregnancy?

A

Pregnancy

elective caesarean section at term is advised if a primary attack of herpes occurs during pregnancy at greater than 28 weeks gestation
women with recurrent herpes who are pregnant should be treated with suppressive therapy and be advised that the risk of transmission to their baby is low
139
Q

What does HPV cause? what can this predispose to?

A

Genital warts (also known as condylomata accuminata) are a common cause of attendance at genitourinary clinics. They are caused by the many varieties of the human papillomavirus HPV, especially types 6 & 11. It is now well established that HPV (primarily types 16,18 & 33) predisposes to cervical cancer.

6 & 11: causes genital warts
16 & 18: linked to a variety of cancers, most notably cervical cancer
140
Q

What are the features of HPV?

A

Features

small (2 - 5 mm) fleshy protuberances which are slightly pigmented
may bleed or itch
141
Q

What is the management of HPV?

A

Management

topical podophyllum or cryotherapy are commonly used as first-line treatments depending on the location and type of lesion
    multiple, non-keratinised warts are generally best treated with topical agents
    solitary, keratinised warts respond better to cryotherapy
imiquimod is a topical cream that is generally used second line
genital warts are often resistant to treatment and recurrence is common although the majority of anogenital infections with HPV clear without intervention within 1-2 years
142
Q

Who is offered the HPV vaccine?

A

The UK has an HPV immunisation programme that provides protection against both the main oncogenic HPV strains (16 & 18) as well as the strains that commonly cause genital warts (6 & 11). The immunisation programme is aimed primarily at 12-13 years olds, both girls and boys but the vaccine is also offered to gay, bisexual, and other men who have sex with men (GBMSM) to protect against anal, throat and penile cancers.

143
Q

How is the HPV vaccine given to 12 and 13 year old girls?

A

All 12- and 13-year-olds (girls AND boys) in school Year 8 are offered the human papillomavirus (HPV) vaccine.

the vaccine is normally given in school
information given to parents and available on the NHS website make it clear that the child may receive the vaccine against parental wishes
since September 2023 one dose is now given instead of two. This change followed evidence from large studies that one dose provided equivalent protection
144
Q

How are:
-eligible GBMSM under age 25
-eligible GBMSM age 25-45
-eligible individuals who are immunosuppressed or those known to have HIV
Given HPV vaccien

A

Other groups

eligible GBMSM under the age of 25 also receive 1-dose, offered through sexual health clinics
eligible GBMSM aged 25 to 45 years receive a 2-dose schedule, offered through sexual health clinics
eligible individuals who are immunosuppressed or those known to be HIV-positive receive a 3-dose schedule
145
Q

What si hepatitis B? how is this spread? what is the incubation period?

A

Hepatitis B is a double-stranded DNA hepadnavirus and is spread through exposure to infected blood or body fluids, including vertical transmission from mother to child. The incubation period is 6-20 weeks.

146
Q

What are 3 features of hep B?
-what are 6 complications of hep B infection?

A

The features of hepatitis B include fever, jaundice and elevated liver transaminases.

Complications of hepatitis B infection

chronic hepatitis (5-10%). 'Ground-glass' hepatocytes may be seen on light microscopy
fulminant liver failure (1%)
hepatocellular carcinoma
glomerulonephritis
polyarteritis nodosa
cryoglobulinaemia
147
Q

Immunisation against hep B
-who is given as a child?
-who are at risk workers who should be vaccinated?
-

A

Immunisation against hepatitis B (please see the Greenbook link for more details)

children born in the UK are now vaccinated as part of the routine immunisation schedule. This is given at 2, 3 and 4 months of age
at risk groups who should be vaccinated include: healthcare workers, intravenous drug users, sex workers, close family contacts of an individual with hepatitis B, individuals receiving blood transfusions regularly, chronic kidney disease patients who may soon require renal replacement therapy, prisoners, chronic liver disease patients
148
Q

What does the hep B vaccine contain? Does everybody respond?

A

Contains HBsAg adsorbed onto aluminium hydroxide adjuvant and is prepared from yeast cells using recombinant DNA technology
around 10-15% of adults fail to respond or respond poorly to 3 doses of the vaccine. Risk factors include age over 40 years, obesity, smoking, alcohol excess and immunosuppression

149
Q

Who is tested for anti-HbS

A

testing for anti-HBs is only recommended for those at risk of occupational exposure (i.e. Healthcare workers) and patients with chronic kidney disease. In these patients anti-HBs levels should be checked 1-4 months after primary immunisation

150
Q

What does each Anti-HBs level indicate:
>100
10-100
<10§

A

Anti-HBs level (mIU/ml) Response
> 100 Indicates adequate response, no further testing required. Should still receive booster at 5 years
10 - 100 Suboptimal response - one additional vaccine dose should be given. If immunocompetent no further testing is required
< 10 Non-responder. Test for current or past infection. Give further vaccine course (i.e. 3 doses again) with testing following. If still fails to respond then HBIG would be required for protection if exposed to the virus

151
Q

What is the management of Hep B?

A

Management of hepatitis B

pegylated interferon-alpha used to be the only treatment available. It reduces viral replication in up to 30% of chronic carriers. A better response is predicted by being female, < 50 years old, low HBV DNA levels, non-Asian, HIV negative, high degree of inflammation on liver biopsy
whilst NICE still advocate the use of pegylated interferon firstl-line other antiviral medications are increasingly used with an aim to suppress viral replication (not in a dissimilar way to treating HIV patients)
examples include tenofovir, entecavir and telbivudine (a synthetic thymidine nucleoside analogue)
152
Q

Hepatitis C - who is at risk? is this common?

A

Hepatitis C is likely to become a significant public health problem in the UK in the next decade. It is thought around 200,000 people are chronically infected with the virus. At risk groups include intravenous drug users and patients who received a blood transfusion prior to 1991 (e.g. haemophiliacs).

153
Q

What kind of virus is Hep C? what is the incubation period?

A

hepatitis C is a RNA flavivirus
incubation period: 6-9 weeks

154
Q

What is the risk of transmission for hep c
-during needlestick injury
-vertical transmission
-breastfeeding
-sexual intercourse

A

Transmission

the risk of transmission during a needle stick injury is about 2%
the vertical transmission rate from mother to child is about 6%. The risk is higher if there is coexistent HIV
breastfeeding is not contraindicated in mothers with hepatitis C
the risk of transmitting the virus during sexual intercourse is probably less than 5%
there is no vaccine for hepatitis C
155
Q

What are clinical features assoc with exposure to hep. C virus?

A

After exposure to the hepatitis C virus only around 30% of patients will develop features such as:

a transient rise in serum aminotransferases / jaundice
fatigue
arthralgia
156
Q

What investigations are used for hep C? what is the natural course of the disease?

A

Investigations

HCV RNA is the investigation of choice to diagnose acute infection
whilst patients will eventually develop anti-HCV antibodies it should be remembered that patients who spontaneously clear the virus will continue to have anti-HCV antibodies

Outcome

around 15-45% of patients will clear the virus after an acute infection (depending on their age and underlying health) and hence the majority (55-85%) will develop chronic hepatitis C
157
Q

How is chronic hep C defined? what are 7 complications of chronic hep C?

A

Chronic hepatitis C may be defined as the persistence of HCV RNA in the blood for 6 months.

Potential complications of chronic hepatitis C

rheumatological problems: arthralgia, arthritis
eye problems: Sjogren's syndrome
cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer
cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)
porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse
membranoproliferative glomerulonephritis
158
Q

What is the management of chronic infection hep C?

A

Management of chronic infection

treatment depends on the viral genotype - this should be tested prior to treatment
the management of hepatitis C has advanced rapidly in recent years resulting in clearance rates of around 95%. Interferon based treatments are no longer recommended
the aim of treatment is sustained virological response (SVR), defined as undetectable serum HCV RNA six months after the end of therapy
currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
159
Q

What are 3 side effects of ribavirin?

A

ribavirin - side-effects: haemolytic anaemia, cough. Women should not become pregnant within 6 months of stopping ribavirin as it is teratogenic

160
Q

What are 5 side effects of interferon alpha?

A

interferon alpha - side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia

161
Q

Hepatitis D
-what is this
- how is this transmitted?

A

Hepatitis D is a single stranded RNA virus that is transmitted parenterally. It is an incomplete RNA virus that requires hepatitis B surface antigen to complete its replication and transmission cycle.

It is transmitted in a similar fashion to hepatitis B (exchange of bodily fluids) and patients may be infected with hepatitis B and hepatitis D at the same time.

162
Q

What is a hepatitis D co-infection vs a super-infection?

A

Hepatitis D terminology:

Co-infection: Hepatitis B and Hepatitis D infection at the same time.
Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.

Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.

163
Q

What is the diagnosis and management of Hep D?

A

Diagnosis is made via reverse polymerase chain reaction of hepatitis D RNA. Interferon is currently used as treatment, but with a poor evidence base.

164
Q

Hep A
-what type of virus is this?
-what is the incubation period?
-What is the transmission?
-Does hep A cause chronic disease?

A

Hepatitis A is typically a benign, self-limiting disease, with a serious outcome being very rare.

Overview

incubation period: 2-4 weeks
RNA picornavirus
transmission is by faecal-oral spread, often in institutions
doesn't cause chronic disease
165
Q

What are the features of hep A infection? 5

A

Features

flu-like prodrome
abdominal pain: typically right upper quadrant
tender hepatomegaly
jaundice
deranged liver function tests
166
Q

Are there complications of hep A?

A

Complications

complications are rare and there is no increased risk of hepatocellular cancer
167
Q

Is there a vaccine available for hep A?

A

Immunisation

an effective vaccine is available
after the initial dose a booster dose should be given 6-12 months later
168
Q

What 6 people should receive hep A immunisation?

A

Who should be vaccinated? (Based on the Green book guidelines)

people travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old
people with chronic liver disease
patients with haemophilia
men who have sex with men
injecting drug users
individuals at occupational risk: laboratory worker; staff of large residential institutions; sewage workers; people who work with primates
169
Q

Hep E
-What kind of virus?
-how is this spread?
-What is the incubation period?

A

RNA hepevirus
spread by the faecal-oral route
incubation period: 3-8 weeks

170
Q

Hep E
-Where is this found in the world?
-What illness does this cause? Is there a mortality assoc?

A

common in Central and South-East Asia, North and West Africa, and in Mexico
causes a similar disease to hepatitis A, but carries a significant mortality (about 20%) during pregnancy

171
Q

Hep E
-Is there complications?
-is there a vaccine?

A

does not cause chronic disease or an increased risk of hepatocellular cancer
a vaccine is currently in development, but is not yet in widespread use

172
Q

Is HIV seroconversion symptomatic? how does this present? is this assoc. with prognosis? when does this occur?

A

HIV seroconversion is symptomatic in 60-80% of patients and typically presents as a glandular fever type illness. Increased symptomatic severity is associated with poorer long term prognosis. It typically occurs 3-12 weeks after infection

173
Q

Give some features of HIV seroconversion? 7

A

Features

sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis
174
Q

What are the two tests that can be done for diagnosis of HIV? when are these indicated?

A

HIV antibodies
may not be present in early infection, but most people develop antibodies to HIV at 4-6 weeks but 99% do by 3 months
usually consists of both a screening ELISA (Enzyme Linked Immuno-Sorbent Assay) test and a confirmatory Western Blot Assay

p24 antigen
a viral core protein that appears early in the blood as the viral RNA levels rise
usually positive from about 1 week to 3 - 4 weeks after infection with HIV

combination tests (HIV p24 antigen and HIV antibody) are now standard for the diagnosis and screening of HIV
if the combined test is positive it should be repeated to confirm the diagnosis
some centres may also test the viral load (HIV RNA levels) if HIV is suspected at the same time

175
Q

How should HIV testing in an asymptomatic patient be done?

A

testing for HIV in asymptomatic patients should be done at 4 weeks after possible exposure
after an initial negative result when testing for HIV in an asymptomatic patient, offer a repeat test at 12 weeks

176
Q

What does antiretroviral treatment for HIV involve? When is treatment initiated?

A

Antiretroviral therapy (ART) involves a combination of at least three drugs, typically two nucleoside reverse transcriptase inhibitors (NRTI) and either a protease inhibitor (PI) or a non-nucleoside reverse transcriptase inhibitor (NNRTI). This combination both decreases viral replication but also reduces the risk of viral resistance emerging

Following the 2015 BHIVA guidelines it is now recommended that patients start ART as soon as they have been diagnosed with HIV, rather than waiting until a particular CD4 count, as was previously advocated.

177
Q

What does an entry inhibitor do in HIV treatment and can you give an example?

A

Entry inhibitors

maraviroc (binds to CCR5, preventing an interaction with gp41), enfuvirtide (binds to gp41, also known as a 'fusion inhibitor')
prevent HIV-1 from entering and infecting immune cells
178
Q

Name 3 Nucleoside analogue reverse transcriptase inhibitors (NRTI) and give their adverse effects

A

tenofovir: used in BHIVAs two recommended regime NRTI. Adverse effects include renal impairment and ostesoporosis
zidovudine: anaemia, myopathy, black nails
didanosine: pancreatitis

179
Q

Give 2 examples of Non-nucleoside reverse transcriptase inhibitors and give the side effects

A

Non-nucleoside reverse transcriptase inhibitors (NNRTI)

examples: nevirapine, efavirenz
side-effects: P450 enzyme interaction (nevirapine induces), rashes
180
Q

Give some examples of protease inhibitors 4
-what are the side effects?

A

Protease inhibitors (PI)

examples: indinavir, nelfinavir, ritonavir, saquinavir
side-effects: diabetes, hyperlipidaemia, buffalo hump, central obesity, P450 enzyme inhibition
indinavir: renal stones, asymptomatic hyperbilirubinaemia
ritonavir: a potent inhibitor of the P450 system
181
Q

What do integrase inhibitors do when treating HIV? give some examples

A

Integrase inhibitors

block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell
examples: raltegravir, elvitegravir, dolutegravir
182
Q

What is advised on mode of delivery for pregnant ladies with HIV?

A

Mode of delivery

vaginal delivery is recommended if viral load is less than 50 copies/ml at 36 weeks, otherwise caesarian section is recommended
a zidovudine infusion should be started four hours before beginning the caesarean section
183
Q

what is used for neonatal antiretroviral therapy?

A

Neonatal antiretroviral therapy

zidovudine is usually administered orally to the neonate if maternal viral load is <50 copies/ml. Otherwise triple ART should be used. Therapy should be continued for 4-6 weeks.
184
Q

Should HIV positive mothers breastfeed?

A

Infant feeding

in the UK all women should be advised not to breast feed
185
Q

Diarrhoea in HIV
-Is this common?
-What are the possible causes? 4

A

Diarrhoea is common in patients with HIV. This may be due to the effects of the virus itself (HIV enteritis) or opportunistic infections

Possible causes

Cryptosporidium + other protozoa (most common)
Cytomegalovirus
Mycobacterium avium intracellulare
Giardia
186
Q

What is the most common infective cause of diarrhoea in HIV patients? what is the incubation period? what is used to diagnosis? what is the rteatement?

A

Cryptosporidium is the most common infective cause of diarrhoea in HIV patients. It is an intracellular protozoa and has an incubation period of 7 days. Presentation is very variable, ranging from mild to severe diarrhoea. A modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium. Treatment is difficult, with the mainstay of management being supportive therapy

187
Q

What can be the cause of diarrhoea in HIV positive patients with a CD4 count below 50? how is diagnosis made? what are typical features? what is the treatment?

A

Mycobacterium avium intracellulare is an atypical mycobacteria seen with the CD4 count is below 50. Typical features include fever, sweats, abdominal pain and diarrhoea. There may be hepatomegaly and deranged LFTs. Diagnosis is made by blood cultures and bone marrow examination. Management is with rifabutin, ethambutol and clarithromycin

188
Q

Kaposi sarcoma in HIV
-what is this caused by?
-how does this present?
-how can respiratory involvement be affected?
-What is the treatment?

A

Kaposi’s sarcoma

caused by HHV-8 (human herpes virus 8)
presents as purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
skin lesions may later ulcerate
respiratory involvement may cause massive haemoptysis and pleural effusion
radiotherapy + resection
189
Q

What is the most common cause of oesophagitis in patients with HIV? what is the treatment?

A

Oesophageal candidiasis is the most common cause of oesophagitis in patients with HIV. It is generally seen in patients with a CD4 count of less than 100. Typical symptoms include dysphagia and odynophagia. Fluconazole and itraconazole are first-line treatments.

190
Q

Toxoplasmosis in HIV
-What are the symptoms?
-what is seen on CT?
-What is the management

A

Toxoplasmosis

accounts for around 50% of cerebral lesions in patients with HIV
constitutional symptoms, headache, confusion, drowsiness
CT: usually single or multiple ring enhancing lesions, mass effect may be seen
management: sulfadiazine and pyrimethamine

Thallium spect negative

191
Q

Primary CNS lymphoma in HIV
-what virus is this assoc. with?
-What is seen on CT?
-What is the treatment?

Thallium spect?

A

Primary CNS lymphoma

accounts for around 30% of cerebral lesions
associated with the Epstein-Barr virus
CT: single or multiple homogenous enhancing lesions
treatment generally involves steroids (may significantly reduce tumour size), chemotherapy (e.g. methotrexate) + with or without whole brain irradiation. Surgical may be considered for lower grade tumours

Thallium spect positive

192
Q

Encephalitis in HIV
-Caused by what?
-what is seen on CT?

A

Encephalitis

may be due to CMV or HIV itself
HSV encephalitis but is relatively rare in the context of HIV
CT: oedematous brain
193
Q

What is the most common fungal infection of the CNS in HIV?
-what are the features

A

Cryptococcus

most common fungal infection of CNS
headache, fever, malaise, nausea/vomiting, seizures, focal neurological deficit
194
Q

What is seen on LP in cryptococcal CNS infection in HIV?

A

CSF
high opening pressure
elevated protein
reduced glucose
normally a lymphocyte predominance but in HIV white cell count many be normal
India ink test positive

195
Q

What is seen on CT in cryptococcal CNS infection in HIV

A

CT: meningeal enhancement, cerebral oedema
meningitis is typical presentation but may occasionally cause a space-occupying lesion

196
Q

PML in HIV
-What is this caused by?
-What does this cause?
-What are the clinical features?
-What are the investigations?

A

Progressive multifocal leukoencephalopathy (PML)

widespread demyelination
due to infection of oligodendrocytes by JC virus (a polyoma DNA virus)
symptoms, subacute onset : behavioural changes, speech, motor, visual impairment
CT: single or multiple lesions, no mass effect, don't usually enhance. MRI is better - high-signal demyelinating white matter lesions are seen
197
Q

AIDS dementia complex
-What is this?
-What is seen on CTB?

A

AIDS dementia complex

caused by HIV virus itself
symptoms: behavioural changes, motor impairment
CT: cortical and subcortical atrophy
198
Q

What is the commonest bacterial cause of infectious intestinal disease in the uk? how is this spread? what is the incubation period?

A

Campylobacter is the commonest bacterial cause of infectious intestinal disease in the UK. The majority of cases are caused by the Gram-negative bacillus Campylobacter jejuni. It is spread by the faecal-oral route and has an incubation period of 1-6 days.

199
Q

Give 3 features of campylobacter

A

Features

prodrome: headache malaise
diarrhoea: often bloody
abdominal pain: may mimic appendicitis
200
Q

Describe the management of campylobacter

A

Management

usually self-limiting
the BNF advises treatment if severe or the patient is immunocompromised. Clinical Knowledge summaries also recommend antibiotics if severe symptoms (high fever, bloody diarrhoea, or more than eight stools per day) or symptoms have last more than one week
the first-line antibiotic is clarithromycin
ciprofloxacin is an alternative although the BNF states that 'Strains with decreased sensitivity to ciprofloxacin isolated frequently'
201
Q

Give 5 complications of campylobacter

A

Complications

Guillain-Barre syndrome may follow Campylobacter jejuni infections
reactive arthritis
septicaemia, endocarditis, arthritis
202
Q

What is the most common protozoal cause of diarrhoea? who is this most common in?

A

Cryptosporidiosis is the commonest protozoal cause of diarrhoea in the UK. Two species, Cryptosporidium hominis and Cryptosporidium parvum account for the majority cases.

Cryptosporidiosis is more common in immunocompromised patients (e.g. HIV) and young children.

203
Q

What are 4 features of cryptosporidium diarrhoea?

A

Features

watery diarrhoea
abdominal cramps
fever
in immunocompromised patients, the entire gastrointestinal tract may be affected resulting in complications such as sclerosing cholangitis and pancreatitis
204
Q

what is the diagnosis of cryptosporidium?

A

Diagnosis

stool: modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium
205
Q

what is the management of cryptosporidium?

A

Management

is largely supportive for immunocompetent patients
if the patient has HIV and is not on antiretroviral therapy then this should be started and often will be enough to resolve the infection
nitazoxanide may be used for immunocompromised patients
rifaximin is also sometimes used for immunocompromised patients/patients with severe disease
206
Q

What is the treatment of c. diff?

A

First episode: oral vancomycin
Second or subsequent episode of infection: oral fidaxomicin

207
Q

What is travellers diarrhoea defined as? What is the most common cause?

A

Travellers’ diarrhoea may be defined as at least 3 loose to watery stools in 24 hours with or without one of more of abdominal cramps, fever, nausea, vomiting or blood in the stool. The most common cause is Escherichia coli.

208
Q

E.Coli
-Who is this most common in?
-what 3 clinical features are seen?

A

Common amongst travellers
Watery stools
Abdominal cramps and nausea

209
Q

Describe what is seen in giardiasis diarrhoea?

A

Prolonged, non-bloody diarrhoea

210
Q

Describe the clinical features of cholera

A

Profuse, watery diarrhoea
Severe dehydration resulting in weight loss
Not common amongst travellers

211
Q

Describe the clinical features of shigella

A

Bloody diarrhoea
Vomiting and abdominal pain

212
Q

What are 2 clinical features of s. aureus gastroenteritis

A

Severe vomiting
Short incubation period

213
Q

What two types of illness are seen in bacillus cereus gastroenteritis?

A

Two types of illness are seen

vomiting within 6 hours, stereotypically due to rice
diarrhoeal illness occurring after 6 hours
214
Q

Describe the clinical features of amoebiasis

A

Gradual onset bloody diarrhoea, abdominal pain and tenderness which may last for several weeks

215
Q

ncubation period

Staphylococcus aureus, Bacillus cereus* ?
Salmonella, Escherichia coli
Shigella, Campylobacter
Giardiasis, Amoebiasis

A

ncubation period

1-6 hrs: Staphylococcus aureus, Bacillus cereus*
12-48 hrs: Salmonella, Escherichia coli
48-72 hrs: Shigella, Campylobacter
> 7 days: Giardiasis, Amoebiasis
216
Q

What is the treatment of salmonella (non-typhoid)?

A

Ciprofloxacin

217
Q

What is the treatment of shigella?

A

Ciprofloxacin

218
Q

What is giardiasis caused by? What are 3 risk factors?

A

Giardiasis is caused by the flagellate protozoan Giardia lamblia. It is spread by the faeco-oral route.

Risk factors

foreign travel
swimming/drinking water from a river or lake
male-male sexual contact
219
Q

What are 7 features of giardiasis?

A

Features

often asymptomatic
non-bloody diarrhoea
    steatorrhoea
bloating, abdominal pain
lethargy
flatulence
weight loss
malabsorption and lactose intolerance can occur
220
Q

What investigations are carried out for giardiasis?

A

Investigations

stool microscopy for trophozoite and cysts: sensitivity of around 65%
stool antigen detection assay: greater sensitivity and faster turn-around time than conventional stool microscopy methods
PCR assays are also being developed
221
Q

What is the treatment of giardiasis?

A

Treatment is with metronidazole.

222
Q

What is enteric fever? what is this caused by?

A

The Salmonella group contains many members, most of which cause diarrhoeal diseases. They are aerobic, Gram-negative rods which are not normally present as commensals in the gut.

Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively. They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia.

223
Q

How is typhoid transmitted?

A

Pathophysiology

typhoid is transmitted via the faecal-oral route (also in contaminated food and water)
224
Q

Describe features of enteric fever? 5

A

Features

initially systemic upset as above
relative bradycardia
abdominal pain, distension
constipation: although Salmonella is a recognised cause of diarrhoea, constipation is more common in typhoid
rose spots: present on the trunk in 40% of patients, and are more common in paratyphoid
225
Q

Give 5 complications of enteric fever

A

Possible complications include

osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
GI bleed/perforation
meningitis
cholecystitis
chronic carriage (1%, more likely if adult females)
226
Q

What is the diagnosis of norovirus?

A

Diagnosis

Clinical history and stool culture viral PCR (polymerase chain reaction).
227
Q

How does salmonella differ from norovirus?

A

Salmonella infection has an incubation period of 6 - 72 hours and is often the result of contact with contaminated animal products, for example, unpasteurized eggs or milk. Unlike norovirus, salmonella gastroenteritis can cause bloody diarrhoea and patients often have a high fever.

228
Q

How does rotavirus differ from norovirus?

A

Rotavirus gastroenteritis causes symptoms very similar to those of norovirus, but predominantly affects children under the age of 5 years.

229
Q

How does e.coli gastroenteritis differ from norovirus?

A

E. coli infection, like Norovirus, causes vomiting and diarrhoea but has a longer incubation period (between 3-4 days but can be up to 10 days following pathogen exposure) and unlike Norovirus, E Coli infection commonly causes severe abdominal cramping and frequently causes bloody diarrhoea.

230
Q

How is norovirus managed?

A

Resolution and Potential Complications

The infection is self-limiting in immunocompetent patients and symptoms generally resolve within 72 hours
Dehydration and electrolyte imbalances may arise as a result of vomiting and diarrhoea, leading to significant morbidity and mortality and patients should be managed supportively with rehydration and electrolyte supplementation where necessary.
231
Q

Where is brucellosis most commonly found in?

A

Brucellosis is a zoonosis more common in the Middle East and in farmers, vets and abattoir workers. Four major species cause infection in humans: B. melitensis (sheep), B. abortus (cattle), B. canis and B. suis (pigs). Brucellosis has an incubation period 2 - 6 weeks.

232
Q

Give 3 features of brucellosis and 4 complications? what is found on blood tests?

A

Features

non-specific: fever, malaise
hepatosplenomegaly
sacroiliitis: spinal tenderness may be seen
complications: osteomyelitis, infective endocarditis, meningoencephalitis, orchitis
leukopenia often seen
233
Q

What is the diagnosis of brucellosis?

A

Diagnosis

the Rose Bengal plate test can be used for screening but other tests are required to confirm the diagnosis
Brucella serology is the best test for diagnosis
blood and bone marrow cultures may be suitable in certain patients, but these tests are often negative
234
Q

What is the management of brucellosis?

A

Management

doxycycline and streptomycin
235
Q

What is cutaneous lava migrans? how is this transmitted?

A

Cutaneous larva migrans is a dermatological condition prevalent in tropical and subtropical regions, largely attributable to cutaneous penetration and subsequent migration of nematode larvae, primarily from the Ancylostoma genus (e.g. Ancyclostoma braziliense). Typically, the transmission vectors are faecal-contaminated soil or sand, posing significant risks to individuals with a history of barefoot beach visits or direct soil contact.

236
Q

Describe the clinical presentation of cutaneous lava migrans

A

The clinical presentation typically involves an intensely pruritic, ‘creeping’, serpiginous, erythematous cutaneous eruption that advances over time. Symptoms can last for weeks to months, potentially leading to secondary bacterial infection due to excessive scratching. Diagnosis is typically clinical, based on exposure history and characteristic skin manifestations.

237
Q

What is the management of cutaneous lava migrans?

A

Treatment options revolve around anthelmintic agents, such as ivermectin or albendazole. Topical therapy with thiabendazole can also be effective, although it’s generally less preferred due to a lower efficacy rate and higher side effect profile.

238
Q

Describe prevention strategies for cutaneous lava migrans

A

Prevention strategies largely involve patient education about appropriate protective measures, particularly avoiding direct skin contact with potentially contaminated soil. Given the zoonotic nature of cutaneous larva migrans, public health measures for animal defecation control can also contribute to reducing the prevalence of this condition.

239
Q

What is dengue fever? what can it progress to? how is it transmitted? what is the incubation period

A

Dengue fever is a viral infection that can progress to viral haemorrhagic fever (other examples include yellow fever, Lassa fever, Ebola).

Aetiology

dengue virus is a RNA virus of the genus Flavivirus
transmitted by the Aedes aegypti mosquito
incubation period of 7 days
240
Q

How is dengue fever classified?

A

Patients with dengue fever can be classified as follows:

dengue fever:
    without warning signs
    with warning signs
severe dengue (dengue haemorrhagic fever)
241
Q

What are warning signs of dengue fever?

A

‘warning signs’ include:

abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)
242
Q

what are 7 clinical features of dengue fever?

A

Dengue fever

fever
headache (often retro-orbital)
myalgia, bone pain and arthralgia ('break-bone fever')
pleuritic pain
facial flushing (dengue)
maculopapular rash
haemorrhagic manifestations e.g. positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis
243
Q

What is severe dengue and what can this result in?

A

Severe dengue (dengue haemorrhagic fever)

this is a form of disseminated intravascular coagulation (DIC) resulting in:
    thrombocytopenia
    spontaneous bleeding
around 20-30% of these patients go on to develop dengue shock syndrome (DSS)
244
Q

What is found on blood tests in dengue fever? what are diagnostic tests?

A

Investigations

typically blood results
    leukopenia, thrombocytopenia, raised aminotransferases
diagnostic tests
    serology
    nucleic acid amplification tests for viral RNA
    NS1 antigen test
245
Q

What is the treatment of dengue fever?

A

Treatment

entirely symptomatic e.g. fluid resuscitation, blood transfusion etc
no antivirals are currently available
246
Q

What is diphtheria? what is the pathophysiology?

A

Diphtheria is caused by the Gram positive bacterium Corynebacterium diphtheriae

Pathophysiology

releases an exotoxin encoded by a β-prophage
exotoxin inhibits protein synthesis by catalyzing ADP-ribosylation of elongation factor EF-2
247
Q

What are 5 clinical features of dengue fever? what does diptheria toxin cause?

A

Diphtheria toxin commonly causes a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue

Possible presentations

recent visitors to Eastern Europe/Russia/Asia
sore throat with a 'diphtheric membrane' - grey, pseudomembrane on the posterior pharyngeal wall
bulky cervical lymphadenopathy
    may result in a 'bull neck' appearanace
neuritis e.g. cranial nerves
heart block
248
Q

What investigations are used for dengue?

A

Investigations

culture of throat swab: uses tellurite agar or Loeffler's media
249
Q

What is the management of dengue?

A

Management

intramuscular penicillin
diphtheria antitoxin
250
Q

What is leishmaniasis caused by? what 3 forms are seen?

A

Leishmaniasis is caused by the intracellular protozoa Leishmania, which are spread by the bites of sandflies. Cutaneous, mucocutaneous leishmaniasis and visceral forms are seen

251
Q

Cutaneous leishmaniasis
-what is this caused by?
-what is seen at the site of the bite?
-how is this diagnosed?
-what is the management?

A

Cutaneous leishmaniasis

caused by Leishmania tropica or Leishmania mexicana
crusted lesion at the site of bite
there may be an underlying ulcer
it is typically diagnosed by doing a punch biopsy from the edge of the lesion allowing for both histology and culture
cutaneous leishmaniasis acquired in South or Central America merits treatment due to the risk of mucocutaneous leishmaniasis whereas disease acquired in Africa or India can be managed more conservatively
252
Q

Mucocutaneous leishmaniasis
-what is this caused by
-how does this differ from cutaneous leishmaniasis?

A

Mucocutaneous leishmaniasis

caused by Leishmania braziliensis
skin lesions may spread to involve mucosae of nose, pharynx etc
253
Q

Visceral leishmaniasis
-what is this caused by?
-where does this occur?
-What clinical features are seen? 8
-What is seen on blood tests?
-what is the gold standard for diagnosis?

A

Visceral leishmaniasis (kala-azar)

mostly caused by Leishmania donovani
occurs in the Mediterranean, Asia, South America, Africa
fever, sweats, rigors
massive splenomegaly. hepatomegaly
poor appetite*, weight loss
    occasionally patients may report increased appetite with paradoxical weight loss
grey skin - 'kala-azar' means black sickness
pancytopaenia secondary to hypersplenism
the gold standard for diagnosis is bone marrow or splenic aspirate
254
Q

Leptospirosis
-what is this caused by?
-when is this usually seen?

A

Leptospirosis is caused by the spirochaete Leptospira interrogans (serogroup L. icterohaemorrhagiae), classically being spread by contact with infected rat urine.

Epidemiology

leptospirosis is commonly seen in questions referring to sewage workers, farmers, vets or people who work in an abattoir
however, on an international level, leptospirosis is far more common in the tropics so should be considered in the returning traveller
255
Q

Describe the early phase of leptospirosis

A

The early phase is due to bacteraemia and lasts around a week

may be mild or subclinical
fever
flu-like symptoms
subconjunctival suffusion (redness)/haemorrhage
256
Q

Describe the second immune phase of leptospirosis. what can this lead to?

A

second immune phase may lead to more severe disease (Weil’s disease)

acute kidney injury (seen in 50% of patients)
hepatitis: jaundice, hepatomegaly
aseptic meningitis
257
Q

Describe the investigations of leptospirosis

A

Investigation

serology: antibodies to Leptospira develop after about 7 days
PCR
culture
    growth may take several weeks so limits usefulness in diagnosis
    blood and CSF samples are generally positive for the first 10 days
    urine cultures become positive during the second week of illness
258
Q

What is the management of leptospirosis?

A

Management

high-dose benzylpenicillin or doxycycline
259
Q

What are the general features of non-falciparum malaria?
-what fever does plasmodium vivax/ovale cause?
-what fever does plamodium malariae cause?
-what is associated with plasmodium malariae?

A

Features

general features of malaria: fever, headache, splenomegaly
Plasmodium vivax/ovale: cyclical fever every 48 hours. Plasmodium malariae: cyclical fever every 72 hours
Plasmodium malariae: is associated with nephrotic syndrome
260
Q

What is the treatment of non-falciparum malaria?

A

Treatment

in areas which are known to be chloroquine-sensitive then WHO recommend either an artemisinin-based combination therapy (ACT) or chloroquine
in areas which are known to be chloroquine-resistant an ACT should be used
ACTs should be avoided in pregnant women
patients with ovale or vivax malaria should be given primaquine following acute treatment with chloroquine to destroy liver hypnozoites and prevent relapse
261
Q

Atovaquone + proguanil (Malarone) (malaria prophylaxis)
-side effects
-when to start
-when to stop

A

GI upset
1 - 2 days
7 days

262
Q

Chloroquine (malaria prophylaxis)
-what is the side effect
-what is this contraindicated in?
-how often is this taken
-when to start
-when to stop

A

Headache
Contraindicated in epilepsy
Taken weekly
1 week
4 weeks

263
Q

Doxycyline
-side effects
-when to start
-when to stop

A

Photosensitivity
Oesophagitis
1 - 2 days
4 weeks

264
Q

Mefloquine (Lariam)
-what arethe side effects
-what is this contraindicated in?
-how often is this taken
-when to start
-when to stop

A

Dizziness
Neuropsychiatric disturbance

Contraindicated in epilepsy
Taken weekly
2 - 3 weeks
4 weeks

265
Q

Proguanil (Paludrine)
Proguanil + chloroquine
-when to start
-when to stop

A

1 week
4 weeks

266
Q

Malaria prophylaxis in pregnancy
-chloroquine
-malarone
-mefloquine
-doxycyline
can any of these be taken?

A

chloroquine can be taken
proguanil: folate supplementation (5mg od) should be given
Malarone (atovaquone + proguanil): the BNF advises to avoid these drugs unless essential. If taken then folate supplementation should be given
mefloquine: caution advised
doxycycline is contraindicated

267
Q

What should be given to children travelling to malaria endemic countries?

A

It is again advisable to avoid travel to malaria endemic regions with children if avoidable. However, if travel is essential then children should take malarial prophylaxis as they are more at risk of serious complications.

diethyltoluamide (DEET) 20-50% has been shown to repel up to 100% of mosquitoes if used correctly. It can be used in children over 2 months of age*
doxycycline is only licensed in the UK for children over the age of 12 years
268
Q

What is schistosomiasis caused by? what are the three main species?

A

Schistosomiasis, or bilharzia, is a parasitic flatworm infection. The three main species of schistosome are S. mansoni, S. japonicum and S. haematobium.

269
Q

what acute manifestations of schistosomiasis exist?

A

Acute manifestations may include:

swimmers' itch
acute schistosomiasis syndrome (Katayama fever)
    fever
    urticaria/angioedema
    arthralgia/myalgia
    cough
    diarrhoea
    eosinophilia
270
Q

Schistosoma haematobium
-what can these worm do?
-what is seen on xray?
-what can this cause?\
-how canthis present and what is this a risk factro for?

A

Schistosoma haematobium

These worms deposit egg clusters (pseudopapillomas) in the bladder, causing inflammation. The calcification seen on x-ray is actually calcification of the egg clusters, not the bladder itself.

Depending on the site of these pseudopapillomas in the bladder, they can cause an obstructive uropathy and kidney damage.

This typically presents as a ‘swimmer’s itch’ in patients who have recently returned from Africa. Schistosoma haematobium is a risk factor for squamous cell bladder cancer.

271
Q

What are the features of schistosoma haematobium?

A

Features

frequency
haematuria
bladder calcification
272
Q

what are the investigations and management of schistosoma haematobium?

A

nvestigation

for asymptomatic patients serum schistosome antibodies are generally preferred
for symptomatic patients the gold standard for diagnosis is urine or stool microscopy looking for eggs

Management

single oral dose of praziquantel
273
Q

What do Schistosoma mansoni and Schistosoma japonicum cause? what complications from these exist?

A

These worms mature in the liver and then travel through the portal system to inhabit the distal colon. Their presence in the portal system can lead to progressive hepatomegaly and splenomegaly due to portal vein congestion.

These species can also lead to complications of liver cirrhosis, variceal disease and cor pulmonale.

274
Q

Schistosoma intercalatum and Schistosoma mekongi - what can these cause?

A

Schistosoma intercalatum and Schistosoma mekongi

These are less prevalent than the other three forms, but are both attributed to intestinal schistosomiasis.

275
Q

What is strongyloides stercoralis? how do these gain access to the body? what illness does this cause?

A

Strongyloides stercoralis is a human parasitic nematode worm. The larvae are present in soil and gain access to the body by penetrating the skin. Infection with Strongyloides stercoralis causes strongyloidiasis.

276
Q

strongyloidiasis
-What are 5 features canthiis cause?

A

Features

diarrhoea
abdominal pain/bloating
papulovesicular lesions where the skin has been penetrated by infective larvae e.g. soles of feet and buttocks
larva currens: pruritic, linear, urticarial rash
if the larvae migrate to the lungs a pneumonitis similar to Loeffler's syndrome may be triggered
277
Q

What is the treatment of strongyloidiasis?

A

Treatment

ivermectin and albendazole are used
278
Q

What are the two main forms of trypanosomiasis?

A

Two main form of this protozoal disease are recognised - African trypanosomiasis (sleeping sickness) and American trypanosomiasis (Chagas’ disease).

279
Q

How many forms of african trypanosomiasis are seen? how are these spread? what are 4 clinical features?

A

Two forms of African trypanosomiasis, or sleeping sickness, are seen - Trypanosoma gambiense in West Africa and Trypanosoma rhodesiense in East Africa. Both types are spread by the tsetse fly. Trypanosoma rhodesiense tends to follow a more acute course. Clinical features include:

Trypanosoma chancre - painless subcutaneous nodule at site of infection
intermittent fever
enlargement of posterior cervical lymph nodes
later: central nervous system involvement e.g. somnolence, headaches, mood changes, meningoencephalitis
280
Q

What is the management of african trypanosomiasis?

A

Management

early disease: IV pentamidine or suramin
later disease or central nervous system involvement: IV melarsoprol
281
Q

What is american trypanosomiasis caused by? what are the clinical features? what are the compliactions?

A

American trypanosomiasis, or Chagas’ disease, is caused by the protozoan Trypanosoma cruzi. The vast majority of patients (95%) are asymptomatic in the acute phase although a chagoma (an erythematous nodule at site of infection) and periorbital oedema are sometimes seen. Chronic Chagas’ disease mainly affects the heart and gastrointestinal tract

myocarditis may lead to dilated cardiomyopathy (with apical atophy) and arrhythmias
gastrointestinal features includes megaoesophagus and megacolon causing dysphagia and constipation
282
Q

What is the management of chagas disease?

A

Management

treatment is most effective in the acute phase using azole or nitroderivatives such as benznidazole or nifurtimox
chronic disease management involves treating the complications e.g., heart failure
283
Q

Zika virus
-How is this transmitted?

A

Zika is a mosquito-borne infection caused by Zika virus, a member of the genus flavivirus and family Flaviviridae. It was first isolated from a monkey in the Zika forest in Uganda in 1947.

Transmission is usually via the bite of an infected Aedes mosquito, although a small number of cases of sexual transmission have been reported. There is increasing evidence of transmission via the placenta from mother to fetus.

284
Q

What are the clinical symptoms of zika virus?

A

The majority of people infected with Zika virus have no symptoms. For those with symptoms, Zika virus tends to cause a mild, short-lived (2 to 7 days) febrile disease. Signs and symptoms suggestive of Zika virus infection may include a combination of the following:

fever
rash
arthralgia/arthritis
conjunctivitis
myalgia
headache
retro-orbital pain
pruritus
285
Q

Give some warning signs of meningitis

A

Senior review if any warning signs are present (please see the Meningitis Research Foundation algorithm link for the full list). Examples include:

rapidly progressive rash
poor peripheral perfusion
respiratory rate < 8 or > 30 / min or pulse rate < 40 or > 140 / min
pH < 7.3 or WBC< 4 *109/L or lactate > 4 mmol/L
GCS < 12 or a drop of 2 points
poor response to fluid resuscitation
286
Q

When should LP be delayed in the management of meningitis?4

A

Lumbar puncture should be delayed in the following circumstances

signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
    focal neurological signs
    papilloedema
    continuous or uncontrolled seizures
    GCS ≤ 12
287
Q

What is the treatment of meningitis?

A

IV antibiotics

3 months - 50 years: BNF recommends cefotaxime (or ceftriaxone)
> 50 years: BNF recommends cefotaxime (or ceftriaxone)  + amoxicillin (or ampicillin) for adults 

IV dexamethasone

the BNF recommend to 'consider adjunctive treatment with dexamethasone (particularly if pneumococcal meningitis suspected in adults), preferably starting before or with first dose of antibacterial, but no later than 12 hours after starting antibacterial; avoid dexamethasone in septic shock, meningococcal septicaemia, or if immunocompromised, or in meningitis following surgery'
288
Q

What is the treatment in each below situation in meningitis:
Initial empirical therapy aged < 3 months
Initial empirical therapy aged 3 months - 50 years
Initial empirical therapy aged > 50 years
Meningococcal meningitis
Pneumococcal meningitis I
Meningitis caused by Haemophilus influenzae
Meningitis caused by Listeria

A

Initial empirical therapy aged < 3 months IVcefotaxime + amoxicillin (or ampicillin)
Initial empirical therapy aged 3 months - 50 years IV cefotaxime (or ceftriaxone)
Initial empirical therapy aged > 50 years IV cefotaxime (or ceftriaxone) + amoxicillin (or ampicillin)
Meningococcal meningitis IV benzylpenicillin or cefotaxime (or ceftriaxone)
Pneumococcal meningitis IV cefotaxime (or ceftriaxone)
Meningitis caused by Haemophilus influenzae IV cefotaxime (or ceftriaxone)
Meningitis caused by Listeria IV amoxicillin (or ampicillin) + gentamicin

289
Q

What is the treatment for meningitis if pen-allergy/cephalosporin allergy?

A

If the patient has a history of immediate hypersensitivity reaction to penicillin or to cephalosporins the BNF recommends using chloramphenicol.

290
Q

Who is prophylaxis offered to for meningitis?

A

Prophylaxis needs to be offered to households and close contacts of patients affected with meningococcal meningitis. Prophylaxis should also be offered to people who have been exposed to respiratory secretion, regardless of the closeness of contact. The risk to contacts is highest in the first 7 days but persists for at least 4 weeks.

291
Q

What is used for meningitis prophylaxis? is vaccianation given? when is no prophylaxis needed?

A

people who have been exposed to a patient with confirmed bacterial meningitis should be given prophylactic antibiotics if they have close contact within the 7 days before onset
oral ciprofloxacin or rifampicin may be used. The Health Protection Agency (HPA) guidelines now state that whilst either may be used ciprofloxacin is the drug of choice as it is widely available and only requires one dose
meningococcal vaccination should be offered to close contacts when serotype results are available, including booster doses to those who had the vaccine in infancy
for pneumococcal meningitis, no prophylaxis is generally needed. There are however exceptions to this. If a cluster of cases of pneumococcal meningitis occurs the HPA have a protocol for offering close contacts antibiotic prophylaxis. Please see the link for more details

292
Q

Body fluid spillages
-what is used?
-how is this used?

A

Generally speaking hypochlorite (chlorine in oxidation state +1) is recommend for the management of body fluid spillage. It is often used in the granular or powder form which is then spread over the affected area.

Chlorine-releasing agents can be a hazard especially if used in large volumes in confined spaces or if mixed with urine. Ensuring adequate ventilation to the area is therefore important.

Other points

personal protective equipment (plastic aprons, gloves, mask, eye protection) is recommended for staff cleaning up body fluids
mops should not be used
293
Q

What is used for suppression of MRSA?

A

Suppression of MRSA from a carrier once identified

nose: mupirocin 2% in white soft paraffin, tds for 5 days
skin: chlorhexidine gluconate, od for 5 days. Apply all over but particularly to the axilla, groin and perineum
294
Q

What is mumps caused by?
-How is this spread?
-what is the incubation period?

A

Mumps is a caused by RNA paramyxovirus and tends to occur in winter and spring

Spread

by droplets
respiratory tract epithelial cells → parotid glands → other tissues
infective 7 days before and 9 days after parotid swelling starts
incubation period = 14-21 days
295
Q

What are 4 clinical features of mumps?

A

Clinical features

fever
malaise, muscular pain
parotitis ('earache', 'pain on eating'): unilateral initially then becomes bilateral in 70%
296
Q

What is the management of mumps?

A

Management

rest
paracetamol for high fever/discomfort
notifiable disease
297
Q

What are 4 complications of mumps?

A

omplications

orchitis - uncommon in pre-pubertal males but occurs in around 25-35% of post-pubertal males. Typically occurs four or five days after the start of parotitis
hearing loss - usually unilateral and transient
meningoencephalitis
pancreatitis
298
Q

What is orf?

A

Orf is generally a condition found in sheep and goats although it can be transmitted to humans. It is caused by the parapox virus.

299
Q

What does orf cause in animals?

A

In animals

'scabby' lesions around the mouth and nose
300
Q

What does orf cause in humans?

A

n humans

generally affects the hands and arms
initially small, raised, red-blue papules
later may increase in size to 2-3 cm and become flat-topped and haemorrhagic
301
Q

How does parvovirus B19 affect pregnant women? what should a pregnant women do if she is exposed? How is this spread? when is a person i=nfectious?

A

Be aware that the virus can affect an unborn baby in the first 20 weeks of pregnancy. If a woman is exposed early in pregnancy (before 20 weeks) she should seek prompt advice from whoever is giving her antenatal care as maternal IgM and IgG will need to be checked. It is spread by the respiratory route and a person is infectious 3 to 5 days before the appearance of the rash. Children are no longer infectious once the rash appears and there is no specific treatment.

302
Q

What are 4 clinical features of rabies?

A

Features

prodrome: headache, fever, agitation
hydrophobia: water-provoking muscle spasms
hypersalivation
Negri bodies: cytoplasmic inclusion bodies found in infected neurons
303
Q

What is the management of an animal bite in at-risk countries for rabies?

A

There is now considered to be ‘no risk’ of developing rabies following an animal bite in the UK and the majority of developed countries. Following an animal bite in at-risk countries:

the wound should be washed
if an individual is already immunised then 2 further doses of vaccine should be given
if not previously immunised then human rabies immunoglobulin (HRIG) should be given along with a full course of vaccination. If possible, the dose should be administered locally around the wound
304
Q

Rubella
-what is this caused by?
-what can happen if contracted during pregnancy?

A

Rubella, also known as German measles, is a viral infection caused by the togavirus. Following the introduction of the MMR vaccine, it is now very rare (typically less than 5 cases in the UK per year). If contracted during pregnancy there is a risk of congenital rubella syndrome

305
Q

When are rubella outbreaks most common?
-What is the incubation period?
-when are individuals infectious in rubella?

A

Basics

outbreaks more common around winter and spring
the incubation period is 14-21 days
individuals are infectious from 7 days before symptoms appear to 4 days after the onset of the rash
306
Q

What are 3 clinical features of rubella?

A

Features

prodrome, e.g. low-grade fever
rash: maculopapular, initially on the face before spreading to the whole body, usually fades by the 3-5 day
lymphadenopathy: suboccipital and postauricular
307
Q

What are 4 complications of rubella?

A

Complications

arthritis
thrombocytopaenia
encephalitis
myocarditis
308
Q

What 4 infections are individuals more susceptable to following splenecotmy?

A

Following a splenectomy patients are particularly at risk from pneumococcus, Haemophilus, meningococcus and Capnocytophaga canimorsus* infections

309
Q

What vaccinations are given to individuals with splenectomy?

A

Vaccination

if elective, should be done 2 weeks prior to operation
Hib, meningitis A & C
annual influenza vaccination
pneumococcal vaccine every 5 years
310
Q

What antibiotics prophylaxis is given to those with splenectomy?

A

Antibiotic prophylaxis

penicillin V: unfortunately clear guidelines do not exist of how long antibiotic prophylaxis should be continued. It is generally accepted though that penicillin should be continued for at least 2 years and at least until the patient is 16 years of age, although the majority of patients are usually put on antibiotic prophylaxis for life
311
Q

Describe changes on blood film following splenectomy

A

Post-splenectomy changes

Platelets will rise first (therefore in ITP, transufsion should be given after splenic artery clamped)
Blood film will change over following weeks, Howell-Jolly bodies will appear
Other blood film changes include target cells and Pappenheimer bodies
Increased risk of post-splenectomy sepsis, therefore prophylactic antibiotics and pneumococcal vaccine should be given.
312
Q

sulfonamides
-How do these work?
-Give 2 examples
-are there non-antibiotic sulfonamides?

A

Sulfonamides are a class of drug that work by inhibiting dihydropteroate synthetase.

Antibiotic sulfonamides:

sulfamethoxazole

+ co-trimoxazole is a combination of sulfamethoxazole + trimethoprim that is used in the management of Pneumocystis jiroveci pneumonia

sulfadiazine
sulfisoxazole

There are also examples of non-antibiotic sulfonamides:

sulfasalazine
sulfonylureas
313
Q

Give 3 adverse effects of co-trimoxazole

A

Adverse effects of co-trimoxazole include:

hyperkalaemia
headache
rash (including Steven-Johnson Syndrome)
314
Q

What is the mechanism of action of tetracycline antibiotics? what is the mechanism of resistance?

A

Examples

doxycycline
tetracycline

Mechanism of action

protein synthesis inhibitors
binds to 30S subunit blocking binding of aminoacyl-tRNA 

Mechanism of resistance

increased efflux of the bacteria by plasmid-encoded transport pumps, ribosomal protection
315
Q

Give 4 adverse effects of tetracyclines

A

Notable adverse effects

discolouration of teeth: therefore should not be used in children < 12 years of age
photosensitivity
angioedema
black hairy tongue
316
Q

What is the mechanism of action of trimethoprim?

A

Mechanism of action

interferes with DNA synthesis by inhibiting dihydrofolate reductase
    may, therefore, interact with methotrexate, which also inhibits dihydrofolate reductase
317
Q

Give 2 adverse effects of trimethoprim?

A

Adverse effects

myelosuppression
transient rise in creatinine: trimethoprim competitively inhibits the tubular secretion of creatinine resulting in a temporary increase which reverses upon stopping the drug
    trimethoprim blocks the ENaC channel in the distal nephron, causing a hyperkalaemic distal RTA (type 4). It also inhibits creatinine secretion, often leading to an increase in creatinine by around 40 points (but not necessarily causing AKI)
318
Q

How does metronidazole work and what are 2 adverse effects?

A

Metronidazole is a type of antibiotic that works by forming reactive cytotoxic metabolites inside the bacteria.

Adverse effects

disulfiram-like reaction with alcohol
increases the anticoagulant effect of warfarin
319
Q

How do you define a ‘clean wound’

A

Wounds less than 6 hours old, non-penetrating with negligible tissue damage

320
Q

How do you define a tetanus prone wound?

A

puncture-type injuries acquired in a contaminated environment e.g. gardening injuries
wounds containing foreign bodies
compound fractures
wounds or burns with systemic sepsis
certain animal bites and scratches

321
Q

How do you define a high-risk tetanus prone wound?

A

heavy contamination with material likely to contain tetanus spores e.g. soil, manure
wounds or burns that show extensive devitalised tissue
wounds or burns that require surgical intervention

322
Q

How do you treat a patient with any wound if they have had a full course of tetanus vaccine with the last dose <10yrs ago?

A

Patient has had a full course of tetanus vaccines, with the last dose < 10 years ago

no vaccine nor tetanus immunoglobulin is required, regardless of the wound severity
323
Q

How do you treat a wound if a patient has had a full course of tetanus vaccines with the last dose >10 yrs ago?

A

Patient has had a full course of tetanus vaccines, with the last dose > 10 years ago

if tetanus prone wound: reinforcing dose of vaccine
high-risk wounds (e.g. compound fractures, delayed surgical intervention, significant degree of devitalised tissue): reinforcing dose of vaccine + tetanus immunoglobulin
324
Q

How do you treat a wound if a patient’s vaccination history is unknown?

A

If vaccination history is incomplete or unknown

reinforcing dose of vaccine, regardless of the wound severity
for tetanus prone and high-risk wounds: reinforcing dose of vaccine + tetanus immunoglobulin
325
Q

what 7 vaccines are live attenuated 7

A

BCG
measles, mumps, rubella (MMR)
influenza (intranasal)
oral rotavirus
oral polio
yellow fever
oral typhoid

326
Q

what 3 vaccines are inactivated?

A

rabies
hepatitis A
influenza (intramuscular)

327
Q

What 3 vaccines are toxoid vaccines?

A

tetanus
diphtheria
pertussis

328
Q

what are 5 subunit and conjugate vaccines?

A

pneumococcus (conjugate)
haemophilus (conjugate)
meningococcus (conjugate)
hepatitis B
human papillomavirus

329
Q
A