Revise Notes Infectious DIsease Flashcards

1
Q

Management

Perform I&D if pus collection/abscess has developed
Minor infection - topical antibiotics - fusidic acid

Oral antibiotics for more severe disease/abscess/pus collection
1st line: PO flucloxacillin or clarithromycin

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Acute Paronychia
Background

Localised, superficial infection of the lateral/proximal skin folds around a nail.
Infection results in painful swelling, or abscess formation.
Aetiology: Staphylococcus aureus most common

Clinical features

Symptoms - painful swelling at base of (usually one) fingernail +/- history of trauma/injury

Examination findings
Red/painful/swollen nail folds
Visible pus

Abscess formation - fluctuance
Digital pressure test causes demarcation of pus

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2
Q

DRE findings

The prostate is tender on examination, and may feel swollen, warm and boggy
DRE must be performed gently and prostate massage should be avoided as it can cause abscess/sepsis.

Investigations

Urine MSU - dipstick, send for MCS

Management

Admit if severely unwell/septic/abscess etc.
Consider urgent referral if immunocompromised/diabetic/urological condition

Antibiotics
1st line: Ciprofloxacin 500mg BD OR ofloxacin 200mg BD
Initial course is 14 days
Use trimethoprim 200mg BD if cipro/oflox are unsuitable

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Acute Prostatitis
Pathophysiology

Acute infection of urinary tract and prostate
Aetiology: E.Coli most common, pseudomonas, klebsiella, enterococcus. Rarely STI (NG/CT)

Clinical features

Urinary symptoms - frequency, urgency, dysuria, fever
Perineal pain

Bladder outflow obstruction due to swelling - urinary retention, voiding symptoms (poor stream, hesitancy, intermittency, straining etc.)

Pain on ejaculation
Lower back pain
Systemic upset, fever, rigours

DRE findings

The prostate is tender on examination, and may feel swollen, warm and boggy
DRE must be performed gently and prostate massage should be avoided as it can cause abscess/sepsis.

DRE findings

The prostate is tender on examination, and may feel swollen, warm and boggy
DRE must be performed gently and prostate massage should be avoided as it can cause abscess/sepsis.

Investigations

Urine MSU - dipstick, send for MCS

Management

Admit if severely unwell/septic/abscess etc.
Consider urgent referral if immunocompromised/diabetic/urological condition
Antibiotics
1st line: Ciprofloxacin 500mg BD OR ofloxacin 200mg BD
Initial course is 14 days
Use trimethoprim 200mg BD if cipro/oflox are unsuitable

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3
Q

Antibacterial Therapy
Though the usual advice is to follow local antimicrobial policy, some questions in the MSRA have historically asked for the most appropriate choice of antibiotic for common infections. The following guidance is recommended by the BNF treatment summaries.

PA = Penicillin allergic

Endocarditis - Blind therapy

Native Valve

Amoxicillin + gentamicin
PA/MSRA: Vancomycin + gentamicin
Prosthetic valve

Vancomycin + Rifampicin + gentamicin

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Meningitis - Empirical therapy

Suspected meningococcal disease, pre-hospital

Benzylpenicillin (PA: cefotaxime)
Age 3 months - 59 years

Cefotaxime (or ceftriaxone)
Age 60+

Cefotaxime + Amoxicillin

Neutropenic sepsis

Anti-pseudomonal cover is important in neutropenic sepsis.

1st line choice may be monotherapy with piperacillin/tazobactam (but see local protocols - gentamicin may be added, alts: include meropenem).

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4
Q

Purulent conjunctivitis

1st line: Chloramphenicol eye drops

Infections of the gastro-intestinal tract

It is worth noting that several of the below GI infections are considered self-limiting, and are often treated conservatively without ABx.

Campylobacter enteritis

If severe/immunocompromised: Clarithromycin
Salmonella

Non-typhoid (Treat if invasive/severe disease): Ciprofloxacin or cefotaxime
Typhoid fever: Cefotaxime (or ceftriaxone)

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Shigellosis

Not usually indicated in mild cases.
If severe: Ciprofloxacin or azithromycin
Clostridioides difficile

First episode of mild, moderate or severe c.diff:

1st line: PO Vancomycin 125mg QDS (10 days)
2nd line: PO Fidaxomicin 200mg BD (10 days)

If considered life-threatening, specialist may offer: PO Vancomycin + IV metronidazole

Further episodes of c.diff:

Within 12 weeks of symptom resolution (relapse): PO Fidaxomicin

More than 12 weeks of symptom resolution (recurrence): PO Fidaxomicin OR Vancomycin

Diverticulitis

If systemically unwell, immunosuppressed, comorbid: Co-amoxiclav (PA: Metronidazole + cefalexin/trimethoprim)

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5
Q

Biliary tract infection

1st line: Ciprofloxacin OR gentamicin OR cephalosporin

Acute sinusitis

If systemically unwell, high risk of complications or prolonged symptoms
1st line: Phenoxymethylpenicillin (co-amoxiclav if very unwell, risk of complications)
PA: Doxycycline OR clarithromycin

Osteomyelitis

1st line: Flucloxacillin
PA: Clindamycin
MSRA: Vancomycin

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Septic arthritis

1st line: Flucloxacillin
PA: Clindamycin
MSRA: Vancomycin
Gonococcal arthritis/Gm -Ve: Cefotaxime

Oropharyngeal infections

Periodontal abscess

Phenoxymethylpenicillin

Gingivitis
Metronidazole

Bacterial sore throat:

1st line: Phenoxymethylpenicillin
PA: Clarithromycin

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6
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A
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7
Q

Community-acquired pneumonia

Low severity:

1st line: PO amoxicillin
PA: clarithromycin, doxycycline
Moderate severity:

1st line: PO amoxicillin
If atypical pathogen suspected, amoxicillin with clarithromycin
PA: clarithromycin, doxycycline

A

High severity:

1st line: PO or IV co-amoxiclav with clarithromycin

Hospital-acquired pneumonia

PO 1st line: co-amoxiclav

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8
Q

Bites (human, cat, dog)

1st line: Co-amoxiclav
PA: Doxycycline AND metronidazole
Cutaneous anthrax

Path: Anthrax spores get through break in skin, following contact with infected animal/animal products

Clinical features:
A raised bump on the skin, which blister and then becomes a painless ulcer with a black eschar in the centre

1st line: Ciprofloxacin or doxycycline

A

Skin infections

Cellulitis & Erysipelas

1st line: Flucloxacillin
PA: Clarithroymcin or doxycycline
If near the eyes or nose - 1st line: co-amoxiclav

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9
Q

Urinary tract infections

LUTI - Men and non-p€regnant women

1st line: Nitrofurantoin or trimethoprim
Treatment duration:
Men - 7 days
Women - 3 days
LUTI - Pregnancy

1st line: Nitrofurantoin
2nd line: Amoxicillin, cefalexin
Prostatitis

1st line: Ciprofloxacin or ofloxacin

A

Acute pyelonephritis

Oral 1st line: Cefalexin OR ciprofloxacin
If pregnant - Cefalexin

Nb. With all of the above guidance, it is important to remember that antibiotics such as tetracyclines and clarithromycin are CI in pregnancy,

so an alternative should be used (e.g. erythromycin).

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10
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11
Q

Cellulitis
Key learning

Commonly affects lower limbs
Most common organisms- Strep. pyogenes, Staph. Aureus

Risk factors- trauma, diabetes, vascular disease
Exam findings- pain, erythema, swelling and warmth around affected site
Management- NICE recommends ERON classification to decide on oral versus intravenous antibiotics

Pathophysiology

Infection dermis and subcutaneous tissue
Most common organisms- Strep. pyogenes, Staph. Aureus
Risk factors

Trauma to affected area
Ulcers
Obesity
Diabetes
Peripheral vascular disease
Immunocompromised
Peripheral neuropathy
Alcohol
Chronic liver disease
Chronic renal disease

A

Clinical Features

Most commonly affects lower limbs
Infected area characterised by pain, erythema, warmth and swelling
Associated fever
Blisters/bullae can form
Investigations

Clinical diagnosis
Bloods
WCC and CRP raised

If septic may have associated renal failure
Swab and send MCS if open wound, ulceration or discharge
XR
May show soft tissue swelling

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12
Q

Cellulitis

A

Management

Eron classification

Class 1- systemically well (no confusion, tachycardia, hypotension) or uncontrolled comorbidities (vascular disease, obesity, diabetes)

Oral antibiotics
Class 2- systemically unwell or has above co-morbidity

Intravenous for 48hrs and consider OPAT (outpatient parenteral antibiotic therapy)
Class 3- systemically unwell or has above co-morbidities which are unstable and therefore reduce response to treatment

Urgent hospital admission for IV antibiotics
Class 4- sepsis or life-threatening (i.e. necrotising fasciitis)

Urgent hospital admission for IV antibiotics
Also consider urgent hospital admission for IV antibiotics if very young or frail, facial, orbital and periorbital cellulitis

Complications

Sepsis
Necrotising fasciitis
Can recur or result in ulceration

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13
Q

Pathophysiology

HIV is an RNA retrovirus, of the lentivirus genus

HIV infects, replicates within and then destroys immune cells including CD4 T cells, macrophages and dendritic cells. The consequence is progressive immunodeficiency.

A

Disease course

  1. Seroconversion phase (primary infection)

The first 2-10 weeks following infection where the body mounts an immune response
Clinical features:
80% develop flu-like symptoms - lethargy, myalgia, sore throat, mouth or genital ulcers, lymphadenopathy, maculopapular rash.
Viral load is very high - high risk of transmission to contacts

  1. Asymptomatic phase

Variable duration - some progress to AIDS within 1 year. In others, the disease progresses more slowly before advanced HIV/AIDS, 10+ years.

  1. Acquired immunodeficiency syndrome

CD4 count < 200 cells/μL
At risk of opportunistic infections/AIDS-defining illnesses

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14
Q

Post-exposure prophylaxis (PEP) hiv

Initiated PEP as soon as possible after exposure, preferably within 24 hours, but can be considered up to 72 hours.
PEP should be continued for 28 days.

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Opportunistic infections

Oral candidiasis

Clinical features

Patches of white/yellow plaque on the tongue, cheeks or palate
Dysphagia
Can be removed from tongue with oral care (unlike hairy leukoplakia)
Oesophageal candidiasis can occur with more advanced immunosuppression

Hairy Leukoplakia

Aetiology

EBV
Clinical features

White plaques on the tongue, with a folded/corrugated appearance
Often affect the lateral borders of the tongue
Hairy - patches of hair from within the folds
Cannot be removed with oral care/toothbrush

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15
Q

Kaposi’s sarcoma

Aetiology

HHV-8
Clinical features

Purple/red papules, macules or plaques appearing on the skin

Lesions can ulcerate and become painful

Can occur within the GIT, respiratory tract and cause bleeding - haematemesis/haematochezia/melaena/ haemoptysis etc.

A

Pneumocystis jirovecii pneumonia (PJP/PCP)

Clinical features

Fever, Dry cough, SOB
Commonly complicated by pneumothorax
CXR: Bilateral infiltrates
Diagnosis

Bronchoalveolar lavage with silver stain
Management:

1st Line: co-trimoxazole (with steroids if hypoxic)

Prophylaxis: CD4 count < 200 - offer prophylactic co-trimoxazole

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16
Q

Cryptosporidium

A

Cryptosporidiosis

Clinical features

Chronic diarrhoea in patient with advanced HIV (CD4 < 200)
Investigations

Stool sample with modified Ziehl-Neelsen stain - Presence of red cysts

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17
Q

Cerebral toxoplasmosis

A

Cerebral toxoplasmosis

Aetiology

Toxoplasma gondi
Clinical features

Headache, fever, confusion
Investigations

CT Head: Multifocal ring enhancing lesions, thallium spect negative
Management

Pyrimethamine + Sulfadiazine

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18
Q

Cans lymphoma

A

CNS lymphoma

Clinical features

Headache, fever, confusion
Investigations

CT Head: Solitary homogeneously enhancing lesions, thallium spect positive

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19
Q

Cryptococcal meningitis

Aetiology

Cryptococcus neoformans (fungus)
Diagnosis

LP with CSF India ink stain positive
Management

Induction regimen with amphotericin B deoxycholate and flucytosine, followed by 1 week of fluconazole

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Progressive multifocal leukoencephalopathy

Aetiology

JC virus causes widespread demyelination within the CNS
Clinical Features

Behavioural, motor and speech disturbance
Investigations

MRI confirms the presence of demyelinating lesions

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20
Q

Diagnosis

A

Antibody tests

ELISA screening to identify antibodies
But can take up to 5-6 weeks to develop antibodies - so early tests can produce false negative result

Antigen test

Tests for p24 antigen
Positive earlier than antibody test (3 weeks)

HIV NATs

Informs us if patient has HIV and can also detect viral load

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21
Q

Management

Offer immediate treatment, irrespective of CD4 count

Triple therapy

Two nucleoside reverse transcriptase inhibitors (NRTIs) plus one of the following as third drug:

Integrase inhibitor (INI)
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Protease inhibitor (PI)

A

NRTIs

Combinations include:
Emtricitabine plus tenofovir
Abacavir plus lamivudine
Side effects: Peripheral neuropathy

NNRTIs (xxviraxx)

Examples: Nevirapine , Efavirenz
PIs (xxnavir)

Examples: Idinavir, nelfinavir
SEs: Metabolic syndrome

INIs (xxtegrxx)

Examples: Raltegravir, dolutegravir

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22
Q

Influenza
Key learning

Acute respiratory illness most commonly influenza A
Occurs during winter months in UK
Symptoms present 2 days after exposure- most commonly runny nose, myalgia, cough, fever

Antiviral drugs (oseltamivir or zanamivir) are not usually recommended unless ALL of the following are met:

Patient at risk of developing complications
Influenza virus is in national circulation
Patient can commence treatment within 48 hours of symptom onset

A

Management

Prevention:

Annual flu vaccine
If influenza confirmed:

Most will self-resolve after around 1 week

Offer anti-viral (oral oseltamivir or nasal zanamivir) if ALL of the following:

Confirmed influenza is circulating by Department of Health and Social Care

Part of ‘at risk’ group:
1.All over 65
2.All under 6 months
3.Essentially any chronic condition of spleen/lungs/heart/kidneys/liver/neurological system or any condition or medication that causes immunosuppression

Treatment can start within 48hrs of symptoms

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23
Q

Influenza
Key learning

Acute respiratory illness most commonly influenza A
Occurs during winter months in Uk

Symptoms present 2 days after exposure- most commonly runny nose, myalgia, cough, fever
Antiviral drugs (oseltamivir or zanamivir) are not usually recommended unless ALL of the following are met:

Patient at risk of developing complications
Influenza virus is in national circulation
Patient can commence treatment within 48 hours of symptom onset

A

Pathophysiology

RNA viruses- Three types

Influenza A
most common and more virulent
can cause epidemics or pandemics as well as more local outbreaks

Influenza B- often co-circulates with Influenza A

Usually less severe except in children (similar severity to Influenza A)

Influenza C- mild similar to common cold

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24
Q

Lyme disease

A

Lyme Disease
Lyme disease can occur following infection by a group of spirochete bacteria, collectively termed Borrelia burgdorferis

Transmitted to humans by Ixodes ticks - so questions may note recent history of hiking/walking etc.

Clinical features & Disease course

The disease course is divided into 3 stages

Stage 1: Early localised lyme

Symptoms: Erythema migrans rash, non-specific flu-like illness
Expanding, target-like rash

Figure 261: Erythema Migrans. Note the bullseye/target-like appearance.
Stage 2: Early disseminated lyme

Symptoms:
Multiple, small secondary erythema migrans lesions
Arthritis
Neurological features - meningitis, CN palsy
Stage 3: Late disseminated lyme

Symptoms:
Lyme arthritis
Neurological complications - peripheral neuropathy, encephalomyelitis

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Lyme Disease Lyme disease can occur following infection by a group of spirochete bacteria, collectively termed Borrelia burgdorferis Transmitted to humans by Ixodes ticks - so questions may note recent history of hiking/walking etc.
Clinical features & Disease course The disease course is divided into 3 stages Stage 1: Early localised lyme Symptoms: Erythema migrans rash, non-specific flu-like illness Expanding, target-like rash Stage 2: Early disseminated lyme Symptoms: Multiple, small secondary erythema migrans lesions Arthritis Neurological features - meningitis, CN palsy Stage 3: Late disseminated lyme Symptoms: Lyme arthritis Neurological complications - peripheral neuropathy, encephalomyelitis
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Management Patients with erythema migrans rash, but no focal symptoms (neuro/arthritis etc) Start oral antibiotics (doxycycline) If no erythema migrans (but clinically suspected), consider starting ABx, and.. Perform ELISA test for lyme If ELISA test is positive or equivocal - perform immunoblot test for Lyme If investigations are positive for lyme disease - Start oral antibiotics Antibiotics in Primary Care 1st line: Doxycycline 100mg BD for 21 days 2nd line: Amoxicillin 1g TDS for 21 days Use amox 1st line in children < 9 years If there are focal neurological, cardiac, dermatological features, or lyme arthritis, antibiotic regimens will be guided by specialist.
Complications of treatment Treatment can trigger a Jarisch-Herxheimer reaction in the first 24 hours of antibiotics (can also occur with treatment of syphilis) due to cytokine release when large numbers of bacteria are killed. Symptoms: malaise, fever & rigours, myalgia, headache, tachycardia. Self-limiting.
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Malaria
Malaria Pathophysiology Aetiology Infection of RBCs by plasmodium parasites Plasmodium falciparum - accounts for 75% of cases and the majority of deaths Non-falciparum causes: P. vivax, P. ovale Transmission: Mosquito borne - Anopheles mosquitoes Infection course Sporozoites enter bloodstream following bite and travel into liver In the liver, sporozoites mature into schizonts which rupture, releasing merozoites Merozoites infect the RBCs, where they mature and divide further Merozoites then cause the RBC to rupture which releases more merozoites to infect other RBCs.
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Clinical features Symptoms Unwell/fever and history of recent travel (most within 2-3/12 of exposure ) High risk area include: African continent, Asia, South America High fever (often > 39), which can be cyclical (p.vivax/ovale/malariae), rigour, sweats Headache, myalgia, lethargy Confusion Jaundice
Malaria
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Investigations Rapid diagnostic test Target two malaria antigens - histidine-rich protein 2 (HRP2), and plasmodium LDH (pLDH) But less sensitive than microscopy Gold standard: Blood film - Thick and thin films Most sensitive, determine the parasite stage and percentage parasitaemia (for falciparum)
Assessment of Severity (Falciparum Malaria) Malaria can be categorised as uncomplicated and complicated/severe Uncomplicated Parasitaemia < 2% with NO end organ dysfunction
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Complicated malaria
Parasitaemia > 2% Parasitaemia < 2% but any of the following: Schizonts on the blood film Cerebral malaria - seizures/low GCS Acidosis (pH < 7.3 or Lac > 4.0) Hypoglycaemia Pulmonary oedema or ARDS Severe anaemia DIC/bleeding Shock Blackwater fever - haemolytic anaemia with resultant haemoglobinuria (dark red urine) Acute renal failure Jaundice Hb < 80
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Mng malaria types
Uncomplicated falciparum malaria 1st line: Oral Artemisinin-based combination treatment Artemether-lumefantrine (Riamet) is drug of choice 2nd line: Quinine plus doxycycline/clindamycin If vomiting - treat as severe Severe/Complicated falciparum malaria Manage in HDU/ITU 1st line: Intravenous artesunate 2nd line: IV quinine (monitor closely for hypoglycemia)
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Non-falciparum malaria Aetiology Plasmodium vivax most common, P. Ovale, P. Malariae Clinical features Fever, headache, splenomegaly 48 hourly cyclical fever = Vivax/Ovale
Acute treatment: 1st line: Artemether-lumefantrine 2nd line: Chloroquine Prevention of Relapse (PV/PO): Primaquine 14 days Treatment of both the active infection and the liver hypnozoite stage is required for PV/PO, or relapse may occur. P. Malariae has no hypnozoite stage - can treat with chloroquine monotherapy Check G6PD levels - Primaquine can induced haemolytic crisis in G6PD deficiency
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Measles Key learning Highly contagious Prodrome of fevers, cough, conjunctivitis Characteristic rash and Koplik’s spots Majority self-limiting but higher mortality in at risk groups Notifiable disease Pathophysiology Highly contagious from prodromal symptoms to four days after onset of rash Spread by direct contact with drops - breathing/coughing/sneezing Caused by morbillivirus of paramyxovirus family Incubation period around 10 days
Epidemiology More likely if not fully immunised or no history of measles infection Most at risk- young adults MMR vaccine has reduced prevalence to 800 cases a year in UK Globally 140000 deaths a year Mortality 2%- higher in immunosupressed Clinical Features Prodromal symptoms - malaise, high fever (39+), cough, conjunctivitis Koplik’s spots are pathognomonic- 2mm red spots with white/blue centres on buccal mucosa Rash Erythematous and maculopapular Begins on face and behind ears then descends down body over 3-4 days Lasts around one week
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Investigations measles Clinical diagnosis so often investigations are not required Options include: Oral fluid testing kit- IgM/IgG Viral RNA Differentials Parvovirus B19- causes fifth disease (erythema infectiosum- slapped cheek syndrome) Scarlet fever Rubella Prevention Vaccination- two doses of MMR
Management Supportive- majority self-limiting Notifiable disease Post-exposure prophylaxis of vulnerable contacts Stay at home until at least 4 days after development of rash Complications Increased susceptibility to opportunistic infections Otitis media Pneumonia Encephalitis Subacute sclerosing panencephalitis Rare degenerative disease of CNS Seizures Decline in motor, cognitive and behavioural function Measles keratoconjunctivitis Can result in blindness
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Meningitis
Pathophysiology Meningitis - inflammation of the inner layers of the meninges (pia/arachnoid mater) Aetiology Viral - enteroviruses most common (coxsackie/echovirus groups), mumps, HSV, EBV, VZV, measles etc. Bacterial Streptococcus pneumoniae (pneumococcal meningitis) Most common cause in adults Neisseria meningitidis - can present with meningitis, meningococcal septicaemia, or both MenB is the commonest causative subgroup Haemophilus influenzae b Listeria - an important cause in neonates and elderly/immunocompromised patients
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Meningitis
Clinical features Symptoms Headache Photophobia/phonophobia Neck ache/stiffness Fever Seizure General malaise, myalgia, lethargy etc. Examination findings Meningism Kernig’s sign - Flex the hip and knee to 90 degrees while pt is led flat - then slowly extend their knee - if pain with extension beyond 135 degs - positive Brudzinski’s sign - flex pts neck, bringing chin to chest whilst led flat. If this causes involuntary flexion of hip and knees (relieves the stretch on meninges) - positive Non-blanching petechial or purpuric rash - suspicious of meningococcal septicaemia Signs of sepsis/shock, neurological deficit
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Pre-hospital management If meningococcal disease is suspected (non-blanching rash etc.) - give parenteral ABx whilst awaiting urgent transfer to hospital IM/IV Benzylpenicillin Only administer ABx to children with suspected meningitis, if urgent hospital transfer is not possible. Investigations Bloods Including whole blood PCR testing for Neisseria meningitidis Lumbar puncture Unless contraindicated, send CSF for WCC/total protein/glucose/ gm stain & MCS
Contraindications for LP Raised intracranial pressure Reduced/fluctuating consciousness Cushing’s response - bradycardia, HTN Papilloedema Focal neurology, abnormal posturing, unresponsive pupils Septic shock CR > 2s, mottled/abnormal complexion, poorly perfused extremities Hypotensive and tachycardic Reduced urine output Meningogococcal septicaemia - Spreading purpura Coagulopathy (e.g. DIC/thrombocytopenia/anticoagulants)
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Lyme mng
Management Patients with erythema migrans rash, but no focal symptoms (neuro/arthritis etc) Start oral antibiotics (doxycycline) If no erythema migrans (but clinically suspected), consider starting ABx, and.. Perform ELISA test for lyme If ELISA test is positive or equivocal - perform immunoblot test for Lyme If investigations are positive for lyme disease - Start oral antibiotics Antibiotics in Primary Care 1st line: Doxycycline 100mg BD for 21 days 2nd line: Amoxicillin 1g TDS for 21 days Use amox 1st line in children < 9 years If there are focal neurological, cardiac, dermatological features, or lyme arthritis, antibiotic regimens will be guided by specialist.
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Lyme diseases RX complication
Complications of treatment Treatment can trigger a Jarisch-Herxheimer reaction in the first 24 hours of antibiotics (can also occur with treatment of syphilis) due to cytokine release when large numbers of bacteria are killed. Symptoms: malaise, fever & rigours, myalgia, headache, tachycardia. Self-limiting
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Management in secondary care Antibiotics Bacterial meningitis Age > 3 months - IV ceftriaxone Age < 3 months OR > 60 years - IV cefotaxime AND amoxicillin or ampicillin The amox/ampicillin is to cover listeria monocytogenes AND - if travel outside UK in last 3 months - add vancomycin to above Meningogococcal septiciaemia IV ceftriaxone
Lumbar Puncture - Interpretation of CSF Bacteria Viral Tuberculosis Fungal Appearance Cloudy Clear Opaque, fibrin web Cloudy WCC > 100 cells/μL Primarily PMNs 10-1000 cells/μL Primarily lymphocytes 50-500 cells/μL Primarily lymphocytes 10-500 cells/μL Protein Elevated (>50mg/dL) Elevated (>50mg/dL) Elevated ++ Elevated Glucose Low (< 40% serum glucose) Normal (>60% serum glucose) Nb. can be low in HSV or mumps Low (< 40% serum glucose) Low Additional Gram stain & MCS PCR for HSV, VZV etc mZN stain for AFB, TB culture, PCR India ink (cryptococcal) Pattern recognition Polymorphonuclear neutrophils + low glucose = Bacterial meningitis Lymphocytes + normal glucose (mumps/HSV can be low) = Viral meningitis Lymphocytes + low glucose + very high protein = TB
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Mumps Aetiology Mumps is caused by a paramyxovirus, with respiratory droplet spread Infection is usually self-limiting after approx. 2 weeks but it can be associated with complications as below. Clinical features Incomplete vaccination history Parotitis - swollen parotid glands - the key feature Starts as unilateral parotitis, before becoming bilateral Serum amylase is elevated Pain on eating, earache Swollen cheeks. Flu-like symptoms - fever, lethargy, myalgia Epididymo-orchitis Red, warm, painful testicular swelling Usually unilateral, but can be bilateral Other complications - pancreatitis, transient hearing loss, aseptic viral meningitis
Management Notifiable disease - HPU Contacts - offer MMR to any non-immunised contacts asap Conservative/symptomatic management To seek medical advice if complications develop (as above) Nb. mumps epididymo-orchitis is conservatively managed without abx/steroids. Patients should isolate and be advised to stay off school or work for 5-7 days after the development of symptoms. Patients are infectious from three days before the onset of symptoms to seven days afterwards.
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Necrotising Fasciitis Key learning Rare but life-threatening soft tissue infection characterized by rapid spread of bacteria through fascial planes, causing tissue necrosis and systemic toxicity. Risk factors- immunocompromised especially, diabetes Clinical features- severe pain out of proportion to physical findings Associated, erythema, oedema, and skin bullae. Predominantly clinical diagnosis Immediate surgical debridement and broad-spectrum antibiotics to prevent complications such as sepsis and limb loss.
Pathophysiology Rapidly spreading severe soft tissue infection characterized by rapid spreading of bacteria through to the deep fascia Often involves mixed aerobic and anaerobic bacteria. Epidemiology Rare but can occur at any age Risk factors: Immunocompromised especially diabetics Causes Type 1- Mix of aerobes and anaerobes. Often post-operatively in diabetics- increased if on SGLT2 inhibitor Type 2- Group A beta-haemolytic strep (strep pyogenes)
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Notifiable Diseases The following diseases must be reported under the Health Protection Regulations 2010:
Acute encephalitis Acute infectious hepatitis Acute meningitis Acute poliomyelitis Anthrax Botulism Brucellosis Cholera COVID-19 Diphtheria Enteric fever (typhoid or paratyphoid fever) Food poisoning Haemolytic uraemic syndrome (HUS) Infectious bloody diarrhoea Invasive group A streptococcal disease Legionnaires’ disease Leprosy Malaria Measles Meningococcal septicaemia Monkeypox Mumps Plague Rabies Rubella Severe Acute Respiratory Syndrome (SARS) Scarlet fever Smallpox Tetanus Tuberculosis Typhus Viral haemorrhagic fever (VHF) Whooping cough Yellow fever
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Meningitis
Steroids Give dexamethasone for bacterial meningitis if > 3/12 - reduces neurological sequelae Do not use if: < 3/12 Septic shock or meningogococcal septicaemia Immunocompromised Contacts No treatment required for contacts of pneumococcal meningitis Meningococcal meningitis or septicaemia Prophylactic antibiotics are indicated in those who have had prolonged close contact in household setting during 7 days preceding onset of symptoms 1st lie: PO ciprofloxacin - 500mg single dose PO for > 12 yrs age Alternative: Rifampicin
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MRSA Background Strains of staphylococcus aureus that are resistant to beta-lactam penicillins (including meticillin, flucloxacillin etc). MRSA can colonise patients - in particular the skin, GIT, nasal passages
Decolonisation Management consists.. Skin decolonisation - chlorhexidine gluconate 4% cleansing solution (OD as bodywash and shampoo on D1/D3) - for 5 days total Nasal decolonisation - Mupirocin 2% ointment - TDS - for 5 days total
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Leprosy
Leprosy (Hansen’s disease) Aetiology Mycobacterium leprae Clinical Features Skin changes - pigmentation may become lighter/hypopigmented OR darker/hyperpigmented, dry and flaky There is classically sensory loss of the affected areas of skin due to damage to sensory neurones - can cause injuries (e.g. burns) due to lack of sensation Can progress to paralysis - e.g. of hands/feet Other signs - loss of eyebrows, saddle-nose deformity, corneal ulcers causing blindness
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Clinical Features Severe pain out of proportion to physical findings Associated erythema, oedema, and rapidly progressing tissue necrosis Systemic symptoms occur LATE- fever, tachycardia, and hypotension If affects perineum= Fournier's gangrene Examination findings: Marked tenderness, crepitus, skin bullae, and areas of necrosis. Investigations Bloods Elevated WCC/CRP Imaging XR- necrosis/surgical emphysema CT/MRI- evaluate extent of tissue involvement
Diagnosis Necrotising Fasciitis Clinical suspicion is crucial, do not wait for imaging to consider surgical management Risk stratify in borderline cases- LRINEC score Management Immediate surgical debridement of necrotic tissue Broad-spectrum antibiotics
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Leptospirosis Pathophysiology Bacteria - Leptospira interrogans Transmission - contact with urine of infected animals - rodents in particular Sewage workers, farmers, vets Clinical features Sudden onset of fever, myalgia and headache Calf tenderness Conjunctival suffusion - redness of the conjunctiva Late/immune phase (> 7 days after onset of symptoms) - immune mediated organ damage: Acute renal failure Pulmonary haemorrhage Liver failure Meningitis Weil’s disease - triad of jaundice, renal failure, haemorrhage
Management Mild disease - doxycycline Severe - IV Benzylpenicillin or ceftriaxone
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Other Bacterial Infections Enteric fever (Typhoid fever) Aetiology Salmonella - gram negative bacillus Salmonella typhi Salmonella paratyphi A & B Clinical Features Foreign travel to endemic areas - South Asia, SE Asia, sub-Saharan Africa Abdominal pain and distension Gradually increasing fever which rises to and plateaus at 39-40 degrees Constipation > diarrhoea
Examination findings Bradycardia Rose spots on trunk - blanching maculopapular lesions Hepatosplenomegaly Mild ascites Diagnosis Blood cultures Management 1st Line: cefotaxime/ceftriaxone
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Botulism Aetiology Clostridium Botulinum Pathophysiology Botulinum toxin irreversibly blocks acetylcholine release at the presynaptic nerve terminal of the NMJ causing paralysis Clinical Features
Normal GCS, normal sensation Symmetric, descending flaccid paralysis of motor neurones and autonomic nervous system Begins with cranial nerves - Dysphagia, diplopia, ptosis, dysphasia Management Botulism Antitoxin
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Chikungunya Alphavirus spread through bite of mosquitos Clinical features: High fever Severe joint pain - commonly bilateral, symmetric polyarthralgia - often knees, ankles, wrists, hands
Zika virus Spread through bite of Aedes mosquitos Infection during pregnancy can cause - microcephaly, teratogenesis
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Pediculosis Pubis Background Pediculosis pubis (pubic lice) are spread through sexual contact, and are most commonly found on pubic and perianal hairs. Clinical features Genital itching - often worse at night Visible lice/eggs present on examination
Examination findings Visible lice (crab-like, approx 1-2mm) Eggs (small, white dots) Maculae ceruleae - blue/red papules at site of lice feeding Management 1st line: Topical insecticide - Permethrin 5% or malathion 0.5% Re-examine after 1 week, and consider repeat treatment if live lice seen
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Threadworm (Pinworm) Pathophysiology Cause: Enterobius vermicularis - a parasitic worm that infests the GIT 2-5mm white worms, with a thread-like appearance Faecal-oral transmission by ingestion of threadworm eggs (invisible to naked eye) Clinical features
Perianal itching is the primary complaint Classically worse at night, which disturbs sleeps May visualise small, white threads in stool/on paper etc. Can cause vulval itching in women too Investigations Adhesive tape test - sent for microscopy Management 1st line: Single dose of mebendazole May need 2nd dose after 2 weeks if persistent infection Children < 6 months and pregnant/breastfeeding women - treat with rigorous hygiene measures alone for 6 weeks Hand washing, fingernail trimming, regular changing of bed linen etc.
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Clinical features History of recent travel/migrants from endemic areas Often asymptomatic / mild, non-specific symptoms if low worm burden Symptoms may include: If significant worm burden - abdominal pain, distension, N&V, change in bowel habit, malabsorption. Loeffler’s syndrome - eosinophilic pneumonitis - inflammatory reaction vs the larvae which migrate into the lungs as above. Symptoms: Cough, wheeze, fever, SOB +/- haemoptysis Rash - urticarial rash as reaction to migrating larvae in the skin Investigations Stool for ova, cysts and parasites FBC might show eosinophilia Management 1st line: Single dose of mebendazole Nb. unlicensed if pregnant/breastfeeding or < 2 yrs
Ascaris lumbricoides Pathophysiology Cause: Ascaris lumbricoides - the largest type of roundworm found in humans One of the most common intestinal worm infections in the world Faecal-oral transmission by ingestion of eggs From the GIT, the larvae are carried to the lungs in the bloodstream. In the lungs they mature, they then ascend the bronchial tree into the oropharynx, where they are swallowed back into the GIT.
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Ascaris lumbricoides Pathophysiology Cause: Ascaris lumbricoides - the largest type of roundworm found in humans One of the most common intestinal worm infections in the world Faecal-oral transmission by ingestion of eggs From the GIT, the larvae are carried to the lungs in the bloodstream. In the lungs they mature, they then ascend the bronchial tree into the oropharynx, where they are swallowed back into the GIT.
Clinical features History of recent travel/migrants from endemic areas Often asymptomatic / mild, non-specific symptoms if low worm burden Symptoms may include: If significant worm burden - abdominal pain, distension, N&V, change in bowel habit, malabsorption. Loeffler’s syndrome - eosinophilic pneumonitis - inflammatory reaction vs the larvae which migrate into the lungs as above. Symptoms: Cough, wheeze, fever, SOB +/- haemoptysis Rash - urticarial rash as reaction to migrating larvae in the skin Investigations Stool for ova, cysts and parasites FBC might show eosinophilia Management 1st line: Single dose of mebendazole Nb. unlicensed if pregnant/breastfeeding or < 2 yrs
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Pelvic Inflammatory Disease Pathophysiology Infection of the upper genital tract, which occurs when infection ascends from the endocervix, resulting in endometritis, salpingitis, oophritis etc. Aetiology: Chlamydia and Gonorrhoea account for roughly 1/4 of cases Others: Mycoplasma genitalium RFs: 4-6 weeks post IUD insertion, age < 25, recent TOP Clinical Features Symptoms Lower abdominal pain Deep dyspareunia Vaginal discharge (often purulent) Vaginal bleeding - IMB, PCB
Examination findings Bimanual exam - adnexal tenderness, cervical excitation/motion tenderness SIRS, pyrexia Investigations Clinical assessment Pregnancy test Test for causative organisms - CT/NG/MG (Nb. negative tests do not exclude PID) Bloods - elevated inflammatory markers The absence of endocervical/vaginal pus cells has a negative predictive value of 95% (but poor PPV), so is useful to r/o PID
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PID
Management BASHH recommend a low threshold for empiric treatment due to (i) lack of definitive diagnostic criteria and (ii) risk of long-term sequelae with delayed treatment (ectopic/infertility). Outpatient antibiotic regimens IM ceftriaxone 1g stat + PO doxycycline 100mg BD + PO metronidazole 400mg BD for 14 days PO ofloxacin + metronidazole for 14 days PO moxifloxacin for 14 days Inpatient antibiotic regimens IV ceftriaxone + IV doxycycline (followed by PO metronidazole + doxycycline) IV clindamycin + IV gentamicin (followed by PO clindamycin + metronidazole
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Rubella (German Measles) Key learning Viral infection Incubation period 14-21 days Rash and non-specific viral symptoms No specific management beyond supportive measures Diagnosis confirmed by lab testing only Urgently refer all women less than 20 weeks pregnant with a rubella-like rash to obstetrics for risk assessment for congenital rubella syndrome Pathophysiology Viral infection (togavirus) Spread by direct contact or droplet from respiratory secretions Epidemiology No cases in 2021 in UK Worldwide 100000 cases of congenital rubella syndrome a year
Clinical Features Incubation period 14-21 days Rash 14-17 days post-exposure Starts on face/neck then becoming generalised Pink/light-red, discrete, maculopapular Mild itch Lasts 3-4 days Lymphadenopathy Arthritis/arthalgia Non-specific viral symptoms (fever, malaise) Rare: Thrombocytopenia Encephalitis Serious complications especially in pregnancy: Congenital rubella syndrome Highest risk in first trimester (8-10 weeks gestation 90% risk) No reported cases beyond 20 weeks gestation Eye defects (cataracts), hearing impairment, cardiac (patent ductus arteriosus), microcephaly, developmental delay, autism, intra-uterine growth restriction
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Rubella Investigations Relies on lab confirmation for diagnosis Serology testing if pregnant Oral fluid sample for others Bloods may show thrombocytopenia and deranged LFTs Prevention Infection or immunisation results in life-long immunity in vast majority Prevention- 2 doses of MMR vaccine
Management Remain infectious from 7 days before symptoms to 4-10 days after onset of rash Most infectious when rash erupting Notifiable disease Specific Non-pregnant Supportive measures Most symptoms self-resolve within a week Avoid contact with pregnant women Pregnant Urgent referral to obstetrics- risk assessment and counselling Supportive and contact avoidance as above No specific treatment for congential rubella syndrome
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Schistosomiasis Aetiology Schistosomiasis is a parasitic infection caused by trematode worms of the genus Schistosoma. It is typically acquired through contact with contaminated freshwater where infected snails release larvae (cercariae) that penetrate the skin of humans. The larvae mature into adult worms in the blood vessels around the intestines or bladder, leading to chronic inflammation, tissue damage, and various clinical manifestations depending on the species involved.
Clinical features: Symptoms Pruritic papular rash - termed swimmer's itch following freshwater exposure A history of swimming especially in freshwater/with travel is a big clue. Fever, malaise, and eosinophilia. Acute Phase: Katayama fever - fever, chills, myalgia, lymphadenopathy, hepatosplenomegaly, and diarrhoea. Chronic infection: Symptoms vary based on species S. haematobium - hematuria, dysuria. Can cause bladder squamous cell carcinoma. S. mansoni and S. japonicum - gastrointestinal symptoms, liver cirrhosis. Examination findings Hepatosplenomegaly, signs of CLD - ascites, portal hypertension.
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Schistosomiasis Aetiology Schistosomiasis is a parasitic infection caused by trematode worms of the genus Schistosoma. It is typically acquired through contact with contaminated freshwater where infected snails release larvae (cercariae) that penetrate the skin of humans. The larvae mature into adult worms in the blood vessels around the intestines or bladder, leading to chronic inflammation, tissue damage, and various clinical manifestations depending on the species involved.
Management Praziquantel - 1st line The treatment of schistosomiasisis with an antiparasitic medication called praziquantel. Effective against all species of Schistosoma. Treatment involves a short course, usually administered as a single dose or over one to two days, depending on the severity and species.
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Sepsis Key learning Life-threatening organ dysfunction due to a dysregulated host response to infection Most common causative organisms: E.coli Staph. Aureus Pseudomonas Risk factors: Age extremes Conditions and medications that cause immunosuppression Clinical features Often non-specific, fevers common and any infective symptoms depending on source Associated with deterioration in NEWS score (i.e. tachycardia, high RR, low saturations, hypotension)
Management- Sepsis 6 bundle within one hour of recognition of sepsis Take blood cultures Check lactate Check urine output/fluid balance Give oxygen to ensure saturation > 94% Give IV fluid bolus Give broad spectrum antibiotics
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Pathophysiology Multifactorial response to infecting pathogen worsened by: Host factors- genetics, age, co-morbidities Pathogen- virulence, burden Environment Septic shock= subset which confers great risk of mortality: Persisting hypotension requiring vasopressors to maintain mean arterial pressure (MAP) > 65mmHg AND Lactate > 2 mmmol/L despite adequate volume resuscitation
Epidemiology Underlying cause or contributing factor to 25000 deaths a year in UK Mortality 25% - increases with delayed diagnosis and lack of prompt management Septic shock mortality- 50% Risk factors Age extremes- < 1 year and > 75 years Frailty Drug abuse including alcohol Recent trauma or surgery Breach of skin including burns, ulcers or indwelling lines Pregnant or post-partum < 6 weeks Immunocompromised Due to underlying condition e.g. HIV, diabetes mellitus, sickle cell, spleen disorders Due to drug treatment e.g. systemic anticancer therapy, steroids, other immunosuppressive drugs
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Causes Common sites of infection causing sepsis include: Respiratory Renal/urinary tract Gastrointestinal Skin Most common causative organisms: E.coli Staph. aureus Pseudomonas Other organisms of note: In children: Neisseria meningitides Haemophilus influenzae Fungal, viral and parasitic causes (rare)
Clinical Features Can be non-specific Malaise Agitation Confusion Fever or hypothermia Specific to infection site, for example: Hypoxic and tachypnoea - respiratory source Dysuria, reduced urine output- urinary source Abdominal pain, vomiting, distension- gastrointestinal source Rash and confusion- meningococcal disease
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Investigations and management sepsis Often first sign is a deterioration in the National Early Warning Score (NEWS) Patients can be risk stratified using the NICE 2024 risk stratification tool As part of the UK Sepsis Trust ‘Sepsis Six’ bundle, all patients should have the following within the first hour following recognition of sepsis: Oxygen to maintain saturations >94% unless contraindicated Measure lactate- higher level can be predictive of higher mortality Blood culture- ideally before antibiotic administration IV broad spectrum antibiotics IV fluid bolus (usually 500mls STAT) Check urine output/fluid balance hourly- low threshold for urinary catheter Other investigations: FBC- WCC high or low (consider neutropenic sepsis), low platelets (consider DIC) CRP- raised in infection/inflammation Renal function- deranged in acute kidney injury/dehydration Clotting screen- coagulopathy/DIC Liver function Glucose CXR Urine MCS/dipstick CT head if neurological deficit
Examination findings GCS- new lower GCS Fever- most common finding Tachycardia Tachypnoea Hypotension Raised capillary refill time Reduced oxygen saturations Skin changes- mottled, pale, cyanosis, cold
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Sepsis complication
Complications Organ dysfunction including: Acute kidney injury Acute respiratory distress syndrome Congestive cardiac failure Liver failure Recurrent and secondary infection i.e. hospital acquired Coagulopathy causing VTE or disseminated intravascular coagulation (DIC) Psychological trauma from long hospital stay
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STIs and Vaginal Discharge Bacterial Vaginosis Pathophysiology
Abnormality of vaginal flora - overgrowth of anaerobic organisms and depletion of lactobacilli Vaginal pH is normally acidic - but becomes more alkaline, with pH > 4.5 Not sexually transmitted, but more prevalent amongst sexually active individuals Significance: BV is associated with complications including misscarriage, preterm labour, PROM, postpartum infections. Clinical features Vaginal discharge (VD) - BV is the most common cause of abnormal VD in women of child-bearing age Characteristically, a thin, grey/white discharge which smells “fishy” There is not normally vaginal pruritus/pain
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Bacterial vaginosis
Amsel criteria The presence of three out of the following 4 indicates a diagnosis of BV: Vaginal pH > 4.5 Positive whiff test - release of a ‘fishy’ odour, with addition of 10% KOH Clue cells > 20% total cell population Characteristic discharge - thin, homogenous Management 1st line: Oral metronidazole 400mg BD for 1 week Alt: If poor compliance - 2g metronidazole stat dose (not if pregnant)
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Trichomoniasis Vaginalis Pathophysiology STI - caused by protozoan Trichomonas Vaginalis The most common non-viral STI in the world (more common than chlamydia and gonorrhoea combined) 90% of cases occur in women Complications of TV infection include W - preterm delivery, low birth weight, PID, infertility M - Prostatitis, infertility
Clinical Features Women 50% asymptomatic Vaginal discharge Variable, but classically described as frothy, yellowy-green Vaginal/vulval pruritus Dysuria Speculum examination: Strawberry cervix, inflammation of vulva/vagina Visible, punctate macular haemorrhages on cervix gives strawberry-like appearance Men: Urethritis - urethral discharge, dysuria, frequency Rarely - symptoms of prostatitis Management 1st line: Oral metronidazole 400mg BD for 1 week Alt: If poor compliance - 2g metronidazole stat dose (not if pregnant) Treat any partners within the last week too.
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Vulvovaginal candidiasis Pathophysiology Overgrowth of candida yeasts, which are part of the normal vaginal flora, causes inflammation of the vagina/vulva. Candida albicans most common. RFs: Recent antibiotic use, diabetes, HIV, steroid use, oestrogen use
Clinical features Vulvovaginitis - itching, soreness Dysuria Vaginal discharge - thick, white ‘curd’ or ‘cheese’ like vaginal discharge Management 1st line: Stat dose of oral fluconazole 150mg Contraindications: Pregnant or breastfeeding 2nd line: Stat dose of clotrimazole 500mg as intravaginal pessary Consider co-prescribing topical clotrimazole cream if vulval symptoms
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Recurrent vaginal candidiasis Defined by BASHH as 4 or more episodes per year Management Confirm the diagnosis of candidiasis - High vaginal swab for MCS Consider induction-maintenance anti-fungal regime: Induction: PO fluconazole every 3 days for 3 doses Maintenance: PO fluconazole weekly for 6 months
Oral candidiasis Clinical features Patches of white/yellow plaque on the tongue, cheeks or palate Dysphagia Management: 1st line: Miconazole oral gel 2nd line: Nystatin suspension If severe: Fluconazole 50mg OD for 14 days
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Clinical Features Painful crops of genital blisters/vesicles which burst, leaving ulcers on the genitalia/perineal region. Primary infection Blisters develop 5-7 days post-exposure/sexual contact Symptoms during primary episode last 2-3 weeks and are more severe than with subsequent recurrent episodes Recurrent episodes may be preceded by prodromal tingling/neuropathic pain in the genital region, buttocks, back or thighs. Dysuria Other symptoms may include vaginal/urethral discharge, systemic upset.
Investigations PCR testing of viral swab taken from base of ruptured vesicle Management Conservative measures: Saline bathing, OTC analgesia Topical lidocaine 5% may help with dysuria Antivirals: First episode: Prescribe oral antivirals (NOT topical) within 5 days of first episode/while new lesions forming 1st line: Aciclovir/ Valaciclovir for 5-10 days Recurrent episodes: Two options depending on frequency. Episodic Tx: If episodes are infrequent (<6/year) - offer a course of antivirals for each episode. Suppressive Tx: If 6 or more episodes per year - offer regular PO antivirals Prescribe for one year max, before reassessment of episode frequency - can continue Tx if episode frequency remains high If first episode of genital herpes during pregnancy, there is a risk of neonatal herpes (highest risk in 3rd trimester) - refer for specialist advice
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Herpes Simplex Pathophysiology Cause: Infection with herpes simplex virus HSV-1 - most common cause of oral herpes HSV-2 - most common cause of genital herpes
Transmitted by contact with infected secretions at mucosal surfaces. Primary infection - initial infection with HSV. Patients are often asymptomatic. Primary infection is followed by viral latency (HSV remains dormant within sensory ganglia) Recurrent herpes - the presence of symptoms, due to the reactivation of HSV.
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Urethritis in Men Background Urethritis is classified as gonococcal or non-gonococcal urethritis (NGU) Causes: Neisseria gonorrhoea NGU: 50% no identifiable cause If identifiable cause - chlamydia, mycoplasma most common
Clinical features Urethral discharge Dysuria Posthitis Balanitis Investigations Investigate for underlying STI including Chlamydia + Gonorrhoea - first-void urine (FVU) sample for NAAT Mycoplasma genitalium Trichomoniasis - urethral swab/FVU for MCS
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Urethritis in Men Background Urethritis is classified as gonococcal or non-gonococcal urethritis (NGU) Causes: Neisseria gonorrhoea NGU: 50% no identifiable cause If identifiable cause - chlamydia, mycoplasma most common
Management Offer empirical ABx for chlamydial infection - doxycycline 100mg BD 7/7 Alt: Azithromycin Consider treating for gonococcal/trichomoniasis as above if suspected Ciprofloxacin/ceftriaxone or metronidazole respectively
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Investigations Send samples for NAATs (nucleic acid amplification tests) or culture Women: Vulvo-vaginal swab Men: First catch urine Management 1st line: If culture sensitivity known - Ciprofloxacin 500 mg PO stat dose Contraindicated in pregnant or breastfeeding women If culture sensitivity not known - Ceftriaxone 1g IM stat dose Alternative: E.g. Needle phobias/CIs Cefixime 400mg PO stat dose + azithromycin 2g PO (e.g. if needle phobic) Gentamicin 240 mg IM stat dose + azithromycin 2g PO Test of cure is recommended in all patients treated for gonorrhoea Partner notification: Men with urethritis - partners within 2 weeks, or most recent partner only if > 2 weeks ago Women and asymptomatic men - partners within 3 months
Gonorrhoea Pathophysiology Cause: Neisseria gonorrhoea (Gm -ve bacteria) Complications: Epididymo-orchitis, prostatitis, PID, infertility Clinical features Most commonly causes an uncomplicated, lower genital tract infection. Women: Urethritis - dysuria Endocervical infection Abnormal vaginal discharge Lower abdominal pain Intermenstrual bleeding Deep dyspareunia Men: Urethritis - mucopurulent discharge, dysuria Symptoms 2-7 days post exposure
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Investigations clamydia Send samples for NAATs (nucleic acid amplification tests) Women: 1st line: Vulvo-vaginal swab Alt: First catch urine if preferred by woman Men 1st line: First catch urine Alt: Urethral swab
Management 1st Line: Doxycycline 100mg BD for 1 week 2nd line: Azithromycin 1g PO stat dose, then 500mg PO OD for 2 days This is also the 1st line in pregnancy Test of cure not routinely indicated, unless poor compliance/pregnant Can offer repeat test in 6 months to check for re-infection Pregnant/ breastfeeding women: Tetracyclines contraindicated 1st Line: Azithromcyin, erythromycin or amoxicillin Test of cure is indicated in pregnancy Complications Fitz-Hugh-Curtis syndrome - perihepatitis secondary to CT - presents with RUQ pain +/- referred shoulder pain Reactive arthritis Epididymo-orchitis Pelvic inflammatory disease
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Chlamydia Pathophysiology The most common bacterial STI Cause: Chlamydia trachomatis Complicated CT: Involvement of upper genital tract causing PID/epididymo-orchitis
Clinical features Commonly asymptomatic - half of men and three quarters of women! Women: Vaginal discharge which may be thick, cloudy, may be yellow in colour, may be malodorous Dysuria Deep dyspareunia Post-coital bleeding Intermenstrual bleeding Pelvic pain, tenderness O/E: Cervical motion tenderness, inflamed cervix +/- contact bleeding Men: Dysuria White, cloudy discharge Lymphogranuloma venereum Cause: Chlamydia trachomatis serovars L1, L2, L3 An ulcerative disease of the genital area which is most common in men who have sex with men (MSM). Symptoms occur in 3 stages: Stage 1: PAINLESS genital ulcers/papules Symptoms include bloody anorectal discharge, tenesmus Stage 2: Tender inguinal lymphadenopathy Stage 3: Strictures/fibrosis/fistulae of anogenital area
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Surgical Site Infection Key learning Common pathogens: Staphylococcus aureus, coagulase-negative Staphylococcus, Pseudomonas, and Escherichia coli. Risk Factors: Prolonged emergency surgery, contaminated wounds, diabetes, immunosuppressive disorders/medications, smoking. Investigations: CT/MRI to assess the extent of infection. Management options: Wound care, IV antibiotics, surgical debridement.
Pathophysiology Occur when bacteria contaminate the surgical wound, leading to local inflammation and tissue damage Most common organisms include: Staphylococcus aureus Coagulase-negative Staphylococcus Pseudomonas Escherichia coli Risk factors Prolonged emergency surgery (> 2 hours) Contaminated or dirty wounds Pre-existing medical conditions- diabetes, immunosuppressive disorders or medications Smoking
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Surgical site infection Presentation Increased pain, swelling, redness, or discharge from the surgical site Associated fever, malaise, and systemic symptoms Examination Findings Signs of local inflammation at the surgical site Erythema Swelling Warmth Tenderness Wound dehiscence or purulent discharge Investigations Bloods including WCC/CRP for infection markers Wound swab for MCS if discharging Imaging- CT/MRI to assess the extent of infection
Management Conservative: Wound care Intravenous antibiotics Surgical intervention if above fails or concern regarding deep infection: Wound debridement Drainage of abscesses Removal of infected implants Complications Delayed wound healing Abscess formation Cellulitis Sepsis and systemic infection
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Syphilis Pathophysiology Cause: Treponema pallidum - a spirochete bacterium Transmission: Sexually transmitted (or vertically/needle sharing etc.) Disease course and clinical features
The disease course is divided into early syphilis and late syphilis. Early syphilis is further categorised into primary, secondary and early latent Primary syphilis Characterised by a chancre - a single firm, indurated ulcer, often associated with regional lymphadenopathy. The ulcer is usually PAINLESS, with well-defined margins Secondary syphilis - systemic features including: Generalised lymphadenopathy Systemic upset - fever, lethargy etc. Snail tract lesions on oral mucosa Condylomata lata - wart-like lesions Maculopapular rash - usually generalised, but may only affect the soles of the feet/palms of the hands - often rough, red/brown spots. Early latent - Confirmed infection but currently asymptomatic
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Late syphilis
Late syphilis (after > 2 years of infection) Late latent infection Tertiary syphilis - uncommon, but characterised by complications such as: Neurosyphilis, inc. tabes dorsalis, general paralysis of the insane (dementia) Gumma - locally destructive nodules/plaques Aortitis with subsequent aneurysm or aortic regurgitation
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Syphilis investigation
Investigations Assessment is complex and should be led by GUM specialists. It involves a combination of the following: Direct tests for syphilis - swabs taken from primary lesion sent for PCR or studied under dark-field microscopy - demonstrate the presence of treponema pallidum. Serological tests: Treponemal tests Examples: EIA, CLIA Detect treponemal IgG and IgM (but cannot differentiate between other, non-venereal types of treponemal infection) NOT useful for monitoring Tx response, as IgG/IgM levels remain +ve lifelong in most people Non-treponemal tests Examples: VDRL antigen test/ RPR Can be used to monitor effect of Tx (with successful Tx, RPR titre declines by fourfold after 6 months)
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Syphilis mng
Management 1st Line: IM Benzathine Benzylpenicillin Complications Complications of treatment - Jarisch-Herxheimer reaction An acute illness which occurs in response to treatment Symptoms: Fever with rigors, headache, general malaise, myalgia, tachycardia - resolves after 24hrs Differentiate from anaphylaxis, as no wheeze/hypotension. Self-limiting - supportive treatment only. Argyll-Robertson Pupils Small irregular pupils with absent pupillary reflex ARP - PRA - pupillary reflex absent Causes: Syphilis, diabetes
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Tuberculosis Background Aetiology Mycobacterium tuberculosis most commonly (others. M. Bovis, M africanum) Transmission: Inhalation of respiratory droplets Terminology Active TB - symptomatic/ progressive disease Active pulmonary TB is most common Other sites may be affected: CNS, LNs, GI, GU etc Disseminated TB = 2+ systems involved Latent TB - asymptomatic, no clinical evidence of TB Reactivation of latent TB to active TB can occur, esp. if patient becomes immunocompromised.
Clinical features 1. A history of risk factors Birth in high prevalence area (> 40 cases/100,000 population) India, Pakistan, Romania, Somalia, Eritrea - highest risk Immunosuppression - HIV, DM, ESRF, malignancy, drugs Living circumstances - homeless shelters, prisons 2. Systemic symptoms of TB Weight loss Fever Night sweats General malaise, lethargy, anorexia 3. System-specific symptoms of TB Symptoms of pulmonary involvement - cough +/- haemoptysis Symptoms of extrapulmonary involvement: Lymphadenopathy, often cervical, supraclavicular - lymphatic TB Bone pain - skeletal TB Abdominal pain - GI/GU TB Urinary symptoms/sterile pyuria - renal TB TB Meningitis Cutaneous TB - erythema nodosum, lupus vulgaris, scarring alopecia Nb. Lupus vulgaris is the most common manifestation of dermatological TB Erythematous flat plaques, which evolve and become painful, ulcerated nodular lesions Most commonly affect the face, nose, mouth
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Investigation TB
Investigations Active TB Suspected Pulmonary TB CXR - bilateral hilar lymphadenopathy, upper lobe fibrosis/cavitation Sputum samples Arrange 3 x early morning sputum samples - for microscopy with ZN staining for acid-fast bacilli and culture Suspected Extra-pulmonary TB CXR Respiratory sample as above Further investigations depend on site of suspicion - x-rays, US, urine samples, echo, CT scans, LP etc
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Latent TB
Latent TB Patients who are asymptomatic, but considered at high risk of infection should be screened. This includes: Patients with contact with a person diagnosed with active TB (e.g. partner/household member) Immunocompromised patients: HIV, organ transplant High-prevalence groups - prisons/homeless shelters Immigrants from high prevalence countries New NHS employees
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Mantoux test
Mantoux test Intradermal tuberculin injection After 2-3 days review the induration If < 5mm = negative 5mm induration or more = positive False negatives can occur in HIV, lymphoma, sarcoidosis, miliary TB, age < 6/12 IGRA test - interferon-gamma release assay Blood test - measure the quantity of IFN-gamma produced in response to M TB antigens
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Complications of TB Treatments
Rifampicin A potent liver enzyme inducer (pcbRas) Hepatitis Orange secretions/urine Isoniazid Peripheral neuropathy (reduce risk with pyridoxine co-prescription) Agranulocytosis Pyrazinamide Hyperuricemia - Gout Ethambutol Optic neuropathy (check visual acuity before treatment) Bilateral painless, symmetric loss of colour vision and central visual acuity
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Management Treatment of Active TB
Initial phase - 2 months - RIPE Rifampicin Isoniazid (with pyridoxine cover) Pyrazinamide Ethambutol Consolidation phase - 4 months - RI Rifampicin Isoniazid (with pyridoxine cover) CNS TB (e.g. TB meningitis) Prolonged treatment regimen (12 months) Also require steroids for 1-2 mont
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Treatment of latent TB
Treatment of Latent TB Options include.. 3 months of Rifampicin and Isoniazid (with pyridoxine cover).. OR Best for patients < 35 yrs - at low risk of hepatotoxicity 6 months of Isoniazid monotherapy (with pyridoxine cover) Best for patients at risk of rifampicin drug interactions (inducer)
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Dengue Fever Pathophysiology Most common in South America Transmitted by Aedes mosquitoes Clinical features
Facial flushing/erythema, or injected oropharynx in first 24-48 hours Maculopapular rash Fever - commonly biphasic Headache with retro-orbital eye pain Haemorrhagic manifestations - petechial rash, bruising, positive tourniquet test, bleeding gums, haematuria Severe dengue - increased vascular permeability - pleural effusions, ascites, then shock and multiorgan failure, severe haemorrhage. Bloods Thrombocytopenia, leukopenia, lymphopenia
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Yellow Fever Pathophysiology Found in Africa, South America Transmitted by Aedes mosquitoes Clinical features
Sudden onset of fever, rigours, flu-like symptoms Bradycardia Most will recover within one week However approx. 15% of infected patients develop severe disease, after a brief period of apparent remission, characterised by: Jaundice Haematemesis Acute renal failure - oliguria
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Viral haemorrhagic fevers
Overview Viral haemorrhagic fevers (VHFs) are a group of viral illnesses characterised by bleeding/haemorrhage. Clinical features Abdominal pain Flu-like symptoms - malaise, lethargy, headache Haemorrhage - Bloody diarrhoea, petecihal rash, bruising/DIC, haematemesis Multi-organ failure
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Warts & Veruccas Pathophysiology Benign lesions caused by infection with human papillomavirus Transmission: Direct skin-to-skin contact or autoinoculation, or indirectly with contaminated surfaces (e.g. swimming pools) Management Conservative management - await spontaneous resolution (months to 2 yrs usually) Consider treatment if unsightly, painful or patient request Cryotherapy Topical salicylic acid
Subtypes and clinical features Common wart Rough, raised, cauliflower-like papules with a hyperkeratotic surface Plantar wart (verrucae) Warts growing on the palms of the hand/soles of the feet. Can be painful Central dark spots (capillary thrombosis) Can be inwardly growing Filiform wart A narrow pedicular base, with a cluster of ‘finger-like’ extensions/fronds Often occur on the face
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