Infectious Diseases Flashcards
What is malaria?
Infectious disease caused by Plasmodium of protozoan parasites (single-celled organisms)
What is the most severe and dangerous type of malaria?
Plasmodium falciparum- Accounts for 80% of malaria causes in the UK
How is malaria transmitted?
Through bites from female Anopheles mosquitoes that carry the disease
Not transmitted in the UK- Is associated with travel to areas where malaria is present
List types of malaria
Plasmodium falciparum (most common and severe form)
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium knowlesi
Outline the life cycle of malaria
Usually spread at night
Feeding mosquito sucks up infected blood- Parasites reproduce in mosquito’s gut, producing sporozoites
Mosquito bites someone, sporozoites are injected- Travel to liver of newly infected person- P. vivax and P. ovale can lie dormant for months or years before reactivating
Parasites mature in liver into merozoites- Enter blood and infect RBCs- Merozoites reproduce, RBCs rupture, releasing merozoites into blood and causing haemolytic anaemia
In P. vivax and P. ovale- Rupture and release of merozoites occurs every 48h, causing fever spike every other day
P. falciparum- Fever spikes more frequently
P. malariae- Fever spikes every 72h
Outline presentation of malaria
Fever (up to 41 degrees C) with sweats and rigors
Fatigue
Myalgia (muscle aches and pains)
Headache
Nausea
Vomiting
What are the signs of malaria on examination?
Pallor due to anaemia
Hepatosplenomegaly
Jaundice (bilirubin released during rupture of RBCs)
What is the most characteristic symptom of malaria?
Fever which spikes very high every 48h
Exposure can be from several years ago
How is malaria diagnosed?
Malaria blood film- Sent in EDTA bottle
3 negative samples taken over 3 consecutive days required to exclude malaria
Outline management of falciparum malaria
Admit
Outline oral management of uncomplicated malaria
Artemether with lumefantrine (Riamet)- 1st choice
Quinine plus doxycycline
Quinine plus clindamycin
Quinine plus clindamycin
Proguanil with atovaquone (Malarone)
Chloroquine (increasing rates of resistance to chloroquine)
Primaquine (can cause severe haemolysis in patients with G6PD deficiency)
Outline IV management of severe or complicated malaria
Admission to HDU or ICU
Artesunate 1st choice (haemolysis common SE)
Quinine dihydrochloride
List complications of P. falciparum malaria
Cerebral malaria
Seizures
Reduced consciousness
AKI
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death
Outline prophylaxis for preventing malaria when travelling to endemic areas
No method 100% effective alone
Use mosquito spray (eg: 50% DEET spray)
Use mosquito nets and barriers in sleeping areas
Seek medical advice if symptoms develop
Take antimalarial medication as recommended
What are the main antimalarial medication options?
Not 100% effective
Proguanil with atovaquone (malarone)- Take from 2d before until 7d after travel to endemic area
Doxycycline- Taken 2d before until 4wks after travel to endemic area
Mefloquine (risk of psychiatric SEs)- Taken wkly from 2wks before to 4wks after travel to endemic area
Chloroquine with proguanil (less often used due to high resistance)
Outline HIV
RNA retrovirus
HIV-1 is most common type
HIV2 mainly found in West Africa
Virus enters and destroys CD4 T-helper cells
Initial seroconversion flu-like illness occurs within few wks of infection- Then asymptomatic until condition progresses to immunodeficiency- May occur yrs after initial infection
Outline transmission of HIV
Unprotected anal, vaginal or oral sexual activity
Mother to child- At any stage of pregnancy, birth or breastfeeding- Vertical transmission
Mucous membrane, blood, or open wound exposure to infected blood/bodily fluids- eg: Sharing needles, needle-stick injuries, blood splashed in eye
List AIDS-defining illnesses
CD4 count dropped to level that allows for unusual opportunistic infections and malignancies
Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia (PCP)
CMV
Candidiasis (oesophageal or bronchial)
Lymphomas
TB
Outline HIV screening
Low threshold for testing
Patients with RFs tested
All patients accessing sexual health/antenatal/substance misuse services offered testing
Verbal consent should be documented
Checks ABs to HIV and p24 antigen
Window period of 45d- Can take up to 45d for +ve test to show
Point of care test- HIV ABs- Give result within mins, have 90d window period
Self-sampling kits- Posted to lab- ABs and p24 antigen
Outline monitoring of HIV
Test CD4 count gives number of CD4 cells in blood- Lower count gives higher risk of infection
500-1200 cells/mm3= Normal
<200 cells/mm3= High risk opportunistic infections
Testing for HIV RNA/ml of blood indicates viral load
Undetectable viral load means level below recordable range (20 copies/ml)
Outline treatment of HIV
Combination of antiretroviral therapy (ART)- Offered to everyone diagnosed with HIV, irrespective of viral load or CD4 count
Genotypic resistance testing- Establish resistance of each HIV strain to different meds to guide treatment
Aims to achieve normal CD4 count and undetectable viral load
List classes of antiretroviral therapy meds
Protease inhibitors (PI)
Integrase inhibitors (II)
Nucleoside reverse transcriptase inhibitors (NRTI)
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Entry inhibitors (EI)
What is the usual starting regime for antiretroviral therapy?
2 NRTIs (eg: Tenofovir plus emtricitabine) plus 3rd agent (eg: Bictegravir)
Outline additional management of HIV
PCP- Prophylactic co-trimoxazole given to all HIV +ve patients with CD4 count<200/mm3
Increased risk developing CVD- Monitor blood lipids and consider statins
Yrly cervical smears- Increased risk HPV and cervical cancer
Vaccinations- Yrly influenza, pneumococcal, HPV, Hep A and B- Avoid live vaccines
Outline reproductive health and HIV
Correct use of condoms
Effective treatment combined with undetectable viral load can prevent spread of HIV
Outline prevention of transmission of HIV during birth
Mother’s viral load determines mode of delivery
<50 copies/ml- Normal vaginal delivery
>50 copies/ml- Consider pre-labour C section
>400 copies/ml- Pre-labour C section
IV zidovudine infusion during labour and delivery if viral load unknown/>1000 copies/ml
Prophylaxis given to baby depending on mother’s viral load:
<50 copies/ml- Zidovudine for 2-4wks
High-risk babies- Zidovudine, lamivudine, nevirapine for 4wks
Outline HIV and breastfeeding
Can be transmitted during breastfeeding
Risk reduced if mother’s viral load undetectable but not eliminated
Outline post-exposure prophylaxis (PEP) of HIV
Post-exposure prophylaxis (PEP)- Used after exposure to reduce risk of transmission- Not 100% effective and must be commenced within <72h
Combination of ART therapy- Emtricitabine/tenofovir (Truvada) and raltegravir for 28d
Outline pre-exposure prophylaxis (PrEP) of HIV
Emtricitabine/tenofovir (Truvada)
Outline TB
Caused by mycobacterium TB (rod-shaped acid-fast bacillus)- Require Zeihl-Neelsen stain- Turns bright red against blue background
What type of staining is used to diagnose TB?
Require Zeihl-Neelsen stain- Turns bright red against blue background
Outline the disease course of TB
Mainly spread by inhaling saliva droplets from infected
Several options:
- Immediate clearance (most cases)
- Primary active TB (active infection after exposure)
- Latent TB (Presence of bacteria w/o symptomatic or contagious)
- Secondary TB (reactivation of latent TB to active infection)
What is miliary TB?
When immune system can’t control infection
Disseminated and severe disease
Outline latent TB
When immune system encapsulates the bacteria and stops progression of the disease
No symptoms and can’t spread the bacteria
Can reactivate, usually due to immunosuppression- Secondary TB
Where is the most common site for TB infection?
Lungs
List sites of extrapulmonary TB
Lymph nodes
Pleura
CNS
Pericardium
GI system
GU system
Bones and joints
Skin (cutaneous TB)
What is a cold abscess?
Firm, painless abscess caused by TB, usually in neck
No inflammation/redness/pain
Outline risk factors for TB
Close contact with active TB
Immigrants from areas with high TB prevalence
People with relatives/close contacts from countries with high rate TB
Immunocompromised (eg: HIV or immunosuppressant meds)
Malnutrition, homelessness, drug users, smokers and alcoholics
Outline the BCG vaccine
Intradermal injection of live attenuated Mycobacterium bovis
Protects against severe and complicated TB, but less against pulmonary TB
Tested with Mantoux before vaccine
Outline presentation of TB
Chronic, gradually worsening symptoms
Most involve pulmonary disease
Cough
Haemoptysis
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on shins caused by inflammation of SC fat)
Spinal pain in spinal TB (Pott’s disease)
Outline investigations of TB
Ziehl-Neelsen stain
2 tests for immune response to TB caused by previous infection/latent TB/active TB- Mantoux test or Interferon-gamma release assay (IGRA)
If disease activity suspected- CXR and cultures
Outline Mantoux test
Inject tuberculin into intradermal space on forearm
Doesn’t contain live bacteria
Creates a bleb under skin- Read after 72h- >5mm is +ve
Outline Interferon-Gamma release Assay (IGRA)
Mixing a blood sample with antigens from M. TB bacteria
After previous contact- WBCs become sensitised to bacteria antigens- Will release interferon-gamma on further contact
Positive- Interferon-gamma is released during test
Outline CXR of TB
Primary TB- Patchy consolidation, pleural effusions and hilar lymphadenopathy
Reactivated TB- Patchy or nodular consolidation with cavitation (gas-filled spaces), typically in upper zones
Disseminated miliary TB- Millet seeds uniformly distributed across lung fields
Outline cultures of TB
Can take several mths
Sputum cultures (3 separate collected)
Mycobacterium blood cultures
Lymph node aspiration or biopsy
If not producing enough sputum:
Sputum induction with nebulised hypertonic saline
Bronchoscopy and bronchoalveolar lavage (saline used to wash airways and collect a sample)
Outline Nucleic Acid Amplification Tests (NAAT)
Assesses genetic material of a pathogen
Detects TB DNA
Faster than traditional culture
Used for- Diagnosing TB in patients with HIV or <16y or RFs for multidrug resistance
Outline treatment of latent TB
Isoniazid and rifampicin for 3mths
Isoniazid for 6mths
Outline treatment of active TB
R- Rifampicin for 6mths
I- Isoniazid for 6mths
P- Pyrazinamide for 2mths
E- Ethambutol for 2mths
Co-prescribe pyridoxine (Vit B6) to prevent peripheral neuropathy caused by isoniazid
What is the main SE of isoniazid and how is this managed?
Peripheral neuropathy
Give pyridoxine (Vit B6)
Other SE- Hepatotoxicity
Outline other management options for TB
Test for other infectious disease (HIV/Hep B/Hep C)
Contact tracing
Isolate patients with active TB (at least 2wks)
Negative pressure rooms in hospitals used to prevent airborne spread
What are the SEs of rifampicin?
Red/orange discolouration of secretions- Urine and tears
Potent inducer of cytochrome P450 enzymes- Reduces effects of drugs metabolised by this system (eg: combined contraceptive)
Hepatotoxicity
What are the SEs of Pyrazinamide?
Hyperuricaemia (high uric acid levels)- Results in gout and kidney stones
Hepatotoxicity
What are the SEs of Ethambutol?
Colour blindness and reduced visual acuity
What is meningitis?
Inflammation of meninges usually due to infection
Meninges- Lining of brain and spinal cord
CSF is contained within meninges (in subarachnoid space)
List the causes of bacterial meningitis
Neisseria meningitidis
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae
Group B Streptococcus (GBS)- Particularly in neonates
Listeria monocytogenes- Particularly in neonates
Outline Neisseria meningitidis
Gram-negative diplococcus bacteria
Typically known as meningococcus
Most common cause of bacterial meningitis
Outline Meningococcal meningitis
Bacteria infects meninges and CSF
Outline Meningococcal speticaemia
Meningococcus bacterial infection in bloodstream
Causes non-blanching rash
What are the most common causes of viral meningitis?
Enteroviruses (eg: Coxsackie virus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)
How is viral meningitis diagnosed?
Viral PCR testing on CSF sample
How is viral meningitis managed?
Aciclovir- Used to treat HSV and VZV
Outline presentation of meningitis
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Outline presentation of meningitis in neonates and babies
Non-specific signs and symptoms
Hypotonia
Poor feeding
Lethargy
Hypothermia
Bulging fontanelle
What are the NICE guidelines for investigations of children with suspected sepsis?
Lumbar puncture
Under 1mth, presenting with fever
1-3mths and are unwell/have low or high WBC count
What are the special tests to perform to look for meningeal irritation?
Kernig’s test
Brudzinski’s test
What is Kernig’s test?
Lie patient on back, flex one hip and knee to 90 degrees, slowly straighten knee whilst keeping hip flexed at 90 degrees
Creates stretch in meninges
If meningitis- Produce spinal pain or resistance to movement
What is Brudzinski’s test
Lie patient flat on back and use hands to lift their head and neck off bed, flexing chin to their chest
Positive test for meningitis- Causes patient to flex their hips and knees involuntarily
Outline the lumbar puncture result of bacterial meningitis
Cloudy
High protein
Low glucose
High WCC (neutrophils)
Bacteria on culture
Outline the lumbar puncture result of viral meningitis
Clear
Mildly raised/normal protein
Normal glucose
High WCC (lymphocytes)
Negative culture
Outline the procedure of a lumbar puncture
Insert needle into L3-L4 or L4/L5 intervertebral space
Spinal cord ends at L1-L2
Outline management of bacterial meningitis
MEDICAL EMERGENCY
Children in primary care with suspected meningitis and non-blanching rash- Urgent benzylpenicillin (IM or IV)
Blood cultures and LP before starting ABs- Meningococcal PCR (gives faster result than blood cultures and still positive after treated with ABs)
<3mths- Cefotaxime plus amoxicillin
>3mths- Ceftriaxone
Aciclovir added if viral meningitis suspected
Vancomycin added if risk of penicillin-resistant pneumococcal infection (recent foreign travel or prolonged AB exposure)
Steroids (dexamethasone) in bacterial meningitis- Reduce frequency and severity of hearing loss and neuro complications
What is used to reduce frequency of hearing loss and neurological complications in meningitis?
Dexamethasone
List complications of hearing loss
Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits- Limb weakness or spasticity
Outline post-exposure prophylaxis of meningitis
Risk highest with close prolonged contact within 7d before onset of illness
Single dose of ciprofloxacin given as soon as possible after diagnosis
Outline Clostridium difficile
Gram positive, rod-shaped, anaerobic bacteria
Infection associated with repeated use of ABs/PPIs/healthcare settings
Spores released in faeces
May colonise intestines w/o causing any symptoms or issues
Produces Toxin A (enterotoxin) and Toxin B (cytotoxin)
List ABs most associated with C. difficile
Clindamycin
Ciprofloxacin (and other fluoroquinolones)
Cephalosporin
Carbapenems (eg: Meropenem)
Outline presentation of C. difficile
Colonisation usually asymptomatic
Infection- Diarrhoea, nausea and abdo pain
Severe infection with colitis- Dehydration, systemic symptoms (eg: Fever, tachycardia, hypotension)
Outline diagnosis of C. difficile
Stool tests:
C. difficile antigen (specifically glutamate dehydrogenase)
A and B toxins (by PCR or enzyme immunoassay)
Outline management of C. difficile
Supportive care and oral ABs
1st line- Oral vancomycin
2nd line- Oral fidaxomicin
Isolate until 48h after last episode of diarrhoea- High recurrence rate
Recurrent cases- Faecal microbiota transplantation
List complications of C. difficile
Pseudomembranous colitis
Toxic megacolon
Bowel perforation
Sepsis
What is Pseudomembranous colitis?
Inflammation of large intestine
Yellow/white plaques form pseudomembranes on inner surface bowel wall
Seen during colonoscopy and confirmed on biopsy
What is Toxic megacolon?
Complication of severe inflammation in large intestine and involves dilation of colon
High risk of bowel rupture
List some post-gastroenteritis complications
Lactose intolerance
IBS
Reactive arthritis
Guillain-Barre syndrome
HUS
Outline general management of Gastroenteritis
Food poisoning- NOTIFIABLE DISEASE
Isolate- Barrier nursing and infection control- 48h after symptoms resolve
Faeces sample- Microscopy, culture and sensitivities
Dehydration- Assess whether need for admission for IV fluids
Oral rehydration salt solution
Antidiarrhoeal drugs- Avoid
Antibiotics- If risk of complications
Oral intake tolerated- Light diet with bland foods
What is oral rehydration salt solution?
Dioralyte sachets mixed with water
Replace losses in risk of dehydration
Contains glucose, potassium and sodium
Outline giardiasis
Parasite in small intestines of mammals- Releases cysts in faeces- May contaminate food/water
Faecal-oral transmission
May cause chronic diarrhoea
Diagnosis- Stool test (NAAT or EIA)
Treat- Tinidazole or metronidazole
Outline staphylococcal aureus as a cause of gastroenteritis
Can produce enterotoxins growing on food (eggs/dairy/meat)
Cause inflammation in intestines
Symptoms- Diarrhoea, vomiting, abdo cramps, fever- Start within hrs of ingestion and settle within 12-24h
Outline Yersinia Enterocolitica
Gram negative bacillus
Pigs are key carriers (raw pork) and contact with infected humans/animals and faeces
Typically affects children- Watery/bloody diarrhoea, abdo pain and fever
Incubation 4-7d- Symptoms last >3wks
Older children/adults present with R sided abdo pain due to mesenteric lymphadenitis (inflammation in intestinal lymph nodes) and fever- Can impersonate appendicitis
Outline Yersinia pestis
Spread through rat flea bites
Causes plague
Outline Bacillus Cereus
Gram positive rod
Spread through contaminated cooked foods- Fried rice/cooked pasta left at room temperature
Toxin cereulide causes abdo cramping and vomiting within 5h of ingestion
Reheating food can kill bacteria but doesn’t destroy the cereulide toxin- Watery diarrhoea
Vomiting within 5h, diarrhoea >8h after ingestion- Symptoms resolve within 24h
Can also occur with infective endocarditis in IV drug users, where heroin is contaminated
What is the most common cause of infective endocarditis in IV drug users?
Staph aureus
Outline salmonella
Spread by eating raw eggs/poultry/food contaminated with infected faeces of small animals
Incubation 12h-3d- Symptoms resolve within 1wk
Symptoms- Watery diarrhoea (may have mucous/blood), abdo pain, vomiting
ABs only necessary in severe cases- Guided by stool culture and sensitivities (eg: Ciprofloxacin)
Outline Shigella
Spread via faeces
Either person-person or through contaminated drinking water/food
Incubation period 1-2d- Symptoms resolve within 1wk
Symptoms- Bloody diarrhoea, abdo cramps, fever
Can produce Shiga toxin- Can cause Haemolytic Uraemic Syndrome
Treat severe cases- Azithromycin or ciprofloxacin
Outline Campylobacter Jejuni
Traveller’s diarrhoea
Gram negative bacteria
Spread- Raw poultry, untreated water, unpasteurised milk
Incubation 2-5d- Symptoms resolve 3-6d
Symptoms- Abdo cramps, diarrhoea with blood, vomiting, fever
ABs considered if severe symptoms or other RFs (HIV or HF)- Clarithromycin (1st line), azithromycin, ciprofloxacin
Outline E. coli
E. coli is normal intestinal bacteria
Spread through contact with infected faeces/unwashed salad/contaminated water
Produces Shiga toxin- Increased risk HUS- Avoid ABs
Outline viral gastroenteritis
Common and highly contagious
Rotavirus
Norovirus
Adenovirus (tends to cause respiratory symptoms)
What is acute gastritis?
Stomach inflammation
Presents with epigastric discomfort, nausea and vomiting
What is enteritis?
Inflammation of intestines
Presents with abdo pain and diarrhoea
What is gastroenteritis?
Inflammation from stomach to intestines
Presents with pain, nausea, vomiting and diarrhoea
What is the most common cause of gastroenteritis?
Virus
Easily spread
Isolate in a healthcare environment
What is the prognosis of gastroenteritis?
Most people recover well
Can rarely be fatal- Especially in very young or old patients, or those with other health conditions
Outline influenza virus
RNA
3 types- A, B, and C
A and B most common
Outbreaks typically occur in winter
Outline influenza vaccination
Yearly required in:
>65y
Young children
Pregnant women
Chronic health conditions- Asthma, COPD, HF, diabetes
Healthcare workers and carers
Outline presentation of influenza
Fever
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache
Dry cough
Sore throat
Coryzal symptoms
What is the typical difference in features between cold and flu?
Flu- Abrupt onset, fever, ‘wiped out’ with muscle aches and lethargy
Common cold- Gradual onset
Outline testing of influenza
Point-of-care tests- Swabs- Detect viral antigens
Viral nasal or throat swabs- PCR analysis
Outline management of influenza
If risk of complications- Oral oseltamivir (twice daily for 5d), inhaled zanamivir (twice daily for 5d)
Treatment needs to be started within 48h of onset of symptoms
Outline criteria for receiving post-exposure prophylaxis of influenza
Started within 48h of close contact with influenza
Increased risk (eg: Chronic disease or immunosuppression)
Not protected by vaccination (eg: <14d since vaccinated)
What are the options for post exposure prophylaxis for influenza?
Oral osetamivir 75mg once daily for 10d
Inhaled zanamivir 10mg once daily for 10d
List complications of influenza
Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening chronic health conditions- COPD and HF
Febrile convulsions (young children)
Encephalitis
What is septic arthritis?
MEDICAL EMERGENCY
Infection in joint
Can occur in original joint or prosthetic joint replacement
Outline presentation of septic arthritis
Usually affects single joint
Rapid onset
Hot, red, swollen and painful
Stiffness and reduced range of motion
Systemic symptoms- Fever, lethargy and sepsis
What is the most common cause of septic arthritis?
Staph aureus
What are the less common causes of septic arthritis?
Neisseria gonorrhoea (gonococcus)- In sexually active individuals- Typically a young patient with single acutely swollen joint- Gram negative diplococcus
Group A strep
Haemophilus influenza
E. coli
What is the difference between Septic arthritis and reactive arthritis?
Disclude septic arthritis first
Reactive arthritis- Urinary or genital symptoms- Typically triggered by urethritis or gastroenteritis and associated with conjunctivitis
What is the difference between Septic arthritis and gout?
Gout- Joint fluid shows urate crystals that are negatively birefringent of polarised light
What is the difference between Septic arthritis and pseudogout?
Pseudogout- Joint fluid shows rod-shaped calcium pyrophosphate crystals that are positively birefringent
What is the difference between Septic arthritis and haemarthrosis?
Bleeding into joint, usually after trauma
Outline management of septic arthritis
Joint aspiration before starting ABs
Sample sent for gram staining, crystal microscopy, culture and AB sensitivities- Joint fluid may be purulent (pus)
Empirical IV ABs continued for 4-6wks
Outline the AB choices for septic arthritis
1st line- Flucloxacillin
Penicillin allergy- Clindamycin
MRSA suspected- Vancomycin
Ceftriaxone- Neisseria gonorrhoea
List possible intra-abdominal infections
Acute diverticulitis- Infection in intestinal diverticula
Acute cholecystitis- With secondary infection in gallbladder
Ascending cholangitis- Infection in bile ducts
Appendicitis
Spontaneous bacterial peritonitis- Infection in fluid in peritoneal cavity
What type of bacteria is E. coli?
Gram-negative
What type of bacteria is Klebsiella?
Gram-negative
What type of bacteria is Enterocolitis?
Gram-positive
What type of bacteria is Streptococcus?
Gram-positive
Which bacteria does Co-amoxiclav cover?
Gram +ve
Gram -ve
Anaerobes
Name types of anaerobic bacteria
Bacteroides
Clostridium
Outline the coverage of amoxicillin plus gentamicin plus metronidazole
Amoxicillin- Gram +ve
Gentamicin- Gram -ve
Metronidazole- Anaerobes
Outline the coverage of ciprofloxacin plus metronidazole
Ciprofloxacin- Gram +ve, Gram -ve
Metronidazole- Anaerobes
Outline coverage of vancomycin plus gentamicin plus metronidazole
Vancomycin- Gram +ve
Gentamicin- Gram -ve
Metronidazole- Anaerobes
Outline Co-amoxiclav
Covers gram +ve, gram -ve, anaerobes
Doesn’t cover pseudomonas or atypical bacteria
Outline quinolones
Ciprofloxacin and levofloxacin
Covers gram +ve, gram -ve, atypical
Don’t cover anaerobes
Usually paired with metronidazole
Outline metronidazole
Anaerobic cover
Inhibits metronidazole
Bactericidal
Outline gentamicin
Covers gram -ve bacteria and some gram +ve cover (staph)
Bactericidal
Outline vancomycin
Gram +ve cover, including MRSA
Combine with gentamicin (gram -ve) and metronidazole (anaerobe cover) in patients with penicillin allergy
Outline cephalosporins
Broad-spectrum cover against gram +ve and gram -ve bacteria
Often avoided due to risk of C. diff infection
Outline Piperacillin with tazobactam and meropenem
Cover gram +ve, gram -ve and anaerobic bacteria
Don’t cover atypical bacteria or MRSA
Usually reserved for very unwell patients and those not responding to other ABs
What is cellulitis?
Infection of skin and soft tissues underneath
May be due to skin trauma, eczema, fungal nail infections or ulcers
Outline presentation of cellulitis
Erythema
Warm/hot to touch
Tense
Thickened
Oedematous
Bullae (fluid filled blisters)
Golden-yellow crust indicates Staph aureus
May be systemically unwell- Sepsis
What are the most common causes of cellulitis?
Staph aureus
Group A strep
Group C strep
MRSA should be considered- Repeated hospital admissions and ABs
Outline Eron classification
Severity of cellulitis
Class 1- No systemic toxicity or comorbidity
Class 2- Systemic toxicity or comorbidity
Class 3- Significant systemic toxicity or significant comorbidity
Class 4- Sepsis or life-threatening infection
Outline management of cellulitis
Class 3 and 4 cellulitis requires admission for IV ABs
1st line- Flucloxacillin- Effective against Staph aureus
Alternatives- Clarithromycin, clindamycin, Co-amoxiclav (1st line for cellulitis near eyes or nose)
What are Lower UTIs?
Infection in bladder
Causing cystitis (inflammation of bladder)
What is pyelonephritis?
Inflammation of kidney resulting from bacterial infection
Affects kidney tissue (parenchyma) and renal pelvis (ureter joins kidney)
Outline UTIs
More common in women- Urethra is shorter
Primary source is faeces
Urinary catheters are a possible source of infection- More challenging to treat
Outline presentation of Lower UTIs
Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Haematuria
Cloudy or foul-smelling urine
Confusion- Commonly only symptom in older and frail patients
Outline presentation of pyelonephritis
Fever
Loin or back pain (bilateral or unilateral)
Nausea or vomiting
Systemic illness
Loss of appetite
Haematuria
Renal angle tenderness
Outline management of UTIs in pregnancy
7d ABs
MSU and MC&S
Nitrofurantoin (avoid in 3rd trimester)
Amoxicillin (only after sensitivities known)
Cefalexin (typical choice)
Why is nitrofurantoin avoided in 3rd trimester of pregnancy?
Risk of neonatal haemolysis
Why is trimethoprim avoided in 1st trimester of pregnancy?
Folate antagonist- Folate essential in early pregnancy for normal development of fetus
Can cause congenital malformations- Neural tube defects (spina bifida)
Outline UTIs and pregnancy
Increased risk of pyelonephritis, premature rupture of membranes and pre-term labour
Outline management of Pyelonephritis
Refer to hospital if features of sepsis
7-10d ABs
Cefalexin
Co-amoxiclav (if culture results available)
Trimethoprim (if culture results available)
Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)
What should you consider if pyelonephritis is not responding to treatment?
Renal abscess
Kidney stone obstructing ureter- Causing pyelonephritis
Outline management of Lower UTIs
Nitrofurantoin- Avoid in patients with eGFR <45
Trimethoprim- Associated with high rates bacterial resistance
Alternatives- Pivmecillinam, amoxicillin, cefalexin
Typical duration:
3d ABs- Simple lower UTIs in women
5-10d ABs- Immunosuppressed women/abnormal anatomy/impaired kidney function
7d ABs- Men/pregnant women/catheter-related UTIs
Outline causes of UTIs
E. coli- Most common
Klebsiella pneumoniae
Enterococcus
Pseudomonas aeruginosa
Staph saprophyticus
Candida albicans (fungal)
Outline investigations of UTIs
Urine dipstick- Nitrites (bacteria in urine), leukocytes (can be infection), RBCs (microscopic/macroscopic haematuria, common sign of infection/bladder cancer/nephritis)
Nitrites better indication of infection than leukocytes
UTI- Nitrites or leukocytes plus RBCs
Dipstick result less reliable in catheterised patients or women >65y
MSU- MC&S
When is an MSU done?
Pregnant patients
Patients with recurrent UTIs
Atypical symptoms
When symptoms don’t improve with ABs
What is sepsis?
Body launches large immune response to infection, causing systemic inflammation and organ dysfunction
Outline pathophysiology of sepsis
Macrophages, lymphocytes and mast cells recognise pathogens- Release cytokines (IL and TNF) that activate immune system- Leads to systemic inflammation and release of NO (causing vasodilation)
Cytokines cause endothelial lining of blood vessels to become more permeable- Fluid leaks out of blood into ECS, resulting in oedema and reduced intravascular volume- Increased gap between blood and tissues- Reduced amount of oxygen that reaches tissue
Activation coagulation system- Deposition of fibrin and formation of thrombi- Compromised organ and tissue perfusion- Consumes platelets and clotting factors- Leads to thrombocytopenia (low platelets) and uncontrolled haemorrhage- DIC
Anaerobic respiration- Raised serum lactate and metabolic acidosis
Outline pathophysiology of disseminated intravascular coagulopathy
Activation of immune system and systemic inflammation
Release of cytokines and increased oedema- Reduced O2 reaching tissues
Activation of coagulation system- Fibrin deposition- Formation of thrombi- Compromised organ and tissue perfusion
Blood clots consume platelets and clotting factors- Thrombocytopenia (low platelets) and uncontrolled haemorrhage
What is seen on an ABG in sepsis?
Raised serum lactate and metabolic acidosis
Outline septic shock
Occurs when arterial BP drops despite adequate fluid resuscitation- Results in organ hypoperfusion
Anaerobic respiration begins and serum lactate level rises
Outline diagnosis of septic shock
Low mean arterial pressure (<65 mmHg) despite fluid resuscitation (requiring vasopressors)
Raised serum lactate (>2mmol/L)
How is septic shock managed?
Aggressive treatment with IV fluids to improve BP and tissue perfusion
High dependency or intensive care
Vasopressors (noradrenaline)- Cause vasoconstriction and increase systemic vascular resistance and MAP- Improves tissue perfusion
Outline sepsis-related organ failure assessment
Assess severity of organ dysfunction- Takes into account signs of organ dysfunction
Hypoxia
Increased oxygen requirements
Requiring mechanical ventilation
Low platelets (thrombocytopenia)
Reduce GCS
Raised bilirubin
Reduce BP
Raised creatinine
List risk factors for sepsis
Any condition causing immune dysfunction/frailty/predisposition to infection
Very young/old patients (<1y or >75y)
Chronic conditions- COPD and diabetes
Chemotherapy, immunosuppressants, steroids
Surgery, recent trauma, burns
Pregnancy and childbirth
Indwelling medical devices, catheters, central lines
Outline presentation of sepsis
NEWS2
Temperature
Heart rate
Respiratory rate
Oxygen sats
Blood pressure
Consciousness level
Additional signs of infection:
Signs of potential sources- Cellulitis, discharge from wound, cough, dysuria
Reduced urine output
Mottled skin
Cyanosis
Arrhythmias (new-onset AF)
A non-blanching rash (meningococcal septicaemia)
Raised RR- Sign of early sepsis
Elderly- Non-specific findings- Confusion, drowsiness, ‘off legs’
Neutropenic/immunocompromised- May have normal obs despite being life-threatening
Outline investigations of sepsis
FBC- WCC and neutrophils
U&Es- Kidney function and AKI
LFTs- Liver function and source of infection
CRP- Assess for inflammation
Blood glucose- Hyperglycaemia and hypoglycaemia
Clotting- Assess for DIC
Blood cultures- Assess for bacteraemia
Blood gas- Lactate, pH, glucose
Urine dipstick and culture
CXR
CT if intra-abdo infection or abscess suspected
LP- Meningitis or encephalitis
Outline management of sepsis
Sepsis protocol and pathway
Assess and start treatment within 1h of presenting
Sepsis 6
Outline sepsis 6
Take:
Serum lactate
Blood cultures
Urine output
Give:
O2- Maintain 94-98% (88-92% in COPD)
Empirical broad-spectrum ABs
IV fluids
What is neutropenic sepsis?
Sepsis with neutrophil count <1x10^9/L
Usually consequence of anti-cancer or immunosuppressant treatment
List medications that may cause neutropenia
Chemotherapy
Clozapine- Schizophrenia
Hydroxychloroquine- RA
Methotrexate- RA
Sulfasalazine- RA
Carbimazole- Hyperthyroidism
Quinine- Malaria
Infliximab- Monoclonal antibody used for various AI conditions
Rituximab- Monoclonal antibody used for various AI conditions and cancers
Outline management of neutropenic sepsis
Low threshold for suspecting neutropenic sepsis in chemotherapy or meds that may cause neutropenia
Any temperature >38 degrees C treated as neutropenic sepsis until proven otherwise
Emergency admission
Neutropenic sepsis policy
Immediate broad-spectrum ABs- Piperacillin with tazobactam
What is the prognosis of septic arthritis?
Mortality of approx. 10%
In OSCEs, treating infections which antibiotic would you give?
Antibiotics according to local antibiotic policy
Which antibiotics inhibit cell wall synthesis?
Antibiotics with beta-lactam ring:
Penicillin
Carbapenems (meropenem)
Cephalosporins
Antibiotics w/o beta-lactam ring:
Vancomycin
Teicoplanin
Which ABs inhibit folic acid metabolism?
Sulfamethoxazole
Trimethoprim
Co-trimoxazole (bactericidal)- Combination sulfamethoxazole and trimethoprim (bacteriostatic)
List ABs that target ribosomes
Inhibit protein synthesis
Macrolides (erythromycin, clarithromycin, azithromycin)
Clindamycin
Tetracyclines (eg: Doxycycline)
Gentamicin
Chloramphenicol
Outline nitrofurantoin
Exclusively used to treat lower UTIs
Bactericidal
Not used to treat pyelonephritis- Only achieves adequate conc. in urine
Outline coverage of amoxicillin
Gram +ve
Strep, listeria, enterococci
Outline coverage of Co-amoxiclav
Gram +ve, gram -ve, anaerobes
Staph, Haemophilus, E. coli
Outline coverage of clarithromycin
Gram +ve, atypicals
Outline coverage of clindamycin
Gram +ve, anaerobes
Outline coverage of gentamicin
Gram -ve
Outline coverage of ciprofloxacin
Gram -ve, atypicals
Outline coverage of metronidazole
Anaerobes
Outline coverage of doxycycline
Gram +ve, Gram -ve, anaerobes, atypicals
Outline coverage of vancomycin
Gram +ve
MRSA
Outline gram stain
Crystal violet stain- Binds to gram +ve- Turns violet
Counterstain- Binds to cell membrane of gram -ve- Turns red/pink
List gram +ve cocci
Staphylococcus
Streptococcus
Enterococcus
List gram +ve rods
Corneybacteria
Mycobacteria
Listeria
Bacillus
Nocardia
List gram +ve anaerobes
Clostridium
Lactobacillus
Actinomyces
Propionibacterium
List positive gram -ve bacteria
Neisseria meningitidis
Neisseria gonorrhoea
Haemophilia influenza
E. coli
Klebsiella
Pseudomonas aeruginosa
Moraxella catarrhalis
List 5 causes of atypical pneumonia
Legionella pneumophilia
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Q fever
Outline Methicillin-Resistant Staphylococcus Aureus (MRSA)
Staph aureus bacteria resistant to beta-lactam ABs (eg: Penicillin, cephalosporin, carbapenems)
Hard to treat
Eradication of MRSA on skin- Chlorhexidine
ABs used to treat- Doxycycline, clindamycin, vancomycin, teicoplanin, linezolid
Outline Extended-Spectrum Beta-Lactamase Bacteria
Developed resistance to beta-lactam ABs (penicillins, cephalosporins, carbapenems)
Produce beta-lactamase enzymes that destroy beta-lactam ring on AB
ESBLs tend to be E. coli or Klebsiella and cause UTIs
Can cause other type of infections such as pneumonia and septicaemia
Usual treatment:
Nitrofurantoin
Fosfomycin
Carbapenems
