Infectious Diseases Flashcards
Diarrhoea
Gastro-enteritis
Dysentery
Subjective - Fluidity and frequency
Objective - >= 3 loose stools/day + features
Obvious - Large bowel inflammation, bloody stools
Bristol Stool Chart Types
1) Separate hard lumps (nuts) - Hard to pass
2) Sausage-shaped but lumpy
3) Sausage but cracks on the surface
4) Sausage/Snake - Smooth and Soft
5) Soft blobs with clear-cut edges
6) Fluffy pieces with ragged edges, mushy stool
7) Watery, no solid pieces
Epidemiology of gastro-enteritis
Contamination of food e.g. chicken + campylobacter (commonest bacterial + foodborne pathogen but viruses are the commonest cause - norovirus)
Isolated cases rather than outbreaks (C. jejuni/ C. coli)
Poor storage of produce
E.g. Bacterial proliferation at room temperature
Travel-related infections e.g. Salmonella (most hospital admissions)
Person-to-person spread e.g. Norovirus
Defences against enteric infections
Hygiene
Stomach acidity - antacids and infection
normal Gut Flora - Cl. difficile diarrhoea
Immunity - HIV - Salmonella
Diarrhoeal illness
Non-inflammatory / Secretory
e.g. Cholera - Secretory toxin-mediated - Vibrio.cholerae
Enterotoxigenic E. coli (travellers’ diarrhoea)
Increases cAMP levels and Cl secretion
Frequent watery stools with LITTLE Abdominal Pain
- Fluid and electrolyte losses
Hyponatraemia due to Na+ loss with fluid replacement by hypotonic solutions
Hypokalaemia due to K loss in stool
Rehydration mainstay of therapy
Inflammatory
Mixed picture
e.g. Shigella (Bacterial) / Amoebic dysentery
Inflammatory toxin damage and mucosal destruction Pain and Fever
Rehydration + Antimicrobials may be appropriate
e.g. C. difficile
Assessing Diarrhoeal illness
Symptoms and their duration
>2/52 unlikely to be infective gastro-enteritis
Risk of food poisoning - Dietary, Contact, Travel history
Assess hydration - Postural BP, skin Turgor, Pulse
Features of inflammation (SIRS) - Fever, raised WCC
Assessing Diarrhoeal illness in Children
Sunken Eyes, No tears
Sunken Fontanelle
Sunken Abdomen
Skin Turgor decreased
Dry Mouth / Tongue
Diarrhoeal illness Investigations
Stool culture
Blood culture
Bacterial culture (selective and enrichment methods)
polymerase chain reaction (PCR)
antigen-detecting enzyme immunoassays (EIAs) immunofluorescence assays (IFAs)
microscopy, serology, and viral culture
Renal function
Blood count - Neutrophilia, Haemolysis
Abdominal X-Ray if abdomen distended, tender
Diarrhoeal illness
*Differential diagnosis
IBD, Carcinoma
Spurious diarrhoea - Secondary to constipation
SEPSIS outside gut - Diarrhoea + Fever
- Lack of Abdo pain/tenderness; against gastroenteritis
- No blood/mucus in stools
Gastroenteritis Treatment
Oral rehydration with salt (Na)/sugar (glucose) solution
IV saline
Campylobacter gastroenteritis
Up to *7 days incubation so dietary history unreliable
Stools negative within 6 weeks
Abdominal pain can be severe
<1% invasive
Post-infection sequelae - Guillain-Barre syndrome, Reactive arthritis
Salmonella gastroenteritis
Salmonella enterica
Symptom onset usually <48 hrs after exposure
Diarrhoea usually lasts <10 days
<5% positive blood cultures
20% patients still have positive stools at 20/52
Prolonged carriage may be associated with gallstones
Post-infectious irritable bowel is common
Screened out as lactose non-fermenters
Then antigen and biochemical tests
Salmonella enteritidis and Salmonella typhimurium
> 50% of these were imported from abroad in 2010
S. typhi and S. paratyphi
Cause enteric fever (typhoid and paratyphoid)
and NOT gastro-enteritis
E.Coli 0157
From contaminated meat or person-to-person spread
Frequent bloody stools
Produces (verocyto-)toxin
E. coli O157 stays in the gut but the toxin gets into the blood - can cause HUS
Treatment supportive – antibiotics NOT indicated
Hemolytic-uraemic syndrome (HUS)
Toxin binds to globotriaosylceramide
Platelet activation stimulated
Micro-angiopathy results
Attach to endothelial, glomerular, tubule, mesangial cells
Characterised by renal failure, haemolytic anaemia and thrombocytopenia.
Abx Treatment Indicated in gastroenteritis for?
Immunocompromised Severe sepsis or invasive infection Valvular heart disease Chronic illness Diabetes
Clostridium difficile diarrhoea
Patient usually gives history of previous antibiotic treatment – the “4 C antibiotics”
Severity ranges from mild diarrhoea to severe colitis
C. Diff produces enterotoxin (A) and
cytotoxin (B) (inflammatory)
Clostridium difficile Treatment
Metronidazole
oral Vancomycin
Fidaxomicin (new and expensive)
Stool transplants
Surgery may be required
Clostridium difficile prevention
Reduction in broad spectrum antibiotic prescribing
Avoid 4 Cs – Cephalosporins, Co-amoxiclav, Clindamycin, Clarithromycin
Antimicrobial Management Team (AMT) and local antibiotic policy
Isolate symptomatic patients
Wash hands between patients
Parasitology
Protozoa and helminths
Diagnosis generally by microscopy
Send stool with request “parasites, cysts and ova please” or P, C and O
Sepsis
Acute change in total SOFA score >2 which reflects an overall mortality risk of approximately 10% in hospital
Sequential (Sepsis-Related) Organ Failure Assessment Score
Systemic illness caused by microbial invasion of normally sterile parts of the body
Life-threatening organ dysfunction caused by dysregulated host response to infection
SIRS
Sepsis
Severe Sepsis
Septic Shock
> =2 of fever >38.0°C or hypothermia <36.0°C,
tachycardia >90 beats/minute,
tachypnoea >20 breaths/minute,
leucocytosis >12109/l or leucopoenia <4109/l
SIRS + Infection
Sepsis + End Organ Damage
+ Hypotension
qSOFA
Promptly identifies patients with suspected infection who are likely to have a prolonged ICU stay / die in hospital
Hypotension (Systolic BP<100mmHg)
Altered Mental Status
Tachypnoea RR >20/min
SEPSIS 6
The Sepsis Six is the name given to a bundle of medical therapies designed to reduce mortality in patients with sepsis.
High Flow Oxygen Blood Cultures IV Abx Fluid challenge (rapid correction of hypovolaemia state) Lactate Measurement Urine Output measurement
Phases in the pathogenesis of sepsis
Release of bacterial toxins
Release of mediators
Effects of specific excessive mediators
Commonly released toxins:
Gram negative
Gram positive
Superantigens
Lipopolysaccharide (LPS)
Microbial-associated molecular pattern (MAMP)
- Lipoteichoic acid
- Muramyl dipeptides
Staphylococcal toxic shock syndrome toxin (TSST)
Streptococcal exotoxins
Transmission rootes and bacteria
Direct contact
e.g. Staphylococcus aureus, coliforms
Respiratory/Droplet
e.g. Neisseria meningitidis, Mycobacteria tuberculosis
Faecal-Oral
e.g. Clostridium difficile, Salmonella sp.
Penetrating Injury
e.g. Group A streptococcus, Bloodborne viruses
ANTIVIRAL THERAPY
Use ASAP and within 48hours of symptom onset
Neuraminidase Inhibitors:
ZANAMIVIR (RELENZA) - Inhaled
Adverse Effects: Rare – occasional bronchospasm
OSELTAMIVIR (TAMIFLU) - Oral
Adverse Effects: Renal dosing needed
Common – Nausea, vomiting, Abd pain, diarrhoea
Less Common – Headache, hallucinations, insomnia
PERAMIVIR (Alpivab®)
Intravenous infusion, for uncomplicated influenza
Favipiravir (Avigan®)
Viral RNA polymerase inhibitor
Beta-d-glucan
Tool to diagnose *invasive fungal infections
eg. *Candidiasis
High NPV (negative predictive value) mean patient almost certaintlhy doesnt have disease
Aspergillus Causes and Pathophysiology
Aspergilloma
- Fungal mass in lung
- Bronchiectasis/ Sarcoidosis
Allergic (Asthma, CF), COPD
Airborne conidia - Inhaled
Neutropenia - low level of neutrophils eg. leukaemia
Hyphal growth and dissemination
Angio-Invasive, Thrombosis, Haemorrhage
Aspergillus Ix if Neutropenic patient
CT Chest in high resolution shows
‘‘halo sign + air crescent sign’’
Blood Molecular Markers, PCR
Galactomannon (component of the cell wall of Aspergillus and is released during growth), NPVHigh?
Aspergillus Ix if non-Neutropenic patient
Sputum Culture
Bronchoalveolar lavage +/- biopsy
Aspergillus Specific IgE and IgG if chronic/allergic
Cryptococcus + Cryptococcosis Symptoms
Meningitis - HIV associated
Headache Confusion Increased ICP - coma Altered Behaviour Visual Disturbance