Clinical Infections
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Clinical Reference Only. This material is intended as a study and clinical reference tool for paramedic students and practitioners. Always follow your service's clinical practice guidelines and consult senior clinical staff for patient care decisions.
Classification of Infectious Agents
Bacteria
Single-celled prokaryotes lacking membrane-bound organelles. Structural differences from human cells allow selective targeting with antimicrobials.
- ●Classified by morphology (cocci, bacilli, spirochetes)
- ●Cell wall composition determines Gram stain result
- ●Can produce exotoxins (secreted) or endotoxins (cell wall component)
- ●Can form spores to survive hostile environments
Structure
- ●Thick outer peptidoglycan layer
- ●No outer lipid membrane
- ●Retains crystal violet stain (purple)
Key Pathogens
- Staphylococcus aureus (inc. MRSA)
- Streptococcus pyogenes (Group A Strep)
- Streptococcus pneumoniae
- Clostridium tetani / botulinum
- Enterococcus spp.
Structure
- ●Thin peptidoglycan layer
- ●Outer lipid membrane (contains LPS/endotoxin)
- ●Does not retain crystal violet (pink)
Key Pathogens
- Escherichia coli
- Pseudomonas aeruginosa
- Neisseria meningitidis / gonorrhoeae
- Klebsiella pneumoniae
- Haemophilus influenzae
Viruses
Non-living infectious agents. Cannot replicate independently — hijack host cell machinery. Classified by nucleic acid type (RNA or DNA) and virion shape.
- ●Outer envelope comprised of lipids (enveloped) or protein coat (non-enveloped)
- ●Virion = released viral particle capable of infecting new host
- ●Highly selective for cell type (tropism)
- ●No cell wall — most antibiotics ineffective
- ●Antivirals target specific viral processes (e.g. neuraminidase inhibitors for influenza)
- ●Can cause lytic, latent or persistent infections
Fungi
Eukaryotic organisms requiring organic carbon for growth. Include single-celled yeasts and multicellular filamentous moulds.
- ●Yeasts replicate asexually via binary fission
- ●Moulds grow via extending filaments (hyphae) forming a mycelium
- ●Aerial hyphae produce spores — readily inhaled
- ●Common in immunocompromised patients (opportunistic)
- ●Target: ergosterol in fungal cell membrane (different to human cholesterol)
- ●Examples: Candida, Aspergillus, Tinea
Parasites
Protozoa
- ●Single-celled eukaryotes
- ●Infective stage = trophozoite
- ●Form cysts to resist hostile environments
- ●Examples: Plasmodium (malaria), Giardia
Helminths (Worms)
- ●Multicellular parasites
- ●Often require more than one host
- ●Classified as flatworms or roundworms
- ●Common in areas of poor sanitation
No Treatment Available
Prions are the most resistant known pathogens. Comprised of only protein — no nucleic acid. Host disease results from conformational change in brain proteins. No pharmacological treatment exists. Removal requires alkaline detergent cleaning plus extended steam sterilisation.
Stages of Infection
Incubation
Agent acclimatises to host and begins to replicate. Host is asymptomatic.
Prodromal
Agent replicates. Immune response activates. Non-specific symptoms — fever, malaise.
Acute
Peak replication. Specific symptoms manifest — cough, rash, lesions, localised pain.
Decline
Pathogen numbers reduce — immune response and medical intervention effective.
Convalescent
Continued resolution. Patient returns to normal function. Immunity may be established.
Chain of Infection — Interactive
Link 1
Infectious Agent
›
Link 2
Reservoir
›
Link 3
Portal of Exit
›
Link 4
Transmission
›
Link 5
Portal of Entry
›
Link 6
Susceptible Host
Infectious Agent
The pathogen causing disease: bacteria, viruses, fungi, parasites, or prions. Characteristics such as virulence, pathogenicity and antimicrobial resistance influence disease severity. Interruption: identify and target the agent with appropriate antimicrobial therapy based on microbiological culture where possible.
Key Pathogens
Staphylococcus aureus / MRSA
Presentations
- Skin/soft tissue infections
- Bacteraemia & sepsis
- Toxic shock syndrome
- Pneumonia
- Endocarditis
Risk Factors
- Skin breaks/wounds
- Indwelling devices
- Healthcare exposure
- Immunocompromise
- IVDU
Treatment
- MSSA: flucloxacillin
- MRSA: vancomycin
- Source control critical
- Blood cultures before antibiotics
Streptococcus pyogenes (Group A Strep)
Presentations
- Strep throat / pharyngitis
- Cellulitis / erysipelas
- Necrotising fasciitis
- Toxic shock syndrome
- Rheumatic fever (post-infection)
Mechanism
- Exotoxin production
- Immune cross-reactivity with heart tissue → rheumatic fever
- Streptolysins damage host cells
Treatment
- Penicillin (first-line)
- Amoxicillin for pharyngitis
- Surgery for NF
- Rheumatic fever: long-term penicillin prophylaxis
Escherichia coli & Gram-Negatives
Key Pathogens
- E. coli — UTI, sepsis
- Pseudomonas aeruginosa — burns, HAI
- Klebsiella — pneumonia, UTI
- Neisseria meningitidis — meningitis
Endotoxin (LPS)
- Component of outer membrane
- Released on cell lysis
- Triggers massive inflammation
- Signs often worsen after antibiotics (more lysis)
Treatment
- Cephalosporins / carbapenems
- Culture-guided therapy critical
- Rising resistance (ESBL, CRE)
Toxic Shock Syndrome (TSS)
Time-Critical Presentation
TSS is a potentially life-threatening condition caused by exotoxins (superantigens) produced by S. aureus or S. pyogenes. Exotoxins trigger massive, dysregulated T-cell activation — can cause rapid deterioration.
Classic Features
- ●High-grade fever (>38.9°C)
- ●Hypotension / shock
- ●Diffuse erythematous blanching rash (resembles sunburn)
- ●Desquamation (skin peeling 1–2 weeks later)
- ●Nausea, vomiting, diarrhoea
- ●Myalgia, disorientation
- ●Mucosal hyperaemia
Management Principles
- ●Aggressive IV fluid resuscitation
- ●Source control (remove tampon, drain abscess)
- ●Anti-staphylococcal antibiotics (vancomycin/clindamycin)
- ●Clindamycin added to inhibit toxin production
- ●Vasopressors for refractory hypotension
- ●ICU admission likely required
Infective Endocarditis
Infection and inflammation of the endocardium. Majority of patients have underlying cardiac conditions. Three critical pathogenic elements:
- 1Endocardial damage — usually from pre-existing cardiac condition or instrumentation
- 2Bacteraemia — blood-borne organisms (dental procedures, IV lines, IVDU) reach damaged surface
- 3Vegetation formation — organisms proliferate, forming infected fibrin-platelet vegetations on valves
Key Signs
New or changed cardiac murmur, Osler's nodes, Janeway lesions, splinter haemorrhages, fever, embolic events (stroke, pulmonary embolism). Significant rate of healthcare-acquired cases. Long-course IV antibiotics required; surgical valve replacement may be needed.
HIV / AIDS
Pathophysiology
HIV (Human Immunodeficiency Virus) infects CD4+ T-helper lymphocytes — the key coordinators of the immune response. Progressive depletion of CD4+ cells leads to immunocompromise and susceptibility to opportunistic infections.
Stage 1: Acute Infection
- Flu-like illness (seroconversion)
- Fever, rash, lymphadenopathy
- High viral load
- Occurs weeks after infection
- Often undiagnosed
Stage 2: Chronic Infection
- Asymptomatic (years)
- Ongoing viral replication
- Gradual CD4 decline
- Person remains infectious
- ART commenced here ideally
Stage 3: AIDS
- CD4 count <200 cells/µL
- AIDS-defining illnesses
- Systemic fungal infections
- Tuberculosis reactivation
- Kaposi sarcoma, PCP
Management Overview
- ●Antiretroviral therapy (ART) — Reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors
- ●ART does not cure HIV but suppresses viral load to undetectable
- ●Undetectable = Untransmittable (U=U)
- ●Pre-exposure prophylaxis (PrEP) for high-risk individuals
- ●Post-exposure prophylaxis (PEP) within 72 hours of exposure
- ●Standard precautions protect against transmission
Influenza
Pathophysiology & Transmission
- ●RNA virus — Influenza A and B most clinically significant
- ●Droplet transmission (coughing, sneezing)
- ●Incubation 1–4 days, infectious 1 day before symptoms
- ●Antigenic drift (minor mutation) — annual vaccine variation
- ●Antigenic shift (major reassortment) — pandemic potential
Clinical Features
- ●Abrupt onset fever, rigors
- ●Severe myalgia and headache
- ●Dry cough, sore throat, rhinorrhoea
- ●Complications: pneumonia, encephalitis
- ●High-risk: elderly, immunocompromised, pregnant, chronic disease
Treatment
Neuraminidase inhibitors (oseltamivir/Tamiflu, zanamivir) reduce duration and severity if started within 48 hours of symptom onset. Most effective in high-risk groups. Annual vaccination remains the most effective preventive measure.
Herpesvirus Family
| Virus | Primary Infection | Latency Site | Reactivation Triggers | Treatment |
|---|---|---|---|---|
| HSV-1 | Cold sores, oral ulcers | Trigeminal ganglion | Stress, fever, UV light | Aciclovir topical/oral |
| HSV-2 | Genital herpes, lesions | Sacral ganglia | Stress, immunosuppression | Aciclovir, valaciclovir |
| VZV | Varicella (chickenpox) | Dorsal root ganglia | Immunocompromise, age | Aciclovir; vaccine available |
| EBV | Glandular fever (mono) | B lymphocytes | Immunocompromise | Supportive; avoid contact sports |
| CMV | Mild flu-like illness | Monocytes/macrophages | Immunocompromise (transplant) | Ganciclovir IV |
COVID-19 & SARS-CoV-2
Key Features
- ●RNA coronavirus — binds ACE2 receptor (respiratory, cardiac, renal)
- ●Droplet and airborne transmission
- ●Wide clinical spectrum: asymptomatic to critical
- ●Classic: fever, cough, anosmia/ageusia
- ●Severe: pneumonia, ARDS, multi-organ failure, coagulopathy
High-Risk Groups & Management
- ●Elderly, obese, immunocompromised, diabetes, cardiovascular disease
- ●Supportive: oxygen, prone positioning, dexamethasone (severe)
- ●Antivirals (nirmatrelvir/ritonavir) for high-risk early in illness
- ●Vaccination highly protective against severe disease
Common Fungal Infections
| Infection | Organism | Presentation | Population | Treatment |
|---|---|---|---|---|
| Candidiasis | Candida albicans | White plaques (oral thrush), genital, systemic | Immunocompromised, antibiotic use, diabetes | Azoles (fluconazole); echinocandins for systemic |
| Tinea (Ringworm) | Dermatophytes | Dry, itchy, raised red rings; affects skin/nails/scalp | Any; close contact, shared facilities | Topical azoles; oral terbinafine for nails |
| Tinea Versicolor | Malassezia | Cosmetic pigment disruption, hypo/hyperpigmented patches | Young adults, warm/humid climates | Topical selenium sulfide or azoles |
| Aspergillosis | Aspergillus | Pulmonary infiltrates, haemoptysis, sinusitis | Severely immunocompromised (transplant, haematological malignancy) | Voriconazole (first-line) |
| Cryptococcus | Cryptococcus neoformans | Meningitis, pneumonia | HIV/AIDS (CD4 <100) | Amphotericin B + flucytosine |
Malaria
Life-Threatening — Notifiable Disease
Malaria is a protozoal infection caused by the Plasmodium genus. P. falciparum causes the most severe disease with risk of cerebral malaria, severe anaemia, and organ failure. Consider in any febrile patient returning from endemic regions.
Life Cycle & Transmission
- ●Transmitted via female Anopheles mosquito bite
- ●Sporozoites → liver (asymptomatic maturation)
- ●Merozoites → RBC invasion → RBC lysis (cyclic fever)
- ●Gametocytes taken up by mosquito to complete cycle
Clinical Features & Management
- ●Cyclical fever, rigors, sweating (48/72 hr cycles)
- ●Severe anaemia, splenomegaly, jaundice
- ●P. falciparum: cerebral malaria, ARDS, renal failure
- ●Artemisinin combination therapy (ACT) — first-line
- ●IV artesunate for severe malaria
- ●Prevention: bed nets, repellent, chemoprophylaxis
Definition (Sepsis-3)
Sepsis = Infection + Organ Dysfunction. Organ dysfunction is identified by an increase in 2 or more SOFA points. It is not simply an excessive inflammatory response — it is a dysregulated response that impairs normal body functioning, regardless of whether inflammation is excessive or not.
Severity Escalation
Pathophysiology
Circulatory Compromise Cascade
1
Systemic inflammation → Nitric oxide (NO) released throughout body
2
NO → Vasodilation — reduces venous return (preload) → ↓ stroke volume & cardiac output. Directly impairs myocardial contractility.
3
↑ Vessel permeability → fluid leaks from intravascular space → reduced circulating volume
4
Coagulopathy — ↑ procoagulant factors, microthrombi in small vessels → impaired capillary perfusion
5
↓ RBC flexibility → impaired oxygen delivery → organ dysfunction → failure if untreated
Common Sources
- ●Lower respiratory tract (pneumonia) — most common
- ●Urinary tract — most common in elderly
- ●Abdominal (bowel perforation, cholangitis)
- ●Skin / soft tissue (cellulitis, NF)
- ●No source found in up to one-third of cases
Risk Factors
- ●Age >65 or very young (<1 year)
- ●Immunocompromised (malignancy, steroids, HIV)
- ●Recent surgery or invasive procedures
- ●Indwelling catheters / IV lines
- ●Diabetes mellitus, chronic renal failure
- ●Alcohol/drug use, pregnancy
qSOFA Score — Interactive Calculator
qSOFA Guidance
Quick SOFA is a rapid bedside screening tool. A score of 2+ indicates need for further investigation for potential sepsis and greater risk of adverse outcomes. qSOFA+ = very likely sepsis. qSOFA− does not rule out sepsis — clinical judgement always applies.
Tachypnoea
Respiratory rate >22 breaths/min (reflects respiratory organ dysfunction)
Altered Mental Status
Any change in conscious level or confusion (reflects CNS dysfunction)
Hypotension
Systolic BP <100 mmHg (reflects cardiovascular dysfunction)
0
/ 3 — Select criteria above
Tick each criterion present in your patient to calculate the qSOFA score.
SOFA Score — Organ Systems
| System | Parameter | Score 1 | Score 2 | Score 3–4 |
|---|---|---|---|---|
| Respiratory | PaO2/FiO2 ratio | <400 | <300 | <200 / <100 (ventilated) |
| Cardiovascular | MAP / vasopressors | MAP <70 | Dopamine <5 | Higher dose vasopressors |
| Renal | Creatinine / UO | 110–170 µmol/L | 171–299 | >300 / UO <0.5mL/kg/hr |
| Liver | Bilirubin | 20–32 µmol/L | 33–101 | >102 / >204 |
| CNS | GCS | 13–14 | 10–12 | <10 / <6 |
| Coagulation | Platelets (×10³/µL) | <150 | <100 | <50 / <20 |
SOFA Score Mortality
Score 2+: organ dysfunction present = sepsis. Score 10+: approximately 50% mortality. Score 14+: approximately 95% mortality. A change of 2+ from baseline confirms organ dysfunction.
Septic Shock Definition
Sepsis + vasopressors required to maintain MAP >65 mmHg + serum lactate >2 mmol/L (despite adequate fluid resuscitation). Practical: hypotension unresponsive to reasonable fluid administration. Mortality 20–24%.
Sepsis 6 Bundle
Aim to complete all six actions within one hour of sepsis recognition.
Take (Measure & Monitor)
- Blood cultures x2 (before antibiotics if possible — do not delay treatment)
- Blood tests — lactate level, FBC, CRP, UEC, LFTs, coagulation
- Urine output measurement (urinary catheter provides most reliable measurement)
Lactate >2 mmol/L indicates tissue hypoperfusion even if BP appears normal
Give (Administer)
- High-flow oxygen (target SpO2 >94%; caution with COPD)
- IV fluid resuscitation — crystalloid 30mL/kg bolus (restores preload)
- Empirical IV antibiotics (broad-spectrum; within 1 hour of recognition)
Vasopressors and inotropes if BP not maintained with IV fluids
Pre-Hospital Management
Transport anyone with suspected infection and abnormal vital signs. Pre-notify receiving hospital for suspected septic shock. Initiate oxygen, IV access and fluid resuscitation en route. Early antibiotic administration is the most time-critical intervention — each hour of delay increases mortality.
Urinary Tract Infections
Pathophysiology & Risk
- ●Bacteria most common cause — predominantly E. coli (opportunistic translocation from GI tract)
- ●Higher risk in females: short urethra, proximity of GU and GI tract openings
- ●Innate defences: acidic urine pH, voiding (shearing force), endogenous microbiota
- ●Healthcare-acquired UTIs: much harder to treat due to antimicrobial resistance
Risk Factors
- ●Indwelling urinary catheters (CAUTI)
- ●Anatomical abnormalities / urological obstruction
- ●Sexual intercourse (females)
- ●Pregnancy
- ●Diabetes mellitus
- ●Incomplete bladder emptying
Lower UTI (Cystitis)
- Infection confined to bladder/urethra
- Dysuria (painful urination)
- Urinary frequency and urgency
- Suprapubic pain or pressure
- Haematuria (blood in urine)
- No systemic features
Upper UTI (Pyelonephritis)
- Infection of renal pelvis and parenchyma
- Flank / loin pain (often severe)
- Fever >38°C, rigors
- Nausea and vomiting
- May have lower UTI symptoms
- Risk of sepsis — IV antibiotics often required
Red Flags — Seek Urgent Assessment
Signs of sepsis (tachycardia, tachypnoea, hypotension, altered consciousness) | Pyelonephritis in pregnancy | Obstruction with infection | Frank haematuria | Urethral or pelvic trauma | Failure to respond to outpatient treatment.
Diagnosis
- ●Mid-stream urine (MSU) for UTI — avoids contamination from colonised distal urethra
- ●Dipstick: leucocytes, nitrites, blood, protein
- ●MC&S (microscopy, culture & sensitivity) guides antibiotic choice
- ●Blood cultures if signs of sepsis
Management
- ●Increased oral fluid intake
- ●Analgesia (paracetamol, NSAIDs)
- ●Antibiotics based on culture sensitivity and site of infection
- ●Uncomplicated lower UTI: trimethoprim or cefalexin (oral)
- ●Pyelonephritis / sepsis: IV cephalosporins or gentamicin
- ●Prevention: post-coital voiding, reduce catheter time in situ
Sexually Transmitted Infections (STIs)
Key Principles
Humans are the natural reservoir for most STI pathogens. Many STIs are asymptomatic, increasing transmission risk. Effective treatment requires microbiological identification. Contact tracing limits spread and prevents reinfection of the index patient.
| Infection | Organism | Presentation | Complications | Treatment |
|---|---|---|---|---|
| Chlamydia | Chlamydia trachomatis | Often asymptomatic; discharge, dysuria, pelvic pain | Pelvic inflammatory disease (PID), infertility, neonatal infection | Azithromycin or doxycycline |
| Gonorrhoea | Neisseria gonorrhoeae | 50% asymptomatic; purulent discharge, dysuria | PID, epididymitis, disseminated gonococcal infection | Ceftriaxone IM (rising resistance) |
| Syphilis | Treponema pallidum | Primary: painless chancre. Secondary: rash, fever. Tertiary: cardiovascular/neurological | Neurosyphilis, cardiovascular syphilis, congenital syphilis | Penicillin (all stages) |
| Genital Herpes | HSV-2 (mainly) | Painful genital ulcers/vesicles, dysuria; recurrent | Neonatal herpes if active during delivery | Aciclovir (no cure; reduces episodes) |
| HPV | Human papillomavirus | Genital warts; often asymptomatic (high-risk strains) | Cervical, oropharyngeal, anorectal cancers (high-risk strains) | No antiviral; wart treatment, vaccination |
| HIV | HIV-1 / HIV-2 retrovirus | Acute: flu-like. Chronic: asymptomatic. AIDS: OIs | AIDS, opportunistic infections, malignancies | Antiretroviral therapy (ART) — lifelong |
Indigenous Population Risk
Indigenous populations carry a disproportionately high risk for STIs in Australia. High rates of asymptomatic chlamydia and gonorrhoea. Culturally safe, non-judgemental care and targeted screening programs are essential. Maternal STI infection can cause devastating consequences for newborns including blindness and stillbirth.
Pneumonia
Classification
By Organism
- ●Bacterial (most common)
- ●Viral (influenza, COVID-19, RSV)
- ●Fungal (immunocompromised)
- ●Aspiration (mixed organisms)
Community Acquired (CAP)
- ●Develops in community setting
- ●Common: S. pneumoniae, Mycoplasma, H. influenzae
- ●Most respond to oral antibiotics
Hospital Acquired (HAP)
- ●Onset >48 hours after admission
- ●Gram-negative and resistant organisms
- ●Higher mortality, broader antibiotics
Transmission Routes
- ●Inhalation of aerosols or respiratory droplets
- ●Spread from upper respiratory tract infection
- ●Aspiration of oropharyngeal secretions
- ●Haematogenous spread (less common)
Clinical Presentation
- ●Cough ± productive (purulent or rust-coloured sputum)
- ●Breathlessness, pleuritic chest pain
- ●Fever, rigors, sweating
- ●Myalgia, malaise, reduced appetite
- ●Auscultation: crackles (crepitations), bronchial breath sounds, reduced air entry
CURB-65 Severity Score — Interactive
Community-acquired pneumonia severity assessment. One point for each criterion present.
✓
C
Confusion
New confusion (abbreviated mental test score ≤8 or acute confusion)
✓
U
Urea
Blood urea >7 mmol/L (renal dysfunction)
✓
R
Respiratory Rate
≥30 breaths per minute
✓
B
Blood Pressure
Systolic BP <90 mmHg OR diastolic BP ≤60 mmHg
✓
65
Age ≥65 years
Age is an independent mortality risk factor
0
/ 5 — Select criteria above
Click each criterion present to calculate the CURB-65 severity score.
Tuberculosis (TB)
Airborne Precautions Required
TB requires standard precautions plus airborne transmission-based precautions (N95 respirator, negative pressure room). Highly infectious — transmitted by aerosols during coughing and sneezing. Notifiable disease in Australia.
Primary TB
- Develops in immunologically naive individuals
- Often asymptomatic or mild respiratory illness
- Ghon complex forms (calcified primary focus)
- Most cases contained by immune response
- Latent TB: no symptoms, not infectious
Secondary (Reactivation) TB
- Arises in previously sensitised hosts
- Reactivation of latent infection (immunosuppression, HIV, malnutrition)
- Classic: productive cough, haemoptysis, night sweats, weight loss
- Cavitating lesions on chest X-ray
- Treatment: RIPE regimen (6 months)
Bacterial Skin Infections
| Infection | Depth | Causative Organism | Features | Management |
|---|---|---|---|---|
| Impetigo | Superficial epidermis | S. aureus, S. pyogenes | Highly contagious; bullous (fluid-filled) or non-bullous (honey-coloured crust); insect bites/eczema predispose | Topical mupirocin; oral flucloxacillin for widespread |
| Folliculitis | Hair follicle | S. aureus | Pustules around hair follicles; shaving, friction predispose | Usually self-limiting; topical antibiotics |
| Erysipelas | Dermis (superficial) | S. pyogenes | Bright red, well-demarcated erythematous rash; systemic infection — fever, chills | Penicillin; hospitalisation often required |
| Cellulitis | Deep dermis + subcutaneous | S. aureus, S. pyogenes | Poorly demarcated erythema, warmth, oedema, tenderness; systemic features; risk with diabetes/immunocompromise | Oral flucloxacillin; IV if systemic, facial or rapidly spreading |
Necrotising Fasciitis
Surgical Emergency — Time-Critical
Necrotising fasciitis is a life-threatening infection involving the subcutaneous tissue and deep fascia. Rapid tissue destruction is caused by bacterial toxins (commonly polymicrobial or Group A Strep). Early recognition and emergency surgical debridement is critical — delay significantly increases mortality.
Warning Signs
- ●Pain disproportionate to visible wound
- ●Rapid spread of erythema beyond initial margins
- ●Skin becomes dusky, blue-grey, then necrotic
- ●Crepitus (gas in tissues) — pathognomonic
- ●Severe systemic sepsis
- ●Anaesthesia of affected skin (nerve destruction)
Management
- ●Immediate hospital transport — pre-notify surgical team
- ●IV access, fluid resuscitation, high-flow oxygen
- ●Blood cultures + broad-spectrum IV antibiotics
- ●Emergency surgical debridement (definitive treatment)
- ●ICU admission post-operatively
Fungal & Parasitic Skin Infections
Tinea (Ringworm)
- Infection of keratinised skin layers
- Keratin is the nutrient source
- Dry, itchy, raised red margins with central clearing
- Tinea pedis (athlete's foot), capitis, unguium (nails)
- Topical or oral antifungals
Candidiasis
- Warm, moist, macerated areas
- Red skin with white edges (satellite lesions)
- Intertrigo, nappy rash, oral thrush
- Risk: diabetes, antibiotics, obesity
- Topical clotrimazole or nystatin
Scabies / Pediculosis
- Scabies: mite burrows into epidermis — intensely pruritic, worse at night
- Burrow tracks between fingers, wrists, genitalia
- Pediculosis: lice of head, body, pubic area
- Highly contagious — contact precautions
- Permethrin cream / ivermectin
Wound Infections
Disruption to skin integrity allows pathogen entry. The inflammatory response to wounding creates serous exudate and tissue damage. Biofilm formation is a hallmark of chronic wounds and significantly impairs antimicrobial penetration.
Wound Infection Spectrum
- ●Colonisation — organisms present without inflammatory response or tissue damage
- ●Infection — organisms replicate, immune response activated, tissue damage occurs
- ●Systemic infection — bacteria enter bloodstream, sepsis risk
Burn Wounds
- ●Significant tissue damage makes burns highly susceptible to infection
- ●Loss of skin barrier function
- ●Infections often healthcare-associated
- ●Strict aseptic technique, wound dressings critical
Meningitis
Classic Triad — Time-Critical
Bacterial meningitis can be fatal within hours. Classic triad: fever + neck stiffness (meningism) + photophobia. Additional: headache, altered consciousness, vomiting, non-blanching petechial/purpuric rash (meningococcal — seek emergency care immediately). Not all features need to be present — if suspected, treat empirically.
Bacterial Meningitis
- Less common but more dangerous than viral
- Key organisms: N. meningitidis, S. pneumoniae, Listeria (neonates/elderly)
- Rapid onset — hours
- CSF: cloudy, high WCC (neutrophils), low glucose, high protein
- Treatment: IV ceftriaxone (empirical) + dexamethasone
- Contact precautions; droplet precautions for meningococcal
- Vaccine-preventable (meningococcal B and ACWY)
Viral Meningitis
- More common — usually less severe
- Key organisms: enteroviruses, HSV, mumps
- Gradual onset — days
- CSF: clear, elevated lymphocytes, normal/low glucose, mildly raised protein
- Treatment: supportive; aciclovir for HSV meningitis
- Usually self-limiting in immunocompetent hosts
Encephalitis
Inflammation and infection of brain tissue itself — less common than meningitis but causes extensive necrosis of brain tissue. Clinical features overlap with meningitis but altered consciousness and focal neurological deficits are more prominent.
- ●Altered consciousness (confusion, stupor, coma)
- ●Focal neurological deficits
- ●Seizures (often the presenting feature)
- ●Personality and behavioural changes
- ●Most common cause: HSV encephalitis (temporal lobe)
- ●Treatment: IV aciclovir (start empirically — do not wait for CSF)
- ●MRI brain + EEG + CSF analysis
- ●Rabies also causes viral encephalitis — vaccine preventable
Other Serious CNS Infections
| Infection | Organism | Mechanism | Key Features | Treatment / Prevention |
|---|---|---|---|---|
| Tetanus | Clostridium tetani | Spores germinate in deep wounds (anaerobic). Neurotoxin (tetanospasmin) blocks inhibitory neurotransmitters → sustained muscle contraction | Lockjaw (trismus), opisthotonus, risus sardonicus, severe spasms, autonomic instability | Wound debridement, tetanus immunoglobulin, metronidazole, muscle relaxants. Vaccine-preventable. |
| Botulism | Clostridium botulinum | Toxin targets the peripheral nervous system at the neuromuscular junction — blocks acetylcholine release → flaccid paralysis | Descending flaccid paralysis, diplopia, dysarthria, dysphagia, respiratory failure | Antitoxin, mechanical ventilation if respiratory compromise. Food-borne, wound, or infant types. |
| Rabies | Rabies virus (lyssavirus) | Replicates in muscle, travels retrogradely along peripheral nerves to brain → encephalitis | Initially flu-like, then agitation, hydrophobia, aerophobia, paralysis, coma — almost universally fatal once symptomatic | Post-exposure prophylaxis (rabies immunoglobulin + vaccine) must be given before symptoms. Vaccine-preventable. |
| Polio | Poliovirus | Faecal-oral transmission. CNS invasion in <1% of cases — destroys anterior horn motor neurons | Majority asymptomatic. Paralytic polio: acute asymmetric flaccid paralysis — may cause permanent disability | No antiviral. Vaccine-preventable (OPV/IPV). Near-eradicated globally. |
| Prion Diseases | Prions (misfolded proteins) | Conformational change in normal brain prion protein (PrP) → progressive neurodegeneration (spongiform encephalopathy) | Rapidly progressive dementia, ataxia, myoclonus, psychiatric symptoms. Universally fatal. | No treatment available. Most resistant known pathogen. Requires alkaline detergent + extended steam sterilisation for decontamination. |
Antibacterial Drug Classes
| Mechanism | Drug Class | Examples | Spectrum | Key Notes |
|---|---|---|---|---|
| Cell Wall Synthesis Inhibition | Beta-lactams — Penicillins | Amoxicillin, flucloxacillin, piperacillin | Gram positive mainly; some broad | Allergy common; bactericidal |
| Beta-lactams — Cephalosporins | Cefalexin (1st), ceftriaxone (3rd) | Broad spectrum; varies by generation | Useful for severe infections and meningitis | |
| Beta-lactams — Carbapenems | Meropenem, ertapenem | Very broad — reserve for resistant organisms | Last-resort; protect from overuse | |
| Glycopeptides | Vancomycin, teicoplanin | Gram positive (inc. MRSA) | IV only; renal monitoring required | |
| Protein Synthesis Inhibition | Macrolides | Azithromycin, clarithromycin | Atypical organisms, Gram positive | Useful for pneumonia, STIs; bacteriostatic |
| Tetracyclines | Doxycycline | Broad; atypicals, STIs | Avoid in pregnancy and children under 12 | |
| Aminoglycosides | Gentamicin, tobramycin | Gram negative | Oto/nephrotoxic; monitor levels | |
| Cell Membrane Disruption | Polymyxins | Colistin | Gram negative MDR organisms | Last-resort; nephrotoxic |
| DNA / Metabolite Inhibition | Fluoroquinolones | Ciprofloxacin, norfloxacin | Broad spectrum; UTI, GI, respiratory | Avoid in children; tendon rupture risk |
| Nitroimidazoles | Metronidazole | Anaerobes, protozoa | Inhibits DNA replication; abdominal infections |
Other Antimicrobial Classes
Antifungals
- Azoles (fluconazole, voriconazole) — inhibit ergosterol synthesis
- Polyenes (amphotericin B) — bind ergosterol, disrupt membrane
- Echinocandins (caspofungin) — inhibit cell wall glucan synthesis
- Target ergosterol (not human cholesterol) — selective toxicity
Antivirals
- Anti-HIV (ART) — reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors
- Influenza — neuraminidase inhibitors (oseltamivir)
- Herpesviruses — aciclovir, valaciclovir (inhibit DNA replication)
- COVID-19 — nirmatrelvir/ritonavir (protease inhibitor)
Antiparasitics
- Antimalarials — artemisinin, chloroquine (inhibit nucleic acid/protein synthesis)
- Antihelminthics — albendazole (inhibit tubulin polymerisation)
- Antiprotozoals — metronidazole (inhibit DNA replication)
- Ectoparasiticides — permethrin, ivermectin
Antimicrobial Stewardship Principles
Antimicrobial stewardship is the safe and effective prescription of antimicrobial agents to improve patient outcomes, reduce adverse effects (including resistance emergence), and ensure cost-effective therapy.
- ●Culture before treatment — collect samples first where possible
- ●Evidence-based indications — treat only where antimicrobials improve outcomes
- ●Narrowest spectrum — minimise collateral damage to normal flora
- ●Appropriate dosage — must achieve therapeutic levels at site of infection
- ●Minimise duration — shorter courses reduce resistance development
- ●Monotherapy preferred in most cases
- ●Resistance arises from overuse, underuse and misuse — including incomplete courses
- ●Resistance spreads via transformation, conjugation (plasmid transfer), and transduction (bacteriophage)
Antimicrobial Resistance — Global Threat
Antimicrobial resistance arises from random mutations and horizontal gene transfer. High-priority resistant organisms include MRSA, VRE, ESBL-producing Enterobacteriaceae, and carbapenem-resistant organisms (CROs). Strict adherence to stewardship and infection control principles is essential in clinical practice.