ACEM Primary
Bacterial and mycobacterial infections
Gram Positives
| Staph aureus S. epidermidis (opportunistic) S. saprophyticus (UTI) | Grape clusters Causes skin infections, osteomyelitis, abscess, sepsis Pneumonia, endocarditis, TSS Virulence factors: Polysaccharide capsule – allows attachment to prosthetic material (valve) and evades host phagocytes Lipase enzyme on surface – degrades lipids, allows abscess formation R for fibrinogen/ fibronectin/ vitronectin – bind host endothelium Protein A – bind FC portion Ig, prevents Ab mediated killing MRSA – resistant to beta lactam Superantigens: lead to TSS, food poisoning Bind to MHC or Tc R beta chain -> cytokine release -> septic shock like syndrome Toxins: a – pore forming, depolarises host cells b – sphingomyelinase (nerve sheath damage) d – detergent like properties g + leucocidin – lyse RBC and WBC Exfoliative toxin A and B – cleave desmoglein 1 -> detach epidermal cells (local = bullous impetigo or systemic = scalded skin syndrome with epidermal desquamation) Morphology: Locally destructive |
| Streptococci | Cocci in pairs or chains Types: Beta haemolytic, Lancefield A = S pyogenes Virulence factors: M protein cross reacts myocardial proteins C5a peptidase evades phagocytosis Exotoxin causing fever and rash Capsule resists phagocytes Causes: Rheumatic fever, pharyngitis, Scarlett fever (3-15 yo) Erysipelas, impetigo Necrotising fasciitis TSS Post streptococcal glomerulonephritis = 1-4 weeks post pharyngeal/ skin infection, T2/3 hypersensitivity: Immune deposits in glomeruli -> complement activation -> inflammation. Sx = malaise, fever, haematuria, red cell casts, proteinuria, oedema and HTN. Clinical course: Adults – worse prognosis = 50% continue to have reduced renal function, hypertension or proteinuria Children – excellent prognosis = recovery complete 6-8 weeks Beta haemolytic, Lancefield B = S agalactiae Commensal in female genital tract Causes chorioamnionitis, and neonatal sepsis/ meningitis Alpha haemolytic = S pneumoniae Has pneumolysin (cell damaging) Causes CAP, meningitis Viridans group – endocarditis S. mutans – dental caries Morphology: Minimal tissue destruction |
| Enterococci | Cause endocarditis, UTI Resistant to vancomycin Antiphagocytic capsule |
| Diphtheria | Corynebacterium diphtheriae = G+ve rod Spread by aerosols or skin exudate Virulence: Toxin blocks host cell protein synthesis Clinical course: Asymptomatic – skin lesions – life threatening Attach mucosa of respiratory tract -> proliferation, exotoxin causes necrosis and fibrinosuppurative exudate which forms membrane -> sloughs off, risk of asphyxiation Exotoxin: Hepatosplenomegaly, fatty change in myocardium, myofibronecrosis, polyneuritis, demyelination Focal necroses in adrenals, liver, kidneys Vaccination protects against toxoid only |
| Listeria | Listeria monocytogenes = G+ve intracellular bacillus Food borne infection Pregnancy – amnionitis, stillbirth, abortion, neonatal sepsis Immunosuppressed – meningitis Virulence: Internalin proteins – binds e cadherins on host epithelia -> endocytosis Listeriolysin – escape phagolysosome |
| Anthrax | Bacillus anthracis – box car shaped G+ve rod Farm/ wild animals and contaminated soil Biologic weapon 3 syndromes: Cutaneous 95% Painless, pruritic papule -> vesicle in 2 days -> oedema and LAD -> ruptures to form black eschar -> recovery Bacteremia is rare Inhalational: Spores inhaled, organisms carried to LN by phagocytes -> gemination -> toxin release: haemorrhagic mediastinitis, bacteremia, meningitis, death 1-2 days. GI Ingested undercooked meat of anthrax infected animal. Mortality >50% Virulence: Antiphagocytic capsule Toxins = A subunit (oedema/ lethal factor) + B (bind to cell membrane) àdysregulated cell growth |
| Nocardia | Aerobic G+ve “beaded” Soil Opportunistic infections in immunosuppressed N Asteroides – resp/ CNS N Brasiliensis – skin Nil granuloma |
Gram negatives
| Neisseria | G-ve diplococci Culture on chocolate agar Virulence: Antigenic variation (OPA/pili proteins) Types: N. meningitidis Meningitis <2 yo. Colonizer of oropharynx Spread via respiratory route 13 serotypes Antiphagocytic capsule. Patients who lack complement protein = high risk dissemination N gonorrheae STI = urethritis, cervicitis, PID Systemic = arthritis, rash Neonates = blindness, sepsis |
| Whooping Cough Bordetella pertussis | G-ve coccobacillus Dx with PCR Vaccination available Pathogenesis: Colonizes brush border of bronchial epithelium and invades macrophages -> endotoxin paralyses cilia -> laryngotracheobronchitis + bronchial mucosa erosion + copious mucopurulent exudate + lymphocytosis |
| Pseudomonas | Aerobic G-ve bacillus Opportunistic in setting of CF, burns, neutropenia Can cause corneal keratitis, endocarditis, osteomyelitis, external otitis Virulence: Pili (adherence proteins) Endotoxin Alginate – slimy biofilm protects from Ab/ complement/ Abx Exotoxin A inhibits protein synthesis Exoenzyme S dysregulates cell growth Phospholipase C lyses RBC, degrades surfactant Elastase degrades Ig and ECM Iron containing compounds toxic to endothelium Morphology: Necrotizing pneumonia (fleur-de-lis pattern = vasculitis) Skin (erythema gangrenosum) Bacteremia and DIC |
| Plague Yersinia pestis | G-ve intracellular bacterium Infected flea -> rodent -> human (aerosol) Proliferate in lymphoid tissue Virulence: Gene complex called YOP virulon -> inactivate actin polymerisation + kills host macrophages Pathogenesis: Bubonic Small pustule from flea bite – Lymphadenopathy (soft pulpy, plum coloured) – infarct and rupture through skin. Necrotizing pneumonia Septicaemia: systemic LAD, focal necrosis organs, DIC |
| Chancroid Haemophilus ducreyi | STI Difficult culture requires silver stain Pathogenesis: 4-7 days = tender, erythematous papule on external genitalia -> irregular ulcer, not indurated 1-2 weeks = LAD, ulcers erode and drain |
| Granuloma inguinale Klebsiella granulomatis | Donovanosis, STI Encapsulated coccobacillus Difficult culture requires Giemsa/ silver (Donovan bodies in macrophages) Pathogenesis: Raised papular lesion in genital mucosa -> ulcerates, indurated painless mass -> scarring + fissures causes lymphatic obstruction. Nil LAD |
Anaerobes
| Clostridia | G+ve anaerobic bacilli Dx culture or toxin assay C perfringens Cellulitis, myonecrosis of surgical wounds Requires tissue death to grow Gas gangrene = necrosis of muscle Release collagenase + hydraluronidase to degrade ECM + alpha toxin phospholipase degrades muscle cells. Oedema + enzymatic necrosis of muscle cells 1-3 days -> fluid exudate, bullous vesicles -> gas bubbles caused by bacterial fermentation appear within gangrenous tissues. C tetani Puncture wounds Neurotoxin “tetanospasmin” -> convulsive contractions of muscle, violent spastic paralysis C botulinum Canned foodsNeurotoxin -> blocks Ach release at NMJ -> flaccid paralysis + respiratory muscles C difficile Overgrowth in gut following Abx -> pseudomembranous colitis |
| Chlamydia trachomatis | G-ve obligate intracellular Elementary body taken up into phagolysosome -> reticular body becomes active and replicates. Urogenital Conjunctival Lymphogranuloma Venereum |
| Rickettsia | Vector borne (lice/ ticks) G-ve rods Stain poorly Typhus = rash, vasculitis -> haemorrhagic rash Scrub Typhus Spotted Fever = generalised haemorrhagic rash including palms/soles Ehrlichiosis – Affects vascular endothelium -> hypovolaemia, shock, oedema, APO, ARF |
Spirochetes
- Gram-negative bacteria
- Corkscrew shape
- Flagella
- Diagnosed on serology
- Syphilis Treponema pallidum
- Silver stain
- Transmitted sexually, transplacentally
- Three stages:
- Primary
- 0-3 weeks: CHANCRE
- Firm, non tender, resolves 3-6 weeks
- Haem/lymph spread
- Secondary (75% untreated patients)
- 2-10 weeks post chancre
- Palmar rash, LAD, condyloma lata (elevated plaques)
- Fever, malaise, weight loss
- Then moves to latent phase
- Tertiary (rare, 30% untreated patients)
- Post 5 years of latency
- Cardiovascular = aortitis, AR, aneurysm
- Neuro = meningovascular, tabes dorsalis
- Gummas
- Primary
- Congenital
- Late abortion, stillbirth
- Infantile = rash, osteochondritis, periostitis, liver/ lung fibrosis
- Childhood = interstitial keratitis, Hutchinson teeth, CN8 deafness
- Lyme Disease Borellia burgdorferi
- Rodents -> people via Ixodes deer ticks
- Stages:
- Tick bite
- Erythema chronicum migrans + LAD
- Early (4-12 weeks)
- Meningoencephalitis + cranial neuritis
- Heart block, peri/myocarditis
- Chronic (2-3 years)
- Destructive arthritis, acrodermatitis atrophicans
- Encephalitis
- Tick bite
Infectious Enterocolitis
| Cholera Vibrio cholerae | G-ve comma shaped bacteria Reservoir in shellfish India, Africa Transmitted in contaminated drinking water Pathogenesis: Remain within intestinal lumen, non invasive = small intestine Preformed enterotoxin (cholera toxin) = binds to GM1 ganglioside and via retrograde transport, activates adenylate cyclase -> increases cAMP -> opens CTFR -> drives chloride + bicarb + Na + water secretion -> watery diarrhoea. Clinical features: Watery diarrhoea (resembles rice water, fishy odour) and vomiting Incubation period 1-5 days Dehydration, hypotension, shock and anuria Mortality without treatment ~50% |
| Campylobacter | G-ve comma shaped, flagellated Reservoir in chicken/ sheep/ cattle Developed countries + traveller’s diarrhoea Transmitted in poultry, milk Pathogenesis: Affects colon Motile and adhere via flagella + cytotoxins cause epithelial damage Clinical features: Watery or bloody diarrhoea Complications: Reactive arthritis GBS (<0.1% patients) – serum Ab to C. jejuni cross react with peripheral/ central nervous system gangliosides |
| Shigellosis | G-ve bacilli, unencapsulated and non motile Reservoir in humans Developing countries Transmitted faecal-oral, food/ water Affects children Pathogenesis: Left colon, ileum Taken up by epithelial cells -> proliferate intracellularly -> escape into lamina propria and are eaten by macrophages -> induce apoptosis, inflammation Virulence plasmids = inject bacterial proteins into host cytoplasm S dysenteriae (serotype I) release Shiga toxin = inhibits protein synthesis, cell death Clinical features: Bloody diarrhoea, fever, abdominal pain IP 4-6 days Complications: HUS – associated with S dysenteriae Reiter syndrome (arthritis, uveitis, conjunctivitis) |
| Salmonella = Non typhoid salmonella S enteriditis | G-ve bacilli (Enterobacteriaceae) Reservoir in farm animals Worldwide Transmission in meat/ poultry/eggs/milk Pathogenesis: Colon and small intestine Virulence gene = transfer bacterial proteins into host cell -> actin rearrangement and bacterial uptake -> growth within phagosomes Flagellin protein = increases inflammation Stool culture for dx Clinical features: Bloody or watery diarrhoea Self limiting Complications: Sepsis Abscess |
| Enteric (typhoid) Fever = Typhoid salmonella S typhi S paratyphi | Reservoir in humans India, Mexico, Phillippines Transmission faecal- oral Pathogenesis: Small intestine Similar to non typhoid salmonella, however can also disseminate via blood/ lymph Clinical features: Bloody diarrhoea, fever, abdominal pain Bacteremia Flu like symptoms Ongoing for ~2 weeks unless Abx given Complications: Chronic infection Carrier state Encephalopathy Myocarditis |
| E COLI | G-ve bacilli Colonise healthy GI tract – subset cause disease |
| Enterotoxigenic (ETEC) | Traveller’s diarrhoea Developing countries Food, faecal- oral Small intestine Sx: Severe watery diarrhoea Produce heat labile toxin and heat stable toxin -> induce chloride and water secretion + inhibit intestinal fluid reabsorption |
| Enterohaemorrhagic (EHEC) | Two types = E coli O157:H7 and non O157:H7 Worldwide Beef, milk produce Colon Sx: Bloody diarrhoea Complications: Dehydration, electrolyte imbalances O157:H7 associated with HUS |
| Enteroinvasive (EIEC) | Developing countries Cheese, food, water Young children Colon Sx: Bloody diarrhoea Complications: HUS |
| Enteroaggregative (EAEC) | Worldwide Unknown transmission Colon Sx: Non bloody diarrhoea, afebrile Prolonged in AIDS patients |
| LEGIONELLA L pneumophilia | G-ve bacteria Causes Legionnaire’s Disease (bronchopneumonia), Pontiac fever (mild flu-like illness) Flourishes in artificial aquatic environments or aspiration of contaminated water Organ transplant patients susceptible Fatality rate 50% in immunosuppressed patients Dx urinary antigens or culture |
Mycobacteria
- Mycobacteria are slender aerobic rods
- Have a waxy cell wall made up of mycolic acid, which retains acid/ alcohol stain = ‘acid fast’ bacteria
- Weakly Gram positive
Mycobacteria tuberculosis
- Reservoir of bacteria is humans with active infection
- M Bovis can also cause intestinal/ oropharyngeal tuberculosis via infected milk, however this is rare following pasteurisation process
- Increased risk in patients who are immunosuppressed, underlying lung disease, malnutrition and poverty
- Airborne transmission
- Infection is different to Disease:
- Infection indicates presence of organisms which may or may not cause clinically significant disease. It occurs in unsensitized host at 0-3 weeks post exposure.
- Primary TB = may present asymptomatic, fever, pleural effusion
- Viable organisms lay within fibrocalcific nodule “Ghon complex” in lower part of upper lobe or upper part of lower lobe
- May be dormant for years
- If immune defences are lowered, then infection may reactivate and progress to communicable disease
- Ghon complex undergoes fibrosis and radiologically detectable calcification, can be seen on CXR as ‘Ranke complex’
- Primary TB = may present asymptomatic, fever, pleural effusion
- Disease indicates damage is occurring in a sensitized host, occurs with immunosuppression
- Primary progressive TB = resembles acute bacterial pneumonia
- Secondary TB = involves apex of both lungs and cavitating lesions. Presents with anorexia, malaise, night sweats, fevers, haemoptysis or pleuritic pain.
- Miliary TB = systemic organ involvement
- Infection indicates presence of organisms which may or may not cause clinically significant disease. It occurs in unsensitized host at 0-3 weeks post exposure.
- Diagnosed via acid fast smears, sputum culture and PCR
- Infection leads to delayed hypersensitivity to M tuberculosis antigens, which can be detected by Mantoux test
- 2-4 weeks post infection, intracutaneous injection of purified protein derivative of M. tuberculosis produces palpable induration that peaks in 48-72 hours –< indicates T cell mediated immunity to mycobacterial antigens
- Does not differentiate between infection and disease
- False negatives = viral infection, lymphoma, sarcoidosis and overwhelming active tuberculous disease
- False positives = prior vaccination with BCG (Bacillus Calmette-Guerin = attenuated strain of M bovis)
Mycobacterium avium-intracellulare complex (MAC)
- M. avium and M. intracellulare are separate species
- Infections they cause are very similar, thus named as a complex
- MAC is common is soil, dust or domestic animals
- Uncommon except in AIDS patients, causes disseminated infections
Mycobacterium leprae
- Caused by M. leprae
- Affects peripheral nerves and skin, resulting in disabling deformities
- Transmitted by aerosol, taken up by alveolar macophages and disseminates haematogenously
- Endemic among poor tropical countries
- Two patterns of disease:
- Tuberculoid leprosy = limited disease, asymmetric involvement of skin and large peripheral nerves
- Lepromatous leprosy = severe disease, symmetric skin thickening/ nodules
Last Updated on August 20, 2021 by Andrew Crofton
Andrew Crofton
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