Clinical Microbiology Revision Notes PDF

Revision: Clinical Microbiology Note: red words are added by Eddrick Loong of 25 Maksim Chan (A&E 23) Blue words are further added by me! Content based on course materials, textbooks and online resources  Exam tips ⬢ Ix: always think about what specimen + what tests (e.g. “sputum for Gram stain, c...

Revision: Clinical Microbiology Note: red words are added by Eddrick Loong of 25 Maksim Chan (A&E 23) Blue words are further added by me! Content based on course materials, textbooks and online resources  Exam tips ⬢ Ix: always think about what specimen + what tests (e.g. “sputum for Gram stain, culture and sensitivity, ZN stain and TB culture) ⬢ Make sure you cover DDx adequately – have you considered virus? TB? Fungus? (e.g. ”stool culture” is NOT enough for GE) ⬢ Mx: Don’t just think about antibiotics – infection control measures, contact tracing, notification, supportive Tx (e.g. hydration / O2 / ICU support) are equally important ⬢ Avoid shorthands as far as possible especially for drug treatments ⬢ Study the pictures – some questions are like spot tests! 2 1 Basic microbiology It is only when you’ve recited a lot of dry facts before you start to develop the “sense” of deducing the answers L Usually tested in MCQ Focus on these for the “basic” bacteria lectures ⬢ Gram positive or negative? ⬢ Colonial morphology – e.g. cocci or rod? ⬢ Recognize common buzzwords (e.g. Streptococcus = “G+ cocci in chains”, Haemophilus = “pleomorphic G- coccobacilli”) ⬢ Tests: make sure you know the algorithms in identifying species ⬢ Oxygen requirement: obligate aerobe (e.g. TB), facultative anaerobe, obligate anaerobe (e.g. Clostridium) ⬢ Common diseases ⬢ Remember at least ONE first-line antibiotic for common bacteria 4  Bacteria blue = aerobic; purple = anaerobic Gram positive Gram negative Cocci Staphylococcus Peptococcus Neisseria Veillonella Streptococcus Peptostreptococcus Moraxella (+Enterococcus) Lactose fermenter MacKonkey red Glucose non-fermenter Bacilli Bacillus Clostridium E. Coli Pseudomonas Bacteroides Listeria Actinomyces Klebsiella Acinetobacter Fusobacterium (Rods) Corynebacterium Lactobacillus Enterobacter Vibrio Curved rods Porphyromonas Nocardia Propionibacterium Serratia Campylobacter Prevotella Erysipelothrix Citrobacter Helicobacter Proteus Hemophilus Shigella Legionella Fastidious Salmonella Bordetella Zoonosis Lactose non-fermenter Brucella MacKonkey orange Yersinia Atypicals: Mycobacterium spp. (weakly G+?), Chlamydia, Mycoplasma, Rickettsia, spirochetes 5 Describe the procedure of Gram stain. What is the difference between structure of G+ and G- bacteria? Staphylococcus 葡萄球菌 = G+ cocci in clusters ⬢ Catalase +ve ⬢ Coagulase +ve = S. aureus ⬢ Coagulase –ve: novobiocin susceptibility test Haemolysis β γ γ yellow red yellow 6  Determination of MRSA: use 30 mcg Determination of VRSA: use 30 cefoxitin disc to screen. Read after 24 mcg vancomycin disc to screen. If hours incubation. If cefoxitin zone ≤ 19 vancomycin zone ≤ 14 mm, it is Staphylococcus aureus ⾦黃葡萄球菌 mm, it is reported as oxacillin-resistant. reported as vancomycin-resistant. Skin / Wound / Bone / Joint infections à S. aureus! Tests: catalase +ve, coagulase +ve Common diseases: abscess within hair follicle coalesced furuncle inflammation of skin around nails ⬢ Skin: impetigo, boils (furuncles), carbuncles, paronychia ⬢ Bone / Joint: osteomyelitis, septic arthritis if caused by S. aureus, ⬢ Others: pneumonia, acute infective endocarditis mostly very severe ⬢ Toxin-mediated: food poisoning, Staphylococcus toxic shock syndrome (tampon use!), scalded skin syndrome Antibiotics of choice: enhance penetration of antibiotic, e.g. in bone / joint infections mediated by Staphylococcal exfoliative toxin ⬢ MSSA: cloxacillin +/- fusidic acid IV cefazolin is also Penicillin resistance in S. aureus ≥ 95% ⬢ MRSA: vancomycin methicillin, cloxacillin, etc. used if resistant to suitable for MSSA Can we give penicillin for Staph? most Staph nowadays are resistant to penicillin (for WWI soldier only lol) 7 Vancomycin is less effective for treatment of S. aureus bacteremia than beta-lactam agents and should not be administered as 1˚ therapy for methicillin-sensitive strains unless the use of a beta-lactam agent is precluded by drug intolerance.  Coagulase negative Staphylococcus Staphylococcus saprophyticus ⬢ Test: catalase +ve, coagulase –ve, novobiocin resistant ⬢ Urinary tract infection Infective endocarditis causative organisms: arranged in descending order of prevalence - Acute IE: Staphylococcus aureus, group A strep (e.g. S. pyogenes) - Subacute IE: Streptococcus viridans - IE with prosthetic heart valve: Staphylococcus epidermidis Staphylococcus epidermidis - IE in IV drug addict: Staphylococcus aureus, HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella) ⬢ Test: catalase +ve, coagulase –ve, novobiocin sensitive ⬢ Normal skin flora → does not normally cause skin infection. Only cause infection when entering into blood, so usually associated with catheter, etc. ⬢ Catheter / Shunt / Prosthesis associated infections also can think of Candida infection ⬢ Infective endocarditis (SBE) 8 Streptococcus 鏈球菌 = G+ cocci in chains / pairs ⬢ Catalase -ve 1. haemolysis → 2. bacitracin / optochin susceptibility test ⬢ Beta-hemolytic: bacitracin susceptibility test ⬢ Alpha-hemolytic: optochin susceptibility test Enterococcus faecium (≠ faecalis) can be resistant to vancomycin Anti-streptolysin O titre !! Entercoccus: aesculin hydrolysis test 9  Streptococcus pyogenes (Group A Strep) Similar to S. aureus but something more~~ Antistreptolysin O titre Tests: catalase -ve, beta-hemolytic, bacitracin sensitive, raised ASOT Common diseases: Blood film picture → neutrophilia with toxic granules most common cause of: ⬢ Skin: impetigo, erysipelas, necrotising fasciitis ⬢ Strep throat (pharyngitis) ⬢ Scarlet fever: pharyngitis, strawberry tongue, sandpaper rash with circumoral pallor Acute rheumatic fever is an acute, immunological mediated, multisystem inflammatory disease that follows, after a few weeks, an episode of group A streptococcal pharyngitis. ⬢ Quinsy (peritonsillar abscess), retropharyngeal abscess immune-⬢ Post-strep diseases: acute post-strep GN (Type III HSR), rheumatic Tx: anti-inflammatory agents mediated diseases fever (Type II HSR) Check ASOT or Anti-Strep DNAase B titre (e.g. aspirin / other NSAIDs) Antibiotics of choice: erythromycin, clarithromycin, azithromycin What is the usual regimen 1st line for penicillin allergic PT: oral penicillinfor Strep throat? ⬢ Penicillin / Macrolides / Clindamycin V 10 days 10  Other Strep species Investigations of infective endocarditis: - Blood culture (3 sets, each aerobe + anaerobe), within 24 h, from 3 distinct Group B: Streptococcus agalactiae CAMP test positive anatomical sites, ≥ 1 h apart ⬢ Test: catalase -ve, beta-hemolytic, bacitracin resistant - Complete blood count with differential ⬢ is: Vaginal flora à MC cause of neonatal meningitis & neonatal S. agalactiae (anaemia, high WBC) sepsis !! - Erythrocyte sedimentation rate (ESR), ⬢ Antibiotic of choice: ampicillin / penicillin rheumatoid factor +ve group “B” = BB → looks like pneumococcus on agar, arranged in pairs neonatal menigitis - ECG: present with conduction defects Group D: most reclassified as Enterococcus spp. - Trans-thoracic / trans-oesophageal echocardiogram: present with vegetation, ⬢ Test: catalase –ve, gamma/non-hemolytic, bile aesculin +ve valvular regurgitation, microabscesses ⬢ Urinary tract infection If the specimen looks like pneumococcus on agar, but Hx shows ⬢ Biliary tract infection biliary tract infection → enterococcus instead of pneumococcus ⬢ Subacute bacterial endocarditis (SBE) Enterococcus faecium → can be vancomycin resistant (VRE) ! ⬢ Antibiotic of choice: ampicillin (Note: Enterococcus is cephalosporin-resistant!) e.g. S. oralis, S. bovis (can cannot use 3rd gen cephalosporins! also cause colorectal CA) Empirical antibiotics: penicillin ± aminoglycoside Monitor Tx: Baseline renal f(x), Viridans streptococci (e.g. gentamicin), intravenous route C-reactive protein, CBC, incl. WBC ⬢ Test: catalase –ve, alpha-hemolytic, optochin resistant DDx: S. aureus, S. epidermidis, viridans strep, enterococcus ⬢ Normal flora of mouth à Dental caries à MC cause of infective endocarditis S/S: - Immune: Osler node, Janeway lesions colon cancer Strep bovis is associated with which cancer? Which Strep in pork handlers? Strep. suis 11 - Haematological: splinter haemorrhage  Streptococcus pneumoniae 肺炎鏈球菌 Mucoid appearance on agar plate + = presence of capsule Tests: catalase –ve, alpha-hemolytic, optochin sensitive, Quellung+, “lancet-shaped diplococci” Common diseases: MC for these 3 diseases DDx ⬢ Community-acquired pneumonia These three often come together: G+ diplococci - S. pneumoniae H.M.S.: ⬢ Acute otitis media AOM C.A.M. G– coccobacilli - H. influenzae - H. influenzae - M. catarrhalis ⬢ Meningitis G– diplococci - M. catarrhalis - S. pneumoniae Prevention of acute otitis media: Complications of acute otitis media: - Conjugated vaccine (1 mark) Capsular organisms: Antibiotics of choice: - Polysaccharide vaccine (1 mark) - Penicillin prophylaxis (1 mark) - Meningitis (1 mark) - Brain abscess (1 mark) (Some Killers Have Pretty Nice ⬢ Penicillin (if sensitive J) - Septic shock (0.5 marks) Capsules) - S. pneumoniae ⬢ Augmentin 1st line not use augmentin, because of low BBB penetration - K. pneumoniae ⬢ 3rd generation cephalosporin (if meningitis) - H. influenzae e.g. ceftriaxone, cefotaxime; if resistant, - P. aeruginosa add IV vancomycin and rifampicin - N. meningitidis Should we give penicillin for S. pneumoniae? - C. neoformans 12 Summary for Gram positive organisms 13  Aerobic G+ rods Cutaneous, pulmonary, GI anthrax; S/S: - Cutaneous: black eschar, lymphadenopathy, fever - Pulmonary: haemorrhagic pneumonia; fatal !! Bacillus spp. normal washing - GI: intestinal obstruction, bloody diarrhoea hands is not effective Bacillius (aerobic) or Clostridium (anaerobic) ⬢ Test: Spore—forming Only 2 bacteria form spores!!!! Prevention: acellular vaccine (USA) = Pulmonary anthrax ⬢ B. anthracis: anthrax, Woolsorter’s disease (ciprofloxacin, doxycycline) ⬢ B. cereus: emetic toxin (“fried rice syndrome”), diarrheal toxin, (beta- lactam resistant: try vancomycin) Abdominal pain and diarrhoea B. cereus secrete emetic toxin → vomiting, rarely diarrhoea Corynebacterium diphtheriae Club-shaped swellings at end of bacilli ⬢ Tests: ”Chinese-character like” on Gram’s stain, volutin granules on Albert stain, black on tellurite medium, Elek test +ve used to test for diphtheria toxin ⬢ Disease: diphtheria (sore throat with pseudomembrane à life- forming grey adherent membrane inflammed tonsils → covered with exudate DTaP: threatening airway obstruction) Albert stain, with green volutin granules diphtheria, tetanus, ⬢ Preventable by DTaP vaccine pertussis Tellurite agar ⬢ Mx: penicillin, diphtheria antitoxin 14  Aerobic G+ rods 1. Group B strep. (most common) (i.e. Streptococcus agalactiae), 2. E. coli, 3. Listeria monocytogenes → BEL B.E.L. Listeria monocytogenes non-spore-forming What are the 3 most common bacteria for neonatal meningitis? ⬢ Test: tumbling mobility at 22 degrees, growth in cold temp dynamic and erratic manner, randomly Tumbling motility: moving in a highly ⬢ Foodborne (unpasteurized milk, ice cream J) changing direction and speed ⬢ Neonatal meningitis, sepsis in pregnant women (pharyngitis, diarrhoea, generalised pain) Normal adults: pneumonia, febrile illness ⬢ Antibiotic: ampicillin + gentamicin (Note: Listeria is cephalosporin-resistant!) another resistant species: enterococcus we do not use antibiotics for adult meningitis (e.g. augmentin, ceftriaxone), to treat neonatal meningitis. Nocardia asteroides (1) Non-spore-forming (2) [microscopy] short filamentous bacilli with Lactobacillus spp. (乳酸桿菌) branching (fungi-like) (3) Semi-acidfast (differentiated from TB) ⬢ Normal commensal in mouth, GI tract, vagina (acidity J) (4) [culture] grow on Sabouraud agar in 3 days (5) Aerobic to microaerophilic ⬢ Often used as probiotic Clinical manifestation – Nocardiosis: (1) Pulmonary nocardiosis → Cavitary pneumonia (~TB); Possible spread to brain → multiple brain abscesses (2) Cutaneous / subcutaneous nocardiosis → Traumatic implantation → cellulitis → mycetoma / eumycetoma (subcutaneous abscess with granules) Treatment: co-trimoxazole 15  Gram negatives / “Coliforms” ⬢ Important tests: glucose F/O, lactose F/O (MacConkey agar), oxidase, urease, special medium (e.g. TCBS) Thiosulfate-citrate-bile salts-sucrose agar cefotaxime, ceftriaxone, ceftazidime, ceftibuten ⬢ Antibiotic (generally): 3rd gen cephalosporin / fluoroquinolones ciprofloxacin, levofloxacin, moxifloxacin, etc. 16  Enterobacteriaceae A large family of Gram negative bacteria, facultative anaerobes normal GI flora ⬢ All are glucose fermenters and oxidase –ve Members of the Enterobacteriaceae are bacilli (rod-shaped), and are ⬢ Differentiated by lactose fermentation (MacConkey agar) typically 1–5 μm in length. Most have many flagella used to move ⬡ Lactose Fermenters (red): E. coli, Klebsiella, Enterobacter about, and they are non spore-formers. ⬡ Lactose Non-fermenters (yellow): Serratia, Citrobacter, Proteus, Shigella, Salmonella + Pseudomonas aeruginosa Escherichia coli ⼤腸桿菌 (ox +ve, glu non-fer.) Example: MacConkey agar (red): E. coli ⬢ Normal to be found in faeces EHEC: produces Shiga toxin The best known strain is ⬢ MC cause of urinary tract infection E. coli O157:H7 ⬢ 2nd MC cause of neonatal meningitis after GBS & neonatal sepsis ! ⬢ Strains: EHEC/EIEC (bloody diarrhea), ETEC (traveller’s diarrhea), EPEC enterohemorrhagic Escherichia coli / enterotoxigenic E. coli: watery diarrhoea enteroinvasive Escherichia coli ETEC -> Heat labile (LT) toxin Enteropathogenic ⬡ E. coli O157:H7, Escherichia coli O104:H4 causes hemolytic microangioplastic haemolytic anaemia uremic acute kidney injury syndrome (MAHA + thrombocytopenia + AKI) if answering Enterobacteriaceae for diarrhoea, must mention the strain of E. Coli (“E. coli causes diarrhoea” doesn’t make sense because E. coli is in normal GI flora and found in stool) NOT all E. coli are pathogenic! In the exam, you must specify the STRAIN 17  Enterobacteriaceae Normal flora of the human intestinal tract Klebsiella pneumoniae Voges- capsulated bacteria can form mucoid colonies Quellung reaction Proskauer test ⬢ Test:lactoselactose F, Quellung+, VP+, form mucoid colonies also urease +ve fermenter ⬢ Community acquired pneumonia, urinary tract infection Enterobacter, Serratia, Citrobacter not common in exam ⬢ Serratia marcescens form red-orange pigmented colonies Proteus mirabilis MARCEscens = MARS → Mars is red colour = red-orange pigmented colonies ⬢ Test: urease +ve, swarming on agar plate composition of struvite stones: ⬢ Urinary tract infection: form struvite stones (Mg, NH4, PO4) PRoteus = PieRRe → stones Shigella spp. human as only host XLD agar, Hektoen agar: Salmonella turns black - Shigella: no change (XLD), green colonies (Hektoen) ⬢ 4 Shigella species: S. dysenteriae, S. flexneri, S. boydii, S. sonnei Differentiating Shigella vs Group A = most pathogenic ⬢ Bacillary dysentery is a notifiable disease since human is only natural Salmonella: Children confirm TN ⬢ Endemic in HK, obligate aerobe therefore, more likely on upper lobe of lung ⬢ Unable to be killed by alveolar macrophages à Form granuloma ⬢ Remain latent à Reactivate and disseminate when immunocompromised Rapid growing: M. abscessus, M. marinum = aquatic habitat water exposure fortuitum, chelonae -> Granuloma w/ cellulitis Non-tuberculous mycobacterium - Runyon classification (Groups 1-4) based on M. kansaii = pulmonary disease pigment production and growth rate skip if you just want a pass MAC = M. avium, intracellulare, chimaera -> MAC pulmonary 22 ⬢ Mycobacterium leprae: cause leprosy, cannot be cultured disease on top of other lung disease e.g AE COPD  Another example of anaerobe: Actinomyces israelii Actinomyces israelii cont’d - Obligate anaerobe, Non-spore-forming Reservoir – normal flora of oral Anaerobes - [microscopy] branching filamentous bacilli - [colony] sulphur granules – white → yellow → brown → black cavity & female genital tract Transmission – endogenous Cover anaerobes when: - [culture] grow on enriched media (BHIA, K1) under anaerobic condition at 37˚C for 7-10 days S/S: lung abscess, CNS involvement Closed-space infections Tx: surgical drainage, if cannot recall, guess this (e.g. abscess) Treatment for anaerobes = metronidazole + drainage debridement, penicillin GI tract involved G+ Clostridium spp. à spore-formers! Clostridium haemolysis → obligate anaerobe, spore-forming, on blood agar ! Gas-producing / Foul- Bacilli subterminal spores smelling ⬢ C. botulinum: botulism (flaccid paralysis, resp. failure), in canned Necrotic tissue / food / honey ( ingrown eyelid (trichiasis), corneal scarring (cicatricial disease) -> keratoconjunctivitis -> blindness 3F (Flies, formite, fingers) Chlamydia What is most common bacterial STD? Chlamydia Serovar D-K ⬢ Chlamydia trachomatis: trachoma, STD (non-gonococcal urethritis, neonatal conjunctivitis), pneumonia, lymphogranuloma venereum L1-L3 Tx = doxycycline + azithromycin (single dose for trachoma) ⬢ Chlamydophila pneumoniae: atypical pneumonia ⬢ Chlamydophila psittaci: atypical pneumonia (notifiable!), contact history with parrot M. pneumoniae Tx → doxycycline + macrolide How is atypical pneumonia “atypical”? Mycoplasma à fried egg colonies on Diene’s stain, cold agglutin test +ve - caused by atypical organisms - flu-like symptoms: non-productive ⬢ Mycoplasma pneumoniae: MC bacterial cause of atypical pneumonia cough, high fever, fatigue, muscle pain, consolidation? (infection site ⬢ Others: M. hominis, M. genitalium, U. urealyticum interstitium not alveolus) Typical: cough, sputum, fever, CXR Cold agglutins are autoAb that Mycoplasma do not have a cell wall lobar consolidation; DDx: Strep. bind to RBC at low temp. → pneumonia, Haemophilus influenzae, → cannot use beta-lactams ! Gram stain no use ! cause clumping of blood at 4˚C Moraxella catarrhalis Myocarditis + pericarditis, Erythema multiforme, Hepatitis & pancreatitis, Myalgia, arthralgia, arthritis Encephalitis, myelitis, Guillain Barre syndrome (polyneuropathy) Cold-agglutinin production ->AIHA!! 24  Tick transmitted organisms examples: (@2 marks) - Borrelia burgdorferi - Rickettsia rickettsii - Rickettsia typhi Treatment for atypicals = doxycycline / macrolide Atypicals Cannot be cultured!! à PCR / Serology Centripetal maculopapular petechial rash amplification of atypical by indirect immunofluoresence - Begin peripherally on ankles & wrist → trunk DNA from blood sample Typical case (R. rickettsia): G– Rickettsial organisms à Weil-Felix test (cross-reaction with Proteus vulgaris) hiking in the woods / bitten bacilli ⬢ R. rickettsia: tick-borne, Rocky Mountain Spotted Fever by dog before → bitten by unknown organism → rash ⬢ R. prowazekii: louse-borne, epidemic typhus recrudescent form of epidemic typhus Brill-Zinsser disease is the ⬢ R. typhi: flea-borne, murine typhus ⬢ O. tsutsugamushi: mite-borne, scrub typhus typical case: sheep in farm, labour → inhalation of Coxiella burnetii ⬢ Coxiella burnetii: Q fever, culture negative endocarditis i.e. pyrexia of unknown origin → chronic state may cause endocarditis usually unable to be cultured Spirochetes à Dark-ground microscopy (Mx: penicillin) G– spirochete ⬢ Treponema pallidum: syphilis ⬢ Borrelia burgdorferi: Lyme disease (erythema migrans) also may have: arthritis, facial nerve palsy ⬢ Leptospira interrogans: Weil’s disease (liver and renal failure), contact history with rat / livestock icteric leptospirosis host of infection: rats / rodents urine can also cause anicteric leptospirosis Dx: serology → leptospira microscopic agglutination test (LMAT), culture of blood, CSF, urine past paper: hiking, walk to creek; water was contaminated by urine of some animals → Leptospira infection 25  Basic virology Classification of viruses RNA virus has less proofreading ability → higher mutation rate ⬢ DNA vs RNA virus: implication on mutation rate à new strains, drug resistance ⬢ Enveloped vs non-enveloped à difficulty to kill Enveloped viruses are more easily destroyed by alcohol as it can disrupt the lipid envelope ⬢ Baltimore classification highest mutation rates: reverse transcriptase viruses → e.g. HIV is resistant to many drugs most common: PCR, serology Diagnostic methods standard”⬢ PCR: most sensitive and specific, but prone to contamination “gold ⬢ IF: detect virus antigen (e.g. Latex agglutination) ⬢ EM: low sensitivity, may not distinguish between similar viruses ⬢ Serology: IgM for acute infection, IgG for immunity i.e. IgG positive after acquiring immunity → Viral culture: require cell lines, identify viruses based on cytopathic effects practice⬢ 26 not common  Basic mycology What agar for fungi? How to prepare skin scrape? Immunocompromised: Old / Frail Poorly controlled DM Yeasts – unicellular fungi germ tube positive: albicans; Long term steroids / germ tube negative: non-albicans immunosuppressants / G+ ⬢ Candida albicans vs non-albicans: differentiated by germ tube test chemotherapy Cannot be ⬢ Pneumocystis jirovecii: diagnosed by Toluidine blue O stain Immunodeficiency e.g. AIDS cultured !! Obligate ⬢ Cryptococcus neoformans: halo appearance on India ink high risk for systemic fungal infection Form mucoid colonies prominent capsules stained brightly on mucin 1. suspend yeast cells in horse serum parasite !! collapsed basketball appearance 2. incubate at 37˚C Moulds – multicellular fungi on Toluidine blue O stain 3. observe for germ tube formation in ⬢ Aspergillus spp.: pulmonary infections wet mount (germ tube = hyphae) → C. albicans is a yeast but ⬢ Dermatophytes: Microsporum, Trichophyton, Epidermophyton reproduce as mould at high temp. ⬢ Zygomycetes: very deadly How to distinguish the dermatophyte species? usually in severely immunocompromised patients Microsporum: macroconidia thick-walled & fusiform Dimorphic fungi can switch between unicellar and multicellular Trichophyton: macroconidia rare Epidermophyton: macroconidia thin-walled & smooth ⬢ Malassezia furfur: cause tinea versicolor Skin scrape / hair samples, want to see if ⬢ Talaromyces marneffei: red-wine colour pigment there is fungus. How to prepare? ⬢ Sporothrix schenckii: cause rose gardener disease - use 10% KOH to wash away the keratin injury by rose thorns → hand swelling For fungal culture we use sabouraud dextrose agar Penicillium is also another dimorphic fungi 27  Basic mycology germ tube test positive: Candida albicans Aspergillus: multicellular, with branching (acute angle branching) (If branching is irregular → think of zygomycetes) Pneumocystis jirovecii on Toluidine blue O stain halo appearance on India ink: cryptococcus neoformans 28 2 Antimicrobials You actually only use a) Sulfatide (sulfolipid in cell envelope) replicate in and release from macrophage b) Cord factor c) Tuberculin (surface protein) along with mycolic acid Inflammatory response (TNF, ROS, TB disease = active TB Stages of TB - Cause delayed-type (type IV) hypersensitivity RNS) + cytotoxicity -> collateral TB infection = chronic TB - Cell-mediated immunity → granulomas & caseation host cell damage ⬢ Primary TB / Pulmonary TB: often asymptomatic; can have fever, cough, hemoptysis, night = granuloma sweats; CXR shows Ghon complex (Ghon focus + hilar LN) Ranke complex = calcified LN ⬢ Latent TB: non-infectious, no clinical manifestations ⬢ Reactivation: can disseminate to extrapulmonary tissues as miliary TB, e.g. TB meningitis, TB spine (Pott’s disease), TB UTI, TB ileus +cardiac cardiac: constrictive pericarditis / tamponade CXR of miliary TB Diagnosis of active TB Hypertonic saline aerosol Solid: Löwenstein-Jensen medium → mucus production ↑ ⬢ CXR Liquid broth culture: Middlebrook AFB smear positive = open TB medium (faster, 1-3 wk) ⬢ Early morning sputum for AFB (ZN stain) + TB culture ⬢ NAAT e.g. GeneXpert MTB Screening for TB: fluoresence stain nucleic acid amplification test (NAAT) NOT subcutaneous by auramine O / rhodamine B Diagnosis of latent TB How to interpret a positive TST? +ve result in ⬢ Tuberculin skin test (TST): intradermal injection of purified protein derivative (PPD) of MTB Mantoux test if Aka Mantoux test Causes of false negatives of TST: size of induration antigen à measure size of induration 48-72h later Causes of false positives of TST: - malnutrition, viral infections (e.g. > 10 mm - BCG vaccine HIV), live vaccines, steroid therapy ⬢ Interferon-gamma release assay (IGRA) NOT erythema induration: slight protrusion on skin; Interferon-γ (IFN-γ) release assays rely on the fact that T- erythema: redness of skin 44 lymphocytes will release IFN-γ when exposed to specific antigens.  Direct Observed Therapy Short-course; Side effect of TB drugs: use of medication is supervised by nurse Tuberculosis (TB) Isoniazid (H): hepatotoxicity, Multi-drug resistant TB: TB that is resistant peripheral neuropathy to at least isoniazid and rifampicin Rifampicin (R): hepatotoxicity, red-orange Treatment of TB What is DOTS? What is MDR-TB? hyper- discolouration of body fluids, 2 months 4 drugs, bilirubinaemia thrombocytopenia ⬢ Active TB: 2 month HRZE + 4 month HR then 4 months 2 drugs Pyrazinamide (Z): gout ⬢ Particular sites may require up to 12 months of treatment Ethambutol (E): retrobulbar ⬢ Latent TB: isoniazid x 6 month (monotherapy) or RI daily / weekly 3 mth neuritis + MDR-TB: Levofloxacin / moxifloxacin + bedaquiline + linezolid + clofazimine / cycloserine / terizidone How to prevent peripheral Infection control: airborne precautions + Double door system, high efficiency particulate air (HEPA) filter neuropathy for isoniazid? ⬢ Negative-pressure isolation rooms with at least 6 air changes per prescribe isoniazid with vitamin B6 hour. Room door should be kept close except entry/exit. ⬢ Personal protective equipment: Fit-tested N95 respirator 3 HRZE + 9 HR: 2 HRZE + 7 HR when: - CNS involvement (+ adjunctive dexamethasone) - Cavitation of initial CXR + positive culture after 2 mth therapy - Miliary TB - Immunocompromised PT (DM, HIV, silicosis) - Pericarditis, peritonitis, genitourinary 2 HRZE + 10 HR: - Bone and joint TB 45 & pyrazinamide RIF = DNA-dependent RNA polymerase inhibitor (kill persisters) -> rpoB mutation, CYP inducer INH = inhibit mycolic acid synthesis + inhibit catalase peroxidase (katG) -> bactericidal for active, bacteristatic for latent [S/E peripheral neuropathy -> relieved by pyridoxine], mutation @katG/ inhA PZA = bactericidal, for subdormant organism in acidic pH (IC bac. in phagosome), mutation @pncA EMB = inhibit cell wall synthesis -> bacteristatic for in vitro / IC bac, mutation @EmbB  Gastroenteritis Complications of C. difficile GE: Pathogenesis of watery diarrhoea: - Toxic megacolon - By toxins → preformed toxins, - Pseudomembranous colitis toxins formed in vivo Common organisms – bloody or watery? - Perforation of colon - Direct invasion Bloody Watery Salmonella can be enterotoxigenic E. coli grouped into: Bacteria Shigella dysenteriae important! ETEC (Traveller’s diarrhea) group - Typhoid / paratyphoid C. difficile accounts for > 25% of antibiotic-associated EHEC (E. coli O157:H7 / O104:H4) Vibrio cholerae important! - Gastroenteritis group diarrhoea; Clostridium difficile – Hx of ABx us Clostridium perfringens Undercooked poultry, Bacillus cereusPreformed chicken / duck eggs, raw Salmonella enteritidis Can also present with watery diarrhoea. neurotoxin milk or food handlers Halophilic (salt-loving) vibrio Campylobacter jejuni Staphylococcus aureus Incubation 1-7 days Fever, headache, Heat-stable & heat-labile enterotoxins Contaminated seafood Vibrio parahaemolyticus Salmonella enteritidis abdominal pain, diarrhoea Incubation 8 hrs - 2 days Explosive diarrhoea, abdominal pain, C. difficile pathogenesis: 1. Antimicrobial therapy (cefotaxime) → disruption of intestinal microbiota. Campylobacter jejuni Mechanism varies; nausea & vomiting Self-limiting 2. Coloniation of C. difficile via faecal oral route. Vibrio parahaemolyticus enterotoxin-like, invasive or cytotoxic 3. C. difficile produces C. difficile toxin A and B → bind to receptors on Virus Rotavirus Reoviridae (group A) intestinal epithelial cells → inflammation + diarrhoea. Prevalence increasing 4. Toxin A directly activates neutrophils → neutrophil chemotaxis to localize in developed world important! in pseudomembranes and the underlying intestinal (colon) mucosal layer → inflammation leading to intestinal fluid secretion and mucosal injury Norovirus Antibiotics if systemic involvement: quinolones 5. Toxin B disrupts the cytoskeleton and induces apoptosis of intestinal Adenovirus Cytomegalovirus + Astrovirus (colonic) epithelial cells. Parasite Entamoeba histolytica important! Giardia duodenalis important! Cryptosporidium Zoonotic infection from under-cooked poultry, raw milk Incubation 1-5 days Non-enveloped, Fever, nausea, abd cramps, diarrhoea mainly affect adults; Cyclospora Reactive arthritis, neuro Cx S/S similar to rotavirus. 46 Self-limiting, erythromycin / quinolones reduces duration of Sx Dx: antigen detection by ELISA What is a bacterial toxin? Bacterial toxins are divided into heat-stable and heat labile toxins: Gastroenteritis - A toxigenic substance secreted by bacteria to facilitate the infection process - Heat stable: withstand 100˚C, 15 min; - Heat labile: destroyed at 60˚C, 15 min - Temperature stability is affected by pH → acidic pH improves stability DCA for Shigella, Salmonella; No. For stool, we use DCA (salmonella? Shigella?), TCBS for Vibrio TCBS (Vibrio?) and stero? MacConkey is not selective Diagnosis Can we culture stool on MacConkey agar? What do we use instead? Skirrow’s for Campylobacter ⬢ Stool / Rectal swab for bacterial culture and OCP (ova, cyst & parasite) Signs and symptoms: - Diarrhoea (watery / bloody) ⬢ Stool / Rectal swab for viral antigen detection (rotavirus) and PCR (norovirus) - Abdominal cramps and pain - Nausea, vomiting ⬢ Blood culture if severe RT-qPCR (real-time quantitative - Loss of appetite Rotavirus: by enzyme immunoassay, latex agglutination polymerase chain reaction) - Headache, fever, muscle Adenovirus: by ELISA ⬢ Food sample for culture (if suspected food poisoning) viral antigen detection ≠ virus aches & weakness, fatigue. isolation (viral culture) - Dehydration ⬢ Stool for C. diff toxin A/B PCR dehydrogenase (GDH) by enzyme immunoassay / nucleic acid amplification test + detection of glucose + Cytotoxic assay by cell culture for C. difficile Notifiable: bacillary dysentery, amoebic dysentery, Treatment Need to mention if asked for Mx ! (e.g. “ABx indicated in selected cases”, don’t write nothing!) cholera, food poisoning, Shiga-toxin producing E. coli ⬢ First-line is always rehydration (ORS oral rehydration solution / IV fluids) +electrolyte maintain fluid and balance !! ⬢ Prudent use of antibiotics: only given if very septic / public health concern due to extending carriage – choices include quinolones / macrolides / tetracyclines / 3rd gen cephalosporins ciprofloxacin azithromycin cefotaxime, ceftriaxone ⬢ Antibiotics are contraindicated for E. coli O157:H7: risk of causing HUS haemolytic-uraemic syndrome a type of enterohaemorrhagic E. coli ⬢ Oral vancomycin / metronidazole for C. diff colitis Triad: Microangiopathic haemolytic anaemia Cannot give via IV: not enough drug excretion into colon OR fidaxomicin + thrombocytopenia + acute kidney injury Amoebic dysentery (by Entamoeba histolytica) → Tx: (systemic) metronidazole, tinidazole + (luminal) paromomycin, iodoquinol 47  Gastroenteritis Rotavirus (Family: Reoviridae) Norovirus (Family: Caliciviridae) aka “Winter vomiting disease” Epi Common in young children (6-24m) Common in adults Rotavirus A, the most Transmitted via faecal-oral route Source: undercooked seafood common species, causes more than 90% of rotavirus (only human-to-human) Transmitted via faecal-oral and infections in humans. respiratory routes → inhalation of aerosols from faeces / vomitus S/S Watery diarrhea +/- vomiting Projectile vomiting +/- diarrhea Dx Stool and rectal swabs for rapid Stool and rectal swabs for RT-qPCR antigen detection (EIA / Latex) Vaccine? Oral vaccination Vaccine N/A RotaRix: monovalent, 2 doses RotaTeq: pentavalent, 3 doses First dose between 6-15w, last dose before 32w Risk of intussusception after 32 weeks a part of the intestine folds into the section immediately ahead of it Why can these viruses withstand the environment of GI tract? 48 because they are non-enveloped  HBP infection Recurrent pyogenic cholangitis causative organisms: - Aerobic G– bacilli → E. coli, Klebsiella spp. - Anaerobic G– bacilli → Bacteroides spp., Clostridium perfringens, Prevotella spp. - Parasite (trematode) → Clonorchis sinensis, Opisthorchis spp., Fasciola hepatica Spectrum of diseases - Parasite (nematode) → Ascaris lumbricoides Acute cholecystitis: infection of Acute cholangitis: infection of bile ducts (e.g. gallbladder (e.g. gallstone obstructing gallstone obstrucgting common bile duct) cystic duct) no jaundice If present w/ recurrent episodes → “Recurrent pyogenic cholangitis” S/S Fever, RUQ pain, Murphy’s sign +gallbladder palpable (40%) Charcot’s triad: fever, RUQ pain, jaundice K1 & K2 Parasites: Organism G-: E. coli, Klebsiella, Enterobacter, … G-: E. coli, Klebsiella, Enterobacter, C. sinensis If CBD stents 87% aerobes (66% G-) G+ (Enterococcus, Streptococcus) Pseudomonas, … Anaerobes: Bacteroides, Clostridia 13% anaerobes (mainly G+) anaerobes G–: Bacteroides spp.,a- & B- haemolytic strep G+: Enterococcus If symptomatic: a) Repeated attacks (chronic G+: Clostridium perfringens infection) of acute cholangitis & pancreatitis + Proteus b) Biliary obstruction & stricture aka pyogenic liver abscess Bacterial liver abscess no jaundice Amoebic liver abscess Parasitic infection S/S High swinging fever, chills, RUQ pain Low grade fever, Usually asymptomatic, Right lobe > left > Pyogenic liver abscess S/S: + markedly diarrhoea,Hxcough, of dysentery Hx of eating poorly caudate / quadrate raised bilirubin, liver enzymes, leukocytosis crackles Hepatomegaly, RUQ pain cooked freshwater fish Organism G-: Klebsiella (MC), E. coli, …+3x gut anaerobes Entamoeba histolytica Clonorchis sinensis Enterococcus is resistant G+: Enterococcus, Streptococcus Look out for travel history !! Chronic infection → recurrent cholangitis, pancreatitis, risk of 49 to cephalosporins ! Esp. to developing countries cholangiocarcinoma ↑ HBP infection Pathophysiology of amoebic liver abscess: 1. Ingestion of amoebic cysts in contaminated food or water Ultrasonography of the 2. Excystation occurs in intestinal lumen. Investigations hepatobiliary system & pancreas3. Trophozoites migrate to colon, binds to colonic epithelium ⬢ USG HBP 1st line and multiply by binary fission. ⬢ Biliary drainage (e.g. USG-guided drainage of pus, ERCP, pigtail) and send specimen for microscopy, Gram stain, C/ST Acute cholangitis: bile for microscopy, culture ⬢ Blood culture or + bile microscopy for flukes ⬢ If suspected amoeba / C. sinensis: serology, stool for OCP (ova, cyst and parasite) Fresh + Resuscitation with IV fluids !! ampicillin: enterococcus; Management 4-6 weeks! What do these antibiotics target at? cefuroxime: coliforms (Escherichia, 2nd gen cephalosporin Klebsiella, Enterobacter) ⬢ Triple antibiotics: IV ampicillin + cefuroxime + metronidazole metronidazole: anaerobes ⬢ Biliary drainage (e.g. USG-guided drainage of pus, ERCP, pigtail) (Bacteroides, Clostridium perfringens) a type of drain ⬢ Lap. cholecystectomy if cholecystitis ⬢ Metronidazole + paromomycin for amoebic abscess against Entamoeba histolytica systemic Tx luminal Tx ⬢ Praziquantel for C. sinensis Mx: + Resuscitation with IV fluids !! 50  Viral hepatitis All viral hepatitis are notifiable! No, Hep B is DNA virus Hepatitis viruses are all RNA viruses – Yes or No? ACUTE Hepatitis A Hepatitis E Zoonotic disease Mortality at extreme ages Genotype 1-4 infect Epi Faecal-oral route (shellfish) Poor hygiene, contam food Faecal-oral route (pig livers) humans, HK = genotype Infectious before symptomatic! 4 zoonosis S/S Children mostly asymptomatic Severity increases with age 2-8 (5) week 2-6w incubation Adult mostly symptomatic (fever, jaundice) High risk in pregnant women incubation AST ALT i.e. Dx Anti-HAV IgM Direct detection by PCR NOT OK (short faecal shedding) Anti-HEV IgM Direct detection by PCR OK !! (long faecal shedding) serology Blood samples for: Anti-HAV IgG: past infection / vaccination Anti-HEV IgG: past infection Vaccine? Monovalent vaccine: inactivated, 2 doses Vaccine N/A Bivalent vaccine (w/ HBV): inactivated, 3 doses Prevention for hepatitis A and E: consume well-cooked food & water Tx: Agents with proven antiviral effect for HAV and HEV are NOT available Hepatitis A S/S: Hepatitis A Hepatitis E - abrupt onset of nausea, vomiting, anorexia, - Incidence decreases over the two last decades - Commonest acute hepatitis in recent years fever, malaise & abdominal pain - Older age group - Most (>80%) young adults are susceptible - dark urine (bilirubinuria); pale stools - Most (>70%) young adults are susceptible - Most local cases are genotype 4 (zoonosis) (lacking bilirubin pigment); jaundice, pruritus Hepatitis E S/S: - scleral icterus, hepatomegaly; right upper Jaundice with malaise, anorexia, nausea, quadrant tenderness to palpation vomiting, abdominal pain, fever & hepatomegaly 51  given mother is screened to be hep B positive (HBsAg positive) → HBV, HCV, HIV see viral load → not suppressed → 3rd trimester: tenofovir. How to prevent HBV vertical transmission? Hepatitis B Hepatitis C No Vaccine ! HIV Group VI: single-stranded RNA viruses with a DNA intermediate (i.e. (+)ssRNA-RT virus) Epi Almost 100% vaccinated, Lower prevalence and disease Main risk groups: MSM, IVDA, mainly vertically transmitted burden than HBV transsexuals, female sex workers i.e. mother to child Routes Vertical: during delivery and breastfeeding No Vaccine for HIV ! Sexual: HIV transmission is enhanced by genital ulcers (e.g. syphilis, HSV) Blood-borne: transfusion, IV drug use, sharps injury, tattoo, … AIDS: severe late-stage HIV infection Clinical Primary infection often 2-6mo Primary infection often Acute: “sero-conversion” – fever, LN, incubation course asymptomatic in children asymptomatic à >80% flu-like symptoms lymphadenopathy Reducing carrier % (30-50% symp. in adults) progress to chronic hepatitis Latent: gradually dropping CD4+ But increasing à Chronic hepatitis à Cirrhosis / HCC higher rate AIDS: viral load increases, CD4 than hep B symptomatic à Cirrhosis / HCC (200x) count 6 mo for chronicity Anti-HCV / HCV RNA HIV 4th-generation immunoassay Ab Acute Hep B: detection of HBsAg (EIA) & IgM anti-HBc HCV core Ag + Anti-HCV IgG = combo HIV Ab differentiation assay Chronic Hep B: persistent detection of HBsAg > 6 mths Tx Interferons Peg Interferons Highly active anti-retroviral Nucleoside analogues: Ribavirin therapy (HAART): e.g. tenofovir, entecavir Protease inhibitors tenofovir/emtricitabine (Truvada) + 3rd drug e.g. NNRTI, integrase inhibitor52 ritonavir, nelfinavir NNRTI: non-nucleoside reverse transcriptase inhibitor Laboratory markers for HBV Chronic carrier → HbsAg + Anti-HBc IgG +ve ⬢ HBsAg: current infection (+ve = there is HBV in your body) ⬢ Anti-HBs IgG: immunity (+ve = you are immune to HBV e.g. vaccinated / recovered) ⬢ Anti-HBc IgM (acute) / IgG (chronic): (+ve = you have been exposed to HBV in some point of life) exposed recently chronic exposure ⬢ HBeAg: correlates with HBV DNA (viral load), indicate the infectivity or severity How to differentiate between vaccine and past infection? Vaccine: - Anti-HBs IgG +ve, - Anti-HBc –ve Past infection: - Anti-HBs IgG +ve, - Anti-HBc +ve 53  Urinary tract infection (UTI) Classification What are the differences in S/S? bladder infection kidney infection ⬢ Lower vs Upper: lower tract (urethritis, cystitis), upper tract (pyelonephritis) ⬢ Uncomplicated vs complicated: Uncomplicated = adult non-pregnant female without structural/neurological dysfunction, Complicated = anyone else (e.g. all men) - Urethritis: dysuria, urgency, frequency, urethral discharge - Cystitis: dysuria, urgency, vesicoureteral reflux frequency, suprapubic pain, Risk factors: female, indwelling catheter, VUR, urinary tract obstruction, diabetes haematuria - Prostatitis: dysuria, urgency, Haematogenous spread frequency, suprapubic pain, (Staph aureus / MTB) Need Quantitative culture -> >10^5 cfu / ml MSU Causative organisms haematuria + obstruction S/S (hesitancy, poor stream…) Gram negatives PPE Gram positives MESS Others Neisseria gonorrhea & Chlamydia trachomatis Escherichia coli (MC) Uropathogenic Staph saprophyticus STD organisms E coli Klebsiella MgNH4PO4 Enterococcus Candida (if catheterized) Proteus (struvite stone!) Staph aureus (esp. if bacteremia) Schistosoma haematobium Apatite (CaPO4) Pseudomonas MTB (esp. if bacteremia) Anaerobes, MTB, Adenovirus, Polyomavirus How to choose urinary specimen? pyelonephritis + septic → UTI may be originated from bloodstream infection → Staph aureus, M. tuberculosis gonococcus, chlamydia bowel symptoms? /acid prostate infection First pass urine (urethritis), mid-stream urine (cystitis), terminal urine (prostatitis) Boric (bacteriostatic) Dip slide in CLED / MacConkey Sterile container, immediate transport (X overgrowth) Catheterized urine, suprapubic Fresh catheterized urine (avoid colonization) urine Filter paper strip method for culture54 Suprapunic urine = from bladder in aseptic technique -> any growth is considered significant (no need >10^5)  Nitrite shows presence of Enterobacteriaceae → produce nitrate reductase Prophylaxis is generally not needed in Leukocyte esterase shows presence of white cells. uncomplicated UTI. Urinary tract infection (UTI) Indications for prophylaxis include: - Immunocompromised / pregnant lady - Children (risk of renal scarring) Investigations What is “significant bacteriuria” for MSU? Prophylaxis for UTI → ⬢ Urine dipstick: nitrite, leukocyte esterase nitrite, leukocyte esterase +ve = UTI nitrofurantoin, co-trimoxazole ⬢ Mid-stream urine: microscopy, Gram stain, C/ST +/- AFB (ZN stain), TB culture ⬢ Blood culture + Complete blood count, renal function test Ultrasound kidney, CT urogram for ⬢ Workup for underlying cause Nitrofurantoin & fosfomycin = urinary tract agents (high urine conc.) if complicated / recurrent (e.g. USG) Proteus → look for struvite stones ! Nitrofurantoin is contraindicated in renal impairment How to collect urine specimen? For patient who was on long-term urinary catheter: PT and G6PD deficiency PT. Use in caution in elderly. - ‘Fresh Catheterised Urine’ catheter is replaced prior to collection Antibiotic treatment - Collect sample from sampling port of the catheter for catheters remaining in situ - Do NOT collect specimen from the collection bag (as it is prone to contamination with biofilm formation) Fosfomycin Lower tract (cystitis) PO Nitrofurantoin (esp. if E. coli) Uncomplicated: 3-5 days E. coli, S. saprophyticus, PO Septrin (trimethoprim-sulfamethoxazole) Complicated: 7 days i.e. co-trimoxazole S. agalactiae PO Augmentin If E. coli resistant to beta-lactams → ciprofloxacin Upper tract (pyelonephritis) IV Augmentin / Tazocin piperacillin- tazobactam IV until afebrile for 24-48h, then finish Enterobacteriaceae, Enterococcus, Pseudomonas or carbapenem for severe cases 14 days PO E. coli, Klebsiella, Proteus Re: foley w/ ESBL Prostatitis PO fluoroquinolones (e..g cipro) ciprofloxacin UTI if afebrile + uncomplicated → PO ciprofloxacin OK! → if no improvement, upgrade to IV 3rd gen cephalosporin (cefotaxime) 55  CNS infection Meningitis: Meningeal infection involving the leptomeninges (arachnoid and pia mater) and subarachnoid space. i.e. stiff neck, pain Kernig: flex the hip and Brudziński: forced neck Clinical presentation when turning, moving, knee to 90˚, if extension is painful → positive sign flexion causes a reflex hip and knee flexion flexing the neck ⬢ Meningeal irritation: nuchal rigidity, Kernig’s sign, Brudzinski’s sign ⬢ Raised ICP: headache, early morning vomiting, papilledema, CN6 palsy, bulging fontanelles (infants) Encephalitis: Inflammation of the brain, resulting in decreased mental state, e.g. ⬢ Neurological deficits: diplopia, seizure, coma confused or stupor, early in course of disease with minimal meningeal signs Haematogenous; contiguous sites (AOM, sinusitis); direct inoculation shunt (skull base #) - Other S/S: fever, headache, seizures Risk factors: skull base #, otitis media, head trauma, CSF shunt, cochlear implant Non-balancing Complications: cerebral edema, CN palsy (e.g. deafness ), hydrocephalus maculopapilar rash 35-37 week do low vaginal and rectal swab → see whether there fever + rash (purpura) → meningococcal is GBS. If yes, If GBS +ve, IV antibiotic (ampicillin) intra-partum septicaemia until proven otherwise Bacterial/Fungal infection – classify by AGE What is “purpura fulminans”? Neonates / Infants Sharply Cellulitis: ill defined edge, demarcated border, incision and drainage i.e. penicillin not ok, need augmentin diffuse erythema, lymphangitis erematoud indurated (preferred over cloxacillin) Necrotising fasciitis: life threatening!! (peau d’orange) @infant, 1: non-blanchable erythema of intact skin ⬢ Warning signs: severe pain out of proportion, presence of haemorrhagic 2:3: partial children, old adult thickness skin loss with exposed dermis full thickness skin loss → extends to subcutaneous fat layer bullae/blisters, rapidly progressing necrosis 4: full thickness skin and tissue loss → exposed muscle / bone ⬢ Clinical diagnosis: always a DDx of cellulitis Causative organisms: S. aureus, S. pyogenes ⬢ Organisms: Strep pyogenes (MC), Vibrio vulnificus, Staph aureus, anaerobes Linezolid!! (Inhibit toxin piperacillin-tazobactam ⬢ production Management: aggressive surgical debridement + big-gun antibiotics (e.g. IV Tazocin of dead tissue / meropenem + metronidazole) to manage possible 2˚ infection due to extensive debridement pyogenic bacteria EXCEPT MRSA, anaerobes !! What is “Fournier’s gangrene”? ampicillin-resistant enterococci, in case in contact with Fournier’s gangrene: necrotising fasciitis stenotrophomonas, atypical, MDRO seawater, e.g. injury when in of the perineum and the scrotum Cellulitis: Infection of dermis and subcutaneous fat. S/S: contact with marine organisms Pseudomonas always - Diffuse area of erythema and oedema If IV drug user + infective endocarditis (e.g. pansystolic murmur) → S. aureus !!! comes out if deep burns -> - Ill-defined edges (c.f. erysipelas) S. pyogenes is less likely + should also present with pharyngitis, - Usually no fluctuation or pus 62 scarlet fever, etc. look for green discharge - Usually accompanied by lymphadenitis / lymphangitis  How to prevent wound infection: Wound infection Wound infection signs and symptoms: - Fever, tachycardia, septicaemic features - Proper patient preparation (nutrition, skin - Wound pain, erythema, swelling, warmth, asepsis) collection / abscess, discharge - Proficient surgical skills Surgical antibiotic prophylaxis – depend on wound classification - Appropriate use of peri-operative antibiotic - Proper wound care ⬢ Usually given ”on call to OT” (IV 30-60min before incision), repeat after 2x half-life of drug (cefuroxime Q3h) Type Examples Organisms Inf. rate Antibiotic prophylaxis Achieve max infection tissue conc at Clean: does not transect GI tract, Thyroidectomy Staphylococcus 1% Not always needed the time when GU tract, respiratory tract Breast surgery spp. Orthopaedics: cefazolin bac contam is Herniotomy Neurosurgery: ceftriaxone 3rd gen most likely for a Consider CSF conc. limited time Clean-contaminated: transect CA stomach Staphylococcus 5% Cefazolin (1st gen ceph) (decisive period)GI tract, GU tract, respiratory CA colon spp. 1GC w/ MSSA coverage (from time of tract but no gross contamination incision - wound 2nd gen ceph closure) -> Contaminated: transect GI tract, Perforated bowel Mixed aerobic + 13% Cefuroxime + Balance: GU tract, respiratory tract with Spillagerepair expected, anaerobic Cholecystectomy during metronidazole protection definite bacterial contamination can’t maintain sterile Acute cholecystitis during high risk period vs reduce Dirty: Known infection Gangrene, Mixed aerobic + 40% Case-by-case Exposure to abscess, NF anaerobic necrotising fasciitis ABx to reduce CTX surgery need maintain ABx conc >MIC till 3 days post-op emergence ofNon-surgical antibiotic prophylaxis cover pneumococcus, meningococcus resistance & S/E of ABx ⬢ Splenectomy (cover encapsulated organisms): penicillin, vaccination (e.g. PCV-13, Hib, Meningococcal ACYW) ⬢ HIV: PCP prophylaxis by co-trimoxazole high risk of infective endocarditis not give penicillin because pen can cover viridans strep but not enterococcus ⬢ Cyanotic heart diseases / Prosthetic heart valves: amoxicillin before dental / respiratory procedures 63 Sexually transmitted infection Remember: contact tracing + treat sexual partners 64  Sexually transmitted infection Another Ix: dark-field microscopy → requires fresh exudate from T. pallidum is an Syphilis: Treponema pallidum chancres (T. pallidum cannot survive outside host for long time) obligate anaerobe ! chancre ≠ chancroid (caused Clinical course S/S by Haemophilus ducreyi) Tx: penicillin Primary syphilis Painless genital ulcer (chancre) Primary/Secondary/Early latent: if painful → think of Herpes infection benzathine pen 2.4 MU IM x 3 doses Secondary syphilis Maculopapular rash over palms and soles Late latent: + hepatitis, osteitis, nephritis, uveitis benzathine pen 4 MU IM weekly x 3 weeks Latent syphilis Asymptomatic slow degeneration of the neural Tertiary syphilis Cardiovascular: aortitis tracts in the DRG of spinal cord IV penicillin G 3-4 MU Q4h x 10-14 days 1. non-treponemal for screening Neuro: tabes dorsalis, general paresis of → 2. treponemal for confirmation the insane, Argyll-Robertson pupils T. pallidum particle agglutination assay → 3. non-treponemal for follow-up Gumma (granulomatous lesions) Monitor drop in titre Fluorescent treponemal T. pallidum Serology antibody absorption hemagglutination assay ⬢ Dx: non-treponemal test (VDRL, RPR) vs treponemal test (FTA-ABS, TPPA, TPHA) venereal disease research laboratory rapid plasma reagin NON-treponemal = NON-specific Gonorrhoea: Neisseria gonorrhoeae