Infectious diseases Flashcards

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1
Q

First thought cellulitis.

A
  • Infection of dermis and subcutaneous tissue
  • caused by: S. aureus, ß-haemolytic streptococci
  • Flucloxacillin
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2
Q

What is the aetiology of cellulitis?

A
  • common causative agents: S. aureus, β-hemolytic streptococci
  • immunocompromised patients or water exposure: may also include GN rods and fungi
  • risk factors:
    • trauma with direct inoculation, recent surgery
    • peripheral vascular disease, lymphedema diabetes, cracked skin in feet/toes (tinea pedis)
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3
Q

What are the clinical features of cellulitis?

A
  • pain, edema, erythema with indistinct borders ± regional lymphadenopathy, systemic symptoms (fevers, chills, malaise)
  • can lead to ascending lymphangitis (visible red streaking in skin along lymphatics proximal to area of cellulitis)
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4
Q

What Ix are ordered for a pt with cellulitis?

A
  • FBC and differential, blood C&S if febrile
  • skin swab ONLY if open wound with pus
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5
Q

What is the Rx for cellulitis?

A
  • Abx
    • Mild/early: di/flucloxacillin 500 mg PO, 6h for 5-10 days OR cephalexin for penicillin sensitivity
    • Severe: flucloxacillin 2g IV, 6h Or cephazolin for penicillin sensitivity
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6
Q

Describe the aetiology and risk factors of a septic joint?

A
  • most commonly caused by Staphylococcus aureus in adults
  • consider coagulase-negative Staphylococcus in patients with prior joint replacement
  • consider Neisseria gonorrhoeae in sexually active adults and newborns
  • most common route of infection is hematogenous
  • risk factors: age >80 yr, DM, RA, prosthetic joint, recent joint surgery, skin infection/ulcer, IV drug use, alcoholism, previous intra-articular corticosteroid injection
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7
Q

What is the clinical presentation of a septic joint?

A
  • inability/refusal to bear weight
  • localized joint pain
  • erythema
  • warmth
  • swelling
  • pain on active and passive ROM
  • ± fever
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8
Q

What investigations should be ordered for a suspected septic joint?

A
  • Bloods: FBC, UEC, LFT, glucose, urate, CRP/ESR, blood cultures
  • Urine: ward test → MCS if positive.
  • x-ray (to rule out fracture, tumor, metabolic bone disease)
  • Joint asperate: MCS, crystals
    • WBC >80,000 with >90% neutrophils, protein level >4.4 mg/dL, joint glucose level << blood glucose level, no crystals, positive Gram stain results
  • Listen for heart murmur (to reduce suspicion of infective endocarditis)
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9
Q

What is the Rx for septic arthritis?

A
  • IV antibiotics, empiric therapy (based on age and risk factors), adjust following joint aspirate C&S results:
    • Flucloxacillin 1g/6h IV - ?empirical
    • Vancomycin 1g/12h IV if MRSA
    • Cefotaxine 1g/8h IV if gonococcal or Gram-ve
  • for small joints: needle aspiration, serial if necessary until sterile
  • for major joints such as knee, hip, or shoulder: urgent decompression and surgical drainage - Ortho referral for arthrocentesis, lavage and/or debridement
  • Give adequate analgesia
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10
Q

What is the classification of a prosthetic joint infection?

A
  • Early (<3 months after surgery) - acquired during implantation
  • Delayed (3 - 12 months after surgery) - acquired during implantation
  • Late (>12 months) - primarily due to haematogenous (sudden onset in a previously well-functioning joint)
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11
Q

What is the aetiology of a prosthetic joint infection?

A
  • Early post-operative: virulent organisms - Staphylococcus aureus but also beta-haemolytic streptococci and aerobic Gram-negative organisms.
  • Chronic infections: are likely to be caused by less virulent organisms, including coagulase-negative staphylococci, Enterococcus species and Propionibacterium species
  • Late acute haematogenous infections: Virluent organisms - Staphylococcus aureus but also beta-haemolytic streptococci and aerobic Gram-negative organisms.
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12
Q

What is the Rx for a prosthetic joint infection?

A
  • Multidisciplinary team approach
  • Abx to culture and sensitivities
    • Empiral Rx use - Vancomycin IV
  • Ortho - tissue biopsy and specimen of synovial fluid intraopertatively
    • removal of prosthesis in some cases
    • exchange arthroplasty
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13
Q

Define S aureus bacteremia.

A
  • S. aureus bacteremia is defined as positive blood cultures for S. aureus; frequently, this occurs in association with correlating symptoms such as fever or hypotension.
  • S. aureus is a leading cause of community-acquired and hospital-acquired bacteremia.
  • Bacteremia may develop as a complication of a primary S. aureus infection such as skin and soft tissue infection, bone and joint infection, or pneumonia.
  • Vascular catheters are a common source of bacteremia.
  • Bacteremia may also lead to subsequent S. aureus infection at a previously sterile site, such as endocarditis or prosthetic device infection.
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14
Q

Whar is your clinical appraoch towards a patient with potential S aureus bacteremia?
Hx and exam

A
  • Hx
    • Portals of entry: skin or soft tissue, indwelling prosthetic devices
    • Symptoms: reflecting metastatic infectyion
      • bone or joint pain
      • protracted fever or sweats
      • abdo pain
      • costovertebral angle tenderness and headache
  • Exam:
    • Cardiac: new regurgitant murmurs or heart failure, stigmata of endocarditis
    • Neuro: focal neuro impairment and baseline neuro incase deficits develop
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15
Q

What is the Rx for S aureus bacteremia?

A
  • ID consult
  • Echo - rule out endocarditis
  • Removal of source
  • Abx
    • Empirical - Vancomycin IV
    • MSSA - flucloxacillin IV q6h or cefazolin 2g IV q8h
    • MRSA - Vancomycin IV
  • Follow-up cultures to document clearance of bacteraemia
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16
Q

Define what a urinary tract infection is?

A
  • symptoms suggestive of UTI + evidence of pyuria and bacteriuria on U/A or urine C&S
    • if asymptomatic + 100,000 CFU/mL = asymptomatic bacteriuria; only requires treatment in certain patients (e.g. pregnancy)
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17
Q

How are UTIs classified?

A
  • uncomplicated: lower UTI in a setting of functionally and structurally normal urinary tract
  • complicated: structural and/or functional abnormality, male patients, immunocompromised, diabetic, iatrogenic complication, pregnancy, pyelonephritis, catheter-associated
  • recurrent/chronic cystisis: ≥3 UTIs/yr
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18
Q

What are the risk factors for getting a UTI?

A
  • stasis and obstruction
    • residual urine due to impaired urine flow e.g. PUVs, reflux, medication, BPH, urethral stricture, cystocele, neurogenic bladder
  • foreign body
    • introduce pathogen or act as nidus of infection e.g. catheter, instrumentation
  • decreased resistance to organisms
    • DM, malignancy, immunosuppression, spermicide use, estrogen depletion, antimicrobial use
  • other factors
    • trauma, anatomic abnormalities, female, sexual activity, fecal incontinence
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19
Q

What are the clinical features of UTI?

A
  • storage symptoms: frequency, urgency, dysuria
  • voiding symptoms: hesitancy, post-void dribbling
  • other: suprapubic pain, hematuria, foul-smelling urine
  • pyelonephritis – if present: typically presents with more severe symptoms (e.g. fever/chills, CVA tenderness, flank pain)
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20
Q

What are the organisms that are usually involved in UTI?

A
  • typical organisms: KEEPS
    • Klebsiella sp.
    • E. coli (90%), other Gram-negatives
    • Enterococci
    • Proteus mirabilis, Pseudomonas
    • S. saprophyticus
  • atypical organisms
    • tuberculosis (TB)
    • Chlamydia trachomatis
    • Mycoplasma (Ureaplasma urealyticum)
    • fungi (Candida)
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21
Q

What are the indications for investigation of UTI?

A
  • pyelonephritis
  • persistence of pyuria/symptoms following adequate antibiotic therapy
  • severe infection with an increase in Cr
  • recurrent/persistent infections
  • atypical pathogens (urea splitting organisms)
  • hx of structural abnormalities/decreased flow
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22
Q

What investigations should be order in UTI?

A
  • U/A, urine C&S
    • UA: leukocytes ± nitrites ± hematuria
    • C&S: midstream, catheterized, or suprapubic aspirate
  • if hematuria present, retest post-treatment, if persistent need hematuria workup
  • U/S, CT scan if indicated
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23
Q

What is the treatment for UTI?

A
  • Non-pregant women/men: trimethoprim 300mg PO for 3 days
  • Pregnant women: cephalexin 500mg PO 12h for 5 days
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24
Q

What microbes usually cause surgical site infections?

A
  • S. aureus
  • E. coli
  • Enterococcus
  • Streptococcus spp.
  • Clostridium spp.
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25
Q

What are the risk factors for a surgical site infection?

A
  • patient characteristics
    • age, DM, steroids, immunosuppression, obesity, burn, malnutrition, patient with other infections, traumatic wound, radiation, chemotherapy
  • other factors
    • prolonged pre-operative hospitalisation, reduced blood flow, break in sterile technique, multiple antibiotics, haematoma, seroma, foreign bodies (drains, sutures, grafts), skin preparation, hypoxaemia, hypothermia
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26
Q

What is the clinical presentation of a surgical site infection?

A
  • typically fever POD #5-8 (Streptococcus and Clostridium can present in 24h)
  • pain, blanchable wound erythema, induration, purulent discharge, warmth
  • complications: fistula, sinus tracts, sepsis, abscess, suppressed wound healing, superinfection, spreading infection to myonecrosis or fascial necrosis (necrotizing fasciitis), wound dehiscence, evisceration, hernia
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27
Q

What can be done as prophylaxis for surgical site infections?

A
  • used to reduce the chance of surgical site infections pre-operative antibiotics for most surgeries (cefazolin ± metronidazole or if β-lactam allergy, clindamycin ± gentamycin)
    • within 1 h pre-incision; can re-dose at 1-2 half-lives (~q4-8h) in the OR
    • not required for low risk elective cholecystectomy, hemorrhoidectomy, fistulotomy, sphincterotomy for fissure
  • generally no need to continue prophylactic antibiotics post-operatively
    • reserve post-operative antibiotics for treatment of suspected or documented intra-abdominal infection
  • normothermia (maintain patient temperature 36-38ºC during OR)
  • hyperoxygenation (consider FiO2 of 80% in OR)
  • chlorhexidine-alcohol wash of surgical site
  • hair removal should not be performed unless necessary; if so, clipping superior to shaving
  • protect skin edges (moistened lap pads); consider delayed primary closure of incision for contaminated wounds
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28
Q

What is the Rx for surgical site infections?

A
  • examination of the wound: inspect, compress adjacent areas, swab drainage for C&S and Gram stain
  • re-open affected part of incision, drain, pack, heal by secondary intention in most cases
  • for deeper infections, debride necrotic and non-viable tissue
  • antibiotics
  • demarcation of erythema only if cellulitis or immunodeficiency
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29
Q

Describe the aetiology of diabetic foot infections.

A
  • neuropathy, peripheral vascular disease, and hyperglycemia contribute to foot ulcers that heal poorly and are predisposed to infection
  • organisms in mild infection: S. aureus, Streptococcus spp.
  • organisms in moderate/severe infection: polymicrobial with aerobes (S. aureus, Streptococcus, Enterococcus, GNB) and anaerobes (Peptostreptococcus, Bacteroides, Clostridium)
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30
Q

What are the clinical features of diabetic foot infections?

A
  • NOT all ulcers are infected
  • consider infection if: probe to bone, ulcer present >30 d, recurrent ulcers, trauma, PVD, prior amputation, loss of protective sensation, renal disease, history of walking barefoot
  • diagnosis of infected ulcer: ≥2 of the cardinal signs of inflammation (redness, warmth, swelling, pain) or the presence of pus
  • ± crepitus, osteomyelitis, systemic toxicity
  • visible bone or probe to bone → osteomyelitis
  • infection severity:
    • mild = superficial (no bone/joint involvement)
    • moderate = deep (beneath superficial fascia, involving bone/joint) or erythema >2 cm
    • severe = infection in a patient with systemic toxicity (fevers, tachypnea, leukocytosis, tachycardia, hypotension)
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31
Q

What investigations need to be order with a patient with a diabetic foot infection?

A
  • curettage specimen from ulcer base, aspirate from an abscess or bone biopsy (results from superficial swabs do not represent organisms responsible for deeper infection)
  • blood C&S if febrile
  • assess for oseteomyelitis by x-ray (although not sensitive in early stages) or MRI if high clinical suspicion
    • if initial x-ray normal, repeat 2-4 wk after initiating treatment to increase test sensitivity
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32
Q

What is the Rx for diabetic foot infection?

A
  • evaluate for early surgical debridement ± revascularization or amputation
  • eliminate/reduce pressure and provide regular local wound care
  • mild to moderate: Amoxycillin + clavulanate 875 + 125 mg PO 12h
  • severe: piperacillin/tazobactam 4 + 0.5 g IV q8h
  • encourage glycemic control
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33
Q

What is the DDx of fever in the returned traveller

A
  • commonly identified causes of fever in returning traveler
    • parasitic: malaria (20-30%)
    • viral: non-specific mononucleosis-like syndrome (4-25%), dengue (5%), viral hepatitis (3%)
    • bacterial: typhoid from Salmonella (2-7%), rickettsioses (3%)
    • diverse group of causative pathogens: traveler’s diarrhea (10-20%), RTI (10-15%), UTI/STD (2-3%)
  • febrile illness in travelers can be caused by routine infections that are common in non-travelers (e.g. URTI, UTI)
  • less commonly, fever can be due to non-infectious causes: e.g. DVT, PE
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34
Q

What information do you want to collect from a patient who is a returned traveller with a fever?

A
  • pre-travel preparation
  • travel itinerary: when, where, why, what, who, how?
    • dates of travel (determine incubation period)
    • season of travel: wet or dry
    • destination: country, region (urban or rural), environment (jungle, desert, etc.)
    • purpose of trip
  • persons visiting friends and family more likely to be exposed to local population and pathogens
    • style of travel: lodgings, camping, adventure traveling
    • local population: sick contacts
    • transportation: use of animals
  • exposure history
    • street foods, untreated water: increased risk of traveler’s diarrhea, enteric fever
    • uncooked meat/unpasteurized dairy: increased risk of parasitic infection
    • body fluids (sexual contacts, tattoos, piercings, IVDU, other injections)
    • increased risk of HBV, HCV, HIV, GC, C. trachomatis, syphilis
    • animal/insect bites: increased risk of malaria, dengue, rickettsioses, rabies
  • fever pattern
  • incubation period: use the earliest and latest possible dates of exposure to narrow the differential diagnosis and exclude serious infections
    • <21 d: consider malaria, typhoid fever, dengue fever, rickettsioses; exclude HBV, TB
    • >21 d: consider malaria, TB; exclude dengue fever, travelers’ diarrhea, rickettsioses
  • body systems affected: GI, respiratory, CNS, skin
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35
Q

What investigations would you order in fever in a returned traveller?

A
  • all travelers with fever should undergo the following tests
    • blood work: FBC, LFT, UECs, thick and thin blood smears x3 (for malaria), blood C&S
    • ƒurine: urinalysis, urine C&S
  • special tests based on symptoms, exposure history, and geography
    • stool: C&S, O&P
    • CXR
    • dengue serology for IgM
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36
Q

Describe the lifecycle of malaria (Plasmodium spp.).

A
  1. Sporozoites enter blood via mosquito bite, infect liver
  2. Hepatic infiltration
  3. Infect red blood cells
  4. Trophozoite divides asexually many times to produce schizont (contains merozoites)
  5. Red blood cell lyses and merozoites attack other red blood cells (chills and fever)
  6. Male and female gametocytes (from merozoites) ingested by mosquito
    during bite
  7. Male and female gametocytes (from merozoites) fuse in mosquito gut; produce ookinete
  8. Ookinete matures into an oocyst which contains individual sporozoites; migrates to mosquito salivary glands
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37
Q

What are the clinical features of malaria?

A
  • flu-like prodrome
  • paroxysms of high spiking fever and shaking chills (due to synchronous systemic lysis of RBCs) (lasts several hours)
    • P. vivax and P. ovale: chills and fever q48h but can be variable
    • P. malariae: chills and fever q72h but can be variable
    • P. falciparum: less predictable fever interval, can be highly variable (>90% ill within 30 d)
  • abdominal pain, diarrhea, myalgia, H/A, and cough
  • hepatosplenomegaly and thrombocytopenia without leukocytosis
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38
Q

What are the complications of malaria?

A
  • P. falciparum: CNS involvement (cerebral malaria = seizures and coma), severe anemia, acute renal failure, ARDS, primarily responsible for fatal disease
  • P. knowlesi, and rarely P. vivax can be fatal
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39
Q

What investigations are order for a pt with malaria?

A
  • microscopy: blood smear q12-24h (x3) to rule out infection
    • thick smear (Giemsa stain) for presence of organisms
    • thin smear (Giemsa stain) for species identification and quantification of parasites
  • rapid antigen detection tests
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40
Q

What is the Rx for malaria?

A
  • P. vivax, P. ovale: chloroquine (and primaquine to eradicate liver forms)
  • P. vivax, chloroquine resistant: primaquine with quinine and doxycycline or tetracycline or mefloquine
  • P. malariae, P. knowlesi: chloroquine
  • P. falciparum: most areas of the world show chloroquine resistance – check local resistance patterns
    • artemisinin combination therapy (e.g. artesunate + doxycycline or clindamycin or atovaquone/proguanil)
    • atovaquone/proguanil combination (Malarone®)
    • quinine plus doxycycline, tetracycline, or clindamycin
    • mefloquine and artemisinin resistance increasing in southeast Asia (check local resistance)
  • prevention with antimalarial prophylaxis, covering exposed skin, bed nets, insect repellant
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41
Q

Describe the epidemiology and risk factors of discitis?

A
  • Most cases occur in >50
  • M>F = 2:1
  • Risk factors:
    • IVD use
    • endocarditis
    • degenerative spine disease
    • prior spinal surgery
    • corticosteroid therepy/immunocompromised state
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42
Q

What are the organisms that responsible for discitis?

A
  • Staph aureus (>50%)
  • Enteric gram -ve bacilli - urinary tract instrumentation
  • Pseudomonas aeruginosa and Candida spp. - associated with IVD
  • Group B and G haemolytic streptococci - esp. in DM
  • TB
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43
Q

What are the clinical features of discitis?

A
  • Back or neck pain - localised to the infected disc space, exacerbated by physical activity or percussion to the affected area.
  • Radiating pain to the abdo, leg, scrotum, groin or perineum
  • Spinal pain that begins insidiously and progressively worsens over weeks>months and worse at night
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44
Q

What Ix should be order for a patient with discitis?

A
  • Bloods: FBC, UECs, LFT, CRP/ESR, blood cultures,
  • Urine: MCS
  • Echo: endocarditis
  • Imaging: CT guided needle bipsy (MCS), MRI
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45
Q

What is the treatment for discitis?

A
  • Abx: pathogen specific - for a min of 6 weeks
    • Staph aureus: cefazolin 2g IV q8h
    • Strep spp: ceftriaxone 1-2g IV q24h
    • Empirial: vancomycin 15-20 mg/kg Q8-12h PLUS a cephalosporin
  • Surgery: used only in patietns with neurological deficits
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46
Q

Define meningitis.

A

Inflammation of the meninges

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47
Q

What are the common organisms in meningitis?

A
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49
Q

What are the risk factors for meningitis?

A
  • lack of immunisation against S. pneumoniae, H. influenzae type b in children
  • haematogenous spread after invasion from a mucosal surface (nasopharynx)
  • parameningeal focus (otitis media, infection, sinusitis)
  • penetrating head trauma
  • anatomical meningeal defects – CSF leaks
  • previous neurosurgical procedures, shunts
  • immunocompromise (corticosteroids, HIV, asplenia, hypogammaglobulinemia, complement deficiency)
  • contact with colonised or infected persons
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50
Q

What are the clinical features of meningitis?

A
  • neonates and children: fever, vomiting, lethargy, irritability, poor feeding
  • older children and adults: fever, H/A, neck stiffness, confusion, N/V, lethargy, photophobia, altered level of consciousness, seizures, focal neurological signs, papilledema
  • petechial rash in meningococcal meningitis, seen more frequently on trunk or lower extremities
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51
Q

What Ix should be done for a pt with meningitis?

A
  • blood work:
    • FBC and differential, UEC (for SIADH), blood C&S
    • CSF: opening pressure, cell count + differential, glucose, protein, Gram stain, bacterial C&S
      • Acid fast bacilli, fungal C&S, cryptococcal antigen in immunocompromised patients, subacute illness, suggestive travel history or TB exposureƒ
      • PCR for HSV, VZV, enteroviruses, WNV if viral cause suspected
  • imaging/neurologic studies:
    • CT, MRI, EEG if focal neurological signs present
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52
Q

Describe the typical CSF profiles for bacterial and viral meningitis?

A
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54
Q

Describe the treatment for bacterial meningitis?

A
  • bacterial meningitis is a medical emergency: do not delay antibiotics for CT or LP
  • empiric antibiotic therapy
    • <2 mo call paeds/ED consultant
    • age >2 mo + adults: ceftriaxone IV
  • Direct Abx therapy: see eTG for specific treatments
  • Dexamethasone IV within 20 min prior to or with first dose of antibiotics
    • continue Q6h for 4 days
55
Q

What are the preventitive measures for meningitis?

A
  • immunizationƒ
    • children: immunization against H. influenzae, S. pneumoniae, N. meningitidis
    • adults: immunization against N. meningitidis in selected circumstances (outbreaks, travel, epidemics) and S. pneumoniae (Pneumovax®) for high-risk groups
  • prophylaxis: close contacts of patients infected with H. influenzae should be treated with rifampin if they live with an inadequately immunized (<4 yr) or immunocompromised child (<18 yr); ciprofloxacin, rifampin, or ceftriaxone if close or household contact of a patient with N. meningitidis
56
Q

Define endocarditis, and how it is classified?

A
  • infection of cardiac endothelium, most commonly the valves
  • classifications: acute vs. subacute, native valve vs. prosthetic valve, right-sided vs. left-sided
  • leaflet vegetations that are comprised of platelet-fibrin thrombi, WBCs, and bacteria
57
Q

What are the risk factors and aetiology of endocarditis?

A
  • predisposing conditions
    • high risk: prosthetic cardiac valve, previous IE, congenital heart disease (unrepaired, repaired within 6 mo, repaired with defects), cardiac transplant with valve disease (surgically constructed systemic-to-pulmonary shunts or conduits)
    • moderate risk: other congenital cardiac defects, acquired valvular dysfunction, hypertrophic cardiomyopathy
    • low/no risk: secundum aterial septal defect (ASD) or surgically repaired ASD < VSD, PDA, MV prolapse, ischemic heart disease, previous CABG
    • opportunity for bacteremia: IVDU, indwelling venous catheter, hemodialysis, poor dentition, DM, HIV
  • frequency of valve involvement MV >> AV > TV > PV
    ƒ but in 50% of IVDU-related IE the tricuspid valve is involved
58
Q

Which microbes are resonsible for endocarditis on native valves?

A
  • Streptococcus1 (36%)
  • S. aureus4 (28%)
  • Enterococcus (11%)
  • S. epidermidis
  • GNB
  • Other:
    • Streptococcus bovis (usually associated with underlying GI malignancy, cirrhosis)
    • Culture-negative organisms including nutritionally-deficient streptococci, HACEK, Bartonella, Coxiella, Chlamydia, Legionella, Brucella
    • Candida
59
Q

Which microbes are resonsible for endocarditis in IVDU?

A
  • S. aureus (68%)
  • Streptococcus (13%)
  • Enterococcus
  • GNB
  • Candida
  • Other:
    • IVDU endocarditis pathogens depend on substance used to dilute the drugs (i.e. tap water = Pseudomonas, saliva = oral flora, toilet water = GI flora)
60
Q

Which microbes are resonsible for endocarditis on Prosthetic Valve
(recent surgery <2 mo)?

A
  • S. aureus (36%)
  • S. epidermidis (17%)
  • Enterococcus
  • GNB
  • Other:
    • Streptococcus bovis (usually associated with underlying GI malignancy, cirrhosis)
    • Culture-negative organisms including nutritionally-deficient streptococci, HACEK, Bartonella, Coxiella, Chlamydia, Legionella, Brucella
    • Candida
61
Q

Which microbes are resonsible for endocarditis on Prosthetic Valve
(remote surgery >2 mo)?

A
  • Streptococcus (20%)
  • S. aureus (20%)
  • S. epidermidis (20%)
  • Enterococcus (13%)
  • Other:
    • Streptococcus bovis (usually associated with underlying GI malignancy, cirrhosis)
    • Culture-negative organisms including nutritionally-deficient streptococci, HACEK, Bartonella, Coxiella, Chlamydia, Legionella, Brucella
    • Candida
62
Q

How is endocarditis diagnosed?

A
  • Modified Duke Criteria
    • definitive diagnosis if: 2 major, OR 1 major + 3 minor, OR 5 minor
    • possible diagnosis if: 1 major + 1 minor, OR 3 minor
63
Q

What are the clinical features of endocarditis?

A
  • systemicƒ
    • fever (80-90%), chills, weakness, rigors, night sweats, weight loss, anorexia
  • cardiac
    • dyspnea, chest pain, clubbing (subacute)
    • regurgitant murmur (new onset or increased intensity)
    • signs of CHF (secondary to acute MR, AR)
  • embolic/vascular
    • petechiae over legs, splinter haemorrhages (linear, reddish-brown lesion within nail bed)
    • Janeway lesions (painless, 5 mm, erythematous, haemorrhagic pustular lesions on soles/ palms)
    • focal neurological signs (CNS emboli), headache (mycotic aneurysm)
      ƒ splenomegaly (subacute)
    • microscopic haematuria, flank pain (renal emboli) ± active sediment
  • immune complex
    • Osler’s nodes (painful, raised, red/brown, 3-15 mm on digits)
    • glomerulonephritis
    • arthritis
    • Roth’s spots (retinal haemorrhage with pale center)
65
Q

What Ix need to be ordered for endocarditis?
And what to expect as the results?

A
  • serial blood cultures: 3 sets (each containing one aerobic and one anaerobic sample) collected from different sites >1 h apart
    • persistent bacteremia is the hallmark of endovascular infection (such as IE)
  • repeat blood cultures (at least 2 sets) after 48 to 72 h of appropriate antibiotics to confirm clearance
  • blood work: FBC (normochromic, normocytic anemia), ESR (increased),
    RF (+), BUN/Cr
  • urinalysis (proteinuria, hematuria, red cell casts) and urine C&S
  • ECG: prolonged PR interval may indicate perivalvular abscess
  • Echo findings: vegetations, regurgitation, abscess
    • TTE (poor sensitivity) inadequate in 20% (obesity, COPD, chest wall deformities)ƒ
    • EE indicated if TTE is non-diagnostic in patients with at least possible endocarditis or if suspect prosthetic valve endocarditis or complicated endocarditis (e.g. paravalvular abscess/perforation) (~90% sensitivity)
66
Q

What is the treatment of endocarditis?

A
  • medicalƒ
    • usually non-urgent and can wait for confirmation of aetiology before initiating treatment: Need ID/micro consult and cardio consult
    • empiric antibiotic therapy if patient is unstable; administer ONLY after blood cultures have been taken
      • first-line empiric treatment for native valve: Gentamicin IV PLUS Benzylpenicillin 1.8 g IV q4h PLUS flucoxacillin 2g IV q4h
      • first line empiric treatment for prosthetic valve: gentamicin IV PLUS flucloxacillin 2g IV q4h PLUS vancomycin IV
    • targeted antibiotic therapy: antibiotic and duration (usually 4-6 wk) adjusted based on valve, organism, and sensitivities
    • monitor for complications of IE (e.g. CHF, conduction block, new emboli) and complications of antibiotics (e.g. interstitial nephritis)
    • prophylaxis only for high risk individuals listed above with dental procedures OR invasive procedure of the respiratory tract that involves incision or biopsy of the respiratory mucosa, such as tonsillectomy and adenoidectomy OR procedures on infected skin, skin structure, or musculoskeletal tissue
      • dental/respiratory: amoxicillin 2g single dose 1h prior;
      • skin/soft tissue: cephalexin single dose 30-60 min prior
  • surgical:
    • most common indication is refractory CHF
    • other indications include: valve ring abscess, fungal etiology, valve perforation, unstable prosthesis, ≥2 major emboli, antimicrobial failure (persistently positive blood cultures), mycotic aneurysm, staphylococci on a prosthetic valve
67
Q

What is the clinical presentation of shingles?

A
  • unilateral dermatomal eruption occurring 3-5 d after pain and paresthesia of that dermatome; may be disseminated in Immunosuppressed (eg HIV, organ transplant)
  • vesicles, bullae, and pustules on an erythematous, edematous base
  • lesions may become eroded/ulcerated and last days to weeks
  • pain is can be pre-herpetic, synchronous with rash, or post-herpetic
  • severe post-herpetic neuralgia often occurs in elderly and may be permanent
  • Hutchinson’s sign: involvement of tip of nose suggests eye involvement
  • distribution: thoracic (50%), trigeminal (10-20%), cervical (10-20%); disseminated in HIV
68
Q

What is the cause and risk factors of shingles?

A
  • caused by reactivation of VZV
  • risk factors: immunosuppression, old age, occasionally associated with hematologic malignancy, stress
69
Q

What investigations can be done on a pt with shingles?

A
  • none required, but can do Tzanck test, direct fluorescence antibody test, or viral culture to rule out HSV
70
Q

What is the management of shingles?

A
  • compress with normal saline, Burow’s, or betadine solution
  • analgesics (NSAIDs, amitriptyline)
  • famciclovir or valacyclovir or acyclovir for 7 d; must initiate within 72 h to be of benefit; IV acyclovir for ophthalmic or disseminated Involvement
  • gabapentin 300-600 mg PO tid for post-herpetic neuralgia
71
Q

What is the incubation period of varicella?

A

0-21 days

72
Q

When is varicella most contagous?

A

1-2 days pre-eruptions and 5 daqys post-eruption

73
Q

What is the route of transmission of varicella?

A

Mainly airborne, but also through direct contact with vesicle fluid.

74
Q

Describe the rash that is associated with varicella?

And the associated features?

A
  • Appearance: groups of skin lesions, polymorphic, from macules to papules to vesicles to crusts
  • Timing: 1-3 d after start of symptoms
  • Distribution: generalized
  • Significant pruritis
  • Enanthem: vesicular lesions which may become pustular or ulcerate
75
Q

What is the management of varicella?

A
  • Supportive : Avoid salicylates (due to risk of Reye syndrome)
  • Consider antivirals
  • Respiratory and contact isolation, report to Public Health
  • Prevention: varicella vaccine
76
Q

What are the outcomes and complications of varicella?

A
  • Skin: bacterial suprainfection, necrotizing fasciitis
  • CNS: acute encephalitis and cerebellar ataxia
  • Systemic: hepatitis, DIC
  • Congenital varicella syndrome if intrapartum infection
77
Q

Describe the classic Hx of gastroenteritis?

A
  • non-specific: diarrhea, vomiting, fever, anorexia, headache, myalgias, abdominal cramps
  • bacterial and parasitic agents more common in older children (2-4 yr)
  • recent infectious contacts: symptoms usually begin 24-48 h after exposure
78
Q

What investigation are done for gastroenteritis?

A
  • not usually necessary in young children
  • stool analysis: leukocytes/erythrocytes suggests bacterial or parasitic etiology; pH <6 and presence of reducing substances suggests viral etiology
79
Q

What are the complications of gastroenteritis?

A
  • viral gastroenteritis usually self-limiting (lasts 3-7 d in most cases)
  • adverse effects related to hypovolemia, shock, tissue acidosis, and rapid onset and overcorrection of electrolyte imbalances
  • death in severe dehydration (rare in developed countries)
80
Q

Describe the aetiology and clinical presentation of both viral and bacterial causes of gastroenteritis?

What are the risk factors and management of both?

A
81
Q

What organisms are responsible for septic athrittis and osetomyelitis is children?

A
82
Q

Describe the aetiology, mechanism of spread and risk factors for osteomyelitis?

A
  • most commonly caused by Staphylococcus aureus
  • mechanism of spread: hematogenous (most common) vs. direct-inoculation vs. contiguous focus.
  • risk factors: recent trauma/surgery, immunocompromised patients, DM, IV drug use, poor vascular supply, peripheral neuropathy.
83
Q

What is the clinical presentation of osetomyelitis?

A
  • symptoms: pain and fever
  • on exam: erythema, tenderness, oedema common ± abscess/draining sinus tract; impaired function/WB
84
Q

How is osteomyelitis diagnosed?

A
  • workup includes:
    • FBC, WBC and diff, ESR, CRP, blood culture, aspirate culture/bone biopsy
  • Imaging:
    • MRI is the imaging modality of choice for demonstrating bone, bone marrow, and soft tissue nabnormalities
    • 99mTc, followed by 111In labeled white cell scan or gallium radioisotope scan
    • plain film
      • visible 8-10 d after process has begun
      • osteomyelitic changes on plain film
        • soft tissue swelling
        • local periosteal reaction
        • pockets of air (from anaerobes) may be seen in th
        • tissues, may also suggest necrotizing
          fasciitis
        • mottled and nonhomogeneous with a classic “moth-eaten” appearance
        • cortical destruction
85
Q

What is the surviving sepsis campaign definition of SIRS?

Definition for sepsis, severe sepsis and septic shock?

A

Systemic inflammatory response syndrome (SIRS) requires 2 or more of the following (the definition differs for children):

  1. T >38 C or <36 C
  2. P >90/min
  3. RR >20/min or PaCO2 <32 mmHg
  4. WCC >12 or >10% immature band form
  • sepsis: SIRS + proven or provable infection
  • severe sepsis: sepsis + signs of end-organ dysfunction and hypoperfusion
  • septic shock: severe sepsis + hypotension (<90 mmHg sBP), despite adequate fluid resuscitation
86
Q

What is the aetiology and pathophysiology of septic shock?

A
  • causative agents are identified in only 50-70% of cases
  • when organisms are identified, GP and GN organisms are the cause in 90% of cases
  • primary bloodstream infection or secondary bacteremia → local immune response → immune cells release pro-inflammatory cytokines → immune response spreads beyond local environment → unregulated, exaggerated systemic immune response → vasodilation and hypotension → involvement of tissues remote from the site of injury/infection resulting in multiple major organ dysfunction → periodic immunoparalysis
87
Q

What are the clincal features of septic shock?

A
  • history: fever, chills, dyspnea, cool extremities, fatigue, malaise, anxiety, confusion
  • physical: abnormal vitals (fever, tachypnea, tachycardia, hypotension), local signs of infection
88
Q

What investigations should be order in septic shock?

A
  • Blood: FBC UECs, BUN, LFTs, ABG, lactate, INR, PTT, FDP,
    blood cultures x3
  • Urine: urinalysis, urine C&S and cultures of any wounds or lines
  • Imaging: CXR (other imaging depends on suspicion of focus of infection)
89
Q

What is the treatment of septicl shock?

A
  • respiratory support: O2 ± intubation
  • cardiovascular support: IV fluids, ± norepinephrine + ICU
  • IV antibiotics (empirical, depends on suspected source)
    • start with broad spectrum antibiotics (piperacillin/tazobactam or meropenem) ± additional agents depending on patient risk factors, suspected etiology of infection, and local microbial
      susceptibilities (± aminoglycoside for drug-resistant GNs or vancomycin for MRSA)
    • narrow once susceptibilities are known
  • hydrocortisone IV in patients with septic shock unresponsive to fluid resuscitation and vasopressors
90
Q

What is the natural Hx of TB?

A
  • inhalation and deposition in the lung can lead to one of the following outcomes:
    • immediate clearance of the pathogen
    • latent TB: asymptomatic infection contained by host immune defenses (represents 95% of infected people)
    • primary TB: symptomatic, active disease (represents 5% of infected people)
    • secondary TB: symptomatic reactivation of previously dormant TB (represents 5-10% of those with latent TB, most often within the first 2-3 yr of initial infection) at a pulmonary or extra-pulmonary site
91
Q

What are the risk factors for developing TB?

A
  • social and environmental factors
    • travel or birth in country with high TB prevalence (e.g. Asia, Latin America, Sub-Saharan Africa, Eastern Europe)
    • Aboriginal, crowded living conditions, low SES/homeless, IVDU
    • personal or occupational contact
  • host factors
    • immunocompromised/immunosuppressed (especially HIV, including extremes of age)
    • silicosis
    • chronic renal failure requiring dialysis
    • malignancy and chemotherapy
    • substance abuse (e.g. drug use, alcoholism, smoking)
92
Q

Describe the clinical features of TB?

A
  • primary infection usually asymptomatic, although progressive primary disease may occur,
    especially in children and immunosuppressed patients
    • secondary infection/reactivation usually produces constitutional symptoms (fatigue, anorexia,
    night sweats, weight loss) and site-dependent symptoms
    • pulmonary TB
      • chronic productive cough ± hemoptysis
      • CXR consolidation or cavitation, lymphadenopathy
      • non-resolving pneumonia despite standard antimicrobial therapy
    • miliary TB
      • widely disseminated spread especially to lungs, abdominal organs, marrow, CNS
      • CXR: multiple small 2-4 mm millet seed-like lesions throughout lung
    • extrapulmonary TB
      • lymphadenitis, pleurisy, pericarditis, hepatitis, peritonitis, meningitis, osteomyelitis (vertebral = Pott’s disease), adrenal (causing Addison’s disease), renal, ovary
93
Q

What Ix should be ordered for TB?

A
  • screening for latent TB
    • Mantoux skin tests
      • diagnose prior TB exposure; can not diagnose or exclude active disease
    • IFN-γ release assay (IGRA):
      • in patients previously infected with TB, T-cells produce increased amounts of IFN-γ when re-exposed to TB antigen
      • detects antigen not present in the BCG vaccine or in most types of non-tuberculous-
        mycobacteria (NTM), therefore fewer false positives
    • American guidelines treat IGRAs as equivalent to the TB skin test and preferable in patients
      with a history of BCG vaccination or who may not return for skin test reading
  • diagnostic tests/investigations for active pulmonary TB
    • morning sputum on 3 consecutive days for acid-fast bacilli smear and culture
    • Bronchoavleolar lavage
    • CXR
      • nodular or alveolar infiltrates with cavitation (middle/lower lobe if primary, apical if secondary)
      • pleural effusion (usually unilateral and exudative) may occur independently of other
        radiograph abnormalities
      • hilar/mediastinal adenopathy (especially in children)
      • tuberculoma (semi-calcified well-defined solitary coin lesion 0.5-4 cm that may be
        mistaken for lung CA)
      • miliary TB
      • evidence of past disease: calcified hilar and mediastinal nodes, calcified pulmonary focus,
        pleural thickening with calcification, apical scarring
94
Q

What is the Rx for active TB infection?

A
  • empiric therapy: INH + rifampin + pyrazinamide + ethambutol + pyridoxine
  • pulmonary TB: INH + rifampin + pyrazinamide + ethambutol + pyridoxine x 2 mo (initiationphase), then INH + rifampin + pyridoxine x 4 mo in fully susceptible TB (continuation phase), total 6 mo
  • extrapulmonary TB: same regimen as pulmonary TB but increase to 12 mo in bone/joint, CNS, and miliary/disseminated TB + corticosteroids for meningitis, pericarditis
  • empiric treatment of suspected MDR (multidrug resistant) or XDR (extensively drug-resistant) TB requires referral to a specialist
    • MDR = resistance to INH and rifampin ± others
    • XDR = resistance to INH + rifampin + fluoroquinolone + ≥1 of injectable, second-line agents
      • very difficult to treat, global public health threat
    • suspect MDR TB if previous treatment, exposure to known MDR index case, or immigration from a high-risk area
  • note: TB is a reportable disease to Public Health
95
Q

How is TB prevented?

A
  • primary prevention
    • airborne isolation for active pulmonary disease
    • BCG vaccine
      • ~80% effective against pediatric miliary and meningeal TB
      • effectiveness in adults debated (anywhere from 0-80%)
      • routine use rarely recommended in American population, however widely used in other
        countries
  • secondary prevention (defer in pregnancy unless mother is high risk)
    • likely INH-sensitive: isoniazid (INH) + pyridoxine (vit B 6 to help prevent INH-associated neuropathy) x 9 mo
    • likely INH-resistant: rifampin x 4 mo
96
Q

Describe what HIV is and the pathophysiology of HIV?

A
  • HIV is a retrovirus that causes progressive immune system dysfunction which predisposes patients to various opportunistic infections and malignancies
  • HIV virion includes an envelope (gp41 and gp120 glycoproteins), matrix (p17) and capsid (p24) enclosing 2 single-stranded copies of RNA + enzymes in its core
  • virion glycoproteins bind CD4 and CXCR4/CCR5 on CD4+ T lymphocytes (T-helper cells) to fuse and enter the cells
  • RNA converted to dsDNA by reverse transcriptase; dsDNA is integrated into host genome
  • virus DNA transcribed and translated using host cell machinery, post-translational modifications include proteolytic activity of virally encoded protease enzymes
  • newly produced virions bud out of host cell, incorporating host cell membrane; additional maturation steps are required before virion is considered infectious
  • exact mechanisms of CD4 depletion incompletely characterized but likely include direct viral cytopathic effects, apoptosis, increased cell turnover
97
Q

Describe the invasion sites by HIV and the medium that is used to do so?

A
98
Q

Describe the natural history of HIV?

A

Acute (Infection) Retroviral Syndrome

  • 40-90% experience an acute “flu-like” illness (may include fever, pharyngitis, lymphadenopathy, rash, arthralgias, myalgias, H/A, GI symptoms, oral ulcers, weight loss) 2-6 wk post-exposure lasting 10-15 d
  • haematologic disturbances (lymphopenia, thrombocytopenia)
  • 10-20% present with aseptic meningitis; HIV RNA and/or p24 may be detected in CSF
  • associated with a high level of plasma viremia and therefore high risk of transmission

Asymptomatic (Latent) Stage

  • during latent phase, HIV infects and replicates in CD4+ T lymphocytes (lymph nodes)
  • normal CD4 count: 500-1,100 cells/mm 3
  • CD4 count drops 60-100 cells/mm 3 per year
  • by 10 yr post-infection, 50% have AIDS, 30% demonstrate milder symptoms, and <20% are asymptomatic if left untreated

AIDS Definition in United States

  • CD4+ T-lymphocyte count of <200 cells/μL OR
  • CD4+ T-lymphocyte percentage of total lymphocytes of <14% OR
  • documentation of an AIDS-defining condition
99
Q

Describe the illnesses that accompany the decreasing CD4 counts?

A
100
Q

How is HIV diagnosed?

A
  • anti-HIV antibodies detectable after a median of 3 wk, virtually all by 3 mo (therefore 3 mo window period)
  • initial screening test (3rd generation antibody test): enzyme linked immunosorbent assay (ELISA) detects serum antibody to HIV; sensitivity >99.5%
  • increasingly, combination p24 antigen/HIV antibody tests (4th generation) used for screening; improved sensitivity in early or acute infection and sensitivity/specificity approach 100% for chronic infection
  • confirmatory test: in positive screen, Western blot confirmation by detection of antibodies to at least two different HIV protein bands (p24, gp41, gp120/160); specificity >99.99%
  • rapid (point of care) antibody tests: higher false positives, therefore need to confirm positive results with traditional serology
  • p24 antigen: detection by ELISA may be positive during “window period”
101
Q

How is HIV managed?

A
  • verify positive HIV test
  • complete baseline history and physical exam, then follow-up every 3-6 mo
  • laboratory evaluation
    • routine CD4 count to measure status of the immune system
    • routine HIV-RNA levels (viral load)
      • also important indicator of effect of ART
    • baseline HIV resistance testing to guide ARV therapy
    • HLA-B*5701 genetic test to screen for abacavir hypersensitivity
    • baseline tuberculin skin test (PPD): induration greater than 5 mm is positive
    • baseline serologies (hepatitis A, B, and C, syphilis, toxoplasma, CMV, VZV)
    • routine biochemistry and hematology, CXR
    • annual fasting lipid profile and fasting glucose (due to HAART side effects)
  • education
    • regular follow-up on CD4 counts and viral loads (q3-6 mo) as well as strict adherence to ART improves prognosis
    • prevention of further transmission through safer sex and clean needles for injection drug use
    • HIV superinfection (transmission of different HIV strains from another HIV+ person) does rarely occur so barrier protection during sex is still recommended
    • discuss importance of disclosing HIV status to partners including risk of criminal prosecution of non-disclosure in jurisdictions where applicable
    • connect to relevant community groups and resources
  • health care maintenance
    • assessment of psychosocial concerns and referral to psychiatry or social work if appropriate
    • vaccines: influenza annually, 23-valent pneumococcal every 5 yr, HBV (if not immune), HAV (if seronegative)
    • annual screening (PAP smear, STDs)
    • management of comorbid conditions and provision of general primary care
102
Q

What is the overall treatment principles of ani-retroviral drugs in the treatment of HIV?

A
  • recommended that all HIV+ patients initiate HAART to prevent disease progression and transmission; strength of evidence supporting that recommendation changes depending on CD4 count and sexual practices (AI evidence that CD4 <350 should be on HAART)
  • patients starting HAART should be committed to treatment and understand the importance of adherence; poor compliance can lead to viral resistance; may defer treatment on the basis of clinical and psychosocial factors on case by case basis
  • initiate ART if opportunistic infection/malignancy, pregnancy, HIV-associated nephropathy, HIV-associated thrombocytopenia, need for hepatitis B therapy in HBV co-infected patients
  • consider starting treatment early if HCV co-infection, high HIV viral load, comorbid conditions (e.g. cardiovascular disease)
  • consider results of baseline resistance testing and complete ART history before (re-)initiating HAART
  • goal: keep viral load below limit of detection i.e. <40 copies/mL (undetectable); viral load should decrease 10-fold within 4-8 wk, be undetectable by 6 mo and restore immunological function
  • strong evidence against intermittent HAART or ‘drug holidays’
  • ART leads to 96% reduction in risk of transmitting HIV to sexual partners
103
Q

What are the target sites for anti-retroviral drugs?

A
104
Q

What are some stratageies that can be used to prevent HIV?

A
  • education, including harm-reduction
    • safer sexual practices: condoms for vaginal and anal sex, barriers for oral sex
    • harm reduction for injection drug users: avoid sharing needles
  • treatment of HIV+ women with HAART during the 2nd and 3rd trimester of pregnancy and AZT during delivery followed by treatment of the infant for 6 wk (decreases maternal-fetal transmission from 25% to <3%)
  • universal blood and body precautions for health care workers
    • post-exposure prophylaxis (PEP) after occupational (e.g. needle-stick injury) and non- occupational (e.g. consensual sex, sexual assault) exposure to HIV: 2- or 3-drug regimen initiated immediately (<72 h) after exposure and continuing for 4 wk
  • recent data has demonstrated efficacy of pre-exposure prophylaxis (oral PrEP or topical microbicides) in preventing HIV although additional data needed
  • ART associated with 96% reduction in risk of transmitting HIV to sexual partners
  • screening of blood and organ donation
105
Q

How does necrotising fasciitis present?

A
  • pain out of proportion to clinical findings and beyond border of erythema
  • oedema, ± crepitus (subcutaneous gas from anaerobes), ± fever
  • infection spreads rapidly
  • patients may rapidly become very sick (tachycardia, hypotension, lightheadedness)
  • late findings
    • skin turns dusky blue and black (secondary to thrombosis and necrosis)
    • induration, formation of hemorrhagic bullae
106
Q

How is necrotising fasciitis diagnosed?

A
  • a clinical/surgical diagnosis – do NOT wait for results of investigations before beginning treatment
  • blood and tissue C&S
  • serum CK (elevated CK usually means myonecrosis – a late sign)
  • plain film x-ray (soft tissue gas may be visualized)
  • surgical exploration for debridement of infected tissue
107
Q

What infections can arise from mammalian bites and there ABx?

A
  • Mammalian
    • Dog and cat: Pasteurella multocida, S. aureus, S. viridans
      • 80% of cat bites, 5% of dog bites become infected
      • amoxicillin + clavulanic acid
    • Human: Eikenella corrodens, S. aureus, S. viridans, oral anaerobes
      • amoxicillin + clavulanic acid
108
Q

What are the main types of hepatitis that can be acquired during travel in South-east asia or south asia and how can they be prevented?

A
109
Q

What is the aetiology of encephalitis?

A
  • identified in only 40-70% of cases
    • when cause is identified, the most common aetiology is viral
      • e.g. HSV, VZV, EBV, enteroviruses, CMV, West Nile, HIV, mumps, measles, rabies, polio
    • bacteria: L. monocytogenes, Mycobacteria, spirochetes (syphillis)
    • parasities: protozoa (e.g. Toxoplasma) and helminths (rare)
    • fungi: e.g. Cryptococcus
    • post-infectious (e.g. acute disseminated encephalomyelitis [ADEM])
110
Q

How is encephalitis diagnosed?

A
  • CSF: opening pressure, cell count + differential, glucose, protein, Gram stain, bacterial C&S, PCR for HSV, VZV, EBV, enteroviruses, and other less common viral etiologies
  • serology: may aid diagnosis of certain causes of encephalitis (e.g. West Nile virus)
  • imaging/neurologic studes: CT, MRI, EEG to define anatomical sites affected
  • invasive testing: brain tissue biopsy may be required for culture, histological examination, and immunocytochemistry (if diagnosis not clear via non-invasive means)
  • findings in herpes simplex encephalitis (must rule out due to high mortality)
    • CT/MRI: medial temporal lobe necrosis
    • EEG: early focal slowing, periodic discharges
111
Q

Illustrate bacterial wall structures in gram +ve and -ve bacteria.

A
112
Q

What is the source of enterobacteriacae and what are 5 medically important genera?

A
  • Large family of facultatively anaerobic Gram-negative bacilli
  • Found in the normal flora of animals and human, as well as soil and water
  • Transmission
    • From other animal or humans and from the inanimate environment
    • Arising from the body’s normal flora when opportunities are provided by medical, surgical or other therapy
    • Medically important genera: E. coli, Klebsiella sp., Proteus sp., Enterobacter sp., Salmonella sp., Shigella sp. And Yersinia sp.
113
Q

Which gram -ve bacteria can be responsible for diarrhoea?

A
  • E. Coli
  • Salmonella sp
  • Shigella sp
114
Q

Who are at ridk of getting a pseudomonas aeroginosa infection?

A
  • Predominantly affecting at risk hospitalised patients
    • Neutropenic patient – particular risk of bacteraemia
    • Long-stay patients (with wounds, drains, IV and urinary catheters, ventilated and multiple antibiotics) – particular infection of catheter associated UTI
    • Burns patients – particular risk of bacteraemia and wound infection
    • Patients with cystic fibrosis or other chronic lung disease – particular risk of respiratory infection, including an acute ventilator associated respiratory infection
    • Other risks – folliculitis and dermatitis from spas and swimming pools, otitis externa (particularly in diabetics), corneal ulcer from contaminated contact lens solutions, endopthalmitis from penetrating injury, and osteomyelitis from puncture wound through shoes into the calcaneous
115
Q

Describe the clincal features of Neisseria meningitides infection?

A
  • Fever, stiff neck, reduced consciousness
  • Petechial rash, a sign of septicaemia, may be present without other signs of meningitis
  • Septic or reactive arthritis may develop
116
Q

What is the Rx for Neisseria meningitides infection?

A
  • 2.4g benzylpenicillin IM before hospitalisation if high suspicion on clinical grounds
  • Give dexamethasone 10mg IV before or with the first dose of antibiotics, then 6-hourly
  • Plus ceftriaxone 4g IV daily
117
Q

Which Abx is associated with an allergic ‘red man syndrome’, characterised by exfoliative dermatitis, Stevens-Johnson syndrome, toxic epidermal necrolysis and vasculitis?

A

Vancomycin

118
Q

Which Abx is associated with an experimental arthropathy in growing animals and therefore contraindicated in patients under 16 years.

A

Ciprofloxacin

119
Q

Which Abx causes a metallic taste. Rarely can cause a peripheral neuropathy?

A

Metronidazole.

120
Q

Which Abx inhibit cell membrane synthesis?

1 examples.

A
  • Lincomycins
121
Q

Which Abx inhibit protein synthesis?

4 examples

A
  • Tetracyclines
  • Macrolides
  • Aminoglycosides
  • Chloramphenicol.
122
Q

Which Abx inhibit DNA formation?

3-4 examples

A
  • Sulphonamides/trimethoprim
  • Quinolones
  • Metronidazole.
123
Q

Which Abx inhibit cell wall synthesis?

4 examples

A
  • Penicillins
  • Vancomycin
  • Cephalosporins
  • Macrolides
124
Q

How is Giardia lamblia transmitted? And what are the risk factors for contracting an infection?

A
  • reservoir: infected humans and other mammals
  • food/waterborne (especially in the Rockies) and fecal-oral transmission of infectious cysts
  • risk factors: travel, camping, institutions, day care centers, MSM
125
Q

What are the clinical features of a Giardia lamblia infection?

A
  • giardiasis (“beaver fever”)
    • symptoms vary from asymptomatic to self-limited mild watery diarrhea to malabsorption syndrome (chronic giardiasis where the parasite coats small intestine and thus prevents fat absorption)
    • nausea, malaise, abdominal cramps, bloating, flatulence, fatigue, weight loss, steatorrhea
    • no haematochezia (no invasion into intestinal wall), no mucus in stool
126
Q

What Ix need to be done in someone with suspected Giardia lamblia infection?

A
  • multiple stool samples (daily x 3 d) for microscopy - 90% sensitivity (1 stool sample - 50% sensitvity, hense 3 is needed), detects cysts and oocytes
  • stool antigen used occasionally
  • occasionally small bowel aspirate or biopsy
127
Q

How is Giradiasis Rx?

A
  • metronidazole
  • good personal hygiene and sanitation, water purification (iodine better than chlorination),
    outbreak investigation
128
Q

What Abx are used to treat ABx-associated colitis (C diff infection)?

A

Vanc or metronidazole

129
Q

Which Abx is the cause of Abx-associated colitis (C diff infection)?

A
  • Clindamycin
  • cephalosporins
  • amoxicillin
130
Q

Which Abx used to mycoplasma pneumoniae?

A

Clarithromycin or erythromycin.

Alternatively tetracycline or doxycycline.

131
Q

WHat is the most common cause of pneumonia in individuals aged 15-30 years?

A

Mycoplasma pneumoniae

132
Q

Extrapulmonary manifestations of Mycoplasma occur in up to 10% of cases of Mycoplasma pneumonia. What are these?

A
  • Haemolytic anaemia: s associated with the presence of cold agglutinins, found in up to 50% of cases of Mycoplasma pneumonia. Diagnosis is based on demonstration of anti-Mycoplasma antibodies in paired sera.
  • Renal failure
  • Hepatitis
  • Myocarditis
  • Meningism and meningitis
  • Transverse myelitis
  • Cerebellar ataxia.
  • Cutaneous manifestations include erythema multiforme.