Surgical Foundations: INFECTIONS Lecture # 3
Hospital acquired infections
January 28, 2014 - Dr. J M A Bohnen
FEVER
Endotoxin → WBCs esp macros secrete cytokines IL-1, TNF, IL-6, IFN to cause fever via PGE2 ,
blocked by ASA. No need to measure temp after elective OR for noninfectious conditions CID
2005;40:1404,1411; nor do blood cultures for postop fever if healthy (no steroids, lines); nor for known
infection unless bacteremia will change rx eg enterococcus, S. aureus JACS 2002;194:477, value of
antipyretics controversial 2007;204:815
OPPORTUNISTIC INFECTIONS:
Bacteria → Local environment ← Systemic Host Defenses
↑
Duration of contamination
Unfavourable local environment, ↓ host defenses allows infection with fewer, less virulent microbes. By
convention, “opportunistic” = infections 2° to ↓ host defenses; but local breaches create opportunities too: surgical
site, UTI, pneumonia, vascular catheters, surgical implants.
Caveat: antibiotic suggestions below are only examples; expert opinion changes often because of resistance, new
therapies and hospital formulary decisions. Consult pharmacy, literature reviews, Sanford.
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SURGICAL SITE INFECTIONS (SSI)
Defns: 1) superficial incision (skin/fat) = “wound” 2) deep incision (fascia/muscle) 3) Space 4) organ
Risks: contaminant load, age, malnut, long preop hosp stay (JACS 2010;211:784), OR duration, remote
infection, skin shave day before, type of OR (esp abd), degree of illness, obesity[JACS 2010;210:381], steroids,
↑blood sugar (many refs, reviewed SurgInf 2011;12:405), periop hypothermia +hypoxemia; smoking; drains;
Etoh overuse JACS2012;215:229
Microbial Etiology S. aureus commonest single bug 20-25%, commonest cause in clean cases, usu endog
patient’s skin, nose, may be exog eg surgeon’s nose. E. coli 2nd commonest; enteric bacteria total more comm.
than S. aureus; P. aeruginosa either endog (gut, skin) or exog (hosp environment). Gm neg anaerobes (eg
Bacteroides) often with enteric gram neg facultatives, esp after bowel OR. Clostridia more likely after trauma,
amputation, ischemia, fecal contamination.
Pathogenesis Bugs + infla ↓ 2 key wound functions, epithelial cover and wound strength → skin dehiscence.
Clinical: usually day 4-8, up to years. Local infla, discharge. Some bugs give typical signs: S. pyogenes early
presentation, cellulitis, little pus, rapid progression to fasciitis; clostridia – like strep, with gas; S. aureus
creamy pus 4-6d postop; coliforms like S. aureus or few signs, may be occult sepsis; gas uncomm. Systemic
fever, ↑WBC though may be absent, esp elderly.
Diagnose Examine wound daily from 48 h postop (earlier if fever or ++pain). Incise inflamed wound after skin
prep, Gram stain, culture pus for surveillance + if antibiotics needed. Putrid odour: gas-forming bugs, likely
anaerobes. Beware underlying deeper infection, check for opening in fascia
Treat May need debride in OR for strep, clostridia, lethal infections which leave dead tissue. Incise wound to
fascia, drain/debride adequately. ≤7 d postop open entire wound; >7d may open just,inflamed segments.
Inspect, feel wound base for connection with deep infection. Pack, record gauze count. Topical rx: NS ok;
follow home care request; if chronic, many options, few definitive trials CID 2009;49:1541. Systemic antibiotics
not indicated unless 1) regional/distant spread (cellulitis, fasciitis) 2) critically ill 3) immunosuppressed (eg
steroids) 4) remote endoprosthesis (eg cardiovasc, hip) 5) 1st 48 hours postop (likely strep/clostridia) 6) consider
for S. aureus because 15% bacteremia, 2x more than other organisms CID 2002;34:305. Till cult/sens back,
cefaz or clox if lo MRSA prev; add AG, quinolone, carbapenem or ceph3 for Gm neg and clinda or metro for
anaerobes. Narrow spectrum when C+S back. SSI in first 48h: hi dose pen G IV 12-24 mU/d; add clinda if
severe, spreading. Mild wound cellulitis, cefazolin alone OK. D/C when responds clinically.
Complications: may upset patient, ruin scar, dehisce fascia, hernia, bacteremia/sepsis, toxic shock; 2°
complications (eg strangulated hernia, infected prosthetic implant) …disaster. Costly hosp stay, absence.
SSI prevention: Try fix modifiable risk factor listed above; next paragraphs add detail pre- intra- and postop
Mangram ICHE 1999; 20:250-278; JACS 2010;211:812
SSI PREVENTION: BEFORE OPERATION
Bacteria: CHG sponge shower x2 (night, a.m.pre-op); rapid ID nasal mupirocin for S. aureus may ↓ S. aureus ssi
in big ORs NEJM 2010;362:9, 75; surveillance, quality improvement. JACS 2007;205:432, 2010;211:705
2012;215:850 ↓ ssi by protocol; bowel prep useless JACS 2010; 211:812 except rectal cancer operations Ann Surg
2010;252:863; minimize preop hosp stay
Local environment: manage/postpone for local infection; smoking abstinence ↓ ssi: Ann Surg 2003;238:1, JACS
2012;215:418; wt loss if poss because ↑BMI → ↑ ssi Heart Lung 2005;34:108, JACS 2011;213:236, 2010;210:381
Host defenses: preop nutrition reduces major infn in major malnut for major OR; resuscitation; control blood
sugar Circulation 2004;109:1497; ↓/dc steroids if possible
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SSI PREVENTION: IN THE OR
Bacteria: 4 min surgeon hand scrub 1st case, 1 min thereafter; etoh hand rub good JAMA 2002;
288:722; WHO rec’s etoh rub or soap wash, not both ICHE 2009;30:611; clip or leave hair ICHE
2005;26:923 no conclusion; NEJM 2006;355:2640 shave may help. Pt skin prep: CHG better than
povidone-iodine NEJM 2010;362:18, 75. Strict asepsis! Gowns/drapes: poor data quality Bull Am Coll
Surg 2007;92:15; masks: poor data re ssi, protect us, may limit bacteria “shedders.” Don’t make holes in
dirty places; prophylactic antibiotics see 2nd lecture
Local environment:
GOOD: MIS better than open JACS 2010; 211:232; WJS 2010 34:2026, 2011;35:2143; local anesth may be
better WJS 2011;35:2596 normothermia NEJM 1996;334:1209, hi inspired oxygen (eg 80%) likely reduces ssi
NEJM 2000;342:161, Lancet 2001;358:876, Arch Surg 2009;144:359 CID 2013;57:1465
BAD: 1) blood: anoxic culture medium; liquid impairs pmns; 2) dead tissue: anoxic culture medium 3) dead
space attracts fluid, anoxic 4) foreign bodies (FB): drains bad in most cases; ↑drain duration → ↑ spine fusion
ssi CID 2011;53:686; long operation JACS 2012;215:512 sutures: tapes better than staples better than sutures;
synthetic better than natural; mono better then multifilament (braided); absorb sim to nonabsorb.
Host Defenses: Blood transfusion increases ssi risk JACS 2009;208:931
SSI PREVENTION: POSTOP
Handwash ICHE 2004; 25:187; avoid bacteremia: D/C Foley, NG, IVs, lines. Fear ssi in 1st 48 hr
HOSPITAL ACQUIRED URINARY INFECTION
Key reference: IDSA Guidelines dx, prevention, rx cather UTI CID 2010;50:625
Risk: catheters. Bacteria ascend around + in catheter, breach urethra/sphincter, adhere to foreign body via
biofilm. ↑ duration → ↑ risk; long preop hosp stay JACS 2010;211:784. Transrectal prostate bx.
Micro: 50% E.coli, resist freq; other Gm neg rods, enterococci, less frequ fungi, coag neg staph. Urine S. aureus:
seek S. aureus bacteremia or renal carbuncle. Candiduria is local or assoc with candidemia; culture blood
Prevent: Minimize pre-op hospital stay. Avoid, limit, remove catheters; sterile technique; prevent backflow:
keep bag below pt. Incontinent, alert co-op male, use condom catheter. Separate catheterized patients. Hosp
staff transmit infections; aggressive infection control works CID 2006; 42:1544. Quinolone 1 dose pretransrectal prost bx though E. coli resistance serious CID 2013;57:267. Unproven: antimicrobial catheter coating,
antibiotic, antiseptic and cranberry prophylaxis, meatal care, catheter irrigation..
Diagnose Significant WBCs in urine (>10/cc or dipstick) implies infection, though catheter, chronic prostatitis,
analgesic nephropathy cause pyuria. Quantitative culture dx controversial. Midstream urine ≥105 bugs/ml in
uncath’d patient (or ≥103 bugs/ml plus symptoms CID 2013;57:719) suggests infection. Instruct patient re
MSU collection. Definition, dx in cath’d patient is controversial. Base dx on “ 100 bugs/ml” and determine if
treatment indicated (see below). Multiple bugs means contam or rarely GI fistula (pneumaturia, esp colovesical
from diverticulitis). Neg urine sediment in cath’d pt excludes UTI JACS 2013;217:162
Treat: D/C catheter →bacteruria gone in a wk in 2/3; if can’t d/c, use antibiotics if renal infection (CVA
tenderness), fever/chills, endoprosthesis. Don’t treat asymp bacteruria unless immunocomp or having procedure.
Change catheter to ↓relapse. Avoid empiric therapy with quin, amox/amp or TMP/SMZ re E.coli resistance;
Hospital data should guide empiric rx of complicated UTI, cath -associated UTI and pyelo [SMH guide, CID
2013;56:641]. Duration 5d to 2 wk depends on clinical response. Acute + chronic prostatitis may complicate,
reviewed CID 2010;50:1641
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POSTOPERATIVE PNEUMONIA; VAP = Ventilator associated pneumonia
VAP care guidelines Can J ID Med Micro 2008;19:19
Local defenses breached: cough, cords, cilia esp VAP.
Risk: Long preop hosp stay JACS 2010;211:784; abd, chest ORs; atelectasis 2° to pain, sedation,
immobilization; aspiration; supine position; previous lung disease; ventilator contamination
Micro: gm neg facult/aerobic rods in half, gm pos cocci esp S. aureus, anaerobes esp aspiration. Community
acquired pneumonias may occur postop esp Strep pneumo + “H flu” in COPD. ↑frequ multi-drug resist bugs
(CID 2013;57:1373]
Prevent: d/c smoking; minimize pre-op hosp stay; mobilize Proph antibiotics don’t help aspiration. VAP:
selective subglottic decontam may work Intensive Care Med 2002;28:432. Elevate head, d/c NG, suck subglottis, po
chlorhexidene Chest 2006;130:251 AJRCCM 2006;173:1297, 1348
Diagnose: Controversial [CID 2013;57(S3):S139]. Suspect if ≥ 2 of temp > 38/<36, ↑ or ↓ wbc, pus in
trach/sputum, ↓ PaO2. Lung infiltrate unreliable. Micro dx: sputum cult unreliable, contam from above. If
approp, culture blood, pleural fluid. VAP: quantitative protected brush or BAL cult, ETT aspirate guide dx
and antibiotics NEJM 2006;355:2619.
Treat: Physio. Start empiric antibiotics within 24h, continue 4 wks for S. aureus, 2 wks for Pseudo, try ≤ 7d
for others; d/c if if dx not confirmed, d/c if other source found NEJM 2004;350:433; JACS 2011;212:476. C + S
result guides switch. Many empiric regimens work, none covers all pathogens, consider scenario esp hosp
sensitiv data. Empiric ceftriaxone/azithro, carbapenem, pip-tazo or levoflox till cult back; if find or suspect
P.aeruginosa, use ceftaz, cefip or carbapenem with 2nd anti-Pseudo drug eg tobra or quin to ↑ effect CCM
2007;35:1888. Aspiration: add clinda or metro. S. aureus: clox or (if MRSA) vanco, linezolid for 3 wk, longer if
metastatic infections. Varies among hosps, communities re resistance patterns
VASCULAR CATHETER INFECTIONS
Key reference, clinical care guidelines: CID 2011;52:1087
Breached defenses, risks: Extraluminal from skin intraluminal hub colonization Biofilms help bugs. Arterial,
PICC, tunneled CVCs: fewer infections than non tunneled CVCs, femoral lines, short IVs >72h esp cutdowns.
Totally implanted best. # of lumens irrel.
Micro: S epi, S. aureus, aerobic gram neg rods, C. albicans commonest, many bact and fungi can cause. TPN
lines: esp S epi, C. albicans
Prevent: In hospital daily CHG baths ↓risk NEJM 2013;368:533 Avoid groin. Use PICC not periph for infusion >1
wk. Sterile insertion, maintenance: hat mask gown gloves drape effective CID 2004;39:1441. Chlorhex beats
pov iodine for CVC insertion+maintenance, both + etoh ok for periph. Examine daily, leave dressing unless
infection, change periph IV q72h. Except burns, frequ CVC or PICC changes no help. Use coated CVCs
(chlorhex/sulfadiazine; minocycline/rifampin) if infection common (controv) CID 2004;39:1829. D/C unnec line
asap. Don’t use topical antibiotic (risk fungi).
Diagnose: If only mild suspicion, severity and IV access a problem, change CVC over wire, culture tip (semiquant or in blood cult tube); if cult pos, decide to retain or d/c CVC. Sick pt, likely CVC infection: remove and
culture CVC. Periph blood cultures carry greater weight than retrograde which can be contaminated. Same bug
on retrograde or CVC tip + periph blood implicates organism. Infections present clinically with “occult”
fever and/or positive blood cultures, especially S. epi, +/or local infla. Milking IV site may express pus.
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Treat: Remove inflamed periph IV. CVC retention does not affect resolution of S. epi bacteremia but ↑ recurrence
CID 2009; 49:1187. Catheter removal usually suffices exc S. aureus. For tunneled CVC + implanted port base
decision to remove catheter on clinical situation; antibiotic lock may work. If pus, I + D. Rarely excise vein.
Antibiotics for sick patient, CVC salvage, endovascular prosthesis, S. aureus. Use vanco till culture back; watch
for fungus. Clox sens S. aureus bacteremia: d/c line + clox 2 wks. Enterococcal bacteremia: 2 wks 1st or
advanced pen or vanco +/- AG – depends on pen or AG resistance – consult Mico, ID. Fluc if fungus.
Prognosis: May be fatal, esp if endovascular prosthesis seeded.
INFECTIONS ASSOCIATED WITH SURGICAL IMPLANTS
CID 2009;49:1036, NEJM 2004;350:1422, 2004;351:1645, CID 2003;36:1284, CID 2001;33:1387
Epiemiol/clinical: Huge clinical, economic burden. U.S. fracture-fixation devices 100,000/yr > vascular graft
16,000 > joint prosth = pacemaker-defibrillator 12,000 > mech heart valve, breast implant, VP shunt etc. Joints:
early (<3 mo) joint pain, infla; delayed (3-24 mo) pain, loosening; late (>24 mo postop) hematogenous from
skin, resp, dental, UTI. Dx and rx challenging and controversial.
Micro/pathog: S. epi, S. aureus commonest. FB → adhesins (inc fibrinogen, fibronectin, collagen) attracts
planktonic (= free floating) bugs which add glycocalyx → biofilm promotes persistence despite antibiotics.
Treatment: Controversial, treatment failure common CID 2012;55:1474, 1481, 2013;56:1, 182. Generally, antibiotics
+/- implant removal. Surgical removal usually for Candida spp, S. aureus , not S. epi. 1) Antibiotics: Vanco for
empiric and S. epi, inadequ for meth-suscept staph. Add rifampin for nonresponding staph; others inc linezolid. 2)
Operate if antibiotics fail; debride + retain, debride + exchange, or remove implant; use antibiotic-impregnated
joint spacers; ensure eradication before reimplant; antibiotics started early may control infection, obviate removal.
ACUTE PAROTITIS
Local defense: Salivary flow flushes oral pathogens.
Micro: S. aureus in 90%;gm neg rods, streptococci, anaerobes.
Risk Factors: Dehydration, impaired oral hygiene, old age, debility. Uncommon with good supportive care.
Diagnosis and Treatment: Diagnosis is clinical, inflamed parotids, hours to weeks following operation, uni- or
bilateral. Gm stain and culture pus from Stensen’s duct.
Treatment: Start antibiotics vs S. aureus and gram neg rods, either clox, cefazolin or vanco, add AG, antianaerobe if not improving. If no better in 3-5 days, may need to drain the gland surgically. Rarely fatal.
BLOOD TRANSFUSION INFECTION
Local defense breach: Skin and blood vessel wall.
Micro: Viral most common, bacterial most acutely lethal. HIV, Hep B, Hep C risk per blood unit now
<1/1,000,000; no West Nile Virus since 2003. Other microbes (HTLV, parvovirus, syphilis, malaria et al) rare or
not pathogenic that we know of [Can Paed Society 2012 http://www.cps.ca/documents/position/transfusion-and-risk-ofinfection-Canada] Bacterial contamination (usually gm neg rods) ↑↑risk if blood unit given over >3 h; if leak in
the system, stop transfusion immediately. Platelets at higher risk because stored at room temp.
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Prevention: Limit transfusion indications, limit duration to 3h/unit.
Diagnosis: Bacterial infection presents as hi fever, chills, vascular collapse and pos culture of transfused
blood. Viral infections present generally as subclinical to fulminant hepatitis with jaundice wks to months
after transfusion. Hep C: 70% asymp, 25% jaundice, 4% nonspecific symptoms; 50% develop chronic
hepatitis, 20% of those get cirrhosis. Post-transfusion hepatitis is in ddx of postop jaundice. Viral serology of
various types estabs dx. Hep B has “window of time” when antibody and surface antigen are neg ,
measurement of core antibody needed to detect hep B.
Treatment: For suspected bacterial infection stop transfusion immediately, obtain gm stain/culture of blood
unit, give broad spectrum antibiotics.
AIDS, HEPATITIS AND THE SURGEON
Hep B is highly transmissible. An unvaccinated surgeon’s risk of death from hep B exceeds that from AIDS,
which has very low risk of transmission Am J Surg 2005;190:249. Seroconversion risk after needle exposure is
0.3% for HIV, up to 10% for Hep C and up to 25% for Hep B. Recombinant Hep B vaccine is safe and
prevents Hep B if antibodies develop. Hep B infection generally confers immunity so vaccination unnec Hep B
booster unnec if antibody detectable. Get Hep B vaccine (unless immune), don’t let patient fluid contact your
mucous membranes or skin breaks. A patient may have HIV yet test neg for AIDS. DON’T RECAP HOLLOW
NEEDLES OR HANDLE SURGICAL NEEDLES. Avoid face and skin exposure to blood: face masks,
impermeable gowns, etc. Double gloving reduces blood exposure JACS 2010;210:325. Surgeon may transmit
Hep B to patients CID 2013;56:218
OPPORTUNISTIC INFECTIONS SECONDARY TO ↓ HOST DEFENSES:
CANDIDA INFECTIONS
Epidemiology C. albicans is commonest. Non-albicans include C. tropicalis and C. glabrata. Most predisposing
factors are iatrogenic: antibiotics, steroids, TPN, IVs, prostheses, abdominal operation, cancer, AIDS,
neutropenia, burns, renal failure, hemodialysis, mechanical ventilation
Path/clinical: colonization  infection  sepsis. Tissue invasion → micro abscesses.
Clinical: mucosal, deep organ and disseminated variants, with overlap:
Mucosal: “Thrush” is oral candidiasis. Esophagitis occurs in hematological/ lymphatic cancer. An otherwise
healthy man with oral or esophageal candidiasis probably has AIDS. Fifty percent with esophagitis have no
thrush. Candida esophagitis: dysphagia and chest pain. Dx with endoscopy/biopsy/culture. Infection elsewhere
in the gut (esp stomach) occurs in patients with cancer. Vaginitis occurs in diabetic and healthy women.
Deep Organ: Any organ, either primarily, or assoc with disseminated infection: meningitis, brain
microabscesses, cardiac (prosthetic valve, myocarditis, pericarditis), urinary, peritonitis, arthritis, osteomyelitis,
ocular. Septic thrombosis of central veins (suppurative thrombo-phlebitis) 2° to TPN. Upper +/or lower GU
tracts in disseminated candidiasis; cystitis may occur without dissemination, generally 2° to catheterization in
patient otherwise at risk for candida. Peritonitis commonly occurs 2° to perit dialysis, also by perf’d viscus.
Mere presence of Candida in perf viscus does not require therapy.
Candidemia: May be benign, secondary to a vascular catheter, clearing on removal of the line, or a sign of
disseminated candidiasis. If impaired host defenses or ill, don’t call candidemia benign till search for
disseminated infection repeatedly neg. Multiple culture candidemia implies disseminated candidiasis.
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Disseminated Candidiasis: Generally when multiple Candida risk factors present. Blood cultures may be neg.
Any organ system may be involved. Endophthalmitis (fluffy white exudates on fundoscopy) is diagnostic of
dissem candidiasis, but only occurs in 5%. Get ophth consult if suspect dissem infection. Renal failure may be
from obstr’n due to fungus ball, dx with CT/US/retrograde. Skin lesions in 13% with dissem infection: embolic
1cm reddish single or mult nodules, bx is diagnostic. Ultimately Dx is clinical. Treatment delay and lack of
source control →↑mortality CID 2012;54:1739
Treatment: Mucosal: Nystatin mouthwash if mild, 500,000 units 5-6 times daily. Oral fluconazole in
immunocomp. Ampho IV rarely needed. UTI without dissem (Candida cystitis): po fluconazole. Deep and
Dissem Infection: For multi-site colonization, prophylax with fluconazole 400 mg/d IV, then po, Treatment
controversial. Remove infected lines. Consensus: remove uninfected lines too. Consult ID. Treat with
fluconazole for any positive blood culture, unless patient had received 2d fluconazole or is clinically unstable,
for which give caspofungin or micafungin x 4-6 wks. C. glabrata generally resistant to fluconazole. Although
ampho toxic, give when nec. Demerol 25-50 mg IV limits rigors. Steroids not indicated. Role of fluconazole vs
liposomal ampho vs ampho vs caspofungin/micafungin/anidulafungin evolving [CID 2012;54: 1110, 1123,];
anidulafungin = fluconazole for invasive candidiasis, NEJM 2007;356:2472 fluc much cheaper.
Operate for Candida abscess, endocarditis or renal obstruction due to a fungus ball.
OVERWHELMING POST – SPLENECTOMY INFECTION (OPSI)
Micro: Uncommon, lethal infection < 2% of kids post-splenectomy; also functional asplenia eg sickle disease.
S. pneumoniae most common, other encapsulated bugs (meningococci, H. influenzae). Nausea, vomiting,
confusion progress rapidly to death within hours despite hi dose pen. Source usually obscure. Blood cultures are
positive, bacteria often seen on blood film.
Prevent: Prophylaxis includes spleen preservation esp in kids, pneumococcal, meningococcal and “H flu”
vaccines before elective or after emergency splenectomy though do not cover all bacterial strains. Repeat pneumo
vaccine q 6 yrs. Vaccine has few side effects. Give kid pen daily for 3 yr after splenectomy. Asplenic patients
should carry amox or amox/clav always, take if fever.
Treat : Ceftriaxone or cefotaxime IV. If Gm stain, cultures grow S. pneumoniae, use pen
OTHER OPPORTUNISTIC INFECTIONS
Solid organ transplant infections: N Engl J Med 2007;357:2601
Infections in solid organ transplant recipients classified by 1) pathogen: viral, bacterial, fungal, protozoal; and
opportunistic or “conventional” 2) onset (1 mo, 6 mo, later) 3) origin in donor or recipient, community or
hospital acquired and 4) technical, related to operation or “medical.” Clinically important: CMV, EBV,
polyomaviruses, pneumocystis, others
Listeria: Gm pos facult rod. Risks: AIDS, steroids, transplant. Causes meningitis. Rx: amp or amp plus genta.
Nocardia: Gm pos branching aerobic, acid-fast rod. Risk: AIDS, steroids, transplant. Causes lung infections
similar to TB, and CNS abscess. Treat with TMP/SMZ or alternates for 6 months, lifelong if AIDS. Drain
abscesses.
Pneumocystis jirovecii: A fungus, formerly protozoan “P. carinii.” Emerg Infect Dis 2004;10:1729 Causes
pneumonia, still nicknamed “PCP.” Risk factors: steroids, cancer, transplant, AIDS. Clinically fever, cough,
↑RR, absence of crackles. CXR: bilat diffuse interstitial pneumonitis. May need BAL, transbronchial or open
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lung bx for dx. Treat with TMP/SMZ, dapsone plus trimethoprim, others. AIDS patients get complications from
TMP/SMZ (fever, neutropenia).
Cryptococcus: Fungus. Risk factors: AIDS, steroids, transplant. Lung and CNS infection NEJM 2013;368:1291.
Rx: antifungals ampho+flucytosine.
Aspergillus: Fungus, can be highly lethal because blood vessel involvement → necrosis. Risk: febrile
neutropenia. Lung, brain. Rx: itraconazole, voriconazole; debride if approp; alternates ampho, caspofungin
NEJM 2009;360:1870
Histoplasmosis: Fungus, affects kidney, liver, pancreas, heart, lung; sometimes lethal; 1-2 years post solid organ transplant;
ampho followed by an azole CID 2013;57:1542
Toxoplasma gondii: Protozoan, can be lethal. Risks: HIV, steroids, transplant. CNS infefctions. Rx:
pyrimethamine and sulfadiazine CID 103;57:1535.
CMV: Risk: AIDS, solid organ and BM transplant. Lung, eye, liver, GI and disseminated infection are the
most common presentations. Rx: ganciclovir and others.
EBV: Hepatitis or dissemin infection in immunocomp host besides infectious mono. Also causes PTLD (posttransplant lymphoproliferative disorders) esp in lung transplant.
VZV: Herpes zoster. If immunocomp, no prev exposure, can dissem, kills. Rx hi dose acyclovir, others
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