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2/7/2018 1 Updates on selected GI infections Joanne Engel, M.D., Ph.D. Professor Depts of Medicine and Microbiology/Immunology UCSF Thanks to Drs. Sarah Doernberg, Bryn Boslett for sharing some slides Disclosures None
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Updates on selected GI infections · – Viral gastroenteritis – Preformed toxin (incubation 2‐7 hours): B. cereus, Staph aureus – Anisakiasis • Non‐GI syndromes – Fish

Aug 05, 2020

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Page 1: Updates on selected GI infections · – Viral gastroenteritis – Preformed toxin (incubation 2‐7 hours): B. cereus, Staph aureus – Anisakiasis • Non‐GI syndromes – Fish

2/7/2018

1

Updates on selected GI infections

Joanne Engel, M.D., Ph.D.Professor

Depts of Medicine and Microbiology/ImmunologyUCSF

Thanks to Drs. Sarah Doernberg, Bryn Boslett for sharing some slides

Disclosures

None

Page 2: Updates on selected GI infections · – Viral gastroenteritis – Preformed toxin (incubation 2‐7 hours): B. cereus, Staph aureus – Anisakiasis • Non‐GI syndromes – Fish

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Updates on:

• Food‐borne GI illnesses with a focus on infectious diarrhea– IDSA 2017 Diarrhea guidelines

– Traveler’s diarrhea will be covered on Friday (Brian Schwartz)

– C. diff was covered yesterday(Sarah Doernberg)

• Abdominal infections

• H. pylori (person‐person)‐– one slide on current treatment recommendations

Diarrhea:  a global cause of disease

• 2nd leading cause of morbidity/mortality worldwide

• In the US

– 200‐375 million episodes/year

– 180 million outpatient visits

– 500,000 hospitalizations

– > 5000 deaths

– Each person has 1‐2 diarrheal illnesses/yr

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Case

• 32 yo female calls your office c/o diarrhea x 2

days.  She notes 8 loose stools in the past 24 

hrs.  She has a low grade temp, mild nausea, 

and has vomited x 2.  She denies bloody 

stools, recent travel, ingestion of unsual foods.  

No sick contacts.

Diarrhea“Passage of 3 or more 

loose or liquid stools per 24 hours, or more 

frequently than is normal for an individual” 

‐WHO

Definitions

AcuteLasts <7 days

Watery vs. bloodyAcute vomiting +/‐ diarrhea = gastroenteritis

ProlongedLasts 7‐13 days

PersistentLasts 14‐29 days

ChronicLasts 30 days or longer

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Differential Dx

• Infectious

• Ischemic

• IBD

• Iatrogenic/Osmotic

• Malabsorption

The players aka “The dirty laundry list”Viral Bacterial Protozoal

Calicivirus (Norwalk, 

Norovirus^, Sapovirus)Salmonella 16.4 Giardia^

Rotavirus Campylobacter 14.3 E. Histolytica^

Adenovirus Shigella^ 2.3 Cryptosporidium^ 1.4

CMV Yersinia 0.3 Microsporidium

AstrovirusE. Coli (shiga toxin)^ 

1.1Cyclospora

Small round virus C. difficile

Corona virus C. perfringens

HSV S. aureus

Bacillus

Vibrio 0.4

Listeria ^low ID50

Chlamydia, GC *cases per 100,000 in US

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Some enteric pathogens are very infectious

Organism Inoculum

Shigella 10‐100

Giardia 30‐100

Cryptosporidium parvum 30‐100

Shigatoxin‐producing E. coli 10‐100

Norovirus 10‐100

Salmonella 103‐105

Campylobacter 103‐106

Cholera 106

ETEC 108

A little goes a long way…

Symptoms: not really specific• Bloody diarrhea

– In USA: Shigella, Campy, Salmonella, Shigatoxin‐producing E. coli

– Consider also: Amoebiasis, Vibrio, Aeromonas, Yersinia, Plesiomonas

• Watery diarrhea– ETEC, enteric viruses, Crytposporidium parvum, Cyclospora cayetanensis

• Fever: Implies inflammation, consider:– Invasive bacteria (Salmonella, Shigella, Campy)

– C. diff

– Noro/rotavirus

• Vomiting– Viral gastroenteritis

– Preformed toxin (incubation 2‐7 hours): B. cereus, Staph aureus

– Anisakiasis

• Non‐GI syndromes– Fish and mushroom toxins, botulism, listeria, typhoid, HAV, toxoplasma, 

brucella Talan D et al., Clin Infect Dis. 2001 Feb 15;32(4):573‐80

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Take a good history

• When & how illness began

• Stool characteristics

• Frequency & quantity

• Presence of dysenteric symptoms

• Symptoms of volume depletion

• Associated symptoms

• Epidemiologic clues

Be a Sherlock Holmes• Travel to developing area

• Food‐handler or caregiver

• LTCF or Day‐care center attendance or employment– “a veneer of feces”

• Recreational water venues

• Consumption of raw meats, eggs, unpasteurized milk/cheese, swimming in or drinking from untreated fresh water

• Farm or zoo animals, reptiles

• Exposure to other ill persons

• Medications, esp antibiotics

• Underlying medical conditions, HIV, IC

• Receptive anal intercourse or oral/anal contact

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Etiology of severe acute gastroenteritis in adults in ER

• Prospective multicenter ER‐based study)

• Pathogens found in ~50%

• Norovirus comprises 50% of identified pathogens; 25% of all cases

0

5

10

15

20

25

30

Iden

tified

 pathogens in ER 

visits

Bresee et al, JID, 2012

When should you do a work‐up?

• Duration >3‐7 days; > 24 hours if associated with blood; “mod‐severe disease”– Fever, bloody or mucoid stools, severe abd cramping or tenderness, signs of sepsis (2017 IDSA guidelines)

• Hospital admission

• Outbreak settings– Even if not useful for rx, can have public health benefit

• Immunocompromised patients

• Risky patients: HCW, food handlers, daycare, LTCF

• Persistent diarrhea

Guerrant RL et al. Clinical Infectious Diseases ; 2001 ; 32 : 331 ‐35Riddle et al, AJG, 2016

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What’s the work‐up• Stool cx for Salmonella, Shigella, Campy, STEC,

– O157 is sorbitol‐;  Non‐0157:H7 STEC are sorbitol +, need to also order Shiga‐toxin by EIA or NAAT

– Shellfish‐assoc or cholera suspectedsalt‐containing media Yersinia if Europe, appendicitis‐like sx, exposure to undercooked pork

– Rectal swab if no stool sample (but less sensitive)

• Blood cultures if septic, suspicion for S. typhi, IC

• C. diff toxin

• Rotavirus Ag (esp in kids)

• Parasites (if persistent or host factors):– Stool O+P

– Giardia Ag

– Coccidia exam (Cyclospora, Isospora, Cryptosporidium)

– Modified trichrome stainMicrosporidia

• STI risks: RPR; GC and Chlamydia (incl LGV work‐up if positive)

Bloody stool w/u

EIA for toxin NAAT for Stx genes

EHECsorbitol negative

STEC

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F/U testing

• F/U cultures in some situations (return to child care, employment, group social activities) as per local health dept regulations 

• Failure to respond to initial rx

FDA approved Multiplex PCR

Riddle et al, AJG, 2016

• Very sensitive and rapid• Does not distinguish between active vs recent past infection• Culture still needed for cases reported to public health (allows for 

epidemiology, abx resistance testing 

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Infectious causes of prolonged diarrhea• Definition

– Prolonged diarrhea: 7‐13 days

– Persistent diarrhea: 14‐29 days

– Chronic diarrhea >30 days, not usually infectious in etiology

• 3% of returning travelers

• Enteric parasites

– Giardia: Freshwater, daycare centers

– E. histolytica

– Cryptosporidium: Human and animal reservoir, drinking water, low inoculum

– Cyclospora: Nepal, Haiti, Peru, Guatemalan rasperries, seasonal

– Isospora

– In HIV, consider Microsporidia, MAC, CMV

• Bacteria: Shigella, enteroaggregative E. coli

• Post‐infectious IBS

– ~10‐15% vs. 2% in the general population

• Brainerd diarrhea

– Acute watery diarrhea > 4 wks no identified cause

– Can occur as outbreaks

– Resolves w/o treatment

Dupont, HL.  JAMA. 2016

Empiric Abx Rx

• Bloody diarrhea:  challenge is to distinguish Shigella from STEC before test results avail.– Freq scant bloody stools, fever, cramps, tenesmus

– EHEC: “all blood, no stool”; 90% bloody at some point, fever rare (non‐invasive bacteria)

• Travel to developing nations T>38.5 and/or signs sepsis (concern for bacterial diarrhea)

• Cipro or azythromycin if STEC not suspected

• IC pts with severe illness and bloody diarrhea

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Ancillary management

• Antimotility agents: Avoid in C. diff, Shigella

• Anti‐emetics if vomiting

• Probiotics:  no clear evidence for efficacy, variability in preps, dose etc– 2017 IDSA recs: “most trials report decrease and diarrhea duration and stool frequency w/sustained benefit across all outcomes”

• Most studies in children

• Efficacy appears greater in viral diarrhea

• Probably no adverse effects

Parker et al, Nutrition, 2018

Case

• 25 attendees of the ID holiday party become ill, and you are suspicious for a foodborne disease

• Median incubation period = 28h

• 90% with vomiting 

• 50% with diarrhea

• 30% with fever

• Recovery occurred in 12‐60 hours

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What is the etiology?

A. Norovirus

B. Shigella sonnei

C. Staphylococcus aureus enterotoxin

D. C. perfringens

E. B. cereus

Foodborne disease by incubation period

• < 2 hours: Chemical agent – scrombroid, ciguatera, mushroom toxins, etc

• 2‐7 hours: Preformed toxin (except C. perfringens)– Staph aureus, B. cereus

• 8‐14 hours: Increased inoculum and C. perfringens– Not necessarily more severe

• > 14 hours: Most viruses and bacteria

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NorwalkRotavirus

Viral diarrhea vs bacterial diarrhea

• Viral diarrhea usually resolves ≤ 3 days

Norovirus

What is the etiology?

A. NorovirusB. Shigella sonnei

– Diarrhea predominates

C. Staphylococcus aureus enterotoxin– Too long an incubation– No fever

D. C. perfringens– Too long incubation– Vomiting is unusual

E. B. cereus– Too long incubation

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Kaplan criteria

• Used to determine if outbreak likely 2/2 Norovirus

• 99% sp, 68% sn if all criteria met

1. Mean/median illness duration of 12‐60 hrs

2. Mean/median incubation period of 24‐48 hrs

3. > 50% of people with vomiting

4. No bacterial agent found

Turcios RM et al., Clin Infect Dis. 2006 Apr 1;42(7):964‐9

Just a little stomach flu…

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Holy sh**

• Single (+) stranded, noneveloped RNA virus

• Caliciviridae family

• Genogroups‐>genotypes‐>strains

• Replicates only in GI tract

• Persists in environment

• Humans are the only reservoir

Glass et al, NEJM, 2009

Norovirus

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Sx

• Inc 12‐48 hrs (mean 33 hrs)

• Sudden onset diarrhea, vomiting, abd pain, malaise, low grade fever

– Profuse and projectile

• Usually self‐limited, resolves ≤ 3 d

– Prolonged and severe sx in elderly, very young, IC pts

– Prolonged asymptomatic shedding

• Up to 8 wks in healthy pts

• Up to 1 yr in severely IC pts

Larry the vomiting robot

Dx

• Not culturable

• Older techniques:  EM, stool ELISA

• Gold standard:  RT‐PCR (since early 1990’s)

– 68% sensitive

– 99% specific

– Available at public health depts, state & national labs, sendouts

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Evolving epidemiology

• Most common cause of gastroenteritis• Leading cause of diarrhea

• Leading cause of foodborne‐associated illnesses

• Responsible for 50% of gastroenteritis outbreaks worldwide

• Greatly under‐reported– Only 1/1562 cases identified

– ~21 million cases/yr US

– ~2.1 million ambulatory visits/yr

– ~71,000 norovirus‐associated hospitalizations costing $493 million/yr (CID 2011: 52, 466)

– ~800 deaths/yr US

– 200,000 deaths annually children <5 developing 

nations

CDCGastanaduy et al, JID, 2013

Norovirus is a moving target• Antigenic shift and drift (like influenza)

– Change in viral capsid affects binding to GI tract oligosaccharides

– New variant‐>new epidemic wave

– New pandemic strain every 2‐4 yrs

• GI, GII, GIV genotypes cause most human infxns

– GII.4 strains predominant since 1990’s

– GII.4 Sydney strain, GII.p17, GII.17

– Continue to evolve q 2‐3 yrs

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Why is norovirus so difficult to contain?

• Highly transmissable:  a little goes a long way…– ID50:  10‐100 virions– Facile 2˚ spread

• Viral shedding precedes clinical illness in >30% of pts • Prolonged shedding

– Up to 8 wks in healthy hosts– Up to 1 yr in IC hosts

• Asymptomatic shedders

– Withstands wide range of temps and persists in environment

– Immunity is short‐lived and not cross‐protective against antigenic variants

Why is norovirus so difficult to contain?

• Multiple modes of transmission– Food

• Globalization of food distribution• Increased # of people who handle the food we eat• Increased consumption of food at risk of contamination (fresh vegetables and fruit)

– Water– Airborne via vomitus

• Susceptibility correlates w/distance from vomiting event

– Contact w/contaminated surfaces– Fomites– Person‐person contact– Resistant to many disinfectants

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Interrupting transmission

• Disinfection– Wipe surface w/detergent to remove particle debris followed by hypochlorite bleach (5000 ppm) as disinfectant

– Other disinfectants less efficient:  (quanternary ammonium compounds, alcohols)

– Alcohol‐based disinfectants are insufficient

• Wash hands for 1 min w/soap & water, rinse for 20 sec, dry w/disposable towels

Interrupting transmission

• Institutional settings– Cohort pts and staff

– Minimize transport, visitors

– Isolation, contact precautions for sick pts (48 hrsafter sx resolve)

– Sick staff stay home until 48 hrs after sx resolve

– Alcohol in, soap& water out

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Vaccine?

• Challenging due to rapid evolution of antigenic variants and short‐lived immunity

• Ligocyte (acquired by Takeda): in phase II clinical trials

• Vaxart: VP1 protein‐based norovirus oral tablet vaccine in phase I trials

Norovirus: The perfect pathogen?

• Highly contagious

• Rapidly & prolifically shed

• Constantly evolving

• Evokes limited immunity

• Only moderately virulent—doesn’t kill host

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Planning your next cruise….Cdc vessel sanitation site

References/Resources

• IDSA Diarrhea guidelines 2017

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CID 2010; 50:133‐164

IDSA guidelines 2009 A few definitions

• Complicated intra‐abdominal infection: “extends beyond hollow viscus of origin into peritoneal space and is associated w/abscess formation or peritonitis”

• And 111 guidelines…

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More definitions

• Mild‐moderate severity community acquired (CA) infection

• Severe CA infection: – age >70

– medical comorbidities 

– poor nutritional status 

– major peritoneal soilage or multiple abscesses

– patient hemodynamically unstable

– source control delayed or not feasible 

• HA associated– invasive device 

– h/o MRSA infxn or colonization 

– h/o surgery, hospitalization, dialysis, or LTHCF in previous 12 mos

Case 

• 44F with no prior medical history presents to ED with several hrs of diffuse abdominal pain and chills. 

• Tc 37.8C, HR 85, BP 140/80, SaO2 100% RA. 

• WBC 16K, other labs normal. UA and pregnancy test negative.  

• Empiric Abx?

• If so, which ones

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Source control

• Diffuse peritonitis due to perforated viscous is a surgical urgency

• If possible, percutaneous drainage of abscesses is preferred– But not if there is a perforated viscous

• Not enough data to support specific approaches– E.g. extent of resection/debridement, anastamosis vs. ostomy, what 

tissue is debrided, wound management technique

• Highly selected patients who are clinically stable with a well‐circumscribed focus of infection may be treated with antibiotics alone, provided that very close follow‐up is possible

Solomkin JS et al., Clin Infect Dis ; 2010 ; 501 : 133 ‐164

Abx selection

• Empiric rx according to predicted flora and likelihood of abx resistance– Narrower spectrum for mild‐mod CA infxns

– Broader coverage (MDR GNR, enterococcus, yeast) for severe HCA infxns

Oral flora

Miami beach for bacteria

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Microbiology

• Organisms identified in 3 randomized prospective studies (N=1237)

• Bacteremia is uncommon– 0‐5%, more likely 

in critical illness

Solomkin JS et al., Clin Infect Dis ; 2010 ; 501 : 133 ‐164

Organism % of pts

Escherichia coli 71

Klebsiella species  14

Pseudomonas aeruginosa 14

Proteus mirabilis 5

Enterobacter species  5

Bacteroides fragilis 35

Other Bacteroides species  71

Clostridium species  29

Prevotella species  12

Peptostreptococcus species  17

Fusobacterium species  9

Eubacterium species  17

Streptococcus species  38

Enterococcus species  23

Staphylococcus aureus 4

Does she need antibiotics now?

• Cholangitis – decreased rates of complication

• Cholecystitis – lack of data, but usually done

• Diverticulitis – no longer routinely recommended in mild uncomplicated disease (but lowest level of evidence)

• Appendicitis – generally yes.

– Select cases: abx preferred over surgery, but this approach still not widely recommended)

IDSA guidelines: Antibiotics indicated as soon as Dx of hollow viscus infection/rupture is made or suspected – within 1 hr for septic patients, within 8 hrs for hemodynamically stable pts

Gastroenterology 2015;149:1944 – 1949.

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Case  continued…

• CT scan ‐> cholecystitis. 

• Surgery planned for tomorrow. 

• NKDA. 

• Which antibiotics? 

Empiric therapy for mild to mod CA infections at UCSF

Severity Drug(s) of First Choice Severe PCN allergy

Mild‐ModerateCA

Ertapenem 1g IV dailyOR

Piperacillin/tazobactam3.375 g IV ‐ 4.5g IV q6h

VancomycinPLUS

Aztreonam 2 g IV q8hPLUS

Metronidazole 500 mg IV q8h

Severe CA

VancomycinPLUS

Piperacillin/tazobactam4.5 g IV q6h

VancomycinPLUS

Aztreonam 2 g IV q8hPLUS

Metronidazole 500 mg IV q8h

Do not need to cover Pseudomonas, Enterococcus, yeastDo cover for enteric gram-negative aerobic and facultative bacilli and entericgram-positive streptococci

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Case continued…

• Ertapenam started

• Successful cholecystectomy

• Doing well POD2, ready for d/c

• How long to continue abx?

Duration of therapy

• If no perforation or evidence of abscess, d/c abx 24 hrsafter surgery –

• No evidence to use abx prophylaxis for the drain!

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Case  continued…

• Pt dc’d home  

• Next day, surgeon calls. Intraoperative tissues sent for culture growing Enterococcus species (among other things) 

• Pt is clinically stable 

• Were cultures appropriate?

• Do you need to restart abx?

• Does enterococcus need to be covered?

Role of intra‐operative cultures

• Cultures optional in low risk CA infection, but “may be of value in detecting epidemiological changes in resistance patterns”

• Anaerobic cultures not necessary if abx regimen covers anaerobes

• Gram stain generally NOT useful in CA infections, but may be useful in HA infections if yeast is shown

• For low risk CA infections, uncovered organisms do not need to be covered unless pt fails to improve

• For severe or HA infections, consider on case‐by‐case basis

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How should micro data guide treatment?

• If good response to source control and initial abx, no need to change even if untreated organisms are found 

• Use micro to guide therapy if not responding well to empirical abx

• For severe or HCA infections, pathogenic potential and density of organisms should be considered

Solomkin JS et al., Clin Infect Dis ; 2010 ; 501 : 133 ‐164

Role of Enterococcus

• Unclear role as pathogen, no good studies

• Found in 20% of intra‐abdominal infections

• Regimens that don’t cover enterococcus work for community acquired infections

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Case• 68M h/o BPH and recent hospital admission two months ago 

for UTI / pyelonephritis treated with ceftriaxone

• Presents w/ T 38.5C, RUQ abdominal pain, WBC 16K, elevated Tbili

• CT scan: acute cholangitis.

• What organisms to cover for empiric Rx?– Pseudomonas?

– Enterococcus?

– Yeast?

Micro of CA vs. HA infectionsMicroorganism CA HA P value

Escherichia coli 159 (72%) 65 (52%) <0.001

Klebsiella spp. 15 (7%) 13 (10%) NS

Enterobacter spp. 28 (13%) 23 (19%) NS

Proteus mirabilis 9 (4%) 7 (6%) NSPseudomonas aeruginosa 11 (5%) 16 (13%) <0.01

Enterococcus faecalis 28 (19%) 31 (33%) <0.05

Enterococcus faecium 16 (11%) 8 (8%) NSEnterococcus (other) 13 (9%) 13 (14%) NS

Streptococcus spp. 74 (50%) 29 (31%) <0.01Staphylococcus aureus 11 (7%) 6 (6%) NS

Bacteroides spp. 74 (56%) 30 (53%) NS

Clostridium spp. 19 (14%) 10 (18%) NSFungi 19 (3%) 13 (4%) NS

Montravers P et al.,  J Antimicrob Chemother2009;63:785‐94

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Empirical coverage severe CA or HA associated infections

Severity Drug(s) of First Choice Severe PCN allergy

Mild‐Moderate

Ertapenem 1g IV dailyOR

Piperacillin/tazobactam3.375 g IV ‐ 4.5g IV q6h

VancomycinPLUS

Aztreonam 2 g IV q8hPLUS

Metronidazole 500 mg IV q8h

Severe

VancomycinPLUS

Piperacillin/tazobactam4.5 g IV q6h

(For hemodynamically unstable health‐care associated infection, consider meropenem)

VancomycinPLUS

Aztreonam 2 g IV q8hPLUS

Metronidazole 500 mg IV q8h

http://idmp.ucsf.edu/hospitalized‐adults‐gastrointestinal‐infections‐secondary‐peritonitis

Case

• Pt undergoes biliary drainage procedure and is recovering uneventfully

• How long to continue abx?

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Abx duration

• If complicated infection (perforation, phlegmon),abx for 4 – 7 d “unless unable to achieve adequate source control” – How short can you go?

• Consider longer duration + reimaging / cultures + change abxif poor clinical response, or in more complex hosts (immunocompromised, etc)

STOP‐IT: Study To Optimize Peritoneal Infection Therapy 

• Open‐label multicenter randomized trial of 518 patients with complicated intra‐abdominal infection 

• Source control intervention was carried out (surgery or drainage)

– Not well specified in study

• Control group: Abx until 2 d post resolution of fever, WBC < 11K, resumption of PO diet. 

• Experimental group: 4 d Abx after source control procedures

• Primary outcome: composite of surgical site infection, recurrent intra‐abdominal infection, or death

• Secondary outcome: Duration of antibiotic therapy

STOP‐IT trial. Sawyer, et al. N Engl J Med. 2015;372(21):1996

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STOP‐IT Results

• No difference in composite primary endpoint – 21.8% of experimental group vs. 22.3% control (p = 0.92)

• Duration of abx 4 d vs 8 d (p = <0.001)

• Adherence to protocol 82% experimental vs 73% control

Conclusion: For patients who achieve source control procedure, 4 days of abx adequate

STOP‐IT trial. Sawyer, et al. N Engl J Med. 2015;372(21):1996

Enterococcus – when to cover in HA

• Definitely: positive blood cultures

• Maybe: Enterococcus recovered in abd fluid cultures in HA infxn

• Per IDSA, strongly consider in: 

‐ Immunocompromised patients

‐ Health care‐associated postoperative peritonitis

‐ Severe sepsis who have previously received cephalosporinsand other broad‐spectrum antibiotics selecting for Enterococcus species

‐ Valvular heart disease or prosthetic intravascular material (risk of endocarditis)

• Do NOT need to empirically cover VRE unless high index of suspicion

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Role of MRSA 

• Quite rare in CA intra‐abd infections – guidelines do NOT recommend empiric coverage

• Per IDSA: “Empiric antimicrobial coverage directed against MRSA should be provided to patients with health care–associated intra‐abdominal infection who are known to be colonized with the organism or who are at risk of having an infection due to this organism because of prior treatment failure and significant antibiotic exposure”

• Would consider adding anti‐MRSA coverage in HD unstable patients (treat as per sepsis guidelines)

Role of Yeast

• C. albicans found in ∼20% of patients with acute perforations of GI tract

• Does not always need to be treated

• Definitely treat:

‐ Positive blood cultures

‐ Immunocompromised patients

‐ GI perforation on PPI

‐ Postoperative infection

‐ Recurrent intra‐abdominal infection

• Consider in: 

– Pancreatitis surgery (empirically)

– Heavy growth from intra‐op cultures

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Anti‐fungal Rx

• C. albicans:  fluconazole

• Rising rates of non‐albicans Candida (C. glabrata, C. krusei, etc)  for HD unstable patients, use echinocandins until yeast ID is known

• C. parapsilosis, C. lusitaniae, C. guilliermondii, C. orthopsilosis have decreased susceptibility to echinocandins! 

Case 

• 26M prev healthy

• high‐speed MVA with blunt trauma, intra‐abdominal perforation. 

• Started on empiric antibiotics and undergoes urgent surgical repair.  

• Now clinically stable.

• Abx for how long?

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Indications for <24 hours of abx Rx

• Traumatic injuries repaired within 12 hrs

• Intra‐op contamination

• Acute upper GI perforations (stomach, duodenum, proximal jejeunem) in absence of antacid therapy or malignancy

• Uncomplicated acute appendicitis with repair

A word on pancreatitis

• 80% of pancreatitis recover within 1 wk – Abx are NOT recommended for acute pancreatitis (mild or severe)

• 20% develop necrotizing pancreatitis  ‐ roughly one‐third of these will develop superinfection (high mortality)

• Dx: Clinical deterioration or lack of improvement after ~10 days of supportive care. FNA for dx/micro recommended. 

• Rx: controversial – empiric antibiotics vs targeted therapy via FNA/drainage vs necrosectomy

• Often involves multiple procedures

• Length of Rx by clinical improvement

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Consistent principles

• Prophylactic abx (< 24 hrs duration)

– Traumatic injuries repaired within 12 hrs

– Intra‐op contamination 

– Acute perfs of stomach, duodenum, proximal jejeunem in absence of antacid therapy or malignancy

– Uncomplicated acute appendicitis

• Treatment abx (>24 hrs):until resolution of clinical signs of infxn

– STOP‐IT study: or 4 days, if adequate source control

• W/u if no response after 5‐7 d of rx

• enterococcus, yeast only need to be treated in specific situations

Intra‐abdominal Infections take‐home

• Source control is crucial

• Cover aerobic and anaerobic GPCs and GNRs

– Enterococcus if HA post‐surgical, immunocompromised, prosthetic material, severe infection, prior cephalosporins

– MRSA if hospital‐acquired or known carrier

– Yeast if HA post‐operative, pancreatitis associated, perf on PPI, immunosuppressed

• Shorter courses of antibiotics may be possible if source control is achieved and symptoms of infection resolve

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Updated treatment recs H. pylori

• Increasing therapy failure for H. pylori

• Overall principles:  similar to TB Rx

– Don’t reuse a drug to which you suspect resistance

– 4 drugs preferred over 3 drugs when clarithro resistance significant

• Recommended 1st line Rx is quadruple therapy x 14 D

– BPMT or PAMC

– Unless known low clarithro resistance or known local efficacy of 3 drug regimens

• Rifabutin regimens restricted to pts who fail 3 prior options

Fallone et al, Gastroenterology, 2016

Recommended regimens

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Potential regimens

Dosing