i- Table 4. Membrane and Cell Wall Compositions

Membrane Sterol Cell Wall 12

Mold: septate hyphae I

Bacteria Peptldoglycan

5

Human Cell

Fungi

Cholesterol

Frgosterol

Z

Chitin (complex glycnpolysaccltariile) &

I

Mechanisms of Fungal Disease 5

• primary fungal infection by:

overgrowth of normal flora (e.g.Candida spp.)

• inhalation of fungal spores

traumatic inoculation into skin

• toxins produced by fungi (e.g.ingestion of aflatoxins)

• allergic reactionsto fungi (e.g. bronchopulmonary aspergillosis)

=

Mold: non-septate hyphae 5

QJ

Figure 4.Common fungus

morphology

Parasitology

Parasite Basics

• parasite:an organism that livesin or on another organism (host) and damagesthe host in the process

• parasites with complex life cycles require more than one host to reproduce

reservoir host:maintains a parasite and may be the source for human infection

• intermediate host:maintains the asexual stage of a parasite or allows development of the parasite

to proceed through the larvalstages

• definitive host allows the parasite to develop to the adultstage where reproduction occurs

• 2 major groups of parasites:protozoa and helminths

• see table 25,ID35 and table 26, ID39 for examples of clinically important parasites

Table 5.Differences Between Protozoa and Helminths

Apicomplex Sporozoite

(no obvious means of locomotion)

Protozoa Helminths

Unicellular

Motile trophozoite,inactive cyst

Multiplication

Eosinophilia unusual

Indefinitelife span

Multicellular

Adult-»egg -»larva

No multiplication inhuman host

Eosinophilia (proportional loeitenloi tissue invasion)*

Definite tile span

Amoeba

(pseudopod)

"Adult Asearii (tounOwoin)docs rot cause eosinophilia: mlgiotory larval pluses ol Ascaris.however,cause high-giade eosinopMta

Characteristics of Parasitic Disease

• symptoms are usually proportional to parasite burden

• tissue damage is due to the parasite and host immune response

• chronic infections may occur with or without overt disease

• immunocompromised hosts are more susceptible to manifestations ofinfection,reactivation oflatent

infections,and more severedisease

• eosinophilia may suggest a parasitic worm infection

Mechanisms of Parasitic Disease

1. mechanical obstruction (e.g. ascariasis, clonorchiasis)

2. competition with host tor resources (e.g. anemia in hookworm disease, vitamin Bi

’

deficiency in

diphyllobothriasis)

3.cytotoxicity leading to abscesses and ulcers (e.g. amoebiasis,leishmaniasis)

4.inflammatory

acute hypersensitivity (e.g.pneumonitisin Loeffler'

ssyndrome)

delayed hypersensitivity (e.g.egg granulomas in schistosomiasis)

cytokine-mediated (e.g.systemic illness of malaria, disseminated strongyloidiasis)

5. immune-mediated injury

autoimmune (e.g.myocarditis of Chagas disease, tissue destruction of mucocutaneous

leishmaniasis)

immune complex (e.g. nephritis of malaria,schistosomiasis)

Ciliate

(cilia)

r

.

Flagellate

(flagella/whip-like)

-

.

Figure 5.Classification of protozoa

based on movement

Parasite sampling may need tobe

repeated on several occasions before

infection can be ruled out

+

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ID6 Infectious Disease Toronto Notes 2023

Transmission of Infectious Diseases

Table 6.Mechanism of Transmission

Mechanism Mode of Transmission Examples Preventative Measure

Contact Direct physical contact, or indirect contact

with a fomite

Skin-to-skin (MRSA)

Sexual (Af.gomtihoeae,C.

liachomatis. HSV, HIV|

Blood - borne (HIV, HBV. HCV)

For patientsin healthcare facilities:

Contact precautions

Barrier precautions

Safe needlestick/sharp practices

Droplet/Contact Respiratory droplets|>5 pm) can be projected Influenza, mumps,

short distances(«2 m|and deposit on mucosal H.meningitidis.Bordetelo pertussis Contact/droplet precautions

surfaces of the recipient je.g. by coughing,

sneezing, or talking):transmission can also

occur by direct physical contact of respiratory

fluids or indirect contact with a fomite

contaminated with respiratory lluids

Airborne droplet nuclei («5 pm) remain

infectious over time and distance

Ingestion ol conlaminated food or water

For patients in healthcare facilities:

Airborne Af tuberculosis, disseminated VZV. For patientsin healthcare facilities:

measles

V. cboleioe.Salmonella. HAV, HtV Prophylactic vaccinations where

available

Ensure clean food/waler supply

For patientsin healthcare facilities:

Contact precautions used loi admitted

patients with fecal incontinence

when stool is unable to be contained

in diapers

Airborne precautions

Food/

Waterborne

Zoonotic/Vector- Disease transmission from animals to humans Direct animal transmission (rabies. Prophylactic medications,vaccinations

either directly or via an insect vector,or 0 fever)

disease transmission from human to human via Arthropod mediated transmission mosquito nets,tick inspection

an insect vector

borne Protective clothing,insect repellent.

(malaria.Lyme disease.West

Nile virus)

Vertical Spread of disease from parent to offspring Congenital syndromes (TORCH

infections)

Perinatal (HIV. HBV. GBS)

Prenatal screening

Prophylactic treatment

Nosocomial Infections

• definition: infections acquired >48 h after admission to a healthcare facility OR within 30 d from

discharge

• risk factors: prolonged hospital stay, antibiotic use,surgery, hemodialysis, intensive care, colonization

with a resistant organism, immunodeficiency

patients with nosocomial infections have higher mortality, longer hospital stays, and higher

healthcare costs

• hand hygiene is an essential precaution

Table 7.Common Nosocomial Infectious Agents

Bacteria Characteristics Manifestation Investigations Management

Admission screening culture Contact precautions

Irom nates and peri-anal region For infection:vancomycin or daptomycin or linezolid

identifies colonization To decolonize: chlorhexidine 2% wash once daily (•rifampin

Culture of infection site (doxycyctine or 1MP/SMX) mupirocin cream BIO to nates) x 7 d

MRSA GP cocci Skin and soft tissue infection

Bacteremia

Pneumonia

Endocarditis

Osteomyelitis U R

Contact precautions’

Ampicillin if susceptible

Otherwise, linezolid. hgccychne.or daptomycin depending on

site of infection

Ho effective decolonization methods identified

Majority are l. loecium

Resistant if minimum

inhibitory concentration ol Bacteremia

vancomycin l$ >32 pg/mL Endocarditis

Meningitis

Releases exotoxins A and B Fever, nausea, abdominal pain

Hypervirulent strain (MAPI,’ Watery diarrhea

BI/027) has been responsible Pseudomembranous colitis

for increase in incidenceand Severe:toxic megacolon

Riskof bowel perforation

Associated with antibiotic use

Leukocytosis

Rarely causes disease in healthy people Rectal or perirectal swab OR

slool culture for colonization

Culture of Infected site

VRE

un

Stool PCR for toxin A and B genes Contact precautions

Stool immunoassay for

toxins A and B (lesssensitive

than PCR)

Abdominal x-ray (may see

colonic dilatation)

Sigmoidoscopy for

pseudomembranes:avoid if

known colonic dilatation

Clostridioides

difficile

(C.difficile)

Stop culprit antibiotic therapy (primarily fluoroquinolones and

clindamycin)

Supportive therapy (IV fluids)

Empiric treatment with either vancomycin orfidaxomicin

If access to empiric treatment is limited,then metronidazole may

be used

severity

For fulminant C. difficile infection (previously called severe),oral

vancomycin is used. IV metronidazole added to regimen if ileus

present

Contact precautions’

Carbapenems or non- jt-ladam antibiotics can be used for empiric

therapy

Extended Spectrum Resistant to most

p-lactam Producers (t-lactam antibiotics Pulmonary infection

(c.g. ESBl producing except carbapenems e.u. Bacteremia

l. cob.K. penicillins, atlreonam , and liver abscessin susceptible patients

pneumoniae)

Carbapcnemase- producing

Enterobacterales

(CPE)

U l l Blood , sputum, urine, or

aspirated body fluid culture

Imaging at infection site (CXR.

CT, 0/S|

cephalosporins Meningitis

Resistant to It'laclam

antibiotics including

caibapcnems

Contact precautions

Colislin.ligecycllnc can be usedvarying on susceptibility

Cefrdcrocol. ceflazidime -avibactam, plazomin are other options

available through the Special Access Program

Ull Blood , sputum, urine,or

aspirated body fluid culture

Imaging at infection site (CXR.

Cl, U/S)

Pulmonary inlection

Bacteremia

liver abscessin susceptible patients

Meningitis

+

'the use of contact precautionsfor VRE and ESBL varies depending on institutional policies."Not available in Canada

ID7 Infectious Disease Toronto Notes 2023

Respiratory Infections When Klebsiella causes pneumonia:

see red currant jelly sputum

Pneumonia

• see Paediatrics, P93

Definition

• infection of the lung parenchyma

Etiology and Risk Factors

• impaired lung defenses

poor cough/gag reflex (e.g.illness, drug-induced)

• impaired mucociliary transport (e.g.smoking, cystic fibrosis)

immunosuppression (e.g.steroids, chemotherapy,AIDS/HIV, DM, transplant, cancer)

• increased risk of aspiration

impaired swallowing mechanism (e.g. impaired consciousness, neurologic illness causing

dysphagia)

• mechanical obstruction

• no organism identified in 75% of hospitalized cases, and >90% of ambulatory cases

3 As of Klebsiella

Aspiration pneumonia

Alcohol use disorder and patients with

diabetes

Abscess in lungs

Aspiration pneumonias more commonly

manifest as infiltrates in the right middle

or lower lobes due to the larger calibre

and more vertical orientation of the right

bronchus

Table 8. Common Organisms in Pneumonia

Healthcare-Associated Infectious aid

Antimicrobial Resistance inCanadian Ante Care

Hospitals

Can CtiEBua Os fea 2020:46^

9-112

Pirpose to describe feSards of realScare

assoc atEd '

factors (HAS) a:dartn.eoia!

res-stance|AH!1horn 2014 to 2018 -

srgs

_rre la-ce

data from tieCanalan lasoco-a tafecim

Surveillance Prog-am.

Methods Data iratecoi lectedfrom 70 Casadiet

sentinel rosprias regardingClessdentes 4T5o e

rfactron(COI).URSA dcodstreeir riectas.Vt£

moods:ream infcrtinus.aMeabapeneruasepradubngEntarcbectrnatece.

Resnlts:tabsper10.000 patent-dap creased

tor MUSA(59%:0.66105.W.023) a'drtf

pcodstrem nfec:ons (143%;0.B-(m.NU)23 j.

Hanerer.COI etas decreased ty125% fhoc

6.16-5.39.

^

0842).Cafepenoaseptakdag

Eatemtectenaceae colonization rcreased by 375%

(0.04-0.19:Nl-014)b.1in'

ecton raxs -erered

kmand stable.

Conclusion:Stacda-dired s

_rre lance data frsacute caretosp talsnaddsor bantnrtroiial

stewantsb p mtl becrucialturtlenrgn rgp-ererton

of HAIsardAMR nCanada.

Community-Acquired Nosocomial Aspiration Immunocompromised Patients Alcohol Use Disorder

Typical Bacteria

Streptococcuspneumoniae

Moraxella colorrholis

Haemophilus influenzae

Staphylococcus aureus

Pneumocystis jimvecii

Fungi (e.g.Cryptococcus)

Hocordia

Klebsiella

Enteric GNS

S.aureus

Oral anaerobes (aspiration)

Enteric GHB

(e.g.f.coli)

Pseudomonas

oeruginoso

S. aureus

(including

MR &A)

Oral anaerobes

(e.g.Bocteroides)

Enteric GNB

S.aureus

Gastric contents

(chemical

pneumonitis)

CMV

HSV IS

GAS IB

Atypical Bacteria

Mycoplasmapneumoniae

Chlamydia pneumoniae

Legionella pneumophila

Viral

Influenza virus

Adenovirus

SARSCoV-2

’See Paediatrics.P93. Table 45.Common Causes and treatment o!Community-Acquired Pneumonia

Clinical Features

• cough (± sputum),fever, pleuritic chest pain, dyspnea, tachypnea, tachycardia

• elderly often present atypically;altered LOG is sometimes the only sign

• evidence of consolidation (dullness to percussion, bronchial breath sounds, crackles)

• features of parapneumonic effusion (decreased air entry, dullnessto percussion)

• complications:ARDS, lung abscess, parapneumonic effusion/empyema, pleuritis ± hemorrhage

Investigations

• pulse oximetry to assess severity of respiratory distress

• CBC and differential, electrolytes, urea,Cr, arterial blood gas (ABG) (if respiratory distress)

• sputum Gram stain/C&S, blood C&S, ± viral detection (influenza testing) ± serology, ± pleural fluid

C&S (if effusion >5 cm or respiratory distress)

• CXR ± CT chest shows distribution (lobar consolidation or interstitial pattern), extent of infiltrate ±

cavitation

• bronchoscopy ± washingsfor:

• (1) severely ill patients refractory to treatment and (2) immunocompromised patients

Treatment

• airway/breathing/circulation, 02, IV fluids, consider salbutamol (nebulized or metered-dose inhaler)

• determine prognosis and need for hospitalization and antibiotics

Criteria for Hospitalization

• along with clinical judgment, validated clinical prediction rules for prognosis can be used to

determine the need for hospitalizations in adults diagnosed with community-acquired pneumonia

(e.g. the CURB-65 Score or Pneumonia Severity Index (PS1))

Forarejortonnosoccna rfrectozs n trallS.

jlease refer D:HEJH 2014:370:1138-208.Coesut

ps cca!hospital statsZcsbrte aosdatolcable

rforaation forper Bertniece.

Diagnosis of Ventilator-AssociatedPneumonia in

CriticallyIIAdultPatients:A Systematic Revien

and Meta-Analysis

Intensite Ca-eBed 2020:46:1170 79

Purpose: To identifyaMcoapantktacccacy of

9e fj.onmg tceasresfordiag'as'g VIP:ptyscal

camration,dies!raingrajby.ecdorracei

asbi-ete (ETA),b-onczoscobicsanj.ng cat-res

(protected specie:trust|PSB) a'dbruncboa'teolar

aiage|BAU|.and CPIS>6.

Study Selection: El g tie otiservatroa st-des

andRCIs oebded >90% patients wer16 y 'o rr.B

measures condcc.eduttelCU.rebdeg talests

urtb niiiEna4la of itrasne raectancal ied£atm.

Resnlts:Ite co:

lectie ses s tnty atdstec:5cdy

of VAP phys ca!eras: setts Srdcgsnere»ot:

fever (66.4% asd 538%.respectively) andpatient

seeretnas(77.0%.39.0%):earp nStratens chest

radngrajby (888%.26.1%tETA(752%.678%).

Among broecboscopic sen- egnettods.PSB 161.4%.

765%):IAI(711%.73.6%).CP1S

-6(738%.66.4%).

Conclusion VAP Tsdiagsossasdpjta-iely

unnecessaryaatimooMusa aay cesut froc

reliance osclassicalctekal measures used in

isolates.

Table 9. CURB- 65 Score -Pneumonia Clinical Prediction Tool

Component' Measurement(s) Points Total Score Mortality Disposition

ri

Confusion

Urea/BUN

Respiratory Rale

Blood Pressure

0-1 <5% Can treat as outpatient

Consider hospitalization

Consider ICU

Altered menial status

Urea >7 mmol/L or BUN >20 mg/dl

>30 brealhs/min

1

1 2-3 5-15%

1 45 15 30%

sBP "

90 mmHg or dBP *60 mmHg

65 or older

1

Age 1 +

*A CRB-55 score may also be applied in community acquired pneumonia.Its criteria depends on clinical assessment alone

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11)8 Infectious Disease Toronto Notes 2023

Table 10. Pneumonia Severity Index - Clinical Prediction Rule for Prognosis

Risk Factor Points Total Score Risk Class Mortality Recommendation

Demographics <51 I 0.1% Consider outpatient

Age (yr)

Age|yr) - 10

Men

Women

Nursing home resident

Coexisting Illness

Neoplastic disease

Liver disease

Congestive heart failure

Cerebrovascular disease

Renal disease

Physical Exam

Altered mental status

Respiratory rater30 breathsfmln

s8P <90 mmHg

T *35‘C or tdO'C

HR »125 bpm

Investigations

Arterial pH<7.35

BUN >30mgfdL

Sodium <130 mmol/L

Glucose»250 mg/dL

Hematocrit <30%

Partial pressure of arterial 02 <60 mmKq

Pleural effusion

•10

5170 II 0.6% Consider outpatient

•30

20

10

10

10

71-90 III 09-2.8% Consider outpatient Lobar Pneumonia

•20

20

•20

•15

•10

91-130 IV 82-9.3% Hospitalize

30

20

20 >130 V 27.0-29.2% Hospitalize

10

10

10

•10

Adapted with permission hum Diagnosis and Treatment of Community-AcquiredPneumonia.February 1.2006. Vol 73.No 3. American Family

Physician Copyright 2006 American Academy of Family Physicians. All Rights Reserved Bronchopneumonia

Table 11. IDSA/ATS Community-Acquired Pneumonia Treatment Guidelines 2019

Setting Circumstances Treatment

Outpatient No comorbidities or risk factors for MRSA or P.aeruginosas Amoxicillin OR

Doxycydine OR

Macrolide (localpneumococcalresistance <25%)

'

Comorbidities1 Amoxicillinlclavulanalc or cephalosporin

* AND

Macrolidezot doxycydine

OR

Respiratory fluoroquinolones

S-lactam?tmacrolide 2

OR respiratory fluoroquinolone5

Severe inpatientpneumonia«and no risk factors for MRSA piactarrf •macrolide )0R

or P. aeruginosas

Nonsevere inpatient pneumonia%td no risk factors for

MRSAorP.aeruginosa1

Inpatient

Interstitial Pneumonia

p-lactairv*

fluoroquinolone s

©Stuart Jantzon 2012

Given different regional resistance patterns,therapy should be based on local epidemiology and site-specific recommendations

Refers to empiric treatment to be started. Appropriate antibiotic therapy should be tailoredIIpothogcri Is Identified

1.Previous respiratory isolation of MRSA or P. uvruymouj or recent hoipltellxatton AND parenteral antibiotic useIn last 3mo t locally validated risk

(actors

2. Macrolide:use azithromycin or clarithromycin

3. Comorbidities:chronic heart, lung, liver,or renal disease.DM,alcohol use disorder,malignancy,asplenia

4. Cephalosporin:celpodoxime or cefuroxime

5.Respiratory fluoroquinolone:moxilloxacin.levofloxacin

6.Severe =1major criterion or >3 minor criteria.Minor criteria:respiratory rate >30 breaths

'min,Pa02/Fi02 ratio 1250.multilobar infiltrates,

confusion/disorientation.BUN >20 mg/dL.WBC <4000/pL due to infection.Pit

*

100000/pL. T *

36’C,hypotension withaggressive fluid

resuscitation. Major criteria:septic shock withvasopressors, respiratory failure withmechanical ventilation

7. (Hactam:ampicillin sulbactam*, cefotaxime.ceftriaxone,cettaroline*

IDSA:Infectious Oiscases Society of America

ATS:American Thoracic Society

’AvailableIn Canada through the Special Access Program

Figure 6. Lobar, broncho-, and

interstitial pneumonia

Diagnosis and Treatment nf Adults with

Community-Acquired Pneumonia:An Official

C linicalPractice Guideline of the American

Thoracic Society and Infectious Diseases Society

ol America

Am JRespr C'

it Care Med 2019:200:e45 e6?

. Ihe Pneumonia Seventy Index is preferredPI*

I

(he CURB 65 tool for determin nq inpatient vs.

outpatient treatment.

• Test for influenza with a rapid influenza motecutar

assay when it iscirculating in the community.

• Obtaining blood CiSocsputum Gram stair.'CiS

routinely in adults with CAP managed m the

outpatient setting is not recommended.

• Ohtairing pre-treatment blood CISand sputum

Cram sUiwUSis recommendednadults with

CAP managed in Ihe hosptal settingwho (1)aie

classified as seme CAP or (2|are be-nq empneaty

healed lor MRSA or P. aeruginosa or (3) were

previously inlected with MRSA or P.aeruginosa

or (4) were hospitalized and receitdparenteral

antibiotics in the last 90 d.

r s

i

-

J

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1D9 Infectious Disease Toronto Notes 2023

Table 12. IDSA/ATS Hospital-Acquired (HAP) and Ventilator-Associated (VAP) Pneumonia Clinical

Practice Guidelines 2016

Setting Treatment

Doesthis Patient hate Community-Acquired

Pneumonia?

Diagnosing Pneumonia by History and Physical

(lamination

JAM*

1997:278:1440 141S

Study. Systematc retie*

of articles assessing the

sensitivity and specificityof clinical eram maneuversfor

the diagnosis of adult conrunity-acquired p-neumor:a.

Results: the presence of fever or immunosuppression

hada positive likelihood ratio (HR|of 2.whilea history

oIdementia had a

-18of 3:however,these hats ate

not confirmatory,the presence of an abnormality «any

vital sign, including tachytardia.tachypnea,or feter

had a -18 ra ng ng trim 2-4.mb ich wasrotsignificantly

ejected by differentcut-points.The absence of vital

sign abnormality had a -LRrangingfrom 0.S-0.8.The

combination of respratory rate <30 bteathsi'mh. heart

rate <100 bpm, andttmperatgre < 37.8‘C hada -18

ol 0.18.findingson chest turn rased the likelihood

ol diagnosis but were uncommonly seen m studies

(e.g.presence of asymmetric respirations essentially

confirmed the d agnoss but wasonly present in 4%

ol patientd.In patientsvhthadinical diagnosis but

normal radiograph,only *10% will develop radiographic

find rigs in 72 It.

Conclusions: Evidence suggests no single item on

clinical tistory or physical eum issufficient to rule m

or out pneumonia without CXR.Vital sign abnormal tes

were correlated with a dagnosisof pneunoria.findings

on chest eucam significantly raised the fekelihoodof

pneumonia but were uncommonly seen in studies.

Clinically suspected HAP (non-VAP) with no increase in likelihood One of:

of MRSA and not at high-risk of mortality pipeiacillin-tazobactam

OR cclepime

OR levolloxacin

OR imipenem

OR meropenem

Clinically suspected HAP (non-VAP) with increasing likelihood of One of:

MRSA and not at high - risk ol mortality pipeiacillin- tazobactam

OR cclepime or ceftazidime

OR levolloxacin or ciprofloxacin

OR imipenem oc meropenem

ORaztreonam*

PLUS one of:

vancomycin or linezolid for MRSA coverage

Clinically suspected HAP (non-VAP) with high -risk of mortality or Two of the following (avoid 2 p-lactams):

pipeiacillin- tazobactam

OR cefepime or ceftazidime

OR levolloxacin or ciprofloxacin

OR imipenem or meropenem

OR aztreonam*

OR amikacin or gentamicin or tobramycin

PLUS cither MRSA or MSSA coverage:

MRSA: vancomycinor linezolid

OR MSSA: pipeiacillin -tazobactam.cclepime. levolloxacin, imipenem.

meropenem

recipient of IV antibiotics in last 90 d

Clinically suspected VAP in units where empiric MRSA coverage One of:

and double antipseudomonal/GN coverage arcappropriate (3-laclam/p-lactamase inhibitor (piperacillinftazobactam)

OR antipseudomonal cephalosporin (cefepime or ceftazidime)

OR antipseudomonal carbapcnem (imipenem or meropenem)

OR monobadam (aztreonam’)

PLUS one of:

antipseudomonal fluoroquinolone (ciprofloxacin or levofloxacin)

OR aminoglycoside (amikacin,gentamicin,or tobramycin )

OR polymyxins(colislin or polymyxin B)

PLUS one of:

vancomycinor linezolid lor MRSA coverage

Refeis to empiric treatment to be started.Appropriate antibiotic therapy should be tailored it pathogen is identified

'Available in Canada through the SpecialAccess Program

Risk factors for mortality include need for ventilatory support due to pneumonia and septic shock

Risk factors for MDR VAP;prior IV antibiotic use within 90 d. septic shock at time of VAP.ARDS preceding VAP.5*

d of hospitaliiation prior to VAP

onset,acute tonal replacement therapy prior to VAP onset

Ravk factors for MDR HAP. MRSA VAP/HAP. ot MDR Ptmutotnonm VAP.'MAP:Prior IV antibiotic use within 90 d

Note;

Indications for MRSA coverage Includes IV antibiotic treatment during thu prior 90dand treatmentIn a unit where prevalence of MRSA of S.

OUtfUS isolates Is not known or Is *20%

Note:These guidelines may be less applicable in Canada given lower rates of antibiotic resistance among common nosocomial pathogens

Prevention

• Public Health Agency of Canada recommends the following

• vaccine for influenza A and B annually for ail ages 2:6 mo

pneumococcal polysaccharide vaccine (Pneumovax*) for all adults £65 yr and in younger patients

>24 mo at high-risk for invasive pneumococcal disease (e.g. functional or anatomic asplenia,

congenital or acquired immunodeficiency)

• pneumococcal conjugate vaccine (Prevnar-13*) for children and adolescents ages 5-17 yr at high

risk for invasive pneumococcal disease and who have not previously received Prevnar-13* (CDC

recommends giving Prevnar-13*

to all adults at high-risk for Invasive pneumococcal disease)

• Pfizer-BioNTech (Comirnaty*) COV1D-I9 vaccine for children ages 5-11 yr, Moderna (Spikevax*)

COVID-19 vaccine (half-dose, 50 pg) for children ages 6-11 yr, and mKNA COV1D-19 vaccine for

all ages >12 vr who do not have contraindications

Beware! Do Not Confuse H. influenzae

with Influenza Virus

H. influenzae, a bacterium (Types A.B.

C. D, E. and F refer to capsule)

Influenza: a virus (Types A and B refer

to strain)

Vacclnesfor Preventing Influenza in Healthy

Adults

Cochrane DB Syst Rev 201S.C00012G9

Study: 5!RCIsand quiuRCIs evaluating mllut

'

zi

vaccines compared to placebo or no Intervention

in healthy individuals16-65 ylo.Observational

comparative studies were not included.

Results:Inactivated nfluenza vaccines reduce

influenza in healthy adultsfrom 2.3% to 0.9% and

reduce influema -kke llnm(ll|from 21.5% to18.1%.

the preventative effect of vaccination issmall,with

71 healthy adults need ngto he vaccinated to prevent

one from experiencing influenza, and 29 need ng

to be vaccinated to prevent onefrom experiencing

III.Vaccination leadsto a small reduction m the risk

of hospitalization from 14.7% to 14.1%,and a sra l

reduction in days off work.Effectiveness of the

influenza vaccine islessin mochers and newborns

compared to the general population.

Conclusions: Influeaza vaccines have a very modest

effect in zeducing influenza, associated symptoms,

hospitalization, and days off work In healthy adults.

Influenza

Definitions and Etiology

• influenza viruses A and B

• influenza A further divided into subtypes based on envelope glycoproteins

• hemagglutinin ( H ) and neuraminidase ( N)

• seasonal (epidemic) influenza

• main circulating influenza viruses: influenza A ( H INI), influenza A ( H3N2), and influenza B

associated with antigenic drift (gradual, minor changes due to random point mutations)

may create a new viralsubtype resulting in a seasonal epidemic (disease prevalence is greater

than expected )

outbreaks occur mainly during winter months (late December to early March )

• pandemic influenza

associated with antigenic shift: abrupt, major changes due to mixing of two different viral strains

from different hosts

may create a new viral strain resulting in a pandemic outbreak (worldwide)

antigenic shift occurs only in type A

• transmission:droplet, possibly airborne

ri

L J

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ID10 Infectious Disease Toronto Notes 2023

Table 13. Difference Between Influenza Strains

Influenza A Influenza B

Host(s)

Antigenic Drift

Antigenic Shift

Epidemics

Pandemics

Humans,birds,mammals

Yes,new strains

Yes.new subtypes

Humans only

Yes,new slrains Acute Myocardiallnfarction alter laboratoryConfirmed Influenza Inlection

H EJM 2018;378:345-353

Purpose:To investigate the association between

laboratory-confirmed influenza iafectnaand

acute Ml.

Methods: Self -controlled case senes, disk interval

defined asfirst 7 d after respiratocy soecimen

collection and control Interval as1 jr before and 1yr

afterthe risk interval.

Results:Increased incidence ratioof an admission for

acute Ml during risk interval vs.control inletval (6.05.

95% Cl 3.86 9.50). No increased incidence alter fd.

Increased incidence ratiosfor acute Ml within I d after

detection of influenza B ItO.tl.95% Cl 4.31-23.38),

influenza A (5.11, 95% Cl 3.02-8.84).and respiratory

syncytial virus(3.51,95% Cl1.11-11.12).

Conclusions:Sigrificantassociaton between

respiratory infections, especially ioDueuia.and

acute Ml.

No

Yes Yes

Yes No

Clinical Features

• incubation period 1-4 d and symptoms typically resolve in 7-10 d

• acute onset of systemic (fever, chills, myalgias, arthralgias, headache, fatigue) and respiratory

symptoms(cough, dyspnea, pharyngitis)

• complications:respiratory (viral pneumonia,secondary bacterial pneumonia, otitis media,sinusitis),

muscular (rhabdomyotysis, myositis), neurologic (encephalitis, meningitis, transverse myelitis,

(vuillain-Barre syndrome)

• severe disease more likely in the elderly, children, pregnant women, immunocompromised patients,

asthma, COPD, cardiovascular disease (CVD), DM, and obesity

Investigations

• diagnosis is primarily clinical based on symptoms during the influenza season

• nasopharyngeal swabs for RT-PCR (gold standard),or rapid antigen detection (DTA, direct fluorescent

antibody) which has lower sensitivity

• lower respiratory specimens for RT-PCR

• serology:rarely used for clinical management

Treatment and Prevention

• primarily supportive unlesssevere infection or high-risk for complications

• neuraminidase inhibitors: oseltamivir (Tamiflu*) or zanamivir (Relenza*) for treatment and

prophylaxis against types A and B or peramivir (Raplvab") for the treatment against types A and B

decreases duration (by -1 d) and severity of symptoms if given within 48 h of onset

treatment beyond 48 h time window may be warranted in immunosuppressed and critically ill

patients

• vaccine for influenza A and B viruses is recommended annually for all ages >6 mo

• vaccine is reformulated each year to reflect circulating influenza A and B strains

High-risk for Complications

• anyone who is hospitalized, patients with severe illness/chronic medical conditions,

immunocompromised patients, children <2 yr, elders >65 yr, pregnant women or women <2 wk

postpartum

COVID-19

Definitions and Etiology

• an acute infectious respirator)'disease caused by the SARS-CoV-2 virus

• SARS-CoV-2 is an enveloped, positive-sense,ssRNA virus

• transmission:droplet and airborne transmission

• incubation period 2-14 d, usually -5 d

Pathophysiology

• invasion of host cells via the viral spike protein which binds to angiotensin-converting enzyme 2

(ACE2) expressed on the surface epithelium of the lungs

• virus induced cytotoxic damage particularly to the alveolar epithelium

• dysregulated immune response can lead to a cytokine storm causing organ failure or death

Clinical Features

• can be asymptomatic (estimated to be I in 3 of those infected)

children are more likely to be asymptomatic or to have mild disease

• most common:fever,fatigue, dry cough

• common:dyspnea,loss ofsmell and/or taste (may vary depending on the variant circulating),loss of

appetite,myalgia

• less common: nausea, vomiting, abdominal pain,sore throat, headache, thromboembolic events

• course: can range front mild disease (lasts l-2 wk) to severe or critical disease (lasts 3-t- wk); may be

complicated by post-COVID condition which is associated with a wide range of diverse symptoms

across multiple organ systems that may fluctuate in intensity,often exacerbated by mental and

physical over-exertion

Diagnosis

• nasopharyngeal swabs for RT-PCR (gold standard) or nasal/oral-nasal swabs for rapid antigen

detection point of care tests which have lower sensitivity

• lower respiratory specimensfor RT-PCR

Treatment (accurate as of April 1, 2022)

• please see updated guidance through the Ontario Science Table (https://covidI9-sciencetable.ca/

science-briefs/#infectious-diseases-clinical-care)

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• for critically ill adults >18 yr requiring ventilatory and/or circulatory support:

• dexamethasone HO or IV for 10 d (or until discharge)

• tocilizumab if on recommended steroid dose » admitted to hospital or diagnosed with (.

'

OVID-19

in hospital within 14 d

• prophylactic low molecular-weight or unfractionated heparin

• for adults >18 yr requiring low-flow supplemental 02:

dexamethasone HO or IV'

for 10 d (or until discharge)

• remdesivir IV for 5 d

• tocilizumab if serum CRH 75 mg/L t disease progression despite 24-48 h of recommended

steroid dose t admitted to hospital or diagnosed with COVID-19 in hospital within 14 d

• prophylactic low molecular-weight or unfractionated heparin

• for mildly ill adults >18 yr who do not require supplemental ()2 in any setting:

• stratify by risk ofsevere disease (i.e. >5% risk of hospitalization)

• for patients with >5% risk of hospitalization:

• nirmatrelvir/ritonavir (Haxlovid) if presenting within 5 d of symptom onset

remdesivir if presenting within 7 d of symptom onset

• for patients with <5% risk of hospitalization: reassurance and self-monitoring of symptoms

Table 14. Risk of Hospitalization in Mildly III Adults >18 yr with COVID-19 (accurate as of April1, 2022)

. Higher risk individuals are those who have a »5% risk of hospitalization if they develop COVID-19.Standard risk individuals are those who have a of hospitalization.

• Indigenous people.Black people,and members of other racialized communities may be at increased risk of disease progression due lo disparate rates of comorbidity,increased barriers to

vaccination,and social determinants of health.They should be considered priority populations for access to COVIO-19 drugs and therapeutics.

Age (Years) Number of Vaccine Doses Risk Factors

Obesity (BMI »30 kg/m2)

Diabetes

Heart disease,hypertension,congestive heart

failure

Chronic respiratory disease,including cystic fibrosis

Cerebral palsy

Intellectual disability

Sickle cell disease

Moderate or severe kidney disease|eGfR '

60 ml/

0 Doses

Higher risk if >3 risk factors 1 Standard risk t

Higher risk il>3 risk factors Higher risk if >3 risk factors Standard risk

Higher risk if >1risk factors Higher risk if >3 risk factors Standard risk

Higher risk Higher risk if >1risk factors Higher risk if >3 risk factors

Higher risk: therapeutics should always be recommended lor immunocompromised individuals not

eipeded lo mountan adequate immune response to COVIO-19 vaccination or SARS- CoV- 2 infection due

lo their underlying immune status,regardless of age or vaccine status U

Higher risk1

1or 2 Doses 3 Doses

«20i Standard risk >

20 to 39

40 to 69

>70

Immunocompromised1individuals

olanyage

min)

Moderate or severe liver disease (e.g.ChildPugh

Class B oi C cirrhosis)

Pregnancy Standard risk Standard risk

1. Evidence for the vilely.ind efficacy of

^

otrovlmob and nirmotrdvlf /rilonavlr (Paxlovid) In children •18 yean of ageI

*

limited While early evidence on ilsk factor

*

for moderate and severe COVIO-19

In children!

*

emerging, theability to reliably predict di

*

ea*

c progression in children remain*

very limited,and the frequency of progrc**

ionI

*

tore. While not routinely recommended In children <18

year*

of age.the u

*

eof the*

e agent*

may be consideredin exceptional circum

*

tanco

*

(e.g.tevora Immunocompromise and/or multiple ti*

k factor*

,clinical progrc**

ion)on a ca*

e-by-ca*

e basis.

Multidisciplinary consultation with Infectious Disease*

(or Pediatric Infectious Diseases) and the tuam primarily responsible for thechild's care is recommended to review the individual consideration

of thesemedications.

2. Examples of Immunocompromised or immunosuppressed individuals include receipt ol treatment lor solid tumours and hematologic malignancies (including individuals with lymphoid malignancies

who arc being monitored without active treatment),receipt olsolid-oigan transplant and takingimmunosuppressive therapy,receipt olchimeric antigen receptor (CAR)- T-cell or hematopoietic stem

cell transplant (within 2 years of transplantation or taking immunosuppression therapy),moderate or severe primary immunodeficiency (e.g.DiGeorge syndrome. Wiskott

-Aldrich syndrome,common

variable immunodeficiency. Good’s syndrome,hyper IgE syndrome),advanced or untrealed HIV Infection,active treatment with high-dose corticosteroids (i.e. £20 mgprednisone or equivalent per

day when administered for >2 weeks),alkylating agents,antimetoboliles.transplant

-ielated immunosuppressive drugs,cancer chemotherapeutic agents classified as severely immunosuppressive,

tumour

-necrosis factor (TNF) blockers,and other biologic agents that are immunosuppressive or immunomodulatory. These individuals shouldhave a reasonable expectation for 1-year survival prior

to SARS-CoV-2 inlection.

3. Therapeutics should always be recommended for pregnant individuals who have received zero vaccinedoses.

Prevention (accurate as of June 7, 2022)

• complete series of mRNA COVID-19 vaccine for all ages >12 yr who do not have contraindications

• Hfizer-BioNTech (Comirnaty*) COVID-19 vaccine for children ages 5-11 yr, Moderna (Spikevax*)

COVID-19 vaccine (half-dose, 50 pg) for children ages 6-11 yr, and mRNA COVID-19 vaccine for all

ages >12 yr who do not have contraindications

Skin and Soft Tissue Infections

Cellulitis

Definition

• acute infection of the skin principally involving the dermis and subcutaneous tissue

Etiology

common causative agents: p-hemolytic streptococci (most common cause of non-purulent cellulitis), S.

aureus, and occasionally S. lugdunensis

• immunocompromised patients or water exposure: may also include CiN rods and fungi

• bite wounds: consider skin tlora of “bitec" and mouth flora of “biter"

• risk factors

• trauma with direct inoculation,recent surgery

peripheral vascular disease, lymphedema, DM, cracked skin in feet/toes (tinea pedis)

Clinical Features

• pain, edema, erythema with indistinct borders ± regional Ivmphadenopathy,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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Investigations

• CBC and differential, blood C&S if patient has malignancy,severe systemic features, or unusual

predisposing factors,such asimmersion injury, animal bites, neutropenia, and severe cell-mediated

immunodeficiency

• skin swab ONLY if open wound with pus

Treatment

• consult local guidelines for appropriate antibiotic therapy

• antibiotics: cephalexin (broader coverage if risk factors for (iN rods)

• if extensive erythema or systemic symptoms, consider cefazolin IV

• if MRSA is suspected, empiric coverage for MRSA may be considered (see A Simplified Look at

Antibiotics, ID46 )

• limb rest and elevation may help reduce swelling

Necrotizing Fasciitis

Definition

• life- and limb-threatening infection of the deep fascia characterized by rapid spread

Etiology

• two main forms

• Type 1: polymicrobial infection - aerobes and anaerobes (e.g. S.aureus, Bacteroides,

Entcrobacterales)

Type 11: monomicrobial infection with GAS,or less commonly S.aureus

Clinical Features

• pain out of proportion to clinical findings and beyond border of erythema

• edema ± crepitus (subcutaneous gas from anaerobes)

• infection spreads rapidly

rapid onset ofsystemic symptoms (e.g. tachycardia, hypotension, lightheadedness,disorientation,

lethargy, ana fever)

• late findings

skin turns dusky blue and black (secondary to thrombosis and necrosis)

• induration,formation of hemorrhagic bullae

loss ofsensation in the affected area (paresthesias)

Investigations

• clinical/surgical diagnosis-do NOT wait for results of investigations before beginning treatment

• blood and tissue C&S

• serum Creatine Kinase (CK) - elevated CK usually means myonecrosis (a late sign)

• plain film x-ray or CT (soft tissue gas may be visualized)

• surgical exploration for debridement of infected tissue

Treatment

• resuscitation with IV' fluids

• emergency surgical debridement to confirm diagnosis and remove necrotic tissue (may require

amputation)

• IV'

antibiotics

unknown organism:meropenem or piperacillin/tazobactam + clindamycin IV ± vancomycin if

MRSA is considered

Type 1 (polymicrobial): piperacillin /tazobactam + clindamycin IV'

Type II (monomicrobial): with confirmed GAS infection, penicillin G + clindamycin IV; with

confirmed S. aureus infection, cefazolin (or doxadllin) + clindamycin IV

with Type II, evaluate for streptococcal toxic shock syndrome and the need for IVIg

Acquired Oral Lesions

Etiology

• infection (e.g. candidiasis,gonococcal infection), HSV

• malignancy (e.g. adenocardnoma,leukoplakia)

• poor oral hygiene (e.g. caries, periodontal disease)

• trauma (e.g. abuse)

• toxic ingestion

• xerostomia (e.g. age, medications)

• systemic diseases (e.g. lichen planus, Behcet disease)

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Table 15. Comparison between Oral Infection vs. Oral Carcinoma

Oral Candidiasis Oral Squamous Cell Carcinoma

Risk Factors Antibiotics, chemotherapy, radiation therapy

Immunocompromised, inhaled corticosteroids

Age -infants,older adults with dentures

Tobacco use (smoked and smokeless)

Betel use

Alcohol

HPV,especially HPV-16

Morphology Pseudomembranous:confluent,white patches or Alesion of three or more weeks duration:

plaques,can be wiped off with a gauze,exposing an Redor red and white lesion

erythematous base

Atrophic candidiasis:red patches localized mainly to

the palate and dorsum of the tongue

Diagnosis Cytology, biopsy, or culture

Treatment Topical antifungal

Ulcer

Lump

Especially when in combination or if indurated (firm on palpation)

Biopsy and histopathologic examination

Referral to ENT

Gastrointestinal Infections

• sec Gastroenterology.Gl 4 and Paediatrics. NO

Traveller’s Diarrhea

• see Gastroenterology.G18

Chronic Diarrhea

• see Gastroenterology.(i19

Peptic Ulcer Disease (Helicobacter pylori)

• see Gastroenterology. Gl 3

Bone and Joint Infections

Septic Arthritis

Definition

• infection of one or more joints by pathogenic microbes

Routes of Infection

• hematogenous (most common)

from distant infection (e.g. abscesses, wound infection, bacteremia)

• direct inoculation via skin/trauma

iatrogenic (e.g.surgery, arthroscopy, arthrocentesis, joint injection)

• trauma (e.g. open wounds around the joint, penetrating trauma)

• contiguousspread (e.g.septic bursitis, osteomyelitis)

Etiology

• gonococcal

N.gonorrhoeae: previously accounted for 75% ofseptic arthritisin young sexually active adults

• non-gonococcal

S. aureus: affects ail ages, rapidly destructive, accountsfor most non-gonococcal cases ofseptic

arthritisin adults (especially in those with rheumatoid arthritis)

Streptococcus spp. (Group A and B)

• GNs: affect neonates, elderly, injection drug users, immunocompromised

.S’, pneumoniae: affects children

Kingclla kingac: affects children <4 yr

• Haemophilus influenzae type B (Hib) now rare due to Hib vaccine: consider in unvaccinated

children

• Salmonella spp.:characteristic ofsickle cell disease

• coagulase- negative Staphylococcusspp.:prosthetic joints

• if culture-negative:partially treated infection (prior to oral antibiotics), reactive arthritis, rheumatic

fever,less common bacterial causessuch asBorrelia spp.(Lyme disease) or Tropheryma whipplei

(Whipple’

s disease), and non-infectious causes

Medical Emergency

Septic arthritis is a medical emergency!

If untreated,rapid joint destruction will

occur

Disseminated Gonococcal Infection

Triad

• Migratory arthralgias

• Tenosynovitis next to inflamed joint

• Pustular skin lesions

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Risk Factors

• gonococcal

• age <40 yr, multiple partners, unprotected intercourse, MSM

• non-gonococcal

• most affected children are previously healthy with no risk factors: occasionally preceding history

of minor trauma

bacteremia (extra-articular infection with hematogenous seeding,endocarditis)

prosthetic joints/recent joint surgery

underlying joint disease (e.g. rheumatoid arthritis,osteoarthritis)

immunocompromised (e.g. DM, chronic kidney disease,alcohol use disorder,cirrhosis)

» loss ofskin integrity (e.g. cutaneous ulcer,skin infection)

• age >80 yr

Clinical Features of Gonococcal Arthritis

• two forms (although often overlap):

» septic arthritisform:local symptoms in involved joint (swelling, warmth, pain,inability to weight

bear,decreased range of motion)

bacteremic form:systemic symptoms of fever, malaise, chills

Clinical Features of Non-Gonococcal Arthritis

• acute onset of pain,swelling, warmth,decreased range of motion ± fever and chills;in children,

refusal to weight bear

• most often in large weight-bearing joints (knee, hip, ankle) and wrists

• usually monoarticular ( polyarticular risk factors: rheumatoid arthritis, endocarditis, GBS)

Investigations

• consider rheumatologic causes for monoarthritis (see Rheumatology,Table 4, RH3)

• gonococcal:blood C&S, as well as endocervical, urethral, rectal, and oropharyngeal testing

• non-gonococcal: blood C&S

• arthrocentesis(synovial fluid analysis) is mandatory, CBC and differential, Gram stain,C&S,examine

for crystals

infectious = opaque, increased WBCs (>15000/mm >.likelihood of infection increases with

increasing WBCs), PMNs >90%, culture positive

• growth of N. gonorrhoeas from synovial fluid issuccessful in <50% of cases

• ± plain x-ray: assess for osteomyelitis, provides baseline to monitor treatment

Treatment

• medical

« empiric IV antibiotics:specific choice depends on clinical scenario and local guidelines;for

most adults, cefazolin ± vancomycin is reasonable; for fully vaccinated children, cefazolin or

cloxacillin IV unless MRSA is a consideration - delay may result in joint destruction

Gram stain and cultures guide subsequent treatment

gonococcal: ceftriaxone (+ azithromycin for concurrent treatment of C. trachomatis),7 d of

therapy usually sufficient

• non-gonococcal: antibiotics against Streptococcusspp. (2-3 wk IV followed by PO), S.aureus (4 wk

IV minimum), or GNB (4 wk, newer evidence suggests early switch to PO issafe and effective)

• surgical intervention if (see Orthopaedic Surgery, OR11)

would considersurgical intervention on all cases ofseptic arthritis if possible

persistent positive joint cultures on repeat arthrocentesis

hip joint involvement, especially in paediatric population

prosthetic joint

• daily joint aspirations until culture sterile

• physiotherapy

Prognosis

• gonococcal:responds well after 24-48 h of initiating antibiotics (usually complete recovery)

• non-gonococcal:in children, generally good outcome if treated promptly; in adults, up to 50%

morbidity (decreased joint function/mobility)

Intra articular steroids are

contraindicated until septic arthritis has

been excluded

IW60F Guidance on the Diagnosis and

Management of toot Infections in Persons with

Oibelts- Recommendationslor Diagnosing

Osteomyelitis

Diabetes Metab Res Rev 2016:32:45 74

Perfotm a probe-to bone test lor an infected open

wound:a negative lest likely rMesootosteomyelitis

in tow-risk patients. while a positive test isIkely

diagnostic in high-risk patients.

In suspected cases,dramatically derated serum

inflammatory markers(especially ESI)are suggestive

olosteomyelitis.

hew in doubt, positive results on microbiological

or histological eram ol an aseptic bone sample are

usually required lor a definitive diagnosis ol bone

infection.

tone infection a probable if there are positive results

on a combination of diagnostic tests(probe-to-bone,

serum nflammatory markers, plain i-ray. MR I.or

radionuclide scanning).

for all cases of non-superlicial drabeticfoot infection ,

plain x-rays of the footshou Id be obtained.

When advanced imaging isrequired for diagnosis.

Mil is preferred.

See Landmark Infectiujs Disease Trials table for more

information on the OVIVA trial.It details whether

oal antibiotic therapy is noninferiorto IV antibiotic

therapy for the management of cmploorthopaedic

infections.

Diabetic Foot Infections

Etiology

• neuropathy, peripheral vascular disease, and hyperglycemia contribute to foot ulcersthat heal poorly,

and are predisposed to infection

• organisms in mild infection:Streptococcusspp.,S. aureus

• organisms in moderate/severe infection: polymicrobial svith aerobes (S. aureus, Streptococcus,

Enterococcus,GNB) and anaerobes(Peptostreptococcus, Bacteroides, Clostridium)

Clinical Features

• not all ulcers are infected

• consider infection if: probe to bone (see below), ulcer present >30 d, recurrent ulcers, trauma, PVD,

prior amputation,loss of protective sensation, renal disease, or history of walking barefoot

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•diagnosis of infected ulcer: 2 of the cardinal signs of inflammation (redness,svarmth,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 (fever, tachypnea, leukocytosis, tachycardia,

hypotension)

Investigations

•curettage specimen from ulcer base, aspirate from an abscess or bone biopsy (resultsfrom superficial

swabs do not represent organisms responsible for deeper infections)

•blood C&S if febrile

•assess for osteomyelitis by x-ray (although not sensitive in early stages) or MKl/bone scan if high

clinical suspicion

•if initial x-ray normal, repeat 2-4 wk after initiating treatment to increase testsensitivity

Treatment

•mild to moderate:cefazolin or cephalexin

severe:options include:1. ceftriaxone + metronidazole;2. piperacillin/tazobactam ± vancomycin; 3.

meropenem ± vancomycin

•optimize glycemic control, pressure offloading, wound care, consider revascularization

• this is empiric treatment, and specific treatment needs to be adjusted based on culture and

response to therapy

Osteomyelitis

• see Orthopaedic Surgery, OR 11

Cardiac Infections

InfectiveEndocarditis

Definition

• Infection of cardiac endothelium, most commonly the valves

classifications:acute vs. subacute, native valve vs. prosthetic valve, right sided vs. left sided

• leaflet vegetations are made of platelet-fibrin thrombi, WBCs, and bacteria

Risk Factors and Etiology

• predisposing conditions

» high-risk:prosthetic cardiac valve, previous infective endocarditis(IE), congenital heart disease

(unrepaired,repaired within 6 mo, or 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 atrial septal defect (ASD) orsurgically repaired ASDcventricular septal

defect (VSD), patent ductus arteriosus (PDA), mitral valve (MV ) prolapse, ischemic heart disease,

previous coronary artery bypass graft (CABG)

* opportunistic bacteremia: IVDU, indwelling venous catheter, hemodialysis, poor dentition, DM,

HIV

• frequency of valve involvement M V»aortic valve (AV)>tricuspid valve (T'V )>pulmonary valve (PV)

in 50% of IVDU-related IE the tricuspid valve is involved

Table 16. Microbial Etiology of Infective Endocarditis Based on Risk Factors

Native Valve IVDU Prosthetic Valve (recent

surgery <2 mo)

Prosthetic Valve (remote

surgery >2 mo)

Strepfococa/5

,(36%)

S. aureus (28%)

Cnterococcus (11%)

5. epidermidis

GNB

Other1

5.aureus

Streptococcus (13%)

[nterococcus

S. aureus (36%)

S. epidermidis (17%)

enterococcus

Streptococcus (20%)

S.aureus(20%)

S. epidermidis (20%)

fnterococcus (13%)

Other1

GNB EM

Candida Other

Other

’