Nosocomial infections

1. NOSOCOMIAL INFECTIONS
Moderator DR ANANYA
SPEAKERS Dr SHRADDHA
Dr GREESHMA

2. CONTENTS
1. NOSOCOMIAL PNEUMONIA
2. INTRA VENOUS CATHETER RELATED INFECTIONS
3. URINARY TRACT INFECTIONS

3. INTRODUCTION
Definition:
Infection acquired in the hospital: > 48 hours after admission
Related to severity of underlying disease, immunosuppression,
invasive medical interventions
Frequently caused by antibiotic-resistant organisms: MRSA, VRE,
resistant Gram- negative bacilli, Candida .
Also influenced by the bacteriological flora prevailing within a
particular unit or hospital
The closed milieu of the ICU provides an environment that is conducive
to the growth and preservation of resistant organisms

4. INCIDENCE
HIGHEST in burn units, surgical ICUs and ICUs for low birth weight neonates (15–30%).
INTERMEDIATE in medical and pediatric ICUs (5–10%),
LOWEST in coronary care units (1–2%)

5. EPIDEMIOLOGY

6. CASE SCENARIO
oA 52 year old male is admitted with a severe headache and is found
to have a subarachnoid hemorrhage from a ruptured aneurysm.
oThe neurosurgeons evacuate the hematoma and clip his aneurysm.
Post-op he remains on a ventilator.
oOn hospital day 5 he spikes a fever to 102o F and is noted to have
copious secretions from his endotracheal tube.
oIncreasing amounts of inspired O2 are required. Blood and sputum
cultures grow highly resistant Enterobacter cloacae.

8. DEFINITION
HAP (or nosocomial pneumonia) is pneumonia that occurs 48 hours
or more after admission and did not appear to be incubating at the
time of admission.
VAP is a type of hospital-acquired pneumonia that occurs more than
48 hours after endotracheal intubation.
This can be further classified into
Early onset (within the first 96 hours of MV)
Late onset (more than 96 hours after the initiation of MV), which is
more commonly attributable to multidrug–resistant pathogens.

9. INCIDENCE
Quoted by the International Nosocomial Infection Control
Consortium suggest that the overall rate of VAP is 13.6 per 1000
VAP is common in critical care patients and is responsible for around
half of all antibiotics given to patients in ICUs.
Time taken to develop VAP from the initiation of MV is around 5 to 7
days, with a mortality rate quoted as between 24% and 76%

10. ETIOLOGY
Common pathogens of HAP and VAP include
Aerobic gram-negative bacilli (e.g. Pseudomonas
aeruginosa, Escherichia coli, Klebsiella
pneumoniae, Enterobacter spp, Acinetobacter spp)
Gram-positive cocci (e.g., Staphylococcus aureus, which includes
methicillin-resistant S. aureus, Streptococcus spp).
Differences in host factors and in the hospital flora of an institution
affect the patterns of the causative pathogens.[

11. RISK FACTORS FOR THE
DEVELOPMENT OF VAP/HAP
Increasing age (.55 years)
Chronic lung disease
Aspiration/ microaspiration
Previous antibiotic therapy, especially broad-spectrum antibiotics
Reintubation after unsuccessful extubation, or prolonged intubation
Acute respiratory distress syndrome
Frequent ventilator circuit changes
Polytrauma patient
Prolonged paralysis
Premorbid conditions such as malnutrition, renal failure, and anaemia

12. PATHOPHYSIOLOGY
The key to the development of VAP is the presence of an ETT or
tracheostomy
Both of which interfere with the normal anatomy and physiology of
the respiratory tract, specifically the functional mechanisms involved
in clearing secretions (cough and mucociliary action).
 Intubated patients have a reduced level of consciousness that
impairs voluntary clearance of secretions, which may then pool in the
oropharynx.
This leads to the macroaspiration and microaspiration of
contaminated oropharyngeal secretions that are rich in harmful
pathogens.

13. Normal oral flora start to proliferate and are able to pass along the
tracheal tube, forming an antibiotic-resistant biofilm which eventually
reaches the lower airways.
 Critically unwell patients exhibit an impaired ability to mount an
immune response to these pathogens, leading to the development of
a pneumonia.
The presence of additional predisposing factors such as pulmonary
oedema in these patients can also accelerate the process

14. Early-onset VAP, occurring within the first four days of MV, is usually
caused by antibiotic-sensitive community-acquired bacteria such as
Haemophilus and Streptococcus.
VAP developing more than 5 days after initiation of MV is usually
caused by multidrug–resistant bacteria such as Pseudomonas
aeruginosa.

15. RISK FACTORS FOR MULTIDRUG–
RESISTANT
HAP/VAP
Intravenous antibiotic use within the previous 90 days
Septic shock at the time of VAP
Acute respiratory distress syndrome (ARDS) preceding the
development of VAP
More than 5 days of hospitalisation prior to the development of
VAP
Patient requiring acute renal replacement therapy prior to the
development of VAP

16. DIAGNOSIS
NOSOCOMIAL pneumonia classically presents with symptoms
such as
Fever
Purulent respiratory secretions
Rising inflammatory markers
Respiratory distress, worsening respiratory parameters
(reduced tidal volume, increased minute ventilation, and
hypoxia).

17. SCORING SYSTEMS

19. CLINICAL EVALUATION
In the guidelines for the management of HAP and VAP by Infectious
Diseases Society of America/American Thoracic Society 2016,
Diagnosis is based upon a presence of
1. New lung infiltrate
2. Clinical evidence that the infiltrate is of an infectious cause
New onset of fever
Purulent sputum
Leukocytosis
Decline in oxygenation

20. BACTERIOLOGIC EVALUATION
For patients with VAP sampling the lower airways to get quantitative
cultures can be done by:
a. Blind tracheobronchial aspiration (TBAS)
b. Bronchoscopy with bronchoalveolar lavage
c. Protected specimen brush (PSB)
For patients with HAP (non-VAP), noninvasive methods for sampling
the lower airways include
i. Spontaneous expectoration
ii. Sputum induction,
iii. Nasotracheal suctioning in a patient who cannot cooperate to
produce a sputum sample.

21. MICROSCOPIC ANALYSIS
Analysis of polymorphonuclear leukocytes and a gram stain.
The microscopy can be helpful in determining a
possible pathogen and the antibiotic selection until the results
of the culture are available.
The presence of abundant neutrophils and the bacterial
morphology may suggest a likely pathogen.

22. QUANTITATIVE CULTURES
Diagnostic thresholds include:
Endotracheal aspirates 1,000,000 colony forming
units (CFU)/mL
Bronchoscopic- or mini-BAL 10,000 CFU/mL
PSB 1000 CFU/mL

23. NEW MOLECULAR DIAGNOSTIC
TESTS
Multiplex polymerase chain reaction assay, which detects
an array of respiratory bacterial pathogens and many
antibiotic resistance genes
 Offer the advantage of rapid identification of pathogens
and resistance patterns for rapid choosing the antibiotic
regimen

24. PRINCIPLES IN TREATMENT STRATEGY
x Promptly start empiric antibiotic therapy after sending respiratory
secretions for culture antibiotic sensitivity and Gram stain– Blood
culture
x Avoid repeating the same antibiotic class if patient has received it
in the past two weeks
x Subsequent modification of antibiotic regime as per culture
sensitivity
x Persevere with the same antibiotic regime if there is a good clinical
response even if this is contrary to culture reports
x Avoid prolonged use of antibiotics ,consider de-escalation of
therapy in appropriate cases
x Stop antibiotics if no growth reported—unless the patient has
severe sepsis and no other cause for sepsis is evident

27. CASE SCENARIOS
•A 45 year old male is admitted for community-acquired
pneumonia.
•He has a long history of IV drug use, but has not used in
several years.
•The intern has difficulty starting a peripheral IV, so places a
femoral venous catheter.
•His cough and fever begin to improve.
•On hospital day 3 he has fever, chills and a WBC of 18,000.
•Blood cultures are positive for vancomycin-resistant
Enterococcus.

28. INTRAVASCULAR CATHETER-
RELATED INFECTION:
•Catheter-related bloodstream infections (CRBSIs)
occur in association with peripheral intravascular (IV)
catheters and central venous catheters (CVCs) .
•CVCs are increasingly used in the inpatient and
outpatient setting to provide long- term venous
access
•Bloodstream infections associated with such catheters
are also known as central line-associated bloodstream
infections (CLABSIs)

29. RISK FACTORS
1) Host factors — Host factors commonly associated with
nosocomial bloodstream infections (BSIs) include the following
● Chronic illness
● Bone marrow transplantation
● Immune deficiency, especially neutropenia
● Malnutrition
● Total parenteral nutrition
● Previous BSI
● Extremes of age
● Loss of skin integrity, as with burns

30. 2) Catheter factors — All intravascular devices confer a risk of
infection, although some (eg, nontunneled central venous
[CVCs] and pulmonary artery catheters, Multiple-lumen
compared with single-lumen peripherally inserted central
catheters) carry greater risk than others (eg, peripheral venous
catheters)
3) Other than the type and location of the catheter, the most
important extrinsic risk factors associated with the development
of CRBSIs include:
● Duration of catheterization (although there is no indication
for routine line changing based on number of catheter days)
● Type of catheter material
● Conditions of insertion
● Catheter-site care
● Skill of the catheter inserter

31. In general, the risk of CLABSI is comparatively elevated in the
following circumstances:
 Femoral or internal jugular placement compared with subclavian
placement
 Use for hyperalimentation or hemodialysis compared with other
indications
 Submaximal compared with maximal (mask, cap, sterile gloves,
gown, large drape) barrier precautions during insertion
 Nontunneled >tunneled insertion>totally implantable device
 Bare compared with antibiotic-impregnated catheter

32. SOURCES OF INFECTION
Bloodstream infection (BSI) associated with central
venous catheters (CVCs) can be attributable to four
major sources:
Most often colonization from the skin or intraluminal
Hub contamination
Less often secondary seeding from a BSI
 Contamination of the infusate

33. Skin colonization
 The most common source of CVC-related infections is
colonization of the intracutaneous and intravascular portions of
the catheter by microorganisms from the patient's skin and
occasionally the hands of health care workers (on insertion or as
a result of manipulation)
Microorganisms gain access to the catheter wound and migrate
along the catheter-subcutaneous tract into the fibrin sheath that
surrounds intravascular catheters.
The biofilm is produced by a combination of host factors (eg,
fibrinogen and fibrin) and microbial products (eg, glycocalyx or
"slime").
Thus, it is not surprising that common skin commensals, such
as S. aureus and coagulase-negative staphylococci, are often

34. Intraluminal contamination — Intraluminal
and/or hub contamination is an important source of
BSI in patients with centrally inserted CVCs that are in
place for more than two weeks or in patients with a
surgically implanted device
Hematogenous seeding — Hematogenous
seeding of the device can occur during a BSI
originating from another focus of infection, often from
a gastrointestinal site
This is most likely to occur in critically ill patients or
those with long-term catheters

35. Infusate contamination — Administration of
contaminated infusate or additives, such as a
contaminated heparin flush, can result in a BSI.
•Organisms may contaminate infusate by several
mechanisms: during manufacture, during solution
preparation, via retrograde contamination from a
contaminated catheter, or handling by health care
workers.
•Infusate-related infections should be suspected when
sepsis occurs in an otherwise low-risk patient
receiving an intravenous solution or when there is a
cluster of primary BSIs with an unusual organism,
often an uncommon gram-negative bacillus.
•The infection is confirmed by the isolation of the same

36. MICROBIOLOGY
General principles — Prior to the 1980s, gram-negative aerobes
were the predominant organisms associated with nosocomial
bloodstream infections (BSIs).
 Since then, gram-positive aerobes (eg, coagulase-negative
staphylococci, S. aureus, and Enterococcus) and Candida
species have increased in relative importance .

37. Special populations — Certain patient populations have a different
epidemiology of BSI with regard to microbial etiology:
•Among burn patients, Pseudomonas aeruginosa is the most
frequently isolated gram-negative pathogen
•In patients with hematologic and nonhematologic malignancies,
gram-negative pathogens predominate
•In hemodialysis patients, gram-positive organisms reflecting skin
microbiome are responsible for most catheter-related infections.

38. ● In the ambulatory setting, children younger than three years or
without recent hospitalization (within the week prior to presentation)
may have an increased likelihood of polymicrobial CLABSIs
● In patients, particularly very young infants, receiving intravenous
lipids, Malassezia furfur, a lipophilic yeast, has been identified as a
cause of BSIs
● In patients receiving a high concentration of glucose in
intravenous hyperalimentation, fungal infections, and Candida
species in particular, are a particular concern.

39. DIAGNOSIS
Diagnostic Tests Performed After Catheter Removal
•Qualitative broth culture has a high sensitivity but a very low
specificity and is unable to distinguish contamination from infection.
•Quantitative culture techniques have been developed for investigating
either the extraluminal part of the catheter (semiquantitative Maki’s
technique) or the intraluminal part.

40. QUANTITATIVE CULTURE OF THE CATHETER
EXIT SITE
•Quantitative culture of the catheter exit site reflects the extraluminal
contamination pathway
•In case of suspicion of CRI, such culture tests rule out this diagnosis,
thereby preventing unnecessary catheter replacement.
•However, routine surveillance culture is useless, as positive cutaneous
culture is closely related to cutaneous clinical signs at the insertion
site.

41. QUANTITATIVE BLOOD CULTURE
•Simultaneous samples drawn through the catheter and through a
peripheral vein without removal or exchange of the catheter are more
accurate in predicting CR-BSI.
•The time to positivity of a blood culture is highly related to the
bacterial concentration in the milieu.
•Therefore, measuring differences in the time to positivity of hub
blood as compared to peripheral blood cultures has been proposed.
•Using a cutoff of 120 minutes, sensitivity and specificity were greater
than 90%.
•Theoretically, this technique only explores the intraluminal route of
infection, but recent reports suggest that it should be used for both
short- and long-term CR-BSI.

42. MANAGEMENT OF CATHETER-RELATED
INFECTIONS
Catheter Removal or a More Conservative Attitude?
•If catheter infection is suspected, the diagnostic strategy must be to
change the catheter or use a more conservative strategy.
•In case of septic shock or severe sepsis of undetermined origin or
when frank local signs of infection are found, the catheter should be
removed
•In the absence of severe sepsis or local signs, two conservative
strategies might be proposed, especially when a new catheter
insertion is hazardous:
 To change the catheter over a guidewire (GWX).
 To perform the watchful waiting strategy.

43. Conservative
•When conservative strategies have been initially decided, the decision
of catheter removal mainly depends on microorganisms and on the
evolution of the patient’s state during the first 48 hours.
•If blood cultures recover S. aureus, enterococci, gram-negative bacilli,
or fungi, the catheter should be removed.
•Overall, conservative strategies are always risky in critically ill patients.
•After a decision is made, patients must be cautiously monitored.
•The catheter must be removed in case of a complicated course

44. ANTIMICROBIAL THERAPY
•When catheter BSI is associated with severe sepsis or shock,
antimicrobial therapy must be administered immediately, together
with catheter replacement.
•Probabilistic treatment should include vancomycin, a broad-spectrum
β-lactamin with activity against P. aeruginosa, and an aminoglycoside.
• In case of previous Candida colonization or high risk there of,
antifungal therapy should be started, preferably with an
echinocandin.

45. CASE SCENARIO
A 67 year old female with poorly controlled hypertension was
admitted because of a right-sided stroke.
She had confusion, limitation of mobility of her left leg, and urinary
incontinence.
A urinary (Foley) catheter was placed and she was evaluated for
rehabilitation.
 4 days later she developed a temp to 103o F and blood pressure of
90/60 and was transferred to the ICU.
Blood and urine cultures grew resistant Klebsiella.

46. NOSOCOMIAL UTI
Up to 25% of hospitalized patients are catheterized at some time
during their hospital stay.
15% colonized (bacteruria)
5-10% per day of catheterization
50% after 14 days
Gram-negative bacilli, VRE, Candida – frequent antimicrobial
resistance

47. The Infectious Diseases Society of America (IDSA) guidelines define
catheter-associated bacteriuria as follows [1]:
● Symptomatic bacteriuria (urinary tract infection [UTI]) – Culture
growth of ≥103 colony forming units (cfu)/mL of uropathogenic
bacteria in the presence of symptoms or signs compatible with UTI
without other identifiable source in a patient with indwelling urethral,
indwelling suprapubic, or intermittent catheterization.
Compatible symptoms include
Fever,
Suprapubic or costovertebral angle tenderness,
Otherwise unexplained systemic symptoms (altered mental status,
hypotension, or evidence of a systemic inflammatory response
syndrome)

48. Risk factors — The duration of catheterization is an important risk
factor for catheter-associated bacteriuria and UTI and is a major
target of prevention efforts
Other risk factors include :
● Female sex
● Older age
● Diabetes mellitus
● Bacterial colonization of the drainage bag
● Errors in catheter care (eg, errors in sterile technique, not
maintaining a closed
drainage system, etc.)

49. PATHOGENESIS
Urinary tract infection (UTI) associated with catheterization may be
extraluminal or intraluminal.
Extraluminal infection occurs via entry of bacteria into the bladder
along the biofilm that forms around the catheter in the urethra .
Intraluminal infection occurs due to urinary stasis because of
drainage failure, or due to contamination of the urine collection bag
with subsequent ascending infection.
Extraluminal is more common than intraluminal infection

50. MOST COMMON CAUSATIVE
PATHOGENS IDENTIFIED WERE:
E. coli —24%
Candida — 24%
Enterococcus — 14%
P. aeruginosa — 10%
Klebsiella — 10%

51. CLINICAL FEATURES
Symptoms and signs — Symptoms of catheter-associated urinary
tract infection (UTI) are protean and do not necessarily refer to the
urinary tract.
Fever is the most common symptom
Localizing symptoms may include
Flank or suprapubic discomfort
Costovertebral angle tenderness
Catheter obstruction.

52. Laboratory findings
Pyuria is a common finding in catheterized patients with bacteriuria,
whether they are symptomatic (ie, have UTI) or not.
By definition, all patients with catheter-associated UTI have
bacteriuria or funguria.
 The vast majority of patients with symptomatic bacteriuria (ie, UTI)
have bacterial culture growth ≥105 cfu/mL or fungal growth in urine.
Specimen collection
Ideally urine samples for culture should be obtained by removing the
indwelling catheter and obtaining a midstream specimen.