NOSOCOMIAL INFECTIONS (HOSPITAL INFECTIONS)
NI = infection acquired in relation to hospital stay, not present at the time of admission.
Important complications of the hospital care with multiple negative impacts:
 worsen prognosis of the patient principal illness
 increas mortality
 prolong the hospital stay
 worsen the patients´ quality of life
 demand expensive investigation, treatment and control measures – increase the cost of care
NI = complicated interaction between the population of susceptible individuals with often serious illnesses and specific hospital environment.
Factors predisposing to hospital infection:
1.
Pre-existing condition
2.
Need for invasive devices ( IV, U, ET)
3.
Effect of surgery (skin wound, tissue trauma, opening colonized viscus, immobilization, implants of foreign material (joint prostheses, arterial graft)
4.
Effect of antibiotic treatment (colonization by resistant bacteria and fungi)
5.
Effect of immunosupressive treatment (corticosteroids, cancer chemotherapy, radiotherapy, transplant immunosupression)
6.
Exposure to health care workers and other pts. who may transmit pathogens
7.
Exposure to pathogens in the hospital environment
Patients in the intensive care units are particularly susceptible to infection for several reasons:
underlying disease is more severe = more disturbing their immune responses
recently underwent anaesthesia and surgery
often had got previous (multiple) antibiotics
barriers to infection are breached by catheterization ant intubation
Epidemiology:
~ 10 % of pts. admitted to hospital
EPIIC Study (European Prevalence of Infection in Intensive Care) Study 1995 prevalence and epidemiology of intensive care-related infections – single day study:
10038 pts. hospitalized at ICUs in 17 Europian countries
20,6 % of patients had an intensive care-related infection : pneumonia other respiratory tract infection
46,9 %
17,8 % urinary tract infection catheter-related infection surgical site infection
17,6 %
12 %
6,9 %
The most frequent pathogens were Staphylococcus aureus, enterobacteria, Pseudomonas
aeruginosa, Acinetobacter spp., coagulase-negative staphylococci, enterococci and candida.
Main groups of NI: catheter-related infections pneumonia respiratory tract infections other than pneumonia surgical site infections urinary tract infections gastrointestinal infections central nervous system infections

Intravascular catheter-related infections
A) Localised - peripheral thrombophlebitis, absces
B) Systemic – bacteraemia, sepsis, endocarditis, metastatic infection
Source of infection :
contamination during insertion of catheter or cannula
later contamination from the skin along the catheter
contamination of catheter hub,taps,line during manipulation
contaminated IV fluids
hematogenous spread from another focus of infection
Influencing factors:
Insertion site : subclavian x jugular x femoral
Catheter characteristics:
Type: central tunnelled, Portacath x central x peripheral
Material: teflon, silicon, polyurethan x PVC, polyethylene surface impregnated with silver, antibiotics
Number of lumen: single-luminar x multiple-luminar
Usage: drugs x nutrition x blood
Microbiology: coagulase-negative staphylococci ( S. epidermidis ), S. aureus, Candida spp., Enterococcus spp., gramnegative rods
Clinical features:
local signs of inflammation at the site of entry – redness, tenderness, swelling, slight purulent exudate – prominent in peripheral lines, less in central lines
systemic signs – fever, rigors and no other source of fever
clinical improvement after catheter removal
elevated inflammatory markers, typical pathogens in blood culture
-
Management of line-related sepsis :
1.
Blood culture: 1. catheter, 2. peripheral – colonization x catheter-related bacteraemia
2.
Catheter removal, culture of the tip – semiquantitative > 15 CFU = infection
(insertion of a new catheter not immediately)
3.
Antibiotics, if symptoms did not resolve after removal, guided by culture results
4.
Long-time catheters (Broviac, Hickman) – catheter treatment, ATB locks
Prevention and control:
1.
Choice of catheter and insertion site
2.
Aseptic and atraumatic insertion (skin disinfection, barrier precautions), fixation to the skin
3.
TPN (all-in-one bags) prepared in the pharmacy under sterile precautions
4.
Minimimize opening of the IV set for additive drugs, every opening strictly aseptic!
5.
Maintaining adequate hygiene and dressing of the insertion site and regular review of insertion site
6.
Replacing giving set and catheter at appropriate intervals
giving set every 72 hours, if lipid emulsions or blood products – 24 hours
catheter – peripheral 48 h, central 7 days, tunnelled line much longer
removal of catheter if not longer necessary
IV teams in hospitals in the USA insert and take care of IV catheters following a strict protocol, and thus minimize the incidence of catheter-related infections.

Hospital – acquired, nosocomial pneumonia
Pneumonia occurring at least 48 h after admission.
The leading hospital acquired infection in ICU, associated with increased morbidity, prolonged mechanical ventilation and ICU-stay, higher antibiotic use and attributable mortality.
Affect 5 % of all hospitalized pts, 25 % of ICU pts, 30 % of mechanically ventilated pts.
Mortality 30-50 %, highest in the elderly and ventilated pts.
Risk factors : age, underlying chronic/acute illness, thoracic or abdominal surgery, immobility, reduced level of consciousness, dysphagia, use of broad-spectrum ATB, mechanical ventilation.
Endotracheal tubes and tracheostomies bypass host respiratory tract defense mechanisms and allow bacteria to be deposited directly into the LRT. Secretions may pool in the subglottic area above the endotracheal cuff and slowly leak into the LRT.
Etiology: in 50 % mixed infection
 early onset 2-5days - similar to CAP – S.pneum., H.infl. S.aureus
, anaerobes
 late onset > 5d – gramnegative bacteria – Enterobacteriacae, S.aureus, other gramnegatives -
Pseudomonas, anaerobes, rarely Legionella sp.
Clinics: fever, purulent respiratory secretions, respiratory symptoms
Diagnosis: new X-ray signs, leukocytosis, neutrophilia, CRP
sputum and blood culture
Ventilator associated pneumonia (VAP) – particular subgroup.
Pseudomonas, Acinetobacter , Klebsiella , S.aureus
, Enterococcus , resistant!
Source of infection:
 endogenous:
GIT: a) retrograde colonization of the upper GIT and pharynx by intestinal flora, facilitated by decreased stomach acidity b) translocation of bacteria through intestinal wall during gut ischaemia hematogenous spread from a distant focus
 exogenous: hands of hospital personnel, tap water, ventilator circuit, nebulizers
Diagnosis is difficult: purulent secretion = infection x local irritation tracheal aspirate culture = infection x colonization x tracheobronchitis fever and leukocytosis = pneumonia x other reasons
(pneumonia with no fever and leukocytosis)
X-ray infiltrate = pneumonia x embolia x edema in CHF x malignancy
Microbiology:
- tracheal aspirate widely used for detection of eti, doubtful value? quantitative bacteriology- cut-off 10 5 - 10 6 /ml
- bronchoscopy with bronchoalveolar lavage 10 4 or protected bronchial brush specimen 10 3 /mL
Studies: correlation 70%, no mortality advantage, more ATB changes.
Endotracheal aspiration with quantification is the simplest and most cost effective method of diagnosing etiology of VAP.
- blood culture, pleural fluid culture

Treatment:
Antibiotic:
early onset and non-ventilated – empirical ATB covering the possible pathogens
late and VAP – guided by culture and sensitivity results, if empirical, then covering the problem pathogens Pseudomonas, Acinetobacter , with respect to the microbiology of the environment
Respiratory support, physiotherapy
Treatment of underlying conditions (CHF, diabetes,...)
Prevention:
Postoperative patients: cough and deep-breathing exercises, patient positioning and early mobilization, effective analgesia
VAP:
1.
Infection control strategies: hand washing, exchange of ventilator circuits, sterile equipment, nontraumatic sterile suctioning
2.
Decrease URT colonization and aspiration of upper GIT contents:
oral cavity hygiene
positioning – upper part elevation
maintain stomach acidity (pH

4) – prevent stress ulcer with sucralfate rather than antacids and
H
2 antagonists, acidificated feeding, good splanchnicus O
2
supply (oxygenation, blood pressure), jejunostomy tubes for long-term feeding
keep appropriate integrity and function of GIT mucosa - early enteral feeding, intermittent vs. continuous, glutamin enriched f., appropriate O
2 supply, prokinetic drugs
improved endotracheal tubes
3.
Antimicrobial prophylaxis – studies with conflicting results (

incidence VAP, no influence on mortality, ↑ ATB resistance):
selective digestive tract decontamination (SDD) – polymyxinE + tobramycin + amphotericin B
local prophylaxis with polymyxin B decreased P.aeruginosa
infection, but fatal pneumonias caused by resistant pathogens occured
systemic prophylaxis
Other respiratory tract infections – tracheobronchitis, sinusitis – frequent in mechanically ventilated pts., risk factor for development NP and sepsis.
Urinary tract infections = urinary catheter-related infections
Prolonged hospital stay and raised expenses , low impact on mortality.
Etiology: gramnegatives – E.coli, Klebsiella pn., Pseudomonas , Proteus spp. enterococci
Candida spp.
Ascending extraluminal or intraluminal route of infection.
Risk factors: length of catheterization (5 %/day), opened drainage system, diabetes, female sex, age above 50 y.

Colonization is often asymptomatic, but there is a risk of ascending infection – pyelonephritis, bacteraemia, sepsis.
Diagnosis: pyuria - > 5 leukocytes per high-power field urine culture – significant bacteriuria ≥ 10 5 CFU/mL
Treatment: catheter removal or change antibiotics in symptomatic UTI
Prevention:
catheterization only when necessary
sterile, atraumatic insertion
closed sterile drainage
maintenance of good patient hygiene
replacing catheter at appropriate intervals
ICU – bacteriological screening – urine culture at appropriate intervals
Surgical site infections (SSI)
= infections in the site of surgery and related bacteraemias.
CDC classification:
Superficial SSI – skin and subcutaneous tissue involved
Deep SSI – deep soft tissue, fascia, muscles
Organ SSI – organs, cavities
Microbiology:
S.aureus
, coagulase-negative staphylococci, enterococci, E.coli, Pseudomonas, Enterobacter
Factors influencing SSI : patient, operation, antimicrobial prophylaxis, surgical team, postoperative care.
Patient: underlying disease (diabetes, malignancy, multiple trauma), immunosupression, malnutrition, obesity. Minimizing the time between admission and surgery will limit the opportunity to acquire resistant hospital pathogens. Preexisting infection should be treated before surgery.
Classification of operations for the purpose of ATB prophylaxis:
1.
Clean - in normally sterile tissue - orthopaedics, neurosurgery, cardiovascular, SSI incidence

2% (staphylococci), antimicrobial prophylaxis is not indicated.
The exception is insertion of prosthetic device , infection may have catastrophic consequences, antimicrobial prophylaxis is indicated . The other prophylactic measures: filtered air to OR, impermeable suits for surgeons, antibiotic-impregnated orthopaedic cement, antibioticimpregnated intravascular prostheses.
Neurosurgical operations on opened meninges carry a risk of meningitis, S.aureus
or gramnegatives, esp. Pseudomonas .
2.
Contaminated
– GIT, RT and UT surgery and endoscopy. Antimicrobial prophylaxis is indicated.
3.
Infected (dirty) – infection already exists - drainage of abscess, excision of perforated bowel.
Appropriate antimicrobial therapy rather than prophylaxis is necessary.
Antibiotic prophylaxis:

ATB bactericidal, effective against considered pathogens, with respect to local resistance, not betalactamases inducers
Short course of prophylaxis – first dose IV at induction of anesthesia, second dose if surgery > 3hours
Prevention of SSI:
Preoperative: minimizing the preoperative hospital stay cutting > shaving of surgical site
ATB prophylaxis, if indicated surgical team clothing and washing
Intraoperative: regardful (tissue-saving) operation technique bleeding control excision of foreign bodies and devitalised tissue isolation of incised bowel minimizing of surgical staff and their movement
Postoperative: aseptic care of the site, sterile covering
Gastrointestinal infections
Antibiotic-associated colitis
Precipitated by previous antibiotic treatment, mainly lincosamides, ampicillins, cephalosporins.
Clostridium difficile toxin A (enterotoxin), toxin B (cytotoxin)
Transmission via spores may cause hospital epidemics.
postantibiotic diarhea, simple colitis
pseudomembranous colitis
toxic megacolon
Diagnosis: clinical: diarhea, fever, abdominal pains, vomiting, related to antibiotic treatment laboratory: Cl.difficile
toxin detection - ELISA antigen detection - latexagglutination
(stool culture on selective agar, cytotoxicity test on tissue culture = „gold standard“, rarely available) colonoscopy – typical morphology with pseudomembranes typical histology in biopsy specimens
Treatment:
stop precipitating ATB
rehydration, diet
ATB: p.o. metronidazol 3-4x 500mg p.o. or vancomycin 4 x 125-250mg if no peristalsis, give i.v. metronidazol treat at least 7 days
probiotic drugs, colestipol
no inhibitors of peristalsis
toxic megacolon - colectomy
Central nervous system infections
CSF shunt-related, rare occurence, mostly Staph. aureus and Pseudomonas , often serious course
(nosocomial ventriculitis) and high mortality.