Hospital-Acquired Infections (HAI) Seminar PDF

2 Hospital-acquired infections (healthcare-associated infections) are nosocomially acquired infections that are not present or might be incubating at the time of admission toa hospital. Z These infections are usually acquired after hospitalization and manifest 48 hours after admissi...

2 Hospital-acquired infections (healthcare-associated infections) are nosocomially acquired infections that are not present or might be incubating at the time of admission toa hospital. Z These infections are usually acquired after hospitalization and manifest 48 hours after admission to the hospital. C The infections are monitored closely by specialised agencies such as the a National Healthcare Safety Network (NHSN) oftheCenter forDisease Control. and Prevention (CDC) in USA o National Institute of Public Health — National Institute of Hygiene (NIZP PZH) in Poland. 2 This surveillance is done toprevent HAI and improve patient safety. CDC/NHSN Suivcilliince Definitions for Specific Types ofInfections 3 HAI infections include: oCentral line-associated bloodstream infections (CLABSI), oCatheter-associated urinary tract infections (CAUTI), Surgical site infections (SSI), oHospital-acquired Pneumonia (HAP), Ventilator-associated Pneumonia (VAP), a Clostridioides difficile infections (CDI). Z Symptoms that favor an HSI include o productive cough, 1 shortness of breath, o abdominal pain, a rebound tenderness, o altered mental status, a palpitations, 1 suprapubic pain, o polyuria, a dysuria, o costovertebral angle tenderness. 0 The impact of hospital-acquired infections is seen notjust at an individual patient level, but also at the community level as they have been linked to multidrug-resistant infections. ñ Identifying patients with risk factors for hospital-acquired infections and multidrug-resistant infections is very important in the prevention and m inimization of these infections. 0 The definitions of Pneumonia have been changed tobetter identify patients at risk for multidrug-resistant (MDR) pathogens. o this, in turn, is aimed atavoiding the overuse ofantibiotics. 0 Healthcare-acquired Pneumonia orHCAP, which was widely used previously, has been made obsolete. 0 The term Hospital-acquired Pneumonia or HAP has replaced HCAP. 0 Hospital-acquired Pneumonia isdefined as "pneumonia that occurs 48 hours or more after admission to the hospital and did not appear to be incubating at the time of admission". Ventilator-associated pneumonia orVAP is defined as "pneumonia that develops more than 48 to 72 hours after endotracheal intubation" S Both HAP and VAP are associated with poorer outcomes and significant morbidity and mortality worldwide. Z The risk for hospital-acquired infections is dependent on: othe infection control practices at the facility, bthe patient's immune status, bthe prevalence of the various pathogens within the community. Z The risk factors for HAI include: immunosuppression, solder age, a length of stay in the hospital, a multiple underlying comorbidities, -frequent visits to healthcare facilities, omechanical ventilatory support, firecent invasive procedures, o indwelling devices, a stay in an intensive care unit (ICU). 2 Receipt of intravenous antibiotics within the last 90 days isone ofthe major risk factors for developing antimicrobial resistance to multiple drugs. 2 While hospitalizations playa major role in the management ofacute illnesses, and they also enhance therisk of susceptible patients for multiple nosocomial and often antimicrobial- resistant pathogens. Z These pathogens can be acquired from: oother patients, a hospital staff, othe hospital facility. 0 The risk is higher among patients in ICU. o ina point prevalence study that included 231,459 patients across 947 hospitals concluded that about 19.5% of patients in ICU had at least one HAI. Z Clostridioides difficile is the organism that causes Clostridioides cfiffici/e colitis (CDI). Z Common organisms forcentral line-associated bloodstream infections (CLABSI) are: a Candida spp (adult ICU), a Enterobacterales (adult wards, pediatric ICU and wards, and oncology wards), a Staphylococcus aureus 0 Common pathogens that are known tocause catheter-associated urinary tract infections (CAUTI) are: oEnferococcz/s spp, a Staphylococcus aureus, a Pseudomonas spp, a Proteus spp, a Kleösiella spp, a Candida spp. Z The common causative organisms forsurgical site infections (SSI) include: S. aureus, ocoagulase-negative Staphylococcus, O Enferococcos spp, we. coli, a Pseudomonas aeruginosa, a Enterobacter spp, a Klebsiella pneumoniae. 2 The most common pathogens forhospital-acquired pneumonia (HAP) and ventilator- associated pneumonia (VAP) are: a S. aureus a Pseudomonas aemginosa, BE. co/i and Klebsiella fi›neumoniae can be seen in higher proportions among pediatric populations 2 Epidemiology 2 In2014, the CDC publisheda multistate point prevalence survey of healthcare-associated infections involving 11,282 patients from 183 US hospitals. oabout 4% ofhospitalized patients suffered from at least one of the HAI. a In absolute numbers, in2011, an estimated 648,000 hospitalized patients suffered from 721,800 infections 2 The dominant infections (in descending order) include o pneumonia (21.8%), o surgical site infections (21.8%), o gastrointestinal infections (17.1%), a urinary tract infections or UTIs (12.9%), o primary bloodstream infection (9.9%, and include catheter-associated bloodstream infections). 2 Among thepathogens causing HAI, C. difficile (12.1%) isthe leading pathogen and is closely followed by Staphylococcus aureus (10.7%), Klebsiella (9.9%), and Escherichia co/i (9.3%). Z Laboratory testing complements the history and clinical examination inelucidating the possible source of infection and revealing evidence of organ dysfunction. oserum levels of lactic acid, liver transaminases, prothrombin time, blood urea nitrogen (BUN), and serum creatinine can support clinical findings of hypoperfusion. Z Other important lab findings include: o low or elevated white cell counts, elevated bands, bands can be elevated in many situations including inflammation, autoimmune disease, metabolic abnormalities, pregnancy, and treatment with granulocyte colony stimulating factors. band counts of 10% have been used clinically as an indicator of serious bacterial illness. o thrombocytopenia, a hypoglycemia, o hyperglycemia, a reduced mixed venous blood saturation. OObtaining samples forcultures before initiation of antibiotics is vital in early identification of the pathogen and the antimicrobial susceptibility pattern. 1 Both the pathogen and the antibiotic susceptibility help narrow down from broad-spectrum antibiotics to specific agents targeted towards the pathogens. 0 Investigations that do not alter clinical decision making orthe clinical course are not usually recommended. o If the pretest probability is high fora HAI such as ventilator-associated pneumonia/ VAP, then tests such as C-reactive protein (CRP) and procalcitonin are considered ancillary and not indicated. oFor patients with HAP/ VAP, recentI DSA guidelines recommend noninvasive sampling with tracheal aspirates as they have been shown tohave non-inferior yield when compared toinvasive samplings such as quantitative tracheal lavage or bronchoscopy. U The Infectious Diseases Society ofAmerica has grouped the bacterial pathogens responsible for hospital-acquired infections (HAI) and referred to as “ESKAPE” pathogens. 0 ESKAPE is an acronym comprising the scientific names ofsixhighly virulent and antibiotic resistant bacterial pathogens including: oEnterococcus faecium, ostaphylococcus aureus, oXie6sie//a pneumoniae, nAcinetobacter baumannii, nPseudomonas aeruginosa, oEnferobacfer spp. 0 This group ofGram-positive and Gram-negative bacteria can evade or’escape’ commonly used antibiotics due to their increasing multi-drug resistance (MDR). «ated raI zaktad ZMechanisms ofdrug resistance fall into several broad categories, including odrug inactivation/alteration omodification of drug binding sites/targets ochanges in cell permeability resulting in reduced intracellular drug accumulation obiofilm formation U Enzyme-mediated antimicrobial inactivation, oirreversibly destroys the active antibiotic site o hydrolytic cleavage ofthe §-Iactam ring by §-Iactamases ocovalently modifies key structural elements ofthe drug to hinder the bacterial target site interaction o aminoglycoside-modifying enzymes that catalyze hydroxyl/amino group modifications; 3 Bacterial target site modification, which prevents the binding or which reduces the affinity of the antibiotic molecule oat the cell surface o LPS modification, o PBP2a expression with reduced §-lactam affinity, o van gene cluster-mediated peptidoglycan modification olntracellularly o 16S RNA methylation 0 Reduced antibiotic accumulation U Oersistence through biofilm-embedded cells which demonstratea markedly higher tolerance to antimicrobial agents than planktonic bacteria. Antimicrobial inactivation Persistenc+ §-lactam modification Èiofilltl f0fM6tiOI^l CHU g l3¢tdîf\BSD CHU Dispersion Antiblotlcs bacteria CH, CHj AMEs, aminoglycoside-modifying Persister cells enzymes; Aminoglytoside modification AACs, aminoglycoside H, Hyd yl acetyltransferases; mod æüon Att¥chment EPS growth EPS maturation Antibiotic ANTs, aminoglycoside nucleotidyltransferases; AMfis APHs, aminoglycoside phosphotransferases; Aminoçlycosîde »* LPS, lipopolysaccharide; E S K A P E Cell wall alterations Porin altérations PBP, penicillin-binding protein; O-Ala D-tue Antlbiotics j. RND, resistance-nodulation- ’ P0rin Porin mutation loss division; MFS, major facilitator superfamily; MATE, multidrug and toxic High- Antibiotics compound extrusion; 165 rRNA methylation * ’k affinlfy SIgR, small multidrug resistance; CHU CH, ABC, ATP-binding cassette; rRNA PACE, proteobacterial methyltransferase antimicrobial compound efflux; COOH (RND, MFS, MAT£. SM4, ABC FACE) Reduced antibiotic accumulation EPS, extracellular polymeric substance.  hated