Dr Rini Latifah SpMK 12 Mei 2016 Page 2 Normal Flora Risk of nosocomial infection R e usable contain e r s Singl e u se conta i n e rs Bact e ria ID: 796237
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Slide1
Infection Control Vs Microrganisme
Dr
Rini
Latifah
SpMK
12 Mei 2016
Slide2Page
2
Normal Flora
Slide3Slide4Risk of nosocomial infection
R
eusable containersSingle-use containers
Bacteria
(
%
)Fungi (%)Bacteria (%)Fungi (%)Bacillus sp (89.2)Alternaria sp (2.5)Bacillus sp (8.1)Aspergillus flavus (1.6)Gram-negative rods (25.0) Aspergillus flavus (2.5)Coagulase-negative Staphlococci (6.5)Aspergillus fumigatus (1.6)Micrococcus sp (2.5)Aspergillus fumigatus (2.5) Aspergillus terreus (1.6)Pseudomonas aeruginosa (0.8) Aspergillus glaucus (1.7) Aspergillus sp (1.6) Pseudomonas sp (1.7)Aspergillus niger (15.0) Cladosporium sp (1.6)Coagulase-negative Staphylococci (30.8)Aspergillus sp (14.2) Penicillium sp (1.6)Staphylococcus aureus , including MRSA (1.7)Aureobasidium pullulans (2.5) Alpha-hemolytic Streptococci (23.3)Cladosporium sp (18.3) Nonhemolytic Streptococci (1.7)Curvularia sp (0.8) Fusarium sp (2.5) Penicillium sp (30.8) Rhodotorula sp (27.5) Trichoderma sp (5.0) Ulcladium sp (0.8) Verticillium sp (0.8)
.
% = percentage of incoming containers that cultured positive for that microorganism. From Neely et al. 2003
Table shows microorganisms
isolated from incoming infectious waste
containers in the USA
Slide5Slide6Slide7Slide8Infeksi HAIsHAP-CAPBlood Stream infectionSurgical
S
ite InfectionCAUTI
Slide9HAP-VAPHospital-Acquired Pneumonia (HAP) : penyakit infeksi parenkim paru yang terjadi ≥ 48 jam setelah dirawat di RS sedangkan pada waktu masuk tidak sedang dalam masa inkubasi infeksi
tersebut
Ventilator-associated pneumonia (VAP) : pneumonia yang muncul setelah 48-72 jam pemasangan selang endotracheal
Slide10Sumber patogen pada infeksi nososkomial saluran nafas
Udara : Aspergillus
Sumber air : Legionella, P.aeruginosa, A.baumaniiMakanan : batang gram – enterikFomite : S.aureus. Batang gram -Endotracheal tubeNasogastric tubeSuction cathetersBronchoscopeRespiratory devicesH.InfluenzaeS.AureusP.AeruginosaMDR strains
Bennett & Brachman’s Hospital Infection. 2007
Slide11PATOGENESIS HAP
Mikroaspirasi
pada pasien yang tidak memakai ventilator : rute utama masuknya bakteri pada saluran nafas bawahPasien sedasi, pasca operasi, abnormalitas menelan risiko aspirasi lebih tinggiAdanya konsentrasi yang tinggi dari refluks bakteri dari lambung atau infeksi sinus dapat teraspirasi dan meningkatkan level kolonisasi bakteri di orofaringKolonisasi di orofaring merupakan sumber utama masuknya bakteri ke paru serta menjadi saluran dari kolonisasi di lambung
Slide12Patogenesis VAPPada pasien dengan ventilator, bakteri memasuki saluran nafas bawah melalui rute :
Inhalasi aerosol
Pengembunan di selang yang terkontaminasiKebocoran bakteri dari endotracheal cuffTrauma lokal dan inflamasi dari ETT meningkatkan kolonisasi trakea serta mengurangi clearance organisme dan sekresi dari sal.nafas bawahPembentukan biofilm oleh bakteri pada lumen ETT meningkatkan risiko embolisasi bakteri ke dalam alveoli setelah prosedur suctioning atau bronkoskopi
Slide13Probable routes of transmission of pathogens leading to VAP
Slide14Urinary Tract Infection(UTI)
Associated Risk
FactorsA history of previous catheter useDuration the catheter is in situLength of stay in hospital prior to catheter insertionLocation of catheter insertion
Slide15Associated Risk FactorsA history of previous catheter use
Duration the catheter is
in situLength of stay in hospital prior to catheter insertionLocation of catheter insertion
Slide16Slide17Slide18Slide19Blood Stream InfectionInfeksi yang terjadi pada hari ke-3/sesudahnya masa perawatan di RS (> 48 jam) dimana terdapat patogen dalam darah yang dikonfirmasi dengan hasil
laboratorium
Faktor resiko yang utama dalam mempangaruhi
infeksi
nosokomial
ini adalah lamanya kateterisasi, level aseptik dan pemeliharaan yang kontinu dari kateter.
Slide20Blood Stream Infections: Sources of organisms
Slide21PATOGEN BSI
Sumber : www.cdc.gov/nhsn/forms/57.108_PrimaryBSI
Slide22Surgical Site Infection
Infection at the site of surgery that occurs within 30 days of surgery if there is no implant (hardware, artificial graft, mesh,
etc) OR occurs within 1 year of the surgery with an implant in placeTypes of SSIs:Superficial incisionalDeep incisionalOrgan or body spaceFrom CDC’s NNIS
Slide23Factors That may Influence SSI Development
Patient
Age Nutritional status Diabetes Smoking Obesity Coexistent infections at a remote body site Colonization with microorganisms Altered immune response
Length of preoperative stay
Slide24Factors That may Influence SSI Development
Operation
Duration of surgical scrub Skin antisepsis Preoperative shaving Duration of operation Antimicrobial prophylaxis Operating room ventilation Inadequate sterilization of instruments Foreign material in the surgical site
Surgical drains
Surgical technique
Slide25Bacterial dose
Virulence
Impaired
host resistance
Risk of Infection
Slide26Acinetobacter Infections in a Hospital Setting
Ubiquitous:
Widely distributed in nature (soil, water, food, sewage) & the hospital environmentSurvive on moist & dry surfaces32 species>2/3 of Acinetobacter infections are due to A. baumaniiHighly antibiotic resistantNumerous mechanisms of resistance to β
-lactams described in A. baumanii
15 aminoglycoside-modifying enzymes described
Quinolone resistance due to mutations in DNA
gyrase
Slide27Major infections due to Acinetobacter
Ventilator-associated pneumonia
Urinary tractBloodstream infection infectionSecondary meningitisSkin/wound infectionsEndocarditisCAPD-associated peritonitisVentriculitis
Slide28Environmental Contamination with Acinetobacter
Bed rails
Bedside tablesVentilatorsInfusion pumpsMattressesPillowsAir humidifersPatient monitorsX-ray view boxesCurtain railsCurtainsEquipment cartsSinksVentilator circuitsFloor mops
Slide29Acinetobacter Transmission in the Hospital Setting
Direct or indirect contact
Contaminated hands of healthcare workersAirborne transmission via aerosol production (e.g., hydrotherapy) may occurSimor AE et al. Infect Control Hosp Epidemiol 2002;23:261-267.
Slide30Acinetobacter spp Skin Colonization
Body site
Hospitalized patients (n=40)
Healthy controls (n=40)
Forehead
33%
13%
Ear35%7%Nose33%8%Throat15%0%Axilla33%3%Hand33%20%Groin38%13%Perineum20%3%Toe web
40%
8%
Any site
75%
42.5%
Seifert H et al. J
Clin
Microbiol
1997;
35:2819-2825.
A.
baumanii
isolated from 2 patients & 1 control only
Slide3131
Opportunistic Fungal Infections
Require
impairment of host immunity
to cause serious infection
Clinical infection -
localized
to severe systemic infectionYeasts:Candida spp. (albicans, tropicalis, parapsilosis, krusei, glabrata, lusitaniae, kefyr, guilliermondii etc.)Cryptococcus neoformansFilamentous fungi: Aspergillus spp. (fumigatus, niger, flavus)Zygomycetes (Rhizopus, Mucor, Rhizomucor, Absidia)Fusarium spp.Penicillium spp. (marneffei)Pseudallescheria boydii (Scedosporium apiospermium)Curvularia spp.
Slide3232
Predisposing Factors (Immunologic)
Cancer
(esp. hematological malignancy)
Key defect:
Neutropenia
Organ Transplantation
(bone marrow, liver, lung, kidney)Key defect: Neutropenia, Impaired T cell functionCellular Immune Dysfunction (AIDS, lymphoma, CMC)Key defect: Impaired T cell function
Slide3333
Predisposing Factors
(Non-Immunologic)
Chemotherapy
(cytotoxic) - mucosal damage of GI, respiratory, GU tracts
Antibiotics
- Broad spectrum; loss of normal flora, esp. anaerobic
Invasive devices - breach skin/mucosal defences, i.e. intravenous lines, urinary catheters, tracheostomiesInvasive procedures - surgery, diagnostic biopsies
Slide3434
Transmission of Opportunistic Fungi
Candida
,
Trichosporon
,
Malassezia
ENDOGENOUSunique straincolonization precedes infectionantibiotic suppression of normal flora, fungal overgrowthEXOGENOUShand carriage health care worker
Slide3535
Transmission of Opportunistic Fungi
Aspergillus
,
Zygomycetes
, other filamentous fungi,
Cryptococcus
EXOGENOUSinhaled conidiaventilation systems, construction, heliports, plants, environmentdirect contact - dressings, arm boards, burns, wounds
Slide36Terima Kasih