Nosocomial infections: Particular Features of
Diagnosis, Prophylaxis and Treatment
(Prepared by Inzhevatkina S.M., Department of (Prepared by Inzhevatkina S.M., Department of Microbiology and Virology of Russian National Research
Medical University NI Pirogov)
Definition of Nosocomial Infection
A nosocomial, or hospital-acquired, infections (NIs) are infections acquired by patients during hospitalization or other type of clinical care facility (infections acquired through outpatient care such as day surgery, dialysis, or home parenteral therapy). Thus, NI is an infection acquired in a therapy). Thus, NI is an infection acquired in a hospital by a patient who was admitted for a reason other than that infection.
NI is usually defined as an infection that is identified at least 48 h following admission, so infections incubating, but not clinically apparent, at admission are excluded. NI onset can occur after
patients have been discharded.
Characteristic features of NI
NI are characterized by high contagiousness, a wide range of pathogens and a variety of ways of their transmission; the possibility of outbreaks at any time of the year, the presence of patients with increased risk of disease and the possibility of relapses. Current studies reported at least 5 of relapses. Current studies reported at least 5 percent of patients became infected during hospitalization. With the increased use of invasive procedures, at least 10 percent of patients now acquire some type of NIs.
Besides harming patients, NI can affect physicians, nurses, hospital personnel and anyone who has contact with the hospital.
Healthcare-Associated Infections (HAI)
Increasing numbers of individuals in
skilled nursing and homecare settings have prompted the more recent use of the term healthcare associated infections (HAI).healthcare-associated infections (HAI).Nevertheless, hospitals remain the major environment associated with HAI.
History of Nosocomial Infections
The problem of nosocomial infections arose in ancienttimes, with the advent of hospitals. One of the main functions ofhospitals before XIX was isolation of infectious patients, whileprevention of hospital infections was practically absent. Thefrequency of wound infection reached 100%. 60% ofamputations resulted in the death of patients. High mortalityamong women who gave birth in hospital: during the outbreakof "maternity fever" in 1765, 95% of women died. Someempirical measures to prevent infections were known in ancienttimes (natural antiseptics, general ideas about the need tomaintain cleanliness), the problem of nosocomial infections wasnot solved until the middle of the XIX century.
History of Nosocomial InfectionsRenaissance Europe had birthing centers, places where
women went to deliver their babies under the guidance of people with medical training. Even as late as the 1840s, the birthing mortality rate (then called childbed fever) sometimes reached 40%. This was because some birthing centers were attached to medical schools, as many are today. Medical universities perform autopsies of cadavers as a part of medical training. The doctors and medical students would medical training. The doctors and medical students would interrupt the dissecting of cadavers to deliver babies. While they might wash their hands between dissections and deliveries, they often didn’t change clothes, and disinfectants were unknown at the time. Tiny particles of decaying flesh and germs from the cadavers were taken to the delivery room with terrible results. Birthing centers that operated without research cadavers had lower mortality rates. Men like Semmelweis, Pasteur, and Lister did research in the 1800’s that linked poor medical hygiene to patient mortality rates.
IGNAZ SEMMELWEIS (1818–1865)Known as the “father of infection control”, Dr Ignaz (or
Ignac) Semmelweis ( was a Hungarian born physician who received his MD degree in Vienna in 1844. In 1847 he was given a 2 year appointment as an assistant in obstetrics with responsibility for the First Division of the maternity service of the vast Allgemeine Krankenhaus teaching hospital in Vienna.There he observed that women delivered by physicians and medical students had a much higher rate (13–18%) of post-delivery mortality (called puerperal fever or 18%) of post-delivery mortality (called puerperal fever or childbed fever) than women delivered by midwife trainees or midwives (2%).
This case-control analysis led Semmelweis to consider several hypotheses. He concluded that the higher rates of infections in women delivered by physicians and medical students were associated with the handling of corpses during autopsies before attending the pregnant women. This was not done by the midwives. He associated the exposure to cadaveric material with an increased risk of childbed fever, and conducted a study in which the intervention was hand washing.
IGNAZ SEMMELWEIS (1818–1865)
IGNAZ SEMMELWEIS suggested hand washing
Dr Semmelweis initiated a mandatory hand washing policy for medical students and physicians. In a controlled trial using a chloride of lime solution, the mortality rate fell to about 2%—down to the same level as the midwives. Later he started washing the medical instruments and the rate decreased to about 1%. His superior, Professor Klein, a member of the academic “old guard”, did not accept his conclusions. The senior staff won and Semmelweis did not get his assistant professorship renewed in 1849. Then he changed jobs at several Universities.
In 1861 he published a book, “The Etiology, Concept, and Prophylaxis of Childbed Fever”, but it was badly written and poorly received by the medical establishment. About 5 years later he died in a public insane asylum at the age of 47.
Statistical data of NINI is the most common complication of
hospitalized patients. In the US, NI are the fourth
most common cause of mortality after
cardiovascular diseases, malignant tumors and
strokes. NI occur in 5-12% of patients, joining the
main disease, worsen the course and prognosis ofprognosis
the disease. NI significantly increase the cost of
treatment, (antibiotics reserve and increase in terms
of hospitalization) Mortality in various nosological
forms ranges from 3.5-60%, and in generalized
forms reaches the same level as in the pre-diabetes
era.
Statistical data of NI for newborns
Infections are the main cause of disease and death of newborns, especially premature mortality (sepsis in the intensive care unit).
Why Increased Cases of NI?Appearance of large hospital complexes with peculiar
ecology: high density of the population represented by
immunodeficient patients, and the medical personnel
comminicates constantly and closely with the patient.
Formation of an artificial mechanism of transmission of
infectious agents associated with medical and diagnostic
invasive medical proceduresinvasive medical procedures.
Extensive use of sophisticated techniques for diagnosis
and treatment requires special methods of sterilization. The
use of devices and equipment often leads to injury of
mucous membranes and skin, forming an unusual entrance
“gate” for infectious agents.
Nosocomial (Hospital) Strain
Definition of “Nosocomial (hospital) strain”
exists only in Russion medicine. Nosocomial
(hospital) strain is a strain of the microorganism
that has changed its genetic properties during
circulation in the hospital as a result of mutations circulation in the hospital as a result of mutations
or gene transfer by conjugation (plasmid) and
acquired several characteristics that are unusual
to the initial "wild" strain that allow it to survive in
a hospital.
Two Classes of NI
NI are divided into two classes, endemic or epidemic.
Most are endemic, meaning that they are at the level of usual occurrence within the setting.
Epidemic infections occur when there is an Epidemic infections occur when there is an unusual increase in infection above baseline for a specific infection or organism.
NIs can occur in people of any age, from newborns to the elderly, no matter what the reason for the initial hospital stay was, although people with poorly functioning immune systems may be more likely to get these infections.
Evolution of Pathogens Causing NI
The evolution of pathogens causing NI depends on
the types of hospitals,
nosological forms of diseases,
peculiarities of surgical interventions, peculiarities of surgical interventions,
methods of diagnosis and treatment, the nature of
antimicrobial measures,
the degree of diversity of hospital bacterial strains for
antimicrobial resistance,
the dependence of the stability on the type of
microorganisms
Evolution of Pathogens Causing NI
increase of the number of species ofpathogens of nosocomial infection due toopportunistic bacteria and fungi;
increase of importance ofincrease of importance ofenterobacteria, non-fermenting gram-negative bacteria (Pseudomonas,Acinetobacter, Alcaligenes, etc.),coagulase-negative staphylococci,enterococci, anaerobes and fungi in the NIetiology;
Evolution of Pathogens Causing NI
penetration of the pathogens of nosocomial infection of new biotopes in the human body, the growing adaptation of bacteria to conditions of existence in them, leading to an increase in recurrent and chronic forms of the disease,
formation in the various hospitals stable bacterial and bacterial-fungal associations of the pathogens of nosocomial infection
R-plasmid (R-factor) is an extrachromosomal DNAmolecule that confers on bacteria resistance to one ormore antibiotics. It consists of two components: theresistance transfer factor (RTF) required for transfer ofthe plasmid between bacteria, and the r-determinants(genes conferring antibiotic resistance). R plasmidswere first isolated from strains of Shigella dysenteriaethat showed resistance to multiple antibiotics. R-plasmids can transfer not only inside the particular
R-plasmids
plasmids can transfer not only inside the particularspecies, but also between different bacterial generaand families.
R-plasmid can be formed and stored inside thenormal gut microbiota and transfer then to thepathogens.
Detection of the nosocomial strain, containing R-factors, should be considered unfavorable to thehospital.
Conjugation is the
main method of transfer of
genes localized in
plasmids. Conjugation can
occur inside the particular
species or between related
R-plasmids
genera. Transmission of
plasmids occurs at a high
frequency, which leads to
the spread of strains with
non-chromosomal
resistance. It's becoming
an epidemic.
The mechanism of bacterial resistance to
chemotherapetic drugs is supplemented by the discovery of
mobile genetic elements (transposones)
Transposons (transposable elements or "jumping
genes“) are small pieces of DNA that encode enzymes that
transpose the transposon, that is, move it from one DNA location to another either on the same molecule of DNA
Mechanism of Resistance
location to another, either on the same molecule of DNA or on a different molecule.
For the formation of nosocomial strains of pathogens,
the ability of transposons (mobile simultaneously with
resistance to transfer genes that determine a number of
virulence factors and several new biochemical properties of
bacteria that allow them to persist in the environment for a
long time) is important.
Classification of NI
The infections most commonly acquired in hospitals are:
1. Surgical wound infection
2. Respiratory tract infection
3. Urinary tract infection (UTI)3. Urinary tract infection (UTI)
4. Bacteraemia
a. primary – due to the direct introduction
of organisms into the blood from, for example,
contaminated intravenous fluids
b. secondary to a focus of infection already present in
the body (e.g. UTI).
5. Other infections (e.g., gastroenteritis and hepatitis).
Comparison of frequencies of different kinds of hospital infection vary in different patient groups, but urinary tract infections are the most common
hospital-acquired infections
More than 200 etiological agents could be the
cause of the NI.
90% of all NI are of bacterial origin.
Viruses, fungi and protozoa are rare etiological
Etiology of NI
agents of NI. Classification of nosocomial
pathogens is based on epidemiological aspects.
The first group of NI agents are traditional agents
that lack specific characteristics in hospital
environment. They are spread in hospitals due to
the high concentration and close communication
hospitalized patients (dysentery, salmonellosis).
Etiology of NI
Streptococci and anaerobic rods had been the
main causative agents of NI in pre-antibiotic era.
Usage of antibiotics had changed the etiological
agents of NI. Currenly the main etiological agents
are opportunists:are opportunists:
Staphylococcus spp. (S.aureus, S.epidermidis,
S.saprophiticus), Enterococcus faecalis,
Enterococcus durans, Escherichia coli, Klebsiella
sp., Proteus mirabilis, Providencia spp,
Acinetobacter, Citrobacter, Serratia marcescens.
‘Opportunists’ are microbes that are unable to cause
disease in healthy people with intact defence mechanisms,
but that can cause infection in compromised patients or when
introduced during the course of invasive procedures.
Currently, coagulase-negative staphylococci, Staphylococcus
aureus, and enterococci account overall for most NI.
Etiology of NIStaphylococci and Escherichia coli are the most
important G+ and G- causes of NI, respectively.
G- m/os such as Escherichia coli and Pseudomonas aeruginosa emerged as important pathogens.
Currently, the development of more potent and broad-spectrum antimicrobials and the increase in invasive medical techniques has been accompanied by an increase in the incidence of:
1. antibiotic-resistant G+ m/os such as coagulase-negative staphylococci, enterococci (especially those resistant to vancomycin; VRE) and methicillin-resistant Staph. aureus (MRSA)
2.multidrug-resistant G- m/os including those producing expanded-spectrum beta-lactamases (ESBLs)
3.Candida. Almost any microbe can cause a hospital infection, though protozoal infections are rare.
Etiology of NIThe general rank order of pathogen importance
is listed for the different infection categories. Although a few species are the most important in
all kinds of hospital infection, predominant pathogens vary in different infections.
Staphylococcus aureus is very important in surgical wound infections and bacteraemia, but surgical wound infections and bacteraemia, but much less important in urinary tract infections. 1/3 of healthy people are permanent carriers of Staphylococcus in the nasopharynx. Medical personnel with infectious lesions of the skin and soft tissues are more dangerous as sources of NI.
The importance of G- rods has increased since the advent of broad-spectrum antibiotics because these organisms often carry multiple antibiotic resistances.
Etiology of NI
Urinary tract infections
E. coli
Candida
EnterococciEnterococci
other G- m/os
(e.g., P.aeruginosa, K.pneumoniae, Serratiaspp., Proteus spp., Enterobacter spp.)
Urinary tract infectionUrinary tract infection (UTI) has been shown to occur
after urinary catheterization. Catheterization is the placement of a catheter through the urethra into the urinary bladder to empty urine from the bladder; or to deliver medication, relieve pressure, or measure urine in the bladder; or for other medical reasons. Normally, a healthy urinary bladder is sterile, with no harmful bacteria or other microorganisms present. Although bacteria may be in or around the urethra, they normally cannot enter the bladder. A catheter, however, they normally cannot enter the bladder. A catheter, however, can pick up bacteria from the urethra and give them an easy route into the bladder, causing infection. Bacteria from the intestinal tract are the most common type to cause UTIs. Patients with poorly functioning immune systems or who are taking antibiotics are also at increased risk for UTI caused by a fungus called Candida . The prolonged use of antibiotics, which may reduce the effectiveness of the patient's own immune system, has been shown to create favorable conditions for the growth of this fungal organism.
Etiology of NI
Surgical wound infections
Staphylococci (Staph. aureus and coagulase-negative)
Str.pyogenesStr.pyogenes
Enterococci
E.coli, P.aeruginosa, Proteus (other G-m/os to a lesser extent)
Anaerobic m/os
Surgical-Site Infection
Invasive surgical procedures increase a patient's risk of getting an infection by giving bacteria a route into normally sterile areas of the body. An infection can be acquired from contaminated surgical equipment or from the hands of health care workers. Following surgery, hands of health care workers. Following surgery, the surgical wound can become infected from contaminated dressings or the hands of health-care workers who change the dressing. Other wounds can also become easily infected, such as those caused by trauma, burns, or pressure sores that result from prolonged bed rest or wheel chair use.
Etiology of NI
Lower respiratory tract infections
Staph.aureus
Str.pneumoniae
P. aeruginosa (other Gram negatives to a P. aeruginosa (other Gram-negatives to a lesser extent, e.g. Haemophilus influenzae, representatives of the family Enterobacteriaceae)
Respiratory viruses
Fungi
Low Respiratory Tract InfectionPneumonia is the second most common type of NI.
Bacteria and other m/os are easily introduced into the throat by treatment procedures performed to treat respiratory illnesses. Patients with chronic obstructive lung disease, for example, are especially susceptible to infection because of frequent and prolonged antibiotic therapy and long-term mechanical ventilation used in their treatment. The infecting m/os can come from contaminated equipment or the hands m/os can come from contaminated equipment or the hands of health care workers as procedures are conducted such as respiratory intubation, suctioning of material from the throat and mouth, and mechanical ventilation. Once introduced through the nose and mouth, m/os quickly colonize the throat area. This means that they grow and form a colony, but have not yet caused an infection. Once the throat is colonized, it is easy for a patient to aspirate the microorganisms into the lungs, where infection develops that leads to pneumonia.
Ventilator-Associated Pneumonia
Ventilator-associated pneumonia is a type of lung infection
that occurs in people who are on mechanical ventilationbreathing machines in hospitals. VAP typically affects
critically ill persons that are in an intensive care unit
(ICU). VAP is a major source of increased illness and death.
Ventilator-Associated Pneumonia
Tracheal intubation
and mechanical
ventilation increase the
risk of pneumonia in 6-
21 times. Nosocomial 21 times. Nosocomial
pneumonia associated
with mechanical
ventilation occurs after
48 hours of intubation
Early-Onset Ventilator-Associated Pneumonia
Early-onset ventilator-associated pneumonia develops in the first 5 days after tracheal intubation. The prognosis is more favorable, the pathogens are sensitive to antibiotics, these are microorganisms colonizing the oropharynx and entering the trachea colonizing the oropharynx and entering the trachea by aspiration. Early initiation of VAP (first 5 days of mechanical ventilation) in patients without previous antibiotic therapy is caused by pneumococci, Haemophilus influenzae, members of the Enterobacteriaceae family without acquiredantibiotic resistance, and methicillin-sensitive S.aureus.
Sputum, Gram stain
Late-onset VAP develops after 5 days of
intubation, the causative agents are nosocomial
microorganisms characterized by resistance to
antibiotics. Such NI is characterized by a high
mortality, caused by pathogens with multiple
Late-Onset Ventilator-Associated Pneumonia
mortality, caused by pathogens with multiple
resistance (P.aeruginosa, Acinetobacter baumanii,
MRSA, and Stenotrophomonas maltophilia).
Risk factor is duration of mechanical ventilation more
than 7 days prior antibiotic therapy.
Selection of pathogens contributes to the
appointment of cephalosporins III generation, fluoroquinolones and imipenem.
Pathogenesis of Ventilator-Associated Pneumonia
The mucosa injury and
inflammation caused by the
endotracheal tube and
contaminated the secret around
the cuff of the tube lead to
increasing colonization of upper increasing colonization of upper
parts of the trachea, and then
lower, increase the risk of
development of tracheobronchitis
and pneumonia. If m/os penetrate
the biofilm formed from fibrin and
fibronectin on the surface of the
intubation tube, they enter the
lungs.
Etiology of NIBacteraemia
Staphylococci (Staph. aureus and coagulase-negative) Gram-positive cocci cause bloodstream infections in most cases (>60%)
Enterococci
Candida (mainly C.glabrata (75% of bacteremias, Candida (mainly C.glabrata (75% of bacteremias, caused by Candida spp.)
K. pneumoniae (other G- m/os to a lesser extent)Rare pathogens:
– Enterobacteriaceae (Enterobacter, Serratia)
– Pseudomonas aeruginosa
– Acinetobacter spp.
Nosocomial Bloodstream InfectionMany hospitalized patients need continuous
medications, transfusions, or nutrients delivered into their bloodstream. An intravenous catheter is placed in a vein and the medications, blood components, or liquid nutritionals are infused into the vein. Bacteria from the surroundings, into the vein. Bacteria from the surroundings, contaminated equipment, or health care workers' hands can enter the body at the site of catheter insertion. A local infection may develop in the skin around the catheter. The bacteria can also enter the blood through the vein and cause a generalized infection. The longer a catheter is in place, the greater the risk of infection.
Catheter-Related Infections
Venous catheterization is currentlyconsidered to be routine by themanipulation conducted in thedepartments of reanimation and intensivedepartments of reanimation and intensivetherapy. At the same time, it can lead tocomplications, including infectious, whichcan be fatal to the patient.
Catheter-Related Infections
There are three ways to spread theinfection.
1. From the skin (the main source ofmicroorganisms) move along the channelcreated by the catheter.by
2. M/os can enter the bloodstreamthrough connections in the infusionsystem.
3. Hematogenous pathway of cathetercolonization M/os may already be in thebloodstream, in the future they adhere onthe surface of the catheter and multiply onit. In this case, the catheter becomes asecondary focus of infection.
Catheter-Related Infections
M/os on the surface of the catheter to form two forms: fixed and planktonic (freely suspended). The fixed form further forms a biofilm consisting of several layers of m/os covered with a common glycoprotein (mucosa) capsule-like structure. The ability to form a glycoprotein layer is most pronounced in coagulase-negative staphylococci. Formation of biofilm begins after adhesion of m/os to the catheter surface.
Formation of Biofilm
Increase in Concentration of Microorganisms inside Biofilm
Protection of microorganisms against antibiotics, chemicals and immune
system inside biofilm
Catheter-Related Infections
The formation of biofilm begins after the
adhesion of m/os to the catheter surface. The
adhesion of m/os on the catheter surface
depends on its physical properties, the adhesive
properties of microorganisms, the presence of
macroorganism proteins. Most m/os are able to
attach to the catheter surface due to non-
specific adhesion mechanisms. However, the
adhesion is much more efficient when the
deposition on the surface of the catheters of
plasma proteins (fibrin, fibrinogen, etc.).
Catheter-Related Infections
Fungi from the genus Candida and S.aureus
can adhere to proteins such as fibronectin and
fibrin. Coagulase-negative staphylococci are
associated only with fibronectin. The ability to
cause local coagulation changes is directly
affected by the chemical nature of the catheter
material. The greatest thrombogenic activity
have polyethylene and polyvinyl chloride, the
least activity have silicone, Teflon and
polyurethane.
There is a relationship between the number
of m/os on the catheter surface, determined by
semi-quantitative or quantitative method, and
the risk of infection. Infection develops when a
Catheter-Related Infections
certain threshold number of m/os on the surface
of the catheter is exceeded, especially in the
form of a freely suspended form. The vast
majority of m/os included in the biofilm are at
rest (do not multiply), which dramatically
increases their resistance to antibacterial drugs.
The initial point of development of catheter-
associated infection is the appearance in
various areas of biofilm foci of "proliferation", the
cause of which to date has not been fully
Catheter-Related Infections
clarified. As a result, the concentration of
planktonic forms of m/os significantly increases
in the bloodstream. In this case, the severity of
the clinical picture of angiogenic infection will
largely be determined by the intensity of the
formation of plankton forms of m/os.
� Most frequent
� – Staphylococcus epidermidis, 37,3%
� Possible
� – Staphylococcus aureus 12,5 %
� Enterococcus spp. 13,5%
Etiology Catheter-RelatedInfections in Bloodstream
� – Enterococcus spp. 13,5%
� – Candida spp.
� Rare
� – Enterobacteriaceae (Enterobacter, Serratia)
� – Pseudomonas aeruginosa
� – Acinetobacter spp.
Staphylococcus aureus, Gram stain
Staphylococcus epidermidis (coagulase-negative staphylococci),
Gram stain
Staphylococcus epidermidis in
tissue, Gram stain
Escherichia coli, Gram stain
Pseudomonas aeruginosa,
Gram stain
Enterobacter spp.,
Gram stain
Acinetobacter calcoaceticus,
Gram stain
Enterococcus faecalis in a Blood Culture, Gram stain
Candida albicans, Gram stain
Candida albicans, Gram stain(dimorphic fungi)
Candida albicans in tissue,
Gram stain
Klebsiella pneumoniae,Gram stain
Klebsiella pneumoniae in tissue,
Gram stain
Klebsiella pneumoniae in tissue, Gram stain
(vivid capsule)
Clostridium difficile, Gram stain
The newest trend for MRSASome infections historically associated
with hospitals are now increasingly seen outside of the healthcare setting
Recent reports in numerous countries have documented the emergence of virulent MRSA strains causing infection in individuals outside of strains causing infection in individuals outside of the healthcare system. These community-associated MRSA (CA-MRSA) can be transported into the healthcare environment, thus blurring the distinction between community-associated and healthcare-associated infection. This has prompted guidelines for differentiating the increasing number of CA-MRSA infections from those associated with healthcare
Etiology of NI (viruses)viruses acquired by the respiratory route, especially influenza, respiratory syncytial virus (RSV), parainfluenza, varicella-zoster virus (VZV); this may also include some of the viral causes of gastroenteritis
viruses acquired by contact with vesicular lesions such as VZV and herpes simplex virus (HSV)
viruses acquired by contact with contaminated fomites such as noroviruses and rotavirus
viruses acquired by contact with blood-contaminated fomites, needlestick injury or splash on mucous membranes, such as hepatitis B virus (HBV), hepatitis C virus (HCV), HIV and human T-cell lymphotropic virus (HTLV). Blood and blood products are not screened or in the rare instance in developing countries where the blood donor was in the early incubation period of infection, thereby escaping detection by the screening assay. The latter is referred to as the window period and may be missed even if a viral genome detection method is used.
Etiology of NI (viruses)
Sources of NIHealthcare-associated infection may be acquired from:
an exogenous source (e.g. from another patient – cross-
infection – or from the environment)
an endogenous source (i.e. another site within the patient –
self- or auto-infection)
Endogenous Source of NIIn endogenous infections NI is associated with the normal
microbiota of the patient, or microbiota, acquired by the patient in the hospital (and which colonizes the patient for a long time).
Infection occurs due to diagnostic and therapeticprocedures in the same biotope or other biotopes (translocation).
Infections occur in the area of surgery if the wound Infections occur in the area of surgery if the wound microorganisms that inhabit the skin, urinary tract of the patient, or his intestines. Infection can also occur with tissue damage (wound) or with inappropriate antibiotic therapy that allows overgrowth of endogenous bacteria like C.difficile.
“Recto-pulmonary" transmission can occur when the intestinal flora penetrates into the respiratory tract, may occur with nosocomial pneumonia.
Exogenous Sources of NI
1. human from other patients or hospital staff, and occasionally visitors
2. environmental from contaminated objects (‘fomites’), food, water or air .
The source may become contaminated The source may become contaminated from an environmental reservoir of organisms, for example, contaminated antiseptic solution distributed for use into sterile containers. Eradication of the source will also require eradication of the reservoir.
Routes of spread of NI (see next scheme)
Hospital infections are spread by the same routes as infections spread in the community (air-borne, droplet, direct contact, indirect contact, and common vehicle transmission).
The reservoir and the source of infection may be human or inanimate and may be one may be human or inanimate and may be one and the same (e.g. a nurse with an infected skin lesion).
If the reservoir and source are distinct (e.g. contaminated distilled water supply used to prepare a variety of pharmaceuticals), both must be eliminated if the spread of infection is to be halted, otherwise the reservoir may continue to contaminate new sources.
2009
2013
Common Vehicle Transmission
Inanimate materials that indirectly transmit pathogens are called vehicle. A single inanimate vehicle or source (surgical instruments, drinking vessels, stethoscopes, bedding, eating utensils, and neckties) serves to spread the pathogen to multiple hosts. The common vehicles are called multiple hosts. The common vehicles are called fomites (s., fomes or fomite). A single source containing pathogens (e.g., blood, drugs, intravenous fluids) can contaminate common vehicle that cause multiple infection. Food, water, and biological fluids (fluids and tissues) are important common vehicle for many human diseases. They often support pathogen reproduction.
Common Vehicle Transmission
Common vehicle transmission means transmission of the nosocomial pathogen via inanimate materials contaminated by the infectious agent to many individuals.
Addition of view from Russian medicine:
NI can be acquired by food-borne, transplacental transmission, during the passage of the fetus in birth canal, and other ways.
Human sources of NI1. people who are themselves infected
2. people who are incubating an infection
3. healthy carriers.
The time period for which a human source is infectious varies with the disease. For example, some infections can be spread during their incubation period, others in the early stages of clinical disease, while others are characterized by a prolonged carrier state even after are characterized by a prolonged carrier state even after clinical cure (e.g. typhoid fever). Carriers of virulent strains of, e.g. Staph. aureus or Strep. pyogenes, may act as sources of hospital infection, although they themselves do not develop clinical disease. The carrier state may persist for a long time and go unnoticed unless there is an outbreak or, depending on the significance of the organism, a single case of infection that is traced to the carrier, e.g. a healthcare worker with chronic hepatitis B.
Particular microorganism may be spread by more than one route
It is important to remember that the same
organism may be spread by more than one
route.
Strep. pyogenes can be spread from patient Strep. pyogenes can be spread from patient
to patient by the airborne route in droplets or
dust, but is also transmitted by contact with
infected lesions, for example on a nurse’s hand.
A patient or healthcare worker with shingles
can transmit VZV to a susceptible person having
direct contact with rash blisters.
Host factors and NIUnderlying disease, certain treatments and invasive
procedures reduce host defenses.The spread of an infectious agent to a new host can result
in a spectrum of responses: from colonization, through subclinical infection, to clinically apparent disease, which may be fatal.
The degree of host response differs in different people depending upon their degree of compromise. depending upon their degree of compromise.
The very young are particularly susceptible because of the immaturity of their immune system. Likewise, the elderly suffer a greater risk of infection because of predisposing underlying disease, impaired blood supply and immobility, which contribute to stasis and therefore to infection in, for example, the lungs. In all age groups, underlying disease and the treatment of that disease (e.g. cytotoxic drugs, steroids) may predispose to infection, while invasive procedures allow organisms easier access to previously protected tissues.
Factors which predispose patients to NI
1. Age. Patients at extremes of age are particularly susceptible.
2. Absence of specific immunity against infection. Patient may lack protective antibodies to, e.g., measles, chickenpox, whooping cough.whooping cough.
3. Presence of underlying disease.
Other (non-infectious) diseases tend to lead to enhanced susceptibility to infection, e.g. hepatic disease, diabetes, cancer, skin disorders, renal failure, neutropenia (can be a result of disease or of treatment)
Factors which predispose patients to NI
4. Presence of other infections. HIV and other immunosuppressing virus infections; patients with influenza prone to secondary bacterial pneumonia; herpes virus lesions may become secondarily infected with staphylococci
5. Specific medicaments. Cytotoxic drugs (including post-transplant immunosuppression) and steroids both lower host defenses; antibiotics disturb normal flora and predispose to invasion by resistant nosocomial pathogens.
Factors which predispose patients to NI
6. (a) Accidental or (b) intentional trauma.
(a) Burns, stab or gunshot wounds, road traffic accidents;
(b) Surgery, intravenous and urinary catheters, peritoneal dialysis
Hospital patients are not all at equal risk of infection. Some factors that predispose to infection can be influenced by, e.g. treating underlying disease, improving specific immunity and avoiding inappropriate use of antibiotics. Other factors such as age are unalterable.
A Variety of Factors Predispose to Wound Infection
Wound infection or wound sepsis is characterized by the presence of inflammation, pus and discharge in addition to the isolation of organisms such as Staph. aureus. Extensive studies of postoperative wound infection have identified a number of predisposing factors:
Prolonged preoperative stay increases the opportunity for the patient to become colonized with antibiotic-resistant for the patient to become colonized with antibiotic-resistant hospital pathogens.
The nature and length of the operation also have an effect.
Wet or open wounds are more liable to secondary infection.
From these studies, it has been possible to identify the patients and operations with greatest risk and apply preventive measures such as prophylactic antibiotic regimens and ultra-clean air in orthopaedic operating theatres.
Risk factors for postoperative infections
1. Length of preoperative stay (Longer stay –more likely to become colonized with virulent and antibiotic-resistant hospital bacteria and fungi)
2. Presence of intercurrent infection(Operating on an already infected site more likely to cause disseminated infection)
3. Length of operation (Longer – greater risk of tissues becoming seeded with organisms from air, staff, other sites in patient)
Risk Factors for Postoperative Infections
4. Nature of operation (Any operation which results in faecal soiling of tissues has higher risk of infection (e.g. postoperative gangrene), ‘adventurous’ surgery tends to carry greater risks)
5. Presence of foreign bodies (shunts, prostheses, e of foreign bodies (shunts, prostheses, or catheters impairs host defenses)
6. State of tissues (Poor blood supply encourages growth of anaerobes; inadequate drainage or presence of necrotic tissue predisposes to infection).
‘High-tech’ surgery is often long and difficult and predisposes the patient to postoperative infection.
Postoperative gangrenous cellulitis. There is a huge area of ulceration filled with gangrenous skin, with sloughing
adjacent to the wound and surrounding cellulitis.
Consequences of NI
1. Severe disease or death.
2. Prolonged hospital stay, which is costly.
3. Necessity of additional antimicrobial therapy, which is costly, exposes the therapy, which is costly, exposes the patient to additional risks of toxicity, and increases selective pressure for resistance to emerge among hospital pathogens
5. The infected patient is the source for another patients, hospital staff and visitors.
Prevention of NI
1. Exclusion of sources of NI.
2. Interruption of the transmission of infection from source to susceptible host (breaking the chain of infection).
3. Improving the host’s ability to resist infection.
Exclusion of Sources of NIThe provision of sterile instruments and dressings, sterile medicaments and intravenous fluids, clean linen and uncontaminated food, and the use of blood and blood products screened for infectious agents.
Many of the sources of infection are human or are objects that become contaminated by humans, in which case exclusion is more difficult. Hospitals must prevent patient contact with staff who are carriers of pathogens. The problem is the detection the members of staff who are carriers of pathogens and their relocation to less hazardous positions.
Exclusion of Sources of NI
Staff must undergo health screening before employment and should have regular health checks (e.g., HIV and hepatitis C). Hepatitis B immunization is compulsory. It is critical to reveal the compulsory. It is critical to reveal the individuals from medical staff that lack immune response to the hepatitis B vaccine.
Recommended work restrictions for staff with infectious diseases.
In the event of a member of staff becoming infected, either in the hospital or outside, he or she should be relieved from direct contact with patients. Kitchen staff should also be relieved from duty if they are suffering from diarrhea or hepatitis A, or have infected lesions on their hands.
Diarrhea (any etiology)
Hepatitis A
Herpes simplex on hands (herpetic whitlow)
Streptococcus pyogenes infections
Staphylococcus aureus skin lesions
Measles
Mumps
Whooping cough
Rubella
Varicella-zoster infections
Upper respiratory tract infections (high-risk patients)
Management of healthcare workers and others who may have been exposed to
viruses
Prophylaxis includes active and/or passive
immunization against hepatitis B and a short
course of antiretroviral therapy for HIV exposure.
The risk of transmission is highest, 33% for The risk of transmission is highest, 33% for
HBV in unimmunized recipients, 0.32% for HIV
after a single needle stick injury, and HCV is
thought to be between 1% and 3%. Special
schemes of preventive therapy is used for such
incidentswith the medical staff.
Breaking the Chain of NI
Breaking the chain of infection can be the structural and the human.
The structure of the hospital and its equipment can play a role in preventing airborne spread of infection and in airborne spread of infection and in facilitating aseptic practices by the staff, but this is of no avail if staff do not use the facilities correctly and do not themselves act positively to prevent the spread of infection.
Control of Airborne Transmission of InfectionVentilation systems and air flow can play an
important role in the dissemination of organisms by the airborne route
Wards comprising separate rooms have been shown to afford some protection against airborne spread, and rooms with controlled ventilation are even better. But sometimes medical personell and their clothing can disseminate the NI infection more effective than airborne spread.
However, Legionella infection is acquired by the airborne route, and air-conditioning systems throughout the hospital should be maintained so as to prevent the multiplication of these organisms. Aspergillus infection in hospitals has been attributed to dissemination of the spores in hospital air, especially when building work is ongoing in the locality.
Legionella pneumophila, Gram stain
Significance of Ventilation SystemsVentilation systems in operating theatres must be
properly installed and maintained to prevent the ingress of contaminated air and to minimize air currents carrying organisms from the staff in the operating room to the operation site. ‘Ultra-clean’ air is air passed through high-efficiency filters to remove bacteria and other particles and has been shown to contribute positively to a reduction in the number of postoperative wound infections developing after long orthopaedic operations.long orthopaedic operations.
Protective isolation can be provided by a single room on a ward or by enclosing the patient in a plastic isolator. With appropriate positive-pressure ventilation, air should flow from the ‘clean’ patient area out of the room or isolator. Staff entering the room or in contact with the patient should wear sterile gowns, gloves and masks to prevent organisms they are carrying or have picked up from other patients from coming in contact with the patient.
Growth of Aspergillus flavus
Breaking the Chain of NIFacilitation of aseptic behaviour. (A
general state of cleanliness throughout the hospital is essential).
Bacteriologically effective handwashing is one of the most handwashing is one of the most important ways of controlling hospital infection. (The hands of staff transmit m/os to patients from septic lesions and healthy carrier sites of other patients, from equipment contaminated by these sources and from carrier sites of the staff themselves).
Contact spread of Opportunist Pathogens
(on example of klebsiellae)
Procedure Number of m/os recovered per hand
Physiotherapy 10–100
Taking blood pressure and pulse 100–1000
Washing patient 10–100
Taking oral temperature 100 1000Taking oral temperature 100–1000
Taking radial pulse 100–1000
Touching shoulder 1000
Touching groin 100–1000
Touching hand 10–100
Extubation 100–1000
Touching tracheostomy 1000
G- rods are not usually part of the resident skin flora except in
moist environments, but are readily carried on hands and can
be transferred from a source to a susceptible patient. This
picture shows an impression of a hand that was inoculated
with approximately 1000 Klebsiella aerogenes
Bacteriologically Effective Handwashing
Staff should therefore wash their hands:
before any procedure for which gloves or forceps are necessary
after contact with an infected patient or one who is colonized with multiply-resistant bacteriacolonized with multiply resistant bacteria
after touching infective material.
While soap and water are adequate in many circumstances, the usage of fast-drying alcohol-based gels and solutions are easier and demonstrate more antibacterial result. Drying hands after any washing procedure is important. A more prolonged and thorough hand decontamination is required before commencing surgery.
Enhancing the host’s ability to resist infection
1. Boosting specific immunity by active (vaccine) or passive (specific Ig) immunization.
2. The appropriate use of prophylactic antibioticsantibiotics.
Note!!! Selective bowel contamination to reduce the aerobic G- flora has been practiced for some time. The aim is to reduce the reservoir of potential pathogens. At the present time, there is still controversy about the efficacy and safety of the procedure.
Enhancing the host’s ability to resist infection
3. Care of invasive devices that breach the natural defenses (e.g. urinary catheters, intravenous lines). For example, the periurethral flora will cause endogenous infection of the bladder in catheterized patients.
The majority of hospital-associated bacteraemias and candidaemias are infusion-related. These infusion-related bacteraemias and candidaemias derive mainly from related bacteraemias and candidaemias derive mainly from vascular catheters. Most bacteraemias associated with invasive devices are caused by the patient’s own skin flora, although this may be a more resistant flora acquired during the patient’s stay in hospital replacing susceptible resident bacteria. Coagulase-negative staphylococci are the most common aetiologic agents, but enterococci, Candida, and various G- rods are also implicated. These infections are largely preventable if appropriate steps are taken.
Enhancing the host’s ability to resist infection
4. Reducing the risks of postoperative infection1) The preoperative length of stay in hospital should be kept to a
minimum.
2) Intercurrent infections should be treated appropriately before
surgery whenever possible (e.g. treatment of UTI before
resection of the prostate).
3) Operations should be kept to the minimum duration consistent
with good operating technique.
4) Adequate debridement of dead and necrotic tissue is essential,
together with adequate drainage and maintenance or re-
establishment of a good blood supply.
5) Prevention of pressure sores and stasis by good nursing
techniques and active physiotherapy minimizes the risks of
developing respiratory tract infection or UTI.
Another rare types of NIs
Other hospital procedures that may put patients at risk for nosocomial infection are gastrointestinal procedures, obstetric procedures, and kidney dialysis. procedures, and kidney dialysis.
Symptoms of NIs
Fever is often the first sign of infection. Other symptoms and signs of infection are rapid breathing, mental confusion, low blood pressure, reduced urine output, and a high white blood cell count. Patients with a UTI may have pain when urinating and blood in the urine. Symptoms of urinating and blood in the urine. Symptoms of pneumonia may include difficulty breathing and inability to cough. A localized infection begins with swelling, redness, and tenderness on the skin or around a surgical wound or other open wound, which can progress rapidly to the destruction of deeper layers of muscle tissue, and eventually sepsis.
Diagnosis of NIs• An infection is suspected any time a hospitalized
patient develops a fever that cannot be explained by the underlying illness. Some patients, especially the elderly, may not develop a fever. In these patients, the first signs of infection may be rapid breathing or mental confusion.
Diagnosis of a hospital acquired infection is • Diagnosis of a hospital-acquired infection is determined by:
• evaluation of symptoms and signs of infection
• examination of wounds and catheter entry sites for redness, swelling, or the presence of pus or an abscess
Diagnosis of NIsLaboratory tests, including complete blood count; urinalysis, looking for white cells or evidence of blood in the urinary tract; cultures of the infected area, blood, sputum, urine, or other body fluids or tissue to find the causative organism. Cultures of blood, urine, sputum, other body fluids, or tissue are especially important in order to identify the bacteria, fungi, virus, or other m/o causing the infection. Once the m/o has been identified, it will be tested again for sensitivity to a has been identified, it will be tested again for sensitivity to a range of antibiotics so that the patient can be treated quickly and effectively with an appropriate medicine to which the causative organism will respond.
Chest x ray may be done when pneumonia is suspected to look for the presence of white blood cells and other inflammatory substances in lung tissue
Review of all procedures performed that might have led to infection
Laboratory Diagnosis of NI1. Bacteriological method
1 stage. Inoculation of clinical specimen on solid medium for obtaining of isolated colonies. Incubation.
2 stage. Study of isolated colonies on plates by cultural and staining properties. Each type of isolated colony should be inoculated on solid isolated colony should be inoculated on solid agar slant. Incubation.
3 stage. Identification of isolated pure culture is based on examination and study of their morphological, staining, cultural, biochemical, antigenic and virulent properties and susceptibility to phages, chemical substrates, antibiotics by disc method, etc.
First stage of isolation of pure
culture
Colony descriptions(cultural=macroscopic properties)
• Colony size (using relative terms such as pinpoint, small, medium, large)
• Form - What is the basic shape of the colony? For example, circular, filamentous, etc.
• Elevation - What is the cross sectional shape of the colony? Turn the Petri dish on end.
• Margin - What is the magnified shape of the edge of the colony?
• Surface - How does the surface of the colony appear? For example, smooth, glistening, rough, dull (opposite of glistening), wrinkled, etc. smooth, glistening, rough, dull (opposite of glistening), wrinkled, etc.
• Opacity - For example, transparent (clear), opaque, translucent (almost clear, but distorted vision, like looking through frosted glass), iridescent (changing colors in reflected light), etc.
• Pigmentation - For example, white, buff, red, purple, etc.
• Changes in agar media resulting from growth (e.g. hemolytic pattern on blood agar, changes in media or colony color due to a change in pH indicators, pitting of agar surface)
• Odor (certain bacteria produce distinct odors)
•
Colony morphology descriptions
Colony morphology descriptions
Many of these criteria given on the picture are
subjective. In the clinical laboratory, careful
determination of colony appearance is important but
should not be the only criteria for making a preliminary
identification.identification.
And then microscopy is used: Gram stain, etc.
Note!!!
Examples of various colony morphologies
Examples of various colony morphologies
Antibiotic Sensitivity Test(disc method)
Susceptibility of Pseudomonas aeruginosa to antibiotics (disc method)
Zones of inhibition for microbial growth around the disks are measured. Diameter of zone indicates the susceptibility or resistance to each
agent: <15 mm mean weak susceptibility; 15-30 mm means medium susceptibility; >30 mm means high susceptibility.
Laboratory Diagnosis of NI2. Molecular-genetic method (molecular hybridization, PCR, and DNA sequencing analysis).
While a comparison of total chromosomal sequences is not a practical option, analysis of a subset of nucleotide sequences is the basis for what one could consider fourth-generation molecular epidemiology. Thus, recent years have seen a variety of sequence-based approaches to assessing microbial relatedness. These have included:
microarrays, capable of comparing bacterial isolates for the microarrays, capable of comparing bacterial isolates for the presence or absence of specific genes (e.g., virulence, antibiotic resistance)
a comparison of specific chromosomal regions in isolates looking for changes in DNA base (A, T, G, or C) coding, termed single nucleotide polymorphisms (SNPs)
multi-locus sequence typing (MLST), where differences in the sequences of several (e.g., 6 or 7) essential ‘housekeeping’ genes serve as the basis for an assessment of isolate relatedness.
Treatment of NIsWhile waiting for these test results, treatment may
begin by penicillin, cephalosporins, tetracyclines, or erythromycin. If bacteria are becoming resistant to these standard antibiotic treatments, especially when patients with chronic illnesses are frequently given antibiotic therapy for long periods of time, more powerful, and more specific antibiotic must be used to which the specific m/o has been shown to respond (vancomycin and imipenem), although shown to respond (vancomycin and imipenem), although some bacteria are developing resistance to these antibiotics as well. development of infection.
Fungal infections are treated with antifungal medications (amphotericin B, nystatin, ketoconazole, itraconazole, and fluconazole).
Viruses do not respond to antibiotics. A number of antiviral drugs have been developed that slow the growth or reproduction of viruses (e.g, acyclovir, ganciclovir, foscarnet, and amantadine).
Prevention of NIs• Adopt an infection control program, which includes quality
control of procedures known to lead to infection, and a monitoring program to track infection rates to see if they go up or down.
• Employ an infection control practitioner for every 200 beds.
• Identify high-risk procedures and other possible sources of infection.
• Strict adherence to hand-washing rules by health care • Strict adherence to hand-washing rules by health care workers and visitors to avoid passing infectious microorganisms to or between hospitalized patients.
• Strict attention to aseptic (sterile) technique in the performance of procedures, including use of sterile gowns, gloves, masks, and barriers.
• Sterilization of all reusable equipment such as ventilators, humidifiers, and any devices that come in contact with the respiratory tract.
• Frequent changing of dressings for wounds and use of antibacterial ointments under dressings.
Normal skin is colonized with bacteria both on the surface and deep in the pores and ducts of the sweat and sebaceous glands. In addition, bacteria may be carried transiently on the skin surface and may be transmitted from a contaminated source to a susceptible patient. Careful handwashing with soap and water removes the transient flora and some of the superficial resident flora. Scrubbing the hands with disinfectants removes more of the resident flora, but the skin surface is recolonized within hours from the normal flora deep in the skin pores.
Prevention of NIs• Remove nasogastric (nose to stomach) and endotracheal
(mouth to stomach) tubes as soon as possible.
• Use of an antibacterial-coated venous catheter that destroys bacteria before they can get into the blood stream.
• Prevent contact between respiratory secretions and health care providers by using barriers and masks as needed.
• Use of silver alloy-coated urinary catheters that destroy bacteria before they can migrate up into the bladder. bacteria before they can migrate up into the bladder.
• Limitations on the use and duration of high-risk procedures such as urinary catheterization.
• Isolation of patients with known infections.
• Sterilization of medical instruments and equipment to prevent contamination.
• Reductions in the general use of antibiotics to encourage better immune response in patients and reduce the cultivation of resistant bacteria.
