hapter 7 The Role of the Microbiology...

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Chapter 7

The Role of the Microbiology

Laboratory Smilja Kalenic

Key Points

Microbes are infectious agents that are not visible to the naked eye; they are widespread in nature. Some cause human diseases. They are divided into bacteria, fungi, viruses, prions, and protozoa. Macroscopic parasites are also included.

Diagnosis of infection by the microbiology laboratory has two important functions: clinical and epi-demiological.

An important innovation in microbiological diagnostics is development of point-of-care tests. This can help overcome the issue of scarce microbiology laboratories in developing countries.

The microbiology laboratory is an essential part of effective infection prevention and control (IPC). The microbiology laboratory should be able to determine the most frequent microbes causing healthcare-associated infections, and perform at least some basic typing of microorganisms for epi-demiologic evaluations.

The microbiology laboratory should produce routine reports for IPC personnel to develop incidence graphs for specific pathogens, antibiotic resistance, wards, and groups of patients.

Microbiologists, understanding the role of normal colonising flora of humans, the pathogenesis of infec-tions, and the characteristics of specific pathogens, can interpret microbiological findings for IPC per-sonnel.

The Role of the Microbiology Laboratory

©International Federation of Infection Control

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IFIC Basic Concepts of Infection Control, 3rd edition, 2016


Basics of microbiology Microbes are living organisms that are not visible to the naked eye. They are divided into bacteria, fungi, viruses, prions, and protozoa. Macroscopic parasites are also included in the group. Microbes are ubiqui-tous in nature, living as free organisms in the environment or on/in plants, animals, and humans, either as normal flora (not causing harming) or as pathogenic microbes (causing diseases). While some microbes are confined to only one host, most microbes can live on/in a wide array of hosts in nature. Plant mi-crobes do not cause disease in humans, however some animal microbes can cause disease in humans (so called zoonotic diseases).

When a microbe encounters a new host and begins to multiply, this phenomenon is usually called coloni-sation. The microbe can remain in balance with the host and no disease will develop. However, if the mi-crobe causes harm and disease, the disease is called an infectious disease (infection). Microbes that usu-ally cause disease in a susceptible host are called primary pathogenic microbes. Microbes that live as nor-mal flora of humans or live in the environment and do not cause disease in an otherwise healthy host are called opportunistic pathogens (can cause disease in an immunocompromised host). When we encounter unusual microbes on skin or non-living surfaces/items, it is called contamination.

Infection can be asymptomatic or symptomatic. During asymptomatic infections, as well as during the incubation period in symptomatic infections, microbes can be shed from an infected host; the host is in-fectious but may not realise it. After an infection, microbes can be present for some time in the host and can be further released, although the person is clinically completely healthy. This state is referred to as a “carrier state” and such persons are called “carriers”.

If infection is caused by microbes that are part of normal flora, we call it endogenous infection; exoge-nous infection is an infection caused by microbes that are not part of the normal flora of that person. Microbes are transmitted from one host to another by a number of pathways: through air, water, food, live vectors, such as mosquitos, indirect contact with contaminated items or surfaces, or direct contact of different hosts, including hands of healthcare workers (HCW).

To cause an infectious disease, a microbe first must enter the human body (portal of entry), either through respiratory, gastrointestinal, or genitourinary tracts, or through damaged or even intact skin. The microbe usually multiplies at the site of entry, then enters through mucous membranes to tissue and sometimes to blood. When in the bloodstream, the microbe can spread throughout the body and enter any susceptible organ. After multiplication, microbes usually leave the body (portal of exit) either through respiratory, gastrointestinal, or genitourinary discharges and seeks a new host. Some microbes are trans-mitted with the help of insect vectors that feed on human blood. Knowing the path of disease develop-ment is essential for a clinical diagnosis. It is also important for timing and ordering the right specimen for microbiological diagnosis, as well as for using the correct measures to prevent spread of microbes. Recog-nition of who might get sick from a certain microbe (susceptible host) also helps with the prevention of disease transmission.

Bacteria Bacteria are the smallest unicellular organisms with all functions of a living organism. They multiply by simple division from one mother cell to two daughter cells. When multiplying on a nutritious solid surface in the laboratory, after some time, they form so called “colonies” that are visible to the naked eye, repre-senting offspring of the same bacteria.

The genetic material (deoxyribonucleic acid or DNA) is situated in one circular chromosome and several

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independent units called plasmids. The chromosome is haploid (only one DNA chain) so every variation can be easily expressed phenotypically. Genetic material is transferred vertically and horizontally be-tween different bacteria. This has important consequences, especially when antibiotic resistance genes are transferred.

Most bacteria are very easily adaptable to any kind of environment. All pathogenic and most opportunis-tic bacteria have many virulence factors that are important in the development of infectious diseases. Some bacteria can sporulate ‘form spores’ – the most resistant form of life we know – if the conditions for the vegetative form is detrimental. When conditions are again favourable, the vegetative forms devel-op from the spore.

Table 7.1 outlines the main groups of pathogenic and opportunistic bacteria that can cause healthcare associated infections (HAI) with their usual habitat, survival in the environment, mode of transmission, infections they cause, and main HAI prevention methods.

Fungi Fungi are unicellular (yeasts) or multicellular (moulds) microorganisms that are widespread in nature. Their cell is so-called “eucaryotic”, meaning they have DNA packed in the nucleus, as any other biological cell in plants and animals. Their chromosome is diploid, so the variations in genome will not be as easily expressed phenotypically as in bacteria. Some species of yeast are part of the normal flora in humans, while moulds are usually living free in nature. Yeasts multiply by budding a new cell from the mother cell (blastoconidia), while moulds multiply asexually (conidia) and sexually (spores). It is important to remember that fungal spores are not as resistant as bacterial spores. Growth on a solid surface will lead to the formation of a colony as for bacteria. Some pathogenic fungi can live as yeast (in the host) and as a mould form (in the environment) so they are called dimorphic fungi.

Table 7.2 outlines the main groups of fungi that can cause HAI with their usual habitat, survival in the environment, mode of transmission, infections they cause, and main HAI prevention methods.

Viruses Viruses are the smallest particles – not cells – capable of reproducing themselves in living cells, either bacterial, plant, or animal cells. Outside a living cell viruses can survive, however they cannot multiply. They consist of one kind of nucleic acid (NA), either DNA or ribonucleic acid (RNA), and a protein coat that protects the NA. Some viruses also have a lipid envelope outside the protein coat, referred to as enveloped viruses; others do not have a lipid envelope (non-enveloped viruses). A virus enters the host cell and the viral NA then takes over the host cell to synthesise viral proteins and NA. It assembles these into a new virus and exits the host cell to enter other host cells. During this pro-cess, host cells are damaged or even destroyed and signs and symptoms of infectious disease appear; infection can be asymptomatic in a portion of the infected population. Some viruses can incorporate their DNA into the host DNA, or can live in some host cells causing no harm – these are called latent in-fections that can become overt in some circumstances, depending on the virus.

Table 7.3 outlines the main groups of viruses that can cause HAI with their usual habitat, survival in the environment, mode of transmission, infections they cause, and main HAI prevention methods.

Prions Prions are protein particles that do not contain any NA (neither DNA nor RNA). They are known to be connected with some neurological diseases (Creutzfeldt-Jakob disease – familial spongiform encephalo-pathy; variant Creutzfeldt-Jakob disease – bovine spongiform encephalopathy, and some other diseases).



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Prions are highly resistant to the usual methods of disinfection and even sterilisation. There is a possibil-ity of iatrogenic transmission of these diseases through transplantation or contamination of instruments with brain tissue, dura mater, cerebrospinal fluid, or blood of a diseased person. Prion diseases are not transmitted from diseased to healthy persons by contact; transmission to a HCW has never been de-scribed.

Parasites Parasites are either 1) microscopic protozoa, i.e., unicellular microorganisms with eucaryotic diploid nu-cleus that can live free in nature and/or live in some animal host including humans, some of them causing infections or 2) they are macroscopic organisms, such as helminths (worms) (endo-parasites) or lice (exo-parasites) that can cause infections – known also as infestations. Although many parasites are widespread in the world and cause some of the most important community-acquired infections (malaria, ascariasis, etc), not many parasites cause HAIs. Table 7.4 outlines the main groups of parasites that can cause HAI with their usual habitat, survival in the environment, mode of transmission, infections they cause, and main HAI prevention methods.

Arthropods Arthropods are a large and very diverse group of animals. They comprise insects, ticks, mites, and some other groups. Arthropods are very important as vectors of microbes (viruses, bacteria, protozoa, and hel-minths) both between humans and between animals and humans. Some of them can also cause a disease in humans called ectoparasitoses, as they only cause skin disease; these arthropods include Sarcoptes scabiei (scab-mite) causing scabies and human lice causing pediculosis. Scabies is a highly contagious skin disease that can be spread rapidly in a health care institution unless very vigorous containment measures are instituted. The habitat of the scab-mite is only human skin; however it can survive in clothing and bedding for several days. The primary method of transmission in health care settings is by direct contact with the skin of an infested person; however transmission through clothing and bedding can also occur. The primary preventive measure is use of Contact Precau-tions (isolation/cohorting) in addition to simultaneous specific treatment of all cases and exposed per-sons in a ward. Environmental cleaning and disinfection and processing of clothing and bedding as infec-tious items are also necessary. Another arthropod that can be transmitted in a health care institution is the louse. There are three types of human lice: head, pubic, and body. Head and pubic lice live on hair and body lice live on clothing (only contacting the body during feeding). Human lice survive a short time in the environment (<3 days for a body louse). Lice are transmitted from person to person by close contact, therefore preventive measures include Contact Precautions, bathing of patients, processing clothing and bedding as infectious items, and specific treatment for head and pubic pediculosis. Generally only head lice are important in health care institutions, specifically in paediatric wards. Many arthropods can bite humans and provoke an allergic reaction to the bite. In the past decades one of them, the bed bug (Cimex lectularius), has resurged in the developed world, including healthcare facili-ties. Bed bugs do not live on humans, they live in the environment. However, it feeds on human blood; this leads to an allergic reaction on the skin. As bed bugs do not live on humans, the primary prevention method is good hygiene and pest control, including vacuuming, heat or cold treatment of the environ-ment, trapping devices, and pesticides.

The role of the microbiology laboratory The isolation and characterisation of microorganisms causing infections performed by the microbiology laboratory has two important functions. The first is clinical - everyday management of infections. The second is epidemiological - knowledge of an infective microbe in a patient can lead to finding its source



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and route of transmission. This allows staff to stop infections from spreading. Furthermore, the microbi-ology laboratory interprets microbiology data for clinicians and for IPC professionals, thus participating in HCW education. The microbiology laboratory also participates in the development of an institution’s anti-biotic policy.

Clinical role Some infections must be quickly diagnosed clinically and treated empirically without knowledge of the causative microorganism or determination of antibiotic susceptibility (e.g., acute meningitis, sepsis, or severe pneumonia). However, if there is a clinical suspicion of infection, laboratory tests may confirm the diagnosis. Most HAIs are caused by bacteria and fungi that can be more antibiotic resistant than commu-nity-acquired pathogens or their susceptibility to antibiotics is less predictable. Etiological diagnosis of HAIs is therefore exceptionally important for targeted antimicrobial chemotherapy. The microbiology laboratory is becoming more important in clinical medicine and in the prevention of HAIs, especially as new or antibiotic-resistant pathogens emerge and new diagnostic technologies are developed. The microbiology laboratory should be able to diagnose the most common infectious agents, especially those causing HAIs. The laboratory should also be able to determine susceptibility to antibiotics for bacteria and fungi (See Tables 7.1.-7.4.). Targeted antimicrobial therapy will lead to better patient outcomes, and as eradication of a pathogen is achieved earlier, the danger of transmission to other pa-tients will be decreased. The right specimens from appropriate sites must be taken using proper techniques (See Tables 7.1.-7.4.). The microbiology laboratory staff can assist in ensuring good specimens by educating other staff in proper collection techniques. Identification of the microorganism and its antibiotic susceptibility should be as precise as possible (identification to the species level). Microbiological diagnostic methods can be divided into two types:

1. Direct methods (smear from specimens, isolation of infectious agents on culture media, or proof of microbial antigens or nucleic acids in the specimen).

2. Indirect methods – proof of immune response to the infectious agents (serology). Indirect methods are usually used for diagnosis of difficult to isolate bacteria and most viruses. It has to be recognised that serologic testing is the confirmation of a diagnosis, not the diagnosis itself. For many microorganisms antibodies take several days to develop, in many cases at least 10-14 days. Serology is mostly considered an epidemiological method, with the clear exception of some viral diseases where it is possible to make a diagnosis of an acute infection based on immunoglobulin class M (IgM), or avidity of class G (IgG), or a combination of antibodies to different viral antigens. An important new technology in microbiology is molecular diagnostics. Diagnosis can be rapid as it is not dependent on waiting for microbial growth in cultures. These tests are sensitive, as they are based on detection of only a few microorganisms; and they are specific, detecting microbe-specific genes.

Infection control role The microbiology laboratory is an essential part of an effective IPC program and has many roles in the control of HAIs: outbreak management, performing additional tests for epidemiologic studies, bacterial and fungal typing, HAI surveillance, and reports about new alert microbes or unusual resistance. All these functions enable the microbiological laboratory to educate not only clinical but also IPC personnel about microorganisms and their role in infection and specifically in HAI. Furthermore, daily communication be-tween laboratory staff and the Infection Control Team (ICT) is vital, allowing for timely and rapid infor-mation sharing about causative agents of HAIs. The clinical microbiologist should ideally be a member of the Infection Control and Antibiotic Stewardship Committees and a member of the ICT. Additional tests during outbreak investigation Sometimes the ICT requires additional data to clarify endemic or epidemic situations. Microbiological



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tests of blood products, environmental surfaces, disinfectants and antiseptics, air, water, hands of per-sonnel, anterior nares of personnel, etc., may be required. During an outbreak or in endemic situations when the causative agent is known, the microbiology laboratory may be able to use selective media for the agent in question to minimise expense and increase the sensitivity of the cultures. To determine the cause of a single-source outbreak, the causative microorganism must be defined. A mi-crobial species may contain subspecies and variants that differ in particular characteristics. For example, individual bacteria from the same species can differ as much as 30% in their genomes. Genetic differences are often phenotypically expressed; however this is not a rule. Typing of bacteria and fungi Microorganism typing determines whether two epidemiologically connected strains are really related or whether they differ from strains that are not epidemiologically connected. If strains are unrelated, the patients do not belong to the same outbreak. If strains are related, it is impossible to state that the pa-tients are involved in an outbreak without epidemiological analysis. Therefore, epidemiology and typing are complementary. Typing methods differ in several important points:

1. Typability, i.e., the method can type most or even all strains of the same species; 2. Discriminatory power, i.e., the method can differentiate well between different types; 3. Inter-laboratory and intra-laboratory reproducibility, i.e., the method can provide the same

typing results in repeated testing by different sites or in different times; 4. The method should be simple, unambiguous to interpret, and inexpensive.

There are two groups of typing methods: phenotyping and genotyping. Phenotyping Using phenotyping methods we can determine physical characteristics that can distinguish different strains of the same species. These methods may be based on antigenic structure (serotyping), physiologic properties/metabolic reactions (biotyping), susceptibility to antimicrobial agents (sensitivity testing), and colicines (colicino-typing) or bacteriophages (phage typing). Phenotyping methods are well standardised with high reproducibility. Discriminatory power is not always high if only a few types exist; however it can be very high if many types exist. These tests are simple and unambiguous to interpret. Many are inexpensive enough to be performed in every microbiology labora-tory. The main objection to phenotyping of bacteria is that bacterial genes are not always expressed. Two phe-notypically different strains can actually have the same genetic background or two phenotypically identi-cal strains can actually differ genetically. Sometimes the emergence of a particular phenotype is specific enough to explain an outbreak. However, if a phenotype is widespread and frequent, genotyping will be required for outbreak management. Genotyping Molecular techniques have revolutionised the potential of the microbiology laboratory because they have very high typability and discriminatory power. Genotyping can demonstrate definitively the relatedness or difference between two isolates of the same species. However, genotyping methods require sophisti-cated and expensive equipment and materials with trained staff. Furthermore, some techniques have a low reproducibility, especially in inter-laboratory comparisons. Result interpretation is not always simple or unambiguous.

Role in the surveillance of HAIs The microbiology laboratory should produce routine periodic reports of isolates to allow the ICT to devel-op incidence graphs for specific pathogens, wards, and groups of patients. These data can be made avail-able immediately if the laboratory is computerised. A ‘baseline incidence’ can be established and any new isolates can then be compared with this incidence. Graphs enable the ICT to discover the beginning of an



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outbreak earlier than it can be discovered clinically. Periodic reports are also important because they demonstrate trends of specific pathogens and can be very useful in planning preventive measures. Alert organism reports The early isolation of a new or unusual microorganism, without any further typing, enables the ICT to take appropriate measures to stop it from spreading. The ICT should identify, together with laboratory personnel, possible ‘alert’ microorganisms, such as multi-resistant or highly pathogenic microorganisms (e.g., methicillin resistant Staphylococcus aureus (MRSA), vancomycin intermediate Staphylococcus aure-us (VISA), vancomycin resistant enterococci (VRE), multidrug resistant (MDR) P.aeruginosa, MDR A.baumannii, MDR M.tuberculosis, C.difficile, extended spectrum beta-lactamase (ESBL) Enterobacteria, carbapenem-resistant Enterobacteria (CRE), E.coli 0127, Legionella spp, penicillin resistant (PR) Strepto-coccus pneumoniae, etc.). Any new isolates should be reported immediately to the wards and the ICT. Alert organism surveillance may be all that can be performed if the facility is understaffed. In addition, laboratory staff may report clustering of infections (two related isolates in different patients in the same time frame).

Interpreting Microbiology Data Microbiologists are required to interpret microbiological data (e.g., results of isolation, identification, sus-ceptibility tests, serology, and typing). To interpret microbiological data for infection in an individual pa-tient, one should first determine if the specimen was correct. The next step is to take into account if the isolated or otherwise proven microorganism is a primary or an opportunistic pathogen. Another factor is the clinical suspicion or working diagnosis. Lastly, understand the actual immune status of the patient at the time of specimen collection. It is relatively easy to interpret the results of so-called primary sterile specimens (e.g., blood, cerebral spinal fluid, or biopsy materials). It is more difficult to interpret results of non-sterile samples (e.g., differ-ent swabs, respiratory specimens, or wound exudates) or specimens that are easy to contaminate (urine). The microbiology laboratory result often is known after antibiotic treatment has already begun, and the patient has improved or not improved in response to the antibiotic. Therefore the concordance of the microbiological result with the patient’s course is another important factor in interpretation of the micro-biological result if dealing with opportunistic microorganisms. It is also important to look for concordance with other laboratory and/or imaging results of the patient. To interpret microbiological data for IPC purposes, the first issue is always to determine if the specimen was correct, either from a patient, healthy contacts, or the environment. Then the microbiologist who understands normal colonising flora of humans, the pathogenesis of infections (incubation period, inocu-lum size, and kind of vehicle), and the characteristics of specific pathogens (natural habitat, resistance to drying or disinfectants, and antibiotics) – can interpret the laboratory data for the ICT. In more complicat-ed outbreaks or an endemic situation, in addition to good microbiology (especially typing) there is a need to include epidemiologic considerations for the correct interpretation of microbiological data. The micro-biologist should be a clinical scientist with appropriate training; the professional background varies from country to country.

Antibiotic policy role Determining antibiotic susceptibility patterns for microorganisms causing HAIs is vital for individual pa-tient care. It can also help in planning antibiotic policy and designing the local antibiotic formulary. The microbiology laboratory should work closely with physicians and pharmacists to determine appropriate antibiotics to be included in susceptibility testing panels. Then the microbiology laboratory should pro-vide restricted antibiotics reports to the wards, according to the formulary. The microbiology laboratory should produce periodic resistance reports for specific wards and for the entire hospital, stratified by pathogen species and infection site. These reports should be available for every physician who prescribes antibiotics; they are very important for the design of local empirical therapy.



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IPC in the laboratory In every clinical laboratory in which biological samples are investigated, the first IPC concern is usually exposure to viruses that are spread through blood and bodily fluids (human immunodeficiency virus [HIV] and hepatitis B and C viruses [HBV, HCV]). It is very important that laboratory workers take all necessary preventive measures against those viruses (see Chapter “Prevention of blood-borne virus infections in patients and personnel”). A clinical microbiology laboratory is usually classified as a biosafety level 2 laboratory. This means that it diagnoses well-characterised agents that do not cause severe or untreatable diseases in healthy adult humans and poses only a moderate potential hazard to personnel and the environment. The laboratory must have limited access. Laboratory workers must have specific training to work with microbes and take all standard precautions with all biological specimens and microbial cultures (hand hygiene, disinfection of the environment, specific precautions with sharps, working in biological safety cabinets if aerosols may be created, proper disposal of waste, and sterilisation of culture material once testing is complete). In some clinical microbiology laboratories, pathogens such as Mycobacterium tuberculosis or Legionella pneumophila are diagnosed. These diagnostics are to be performed in a biosafety level 3 laboratory (agents which may cause serious or potentially lethal disease in healthy adult humans after inhalation, but for which vaccine or other treatment exists). Sometimes it is not possible to have a level 3 facility; therefore these microbes may be diagnosed in a level 2 laboratory. In that case, laboratory workers must be properly educated and wear appropriate personal protective equipment (PPE), the filtered exhaust air from the laboratory room is to be discharged to the outdoors, the room has negative air pressure, and all recommended practices for biosafety level 3 are rigorously followed.

Point of care microbiological tests The main problem of microbiological diagnostics in low resource countries is the lack of nearby microbiol-ogy laboratories; these are typically not sited outside of major urban areas. Therefore, it is very important to develop point of care (POC) microbiological tests that are sensitive and specific enough, rapid, easy to perform for HCWs that have no specific education in laboratory procedures, do not require special equip-ment, unambiguous to interpret, and affordable. Several such tests are already in use (for the diagnosis of malaria, HIV, HCV, syphilis, measles, respiratory viruses, and tuberculosis), however much more has to be done in this field. Especially important tests from the point of view of HAI prevention and control are tests for diagnosing pathogens causing HAIs, as well as antibiotic sensitivity to identify multidrug resistant strains to rapidly stop their spread. Staff performing the POC tests must also be provided education on PPE, hazards of specimens, and good methods to dispose of specimens and tests once the testing is com-pleted.

Minimal Requirements for Microbiology Laboratories in the Control of HAIs

1. Should be sited inside the hospital; if this is not possible, then negotiate a contract for diag-nostic microbiology with the nearest laboratory.

2. Should be available every day, including Sundays and holidays, ideally on a 24-hour basis. 3. Should be able to examine blood, cerebrospinal fluid, urine, stool, wound exudates or swab,

and respiratory secretions, and perform serological tests (at least HIV, HBV, HCV). 4. Should be able to identify common bacteria and fungi that can cause HAIs to the species

level (Staphylococcus aureus, Escherichia coli, Salmonella, Shigella, Pseudomonas aerugino-sa, Klebsiella pneumoniae, Streptococcus pyogenes (Group A streptococci), Streptococcus agalactiae (Group B streptococci), enterococci, Campylobacter jejuni/coli, Enterobacteri-aceae, Neisseria meningitidis, Candida albicans, Aspergillus spp, etc.), besides other com-mon microorganisms that cause severe community-acquired infections (Streptococcus pneu-moniae, Neisseria gonorrhoeae, Vibrio cholerae, Corynebacterium diphtheriae).

5. Should be able to perform susceptibility testing for relevant antibiotics using disc-diffusion



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methodology. 6. Should be able to perform basic typing - serotyping (for salmonellae, shigellae, N. meningiti-

dis) and biotyping (e.g., for S. typhi). 7. Should have quality assurance procedures (both internal quality control and external quality

control [national or international]). 8. Should have a clinical microbiologist who is able to communicate well with clinical and ICT

staff. 9. May have the ability to perform simpler genotyping methods or access to genotyping meth-

ods centrally at state or regional laboratories. The central laboratory can then assist with epidemiological investigations of HAIs.

References and Further Reading

1. Baron EJ, Miller M, Weinstein MP, et al. A guide to utilization of the microbiology laboratory for diag-

nosis of infectious disease: 2013 recommendations by the Infectious Diseases Society of America (IDSA) and the American society for Microbiology (ASM). Clin Infect Dis 2013; 57:e22-121.

2. Brooks K, Ready Reference to microbes, 3rd ed., Association for Professionals in Infection Control and Epidemiology, Inc., Washington, DC, 2012.

3. Brown M. Microbiology basics. In: APIC Text of Infection Control and Epidemiology, 4th Edition, Clini-cal Editor Grota P. Washington, DC, Association for Professionals in Infection Control and Epidemiolo-gy, Inc., 2014: Chapter 24.

4. Chosewood LC, Wilson DE (editors) (2009). Biosafety in Microbiological and Biomedical Laboratories (5th ed.). http://www.cdc.gov/biosafety/publications/bmbl5/BMBL.pdf [Accessed 1 September 2015]

5. Damani N. Manual of infection prevention and control, 3rd Ed., Oxford University Press, Oxford, UK, 2012.

6. Diekema DJ, Pfaller MA. Prevention of health care-associated infections. In Manual of Clinical Micro-biology, 11th Ed., Jorgensen JH and Pfaller MA, Editors in Chief, ASM Press, Washington, DC, 2015:106-119.

7. Diekema DJ, Saubolle MA. Clinical microbiology and infection prevention. J Clin Microbiol 2011; 49:S57-S60.

8. Gastmeier P, Schwab F, Baerwolff S, Rueden H, Grundmann H. Correlation between the genetic diver-sity of nosocomial pathogens and their survival time in intensive care units. J Hosp Infect 2006; 62:181-186.

9. Gerner-Schmidt P, Hyytia-TreesE, Rota PA. Molecular Epidemiology. In Manual of Clinical Microbiolo-gy, 10th Ed., Versalovic J, Editor in Chief, ASM Press, Washington, DC, 2011:100-123.

10. Guidance for Control of Carbapenem-resistant Enterobacteriaceae (CRE) 2012 CRE Toolkit, Centers for Disease Control and Prevention, Atlanta, GA, USA. http://www.cdc.gov/hai/organisms/cre/cre-toolkit/ [Accessed 27 August 2015]

11. Iram S, Zeenat A, Yusuf NW, Aslam M. Rapid diagnosis of tuberculosis using Xpert MTB/RIF assay– Report from a developing country. Pak J Med Sci 2015; 31:105-110.

12. Kalenic S, Budimir A. The role of microbiology laboratory in healthcare-associated infection preven-tion. Int J Infect Control 2009; 5(2).

13. Kramer A, Schwebke I, Kampf G. How long do nosocomial pathogens persist on inanimate surfaces? A systematic review. BMC Infect Dis 2006; 6:130. http://www.biomedcentral.com/1471-2334/6/130 [Accessed 1 September 2015]

14. Kulich PA, Taylor DL. The Infection Preventionist’s Guide to the Lab. Washington DC, Association for Professionals in Infection Control and Epidemiology, Inc., 2012.

15. Memish ZA, Al-Tawfiq JA, Alhakeem RF, et al. Middle East respiratory syndrome coronavirus (MERS-CoV): A cluster analysis with implications for global management of suspected cases. Travel Med In-fect Dis 2015; pii:S1477.

16. Moore C. Point-of-care tests for infection control: should rapid tests be in the laboratory or at the front line? J Hosp Infect 2013; 85(1):1-7.

17. Murray PR. The clinician and the Microbiology Laboratory. In: Mandell, Douglas and Bennett’s Princi-



http://www.cdc.gov/od/ohs/biosfty/bmbl4/bmbl4toc.htm

http://www.cdc.gov/biosafety/publications/bmbl5/BMBL.pdf

http://www.cdc.gov/hai/organisms/cre/cre-toolkit/

http://www.cdc.gov/hai/organisms/cre/cre-toolkit/

http://www.biomedcentral.com/1471-2334/6/130

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ples and Practice of Infectious Diseases, 8th Ed., Bennett JE, Dolin R, Blaser MJ, Editors, Elsevier Saun-ders, Philadelphia, 2015:191-223.

18. Peeling RW, Mabey D. Point-of-care tests for diagnosing infections in the developing world. Clin Mi-crobiol Infect 2010; 16:1062-1069.

19. Pereira-Neves A, Benchimol M.Trichomonas vaginalis: in vitro survival in swimming pool water sam-ples. Exp Parasitol 2008; 118:438-41.

20. Peterson LR, Hamilton JD, Baron EJ, et al. Role of clinical microbiology laboratory in the management and control of infectious diseases and the delivery of health care. Clin Infect Dis 2001; 32:605-611.

21. Robertson LJ, Campbell AT, Smith HV. Survival of Cryptosporidium parvum oocysts under various en-vironmental pressures. Appl Environ Microbiol 1992; 58:3494-3500.

22. Shonhai A, Warrener L, Mangwanya D, et al. Investigation of a measles outbreak in Zimbabwe, 2010: potential of a point of care test to replace laboratory confirmation of suspected cases. Epidemiol In-fect 2015; 13:1-9.

23. Smyer J. Laboratory testing and diagnostic. In: APIC Text of Infection Control and Epidemiology, 4th Edition, Clinical Editor, Grota P. Washington DC, Association for Professionals in Infection Control and Epidemiology, Inc., 2014: Chapter 25.

24. Soun VV, Eidson M, Wallace BJ, et al. Antemortem diagnosis of New York human rabies case and re-view of U.S. cases. Intl J Biomed Sci 2006; 2: 434-45.

25. Stratton CW IV, Greene JN. Role of the Microbiology Laboratory and Molecular Epidemiology in Healthcare Epidemiology and Infection Control. In: Hospital Epidemiology and Infection Control, 4rd Ed., Mayhall CG, Editor, Lippincott, Williams & Wilkins, Philadelphia, 2012:1418-1431.

26. Studdiford JS, Conniff KM, Trayes KP, Tully AS. Bedbug infestation. Am Fam Physician 2012; 86:653-658.

27. Williams J. Bed bugs in hospitals: more than just a nuisance. CMAJ 2013; 185:E524.


While the advice and information in this chapter is believed to be true and accurate, neither the authors

nor the International Federation of Infection Control can accept any legal responsibility or liability for any

loss or damage arising from actions or decisions based on this chapter.

Published by the International Federation Of Infection Control

47 Wentworth Green

Portadown, BT62 3WG, N Ireland, UK

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©International Federation of Infection Control, 2016. All rights reserved.

http://www.ncbi.nlm.nih.gov/pubmed/17949719

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reve

nti

ve

mea

sure

s**

Aci

net

ob

act

er

ba

um

an

nii

MD

R s

trai

ns

Hu

man

s: m

ois

t p

arts

of

skin

, ga

stro

inte

sti-

nal

(G

I) t

ract

3 d

ays

– 5

m

on

ths

Air

; in

dir

ect*

**

and

dir

ect

con

tact

U

rin

ary

trac

t in

fecti

on

(U

TI),

se

psi

s,

men

ingi

tis,

p

ne

um

on

ia

Uri

ne,

blo

od

, ce

reb

ral s

pin

al

flu

id (

CSF

),

spu

tum

, asp

irat

es

Co

nta

ct p

reca

uti

on

s

Bo

rdet

ella

p

ertu

ssis

H

um

ans:

nas

o-

ph

aryn

geal

m

uco

sa

(pati

ents

)

3-5

day

s D

rop

lets

P

ertu

ssis

N

aso

ph

aryn

geal

(N

P)

swab

D

rop

let

pre

cau

tio

ns

Ca

mp

ylo

ba

c-te

r je

jun

i, C

.co

li

H

um

ans,

an

imal

s: G

I tr

act

Up

to

6 d

ays

Faec

al-o

ral,

wat

er,

foo

d

Dia

rrh

oea

St

oo

l C

on

tact

pre

cau

tio

ns

Safe

fo

od

an

d w

ater

Clo

stri

diu

m

diffi

cile

H

um

ans:

GI

trac

t H

igh

ly

resi

stan

t (s

po

res

– 5

m

on

ths)

Faec

al-o

ral;

ind

irec

t an

d d

irec

t co

nta

ct

Clo

stri

diu

m

diffi

cile

infe

c-ti

on

s (C

DI)

Sto

ol

Co

nta

ct p

reca

uti

on

s U

se o

f so

ap a

nd

wat

er f

or

han

d h

ygie

ne

rath

er t

han

al

coh

ol-

bas

ed s

aniti

zer

Cle

an h

and

s o

f p

atie

nts

P

rud

ent

use

of

anti

bio

tics

Clo

stri

diu

m

teta

ni

En

viro

nm

ent:

ea

rth

, du

st

Hig

hly

re

sist

ant

(sp

ore

s)

Ente

rin

g u

mb

ilica

l co

rd w

ou

nd

(o

n

dir

ty in

stru

men

ts)

Teta

nu

s

Ster

ilisa

tio

n o

f in

stru

men

ts f

or

um

bili

cal c

ord

Co

agu

lase

n

egati

ve

stap

hyl

oco

cci

Met

hic

illin

re

sist

ant

CN

S (M

RSE

)

Hu

man

s: s

kin

, m

uco

us

m

emb

ran

es

ND

C

on

tact

(d

irec

t,

ind

irec

t)

end

oge

no

us

Diff

eren

t

infe

ctio

ns

in

imm

un

oco

m-

pro

mis

ed h

ost

Diff

eren

t

spec

ime

ns

dep

en

din

g o

n

infe

ctio

n

Stan

dar

d p

reca

uti

on

s

Co

ryn

eba

cte-

riu

m

dip

hth

eria

e

H

um

ans:

NP

m

uco

sa

(pati

ents

, ca

rrie

rs)

7 d

ays

– 6

m

on

ths

Dro

ple

ts, c

on

tact

(d

irec

t, in

dir

ect)

NP

sw

ab; t

hro

at

swab

D

rop

let

pre

cau

tio

ns;

sin

gle

roo

m/c

oh

orti

ng

Co

nta

ct p

reca

uti

on

s (h

ealt

hca

re w

ork

er [

HC

W]

vacc

inati

on

)

Tab

le 7

.1. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f b

acte

ria

po

ten

tial

ly c

ausi

ng

HA

I


12


Bac

teri

a M

ulti

dru

g re

-si

stan

t st

rain

s (M

DR

)

Hab

itat

Su

rviv

al in

th

e en

viro

n-

men

t (d

ry

surf

ace

s)13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r d

iagn

osi

s o

f

infe

ctio

n/

colo

nis

atio

n

Mai

n p

reve

nti

ve

mea

sure

s**

Ente

roco

ccu

s sp

ecie

s

Gly

cop

epti

de

resi

stan

t e

nte

r-o

cocc

i (G

RE)

Hu

man

s: G

I tr

act,

ge

nit

ou

rin

ary

trac

t

5 d

ays

– 4

m

on

ths

Ind

irec

t an

d d

irec

t co

nta

ct;

end

oge

no

us

UTI

, sep

sis

Uri

ne,

blo

od

, st

oo

l C

on

tact

pre

cau

tio

ns

Ente

rob

acte

r sp

ecie

s

Exte

nd

ed

spec

tru

m β

la

ctam

ase

stra

ins

(ESB

L),

mu

ltid

rug

re

sist

ant

(MD

R)

Envi

ron

men

t,

hu

man

GI t

ract

N

D

Co

nta

ct, f

oo

d

UTI

, sep

sis,

w

ou

nd

in

fecti

on

Uri

ne,

blo

od

, w

ou

nd

exu

dat

e,

sto

ol

Co

nta

ct p

reca

uti

on

s P

rud

ent

use

of

anti

bio

tics

(a

void

ing

the

use

of

3rd

ge

ne

rati

on

cef

alo

spo

rin

s)

Esch

eric

hia

co

li ES

BL

stra

ins

Car

bap

en

em

resi

stan

t

ente

rob

acte

ria

(CR

E)

Hu

man

s: G

I an

d

gen

ito

uri

nar

y tr

act

1.5

ho

urs

–

16

mo

nth

s Fa

ecal

-ora

l, in

dir

ect

and

dir

ect

con

tact

, fo

od

, wat

er,

end

oge

no

us

UTI

, sep

sis,

p

ne

um

on

ia,

per

ito

niti

s,

neo

nat

al

men

ingi

tis

Uri

ne,

blo

od

, sp

utu

m,

asp

irat

es,

CSF

, w

ou

nd

ex

ud

ate,

sto

ol

Co

nta

ct p

reca

uti

on

s Sa

fe f

oo

d a

nd

wat

er

Pru

den

t u

se o

f an

tib

ioti

cs

(avo

idin

g th

e u

se o

f 3

rd

gen

era

tio

n c

efal

osp

ori

ns

and

car

bap

enem

s)

Hel

ico

ba

cter

p

ylo

ri

G

astr

ic

mu

cosa

of

h

um

ans

Less

th

an 9

0

min

ute

s C

on

tam

inat

ed G

I en

do

sco

pes

A

cute

an

d

chro

nic

ga

stri

tis

Bio

psy

mat

eria

l; u

rea

bre

ath

te

st; s

too

l fo

r an

tige

n

det

ecti

on

Pro

per

ly d

isin

fect

ed

GI

end

osc

op

es

Kle

bsi

ella

pn

eum

on

iae

ESB

L st

rain

s C

RE

Hu

man

s: G

I tr

act;

hu

mid

en

viro

nm

en

t

2 h

ou

rs –

m

ore

th

an 3

0

mo

nth

s

Ind

irec

t an

d d

irec

t co

nta

ct,

end

oge

no

us

UTI

, sep

sis

(neo

nat

al

un

its)

, p

ne

um

on

ia

Uri

ne,

blo

od

, sp

utu

m,

asp

irat

es,

sto

ol

Co

nta

ct p

reca

uti

on

s P

rud

ent

use

of

anti

bio

tics

(a

void

ing

the

use

of

3rd

ge

ne

rati

on

cef

alo

spo

rin

s an

d c

arb

apen

ems)

Leg

ion

ella

pn

eum

op

hila

W

ater

(n

atu

ral

wat

ers,

tap

w

ater

, sh

ow

er h

ead

s,

coo

ling

tow

ers,

h

ot

wat

er t

anks

, h

um

idifi

ers

res-

pir

ato

ry t

her

apy

eq

uip

men

t)

NA

A

ero

sols

fro

m

envi

ron

me

nta

l w

ater

so

urc

es

(usu

ally

war

m

wat

er in

ho

spit

als)

; n

o p

erso

n-t

o-

per

son

tra

nsm

issi

on

Legi

on

nai

re’s

d

isea

se

Spu

tum

, blo

od

fo

r se

rolo

gy;

uri

ne

Hyp

erch

lori

nati

on

of

wat

er

or

hea

tin

g to

at

leas

t 5

5°C

N

o p

atien

t is

ola

tio

n n

eed

ed

Tab

le 7

.1. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f b

acte

ria

po

ten

tial

ly c

ausi

ng

HA

I


13


Tab

le 7

.1. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f b

acte

ria

po

ten

tial

ly c

ausi

ng

HA

I

Bac

teri

a M

ulti

dru

g re

sist

ant

stra

ins

(MD

R)

Hab

itat

Su

rviv

al in

th

e en

viro

n-

men

t (d

ry

surf

ace

s)13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r d

iagn

osi

s o

f

infe

ctio

n/

co

lon

isati

on

Mai

n p

reve

nti

ve

mea

sure

s**

List

eria

m

on

ocy

tog

enes

So

il,

vege

tab

les,

h

um

an G

I tr

act

(rar

ely)

; h

um

an b

irth

ca

nal

1 d

ay -

m

on

ths

Co

nta

min

ated

fo

od

; p

erin

atal

tr

ansm

issi

on

; co

nta

ct

wit

h c

on

tam

inat

ed

equ

ipm

ent

in

n

urs

erie

s

Men

ingi

tis,

b

acte

raem

ia

Blo

od

, CSF

Sa

fe f

oo

d

Stan

dar

d p

reca

uti

on

s in

n

urs

erie

s

Myc

ob

act

eriu

m

tub

ercu

losi

s

MD

R s

trai

ns

Extr

emel

y D

R

stra

ins

(XD

R)

Res

pir

ato

ry

trac

t o

f

pati

ents

1 d

ay –

4

mo

nth

s A

irb

orn

e, d

rop

lets

Tu

ber

culo

sis

spu

tum

A

irb

orn

e p

reca

uti

on

s (i

f n

ot

po

ssib

le, t

he

n d

rop

let

iso

la-

tio

n)

(HC

W v

acci

nati

on

)

Nei

sser

ia

men

ing

itid

is

N

P m

uco

sa o

f h

um

ans

ND

D

rop

lets

A

cute

m

enin

giti

s C

SF

Dro

ple

t p

reca

uti

on

s

Ch

emo

pro

ph

ylax

is

Pro

teu

s sp

ecie

s ES

BL

GI fl

ora

of

hu

man

s 1

-2 d

ays

End

oge

no

us,

co

nta

ct

(dir

ect

and

ind

irec

t)

UTI

, sep

sis

Uri

ne,

blo

od

, st

oo

l C

on

tact

pre

cau

tio

ns

Pse

ud

om

on

as

aer

ug

ino

sa

MD

R a

nd

pan

-dru

g

resi

stan

t (P

DR

) st

rain

s

Hu

man

s: G

I tr

act,

hu

mid

sk

in r

egi

on

s;

ub

iqu

ito

us

in

hu

mid

en

viro

nm

en

t,

(wat

er, s

oil,

p

lan

ts)

6 h

ou

rs t

o 1

6

mo

nth

s D

irec

t an

d in

dir

ect

con

tact

(h

um

id

item

s: p

oo

rly

d

isin

fect

ed it

ems,

ve

nti

lato

r ci

rcu

its)

Diff

eren

t u

sual

ly

seve

re

infe

ctio

ns

in

ho

spit

alis

ed,

esp

ecia

lly

imm

un

oco

m-

pro

mis

ed

pati

ents

Diff

eren

t

spec

ime

ns

de-

pen

din

g o

n

infe

ctio

n

Stan

dar

d p

reca

uti

on

s M

DR

/PD

R s

trai

ns:

co

nta

ct

pre

cau

tio

ns

Pru

den

t u

se o

f an

tib

ioti

cs

Salm

on

ella

sp

p

G

I tra

ct o

f h

um

ans

and

an

imal

s

NA

Fa

ecal

-ora

l, w

ater

, fo

od

D

iarr

ho

ea,

sep

sis

Sto

ol,

blo

od

Safe

fo

od

an

d w

ater

St

and

ard

pre

cau

tio

ns

Salm

on

ella

ty

ph

i

G

I tra

ct o

f h

um

ans

6 h

ou

rs –

4

wee

ks

Faec

al-o

ral,

wat

er,

foo

d

Typ

ho

id f

ever

St

oo

l, b

loo

d

Safe

fo

od

an

d w

ater

St

and

ard

pre

cau

tio

ns

Salm

on

ella

ty

ph

imu

riu

m

G

I tra

ct o

f h

um

ans

and

an

imal

s

10

mo

nth

s –

4.2

yea

rs

Faec

al-o

ral,

wat

er,

foo

d

Dia

rrh

oea

, se

psi

s St

oo

l, b

loo

d

Safe

fo

od

an

d w

ater

St

and

ard

pre

cau

tio

ns


14


Tab

le 7

.1. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f b

acte

ria

po

ten

tial

ly c

ausi

ng

HA

I

Bac

teri

a M

ulti

dru

g re

sist

ant

stra

ins

(MD

R)

Hab

itat

Su

rviv

al in

th

e en

viro

n-

men

t (d

ry

surf

ace

s)13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

ass

o-

ciat

ed in

fecti

on

s Sp

ecim

ens

for

dia

gno

sis

of

in

fecti

on

/

colo

nis

atio

n

Mai

n p

reve

nti

ve

mea

sure

s**

Serr

ati

a

ma

rces

cen

s

H

um

ans:

GI t

ract

; h

um

id e

nvi

ron

-m

ent

3 d

ays

– 2

m

on

ths;

on

d

ry fl

oo

rs 5

w

eeks

Ind

irec

t an

d d

irec

t co

nta

ct,

con

tam

inat

ed

intr

aven

ou

s fl

uid

s (e

spec

ially

hep

arin

so

luti

on

s)

Sep

sis,

wo

un

d

infe

ctio

n

Blo

od

, wo

un

d

exu

dat

e

Stan

dar

d p

reca

uti

on

s

Shig

ella

sp

ecie

s

GI t

ract

of

hu

man

s 2

day

s –

5

mo

nth

s Fa

ecal

-ora

l, w

ater

, fo

od

D

iarr

ho

ea

sto

ol

Safe

fo

od

an

d w

ater

C

on

tact

pre

cau

tio

ns

Sta

ph

ylo

cocc

us

au

reu

s

Met

hic

illin

re

sist

ant

S.

au

reu

s (M

RSA

)

Hu

man

s: s

kin

, m

uco

us

mem

-b

ran

es

7 d

ays

- 7

m

on

ths

Dro

ple

ts, d

irec

t an

d

ind

irec

t co

nta

ct,

med

ical

eq

uip

men

t;

end

oge

no

us

Skin

infe

ctio

ns,

p

ne

um

on

ia,

se

psi

s, o

steo

mye

-liti

s

Swab

s, s

pu

tum

, n

ares

, blo

od

, as

pir

ate

s, b

iop

sy,

wo

un

d e

xud

ate,

p

eria

nal

sw

ab,

sto

ol

Co

nta

ct p

reca

uti

on

s P

rud

ent

use

of

an

tib

ioti

cs (

avo

id

cip

rofl

oxa

cin

)

Stre

pto

cocc

us

ag

ala

ctia

e G

rou

p B

st

rep

toco

ccu

s (G

BS)

H

um

ans:

bir

th

can

al

ND

In

trap

arta

l; d

irec

t an

d in

dir

ect

con

tact

in

de

liver

y ro

om

an

d n

urs

erie

s

Sep

sis

and

men

ingi

tis

of

n

ewb

orn

Blo

od

, CSF

, vag

inal

sw

ab

An

tib

ioti

c p

rop

hyl

axis

d

uri

ng

del

iver

y w

hen

in

dic

ate

d

Stan

dar

d p

reca

uti

on

s

Stre

pto

cocc

us

pyo

gen

es

Gro

up

A

stre

pto

cocc

us

(GA

S)

H

um

ans:

oro

ph

a-ry

nge

al m

uco

sa

3 d

ays-

6.5

m

on

ths

Dro

ple

ts, c

on

tact

, en

do

gen

ou

s P

har

yngi

tis

(“st

rep

th

roat

”),

surg

ical

wo

un

d

infe

ctio

n

Oro

ph

aryn

geal

sw

ab, w

ou

nd

ex

ud

ate

Staff

wit

h G

AS

infe

ctio

ns

or

carr

iers

of

GA

S sh

ou

ld

no

t w

ork

in t

he

o

per

atin

g th

eatr

e

Vib

rio

ch

ole

rae

G

I tra

ct o

f h

um

ans;

w

ater

1

– 7

day

s Fa

ecal

-ora

l, w

ater

, ra

w s

eafo

od

C

ho

lera

st

oo

l Sa

fe w

ater

an

d f

oo

d

Stan

dar

d p

reca

uti

on

s

Yers

inia

en

tero

coliti

ca

G

I flo

ra o

f m

any

an

imal

s, c

ause

s

dia

rrh

oea

in y

ou

ng

anim

als;

rar

ely

hu

man

s as

car

rier

s

ND

B

loo

d t

ran

sfu

sio

n in

h

osp

ital

s; f

aeca

l-o

ral i

n t

he

co

mm

un

ity

Bac

tera

emia

co

n-

nec

ted

to

blo

od

tr

ansf

usi

on

;

dia

rrh

oea

in t

he

com

mu

nit

y

Blo

od

, sto

ol

Safe

blo

od

pro

du

cts

Stan

dar

d p

reca

uti

on

s

* Su

rviv

al is

bett

er if

co

nd

itio

ns

are

hu

mid

fo

r m

ost

mic

roo

rgan

ism

s (e

xcep

tio

n b

ein

g St

ap

hyl

oco

ccu

s a

ure

us)

, an

d

if m

icro

org

anis

m is

in b

iolo

gica

l mat

eria

l (b

loo

d, f

aece

s, w

ou

nd

exu

dat

e), i

f th

e te

mp

erat

ure

is lo

wer

an

d if

bac

te-

ria

are

in h

igh

er n

um

ber

s **

See

“Is

ola

tio

n p

reca

uti

on

s”

***

wh

ene

ver

ind

irec

t co

nta

ct is

invo

lved

, it

is m

ost

fre

qu

en

tly

by

han

ds

of

hea

lth

care

wo

rker

s N

D =

no

t d

on

e; N

A =

no

t ap

plic

able


15

Tab

le 7

.2. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f fu

ngi

po

ten

tial

ly c

ausi

ng

HA

I


Fun

gi

Hab

itat

Su

rviv

al in

th

e en

viro

nm

ent

(dry

su

rfac

es)

13

*

Tran

smis

sio

n

in h

ealt

hca

re

Hea

lth

care

ass

oci

ated

in

fecti

on

s Sp

ecim

ens

for

dia

gno

-si

s o

f in

fecti

on

/co

lon

isati

on

Mai

n p

reve

nti

ve m

easu

res*

*

Ca

nd

ida

alb

i-ca

ns

(yea

st)

Soil,

an

imal

s,

hu

man

s,

inan

imat

e

ob

ject

s

1-1

20

day

s D

irec

t an

d

ind

irec

t**

* co

nta

ct,

end

oge

no

us

Diff

eren

t o

pp

ort

un

isti

c in

fecti

on

s D

iffer

ent

spec

imen

s

dep

en

din

g o

n in

fecti

on

St

and

ard

pre

cau

tio

ns

Ca

nd

ida

gla

-b

rata

(ye

ast)

Soil,

an

imal

s,

hu

man

s,

inan

imat

e

ob

ject

s

10

2-1

50

day

s D

irec

t an

d

ind

irec

t co

nta

ct,

end

oge

no

us

Diff

eren

t o

pp

ort

un

isti

c in

fecti

on

s D

iffer

ent

spec

imen

s

dep

en

din

g o

n in

fecti

on

St

and

ard

pre

cau

tio

ns

Ca

nd

ida

pa

ra-

psi

losi

s (y

east

)

Soil,

an

imal

s,

hu

man

s,

inan

imat

e

ob

ject

s

14

day

s D

irec

t an

d

ind

irec

t co

nta

ct,

end

oge

no

us

Diff

eren

t o

pp

ort

un

isti

c in

fecti

on

s D

iffer

ent

spec

imen

s

dep

en

din

g o

n in

fecti

on

St

and

ard

pre

cau

tio

ns

Asp

erg

illu

s sp

ecie

s (m

ou

ld)

Ub

iqu

ito

us

in

soil,

wat

er,

foo

d, d

ecay

ing

mat

eria

l, o

utd

oo

r an

d

ind

oo

r ai

r

Co

nid

ia a

nd

sp

ore

s ar

e

resi

stan

t fo

rms

Inh

alati

on

, (c

on

tact

) P

neu

mo

nia

, dis

sem

inat

-ed

infe

ctio

ns

in s

ever

ely

imm

un

oco

mp

rom

ised

p

atien

ts

Spu

tum

, diff

eren

t o

the

r sp

ecim

en

s d

epe

nd

ing

on

in

fecti

on

Pro

tecti

ve is

ola

tio

n o

f su

scep

ti-

ble

pati

en

ts

Co

nta

inm

ent

of

area

s w

her

e co

nst

ructi

on

/ re

no

vati

on

is in

p

roce

ss t

o r

edu

ce e

xpo

sure

****

Sa

fe t

ap w

ater

, fo

od

an

d d

rin

ks

Mu

cor

(mo

uld

) So

il, p

lan

ts,

fru

its,

an

imal

ex

cret

a, f

oo

d

Co

nid

ia a

nd

sp

ore

s ar

e

resi

stan

t fo

rms

Inh

alati

on

D

iffer

ent

op

po

rtu

nis

tic

infe

ctio

ns

in

imm

un

oco

mp

rom

ised

p

atien

ts (

zygo

myc

osi

s)

Diff

eren

t sp

ecim

ens

d

epe

nd

ing

on

infe

ctio

n

Pro

tecti

ve is

ola

tio

n o

f su

scep

ti-

ble

pati

en

ts

Co

nta

inm

ent

of

area

s w

her

e co

nst

ructi

on

/ re

no

vati

on

is in

p

roce

ss t

o r

edu

ce e

xpo

sure

****

Sa

fe f

oo

d a

nd

dri

nks

Rh

izo

pu

s (m

ou

ld)

Soil,

pla

nts

, fr

uit

s, a

nim

al

excr

eta,

fo

od

Co

nid

ia a

nd

sp

ore

s ar

e

resi

stan

t fo

rms

Inh

alati

on

D

iffer

ent

op

po

rtu

nis

tic

infe

ctio

ns

in

imm

un

oco

mp

rom

ised

p

atien

ts (

zygo

myc

osi

s)

Diff

eren

t sp

ecim

ens

d

epe

nd

ing

on

infe

ctio

n

Pro

tecti

ve is

ola

tio

n o

f su

scep

ti-

ble

pati

en

t

Co

nta

inm

ent

of

area

s w

her

e co

nst

ructi

on

/ re

no

vati

on

is in

p

roce

ss t

o r

edu

ce e

xpo

sure

****

Sa

fe f

oo

d a

nd

dri

nks

*Su

rviv

al is

bett

er in

low

tem

per

atu

re, h

igh

hu

mid

ity

and

pre

sen

ce o

f se

rum

or

alb

um

in;

** S

ee “

Iso

lati

on

pre

cau

tio

ns”

**

* W

hen

eve

r in

dir

ect

co

nta

ct is

invo

lved

, it

is m

ost

fre

qu

en

tly

by

han

ds

of

hea

lth

care

wo

rker

s **

** S

ee “

Hea

lth

car

e fa

cilit

y d

esig

n, c

on

stru

ctio

n a

nd

ren

ova

tio

n”


16


Tab

le 7

.3. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f vi

ruse

s p

ote

nti

ally

cau

sin

g H

AI

Vir

us

Hab

itat

Su

rviv

al in

th

e en

viro

nm

ent

(dry

su

rfac

es)

13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r

dia

gno

sis

of

in

fecti

on

**

Mai

n p

reve

nti

ve

mea

sure

s**

*

Ad

eno

viru

s Se

vera

l typ

es

Hu

man

s, w

ater

, fo

mit

es (

e.g.

, o

ph

thal

mo

logi

cal

equ

ipm

ent

and

so

luti

on

s),

envi

ron

me

nt

7 d

ays

– 3

mo

nth

s D

irec

t an

d in

dir

ect*

***

con

tact

Ey

e in

fecti

on

s,

resp

irat

ory

in

fecti

on

s

Co

nju

ncti

val s

wab

N

P s

wab

St

and

ard

pre

cau

tio

ns

Sep

arat

e ey

e d

rop

s fo

r ev

ery

pati

ent

Co

ron

avir

us

Hu

man

s

3 h

ou

rs

D

rop

lets

D

irec

t an

d in

dir

ect

co

nta

ct

Res

pir

ato

ry

infe

ctio

ns

Dia

rrh

oea

Seru

m s

amp

le

Res

pir

ato

ry s

amp

le

Sto

ol s

amp

le

Dro

ple

t p

reca

uti

on

s C

on

tact

pre

cau

tio

ns

Co

ron

avir

us:

SA

RS

(Se

vere

Acu

te

Res

pir

ato

ry

Syn

dro

me)

-Co

V

An

imal

s H

um

ans

SAR

S vi

rus:

72

-96

h

ou

rs

Dro

ple

ts

Dir

ect

and

ind

irec

t

con

tact

Fa

ecal

-ora

l ?

Seve

re r

esp

ira-

tory

infe

ctio

ns

Seru

m s

amp

le

Res

pir

ato

ry s

amp

le

Air

bo

rne

pre

cau

tio

ns

(if

no

t p

oss

ible

th

en d

rop

let

p

reca

uti

on

s) p

lus

con

tact

p

reca

uti

on

s

Co

ron

avir

us:

M

ERS

(Mid

dle

Eas

t R

esp

irat

ory

Sy

nd

rom

e)-C

oV

An

imal

s H

um

ans

ND

D

rop

lets

D

irec

t an

d in

dir

ect

co

nta

ct

Seve

re

resp

irat

ory

in

fecti

on

s

Res

pir

ato

ry s

amp

le

Air

bo

rne

pre

cau

tio

ns

(if

no

t p

oss

ible

th

en d

rop

let

p

reca

uti

on

s) p

lus

con

tact

p

reca

uti

on

s

Co

xack

ie B

vir

us

Hu

man

s >2

wee

ks

Faec

al-o

ral;

dir

ect

and

in

dir

ect

con

tact

G

ene

raliz

ed

dis

ease

of

new

bo

rn

Seru

m s

amp

le

Blo

od

CSF

Stan

dar

d p

reca

uti

on

s

Cyt

om

egal

ovi

rus

Hu

man

s 8

ho

urs

B

loo

d p

rod

uct

s, ti

ssu

e an

d o

rgan

s fo

r tr

ansp

lan

-ta

tio

n; m

uco

sal c

on

tact

w

ith

sec

reti

on

s an

d e

x-cr

etio

ns

Hu

ge r

ange

of

diff

ere

nt

dis

-ea

ses

Seru

m s

amp

le

Safe

blo

od

pro

du

cts

and

ti

ssu

es/

org

ans

for

tr

ansp

lan

tati

on

Ebo

la (

Mar

bu

rg)

Hu

man

s A

nim

als

ND

D

irec

t co

nta

ct

Blo

od

, sec

reti

on

s,

resp

irat

ory

dro

ple

ts,

sem

en, c

on

tam

inat

ed

syri

nge

s an

d n

eed

les,

ae

roso

ls

Hae

mo

rrh

agic

fe

ver

Seru

m s

amp

le, b

loo

d

Air

bo

rne

pre

cau

tio

ns

(if

no

t p

oss

ible

th

en d

rop

let

p

reca

uti

on

s) p

lus

con

tact

p

reca

uti

on

s


17


Tab

le 7

.3. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f vi

ruse

s p

ote

nti

ally

cau

sin

g H

AI

Vir

us

Hab

itat

Su

rviv

al in

th

e en

viro

nm

ent

(dry

su

rfac

es)

13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r ‘d

iagn

osi

s o

f

infe

ctio

n**

Mai

n p

reve

nti

ve

mea

sure

s**

*

Hep

atiti

s A

vir

us

Hu

man

s 2

ho

urs

– 6

0 d

ays

Faec

al-o

ral

Hep

atiti

s A

Se

rum

sam

ple

Sa

fe f

oo

d a

nd

wat

er

Stan

dar

d p

reca

uti

on

s

Hep

atiti

s B

vir

us

Hu

man

s >1

wee

k B

loo

d, b

od

ily fl

uid

s, ti

ssu

e an

d o

rgan

s fo

r

tran

spla

nta

tio

n

Hep

atiti

s B

Se

rum

sam

ple

Sa

fe b

loo

d p

rod

uct

s an

d

tiss

ue

s/o

rgan

s fo

r

tran

spla

nta

tio

n

Hep

atiti

s C

vir

us

Hu

man

s N

A

Blo

od

, bo

dily

flu

ids,

tiss

ue

and

org

ans

for

tr

ansp

lan

tati

on

Hep

atiti

s C

Se

rum

sam

ple

Sa

fe b

loo

d p

rod

uct

s an

d

tiss

ue

s/o

rgan

s fo

r

tran

spla

nta

tio

n

Her

pes

sim

ple

x vi

rus

Hu

man

s 4

.5 h

ou

rs –

8

wee

ks

Dro

ple

ts, c

lose

co

nta

ct

Diff

eren

t m

u-

cosa

l an

d s

kin

in

fecti

on

s

Lesi

on

sw

ab

CSF

If

infe

cted

, HC

W s

ho

uld

no

t ca

re f

or

susc

epti

ble

per

son

s (n

ewb

orn

, im

mu

no

com

pro

mis

ed)

HIV

H

um

ans

>7 d

ays

Blo

od

, bo

dily

flu

ids,

tiss

ue

and

org

ans

for

tr

ansp

lan

tati

on

AID

S Se

rum

sam

ple

Sa

fe b

loo

d p

rod

uct

s an

d

tiss

ue

s/o

rgan

s fo

r

tran

spla

nta

tio

n

Infl

uen

za v

iru

s H

um

ans

1-2

day

s D

rop

lets

, dir

ects

an

d

ind

irec

t co

nta

ct, H

CW

as

sym

pto

mati

c o

r

asym

pto

mati

c d

isea

sed

p

erso

ns

Infl

uen

za

NP

sw

ab

Dro

ple

t p

reca

uti

on

s H

CW

vac

cin

atio

n

No

rovi

rus

Hu

man

s 8

ho

urs

– 7

day

s Fa

ecal

-ora

l, d

irec

t an

d

ind

irec

t co

nta

ct, a

ero

sols

fr

om

vo

mit

us

Dia

rrh

oea

St

oo

l C

on

tact

pre

cau

tio

ns

Rab

ies

viru

s D

ogs

(an

d o

ther

an

imal

s); h

um

ans

Inac

tiva

ted

so

on

b

y d

ryin

g24

Saliv

a an

d o

ther

bo

dy

flu

ids

and

sec

reti

on

s o

f p

atien

t th

rou

gh c

on

tact

w

ith

op

en w

ou

nd

s, s

kin

ab

rasi

on

s o

r m

uco

us

mem

bra

ne

s H

um

an b

ite/

scra

tch

Aer

oso

l tra

nsm

issi

on

?

Rab

ies

Co

rnea

l im

pre

ssio

n

Skin

bio

psy

Sa

liva

CN

S ti

ssu

e at

au

top

sy

Dro

ple

t p

reca

uti

on

s an

d c

on

-ta

ct p

reca

uti

on

s P

ost

-exp

osu

re p

rop

hyl

axis

in

per

son

s w

ho

wer

e ex

po

sed

to

sal

iva

and

oth

er b

od

y

flu

ids

and

sec

reti

on

s o

f

pati

ent

or

wer

e b

itten

/sc

ratc

hed

by

pati

ent


18


Tab

le 7

.3. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f vi

ruse

s p

ote

nti

ally

cau

sin

g H

AI

Vir

us

Hab

itat

Su

rviv

al in

th

e en

viro

nm

ent

(dry

su

rfac

es)

13

*

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r d

iagn

osi

s o

f in

fecti

on

**

Mai

n p

reve

nti

ve

mea

sure

s**

*

Res

pir

ato

ry

syn

cyci

al v

iru

s

Hu

man

s U

p t

o 6

ho

urs

D

rop

lets

, dir

ect

and

in

dir

ect

con

tact

A

cute

re

spir

ato

ry

infe

ctio

ns

in

you

ng

child

ren

NP

exu

dat

e

Dro

ple

t p

reca

uti

on

s

Ro

tavi

rus

Hu

man

s 6

-60

day

s Fa

ecal

-ora

l, d

irec

t an

d in

dir

ect

co

nta

ct

Dia

rrh

oea

St

oo

l C

on

tact

pre

cau

tio

ns

Ru

bu

la v

iru

s H

um

ans

ND

D

rop

lets

M

um

ps

(par

oti

tis)

Se

rum

sam

ple

D

rop

let

pre

cau

tio

ns

H

CW

vac

cin

atio

n

Ru

biv

iru

s H

um

ans

ND

D

rop

lets

R

ub

ella

(G

erm

an

mea

sles

)

Seru

m s

amp

le

Dro

ple

t p

reca

uti

on

s

HC

W v

acci

nati

on

Mo

rbill

ivir

us

Hu

man

s N

D

Dro

ple

ts

Mea

sle

s Se

rum

sam

ple

D

rop

let

pre

cau

tio

ns

H

CW

vac

cin

atio

n

Var

icel

la-z

ost

er

viru

s

Hu

man

s N

D

Dro

ple

ts, c

lose

co

nta

ct

Var

icel

la

Seru

m s

amp

le

Dro

ple

t/ai

rbo

rne

pre

cau

tio

ns

HC

W v

acci

nati

on

* Su

rviv

al is

bett

er in

low

te

mp

erat

ure

, pre

sen

ce o

f b

iolo

gica

l mat

eria

l an

d if

vir

use

s ar

e in

hig

her

nu

mb

ers

** D

iagn

osi

s is

per

form

ed u

sin

g se

rolo

gy, i

f ap

plic

able

an

d if

lab

ora

tory

can

per

form

dir

ect

dia

gno

stics

, it

will

be

mo

stly

an

tige

n d

etec

tio

n o

r n

ucl

eic

acid

det

ecti

on

in t

he

sam

ple

fro

m in

fecti

ou

s si

te, r

arel

y vi

rus

iso

lati

on

**

* Se

e “I

sola

tio

n p

reca

uti

on

s”

****

wh

ene

ver

ind

ire

ct c

on

tact

is in

volv

ed, i

t is

mo

st f

req

uen

tly

by

han

ds

of

hea

lth

care

wo

rker

s N

A =

no

t ap

plic

able

; ND

= n

ot

do

ne;

HC

W =

hea

lth

care

wo

rker


19


Tab

le 7

.4. C

har

acte

risti

cs o

f m

ain

gro

up

s o

f p

aras

ite

s p

ote

nti

ally

cau

sin

g H

AI

Par

asit

e

Hab

itat

Su

rviv

al in

th

e en

viro

nm

ent

Tran

smis

sio

n in

h

ealt

hca

re

Hea

lth

care

as

soci

ated

in

fecti

on

s

Spec

imen

s fo

r d

iagn

osi

s o

f in

fecti

on

Mai

n p

reve

nti

on

met

ho

ds*

Cry

pto

spo

rid

ium

(p

roto

zoa)

Hu

man

s 2

ho

urs

on

dry

su

rfac

e13

lon

gevi

ty in

w

ater

21

Faec

al-o

ral,

wat

er,

foo

d

Dia

rrh

oea

St

oo

l Sa

fe w

ater

an

d f

oo

d

Stan

dar

d p

reca

uti

on

s

Pla

smo

diu

m

spec

ies

(pro

tozo

a)

Live

r,

eryt

hro

cyte

s o

f d

isea

sed

per

son

NA

M

osq

uit

o-b

orn

e in

th

e co

mm

un

ity;

in

fect

ed b

loo

d

Mal

aria

B

loo

d

Safe

blo

od

pro

du

cts

Tric

ho

mo

na

s va

gin

alis

(p

roto

zoa)

Vag

inal

mu

cosa

Se

vera

l ho

urs

in

hu

mid

en

viro

nm

en

t19

Sexu

ally

tr

ansm

itted

in t

he

com

mu

nit

y;

con

tam

inat

ed

med

ical

eq

uip

men

t in

gyn

aeco

logy

Vag

inal

in

fecti

on

in

wo

men

Vag

inal

dis

char

ge

Dis

infe

cted

/ste

rilis

ed

med

ical

eq

uip

men

t in

gyn

aeco

logy

Ente

rob

ius

ve

rmic

ula

ris

(hel

min

th)

Inte

stin

al t

ract

of

dis

ease

d p

erso

n

Fa

ecal

-ora

l,

in

gesti

on

of

par

a-si

te e

ggs

that

can

co

nta

min

ate

envi

ron

me

nt;

airb

orn

e

Ente

rob

iasi

s P

eria

nal

tap

e

Stan

dar

d p

reca

uti

on

s C

han

gin

g lin

en a

nd

pati

ent

clo

thes

wit

ho

ut

crea

tin

g

aero

sols

* Se

e “I

sola

tio

n p

reca

uti

on

s”


hapter 7 The Role of the Microbiology...

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