Airborne Superbugs: Can Hospital-Acquired Infections Cause Community Epidemics?

Much attention has been focused recently on pathogenic microorganisms and the threat these microorganisms are to communities. Especially problematic are microorganisms that have developed resistance to antibiotic treatment and that have begun to spread beyond the bounds of hospital walls. The most dangerous are those that may spread by the airborne route, which include methicillin-resistant Staphylococcus aureus (MRSA) and multidrug-resistant tuberculosis (XTB). Pathogens that develop pan-drug resistance (PDR) might be considered “superbugs” because they are virtually invulnerable to standard drug treatments. Once these microbes develop immunity to antibiotic treatment and cause outbreaks in hospital environments they may, and have on occasion, spread into local communities. How great an epidemic threat these microorganisms are to communities is a question worth examining in more detail.

Airborne nosocomial infections

Nosocomial, or hospital-acquired, infections have been around as long as hospitals have been operating. But it is only in the last few decades that antibiotic and other treatments for these diseases have begun failing (ASM, 1994). The failure of any treatment leads to further spread if the infection cannot be contained by other means, such as quarantine. Airborne epidemics can spread rapidly and pervasively through a non-immune population (Weinstein, 2004). Thanks to favorable indoor environments airborne epidemics tend to be self-perpetuating, as opposed to foodborne and waterborne epidemics, which tend to be local and short-lived. Most of the drug-resistant pathogens circulating today are capable of airborne transmission (Kowalski, 2006).

Table 1 identifies all of the nosocomial agents that may transmit at least partly by the airborne route, and these include bacteria, viruses, and fungi (Kowalski 2006). These microbes are ranked by estimated order of occurrence and are classified as contagious, noncontagious and endogenous (present as part of normal human flora). The primary infections caused are identified, including surgical site infections (SSI).

Because the types of drug treatment differ between these three groups, the nature of the drug resistance also varies. But one factor is common to all these microbes—increasing drug resistance tends to facilitate their multiplication and spread, sometimes beyond the bounds of hospital walls.

The reasons for the resurgence of infectious diseases are complex and include factors such as increased urbanization and crowding, environmental changes, and worldwide commerce and travel (Pimentel et al, 1998, Platt, 1996) contribute to the resurgence. Some specific causes are population growth and an enormous number of susceptible people living in poor and crowded urban areas, inadequate and deteriorating public health infrastructures worldwide and misuse of antibiotics or other drugs, which can hasten the evolution of resistant microbes (Ewald, 1994). Misusing drug includes prescribing them without proper indications, prescribing the wrong drugs or the wrong doses and having poor patient compliance with treatment regimens (WHO “World Heath Organization Fact Sheet No. 194”).

Bacteria that cause respiratory infections have been developing increased drug resistance over the past few decades (WHO “World Heath Organization Fact Sheet No. 194”). Other non-respiratory bacteria have experienced the same drug-resistance and increasing incidence. Viral respiratory pathogens represent a significant fraction of nosocomial infections and are subject to rapid evolutionary change (Ewald, 1994). Fungal pathogens also have been on the rise recently, in part due to the prevalence of immunodeficiency diseases that facilitate their spread (Ampel, 1996).

The public often imagines that doctors have unlimited arsenals of weapons to fight microbial infections, but in fact, there are a mere seven classes of antibiotics, a similarly small number of fungicidal agents, and there are less vaccines than there are viruses (Ryan, 1994). The result is that as each new treatment becomes ineffective, the arsenal of treatments begins shrinking to dangerously low levels. Some predict that one day new medicines will become obsolete faster than new ones are developed.

Increasing drug resistance

Some microbes possess the abilities to resist one or more types of treatments, while others may be multi-drug resistant (MDR). Still, others are subject to the phenomenon of pan-drug resistance, which is defined as those microbes that resist all seven major classes of antimicrobial agents: penicillins, cephalosporins, carbapenems, monobactams, quinolones, aminoglycosides and polymyxins (Falagas and Kasiakou, 2005). Drug resistance is defined in terms of an IC50 value, or the concentration that causes 50% growth inhibition, and resistance is defined as a 10-fold increase in IC50 values (Andre et al 2004, Andersson et al 2003).

A wide body of evidence is available regarding the drug resistance of individual species of nosocomial pathogens. A selection of data and representative sources are provided here as examples of the scope of the problem.

At least 11 major microbes, including species of Streptococcus and Staphylococcus, already are highly resistant to standard antibiotic treatment (Pimentel et al 1998). Rapid increase in drug resistance by disease organisms is caused by the widespread use and overuse of more than 300 antibiotics by the medical profession (ASM “Report of the ASM task force on antibiotic resistance”). In addition, one-half of the antibiotics used in the United States to treat humans also are used to treat disease-infected domestic animals. The concurrent use of antibiotics for both humans and livestock enhances selection for drug-resistant microbes, further exacerbating the problem of antibiotic resistance (Pimentel et al, 1998).

Although drug resistance often has been associated with nosocomial infections, innate resistance of bacteria is increasingly being reported. MDR Haemophilus influenzae are being increasingly reported from all over the world (Jain, 1997). Alcaligenes and Acinetobacter species have acquired a wide range of drug resistance. Multidrug resistant strains of Acinetobacter baumannii, Pseudomonas aeruginosa , and Klebsiella pneumoniae , have been recognized among casualties returning from battlefields (Davis et al, 2005). Clinically isolated Pseudomonas aeruginosa have acquired resistance to fluoroquinolones and amikacin, approximately 20% and 5%, respectively.

Dr. William Jarvis of the Centers for Disease Control & Prevention warns that, “In at least 70% of the hospital-acquired infections that occur, the organism is resistant to at least one antibiotic.” Bacteria acquire up to 90% of their genetic material from distantly related bacteria species, according to new research from the University of Arizona in Tucson. It is even possible for unrelated species to exchange bits of genetic information that allow them to develop drug resistance.

The drug resistance of streptococcal infections, which can cause Scarlet Fever, has increased from 0.8% to 28% in the past decade, according to figures from the Institute of Environmental Science and Research in New Zealand. MRSA has shown up outside hospital settings and has even become a problem in athletics, where it may contaminate sports equipment and facilities (”Benching Bacteria from Athletics: New Sporting Goods Line Answers Call for Protection Against Antibiotic-Resistant Staph Infections”). Multidrug-resistant tuberculosis has caused a resurgence in this disease worldwide, and close to one million people die each year from this disease, once thought to be under control in the West (WHO Europe “World Health Organization Europe Fact Sheet 07/02”). Burkholderia pseudomallei , the causative agent of melioidosis, has shown increasing resistance to antibiotics and has resulted in severe problems with treatment regimes, leading to intensification of the search for new drugs (Perumal et al, 2006).

The evolution of drug resistance in microbes can be surprisingly rapid. In 1979, only 6% of European pneumococcus strains were resistant to penicillin, but one decade later that percentage had grown to 44% (Platt, 1996).

Viruses are treated with vaccines and antiviral agents, not with antibiotics, and these have generally remained effective over the years. The trouble is that each new variant of a virus generally requires a specific antiviral agent and a specific vaccine (Ryan, 1994). Viruses can mutate rapidly, more rapidly than any bacteria, and a vaccine must be quickly developed at the first appearance of any new variant or virus (ASM “Report of the ASM task force on antibiotic resistance”). The greatest concern with viruses is not their abilities to resist treatment, but their propensity to cause explosive epidemics before a vaccine or effective treatment can be developed. Influenza and SARS virus are two examples of viruses that can cause high fatality rates without treatment.

A major problem with antiviral drugs is the high frequencies of drug-resistant mutants. There are experimental and clinically approved drugs that are effective, dramatically reducing virus yields or providing good relief of symptoms in patients, but the drugs ultimately have limited usefulness, because viruses that escape the initial inhibition are frequently drug-resistant (Huang, 2005). The rapid development of drug resistance by retroviruses and RNA viruses is due to their high mutation rates. That is, viruses can mutate into viruses faster than new vaccines can be developed. Indeed, it is not unreasonable to propose that the large diversity of RNA viruses is in large part due to their high mutation rates, which allow them to mutate and adapt to new niches very rapidly.

A recent report on the global prevalence of adamantane-resistant influenza A viruses indicated a significant increase of drug resistance, from 1.8% during the 2001-02 influenza season to 12.3% during the 2003-04 season (Bright et al, 2005). Vaccines can become ineffective due to slight changes in the viruses.

Over the past decade, the increasing incidence of serious fungal infections, along with increased antifungal drug use, has led to the emergence of drug-resistant fungal pathogens. Antifungal drug resistance has been reported by a number of researchers in pathogenic fungi including Histoplasma capsulatum, Cryptococcus neoformans , and other fungal species (VandenBossche et al, 1998). Although such fungal infections are not normally nosocomial, they are associated with human immunodeficiency virus (HIV) and, also illustrate how hospital treatment may enhance some community-acquired infections.

Antifungal drug resistance has become an increasing problem with the development of a larger compendium of antifungal agents. Fungal diseases are increasing among patients infected with (HIV) type 1. Increasing evidence suggests that prolonged use of these antifungal drug treatments results in both clinical and microbiologic resistance (Ampel et al, 1996).

Community spread

Microbes that exist environmentally or as endogenous microflora in humans may develop drug resistance and when such infections hail from the community rather than from hospitals, they are referred to as community-acquired infections. Increasing drug resistance has occurred among such community-acquired microbes such as Haemophilus , Cardiobacterium , members of the Enterobacteriaceae, Pseudomonas species and others (Baddour et al, 2005).

MRSA has been reported in prisons, sports facilities and residential homes.

The MRSA superbug is no longer confined to hospitals and new strains are killing young, healthy people (Moellering, 2006). Necrotising fasciitis, better known as a flesh-eating disease, will kill one in five patients even with treatment. The CDC has warned that outbreaks from small pets like hamsters, mice and rats have sickened many people in various states with dangerous multidrug-resistant bacteria. Farm animals also have been found to be infected and these carriers provide yet another reservoir, outside of communities and hospital environments, in which superbugs may develop drug resistance and mutate or evolve into new variants (Pimentel et al, 1998).

The multifaceted problem of drug resistance in nosocomial pathogens threatens to extend explosively beyond the boundaries of health care settings and we are witnessing their occurrences in communities, prisons, athletic facilities, agricultural environments and even battlefields. It may be time to consider more drastic solutions than drug treatment alone, and options may include disease management methods such as quarantine and health education, and engineering methods such as air treatment. The latter approach has great unexplored potential. Although it may not be a complete solution, it may, if implemented on a wide enough basis, be capable of limiting epidemics and providing healthy, safe environments in which to live and work.

Pathogen	Group	Type	Annual Cases	Increasing Drug Resistance	Primary Infections
Table 1: Potential Airborne Agents of Nosocomial Infections in the United States. Adapated from Aerobiological Engineering Handbook: A Guide to Airborne Disease Control Technologies, by W.J. Kowalski, PhD, PE. *China only
Acinetobacter	Bacteria	Endogenous	147	Yes	SSI, meningitis
Alcaligenes	Bacteria	Endogenous	rare	Yes	SSI
Bacteroides fragilis	Bacteria	Endogenous	uncommon	Yes	bacteremia, SSI
Bordetella pertussis	Bacteria	Contagious	6,564	Yes	Whooping cough
Burkholderia pseudomallei	Bacteria	Noncontagious	rare	Yes	melioidosis
Cardiobacterium	Bacteria	Endogenous	rare	Yes	endocarditis
Chlamydia pneumoniae	Bacteria	Contagious	uncommon	No	pneumonia
Corynebacterium diphtheriae	Bacteria	Contagious	10	Yes	diphtheria
Haemophilus influenzae	Bacteria	Contagious	1,162	Yes	SSI, pneumonia, meningitis
Haemophilus parainfluenzae	Bacteria	Endogenous	rare	Yes	pneumonia, meningitis
Klebsiella pneumoniae	Bacteria	Endogenous	1,488	Yes	SSI, pneumonia
Legionella pneumophila	Bacteria	Noncontagious	1,163	?	pneumonia
Moraxella	Bacteria	Endogenous	rare	Yes	otitis media
Mycobacterium tuberculosis	Bacteria	Contagious	20,000	Yes	TB
Nocardia asteroides	Bacteria	Noncontagious	uncommon	Yes	nocardiosis
Nocardia brasiliensis	Bacteria	Noncontagious	uncommon	Yes	nocardiosis
Pseudomonas aeruginosa	Bacteria	Noncontagious	2,626	Yes	SSI, pneumonia
Serratia marcescens	Bacteria	Endogenous	479	Yes	SSI, pneumonia, bacteremia
Staphylococcus aureus	Bacteria	Endogenous	2,750	Yes	SSI, pneumonia
Streptococcus pneumoniae	Bacteria	Contagious	500,000	Yes	pneumonia, meningitis
Streptococcus pyogenes	Bacteria	Contagious	213,962	Yes	Scarlet fever, SSI
Aspergillus	Fungi	Noncontagious	666	Yes	Aspergillosis
Blastomyces dermatitidis	Fungi	Noncontagious	rare	?	Blastomycosis
Coccidioides immitis	Fungi	Noncontagious	uncommon	?	coccidioidomycosis
Cryptococcus neoformans	Fungi	Noncontagious	high	Yes	cryptococcosis
Histoplasma capsulatum	Fungi	Noncontagious	1,000	Yes	Histoplasmosis
Mucor plumbeus	Fungi	Noncontagious	rare	No	mucormycosis
Pneumocystis carinii	Fungi	Noncontagious	rare	Yes	pneumocystosis
Rhizopus stolonifer	Fungi	Noncontagious	rare	No	zygomycosis
Influenza A virus	Virus	Contagious	2,000,000	Yes	flu
Measles virus	Virus	Contagious	500,000	No	measles
Parainfluenza virus	Virus	Contagious	28,900	?	flu, pneumonia
Respiratory Syncytial Virus	Virus	Contagious	75,000	No	RSV
Rubella virus	Virus	Contagious	3,000	?	rubella
SARS virus	Virus	Contagious	10*	?	SARS
Varicella-zoster virus	Virus	Contagious	46,016	Yes	VZV

UV Germicidal Irradiation for Buildings: Formal Engineering Guidance on the way

By Forrest Fencl, president, UV Resources, Huntington Beach, Calif.

Hospitals are good examples of where dilution ventilation has limitations in reducing microbial contaminants; instead it’s become an energy concern. As infectious agents are “viable particles”, lessons learned from prescriptive spaces such as submarines, space stations and cleanrooms may provide researchers and practitioners with a focus on proven remediation of contaminated space air. One such treatment, ultraviolet germicidal irradiation (UVGI), has existed commercially since the 1930s, for lesser-known product and surface treatment.

Does UVGI kill all microbes?

Of interest, science has not uncovered a microorganism that’s resistant to the damaging effects of mechanically generated 254 nm germicidal UV energy, including the superbugs mentioned here. Another building type suffering from similar drug-resistant pathogens are the nation’s jails and prisons. Here, ventilation strategies that include air filtration, UVGI (both in-duct and upper air) and space pressure differential relationships have proved significant in the reduction of cross-infection rates.

What’s the best approach for hospitals?

Three methods of applying UV-C significantly reduce troublesome microbes and their resulting nosocomial effects in healthcare venues. All can be applied in any or all space applications.

A reservoir and therefore source of fungi occurs in any air handling unit where various species proliferate on damp coils and in drain pans and then disperse throughout the air conveyance system infecting immuno-compromised persons. UV-C lamps placed downstream of the coil bathe it, the drain pans and plenum surfaces to drastically reduce their numbers. Fungi sources that remain are found in return and makeup air where air filtration and coils arrest nearly 99% of them. However, the reservoir is gone.

Other airborne pathogens result from transient, un-typed persons occupying waiting rooms. Contagions transfer from occupant to occupant and to the return, to be circulated (spread) to other patient areas where immune-deficient individuals may be confined for potentially unrelated care. Here, upper air UVGI systems are the most effective at inactivating the greater number of these particles.

Patient-sourced and drug-resistant superbugs are returned in various concentrations to the AHU, which carries them throughout the air conveyance system to all other spaces occupied by other patients and hospital personnel. AHU air filters can play a significant role in reducing concentrations of nosocomial pathogens. However, properly located UVGI in the AHU can kill or inactivate both airborne and surface microbes as well as those caught and exposed on filter media, thus drastically reducing their concentrations, and especially their viability when and if dispersed to any space.

Historically, engineers needing to apply UVGI lacked specific guidance for systems design, sizing and specification. ASHRAE recently undertook the process of approving UVGI as a required technology through the establishment of a standing technical committee. TC 2.9 was formed and the new committee is at work, among other things, writing a chapter for the 2008 Systems and Equipment handbook to address these very things.

UV-C technology at large

UV-C’s rising popularity beyond ASHRAE spawned research analogous to the technical committee’s goals by lesser publicized organizations such as the Air Purification Consortium (APC), the Air Cleaning Industry Expert Advisory Panel (ACIEAP) and The National Center for Energy Management and Building Technologies (NCEMBT). NCEMBT improves the efficiency, productivity and security of the U.S. building stock (no small challenge!). UV-C energy is crucial to achieving each of their goals, whether to save energy, reduce maintenance or to reduce absenteeism. Also, group members are involved in high-stakes projects such as Homeland Security where application methodologies of UVGI are crucial to preclude large scale destruction resulting from terrorist activities.

The worldwide UV organization is the International Ultraviolet Association (IUVA), whose key U.S. members are the same highly qualified participants noted before, each with their unique area of expertise. Prior to the creation of ASHRAE’s TC 2.9, IUVA started an aggressive program of producing draft Standards and Guidelines for UVGI that included Air and Surface Disinfection, Testing and Commissioning of In-Duct Air Treatment Systems, Installation of Air Disinfection Systems (New Building Construction) and In-Duct Air Disinfection Systems. With ASHRAE covering these same areas, IUVA has stopped its efforts for now. In either case, Standards, Guidelines and under-written independent testing and verification is moving faster than other HVAC technologies of recent history.

Not covered here are other known microbial pathways such as lobbies, elevators, elevator shafts, stairwells, laundry chutes, and emergency entrances and corridors. However, they too can be effectively and affordably treated with UVGI. As the efforts of ASHRAE, IUVA and other organizations promulgate their standards and guidelines, UVGI application will increase, which does not bode well for superbugs anywhere.

Suggested Reading on Superbug Control

By Michael G. Ivanovich, Editor-in-Chief

While reading this article on superbugs, you probably have been wondering how to kill them. Designing infection control systems for hospitals requires integrating HVAC and air-pressure-control systems with dedicated infection-control systems, and minimizing unplanned airflows through building envelopes and interior spaces. It can also mean, as Forest Fencl describes in his sidebar on p. 34, applying ultraviolet germicidal lights. To help engineers research and apply infection-control systems, engineers can obtain the documents below as a starting point, and look to future articles in CSE .

Design guides

“Guideline for Hand Hygiene in Health-Care Settings,” Centers for Disease Control Mobidity and Morality Weekly Report, 25 Oct. 2002: 1-44.

“Guidelines for design and construction of hospital and health care facilities,” American Institute of Architects (2006) Available at

“Guidelines for Environmental Infection Control in Health Care Facilities,” Centers for Disease Control (2003) Available at

“HVAC design manual for hospitals and clinics,” American Societyof Heating, Refrigerating and Air-Conditioning Engineers. (2003) Available at

Technical articles

Fencl, Forrest B. “UVC Energy: How Does It Work?” HPAC Engineering (2007) Available at

Kowalski, W. “Air-Treatment Systems for Controlling Hospital- Acquired Infections,” HPAC Engineering (2007).

Streifel, Andrew J. “Pressure Management in Health-Care Facilities,” HPAC Engineering (2006).

Miscellaneous

Hayden II, Charles S., G. Scott Earnest and Paul A. Jensen, “Devel- opment of an Empirical Model to Aid in Designing Airborne Infection Isolation Rooms,” Journal of Occupational and Environmental Hygiene (2007).

March, David. “’Superbug’ Outside Hospital Poses Risk to Caregiv- ers Inside,” The JHU Gazette 18 Sept. 2006. Available at

Miller, Shelly, et. al. “Efficacy of Ultraviolet Irradiation in Controlling the Spread of Tuberculosis,” Centers for Disease Control and the National Institute for Occupational Safety and Health 19 Oct. 2002. Available at

Saravia, Stefan A., Peter C. Raynor and Andrew J. Streifel, “A perfor- mance assessment of airborne infection isolation rooms,” American Journal of Infection Control 35.5 (2007): 324-331.

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