Wing Hong Seto
Wilina Lim
Introduction
Acute respiratory viral infections are frequent causes of hospital admission, and nosocomial clusters of these diseases are frequent occurrences. Despite the large number of viruses causing these infections and the large number of admissions with such infections, the size of the problem worldwide is not known. Determining the extent of this problem is complicated by the lack of laboratory diagnostic capabilities. However, in recent years, many hospitals have established rapid viral diagnosis capacity. At Queen Mary Hospital in Hong Kong, such capacity has existed since 1995. The number of viral laboratory diagnoses made at this 1,400-bed teaching hospital in Hong Kong during 2003 to 2005 illustrates the magnitude of respiratory viral infections (Table 41-1). As shown, influenza and respiratory syncytial virus (RSV) account for the majority of positive specimens and together account for about 70%. The majority of these patients are children and in adults, many are elderly. It is obvious that the practice of infection control for these patients has its own particular challenges and demands.
This chapter is divided into two sections. The first section provides vital background information on the viruses as it pertains to infection control; the second covers the strategies for infection control.
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TABLE 41-1 |
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The Viruses
Although deaths from acute viral respiratory illness gradually decreased until they nearly ended in developed countries, morbidity associated with respiratory illness continues to be a major societal burden. The large number of infectious agents involved makes successful vaccination difficult and development with antivirals for treatment of these infections slow. Implementation of nonpharmaceutical intervention is essential to limit the spread of
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acute viral respiratory pathogens in hospital settings and community.
Most of the respiratory viral pathogens are subject to marked seasonal influence. Seasonality for a specific agent may be different for different regions, especially when the climates are different. Although the underlying mechanisms still remain largely unexplained, the seasonality for many infectious diseases is stable and well documented [1,2]. Knowledge of seasonal and cyclical variations in the incidence of diseases not only is useful in clinical management of patients but also is essential for the design and implementation of preventive strategies.
To devise effective infection control measures, it is essential to understand factors that affect the spread of respiratory virus pathogens, which include these:
Influenza
Influenza is a highly transmissible acute respiratory pathogen that can spread rapidly causing local outbreaks or widespread epidemics. It begins with sudden onset of fever with sore throat, dry cough, headache, myalgia, and malaise. The clinical presentation of the infection ranges from asymptomatic infection or mild pharyngitis to pneumonia with fatal outcome. All age groups are at risk for infection with infants and children having the highest infection rates. Infection can be life threatening in the elderly and patients with predisposing heart and chronic chest disease.
Influenza viruses belong to the family Orthomyxoviridae. They are divided into types A, B, and C. Influenza A virus gives rise to pandemics. The virus contains 8 segments of RNA corresponding to genes of the virus. The surface of the virus particle has H and N proteins. In influenza virus A, there are 16 subtypes of H and 9 of N. Aquatic birds are the prime reservoir of all subtypes. Swine, horses, and seals also can be infected with influenza virus. Variation occurs frequently in the genes of the influenza viruses, leading to an unstable surface that alters constantly, evading existing human body defenses and causing epidemics and pandemics. The first type of variation occurs as a result of accumulation of point mutation in the H and N genes of surface proteins, called antigenic drift. This change is responsible for the interepidemic outbreaks. A radical change called antigenic shift occurs when genetic materials are swapped between two different strains infecting the same host. The new virus created has led to major pandemic strains, including the Asian flu H2N2 in 1957 and Hong Kong flu H3N2 in 1968. The Hong Kong flu virus in 1968 had two gene segments changed as compared to the H2N2 virus. The H3 and H2 surface protein differed in more than 60% of their amino acids. The conservation of the other surface protein, the neuraminidase, in the 1968 H3N2 virus may have provided some protection to the population, which had been exposed to H2N2 viruses, and this may explain the lower morbidity and mortality compared with the pandemic in 1957 [3].
The pandemic of 1918 was said to be the greatest medial holocaust on history; it killed more people in a few months than World War I did in four years and more people than anything else in history during the period of one year or less. It originated in the United States and spread to Europe, Africa, and Asia. Within a few cycles of infection, it was apparent that the disease had become more virulent with a 10-fold increase in the death rate among those infected. During the pandemic, it is estimated that 50% of the world population was infected with a total mortality >40–50 million. Deaths occurred mainly in the 20–40 year age group, which is distinct from the experience of all other recorded influenza epidemics. The pandemic was caused by an influenza A H1 virus that is closely related to the virus later found in pigs and that remains an infection of the species to the present time. Recent analysis of lung samples obtained from patients who died from the disease in 1918 shows that the virus appeared to be transmitted unchanged from avian source to humans [4].
The pandemic of Hong Kong flu in 1968 began in China in July, spread to Hong Kong in the same month, reached its maximum intensity in 2 weeks, and lasted some 6 weeks in total. About 15% of the population in Hong Kong was affected, but the mortality rate was low and the clinical symptoms were mild. The epidemic was quickly identified as having been caused by a new virus subtype, designated influenza A H3 [5]. The H3 gene was derived from gene swapping from avian source against which the population had no immunity. However, an antibody to this new virus was identified in blood collected before 1968 in elderly persons alive during the 1898 pandemics, suggesting the two pandemics were caused by related viruses [6].
Influenza is subject to marked seasonal influence and usually has predilection for the winter in temperate climates [7,8]. In the subtropics and tropics, influenza can occur throughout the year, but an increase of influenza is generally observed in late winter/early spring and in the tropics again in the summer months or during the rainy seasons [9,10]. The magnitude of seasonal variation is unpredictable, depending on virus characteristics and herd immunity (Figure 41-1).
Depending on the size of the infecting dose, the incubation period is from 24 to 96 hours. [11]. Viral shedding begins 1 day before the illness onset and continues for 3 to 5 days in adults, with longer periods in persons with severe illness and children [12].
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Avian Influenza
Avian influenza viruses do not normally infect species other than birds. The first documented influenza A (H5N1) infection in humans occurred in Hong Kong in 1997 with six deaths among 18 reported cases, coinciding with outbreaks among poultry [13]. In February 2003, H5N1 infection again was diagnosed in a father and son who returned from Fujian province China [14]. With unprecedented outbreaks of H5N1 among poultry reported in Southeast Asia and human H5N1 infections starting at the end of 2003 [15], as of June 2006, 224 human infections with H5N1 virus had been confirmed in 10 countries with 127 deaths. So far, transmission of virus from avian to humans appears very inefficient and sustained transmission from human-to-human has not occurred. Human disease caused by H5N1 influenza virus typically presents as a rapidly progressing viral pneumonia, often with evidence of marked lymphopenia, leucopenia, and mild to moderate liver dysfunction. The disease may progress to acute respiratory distress syndrome, multiple organ dysfunction, and death. Evidence is consistent with bird-to-human, possibly environment-to-human and limited, nonsustained human-to-human transmission [16].
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Figure 41-1 Influenza Virus Isolates, Government Virus Unit, Hong Kong, 1991–2003. |
As with other enveloped respiratory viruses, influenza viruses could be easily inactivated by heating to 56°C lipid solvents or oxidizing agents [17].
Respiratory Syncytial Virus
RSV is the most important respiratory pathogen in childhood; it is responsible for bronchiolitis and pneumonia in infancy throughout the world. Outbreaks of lower respiratory tract disease in nursing homes and institutions for disabled persons have been reported.
RSV belongs to the family Paramyxoviridae and is classified in the genus Pneumovirus. It is an RNA virus with a lipo-protein coat. RSV is a major cause of healthcare-associated infection (HAI) and a particular hazard for premature infants, infants with congenital cardiac and lung disease, and immunodeficient infants, children, and adults. It has been estimated that about 50% of infants will acquire RSV infection during their first year of exposure. Severe RSV disease that requires hospitalization occurs approximately 30% more often among male infants than among female infants. The rate of HAI for infants and children during an RSV season has been reported to range from 26 to 47% in newborn units and for 20–40% for older children [18]. In temperate climates, RSV epidemics occur in late fall, winter, or early spring but are absent during the summer. In contrast, high RSV disease rates occur annually in spring and summer in tropical Hong Kong. The number of RSV isolates begins to rise in March, peaks sharply in April, and remains at a considerably high level until September. Of RSV isolates, 90% are from children under 2 years of age [19].
The incubation period is approximately 5 days, and the illness lasts for 5 days. Patients infected with RSV shed large amounts of virus in their respiratory secretions with a duration of shedding ranging from 1 to 21 days [18]. Virus shedding correlates with severity of disease, and virus transmission has been documented to occur most commonly through contact with infected droplets or fomites. Hospital staff spread the virus by touching secretions or contaminated objects while caring for infected infants. RSV can survive for up to 6 hours on environmental surfaces but can easily be inactivated with alcohol, detergent, or oxidizing agents [20].
Parainfluenza
Human parainfluenza viruses (HPIVs) are common respiratory tract pathogens that can infect persons of any age. They are enveloped RNA viruses with four genetically and
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antigenically different types, HPIV type 1 to 4 (HPIV1 to 4). HPIV1 and HPIV3 belong to the genus Respirovirus within the family Paramyxovirus, whereas HPIV2 and HPIV4 belong to the genus Rubulavirus. HPIV1 is the principal cause of croup; HPIV3 causes bronchiolitis and pneumonia in infants. HPIV1, 2, and 3 may cause lower respiratory tract infections in young children and immunocompromised hosts, and upper respiratory tract infections in older children and adults [21]. In particular, HPIV1 and HPIV3 have been identified as important causes of outbreaks of respiratory tract infections, especially in institutional settings [22]. In contrast, HPIV4 has been regarded as less clinically important and associated with milder respiratory illness and has rarely been reported to cause major outbreaks of respiratory tract infection.
Parainfluenza viruses can be isolated worldwide throughout the year in temperate and tropical climates [23]. In tropical climates of Hong Kong, these viruses are recovered throughout the year with increased incidence in the winter [24]. This is particularly so for HPIV 1. Interestingly, this also holds true for the incidence of HPIV 3, which is in contrast to the reports from the temperate zone for this virus. In temperate climates, the predilection for diseases by HPIV 1 and 2 is the autumn or winter and for HPIV 3 diseases for the spring or summer [1,23,25]. In some countries, there is evidence of mutual exclusion for HPIV 1 and 2 on the one hand and HPIV 3 on the other [23,24].
HPIV has an incubation period ranging from 3–6 days. The virus can be excreted for 3–10 days following primary infection. It is transmitted through respiratory droplets or person-to-person contact. The virus remains viable on surfaces for several hours and in aerosols for 1 hour. It is readily inactivated by heat, detergents, or oxidizing agents [25].
Respiratory Adenovirus Diseases
Human adenoviruses belong to the family Adenoviridae. They are double-stranded, non-enveloped DNA viruses. Adenoviruses cause upper respiratory illnesses including common colds, pharyngitis, and tonsillitis and occur mainly in infants and young children. They are mainly associated with adenovirus types 1 through 7. Severe pneumonia occurs in infants and children. Outbreaks of pharyngo-conjunctival fever in children associated with swimming pools and acute respiratory illness among military recruits have been reported.
Adenoviruses are circulating worldwide around the year. Adenoviruses causing respiratory tract disease are recovered throughout the year in tropical climates of Hong Kong with adenovirus 3 being the most commonly isolated serotype. Decreased incidence is noted in this region in the months of August, September, and October. In moderate climates, the so-called endemic adenoviruses (types 1, 2, 5, and 6) can be detected year-round [26]. In contrast, some marked seasonal prevalence has been reported for the epidemic adenoviruses 3, 4, or 7. For instance, in the 1960s, the highest rates of respiratory adenovirus disease among military recruits in the United States, usually caused by these epidemic adenoviruses, were found in winter and spring. In other countries, however, adenoviruses 3 and 7 epidemics have been described to be most frequent in summer [1,26,27].
The incubation period ranges from 6–9 days, and the virus is first excreted from the respiratory tract. Then it disappears from this site but is found intermittently in fecal specimens for an extended period. The virus can survive for a long time in the environment. It is resistant to detergents and lipid solvents but can be inactivated by heat and oxidizing agents. The mode of transmission is primarily through respiratory droplets or direct hand contacts.
Rhinovirus Disease (Common Cold)
Rhinoviruses belong to the family Picornaviridae. They are non-enveloped RNA viruses that cause a typical common cold characterized by rhinorrhea, nasal obstruction, sneezing, pharyngeal discomfort, and cough. Symptoms last from 5 to 7 days. In asthmatic, bronchitic, or immunocompromised individuals, illness may exacerbate asthma or bronchitis or cause lower respiratory tract infection. More than 100 serotypes of rhinovirus cause the common cold. In temperate climates, rhinovirus disease peaks in early autumn (September) and spring [28,29]. After September, the incidence decreases but remains fairly high until the end of the winter and in spring and summer [de Jong, unpublished]. In the tropics, rhinovirus infection coincides with the rainy season in May and June and ends in November and December. Prevalent serotypes change from year to year with multiple serotypes circulating in a given area at any time.
The incubation period of rhinovirus infection is 2–3 days with peak virus shedding coinciding with the acute rhinitis on day 3. The virus can be isolated from 1 day before to 6 days after the onset of cold symptoms. Rhinovirus is present in highest titers in the nose of infected persons and constantly contaminates their hands and the environment. Close personal contact appears necessary for the virus to spread effectively from an infected to susceptible person. In experiments, virus shedding peaked on the third day and fell to low level detectable for up to two weeks [28]. Rhinoviruses are transmitted by direct hand contacts or by large droplets. The rhinovirus is not inactivated by lipid solvents, alcohols, or phenolics but is easily inactivated by heat or oxidizing agents.
Human Metapneumovirus (HMPV)
HMPV is a recently discovered respiratory pathogen of the family Paramyxoviridae belonging to the subfamily Pneumovirinae. Clinical features associated with HMPV were found to be similar to those of RSV. Clinical symptoms from HMPV-infected children have included nonproductive cough, nasal congestion, wheezing, bronchiolitis, and pneumonia. There is evidence of HMPV infection in
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approximately 2.2% of patients with influenza-like illness that are negative for RSV and influenza [30]. Studies have found that HMPV-infected children are significantly older (median age 11.5 months) than RSV-positive children (median age 3 months) [34]. Seroepidemiologic data in the Netherlands showed that all children are seropositive for HMPV antibody by 10 years of age [31]. Much like RSV, previous studies, all from temperate regions, have reported HMPV to be a virus with a winter–spring seasonality while in the tropical region such as in Hong Kong, HMPV virus activity is detected in the spring and summer months [32]. There are no clinical data on incubation period, virus shedding, and documented routes of transmission, although HPMV is thought to be transmitted like RSV through contacts and respiratory droplets.
“Classical” Coronavirus Diseases
Human coronaviruses are enveloped RNA viruses of the coronaviridae virus family that cause a cold-like respiratory illness indistinguishable from those caused by other types of respiratory viruses. Coronavirus diagnostics of the “classical” human coronavirus types 229E and OC43 have not often been included in studies of respiratory virus diseases. These viruses were shown to be responsible for up to one-third of common colds [33]. In the United States, France, and Finland, isolation and antibody titre increases are rarely reported outside the period from December through May [34,35]. In children, two peaks of disease in late autumn to early winter and early summer were detected [36]. In the United States, outbreaks of type 229E follow a 2–4-year cycle and outbreaks due to type OC43 occur every other year when the incidence of 229E is low [36]. Rarely do sizeable epidemics of types 229E and OC43 occur in the same year, indicating a seasonal interference phenomenon similar to that observed with HPIVs.
All age groups are susceptible to infection. The incubation period ranges from 2–4 days. Virus shedding lasts for 1–4 days after onset of illness. Classical coronaviruses may be transmitted by droplet nuclei and large-droplet aerosol [37]. Studies show that coronavirus 229E can survive for 3 hours after drying on three different surfaces—aluminum, cotton gauze sponges, and latex gloves—but coronavirus OC 43 survived 1 hour or less [37].
Severe Acute Respiratory Syndrome (SARS)
A novel coronavirus identified as the putative cause of SARS in March 2003 was named as SARS-associated coronavirus (SARS-CoV) [38]. The incubation period ranges from 4–5 days. The primary mode of transmission of SARS appeared to be direct mucus membrane contact with infectious droplets and through exposure to fomites. The rate and quantity of viral shedding is low in the initial few days of the illness but rises significantly after 6 days to peak at 6–14 days after onset of illness. Maximal viral shedding occurred earlier (6–11 days) in respiratory secretions than in feces (9–14 days) but declined more rapidly. This pattern in which maximal viral shedding occurs at the onset of symptoms has not been seen for any other respiratory virus. Because maximal virus shedding appears to reach a maximum 6–14 days after onset, hospital workers are particularly prone to infection because most SARS patients are hospitalized. Because patients are unlikely to be highly infectious in the first few days of illness, early and simple isolation measures including home quarantine likely would be effective. This very characteristic might have played an important part in the eventual containment of the worldwide SARS outbreak because the most infectious patients would have been hospitalized and isolated [39].
Studies demonstrated that SARS-CoV contaminates a variety of environmental surfaces in healthcare settings [40]. Surfaces can become contaminated by indirect transfer of SARS-CoV through gloves and gowns. Transmission efficiency appears to be greatest from severely ill patients or those experiencing rapid clinical deterioration, usually during the second week of illness. SARS-CoV can survive in respiratory samples for 5 days at room temperature and up to 3 weeks at 4°C. In diarrheal stool, SARS-CoV can survive for a few days at room temperature [41]. With a high virus load at a concentration of 106 TCID50 / ml of SARS-CoV, it is notable that fecal droplets containing SARS-CoV remained infectious for 4–5 days. Common disinfectants used in hospital and laboratory settings had been generally found to be effective in virus inactivation [41,42]. Ordinary household detergent, hypochlorite solution, and peroxygen compound at concentrations normally used in the laboratory have been shown to inactivate SARS-CoV within 5 minutes [41].
Obviously, no seasonal pattern can be inferred for SARS at present. It is possible only to compare the dates of the reported detections of the illness with the seasonality of classical coronavirus disease. The first case of SARS was recorded in November 2002 in Guangdong province in China, where the outbreak peaked in February 2003 and disappeared in May 2003. In Hong Kong, the syndrome was first detected in February 2003, outbreaks occurred in March, diminished in magnitude in April, and disappeared by June 2003. These observations are compatible with a seasonal pattern similar to that of the classical coronavirus disease described previously. If so, there is the interesting possibility of seasonal interference between SARS-CoV and the classical coronaviruses, similar to that observed with the HPIVs 1–3 and the classical coronaviruses 229E and OC43.
Strategies for Infection Control
Understanding the Modes of Transmission
In developing effective strategies for infection control, it is critical to understand the mode of transmission of these pathogens. Because these pathogens infect the lungs and
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the virus can be dissimilated into the air by coughing, it was assumed that the primary route of transmission was airborne. It is evident now that this is not the case. An infected person's cough would produce large droplets of >5µ, because the lungs would be highly congested with fluid, and these large droplets would generally fall to the ground within 1 meter of the patient [43]. Consequently, infection control precautions are necessary only when the healthcare worker comes within 1 meter of the patient. This is the theoretical concept behind the recommendations under “droplet precautions,” which will be discussed later.
Some of these respiratory viral diseases (e.g., RSV, HPIVs, and Adenoviruses) emit a vast amount of viral particles in their secretions. These could result in extensive contamination of the patients' environment, and infection control precautions would have to extend beyond the 1 meter perimeter [43]. The isolation measures for these pathogens is designated “contact precautions,” which will also be discussed later. Nevertheless, the patient generally does not cough out droplets nuclei of <5µ, and, therefore, infectious material is not disseminated for a long distance through the air. Thus, “airborne precautions” are generally not necessary. There are no precise clinical data on transmission of HMPV, but because of its similarity to RSV [44], general consideration is that “contact precautions” are required for infections caused by this agent [32,45].
Presently, none of these acute respiratory viral pathogens is classified as airborne and, as listed in the guideline of the Centers for Disease Control and Prevention (CDC), airborne infections only include pulmonary tuberculosis, varicella, and measles [43]. This fact is important because it means that none of these acute respiratory viral infections requires isolation in a negative pressure isolation room, which often is available only in limited numbers in any hospital. However, it should be noted that these respiratory virus infections may spread by the airborne route under special circumstances described as “opportunistic airborne infections” by Roy et al. [47]. They also stressed that such diseases do not require “airborne infection isolation.” Rather, one should be alert to those special circumstances in which airborne transmission may be possible and, as in SARS, special precautions such as wearing an N95 respirator are already mandated for high-risk procedures.
Infection Control Measures
The general principles in the infection control measures for these diseases will be discussed together, but special attention will be given to influenzae, avian influenza, and SARS because of the many current issues relate to these diseases.
General Measures
Guidelines for the prevention of transmission of acute respiratory viruses in the hospital are available and should be consulted [47]. The details will not be repeated here, but the key elements will be emphasized.
The key infection control measures that are generally needed for all respiratory viral agents include rigorous hand hygiene, standard precautions, and “cough etiquette.” Hand hygiene is extremely important, and every hospital should implement the WHO hand-hygiene guidelines [48]. Data show that the alcohol hand rubs are effective against all respiratory viruses. Standard precautions are the measures adopted for all patients to reduce the risk of blood borne pathogen transmission [43]. For respiratory viral infections, it is particularly important as part of standard precautions that healthcare workers use a surgical mask and eye protection when there is significant risk of contamination from patients with cough. “Cough etiquette” is a measure to contain respiratory secretions from patients with cough [47]. Such patients should be provided with tissues to cover their mouth and nose while coughing. An alternative is to provide ample surgical masks for the patients.
A key element of all of these measures is to obtain compliance from staff and patients. Therefore, staff and patient education must be conducted at all times.
Specific Measures
Specific measures vary, depending on the pathogen (Table 41-2).
Surveillance is extremely useful so that hospitals are alerted to outbreaks circulating in the community. This is helpful for early diagnosis and isolation of patients. A system to alert infection control personnel when there are ≥3 patients with influenzalike illnesses from a single ward also is extremely useful. Immediate assessment of the possibility of an outbreak should be initiated, and early isolation or discharge of patients can be undertaken [47].
Appropriate isolation precautions are discussed in another chapter. The two main precautions for acute viral respiratory infections are droplets precautions and contact precautions. It is important to stress that standard precautions and strict hand hygiene are integral parts of all of these precautions.
The key element of droplets precautions is wearing a surgical mask whenever healthcare workers come within 1 meter of the patient; for contact precautions, the CDC guideline recommends wearing a gown and gloves on entering the patient's room [43]. In the context of respiratory infections, there are variations in the practice of contact precautions, and many hospitals recommend that staff wear a surgical mask, gloves, and a gown only when performing patient care.
The availability of rapid viral diagnosis can be of great help to ward staff and the infection control team. At Queen Mary Hospital, the initiation of such a service has been cost effective [49].
Quarantine is an infection control measure recommended for some severe infectious diseases, but it should be noted that there is no such recommendation in any
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guidelines for the present list of acute viral respiratory infections [43]. Quarantine involves the segregation of healthy contacts and was the policy regarding SARS in many countries. Such a drastic measure for SARS was basically carried out for the sake of caution, but the present evidence certainly does not support the need for quarantine. Subclinical infection is virtually nonexistent [51], and even mildly symptomatic patients have not been reported [51]. Furthermore, asymptomatic carriers of the virus have not been identified, and it has been reported that SARS almost exclusively manifests as a florid clinical syndrome [51]. It has been documented that the viral load reaches its peak only in the second week of illness and that transmissibility of the SARS-CoV in the early phase of disease is relatively low [52].
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TABLE 41-2 |
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Special Cohorting Precautions
Cohorting is the process of isolating patients with the same diagnosis in the same isolation room. Because significant surge of these viral infections occurs especially in the winter months, cohorting often is necessary.
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However, many hospitals often have the problem of having large numbers of patients with respiratory syndromes severe enough for admission, especially among pediatric patients, with insufficient isolation capacity. A possible solution that is practiced in Queen Mary Hospital is to put all of these patients on droplets precautions until there is a clear diagnosis. The steps needed are relatively simple. They include ensuring that all beds are at least 1 meter apart and having healthcare workers wear masks whenever they are within 1 meter of the patient. Patients are advised not to leave their beds without permission, and the common play area commonly seen in pediatric wards is eliminated. Furthermore, there is no sharing of specific patient care equipment, such as stethoscopes, and patient medical records are not placed by the bedside but at the nursing station. When a diagnosis is established, infected patients are taken from this area and placed under the appropriate precautions in the isolation unit. Such cohorting of respiratory illnesses in the pediatric units has been shown to successfully reduce nosocomial respiratory viral infections [53,54]. Similar surges may also be encountered in adults and perhaps such measures may also be adapted with care. However, when toilets are shared, it is important to ensure proper disinfection and adequate hand hygiene after use.
Influenzae
Controversy surrounds the mode of transmission of Influenza, especially with an outbreak report suggesting that it could be airborne [56]. However, recent reviews suggest that the basic mode of transmission is still considered to be droplets [56,57,58]. Presently, influenzae listed in the CDC guidelines requires droplets precautions [43], and, similarly, the World Health Organization (WHO) recommends that standard precautions and droplet precautions suffice for patients infected with Influenza [59]. However, in a new WHO guideline, both “droplets” and “contact precautions” are recommended [73].
Annual vaccination with trivalent inactivated vaccine is the primary means of prevention and control of seasonal influenza. Antiviral drugs, the amantadine and neuraminidase inhibitors, have been used for chemoprophylaxis of influenza.
There are two main types of attenuated vaccine, namely the inactivated and the live. The CDC recently published its recommendations for influenza prophylaxis [61] and for vaccination of healthcare workers [61]. CDC now recommends that all healthcare workers be vaccinated for influenza unless there are medical contraindications. However, this policy must be taken with caution from an international perspective because in some countries, the mortality for influenzae is not as high as that in the United States. At Queen Mary Hospital, there were only three deaths from influenza from 2003 to 2005 (Table 41-1). Presently, the hospital recommends vaccines for healthcare workers caring for patients in high-risk groups (Table 41-2).
Chemoprophylaxis may be appropriate in certain persons such as those who cannot tolerate the vaccine as in persons with hypersensitivity. Antivirals also can be used if immediate protection is needed because the vaccine requires about 2 weeks before antibodies develop. These agents are especially useful when there is a there is a rapidly growing outbreak in a long-term care facility [62].
The dosages of the drugs for Chemoprophylaxis [60] follow:
Avian Influenzae
The WHO has published its interim guideline for infection control measures for avian influenza (AI) [59]. It is a comprehensive guideline that covers many aspects of AI. It is important to point out that the general consensus regarding AI mode of transmission is via droplets. Furthermore, studies had shown that human-to-human spread is possible but a rare event [59]. However, on the side of caution, the WHO has recommended that wherever possible, if facilities are available, airborne precautions may be adopted in view of the high mortality reported and the fact that presently, the number of cases is limited [59]. It should be emphasized, however, that the evidence supports droplets as the mode of transmission, and in practice, droplets precautions should suffice.
The first community outbreak of AI was reported in Hong Kong in 1997 [13] and was successfully controlled with no hospital clusters reported. As an example of how AI can be managed in the hospital, the present protocols for Hong Kong public hospitals are reported in Table 41-3.
Severe Acute Respiratory Syndrome (SARS)
When SARS was first reported, the emotional response was intense and widespread. This is understandable, because it was a new disease with more than 1,700 healthcare workers infected. Nevertheless, this was not the optimal environment for objective information collection and rational precaution determination. Now there has been ample time for proper evaluation of the evidence resulting from that outbreak.
Studies conducted in Hong Kong clearly demonstrated that infection control measures are effective. A case-control study on staff providing direct patient care to 11 proven SARS patients has been reported, comparing the infection control precautions of the 241 noninfected staff with
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the 13 infected staff [64]. Four specific measures were specifically studied: (1) the washing of hands and the wearing of (2) masks, (3) gowns, and (4) gloves. The results showed that if proper droplet and contact precautions were undertaken by the staff, as recommended in the CDC guidelines [43], they would be significantly protected. None of the 69 staff reporting the practice of all four measures was infected. In contrast, all 13 infected staff who omitted at least one of the measures (ρ < 0.0224 Fisher's two-tailed) became infected [64].
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TABLE 41-3 |
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Although standard infection control measures will prevent transmission of SARS-CoV, the correct practices must be inculcated in a properly organized program for the entire hospital. The SARS outbreak in Hong Kong ultimately infected 405 healthcare workers [51], or 23% of the 1,755 cases. However, at Queen Mary Hospital, only two nurses were infected, and no definite nosocomial infections were reported among patients. Hospital personnel participated fully in the care of SARS patients, admitting a total of 704 patients to the cohort wards during the outbreak period of which at least 52 patients were confirmed cases of SARS. The strategy and infection program for the control of SARS at Queen Mary Hospital have been described elsewhere [65,66] and will not be repeated in this chapter. Nevertheless, the salient strategic features of the program are summarized in Table 41-4. This approach may be a model for others to incorporate into their hospital policy.
Can SARS Be Airborne?
There is much controversy in the literature regarding the transmission of SARS-CoV, and it would be worthwhile to review the scientific data pertaining to airborne transmission of SARS-CoV and to assess the weight of the evidence. There are basically two research studies on this subject published in the reference literature.
The first is a Hong Kong study by Yu et al. [67] that used computerized fluid dynamics modeling to show that SARS-CoV could be transmitted by the airborne route in the Amoy Garden outbreak. It was an elegant study but is basically a simulation, and the level of evidence is not comparable to actual epidemiological comparative studies involving real patients with concomitant controls. The authors correctly point out in their conclusions that their study only “supports the probability of an airborne spread of SARS in the outbreak in Amoy Gardens.”
In an editorial regarding the article by Yu et al., Roy et al. [46] stated that “Hydraulic aerosol experiments combined with aerosol and epidemiologic modeling clearly implicated airborne transmission within the apartment complex.” However this “should not be considered to represent evidence that airborne infections necessarily cause explosive outbreaks.”
It is important to note that Roy et al. also stated that airborne transmission should be classified into
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obligate, preferential, and opportunistic [46] categories. Obligates are those that under natural conditions spread by the airborne route. Preferentials are those that only predominately spread by air but can also spread through the other routes. Finally, the opportunistics are those that naturally spread by nonairborne routes but under certain special environmental conditions may spread by the airborne route: Roy et al. allocated “SARS to be opportunistically airborne transmission.”
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TABLE 41-4 |
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The second study is by Booth at al. [68] who had taken air samples in isolation rooms of SARS patients in Toronto. It should be noted that only 1 sample of 10 was positive initially and the other two were detected only after 100-fold concentration. The samples also were positive only by polymerase chain reaction (PCR) indicating viral nucleic material but all cultures were negative, indicating that they are not viable virus able to cause disease. Another method of air sampling also was done in the study, but all 28 samples were negative. The authors rightly pointed out that the data simply “suggest that SARS-CoV could be an opportunistically airborne infection.”
In contrast, evidence that SARS-CoV is not airborne transmitted is rather substantial. Many reports indicate a lack of transmission in spite of unprotected extended exposures [69,70,71]. With the weight of evidence, the general consensus is that SARS-CoV simply does not behave like an airborne-transmitted pathogen.
References
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