In November 2002, the first case of severe acute respiratory syndrome (SARS) was reported in the Guangdong Province in China (Lau and Peiris, 2005). Over the next few months, SARS cases were reported in over two dozen countries in Asia, South America, Europe, and North America (CDC, 2004a). The biggest concentration of SARS cases appeared in Singapore, Hong Kong, Taiwan, and Canada (Totura and Baric, 2012). By July of 2003 the epidemic had been controlled through health measures. Overall, there were 8,096 confirmed SARS cases with a mortality rate of 9.6%.
SARS Etiology and Clinical Presentation
SARS is a respiratory disease caused by a coronavirus infection, a virus consisting of a protein capsule containing an RNA viral genome (Totura and Baric, 2012). Believed to transmissible between humans through respiratory aerosols and physical contact, the febrile disease initially presents with a cough and sore throat. These symptoms are consistent with the virus entry point being respiratory ciliated epithelial cells.
What distinguished SARS from seasonal influenza is that most patients developed pneumonia (CDC, 2004a) and approximately 25% progressed to acute respiratory distress syndrome (ARDS) (Totura and Baric, 2012). The elderly were most susceptible to developing ARDS (50%) and ARDS patients had a mortality rate over 50%. ARDS in SARS patients was characterized by pulmonary edema, severe hypoxia, an immune infiltrates in the lungs. Further worsening of the disease led to multiple organ failure and then death.
Using retrospective serological analysis, the first index SARS case was traced to an adult male in Foshan, just west of Guangzhou (Zhao, 2007). He was hospitalized on November 12, 2002 and had infected his wife and three other relatives. The first confirmed case of SARS was a chef working in Shenzhen and he was hospitalized on 15 December, 2002. As a result, seven hospital staff and one patient were infected. During the end of December and the beginning of January, atypical pneumonia cases sprang up throughout the Pearl River Delta surrounding the main city of Guangzhou. The SARS case map in the Pearl River Delta region between mid-November 2002 and mid-January 2003 does not indicate a clear spread pattern, but only isolated cases. However, it was clear that all cases were west of the capital city, Guangzhou, an area undergoing rapid economic development, including a blossoming trade in exotic animals.
Beginning about mid-January, the number of SARS cases increased 5-fold (Zhao, 2007). The relatives of infected individuals and hospital staff began to be infected at an alarming rate in China. A patient traveled to Hong Kong and stayed in a hotel, where it is believed he infected hotel guests and staff (Figure 1). This event is believed to be the primary one leading to the global spread of SARS to Singapore, Taiwan, Canada, and Europe.
COMMUNICABLE DISEASE/COMMUNITY NURSING
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Figure 1: Spread of SARS during 2003 Global Outbreak. Left Panel: the initial spread through the Pearl River Delta region to Hong Kong. Right Panel: Once SARS had arrived in Hong Kong, it then spread to Taiwan, Canada, Europe, and the rest of China.
Researchers retrospectively identified the likely zoonotic reservoirs of the disease by examining the epidemiological data of the infected individuals in the Guangzhou region (Zhao, 2007). The increasing affluence of the western Pearl River Delta region had fostered an increased in trade in exotic animals for pets and restaurant fare. Of the 10 independent index cases occurring in this region, at least six had handled animals. Serological tests of a number of animal species, including chickens, pigs, snakes, bats, monkey, ferret, rabbit, cats, and rats revealed no virus or were inconclusive; however, experiments with palm civets and raccoon dogs revealed that these species were very efficient in transmitting the disease through saliva. Retrospective testing of civet farm workers in the region revealed that 40-78% were seropositive for SARS. The implications of this result are that most individuals infected with SARS from wild animals remained asymptomatic.
The SARS genomic sequencing studies also revealed that the civet-derived virus was not very pathogenic, but once the virus has begun to replicate in human hosts, it quickly became virulent (Zhao, 2007). Once this pattern was revealed, the Chinese government instituted a permanent ban on wild animal markets in the Pearl River Region. This resulted in a dramatic decline in SARS seropositivity in animal and restaurant workers, from 25% in 2003 to 5% by mid-2004.
Based on the above epidemiological analysis, my community would not be the source of a future SARS outbreak because a wild animal market does not exist. However, given the global nature of travel in the modern world the threat of SARS in my community is not zero. SARS could emerge again in Asia or anywhere wild animals are handled. There are a number of zoos and wild animal parks across the United States that could be a source of SARS. While quarantine procedures and serological testing will probably prevent such an event from occurring, the smuggling of exotic animals in the United States does occur. Luckily, the virus needs time to adapt to a human host before it becomes virulent enough to cause severe disease and spread rapidly through human hosts. With the world now on guard against another SARS outbreak, the chances are increased that infected individuals will be tested and quarantined before the disease can spread.
Since researchers have shown that SARS infections resulting from human to human transmission are much more pathogenic than SARS infections from animal reservoirs, the Centers for Disease Control and Prevention (CDC) have established different reporting guidelines for each route of transmission (CDC, 2004b). The two reporting categories are atypical pneumonia in the absence of a SARS outbreak anywhere in the world and atypical pneumonia during a SARS outbreak somewhere in the world.
In the absence of a SARS outbreak anywhere in the world, patients with radiologically-confirmed cases of pneumonia or ARDS should be reported to health authorities as suspected SARS if they have certain risk factors. These risk factors include travel to China, Hong Kong, or Taiwan or close contact with anyone who has traveled to these locations within the last 10 days. Although no SARS cases have been reported in these locations since 2004, the banned wild animal market may have transitioned to a black market. Another risk factor is working in a profession with an increased risk of SARS exposure, such as healthcare workers and laboratory personnel doing research studies on the SARS virus. Finally, any patient in a geographic location where a cluster of undiagnosed atypical pneumonia has emerged should be considered a suspected SARS patient until proven otherwise. For example, two healthcare workers who develop atypical pneumonia in the same facility would represent a SARS cluster until laboratory tests proved otherwise.
Since the family in the vignette has confirmed SARS and a cluster of atypical pneumonia cases have emerged in the community, this would shift the reporting method to the second category. First, the hospitalized patients should be isolated and droplet control procedures implemented immediately (CDC, 2004b). Since the family members have confirmed SARS, the treating physician is required to immediately report the laboratory results to the state and local health agencies by telephone (CDC, 2004c). This will in turn trigger a response to confirm the SARS diagnosis, identify all persons who may have come into contact with the SARS patients in the last 10 days, and implement isolation procedures for confirmed and suspected SARS patients. The local and state health departments in turn will report this information to the CDC. Since a confirmed cluster of SARS cases has emerged, CDC guidelines require that the CDC be notified by telephone as well. The CDC will in turn notify the World Health Organization that a SARS outbreak has occurred in the United States.
Management of Respiratory Patients during Poor Air Quality Events
Outdoor air pollution represents a significant risk for premature death for all people, but during short-term increases in air pollution patients suffering from respiratory and cardiovascular disease will disproportionately visit emergency rooms and be admitted to hospitals due to respiratory and cardiovascular distress (reviewed by Abelsohn and Stieb, 2011). The primary outcome of increased air pollution levels for patients with asthma, chronic obstructive pulmonary disease, and heart disease, is an exacerbation of symptoms and increased mortality. The symptoms that can develop can include pulmonary inflammation, obstruction, infections, and allergic symptoms. For cardiovascular patients, heart rhythms, blood pressure, vascular tone, and clotting activity can be altered. Overall, these symptoms are consistent with an air pollution-induced increase in systemic inflammation.
The main pollutants of concern are ozone, particulate matter (< 2.5 ?m in diameter), and nitrogen oxides (reviewed by Abelsohn and Stieb, 2011). The main source of these pollutants is roadways, but the concentration of these pollutants drop off considerably after about 150 meters distance. Persons with respiratory and cardiovascular disease should therefore avoid spending time near roadways, especially during periods of elevated pollution levels.