INTRODUCTION — In February 2003, the World Health Organization (WHO) reported about 300 cases of a rapidly progressive respiratory illness in the Guangdong Province of China with five deaths. Over the next month, similar cases were reported from Hong Kong, Vietnam, Singapore, and Canada [1]. By the end of the worldwide outbreak in July 2003, a total of 8096 cases were reported, with 774 deaths and a case-fatality rate of 9.6 percent [2]. WHO termed the disease "severe acute respiratory syndrome" (SARS) and the identified case was a novel coronavirus termed SARS coronavirus (SARS-CoV). Once another novel coronavirus emerged in 2019 and was designated SARS-CoV-2, SARS-CoV became known as SARS-CoV-1.
No cases of SARS-CoV-1 have been reported since mid-2004. However, re-emergence of SARS and SARS-CoV-1 is theoretically possible, even in the presence of the Middle East respiratory syndrome coronavirus (MERS-CoV) and SARS-CoV-2, the cause of coronavirus disease 2019 (COVID-19).
The case definition, epidemiology, etiology, clinical manifestations, diagnosis, treatment, and prevention of SARS will be reviewed here. Coronaviruses, including MERS-CoV and SARS-CoV-2, are discussed in detail separately. (See "Coronaviruses" and "Middle East respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology" and "COVID-19: Epidemiology, virology, and prevention".)
CASE DEFINITIONS — During and in the immediate aftermath of the SARS epidemic, both the World Health Organization (WHO) and the United States Centers for Disease Control and Prevention (CDC) issued case definitions for SARS. The WHO definition was subsequently updated and notes that in the absence of current SARS activity in humans, laboratory confirmation using reliable and experienced laboratories, such as those at the WHO and the CDC, is a critical component of the case definition [3]. The updated WHO definition is outlined here for historical reasons and in the event of a re-emergence.
According to the WHO, a case of SARS is notifiable if it occurs in an individual with laboratory confirmation of infection who either meets the clinical case definition or has worked in a laboratory with live SARS coronavirus or with clinical specimens infected with SARS coronavirus [3].
The clinical case definition used by the WHO includes:
●A history of fever or documented fever and
●One or more symptoms of lower respiratory tract illness (cough, difficulty breathing, shortness of breath) and
●Radiographic evidence of lung infiltrates consistent with pneumonia or acute respiratory distress syndrome (ARDS) or autopsy findings consistent with the pathology of pneumonia or ARDS without an identifiable cause and
●No alternative diagnosis fully explaining the illness
Laboratory diagnostic tests that are required include one or both of the following:
●Detection of virus by an assay for viral RNA (reverse-transcriptase polymerase chain reaction) present in two separate samples or by virus culture from any clinical specimen. These two samples can be obtained from either two separate sites (eg, nasopharyngeal and stool) or from the same site but at different times (eg, sequential nasopharyngeal aspirates).
●Detection of antibody (a rise in antibody titer, either from negative to positive or at least a fourfold increase) by enzyme-linked immunosorbent assay and/or immunofluorescent assay.
EPIDEMIOLOGY — Cases of SARS were first noted in Guangdong Province, China, in November 2002. Between November 16, 2002, and February 28, 2003, 792 cases were reported in this province [4,5]. Healthcare workers and their contacts appeared to be disproportionately affected by the outbreak.
The index case for the illness in Hong Kong was a physician from Guangdong Province who traveled to Hong Kong five days after the onset of symptoms [6]. Other cases in Hong Kong developed in those with contact with the index or secondary cases, including individuals staying at the same hotel as the index patient. The index cases in Singapore, Thailand, Vietnam, and Canada were in travelers returning from Guangdong Province or Hong Kong.
The illness had many epidemiologic and clinical features of an infection, and early efforts to find an associated pathogen quickly centered around a new viral strain from the coronavirus family, first identified in February and March 2003 [7-9]. The virus spread rapidly from southern China and Hong Kong to Vietnam, Thailand, and Singapore, and then to Europe, Canada, and the United States.
Local epidemics in Hong Kong, Singapore, Toronto, and parts of China through March led the World Health Organization (WHO) and the United States Centers for Disease Control and Prevention (CDC) to issue several travel advisories on or around April 1, 2003. These were combined with extraordinary efforts at containment through application of infection-control practices, particularly in hospitals. By July 2003, no new cases were reported worldwide and the WHO lifted its last remaining travel advisory.
During the remainder of 2003 and the first half of 2004, four small outbreaks of SARS were documented following the apparent end of the epidemic. Three outbreaks were related to laboratory transmission of the epidemic virus, and one was presumably from contact with animal sources. Since mid-2004, no cases have been reported. (See 'Intermediate host and reservoir' below.)
Most illnesses occurred in adults [10]. Children 12 years or older had a clinical presentation similar to adults, whereas younger children had milder disease [11,12]. No fatal cases were reported among children.
Scope of outbreak — The 2002 to 2003 outbreak resulted in 8096 cases with 774 deaths and a case-fatality rate of 9.6 percent [2]. Older age was associated with a higher mortality rate, being as high as 43 percent in patients age 60 or older in Hong Kong compared with 13 percent in younger patients [13].
Cases of SARS occurred in 29 countries in Asia, Europe, and North America. China, including Hong Kong, had 83 percent of all cases. The United States had 27 probable cases with no secondary cases and no deaths. In Canada, mainly in Toronto, there were 251 cases (5 imported and the rest secondary) with 43 deaths [2].
The small outbreaks that followed the major SARS epidemic are of considerable interest as models of possible future SARS outbreaks [14]. Two outbreaks that presumably originated in laboratories working with the SARS coronavirus involved only a single case with no secondary spread [14,15]. In a third laboratory-based outbreak that occurred in China in April 2004, there were nine cases in three generations of contacts and one death [16]. A fourth outbreak, in December 2003 and January 2004, consisted of four relatively mild and epidemiologically separate cases, all in Guangdong Province in southern China, and all presumably from contact with infected animals, probably palm civets [14,17,18].
These small outbreaks illustrate several important principles:
●There must be strict control of laboratory strains.
●Laboratory strains, presumably because they represent strains that have been adapted to spread among humans, can cause outbreaks; in contrast, animal-derived strains are less likely to cause outbreaks without some period of adaptation.
●Control of possible animal intermediaries is important in preventing reemergence of SARS. Since 2004, China has banned all consumption of palm civets [19].
Intermediate host and reservoir — Animals eaten as exotic foods in southern China were probably intermediate hosts. The Chinese government launched an effort to kill palm civets, a cat-like creature considered a culinary delicacy in China that was sometimes infected by a coronavirus similar to the SARS coronavirus. A direct link between civets and SARS has not been confirmed, although molecular studies have suggested that SARS coronaviruses isolated early in the epidemic were closely related to palm civet coronaviruses [20-22].
Two studies demonstrated infection of a relatively high percentage of horseshoe bats (genus Rhinolophus) in China with viruses that have nucleotide sequences closely related to SARS [23,24]. In a later study, the genomes of two novel bat coronaviruses from horseshoe bats in China were sequenced and found to resemble SARS coronavirus more than any previously identified bat coronavirus [25]. In addition, two replicating bat coronaviruses, SARS-like coronaviruses WIV1 [25] and WIV16 [26], were isolated from Rhinolophus sinica feces in tissue culture. Both viruses use angiotensin-converting enzyme 2 (ACE2) from humans, civets, and Chinese horseshoe bats for cell entry; ACE2 is a functional receptor for SARS coronavirus. Studies of the sequences and functions of the receptor-binding region of the S gene, the open reading frame 3A, and the hypervariable open reading frame 8 have added further evidence of a close genetic relationship between certain Rhinolophus bat coronaviruses (particularly bats found through intensive study of a cave in Yunnan province of China) and the virus that caused the SARS epidemic [27,28]. These findings suggest that bats are likely to be an important reservoir for this virus. Moreover, coronaviruses resembling the SARS coronavirus, as well as others closely related to the Middle East respiratory syndrome coronavirus, have been found in bats on several continents outside Asia [29-32]. (See "Middle East respiratory syndrome coronavirus: Virology, pathogenesis, and epidemiology", section on 'Bats'.)
Transmission — Based upon the clusters of cases in Hong Kong and Canada, SARS coronavirus clearly spread from person to person and could be acquired from face-to-face contact, suggesting droplet spread [6,33-35]. Because of the rapid and extensive spread of SARS in Hong Kong, there has also been speculation that other dissemination modes, such as fecal-oral or airborne spread, might occur. Airborne spread is the most likely explanation for "superspreader" events, including the small outbreak that occurred on an aircraft [36] and, possibly, the large, explosive outbreak in Amoy Gardens and surrounding residential building complexes in Hong Kong [37,38]. Superspreaders are individuals who are responsible for a disproportionately large number of transmission events [39].
Transmission to healthcare workers has been a common feature of most SARS outbreaks. A possible contributing factor is that peak viral shedding in respiratory secretions, as determined by polymerase chain reaction (PCR), occurs 6 to 11 days following the onset of illness, at a time of severe respiratory symptoms [40,41]. This late viral excretion peak is unusual for a respiratory virus.
Fomites are another possible contributor to nosocomial transmission. SARS virus RNA is present in stool and was detected on a variety of hospital surfaces (eg, hospital bed tables, television remote controls, refrigerator doors) during outbreaks [33,42]. Fomites have also been implicated in an analysis of an outbreak of SARS aboard an airplane [43]. This emphasizes the need for strict surface hygiene practices.
Molecular epidemiology — It is likely that, after one or more instances of spread from animals to humans, the SARS coronavirus adapted through mutation, deletions, and possibly recombination, until it transmitted readily among humans. The virus that spread worldwide was derived primarily from a single infected individual who traveled from Guangdong Province to Hong Kong and infected numerous individuals in a superspreading event [44]. The virus that was epidemic in China and produced the majority of probable infections was more variable [19,45].
Incubation period — The incubation period for SARS is usually two to seven days [13]. Approximately 95 percent of patients will develop symptoms within 10 days [13]. Thus, after possible exposure, an individual should be monitored for the development of symptoms for at least 10 days. There is also an apparent association between more severe clinical manifestations and a shorter incubation period [46].
Prognostic features — Epidemiologic studies have identified a number of risk factors for poor outcomes in patients with SARS. These include:
●Older age [10,13,41]
●Diabetes, chronic hepatitis B, and other underlying comorbid conditions [10,41,47]
●Atypical presenting symptoms [10]
●Elevated serum lactate dehydrogenase on admission [10,48]
Relatively few infections and no deaths were reported in children or adolescents in a survey from Hong Kong [10].
ETIOLOGY — Early in the course of the investigations, it was suspected that SARS was a viral respiratory illness. A novel coronavirus was detected in specimens from a number of patients with SARS, and the virus was sequenced and fulfilled Koch's postulates, including causing severe respiratory disease in inoculated cynomolgus macaques [49-52]. Coronaviruses are usually agents of the common cold and generally do not cause severe respiratory disease. (See "Coronaviruses".)
Investigators at the United States Centers for Disease Control and Prevention identified a novel coronavirus in cell cultures inoculated with specimens from two patients in Thailand and Hong Kong [8]. At the same time, coronaviruses were isolated from index cases in Germany and Hong Kong [7,9]. Preliminary sequence analysis suggested that the viruses were similar and represented a previously undescribed coronavirus.
The SARS coronavirus genome has an organization similar to that of other coronaviruses [50]. It has been classified as a lineage B beta-coronavirus (with several bat coronaviruses) [53]. Through a variety of clinical, animal, and laboratory studies, the etiologic association between the SARS coronavirus and SARS has been clearly established [49].
PATHOGENESIS — Knowledge of the pathogenesis and immune responses to SARS coronavirus is limited. Autopsy studies of patients who died during the first 10 days of illness confirm that the lung is an early target [54]. Virus was consistently found in the lung and intestinal tract [8,9]. In fatal cases, virus was found in multiple organs, including the brain.
The adaptive immune system is probably critical to recovery from SARS, as demonstrated in experiments in mouse models [55]. It is also likely that the innate immune system, including the complement system [56], plays a role, both in defense against and in the pathogenesis of SARS. Genetic studies have pointed to the interleukin 12 receptor and the mannose-binding lectin as potential important first lines of defense [57,58].
Angiotensin-converting enzyme 2 (ACE2) and CD209L (L-SIGN) are functional receptors for SARS [59,60]. In an animal model, infection of ACE2 knockout mice led to recovery of low quantities of infectious virus compared with large amounts in the wild-type mice [61]. The authors of this report hypothesized that infection with SARS results in downregulation of ACE2 and subsequent lung pathology, since ACE2 has a key protective role in acute lung injury. Several cellular proteolytic enzyme systems also facilitate entry of virus into the cell [62,63].
CLINICAL MANIFESTATIONS
Signs and symptoms — SARS is an unusual respiratory viral disease since the prodrome is often somewhat prolonged, lasting for three to seven days, and is characterized by fever (temperature ≥100.5ºF [>38ºC]) malaise, headache, and myalgias [64]. Unlike virtually all other respiratory viral prodromes, most patients have no upper respiratory symptoms during this stage. At the end of this prodrome, the respiratory phase typically begins with a nonproductive cough. Dyspnea may follow and may progress to respiratory failure, with progressive pulmonary infiltrates on chest radiograph, necessitating mechanical ventilation.
A comprehensive review of the clinical manifestations associated with SARS summarizes data from 752 patients from mainland China (190 cases), Hong Kong (388 cases), Canada (154 cases), and Singapore (20 cases) [5]. The most common symptoms and signs on presentation to hospital were:
●Fever – 100 percent
●Cough – 66 percent
●Chills and/or rigors – 52 percent
●Myalgias – 49 percent
●Dyspnea – 46 percent
●Headache – 39 percent
Other less common symptoms were diarrhea (20 percent) and chest pain or pleurisy (22 percent). Sore throat and rhinorrhea were seen in 17 and 14 percent, respectively. Symptoms observed in 346 laboratory-proven cases in Taiwan were similar [65]. All respiratory symptoms (cough, dyspnea, pleuritic pain) became more common and severe as the disease progressed. Approximately 25 percent of patients required transfer to the intensive care unit (ICU), usually for mechanical ventilation [6,41,47,66-68]. Death was usually caused by a combination of adult respiratory distress syndrome and multiorgan failure.
Asymptomatic infection during the large SARS epidemic was infrequent, although animal handlers in southern China were found to have a high rate of antibody with no history of typical illness [45].
Laboratory findings — The most common laboratory abnormalities were depressed total lymphocytes (66 percent) and elevated lactate dehydrogenase (LDH; 46 percent) and alanine aminotransferase (44 percent) [5]. Thrombocytopenia was present in 30 percent, usually as the respiratory phase peaked. High LDH was associated with a poor outcome [10,48].
Imaging — Chest radiograph patterns ranged from normal to diffuse interstitial infiltrates characteristic of acute respiratory distress syndrome [69,70]. Bilateral peripheral infiltrates were common, usually in the middle or lower lung zones (image 1) [71].
Computed tomographic (CT) scanning can show parenchymal abnormalities in patients with apparently normal chest radiographs (image 2) [72]. Infiltrates are usually ground glass in character and peripheral in location.
Long-term follow-up pulmonary CT studies in SARS survivors demonstrate persistent abnormalities seven years after infection, with reticulation and interlobular thickening replacing ground-glass opacities in most subjects and mild to moderate changes in pulmonary function tests [73].
Pregnancy — Information about the effect of SARS on pregnant women and their fetuses is limited. Two reports from the same group at a hospital in Hong Kong suggested that pregnant women with SARS had a higher mortality rate and higher rates of both intubation and ICU admission than nonpregnant women with SARS but that transmission of the virus to the infant did not occur [74,75]. Complications, such as miscarriages, preterm deliveries, and small for gestational age neonates, were frequent.
PATHOLOGY — Diffuse alveolar damage with varying degrees of organization is seen on pathologic examination in patients with SARS who have acute lung injury [54,76]. Severe disease with lung injury is believed to reflect an excessive host response with production of large quantities of proinflammatory cytokines ("cytokine storm") [77]. Histologic features vary with the stage of disease:
●In the early phase, hyaline membranes, interstitial and intraalveolar edema, and vascular congestion are present.
●In the organizing phase, fibroblast proliferation occurs both in the interstitium and alveolar spaces.
●In the organizing phase, the majority of fibroblast proliferation occurs within alveolar septa.
DIAGNOSIS — During the 2002 to 2003 epidemic, the United States Centers for Disease Control and Prevention supplied reagents to laboratories in the United States to test for serum coronavirus antibodies from paired acute and convalescent samples from suspected cases. Because of justified concerns about false-positive diagnostic tests, the World Health Organization (WHO) requires that positive laboratory tests from suspected cases be repeated and confirmed in central WHO laboratories.
When SARS is suspected, specimens for polymerase chain reaction (PCR) testing should be obtained from at least two sites, such as the respiratory tract, stool, and serum or plasma. PCR testing should be performed as early in the illness as possible and, if symptoms progress or persist, be repeated five to seven days later. Acute and convalescent serum should also be collected for serologic testing. The results required to establish the diagnosis of SARS are discussed above. (See 'Case definitions' above.)
Serologic testing — Serum antibody, usually measured by enzyme-linked immunosorbent assay, is the most sensitive of available tests. However, antibodies typically develop several weeks into the illness, making serologic testing less useful for diagnosis during the acute phase. As an example, the mean time to seroconversion was 19 and 20 days in two series [41,78], and a small number of patients failed to develop antibody even later in the illness.
Due to the antigenic similarity among coronaviruses, antibodies to SARS coronavirus sometimes develop after other respiratory coronavirus infections [79,80]. Thus, serologic testing for SARS may give false-positive results.
Polymerase chain reaction — Reverse-transcriptase PCR (RT-PCR), including quantitative real-time RT-PCR, was performed on respiratory, stool, and serum or plasma samples in many patients with SARS, but no systematic study has been performed to determine the relative value of each type of specimen at various stages of illness.
The following findings have been observed:
●RT-PCR assays performed on samples obtained early in the illness had sensitivities as low as 50 percent [81,82]. Optimization using real-time PCR increased the sensitivity in some studies.
●The sensitivity of serum or plasma appears to be greatest early in the illness (between one and seven days after onset of fever) and diminishes markedly with time [83].
●Nasopharyngeal aspirates may, if all conditions are optimized, be sensitive at the time of admission to the hospital [84] but appear to be most sensitive at the time of peak respiratory symptoms, usually during the second week of illness [41,82]. In one study that included 75 patients, 32 percent had a positive RT-PCR assay three days following the onset of illness compared with 68 percent at day 14 [41].
●Stool samples remain PCR positive for the longest period, with 65 of 67 samples (97 percent) in one report being positive a mean of 14 days after illness onset [41].
●Both serum and respiratory virus titers as measured by real-time RT-PCR have been correlated with prognosis, with higher titers associated with worse prognosis [85].
TREATMENT — No specific treatment is recommended except for meticulous supportive care [86]. As with other viral infections, antibacterial agents are ineffective. In addition, no antiviral agents have been found to provide benefit for treating SARS. During the epidemic, most patients were treated with high-dose glucocorticoids and ribavirin, but most experts now agree that neither treatment had a clear beneficial effect, and immediate and late toxicities were common [87,88]. Lopinavir-ritonavir may have some activity against the virus in vitro, but its clinical efficacy has not been established [89]. Remdesivir (GS-5734), has in vitro activity against the SARS and MERS coronaviruses [90].
PREVENTION — Stringent infection-control practices are crucial for the prevention of SARS, since other modalities such as a vaccine and monoclonal antibodies remain in development.
Infection control — The control of SARS through the rigorous application of barrier methods represents one of the landmark accomplishments of infectious diseases epidemiology and public health coordination. One of the characteristics of the infection, namely the low contagiousness of patients during the prodrome, probably contributed to the success of control efforts, since patients could, in the outbreak situation, be identified and placed on precautions before they became most infectious to contacts. But the disappearance of SARS in July 2003, only nine months after it had first been detected, was a substantial international public health accomplishment. Isolation of patients, rigorous use of masks, gloves, and gowns, closure of schools, hospitals, and clubs, and quarantine of exposed individuals probably all contributed to containment of the outbreak [91-93].
Both surgical masks and N95 respirators were demonstrated to be useful in blocking the spread of SARS, with no added advantage to N95 respirators over masks [94].
Vaccine development — Efforts are underway to prepare a vaccine for the prevention of SARS, and a large number of candidate vaccines have been developed [95]. Most efforts have concentrated on developing antibody (either secretory or systemic, or both) to the surface S glycoprotein, since neutralizing antibody is directed against the receptor-binding portion of this molecule (figure 1). There is controversy regarding the potential inclusion of the M protein as a component of a vaccine. Although the M protein is an immunodominant protein and may be important as a target of cell-mediated immunity, there is disagreement about its capacity to induce neutralizing antibody and therefore its importance as an antigen in a preventive vaccine [96-98]. There is some concern that, by analogy with some animal coronavirus diseases, immunization might cause paradoxically severe disease on subsequent exposure to natural infection.
The following illustrate several approaches that have been evaluated:
●A recombinant receptor-binding domain S glycoprotein vaccine produced in fungi, bacteria, or insect or mammalian tissue culture protects mice fully with no evidence of paradoxically severe disease [99,100].
●DNA vaccine approaches have induced antigen-specific antibody and cellular immune responses as well as protection in murine models [101].
●Intranasal immunization of monkeys with an attenuated parainfluenza virus that expressed the SARS spike protein resulted in no viral shedding after exposure to the SARS virus [102].
In contrast, the following are models of vaccines that produced paradoxically severe disease on subsequent exposure to the SARS coronavirus:
●Mice immunized intradermally with vaccinia virus constructs containing the nucleoprotein gene of the SARS coronavirus developed severe pneumonia following subsequent intranasal exposure to SARS coronavirus itself, in contrast with those immunized with vaccinia virus constructs containing the S protein gene, who were protected [103].
●Macaques immunized with modified vaccinia Ankara (MVA) encoding full-length SARS spike protein and then challenged with live SARS virus developed greater histologic evidence of acute lung injury than animals challenged after receiving MVA alone [104].
Tests of these candidate vaccines have not been carried out in human subjects.
Monoclonal antibodies — Administration of monoclonal antibodies is another potential approach to the prevention of SARS, although none are available for clinical use. Humanized monoclonal antibodies directed at specific portions of the S glycoprotein have been developed singly and in combination to effectively neutralize virus in vitro and prevent infection in animal models, as illustrated by the following examples (figure 1):
●Human monoclonal antibody to the S1 domain of the spike protein led to potent neutralization of SARS coronavirus in vitro [105].
●Several widely conserved amino acids in the receptor-binding domain in the S1 region of the S glycoprotein have been identified that are critical in neutralization of the virus [106].
●A combination of two noncompeting human monoclonal antibodies broadened protection in vitro by reducing immune escape [107].
SUMMARY AND RECOMMENDATIONS
●In February 2003, the World Health Organization (WHO) reported about 300 cases of a rapidly progressive respiratory illness in the Guangdong Province of China with five deaths. Over the next month, similar cases were reported from Hong Kong, Vietnam, Singapore, and Canada. The illness was termed severe acute respiratory syndrome (SARS) and was found to be caused by a novel coronavirus, designated SARS coronavirus (SARS-CoV) and later called SARS-CoV-1. The outbreak resulted in a total of 8096 cases with 774 deaths and a case-fatality rate of 9 to 12 percent. (See 'Introduction' above and 'Epidemiology' above.)
●Since mid-2004, no cases of SARS-CoV-1 have been reported. The information presented here is mainly of historical interest, although re-emergence of SARS and SARS-CoV-1 is theoretically possible. (See 'Introduction' above.)
●If SARS is suspected, specimens for polymerase chain reaction (PCR) testing should be obtained from at least two sites, such as the respiratory tract, stool, and serum or plasma. PCR testing should be performed as early in the illness as possible and, if symptoms progress or persist, be repeated five to seven days later. Acute and convalescent serum should also be collected for serologic testing. The results required to establish the diagnosis of SARS are discussed above. (See 'Case definitions' above.)
●Animals eaten as exotic foods in southern China, particularly the palm civet, may have been intermediate hosts. Some data have raised the possibility that bats are likely to have been a reservoir for this virus. (See 'Intermediate host and reservoir' above.)
●Based upon the clusters of cases in Hong Kong and Canada, SARS coronavirus clearly spread from person to person and could have been acquired from face-to-face contact, suggesting droplet spread. Other modes of spread, such as fecal-oral, airborne, and fomites might also have been possible. (See 'Transmission' above.)
●SARS begins with a prodrome lasting for three to seven days characterized by fever, malaise, headache, and myalgias. At the end of this prodrome, the respiratory phase typically begins with a nonproductive cough. Dyspnea may follow and may progress to respiratory failure. (See 'Signs and symptoms' above.)
●Diffuse alveolar damage with varying degrees of organization was seen on pathologic examination in patients with SARS who had acute lung injury. (See 'Pathology' above.)
●Treatment of SARS consisted of meticulous supportive care, including mechanical ventilation when indicated. Neither antivirals nor glucocorticoids had demonstrated efficacy for SARS. (See 'Treatment' above.)
●Meticulous infection-control practices were crucial for the prevention of SARS, since other modalities such as a vaccine and monoclonal antibodies were not available. (See 'Prevention' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟