Version May 2024
INTRODUCTION — The Bacillus cereus group is comprised of 22 closely related species. Most human non-anthracis Bacillus spp infections are caused by B. cereus sensu stricto, although infections with other species within the B. cereus group have also been described [1-3]. Not all isolates are associated with invasive disease; however, B. cereus has been associated with nosocomial and opportunistic infection, particularly in immunocompromised patients, intravenous drug users, and patients with indwelling or implanted devices. B. cereus is also associated with syndromes such as food poisoning due to toxin production.
Issues related to B. cereus and other non-anthracis Bacillus species will be reviewed here. Issues related to Bacillus anthracis are discussed separately. (See "Microbiology, pathogenesis, and epidemiology of anthrax" and "Clinical manifestations and diagnosis of anthrax" and "Treatment of anthrax".)
MICROBIOLOGY — Members of the B. cereus group are catalase-positive, aerobic (or facultatively anaerobic), spore-forming gram-positive environmental bacilli [4]. Occasionally, B. cereus may appear gram variable or even gram negative with age. In Gram stains of body fluids, B. cereus appears straight or slightly curved with square ends arranged either alone or in short chains. Junctions between members of the chain are clearly visible. Gram staining of B. cereus taken from agar colonies tends to have a more uniform bacillary appearance ranging in size from 3 by 0.4 microns up to 9 by 2 microns. B. cereus present in tissue sections may appear long and filamentous. Spores are not always visible on Gram stain but, when apparent, they are located centrally, do not distort the bacillary shape, and are clear in appearance. Spores can be stained using specific dyes (eg, malachite green) that are absorbed by spores in the presence of heat.
In some cases, a gram-positive bacillus isolated from blood culture may initially be mistaken for Listeria monocytogenes, leading to delay in appropriate management.
Bacillus species are easily recovered on blood and chocolate agars and grow optimally at environmental temperatures (25 to 37°C). All species except B. anthracis are motile and beta-hemolytic on blood agar. Colonies have an irregular perimeter and appear dull gray and opaque on sheep blood agar. On egg yolk agar, members of the B. cereus group produce a zone of opacification due to lecithinase production.
Individual species within the B. cereus group cannot usually be differentiated by diagnostic laboratories (with the exception of B. anthracis, which is nonmotile and nonhemolytic). Newer methods for identifying microorganisms such as matrix-assisted light desorption/ionization-time of flight mass spectrometry can reportedly differentiate among some members of the B. cereus group (eg, among B. cereus sensu stricto, B. anthracis, and Bacillus thuringiensis), but this may require enhanced databases and identification algorithms [5,6]. Therefore, distinguishing individual species within the B. cereus group usually requires specialized molecular testing by a reference laboratory [7].
Phenotypic differences between member species of the B. cereus group are largely due to the presence of extrachromosomal plasmids [8-10]. For example, B. thuringiensis carries a plasmid that encodes toxins that are pathogenic for a variety of insects. The presence of this plasmid in B. thuringiensis forms the basis for its use as a commercial larvicide and insecticide.
The importance of plasmids and mobile genetic elements is also illustrated by a B. cereus species (B. cereus bv anthracis) causing B. anthrax-like disease that has been identified in nonhuman primates in Cameroon and Côte d'Ivoire [11,12]. Other B. cereus isolates containing B. anthracis toxin genes (eg, B. cereus G9241) have been identified in patients with respiratory illnesses or cutaneous infection, including one patient with a facial lesion resembling an anthrax-like eschar and a series of patients with inhalational diseases associated with metalwork [13-18]. Whole-genome sequencing has suggested a potential correlation between genetic differences among B. cereus strains and disease manifestations [19].
Susceptibility testing — A variety of methods have been used to evaluate the susceptibility of Bacillus spp isolates to a range of antibiotics [20-23]. In one study, 89 blood culture isolates of non-anthracis Bacillus spp (including 54 isolates of the B. cereus group) underwent antibiotic susceptibility testing against 18 different antibiotics by disk diffusion and broth microdilution [22]. All isolates of B. cereus were susceptible to chloramphenicol, ciprofloxacin, gentamicin, imipenem, and vancomycin but resistant to penicillin, oxacillin, and cephalosporins. Variable susceptibilities were observed against clindamycin, tetracycline, and erythromycin. Isolates of Bacillus spp other than the B. cereus group were more sensitive to penicillins than those of the B. cereus group (75 to 90 percent were susceptible to penicillin, cephazolin, cefotaxime, and oxacillin). All isolates were susceptible to chloramphenicol, imipenem, and vancomycin. An additional study evaluated susceptibility of 56 isolates (from a variety of sites); all isolates were reported as susceptible to vancomycin, teicoplanin, pristinamycin, and gentamicin [24].
In another study of susceptibility for isolates of B. cereus, B. mycoides, B. pseudomycoides, and B. thuringiensis, most B. cereus isolates were resistant to amoxicillin, ampicillin, ceftriaxone, penicillin, and oxacillin [21]. Resistance to meropenem and clindamycin was observed in 14 and 17 percent of isolates, respectively. All isolates were susceptible to the following antibiotics: chloramphenicol, ciprofloxacin, clarithromycin, daptomycin, gatifloxacin, gentamicin, levofloxacin, linezolid, moxifloxacin, quinupristin-dalfopristin, rifampicin, streptomycin, tetracycline, tigecycline, and vancomycin. The majority of B. mycoides, B. pseudomycoides, and B. thuringiensis isolates exhibited resistance to penicillins and cephalosporins. Most of the isolates tested were resistant to trimethoprim-sulfamethoxazole at 30°C [21].
PATHOGENESIS — B. cereus is highly adaptable to environmental conditions (such as pH and changing oxygen conditions) in the human gastrointestinal tract [25]. The pathogenic potential of the B. cereus group is largely due to a variety of secreted enzymes and toxins. Two different types of enterotoxins are produced by B. cereus: the diarrheal enterotoxin and the emetic toxin [25]. The transcriptional virulence regulator phospholipase C regulator (PlcR) controls the expression of most virulence factors (eg, enterotoxins, hemolysins, phospholipases, and proteases) by binding upstream of controlled genes to a sequence called the PlcR box [26-28].
EPIDEMIOLOGY — Members of the B. cereus group are saprophytic environmental bacteria that are ubiquitous in nature. In particular, members of the B. cereus group are abundant in soil, fresh water, marine water, and the intestinal tract of soil-dwelling insects. The capability for spore formation means that B. cereus can survive in the environment for extended periods and withstand extremes of temperature. Spores and vegetative bacteria frequently contaminate food. Not surprisingly, therefore, B. cereus is found as a transient but normal component of the human gastrointestinal flora. Stool recovery rates in healthy asymptomatic individuals range from 0 to 43 percent, and the strains recovered are similar to those recovered from the food supply [29].
Isolates of B. cereus are often considered contaminants when cultured from clinical specimens/sterile sites. However, B. cereus can also be an important cause of infection, particularly in patients with prosthetic devices, neonates, immunosuppression, and intravenous drug users. The association between intravenous drug use and bacteremia with B. cereus is due to contamination of needles and injected material with B. cereus. In several studies, Bacillus species were the organisms most frequently recovered from samples of street heroin and intravenous drug paraphernalia [30-32]. B. cereus has also been associated with contamination of alcohol-containing antiseptic wipes [33].
Pseudo-epidemics — Bacillus species are common blood culture contaminants, accounting for 0.1 to 0.9 percent of all blood cultures submitted [34]. Contamination of cerebrospinal fluid has also been described [35]. One multicenter study from Israel suggested that isolation of Bacillus species from blood culture is seasonal, peaking during late summer and early autumn; the underlying reasons for this observation are uncertain [36].
Sharp increases in the rate of contamination of clinical specimens are known as pseudo-epidemics. Pseudo-epidemics of B. cereus in the hospital setting have been linked to contaminated ethanol solution [37], contaminated hospital linen [38], contaminated blood culture media [39], contaminated gloves [40], and hospital construction [41].
Hospital outbreaks — Genuine hospital outbreaks of B. cereus infections have also been reported, usually linked to contaminated medical equipment, such as ventilators and dialysis circuits, and are occasionally linked to construction [42-45]. It is important to differentiate genuine hospital outbreaks from pseudo-epidemics, although both may occur concurrently. Alcohol-based hand rubs have been found to be an ineffective form of hand hygiene for removing B. cereus spores. Handwashing with soap and water and 2% chlorhexidine gluconate have been found to be effective [46,47].
Reports of B. cereus-related sepsis in neonates have been associated with suspected contaminated parenteral nutrition and changes in hospital linen sterilization practices [48,49].
CLINICAL SYNDROMES
Food poisoning — B. cereus is able to persist in food processing environments due to its ability to survive at extreme temperatures as well as its ability to form biofilms and spores. B. cereus has been recovered from a wide range of foods, including rice, dairy products, spices, bean sprouts, and other vegetables. Fried rice is an important cause of emetic-type food poisoning associated with B. cereus in the United States. The organism is frequently present in uncooked rice, and heat-resistant spores may survive cooking. Cooked rice subsequently at room temperature can allow vegetative forms to multiply, and the heat-stable toxin that is produced can survive brief heating such as stir frying [50].
Two distinct types of toxin-mediated food poisoning are caused by B. cereus, characterized by either diarrhea or vomiting, depending on which toxin is involved. The diarrheal toxin is produced by vegetative cells in the small intestine after ingestion of either bacilli or spores. The emetic toxin is ingested directly from contaminated food [26,51]. Both toxins cause disease within 24 hours of ingestion.
Diarrheal syndrome — The diarrheal syndrome is characterized by abdominal cramps and copious diarrhea, usually beginning 8 to 16 hours after ingestion and resolving within 24 hours. Vomiting is uncommon. The diarrheal syndrome is caused by at least three pore-forming cytotoxins/enterotoxins that are secreted by ingested vegetative cells: hemolysin BL, nonhemolytic enterotoxin, and cytotoxin K [26]. The diarrheal cytotoxins are heat labile; their viability is considerably reduced by adequately heating food [52]. Foods that have been linked to diarrheal toxin-mediated disease caused by B. cereus include meats, vegetables, and sauces. The infective dose of toxin-producing B. cereus for diarrheal disease is 105 to 108 colony-forming unit cells per gram of food [26].
Emetic syndrome — The emetic syndrome is caused by direct ingestion of the toxin cereulide, which is a small ring-formed peptide encoded by plasmid deoxyribonucleic acid (DNA). The number of viable spores and vegetative bacteria that produce diarrheal toxin is reduced by heating, although spores associated with emetic toxin are capable of surviving heat processing [52]. Cereulide is heat stable and resistant to gastric conditions. The ingested toxin itself may therefore cause disease despite sufficient heating to kill B. cereus.
The emetic syndrome is characterized by abdominal cramps, nausea, and vomiting. Diarrhea also occurs in about one-third of individuals. Symptom onset is usually within one to five hours of ingestion, but it can also occur within half an hour and up to six hours after ingestion of contaminated food [53]. Symptoms usually resolve in 6 to 24 hours. Rice-based dishes in particular have been implicated in emetic toxin-mediated disease, usually as a result of cooling fried rice dishes overnight at room temperature followed by reheating the next day. The infective dose of cereulide required to cause symptoms is 8 to 10 micrograms per kilogram of body weight [26].
The main differential diagnosis is Staphylococcus aureus enterotoxin-related gastroenteritis, which is also emetic but usually accompanied by diarrhea. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Vomiting'.)
Bacteremia and endocarditis — Differentiating true bacteremia from contamination due to Bacillus spp can be difficult. Most Bacillus species recovered from blood cultures are regarded as contaminants, although Bacillus species also cause true bloodstream infection.
True bacteremia is likely present if Bacillus spp is isolated from both bottles of a single set of blood cultures or isolated repeatedly from multiple blood cultures [54,55]. A retrospective review of Bacillus species blood isolates in one hospital over a five-year period concluded that 5 to 10 percent of isolates represented clinically significant pathogens [54].
Bacillus bacteremia associated with injection drug use has been reported [56]. Many bloodstream infections with Bacillus species in adults in the absence of injection drug use are due to central line-related infections or mucosal compromise and neutropenia; a significant proportion of patients have underlying malignancy or immunosuppression. The rate of relapse is high in settings where antimicrobial therapy is administered but the central line is not removed [24,57-61]. There have been reports of B. cereus transmitted in a hematopoietic cell transplantation product [62] and a report of bacteremia following rhabdomyolysis following autologous bone marrow transplantation [63]. One study noted an increase in the rate of B. cereus bloodstream infection during summer [64]. (See 'Bacteremia and endocarditis' below.)
There are a number of reports of Bacillus spp bacteremia and invasive infections in neonates [45,65-67].
In general, neonates and infants with bacteremia due to Bacillus spp should also be evaluated for central nervous system (CNS) involvement. In one review including 145 invasive neonatal B. cereus infections, the most common focus was blood stream infection, followed by CNS infection, respiratory tract, skin and soft tissue, gastrointestinal, and osteoarticular infection (69, 36, 18, 136, and 2 instances, respectively) [51]. (See 'Central nervous system infection' below.)
Endocarditis due to B. cereus is associated with intravenous drug use [32,68,69], central venous catheters [70,71], prosthetic heart valves [72,73], and pacemakers [60,74]. B. cereus native valve endocarditis in the absence of underlying valvular abnormalities or other risk factors is rare [72,75]. Complications associated with B. cereus prosthetic valve endocarditis include thromboembolic events and valvular dysfunction [76].
Respiratory infection — B. cereus spp has been associated with severe respiratory infection in metalworkers resembling inhalational anthrax [18]. In one series including nine patients, seven had infection associated with a B. cereus spp with virulence factors/toxins on a plasmid similar to that found in B. anthracis.
Musculoskeletal infection — Soft tissue and bone infection due to B. cereus has been associated with trauma, intravenous drug use, and immune compromise [32,60]. Musculoskeletal infections with B. cereus have been reported after a wide variety of trauma mechanisms including:
●Gunshot wounds [77]
●Tropical traumatic wounds acquired in Costa Rica [78]
●Open fractures with environmental contamination [79]
●Postoperative and traumatic orthopedic wounds [80]
●Bear bites [81]
●Plaster-associated wound infection [82]
●Burn wounds infected by contaminated water [83]
●Scalp infection [84]
●Cellulitis from contaminated heroin [85]
Necrotizing soft tissue infection due to B. cereus may resemble clostridial infection. It has been described in the setting of injection drug use, diabetes mellitus, immune compromise, trauma, and as a result of subcutaneous injection of contaminated heroin [32,86-88]. Superinfection with Bacillus spp has also been described in the setting of chronic osteomyelitis due to S. aureus [89].
Central nervous system infection — Central nervous system infections due to Bacillus spp have been described in adults and neonates. Manifestations have included cases of infected subarachnoid hemorrhage, meningoencephalitis, and brain abscess [90-94]. CNS infections due to Bacillus spp in adults have been associated with hematologic malignancy and neurosurgery. The risk of infection may be increased in the setting of external ventricular drains and other implanted devices [57,70,95].
CNS infection has also been described among children and neonates. In one small series of four children with B. cereus bacteremia and CNS infection in the setting of leukemia, risk factors for fulminant disease included neutropenia, relapsed disease, induction chemotherapy, use of corticosteroids or third-generation cephalosporins, recent hospitalization, and recent lumbar puncture with intrathecal chemotherapy [93]. The mechanism of CNS infection in these cases is most likely attributable to chemical arachnoiditis induced by intrathecal chemotherapy with secondary seeding in the setting of bacteremia (rather than introduction of Bacillus spp at the time of lumbar puncture) [93].
Neonates may also have CNS involvement in the setting of B. cereus bacteremia [66,96,97]. In one review including 21 cases of neonatal bacteremia, 11 also had evidence of CNS infection [65].
Ocular infection — Ocular manifestations include endophthalmitis panophthalmitis and keratitis.
Endophthalmitis due to Bacillus species is a serious condition that progresses rapidly and can threaten vision within hours of the onset of symptoms [98-101]. Ocular trauma accounts for 70 to 87 percent of cases of B. cereus endophthalmitis [99,100,102]; the remaining cases occur secondary to hematogenous seeding [30,99,100] or as a complication of ocular surgery [100]. Endophthalmitis due to B. cereus is associated with poor outcomes. In a series of 15 cases of endophthalmitis due to Bacillus species (most patients due to penetrating ocular injuries) with relatively early initiation of treatment, poor visual outcomes occurred in approximately one-half of patients [100]. Similarly, in a review of 82 cases of Bacillus spp endophthalmitis, 46 percent of patients were left with either perception of light only or no perception of light [103].
Keratitis caused by Bacillus spp usually occurs in the setting of traumatic corneal abrasions but can also occur as a complication of wearing contact lenses or cataract surgery. Keratitis usually has a more indolent clinical course than endophthalmitis; patients may present weeks or months after the initial corneal trauma [2,104,105].
DIAGNOSIS — Outbreaks of B. cereus food poisoning usually obtain laboratory confirmation through specialized public health reference laboratories rather than laboratories providing routine diagnostic services. Besides culture of B. cereus from stool, several commercial assays can be used to detect the diarrheal toxin. These include a reverse passive latex agglutination test [106], immunochromatographic tests, and polymerase chain reaction (PCR) that targets the gene itself [107,108]. PCR assays have also been used successfully for diagnosis of emetic foodborne B. cereus infection. As the emetic toxin is heat stable, it can cause disease despite heating the food sufficiently to kill B. cereus. Thus, culture of vomitus may be negative for B. cereus despite the presence of emetic toxin.
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of gastrointestinal illness due to B. cereus can be narrowed based on the incubation period and duration of illness.
●Diarrheal syndrome – Clostridium perfringens can cause a rapid onset illness with both diarrhea and vomiting within 8 to 16 hours due to enterotoxin released in the small bowel by vegetative cells. Acute diarrheal illness due to both C. perfringens and B. cereus typically resolves within 24 hours [109,110]. The diagnosis is established by testing food or stool for C. perfringens toxin. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Clostridium perfringens'.)
The incubation periods of many other bacterial causes of foodborne diarrheal illnesses are generally longer than for B. cereus (8 to 16 hours); these include Campylobacter spp, Escherichia coli producing Shiga toxin, Shigella spp, and Salmonella spp, with incubation periods of one day to one week. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings".)
●Emetic syndrome – Acute emesis due to gastrointestinal infection can be caused by bacterial or viral infection. The most important viral cause is norovirus (incubation period 24 to 48 hours) [111]. In general, viral gastroenteritis may be diagnosed based on clinical manifestations alone, although establishing the etiology in an outbreak setting (generally via polymerase chain reaction) may be useful. (See "Norovirus", section on 'Diagnosis'.)
Bacterial causes of acute emesis involve ingestion of preformed enterotoxins; the most important bacterial cause is S. aureus. The onset of emesis due to preformed enterotoxins of S. aureus is usually within six hours and frequently accompanied by stomach cramps and, less commonly, diarrhea; fever is not a generally a feature. Both B. cereus and S. aureus infections typically last less than 12 hours [109,112]. Vomitus and/or food can be tested for the S. aureus enterotoxin, but the diagnosis of food poisoning due to S. aureus is usually clinical. (See "Causes of acute infectious diarrhea and other foodborne illnesses in resource-abundant settings", section on 'Vomiting'.)
TREATMENT
Empiric antibiotic therapy — Antibiotics are not indicated for treatment of food poisoning caused by B. cereus. Empiric antibiotic therapy is warranted for treatment of other clinical syndromes, including bacteremia, device-related infections, endocarditis, musculoskeletal infection, central nervous system (CNS) infection, and ocular infection. Once in vitro susceptibility testing is available, antibiotic selection for treatment of Bacillus spp infections should be guided by these results. (See 'Susceptibility testing' above.)
Most B. cereus isolates produce beta-lactamases and are resistant to penicillins and cephalosporins. For this reason, penicillins and cephalosporins should not be used for empiric treatment of Bacillus spp infection. Prior to the availability of susceptibility testing, vancomycin is generally considered the preferred antibiotic choice. Alternative agents that have in vitro activity against Bacillus spp include aminoglycosides, carbapenems, and fluoroquinolones. Clindamycin should not be used until the results of susceptibility testing become available; there is in vitro evidence of both outright and inducible clindamycin resistance among clinical isolates of B. cereus [21].
Data are limited regarding use of combination therapy. Bactericidal synergy between gentamicin and clindamycin as well as gentamicin and vancomycin has been observed [23]. Some reports of serious infections due to non-anthracis Bacillus spp have described treatment with vancomycin or clindamycin, plus or minus an aminoglycoside [30,76,98,113].
Food poisoning — Treatment of food poisoning due to B. cereus consists of supportive care; antibiotics are not indicated [1,2]. There is a report of gastroenteritis in an immunocompromised patient in which B. cereus gastroenteritis was associated with rhabdomyolysis in which antibiotics were used [114].
Bacteremia and endocarditis — Treatment of bacteremia due to Bacillus spp consists of intravascular catheter removal (if present) and antibiotic therapy [115]. Appropriate therapy consists of vancomycin (or alternative agent to which the isolate is known to be susceptible) for 7 to 14 days following catheter removal [116]. Data on duration of therapy are limited; seven days is generally sufficient in the setting of clinical resolution of symptoms. Evidence of persistent bacteremia and/or fever warrants longer duration of therapy together with investigation for metastatic site(s) of infection.
Poor outcomes due to B. cereus bacteremia have been described among neonates and infants; in one study with 22 patients, the mortality rate was 60 percent [65]. In general, neonates and infants with bacteremia due to Bacillus spp should also be evaluated for CNS involvement.
Data on management of endocarditis due to Bacillus spp are limited to case report literature [68,71,72,76,117-119]. In general, treatment consists of vancomycin (or alternative agent to which the isolate is known to be susceptible) for at least six weeks. Management of prosthetic valve endocarditis usually requires valve replacement in addition to antimicrobial therapy [72]. Management of pacemaker-associated B. cereus endocarditis is also limited to case reports [74,120]. (See "Antimicrobial therapy of left-sided native valve endocarditis" and "Antimicrobial therapy of prosthetic valve endocarditis".)
Musculoskeletal infection — Treatment of musculoskeletal infection due to Bacillus spp consists of debridement and antimicrobial therapy. Appropriate antimicrobial therapy consists of vancomycin (or alternative agent to which the isolate is known to be susceptible) [1,89]. Treatment of osteomyelitis generally requires a prolonged course of therapy (6 to 12 weeks) [32,89].
Central nervous system infection — Treatment of CNS infection due to Bacillus spp usually consists of combination therapy with vancomycin and an aminoglycoside. Depending upon susceptibility results, a carbapenem may be a suitable alternative. The duration of treatment should be tailored to individual patient circumstances; in general, meningoencephalitis should be treated for at least 14 days, and brain abscesses should generally be treated for at least six weeks. Clindamycin should not be used to treat CNS infections because it is bacteriostatic and does not attain therapeutic concentrations in the cerebrospinal fluid.
The presence of external ventricular drains increases the risk of infection with Bacillus spp [57]. In the setting of infection, these devices should be removed if present [121].
Ocular infection — Treatment of endophthalmitis and panophthalmitis due to Bacillus spp consists of surgical management together with antimicrobial therapy (intraocular and systemic administration) [99,100,116,122]. Early initiation of treatment is critical. Appropriate antimicrobial therapy consists of vancomycin (with or without an aminoglycoside) [116]. Clindamycin is an acceptable alternative agent if the isolate is known to be susceptible; parenteral or subconjunctival administration of clindamycin can achieve therapeutic levels in the iris, choroid, and vitreous. Some data suggest that combination therapy with gentamicin and vancomycin or clindamycin may be synergistic [122]. Bacillus spp are uncommon isolates in the context of keratitis, and treatment of keratitis due to Bacillus spp is not standardized. Topical treatment with topical fluoroquinolones, aminoglycosides, and cephalosporins has been reported as being successful but should be guided by the susceptibility profile [104,123].
SUMMARY AND RECOMMENDATIONS
●Most human Bacillus infections are caused by B. cereus, although infections with other species within the B. cereus group have also been described. Members of the B. cereus group are catalase positive, aerobic (or facultatively anaerobic), spore-forming gram-positive bacilli. Bacillus species are easily recovered on blood and chocolate agars and grow optimally at environmental temperatures. (See 'Introduction' above and 'Microbiology' above.)
●Members of the B. cereus group are abundant in the environment. Spore formation enables B. cereus to survive in the environment for extended periods and withstand extremes of temperature. Spores and vegetative bacteria can contaminate food, causing gastrointestinal illness. The organism can also contaminate drug injection paraphernalia as well as prosthetic devices and other health care equipment. (See 'Epidemiology' above.)
●Bacillus species are common blood culture contaminants. Genuine hospital outbreaks of B. cereus infections have also been reported, usually linked to contaminated medical equipment, such as ventilators and dialysis circuits. (See 'Pseudo-epidemics' above and 'Hospital outbreaks' above.)
●Two distinct types of toxin-mediated food poisoning are caused by B. cereus, characterized by either diarrhea or vomiting, depending on which toxin is involved. The diarrheal toxin is produced by vegetative cells in the small intestine after ingestion of either bacilli or spores. The emetic toxin is ingested directly from contaminated food. Both toxins cause disease within 24 hours of ingestion. (See 'Food poisoning' above.)
●Other clinical syndromes caused by B. cereus include bacteremia, endocarditis, musculoskeletal infection, central nervous system (CNS) infection, and ocular infection. There are several reports of neonatal bacteremia and CNS infection due to Bacillus spp. (See 'Clinical syndromes' above.)
●Antibiotic therapy is not indicated for treatment of toxin-mediated food poisoning caused by B. cereus. Antibiotic therapy is warranted for treatment of bacteremia, device-related infections, endocarditis, musculoskeletal infection, CNS infection, and ocular infection. (See 'Empiric antibiotic therapy' above.)
●Most B. cereus isolates produce beta-lactamases and are resistant to penicillins and cephalosporins. Prior to the availability of susceptibility testing, we suggest that vancomycin be included in empiric treatment regimens (Grade 2C). Alternative agents that have in vitro activity against Bacillus spp include aminoglycosides, carbapenems, and fluoroquinolones. Clindamycin resistance has been described, so this agent should not be used in the absence of susceptibility data. (See 'Empiric antibiotic therapy' above.)
آیا می خواهید مدیلیب را به صفحه اصلی خود اضافه کنید؟
