Introduction
Bacillus cereus is a Gram-positive, aerobic-to-facultative,spore-forming rod widely distributed environmentally and bearinga close phenotypic and genetic (16S rRNA) relationships to several other Bacillus species, especially B. anthracis .
The bacterium exists as a spore former and vegetative cell innature and as a vegetative cell when colonizing the human body.
Transmission electron microscopy ofthe vegetative cell reveals a cytoplasmic membrane surroundingthe cellular content . In addition, some strains containan outermost crystalline surface protein (S layer). The core of the spore is surrounded by the inner membrane, cortex,and inner and outer coats.
While devoid of metabolic activity,the B. cereus spore is refractory to extreme environmental conditionsinclusive of heat, freezing, drying, and radiation and may beregarded as the infective agent for this bacterium. In keeping with its close relationship to B. anthracis , thesurface antigens of the spore share epitopes with B. anthracis spores as determined serologically by cross-agglutination.
In the food industry the spores of B. cereus are particularlytroublesome because spores can be refractory to pasteurizationand gamma radiation, and their hydrophobic nature allows themto adhere to surfaces.
Epidemiology
The natural environmental reservoir for B. cereus consists of decaying organic matter, fresh and marine waters, vegetablesand fomites, and the intestinal tract of invertebrates ,from which soil and food products may become contaminated, leadingto the transient colonization of the human intestine . Spores germinate when they come into contact with organic matter orwithin an insect or animal host.
B. cereus may be the most common aerobic spore bearer in manytypes of soil and in sediments, dust, and plants. B. cereus is also frequently present in food production environments dueto the adhesive nature of its endospores. This characteristicenables the bacterium to spread to all kinds of food. Because of the ubiquitous distribution of B. cereus in foodproducts, the bacterium is ingested in small numbers and becomespart of the transitory human intestinal flora. It is unclear, however, if the recovery of B. cereus in cultures of stool specimens is a function of germinating spores or thegrowth of vegetative cells.
Bacterial Morphology
Members of the B. cereus group exclusive of B. anthracis display a range of morphological forms depending upon the milieu in which they are observed. In Gram-stained smears of body fluids B. cereus presents as straight or slightly curved slender bacilli with square ends singly or in short chains.
Colony Morphology
When grown under aerobic conditions on 5% sheep blood agar at 37°C, B. cereus colonies are dull gray and opaque with a rough matted surface. Colony perimeters are irregular and represent the configuration of swarming from the site of initial inoculation, perhaps due to B. cereus swarming motility. Zones of beta-hemolysis surround and conform to the colonymorphology.
Pathogenesis
The pathogenicity of B. cereus, whether intestinal or nonintestinal, is intimately associated with tissue-destructive/reactive exoenzyme production. Bacillus cereus produces one emetic toxin (ETE) and three different enterotoxins: HBL, Nhe,and EntK. Two of the three enterotoxins are involved in food poisoning.
They both consist of three different protein subunits that act together. One of these enterotoxins (HBL) is also a hemolysin; the second enterotoxin (Nhe) is not a hemolysin. The third enterotoxin (EntK) is a single component protein that has not been shown to be involved in food poisoning. All three enterotoxins are cytotoxic and cell membrane active toxins that will make holes or channels in membranes. The emetic toxin (ETE) is a ring-shaped structure of three repeats of four amino acids with a molecular weight of 1.2 kDa. It is a K+ ionophoric channel, highly resistant to pH between 2 and 11, to heat, and to proteolytic cleavage. The nonhemolytic enterotoxin (Nhe) is one of the three-component enterotoxins responsible for diarrhea in Bacillus cereus food poisoning. Nhe is composed of NheA, NheB and NheC. The three genes encoding the Nhe components constitute an operon. The nhe genes have been cloned separately, and expressed in either Bacillus subtilis or Escherichia coli. Separate expression showed that all three components are required for biological activity. The hemolytic enterotoxin, HBL, is encoded by the _hbl_CDA operon.
The three protein components, L1, L2 and B, constitute a hemolysin. B is for binding; L1 and L2 are lytic components. This toxin also has dermonecrotic and vascular permeability activities, and it causes fluid accumulation in rabbit ileal loops.
Gastrointestinal infection
The bacterium causes two types of gastrointestinal disease, the diarrhoeal and the emetic syndromes, which are caused by very different types of toxins.
| INCUBATION PERIOD | COMMON SYMPTOMS |
|---|
| 1-6 hrs (vomiting) | Nausea and diarrhoea. Typically |
| 6-24 hrs (diarrhoea) | resolves within 24 to 48 hours |
- In the emetic syndrome vomiting is caused by the emetic toxin. The course of the disease is characteristic, with nausea and emesis occurring only a few hours after the meal. The incubation time was originally described as 1-5 h, but more recently to be as short as 0.5 h, and up to 6 h. The duration of the emetic disease is normally 6-24 h. The most important differential diagnosis is intoxication with Staphylococcus aureus enterotoxins, which causes similar symptoms; however, in this disease emesis is commonly accompied by diarrhoea. Several severe and even lethal cases of emetic foodborne B. cereus disease have been reported.
- The diarrhoeal disease is caused by one or more protein enterotoxins, thought to elicit diarrhoea by disrupting the integrity of the plasma membrane of epithelial cells in the small intestine. The diarrhoeal syndrome is easily confused with the foodborne disease caused by another sporeforming bacterium, Clostridium perfringens, and typically presents with abdominal pain, watery diarrhoea and occasionally nausea and emesis. The incubation time is over 6 h, normally in the range of 8-16 h, and on average 12 h, but in rare cases longer incubation times have been observed. The duration of the disease is normally 12-24 h but cases lasting several days have been reported.
Non gastro-intestinal infections
In addition to food poisoning, B. cereus causes a number of systemic and local infections in both immunologically compromised and immunocompetent individuals. Among those most commonly infected are neonates, intravenous drug abusers, patients sustaining traumatic or surgical wounds, and those with indwelling catheters. The spectrum of infections include fulminant bacteremia, central nervous system (CNS) involvement (meningitis and brain abscesses), endophthalmitis, pneumonia, and gas gangrene-like cutaneous infections, to name a few.
Therapy
The clinical spectrum of B. cereus infections is multifaceted,and therapeutic options usually revolve around the antibioticsusceptibility pattern of the isolated strain. In general, most B.cereus isolates are resistant to penicillins and cephalosporinsas a consequence of -lactamase production. In the settingof a suspected B. cereus infection, empirical therapy may benecessary while awaiting the antibiotic susceptibility testingprofile. Resistance of B. cereus to erythromycin, tetracycline,and carbapenem has been reporte, which may complicatethe selection of an empiricaltreatment choice.
Most authors stated that "the drug of choice for B. cereus infectionsappears to be vancomycin" and that broad-spectrum cephalosporinsand ticarcillin-clavulanate should be avoided in the empiricaltreatment of patients with suspected B. cereus infection.
Resistance to penicillin, ampicillin, cephalosporins,and trimethoprim is constant, while susceptibility to clindamycin,erythromycin, chloramphenicol, vancomycin, the aminoglycosides,and tetracycline is usually observed. Susceptibility to ciprofloxacin was uniform, and it has been shown to be highly effective inthe treatment of B. cereus wound infections.
References:
- Schneider et al., "Preventing Foodborne Illness: Bacillus cereus and Bacillus anthracis ". Florida Cooperative Extension Service, University of Florida. November, 2004.
- Medical microbiology, Patrick R. Murray, Ken S. Rosenthal, Michael A. Pfaller, Mosby/Elsevier, 2009.
- Bottone EJ. Bacillus cereus, a volatile human pathogen. Clin Microbiol Rev. 2010 Apr;23(2):382-98.
- Stenfors Arnesen LP, Fagerlund A, Granum PE. From soil to gut: Bacillus cereus and its food poisoning toxins. FEMS Microbiol Rev. 2008 Jul;32(4):579-606
- FDA
- Defending Food Safety
- wikipedia.com
Anna Garofalo
Pietro Perduca
