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Clostridium Information and Courses from MediaLab, Inc.

These are the MediaLab courses that cover Clostridium and links to relevant pages within the course.

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Case Studies in Clinical Microbiology
Review 1

Garbutt JM. Littenberg B. Evanoff BA. Sahm D. Mundy LM. Enteric carriage of vancomycin-resistant Enterococcus faecium in patients tested for Clostridium difficile. Infection Control & Hospital Epidemiology. 20(10):664-70, 1999 OBJECTIVE: To identify independent risk factors for enteric carriage of vancomycin-resistant Enterococcus faecium (VREF) in hospitalized patients tested for Clostridium difficile toxin. PATIENTS: Convenience sample of 215 adult inpatients who had stool tested for C. difficile between January 29 and February 25, 1996. RESULTS: 41 (19%) of 215 patients had enteric carriage of VREF. Five independent risk factors for enteric VREF were identified: (1) history of prior C. difficile infection, (2) parenteral treatment with vancomycin for > or = 5 days, (3) treatment with antimicrobials effective against gram-negative organisms, (4) admission from another institution, and (5) age > 60 years. These risk factors for enteric VREF were independent of the patient's current C. difficile status. CONCLUSIONS: Antimicrobial exposures are the most important modifiable independent risk factors for enteric carriage of VREF in hospitalized patients tested for C. difficile.

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Case History

A 63-year-old man was seen in the emergency room with the complaints of sudden onset of fever, chills, and abdominal pain, accompanied by mild diarrhea. The blood pressure was 140/84, the pulse rate 82/minute, and the body temperature 39.8C. A blood sample was drawn for a complete blood count, and a blood culture. A second blood culture was drawn from the opposite arm, with 10 mL of blood being placed into each an aerobic and an anaerobic bottle, following customary practice. The complete blood count revealed a hemoglobin of 15.8 mg/dL, a hematocrit of 45%, and a white blood count of 4.2/L. The neutrophils were 39%, lymphocytes 45%, monocytes 10%, eosinophils 4% and basophils 2%. The platelet count was 255/L. The patient was admitted to the hospital for further work-up and empiric antibiotic therapy. Within 24 hours after admission, the body temperature had decreased to 38.2C, although the mild diarrhea persisted. A stool toxin test for Clostridium difficile was negative and neither enteric pathogens nor Campylobacter species were recovered in stool culture after 24 hours incubation. Fecal neutrophils were not seen on direct examination. The anaerobic blood culture became positive 36 hours after inoculation.

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Gas gangrene may be seen in infections with all the following clostridia EXCEPT:View Page
The Gram stain shown in the image was prepared from a positive anaerobic blood culture bottle after 36 hours incubation. Based on the morphology of the bacterial cells (some with spores, noted by the blue arrows), what the most likely identification?View Page
Colony Morphology

The growth observed on the anaerobic blood agar plate after 48 hours incubation (see upper image), revealed a spreading colony. The spreading nature of the colony is better observed in the lower image. No growth was observed on subcultures incubated aerobically indicating that this isolate is truly an anaerobe (although aerotolerance studies would be needed for confirmation). The spreading nature of the colony and the lack of hemolysis are highly suggestive of Clostridium septicum. However, biochemical confirmation is necessary.

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Clostridium Quad Plate

Key reactions for the identification of Clostridium septicum are demonstrated in the two quadrant plates shown in the images to the right. Included in the upper image are reactions for milk (casein) proteolysis (12 o'clock quadrant), glucose fermentation, DNAse hydrolysis, and starch hydrolysis respectively reading clockwise. The media in the quadrant plate shown in the lower image include gelatin hydrolysis (2 o'clock quadrant) and fermentation of each of mannitol, lactose, and rhamnose respectively, reading clockwise. Milk (casein) hydrolysis and glucose fermentation are key reactions for the identification in the upper plate, including no proteolysis of milk, fermentation of glucose (yellow red color along the inoculation streak), positive DNAse (reddish clearing around the streak) ,and a negative reaction for starch. Key reactions in the lower plate include hydrolysis of gelatin, fermentation of lactose (yellow pigment), and negative reactions for mannitol and rhamnose (no pigment). Most strains of C. perfringens hydrolyze starch and produce proteolysins of milk, the key reactions that distinguish C. septicum (negative). Reactions to the other tests do not distinguish between the two.

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Clostridium septicum RapID ANA

The definitive identification of C. septicum can be made using a profile of biochemical reactions, as is contained in the RapID ANA strip seen in the image. The upper set of tubules are reactions before addition of reagents; the bottom set of reactions after reagents are added. The upper set of letter codes is used to read the reactions before addition of reagents; the lower set of labels indicate the tests to read following addition of reagents. Of all the reactions included, only ONPG and NAG in the upper set are positive. The biotype number derived from this profile of reactions, 014000 codes for Clostridium septicum, thus confirming the identification.

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Review 1

Lorimer JW. Eidus LB.: Invasive Clostridium septicum infection in association with colorectal carcinoma. Canadian Journal of Surgery. 37:245-9, 1994 The association between invasive Clostridium septicum infection and colorectal carcinoma is examined by the presentation of three cases and a review of the literature. In the first two cases the patients presented with nontraumatic metastatic clostridial gas gangrene. In the third case a patient with chemotherapy-induced myelosuppression from concomitant multiple myeloma had a necrotizing transmural infection of the right colon. The apparent portal of entry of Clostridium septicum was an occult carcinoma of the ascending colon. The increasing evidence for a strong link between this organism and some cases of neutropenic enterocolitis is reviewed.

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Review 2

Citron DM. Appelbaum PC.: How far should a clinical laboratory go in identifying anaerobic isolates, and who should pay? Clinical Infectious Diseases. 16 Suppl 4:S435-8, 1993 Identification of anaerobic bacteria in specimens from sites of infection due to mixed organisms can be time-consuming and expensive. Laboratories should limit anaerobic workups by testing only those specimens that have been properly collected and transported to the laboratory. Use of selective and differential media for initial processing can provide rapid and relevant information to the clinician. Anaerobes isolated from normally sterile sites and sites of serious infection should always be completely identified. Group-or genus-level identifications may suffice in other instances. The Bacteroides fragilis group of organisms should always be identified because of their virulence and resistance to many antimicrobial agents. Some of the other organisms that warrant identification include Clostridium septicum (associated with gastrointestinal malignancy); Clostridium ramosum, Clostridium innocuum, and Clostridium clostridioforme (which are resistant to antibiotics); Clostridium perfringens (a cause of myonecrosis and gas gangrene,potentially serious infection); anaerobic cocci (which may be resistant to metronidazole and clindamycin); and fusobacteria (which may be virulent and resistant to clindamycin and penicillin).

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Review 3

Kornbluth AA. Danzig JB. Bernstein LH.: Clostridium septicum infection and associated malignancy. Report of 2 cases and review of the literature. Medicine. 68(1):30-7, 1989 We report 2 patients with myonecrosis due to Clostridium septicum and associated colon carcinoma and have reviewed the English language literature for all reported cases of atraumatic C. septicum infection. A total of 162 cases of C. septicum infection have been reported. Eighty-one percent of these patients had an associated malignancy. Thirty-four percent of all patients had associated colon carcinoma, while 40% had a hematologic malignancy. Thirty-seven percent of reported patients had an occult malignancy at the time of their infection with C. septicum. In many patients, the portal of entry was found in the large intestine. In a particularly lethal form (79% mortality) of C. septicum infection, known as "distant myonecrosis," infection metastatic from the initial site of infection causes severe myonecrosis, gangrene, and often death within hours of clinical detection. Overall, survival of patients with C. septicum infection is only 35%. Review of all cases of C. septicum infection suggests several conclusions. 1) Patients with malignancy, particularly colonic or hematologic, and patients with cyclic neutropenia who develop signs and symptoms of sepsis, especially with associated findings of abdominal pain or pain in an extremity, should be treated for possible clostridial infection. 2) C. septicum infection does not appear to be a result of a single specific defect in either humoral or cell-mediated immunity. Rather, it may occur in patients who are granulocytopenic and therefore prone to an enterocolitis. 3) Patients in whom an infection with C. septicum is found must undergo a vigorous search for malignancy.

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Match the species of anaerobes and frequently associated conditions.View Page
Each of the following statements is true concerning Clostridium septicum infections EXCEPT:View Page
A Brown and Brenn gram stain was performed on one of the tissue biopsy specimens. Organisms were seen as shown in the image. Based on the history and the appearance of the bacteria, the most likely identification is:View Page

Introduction to Bioterrorism
Category A Agents

Category A agents include: Smallpox (variola major) Anthrax (Bacillus anthracis) Plague (Yersinia pestis) Botulism (Clostridium botulinum toxin) Tularaemia (Francisella tularensis) Ebola hemorrhagic fever Marburghemorrhagic fever Lassa fever Argentine hemorrhagic fever

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Category B Agents

Category B agents include:Q Fever (Coxiella burnetii)Brucellosis (Brucella sp.)Glanders (Burkholderia mallei)Venezuelan encephalomyelitisEastern and western equine encephalomyelitisRicin toxin from castor beans (Ricinuscommunis)Epsilon toxin of Clostridium perfringensStaphylococcus enterotoxin B

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Microbiology / Serology Question Bank - Review Mode (no CE)
Which of the following are not considered normal flora of the gastrointestinal tract:View Page
Which of the following organisms are gram negative:View Page
Which of the following organisms is most likely to be associated with gas gangrene:View Page

Molecular Methods in Clinical Microbiology
Clinical Significance

Clostridium difficile is the cause of antibiotic associated diarrhea (AAD) and pseudomembranous colitis (PMC). PMC is an inflammatory disease of the colon caused by toxins of C. difficile.C. difficile produces two potent toxins: Toxin A (TcdA), an enterotoxinToxin B (TcdB), a cytotoxin It is the production of these toxins in the gastrointestinal tract that ultimately leads to disease. There is a relationship between toxin levels, the development of pseudomembranous colitis (PMC), and the duration of diarrhea. For many years, toxin A was regarded as more important than toxin B in the disease process. Later on, disease producing strains producing only toxin B were identified. These strains produced serious disease, and toxin B was found to be responsible for more serious damage to intestinal cells.

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Previous Methodologies: Culture and Cell Cytotoxicity Neutralization Assay (CCNA)

CultureBacterial culture, utilizing selective/differential media, is an effective method for recovering Clostridium difficile. Its drawbacks are the length of time required (up to four days), as well as the inability to distinguish toxigenic strains from non-toxigenic strains. Positive cultures require follow-up testing for the ability to produce toxin.Cell Cytotoxicity Neutralization Assay (CCNA) This assay detects the presence of C. difficile toxin in fecal samples. A filtrate of stool sample is prepared and inoculated onto sensitive tissue culture cells. Typically human fibroblast cells are utilized; if toxin is present in the filtrate, it causes the fibroblasts to round up in a characteristic cytopathic effect. To verify that the cytopathic effect is caused by C. difficile toxin (and not some other toxic component or viral agent), the filtrate is also inoculated in parallel onto a second set of tissue culture cells, to which C. difficile specific anti-toxin has been added. Absence of cytopathic effect in the second set of cell cultures provides evidence that the cellular changes in the first set were caused by C. difficile toxin. Although CCNA is considered a gold standard for the detection of C. difficile toxin, it is labor intensive, requires the use of cell cultures, and requires at least 48 hours of incubation.

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Several methods of detection are available for the detection of Clostridium difficile in clinical samples. Which methods have the capability for detection in less than 48 hours? (Choose all that apply.)View Page
What statements are TRUE about the glutamate dehydrogenase (GDH) assay for Clostridium difficile? (Choose all that apply.)View Page

Multi-drug Resistant Organisms: MRSA, VRE, and Clostridium difficile
Clostridium difficile

Another organism that has more recently become problematic is Clostridium difficile. Usually, normal gut flora resist overgrowth and colonization by this organism. However, antibiotic use that suppresses the normal gut flora, allows proliferation of C. difficile. The organism releases toxins that cause inflammation and damage to the mucosal lining of the colon, leading to severe diarrhea. An antibiotic-resistant strain has developed that can result in colitis, sepsis, and death. Elderly patients, patients with severe underlying illness, and patients undergoing immunosuppressive therapy are at higher risk of becoming infected since their immune response to the bacteria and its toxins is diminished.

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Laboratory Detection of Clostridium difficile

Several laboratory methods are currently available to aid in the detection of C. difficile, including culture for toxigenic C. difficile (considered the "gold standard" for viable C. difficile detection), detection of Toxin A, B, or both, and molecular detection methods. These methods differ in their sensitivity and specificity and should always be used in conjunction with clinical considerations. To make the diagnosis, it is usually only necessary to submit 1-2 diarrhetic (non-formed) stools per episode. Once positive for C. difficile by any laboratory method, there is no need for follow-up assays to make sure the organism or toxins are absent from the initial episode. If assays are performed for subsequent episodes, culture or tissue culture assay for Toxin B are probably most appropriate to avoid the possibility of detecting the initial antigen, toxin, or gene.

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Clostridium Species

Clostridium are gram-positive or gram-variable, spore-forming, catalase-negative anaerobic bacilli. More than 100 species are currently recognized, though relatively few are encountered in properly collected clinical specimens from humans. There are three types of infection associated with Clostridium species: Non-invasive: Toxin-mediated Invasive: Progressive infection with tissue destruction Purulent disease: Closed space (e.g., in the peritoneal cavity) mixed infection with multiple organisms.Clostridium are well known as the agents of these classic toxin-mediated diseases : DISEASE TOXIN INVOLVED CAUSATIVE ORGANISM Tetanus or "lock jaw" Tetanospasmin Clostridium tetani Myonecrosis/Gas gangrene Exotoxins Clostridium perfringens Botulism (severe food poisoning) Botulin Clostridium botulinum

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References

Clinical and Laboratory Standards Institute (CLSI). Performance Standards for Antimicrobial Susceptibility Testing, Twenty-Third Informational Supplement. CLSI document M100-S23. CLSI. Wayne, PA: 2013.Fenner L, Widmer AF, Goy G, Rudin S, Frei R . Rapid and reliable diagnostic algorithm for detection of Clostridium difficile. JCM, 2008; 46(1): 328-330.Forbes BA, Sahm DF, Weissfeld AS, eds.Bailey & Scott's Diagnostic Microbiology. 11th ed. Mosby; 2002.Gillespie SH, Hawkey PM, eds. Principles and Practice of Clinical Bacteriology. 2nd ed. West Sussex, England: John Wiley & Sons Ltd; 2006.Isenberg HD. Clinical Microbiology Procedures Handbook. 2nd ed. Washington, DC: ASM Press; 2004.Healthcare-associated infections. CDC website. Available at: http://www.cdc.gov/hai/. Accessed June 18, 2013.Vancomycin resistant Enterococci and the clinical laboratory. CDC website. Available at: http://www.cdc.gov/HAI/settings/lab/VREClinical-Laboratory.html. Accessed June 18, 2013.

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Clostridium difficile

Most Clostridium infections arise from endogenous sources. That is, many of the Clostridium species that are associated with disease in humans are part of the normal intestinal microflora, which is true of Clostridium difficile.The organism was originally isolated in 1935 as a component of the normal intestinal flora of healthy newborns. It was dubbed difficile because the organism grows slowly and is difficult to culture. Early investigators also noted that the organism produced a potent toxin, but the relationship between C. difficile antibiotic-associated diarrhea (AAD) and pseudomembranous colitis (PMC) was not elucidated until the 1970's. PMC is an inflammatory disease of the colon caused by toxins of Clostridium difficile. Normal intestinal flora is an important factor in host response to an infectious microorganism. Resistance to intestinal infection is significantly reduced when there is a reduction in the normal flora as a result of antibiotic treatment. The most common manifestation of this decreased host resistance is the development of PMC.

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C. difficile Toxin A and Toxin B

Clostridial toxins are among the largest bacterial toxins reported to date and C. difficile produces two potent toxins: Toxin A ((TcdA), an enterotoxin and Toxin B (TcdB), a cytotoxin. It is the production of these toxins in the gastrointestinal tract that ultimately leads to disease. There is a relationship between toxin levels, the development of pseudomembranous colitis (PMC), and the duration of diarrhea. Levels of Immunoglobulin G against TcdA correlate directly with protection from disease following colonization, suggesting that a robust immune response is sufficient for protection from C. difficle-associated diarrhea (CDAD). The role of TcdB is not as well understood. Naturally occurring Toxin A negative/Toxin B positive (TcdA-TcdB+) strains have been identified from clinical isolates, which are capable of causing disease, even extensive PMC, suggesting a role for TcdB in CDAD. Toxin A had always been regarded as more important than Toxin B in infection. However, recent work utilizing mutant C. difficile, strains which did not, or could not produce Toxin A, and which were capable of producing very serious disease has led researchers to completely rethink the roles of Toxin A and Toxin B in CDAD. Toxin B was found to be responsible for the more serious damage to intestinal cells. In addition to the primary virulence factors (Toxin A and Toxin B ), Clostridium difficile also produces a third toxin, binary toxin (CDT). The prevalence of CDT in clinical isolates varies widely and its clinical relevance and role in pathogenicity are still not well defined.

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Pathogenisis of C. Difficile-Associated Diarrhea

Clostridium difficile is the leading cause of hospital-acquired diarrhea in the United States, with the number of cases rising annually over the last three decades. This is largely due to the increased frequency of antibiotic usage, the development of better detection methods, and the fact that hospital environments are increasingly contaminated with spores of C. difficile. The definition of C. difficile diarrhea includes > 6 episodes of non-formed diarrheic stool per 24 hours, along with prior antibiotic treatment. At least three events must occur in the pathogenesis of C. difficile-associated diarrhea (CDAD): Alteration of the normal fecal flora Colonic colonization with toxigenic C. difficile Growth of the organism with elaboration of its toxins"Colonization resistance" is the term used to describe the mechanism by which indigenous flora control overgrowth of C. difficile. This resistance may be compromised by the use of antimicrobial compounds, underlying illness, or therapeutic procedures. Infection begins with the ingestion of either the organism itself or spores, usually via the fecal-oral route. Spores in particular are able to survive the acidity of the stomach and germinate in the colon to produce vegetative organisms. Toxinogenic strains subsequently produce Toxin A, Toxin B, and/or the Binary Toxin leading to colitis, pseudomembrane formation, and watery diarrhea. Significant complications of the clinical disease associated with infection are hypoalbuminemia, toxic megacolon (acute toxic colitis with dilatation of colon), and pseudomembranous colitis (PMC).

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Risk factors for Clostridium difficile Infection

The incidence of C. difficile infection varies considerably but is increasing worldwide, largely due to widespread use of broad-spectrum antibiotics. The risk factors associated with C. difficile infection and colitis are: Antimicrobial use length of course multiple antibiotics Hospitalization length of stay illness & weakness presence of spores in hospitals and long-term care facilities(LTCF) Age Advanced age > 65 (weakened immune systems Young children (immature immune systems) Underlying disease (weakened immune system) Use of proton pump inhibitors, gastric acid suppressants, or anti-ulcer medications that decrease acidity levels in stomach/GI tract, which can alter normal flora and allow C. difficile to proliferate Chemotherapeutic drugs (weakened immune system) Laxative use Gastrointestinal (GI) surgery or non-surgical invasive procedures such as intubation

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Clostridium difficile-associated Diarrhea

Clostridium difficile-associated diarrhea (CDAD) is a unique hospital infection that occurs almost entirely in patients who have received previous antimicrobial treatment. Anaerobic gut flora are crucial to colonization resistance, so any disruption of the normal colonic flora (through illness, therapeutic procedures or, most commonly, antibiotic use) is essential to the pathogenesis of C. difficile infection. The association of CDAD with antibiotic use is significant. Early attention (1970s) focused on clindamycin but later on (1980s,1990s & continuing today) the cephalosporins, especially third generation, and broad spectrum penicillins (e.g., amoxycillin/ampicillin) were also implicated. The risk of CDAD is increased if C. difficile is resistant to the particular antimicrobial. In the case of clindamycin, C. difficile resistance is variable. Risk of infection due to a clindamycin-resistant strain increases with use of the drug. For the third generation cephalosporins, C. difficile is universally resistant; thus, any toxigenic strain is capable of causing CDAD during cephalosporin use. Other less commonly implicated antibiotics are the macrolides, e.g., erythromycin, azithromycin, clarithromycin. However, prolonged courses of any antibiotics will increase the risk of disease. Even those antibiotics used to treat colitis (metronidazole, for example) have sometimes been reported to cause CDAD.The fluoroquinolones have been in use since the 1980s. Ciprofloxacin was approved in 1987, but it is only in recent years with the emergence of the epidemic strain 027/NAP1/BI, which is resistant to the fluoroquinolones, that this class of drugs has been implicated in Clostridium difficile disease. The fluoroquinolones were initially considered to be low risk but their use has been increasing, both with hospital inpatients and in the community, and fluoroquinolones are now implicated as a risk factor for C. difficile infection. The newer fluoroquinolones, e.g., gatifloxacin, moxifloxacin, have better activity against anaerobes, but poor in vitro activity against C. difficile, thus increasing the likelihood of CDAD. The CDC now recommends that all fluoroquinolones, as a class, be used sparingly as each poses an increased risk for CDAD.

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C. difficile disease is more likely to occur when:View Page

Packaging and Shipping Infectious Materials (retired July 2013)
Category A Definition and Examples

A category A infectious substance is in a form that is capable of causing permanent disability or life-threatening or fatal disease in otherwise healthy humans or animals when exposure to it occurs. Exposure would occur if the substance were released from its protective packaging and a human or animal came into contact with it. Some examples of category A infectious substances are listed below. A more comprehensive list is included as a PDF attachment on this page.Bacillus anthracis (cultures only) Brucella abortus (cultures only) Brucella melitensis (cultures only) Burkholderia mallei (cultures only) Clostridium botulinum (cultures only) Creutzfeldt-Jakob disease (CJD) brain tissue specimens Dengue virus (cultures only) Escherichia coli, verotoxigenic (cultures only) Ebola virus Francisella tularensis (cultures only) Hantaviruses causing hemorrhagic fever with renal syndrome Herpes B virus (cultures only) Human immunodeficiency virus (cultures only) Lassa virus Mycobacterium tuberculosis (cultures only) Poliovirus (cultures only) Rabies and other lyssaviruses (culture only) Shigella dysenteriae type I (cultures only) West Nile virus (cultures only) Yersinia pestis (cultures only)New and emerging pathogens should also be classified as category A until or unless additional information is received to move them to category B. For example, in 2009, shipments of Influenza A 2009 H1N1 subtype specimens were initially placed into category A until sufficient information allowed them to be moved to category B. This is not an exhaustive list. Sometimes, deciding on the classification of an infectious substance requires professional judgement and involves knowing the medical history or symptoms of the source patient or animal and/or knowing the local epidemiological conditions at the time the patient specimen or culture was obtained. If there is doubt as to whether or not a substance meets the criteria of category A, it must be treated as a category A substance for shipping.

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Preliminary Identification of the Primary Select Agents of Bioterrorism
Toxins

Toxin Comment Most Likely Means of Dissemination Primary Route of Entry General Signs and Symptoms Laboratory Testing Botulism toxin: Gram stained image of C. botulinum courtesy of CDC Produced by Clostridium botulinum Could be purified and used in a bioterrorist event to contaminate food or aerosolized to cause disease Aerosol Food contamination Inhalation Ingestion Difficulty speaking or swallowing Blurred or double vision Drooping eyelids (ptosis) Dilated pupils Dry mouth, decreased gag reflex Weakening of the reflexes (hyporeflexia) Abnormal sensations such as numbness, tingling, and progressive arm or leg weakness Flaccid paralysis Culture, anaerobic Digoxigen-labeled IgG ELISA to detect A, B, E, and F toxins Mouse Bioassay for all toxin types and to confirm DIG ELISA Ricin toxin: Extracted from Castor beans Inhibits protein synthesis Causes death approximately 72 hours after initial exposure As an aerosol Inhalation Fever Cough Chest tightness Dyspnea Cyanosis Gastroenteritis Necrosis Antibody detection in clinical specimens Clinical testing not performed unless known exposure has occurred

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Transfusion Reactions
Sources of Contamination

Possible means of blood component bacterial contamination involve the blood donor, the collection process, the collection pack, and blood processing. Most bacteremic individuals are symptomatic and would not be accepted as donors. In the United States, a person cannot donate if their temperature is higher than 37°C. Sometimes a donor may be in an incubation period or in the recovery phase of bacterial infection and this may lead to contamination of their blood products. Most of the organisms isolated from platelet concentrates are normal skin flora which entered the bag during venipuncture when skin is not disinfected properly. Some organisms may even remain viable on the skin after disinfection. The donor's skin may also contain unusual pathogens. Clostridium perfringens was linked to a donor who had recently changed a child's diaper. Blood bags can be contaminated on the outer surfaces. The bacteria can enter the unit at the time of blood donation either through suction into the needle or contamination of the phlebotomist's hands and then on the donor's skin. Contamination during blood processing can occur from thawing frozen products in a contaminated water bath. Bacteria can enter the unit through microcracks in the bags or through pooling.

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