scholarly journals Wound Botulism Caused by Botulinum Neurotoxin Type A in a Chronic Parenteral Drug Abuser

2020 ◽  
Vol 12 (3) ◽  
pp. 422-427
Author(s):  
Sohun Awsare ◽  
David Chirikian ◽  
Forshing Lui

Botulism is an acute paralytic disease caused by botulinum neurotoxin (BoNT)-mediated inhibition of neurosignaling at the neuromuscular junction. BoNTs are produced by gram positive, anaerobic, spore-forming bacteria from the genus <i>Clostridium,</i>most commonly<i> Clostridium botulinum</i>. Over the last decade, a previously uncommon form of botulism, wound botulism, has increased in prevalence possibly due to the rise in parenteral drug abuse. A 53-year-old patient with a history of drug abuse presents to a rural emergency department with rapidly progressing lower extremity weakness over the past few days. He reports a recent heroin injection into right buttock and diffuse skin-popping scarring was observed throughout. The patient was treated with heptavalent botulinum antitoxin obtained from the Center for Disease Control and Prevention (CDC). A right thigh abscess culture was positive for<i> Clostridium tertium</i>, a left hip abscess culture was positive for methicillin-susceptible <i>Staphylococcus aureus</i> (MSSA), and blood culture confirmed multi-microbial bacteremia caused by <i>Staphylococcus epidermidis</i> and <i>Streptococcus mitis</i>. Serum analysis was positive for BoNT type A from a suspected concurrent<i> Clostridium botulinum</i> infection as <i>C. tertium</i> is not known to produce BoNT type A. This case report highlights the importance of early antitoxin treatment for patients with suspected wound botulism.

2005 ◽  
Vol 10 (9) ◽  
pp. 5-6 ◽  
Author(s):  
D Akbulut ◽  
J Dennis ◽  
M Gent ◽  
K A Grant ◽  
V Hope ◽  
...  

Wound infections due to Clostridium botulinum were not recognised in the UK and Republic of Ireland before 2000. C. botulinum produces a potent neurotoxin which can cause paralysis and death. In 2000 and 2001, ten cases were clinically recognised, with a further 23 in 2002, 15 in 2003 and 40 cases in 2004. All cases occurred in heroin injectors. Seventy cases occurred in England; the remainder occurred in Scotland (12 cases), Wales (2 cases) and the Republic of Ireland (4 cases). Overall, 40 (45%) of the 88 cases were laboratory confirmed by the detection of botulinum neurotoxin in serum, or by the isolation of C. botulinum from wounds. Of the 40 cases in 2004, 36 occurred in England, and of the 12 that were laboratory confirmed, 10 were due to type A. There was some geographical clustering of the cases during 2004, with most cases occurring in London and in the Yorkshire and Humberside region of northeast England.


2001 ◽  
Vol 67 (12) ◽  
pp. 5694-5699 ◽  
Author(s):  
Miia Lindström ◽  
Riikka Keto ◽  
Annukka Markkula ◽  
Mari Nevas ◽  
Sebastian Hielm ◽  
...  

ABSTRACT Botulism is diagnosed by detecting botulinum neurotoxin andClostridium botulinum cells in the patient and in suspected food samples. In this study, a multiplex PCR assay for the detection of Clostridium botulinum types A, B, E, and F in food and fecal material was developed. The method employs four new primer pairs with equal melting temperatures, each being specific to botulinum neurotoxin gene type A, B, E, or F, and enables a simultaneous detection of the four serotypes. A total of 43 C. botulinum strains and 18 strains of other bacterial species were tested. DNA amplification fragments of 782 bp for C. botulinum type A alone, 205 bp for type B alone, 389 bp for type E alone, and 543 bp for type F alone were obtained. Other bacterial species, including C. sporogenes and the nontoxigenic nonproteolytic C. botulinum-like organisms, did not yield a PCR product. Sensitivity of the PCR for types A, E, and F was 102 cells and for type B was 10 cells per reaction mixture. With a two-step enrichment, the detection limit in food and fecal samples varied from 10−2 spore/g for types A, B, and F to 10−1 spore/g of sample material for type E. Of 72 natural food samples investigated, two were shown to contain C. botulinum type A, two contained type B, and one contained type E. The assay is sensitive and specific and provides a marked improvement in the PCR diagnostics of C. botulinum.


Blood ◽  
2019 ◽  
Vol 134 (Supplement_1) ◽  
pp. 4991-4991 ◽  
Author(s):  
Juskaran Chadha ◽  
Randy L. Levine ◽  
Omer Ilyas

Background Immunoglobulin (IVIG) is used to treat autoimmune conditions, but there are reports of brisk hemolysis within 48 hours (hrs) of treatment due to anti-A isohemogglutinins(1). Despite these reports, hemolysis remains an unrecognized side effect of IVIG. Methods We presented a series of 3 cases of IVIG-induced hemolysis in patients with autoimmune neurological disorders. In the investigative phase, we traced the cases to a common IVIG lot number. The sample was tested to determine the anti-A titer levels. Case Studies (See Table 1) Case 1 75-year-old man presented with SOB and dysarthria from myasthenia gravis (MG). He received IVIG for 4 days. He developed a hemolytic anemia with 3 g drop in hemoglobin (Hb) 48 hours later. He needed a pRBC transfusion and folic acid. Case 2 59-year-old female with history of MG treated with IVIG at another hospital until 3 months earlier in crisis, with SOB and dysphagia. She received IVIG for 5 days and rituximab. She improved and was discharged, but returned to the ER 7 days later with SOB. Her Hb fell to 8.0 g/dL from 13 g/dL on last admission. She required a pRBC transfusion, folic acid, and vitamin B12 with improvement of SOB. Case 3 20-year-old female admitted for lower extremity weakness, diagnosed with presumed syndrome (GBS). She received IVIG for 4 days. On the 5th day, her Hb fell from 15 g/dL to 9 g/dL. She began prednisone, folic acid, and vitamin B12 with improvement in her Hb. Conclusions Although acute hemolysis is well described in the literature, it is under recognized, as exemplified by the first two cases. Their initial SOB was due to MG, so when SOB recurred, they were misdiagnosed with recurrent MG. A hemolytic anemia was later suspected, and a work up revealed a positive DAT. The initial eluate was negative against type O panel cells, suggesting a drug related hemolysis. It was only when the eluate was tested against type A cells that the etiology became clear. The third patient's hemolytic reaction was then rapidly identified. These cases remind us to consider IVIG induced anti-A hemolysis in patients who are blood type A and AB, and to evaluate the eluate against the appropriate reagent cells. These patients should receive specific IVIG that is low in anti-A isohemagglutinins. Since the second patient did not hemolyze from earlier exposure to IVIG, she likely received a low titer product. Disclosures No relevant conflicts of interest to declare.


2018 ◽  
Vol 10 (1) ◽  
Author(s):  
Paris A. Cook ◽  
Aimee Mishler ◽  
Dan Quan ◽  
Ashley Parrish-Garcia

Botulism is caused by toxin production from many species of Clostridium, most commonly Clostridium botulinum as well as C. baratii and C. butyricum. Development of wound botulism is associated with injection drug users but has also been described in traumatic injuries with exposure to soil. A patient presented to the emergency department with a complaint of descending, progressive weakness. He recently reported skin popping with heroin injections. Heptavalent botulinum antitoxin was obtained from the Center for Disease Control and Prevention. On hospital day seven, the anaerobic wound cultures resulted with growth of Clostridium subterminale.


1984 ◽  
Vol 3 (4) ◽  
pp. 319-320 ◽  
Author(s):  
J. Romero-Vivas ◽  
A. Guerrero ◽  
L. M. Buzon ◽  
J. Berenguer ◽  
J. Martinez-Beltran ◽  
...  

2006 ◽  
Vol 72 (2) ◽  
pp. 1231-1238 ◽  
Author(s):  
Shashi K. Sharma ◽  
Joseph. L. Ferreira ◽  
Brian S. Eblen ◽  
Richard C. Whiting

ABSTRACT An amplified enzyme-linked immunosorbent assay (ELISA) for the detection of Clostridium botulinum complex neurotoxins was evaluated for its ability to detect these toxins in food. The assay was found to be suitable for detecting type A, B, E, and F botulinum neurotoxins in a variety of food matrices representing liquids, solid, and semisolid food. Specific foods included broccoli, orange juice, bottled water, cola soft drinks, vanilla extract, oregano, potato salad, apple juice, meat products, and dairy foods. The detection sensitivity of the test for these botulinum complex serotypes was found to be 60 pg/ml (1.9 50% lethal dose [LD50]) for botulinum neurotoxin type A (BoNT/A), 176 pg/ml (1.58 LD50) for BoNT/B, 163 pg/ml for BoNT/E (4.5 LD50), and 117 pg/ml for BoNT/F (less than 1 LD50) in casein buffer. The test could also readily detect 2 ng/ml of neurotoxins type A, B, E, and F in a variety of food samples. For specificity studies, the assay was also used to test a large panel of type A C. botulinum, a smaller panel of proteolytic and nonproteolytic type B, E, and F neurotoxin-producing Clostridia, and nontoxigenic organisms using an overnight incubation of toxin production medium. The assay appears to be an effective tool for large-scale screening of the food supply in the event of a botulinum neurotoxin contamination event.


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