1. Insert Program or Hospital Logo Introduction Rapidly progressing infantile botulism can be a deadly disease if supportive care is not given early in the disease process. Case reports of babies dying in their sleep secondary to rapidly progressing infantile botulism were often times initially thought to be due to SIDS. In order to avoid devastating outcomes, it is important to diagnose and treat these with botulism immunoglobulin as early as possible. Infantile botulism does present in areas where it is not endemic in the soil such as in our case in Central Texas. It is therefore important to keep our differential diagnoses broad in a patient with rapidly progressing generalized muscle weakness without a known cause. Infantile Botulism in a 10 day old Shana Godfred-Cato, DO, PGY-2, Samira Armin, MD & Deborah Douty, MD, McLane Children’s Scott & White and Texas A&M Health Science Center College of Medicine, Temple, TX Results Abstract Infantile Botulism is a life threatening condition in which the botulism toxin causes muscle weakness, including the muscles of respiration which can lead to death if respiratory support is not given. Infantile botulism is more common in the western United States due to Clostridium botulinum presence in the soil. In Central Texas Clostridium botulinum is not endemic in the soil. This case is unique due to the patient’s age, the rapid course of illness as well as the unknown exposure to the toxin. The infant was breastfed as well as formula fed with no other foods introduced and no exposures noted by family. Possible exposures were identified to be tea with honey consumed by the patient’s mother (though she did not share this with the infant ) or possibly from soil, which was introduced into the baby’s mouth after her toddler brother was found to have his hands inside the patient's mouth after playing outside. Case report A 10 day old female with no significant past medical, family and an unremarkable birth history presented to the Children’s ER with decreased feeding, stooling and lethargy for 2 days. Her mother reported the child had been at home with no sick contacts and developed poor feeding and worsening weakness for 2 days prior to presentation. The infant required a glycerin suppository to stool 3 days prior to presentation. The infant lives with her parents and older brother on a ranch, with no indoor pet exposure. Upon initial assessment her vital signs were normal and there were no notable findings on examination. She was initially admitted to the general med/surg floor but within a few hours, developed respiratory distress and was transferred to the pediatric intensive care unit. There, was intubated secondary to respiratory muscle weakness and failure to protect her airway. This occurred less than 24 hours after admission and she required extensive rescucitation. Conclusions Botulism infection is caused from exposure to the toxin C. botulinum types A through G. The toxin is ingested and binds to the neuromuscular junction irreversibly. An equine antitoxin used for adult patients was not used for infantile botulism due to side effects 1 Therefore, a human derived immunoglobulin was developed, “Botulism immune globulin intravenous (Human) (BIG – IV), a human derived botulism antitoxin that neutralizes botulism toxin.” 1 Research shows that administration of BIG-IV during the first few days after hospital admission decreases the length of hospital admission and the number of days in the intensive care unit and on a ventilator. 1 Unique aspects of our case include the patient’s age at presentation and the rapid course of development of this disease as well the unknown exposure to C. botulinum. The patient was living in central Texas in an area not known to be endemic to C. botulinum. The exposure itself will likely remain unknown as the state of Texas chose not to test the patient’s home/environment for C. botulinum. This case serves as a good reminder to always keep differential diagnoses broad in unusual patient presentations. References 1.Arnon, S. (2006). Creation and development of the public service orphan drug human botulism immune globulin. pediatrics, 119(4), 785-789. 2.Arnon SS, Barzilay EJ. Clostridial Infections: Botulism and infant botulism. In: Pickering LK, Baker CJ, Kimberlin DW, Long SS, eds. The Red Book: 2009 report of the Committee on Infectious Diseases. Elk Grove Village: American Academy of Pediatrics; 2009:259--62. 3.Arnon SS, Schechter R, Maslanka SE, Jewell NP, Hatheway CL, Human Botulism Immune Globulin for the treatment of infant botulism. N Engl J Med. 2006;354:462-471 4.California Department of Public Health. (2010). specimen collection. Retrieved from http://www.infantbotulism.org/ 5.Hurst, D., & Marsh, W. (1993). Early severe infantile botulism. The Journal of pediatrics, 122(6), 909-911. Retrieved from http://www.infantbotulism.org/physician/Hurst_and _Marsh.pdf Texas Pediatric Society Electronic Poster Contest Due to her unexplainable clinical status, a large differential was developed. After extensive lab and imaging testing was negative, the diagnosis of infantile botulism was entertained. The California department of public health was contacted as they are the leading experts in infantile botulism and together it was agreed upon that botulism was a likely diagnosis and treatment should be initiated. A stool sample was sent to the California laboratory as well as the Texas state lab in Austin for diagnosis. Botulism immune globulin intravenous (BIG-IV) was ordered, shipped overnight and administered to the patient the following day. The stool sample confirmed; fecal botulinum toxin test and culture- C. botulinum type A. During this time respiratory and nutritional support was given. Over the course of the next days and weeks, the child regained strength and was successfully extubated and the nasogastric tube was removed. Photo from: www.natural-homerededies.com Clostridium botulinum http://www.cdc.gov/nationalsurveillance/PDFs/Botulism_C STE_2011.pdf