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Year : 2009  |  Volume : 52  |  Issue : 4  |  Page : 592
A six month-old girl with botulism due to honey ingestion

Infectious Diseases and Tropical Medicine Department, Loghman Hospital, Shaheed Beheshti Medical University, Tehran, Iran

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Date of Web Publication1-Oct-2009

How to cite this article:
Vahdani P, Abbasi F, Mojarad MA, Velayati AA, Boloorsaz MR, Musavipour F, Vahdani G. A six month-old girl with botulism due to honey ingestion. Indian J Pathol Microbiol 2009;52:592

How to cite this URL:
Vahdani P, Abbasi F, Mojarad MA, Velayati AA, Boloorsaz MR, Musavipour F, Vahdani G. A six month-old girl with botulism due to honey ingestion. Indian J Pathol Microbiol [serial online] 2009 [cited 2022 Jul 4];52:592. Available from: https://www.ijpmonline.org/text.asp?2009/52/4/592/56139


Botulism is a potentially fatal infectious disease induced by a neurotoxin secreted by Clostridium botulinum. This neurotoxin inhibits the normal release of acetylcholine in the synaptic cleft, inducing presynaptic neuromuscular blockade. [1] It affects both the peripheral nervous system, causing diffuse paralysis, and the autonomous nervous system, inducing vegetative disturbances which worsen the vital prognosis. [2] The patient was a six month-old girl who was referred to our hospital with bilateral ptosis, poor feeding, and weakness. The patient was admitted in the hospital due to muscle hypotonicity. Lumbar puncture was done, cerebrospinal fluid (CSF) was normal. Due to muscle weakness, electromyography (EMG) and nerve conduction velocity (NVC) study were done to rule out neuromuscular disorders. Both EMG and NVC were normal. Brain magnetic resonance imaging (MRI) was normal. With impression of encephalitis, lumbar puncture was performed again. CSF was normal. The patient was then admitted to our hospital. She was the first child of a G1P1A0 healthy mother with birth weight of 2700 gm. Vaccination was complete. She had history of eating honey three weeks ago. The honey was not pasteurized. Three kilograms of this honey was taken from a village vendor by baby's father one year ago. It had been stored for about one year. She had been constipated for two weeks. On physical examination, her measurements were as: weight= 5630 gm, head circumference = 41 cm, and height= 66 cm. T=36.5΀C, pulse rate=120/min, respiratory rate=24/min. She was conscious and orient, bilateral ptosis was obvious, eye movements were normal. She was floppy and was not able to hold her neck. Gag reflex was weak. Examination of heart, lungs, abdomen was normal. Deep tendon reflex (DTR) of upper and lower extremities was normal. There was no sensory level. Tonicity of muscle was decreased. Lab data was as follow:

Complete blood count: WBC (white blood count) = 10800, Hb (hemoglobin) = 10 g/dl, Platelet= 356000, FBS (fasting blood sugar) = 70 mg/dl, Urea= 20 mg/dl, Cr= 0.6 mg/dl, Ca= 8.7 mg/dl, Na= 136 meq/dl, K= 4.3 meq/dl, arterial blood gas was normal, urine analysis was normal. Chest-x-ray was normal. There was no infiltration, lungs fields were clear. Shadow of heart was normal. With impression of botulism, conservative management started for her. Oral feeding discontinued and nasogasteric tube was inserted. Laxative was started for her. Stool was evaluated for botulinum toxins that was positive for botulinum toxin-A. The honey was not available for botulism analysis. Due to delayed diagnosis and improvement of general condition with conservative management, botulinum anti-toxins did not started for her. Ptosis and muscle weakness gradually disappeared and constipation improved. Gag reflex got normal gradually. She was discharged to home with follow up while she was able to sit and hold the neck.

Botulism has four naturally occurring syndromes: food borne, wound, infant botulism, and adult intestinal toxemia. [3] Infant botulism results from the absorption of heat-labile neurotoxin produced in situ by ingested C. botulinum. Honey and environmental exposure are the main sources of acquisition of the organism. Clinical manifestations are owing to progressive neuromuscular blockade, initially of muscles innervated by cranial nerves and later of the trunk, extremities, and diaphragm. Presynaptic autonomic nerves are also affected. Diagnosis is made on clinical grounds and is confirmed by recovery of the organism or by detection of toxin in the stool. [4] In our case, diagnosis was made upon history of honey ingestion, clinical manifestation such as bilateral ptosis, weakness, constipation, and recovery of botulinom toxin-A from stool. Management of botulism includes supportive intensive care and administration of human botulinum immunoglobulin in severe cases. [4] In a botulism outbreak in Taiwan, none of the patient received antitoxin administration because of delayed diagnosis. [5] We did not use anti-toxin in our patient because of delayed diagnosis.

   References Top

1.Gentil A, Soichot P, Maugras C, Lemesle-Martin M, Bιjot Y, Rouaud O, et al. Botulism has not disappeared. Presse Med 2008;37:789-92.  Back to cited text no. 1      
2.Kissani N, Najib J, Amine M, Slassi I, Abid A. Food-born botulism in children in Morocco: Report of 5 cases. Arch Pediatr 2007;14:1324-7.  Back to cited text no. 2      
3.Brook I. Botulism: The challenge of diagnosis and treatment. Rev Neurol Dis 2006;3:182-9.  Back to cited text no. 3      
4.Brook I. Infant botulism. J Perinatol 2007;27:175-80.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Tseng CK, Tsai CH, Tseng CH, Tseng YC, Lee FY, Huang WS. An outbreak of foodborne botulism in Taiwan. Int J Hyg Environ Health 2009;212:82-6.  Back to cited text no. 5      

Correspondence Address:
Farhad Abbasi
Infectious Diseases and Tropical Medicine Research Center, 7th floor, Faculty of medicine, Shaheed Beheshti Medical University, Chamran Highway, Evin, Tehran, PO Box: 19835-159
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.56139

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1 Two cases of type A infant botulism in Grenoble, France: No honey for infants
Hoarau, G., Pelloux, I., Gayot, A., Wroblewski, I., Popoff, M.-R., Mazuet, C., Maurin, M., Croizé, J.
European Journal of Pediatrics. 2012; 171(3): 589-591


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