case study botulism answers

Case Presentation

Sarah, a twenty-one year old student at Iowa State University had spent Thanksgiving day with relatives at her grandparents' farm. During her drive back to campus on Friday morning her vision became blurry, and she was forced to pull over to the side of the road. As she sat in her car, her vision worsened. She opened the car hood in hope of attracting aid and tried to relax. In a short time, a highway patrol officer pulled over and approached Sarah. By this time, Sarah was having trouble swallowing and speaking clearly. The officer helped Sarah to his car and rushed her to the emergency room at a nearby hospital.

In the ER, Sarah was able to describe her symptoms to a physician. The physician made note of what Sarah had eaten during the last 24 hours and was especially interested in the fact that Sarah's grandmother canned all of her own vegetables. The physician observed that Sarah's breathing was becoming labored. She ordered Sarah's blood sampled, her gastrointestinal tract pumped, and a mechanical respirator prepared for use. Fearing that Sarah suffered from a case of botulism, she asked that Sarah's grandparents be contacted and samples of the Thanksgiving meal retained, if possible, and sent to a local clinic for analysis.

Case Background

Botulism is a form of food poisoning caused by exposure to a toxin called botulin. Botulin is produced by , a spore forming, anaerobic bacterium that can contaminate food. Whereas commercially canned foods are specifically heated to destroy botulinum spores, home canned foods that are not boiled for a half-hour prior to canning may be contaminated.

The botulin toxin binds to the presynaptic membranes at motor end plates and prevents the release of acetylcholine from motor neurons, thereby preventing synaptic transmission and muscle contraction. Treatment includes bed rest, and if required, mechanical respiration, and/or administration of drugs to promote acetylcholine release. The mortality rate for botulism is about 15 percent and the cause of death is suffocation.

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Case Report

Food-borne botulism: still actual topic, waldemar brola.

1 Neurology Department with Stroke Unit, Specialist Hospital in Konskie, Konskie, Poland

Malgorzata Fudala

Szymon gacek.

2 Neurology Department with Stroke Unit, District Hospital Bedzin—Czeladz, Czeladz, Poland

Pawel Gruenpeter

Even though since the mid-1990s the number of food-borne botulism cases has systematically decreased and it now occurs in Poland relatively rarely, it is still a real epidemiological problem. There are about 30 cases of botulism in Poland a year, which ranks Poland the first among the European Union. In most cases the symptomatology of botulism is typical, however it does not always fully coincide with the one described in medical manuals which emphasise the dramatic clinical course of botulism with its frequent fatal consequences. Diagnosis of botulism may be difficult because of its rare prevalence and a variable clinical course, especially in old patients. Authors of this paper describe two cases of botulism and diagnostic problems associated with it.

Cases of food-borne botulism are presently uncommon in countries of the European Union; however, in Poland still over 30 cases of food-borne botulism emerge every year. Labour-related emigration to numerous European countries and still persistent tradition of preparing home-made tinned food in polish households may be the cause of emergence of botulism in countries in which it was absent for years. It is worthwhile reminding the symptoms of this dangerous poisoning and difficulties concerning its diagnosis and treatment.

Case presentation

A 71-year-old woman presented with a 2-day history of stomach ache, nausea and vomiting before diplopia appeared. Upon neurological examination diplopia was found when looking from side to side, with no signs of other cranial nerves involvement or central nervous system damage. Biochemical and haematological investigations were normal apart from mildly lowered level of potassium (2.6 mmol/l). Abdominal ultrasound and CT head scan were normal too. The next day (fourth day since the first symptoms) the patient's conditions suddenly deteriorated. Total bilateral ptosis occurred with ophthalmoparesis to all directions, dilated fixed pupils, hoarseness, dysphagia and mouth dryness. A more detailed interview revealed that on the day before the first symptoms appeared, the patient ate homemade marinated mushrooms. Serology for botulinum toxin was performed. The patient was provided symptomatic treatment to regain water–electrolyte balance. Shoulder paresis and breathing difficulties were observed, but there was no necessity to start mechanical ventilation. Owing to the quickly deteriorating general condition of the patient, a decision was made to immediately administer a polyvalent ABE botulinum antitoxin (150 ml intravenously). To avoid allergic reaction, the patient was also given 70 mg of prednisolone. The patient had no difficulty in breathing, but her general condition did not improve. The next day an additional dose of 80 ml antitoxin was given intramuscularly. The patient was fed through a gastric tube. On day 6 of hospitalisation the patient was stable and neurological symptoms were subsiding. Serological tests confirmed the presence of botulinum toxin type B/E in the blood. The patient was discharged after 21 days in a good general condition with no neurological symptoms.

A 29-year-old patient was presented with diplopia, vertigo and gait abnormality for the previous 4 days preceded by nausea and stomach ache. Neurological examination revealed mild divergent strabismus of the left eye, bilateral ptosis, diplopia when looking from side to side, increased deep reflexes in lower limbs, mild left-sided ataxia and a positive Romberg's test. CT head scan was normal. Cerebrospinal fluid analysis revealed protein and glucose levels to be within their normal reference ranges; cellular pleocytosis was 17/µl and absence of oligoclonal bands, IgG and IgM antibodies for Borrelia burgdorferi were not detected. Oligoclonal bands were not found. An MRI of the head and chest x-ray were normal. There were no antibodies found for acetylcholine receptors. Mycobacterium tuberculosis infection was excluded. On the third day of hospitalisation, the patient's condition exacerbated when difficulty in swallowing solid food was observed. The patient also complained of mouth dryness and persistent constipation. Further, a detailed history revealed that the patient had eaten tinned meat about 24 h before the first gastrointestinal symptoms occurred. Serum for botulinum toxin collected on day 11 of hospitalisation showed type B botulinum toxin. ABE anti botulinum serum was not given because of satisfactory general condition of the patient and the period of time that had already passed from the onset of infection. The patient was treated symptomatically. Fluids were introduced intravenously to preserve proper electrolyte balance. During a few days of hospital treatment, gradual recession of neurological symptoms was observed.

Outcome and follow-up

The ‘Case 1’ patient was discharged after 21 days in a good general condition with no neurological symptoms. During the first year following hospitalisation she complained of fatigability, periodically recurrent mood changes and habitual constipation, but there were no abnormalities found upon neurological examination.

The ‘Case 2’ patient was provided conservative treatment for the next few days after the final diagnosis and then discharged from hospital in a good general condition. In the course of 1-year outpatient observation there were no signs of neurological symptoms or any further complications.

Botulism is caused by neurotoxins produced by anaerobic sporogenic Clostridium botulinum , or more rarely by Clostridium butyricum , Clostridium baratii or Clostridium argentinese. 1 2 Eight botulinum toxins were identified on the basis of amino acid compositions and antigenic properties: A, B, Cα, Cβ, D, E, F, G. Botulinum poisoning in humans is usually caused by toxins of A,B,E and sometimes F type. 1–3 Clinical symptoms of botulism occur owing to inhibited release of acetylcholine in neuromuscular connections of motoneurons and synapses of parasympathetic nervous system. 3 Most cases of botulism in Europe result from ingestion of contaminated (type B toxin) homemade tinned meat. 4 Clinical signs of botulism appear after incubation period which lasts several hours—8 days. 2 3 They are usually preceded by nausea, vomiting, stomach ache and loose stools. Clinical botulism includes symmetrical cranial nerves palsy with secondary symmetrical ascending flaccid paralysis, which can lead to respiratory arrest. Symptoms develop in a few hours to a few days and need several weeks or months to subside. 3 5 The most common complications in botulism are aspiration pneumonia and urinary tract infections. 3 Death rate amounts to 7–10%. 1–3

Classic botulism is nowadays a rare condition. In Europe there are only sporadic cases of it, in USA there are about 110 cases of botulism a year, most of which are cases of infant botulism. 5 In Great Britain, in the past 80 years there have been only 62 cases of food-borne botulism. 6 However, in these countries wound botulism in drug addicts seems to be a growing problem. In 2006, in Ireland the first in 20 years case of food-borne botulism was diagnosed in a man of Polish nationality who got poisoned after ingesting homemade food sent to him from Poland. 6 In a Munich Clinic of Toxicology there were two cases described of such poisoning in 1999 and 2006. 6 In Poland, over the last 10 years, however, there have been about several dozen cases of botulism every year. In mid-1990s there were over 100 cases, and in 2009–2010 about 30. 7 The two cases described in this article were registered in 2010 in two different neurological wards.

Even though recognising botulism on the basis of clinical picture and epidemiological history is relatively easy, it is not always remembered that botulism is still a possibility. Moreover, the course of this disease is sometimes untypical, especially in older people. In the two cases described above, the delay in treatment was owing to several factors: long incubation period, mildly symptomatic course and mistaken preliminary diagnosis (both cases were at first diagnosed as gastroenteritis). The fact that the patient had eaten mushrooms additionally blurred the clinical picture. Literature review shows that food-borne botulism caused by marinated mushrooms is not as rare as it may seem. 8 9

Even though botulinum intoxication is rare, it should always be taken into account in differential diagnosis, because early diagnosis may turn out to be crucial for a successful treatment. Development of diagnostics extorts performing numerous detailed tests which is both time-consuming and expensive. The cases described in this paper were treated in two different ways and the final result was successful in both of them. The use of antibotulinum serum is still problematic, since it should be administered in the early stages, whereas its availability is limited. On the other hand, if the treatment is not successful, patients or their families may lodge a complaint that the serum was not used, thus it is advised to treat every case individually.

Learning points

• Consider botulism as a cause of patient's cranial nerves palsy and ascending flaccid paralysis.
• Ask the patient of ingesting homemade marinated food—if yes, collect serum for toxin detection.
• Antibotulinum serum treatment is not required in every case of botulism.

Competing interests: None.

Patient consent: Obtained.

Provenance and peer review: Not commissioned; externally peer reviewed.

• Case report
• Open access
• Published: 20 December 2021

Botulism outbreak in a rural Ethiopia: a case series

• Tigist Bacha   ORCID: orcid.org/0000-0002-8322-1612 1 ,
• Ermias Abebaw 7 ,
• Ayalew Moges 7 ,
• Amsalu Bekele 2 ,
• Afework Tamiru 3 ,
• Ishmael Shemsedin 4 ,
• Dawd S. Siraj 5 ,
• Daddi Jima 6 &
• Wondwossen Amogne 2  

BMC Infectious Diseases volume  21 , Article number:  1270 ( 2021 ) Cite this article

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Foodborne botulism, a toxin-mediated illness caused by Clostridium botulinum, is a public health emergency. Types A, B, and E C. botulinum toxins commonly cause human disease. Outbreaks are often associated with homemade and fermented foods. Botulism is rarely reported in Africa and has never been reported in Ethiopia.

Case presentation

In March 2015, a cluster of family members from the Wollega, Oromia region, western Ethiopia presented with a symptom constellation suggestive of probable botulism. Clinical examination, epidemiologic investigation, and subsequent laboratory work identified the cause of the outbreak to be accidental ingestion of botulinum toxin in a traditional chili condiment called “Kochi-kocha,” cheese, and clarified butter. Ten out of the fourteen family members who consumed the contaminated products had botulism (attack rate 71.4%) and five died (case fatality rate of 50%). Three of the patients were hospitalized, they presented with altered mental status (n = 2), profound neck and truncal weakness (n = 3), and intact extremity strength despite hyporeflexia (n = 3). The remnant food sample showed botulinum toxin type A with mouse bioassay and  C. botulinum type A with culture. Blood drawn on day three of illness from 2/3 (66%) cases was positive for botulinum toxin type-A. Additionally, one of these two cases also had  C. botulinum type A cultured from a stool specimen. Two of the cases received Botulism antitoxin (BAT).

These are the first confirmed cases of botulism in Ethiopia. The disease occurred due to the consumption of commonly consumed homemade foods. Definite diagnoses of botulism cases are challenging, and detailed epidemiologic and laboratory investigations were critical to the identification of this case series. Improved awareness of botulism risk and improved food preparation and storage may prevent future illnesses. The mortality rate of botulism in resource-limited settings remains high. Countries should make a concerted effort to stockpile antitoxin as that is the easiest and quickest intervention after outbreak detection.

Peer Review reports

Foodborne botulism, a toxin-mediated illness caused by  C. botulinum, is a public health emergency. C. botulinum is a heterogeneous group of gram-positive, rod-shaped, spore-forming, obligate anaerobic bacteria. It is ubiquitous and easily isolated from the surfaces of vegetables, fruits, and seafood, and exists in soil and marine sediment worldwide. The bacterium produces lethal toxins types A, B, E, and F [ 1 , 2 , 3 ].

Clostridium botulinum toxins cause human disease, with toxin type A accounting for over half of all cases [ 4 , 5 ]. Other Clostridium species such as toxigenic strains of Clostridium baratii , Clostridium butyricum , and Clostridium argentinensis less commonly produce botulinum neurotoxins [ 6 ] . There are multiple transmission mechanisms. Foodborne botulism happens when  C. botulinum grows and produces toxins in food before consumption. Unlike foodborne botulism, infant botulism occurs when infants ingest C. botulinum spores, which germinate in the gut and release toxins. Wound botulism is rare and occurs when spores get into an open wound. Inhalation botulism is associated with accidental or intentional events (such as bioterrorism), resulting in the release of toxins in aerosols. There is no human-to-human transmission of botulism [ 3 ].

Botulism outbreaks are often associated with improperly processed homemade and fermented foods. Diagnosis is made in a cluster of cases with acute, bilateral cranial neuropathies and symmetrical descending motor weakness without fever and loss of consciousness. Mouse bioassay is the gold standard for diagnosis [ 7 ].

Foodborne botulism is rarely reported in Africa and never before in Ethiopia. It is due to its rare occurrence, low clinical index of suspicion, and limited diagnostic capacity [ 1 , 8 ].

Kenya reported two foodborne botulism outbreaks that occurred 1 year apart. The first cases were reported among Kenyan nomads in 1978 when a C. botulinum TypeA outbreak from traditionally prepared milk caused six deaths [ 9 ]. One year later, another outbreak in Kenya was caused by eating contaminated termites [ 8 ], and five of six cases were fatal. In April 1991, over 90 patients were admitted to the Cairo hospital with symptoms consistent with botulism [ 10 ]. Samples of implicated food subsequently grew C. botulinum . Eighteen of the patients (20%) died of the illness. In February 2002, two siblings (aged eight and 12 years old) from South Africa developed acute flaccid paralysis and died. The implicated cause was a preformed toxin in canned food that was commercially produced in South Africa [ 11 ]. In October 2008, botulism was reported in three Ugandan boarding-school students [ 12 ]. Morocco reported 15 cases of food-borne botulism in 1999 [ 13 ]. Finally, a suspected outbreak of botulism affecting three patients in a family of six was reported in Nigeria after the family ate a home-cooked meal of pounded yam with fresh fish pepper soup. The clinical presentation of the three affected cases was consistent with botulinum poisoning. Two of the affected cases died. The third case survived after the administration of appropriate antitoxin. Samples were tested but did not show C. botulinum [ 1 ].

From 1986 to 2015, 466 confirmed cases of botulism were recorded in Italy (421 were food-borne). The most frequently seen form of botulism is due to the consumption of improperly canned foods at home, and 50% of such cases were registered in Europe. Itsuggests the need to raise public awareness of the risk of foodborne botulism, especially concerning home-preserved foods, as well as improving the training of health providers to ensure a quick and accurate diagnosis of botulism [ 14 ]. This case series describes an outbreak of foodborne botulism in a rural community from the west Wollega, Oromia region, western Ethiopia.

A case of botulism is defined as symptoms, signs, and neuro-diagnostic studies consistent with botulism [ 9 ]. Cases symptoms were identified through interactive interviews, medical record reviews, and systematic clinical examinations and by accounts of symptoms reported by family members in the cases of deaths before the investigation began. Cases with atypical presentations for botulism were evaluated with electrodiagnostic and cerebrospinal fluid (CSF) testing to determine if findings were consistent with an alternative illness. Laboratory diagnostic testing was performed on biological specimens and food samples.

Confirmed cases are defined as botulinum toxin is detected from a biologic specimen (serum or stool) or C. botulinum is cultured from stool. Serum, stool, and food samples were tested by mouse bioassay and mass spectrometry for different types of botulinum neurotoxin (BoNT); food and stool samples were cultured for isolation of botulinum toxin-producing clostridium. BoNTs are synthesized mostly by Clostridium species named Clostridium botulinum and more rarely by other Clostridium species such as toxigenic strains of Clostridium baratii type F, Clostridium butyricum type E, and Clostridium argentinensis [ 15 , 16 ]. Botulinum isolates were further characterized by Whole genome sequencing (WGS).

These case definitions were set in line with the Ethiopian Public Health Emergency Management guidelines developed by the Ethiopian Public health institute (EPHI). EPHI is the institution responsible for dealing with outbreaks/surveillance in Ethiopia [ 17 ]. The Oromia Regional State Health Bureau and EPHI, together with US Center for Disease Prevention and Control (CDC), investigated the described outbreak. The cases were reported from Oromia Region, West Wollega, West Ethiopia.

Description of the outbreak

The outbreak occurred in a family of 14 members after a celebration where homemade cultural food was served. The first reported onset of symptoms (n = 2 cases) was on March 8, 2015, one day after the ceremony. A cluster of 10 cases of probably 14 family members fulfilled the clinical diagnostic criteria with an attack rate of 71.4% (Table 1 ). The median age of the cluster was 19 years old (range 4–45 years) and six (60%) were female. The onset of symptoms was marked with fatigue, headache, dysphagia, vomiting, blurred vision, and slurred speech. Physical findings included bradycardia, cranial nerve palsies (ptosis, dysarthria, dysphonia, dysphagia), and bilateral upper and lower extremity weakness. Five of the ten symptomatic cases died (case fatality rate 50%); three died before they arrived at district hospital (one at home and two on the way to the hospital), two died at the district hospital where intensive care unit (ICU) and mechanical ventilators were not available. Three cases were referred to a tertiary care facility in Addis Ababa where two were admitted to the ICU; one required mechanical ventilator support. The remaining six (2 symptomatic and 4 asymptomatic) were observed at the district hospital and discharged.

Clinical manifestations

The clinical data are summarized in (Table 2 ). The onset was abrupt. Symptoms with the highest frequency were fatigue (9/10), difficulty opening eyes (9/10), headache (8/10), dysphagia (8/10), slurred speech (7/10), visual disturbance (7/10), difficulty supporting the head (7/10), and vomiting (6/10). Those who were hospitalized demonstrated altered mental status (n = 2), profound neck and truncal weakness (n = 3), and intact extremity strength (n = 3). Additionally, they had hyporeflexia and autonomic findings including diarrhea and reactive pupils without mydriasis (n = 1). A 4-year-old child who survived the illness had a classic presentation of descending paralysis that started with headache, vomiting, and blurred vision, followed by dysphagia and upper and lower extremity weakness. An adult case, which required mechanical ventilation also, had classic descending paralysis. Two adult ‘patients’ received 20 mL of BAT as an intravenous I.V. infusion.

Among the survivors, three of the patients with severe disease were referred to tertiary care. Of those, one adult patient was discharged with residual weakness of the extremities. The 4 year old child had improved body weakness but had still bilateral ptosis. The third patient's muscle weakness fully recovered, returning to a fully functional status. Six patients, who were observed at a nearby district hospital for a few days were discharged with no neurologic sequelae or functional abnormalities.

Clinical laboratory testing

Serum and stool samples were tested by mouse bioassay and mass spectrometry for botulinum neurotoxin. Food and stool samples were cultured for isolation of C. botulinum . Foods suspected to be contaminated by the toxin and accessible at the affected households were collected; minimal gelatin phosphate buffer was added and the specimens with detected botulinum toxin were cultured for botulinum toxin-producing clostridia. Blood drawn on the third day of illness from two of the cases was positive for botulinum toxin type A. One of the two cases also had C. botulinum type A cultured from a stool specimen.

Three patients had electromyography (EMG) that confirmed neuromuscular dysfunction severely affecting the face and proximal upper extremity muscles. The 4 year old child had a lumbar puncture with CSF that showed 3 nucleated cells, protein = 37.7 gm/dl, glucose = 98 mg/dl, Gram stain, and culture showed no organism.

Food vehicle investigation

An extensive dietary history was taken in all cases with a clinical diagnosis of botulism. The extended family shared a common food source and were served from the same plate. One day before the first onset of symptoms, nine of the family members with clinical diagnosis ate sorghum porridge with cheese and yogurt for lunch. The cheese was kept for an indefinite time in a tightly sealed container. A traditional food called “kochi-kocha” and butter were added to the cheese prior to eating. One family member ate the kochi-kocha with bread (no sorghum porridge) and did not get ill. The chili condiment “Kochi-Kocha” (which is made from fresh green chili, clarified butter, ginger, garlic, salt, “Besobila Footnote 1 ” and “Tenaadam Footnote 2 ”), and clarified butter were both kept at room temperature in airtight sealed plastic containers separately for an average of 3 days. On the same day, all household members ate Injera (a national staple made of fermented Teff) and bean stew prepared with clarified butter for breakfast and dinner.

Food vehicle laboratory testing

The testing revealed C. botulinum toxin from the chili condiment “Kochi-Kocha” and the clarified butter. The “Kochi-Kocha” was also positive by mouse bioassay for botulinum toxin type A. A very tiny remnant of clarified butter that was collected from the empty container was found to be weakly positive. C. botulinum type A was cultured from two dried specimens which contain milk and cheese collected from gourd containers (Table 3 ).

The clinical specimens and food specimens, i.e., dried cheese, dried milk, clarified butter, and a chili condiment, contained either BoNT type A or C. botulinum type A. The A2 subtype of the BoNT gene was identified in all C. botulinum isolates. Whole genome sequencing and single nucleotide polymorphism (SNP) analysis showed that the isolates from the samples (both clinical sample and food sample) are related and have a common ancestor. However, it should be noted that the result couldn’t definitively confirm the source of the spores as there was a possibility of cross-contamination during food preparation.

Public health measures

All food items used in the preparation of the implicated meal served in the ceremony were removed from the house and destroyed. The remaining family members were oriented to appropriately clean utensils in the house before using them for food preparation. Heath extension workers in the area were trained about the natural reservoir, mode of transmission, the natural history of C. botulinum, and how it can be prevented so that they will promote awareness in their regular communication with the community.

Discussion and conclusion

This case report describes the first proven cases of foodborne botulism in Ethiopia. The outbreak was caused by toxin type A botulinum toxin. The case fatality rate of the outbreak was 50% and the attack rate was 71.4%. This is similar to other case reports of foodborne botulism reported elsewhere [ 9 , 12 , 13 , 18 , 19 ]. Botulinum toxin is a highly poisonous neurotoxin synthesized by the bacteria  C. botulinum . The initial consideration of botulism based on its clinical presentation and clustering of the cases is the most important step to diagnosis and quickly managing clinical care.

Symptoms of foodborne botulism usually begin 12 to 36 h after ingestion of the preformed toxin [ 7 ]. In our cases, the incubation period varied between 1 to 3 days. Incubation periods as long as 1 week are seen when the volume of the preformed toxin inoculum is small. Symptoms predominantly include the involvement of the gastrointestinal tract and the central nervous systems [ 20 ]. As recognized during the previous foodborne botulism outbreaks, the attack rate is not 100% [ 19 , 21 ]. In our case series, the attack rate of 70% among those who ate is explained by an uneven distribution of the toxin in the food, a dose–response relationship, or unrecognized host factors that confer resistance to the toxin.

Clinical presentation and demonstration of toxin in the blood, stool, vomitus of a suspected case, or food items help to make the diagnosis of foodborne botulism [ 13 ]. In this outbreak, as is common in foodborne botulism, diarrhea was a common early symptom [ 2 ]. Diarrhea is caused by toxins other than botulinum toxin including bacteria and/or viruses contaminating the same source of food. Pupils could be reactive without mydriasis, as in the described cases, because the parasympathetic fibers in the oculomotor nerve were spared. Altered mental status in cases of botulism could be due to lack of adequate oxygenation, infection, or other metabolic disorders [ 22 ].

Clinical signs and symptoms and epidemiologic investigation of cases are critical, especially when laboratory test results may be delayed or unavailable. The differential diagnosis of food-borne botulism includes myasthenia gravis, tick paralysis, Guillain–Barre syndrome, poliomyelitis, stroke, and heavy metal intoxication [ 4 ].

In our report, all cases consumed cheese with “Kochi-Kocha,” which was made from chili and butter. Botulinum toxin type A was identified from the cheese, butter, and chili. All foods were stored in sealed containers which can create an oxygen-free environment, thereby favoring the germination of clostridium. Fats can provide the low acidity environment necessary for anaerobic bacteria need for spore germination and toxin elaboration. The plastic sealed containers facilitate the anaerobic environment. The chili is grown in soil and can harbor bacterial spores. There was also the possibility of cross-contamination of toxins while serving the food.

Due to the limited diagnostic capacity, the prevalence of the disease in Ethiopia is not well known. Early recognition of botulism is critical for the treatment of cases and to limit the extent of the outbreak by potentially identifying the possible contaminated food sources. The mainstay of treatment is respiratory support with over 34% requiring mechanical ventilation [ 5 , 14 ], a major limitation in Ethiopia. Botulism antitoxin (BAT) when given early in the disease process can neutralize circulating botulinum toxin, stopping the further progression of the disease. Unfortunately, antitoxin does not reverse the damage that has already been occurred [ 23 ]. Unfortunately, BAT is not readily available in Ethiopia.

Our investigation has limitations. Investigators were not able to interview or examine all the cases. It was also not possible to collect biological samples from all of the cases. The informants about the symptoms of the cases might have recall bias.

The mortality rate of botulism in developing countries with limited resources remains high. Important contributing factors include delay in diagnosis, lack of antitoxin, and the limited presence of an intensive care support system that providers for ventilator support. Countries should make a concerted effort to stockpile antitoxin, as that is the easiest and quick way of intervening upon outbreak detection.

This outbreak investigation can be considered a baseline for public health teams on how to detect and respond to similar outbreaks in the future. At the Ministry of Health and Regional Health Bureau level, a combined strategy of disease surveillance, recognition, confirmation, and treatment has to be devised to assess the extent of botulism and develop prevention strategies for this newly confirmed disease in Ethiopia. There should be a strong partnership between clinicians and public health authorities at all levels for rapid detection of possible clusters of botulism and complete investigation to identify the primary source of infection and the specific process of the risk introduction of the bacilli into the implicated food. Efforts should also be made to inform communities about the risk of food storage practices and the types of food liable for spore contamination. Systematic ongoing surveillance using standardized botulism case definition must be introduced and integrated with the existing acute flaccid paralysis surveillance system. It is also essential to establish a system of referral and logistics where patients suspected of botulism could easily be transported for inpatient admission to provide care such as mechanical ventilation, botulism antitoxin, and nutritional rehabilitation.

Availability of data and materials

The data sets used and/or analyzed during the current study are available from the corresponding author on reasonable request. Data is archived from the Ethiopian Public health institute.

A local herb whose scientific name is Ocimum sanctum/tenuiflorum .

Another local herb is considered to have medicinal value and is used as a flavoring additive. Its scientific name is Rutachalepensis L.

Abbreviations

Botulism antitoxin

Center for disease control and prevention

Cerebrospinal fluid

Electromyography

Ethiopian Public health Institute

Intensive Care Unit

Whole genome sequencing

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Acknowledgements

The authors would like to thank the Federal Ministry of Health, Ethiopian Public Health Institute, Oromia Regional State Health Bureau, and Tikur Anbessa Specialized Hospital and Saint Paul hospital for providing detailed patient information. Our special thanks go to the US CDC of Atlanta and Ethiopia for the facilitation of laboratory testing. The authors focused on the clinical presentation of these patients and the authors acknowledge Ethiopian Public Health Institute conducted the fieldwork in collaboration with the CDC and Tikur Anbessa Specialized Hospital.

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Department of Pediatrics and Child Health, Saint Paul, Millennium Medical College, Addis Ababa, Ethiopia

Tigist Bacha

Department of Internal Medicine, College of Health Sciences, School of Medicine, Addis Ababa University, Addis Ababa, Ethiopia

Amsalu Bekele & Wondwossen Amogne

Department of Public Health, Institute of Health Sciences, Wollega University, Nekemte, Ethiopia

Afework Tamiru

Department of Emergency Medicine and Critical Care, Saint Paul, Millennium Medical College, Addis Ababa, Ethiopia

Ishmael Shemsedin

Division of Infectious Diseases, University of Wisconsin-Madison School of Medicine and Public Health, Madison, USA

Dawd S. Siraj

Ethiopian Public Health Institute, Addis Ababa, Ethiopia

Department of Pediatrics and Child Health, College of Health Sciences, Addis Ababa University, Addis Ababa, Ethiopia

Ermias Abebaw & Ayalew Moges

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TB and EA performed the search and collection of the cases. TB performed the case and data analysis and literature search and wrote the manuscript. TB, EA, AM, AT, AB, IS, DS, DJ, and WA helped with case analysis, refining the manuscript, and making the final corrections to the article. All authors read and approved the final manuscript.

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Correspondence to Tigist Bacha .

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Bacha, T., Abebaw, E., Moges, A. et al. Botulism outbreak in a rural Ethiopia: a case series. BMC Infect Dis 21 , 1270 (2021). https://doi.org/10.1186/s12879-021-06969-w

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Received : 14 December 2020

Accepted : 10 December 2021

Published : 20 December 2021

DOI : https://doi.org/10.1186/s12879-021-06969-w

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