Food Borne Botulism is a rare disease which has been reported from Spain, Canada, Taiwan, China and Romania [1-4]. Few cases of food borne botulism are also reported from Iran [5-7].

Botulism was named after the Latin Botulus in 1820, although Clostridium Botulinum (CB) was first cultured by Van Ermengen in 1898 in Belgium [8]. CB is a gram-positive anaerobic bacterium [9]. The species C. botulinum is divided into four physiological groups (I-IV), which produce BoNTs of seven different serotypes (A-G). Physiological group I (proteolytic) includes C. botulinum strains producing toxins of serotype A, B or F and is mainly associated with human cases. Physiological group II (non-proteolytic) consists of strains producing toxins of serotype B, E or F; these strains also cause human botulism [10].

During the disease, nerve tissues collect botulinum toxin from blood which affect muscle nerve junction. As a result, inhibition of neural signaling and flaccid paralysis occur due to acetylcholine release inhibition [8]; however, sensory nerves are not affected [11].

Early symptoms of digestive poisoning with this bacterium include nausea, vomiting, abdominal pain and discomfort that occur between 12 hours to 4 days after food consumption [12]. Initial clinical manifestations include dry mouth, dysphagia, pupil dilatation, Diplopia and ptosis. During the clinical phase, a progressive, symmetric and descending muscle weakness could be observed and may lead to decreased muscle tone, urinary retention, weakness and dyspnea. Nerve palsy usually begins from III and IV central nerves. A decrease in deep tendon reflexes and constipation will then follow [16]. If untreated, respiratory failure could cause death [10].

Definite diagnosis of food botulism is possible via discovering botulinum toxin in serum, stool, gastric and intestinal contents or patient food, or noticing bacteria in the stool, stomach and intestinal contents [13]. It is also possible to inject the obtained substance to mice peritoneum and observe the consequences including paralysis or death [14]. However, these processes are time consuming [12]. In addition, in some outbreaks it is shown that toxin is undetectable in up to a third of cases [14]. Consequently, clinical findings play a crucial role in diagnosis. EMG is also useful for diagnosis [15]. CT scan and Lumbar puncture can exclude brain lesions and infections [10].

This study aimed to find clinical and paraclinical findings of botulism poisoning in Mashhad over an eight - year period.

Subjects and design

All hospital-referred botulism poisoned patients’ files were screened retrospectively from 21 March 2003 to 20 March 2010 in Imam Reza Mashhad University Hospital in Iran. Data related to patients who were discharged with another diagnosis (six cases) were excluded.

Clinical samples were collected and testing to presence of BoNT toxin from all cases related to clinical symptoms.

In addition, to find the period of time that patients have been free from symptoms after discharging, all selected patients were contacted in early 2011. This study was approved by Ethics Committee, Mashhad University of Medical Sciences.

Spreadsheets were designed for clinical, para-clinical and sociodemographic variables. Patients were divided into two groups, namely sporadic if just one case admitted and outbreak if more than one related case was admitted. Clinical and para-clinical findings’ of sporadic and epidemic botulism groups were compared. All patients but two due to hypersensitivity received antitoxin.

Diagnosis

Diagnosis was made based on history, clinical findings, respond to antidote and laboratory test for botulism.

Statistics

To analyze the obtained data t-test and chi-square were used capitalizing upon SPSS 11.5 for the statistical analysis. A probability value of less than 0.05 was considered statistically significant.

Socio-demographic

In total, 45 cases with botulism were investigated. Incidence of Botulism in Khorasan-Razavi province with a population of almost 6 million (16) varied from 1.7×10⁵ to 35.3×10⁵ from 2003 to 2010 (mean 9.8× 10⁵). No gender preferences were observed (Male % =49.9). Mean age (SD) was 39.5 (17.0) years with a minimum of 3 and a maximum of 70 years. Among them no cases died under treatment. The mean (SD, Min-Max) lag time between exposure and admission was 40.2 (33.6, 2 to 110) hours. Duration of admission was 5.3 (7.1, 1-46) days. Patients were cleared from all symptoms and signs after discharging in 8.3 (9.6, 0-39) weeks. Frequency was not different in cases living in rural or urban areas. The total number of reported cases in 2006 and 2010 were higher than other years. These cases happened more frequently in autumn and early winter (Figure 1,2). Laboratory evaluation was positive for botulism in 44.4% of food and clinical samples. The found toxin subgroup was A and B.

Figure 1: Frequency of cases in the period of study (n=45).

Figure 2: Frequency of cases in different months (n=45).

Clinical findings

On admission, vital signs (pulse, blood pressure, respiratory rate and body temperature) were within normal ranges in 37 cases and 8 (18%) cases that presented with severe clinical manifestation and needed mechanical ventilation.

In sporadic cases, most common clinical symptoms were difficult speech (92%), ptosis (91%), diplopia (67%) and nausea (58%) on admission (Table 1).

Table 1: Frequency of signs and symptoms at the time of administration in all years study

General weakness (92%), dizziness (70%) and constipation (25%) were also the most frequent signs in this group on admission (Table 1).

Most clinical symptoms in outbreak group were dysphagia (94%), ptosis (91%), diplopia (87%) and difficult speech (74%) on admission (Table 1).

General weakness (84%), dizziness (80%) and constipation (47%) were also the most frequent signs in outbreak group on admission (Table 1).

There were two outbreaks of botulism in 2003 and 2010. In these cases, lag time between exposure and admission (P=0.026), headache (P=0.026) and dysphagia (0.002) were significantly different from sporadic cases. Other clinical and para-clinical findings were not significantly different between these two groups.

Mean incidence was 0.98× 106. In other reports their incidence was lower. For example, an incidence of 0.03× 106 has been reported from Georgia, which increased in recent years [17]. This disease is far less common in the United States (0.001× 105) [18]. Reported case fatality rates vary in literature from 0% to 17% [17,19,20]. No deaths reported in this case series were similar to other studies [21,22]. Male to female ratio was rather similar in this study to Georgian, US and Tehran’s studies [17,18,23]. Age range of patients was from 3 to 78 years (in Texas) [22] and 1- 66 years (from Tehran) which are similar to our findings [23].

Laboratory confirmation was more common in this study in comparison to Georgian study (17%) [17] and less common in comparison to Tehran study [23] . It should be taken into account that in many cases, laboratory confirmation is available in later stages. As a result, clinical manifestation and response to antitoxin could be more useful tools in diagnosis.

Lag time from exposure to admission in this study was 40.2 (33.6) hours, which are rather similar to other studies [19,24]. Patients were cleared from symptoms in 8.3 (9.6) weeks, which is rather shorter than some other studies [25].

Clinical findings including ptosis, general weakness and diplopia are the most common findings followed by dysphagia, difficult speech, dizziness, blurred vision and dry mouth in this study. This is rather similar to Meyers et al. and Kalluri’s studies from USA [21,22]. However, in the present report dry mouth, constipation and mydriasis have been observed less frequently in contrast to Zilker report from Germany [19]. Severity of clinical manifestation may vary in different cases due to botulism [19], making it difficult to compare different reports.

Vital signs on admission in a report from East Coast of the United States were normal. Also clinical laboratory tests included potassium and creatinine were reported to be abnormal in 50% of cases [19]. This is different from our study.

Higher incidence of foodborne botulism in winter has been reported [17], which is different from the present study. As the total number of cases is limited in these studies, this could be a result of outbreaks in certain time of the year.

In this study 18% of cases needed mechanical ventilation on admission. This is proportionate to other reports (6% to 33%) [17,19].

In a comparison between sporadic and outbreak cases, all clinical findings but headache and dysphagia were similar.

In conclusion, foodborne botulism is rare, but it more frequently happens in middle-income countries such as Iran. Based on this study most signs and symptoms were in central nervous system that lead to misdiagnosis. On the other hand if there are more than one case the lag time between exposure and admission would be less due to earlier diagnosis. There is no significant difference between sporadic and epidemic groups to use for conclusion. The result of this study could be used as a clinical guideline for diagnosis of botulism in this area. If antitoxin is applied, foodbonre botulism is not fatal.

We would like to acknowledge the kind co-operation of Vice Chancellor for Research, Mashhad university of Medical Sciences.

None to be declared.