On spring, Egyptians’ celebration of eastern festival is accompanied with eating Feseekh (salted fish). However, unexpected outbreak occurred in Autumn and it was justified by contamination of marine mullet meat during that time, where some of those contaminated fish were taken by some individuals and salted in their homes. (Veterinarians warn of the mass death of fish in Lake Rashid 2019).
The outbreak started with a 1.5-year-old child referred from Pediatric University Hospital to APC for differential diagnosis. She presented with paralytic ileus that raised the suspicion of intussusception and surgical abdomen. On examination the surgical emergency was eliminated. A similar scenario was mentioned by Spini et al (2015).
Due to the unusual young age of the child with the absence of the common paralytic manifestations of botulism, pediatricians doubted botulism. Pisani et al (2009) had explained a similar situation as the initial symptoms of the disease are often like several diseases and therefore differential diagnosis is very difficult and rarely suspected by the pediatrician.
Although the highest percentage of the patients were in the middle age group (20 - < 40 years), extremes of age were also involved, and females outnumbered males. This could be explained by the Egyptian culture where the ladies prepared the meals to the families as well as tasting it before meals. All family members gathered for celebration and ate the same food so different ages are usually affected.
APC is serving Alexandria and all-around governorates (Elbehira, Kafr el-Sheikh, Marsa Matrouh, etc.). As the accident of contamination of the mullet fish meat occurred in Elbehira governorate so, all patients were directed to APC as in all other poisons.
In the current work, 91.5% of the cases had no previous medical or surgical history. Past medical and surgical history was taken to exclude neurological diseases, previous stroke, and other gastrointestinal problems. All patient’s symptoms started to appear after eating the Feseekh meal. All the participated cases presented to the hospital from six hours up to nine days after Feseekh ingestion with a mean of 1.70 ± 1.49 days. In their systematic review, Fleck-Derderian et al (2017) reported a median duration between exposure and symptom onset as approximately one day. This difference is expected due to the long incubation period of foodborne botulism which would reach up to 16 days.
The mouse lethal test (MLT) is the standard procedure for detection of botulism. Mouse bioassay test was carried out to 82 out of 94 cases. The results delivered several days after the clinical diagnosis revealed that 87.8% of cases were negative despite presence of clinical neurological manifestations. These negative results could be explained by the long period between the Feseekh ingestion and the withdrawal of serum sample as the samples were obtained from patients at the time of admission and many patients admitted to hospital few days after the appearance of symptoms. This result is in accordance with Temeri et al (2011) who stated that many clinical specimens have low levels of toxin which may not be evident within 4 days.
Although the clinical syndrome of botulism is distinctive, it needs a high index of suspicion to be diagnosed. In the current study, patients were presented with mydriasis (29.8%), blurred vision (14.9%), ptosis (11.7%), dysphagia (24.5%) and muscle weakness in 21.3% of patients. This is in accordance with Gaware et al (2011) who reported these symptoms as the classic for botulism.
On contrary to most of previous studies on Botulism that recommend early antitoxin administration to reduce mortality Gaware et al (2011), Kongsaengdao et al (2006) and Yu (2015). The current study aimed to manage the resources and to decrease the exposure of the patients to the side effects of the unnecessary administration of antitoxin. Thus, the patients in current study were classified at the time of admission into three groups. Only twenty patients -group C1- who presented with severe evident neurological symptoms; ptosis, muscle weakness or respiratory muscle affection with hypoventilation were given the BAT immediately. While the rest of patients didn’t receive the BAT immediately but they were put under close observation.
Patients in group A who presented to hospital with just a history of Feseekh ingestion as members of their family ate the same meal and developed botulism manifestations and also patients in group B who presented with only gastroenteritis didn’t develop any additional symptoms during their period of hospitalization and did not need to receive the BAT. Moreover, patients in group C2 who presented with mild cranial deficit didn’t receive the BAT immediately as most of cranial deficits complain of patients in group C2 might be just a subjective feeling due to the fear or anxiety that result from the warnings spread at that time on the media or due to their affection by other patients in the outbreak.
However, in order to identify patients likeliest to benefit from the antitoxin treatment, patients in group C2 were categorized according to the number of cranial deficit signs on initial assessment to anticipate the deterioration and to predict who would need the antitoxin administration which may be valuable for further development of guidelines. The initial assessment of cases with suspected food-born botulism is very important.
In our opinion, this classification reduced the unnecessary administration of the HBAT to 60 patients who were managed by supportive treatment only. This protocol helped avoidance of many side effects of the antitoxin including the most severe ones as anaphylaxis and hypersensitivity reactions and other delayed allergic reactions as serum sickness. Schussler et al (2017) reported anaphylactic reactions in 1%-2% of botulinum antitoxin recipients that would be severe enough and necessitate intensive care.
Also, this is very important for prioritizing antitoxin treatment when its availability is limited especially in outbreaks where the number of patients is large and unpredicted. This was contradictory to O'Horo et al (2017), in their systematic review, as they could not identify patients likeliest to benefit from the antitoxin treatment. But this was in agreement with Anderson et al (2019) and Barker et al (2019).
In addition, after receiving the first dose of HBAT, (17.7%) of the cases showed no improvement and (26.4%) showed temporary improvement and relapsed later which necessitated the administration of further HBAT doses. These results may be explained by the mechanism of HBAT; it interacts only with unbound toxin, patients who admitted early were improved on one vial, while those arrived late needed second and third vials and 2 of them died in the hospital. (O'Horo et al 2017; Anderson et al 2019; Barker et al 2019). Those who suffered rebound after initial improvement were mentioned in a study of Fagan et al (2011).
The only drawback of the current protocol is prolongation of hospitalization due to monitoring of the patients which reaches up to 12 days in some cases to avoid missing the unpredicted side effects of the antitoxin.
Following the theory in current study, complete recovery occurred in (87.2%). Complications were present in 10.6% of patients while death occurred only in two cases (2.2%). All those 10.6% of patients who discharged with complications received the HBAT. They complained of persistent dry mouth with a very mild dysphagia not interfering with fluid, solid or semisolid food ingestion. Some complained of constipation which improved also with the usage of laxatives. This is like Gottlieb et al (2007) who concluded that previous symptoms of cholinergic autonomic blockade that are prominent during botulism as dry mouth would persist for a long-term later.
Regarding the two cases who died, both were in group C1 with evident neurological paralysis, they received the antitoxin, and both were in need for mechanical ventilation in ICU. They arrested in the ICU; one after 2 days and the other after 4 days without receiving any further doses of HBAT. According to the critical care physicians the cause of death was a superadded chest infection. This point is very important as the appropriate supportive care is still the cornerstone in recovery and survival after botulism. As those cases suffered respiratory compromise so a high-quality intensive care is needed. This is in accordance with Sheth et al (2008).