Download Silent Murder associated with home-canned

Silent Murder associated with
home-canned-preserved bamboo shoots.
Yotsawee Chotechuang , M. D.
Teeraya
Puavilai
, M.D.
Pornthep Worawongprapa , M.D.
Department of Internal Medicine, Lampang hospital.
ABSTRACT
Seven patients from the same residential area came to Lampang hospital with the same clinical
presentation of progressive dysphagia, dysarthria, paralysis and bilateral ptosis preceded by abdominal
cramps, nausea, vomiting, and diarrhea after all of them had eaten home-canned-preserved bamboo
shoots bought
from the weekend central-village market.
Although botulism was rare but potentially fatal illness. Prompt recognition of clinical
syndrome plays an important role in decreasing morbidity and mortality rates. This report provided a
clinical overview, progression and management in one of seven patients who was suffered from
botulism and brief review literature about thi.s disease. We hope that this report will be advantage for
physicians and healthcare workers to prevent misdiagnosis and delay treatment in the patients with
these clinical syndrome.
Key words: Foodborne Botulism, Home-canned-preserved bamboo shoots.
INTRODUCTION
Preserved bamboo shoots (cooked and uncooked) was a kind of cultural favorite foods of Thai
Northern people. One day on November 2003, seven patients from the same Tambon, District and
Province, came to hospital with the same clinical presentation of progressive dysphagia, dysarthria,
paralysis and bilateral ptosis preceded by abdominal cramps, nausea, vomiting, diarrhea after all of
them had eaten home-canned-preserved bamboo shoots which bought from the weekend central-village
market. What's happen to them?
PRESENTATION OF CASE
A 36-year-old woman, couple, agriculture, in Sobprap District, Lampang Province was
admitted to Lampang hospital on 26 November 2003 because of having diarrhea followed by multiple
cranial-nerve palsies.
Three days prior to admission, she had watery diarrhea, nausea, vomiting, abdominal pain,
weakness and fatigue around six hours after ingestion home-canned-preserved bamboo shoots which
she bought from the weekend central-village market. She had no fever (No medications had been
taken).
The next day, she began to have difficulty in drinking water and swallowing both liquid and
soft food. Blurred vision was noted. She could walk well at that time. She was taken to a private
hospital where computer tomographic (CT) scan was performed, and unremarkable result. She was
admitted to the hospital and got nasogastric tube for feeding, supportive and symptomatic treatment
while observing her neurological sign.
Approximately 24 hours after admission, she complained perioral numbsness and
worsening dysphagia. Her speech became severe slurred. Bilateral ptosis was seen but she could move
her eyes in all directions. She was unable to stand, walk, and write complete coherent sentences. She
complained that her legs was more severe weakness than her arms. Then she was transferred to
Lampang hospital.
The patient had no history of underlying diseases, exposure to pets or ticks, recent foreign
travel, use of alcohol or drugs, previous neurologic problems, and loss of vision. Physical examination
revealed that the temperature was 3 6 . 5 ' ~ ,the pulse rate was 82 Imin, the respiratory rate was 20 Imin
and the blood pressure was 120180 mmHg. General physical examination showed no abnormalities.
On neurological examination, the patient was drowsy, bilateral ptosis and countable fingers.
She gave appropriate positive or negative response by turning either thumb up or down. Both pupils
were 3 mm. in diameter and equally reacted to light. Extraocular movement was normal. Facial
sensation and hearing were intact. Uvula was in midline position. She could not protrude her tongue.
Sternocleidomastoid strength was 315 bilaterally. Decreased in gag reflex was noted. Proximal muscle
strength was 315 in both arms and legs. Vibratory, pinprick, light touch, joint position, and temperature
sensations were intact. All deep tendon reflexes were l+.Plantar responses were flexion. Stiffness of
neck was absent. The patient could not cooperate during tests of coordination.
Four hours after admission, her consciousness was down to stuporous. She used abdominal
muscle to respiration. the respiratory rates was 32 to 35 /min and secretion sound was heard on both
lungs. She was intubated endotracheal tube and transferred to intensive care unit.
The results of laboratory tests throughout the course of the patient's illness was showed in
Tables 1 to 3.
A chest radiograph showed alveolar infiltration in right lower lung field, findings consistent
with the presence of suspected aspiration pneumonia. A cranial CT scan showed unremarkable study.
Hemoculture, sputum examination and sputum culture were done. Empirical antibiotics were Ceftriaxone
2 gm. intravenous once daily and .Metronidazole 500 mg, intravenous every eight hours per day.
Specimens of stool and urine were obtained. for culture and toxin studies. Botulinum antitoxin was not
administered due to it was not available in Thailand.
TABLE 1. Hematologic Laboratory values on admission in Lampang Hospital.
VARIABLE
ON ADMISSION
DAY 6
12.9
11.8
24,800
26,400
Neutrophils
90
85
Lymphocytes
6
7
Platelet count (per mm3)
229,000
271,000
Red cell morphology
NCNC*
NCNC*
Hemoglobin (g %)
Hematocrit (%)
MCV (pm3)
White-cell count (per mm3)
Differential count (%)
Monocytes
Bands
-
*
Normocytic Nornlochrornic.
TABLE 2. Blood Chemical values.
VARIABLE
ON ADMISSION
Glucose, (mgldl)
BUN (mgldl)
DAY 6
160
6
Creatinine (mgldl)
0.6
Sodium (mEq1L)
132
Potassium (mEq/L)
3.6
Chloride (mEq/L)
105
Carbon dioxide (mEq/L)
26
Albumin (gmldl)
3.3
Calcium (mgldl)
8.9
Phosphorus (mgldl)
3.5
Magnesium (mgldl)
2.9
TABLE 3. Results of Lumbar puncture.
VARIABLE
Appearance of fluid
FINDING
Clear, colorless
Cells (per mm3)
No cell
Glucose (mg%)
97 ( log* )
Protien (mg%)
38
Stained smear
No microorganism
* Plasma glucose.
On the second hospital day, the temperature was 3 7 . 5 ' ~to 3 8 . 2 ' ~ ,the blood pressure was
110170 mmHg. Drowsiness and complete external ophthalmoplegia were presented. Bilateral pupils
were 3 mm. in diameter and sluggish react to light. Bilateral ptosis persisted. Both arms and legs were
flaccid. Bilateral muscle strength was 115 in proximal and 415 in distal of upper extremities. Both her
legs; muscle strength was 015 in proximal and 315 in distal. Deep tendon reflexes of her arms remained
l+. Knee and ankle jerks were areflexia. Plantar responses were flexion. Pyridostigmine Bromide (360 mg
daily) were administered.
On the fifth day, she was stuporous. The temperature was 3 6 . 7 ' ~ .The pulse rate was 120 Imin
The blood pressure was 90160 mmHg. Bilateral ptosis persisted. The cranial-nerve deficits and bilateral abnormal pupils were unchanged. Generalized flaccid and hyporeflexia was noted. The hemoculture
was no growth in two days. Motor conduction studies was not performed due to unstable hemodynamics of this patient.
On the sixth day, her neurological signs were unchanged. Her vital signs was unstable.
Inotropic agents were administered. She had sudden cardiac arrest and the cardiopulmonary
resuscitation was performed. Postmortem study was not performed.
DISCUSSION
This patient had acute, afebrile, and bilateral cranial-nerve paralysis that worsened over the
period of hours. In patients with muscle weakness could be explained by a lesion at one of four sites:
ea
the central motor neurons and their descending tracts, the nerves, the neuromuscular junctions, or the
muscles themselves"'.
Primary muscle disease can result in oropharyngeal weakness, and ptosis can occur in cases of
primary muscle disease, but it would be exceptional for myopathy to evolve over a period of two or
three days. Furthermore, oculomotor paralysis is not typical feature of muscle disease, except in cases
of progressive external ophthalmoplegia (a type of mitochondria1 myopathy), thyroid ophthalmopathy,
and oculopharyngeal dystrophy, all of which are ingravescent processes. Muscle disease is therefore
unlikely because of the rapid in progression, distribution, and severity of the weakness in this case.
Polymyositis is usually insidious and only rarely fulminant. Proximal-limb weakness and facial
weakness are common manifestations, and dysphagia occurs in more than 25 percent of cased2'.
Although muscle tenderness and cramping are common, the absence of pain is not unusual. The
deterioration in this patient, however would be exceptional even for fulminant polymyositis. Ptosis is
rare in polymyositis. Periodic paralysis, which includes a group of disorders that cause rapid and
profound weakness, frequently with loss of reflexes, tends to occur in the first few decades of life.
Involvement of cranial nerves is infrequent, and involvement of ocular muscles is very rare.
Disorders of the neuromuscular junction could explain this patient's illness, because they
preferentially involve ocular and cranial muscles - the ones with the lowerest threshold for synaptic
failure. The most common neuromuscular disorder, Myasthenia gravis, may progress rapidly, causing
ptosis and oropharyngeal, oculomotor, proximal-limb weakness and respiratory failure. Until the
reflex and sensory loss became evident later in course of the disease, myasthenia gravis was a
defensible diagnosis. However, the pupils are not overtly affected in patients with myasthenia gravis,
and total ophthalmoplegia is uncommon with this disorder. Another disease of neuromuscular junction
which generally begins with a nasal voice, dysarthria,
that warrants consideration is ~otulism'~',
dysphagia and ptosis. In this case, the evolution of neurologic signs over a period of hours, and then
days, after a gastrointestinal illness is also suggestive of botulism, caused by a toxin synthesized
by Clostridium botulinum. Ophthalmoparesis, facial weakness, and bulbar palsy are the most common
initial symptoms of the disease. Despite pharyngeal weakness, a gag reflex is often preserved, as in this
case. Dilatation of the pupils is common but may be absent, in one series, less than half the patients
had dilated pupils'4'. Limb weakness and respiratory compromise may follow, although respiratory
weakness can occur without severe limb weakness. Reflexes may be depressed or absent. Sensation
and cognition are almost always preserved.
Evidences which strongly support the diagnosis
of botulism in this patient: First, history of ingestion of home-canned-preserved bamboo shoots
which prone to contaminate with botulinum toxin and had evidence of outbreak of foodborne
(home-canned-preserved bamboo shoots) botulism in Northern of Thailand in 1998'~'. Second,
the neighborhood and her friends from the same village had clinically signs and symptoms of illness
like her, by all of the neurologic signs changed over a period of hours, the interval less than 24 hours,
after the gastrointestinal illness, and every patients had an important history of ingestion home-cannedpreserved bamboo shoots which they bought from the same sources and on the same day like her
that preferably thought to botulism first, because botulism may occur in the clusters of people ingesting
the same tainted food, but sporadic cases are not unusual. Third, she was afebrile, eventhough there
is no mention of prominent dryness of the mouth and throat, which typical of the early stage
of botulism, botulism could not be ruled out in this patient. The diagnosis of botulism can be made
by injecting a sample of the patient's serum or a preparation of tainted food into mice intraperitoneally.
The test is positive if the mouse becomes paralyzed and dies"'. But this procedure is not widely
available. Another weakness due to neuromuscular junction dysfunction is seen in the Lambert-Eaton
syndrome"', but it was progressed slowly, and cranial-nerve involvement was usually not as
conspicuous as in this case, and respiratory failure is rare. Hypermagnesemia and the administration
to an Aminoglycoside or Polymixin can cause neuromuscular
in this case.
but neither was a factor
Any acute weakness of cranial musculature demands a consideration of disease of the cranial-nerve
nuclei in brain stem, especially the common problem of infarction of pons and midbrain from
occlusion of the basilar artery. It was also difficult to conceive of a process that affects the widely
dispersed brain-stem nuclei innervating the ocular, facial, and oropharyngeal muscles but spare the
adjacent corticospinal tracts. Involvement of the corticospinal tracts is almost essential for the
diagnosis of occlusion of the midbasilar artery. Exception to these rule include Wernicke's disease that
involves the brain-stem nuclei and causes ophthalmoplegia and syringobulbia, with may affect several
cranial-nerve nuclei, but neither disease explains the other features of this patient's illness. Bulbar
poliomyelitis could account for the pattern of destruction of brain-stem motor neurons in this patient,
but it rarely causes ophthalmoplegia and was unlikely because of the absence of fever during early
phase of the neurologic illness and the normal cerebrospinal fluid findings.
The syndrome of acutely advancing ocular, facial, and oropharyngeal weakness coupled with
limb weakness is acute inflammatory demyelinating polyneuropathy (Guillain-Bank syndrome).
Predominant weakness of the ocular and oropharyngeal muscles characterized one of several variants
of the Guillain-BmC syndrome in which weakness was purely or predominantly regional. All these
variants are linked to the typical form of the Guillain-BmC syndrome by the presence of generalized
areflexia weakness; shared electromyographic features, which may abnormal only in weakened
regions; and elevated cerebrospinal fluid protien level in some cases. The differential between botulism
and Guillain-BmC syndrome and its variants was showed in Table 4. Other causes of cranial
polyneuropathy do not satisfactorily explain an acute symmetric paralysis involving cranial nerves I11
through XII. Neoplastic meningeal infiltration evolves more gradually, affects the nerves unilaterally
or asymmetrically, and results in abnormalities in the cerebrospinal fluid. Infectious disease and
noninfectious granulomatous diseases, such as tuberculosis, fungal infections, syphillis, Lyme disease,
sarcoidosis, Wegener's granulomatosis, and idiopathic granulomatous disease, can cause cranial
polyneuropathy, but not as acute and severe as in this case. Diptheria may associated with the cranial
neuropathy but rare and exudative pharyngeal membrane was not detect in this patient. From many
reasons above, the differential diagnosis of this patient were Botulism, Guillain-BmC syndrome and its
variants, Myasthenia gravis, respectively. All of them can be distinguished by their electromyographic
studies, but limit in this case due to complications from aspiration pneumonia with respiratory failure.
Guillain-BmC syndrome, the result was initially be normal or almost normal. Myasthenia gravis, by
demonstrating the absence of a decrement in muscle contraction with repetitive nerve stimulation.
Botulism, by demonstrating the absence of an increment in muscle contraction.
Seven patients who were suffered from botulism in Larnpang hospital, between November to
December 2003, the median age was 40 years (range from 29 to 59 years), and six patients were
female. They had symptoms include diarrhea ( l o o % ) , nausea ( l o o % ) , vomiting ( l o o % ) ,
dysphagia(lOO%), dysphonia (loo%), dysarthria (loo%), symmetrical paralysis (loo%), bilateral
ptosis(100%), perioral numbness (14%).0ne patient had associated with positive Tensilon test. Four
patients required mechanical ventilation (57%). The onset of neurologic symptoms in these patients
was three days after ingestion contaminated foods (range from 2 to 5 days). The sequence of signs and
symptoms of foodborne botulism in order of onset as showed in Table 5. Two patients died from
aspiration pneumonia and respiratory failure. Length of hospitalization was' 20 days (range from 9 to
40 days). All patients came from the same Tambon in Soprap District, Lampang. They had the same
history of home-canned-preserved bamboo shoots ingestion bought from the same village market.
TABLE 4. Differentiating Botulism from the Guillain-BarrC Syndrome.
Variable
Fever
Guillain-Bw 6
Variant of
Syndrome
Guillain-Bmt5
Absent
May be present
May be present
Dilated
Normal
Normal
Botulism
Motor
Pupils
or umeactive (50%)
Ophthalmoplegia
Present early
Present late
Present late
Paralysis
Descending
Ascending
Ascending
DTRs
Preseentlabsent
Absent
Absent
Ataxia
Absent
Present
Present
Paresthesia
Absent
Present
Present
CSF protien
Normal
Elevated
Elevated
Adapted from Reference number 6.
Abbreviations: DTRs, Deep tendon reflexes; CSF, cerebrospinal fluid.
TABLE 5. Sequence of symptoms and signs of seven patients in order of onset after ingestion
home-canned preserved bamboo shoots.
T i e after ingestion
signs and symptoms
6 - 24 hours
Nausea, Vomiting, Diarrhea, Diz7.iness.
48 - 72 hours
Mucus throat, Difficult swallowing food, Slurred speech,
Bilateral ptosis
72 - 96 hours
Progressive dysphagia Unsteady gait, Extreme weakness,
Respiratory failure
CLINICAL DIAGNOSIS
Botulism
LITERATURE REVIEW
Botulism is a paralyzing disease caused by the potent neurotoxin of bacterium Clostridium
botulinum. The name botulism is derived from the Latin word botulus, meaning sausage'"'. In the
early part of the nineteenth century, Justinus Kerner of Germany reported cases of botulism from
ingestion of improperly smoked sausage and found ingestion of an extract from the sausage reproduced
clinical botulism. Kerner hypothesized that the toxic substance found in the sausages was "fatty
acid"lll'12). Not until 1895, Professor Emile van Ermengen of Ghent identified a bacterial toxin to be
the cause of botulism. Professor van Ermengen isolated an aerobic bacterium from the ham and
reproduced the disease in laboratory animals by injection of a toxin produced by the bacteria.
Clostridium botulinum is a spore-forming, obligate anaerobe whose natural habitat is soil,
from which it can be isolated without undue difficulty. Botulinum toxin exists in 7 distinct antigenic
types that have been assigned the letters A through G. The toxin types are defined by their absence of
cross-neutralization (eg, anti-A antitoxin does not neutralize toxin type B-G). Human botulism is
primarily caused by strains of C. botulinum that produce toxin types A,B,and E. Neurotoxigenic
strains of C. baratii (which produce type F toxin) and C. butyricum (which produce type E toxin) also
have been implicated in human botulism. Strains of C. botulinum that produce type C or D toxin for
the most part cause botulism only in nonhuman species. Botulinum toxin is a simple dichain polypeptide that consists of 100-kd "heavy" chain joined by a single disulfide bond to a 50-kd "light" chain.
The toxin's light chain is a zn2' containing endopeptidase that blocks acetylcholine-containing vesicles
from fusing with the terminal membrane of the motor neuron, resulting in flaccid muscle paralysis'13'
The lethal dose of botulinum toxin for humans is not known but can be estimated from primate
studies. By extrapolation, the lethal amounts of crystalline type A toxin for 70-kg human would
be approximately 0.09-0.15 p g intravenously or intramuscularly, 0.70-0.90 p g inhalationally, and
70 p g orally"3'.
Four clinical forms of botulism occur in human: foodborne botulism; wound botulism; infant
botulism (infant intestinal colonization); and rarely, adult infectious botulism (adult intestinal
colonization).
Clostridium botulinum. organisms cause food poisoning because the heat-resistant spores
survive food preservation methods that kill nonsporulating organisms; the bacterial spore are resistant
to heat and may survive the home-canning process at the temperatures below 120 o ~ ' 1 4 They
'.
subsequently produce a potent neurotoxin under anaerobic, low acid (pH > 4.6), and low solute
conditions. Recently identified vehicles for foodborne botulism are showed in Table 6.
The classic picture of botulism is that of a patient in whom acute, bilateral cranial neuropathies
develop in association with symmetric descending weakness. The CDC suggests attention to the
following cardinal features: (1) fever is absent (unless a complicating infection occurs), (2) the
neurologic manifestations are symmetric, (3) the patient remains responsive, (4) the heart rate is
normal or slow in the absence of hypotension, and (5). Sensory deficits do not occur (except for
blurred ~ision)."~'
Disease manifestations are similar regardless of botulinum toxin type. Some patients
may be mildly affected, while others may be so paralyzed that they appear comatose and required
months of ventilatory ~ u ~ ~ o r t ' ' ~ ' .
Foodborne botulism usually develops between 12 and 36 hours after toxin ingestion. The
patient initially complains of nausea and a dry mouth, and diarrhea may occur at this stage. Evidence
of cranial nerve dysfunction most commonly starts with the eyes; parasympathetic involvemerit causes
blurred vision from pupillary dilatation, or nerves 111, IV or VI may be involved. Pupillary reactions
may remain abnormal for months after motor recovery. Nystagmus is occasionally noted, usually
in type A disease. Lower cranial nerve dysfunction is manifested as dysphagia, dysarthria, and
hypoglossal weakness. Weakness then spreads to upper extremities, the trunk, and the lower extremities.
Respiratory dysfunction may result from either airway obstruction or diaphragmatic weakness. Patients
who requiring mechanical ventilation, mean periods of 58 days (type A) and 26 days (type B) for
ventilatory weaning. Recovery may not begin for up to 100 days. Botulinum toxin inhibition of
acetylcholine release affects the parasympathetic and sympathetic systems, as well as the
neuromuscular junction.
TABLE 6. Vehicles Associated with foodborne Botulism.
Home-canned or home-processed low-acid (pH > 4.6) foods.
Vegetables
Whale or seal products
Fermented or salted fish products
Meats
Fish
Relish
Salsa
Bamboo shoots
Chili
pepper
Baked potatoes in .aluminum foil
Garlic in oil
Yogurt
Sauteed onions kept under butter sauce
Commercial cheese sauce
Adapted from Reference number 16.
Autonomic problems may include gastrointestinal dysfunction, alterations in resting heart rate,
loss of responsiveness to hypotension or postural change, hypothermia, or urinary retention. Common
signs and symptoms are showed in Table 7.
The rapidity of onset and severity of botulism depend on the rate and amount of toxin
absorption. Symptoms of foodborne botulism may begin as early as 2 hours or as long as 8 days after
ingestion of toxin'13'. Typically, cases present 12 to 72 hours after the implicated'meal. In severe cases,
extensive respiratory muscle paralysis leads to ventilatory failure have required ventilatory support for
up to 7 month before return of muscular function, but ventilatory support is most commonly needed
for 2 to 8 weeks. The toxin is readily inactivated by heat ( 2 8 5 ' ~for 5 ~ninutes)'~~'.
Thus, foodborne
botulism is always transmitted by foods that are not heated.
Specific tests that helpful in diagnosing botulism are summarized in Table 8. Edrophonium (or
~ensilon)'~'
test, occasionally used to differentiate myasthenia gravis from suspected botulism but in
rare cases, early course of botulism, there is a limited improvement in strength, which is farless
dramatic than occurs in myasthenia gravis'17'. Electromyographic pattern in botulism characterized by
brief, small, abundant motor unit action potentials (BSAPs). Repetitive nerve stimulation at high rates
(20 Hz or greater, as compared with the 4-Hz rate in the diagnosis of myasthenia gravis). Sample of
serum, stool, vomitus, gastric contents and suspected foods should be sent for anaerobic culture
(C. botulinum) and toxin assay.
Respiratory compromise is the usual cause of death from botulism. To prevent or treat this
complication, hospital admission of the patient and of all individuals exposed to a possible source is
mandatory. Close monitoring of respiratory status by using parameters such as vital capacity, peak
expiratory flow rate (PEFR), negative inspiratory force (NIF), pulse oximetry, and the presence or
absence of gag reflex is essential to determine the need for intubation or tracheostomy as the patient
begins to manifest signs of bulbar paralysis. Gastric decontamination should be initiated only for an
asymptomatic person who has very recently ingested a known contaminated foods. Sorbitol is
preferable to magnesium salts, which may potentially depress neuromuscular transmi~sion'~'.
In human,
the efficacy of the type specific antitoxin to type B strain toxin is unknown whereas the type-specific
antitoxins to A and E q e probably beneficial. Antitoxin can prevent paralysis but does not affect
already paralyzed muscles. The benefits must always weighed against the high incidence of
anaphylaxis and serum sickness from the equine antitoxin. Botulinum antitoxins types A, B, AB
(bivalent), E, ABE (trivalent), F are available. Although specific foods tend to correlate relatively well
with botulinum type, trivalent antitoxin (7500 U type A, 5500 U type B, and 8500 U type E) should
be administered. Guanidine which used to enhance acetylcholine release is no longer recommended to
and intravenous immune globulin'22' have been given
treat botulism6. steroid1', plasmapheresis,'19~20'21'
to a small numbers of patients with ambiguous benefit. Further treatment strategies are being developed to include a
F(ab)2 despeciated heptavalent immune globulin, human botulism immune
globulin.
SUGGESTION
Botulism remains one of the rarest poisonings, while its etiologies have become increasing
diverse. The most important aspect of foodborne botulism is prevention. One of many questions should
be answer. Is the Thailand's health care system better for every Thai and foreign people? The best of
medical center in the Southeast Asia will be only dream project or it can be reality. A valuable lesson
from outbreak of foodborne botulism may be only one piece of jigsaws for the direction in sustainable
development of Thai health care system in the future.
TABLE 7. Commonly Reported Clinical Symptoms and Physical Findings in Botulism .
Symptoms
Gastrointestinal:
Nausea Diarrhea (early) constipation (late) Abdominal cramps Vomiting
Neurologic :
Blurred vision Dysphagia
Dry mouth Diplopia Dysarthria Arm weakness
leg weakness Dyspnea
Miscellaneous:
Fatigue
Sore throat Dizziness
Physical findings
Ptosis Tongue weakness Extraocular muscle weakness Hypoactive gag reflex. Pupils fixed or dilated
Extremity weakness - Symmetric, Proximal to distal, Descending pattern
Nystagmus
Hypoactive deep-tendon reflexes
Adapted from Reference number 9.
TABLE 8. Tests that are useful in the diagnosis Botulism.
Test
ResuIt Consistent with botulism
Initial test
Brain imaging
Normal
Lumbar puncture
Normal
Electromyography
Decreased amplitude of action in involved muscle group potential
Rapid repetitive pattern
Facilitation (increasing electromyography of action potential
amplitude , 20-50 Hz)
Confirmatory test
Mouse inoculation test for toxin (serum, stool , food)
Positive
Stool culture for Clostridium botulinum.
Positive
Adapted from Reference number 9.
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