Page 791 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition
P. 791

750 SECTION | XI Bacterial and Cyanobacterial Toxins




  VetBooks.ir  associated with contamination of water supplies by rotting  cell volume and total plasma protein. Bicarbonate loss
                                                                from excessive ptyalism may lead to a metabolic acidosis.
             organic matter containing the botulism toxin or bacteria.
                                                                Increases in muscle enzymes such as aspartate transami-
             Toxicoinfectious and wound botulism are occasional
             causes. As with horses wet, soil-contaminated, alkaline,  nase and creatinine kinase may be present due to muscle
             anaerobic hay wrapped in plastic bags provides ideal  atrophy or trauma resulting from prolonged lateral recum-
             incubation conditions for C. botulinum (Martin, 2003).  bency. Electrolyte abnormalities and hyperglycemia may
                                                                also be detected. One study documented indicators of
                                                                renal failure in a herd poisoned by botulinum toxin B;
             Clinical Signs, Diagnosis, and Treatment           increased γ-glutamyl transpeptidase, urea, creatinine, and
             Bovine botulism usually presents as a herd outbreak. The  phosphorus were also detected.
             classical signs of bovine botulism resemble those in horses;  As with other species, there are no definitive gross
             however, cattle exhibit a more gradual progression of clini-  pathological or pathognomonic histological signs of botu-
             cal signs, improving the prognosis and probability of  lism. Aspiration pneumonia and pulmonary emphysema
             recovery (Whitlock et al., 1989; Whitlock and Williams,  are the most frequent sequelae of botulism in cattle
             1999). The lower susceptibility of cattle to feed-associated  (Galey et al., 2000; Heider et al., 2001; Braun et al.,
             botulism is likely due to presystemic elimination by the  2005). Other lesions, such as gastric ulcerations, thick-
             rumen microflora (Allison et al., 1976). The clinical course  ened intestinal mucosa, hepatic lipidosis, suppurative
             ranges from 2 to 30 days, depending on exposure dose,  rumenitis, and renal failure, have been documented in
             duration and treatment. Early botulism may be confused  concurrence with botulism; however, these findings are
             with milk fever because generalized muscle weakness,  not consistent in all cases of bovine botulism.
             increased ataxia, muscle tremors and herd outbreaks may  Botulism in cattle is usually a presumptive field diag-
             occur in both conditions. Cattle with botulism also exhibit  nosis made on the basis of clinical signs and the ruling
             depression, dysphagia, decreased tongue and jaw tone,  out of other diseases. Differential diagnoses include hypo-
             hypersalivation, dehydration, decreased tail tone, decreased  calcemia, hypomagnesia, hypokalemia, hypophosphate-
             pupillary light responses, and mydriasis. Rumen contrac-  mia, listeriosis, lead poisoning, polioencephalomalacia,
             tions decrease and constipation may develop. Diarrhea and/  ionophore toxicity, nutritional or plant toxin-induced
             or putrid-smelling faces may also be noted. Cattle with bot-  myopathies, molds, organophosphate poisoning, and tick
             ulism tend to spend significant amounts of time in sternal  paralysis. Clinical diagnosis is usually made through the
             recumbency. At terminal stages of botulism, cattle are lat-  detection of neurological deficiencies in light of relatively
             erally recumbent, exhibit abdominal breathing patterns, and  unremarkable laboratory diagnostic findings. The neuro-
             finally succumb from respiratory failure. Vital signs are  logical examination should assess cranial nerve responses,
             often normal in early stages of botulism; however, as the  gait, posture, and attitude. Specifically, a tongue tone test,
             disease progresses, increased heart and respiratory rates  tongue stress test, and a jaw tone test should be per-
             may be noted, whereas body temperature may decrease.  formed. The tongue stress test is performed by placing a
                A syndrome resembling equine dysautonomia has   hand at the base of the cow’s tongue and putting pressure
             been described in German cattle, and a link to botulinum  on the tongue followed by an assessment of muscular
             toxins has been proposed. These cattle may present with a  tone. The tongue tone test is performed as in the horse.
             subclinical to chronic “visceral” disease. Nonspecific  Cattle with botulism will exhibit weak tongue strength.
             symptoms such as weight loss, decreased milk production,  The jaw test is performed by grasping the mandible near
             depression, alternating constipation and diarrhea, edema,  the symphysis and attempting to move the mandible lat-
             laminitis, ataxia, retracted abdomen, emaciation, tachyp-  erally. This test assesses the strength of the masseter mus-
             nea, and unexpected death are associated with this syn-  cles. A “loose” jaw is suggestive of botulism.
             drome (Bo ¨hnel et al., 2001). In cattle exhibiting these  A definitive diagnosis is made by identifying toxin in
             symptoms, Bo ¨hnel and associates demonstrated the pres-  the  patient’s  serum,  ruminal  fluid,  or  tissues.
             ence of both C. botulinum and botulinum toxin in lower  Identification of botulinum toxin or C. botulinum in sus-
             GI tract contents. Furthermore, neither botulinum toxin  pect feedstuffs previously consumed by clinically ill ani-
             nor C. botulinum was isolated from asymptomatic herds.  mals may further support a diagnosis. Isolation of
             This study hypothesized that small levels of C. botulinum  botulinum toxin from the rumen may prove difficult
             colonized the lower intestinal tract and created a low-  because the toxin is often diluted by rumen contents and/
             level, chronic exposure of botulinum toxin. This low-level  or degraded by ruminal microbes. Similar to botulism in
             of toxin may not reach the systemic circulation, and thus  other species, the MBA is the gold standard for a defini-
             toxin may only disrupt nearby parasympathetic ganglionic  tive diagnosis in cattle; however, as in horses, the MBA
             innervation of the GI tract, altering intestinal function.  is often not sensitive enough to detect the low levels of
                In cases of bovine botulism, clinical pathology may  toxin in the general circulation. The MBA may also be
             reveal signs of dehydration such as increases in packed  used to detect toxin in rumen contents, the liver and other
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