Trivalent (serotypes A, B, E) botulinum antitoxin is derived from equine sources using whole antibodies. The second antitoxin is heptavalent botulinum antitoxin (serotypes A, B, C, D, E, F, G), which is derived from equine antibodies that have been altered to make them less immunogenic. This antitoxin is effective against all main strains of botulism. Mechanism of action
Botulinum toxin exerts its effect by cleaving key proteins required for nerve activation. First, the toxin binds specifically to nerves that use the neurotransmitter acetylcholine. Once bound to the nerve terminal, the neuron takes up the toxin into a vesicle by receptor-mediated endocytosis. As the vesicle moves farther into the cell, it acidifies, activating a portion of the toxin that triggers it to push across the vesicle membrane and into the cell cytoplasm. BoNTs recognize distinct classes of receptors simultaneously (gangliosides, synaptotagmin and SV2). Once inside the cytoplasm, the toxin cleaves SNARE proteins (proteins that mediate vesicle fusion, with their target membrane bound compartments) meaning that the acetylcholine vesicles cannot bind to the intracellular cell membrane, preventing the cell from releasing vesicles of neurotransmitter. This stops nerve signaling, leading to paralysis.The toxin itself is released from the bacterium as a single chain, then becomes activated when cleaved by its own proteases. The active form consists of a two-chain protein composed of a 100-kDa heavy chain polypeptide joined via disulfide bond to a 50-kDa light chain polypeptide.
Motor speech disorders are a class of speech disorders that disturb the bodys natural ability to speak due to neurologic impairments. These neurologic impairments make it difficult for individuals with motor speech disorders to plan, program, control, coordinate, and execute speech productions. Disturbances to the individuals natural ability to speak vary in their etiology based on the integrity and integration of cognitive, neuromuscular, and musculoskeletal activities. Speaking is an act dependent on thought and timed execution of airflow and oral motor / oral placement of the lips, tongue, and jaw that can be disrupted by weakness in oral musculature (dysarthria) or an inability to execute the motor movements needed for specific speech sound production (apraxia of speech or developmental verbal dyspraxia). Such deficits can be related to pathology of the nervous system (central and /or peripheral systems involved in motor planning) that affect the timing of respiration, phonation, prosody, and articulation in isolation or in conjunction. Dysarthria
Dysarthria is  the reduced ability to motor plan volitional movements needed for speech production as the result of weakness/paresis and/or paralysis of the musculature of the oral mechanism needed for respiration, phonation, resonance, articulation, and/or prosody. Apraxia
There are two types of Apraxia. Developmental (or Childhood Apraxia of speech) or acquired Apraxia. Childhood apraxia of speech (CAS) is a neurological childhood speech sound disorder that involves impaired precision and consistency of movements required for speech production without any neuromuscular deficits (ASHA, 2007a, Definitions of CAS section, para. 1).