[yorkiegirl2]

Tetanus
Tetanus is a bacterial disease caused by Clostridium tetani that can affect all domestic animals and people. Disease occurs as a result of localization of tetanus spores in an anaerobic environment, such as a necrotic wound with suppuration, with conversion to a vegetative, toxin-producing form. Infection most frequently occurs following an injury, but may also develop after surgical procedures, such as ovariohysterectomy [149-152]. Organisms produce the exotoxin tetanospasmin within 4 to 8 hours, which travels via peripheral nerves (alpha motor neurons) to the CNS [153]. A trans-synaptic migration of tetanus toxin occurs in spinal cord motor neurons. Small amounts of toxin may be spread hematogenously to the CNS. Tetanus neurotoxin appears to prevent synaptic vesicles from fusing with the cell membrane and prevents the release of neurotransmitters [154,155]. It is active at the neuromuscular junction, autonomic terminals, and in inhibitory neurons in the CNS, with the central effects usually predominating the clinical picture. Toxin causes disinhibition on gray matter gangliosides [106] and binds the release of inhibitory neurotransmitters from interneurons (glycine) and from descending upper motor neuron pathways (gamma aminobutyric acid) resulting in release of spinal cord and brainstem motor neurons from inhibition and subsequent hyperexcitability [156,157]. In people, at high concentrations, tetanus toxin acts like botulism toxin in that it inhibits the release of acetylcholine at cholinergic synapses [106].
Considerable species differences exist in susceptibility to tetanus. The dog is much less susceptible than the horse, and tetanus is seen less commonly in cats than in dogs. Clinical signs usually are observed within 4 to 12 days of infection [158-162], although extensor rigidity and ptyalism were observed in one dog 3 weeks after a routine ovariohysterectomy [151]. Frequently seen signs include stiffness of gait with extensor rigidity in all limbs, dyspnea, and spasms of the masticatory and pharyngeal muscles resulting in trismus and dysphagia. The tail may be elevated, facial muscles may be contracted to give a sneering expression ("risus sardonicus") with wrinkling of the forehead and puckering of the skin around the eyes, and the third eyelid may be protruded. Earflaps are usually held in an erect fashion, although low carriage has been noted early in the condition in some animals [163]. Animals may assume a "sawhorse" stance. In severe disease, the animal may be recumbent and opisthotonic. Affected animals are hypersensitive to external stimuli and reflex muscle spasms may occur. Autonomic involvement, such as bradyarrhythmias [164], or tachycardia/tacchyarrhythmias [165], may result from increased vagal tone or adrenergic stimulation, respectively. Death results from respiratory failure.
Localized tetanus may also be seen in dogs and cats with a localized limb injury and is usually characterized by stiffness in one limb before gradually spreading to involve the opposite limb and eventually, the entire body [162]. Tetanus in cats and dogs may remain localized to one of the thoracic limbs, which is held in rigid extension and caudally deflected (elbow extension and carpal flexion or extension) due to continuous involuntary muscle spasms [166,167]. Intermittent spasms may be superimposed upon the tonic rigidity. In one of the affected cats, the neck became twisted to the side [166]. The affected limb does not appear to be painful. Localization to both thoracic limbs, along with mild trismus and forehead wrinking, has been seen in one affected cat [213].
Potential complications include bony fractures from spasms or seizures, dyspnea from laryngeal spasms, inhalation pneumonia from dysphagia, and decubital ulcers. Urinary and fecal retention may be associated with anal and urethral sphincter/bladder spasms. In such instances, urinary stasis may lead to hemorrhagic, purulent cystitis [168,169]. Gastric and intestinal bloating may also occur [169]. Transient megaesophagus and/or hiatal hernia have been reported in association with gastro-esophageal reflux and regurgitation [170,171]. It has been reported that the hiatal hernia developed approximately 2 weeks after the beginning of clinical signs of tetanus [171,172]. Tetanus has been reported as a complication in dogs during parturition [173] and pregnancy [174].
To my knowledge, structural changes in the CNS or PNS have not been reported in dogs or cats. In people, degenerative changes may be found in the cerebral cortex and brainstem, along with hemorrhage, demyelination, and gliosis in chronic cases [106]. Diagnosis of the severe form of tetanus is largely based on characteristic clinical data. Mild forms of the disease may be difficult to diagnose since there are no specific ancillary aids available. There is a lack of the usually observed electrical silence following needle insertion in electromyographic studies. Nerve conduction studies are normal. Megaesophagus and/or hiatal hernia in animals with tetanus can be diagnosed radiographically [170].
Since tetanus is often mild or localized in dogs and cats, prognosis is usually favorable with treatment, which consists of penicillin G (e.g., 20,000 to 100,000 units/kg, qid, IV, as the aqueous potassium or sodium salt or IM, as the procaine salt), and immediate administration of tetanus antitoxin (TAT) (e.g., 100 to 1,000 IU/kg IV) [160]. Antibiotic therapy is aimed at any remaining vegetative C. tetani organisms in the wound, while the antitoxin is given to neutralize any toxin that remains unbound to the CNS. A test dose (e.g., 0.1 - 0.2 ml) of TAT can be given SC 20 minutes prior to the intravenous dosage and the animal observed for any anaphylactic reaction. If a wound is present, radical debridement and excision of all infected or necrotic-appearing tissue should be performed, along with peroxide irrigation to reverse the anaerobic state, and local intramuscular instillation of 1,000 units of TAT and 1,000,000 units of procaine penicillin G, in and around the wound site. Metronidazole is also effective (at 10 mg/kg, PO, tid, in dogs, and at 250 mg, PO, sid or bid, in cats). Antibiotic therapy should be continued for at least 10 days. Chlorpromazine (e.g., 0.5 - 2.0 mg/kg IM, IV, or PO, bid or tid, in dogs and cats) and pentobarbital (e.g., 3 - 15 mg/kg, IV or IM, every 2 - 3 hours, in dogs and cats) can be used to control reflex spasms and convulsions. Tracheostomy may be needed if laryngeal spasms are severe [22]. Esophagostomy or gastrostomy tubes or gastric tube feeding may be necessary if trismus prevents feeding or if megaesophagus and/or hiatal hernia are present along with gastro-esophageal reflux and regurgitation [22,171].
Prompt treatment usually results in a favorable prognosis [150,161,171], although complete remission of clinical signs in dogs and cats with generalized or localized tetanus may take 3 to 5 months [166]. A guarded to poor prognosis has also been reported in severely affected animals [22,169]. Megaesophagus and/or hiatal hernia tend to resolve with resolution of the tetanus [170], although, in one report, all dogs with this complication that were fed normally, died [171]. Nursing care is important to monitor nutritional and fluid balance.

Thallium
Thallium poisoning, from ingestion of thallium-containing rodenticides, may produce vomiting, bloody diarrhea, salivation, anorexia, depression, paralysis, trembling, dyspnea, and death in 3 - 5 days [175]. Degenerative changes have been observed in peripheral nerves [176]. Today, thallium toxicosis is relatively rare as rodenticides containing it are banned in the USA. Thallium toxicosis can be confirmed by detection of thallium in the urine, using colorimetric analysis. Treatment involves use of diphenylthiocarbazone (dithizone) to increase the rate of thallium excretion from the body, administration of antibiotics, fluid therapy, warm-water enemas, and oral administration of activated charcoal slurries [177,178].