Dog distemper symptoms - Canine distemper

Widespread vaccination has substantially decreased the incidence of dog distemper virus infections in many regions, but outbreaks still occur among unvaccinated dogs and sporadically in vaccinated dogs. Canine distemper is usually seen as a multisystemic disease that may include multifocal progressive involvement of the central nervous system. Dog distemper symptoms vary, depending on virulence of the virus stain, environmental conditions, host age and immune status.

Young, unvaccinated dogs are most commonly affected by severe generalized canine distemper. In these dogs, there may initially be overt nonneurologic signs, including ocular and nasal discharge, coughing, dyspnea, vomiting and diarrhea. Neurologic signs begin 1 to 3 weeks after dogs start to recover from systemic illness and may include hyperesthesia, cervical rigidity, seizures, cerebellar or vestibular signs, tetraparesis, and ataxia. Seizures can be of any type, depending on the region of the brain affected, "chewing-gum" seizures caused by polioencephalomalacia of the temporal lobes are commonly described.

Myoclonus, a repetitive rhytmic contraction of a group of muscles resulting in repetitive flexion of a limb or contractions of the muscles of mastication, is often referred to as canine distemper chorea and is most commonly associated with distemper encephalomyelitis. In young dogs infected while their permanent teeth are developing, enamel hypoplasia (brown discoloration) of the teeth will be noted. Older dogs may develop a more subacute to chronic encephalomyelitis with neurologic signs, including progressive tetraparesis or vestibular dysfunction, in the absence of systemic signs. Dog distemper symptoms and most infections are probably subclinical or are associated with mild signs of upper respiratory tract infection that resolves without therapy.
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Bacterial infection of the central nervous system (CNS) is rare in dogs. It may result from local extension of infection from adjacent structures such as ears, eyes, sinuses, nasal passages, or areas of osteomyelitis. Hematogenous dissemination from extracranial foci may also occur in animals with bacterial endocarditis, omphalophlebitis, prostatitis, metritis, diskospondylitis, pyoderma or pneumonia. Local extensions and hematogenous dissemination of bacterial infection to the CNS may be most common in dogs with underlying immunodeficiency. Bacteria most often implicated include Straphylococcus aureus, Straphylococcus epidermitis, Straphylococcus albus, Pasteurella multocida, Actinomyces and Nocardia.

Clinical signs of bacterial meningitis in dogs may include cervical rigidity, hyperesthesia, pyrexia, vomiting, and bradycardia; seizures may also occur. Additional neurologic deficits, such as paresis, paralysis, hyperreflexia, blindness, mystagmus, and head tilt, are common; these suggest parenchymal involvement. The clinical course is variable. However, once the meningitis occurs in dogs, it can progress rapidly. Physical examination of a dog with bacterial meningitis may reveal a focus of underlying infection. These animals are almost systemically ill. Shock, hypotension, and disseminated intravascular coagulation may be present.

Bacterial meningitis in dogs is a life-threatening infection and requires rapid and aggressive treatment. Appropriate therapy of central nervous system infections is based on identification of the causative organism and choosing an appropriate antimicrobial agent. Chloramphenicol, trimethoprim-sulfadiazine, and the quinolones can penetrate into the CNS in therapeutic concentrations. Metronidazole is also effective and is the drug of choice whenever anaerobic infection is likely. In the presence of inflammation, ampicillin, penicillin, and amoxicillin with clavulonic acid also reach adequate concentrations. Although some of the third-generation cephalosporins (cefotaxime) are expensive, most penetrate the CNS well and are effective against many infectious agents, including gram-negative bacteria.

The response to antibiotic therapy is variable, and relapses are common. The prognosis should be considered guarded, because even with appropriate therapy many animals die. However, treatment should be attempted, because some cases respond dramatically to therapy and have complete resolution of their neurologic defects.

We also recommend this natural balanced real-meat dog food and natural dietary supplement for recovery.

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Seizures in dogs

A seizure or convulsion is the clinical manifestation of excessive hypersynchronous electrical activity in the cerebral cortex. This electrical event results is a loss or derangement of counsciousness, altered muscle tone, jaw chomping or trismus, salivation, and often involuntary urination and defecation. Most dogs have tonic-clonic, generalized (symmetric) motor seizures in which the animal experiences a period of extremely increased extensor muscle tone (tonus), falls into lateral recumbency, and then has periods of tonus alternating with periods of relaxation (clonus), resulting in rhythmic contractions of muscles manifested as paddling or jerking of the limbs and chewing movements.

The actual seizures in dogs may be preceded by minutes to hours of unusual behavior (preictal phase), including hiding, attention seeking, or agitation. In some dogs, seizures start during sleep or may be triggered by a specific stimulus or event (repetitive noise, flickering light). Estrus, certain drugs (especially phenothiazines), stress, and excitement can all precipitate seizures in dogs. In most animals, each seizure is followed by a short period of disorientation (postictal phase), during which ataxia, blindness, pacing and delirium are common.

Less common than generalized, symmetric tonic-clonic seizures in dogs are focal partial motor seizures. These seizures arise in part of one cerebral hemisphere, resulting in asymmetric signs that may include turning of the head away from the side of the lesion and focal twitching or tonic-clonic contractions of the contralateral facial or limb muscles. These seizures may ultimately become generalized. Although it is often stated that partial motor seizures in dogs are usually associated with structural brain disease, close observations of animals with idiopathic epilepsy reveals that many experience focal seizures with secondary generalization.

Psychomotor seizures in dogs are focal seizures manifested as stereotypic paroxysms of abnormal behavior such as rage, hysteria, hyperesthesia, self-mutilation, tail chasing, and fly biting. Withouth event-triggered electrodiagnostic testing, however, it is very difficult to distinguish these seizures from compulsive stereotypic behavior. In some cases, consciousness is impaired (complex focal seizures) or the seizure progresses to a generalized symmetric tonic-clonic seizure, aiding diagnosis of seizures in dogs.