dysautonomia in havanese puppies

dysfunction
havanese puppies

dysautonomia in havanese puppies

canine dysautonomia may be a noncontinuous, typically fatal illness that seldom affects teams of connected animals. Four 0-week-old havanese puppies from a litter of five developed clinical signs of canine dysautonomia. The four affected dogs were exposed to an out of doors surroundings, whereas the fifth littermate wasn't exposed to the outside and remained clinically healthy Clinical signs of dysautonomia developed 10–16 days when going outside the house. an unrelated dog conjointly developed dysautonomia when exposure to one of the affected havanese littermates

all five dogs had morphological changes consistent with dysautonomia (widespread vegetative cell degeneration in involuntary ganglia, choose neural structure nuclei, and ventral horn motor neurons. differential diagnoses were excluded through negative materia medica analysis, fecal parasite screening, negative Canine distemper virus reverses transcription enzyme chain reaction, fluorescent protein testing, tried virus isolation, and microscopy. The five affected dogs were within the Kansas town, Missouri space, wherever there's a high incidence of dysautonomia.

canine dysautonomia may be a noncontinuous idiopathic disorder that generally affects individual dogs and leads to a progressive clinical illness of the involuntary system. the illness sometimes culminates in death or kill it absolutely was 1st according to the united kingdom in 1983.8 the primary case within the united state was reported in 1991 in a dog from glenrock, Wyoming.10 Most reported U.S. cases have occurred in Missouri, Kansas, Wyoming, Colorado, North Dakota, Montana, Iowa, and western Tennessee.1 Additionally, the Wyoming State Veterinary Laboratory (WSVL; Laramie, Wyoming) has received reports from owners and clinicians of suspect dysautonomia dogs from southern Illinois, Nebraska, western Kentucky, Minnesota, Alaska, the Texas panhandle, and Canada (Ontario and Alberta). The cause is unknown. The outcome is generally fatal (>92%).2 Rare cases of survival may be the result of exposure-dose-response or variable individual resistance in affected dogs.


Possible causes include autoimmunity, environmental toxins, venomous organisms, and microorganisms and/or biotoxins. The risk factor most commonly associated with dysautonomia is residing in rural areas (<5,000 people).

1 Most cases occur in spring and fall months, possibly suggesting an association with rainfall.

Dysautonomia most often affects young dogs (median age:18 months). there is 1 published report of multiple littermates being affected with dysautonomia. notwithstanding this publication, the WSVL is aware of 5 unpublished multicase households; 2 in Wyoming, 2 in Kansas, and 1 in missouri. Diagnosis is established by characteristic clinical signs and based on lesions in autonomic neurons, spinal cord, and in specific cranial nerves.

widespread degeneration of neurons accounts for clinical signs of vomiting, diarrhea, regurgitation, absent or reduced anal tone, distended bladder, dilated pupils, megaesophagus, and prolapsed third eyelids.

a schirmer tear test to document reduced tear production and pilocarpine-induced miosis are helpful confirmatory clinical tests. additionally, an intradermal histamine injection may show a reduced wheal-and-flare response. Also, the injection of atropine has proven to be unsuccessful in increasing the heart rate in affected dogs (Mankin J, Packer R. Dysautonomia).

dysautonomia was diagnosed by a clinical veterinarian in two 75-day-old Havanese puppies in a litter of 5 from a healthy 4-year-old dam in a suburban 
City, MO. The puppies were clinically normal, up to date on vaccinations, and fed a commercial diet. This was the dam’s second litter, and she was current on vaccinations. demographic characteristics of the 5 dogs eventually affected are presented in the owner had outside surroundings for 4 years. There were 9 adult Havanese dogs on the property that were clinically normal and current on vaccinations; all 9 remained
unaffected. Breeding females had produced 6 litters (18 animals total) prior to this affected litter without complications.

The breeder was considered by the clinical veterinarian to be experienced and conscientious.
The Havanese puppies were born on January 4, 2014, and weaned 6 weeks later. Of 5 dogs in the litter, 4 were allowed outside at the breeder’s residence. A fifth, unaffected dog, was sold and moved off the property minutes prior to the 4 littermates gaining access to outside. The 4 littermates had one-time access to defined areas (<5 m2 ) in the front and back yards for a brief period (<5 min total). All 4 littermates had simultaneous access to this one defined area
of patchy grass with new topsoil applied 6 months prior.

These dogs (B–E) exhibited clinical signs of dysautonomia 10–16 days after the outdoor exposure. All affected dogs developed vomiting and 1 or more other clinical signs, including crusty nares, straining to defecate and urinate, absent anal tone, rhinorrhea, prolapsed third eyelids, and hindlimb ataxia. dogs B and C were treated unsuccessfully with antibiotics, antiemetics, and steroids. dogs and were untreated.

The 4 littermates either died or were euthanized 3–9 days after clinical signs developed. a diagnosis of dysautonomia was established morphologically based on neuronal degeneration in multiple parasympathetic and/or sympathetic ganglia
(cranial mesenteric, splanchnic, and adrenal), and in submucosal and myenteric plexuses. There was widespread degeneration of large motor neurons in the ventral horn at all levels of the spinal cord, accompanied by degeneration in ventral spinal nerve roots. 

unequivocal neuronal degeneration was absent in spinal intermediolateral and intermediomedial nuclei; dorsal root ganglia were unaffected. Bilaterally symmetrical degeneration was present in facial and hypoglossal nuclei. additionally, 3 of the 4 dogs had histiocytic alveolitis (dogs C–E). Ancillary testing for Canine distemper virus was negative by indirect fluorescence microscopy (third eyelid) and polymerase chain reaction (PCR; brain and spleen), attempted virus isolation (lung, liver, spleen, kidney, cerebral cortex, posterior medulla oblongata, and stellate ganglia), negative stain electron microscopy (lung, liver, spleen, kidney, cerebral cortex, brainstem, and thoracic ganglia), and aerobic bacterial culture (lung).

dog G was an unrelated 16-week-old Golden Retriever– Poodle cross that was co-housed with dog D. Dog G was domiciled in south-central Missouri, which is recognized to be on the southern border of the known dysautonomia affected zone. dog G had never visited the affected property in Jackson County, Missouri. After comingling with dog G for 10 days, dog D became symptomatic for dysautonomia.

Seven days later, similar signs developed in dog G and this dog was subsequently euthanized after a clinical course of 4 days. Lesions were consistent with dysautonomia in dogs D and G. Clinical signs and lesions in these cases were consistent with previously published accounts of dysautonomia.2,4 All affected animals were presented with vomiting and straining to defecate and urinate. this is the second reported episode of dysautonomia in littermates.5 In the previous report, the dam developed dysautonomia shortly after multiple littermates to which she gave birth developed clinical signs. 

The Havanese dam in the current episode remained clinically healthy, as did the other 9 adult animals on the property and unaffected littermate F. While the age of this litter that was affected is lower then the median previously reported, WSVL personnel have confirmed cases in dogs as young as 6 weeks of age as well as multicase households in which adult dogs were affected. several possibilities are suggested by this cluster of 4 cases of dysautonomia in 1 household over 5 days. One is that the episode of dysautonomia has a genetic basis.

This is unlikely, as there were no previous or subsequent cases of dysautonomia in these dogs, and dysautonomia affects multiple breeds.3 The history in the current episode is more consistent with a point-source exposure to an unknown toxic compound or infectious agent, possibly related to exposure to an outdoor environment.

The only factor common to the 4 affected littermates was access to exposed soil for a brief period. The current episode is suggestive of exposure to an environmental component in the soil, either toxic or infectious. One possible
explanation is exposure to a soil-borne agent that selectively targets autonomic and lower motor neurons. Clostridial toxins have been proposed in the past as the basis for equine dysautonomia (grass sickness), although no clear association has been documented.6,7,9 It is noteworthy that an unrelated housemate of 1 affected Havanese puppy developed dysautonomia shortly after the former was introduced into the household. It was not possible to resolve whether this was coincidence or horizontal transmission of a toxin or infectious agent.

There may have been an earlier case of dysautonomia on the property. in December 2012, a 10-year-old, female, border collie–australian cattle dog cross (dog A) developed intractable vomiting, coughing, and a hoarse bark. Subsequently, upper airway inflammation and urinary incontinence developed. The dog was treated without success and was euthanized 188 days later. Unfortunately, no autopsy was performed to establish whether dysautonomia was the basis for illness. Investigation of clusters of canine Dog D with clinical signs for 3 days. a widespread degeneration of ganglionic neurons, with chromatolysis, intracytoplasmic
vacuolation, and atrophy. Note mild disseminated ganglioneuritis. 

Celiacomesenteric ganglion. Hematoxylin and eosin (HE). B, chromatolysis and atrophy of ventral horn neurons; cervical spinal cord. HE.
dysautonomia in households may be a useful approach for developing testable hypotheses for the basis of the disease.


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