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Thoracic ultrasonography of tick-paralyzed dogs / Gülersoy et al._____________________________________________________________________
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INTRODUCTION
Tick paralysis, a case of acute flaccid paralysis characterized by
vomiting, regurgitation and sudden onset of lower motor neuron
weakness and respiratory failure in severe cases, is a signicant
veterinary problem in certain parts of the world [1].
A wide variety
of domestic animals are affected, including horses, cattle, dogs,
cats, sheep, and poultry [2].
After attaching to the host, ticks
typically undergo a latent period of 3-6 days (d), during which they
engorge and their salivary glands enlarge, producing a neurotoxin.
Paralysis signs usually result from the engorgement of a single
tick, although multiple ticks may also contribute, and occasionally,
no tick is found [3]. Early clinical signs typically include hind limb
ataxia, which often progresses to quadriplegia [4].
In addition to
the non–specic clinical ndings observed in tick paralysis cases,
mortality rates can reach up to 100% in untreated cases due to
complications involving the cardiovascular, gastrointestinal, and
respiratory systems. The major clinical abnormality and cause of
mortality in tick paralysis cases is respiratory failure [5]. Current
hypotheses explaining the development of respiratory failure
in tick paralysis involve neuromuscular blockade of respiratory
muscles, potentially leading to hypoventilation. This effect may
be exacerbated by central respiratory depression. Additionally,
paralysis of the pharynx and larynx can result in upper airway
obstruction, while pulmonary parenchymal disease may also
contribute [6]. Pulmonary parenchymal disease in tick paralysis
is commonly linked to cardiogenic pulmonary edema resulting
from the tick’s salivary toxin. Aspiration pneumonia is a common
complication in patients with tick paralysis–related lung disease. It
is related to dysfunction of the esophagus, pharynx, and larynx, all of
which are frequently observed in patients with tick paralysis [2, 7].
During the last decade, thoracic ultrasonography has seen
increased use as both a diagnostic and monitoring tool. Previous
descriptions have detailed the identication of lung consolidations
on thoracic ultrasonography, characterized by either a tissue sign
involving the full width of the lung lobe or a shred sign affecting part
of the lung lobe’s width, along with an increased number of B–lines
and the presence of pleural effusion [8, 9]. In Veterinary Medicine,
point–of–care (POC) thoracic ultrasonography has been used to
identify pulmonary hemorrhage, congestive heart failure, and
alternative causes of alveolar–interstitial syndrome [10].
Thoracic
ultrasonography has shown promising diagnostic performance in
critically ill patients experiencing respiratory failure from various
causes. It was reported that it offers more valuable clinical insights
compared to physical examination and bedside radiography [11,
12]. Nevertheless, there is currently no study examining thoracic
ultrasonography ndings in dogs with acute flaccid paralysis due
to tick paralysis.
Discerning the primary pathological processes is essential for guiding
treatment and determining prognosis for patients. Managing clinical
cases related to pulmonary disease poses signicant challenges for
veterinarians and often carries a poor prognosis. Therefore, early
recognition of pulmonary edema and parenchymal disease is crucial
for improving survival rates. Considering that the leading cause of
mortality in tick paralysis cases are respiratory abnormalities such as
pulmonary edema, aspiration pneumonia and respiratory failure, the
purpose of this study is to describe thoracic ultrasonography lesions
in dogs with tick paralysis and to identify patterns that may aid in
diagnosis, treatment planning, and prognosis prediction.
MATERIALS AND METHODS
This study received approval from the Local Ethics Committee
for Animal Experiments at Harran University on 09/05/2022 with
session 2022/003 and decision number 01-06. All animal owners
gave their consent for participation in the study.
Animals
The Patient group for this study consisted of 48 dogs (Canis
lupus familiaris), each displaying symptoms indicative of acute
flaccid paralysis, including anorexia, regurgitation, ataxia, abnormal
vocalization, and weakness in standing, and all were found to have
ticks upon examination. The Healthy group comprised 10 clinically
healthy dogs admitted for vaccination and/or check–up purposes.
All animals were admitted to the animal hospital of Veterinary
Faculty, Harran University.
Inclusion/Exclusion Criteria and Forming Groups
The inclusion criteria for the tick–paralyzed dogs required that
dogs have no history of prior diseases other than tick paralysis—
including respiratory, cardiovascular, or gastrointestinal disorders
that could cause vomiting, diarrhea, anorexia, labored breathing,
or rapid fatigability—have not been treated with antiparasitic
medication within the past month, and exhibit signs of acute
flaccid paralysis. The accepted clinical ndings for acute flaccid
paralysis include sudden onset weakness that intensies within
a few days, characterized by weakness in respiratory muscles
and swallowing ability. Additionally, there is typically an absence
of spasticity, hyperreflexia, clonus, extensor plantar reflexes,
and muscle contraction due to impairment of motor pathways
extending from the cortex to muscle bers [13].
The primary differential diagnosis for the clinical manifestations
observed in the dogs included in the study and suspected
of tick paralysis involved considering common lower motor
neuron conditions in dogs, including botulism, acute idiopathic
polyneuropathy, and snake envenomation [14]. In summary,
botulism can occur in dogs following the consumption of rotten food
or carcasses; however, this was not the case for the dogs described
here, as they are solely fed commercial dry dog food. Clinically, it
is marked by difculties in grasping and swallowing food, along
with drooling. Acute idiopathic polyneuropathy has been observed
in dogs that have come into contact with raccoon saliva or have a
history of systemic illness. It is characterized by hyperesthesia and
neurogenic muscle atrophy enduring for over ve to seven days [3,
14]. Although acute idiopathic polyradiculoneuritis can involve the
cranial nerves and result in partial or complete respiratory paralysis
due to the involvement of intercostal or phrenic nerves, the majority
of clinical symptoms are usually limited to the limbs [15]. Typically,
the respiratory pattern in the neuromuscular paralysis conditions
mentioned is rapid and shallow. In contrast, the present cases
exhibited a slow respiratory pattern with a notable expiratory
effort, resembling what is seen in tick paralysis [3]. Myopathy
was also excluded, as it is manifests as proximal weakness or
fatigue, preserved sensitivity, and followed by a loss of reflexes,
typically following signicant atrophy [16]. While the neurological
manifestations discussed here share similarities with those of
other lower motor neuron diseases, they closely resemble the
ndings typically associated with tick paralysis [17], the cases