
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