{"version":"1.0","provider_name":"TBE Book","provider_url":"https:\/\/tbenews.com\/tbe","author_name":"IT","author_url":"https:\/\/tbenews.com\/tbe\/author\/brianong\/","title":"Chapter 10: TBE in animals - TBE Book","type":"rich","width":600,"height":338,"html":"<blockquote class=\"wp-embedded-content\" data-secret=\"EXT3t1HCSz\"><a href=\"https:\/\/tbenews.com\/tbe\/chapter-10-tbe-in-animals\/\">Chapter 10: TBE in animals<\/a><\/blockquote><iframe sandbox=\"allow-scripts\" security=\"restricted\" src=\"https:\/\/tbenews.com\/tbe\/chapter-10-tbe-in-animals\/embed\/#?secret=EXT3t1HCSz\" width=\"600\" height=\"338\" title=\"&#8220;Chapter 10: TBE in animals&#8221; &#8212; TBE Book\" data-secret=\"EXT3t1HCSz\" frameborder=\"0\" marginwidth=\"0\" marginheight=\"0\" scrolling=\"no\" class=\"wp-embedded-content\"><\/iframe><script>\n\/*! This file is auto-generated *\/\n!function(d,l){\"use strict\";l.querySelector&&d.addEventListener&&\"undefined\"!=typeof URL&&(d.wp=d.wp||{},d.wp.receiveEmbedMessage||(d.wp.receiveEmbedMessage=function(e){var t=e.data;if((t||t.secret||t.message||t.value)&&!\/[^a-zA-Z0-9]\/.test(t.secret)){for(var s,r,n,a=l.querySelectorAll('iframe[data-secret=\"'+t.secret+'\"]'),o=l.querySelectorAll('blockquote[data-secret=\"'+t.secret+'\"]'),c=new RegExp(\"^https?:$\",\"i\"),i=0;i<o.length;i++)o[i].style.display=\"none\";for(i=0;i<a.length;i++)s=a[i],e.source===s.contentWindow&&(s.removeAttribute(\"style\"),\"height\"===t.message?(1e3<(r=parseInt(t.value,10))?r=1e3:~~r<200&&(r=200),s.height=r):\"link\"===t.message&&(r=new URL(s.getAttribute(\"src\")),n=new URL(t.value),c.test(n.protocol))&&n.host===r.host&&l.activeElement===s&&(d.top.location.href=t.value))}},d.addEventListener(\"message\",d.wp.receiveEmbedMessage,!1),l.addEventListener(\"DOMContentLoaded\",function(){for(var e,t,s=l.querySelectorAll(\"iframe.wp-embedded-content\"),r=0;r<s.length;r++)(t=(e=s[r]).getAttribute(\"data-secret\"))||(t=Math.random().toString(36).substring(2,12),e.src+=\"#?secret=\"+t,e.setAttribute(\"data-secret\",t)),e.contentWindow.postMessage({message:\"ready\",secret:t},\"*\")},!1)))}(window,document);\n\/\/# sourceURL=https:\/\/tbenews.com\/tbe\/wp-includes\/js\/wp-embed.min.js\n<\/script>\n","thumbnail_url":"https:\/\/tbenews.com\/tbe\/wp-content\/uploads\/2024\/06\/Chapter-10-TBE-IN-ANIMAL-2-scaled.jpg","thumbnail_width":2560,"thumbnail_height":1709,"description":"Chapter 10:TBE in animals Martin Pfeffer, Hannah M. Schmuck, Michael Leschnik Key points Introduction While tick-borne encephalitis (TBE) is well documented as a public health threat, the veterinary aspects of this zoonotic disease are little recognized. TBE in animals has, for very long, been considered to be a problem exclusive to domestic ruminants due to their known potential to transmit tick-borne encephalitis virus (TBEV) via raw milk and raw milk products to consumers. While clusters of such cases continuously declined with the invention of milk pasteurization and overall improvements in hygiene management in cattle farming, goats and sheep flocks are still kept in traditional grazing farms where they are exposed to TBEV-infected ticks.1,2 In other words, even in industrialized countries, consumption of raw milk products continues to be a risk factor to acquire a TBEV infection. As society continues to exhibit a trend towards a preference for \u201cnatural products\u201d (assuming consumers can afford these), alimentary TBEV infections may be observed more frequently in the future. While this is a \u2018direct\u2019 zoonotic aspect of TBE (besides the tick bite of course), animals play a role in TBEV transmission in many other ways; either as diseased dead-end hosts, as infected animals without obvious burden of disease, or in maintaining and spreading the virus itself. Dogs Canine TBEV infection is a frequent event in endemic areas, with a calculated annual risk of about 11.6%.3 &nbsp;Total seroprevalence in the canine population has been examined in several countries: Switzerland 3.6\u20135.9%,4 Greece 1\u20138%,5 Germany 2.1\u2013 42.7%,6,7 Belgium 0.1%,8 Denmark 4.8\u201330%,9 Czech Republic 3.3\u201311.3%,10,11 Norway 16.4%,12 Finland 6\u201340%,13 and Austria 13.3\u201324%.3,14 Since inclusion criteria were different regarding the presence of clinical symptoms, residence, and tick-exposure of the examined dogs, results are difficult to compare (Table 1). Different test systems (enzyme-linked immunosorbent assay [ELISA], serum neutralization test [SNT]) used in these studies clearly influenced the results too. TBE has always been stated to be a tick-borne infection, mainly transmitted by ticks of the genus Ixodes; however, Dermacentor reticulatus ticks may play an important role in transmission to dogs.15 There has been one single case of a dog from the Czech Republic with a TBE-infection suspected to be due to consumption of raw goat milk.10 Regardless of the way dogs get infected, a recent study showed that walking a dog is a risk factor for human infections.16 Table 1: Serosurveillance studies for TBE virus and TBE virus antibodies in dogs since 2010 n.d. = not determined, SNT = serum neutralization test, Ab = antibodies, * showing the difference between nonendemic areas (1.1% in northern Germany) and endemic areas (22.1% in southern Germany) Source data Figure 1: A Rottweiler during recovery after chronic disease over 3 months \u2013 remarkable weight loss due to systemic muscle atrophy Figure 2: Acute head pressing with concurrent compulsive walking and disorientation on day 2 of a dog with TBE Figure 3: A male Spitz with central vestibular dysfunction and left-sided Horner syndrome during acute TBE Course of TBE Despite frequent TBEV infections in dogs, most of them do not develop any clinical signs.17 Dogs seem to be less susceptible than humans, although a lethal outcome within the first week of disease is documented in 16\u201350% of clinically symptomatic cases. Infection may lead to an acute course of the disease, with complete remission of symptoms within 1\u20132 weeks (31\u201359%). Infrequently, prolonged disease courses are described with long time period to remission (12\u201325%). These dogs frequently suffer from late sequela\u2013like paresis, muscle atrophy, epileptic seizures, or blindness (Figure 1).10,18,19,27,28 Clinical pictures After an estimated incubation period of 5\u20139 days, first clinical symptoms occur and develop to a maximum level within 48 hours. Initially, most dogs are depressed and show non-specific signs such as salivation and vomiting (25%), refusal to eat, and are reluctant to move due to generalized weakness, although some dogs show compulsive walking, circling to one side (25%), unusual behavior (70\u201391%), and head pressing (Figure 2).10,27-30 The elevated body temperature (42\u201366%) may initially be classed as fever; later on, it is more likely a result of non-voluntary excessive muscle contraction (e.g., seizures, loss of inhibition by upper motor neuron damage). Seizures are a principal result of cerebral damage due to TBEV infection and are observed in 12\u201333% of canine cases.28,30 Neurological symptoms like paresis (8\u201338%), vocalization due to painful perception of active and passive back movement (21\u201366%), and deficits of the cranial nerves (16\u201350%) (Figure 3) develop within a few hours thereafter.28,30,31 Blindness due to papillitis, optic nerve inflammation, or chiasma opticus neuritis may become the dominant symptom and systemic signs may diminish. Visual deficits may be the major clinical sign of disease and result from detachment of peripapillary retina, peripapillary hemorrhages, and inflammatory edema.32,33 Degeneration and demyelination of cranial nerves is certainly initiated by the virus\u2019 neurotropism. Later on, secondary immune reaction to neural tissue may prolong the period of damage and lead to irreversible symptoms such as retinal and optic disc atrophy. Other cranial nerve deficits like trigeminal dysfunction, resulting in reduced facial sensation and chewing muscle atrophy, vestibular signs (nystagmus and positional strabismus, Figure 4), and facial palsy, are observed. Figure 4: A comatose dog in lateral recumbency with severe brain stem encephalitis leading to anisocoria and left-sided strabismus Major involvement of the spinal cord results in mostly symmetrical paresis, muscle twitching, and proprioceptive dysfunction (38-50%), which may also be present as an exclusive symptom and may occur asymmetrically (Figure 5).10,28,30,31 Figure 5: A case of canine TBE with hemiparesis and spontaneous dorsal paw placement There is no significant breed, gender, or age predisposition, although most cases are described in adult middle- to large-breed dogs. Rottweilers and Huskies are overrepresented in the literature14,31,32 (Table 2). Brainstem symptoms like arrhythmical breathing pattern may be present in comatose dogs, especially in severe cases with guarded prognosis. Video: Comatose dog of Figure 4 with arhythmical breathing indicative of brain stem lesion Involvement of the brainstem may result in symptoms like arrhythmical breathing and disorder of other vital functions. Prognosis of such severe cases"}