Altre patologie

Tetano

Una malattia che non conoscevamo affatto, se non per vaga informazione sugli umani, fino a quando il nostro Jason ne è stato colpito facendoci spaventare a morte. L'articolo in Italiano è di Giordano, comproprietario di Jason. L'articolo in Inglese mi è stato spedito dalla mia cara amica Michele dell'allevamento Rockland per cercare di non farmi perdere le speranze...

Una brutta avventura…a lieto fine!

Vi voglio raccontare della disavventura in cui ci siamo trovati qualche mese fa..

I primi giorni dello scorso luglio notai che nel mio cucciolone di siberian di 8 mesi c’era qualcosa che non andava: era apatico, mangiava svogliatamente e lasciava gran parte delle crocchette nella ciotola; La prima cosa che ho pensato è stata semplicemente che era estate, c’era un gran caldo e che fosse normale un calo di appetito. 

Vedendo però che la “svogliatezza” e l’inappetenza continuavano, mi sono rivolto al mio veterinario che ha fatto tutti i controlli del caso senza riscontrare nessuna anormalità nei valori. Per assurdo questa normalità mi dava ancora di più inquietudine..sentivo, sapevo che c’era qualcosa che non andava: lui era il mio cane e conoscevo di lui ogni respiro, ogni sua espressione, ogni suo comportamento.

 Di fronte a ciò abbiamo deciso di aspettare se la situazione fosse evoluta in qualche modo: e così purtroppo è stato. 

Il giorno dopo mi sono trovato davanti ad uno “spettacolo” allarmante: le articolazioni del mio cane si stavano irrigidendo, le orecchie si erano avvicinate e quasi si toccavano, gli occhi guardavano uno a destra e l’altro a sinistra.

Tutto il corpo del mio cucciolo era sottoposto a contrazione. 

Davanti a questa situazione mi sono sentito crollare il mondo addosso; avevo da poco perso il mio primo siberian per un tumore al fegato e avevo come l’impressione che sarebbe successo qualcosa anche a lui..non avevo mai visto nulla del genere e non sapevo cosa pensare.

Nella mia testa apparivano mille possibili cause, temevo qualche problema neurologico o peggio un tumore al cervello. Ero disperato.

Senza aspettare un istante sono corso come un matto dal mio veterinario che prontamente (per fortuna) ha riconosciuto i sintomi tipici dell’infezione da tetano (l’espressione tipica del viso con lo strabismo degli occhi e le orecchie vicine è chiamata in veterinaria “sorriso sardonico”).

Mi ha guardato come per dirmi che non sarebbe stato facile ma era possibile fare qualcosa. Dalla nostra parte avevamo il fattore tempo, avevamo scoperto abbastanza presto l’infezione.

Come è solito fare il mio veterinario mi ha chiamato da parte e mi ha parlato della situazione che avevamo davanti e di ciò che c’era da fare, mi ha detto che sarebbe stata una battaglia lunga e che il mio ruolo sarebbe stato, specie nei primi giorni, essenziale.

E’ intervenuto subito con un’iniezione antitetanica e  con degli antibiotici per combattere l’infezione che si ormai si era propagata.

Nel frattempo lo vedevo lì inerme sotto flebo che mi guardava con quell’espressione così innaturale per lui.

Piero, il mio veterinario mi ha raccomandato di fargli mangiare degli omogeneizzati di carne bianca.

Omogeneizzati perché il motivo per cui il cane non mangiava, oltre chiaramente al malessere, era che la contrazione dei muscoli gli impediva di masticare le crocchette. 

Ed inoltre mi disse che era fondamentale somministrargli dei sedativi e  dei miorilassanti (Muscoril o Valium), in quanto specie nella fase critica della malattia c’è il rischio che la contrazione potesse interessare gli organi vitali dell’animale con effetti letali. 

Ricordo bene quelle calde notti d’estate con lui che dormiva in fondo al mio letto con il respiro affannato e gli spasmi che ogni tanto lo scuotevano in tutto il corpo. Dovevo vegliare controllando che il cane non avesse crisi altrimenti dovevo essere pronto ad intervenire con le iniezioni di valium.   

Le terapie sono andate avanti per un mese e grazie a Dio la cosa si è risolta per il meglio. Se tutto va bene il cane reagisce abbastanza presto anche se i  sintomi esteriori necessitano anche di 30/40 giorni per scomparire del tutto. 

Il mio veterinario ha detto “ironicamente” che sono stato fortunato perché comunque il tetano nei cani è abbastanza raro e che sono anche stato fortunato nel vero senso della parola perché siamo riusciti a capire in tempo la malattia perché altrimenti le possibilità di sopravvivenza sarebbero state molto basse. 

Inoltre, sia io che Monia, anche per sentirci più tranquilli, cercavamo di raccogliere più informazioni e notizie possibili sulla malattia: cercavamo su internet, abbiamo chiamato praticamente tutti i veterinari che conoscevamo per avere chissà forse solo delle conferme che stavamo facendo la cosa giusta, volevamo sapere  tutto sulla malattia, come si manifestava e perché, come fare del nostro meglio nello stare vicini al cane e come sarebbe stata la lunga strada della guarigione. 

In tutta questa ricerca ho scoperto che il tetano è una malattia infettiva causata dal Clostridium tetani e che dà come sintomi contrazioni dei muscoli scheletrici fino alla paralisi, e anche di tutti i muscoli relativi a organi e tessuti.
Il Clostridium tetani è un germe in grado di dar luogo a delle spore che dovendo resistere a svariate situazioni, sono molto resistenti ai fattori ambientali e nel tempo. Una volta penetrato nell'organismo recettivo attraverso qualsiasi tipo di ferita, anche la più insignificante, la spora da origine alla forma vegetativa che replicandosi produce la tossina tetanica responsabile della sintomatologia nervosa, infatti essa attacca le cellule nervose che trasmettono ai muscoli l’impulso alla contrazione e ne produce lo spasmo costante.

 Nel cane il tetano dà la seguente sintomatologia: trisma (contrazione spasmodica delle mascelle con conseguente impossibilita' di aprire la bocca), gli occhi infossati ed il cosiddetto "risus sardonicus" (orecchie diritte ed immobili, cute della faccia corrugata, angoli della bocca retratti e occhi socchiusi), contrattura dei muscoli del collo e degli arti. Il decorso della malattia è vario (da 2 gg a 15 gg) e la morte sopravviene di solito per asfissia causata dallo spasmo della glottide o dalla paralisi dei muscoli respiratori.

Il trattamento prevede il ricovero dell’animale in ambiente molto tranquillo, possibilmente al buio.
La terapia prevede la somministrazione di antibiotici, neuroprotettori, siero antitetanico, sedativi.
Prima di somministrare il siero è il caso di testare l’ipersensibilità dell’animale, diversamente si rischiano shock anafilattici.
E’ possibile prevenire l’infezione somministrando il vaccino pratica da considerare soprattutto nelle zone dove il tetano e' una realta' ben presente (zone tetagene, presenza di cavalli, pecore..), tuttavia bisogna considerare che il vaccino e' stato messo a punto per l' uomo e non per i cani e che gli effetti collaterali devono essere considerati con la massima attenzione. 

Mi scuso se ho scritto delle imprecisioni in questo articolo e qualcuno “rabbrividerà” leggendo qualche espressione magari poco tecnica, ma non sono un veterinario e ho cercato di riportare la mia esperienza nel modo più completo possibile.

Giordano Tarara

L'articolo spedito da Michele, USA

“Tucker” Gold, a four-month-old intact male Bull Mastiff puppy, presented to the Emergency Service of the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania on September 2, 2003 with a twenty-four hour history of trismus, risus sardonicus, difficulty standing, trembling, and dysphagia. A diagnosis of tetanus was made based on history and clinical signs. Despite progression to generalized tetanus and complications due to acute upper airway obstruction and pneumonia, Tucker improved with medical treatment and intensive nursing care. A rare and potentially fatal disease, tetanus is caused by the neurotoxin tetanospasmin produced by Clostridium tetani. This paper will discuss the etiology, pathogenesis, diagnosis, treatment and a case presentation of tetanus.

Tetanus is a painful, debilitating, and potentially fatal disease caused by one of the most potent toxins known, the neurotoxin tetanospasmin.1 Produced by Clostridium tetani, a 0.4-0.6 μm x 2.5-5.0 μm, motile, gram positive, nonencapsulated, obligately anaerobic, sporeforming bacillus, the potency of tetanospasmin is due primarily to its strict neurospecificity.1,2 The clinical signs of tetanus are due to the action of tetanospasmin resulting in the inhibition of neurotransmitter release, specifically glycine and gamma-aminobutyric acid at the level of the spinal cord and brainstem. Clostridium tetani is present ubiquitously in the environment and can be routinely isolated from the intestinal tract and feces of many domestic animals, including canines.2 In the presence of adverse environmental conditions, the bacilli of Cl. tetani produce round terminal spores. These spores are able to survive in the environment for months to years, in the absence of direct sunlight, and are resistant to boiling water and chemical and physical inactivation.2 The vegetative form, however, is susceptible to heat and numerous disinfectants.3 Tetanus is a rare disease in the canine due to their natural resistant to tetanospasmin. Consequently, the prevalence of disease in canines is low compared to other domestic animals. Equines are the most susceptible species. If the amount of toxin required to produce clinical illness is arbitrarily set at “1” for equines, humans require three times the amount, canines require 600 times the amount, and felines require 7,200 times the amount of toxin to produce clinical signs.2 Species sensitivity to tetanospasmin is believed to be due to the difference in ability of the toxin to bind to peripheral neurons of different species; direct injection of the identical dose per unit body weight of toxin into the central nervous system produces similar clinical signs in domestic animals.3 However, another theory states that the variation of susceptibility is due to the amino acid sequence of docking proteins involved in neurotransmitter release.4 Vulnerability of the docking proteins to cleavage by tetanospasmin, resulting in inhibition of neurotransmitter release, varies between different species. 4 Due to the poor absorption of tetanospasmin across mucous membranes, destruction of the toxin by gastric juices, and inability of the toxin to cross the placenta as result of its high molecular weight, the most common route of entry for tetanospasmin is from a wound site.1,2 Tetanus develops as a result of contamination of necrotic wounds with spores from Clostridium tetani. Once traumatized tissue has become contaminated with spores, the spores can remain dormant for several months until necrosis of the tissue provides the strict anaerobic environment necessary for germination to the vegetative, toxin-producing form.5 The organism usually remains at the site of introduction due to its preference for devitalized tissue.2 Once the spores have germinated, rapid vegetative growth takes place and three exotoxins are produced at the site of infection.1,5 However, minimal toxin is released prior to bacterial cells lysis.5

The genus Clostridium can be separated into two groups based on pathogenesis: the tissue-invading, enterotoxigenic group and the toxin-forming, noninvasive group.1 The species of the first group can invade and proliferate in tissues of the host animal. They are able to produce toxins, termed enterotoxins when elaborated in the intestines; however, their toxins are less potent than that of the second group.1 The pathogenicity of the noninvasive second group, including Cl. tetani, is based solely on the production of potent toxins produced either outside the body of the host or within localized areas in the body of the host.1 Numerous different strains of C. tetani exist, varying from completely non-toxigenic to very highly toxigenic; however, the toxin produced by all strains is identical and antigenically homogenous.3,6 Toxigenic strains of Cl. tetani produce three exotoxins: tetanospasmin, tetanolysin, and a peripherally acting toxin.1,5 Tetanospasmin, a metalloprotease which enters neurons and blocks neurotransmitter release at the level of the brain and spinal cord, is responsible for the majority of clinical signs seen in tetanus. Tetanolysin, also known as hemolysin, results in the hemolysis of red blood cells during rapid growth of Cl. tetani in vitro. However, the significance of tetanolysin is debated. There is belief that tetanolysin is not clinically significant.2,6 On the other hand, there is also belief that tetanolysin causes local tissue necrosis which results in a favorable environment for germination of the spores of Cl. tetani and proliferation of the vegetative form.1,7 The third exotoxin is a peripherally acting nonspasmogenic toxin whose action is poorly defined.1 By rendering the neuromuscular junction hyperexcitable, the peripherally acting nonspasmogenic toxin is believed to potentiate the action of tetanospasmin.7 The toxigenesis of tetanus is plasma mediated.6 Toxigenic strains of Clostridium tetani contain a plasmid responsible for the production of a single inactive 150 kD polypeptide chain released locally into tissues by bacterial lysis.3,4 Once released, it is cleaved by bacterial and host proteolytic enzymes to yield the active neurotoxin, tetanospasmin.3,4 Tetanospasmin is composed of a dimer consisting of a 100 kD heavy chain and a 50 kD light chain bound by a single interchain disulfide bond.2,6 The toxin contains three functional regions: the carboxyterminal half of the heavy chain responsible for neurospecific binding,4,6 the amino-terminal half of the heavy chain responsible for the internalization of the toxin,3,4 and the zinc-dependent endopeptidase activity of the light chain which is responsible for the proteolysis of synaptobrevin, a vesicle associated membrane protein necessary for neurotransmitter release.3,6 The major sites of action of tetanospasmin are at the synapses of the alpha motor neuron with the inhibitory Renshaw interneuron, preventing the release of the inhibitory neurotransmitter glycine, and with the inhibitory interneurons of the brainstem, preventing the release of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA).6 The neurospecificity of tetanospasmin is due to the toxin’s affinity for binding to gangliosides located on the neuronal plasma membrane and the high affinity nerve terminal membrane protein receptors have for the toxin.1,6 Tetanospasmin binds to gangliosides and protein receptor located at the telodendron of the alpha motor neuron.4 The toxin is then internalized and migrates by retrograde transport within the motor axon at a rate of 75-250 mm per day.2 Once the toxin reaches the neuronal cell body within the central nervous system, it continues to migrate to the dendrites and is released into the intersynaptic space between the alpha motor neuron and the inhibitory interneuron.4 The toxin then binds to gangliosides concentrated at the synaptic membrane of the inhibitory interneurons and is internalized within a vesicle.4 Acidification of the internalized vesicle allows subsequent translocation of the tetanospasmin light chain into the cytoplasm.6 The endopeptidase activity of the light chain is then responsible for the cleavage of synaptobrevin, a specific protein molecule (“docking protein”) required for neurotransmitter exocytosis.4,6 It is believed that in addition to preventing exocytosis as a result of cleavage of synaptobrevin, tetanospasmin may also prevent further neurotransmitter release by crosslinking synaptic vesicles to the cytoskeleton.4 The effects of tetanospasmin within the inhibitory interneuron prevents the exocytosis of neurotransmitter for several weeks; the effects may even be permanent.6 As a result of inhibition of the release of glycine in the spinal cord and/or GABA in the brainstem, the postsynaptic alpha motor neurons lose their inhibition and are constantly activated. This results in the sustained contraction of the muscles supplied by the affected neurons. Due to the irreversible nature of the action of tetanospasmin, clinical recovery is prolonged and requires the development of new interneuronal synapses to replace those that were inactivated by tetanospasmin.2,6 Two forms of tetanus have been described: localized, also known as ascending tetanus, and generalized, also known as descending tetanus. In localized tetanus, such as in one limb, tetanospasmin binds to regional alpha motor neurons adjacent to the wound and tetanus develops first in the muscles of the affected limb.1 Tetanospasmin can spread to the inhibitory interneurons from one ventral horn of the spinal cord grey matter to the contralateral ventral horn, affecting the contralateral limb. The toxin may then continue to spread within the spinal cord and ascend to the brain.1,3,7 In localized tetanus, intracranial signs, such as spasticity of the facial muscles and/or respiratory arrest, develops during the later stages of the disease.2,8 In generalized tetanus, tetanospasmin spreads from the infected site by diffusing into adjacent muscles, the toxin is then transported via lymphatics from which it enters the bloodstream, and binds to alpha motor neurons throughout the body.3,6,7 Intracranial signs develop during the early stages of the disease with generalized tetanus and usually precedes generalized muscular hyperactivity.2 This is believed to be due to the shorter distance tetanospasmin must travel to the brainstem nuclei via retrograde axonal transport in the cranial nerves as compared to nerves of the limbs; consequently, tetanospasmin is rapidly delivered to the brain.3 The muscles of the neck, trunk and limbs subsequently become affected as the toxin reaches the spinal cord via peripheral alpha motor neurons.

Clinical signs due to wound infection with Clostridium tetani generally occurs within five to ten days after infection, but can range from days to a month after infection.6 Due to the innate resistance of canines to tetanospasmin, the incubation period may be as long as three weeks. As a result, the wound that served as the initial site of introduction of Cl. tetani may be healed by the time clinical signs are observed.8,9 Tetanus is characterized by severe tonic contractions of voluntary muscles superimposed upon muscular rigidity.6,9 With generalized tetanus, the gait is generally stiff if ambulatory and a characteristic “sawhorse” stance with an extended, rigid tail may be present with difficulty in standing or laying down due to extensor muscle rigidity.2,4 Painful reflex muscle spasms occur which is exacerbated by external stimuli. As a result of hyperesthesia, mild stimulation can result in generalized tonic contraction of all muscles with opisthotonus.2 Rectal temperature can be increased due to excessive muscular activity. Progression of the disease may make voluntary movements impossible with extensor rigidity of all four limbs resulting in recumbency.4  Intracranial signs due to the action of tetanospasmin on cranial motor nuclei are characteristic for tetanus. Trismus due to contraction of the masticatory muscles, risus sardonicus due to the retraction of the lips, dorsomedial retraction of the ears, and excessive wrinkling of the skin of the forehead are observed. Prolapse of the third eyelid and enophthalmos is due to retraction of the globe from hypertonic extraocular muscles.2,8 Miosis, dysphagia, ptyalism and laryngeal spasms may also be noted. Tetanospasmin may also produce sympathetic and parasympathetic hyperactivity.3 While sympathetic hyperactivity, such as tachycardia, cardiac arrhythmias, and peripheral vasoconstriction, are seen in humans due to increased catecholamine release associated with adrenergic stimulation, it is rarely reported in canines.3 However, the effects of parasympathetic hyperactivity, due to the action of tetanospasmin in the parasympathetic cardiac inhibitory center of the nucleus ambiguous resulting in increased vagal tone, have been observed in canines including bradyarrhythmias, arterioventricular block, sinus arrest, and ventricular escape beats.3 Complications from tetanus include decubital ulcers as a result of recumbency, regurgitation due to dysphagia, megaesophagus, hiatal hernia, dysuria and urine retention due to hypertonic urethral sphincter, and constipation and gaseous distention due to hypertonic anal sphincter.2 The two most severe complications may culminate in death as the disease progresses: respiratory failure secondary to the spasm of respiratory muscles, increased airway secretions, or central respiratory arrest from medullary intoxication and aspiration pneumonia secondary to dysphagia or increased airway secretions.2,3

The presumptive diagnosis of tetanus is based primarily on history, clinical signs and response to treatment. On physical examination, a recent or healed wound may be evident; however, absence of a detectable wound at the time of presentation is not uncommon with tetanus in canines.7 Unfortunately, it is difficult to definitively confirm the diagnosis. Even if a wound is present, isolation of Cl. tetani from wounds can be difficult and often fails due to the low concentration of Cl. tetani present in the wound and the strict anaerobic conditions required for culture.7 Gram staining of samples from the wound may reveal gram-positive rods and darkstaining spherical endospores but this is of limited diagnostic value. The morphology of the sporulated and vegetative forms of Cl. tetani, as observed on gram stain, are similar to other anaerobic bacteria; Cl. tetani does not have characteristic features to make a definitive identification.1,3 Furthermore, Cl. tetani, may be present in a wound as a contaminant and some strains of Cl. tetani are non-toxigenic so their presence is of no pathologic significance.3,6 Results from hematology, serum biochemistry and cerebrospinal fluid are often within normal limits. If a wound or pneumonia is present, a neutrophilic leukocytosis with left shift may be observed. Creatine kinase (CK) and aspartate aminotransferase (AST), enzymes present in muscle, may be elevated due to muscle trauma as a result of hypertonicity and prolonged recumbency.2 Thoracic radiographs may reveal hiatal hernia, megaesophagus, and aspiration pneumonia as complications due to tetanus. Muscle spasms due to tetanus may be inhibited by general anesthesia, however electromyographic changes are present revealing abnormal persistent electrical motor unit discharges rather than the normal period of electrical silence after insertion of a needle into the affected muscle.2 Measurements of serum antibody titers may be helpful in confirming tetanus but have had equivocal results when used in cats.8

Treatment of tetanus in severely affected animals can be cost prohibitive and extremely time consuming. Recovery from tetanus is affected by the dose of toxin exposure, onset of treatment, and presence of secondary complications.4 Although mild or localized tetanus may resolve without treatment, untreated generalized tetanus can be fatal. The objectives of treatment include: neutralizing circulating toxin, eliminating further production of tetanospasmin, and supportive care.3,7,10 The first concern when treating tetanus is neutralizing any toxin that is not bound to the central nervous system. Antitetanus equine serum (ATS), derived from the sera of hyperimmunized horses, exerts its effects by neutralizing unbound toxin either circulating in the blood or present in the wound.1,2,4 Antitetanus equine serum is given intravenously over 15-30 minutes at a dose of 25-110 IU/kg for canines.4 Due to the high prevalence of anaphylaxis with intravenous ATS treatment, an initial test dose of 0.1-0.2 ml of ATS is given subcutaneously or intradermally 30 minutes prior to treatment. If a wheal develops at the site of injection, the patient should be medicated with a prophylactic dose of antihistamines and corticosteroids prior to further treatment.3 Only a single dose of ATS is required since therapeutic blood levels are present in canines for 14 days after treatment.2,10 Local intramuscular injection of 1000 units of ATS around and proximal to the wound may be beneficial in neutralizing unbound toxin.2 Unfortunately, once tetanospasmin is bound to the gangliosides of the alpha motor neuron, the reaction is extremely difficult to reverse.1 Furthermore, once the toxin is internalized, it is no longer accessible for neutralization by antitoxin.4 Consequently, the disease continues to progress after administration of ATS. Recovery is slow, progressive, and does not occur until new interneuronal synapses develop to replace those that were inactivated by toxin.2 In order to prevent further production of tetanospasmin, local and parenteral antibiotic therapy is initiated to eradicate the vegetative form of Cl. tetani. Although penicillin is a known antagonist of GABA, penicillin G is the drug of choice for eliminating the vegetative form. Duration of treatment in canines is ten days at a dose of 20,000-100,000 U/kg every 6-12 hours.2 A portion of the dose can be given intramuscularly adjacent to the wound site as form of local treatment.2 Other antibiotics which may be efficacious include tetracycline, clindamycin, erythromycin and metronidazole. Metronidazole has a higher risk for neurotoxicity but may be more effective than penicillin G.2 Metronidazole is the drug of choice for deep-seated and contaminated wounds due to its ability to penetrate necrotic tissues without losing its effectiveness.10 Sedatives are used in order to control the painful tonic muscle spasms and muscular rigidity associated with tetanus. The preferred agents include a combination of phenothiazine, specifically chlorpromazine, and barbiturates.2 Although phenothiazines lower the seizure threshold, tetanus is the one exception to the use of phenothiazines in seizure prone animals due to their efficacy. Phenothiazines are though to work at the level of the brainstem to depress descending excitatory input on the lower motor neurons within the spinal cord and is a potentiator of barbiturate anesthesia.2 Barbiturates depress the motor areas of the brain and abolish spontaneous spinal cord neuronal activity.3 Possible muscle relaxants include derivatives of benzodiazepine, which are GABA agonists and therefore indirectly antagonize the effects of the tetanospasmin, and the central acting muscle relaxant methocarbamol. Once the patient has been initially treated with ATS, antimicrobials and sedatives, the wound, if present, should be debrided, flushed, and cleaned. Hydrogen peroxide is beneficial due to its ability to increase oxygen tension which results in the inhibition of obligate anaerobes.2 If tissue necrosis or abscess is present, surgery may be required in order to decrease the source of toxin production.2 Supportive care is critical in the successful treatment of tetanus. Patients should be placed in a dark, quiet environment and all treatments should be coordinated so that minimal stimulation and handling occurs.2 The patient should be placed on thick, soft bedding and turned regularly to prevent decubital ulcers and hydrostatic pulmonary congestion.3 Force feeding of food may be required due to trismus. If dysphagia is present, an esophagostomy or gastrostomy tube may be required for feeding. Laryngeal spasm may result in respiratory obstruction necessitating a tracheostomy. Urinary catheterization and enemas may be required due to hypertonic urethral and anal sphincters. Hyperthermia due to generalized muscle contraction must be monitored and treated. Prognosis is related to the incubation period, period of onset, severity of clinical signs, and secondary complications.4,7 A short incubation period, short period of onset, and rapid progression of signs results in a poor prognosis.7 Furthermore, the required supportive care is prolonged, extensive and costly. For patients with respiratory compromise, positive-pressure ventilation may be required which is often cost prohibitive for veterinary patients. Due to the cost and intensive patient care required, many owners elect euthanasia. However, if cost is not a factor and intensive supportive care can be provided, a favorable outcome may be achieved. With rapid and appropriate initiation of therapy, most canines have a self-limiting course of disease. Initial improvement may be seen one week after initiation of treatment with gradual recovery in three to four weeks.2

Tucker Gold, a four-month-old intact male Bull Mastiff puppy, presented to the Emergency Service of the Matthew J. Ryan Veterinary Hospital of the University of Pennsylvania on September 2, 2003 with a twenty-four hours history of trismus, risus sardonicus, rigid tail, difficulty standing, trembling and dysphagia. History revealed Tucker to be from a one pet household, an indoor only dog with supervised access outdoors, current on all his vaccinations including rabies, on heartworm preventative, and no history of previous conditions, problems or surgeries were noted. On presentation, Tucker was bright, alert and responsive with normal vital parameters (temperature, respiratory rate, and heart rate). On physical examination bilateral miosis, trismus, risus sardonicus, dorsomedially retracted ears, wrinkles present on the forehead, ptyalism due to dysphagia, muscle tremors, increased muscle tone in all four limbs, and a stiff gait were noted. Oral examination revealed diffuse yellow discoloration and pulp exposure of all deciduous canines. No other wounds or signs of trauma were noted. Complete blood count, chemistry panel, urinalysis and acid-base status were unremarkable. A diagnosis of tetanus was made based on history and clinical signs. Although a long list of differentials could be made for each individual item on the problem list, the combination of clinical signs with which Tucker presented is classic for tetanus, especially the risus sardonicus, trismus, wrinkled forehead and the dorsomedially retracted ears. Treatment was initiated with tetanus antitoxin, penicillin G, intravenous fluids, diazepam, and minimal stimulation in a dim, quiet room with cotton placed in both ears. Within two days of presentation, Tucker’s clinical signs had worsened. Muscle tone in his face and limbs had significantly increased since initial presentation. As a result, he was unable to stand or walk on his own; with assistance, he was able to exhibit a “sawhorse” stance. His muscle tremors increased in severity, resulting in hyperthermia of 107°F. He had a good appetite but had difficulty eating due to trismus and dysphagia. Tucker was moved to the intensive care unit and treated aggressively with sedatives and muscle relaxants, including a constant rate infusion of midazolam and intravenous methocarbamol, phenobarbital, and acepromazine. Treatment with metronidazole was initiated and given concurrently with penicillin G. Nutritional support was provided with total parenteral nutrition. Thoracic radiographs and baseline tracheal wash confirmed the absence of pneumonia. In the absence of any wounds, all four deciduous canines were removed in the event that they represented the route of entry and persistent infection by Cl. tetani. Histopathology of the teeth and the surrounding tissue revealed organisms morphologically consistent with Cl. tetani. However, anaerobic culture of the teeth and surrounding tissue failed to grow the organism. Due to the difficulty in culturing Cl. tetani, a negative result does not rule out infection. During Tucker’s first week of hospitalization, his generalized tetanus continued to progress. He remained in lateral recumbency and opisthotonus was occasionally observed. During this time, Tucker developed pneumonia and suffered from an episode of acute upper airway obstruction due to excessive mucous production. He became cyanotic, bradycardic, his arterial blood gas values deteriorated to a PaCO2 of 60 mmHg and PaO2 of 57 mmHg, and ventricular premature complexes were observed on electrocardiogram. He was placed on positive-pressure ventilation for 36 hours, after which time he was able to breathe on his own and maintain blood gas values within normal limits. Tracheal wash revealed the presence of severe suppurative inflammation with bacterial infection and Pseudomonas aeruginosa and Escherichia coli were identified on culture. A neutrophilic (32 thou/μl) leukocytosis (39 thou/μl) with no bands was present but resolved over the next few days. Treatment with Timentin (ticarcillin and clavulanate) was initiated with complete resolution of clinical and radiographic signs over the following week. Despite progression to generalized tetanus and complications due to pneumonia and acute upper airway obstruction resulting in the use of mechanical ventilation, Tucker improved with medical treatment and intensive nursing care. Two weeks after presentation, the severity of Tucker’s clinical signs began to decrease and he continued to improve steadily. His improvement was facilitated by the use of an orthopedic sling, which allowed him to partially bear weight and move his limbs with assistance. After twenty-four days of hospitalization, Tucker was able to eat, drink, and ambulate on his own, and was therefore discharged to the care of his owners with instructions for moderate exercise. All sedatives, muscle relaxants, and antibiotics were discontinued prior to discharge. On recheck examination two weeks later, Tucker was doing extremely well with almost complete resolution of clinical signs.

Due to the low concentration of tetanospasmin necessary to induce clinical signs, neither exposure to tetanus nor infection and recovery from tetanus leads to the development of immunity.2 In susceptible species, such as humans and equines, antibody formation is stimulated by vaccination with tetanus toxoid, derived from inactivation of tetanospasmin with formaldehyde, to prevent tetanus and to prophylactically boost the immune response in situations of possible exposure.2,6 However, active immunoprophylaxis is not recommended for canines due to their natural resistance. For canines, proper wound management involving thorough debridement, flushing and cleansing, and rational antibiotic therapy should minimize the occurrence of tetanus.2, 4

1. The Genus Clostridium. In: Gillespie, JH, Timoney JF, Scott FW, et al, eds. Hagen and Bruner’s Infectious Diseases of Domestic Animals. 8th Ed. Ithaca, NY: Comstock Publishing Associates, 1988;214-218.

2. Greene CE. Tetanus. In: Greene CE, ed. Infectious Diseases of the Dog and Cat. 2nd ed. Philadelphia: WB Saunders Co, 1998;267-273.

3. Merrett DJ. Canine tetanus. Veterinary Annual 1993;33:209-219.

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