Pulmonary Histopathology in Cats and Dogs with Fatal Tick Paralysis.

The objective of this study was to evaluate critically the nature and prevalence of histological pulmonary lesions in dogs and cats that had died or were euthanized because of tick paralysis. A retrospective and prospective case study of 11 cats and 23 dogs was carried out. Retrospective cases were gathered from the Veterinary Laboratory Services database at The University of Queensland (UQ). Prospective cases were provided by Veterinary Specialist Services and UQ VETs Small Animal Hospital. Lung and other tissue samples were collected for histopathological analysis. All tick intoxicated animals demonstrated evidence of pulmonary parenchymal changes: alveolar oedema, interstitial and alveolar congestion and alveolar fibrin exudation. Eleven of 23 (48%) dogs exhibited mild to severe bronchopneumonia. A lower rate (18%) of bronchopneumonia was found in cats, with one case of aspiration pneumonia. A novel pulmonary histological grading scheme was developed to evaluate the correlation between clinical presentation and histopathological changes. Novel extrapulmonary lesions in cats included hepatic necrosis and acute renal tubular necrosis attributed to hypoxia. We concluded that both dogs and cats with high clinical grade tick paralysis are extremely likely to have pulmonary pathology. High-protein oedema and fibrin exudation are predicted to be present in most cases of canine and feline tick paralysis.

Pathology of Fatal Australian Black Snake (Pseudechis sp) Envenomation in Two Adult Dogs.

Black snakes (Pseudechis spp) are a genus of venomous Australian elapid snakes that can cause major clinical envenomation in companion animals, which may be fatal, even with appropriate antivenom treatment. Despite its clinical significance, there is little published information on the pathology of black snake envenomation. We report the gross and microscopic lesions associated with black snake envenomation in two dogs, one with a definitive immunological species identification of red-bellied black snake (RBBS; Pseudechis porphyriacus), the other with a black snake immunotype on a venom detection kit. Both dogs were located in a geographical area where the RBBS is found. The prominent gross findings in both cases included icterus, localized facial oedema in the region of the presumed bite wound, pigmenturia and multicavitary serosanguineous effusions. Histopathology of the confirmed RBBS case revealed acute renal tubular necrosis with haemosiderosis, marked splenic haemosiderosis and centrilobular to midzonal hepatocellular necrosis with severe cholestasis. Defining the spectrum of lesions of elapid snake envenomation improves understanding of the pathogenesis, which may lead to improved patient outcomes and post-mortem diagnosis.

Delayed antivenom for life-threatening tiger snake bite: Lessons learnt.

An adolescent victim of an urban snakebite developed respiratory failure, rhabdomyolysis and consumption procoagulopathy but recovered with two vials of tiger snake antivenom administered after a delay of 48 hours. The clinical significance of a post-bite collapse was not initially appreciated. Tiger snake (Notechis spp.) venom antigen was measurable in blood before antivenom but not after whereas antivenom was measurable in blood for nine ensuing days. This case adds to growing evidence that further pharmacokinetic research of venom-antivenom interaction is required to establish the correct dose and timing of tiger snake antivenom. Antivenom therapy, even when delayed, facilitates recovery from snake envenomation.

Coagulation factor activity patterns of venom-induced consumption coagulopathy in naturally occurring tiger snake (Notechis scutatus) envenomed dogs treated with antivenom.

BACKGROUND: Venom-induced consumption coagulopathy (VICC) from tiger snake (Notechis scutatus) envenomation results in a dose-dependent coagulopathy that is detectable on coagulometry. However, individual coagulation factor activities in dogs with tiger snake envenomation have not been determined. This study aimed to characterise VICC and the time course of recovery in tiger snake envenomed dogs and to investigate an association between tiger snake venom (TSV) concentrations and factor activity. METHODS: This was a prospective, observational, cohort study. The study cohort was 11 dogs of any age, breed, sex, body weight >10 kg, confirmed serum TSV on ELISA and treated with antivenom. Blood was collected at enrolment before antivenom administration, then at 3, 12 and 24 h after antivenom administration. Tiger snake venom concentrations were detected with a sandwich ELISA. Fibrinogen was measured using a modified Clauss method, and coagulation factors (F) II, V, VII, VIII and X were measured with factor-deficient human plasma using a modified prothrombin (PT) and activated partial thromboplastin (aPTT) method. Linear mixed models, with multiple imputations of censored observations, were used to determine the effect of time and TSV concentration on the coagulation times and factor activity. This cohort was compared to 20 healthy controls. RESULTS: At enrolment, there were severe deficiencies in fibrinogen, FV and FVIII, with predicted recovery by 10.86, 11.75 and 13.14 h after antivenom, respectively. There were modest deficiencies in FX and FII, with predicted recovery by 20.57 and 32.49 h after antivenom, respectively. No changes were detected in FVII. Prothrombin time and aPTT were markedly prolonged with predicted recovery of aPTT by 12.58 h. Higher serum TSV concentrations were associated with greater deficiencies in FII, FV and FVIII, and greater prolongations in coagulation times. The median (range) serum TSV concentration was 57 (6-2295) ng/mL. CONCLUSIONS: In tiger snake envenomed dogs, we detected a profound, TSV-concentration-related consumption of select coagulation factors, that rapidly recovered toward normal. These findings allowed further insight into tiger snake VICC in dogs.

Review article: Let us talk about snakebite management: A discussion on many levels.

We want to discuss antivenom use in snakebite clinical practice guidelines. Coronial reviews in Victoria of two cases of snakebite envenomation, one described in detail below, prompted us to submit this paper for a wider audience and debate. Venom and antivenom levels were measured in the case detailed below, but not in the other. The coroner received conflicting and varied advice from experts regarding the dose of antivenom. The Victorian Department of Health and Human Services and the Australasian College for Emergency Medicine were instructed to review snakebite management guidelines, particularly with respect to antivenom dosage. The discussion that took place among medical experts led to considerable media attention. We discuss the potential fallout when there is no consensus among medical experts.

Severe acute pulmonary haemorrhage and haemoptysis in ten dogs following eastern brown snake (Pseudonaja textilis) envenomation: Clinical signs, treatment and outcomes.

This report describes a series of ten cases of fulminant pulmonary haemorrhage in dogs following envenomation by the eastern brown snake (Pseudonaja textilis) in south eastern Queensland, Australia. All cases were presented for veterinary treatment during 2011-2018 at a specialist veterinary emergency centre. Each case received prompt antivenom treatment and supportive care. Pulmonary haemorrhage was diagnosed based on clinical examination; overt haemoptysis; thoracic radiographic demonstration of a diffuse alveolar pattern; and, the presence of venom induced consumptive coagulopathy. The median elapsed time from hospital admission to onset of haemoptysis was 2 h (range 0-18 h). In 80% (8/10) of cases endotracheal intubation was required, whilst 20% (2/10) were successfully treated with mask oxygen supplementation alone, and 40% (4/10) received mechanical ventilation; but only 25% (1/4) of these survived to hospital discharge. Fresh frozen canine plasma was administered to 70% (7/10) of cases and 43% (3/7) of these survived. Of the total number of cases presented for treatment, 30% (3/10) survived to hospital discharge, 60% (6/10) were euthanised due to poor prognosis and 10% (1/10) died from cardiac arrest. Initial serum brown snake venom antigen levels were retrospectively measured from frozen serum samples by venom specific sandwich ELISA in two dogs at 154 ng/mL (survived) and 3607 ng/mL (euthanised); no free venom was detected post-antivenom. Dogs that survived were discharged from hospital without apparent complications. Pulmonary haemorrhage is an uncommon event following envenomation by P. textilis in dogs and has not been described in similarly envenomed humans. This case series highlights the potential for fulminant and fatal pulmonary haemorrhage in dogs following eastern brown snake envenomation.

Red-bellied black snake (Pseudechis porphyriacus) envenomation in the dog: Diagnosis and treatment of nine cases.

The clinical signs, biochemical changes and serum and urine venom concentrations for a series of nine cases of Red bellied black snake [RBBS] (Pseudechis porphyriacus) envenomation in eight dogs seen in a regional Australian veterinary hospital are described. Although the resulting envenomation syndrome was, in most cases, relatively mild and responded rapidly to intravenous administration of a novel bivalent caprylic acid purified whole IgG equine antivenom for tiger (Notechis scutatus) and brown snake (Pseudonaja textilis), one fatality prior to antivenom treatment was recorded. The latter case occurred within 1 h of envenomation prior to receiving antivenom treatment. Intravascular haemolysis, pigmenturia, bite site swelling, lethargy, and generally mild coagulopathy were present in most cases. Detectable RBBS venom specific components were found in serum, bite site swab or urine using a standard sandwich ELISA approach. Serum levels fell within the range previously reported for human RBBS envenomation cases (6-79 ng/ml) whilst bite site and urine samples varied more markedly (8.2 to >5000 ng/ml and 2.2-1300 ng/ml respectively). No venom was detected from serum after antivenom treatment. The envenomation syndrome in dogs is similar to what is described for humans, with the exception of the presence of potentially severe venom induced consumption coagulopathy in one case (aPTT > 300 s and fibrinogen < 0.43 g/L) and potential for fatal outcomes. This series represents the largest and most detailed examination of RBBS envenomation in animals yet reported. It reinforces the emerging view that the potential severity of this envenomation has been underappreciated by veterinary practitioners and highlights the possibility of severe venom induced consumption coagulopathy in canine cases.

Successful use of camelid (alpaca) antivenom to treat a potentially lethal tiger snake (Notechis scutatus) envenomation in a dog.

This report describes a confirmed clinical case of tiger snake (Notechis scutatus) envenomation in a domestic dog that was successfully treated with a novel polyvalent camelid (alpaca; Llama pacos) antivenom. Samples collected from the dog were assayed for tiger snake venom (TSV) using a highly sensitive and specific ELISA. The TSV concentration in serum and urine at initial presentation was 365 ng/mL and 11,640 ng/mL respectively. At the time of initial presentation whole blood collected from the dog did not clot and the Prothrombin Time was abnormally increased (>300 s). Serum was also visibly hemolysed. The dog was administered antihistamine, dexamethasone and 4000 Units (sufficient to neutralise 40 mg of TSV) of a novel polyvalent alpaca antivenom diluted in 0.9% NaCl. At 4 h post-antivenom treatment the dog's clinical condition had improved markedly with serum TSV concentrations below the limit of detection (<0.015 ng/mL), consistent with complete binding of venom antigens by the alpaca antivenom. Coagulation parameters had begun to improve by 4 h and had fully normalised by 16 h post-antivenom. Venom concentrations in both serum and urine remained undetectable at 16 h post-antivenom. The dog made a complete recovery, without complications, suggesting that the alpaca-based antivenom is both clinically safe and effective.

Fatal presumed tiger snake (Notechis scutatus) envenomation in a cat with measurement of venom and antivenom concentration.

A fatal outcome of a presumed tiger snake (Notechis scutatus) envenomation in a cat is described. Detectable venom components and antivenom concentrations in serum from clotted and centrifuged whole blood and urine were measured using a sensitive and specific ELISA. The cat presented in a paralysed state with a markedly elevated serum CK but with normal clotting times. The cat was treated with intravenous fluids and received two vials of equine whole IgG bivalent (tiger and brown snake) antivenom. Despite treatment the cat's condition did not improve and it died 36 h post-presentation. Serum concentration of detectable tiger snake venom components at initial presentation was 311 ng/mL and urine 832 ng/mL, this declined to non-detectable levels in serum 15-min after intravenous antivenom. Urine concentration of detectable tiger snake venom components declined to 22 ng/mL at post-mortem. Measurement of equine anti-tiger snake venom specific antibody demonstrated a concentration of 7.2 Units/mL in serum at post-mortem which had declined from an initial high of 13 Units/mL at 15-min post-antivenom. The ELISA data demonstrated the complete clearance of detectable venom components from serum with no recurrence in the post-mortem samples. Antivenom concentrations in serum at initial presentation were at least 100-fold higher than theoretically required to neutralise the circulating concentrations of venom. Despite the fatal outcome in this case it was concluded that this was unlikely that is was due to insufficient antivenom.