Roundworms (Ascariasis) in Dogs - Veterinary Consult PDF

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roundworms veterinary_medicine animal_health parasitology

Summary

This document provides a veterinary consultation on roundworms (ascariasis) in dogs. It discusses the basics of the condition, including causes, diagnosis, and treatment options. The document also covers prevention methods and potential complications.

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1212 Blackwell’s Five-Minute Veterinary Consult Roundworms (Ascariasis) weakness, lethargy, pallor, enteritis) or dogs. Selamectin 6 mg/kg, topically, once...

1212 Blackwell’s Five-Minute Veterinary Consult Roundworms (Ascariasis) weakness, lethargy, pallor, enteritis) or dogs. Selamectin 6 mg/kg, topically, once Strongyloides (diarrhea); coccidiosis, giardiasis; (T. cati, cats): dogs, extra-label. examine feces for eggs or larvae. CONTRAINDICATIONS/POSSIBLE BASICS Physaloptera. INTERACTIONS OVERVIEW CBC/BIOCHEMISTRY/URINALYSIS N/A Ascariasis caused by Toxocara canis (dogs), Usually normal. T. cati (cats), and Toxascaris leonina (dogs, cats); Baylisascaris (raccoons) can infect dogs OTHER LABORATORY TESTS and causes neural larval migrans in people. N/A Transplacental transmission of T. canis IMAGING ­ FOLLOW-UP larvae from bitch to pups causes prenatal N/A PATIENT MONITORING infection; transmammary transmission of Repeat post-treatment fecal exams on DIAGNOSTIC PROCEDURES larvae occurs with both Toxocara spp.; no puppies/kittens and/or repeat anthelmintic Fecal flotation to detect eggs: ◦ Toxocara transplacental or transmammary transmission treatment every 2–3 weeks until old enough eggs spherical pitted outer shell membrane, with Toxascaris. In first month of life, single dark cell filling interior, 80–85 μm for monthly anthelmintic product. infected neonatal pups may develop (T. canis), ~75 μm (T. cati). ◦ Baylisascaris PREVENTION/AVOIDANCE abdominal pain and rapidly deteriorate before eggs similar to T. canis eggs but smaller Minimize environmental contamination, Toxocara eggs appear in feces. Older pups (~76 × 60 μm), more finely pitted shell. treat infected dogs/cats with anthelmintic, and kittens can acquire by ingesting eggs ◦ Toxascaris eggs ovoid, smooth exterior shell dispose of feces promptly. Prevent dogs/cats spread by dams with postgestational membrane, 1–2 cells with light-colored from hunting or ingesting transport hosts. infection; dams can be infected by ingesting cytoplasm; cells do not fill interior of egg; Extra-label treatment of dam with adulticide/ immature worm stages in pups’ feces or 80 × 70 μm in diameter. Necropsy of larvicide anthelmintic to remove intestinal vomitus or by predation on vertebrate siblings—identify ascarids by size, appearance. stages and decrease vertical transmission. transport hosts. Adult ascarids occur in Fecal ELISA—commercial test detects lumen of small intestine; larval stages of POSSIBLE COMPLICATIONS antigen produced by adult and immature Toxocara spp. may migrate in liver and lungs. Transplacental transmission of large numbers roundworms of both sexes; can detect If numerous, ascarids (up to 10–12 cm of larvae can result in fetal death or birth of prepatent infection. long) can distend intestine and cause colic, weak, nonviable offspring. R interference with gut motility, inability to utilize food, intestinal rupture. EXPECTED COURSE AND PROGNOSIS Prognosis good after anthelmintic treatment; SIGNALMENT guarded with severe prenatal T. canis infection. Dog and cat. Important in puppies/kittens ­ TREATMENT Generally outpatient. Acute severe cases due to in utero/transmammary transmission. treated as inpatients; provide parenteral fluids. SIGNS Alert client to possibility of sudden death or Abdominal distension; often with palpable chronic debilitation. Treat dam with ­ MISCELLANEOUS intestinal distension. Colic. Weakness, loss adulticide/larvicide anthelmintic to remove of condition, cachexia; poor nursing or AGE-RELATED FACTORS intestinal stages and limit transmission to appetite; scant feces. Coughing due to larval Greater concern in neonates. subsequent litters. lung migration. Entire litter may be affected. ZOONOTIC POTENTIAL CAUSES & RISK FACTORS Visceral larva migrans, ocular larva migrans, Dormant Toxocara larvae in dam’s tissues is neural larva migrans, chronic abdominal or infection reservoir for puppies during cutaneous problems may follow ingestion of ­ MEDICATIONS infective Toxocara spp. or Baylisascaris eggs by gestation; queen becomes infected during late pregnancy or lactation and transfers to kittens DRUG(S) OF CHOICE humans; advise clients to practice good via transmammary route. Access to infected Adulticide/Larvicide Anthelmintics hygiene after handling feces. Most likely transport hosts. Concurrent enteric Fenbendazole 50 mg/kg PO q24h for cause of neural larva migrans is Baylisascaris; infections. Toxocara larvae undergo extensive 3 days. Milbemycin oxime 0.5 mg/kg virtually all raccoons become infected with migration and can cause granulomatous (dogs) or 2 mg/kg (cats) PO q30 days. Baylisascaris and therefore extreme caution inflammation (visceral larva migrans). Visceral Moxidectin (dogs) 2.5 mg/kg, topically, should be exercised with clients having larva migrans caused by ascarids is cause of q30 days. Moxidectin (in combination raccoons as “pets.” human morbidity. Somatically arrested with imidacloprid) 10 mg/kg, topically, q30 INTERNET RESOURCES larvae in small vertebrates are source of days. Emodepside 3 mg/kg, or praziquantel http://www.capcvet.org http://www.cdc.gov infection for dogs/cats that hunt. 12 mg/kg, topically once for cats ≥8 weeks ­Suggested Reading old; repeat in 30 days if cat is reinfected. Bowman DD. Georgis’ Parasitology for Adulticide Anthelmintics Veterinarians, 9th ed. St. Louis, MO: Pyrantel pamoate 5 mg/kg PO (dogs) or Saunders, 2009, pp. 197–198, 201–208. ­ DIAGNOSIS 10–20 mg/kg PO (cats, extra-label). Authors Matt Brewer and Jeba R.J. Jesudoss Pyrantel/praziquantel, label dose for cats. Chelladurai DIFFERENTIAL DIAGNOSIS Febantel/praziquantel/pyrantel, label dose Consulting Editor Amie Koenig Transmammary perinatal infection of neonates with hookworms (anemia, melena, for dogs. Ivermectin/pyrantel, label dose for Canine and Feline, Seventh Edition 1213 Sago Palm Toxicosis CBC/BIOCHEMISTRY/URINALYSIS sago palm toxicosis available. Can be given Anemia. Elevated serum liver enzymes for supportive therapy. N-Acetylcysteine— (alanine transaminase, aspartate transaminase, antioxidant; no data on efficacy in sago palm ­ BASICS alkaline phosphatase, bilirubin). toxicosis available. A glutathione precursor OVERVIEW Hypoalbuminemia. Hypoglycemia. that can be included in the treatment regimen Cycad palms, also called sago palms, belong Glucosuria, hemoglobinuria, myoglobinuria, for acute fulminant hepatic failure at 140 mg/ in the family Cycadaceae. Native to tropical bilirubinuria, proteinuria, and increased urine kg IV load, followed by 70 mg/kg IV q6h for and subtropical regions but have become specific gravity. 7 treatments. popular ornamental plants in the United OTHER LABORATORY TESTS CONTRAINDICATIONS/POSSIBLE States. Cycas revoluta, Cycas circinalis, and Ammonia tolerance test—hyperammonemia. INTERACTIONS Zamia floridana are the most common species. Prolonged prothrombin time/partial N/A Contain the toxins cycasin, betamethylamino-l- thromboplastin time. alanine, and an unidentified high-molecular- weight compound. Toxins present in all parts IMAGING of the plant; highest concentrations in seeds. N/A Cycasin is metabolized by the intestinal flora DIAGNOSTIC PROCEDURES ­ FOLLOW-UP to the active hepatotoxic, carcinogenic, History of cycad palm ingestion and presence PATIENT MONITORING mutagenic, teratogenic, and neurotoxic of appropriate clinical signs. Identification of Liver enzymes/function. Coagulation status. compound methylazoxymethanol (MAM). plant in ingesta or feces. Biopsy and histo­ Cycad toxicosis has been documented in pathology of liver—hepatic necrosis. PREVENTION/AVOIDANCE several animal species (dogs and ruminants) Necropsy—hepatic centrilobular necrosis. Deny access to sago palms. and humans. In dogs, gastrointestinal (GI) POSSIBLE COMPLICATIONS PATHOLOGIC FINDINGS disturbances and hepatic damage predominate; Hepatic encephalopathy. Disseminated Detection of cycad palm material in GI nervous system involvement is less common. intravascular coagulation. Renal failure. tract and/or in feces. Gross detection of SIGNALMENT liver enlargement. Histologic detection of EXPECTED COURSE AND PROGNOSIS Dogs—no breed, sex, or age predilection. centrilobular and midzonal coagulative Dogs develop vomiting within minutes, Cats—no cases reported. hepatocellular necrosis. followed by further GI upset. Changes in SIGNS clinical laboratory values occur after 24–48 GI disturbances such as vomiting, diarrhea, hours. Nadir serum albumin levels and and abdominal pain. Signs associated with nadir platelet counts are important prognostic S hepatic damage (ecchymoses, petechiae, ­ TREATMENT indicators. Liver failure within a few days. hemorrhage, edema, etc.). Gait Prognosis is poor to guarded. No antidote available. GI decontamination abnormalities; paresis/paralysis; tremors. with activated charcoal can be attempted but Depression, coma, and death. efficacy is unknown. Supportive care CAUSES & RISK FACTORS including close monitoring and, depending on Access to and ingestion of cycad palm. the severity of clinical signs, IV fluids, correction ­ MISCELLANEOUS of electrolyte imbalances and hypoglycemia, vitamin K1, and plasma transfusions. ABBREVIATIONS GI = gastrointestinal. MAM = methylazoxymethanol. ­ DIAGNOSIS INTERNET RESOURCES DIFFERENTIAL DIAGNOSIS http://www.petpoisonhelpline.com/poison/ ­ MEDICATIONS sago-palm/ http://www.aspca.org/pet-care/ Other Causes of Acute GI Upset DRUG(S) OF CHOICE animal-poison-control/toxic-and-non-toxic- Infectious. Metabolic. Toxic. Dietary. Activated charcoal—multi-dose activated plants/fern-palm Other Causes of Acute Liver Failure charcoal at 1–4 g/kg PO q4–6h for 2–3 days Microcystins (hepatotoxic blue-green algal ­Suggested Reading post ingestion. Mix activated charcoal in water Albretsen JC, Khan SA, Richardson JA. toxins)—access to water with algal bloom, at 1 g/5−10 mL of water. IV fluids— Cycad palm toxicosis in dogs: 60 cases algal material on legs or in stomach contents, maintain hydration, induce diuresis, correct (1987–1997). J Am Vet Med Assoc 1998, detection of microcystins in stomach contents. hypoglycemia. Dextrose—50% dextrose 213(1):99–101. Amanitin—access to mushrooms (Amanita, 1 mL/kg IV slow bolus (1–3 minutes). Clarke C, Burney D. Cycad palm toxicosis in Galerina, and Lepiota spp.), GI signs between Vitamin K1—0.5–1.5 mg/kg SC or IM 14 dogs from Texas. J Am Anim Hosp 6 and 24 hours after ingestion. Cocklebur q12h; 1 mg/kg PO q24h. Blood products— Assoc 2017, 53:159–166. (Xanthium spp.)—access to cocklebur (only dependent on hemostatic test results. Ferguson D, Crowe M, McLaughlin L, et al. seeds and two-leaf cotyledon stage are toxic). ALTERNATIVE DRUG(S) Survival and prognostic indicators for cycad Aflatoxins—access to moldy food. S-Adenosylmethionine—antioxidant and intoxication in dogs. J Vet Intern Med Acetaminophen overdose. Xylitol—access hepatoprotectant; no data on efficacy in sago 2011, 25(4):831–837. to xylitol-containing products (sugar-free palm toxicosis available. Dose 20 mg/kg PO Authors Adrienne C. Bautista and Birgit gum, chewable vitamins, baked goods); initial q24h. Ascorbic acid and cimetidine— Puschner hypoglycemia. Severe acute pancreatitis. hepatocyte protectors; no data on efficacy in Consulting Editor Lynn R. Hovda

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