IN ANIMALS continued
and swallowed and develop as egg-producing adults in the gut. Therefore, clinical disease caused by T. canis infestation typically affects young dogs less than one year of age. Patent egg-shedding infestations in older dogs are uncommon, due to a degree of acquired immunity. PREVALENCE AND RISK FACTORS • Companion animal roundworms are distributed worldwide. The prevalence of T. canis in Australia has been reported as 1.2% in domestic pet dogs and 29.4% in Aboriginal community and wild dogs. 4,5 The prevalence of T. cati in domestic cats in Australia has been reported as 3.2%. 5 CLINICAL DISEASE • Heavily infested puppies, and to a lesser extent kittens, can have a classic ‘pot-bellied’ appearance, with clinical signs including ill thrift, abdominal discomfort, anorexia, diarrhoea and vomiting. Young animals may have significant worm burdens due to their limited resilience to infestation, leading to biliary obstruction, intussusception and/or intestinal obstruction. • Heavy infestations in neonatal pups may result in pneumonia and acute death.
• Female roundworms are highly fecund, laying up to 200,000 eggs per day. 6 The eggs are environmentally resistant and can survive a range of temperatures. 7 • The prepatent period of T. canis varies depending on how the larvae are acquired. For transplacental or lactogenic infections, adults develop to patency within three or four weeks respectively, compared to approximately five weeks after ingestion of embryonated eggs from the environment. 8 For T. cati the prepatent period varies between approximately five to eight weeks regardless of route of transmission. 3,9 This is the primary reason kittens are less susceptible to clinical effects of T. cati infection than pups are to T. canis .
DIAGNOSIS • Faecal tests for specific parasite antigens combined with centrifugal faecal flotation has been shown
to assist in the diagnosis of infestation. In standard faecal flotations, detection of thick shelled pitted eggs enables identification to the genus level. The absence of eggs in samples does not rule out infestation.
TRANSMISSION
• Human infection occurs through accidental ingestion of eggs from contaminated water, food or soil or via consumption of undercooked viscera, snails and meat sources containing infective larvae. 10 • Infective, sticky-coated eggs from the environment may also contaminate the fur of animals and pose a direct source of infection to humans in close physical contact. 11 • Toxocara eggs are highly resistant to chemical disinfectants and can survive for years in the environment. Eggs possess a sticky outer coating making their removal from surfaces difficult.
IN HUMANS
PREVALENCE AND RISK FACTORS • A meta-analysis of published data on the seroprevalence of toxocariasis worldwide estimated that 7.0% of Australians are seropositive for Toxocara antibodies, indicating current or prior infection. 12 • The primary risks for Toxocara infection in humans is puppy ownership, pica behaviours and low socioeconomic status given the major source of infection is via the ingestion of embryonated eggs from the environment. Young children, pet owners and individuals in regular contact with companion animals are also at increased risk of exposure.
• Zoonotic roundworms cannot complete their life cycle in humans, however developing larvae can migrate through the body and cause disease. CLINICAL DISEASE • Most people infected with Toxocara have asymptomatic infections, however a number of clinical syndromes are recognised, associated with the host’s immune response to the migrating larvae and the larval burden. • The clinical syndromes of toxocariasis in humans include visceral larva migrans (VLM), ocular larva migrans (OLM),
CONTENTS
85 Companion Animal Zoonoses Guidelines
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