This might sound silly but can dogs get worms from eating the soil? Aspen was eating some around the orange tree yesterday and the day before.
How do you know if they have had them or not? Not every case shows symptoms of carrying worms. BUT they can still carry them and infect others (dogs and humans). A fecal test must be preformed to conclude whether a dog is infected or not. I do NOT think its wise to assume that a dog is not infected or not.My dogs appear to be eating dirt from time to time. I don't know if they are eating worms, bugs or just dirt. They have never had worms. I wouldn't worry about it.
How do you know its not a big deal? Do you know what these worms do to your dog?Even if they do get worms, its not a big deal.
http://en.wikipedia.org/wiki/Hookworm#PathologyHookworm infection is generally considered to be asymptomatic, but as Norman Stoll described in 1962, hookworm is an extremely dangerous infection because its damage is “silent and insidious.” There are general symptoms that an individual may experience soon after infection. Ground-itch, which is an allergic reaction at the site of parasitic penetration and entry, is common in patients infected with N. americanus. Additionally, cough and pneumonitis may result as the larvae begin to break into the alveoli and travel up the trachea. Then once the larvae reach the small intestine of the host and begin to mature, the infected individual will suffer from diarrhea and other gastrointestinal discomfort. However, the “silent and insidious” symptoms referred to by Stoll are related to chronic, heavy-intensity hookworm infections. Major morbidity associated with hookworm is caused by intestinal blood loss, iron deficiency anemia, and protein malnutrition. They result mainly from adult hookworms in the small intestine ingesting blood, rupturing erythrocytes, and degrading hemoglobin in the host. This long-term blood loss can manifest itself physically through facial and peripheral edema; eosinophilia and pica caused by iron deficiency anemia are also experienced by some hookworm-infected patients. Recently, more attention has been given to other important outcomes of hookworm infection that play a large role in public health. It is now widely accepted that children who suffer from chronic hookworm infection can suffer from growth retardation as well as intellectual and cognitive impairments. Additionally, recent research has focused on the potential of adverse maternal-fetal outcomes when the mother is infected with hookworm during pregnancy.
The disease was linked to nematode worms (Ankylostoma duodenalis) from one-third to half an inch long in the intestine chiefly through the labours of Theodor Bilharz and Griesinger in Egypt (1854).
The symptoms can be linked to inflammation in the gut stimulated by feeding hookworms, such as nausea, abdominal pain and intermittent diarrhea, and to progressive anemia in prolonged disease: capricious appetite, pica (or dirt-eating), obstinate constipation followed by diarrhea, palpitations, thready pulse, coldness of the skin, pallor of the mucous membranes, fatigue and weakness, shortness of breath and in cases running a fatal course, dysentery, hemorrhages and edema.
Blood tests in early infection often show a rise in numbers of eosinophils, a type of white blood cell that is preferentially stimulated by worm infections in tissues (large numbers of eosinophils are also present in the local inflammatory response). Falling blood hemoglobin levels will be seen in cases of prolonged infection with anemia.
In contrast to most intestinal helminthiases, where the heaviest parasitic loads tend to occur in children, hookworm prevalence and intensity can be higher among adult males. The explanation for this is that hookworm infection tends to be occupational, so that plantation workers, coalminers and other groups maintain a high prevalence of infection among themselves by contaminating their work environment. However, in most endemic areas, adult women are the most severely affected by anemia, mainly because they have much higher physiological needs for iron (menstruation, repeated pregnancy), but also because customarily they have access to much poorer food than the men.
An interesting consequence of this in the case of Ancylostoma duodenale infection is translactational transmission of infection: the skin-invasive larvae of this species do not all immediately pass through the lungs and on into the gut, but spread around the body via the circulation, to become dormant inside muscle fibers. In a pregnant woman, after childbirth some or all of these larvae are stimulated to re-enter the circulation (presumably by sudden hormonal changes), then to pass into the mammary glands, so that the newborn baby can receive a large dose of infective larvae through its mother's milk. This accounts for otherwise inexplicable cases of very heavy, even fatal, hookworm infections in children a month or so of age, in places such as China, India and northern Australia. (An identical phenomenon is much more commonly seen with Ancylostoma caninum infections in dogs, where the newborn pups can even die of hemorrhaging from their intestines caused by massive numbers of feeding hookworms. This also reflects the close evolutionary link between the human and canine parasites, which probably have a common ancestor dating back to when humans and dogs first started living closely together
Dogs are able to get worms from eating the soil. Hookworm and roundworm and whipworm (type of roundworm) eggs are able to survive in the soil and infect dogs who ingest them, as well as people.There are four modes of infection associated with this species. The basic form is typical to all ascaroides, the egg containing the L2(the second larval developmental stage), being infective, at optimal temperature and humidity, four weeks after secreted in the faeces to the environment. After ingestion, and hatching in the small intestine, the L2 travel through the portal blood stream into the liver and lungs. Such migratory route is known as entero-hepatic-pulmonar larval migration. The second molt takes place in the lungs, the now L3 returns via the trachea and into the intestines where the final two molts take place. This form of infection occurs regularly only in dogs of up to three months of age. In older dogs, this type of migration occurs less frequently and at six months it is almost ceased. Instead, the L2 travel to a wide range of organs including the liver, lungs, brain, heart and skeletal muscles, as well as to the walls of the gastrointestinal tract. In pregnant bitch,parental infection occurs when larvae becoming mobilized at approximately, three week prior to parturition, and migrate to the lungs of the foetus where they molt into L3 just prior to birth. In the newborn pup the cycle is completed when the larva migrates through the trachea and into the intestinal lumen, where the final molts take place. Once infected, a bitch will usually harbor sufficient larvae to subsequently infect all of her litters, even if she never again encounters an infection. A certin amount of the bitch's dormant larvae penetrate into the intestinal lumen, where molting into adulthood take, yet again, place, thus leading to a new release of eggs containing L1 larvae. The suckling pup may be infected by the presence of L3 in the milk during the first three weeks of lactation. There is no migration in the pup via this route. L2 may also be ingested by a variety of animals where it stays in a dormant stage inside the animals tissue until the intermediate host has been eaten by a dog, when subsequent development is confined to the gastrointestinal tract.
http://en.wikipedia.org/wiki/Trichuris_vulpis#Pathology.2FSymptomsBecause the eggs of T. vulpis eggs are very resistant from desiccation, they can live in soil for up to seven years . Once ingested by the canine, the eggs hatch and the resulted larvae live in the small intestine. At this point, though infected, the canine is still asymptomatic. When adult form, T. vulpis live primarily in the cecum with its anterior end attached to the superficial mucosa and its posterior end extended to the cecal lumen where it consumes the canine’s blood, tissue fluid, and mucosal epithelium. Severe infections include symptoms such as bloody diarrhea, weight loss, dehydration, and anemia, and in extreme cases, death.
I don't worry about it. You sound like you work for a vet. :biggrin:I do NOT think its wise to assume that a dog is not infected or not.
I've owned dogs for a zillion years. One of them had worms one time. Don't remember which kind. One trip to the vet and they were gone. You sound like you work for a vet. :biggrin:How do you know its not a big deal? Do you know what these worms do to your dog?
See the part about the zillion years.Dogs are able to get worms from eating the soil. Hookworm and roundworm and whipworm (type of roundworm) eggs are able to survive in the soil and infect dogs who ingest them, as well as people.
My "kid" is old enough to be your father. :biggrin:I *highly* recommend getting your dog tested once annually or biannually to make sure they don't have these worms because the transmission to humans can happen, and is fairly regular in the warmer, southern parts of the US. In most cases dogs test negative for these guys, but to me its better to make sure...especially if you have kids.
This is the response to this as that I thought you would bring, lame and weak. The number of dogs that you have owned doesn't amount to much in the grand scheme of things in a demographic way, even if your son is "old enough to be my father." You should bring a more valid post to the argument than "None of my dogs have ever had them, so its not a problem."I don't worry about it. You sound like you work for a vet. :biggrin:
I've owned dogs for a zillion years. One of them had worms one time. Don't remember which kind. One trip to the vet and they were gone. You sound like you work for a vet. :biggrin:
See the part about the zillion years.
My "kid" is old enough to be your father. :biggrin: