D) The egg must come into contact with water.
Life cycle of Paragonimiasis
The eggs are excreted unembryonated in the sputum, or alternately they are swallowed and passed with stoolThe number 1. In the external environment, the eggs become embryonatedThe number 2, and miracidia hatch and seek the first intermediate host, a snail, and penetrate its soft tissuesThe number 3. Miracidia go through several developmental stages inside the snailThe number 4: sporocystsThe number 4a, rediaeThe number 4b, with the latter giving rise to many cercariaeThe number 4c, which emerge from the snail. The cercariae invade the second intermediate host, a crustacean such as a crab or crayfish, where they encyst and become metacercariae. This is the infective stage for the mammalian hostThe number 5. Human infection with P. westermani occurs by eating inadequately cooked or pickled crab or crayfish that harbor metacercariae of the parasiteThe number 6. The metacercariae excyst in the duodenumThe number 7, penetrate through the intestinal wall into the peritoneal cavity, then through the abdominal wall and diaphragm into the lungs, where they become encapsulated and develop into adultsThe number 8. (7.5 to 12 mm by 4 to 6 mm). The worms can also reach other organs and tissues, such as the brain and striated muscles, respectively. However, when this takes place completion of the life cycles is not achieved, because the eggs laid cannot exit these sites. Time from infection to oviposition is 65 to 90 days. Infections may persist for 20 years in humans. Animals such as pigs, dogs, and a variety of feline species can also harbor P. westermani.
B) Aquatic, migratory birds.
Cercarial dermatitis is caused by the cercariae of certain species of schistosomes whose normal hosts are birds and mammals other than humans. These cercariae seem to have a chemotrophic reaction to secretions from the skin and are not as host-specific as other types of schistosomes. They attempt to, and, sometimes may actually, enter human skin. The penetration causes a dermatitis which is usually accompanied with intense itching, but the cercariae do not mature into adults in the human body. Cases of cercarial dermatitis can occur in both fresh and brackish water environments. One species of schistosome often implicated in cases of cercarial dermatitis is Austrobilharzia variglandis, whose normal hosts are ducks. The snail, Nassarius obsoletus, is the intermediate host for this species and can be found at marine beaches in temperate climates. Cercarial dermatitis should not be confused with seabather's eruption, which is caused by the larval stage of cnidarians (e.g., jellyfish). The areas of skin affected by seabather's eruption is generally under the garments worn by bathers and swimmers where the organisms are trapped after the person leaves the water. Cercarial dermatitis occurs on the exposed skin outside of close-fitting garments.
Life cycle of Cercarial Dermatitis
Hosts of avian schistosomes can be either year-round resident or migratory birds, including seagulls, shorebirds, ducks, and geese. Adult worms are found in the blood vessels and produce eggs that are passed in the feces The Number 1 On exposure to water, the eggs hatch and liberate a ciliated miracidium that infects a suitable snail (gastropod) intermediate host. The Number 2. The parasite develops in the intermediate host The Number 3 to produce free-swimming cercariae that are released under appropriate conditions and penetrate the skin of the birds and migrate to the blood vessels to complete the cycle The Number 4. Humans are inadvertent and inappropriate hosts; cercariae may penetrate the skin but do not develop further The Number 5. A number of species of trematodes with dermatitis-producing cercariae have been described from both freshwater and saltwater environments, and exposure to either type of cercaria will sensitize persons to both
C) Tapeworm infection.
aka: Dipylidium caninum
Dipylidium caninum (the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.
Life cycle of Dipylidium caninum
Gravid proglottids are passed intact in the feces or emerge from the perianal region of the host The number 1. Subsequently they release typical egg packets The number 2. On rare occasions, proglottids rupture and egg packets are seen in stool samples. Following ingestion of an egg by the intermediate host (larval stages of the dog or cat flea Ctenocephalides spp.), an oncosphere is released into the flea's intestine. The oncosphere penetrates the intestinal wall, invades the insect's hemocoel (body cavity), and develops into a cysticercoid larva The number 3. The larva develops into an adult, and the adult flea harbours the infective cysticercoid The number 4. The vertebrate host becomes infected by ingesting the adult flea containing the cysticercoid The number 5. The dog is the principal definitive host for Dipylidium caninum. Other potential hosts include cats, foxes, and humans (mostly children) The number 6, The number 7. Humans acquire infection by ingesting the cysticercoid contaminated flea. This can be promulgated by close contact between children and their infected pets. In the small intestine of the vertebrate host the cysticercoid develops into the adult tapeworm which reaches maturity about 1 month after infection The number 8. The adult tapeworms (measuring up to 60 cm in length and 3 mm in width) reside in the small intestine of the host, where they each attach by their scolex. They produce proglottids (or segments) which have two genital pores (hence the name "double-pored" tapeworm). The proglottids mature, become gravid, detach from the tapeworm, and migrate to the anus or are passed in the stool The number 1.
B) prevent them from ingesting sheep viscera.
This is also a tapeworm.
Echinococcus granulosus, also called the hydatid worm, hyper tape-worm or dog tapeworm, is a cyclophyllid cestode that parasitizes the small intestine of canids as an adult, but which has important intermediate hosts such as livestock and humans, where it causes cystic echinococcosis, also known as hydatid disease. The adult tapeworm ranges in length from 3 mm to 6 mm and has three proglottids ("segments") when intact—an immature proglottid, mature proglottid and a gravid proglottid. The average number of eggs per gravid proglottid is 823. Like all cyclophyllideans, E. granulosus has four suckers on its scolex ("head"), and E. granulosus also has a rostellum with hooks. Several strains of E. granulosus have been identified, and all but two are noted to be infective in humans
A) Tracheal migration.
Toxocariasis is an infection transmitted from animals to humans (zoonosis) caused by the parasitic roundworms commonly found in the intestine of dogs (Toxocara canis) and cats (T. cati).
Who is at risk for toxocariasis?
Anyone can become infected with Toxocara. Young children and owners of dogs or cats have a higher chance of becoming infected.
Approximately 13.9% of the U.S. population has antibodies to Toxocara. This suggests that tens of millions of Americans may have been exposed to the Toxocara parasite.
How can I get toxocariasis?
Dogs and cats that are infected with Toxocara can shed Toxocara eggs in their feces. You or your children can become infected by accidentally swallowing dirt that has been contaminated with dog or cat feces that contain infectious Toxocara eggs. Although it is rare, people can also become infected from eating undercooked meat containing Toxocara larvae.
What are the clinical manifestations of toxocariasis?
Many people who are infected with Toxocara do not have symptoms and do not ever get sick. Some people may get sick from the infection, and may develop:
Ocular toxocariasis: Ocular toxocariasis occurs when Toxocara larvae migrate to the eye. Symptoms and signs of ocular toxocariasis include vision loss, eye inflammation or damage to the retina. Typically, only one eye is affected.
Visceral toxocariasis: Visceral toxocariasis occurs when Toxocara larvae migrate to various body organs, such as the liver or central nervous system. Symptoms of visceral toxocariasis include fever, fatigue, coughing, wheezing, or abdominal pain.
How serious is infection with Toxocara?
In most cases, Toxocara infections are not serious, and many people, especially adults infected by a small number of larvae (immature worms), may not notice any symptoms. The most severe cases are rare, but are more likely to occur in young children, who often play in dirt, or eat dirt (pica) contaminated by dog or cat feces.
How is toxocariasis spread?
The most common Toxocara parasite of concern to humans is T. canis, which puppies usually contract from the mother before birth or from her milk. The larvae mature rapidly in the puppy's intestine; when the pup is 3 or 4 weeks old, they begin to produce large numbers of eggs that contaminate the environment through the animal's feces. Over a 2 to 4 week time period, infective larvae develop in the eggs. Toxocariasis is not spread by person-to-person contact like a cold or the flu.
B) fecal flotation.
These guidelines address transmission of intestinal ascarids and hookworms from dogs and cats to people and recommend counseling of dog and cat owners and well-timed preventive anthelmintic treatments for pets.
Ascarids and Hookworms
Ascarids (Toxocara spp.) and hookworms (Ancylostoma spp. and Uncinaria stenocephala), the common intestinal roundworms of dogs and cats, can cause larva migrans syndromes in persons who accidentally ingest eggs or larvae or have direct skin contact with hookworm larvae in soil contaminated with the feces of infected animals.
Pups and kittens are often infected by transfer of larvae from their dams in utero (T. canis) or via milk (A. caninum, T. cati, and to a lesser extent, T. canis), (1,2) and the tissue-migrating and early intestinal stages of these worms may cause severe, sometimes life-threatening, disease in the first few weeks of the animal's life. Furthermore, pups and kittens may have patent intestinal infections as early as the first 2 (hookworms) to 3 (ascarids) weeks of life, and may contaminate their environment with huge numbers of infective eggs and larvae.
The prevalence of these infections varies with climatic conditions; however, they are present in all parts of the contiguous United States and must be viewed as a potential public health hazard (3-6).
Zoonotic Transmission and Human Disease
When zoonotic ascarids and hookworms infect humans, the parasites rarely mature in the intestine; rather, the larval worms migrate in the host's tissues (larva migrans). The characteristics of the particular tissues and organs in which the larvae migrate determine the signs and symptoms humans have.
The common ascarid of dogs, T. canis, has long been recognized as a cause of larva migrans syndromes in children. The ascarid of cats, T. cati, can also cause disease in humans, although for reasons partly related to the "toilet behavior" of cats, it does so less frequently than T. canis. When the eggs are accidentally ingested, they hatch, and infective-stage larvae migrate through human liver, lungs, and other organs and tissues where they produce damage and induce allergic responses. Infection may leave children with permanent visual or neurologic damage.
In the United States, the popularity of pets together with high ascarid and hookworm infection rates in dogs and cats, especially pups and kittens, result in widespread contamination of soil with infective-stage larvae. Epidemiologic studies have implicated the presence of dogs, particularly pups, in the household and pica (dirt eating) as the principal risk factors for human toxocaral disease. Children's play habits and attraction to pets put them at high risk for ascarid and hookworm infection.
Hookworms of dogs and cats, A. caninum, A. braziliense, A. tubaeforme, and U. stenocephala, can also infect people when larvae in soil are ingested or directly penetrate the skin on contact (4). Cutaneous larva migrans syndromes, characterized by progressive, intensely pruritic, linear eruptive lesions caused by prolonged migration of the larvae in the skin, are the most common manifestation of zoonotic hookworm infection. A. caninum larvae may penetrate into deeper tissues, however, and induce symptoms of visceral larva migrans or migrate to and partially mature in the intestine, inducing eosinophilic enteritis (7,8).
D) skin penetration.
Many hookworms infecting animals can invade and parasitize humans (A. ceylanicum) or can penetrate the human skin (causing cutaneous larva migrans), but do not develop any further (A. braziliense, A. caninum, Uncinaria stenocephala). Occasionally A. caninum larvae may migrate to the human intestine, causing eosinophilic enteritis. Ancylostoma caninum larvae have also been implicated as a cause of diffuse unilateral subacute neuroretinitis.
CLM life cycle
Cutaneous larval migrans (also known as creeping eruption) is a zoonotic infection with hookworm species that do not use humans as a definitive host, the most common being A. braziliense and A. caninum. The normal definitive hosts for these species are dogs and cats. The cycle in the definitive host is very similar to the cycle for the human species. Eggs are passed in the stool The number 1, and under favorable conditions (moisture, warmth, shade), larvae hatch in 1 to 2 days. The released rhabditiform larvae grow in the feces and/or the soil The number 2, and after 5 to 10 days (and two molts) they become filariform (third-stage) larvae that are infective The number 3. These infective larvae can survive 3 to 4 weeks in favorable environmental conditions. On contact with the animal host The number 4, the larvae penetrate the skin and are carried through the blood vessels to the heart and then to the lungs. They penetrate into the pulmonary alveoli, ascend the bronchial tree to the pharynx, and are swallowed. The larvae reach the small intestine, where they reside and mature into adults. Adult worms live in the lumen of the small intestine, where they attach to the intestinal wall. Some larvae become arrested in the tissues, and serve as source of infection for pups via transmammary (and possibly transplacental) routes The number 5. Humans may also become infected when filariform larvae penetrate the skin The number 6. With most species, the larvae cannot mature further in the human host, and migrate aimlessly within the epidermis, sometimes as much as several centimeters a day. Some larvae may persist in deeper tissue after finishing their skin migration.
C) only the females are parasitic.
Pinworm Infection FAQs
What is a pinworm?
What are the symptoms of a pinworm infection?
Who is at risk for pinworm infection?
How is pinworm infection spread?
Can my family become infected with pinworms from swimming pools?
My little kids like to co-bathe - could this be how they are becoming infected?
Did my pets give me pinworms / can I give pinworms to my pets?
How is pinworm infection diagnosed?
How is pinworm infection treated?
Should family and other close contacts of someone with pinworm also be treated for pinworm?
What should be done if the pinworm infection occurs again?
How can pinworm infection and reinfection be prevented?
What is a pinworm?
A pinworm ("threadworm") is a small, thin, white roundworm (nematode) called Enterobius vermicularis that sometimes lives in the colon and rectum of humans. Pinworms are about the length of a staple. While an infected person sleeps, female pinworms leave the intestine through the anus and deposit their eggs on the surrounding skin.
What are the symptoms of a pinworm infection?
Pinworm infection (called enterobiasis or oxyuriasis) causes itching around the anus which can lead to difficulty sleeping and restlessness. Symptoms are caused by the female pinworm laying her eggs. Symptoms of pinworm infection usually are mild and some infected people have no symptoms.
Who is at risk for pinworm infection?
Pinworm infection occurs worldwide and affects persons of all ages and socioeconomic levels. It is the most common worm infection in the United States. Pinworm infection occurs most commonly among
school-aged and preschool-aged children,
institutionalized persons, and
household members and caretakers of persons with pinworm infection.
Pinworm infection often occurs in more than one person in household and institutional settings. Child care centers often are the site of cases of pinworm infection.
How is pinworm infection spread?
Pinworm infection is spread by the fecal-oral route, that is by the transfer of infective pinworm eggs from the anus to someone's mouth, either directly by hand or indirectly through contaminated clothing, bedding, food, or other articles.
Pinworm eggs become infective within a few hours after being deposited on the skin around the anus and can survive for 2 to 3 weeks on clothing, bedding, or other objects. People become infected, usually unknowingly, by swallowing (ingesting) infective pinworm eggs that are on fingers, under fingernails, or on clothing, bedding, and other contaminated objects and surfaces. Because of their small size, pinworm eggs sometimes can become airborne and ingested while breathing.
Can my family become infected with pinworms from swimming pools?
Pinworm infections are rarely spread through the use of swimming pools. Pinworm infections occur when a person swallows pinworm eggs picked up from contaminated surfaces or fingers. Although chlorine levels found in pools are not high enough to kill pinworm eggs, the presence of a small number of pinworm eggs in thousands of gallons of water (the amount typically found in pools) makes the chance of infection unlikely.
My little kids like to co-bathe - could this be how they are becoming infected?
During this treatment time and two weeks after final treatment, it is a good idea to avoid co-bathing and the reuse or sharing of washcloths. Showering may be preferred to avoid possible contamination of bath water. Careful handling and frequent changing of underclothing, night clothes, towels, and bedding can help reduce infection, reinfection, and environmental contamination with pinworm eggs. These items should be laundered in hot water, especially after each treatment of the infected person and after each usage of washcloths until infection is cleared.
Did my pets give me pinworms / can I give pinworms to my pets?
No. Humans are considered to be the only hosts of E. vermicularis which is also known as the human pinworm.
How is pinworm infection diagnosed?
Itching during the night in a child's perianal area strongly suggests pinworm infection. Diagnosis is made by identifying the worm or its eggs. Worms can sometimes be seen on the skin near the anus or on underclothing, pajamas, or sheets about 2 to 3 hours after falling asleep.
Pinworm eggs can be collected and examined using the "tape test" as soon as the person wakes up. This "test" is done by firmly pressing the adhesive side of clear, transparent cellophane tape to the skin around the anus. The eggs stick to the tape and the tape can be placed on a slide and looked at under a microscope. Because washing/bathing or having a bowel movement can remove eggs from the skin, this test should be done as soon as the person wakes up in the morning before they wash, bathe, go to the toilet, or get dressed. The "tape test" should be done on three consecutive mornings to increase the chance of finding pinworm eggs.
Because itching and scratching of the anal area is common in pinworm infection, samples taken from under the fingernails may also contain eggs. Pinworm eggs rarely are found in routine stool or urine samples.
B) pulmonary arteries and right ventricle.
What are Dirofilaria?
Dirofilaria are long, thin parasitic roundworms that infect a variety of mammals. Infection is transmitted by mosquito bites. There are many species of Dirofilaria, but human infection is caused most commonly by three species, D. immitis, D. repens, and D. tenuis. The main natural hosts for these three species are dogs and wild canids, such as foxes and wolves (D. immitis and D. repens) and raccoons (D. tenuis). D. immitis is also known as "heartworm." D. repens is not found in the United States, and D. tenuis appears to be restricted to raccoons in North America.
What is dirofilariasis?
Dirofilariasis is the disease caused by Dirofilaria worm infections. In dogs, one form is called "heartworm disease" and is caused by D. immitis. D. immitis adult worms can cause pulmonary artery blockage in dogs, leading to an illness that can include cough, exhaustion upon exercise, fainting, coughing up blood, and severe weight loss.
Like dogs, humans become infected with Dirofilaria through mosquito bites. In persons infected with D. immitis, dying worms in pulmonary artery branches can produce granulomas (small nodules formed by an inflammatory reaction), a condition called "pulmonary dirofilariasis." The granulomas appear as coin lesions (small, round abnormalities) on chest x-rays. Most persons with pulmonary dirofilariasis have no symptoms. People with symptoms may experience cough (including coughing up blood), chest pain, fever, and pleural effusion (excess fluid between the tissues that line the lungs and the chest cavity). Coin lesions on chest x-rays are not diagnostically specific for pulmonary dirofilariasis. Therefore, discovery of these lesions have led to invasive diagnostic procedures to exclude other, more serious causes, including cancer. Rarely, D. immitis worms have been found in humans outside the lungs, including in the brain, eye, and testicle. A review of cases of human dirofilariasis in the United States published in 2005 lists a total of 81 cases reported in the literature since 1941, the year of the first reported case
D. repens, which is not found in the United States, is the leading cause of human dirofilariasis in Europe. Both D. immitis and D. repens have been found to cause human dirofilariasis in other parts of the world. Among persons infected with D. repens and D. tenuis, the most common findings have been nodules under the skin and under the conjunctiva of the eye. The prevalence of Dirofilaria infection in humans who have no symptoms from their infection is unknown.
The larvae that enter the body through a mosquito bite often do not survive the passage through tissue under the skin and when they do survive, the adult worms remain sexually immature. Therefore, Dirofilaria infection in humans does not result in the production of microfilariae and humans are not able to transmit the infection to other hosts. This is unlike the infection in other mammalian hosts, such as dogs. In these hosts, the infection can be transmitted to other hosts because microfilariae are produced and then ingested by mosquitoes in blood meals.
D. immitis is commonly reported as the cause of human dirofilariasis in the United States. In the United States, infection in dogs and humans is most common in the east and southeast. D. repens, not found in the United States, is the Dirofilaria species most commonly reported to cause human dirofilariasis in Europe. Both species have been found to cause human dirofilariasis in other parts of the world.
How is dirofilariasis transmitted?
The definitive mammalian hosts for Dirofilaria are primarily domestic dogs, wild canids (such as wolves and foxes), and raccoons. In these hosts, sexually mature worms produce microfilariae that circulate in the blood and are ingested by mosquitoes during a blood meal. In mosquitoes, the microfilariae develop into larvae that migrate to the proboscis (the long, tubular part of the mouth of the mosquito that punctures the skin during a blood meal), where they are ready to infect another host during a blood meal. Several types of mosquitoes are capable of transmitting Dirofilaria infection, including Aedes, Anopheles, and Mansonia.
Humans and a wide range of other mammals are accidental hosts that play no role in the transmission of Dirofilaria. In these hosts, Dirofilaria larvae can develop into adult worms but the worms remain sexually immature and no microfilariae are produced.
What are the signs and symptoms of dirofilariasis?
Human infections with D. immitis can result in areas of inflammation induced by dying adult worms in pulmonary arteries that appear as coin lesions on chest x-rays. Coin lesions can also be caused by cancer and other serious diseases, and a coin lesion discovered accidentally on chest x-ray usually leads to an invasive procedure to learn the cause. Most human cases of pulmonary dirofilariasis are diagnosed from samples taken during these procedures. Most reported cases of D. immitis infection in humans have been in persons with no symptoms. People with symptoms can have cough (including coughing up blood), chest pain, fever, and pleural effusion (excess fluid between the tissues that line the lungs and the chest cavity). Rarely, D. immitis worms have been found in humans at outside the lungs, including the brain, eye, and testicle. When D. repens and D. tenuis infection is reported in humans, it is generally as the cause of nodules under the skin, but on occasion, worms are found in the conjunctiva.
Where is dirofilariasis found?
Dirofilariasis is found throughout the world where Dirofilaria species are common. In the United States, canine dirofilariasis has been reported from all states, and D. tenuis in raccoons is common in many areas where raccoons are found. Canine and human dirofilariasis are most prevalent in eastern and southeastern states, although rates are increasing rapidly in a number of western states. D. immitis is the Dirofilaria species most commonly reported to cause dirofilariasis in humans in the United States. D. repens is the Dirofilaria species most commonly reported to cause dirofilariasis among humans in Europe. One or both of these species have been found to cause human dirofilariasis in other parts of the world.
How is it diagnosed?
In humans, dirofilariasis is diagnosed most frequently by the examination of tissue from areas of inflammation in the lung obtained as part of the diagnostic investigation of coin lesions (small, round abnormalities) on chest x-rays or from the examination of tissue in nodules under the skin. Blood tests are not yet helpful in the diagnosis of dirofilariasis in humans.
Can dirofilariasis be transmitted person-to-person?
No. Dirofilariasis is transmitted neither person-to-person nor person-to-mosquito-to-person. The transmission of dirofilariasis requires mosquitoes as the intermediate host as well as the production of microfilariae, which does not take place in humans.
How can I prevent dirofilariasis?
Dirofilariasis can be prevented by avoiding mosquito bites in areas where mosquitoes may be infected with Dirofilaria larvae. The risk of such mosquito bites can be reduced by leaving as little skin exposed as possible, by the use of insect repellent when exposed to mosquitoes, and by sleeping under an insecticide-treated bednet in areas where Dirofilaria-infected mosquitoes bite at night and have access to sleeping areas.
Life Cycle of D. immitis
During a blood meal, an infected mosquito (Aedes, Culex, Anopheles, Mansonia) introduces third-stage filarial larvae of Dirofilaria immitis into the skin of the definitive host, which is usually a domestic dog or coyote in the United States (although a wide variety of other animals can also be infected, including felids, mustelids, pinnipeds, beaver, horses, and humans), where they penetrate into the bite wound The number 1. In the definitive host, the L3 larvae undergo two more molts into L4 and adults. Adults reside in pulmonary arteries, and are occasionally found in the right ventricle of the heart The number 2. Adult females are usually 230-310 mm long by 350 µm wide; males are usually 120-190 mm long by 300 µm wide. Adults can live for 5 - 10 years. In the heart, the female worms are capable of producing microfilariae over their lifespan. The microfilariae are found in peripheral blood The number 3. A mosquito ingests the microfilariae during a blood meal The number 4. After ingestion, the microfilariae migrate from the mosquito's midgut through the hemocoel to the Malpighian tubules in the abdomen The number 5. There the microfilariae develop into first-stage larvae The number 6 and subsequently into third-stage infective larvae The number 7. The third-stage infective larvae migrate to the mosquito's proboscis The number 8 and can infect another definitive host when it takes a blood meal The number 1. In humans The number 9, D. immitis larvae tend to follow the same migratory pathway as in the canine host, ending up in the lungs, where they often lodge in small-caliber vessels, causing infarcts and typical "coin lesions" visible on radiographs.
D) Tunneling into the host's epidermis.
Sarcoptes scabiei mites in a skin scraping, stained with lactophenol cotton-blue
Sarcoptes scabiei mites in a skin biopsy, stained with H&E.
Sarcoptes scabiei mite in a skin biopsy, stained with H&E.
Sarcoptes scabiei var. hominis, the human itch mite, is in the arthropod class Arachnida, subclass Acari, family Sarcoptidae. The mites burrow into the upper layer of the skin but never below the stratum corneum. The burrows appear as tiny raised serpentine lines that are grayish or skin-colored and can be a centimeter or more in length. Other races of scabies mites may cause infestations in other mammals, such as domestic cats, dogs, pigs, and horses. It should be noted that races of mites found on other animals may cause a self-limited infestation in humans with temporary itching due to dermatitis; however they do not multiply on the human host.
Life cycle of Sarcoptes scabiei
Sarcoptes scabiei undergoes four stages in its life cycle: egg, larva, nymph and adult. Females deposit 2-3 eggs per day as they burrow under the skin The number 1. Eggs are oval and 0.10 to 0.15 mm in length The number 2 and hatch in 3 to 4 days. After the eggs hatch, the larvae migrate to the skin surface and burrow into the intact stratum corneum to construct almost invisible, short burrows called molting pouches. The larval stage, which emerges from the eggs, has only 3 pairs of legs The number 3 and lasts about 3 to 4 days. After the larvae molt, the resulting nymphs have 4 pairs of legs The number 4. This form molts into slightly larger nymphs before molting into adults. Larvae and nymphs may often be found in molting pouches or in hair follicles and look similar to adults, only smaller. Adults are round, sac-like eyeless mites. Females are 0.30 to 0.45 mm long and 0.25 to 0.35 mm wide, and males are slightly more than half that size. Mating occurs after the active male penetrates the molting pouch of the adult female The number 5. Mating takes place only once and leaves the female fertile for the rest of her life. Impregnated females leave their molting pouches and wander on the surface of the skin until they find a suitable site for a permanent burrow. While on the skin's surface, mites hold onto the skin using sucker-like pulvilli attached to the two most anterior pairs of legs. When the impregnated female mite finds a suitable location, it begins to make its characteristic serpentine burrow, laying eggs in the process. After the impregnated female burrows into the skin, she remains there and continues to lengthen her burrow and lay eggs for the rest of her life (1-2 months). Under the most favorable of conditions, about 10% of her eggs eventually give rise to adult mites. Males are rarely seen; they make temporary shallow pits in the skin to feed until they locate a female's burrow and mate.
Transmission occurs primarily by the transfer of the impregnated females during person-to-person, skin-to-skin contact. Occasionally transmission may occur via fomites (e.g., bedding or clothing). Human scabies mites often are found between the fingers and on the wrists.
Scabies mites are distributed worldwide, affecting all races and socioeconomic classes in all climates.
When a person is infested with scabies mites for the first time, symptoms may not appear for up to two months after becoming infested; however, an infested person can still transmit scabies during this time. If a person has had scabies before, they become sensitized to mites and symptoms generally occur much sooner, within 1 to 4 days. Mites burrowing under the skin cause a rash, which is most frequently found on the hands, particularly the webbing between the fingers; the folds of the wrist, elbow or knee; the penis; the breast; and/or the shoulder blades. Except in crusted (Norwegian) scabies, burrows and mites may be as few as 10-15 in number and can be difficult to find. A papular "scabies rash" may be seen in skin areas such as the buttocks, scapular region and abdomen, where female mites are absent; this may be a result of sensitization from a previous infection. Severe itching, especially at night and frequently over much of the body, including areas where mites are undetectable, is the most-common symptom of scabies. A more severe form of scabies that is more common among persons who are immunocompromised, elderly, or institutionalized is called crusted (Norwegian) scabies and is characterized by vesicles and formation of thick crusts over the skin, accompanied by abundant mites but only slight itching. Complications due to infestation are usually caused by secondary bacterial infections.
The harvest mite, Trombicula autumnalis, is a species of mite of the family Trombiculidae. Their larvae live parasitically; they infect all domestic mammals, humans, and some ground-nesting birds. Wikipedia
Scientific name: Trombicula autumnalis
Higher classification: Neotrombicula
Trombicula is a genus of harvest mites (also known as red bugs, scrub-itch mites, berry bugs, or in their larval stage, as chiggers or chigoe) in the Trombiculidae family. In their larval stage, they attach to various animals, including humans, and feed on skin, often causing itching.
Trombicula autumnalis are surface mites found worldwide. It will attack and parasitise any animal including humans, causing parasitic skin infestation (trombiculidiasis). Only the larval stage is parasitic however, and adult mites are found living in the soil.
The mites are bright orange in colour and hairy. They have six legs and no spiracles. They breathe through their cuticle.
The lifecycle of Trombicula autumnalis mites lasts around 50 to 70 days. The nymphal and adult stages are free-living in the soil. Eggs are laid in soil and once hatched, larvae climb up vegetation in search of a host to attach to. As the name suggests, numbers are greatest in 'harvest' time, late summer, in temperate climates and all year round in the tropics.
The larvae insert their mouthparts into the host's skin and inject cytolytic enzymes. They then feed on partly digested host tissue causing irritation and potentially a hypersensitivity reaction. The Mites are mainly found on the head, ears and flanks of pets and can be found on the face and limbs of grazing animals, depending upon the host height.
The animal will show signs of intense pruritus and orange to red coloured larvae may be visible on the skin. There will be a erythematous, papular rash and also crusting and scaling.
Clinical signs and the time of year is indicative of the parasite. On physical examination, it is likely the parasite will be seen. Skin scraping, coat brushing or a tape strip may reveal the presence of the mite. Microscopically, the skin will appear hyperplastic with superficial perivascular dermatitis and the presence of eosinophils and mast cells.
a parasitic coccidian protozoan found in the intestinal tract of many vertebrates, where it sometimes causes disease.
What is cryptosporidiosis?
Cryptosporidiosis is a diarrheal disease caused by microscopic parasites, Cryptosporidium, that can live in the intestine of humans and animals and is passed in the stool of an infected person or animal. Both the disease and the parasite are commonly known as "Crypto." The parasite is protected by an outer shell that allows it to survive outside the body for long periods of time and makes it very resistant to chlorine-based disinfectants. During the past 2 decades, Crypto has become recognized as one of the most common causes of waterborne disease (recreational water and drinking water) in humans in the United States. The parasite is found in every region of the United States and throughout the world.
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How is cryptosporidiosis spread?
Cryptosporidium lives in the intestine of infected humans or animals. An infected person or animal sheds Crypto parasites in the stool. Millions of Crypto germs can be released in a bowel movement from an infected human or animal. Shedding of Crypto in the stool begins when the symptoms begin and can last for weeks after the symptoms (e.g., diarrhea) stop. You can become infected after accidentally swallowing the parasite. Cryptosporidium may be found in soil, food, water, or surfaces that have been contaminated with the feces from infected humans or animals. Crypto is not spread by contact with blood.
Crypto can be spread:
By putting something in your mouth or accidentally swallowing something that has come into contact with stool of a person or animal infected with Crypto.
By swallowing recreational water contaminated with Crypto. Recreational water is water in swimming pools, hot tubs, Jacuzzis, fountains, lakes, rivers, springs, ponds, or streams. Recreational water can be contaminated with sewage or feces from humans or animals.
By swallowing water or beverages contaminated with stool from infected humans or animals.
By eating uncooked food contaminated with Crypto. Thoroughly wash with uncontaminated water all vegetables and fruits you plan to eat raw. See below for information on making water safe.
By touching your mouth with contaminated hands. Hands can become contaminated through a variety of activities, such as touching surfaces (e.g., toys, bathroom fixtures, changing tables, diaper pails) that have been contaminated by stool from an infected person, changing diapers, caring for an infected person, changing diapers, caring for an infected person, and handling an infected cow or calf.
By exposure to human feces through sexual contact.
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What are the symptoms of cryptosporidiosis?
The most common symptom of cryptosporidiosis is watery diarrhea. Other symptoms include:
Stomach cramps or pain
Some people with Crypto will have no symptoms at all. While the small intestine is the site most commonly affected, Crypto infections could possibly affect other areas of the digestive tract or the respiratory tract.
How long after infection do symptoms appear?
Symptoms of cryptosporidiosis generally begin 2 to 10 days (average 7 days) after becoming infected with the parasite.
How long will symptoms last?
In persons with healthy immune systems, symptoms usually last about 1 to 2 weeks. The symptoms may go in cycles in which you may seem to get better for a few days, then feel worse again before the illness ends.
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Who is most at risk for cryptosporidiosis?
People who are most likely to become infected with Cryptosporidium include:
Children who attend day care centers, including diaper-aged children
Child care workers
Parents of infected children
People who take care of other people with cryptosporidiosis
Backpackers, hikers, and campers who drink unfiltered, untreated water
People who drink from untreated shallow, unprotected wells.
People, including swimmers, who swallow water from contaminated sources
People who handle infected cattle
People exposed to human feces through sexual contact
Contaminated water may include water that has not been boiled or filtered, as well as contaminated recreational water sources (e.g., swimming pools, lakes, rivers, ponds, and streams). Several community-wide outbreaks of cryptosporidiosis have been linked to drinking municipal water or recreational water contaminated with Cryptosporidium.
Selected zoonotic infectious diseases of dogs and cats*
Route of human exposure Agent Principal clinical syndromes Human surveillance mechanisms
Bites, scratches, or contact with exudates:
Bartonella spp.† (bacteria) Cats and dogs: subclinical fever, hyperglobulinemia, endocarditis, myocarditis, epistaxis, granulomatous rhinitis, uveitis, lymphadenopathy; humans: fever, malaise, endocarditis, myocarditis, meningitis, encephalopathy, lymphadenopathy, pulmonary granulomata, neuroretinitis, bacillary angiomatosis, bacillary peliosis None
Capnocytophaga canimorsus (bacterium) Cats and dogs: subclinical oral carriage; humans: bacteremia None
Francisella tularensis‡ (bacterium) Cats: septicemia, pneumonia; humans: ulceroglandular, oculoglandular, glandular, pneumonic or typhoidal (depending on route of inoculation) NNDSS
Staphylococcus spp.§ (methicillin resistant) (bacterium) Cats, dogs, and humans: subclinical cutaneous infections, bacteremia None
Yersinia pestis‡ (bacterium) Cats and humans: bubonic, bacteremic, or pneumonic (depending on route of inoculation and success of initial therapy) IHR (pneumonic only), NNDSS
Rabies (virus) Cats, dogs, and humans: progressive CNS disease NNDSS, WAHID
Dermatophytes (fungi) Cats and dogs: superficial dermatologic disease; humans: superficial dermatologic disease and deep tissue infections in immunocompromised patients None
Sporothrix schenkii‡ (fungus) Cats and humans: draining cutaneous tracts None
Contact with infected feces (ingestion unless otherwise indicated):
Campylobacter jejuni and C. coli (bacteria) Cats, dogs, and humans: diarrhea and vomiting WAHID, FoodNet
Escherichia coli (bacterium) Cats, dogs, and humans: diarrhea and vomiting WAHID (STEC), NNDSS (STEC), FoodNet (STEC)
Salmonella spp. (bacterium) Cats, dogs, and humans: diarrhea and vomiting WAHID, NNDS, FoodNet
Helicobacter spp.¶ (bacterium) Cats and dogs: vomiting; humans: reflux disease and vomiting None
Yersinia enterocolitica (bacterium) Cats and dogs: subclinical infection or abdominal pain, vomiting and diarrhea; humans: diarrhea and vomiting FoodNet
Entamoeba histolytica# (ameba) Dogs and humans: diarrhea and vomiting None
Ancylostoma braziliense, Uncinaria stenocephala, A. caninum (dog only) and A. tubaeforme (cat only)** (hookworms) Cats and dogs: blood-loss anemia, diarrhea, unthrifty; humans: cutaneous larva migrans, eosinophilic enteritis None
Baylisascaris procyonis (roundworm) Dogs: failure to thrive; humans: visceral larva migrans, CNS disease None
Toxocara canis (dogs) and T. cati (cats)†† (roundworms) Cats and dogs: vomiting, diarrhea, failure to thrive; humans: ocular and visceral larva migrans None
Strongyloides stercoralis‡‡ (threadworm) Cats and dogs: bloody diarrhea, blood-loss anemia, failure to thrive; humans: polysystemic disease None
Echinococcus multilocularis (cestode) Cats and dogs: subclinical infection; humans: polysystemic hydatid disease WAHID
Echinococcus granulosus (cestode) Dogs: subclinical infection; humans polysystemic disease WAHID
Cryptosporidium spp.§§ (coccidian) Cats, dogs, and humans: diarrhea and vomiting NNDSS, FoodNet, CryptoNet
Toxoplasma gondii¶¶ (coccidian) Cats: rarely diarrhea, polysystemic disease; dogs: neuromuscular and rarely polysystemic disease; humans: occular, CNS, and polysystemic disease WAHID
Giardia spp.## (flagellate) Cats, dogs, and humans: diarrhea and vomiting NNDSS
Contact with infected respiratory or ocular secretions:
Bordetella bronchiseptica (bacterium) Cats and dogs: sneezing and coughing; humans: pneumonia in immunosuppressed patients None
Chlamydophila felis (bacterium) Cats: conjunctivitis, sneezing; humans: conjunctivitis None
F. tularensis*** (bacterium) Cats: septicemia, pneumonia; humans: ulceroglandular, oculoglandular, glandular, pneumonic or typhoidal (depending on route of infection) None
Streptococcus group A (bacterium) Cats and dogs: subclinical transient carrier; humans: strep throat, septicemia None
Y. pestis*** (bacterium) Same as entry under bites, scratches, or contact with exudates None
Influenza A virus Cats and dogs: respiratory disease, systemic disease; humans: respiratory disease WHO Global Influenza Program
Contact with infected genital secretions:
Brucella canis††† (bacterium) Dogs: orchitis, epididymitis, abortion, stillbirth, vaginal discharge, uveitis, fever; humans: fever, arthralgia, headache, fatigue, myalgia, weight loss, arthritis/spondylitis, meningitis or focal organ involvement (endocarditis, orchitis/epididymitis, hepatomegaly, splenomegaly) WAHID, NNDSS
Coxiella burnetti*** (rickettsia) Cats: subclinical, abortion or stillbirth; humans: fever, pneumonitis, lymphadenopathy, myalgia, arthritis NNDSS
Contact with infected urine:
Leptospira spp.(bacteria) Dogs: fever, vomiting, pulmonary hemorrhage, renal and hepatic dysfunction, encephalopathy, uveitis; humans: fever, headache, myalgia, meningitis, pulmonary/hepatic and renal dysfunction, hemorrhagic complications WAHID, some U.S. states
Bartonella spp.† (bacterium) Same as entry under bites, scratches, and contact with exudates None
Y. pestis (bacterium) Same as entry under bites, scratches, and contact with exudates None
Rickettsia felis (rickettsia) Cats: subclinical, fever; humans: fever, CNS disease None
Rickettsia typhi (rickettsia) Cats: subclinical; humans: fever, polysystemic disease None
Borrelia burgdorferi (bacterium) Dogs: subclinical infection, fever, polyarthritis, nephropathy; humans: polyarthropathy, cardiac and CNS disease NNDSS
Anaplasma phagocytophilium (rickettsia) Cats and dogs: fever, polyarthritis; humans: fever, polysystemic disease NNDSS
Ehrlichia spp. (rickettsia) Dogs: subclinical infection, fever, polysystemic disease; humans: fever, polysystemic disease NNDSS
Rickettsia rickettsii (rickettsia) Dogs: subclinical infection, fever, polysystemic disease; humans: fever, polysystemic disease NNDSS
Leishmania infantum and L. chagasi (protozoa) Cats and dogs: cutaneous lesions and polysystemic disease; humans: polysystemic (visceral) disease None.
D) the respiratory tract.
The pentastomes are a group of worm-like parasites that infect many different species of fish. Infections have been found in several families of fish including the Cichlidae (tilapia), Cyprinidae (danios), Cyprinodontidae (flagfish), and Poecilidae (mosquitofish, swordtails, mollies, platies).
What are pentastomes?
Pentastomes, also called "tongue worms," look like small conical-shaped worms, but are actually are arthropods, related to spiders and mites. Unlike their relatives, however, pentastomes are internal parasites, generally living in the lungs and respiratory tract of reptiles. The adults range in size from 0.8 to 4.5 inches. There are over 70 different species of pentastomes and they commonly infect snakes, lizards, and crocodilians. The most common species in reptiles include:
Armillifer in pythons and vipers
Porocephalus in boas and rattlesnakes
Kiricephalus in colubrid snakes
Sebekia in crocodilians
Raillietiella in lizards and snakes
What is the life cycle of pentastomes?
The adult worms live in the respiratory tract of a reptile where they mate, and the females lay eggs. The eggs are coughed up by the reptile, swallowed, move through the digestive system, and are expelled in the feces. The eggs develop into larvae in the environment, and are eaten by an intermediate host, usually a bird or rodent. The larvae develop into nymphs within that host. When the host is eaten by a reptile, the nymphs are released, burrow through the intestine, and migrate to the lungs where they develop into adults.
What clinical signs are associated with a pentastome infestation?
Some animals with a pentastome infestation may not show any signs of disease. In others, the parasite can cause severe lesions in the lungs, and even death. Reptiles may have dyspnea (difficulty breathing), lethargy, and a loss of appetite. Secondary bacterial infections may occur. In severe infections, aneurysms may develop. Occasionally, the adult worms may burrow through the lung and protrude from the skin.
How is a pentastome infestation diagnosed?
Diagnosis may be made by finding the eggs in the feces or respiratory secretions.
How is a pentastome infestation treated and controlled?
There is currently no effective treatment for pentastome infestations. Infestations can be controlled through good hygiene and feeding parasite-free prey.
Do pentastomes pose a risk to humans?
Yes. Humans can act as intermediate hosts, becoming infected by having their hands contaminated from the feces or saliva of the reptile, and accidentally ingesting the eggs. Handling fecal contaminated water, dishes, and other equipment may also result in accidental transmission. Usually, there are no clinical signs, however, some people may develop localized inflammation. The larvae can encyst in various tissues, causing abdominal pain, vomiting, constipation, diarrhea, and a tender abdomen. In isolated cases, septicemia may occur.
To prevent transmission of pentastomes, as well as other zoonoses such as salmonellosis, it is important for owners and handlers of reptiles to use good hygiene, including handwashing. To learn more about protective measures see Salmonella & Its Risk to Reptile Owners.
A) 1 teaspoon.
Fecal Exam Procedures
Fecal examination procedures likely to be accepted and implemented in most veterinary practices include flotation (centrifugal or passive), sedimentation, and direct examination (direct smear). Only flotation and sedimentation are concentration procedures. Direct smears have poor sensitivity because of the small amount of feces examined, but may be useful for demonstrating motile organisms. CAPC recommends that feces be routinely screened by a centrifugal flotation method, which is consistently more sensitive than simple flotation. Accuracy of centrifugal flotation techniques depends on procedural details and specimen attributes.
Gross examination. Specimens should be examined grossly for the presence of blood, mucus, intact worms, or tapeworm segments.
Sample size and preparation. Specimen size should be at least 1 gram of formed feces (1 cubic centimeter or a cube about one-half inch on a side). If feces are soft, sample size should be 2 grams. If it is slurry-like, the sample should be 4 grams. For liquid feces, a sample of 6 grams or greater might be appropriate. Inadequate sample size (e.g., fecal loop sample) may result in false-negative results. To remove large fecal debris, sieving is recommended prior to centrifugation. The sample is sieved through cheesecloth or a tea strainer after mixing with water or flotation solution. Passive flotation kits typically include a device that prevents larger particles from floating to the surface.
Flotation solution. Both the type and concentration of sugar or salt solutions used can affect recovery of diagnostic stages of parasites from feces. Common flotation solutes include sodium nitrate, zinc sulfate, sucrose (usually granulated sugar), magnesium sulfate, and sodium chloride. These solutes can be mixed at varying concentrations with water to achieve flotation solutions with different densities. Flotation solutions with higher densities are capable of floating heavier (denser) parasite stages. However, higher density flotation solutions also float many other fecal particles that can render preparations more difficult to examine and can collapse thin-shelled parasite stages, making them difficult to identify or causing them to float poorly. More viscous solutions, such as Sheather's sugar (sucrose) solution, are more efficient for centrifugation. Most salt solutions dry very quickly, crystallizing on slides and obscuring observation.
Centrifugation. Centrifugation of sieved feces may be performed in flotation solution either with a coverslip placed on top of a filled tube or with the coverslip added after the centrifuge has stopped. In the latter case, the tube is spun near-full, and then the tube is filled to form a reverse meniscus, the coverslip is added, and the tube is allowed to sit a few minutes longer.
Centrifugation with the coverslip on the tube works best when a sugar flotation medium is used. Alternate methods for sampling the reverse meniscus include loops or glass rods that can be flamed between samples; however, this approach is less efficient than centrifuging with the coverslip in place.
Slide examination. The entire area under the coverslip should be examined. It is helpful to focus on a small air bubble to obtain the correct focal plane. The edge of the coverslip can be sealed with nail polish to prevent drying and to allow examination of the specimen under oil immersion. Sucrose preparations can be stored in high humidity in a refrigerator for hours to days without significantly altering the morphology of most common helminth eggs.
Although routine fecal examination should always include centrifugation, at times, other examination methods are needed to reach a diagnosis. For example, motile trophozoites and nematode larvae can be observed using the direct smear method. Certain nematode, trematode, and tapeworm eggs will not float in less dense flotation solutions and are better demonstrated using sedimentation. The Baermann funnel method may aid in diagnosis of a feline lungworm (Aelurostrongylus abstrusus) infection. Stained direct smears are useful for diagnosis of a protozoal infection such as giardiasis or trichomoniasis. Specimens to be examined for protozoa can first be fixed using a commercial fixative such as Proto-fix™ or a fixating stain such as MIF (merthiolate-iodine-formalin). Fecal antigen detection tests are useful for diagnosis of giardiasis and cryptosporidiosis.
Almost any animal species can be infected by trematode parasites. Trematode eggs are often too heavy to float in a flotation solution. Similarly, Eimeria leuckarti, a coccidian parasite of horses and donkeys is very heavy and can only be detected in sediments.
Infection with Eimeria leuckarti, a coccidian parasite of the small intestine of horses and donkeys, occurs throughout the world. However, it is a rarely reported infection because the oocysts do not rise to the surface on the usual flotation media and infection is often overlooked. The infection has only been reported twice in Australia, once in Tasmania and once in Victoria, but is believed to be much more common. The infection is usually symptomless, however, severe diarrhoea and deaths have been reported. The Department of Agriculture and Food's Animal Health Laboratories have only seen this parasite once in more than 2000 horse samples examined for the presence of liver fluke infection.
There are several important diseases of trematodes in domestic animals and the most important ones are briefly described below:
Fascioliasis, the disease caused by infection with liver fluke, occurs in all herbivorous animals including pigs, kangaroos and humans. It is found in temperate high-rainfall regions all over the world, according to the distribution of freshwater snail intermediate hosts.
Recorded prevalence rates of liver fluke infection in cattle in endemic areas vary from about 10% in Europe to 95% in southern Latin America. Liver fluke infection in humans can reach a prevalence of 90% (the Lao People's Democratic Republic).
In eastern Australia, liver fluke infection occurs from south-eastern Queensland to southern Victoria and Tasmania. In South Australia, small endemic areas occur in the high-rainfall areas (irrigated pasture adjacent to the Murray river). In Western Australia outbreaks have occurred, but the parasite has not become established.
Fascioliasis is caused by flukes of the genus Fasciola. F. hepatica occurs in most countries and is the only species present in Australia. F. gigantica is the more common liver fluke in Africa and Asia and Fascioloides magna infects wild and domestic ruminants in North America.
F. hepatica is a leaf-shaped, greyish-white parasite with one ventral sucker and can grow to 20 - 50 millimetres in length and 4 - 13 mm in width. F. hepatica is hermaphroditic and only one fluke is necessary to establish a patent infection. Each adult fluke can produce 20,000 eggs per day and may live for 10 years or more. Adults produce 200 times more eggs in sheep than in cattle where the egg production per adult fluke is only about 100 eggs per day. Eggs deposited in faeces hatch and release a miracidium, which infects freshwater snails. Cercaria develop and are released from the snail 4 to 7 weeks later. Cercaria encyst on vegetation as metacercaria, which are eaten by the host. The metacercaria excyst, immature flukes travel through the wall of the small intestine and migrate through the liver parenchyma to the bile ducts. They develop to egg-laying adult flukes in the main bile ducts about 8 - 10 weeks after infection.
The main intermediate hosts for F. hepatica are snails of the genus Lymnaea. Lymnaea (Pseudosuccinea) columella is an important intermediate host in many warm countries and until recently was the only intermediate host for F. hepatica present in Western Australia. L. viridis is an important intermediate host in New Guinea and in the Philippines, has been recorded in Brisbane (Queensland) and more recently also in Western Australia. L. tomentosa is an important intermediate host in Europe and also the eastern States of Australia.
Sheep may suffer severe liver damage and death is not uncommon. Affected animals are anaemic, hypo-proteinaemic, jaundiced and show signs of peritonitis. Fascioliasis in cattle is usually a chronic disease associated with low weight gains and decreased milk production. It can be the cause of significant economic losses through liver condemnation at slaughter.
Pathological changes due to migration of immature flukes are termed acute or subacute fascioliasis, and the response to adult flukes in the bile ducts, chronic fascioliasis. Both changes can be present in the same animals. Migratory flukes cause traumatic lesions to the liver parenchyma forming tortuous tracts that appear in cross sections as 2 - 3 mm diameter haemorrhagic foci. Microscopically, there is haemorrhagic necrosis infiltrated with eosinophils, histiocytes and giant cells. Repair of the lesion results in irregular hepatic fibrosis. In cattle, there may be massive fibrous thickening of the bile ducts in response to adult flukes. This is associated with cholangio-hepatitis and sometimes mineralisation. In most species, however, there is little thickening of the bile duct walls.
Diagnosis in individual animals relies on the demonstration of F. hepatica eggs in the faeces using the sedimentation technique. Eggs are thin-walled, golden yellow, have an operculum and measure 140 x 80 microns. They can be difficult to differentiate from paramphistome eggs. The sedimentation technique used in cattle only detects about 30% of all animals shedding eggs. Diagnosis of infection during the pre-patent period (8 weeks) is not possible.
Intestinal paramphistomiasis caused by paramphistomes, or stomach flukes, is a severe debilitating disease of young cattle between 6 and 18 months of age.
The clinical disease of severe ill-thrift and diarrhoea is caused by massive numbers of immature flukes that colonise the anterior small intestine causing severe damage to the intestinal mucosa. Adult flukes are found in the rumen and reticulum and generally cause no harm. The parasite has an indirect life cycle with planorbid snails as intermediate hosts.
B) Baermann technique.
What is a fecal Baermann test?
" Some parasites pass larvae instead of eggs..."
A fecal Baermann is a specialized test for detecting certain types of parasites or "worms" in stool material. Many parasites pass their eggs in the host's stool, and infection is easily diagnosed by examining the stool for the presence of parasite eggs. (See handout "Fecal Flotation"). However, some parasites pass larvae instead of eggs; larvae cannot be detected by routine stool examination, and a special technique called a fecal Baermann is required to find them.
How does the test work?
fecal_baermann-1Stool material is mixed with water in a special filtering apparatus, and allowed to stand for 1-2 hours. The larvae sink to the bottom of the apparatus, where they are collected and examined. The type of parasitic infection can be determined by identifying the larvae.
What sample is needed?
A small amount of fresh stool material is all that is needed; ideally, the stool sample should be no more than 24 hours old, and should be as free as possible of grass, gravel, kitty litter etc. The sample can be collected in any clean container with a tightly fitting lid; this may be a container brought from home, such as a clean margarine tub, or a container provided by your veterinarian.
When should a fecal Baermann be performed?
"The most common parasitic infection diagnosed using a Baermann test is lungworm, which typically causes signs of coughing."
A fecal Baermann should be performed whenever there is a suspicion that a pet is infected with a parasite that passes larvae, rather than eggs, in the stool. The most common parasitic infection diagnosed using a Baermann test is lungworm, which typically causes signs of coughing. This parasitic worm lives in the lung, and releases larvae into the lung tissue. The host then coughs up the larvae and swallows them, ultimately passing them out in the stool. A fecal Baermann is necessary to diagnose this parasitic infection.
fecal smear to detect the Giardia
What is Giardia?
Giardiasis is an intestinal infection of man and animals caused by a protozoan parasite Giardia intestinalis (also known as Giardia lamblia).
"...it is not a "worm", bacteria or virus."
Giardia is a simple one-celled parasitic species; it is not a "worm", bacteria or virus. The parasite occurs worldwide and is a common cause of "Traveler's Diarrhea" in people. Outdoor enthusiasts who inadvertently consume contaminated water may develop "beaver fever", which is another name for giardiasis in people. Other examples of protozoan parasites that can cause enteric (intestinal) disease are Coccidia, Cryptosporidia and Toxoplasma.
Giardiasis can be an important cause of illness, especially diarrhea, in animals and man. However, the majority of dogs infected with Giardia do not have diarrhea, vomiting or any other signs of illness.
The Giardia organism has two forms. A fragile, feeding form exists in the gut of infected animals, while a hardy cystic form is shed in feces and can survive several months in the environment, particularly in water and damp environments.
What are the clinical signs of Giardiasis?
These microscopic parasites attach themselves to the intestinal wall and the damage causes an acute (sudden-onset) foul-smelling diarrhea. The stool may range from soft to watery, often has a greenish tinge to it, and occasionally contains blood. Infected dogs tend to have excess mucus in the feces. Vomiting may occur in some cases. The signs may persist for several weeks and gradual weight loss may become apparent.
"The disease is not usually life threatening unless the dogs' immune system is immature or immunocompromised."
The diarrhea may be intermittent. Most dogs do not have a fever but may be less active. The disease is not usually life threatening unless the dogs' immune system is immature or immunocompromised.
If your pet is showing these symptoms do not wait for symptoms to get worse. It's better to contact your local VCA Veterinarian. We offer a free first exam* for new clients.
How do dogs get giardiasis?
giardia-1A dog becomes infected with Giardia when it swallows the cyst stage of the parasite. In susceptible dogs, once the cyst passes into the dog's intestines; it goes through transformation to the trophozoite or feeding form and attaches to the intestinal wall to feed. If sufficient numbers are present, clinical signs of damage to the intestinal wall will develop. Trophozoites reproduce by dividing, and some transform into the cystic form. Eventually, the dog passes cysts in its stool.
"Giardiasis can be transmitted by eating or sniffing the cysts from contaminated ground, or by drinking contaminated water."
These cysts are immediately able to infect another animal. Giardiasis can be transmitted by eating or sniffing the cysts from contaminated ground, or by drinking contaminated water.
When Giardia cysts are found in the stool of a healthy adult dog without diarrhea, they are generally considered a transient, insignificant finding. However, in puppies and debilitated adult dogs, they may cause severe, watery diarrhea that may be fatal if left untreated.
The likelihood of developing disease increases when large numbers of cysts are present in the environment from fecal contamination. Giardiasis is a common occurrence in environments that are densely populated, such as kennels, pet stores, or animal shelters.
How is giardiasis diagnosed?
"...require a special zinc sulfate flotation solution for detection."
A routine fecal flotation test may fail to detect these tiny cysts, which are shed inconsistently in the feces, and which often require a special zinc sulfate flotation solution for detection. Occasionally, the parasites may be seen on a direct smear of the feces. If your veterinarian suspects giardiasis, a sample of stool may be analyzed for the presence of Giardia specific antigens (cell proteins). Many cases are presumptively diagnosed on the basis of medical history and clinical signs suggestive of giardiasis.
How is giardiasis treated?
The most common drug used to kill Giardia is metronidazole, an antibiotic. It is normally given for five to seven days to treat giardiasis. Another antiparasitic drug, fenbendazole, is suggested as a potentially useful treatment, especially when used in conjunction with metronidazole. This combination is usually administered to cats with refractory diarrhea (diarrhea that hasn't responded to treatment). Supportive treatment with other drugs may be needed as supplemental therapy if dehydration or severe diarrhea is present. Some dogs may require follow-up tests and treatments based on their condition and severity of infection.
What is the prognosis for Giardiasis?
The prognosis is good in most cases. Debilitated or geriatric animals and those with incompetent immune systems are at increased risk for complications, including death.
Can my dog give a Giardia infection to me or my family?
giardiaGiardia can cause diarrhea in humans and can potentially be passed from dogs to humans. In the past, it was assumed that cats and dogs, along with wildlife, were an important source of infection for humans.
"...contaminated municipal water supplies are responsible for many outbreaks. "
However, human-to-human transmission is also important and contaminated municipal water supplies are responsible for many outbreaks.
If your dog is diagnosed with giardiasis, environmental disinfection and good personal hygiene are important to prevent accidental spread to humans. In particular, people with immunodeficiency, such as AIDS or cancer, or who are undergoing chemotherapy, should use extreme care, especially when handling feces or after administering medications.
For environmental disinfection, you can use chlorine bleach at 1:32 or 1:16 dilutions, or 1-2 cups in a gallon of water (60-120 mls/L). However, be sure that the affected surfaces can be safely treated with bleach. Lysol® and quaternary ammonium compounds (Parvosol®, etc.) are also reported to be effective in killing the cysts. Giardia cysts are susceptible to drying so try to keep your environment as dry as possible. For best results, thoroughly clean the pet's living and sleeping areas and then allow the areas to dry out for several days before reintroducing pets.
Toxascaris leonina, Toxascaris canis, and Toxocar cati
The ascarids Toxocara canis, Toxocara cati, and Toxascaris leonina are probably the most common gastrointestinal helminths encountered in small animal practice. Both T. canis and T. cati can cause serious disease in kittens and puppies; T. leonina is generally less pathogenic. Prenatal transmission assures that virtually all puppies are born infected with T. canis. Transmammary transmission is probably the major route of infection for kittens with T. cati. In addition, all three species of worm produce resistant eggs and use paratenic hosts to facilitate transmission. Much is now known about the complex biology and life history of T. canis. However, many questions, such as those concerning the mechanisms of larval survival within host tissues and of larval reactivation and migration during pregnancy, await further study. The mechanism of resistance to ascarid infections in cats and dogs has not been clearly defined. Ascariasis is traditionally thought to be a disease of young animals, with older animals being considered immune. However, at least in the case of T. canis, adult dogs can be repeatedly infected. A wide range of anthelmintics is available with extremely high efficacy against patent ascarid infections. The problem of prenatal infection with T. canis may be overcome by strategic use of the newer benzimidazole-carbamates, and the production of ascarid-free puppies now seems possible. However, complete larvicidal activity against somatic stages has not been convincingly demonstrated. Visceral larva migrans-like syndromes are now being recognized in dogs and cats. In addition, visceral larva migrans in children due to T. canis continues to be a significant zoonotic disease in North America and underscores the need for the veterinary profession to control ascarid infections in cats and dogs at every opportunity.