Ancylostoma caninum, commonly Dog hookworm, is a parasitic nematode hookworm that infects dogs. The larval stage penetrates the skin and makes it way through the circulatory system into the digestive tract, where adult forms lay eggs that are passed through the feces. Common symptoms include anemia and diarrhea. Newborn pups can die of hemorrhaging from their intestines caused by massive numbers of feeding hookworms. A. braziliense and Uncinaria stenocephala are different species of hookworm which can infect dogs and cause similar symptoms.  The parasite can also affect humans. It occasionally develops into an adult to cause eosinophilic enteritis in people, and their invasive larvae can cause an itchy rash called cutaneous larva migrans. Vaccination may soon be possible.

For more information view the source:Wikipedia

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Ancylostoma tubaeforme is a hookworm that infects cats. Infection can occur by penetration of the skin, eating other hosts such as birds, or by directly consuming the organism. This hookworm can also infect humans, causing a dermatitis. Ancylostoma tubaeforme along with Ancylostoma braziliense are the two most common hookworms to infect cats, causing anemia and also compromising the immune system.

For more information view the source:Wikipedia

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Cryptosporidium is a microscopic parasite that causes the diarrheal disease cryptosporidiosis. Both the parasite and the disease are commonly known as "Crypto."

There are many species of Cryptosporidium that infect humans and animals. 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 tolerant to chlorine disinfection.

While this parasite can be spread in several different ways, water (drinking water and recreational water) is the most common method of transmission. Cryptosporidium is one of the most frequent causes of waterborne disease among humans in the United States.

EPIDEMIOLOGY & RISK FACTORS

Crypto lives in the intestine of infected humans or animals. An infected person or animal sheds Cryptosporidium parasites in the stool. Millions of Crypto parasites can be released in  a bowel movement from an infected human or animal. Shedding 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. Crypto 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 in contact with the  stool of a person or animal infected with Crypto.

Recreational water can be contaminated with sewage or feces from humans or animals.    

• By swallowing water or beverages contaminated by stool from infected humans or animals.
• By  eating uncooked food contaminated with Crypto. All fruits and  vegetables you plan to eat raw should be thoroughly washed with  uncontaminated water.
• 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, and
• handling an infected cow or calf.
• People with greater exposure to contaminated materials are more at risk for infection, such as:    
• 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
• International travelers
• 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. Several community-wide outbreaks of cryptosporidiosis have  been linked to drinking municipal water or recreational water  contaminated with Cryptosporidium.

Cryptosporidium parasites are found in every region of the United States and throughout  the world. Travelers to developing countries may be at greater risk for  infection because of poorer water treatment and food sanitation, but  cryptosporidiosis occurs worldwide. In the United States, an estimated 748,000 cases of cryptosporidiosis occur each year.

Once  infected, people with decreased immunity are most at risk for severe  disease. The risk of developing severe disease may differ depending on  each person's degree of immune suppression.

BIOLOGY

Causal Agent:

Many species of Cryptosporidium exist that infect humans and a wide range of animals. Although Cryptosporidium parvum and Cryptosporidium hominis (formerly known as C. parvum anthroponotic genotype or genotype 1) are the most prevalent species causing disease in humans, infections by C. felis, C. meleagridis, C. canis, and C. muris have also been reported.

Life Cycle:

Sporulated oocysts, containing 4 sporozoites, are excreted by the infected host through feces and possibly other routes such as respiratory secretions. Transmission of Cryptosporidium parvum and C. hominis occurs mainly through contact with contaminated water (e.g., drinking or recreational water). Occasionally food sources, such as chicken salad, may serve as vehicles for transmission. Many outbreaks in the United States have occurred in waterparks, community swimming pools, and day care centers. Zoonotic and anthroponotic transmission of C. parvum and anthroponotic transmission of C. hominisoccur through exposure to infected animals or exposure to water contaminated by feces of infected animals. Following ingestion (and possibly inhalation) by a suitable host, excystation occurs. The sporozoites are released and parasitize epithelial cells of the gastrointestinal tract or other tissues such as the respiratory tract. In these cells, the parasites undergo asexual multiplication (schizogony or merogony) and then sexual multiplication (gametogony) producing microgamonts (male) and macrogamonts (female). Upon fertilization of the macrogamonts by the microgametes, oocystdevelop that sporulate in the infected host. Two different types of oocysts are produced, the thick-walled, which is commonly excreted from the host, and the thin-walled oocyst, which is primarily involved in autoinfection. Oocysts are infective upon excretion, thus permitting direct and immediate fecal-oral transmission.

Life cycle image and information courtesy of DPDx.

DISEASE

Symptoms of cryptosporidiosis generally begin 2 to 10 days (average  7 days) after becoming infected with the parasite. The most common  symptom of cryptosporidiosis is watery diarrhea. Other symptoms include:

• Stomach cramps or pain
• Dehydration
• Nausea
• Vomiting
• Fever
• Weight loss

Some people with Crypto will have no symptoms at all.

Symptoms  usually last about 1 to 2 weeks (with a range of a few days to 4 or  more weeks) in persons with healthy immune systems. Occasionally,  people may experience a recurrence of symptoms after a brief period of  recovery before the illness ends. Symptoms can come and go for up to 30  days.  While the small intestine is the site most commonly affected, Cryptosporidium infections could possibly affect other areas of the digestive tract or the respiratory tract. People  with weakened immune systems may develop serious, chronic, and  sometimes fatal illness. Examples of people with weakened immune  systems include:

• people with AIDS;
• those with inherited diseases that affect the immune system; and
• cancer and transplant patients who are taking certain immunosuppressive drugs.

The risk of developing severe disease may differ depending on each person's degree of immune suppression.

DIAGNOSIS

Diagnosis of cryptosporidiosis is made by examination of stool samples. Because detection of Cryptosporidium can be difficult, patients may be asked to submit several stool samples  over several days. Most often, stool specimens are examined  microscopically using different techniques (e.g., acid-fast staining,  direct fluorescent antibody [DFA] , and/or enzyme immunoassays for  detection of Cryptosporidium sp. antigens).

Molecular  methods (e.g., polymerase chain reaction – PCR) are increasingly used  in reference diagnostic labs, since they can be used to identify Cryptosporidium spp. at the species level.  Tests for Cryptosporidium are not routinely done in most laboratories; therefore, health care  providers should specifically request testing for this parasite.

PREVENTION AND CONTROL

• Practice good hygiene
• Wash hands with soap and water for at least 20 seconds, rubbing hands together vigorously and scrubbing all surfaces:             
• Before preparing or eating food
• After using the toilet
• After changing diapers or cleaning up a child who has used the toilet
• Before and after tending to someone who is ill with diarrhea
• After handling an animal or animal waste
• At child care facilities
• To reduce the risk of disease transmission, children with diarrhea should be excluded from child care settings until the diarrhea has stopped.
• At recreational water venues (pools, interactive fountains, lakes, ocean)
• Protect others by not swimming if you are experiencing diarrhea (this is essential for children in diapers). If diagnosed with cryptosporidiosis, do not swim for at least 2 weeks after diarrhea stops.
• Shower before entering the water.
• Wash children thoroughly (especially their bottoms) with soap and water after they use the toilet or their diapers are changed and before they enter the water.
• Take children on frequent bathroom breaks and check their diapers often.
• Change diapers in the bathroom, not at the poolside.
• Around animals
• Minimize contact with the feces of all animals, particularly young animals.
• When cleaning up animal feces, wear disposable gloves, and always wash hands when finished.
• Wash hands after any contact with animals or their living areas.
• Wash hands after gardening, even if wearing gloves.
• Immunocompromised persons
• Avoid close contact with any person or animal that has cryptosporidiosis. Cryptosporidiosis can become a life threatening disease for immunocompromised persons.
• Do not handle animal feces because infection can be life threatening for immunocompromised persons.
• Avoid Water That Might Be Contaminated
• You may not be protected in a chlorinated recreational water venue  (for example, swimming pool, water park, water play area, splash pad, spray pad) because Cryptosporidium is chlorine-resistant and can live for days in chlorine-treated water.
• Do not swallow water while swimming in swimming pools, hot tubs, interactive fountains, lakes, rivers, springs, ponds, streams or the ocean.
• Reduce  contamination of treated recreational water venues by having pool operators install in-line secondary disinfection systems (for example, ultraviolet light, ozone) to inactive this chlorine-tolerant parasite.
• Do not drink untreated water from lakes, rivers, springs, ponds, streams, or shallow wells.
• Do not drink inadequately treated water or ice made from water during communitywide outbreaks caused by contaminated drinking water.
• Do not use or drink inadequately treated water or use ice when traveling in countries where the water supply might be unsafe.
• If the safety of drinking water is questionable (for example, outbreak, poor sanitation, lack of water treatment systems):             
• Drink bottled water
• Disinfect it by heating the water to a rolling boil for 1 minute, or
• Use a filter that has been tested and rated by National Safety Foundation (NSF) Standard 53 or NSF Standard 58 for cyst and oocyst reduction; filtered water will need additional treatment to kill or inactivate bacteria and viruses

For more information view the source:Center for Disease Control

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Dipylidium caninum, also called the cucumber tapeworm or the double-pore tapeworm, is a cyclophyllid cestode that infects organisms afflicted with fleas, including canids, felids, and pet-owners, especially children. Adult worms are about 18 inches long. Eggs (or “egg clusters” or “egg balls”) are passed in the host's feces and ingested by fleas, which are in turn ingested by another mammal after the tapeworm larvae partially develop. Examples of fleas that can spread D. caninum include: Ctenocephalides canis and Ctenocephalides felis.

As in all members of family Dipylidiidae, proglottids of the adult have genital pores on both sides (hence the name double-pore tapeworm). Each side has a set of male and female reproductive organs. The scolex has a rostellum with four rows of hooks, along with the four suckers that all cyclophyllid cestodes have. In cats, sometimes proglottids are visible hanging out of a cat's anus.

Inside fleas, eggs hatch and form oncosphere larvae that move through the wall of the flea intestine into the body cavity where they become cysticercoid larvae, which are infective to mammal hosts.

In children, infection causes diarrhea and restlessness. As with most tapeworm infections, the drugs of choice are niclosamide or praziquantel. The best way to prevent human infection is to treat infected animals and to kill fleas.

Although, D. Caninum is usually transferred via a flea, Trichodectes canis, the chewing louse of dogs, can also be the intermediate host for the tapeworm.

FAQs

What is the most common kind of tapeworm dogs and cats get?

The most  common tapeworm of dogs and cats in the United States is called Dipylidium caninum.  Infection is common and found throughout the world.

How did my pet get the Dipylidium tapeworm?

By swallowing a flea infected with a tapeworm larvae. A dog or cat may swallow a flea while self-grooming. Once the flea is digested by the dog or cat, the larval  tapeworm is able to develop into an adult tapeworm.

The adult tapeworm is made up of many small segments, called proglottids, each about the size of a grain of rice. Adult tapeworms may measure 4-28 inches in length. As the tapeworm matures inside the intestine, these segments (proglottids) break off and pass into the stool.

How would I know if my pet has a tapeworm infection?

Although cats and  dogs are rarely ill as a result of a Dipylidium tapeworm  infection, the proglottids can sometimes be seen crawling near the anus or on  the surface of a fresh bowel movement. Proglottids contain tapeworm eggs; these  eggs are released into the environment when the proglottid dries out. The dried  proglottids are small (about 2 mm), hard and yellowish in color and can  sometimes be seen stuck to the fur around the pet's anus.

What kind of problems do tapeworms cause for the dog?

Tapeworms are not  usually harmful to your pet. Weight loss may occur if your pet is heavily  infected. Sometimes, an infected dog will & quot; scoot & quot; or drag its anus  across the ground or carpet because the segments are irritating to the skin in  this area.

Occasionally, a  portion of this tapeworm will be passed when the dog vomits. If this happens, a  worm several inches long may be seen.

How is tapeworm infection diagnosed in my pet?

Tapeworm infection  is usually diagnosed when the moving segments are seen crawling around the anus  or in a bowel movement. Dipylidium tapeworm eggs are  rarely released into the feces and are therefore not usually detected by  routine fecal exams performed by your veterinarian. Because of this,  veterinarians depend on you to notify them of possible tapeworm infection in  your pet.

Can I get a tapeworm infection from my pet?

Yes; however, the risk of infection with this  tapeworm in humans is very low. For a person to become infected with Dipylidium, he or she must  accidentally swallow an infected flea. Most reported cases involve children.  The most effective way to prevent infections in pets and humans is through flea  control. A child who is infected will usually pass proglottids (or what appears  as rice) in a bowel movement or find them stuck to the skin around the anal  area.

How is tapeworm infection treated?

Treatment for both animals and humans is simple and very effective. A prescription drug called praziquantel is given, either orally or by injection (pets only). The medication causes the tapeworm to dissolve within the intestine. Since the worm is usually digested before it passes, it may not be visible in your dog's stool. The drugs are generally well-tolerated.

What should I do if I think my child is infected with tapeworms?

See your health care provider for diagnosis and treatment.

How can tapeworm infection be prevented?

To reduce the likelihood of infection you should:

• Control fleas on your pet, and in their indoor and outdoor environments.
• Have your veterinarian treat your dogs and cats promptly if they have tapeworms.
• Clean up after your pet, especially in playgrounds and public parks. Bury the feces, or place it in a plastic bag and dispose of it in the trash.
• Do not allow children to play in areas that are soiled with pet or other animal feces.
• Teach children to always wash their hands after playing with dogs and cats, and after playing outdoors.

BIOLOGY

Causal Agent:

Dipylidium caninum (the double-pored dog tapeworm) mainly infects dogs and cats, but is occasionally found in humans.

Life Cycle:

Gravid proglottids are   passed intact in the feces or emerge from the perianal region of the host. Subsequently they release typical egg packets. 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 larva develops into an adult, and the adult flea harbours the   infective cysticercoid. The vertebrate host becomes infected by ingesting the adult flea   containing the cysticercoid. The dog is the principal definitive host for Dipylidium   caninum. Other potential hosts include cats, foxes, and humans (mostly   children). 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 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.

Life cycle image and information courtesy of DPDx.

For more information view the source:Center for Disease Control

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The genus Echinococcus includes six species of cyclophyllid tapeworms to date, of the family Taeniidae. Infection with Echinococcus results in hydatid disease, also known as echinococcosis.  Echinococcus is triploblastic, i.e. it has 3 layers- outermost ectoderm, middle mesoderm and inner endoderm. Anus is absent; and no digestive system. Body is covered by tegument and the worm is divided into scolex, short neck and 3-6 proglottids. Body is ribbon-like.  In humans, this causes a disease called echinococcosis. There are 3 types of echinococcosis i.e. cystic echinococcosis caused by Echinococcus granulosus, alveolar echinococcosis caused by E. multilocularis and polycystic echinococcosis caused by E. vogeli and/or E. oligarthrus. Incubation period is usually long and can be up to 50 years. Cystic echinococcosis is mostly found in South and Central America, Africa, the Middle East, China, Italy, Spain, Greece, Russia and the West of the United States (e.g. Arizona, New Mexico and California).  Echinococcosis is a zoonosis; humans are dead-end hosts. The definitive hosts are carnivorous predators - dogs, wolves, foxes, lions. The adult tapeworm lives in their small intestine and delivers eggs that are excreted with the stool. The intermediate hosts are infected by ingesting eggs. Sheep, goat, cattle, camel, pig, wild herbivores and rodents are the usual intermediate hosts, but humans can also be infected.  The egg hatches in the digestive system of the intermediate host, producing planula larva. It penetrates the intestinal wall and is carried by bloodstream to liver, lung, brain or another organ. It settles there and turns into a bladder-like structure called hydatid cyst. From the inner lining of its wall, protoscoleces (i.e. scoleces with invaginated tissue layers) bud and protrude into the fluid that is filling the cyst.  After the death of the normal intermediate host, its body can be eaten by carnivores suitable as definitive hosts. In their small intestine, protoscoleces turn inside out, attach and give rise to adult tapeworms, completing the life cycle.  In humans, the cysts persist and grow for years. They are regularly found in the liver (and every possible organ: spleen, kidney, bone, brain, tongue and skin) and are asymptomatic until their growing size produces symptoms or are accidentally discovered. Disruption of the cysts (spontaneous or iatrogenic e.g. liver biopsy) can be life threatening due to anaphylactic shock.  Cysts are detected with ultrasound, CT or other imaging techniques. Anti-echinococcus antibodies can be detected with serodiagnostic tests e.g. Indirect Fluorescent Antibody (IFA) Test, CF (complement fixation), ELISA, Western Blot and other methods.

For more information view the source:Wikipedia

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HELMINTHS: STRUCTURE, CLASSIFICATION, GROWTH, DEVELOPMENT, PATHOGENESIS, AND DEFENSES

General Concepts

The helminths are worm-like parasites. The clinically relevant groups are separated according to their general external shape and the host organ they inhabit. There are both hermaphroditic and bisexual species. The definitive classification is based on the external and internal morphology of egg, larval, and adult stages.

Flukes (Trematodes)

Adult flukes are leaf-shaped flatworms. Prominent oral and ventral suckers help maintain position in situ. Flukes are hermaphroditic except for blood flukes, which are bisexual. The life-cycle includes a snail intermediate host.

Tapeworms (Cestodes)

Adult tapeworms are elongated, segmented, hermaphroditic flatworms that inhabit the intestinal lumen. Larval forms, which are cystic or solid, inhabit extraintestinal tissues.

Roundworms (Nematodes)

Adult and larval roundworms are bisexual, cylindrical worms. They inhabit intestinal and extraintestinal sites.

Classification

Helminth is a general term for a parasitic worm. The helminths include the Platyhelminthes or flatworms (flukes and tapeworms) and the Nematoda or roundworms.

Characteristics

All helminths are relatively large (> 1 mm long); some are very large (> 1 m long). All have well-developed organ systems and most are active feeders. The body is either flattened and covered with plasma membrane (flatworms) or cylindrical and covered with cuticle (roundworms). Some helminths are hermaphrodites; others have separate sexes.

Epidemiology

Helminths are worldwide in distribution; infection is most common and most serious in poor countries. The distribution of these diseases is determined by climate, hygiene, diet, and exposure to vectors.

Infection

The mode of transmission varies with the type of worm; it may involve ingestion of eggs or larvae, penetration by larvae, bite of vectors, or ingestion of stages in the meat of intermediate hosts. Worms are often long-lived.

Pathogenesis

Many infections are asymptomatic; pathologic manifestations depend on the size, activity, and metabolism of the worms. Immune and inflammatory responses also cause pathology.

Host Defenses

Nonspecific defense mechanisms limit susceptibility. Antibody- and cell-mediated responses are important, as is inflammation. Parasites survive defenses through many evasion strategies.

Introduction

Helminth is a general term meaning worm. The helminths are invertebrates characterized by elongated, flat or round bodies. In medically oriented schemes the flatworms or platyhelminths (platy from the Greek root meaning “flat”) include flukes and tapeworms. Roundworms are nematodes (nemato from the Greek root meaning “thread”). These groups are subdivided for convenience according to the host organ in which they reside, e.g., lung flukes, extraintestinal tapeworms, and intestinal roundworms. This chapter deals with the structure and development of the three major groups of helminths.

Helminths develop through egg, larval (juvenile), and adult stages. Knowledge of the different stages in relation to their growth and development is the basis for understanding the epidemiology and pathogenesis of helminth diseases, as well as for the diagnosis and treatment of patients harboring these parasites.

Platyhelminths and nematodes that infect humans have similar anatomic features that reflect common physiologic requirements and functions. The outer covering of helminths is the cuticle or tegument. Prominent external structures of flukes and cestodes are acetabula (suckers) or bothria (false suckers). Male nematodes of several species possess accessory sex organs that are external modifications of the cuticle. Internally, the alimentary, excretory, and reproductive systems can be identified by an experienced observer. Tapeworms are unique in lacking an alimentary canal. This lack means that nutrients must be absorbed through the tegument. The blood flukes and nematodes are bisexual. All other flukes and tapeworm species that infect humans are hermaphroditic.

With few exceptions, adult flukes, cestodes, and nematodes produce eggs that are passed in excretions or secretions of the host. The various stages and their unique characteristics will be reviewed in more detail as each major group of helminths is considered.

Helminths - worms - are some of the world's commonest parasites (see Ch. 86). They belong to two major groups of animals, the flatworms or Platyhelminthes (flukes and tapeworms) and the roundworms or Nematoda. All are relatively large and some are very large, exceeding one meter in length.

Their bodies have well-developed organ systems, especially reproductive organs, and most helminths are active feeders. The bodies of flatworms are flattened and covered by a plasma membrane, whereas roundworms are cylindrical and covered by a tough cuticle. Flatworms are usually hermaphroditic whereas roundworms have separate sexes; both have an immense reproductive capacity.

The most serious helminth infections are acquired in poor tropical and subtropical areas, but some also occur in the developed world; other, less serious, infections are worldwide in distribution. Exposure to infection is influenced by climate, hygiene, food preferences, and contact with vectors. Many potential infections are eliminated by host defenses; others become established and may persist for prolonged periods, even years. Although infections are often asymptomatic, severe pathology can occur. Because worms are large and often migrate through the body, they can damage the host's tissues directly by their activity or metabolism. Damage also occurs indirectly as a result of host defense mechanisms. Almost all organ systems can be affected.

Host defense can act through nonspecific mechanisms of resistance and through specific immune responses. Antibody-mediated, cellular, and inflammatory mechanisms all contribute to resistance. However, many worms successfully avoid host defenses in a variety of ways, and can survive in the face of otherwise effective host responses.

Flukes (Trematodes)

A dorsoventrally flattened body, bilateral symmetry, and a definite anterior end are features of platyhelminths in general and of trematodes specifically. Flukes are leaf-shaped, ranging in length from a few millimeters to 7 to 8 cm. The tegument is morphologically and physiologically complex. Flukes possess an oral sucker around the mouth and a ventral sucker or acetabulum that can be used to adhere to host tissues. A body cavity is lacking. Organs are embedded in specialized connective tissue or parenchyma. Layers of somatic muscle permeate the parenchyma and attach to the tegument.

Flukes have a well-developed alimentary canal with a muscular pharynx and esophagus. The intestine is usually a branched tube (secondary and tertiary branches may be present) consisting of a single layer of epithelial cells. The main branches may end blindly or open into an excretory vesicle. The excretory vesicle also accepts the two main lateral collecting ducts of the excretory system, which is of a protonephridial type with flame cells. A flame cell is a hollow, terminal excretory cell that contains a beating (flamelike) group of cilia. These cells, anchored in the parenchyma, direct tissue filtrate through canals into the two main collecting ducts.

Except for the blood flukes, trematodes are hermaphroditic, having both male and female reproductive organs in the same individual. The male organ consists usually of two testes with accessory glands and ducts leading to a cirrus, or penis equivalent, that extends into the common genital atrium. The female gonad consists of a single ovary with a seminal receptacle and vitellaria, or yolk glands, that connect with the oviduct as it expands into an ootype. The tubular uterus extends from the ootype and opens into the genital atrium. Both self- and cross-fertilization occur. The components of the egg are assembled in the ootype. Eggs pass through the uterus into the genital atrium and exit ventrally through the genital pore. Fluke eggs, except for those of schistosomes, are operculated (have a lid).

The blood flukes or schistosomes are the only bisexual flukes that infect humans. Although the sexes are separate, the general body structure is the same as that of hermaphroditic flukes. Within the definitive host, the male and female worms inhabit the lumen of blood vessels and are found in close physical association. The female lies within a tegumental fold, the gynecophoral canal, on the ventral surface of the male. The medically important flukes belong to the taxonomic category Digenea. This group of flukes has a developmental cycle requiring at least two hosts, one being a snail intermediate host. Depending on the species, other intermediate hosts may be involved to perpetuate the larval form that infects the definitive human host.

Flukes go through several larval stages, each with a specific name, before reaching adulthood. Taking into account variations among species, a generalized life cycle of digenetic flukes runs the following course. Eggs are passed in the feces, urine, or sputum of humans and reach an aquatic environment. The eggs hatch, releasing ciliated larvae, or miracidia, which either penetrate or are eaten by a snail intermediate host. In rare instances land snails may serve as intermediate hosts. A saclike sporocyst or redia stage develops from a miracidium within the tissues of the snail.

The sporocyst gives rise either to rediae or to a daughter sporocyst stage. In turn, from the redia or daughter sporocyst, cercariae develop asexually and migrate out of the snail tissues to the external environment, which is usually aquatic.

The cercariae, which may possess a tail for swimming, develop further in one of three ways. They either penetrate the definitive host and transform directly into adults, or penetrate a second intermediate host and develop as encysted metacercariae, or they encyst on a substrate, such as vegetation, and develop there as metacercariae. When a metacercarial cyst is ingested, digestion of the cyst liberates an immature fluke that migrates to a specific organ site and develops into an adult worm.

Tapeworms (Cestodes)

As members of the platyhelminths, the cestodes, or tapeworms, possess many basic structural characteristics of flukes, but also show striking differences.

Whereas flukes are flattened and generally leaf-shaped, adult tapeworms are flattened, elongated, and consist of segments called proglottids. Tapeworms vary in length from 2 to 3 mm to 10 m, and may have three to several thousand segments.

Anatomically, cestodes are divided into a scolex, or head, which bears the organs of attachment, a neck that is the region of segment proliferation, and a chain of proglottids called the strobila. The strobila elongates as new proglottids form in the neck region. The segments nearest the neck are immature (sex organs not fully developed) and those more posterior are mature. The terminal segments are gravid, with the egg-filled uterus as the most prominent feature.

The scolex contains the cephalic ganglion, or “brain,” of the tapeworm nervous system. Externally, the scolex is characterized by holdfast organs. Depending on the species, these organs consist of a rostellum, bothria, or acetabula. A rostellum is a retractable, conelike structure that is located on the anterior end of the scolex, and in some species is armed with hooks. Bothria are long, narrow, weakly muscular grooves that are characteristic of the pseudophyllidean tapeworms. Acetabula (suckers like those of digenetic trematodes) are characteristic of cyclophyllidean tapeworms.

A characteristic feature of adult tapeworm is the absence of an alimentary canal, which is intriguing since all of these adult worms inhabit the small intestine. The lack of an alimentary tract means that substances enter the tapeworm across the tegument. This structure is well adapted for transport functions, since it is covered with numerous microvilli resembling those lining the lumen of the mammalian intestine. The excretory system is of the flame cell type.

Cestodes are hermaphroditic, each proglottid possessing male and female reproductive systems similar to those of digenetic flukes. However, tapeworms differ from flukes in the mechanism of egg deposition. Eggs of pseudophyllidean tapeworms exit through a uterine pore in the center of the ventral surface rather than through a genital atrium, as in flukes. In cyclophyllidean tapeworms, the female system includes a uterus without a uterine pore. Thus, the cyclophyllidean eggs are released only when the tapeworms shed gravid proglottids into the intestine. Some proglottids disintegrate, releasing eggs that are voided in the feces, whereas other proglottids are passed intact.

The eggs of pseudophyllidean tapeworms are operculated, but those of cyclophyllidean species are not. Eggs of all tapeworms, however, contain at some stage of development an embryo or oncosphere. The oncosphere of pseudophyllidean tapeworms is ciliated externally and is called a coracidium. The coracidium develops into a procercoid stage in its micro-crustacean first immediate host and then into a plerocercoid larva in its next intermediate host which is a vertebrate. The plerocercoid larva develops into an adult worm in the definitive (final) host. The oncosphere of cyclophyllidean tapeworms, depending on the species, develops into a cysticercus larva, cysticercoid larva, coenurus larva, or hydatid larva (cyst) in specific intermediate hosts. These larvae, in turn, become adults in the definitive host.

Roundworms (Nematodes)

In contrast to platyhelminths, nematodes are cylindrical rather than flattened; hence the common name roundworm. The body wall is composed of an outer cuticle that has a noncellular, chemically complex structure, a thin hypodermis, and musculature. The cuticle in some species has longitudinal ridges called alae. The bursa, a flaplike extension of the cuticle on the posterior end of some species of male nematodes, is used to grasp the female during copulation.

The cellular hypodermis bulges into the body cavity or pseudocoelom to form four longitudinal cords—a dorsal, a ventral, and two lateral cords—which may be seen on the surface as lateral lines. Nuclei of the hypodermis are located in the region of the cords. The somatic musculature lying beneath the hypodermis is a single layer of smooth muscle cells. When viewed in cross-section, this layer can be seen to be separated into four zones by the hypodermal cords. The musculature is innervated by extensions of muscle cells to nerve trunks running anteriorly and posteriorly from ganglion cells that ring the midportion of the esophagus.

The space between the muscle layer and viscera is the pseudocoelom, which lacks a mesothelium lining. This cavity contains fluid and two to six fixed cells (celomocytes) which are usually associated with the longitudinal cords. The function of these cells is unknown.

The alimentary canal of roundworms is complete, with both mouth and anus. The mouth is surrounded by lips bearing sensory papillae (bristles). The esophagus, a conspicuous feature of nematodes, is a muscular structure that pumps food into the intestine; it differs in shape in different species.

The intestine is a tubular structure composed of a single layer of columnar cells possessing prominent microvilli on their luminal surface.

The excretory system of some nematodes consists of an excretory gland and a pore located ventrally in the mid-esophageal region. In other nematodes this structure is drawn into extensions that give rise to the more complex tubular excretory system, which is usually H-shaped, with two anterior limbs and two posterior limbs located in the lateral cords. The gland cells and tubes are thought to serve as absorptive bodies, collecting wastes from the pseudocoelom, and to function in osmoregulation.

Nematodes are usually bisexual. Males are usually smaller than females, have a curved posterior end, and possess (in some species) copulatory structures, such as spicules (usually two), a bursa, or both. The males have one or (in a few cases) two testes, which lie at the free end of a convoluted or recurved tube leading into a seminal vesicle and eventually into the cloaca.

The female system is tubular also, and usually is made up of reflexed ovaries. Each ovary is continuous, with an oviduct and tubular uterus. The uteri join to form the vagina, which in turn opens to the exterior through the vulva.

Copulation between a female and a male nematode is necessary for fertilization except in the genus Strongyloides, in which parthenogenetic development occurs (i.e., the development of an unfertilized egg into a new individual). Some evidence indicates that sex attractants (pheromones) play a role in heterosexual mating. During copulation, sperm is transferred into the vulva of the female. The sperm enters the ovum and a fertilization membrane is secreted by the zygote. This membrane gradually thickens to form the chitinous shell. A second membrane, below the shell, makes the egg impervious to essentially all substances except carbon dioxide and oxygen. In some species, a third proteinaceous membrane is secreted as the egg passes down the uterus by the uterine wall and is deposited outside the shell. Most nematodes that are parasitic in humans lay eggs that, when voided, contain either an uncleaved zygote, a group of blastomeres, or a completely formed larva. Some nematodes, such as the filariae and Trichinella spiralis, produce larvae that are deposited in host tissues.

The developmental process in nematodes involves egg, larval, and adult stages. Each of four larval stages is followed by a molt in which the cuticle is shed. The larvae are called second-stage larvae after the first molt, and so on.

Infection

Transmission of Infection

Helminths are transmitted to humans in many different ways. The simplest is by accidental ingestion of infective eggs (Ascaris, Echinococcus, Enterobius, Trichuris) or larvae (some hookworms). Other worms have larvae that actively penetrate the skin (hookworms, schistosomes, Strongyloides). In several cases, infection requires an intermediate host vector. In some cases the intermediate vector transmits infective stages when it bites the host to take a blood meal (the arthropod vectors of filarial worms); in other cases, the larvae are contained in the tissues of the intermediate host and are taken in when a human eats that host (Clonorchis in fish, tapeworms in meat and fish, Trichinella in meat). The levels of infection in humans therefore depend on standards of hygiene (as eggs and larvae are often passed in urine or feces), on the climate (which may favor survival of infective stages), on the ways in which food is prepared, and on the degree of exposure to insect vectors.

Host Factors Influencing Susceptibility

Human behavior is a major factor influencing susceptibility to infection. If the infective stages of helminths are present in the environment, then certain ways of behaving, particularly with regard to hygiene and food, will result in greater exposure. Because helminths, with few exceptions (Strongyloides, Trichinella, some tapeworm larvae), do not increase their numbers by replication within the same host, the level of infection is directly related to the number of infective stages encountered. Obviously, not every exposure results in the development of a mature infection. Many infective organisms are killed by the host's nonspecific defense mechanisms. Of those that do become established, many are destroyed or eliminated by specific defenses. The number of worms present at any one time therefore represents a dynamic balance between the rate of infection and the efficiency of defense. This balance (which reflects the host's overall susceptibility) is altered by changes in the host's behavior and ability to express forms of defense. Children are more susceptible to many helminths than are adults, and frequently are the most heavily infected members of a community. The waning of immune competence with age may also result in increased levels of infection. Individuals differ genetically in their ability to resist infection, and it is well known that in infected populations, some individuals are predisposed to heavier infections than others. Changes in diet may affect susceptibility, as do the hormonal-immune changes accompanying pregnancy and lactation. An important cause of increased susceptibility is the immune suppression that accompanies concurrent infections with some other pathogens and the development of certain tumors. Similarly, immunosuppressive therapies (irradiation, immunosuppressant drugs) may enhance susceptibility to helminth infection. A particular hazard in immunocompromised patients is the development of disseminated strongyloidiasis, in which large numbers of larvae develop in the body by autoinfection from relatively small numbers of adult Strongyloides stercoralis. It is interesting that the human immunodeficiency virus does not result in an overall increase in susceptibility to helminth infection.

Parasite Factors Influencing Susceptibility

The ability of hosts to control infection is offset by the ability of parasites to avoid the host's defenses and increase their survival. In addition to their ability to evade specific immune defenses (see below), many worms are unaffected by the host's attempts to limit their activities or to destroy them simply because they are large and mobile. Many important species measure several centimeters in length or diameter (Ascaris, hookworms, hydatid cysts, Trichuris) and others may exceed one meter in length (tapeworms). Size alone renders many defense mechanisms inoperative, as does the tough cuticle of adult roundworms. The ability of worms to move actively through tissues enables them to escape inflammatory foci.

Many of the pathogenic consequences of worm infections are related to the size, movement and longevity of the parasites, as the host is exposed to long-term damage and immune stimulation, as well as to the sheer physical consequences of being inhabited by large foreign bodies.

Pathogenesis

Direct Damage from Worm Activity

The most obvious forms of direct damage are those resulting from the blockage of internal organs or from the effects of pressure exerted by growing parasites. Large Ascaris or tapeworms can physically block the intestine, and this may occur after some forms of chemotherapy; migrating Ascaris may also block the bile duct. Granulomas that form around schistosome eggs may block the flow of blood through the liver, and this may lead to pathological changes in that organ and elsewhere. Blockage of lymph flow, leading to elephantiasis, is associated with the presence of adult Wuchereria in lymphatics. Pressure atrophy is characteristic of larval tapeworm infections (hydatid cyst, the larva of Echinococcus granulosus) where the parasite grows as a large fluid-filled cyst in the liver, brain, lungs, or body cavity. The multilocular hydatid cysts caused by Echinococcus multilocularis have a different growth form, metastasizing within organs and causing necrosis. The larvae of Taenia solium, the pork tapeworm, frequently develop in the central nervous system (CNS) and eyes. Some of the neurological symptoms of the resulting condition, called cysticercosis, are caused by the pressure exerted by the cysts.

Intestinal worms cause a variety of pathologic changes in the mucosa, some reflecting physical and chemical damage to the tissues, others resulting from immunopathologic responses. Hookworms (Ancylostoma and Necator) actively suck blood from mucosal capillaries. The anticoagulants secreted by the worms cause the wounds to bleed for prolonged periods, resulting in considerable blood loss. Heavy infections in malnourished hosts are associated with anemia and protein loss. Protein-losing enteropathies may also result from the inflammatory changes induced by other intestinal worms. Diversion of host nutrients by competition from worms is probably unimportant, but interference with normal digestion and absorption may well aggravate undernutrition. The tapeworm Diphyllobothrium latum can cause vitamin B12 deficiency through direct absorption of this factor.

Many helminths undertake extensive migrations through body tissues, which both damage tissues directly and initiate hypersensitivity reactions. The skin, lungs, liver, and intestines are the organs most affected. Petechial hemorrhages, pneumonitis, eosinophilia, urticaria and pruritus, organomegaly, and granulomatous lesions are among the signs and symptoms produced during these migratory phases.

Feeding by worms upon host tissues is an important cause of pathology, particularly when it induces hyperplastic and metaplastic changes in epithelia. For example, liver fluke infections lead to hyperplasia of the bile duct epithelium. Chronic inflammatory changes around parasites (for example, the granulomas around schistosome eggs in the bladder wall) have been linked with neoplasia, but the nature of the link is not known. The continuous release by living worms of excretory-secretory materials, many of which are known to have direct effects upon host cells and tissues, may also contribute to pathology.

Indirect Damage from Host Response

As with all infectious organisms, it is impossible to separate the pathogenic effects caused strictly by mechanical or chemical tissue damage from those caused by the immune response to the parasite. All helminths are “foreign bodies” not only in the sense of being large and invasive but also in the immunologic sense: they are antigenic and therefore stimulate immunity. An excellent illustration of this interrelation between direct and indirect damage is seen in the pathology associated with schistosome infections, especially with Schistosoma mansoni. Hypersensitivity- based,granulomatous responses to eggs trapped in the liver cause a physical obstruction to blood flow, which leads to liver pathology. Hypersensitivity-based inflammatory changes probably also contribute to the lymphatic blockage associated with filarial infections (Brugia, Wuchereria).

Immune-mediated inflammatory changes occur in the skin, lungs, liver, intestine, CNS, and eyes as worms migrate through these structures. Systemic changes such as eosinophilia, edema, and joint pain reflect local allergic responses to parasites. The pathologic consequences of immune-mediated inflammation are seen clearly in intestinal infections (especially Strongyloides and Trichinella infections). Structural changes, such as villous atrophy, develop. The permeability of the mucosa changes, fluid accumulates in the gut lumen, and intestinal transit time is reduced. Prolonged changes of this type may lead to a protein-losing enteropathy. The inflammatory changes that accompany the passage of schistosome eggs through the intestinal wall also cause severe intestinal pathology. Heavy infections with the whipworm Trichuris in the large bowel can lead to inflammatory changes, resulting in blood loss and rectal prolapse.

The severity of these indirect changes is a result of the chronic nature of the infection. The fact that many worms are extremely long-lived means that many inflammatory changes become irreversible, producing functional changes in tissues. Three examples are the hyperplasia of bile ducts in long-term liver fluke infections, the extensive fibrosis associated with chronic schistosomiasis, and the skin atrophy associated with onchocerciasis. Severe pathology may also result when worms stray into abnormal body sites.

Defenses Against Infection

Nonspecific Resistance

Infective stages attempting to enter via the mouth or through the skin are opposed by the same non-specific defenses that protect humans from invasion of other pathogens. Following oral ingestion, parasites must survive passage through the acid stomach to reach the small bowel. The natural parasites of humans are adapted to do this, but opportunistic parasites may be killed. Similarly, natural parasites are adapted to the environmental conditions of the bowel (and in many cases require them as cues for development), but accidental parasites may find them inappropriate. Penetration into the intestinal wall may trigger inflammatory responses that immobilize and kill the worm. This may itself lead to serious pathology (as in Anisakis infection). Worms entering through the skin must survive the skin secretions, penetrate the epidermal layers, and avoid inflammatory trapping in the dermis. Invasion of humans by the larvae of dog and cat hookworms (Ancylostoma spp.) results in dermatitis and “creeping eruption” as the worms become the focus of inflammatory reactions that form trails in the skin.

Once in the tissues, worms need the correct sequence of environmental signals to mature. Absent or incomplete signals constitute a form of nonspecific resistance that may partially or completely prevent further development. The parasite may not die, however; indeed, prolonged survival at a larval stage may result in pathology from the continuing inflammatory response (e.g. Toxocara infection).

Specific Acquired Immunity

There is no doubt that specific immunity is responsible for the most effective forms of host defense, although the dividing line between nonspecific and specific mechanisms is difficult to draw with precision. All helminths stimulate strong immune responses, which can easily be detected by measuring specific antibody or cellular immunity. Although these responses are useful for diagnosing infection, they frequently appear not to be protective. The high prevalence of helminth infection in endemic areas (sometimes approaching 100 per cent), and the fact that individuals may remain infected for many years and can easily be reinfected after they are cured by chemotherapy, suggest that protective immunity against helminths is weak or absent in humans. However, some degree of immunity does appear to operate, because the intensity of infection often declines with age, and many individuals in endemic areas remain parasitologically negative and/or clinically normal. Evidence from laboratory studies provides some clues as to the mechanisms involved. Antibodies that bind to surface antigens may focus complement- or cell-mediated effectors that can damage the worm. Macrophages and eosinophils are the prime cytotoxic effector cells, and IgM, IgG and IgE are the important immunoglobulins. Antibodies may also block enzymes released by the worm, thus interfering with its ability to penetrate tissues or to feed. Inflammatory changes may concentrate effector cells around worms, and the release of cellular mediators may then disable and kill the worm. Encapsulation of trapped worms by inflammatory cells may also result in the death of the worm, although this is not always the case. Intestinal worms can be dislodged by the structural and physiologic changes that occur in the intestine during acute inflammation. It has long been suspected that IgE-mediated hypersensitivity reactions, involving mast cells and basophils, contribute to this process, but the evidence is still circumstantial. Despite the abundance of IgA in the intestinal lumen, there is no conclusive evidence that it is involved in protective immunity in humans, although some field and laboratory data suggest it is.

Avoidance of Host Defenses

Despite their immunogenicity, many helminths survive for extended periods in the bodies of their hosts. Some of the reasons have already been mentioned (size, motility), but we now know that worms employ many sophisticated devices to render host defenses ineffective. Some worms (schistosomes) disguise their outer surface by acquiring host molecules which reduce their antigenicity; intrinsic membrane changes also make these worms resistant to immune attack. Filarial nematodes acquire serum albumin on their cuticle, which may act as a disguise. Many worms release substances that depress lymphocyte function, inactivate macrophages, or digest antibodies. Larval cestodes appear to prolong their survival by producing anticomplement factors which protect their outer layers from lytic attack. Antigenic variation in the strict sense is not known to occur, but many species show a stage-specific change of antigens as they develop, and this phenomenon may delay the development of effective immune mechanisms. All helminths release relatively large amounts of antigenic materials, and this voluminous production may divert immune responses or even locally exhaust immune potential. Irrelevant antibodies produced by the host may block the activity of potentially protective antibodies, as has been shown to be the case in schistosome infections.

It is striking that many helminth infections are associated with a degree of immune suppression, which may affect specific or general responsiveness. Many explanations have been proposed for this immune suppression, including antigen overload, antigenic competition, induction of suppressor cells, and production of lymphocyte-specific suppressor factors. Reduced immune responsiveness may not only prolong the survival of the original infecting worm species but increase the host's susceptibility to other pathogens. Epidemiologic evidence also raises the possibility that infections acquired early in life—before or shortly after birth—may induce a form of immune tolerance, allowing heavy worm burdens to accumulate in the body.

The subtlety with which parasitic worms manipulate the host's immune system not only increases their importance as pathogens but also creates formidable problems for their control and eradication.

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Cystoisospora is a genus of parasitic protozoa belonging to the phylum Apicomplexa.

TAXONOMY

This genus was originally created by Frenkel in 1977. Its use was discontinued but was resurrected in 2005 by Barta et al. This genus is currently used to group species that have tetrasporozoic, diplosporocystic oocysts without Stieda bodies in their sporocysts. These species infect the entrocytes of mammals and are transmitted by the orofaecal route.  DNA analysis has shown that this genus belongs to the family Sarcocystidae.  The type species of this genus is Cystoisospora felis Wenyon 1923.

LIFE CYCLE

These parasite has been isolated from dogs, cats and raccoons. C. belli has been isolated from immunosuppressed humans - particularly those with HIV infection.  These parasites normally infect the entrocytes of the small intestine and are spread by the orofaecal route. The definitive hosts are cats but other species including various species of rodents may be infected. No further development occurs in these paratenic hosts and the parastites remain dormant until ingested by a definitive host.

EPIDEMIOLOGY

This genus has been recorded worldwide. C. felis and C. rivolta occur in up to 40% of cats in some tropical countries.

CLINICAL

Clinical signs include watery diarrhoea, vomiting, fever and weight loss. The diagnosis is made by microscopic examination of the stool. Distinguishing between the species of Cystoisospora is most easily done with PCR. This method can also be used to make the diagnosis.  Treatment is based on trimethoprim-sulfonamides with clindamycin or toltrazuril for resistant strains.

PREVENTION

Hygiene on the premises is important in prevention. Good litter tray hygiene is also critical in multi-cat households. Utensils, runs, cages and other implements should be steam-cleaned or washed in boiling water. Because of the importance of paratenic hosts such as cockroaches, insect control is critical. 

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Taenia is a genus of tapeworm that includes some important parasites of livestock. Members of the genus are responsible for taeniasis and cysticercosis in humans. There are more than 100 species recorded. They are morphologically characterized by a ribbon-like body composed of a series of segments called proglottids; hence the name Taenia (Greek tainia meaning ribbon, bandage or stripe). The anterior end of the body is the scolex. Not all members of the genus Taenia have an armed scolex (hooks and/or spines located in the "head" region), for example, Taenia saginata has an unarmed scolex, while Taenia solium has an armed scolex.  Proglottids have central ovary, with a vitellarium (yolk gland) posterior to it. As in all cyclophyllid cestodes, there is genital pore on the side of the proglottid. Eggs are released when proglottid deteriorates, and so a uterine pore is unnecessary.

SELECTED SPECIES

Taenia asiatica  Asian Taenia. Humans as definitive hosts, pigs and rarely cattle, as intermediate hosts. Taenia crassiceps Taenia gonyamai, parasite of antelope (larval-) and lions (adult forms). Taenia mustelae, which infects small carnivorans. Taenia pisiformis, which is common in wild dogs and in rabbits, who serve as intermediate hosts. Taenia rileyi, which infects bobcats. Taenia saginata  beef tapeworm. Infects cattle and humans, and can only reproduce while in the human gut. Taenia solium  Pork Tapeworm. Like T. saginata humans serve as its primary host, and it can only reproduce by the dispersal of proglottids while in the gut. These reinfect pigs when human faeces is improperly disposed of. This infection is most common in parts of Africa. Taenia taeniaeformis, which uses rodents as intermediate hosts and then inhabits cats as the definitive host.

LIFE CYCLE

The life cycle begins with either the eggs or the gravid proglottids being passed in the feces, which can last for days to months in the environment (1). Then, cattle or pigs ingest the contaminated vegetation with eggs or proglottids (2). The oncospheres hatch in the small intestine of the cattle or pig (3) and invade the intestinal wall to travel to the striated muscles to develop into cysticerci. Humans can become infected when eating raw beef or pork meat (4). In the human, the cysticercus develop into adults in two months in the intestines. Using their scolex, they attach to the small intestine (5) where they reside(6). Taenia saginata are about 1,000-2,000 proglottids long with each gravid proglottid containing 100,000 eggs, while Taenia solium contain about 1,000 proglottids with each gravid proglottid containing 50,000 eggs.

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Taenia solium, also called the pork tapeworm, is a cyclophyllid cestode in the family Taeniidae. It infects pigs and humans in Asia, Africa, South America, parts of Southern Europe and pockets of North America. In the larval stage, it causes cysticercosis which is a major cause of seizures in humans. Like all cyclophyllid cestodes, T. solium has four suckers on its scolex ("head"). T. solium also has two rows of hooks.

DESCRIPTION

T. solium is normally 2 m to 3 m in length, but can become very large, over 50 m long in some situations. T. solium has a very similar life cycle to Taenia saginata. Cysticerci have three morphologically distinct types. The common one is the ordinary "cellulose" cysticercus which has a fluid filled bladder that is 0.5 cm to 1.5 cm in length and an invaginated scolex. The intermediate form has a scolex while the "racemose" has no evident scolex but are believed to be larger and much more dangerous. They are 20 cm in length and have 60 ml of fluid and 13% of patients might have all three types in the brain. Humans are usually infected through eating infected pork, fostering adult tapeworms in the intestine, and passing eggs through feces, but autoinfection is also possible. In that case, a cysticercus (a larva sometimes called a "bladder worm") develops in the human and the human acts like an intermediate host. This happens if eggs get to the stomach, usually as a result of contaminated hands, but also due to retroperistalsis. Cysticerci often occur in the central nervous system, which can cause major neurological problems like hydrocephalus, paraplegy, meningitis, convulsions and even death. The condition of having cysticerci in one's body is called cysticercosis. Eggs can be diagnosed only to the family level, but if a proglottid's uterus is stained with India ink, the number of visible uterine branches can help identify the species: unlike the Taenia saginata uteri, T. solium uteri have only five to ten uterine branches on each side. Infection with T. solium adults is treated with niclosamide, which is one of the most popular drugs for adult tapeworm infections, as well as for fluke infections. As cysticercosis is a major risk, it is important to wash one's hands before eating and to suppress vomiting if a patient may be infected with T. solium. If neurocysticercosis occurs the drug of choice is either albendazole or praziquantel. These drugs damage the parasites skin internally causing it to disintegrate and is then removed by the host's immune system. Infection may be prevented with proper disposal of human feces around pigs, cooking meat thoroughly and/or freezing the meat at -10 ?C for 5 days. Most cases occur because infected food handlers contaminate the food.

PATHOGENESIS

Ingestion of T. solium eggs or proglottid rupture within the host intestine can cause larvae to migrate into host tissue and cause cysticercosis. This is the most frequent and severe disease caused by T. solium. In symptomatic cases, a wide spectrum of symptoms may be expressed including headaches, dizziness and occasional seizures. In more severe cases, dementia or hypertension due to perturbation of the normal circulation of cerebrospinal fluid can occur. The severity of cysticercosis depends on location, size and number of parasite larvae in tissues, as well as the host immune response. Other symptoms include sensory deficits, involuntary movements and brain system dysfunction. In children ocular location of cysts is more common than cystation in other locations of the body. If a person is heavily infected with T. solium, it can lead to neurocysticercosis which can lead to epilepsy, seizures, lesions in the brain, blindness and tumor like growths. This kind of patient will also show the low level of eosinophils when they run the blood test.

DIAGNOSIS

Diagnosis requires biopsy of the infected tissue and examination of feces. T. solium eggs and proglottids found in feces diagnoses taeniasis and not cysticercosis. Cysticercosis is diagnosed primarily on confirming the presence of hooks on the scolex of T. solium. Radiological test such as X-ray, CT scans which demonstrate "ring-enhancing brain lesions", and MRIs can also be used to detect diseases. X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues and CT scans and MRIs are used to find lesions in the brain.

TREATMENT

PZQ (praziquantel) is the drug of choice for the treatment of T. solium infection. Some consider Niclosamide to be the drug of choice for all types of Tapeworms. For cysticercosis, one can be treated with albendazole combining with steroid to reduce the inflammation. Surgical intervention may be necessary to treat CNS lesions. Albendazole appears to be more effective and a safe drug for Neurocysticercosis, infection of the brain with T. solium larvae.

PREVENTION AND CONTROL

The best way to avoid getting tapeworms is to not eat under-cooked pork. Moreover, a high level of personal hygiene and prevention of fecal contamination of pig foods also plays a major role in prevention of getting the parasites.

EPIDEMIOLOGY

T. solium is found worldwide, however, it has shown to be more common in cosmopolitan areas. Because pigs are intermediate hosts of the parasite, completion of the life cycle occurs in regions where humans live in close contact with pigs and eat undercooked pork. Cysticercosis is often seen in areas where poor hygiene allows for contamination of food, soil or water supplies. Prevalence rates in the United States have shown that immigrants from Mexico, Central and South America and South-east Asia account for most of the domestic cases of cysticercosis. Taeniasis and cysticercosis are very rare in predominantly Muslim countries, as Islam forbids the consumption of pork. It is important to note that human cysticercosis is acquired by ingesting T. solium eggs shed in the feces of a human tapeworm carrier via gravid proglottids, and thus can occur in populations that neither eat pork nor share environments with pigs, although, as stated, the completion of the life cycle can occur only where humans live in close contact with pigs and eat pork. In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions which were found to have been caused by cysticercosis from T. solium. In keeping with their religion, none of the patients ate pork; additionally, none had any history of recent foreign travel. Several immediate family members of these four patients with seizures were found to have cysticercus antibodies. The families of the four patients had all employed housekeepers from Latin American countries, and one of the housekeepers tested positive for cysticercus antibodies, leading to the conclusion that the housekeepers were the most likely source of the infections.

LIFE CYCLE

This infection is caused by ingestion of eggs shed in the feces of a human tapeworm carrier. Pigs and humans become infected by ingesting eggs or gravid proglottids. Humans are infected either by ingestion of food contaminated with feces containing eggs, or by autoinfection. In the latter case, a human infected with adult T. solium can ingest eggs produced by that tapeworm, either through fecal contamination or, possibly, from proglottids carried into the stomach by reverse peristalsis. Once eggs are ingested, oncospheres hatch in the intestine, invade the intestinal wall, and migrate to striated muscles, as well as the brain, liver, and other tissues, where they develop into cysticerci. In humans, cysts can cause serious sequelae if they localize in the brain, resulting in neurocysticercosis. The parasite life cycle is completed, resulting in human tapeworm infection, when humans ingest undercooked pork containing cysticerci. Cysts evaginate and attach to the small intestine by their scolex. Adult tapeworms develop, (up to 2 to 7 m in length and produce less than 1000 proglottids, each with approximately 50,000 eggs) and reside in the small intestine for years.

 

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Toxascaris leonina is a common parasitic roundworm found in dogs, cats, foxes, and related host species. Toxascaris leonina, or T. leonina, is an ascarid nematode, a worldwide distributed helminth parasite which is in a division of eukaryotic parasites that, unlike external parasites such as lice and fleas, live inside their host. The definitive hosts of T. leonina include canids (dogs, foxes, etc.) and felines (cats), while the intermediate hosts are usually rodents, such as mice or rats. Infection occurs in the definitive host when the animal eats an infected rodent. While T. leonina can occur in either dogs or cats, it is far more frequent in cats.

LIFE CYCLE

The life cycle of T. leonina is fairly simple. Eggs are ingested and hatch in the small intestine. The juveniles then penetrate the mucosal lining of the small intestine. After growth and molt, they return to the intestinal lumen and mature. The adult female worm lays eggs which are passed in the feces of the dog. The eggs become infective after 3–6 days in the environment. Rodents are usually the intermediate hosts of T. leonina. The rodent ingests the eggs and, once the eggs are hatched, the larvae migrate through the tissues of the rodent. The definitive host is then infected with this parasite when it eats an infected rodent.  The egg of the T. leonina is usually more oval than round. The prepatent period for T. leonina is two to three months. The adult worms are usually 3-4 inches long and can be seen in the feces and vomit of the animal.  Toxascaris leonina differs from other Toxocara in that the larvae do not migrate through the lungs; but rather, the entire developmental cycle occurs in the gut.

SYMPTOMS OF INFECTION

Roundworms absorb the nutrients from the animal, which can interfere with digestion and can also damage the lining of the intestine. Animals may not show any outward symptoms of roundworms at all, or in other, usually more severe cases, animals may have diarrhea, vomiting, loss of appetite, experience thinning, dull coats, and in puppies or kittens, can develop distended abdomens, or "pot-belly" appearance.  Infection symptoms are similar to infection by other Toxacara species (T. canis, T. cati). It is a common cause of diarrhea in young animals and can cause vomiting as well. Sometimes the worms themselves are vomited up, which can be alarming as they can be quite large with females reaching lengths of up to seven inches. The worms consume the host's food and can lead to lethargy and a classical pot-bellied appearance. Extreme cases of severe infections can lead to pneumonia as the worms migrate, and if there are enough worms the intestine can become obstructed.

PREVENTION AND TREATMENT

It is recommended to de-worm all puppies and kittens at 6 weeks and repeat treatment 2–4 weeks after the first treatment. T. leonina roundworm infections are treated with the same medication protocol as the T. canis or T. cati roundworm infections (see Toxocariasis). Therefore, when eggs are seen on a fecal flotation exam, or fecal swab, it is not necessary to determine which species is present. Roundworm infections are treated with medication, called "de-wormers", and includes such drugs as fenbendazole, pyrantel, milbemycin oxime, and piperazine.  To prevent reinfection of parasitic roundworms, it is recommended that anything that the animal has been in contact with should be cleaned thoroughly or replaced, including bedding and kennels. It is also strongly recommended that outside areas where defecation may occur be cleaned, as well as all feces removed daily from outdoor pet runs, crates, and the yard.

RISK IN HUMANS

Humans are usually not infected with T. leonina; however, this parasite has been found in humans in a few instances and is a cause of visceral larva migrans in children, though less frequently implicated than is Toxocara canis, the most common roundworm parasite found in dogs.

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Toxocara canis (also known as dog roundworm) is worldwide distributed helminth parasite of dogs and other canids. T. canis are gonochorists, adult worms measure from 9 to 18 cm, are yellow-white in color, and occur in the intestine of the definitive host. In adult dogs, the infection is usually asymptomatic. By contrast, massive infection with T. canis can be fatal in puppies. As paratenic hosts, a number of various vertebrates, including humans, and some invertebrates can become infected. Humans are infected, like other paratenic hosts, by ingestion of embryonated T. canis eggs. The disease caused by migrating T. canis larvae (toxocariasis) results in two syndromes: visceralis larva migrans and ocularis larva migrans. Owing to transmission of the infection from bitches to puppies, preventive anthelmintic treatment of newborn puppies is strongly recommended. Several antihelmintic drugs are effective against adult worms, for example pyrantel, fenbendazole, selamectine etc.

MOPHOLOGY

Adult T. canis have round body with spiky cranial and caudal part, covered by yellow cuticula. Cranial part of the body contains two lateral alae (length 2.5 mm, width 0.2 mm). Male worms measure 9-13 - 0.2-0.25 cm and female worms 10-18 - 0.25-0.3 cm. T. canis eggs have oval or spherical shape with granulated surface, thick-walled, and measures from 72 to 85 -m.

LIFE CYCLE

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 bitches prenatal infection can occur, where larvae become mobilized (at approximately three weeks prior to parturition) and migrate to the lungs of the foetus, here molting 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 certain 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.

TRANSMISSION TO HUMANS

A 2003 study found that humans can be infected by this roundworm, a condition called toxocarosis, just by stroking an infected dog's fur. In humans, this parasite usually grows in the back of the eye, which can result in blindness, or in the liver or lungs. However, a 2004 study showed that, of 15 infected dogs, only 7 had eggs in their coat, and that no more than one egg was found on each dog. Furthermore, only 4% of those eggs were infectious. Given the low concentration of fertile eggs on infected dogs' coats (less than 0.00186% per gram), it is plausible that such eggs were transferred to the dog's coat by contact with fecal deposites in the environment, making dog coats be passive transport hosts.  The risk of being infected by petting a dog is extremely limited and, since a single infected puppy can produce more than 100,000 roundworm eggs per gram of feces, humans are much more likely to be infected by contact with feces than contact with fur. As such, there is little reason for humans to fear infection as long as basic hygiene, like hand-washing, is followed.  There are several treatments, all of which are cheap and easily-accessible by the average dog owner, than can prevent a dog from becoming infected or rid an infected pet of its roundworm parasites. 

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Toxoplasma gondii is a species of parasitic protozoa in the genus Toxoplasma.  The definitive host of T. gondii is the cat, but the parasite can be carried by many warm-blooded animals (birds or mammals, including humans). Toxoplasmosis, the disease of which T. gondii is the causative agent, is usually minor and self-limiting but can have serious or even fatal effects on a fetus whose mother first contracts the disease during pregnancy or on an immunocompromised human or cat. 

LIFE CYCLE

The life cycle of T. gondii has two phases. The sexual part of the life cycle (coccidia like) takes place only in cats, both domestic and wild (family Felidae), which makes cats the parasite's primary host. The second phase, the asexual part of the life cycle, can take place in other warm-blooded animals, including cats, mice, humans, and birds. The hosts in which asexual reproduction takes place is called the intermediate host. Rodents are the typical intermediate host. In both kinds of hosts, the Toxoplasma parasite invades cells and forms a space called a vacuole. Inside this specialized vacuole, called a parasitophorous vacuole, the parasite forms bradyzoites, which are the slowly replicating versions of the parasite. The vacuoles containing the reproductive bradyzoites form cysts mainly in the tissues of the muscles and brain. Since the parasites are inside cells, they are safe from the host's immune system, which does not respond to the cysts.  Toxoplasma's resistance to anti-toxoplasmosis medication varies, but the cysts are very difficult to eradicate entirely. Inside the vacuoles, T. gondii replicates itself (by endodyogeny) until the infected cell fills with parasites and bursts, releasing tachyzoites, the motile, asexually reproducing form of the parasite. Unlike the bradyzoites, the free tachyzoites are usually efficiently cleared by the host's immune system, although some of them manage to infect cells and form bradyzoites, thus maintaining the infection.  Tissue cysts are ingested by a cat (e.g., by feeding on an infected mouse). The cysts survive passage through the stomach of the cat and the parasites infect epithelium of the small intestine where they undergo sexual reproduction and oocyst formation. Oocysts are shed with the feces. Animals and humans that ingest oocysts (e.g., by eating unwashed vegetables) or tissue cysts in improperly cooked meat become infected. The parasite enters macrophages in the intestinal lining and is distributed via the blood stream throughout the body.  Similar to the mechanism used in many viruses, Toxoplasma is able to dysregulate host’s cell cycle by holding cell division before mitosis (the G2/M border). This dysregulation of the host’s cell cycle is caused by a heat-sensitive secretion (with a molecular mass larger than 10 kDa). Infected cells secrete the factor which inhibits the cell cycle of neighboring cells. The reason for Toxoplasma’s dysregulation is unknown, but studies have shown that infection is preferential to host cells in the S-phase and host cell structures with which Toxoplasma interacts may not be accessible during other stages of the cell cycle.  Acute stage Toxoplasma infections can be asymptomatic, but often give flu-like symptoms in the early acute stages, and like flu can become, in very rare cases, fatal. The acute stage fades in a few days to months, leading to the latent stage. Latent infection is normally asymptomatic; however, in the case of immunocompromised patients (such as those infected with HIV or transplant recipients on immunosuppressive therapy), toxoplasmosis can develop. The most notable manifestation of toxoplasmosis in immunocompromised patients is toxoplasmic encephalitis, which can be deadly. If infection with T. gondii occurs for the first time during pregnancy, during an activity such as changing cat litter of a cat infected with T. gondii (uptake of cyst by inhalation, followed by ingestion as the mucus is cleared), the parasite can cross the placenta, possibly leading to hydrocephalus or microcephaly, intracranial calcification, and chorioretinitis, with the possibility of spontaneous abortion (miscarriage) or intrauterine death. An in vitro study showed that ivermectin significantly inhibited T. gondii replication.

EPIDEMIOLOGY

The rates of positive sero-prevalence in women at child-bearing age between 1990 and 2000 were 58% in Central European countries, 51–72% in several Latin-American countries and 54–77% in West African countries. Low seroprevalence, 4–39%, was reported in southwest Asia, China and Korea as well as in cold climate areas such as Scandinavian countries (11–28%).  T. gondii has also been linked to pre-natal depression, as well as increased anxiety and depression during pregnancies. It has also been linked with mood disturbances in nonpregnant populations, including schizophrenia and suicidal behavior.

TOXOPLASMOSIS

T. gondii infections have the ability to change the behavior of rats and mice, making them drawn to, rather than fearful of, the scent of cats. This effect is advantageous to the parasite, which will be able to sexually reproduce if its host is eaten by a cat. The infection is widespread in the brain, with more cysts targeting the parts of the brain corresponding to fear. The widespread nature of the infection causes many previously unnoticed symptoms in the rats.  Studies have also shown behavioral changes in humans, including lower reaction times and a sixfold increased risk of traffic accidents among infected, RhD-negative males, as well as links to schizophrenia including hallucinations and reckless behavior. Recent epidemiologic studies by Stanley Medical Research Institute and Johns Hopkins University Medical Center indicate that infectious agents may contribute to some cases of schizophrenia.  A study of 191 young women in 1999 reported higher intelligence and higher guilt proneness in Toxoplasma-positive subjects.  The prevalence of human infection by Toxoplasma varies greatly between countries. Factors that influence infection rates include diet (prevalence is possibly higher where there is a preference for less-cooked meat) and proximity to cats.  According to Merck the standard treatment for toxoplasmosis is pyrimethamine, but most immunocompetent asymptomatic people infected with T. gondii, with the exception of neonates and pregnant women, require no treatment.

HISTORY

The organism was first described in 1908 in Tunis by Charles Nicolle and Louis Manceaux within the tissues of the gundi (Ctenodactylus gundi). In the same year it was also described in Brazil by Alfonso Splendore in rabbits.  

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Trematodes

Definition: Trematoda is a class within the phylum Platyhelminthes that contains two groups of parasitic flatworms, commonly referred to as "flukes".

• Schistosoma

• Fasciola

• Paragonimus westermani

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Trichuris vulpis is whipworm that lives in the large intestine of canines in its adult stages. Out of different types of worms, Trichuris vulpis is one of the smaller worms with a size ranging from 30-50 mm in length . As the name suggests, the worm has a whip-like shape with distinct features including a small, narrow anterior head, which is the digestive part of the worm, and a larger posterior tail, which is the reproductive part of the worm. Eggs from T. vulpis are oval shaped with bipolar plugs and contain a thick outer shell. Their sizes range from 72-90 um in length and 32-40 um in width. Because of their thick outer shell, T. vulpis eggs are very resistant to environmental extremes such as freezing or hot temperatures, thus allowing for their long viability in the outside world. 

LIFE CYCLE

The life cycle of Trichuris vulpis begins with the adult whipworms living in the large intestines of dogs. T. vulpis lay many eggs in the large intestine and are released in the feces into the outside environment. When eggs are released into the outside environment, these unembryonated eggs are able to form embryos in the soil in about 2-4 weeks, at which point they become infective when ingested by the new host . An infective larva develops within the egg before it is even ingested by the new host.  Another canine becomes a new host by ingesting the egg containing the larva. Once ingested, the egg gets into the small intestine where it hatches to release its larva. The larvae invade the small intestinal mucosa and remain there for about 15 days. Afterward, the larva then travel from the small intestine into the large intestine where they go through several stages to become an adult whipworm in the large intestine. Once an adult, their whip-like shape containing a narrow anterior head allows them to burrow through the large intestinal walls while their posterior reproductive end protrudes them into the lumen. Adult whipworms live inside the cecum, colon, and rectum for about three months before they lay eggs intermittently to be released in feces where they can become infective to another host.

EPIDEMIOLOGY

T. vulpis infects canines worldwide. In the United States, it has been reported that 14.3% of shelter dogs are infected with this parasite . Though rare, there are some cases of human infection. The eggs of T. vulpis are prevalent in shady moist soil areas that have been contaminated by canine feces.

PATHOLOGY AND SYMPTOMS

Because 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 canines blood, tissue fluid, and mucosal epithelium. Severe infections include symptoms such as bloody diarrhea, weight loss, dehydration, and anemia, and in extreme cases, death.

DIAGNOSIS

Infection of this parasite can be confirmed with detection of eggs in the canines feces. However, this is difficult because egg production is usually small, its shedding is periodic, and its structure is dense which prevents from floating. Symptoms may appear before the eggs are shed in the feces due to the long prepatent period.

PREVENTION AND CONTROL

Keeping canines away from contaminated areas, especially areas where there are feces can prevent them from contracting T. vulpis. There is no effective way to kill the parasite's eggs in the soil, so it is might be necessary to replace the soil and cleaning out litter boxes and kennels frequently. People cleaning these areas should wear gloves and wash their hands after task.  Dogs should have fecal examinations and deworming as necessary. If a dog is detected to be infected with T. vulpis, it should be treated immediately to prevent infection of other dogs. 

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Uncinaria stenocephala is a nematode that parasitizes dogs, cats, and foxes as well as humans. It is rare to find in cats in the United States. The common name is the northern hookworm of dogs.

LIFE CYCLE

The host ingests an infective third stage larva. The larva matures to the adult in the small intestine. Eggs are laid in the small intestine and pass out with the feces. The prepatent period is about 15 to 17 days. The eggs hatch in the soil and the larvae molt twice to reach the infective third-stage.  Adult worms may live for 4 to 24 months in the small intestine. Dog and cat hookworms range in size from 10 to 20 mm by 0.4 to 0.5 mm and the eggs are 71 to 93 m by 35 to 58 m.  Adult parasites are most often found in their hosts' small intestine.

DIAGNOSIS

Diagnostic Stage:

Eggs are found in fecal flotation. Eggs measure 75 um long by 45 um wide.

Common Diagnostic Test:

Fecal float to recover eggs.

Clinical Signs:

All hookworms suck blood, they are capable of removing 0.1mls of blood per worm, per 24 hour period. Light infections are asymptomatic. Infected pups may present with pale mucus membranes and anemia, ill thrift, failure to gain weight, poor hair coat, dehydration, and dark, tarry diarrhea (melena). Puppies harboring many worms will develop an acute normocytic, normochromic anemia followed by hypochromic, microcytic anemia due to iron deficiency. Without immediate intervention, these animals may die of the infection. Those that survive may continue as "poor doers" with chronic anemia. 

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Wuchereria bancrofti is a parasitic filarial nematode (roundworm) spread by a mosquito vector. It is one of the three parasites that cause lymphatic filariasis, an infection of the lymphatic system by filarial worms. It affects over 120 million people, primarily in Africa, South America, and other tropical and subtropical countries. If the infection is left untreated, it can develop into a chronic disease called elephantiasis. Limited treatment modalities exist and no vaccines have been developed.

BIOLOGY

CAUSAL AGENTS

Filariasis is caused by nematodes (roundworms) that inhabit the lymphatics and subcutaneous tissues.  Eight main species infect humans.  Three of these are responsible for most of the morbidity due to filariasis: Wuchereria bancrofti and Brugia malayi cause lymphatic filariasis, and Onchocerca volvulus causes onchocerciasis (river blindness).  The other five species are Loa loa, Mansonella perstans, M. streptocerca, M. ozzardi, and Brugia timori.  (The last species also causes lymphatic filariasis.)

LIFE CYCLE

Infective larvae are transmitted by infected biting arthropods during a blood meal.  The larvae migrate to the appropriate site of the host's body, where they develop into microfilariae-producing adults.  The adults dwell in various human tissues where they can live for several years.  The agents of lymphatic filariasis reside in lymphatic vessels and lymph nodes; Onchocerca volvulus in nodules in subcutaneous tissues; Loa loa in subcutaneous tissues, where it migrates actively; Brugia malayi in lymphatics, as with Wuchereria bancrofti; Mansonella streptocerca in the dermis and subcutaneous tissue; Mansonella ozzardi apparently in the subcutaneous tissues; and M. perstans in body cavities and the surrounding tissues.  The female worms produce microfilariae which circulate in the blood, except for those of Onchocerca volvulus and Mansonella streptocerca, which are found in the skin, and O. volvulus which invade the eye.  The microfilariae infect biting arthropods (mosquitoes for the agents of lymphatic filariasis; blackflies [Simulium] for Onchocerca volvulus; midges for Mansonella perstans and M. streptocerca; and both midges and blackflies for Mansonella ozzardi; and deerflies [Chrysops] for Loa loa).  Inside the arthropod, the microfilariae develop in 1 to 2 weeks into infective filariform (third-stage) larvae.  During a subsequent blood meal by the insect, the larvae infect the vertebrate host.  They migrate to the appropriate site of the host's body, where they develop into adults, a slow process than can require up to 18 months in the case of Onchocerca.

LIFE CYCLE OF WUCHERERIA BANCROFTI

Different species of the following genera of mosquitoes are vectors of W. bancrofti filariasis depending on geographical distribution.  Among them are: Culex (C. annulirostris, C. bitaeniorhynchus, C. quinquefasciatus, and C. pipiens); Anopheles (A. arabinensis, A. bancroftii, A. farauti, A. funestus, A. gambiae, A. koliensis, A. melas, A. merus, A. punctulatus and A. wellcomei); Aedes (A. aegypti, A. aquasalis, A. bellator, A. cooki, A. darlingi, A. kochi, A. polynesiensis, A. pseudoscutellaris, A. rotumae, A. scapularis, and A. vigilax); Mansonia (M. pseudotitillans, M. uniformis); Coquillettidia (C. juxtamansonia).  During a blood meal, an infected mosquito introduces third-stage filarial larvae onto the skin of the human host, where they penetrate into the bite wound .  They develop in adults that commonly reside in the lymphatics .  The female worms measure 80 to 100 mm in length and 0.24 to 0.30 mm in diameter, while the males measure about 40 mm by .1 mm.  Adults produce microfilariae measuring 244 to 296 um by 7.5 to 10 um, which are sheathed and have nocturnal periodicity, except the South Pacific microfilariae which have the absence of marked periodicity.  The microfilariae migrate into lymph and blood channels moving actively through lymph and blood .  A mosquito ingests the microfilariae during a blood meal .  After ingestion, the microfilariae lose their sheaths and some of them work their way through the wall of the proventriculus and cardiac portion of the mosquito's midgut and reach the thoracic muscles .  There the microfilariae develop into first-stage larvae  and subsequently into third-stage infective larvae .  The third-stage infective larvae migrate through the hemocoel to the mosquito's prosbocis  and can infect another human when the mosquito takes a blood meal.

GEOGRAPHIC DISTRIBUTION

Among the agents of lymphatic filariasis, Wuchereria bancrofti is encountered in tropical areas worldwide; Brugia malayi is limited to Asia; and Brugia timori is restricted to some islands of Indonesia.  The agent of river blindness, Onchocerca volvulus, occurs mainly in Africa, with additional foci in Latin America and the Middle East.  Among the other species, Loa loa and Mansonella streptocerca are found in Africa; Mansonella perstans occurs in both Africa and South America; and Mansonella ozzardi occurs only ins the Americas, from Mexico south to South America and in the Caribbean. 

CLINICAL FEATURES

Most infections are probably asymptomatic, as indicated by serologic surveys.  Manifestations of disease include fever, chills, sweating, myalgias, fatigue, hepatosplenomegaly, and hemolytic anemia.  Symptoms typically occur after an incubation period of 1 to 4 weeks, and can last several weeks.  The disease is more severe in patients who are immunosuppressed, splenectomized, and/or elderly.  Infections caused by B. divergens tend to be more severe (frequently fatal if not appropriately treated) than those due to B. microti, where clinical recovery usually occurs.

LABORATORY DIAGNOSIS

Identification of microfilariae by microscopic examination is the most practical diagnostic procedure. Examination of blood samples will allow identification of microfilariae of Wuchereria bancrofti, Brugia malayi, Brugia timori, Loa loa, Mansonella perstans, and M. ozzardi.  It is important to time the blood collection with the known periodicity of the microfilariae.  The blood sample can be a thick smear, stained with Giemsa or hematoxylin and eosin.  For increased sensitivity, concentration techniques can be used.  These include centrifugation of the blood sample lyzed in 2% formalin (Knott's technique), or filtration through a Nucleopore® membrane. Examination of skin snips will identify microfilariae of Onchocerca volvulus and Mansonella streptocerca.  Skin snips can be obtained using a corneal-scleral punch, or more simply a scalpel and needle.  The sample must be allowed to incubate for 30 minutes to 2 hours in saline or culture medium, and then examined for microfilariae that would have migrated from the tissue to the liquid phase of the specimen.

For more information view the source:Center for Disease Control

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