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127 Cards in this Set
- Front
- Back
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General morphology of nematodes
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Elongate, cylindrical (vermiform) organisms.
Bilaterally symmetrical Pseudocoelomate Unsegmented Lack circulatory and respiratory system Usually have separate sexes One or two gonads Have a body wall composed of cuticle, hypodermis, and a layer of muscle cells |
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Body wall of nematodes
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Cuticle
Hypodermis - Expanded inwardly to form dorsal, ventral and lateral chords at the dorsal and ventral midlines, and in the lateral fields Muscles - elongate and spindle shape |
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Pinworm geographic distribution
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Worldwide, w/ infections more frequent in school- or preschool-aged children and in crowded conditions. Not a disease of poverty.
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Pinworm morphology
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Anterior end of both sexes has cuticular inflations. Tail of female is long and pointed, whereas the mail is bluntly rounded and very short. There are prominent alae in adults of both sexes.
Muscular pharynx divided into corpus, isthmus and bulb. |
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Life cycle of pinworm
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Adult worms inhabit the cecum and small intestine. When the female is ready to lay eggs, she crawls out of the anus and deposits the eggs on the perianal and perineal skin.
Eggs mature in about 6 hours at body temperature, contain the L3 stage larva, at which time they are immediately infective. Infective eggs are transferred to another host or to reinfect the same host. Infected eggs that are ingested, hatch and the larvae move through the small intestine to the cecum where they develop into adult, sexually mature worms in about 4-6 wks. |
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Pinworm pathology
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Infection is relatively innocuous - often asymptomatic. Common sxs: "itchy bottom" in pre-school and older children.
Occasionally, female worms migrate into the human vagina and onward into the reproductive tract, and sometimes into the peritoneal cavity. When the worm dies, a granulomatous lesion may form. |
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Pinworm diagnosis
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Female pinworm releases large numbers of mature eggs on the perianal skin at night. "scotch tape" preparation should be collected first thing in the morning before the child has defecated or washed.
Eggs usually not found in feces. |
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Pinworm treatment
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Albendazole 400 mg
Mebendazole 100 mg Pyrantel pamoate, 11 mg/kg |
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Ascariasis (Roundworm)
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Geographic Distribution: Most common human helminthic infection.
Endemicity is governed by the existence of poor sanitation. This includes both personal practice and agricultural practices involving the use of human feves ("night soil") as fertilizer for food crops. |
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Ascaris lumbricoides morphology
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Very large worms. Cuticle is smooth and transversely striated.
Most fertilized eggs have mammillations, some are decorticated. |
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Ascaris lumbricoides life cycle
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Soil-transmitted parasite (geo-helminth).
Adult worms live in the small intestine. Fertile eggs must embryonate in suitable soil conditions before they are infectious for other people. The eggs develop over a 3-wk period into an infectious secondary stage larva (L2) that remains within the eggshell. If the embryonated egg, which is the infective stage of the life cycle, is ingested by a human, the egg hatches in the upper small intestine, freeing the L2 larvae. The L2 larvae penetrates the gut wall, and enters the venous blood supply or lymphatics. It migrates to the lungs, molts to the L3 stage which enters an alveolus. Here it undergoes another molt, migrates up the bronchi to the trachea, and passes onto and down the esophagus. Final development to the adult stage occurs in the small intestine. |
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How long is the ascaris lumbricoides prepatent period?
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10-12 weeks
Adult worms live for about one year, sometimes as long as 2 |
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Ascaris lumbricoides pathology
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Pathology d/t adults: Heavy infections may cause abdominal discomfort, NV. Presence of many worms may cause potentially fatal bowel obstruction. Migration stimulated by stress - migrate into small lumens. Sensitive to anaesthetics. Failure to thrive and learn.
Pathology d/t larvae: Loeffler's syndrome. |
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Diagnosis of ascaris lumbricoides
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Eggs in feces, recognition of worms spontaneously expelled by the infected person or recovered in surgery, or recognition of parasites in biopsy specimens.
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Treatment of ascaris lumbricoides
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Albendazole 400 mg
Mebendazole 100 mg Pyrantel, levamisole or piperazine |
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Toxocara canis and catis
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Most common cause of visceral larva migrans
Widely reported throughout the world. Most frequently seen in children of dirt eating age |
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Toxocara canis life cycle
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Shed in feces of dog and develop in moist, shaded areas over a period of about three weeks to the infective stage. Transmission is accomplished by ingestion of the infective, embryonated egg.
Assuming a dog has never been infected w/ Toxocara, the 1st time it is infected the worm develops as for ascaris in humans. If a previously infected dog ingests infective eggs, the larvae hatch and remain in the dog's tissues as dormant, second stage larvae. If infected dog becomes pregnant, transplacental infection of fetus will occur. Transmammary infection also occurs. If another animal eats infective eggs of Toxocara, second stage somatic larvae will develop in this intermediated host. The larvae may be transmitted up chain by paratenic hosts. When humans ingest eggs, they can also be infected w/ second stage somatic larvae to T. canis. |
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Toxocara canis in human host
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Eggs hatch in the small intestine, the larvae penetrate the intestinal mucosa and migrate via the bloodstream or lymphatics to the liver, lungs and other organs where they seem to be at a "dead end". Instead of becoming dormant, they will wander through these tissues and organs, eliciting a host inflammatory response to their presence.
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Toxocara pathology
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Infected individuals may be asyptomatic, or may present w/ a typical syndrome of chronic hyper-eosinophilia, hematomegaly, LAD, hyperglobulinemia and pulmonary infiltrates.
Sxs will vary in degree of severity depending in part on the size of the inoculum. Greatest concentration typically occurs in the liver. |
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Ocular Larva Migrans
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In rare cases, the wandering larva will enter the orgic of the eye. Usually unilateral. Sxs include visual difficulties, retinochoroidiasis, and peripheral retininitis. May be mistaken for retinoblastoma.
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Dx of VLM
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Usually established on clinical grounds, i.e. eosinophilia, hepatomegaly, hyperglobulinemia. Some pts exhibit transient or chronic pulmonary inflammation. Serological tests do exist, but up to 20% of persons in certain populations may be seropositive w/o a h/o disease, presumably d/t prior asymptomatic infection.
Definitive dx: demonstration of larvae in tissues. |
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VLM Tx
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Tx is disappointing.
Mild disease is usually self-limiting Mebendazole is usually ineffective Albendazole and ivermectin may have a role Corticosteroids may be indicated to reduce inflammatory effects |
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Baylisascaris Procyonis
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Natural and common parasite of raccoons that can cause VLM in humans.
Ascarid nematode w/ typical ascarid life cycle. Adult roundworms live in raccoon's small intestine, eggs are passed in feces, and it takes approximately one month for the eggs to become infective once passed. When the eggs are infested by humans, the larvae of Baylisascaris procyonis migrate extensively into the viscera, eyes and CNS. Eosinophilic meningoencephalitis is frequently fatal. |
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Sero-Dx of Baylisascaris procyonis
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Experimental baylisascaris-specific, ELISA-type test is available.
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Prevention of Baylisascaris procyonis
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Don't keep raccoons as pets or entice them to frequent the backyard!!
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Tx of Baylisascaris procyonis
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Benzmidazoles and ivermectin have both been used, and don't appear to be uniformly effective
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Anisakiasis
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Human disease caused by ingestion of nematode larvae belonging to ascaridoid family Anisakidae. Typically, humans acquire the infection by eating undercooked or uncooked seafood dishes.
3 types of anisakid nemotodes have been implicated in human disease: 1. Anisakis spp. 2. Pseudoterranova spp 3. Contracaecum spp (much less common) |
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Anisakis life cycle
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Adult worms live in the stomachs of marine mammals and marine birds, reptiles and fishes. Eggs are discharged in seawater, develop and hatch, and the liberated larvae are ingested by krill and develop to the third stage larva. The krill are eaten by a variety of fish.
In the infected fish, the larvae migrate from the gut into the body cavity, viscera, and musculature. Larvae move from fish --> fish up the food chain. The larvae remain ineffective in these paratenic hosts, but do not develop further. Ultimately, the parasite completes its life cycle when the infected fish is eaten by a marine mammal Human infection is accidental. |
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Pathology
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2 forms of anisakiasis: non-invasive or invasive.
Non-invasive: usually asymptomatic and involves no tissue penetration by the worm. "tingling throat syndrome". Generally, larvae beloning to the genus Pseudoterranova are non-invasive. Invasive anisakiasis: occurs when larvae attach to, embed in, or penetrate human tissues. Anisakis larvae are more likely to penetrate tissues. The larvae have been located in the mucosa or submucosa of the stomach and intestine, and can migrate to other sites including the omentum, pancreas, liver and possibly lung. |
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Ansikasis Sxs
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May be acute, but are often vague. pt can present w/ appendicitis-like pain. Often mis-dx'd as acute abdomen; gastric tumor or cancer, ileitis; diverticulitis; stomach tumor.
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Anisakis Tx
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Fiber-optic endoscopy w/ biopsy forceps
Surgical removal may be necessary. |
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What is characteristic of trichuroids?
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An esophagus composed of a simple tube embedded in a linear row of secretory cells called stichocytes - collectively known as the stichosome
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Trichuris trichiura distribution
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Whipworm
Worldwide distribution, especially in the tropics, occurs also in sub-tropics. Often occurs in combination w/ ascaris. |
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Trichuris trichiura biology
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Adult whipworms live in the colon, caecum, and appendix, w/ the anterior 60% of their body embedded in the muscosal epithelium and the remainder of the body hanging free in the gut lumen of the host cell.
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Life cycle
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Female produces eggs while in the large intestine that pass out of the body with the fecal stream. The fertile egg is unembryonated when discharged from the body.
Eggs develop in the soil. About 3 weeks is required for the ovum to develop to the infective stage. The egg requires a warm, moist environment/soil for development. Infection is accomplished by ingestion of the embryonated egg. They enter hatch in small intestine and make way down to large intestine, where they burrow into the mucosa. Pre-patent development requires about 3 months. The adult worms may live for several days. |
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Morphology of Trichuris trichiura
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Adult: Stichosome which is made up of stichocytes: secretory cells which line the esophagus and produce various proteins for parasite function.
Bacillary band: row of columnar cells on ventral surface protected by cuticle; some secretory function; may be responsible for nutrient uptake from environment via pores in cuticles. Egg: Bipolar knobs or plugs |
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Pathology
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Clinical disease usually occurs only in heavily infected individuals. Infections w/ small numbers of worms are typically asymptomatic. Heavier infections may cause abdominal pain, diarrhea, sometimes dysentery, weight loss and tenesmus. Moderate peripheral blood eosinophilia is common. Stools may have Charcot-Leyden crystals. Severe anemia may occur.
Prolapse of rectum. Chronic infection can produce long term deficits in child cognitive and intellectual development. |
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Dx of Trichuris trichiura
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Finding eggs in feces. Adult worms may be seen during sigmoidoscopy.
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Tx for Trichuris trichiura
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Albendazole 400 mg
Mebendazole 100 mg |
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Capillaria Philippinensis
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Zoonotic infections in humans; fish eating birds are definitive hosts
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Geographical distribution of Capillaria philippinensis
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First cases reported in Philippines, other infections have been reported from Thailand, Japan, Taiwan, Iran and Egypt
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Life cycle of Capillaria philippinensis
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Natural definitive hosts are probably fish eating birds, wherein the adult worms inhabit the intestinal mucosa. Effs passed in bird feces. Small fish are the natural intermediate hosts, and harbor the larvae, which are infectious for birds (and humans)
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Transmission of Capillaria philippinensis to humans
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Results form eating raw freshwater fish, crustacea. Larvae are found in the intestines of the fish and are infectious within the human bowel, leading to the auto-infectious cycle.
Adult worms inhabit the mucosa of the small intestine, primarily the jejunum |
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What is unusual about Capillaria philippinensis
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Internal autoinfection can take place, causing an overwhelming and fatal infection.
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Pathology of Capillaria philippinensis
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Causes illness that may lead to death if untreated. Sxs include abdominal pain, flatulence, persistent intermittent diarrhea accompanied by weight loss.
Early tx is important in order to avoid internal autoinfection. Worms in all stages of development can be seen in intestinal crypts. |
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Tx for Capillaria philippinensis
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Albendazole, 400 mg
Mebendazole 200 mg Thiabendazole 25 mg/kg |
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Capillaria hepatica
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Natural parasite of wild animals, mostly rodents, in which it inhabits the liver.
Humans are accidental hosts and the infection presents w/ a clinical picture of VLM. Infection primarily occurs in children of dirt eating age. Distribution is worldwide, but is uncommon |
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Capillaria hepatica Biology
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Adult worms inhabit the parenchyma of the liver where they burrow. The female leaves a trail of eggs in these burrows.
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Life cycle of Capillaria hepatica
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Adult worms in liver parenchyma. Females produce unembryonated eggs, which are trapped in fibrous trails in the liver. For the cycle to continue, the infected host must be eaten by a predatory animal in order for the eggs to be released. The eggs reach the external environment with the feces of the predator. The eggs embryonate in the soil to reach the infective stage, which takes a period of a few weeks.
When the infective eggs are ingested by another host, including humans, the eggs hatch and migrate via the blood stream to the liver, where they reach sexual maturity in about 3-4 weeks. The infection remains occult. |
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Pathology of Capillaria hepatica
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Mild infections involving a few worms probably go unnoticed. Severe infections may result in fever, hepatomegaly, and hypereosinophilia. Clinical picture is similar to VLM.
Adult worms die after a few weeks, but the eggs remain trapped in fibrous tracts of the liver parenchyma. |
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Dx of Capillaria hepatica
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Depends on finding effs in liver biopsy specimen from a pt suspected of having the infection.
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Eustrongylides
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Nematode parasites of birds that have rarely been reported in humans. Most cases have been reported after the ingestion of live minnows... Presentation is similar to that of invasive anisakiasis w/ acute abdominal pain; the third stage larvae however are much larger and very active after ingestion.
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Trichinella spiralis
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Natural parasites of rodents, pigs, and a variety of wild animals - wild boar, bears, walruses and other carnivores.
Humans are incidental hosts for Trichinella. |
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Trichinella species distribution
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Worldwide distribution but are most prevalent in humans in part of Europe and NA; in East Africa, Asia, especially in China and parts of South America.
T. spiralis is the most important of the Trichinella spp in most parts of the world, because of its near-cosmopolitan distribution and its high pathogenicity. |
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Biology of Trichinella Spp.
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Unusual in that they live all or part of their lives as intracellular parasites. Both the adults and the infective larvae occur in the same host, but a two-host cycle is essential for transmission.
As with other trichuroids, these parasites have a stichosome that ca be seen in the adult and in infective stages. |
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Trichinella life cycle
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Adult worms live in the intestinal mucosa. They are minute. These parasites actually live within a row of columnar epithelial cells - they are intra-multi-cellular organisms.
Host immunity develops relatively rapidly, resulting in expulsion of adults from the host; hence patency is otly several weeks to a few months. While in the host, the female discharges minute larvae into the mucosa. The larvae migrate via the blood stream to the skeletal muscles and other organs of the body. Larvae only mature in striated muscle. They mature to infectivity in 3-4 weeks. They become encapsulated in the muscle and remain alive and infectious for many months, even years. They eventually die and become calcified in the tissues, unless the infected muscle is ingested by a carnivore. Infective larvae ingested by a carnivorous host burrow into the intestinal epithelium and mature very rapidly to the adult stage by the sixth day. Peak larval production reached by about 2 wks after infection, and may continue for up to 4 months. Adult worms live only a few weeks to a few months and then die. |
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Pathology of Trichonella
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Correlates w/ parasite lifecycle. Light infections are generally asymptomatic. However, GI upset after eating infected pork followed by muscular pains a few days later is not common.
During intestinal phase of infection, inflammation of the small intestine may cause NVD, abdominal cramps, all mimicking food poisoning. During muscle invasion, there may be severe myositis, facial edema, fever, and/or peripheral eosinophilia that may last for days to weeks. Myocarditis is a grave manifestation and may cause death. Encapsulation of infective larvae in striated muscle tissue begins at about the end of the third week, ad this marks the beginning of the convalescence period in humans. |
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Tx for Trichonella
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To eliminate adults and halt production of larvae: Mebendazole, 400 mg
Albendazole 400 mg No drug, including ivermectin, has been shown to treat myopathic phase of disease, which is treated w/ corcitosteroids, analgesics and antipyretics. Antihelminthic therapy w/o corticosteroids may worsen condition. |
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Hookworms
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Necator americanus
Ancylostoma duodenale Endemicity is limited for the most part to subtropical and tropical regions of the earth, regions that are non-arid, typically rural, and where levels of sanitation are poor. |
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Necatur americanus
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The most common hookworm worldwide. No known significant reservoir hosts.
Prevailing hookworm species of the Western Hemisphere, central and southern Africa, southern Asia, southern China, and Indo-Pacific islands. |
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Ancylostoma duodenale
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More geographically restricted. No known significant reservoir hosts.
Predominates in northern Asia, north Africa, the Middle East, Mediterranean regions, west coast of South America, and northern Australia. It also occurs in areas where N. americanus is the dominant species. |
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Hookworm Morphology
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Live in the upper small intestine attached to the mucosa. They have a well developed buccal capsule that, in the case of Necator, is armed with cutting plates or that, in the case of Ancylostoma, is armed with teeth.
Males possess copulatory bursa that is a broad, translucent, membranous structure supported by fleshy rib-like rays. |
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Hookworm Life Cycle
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Adult worms attach to mucosa of small intestine w/ buccal capsule filled with a plug of mucosa. Release proteolytic enzymes and anti-coagulants into the buccal capsule. They suck blood and also cause loss of blood from hemorrhage at site of attachment.
Female produces eggs that pass out in the fecal stream. Eggs embryonate and hatch in soil after about 24-48 hours under favorable conditions. Larva that hatches from the egg is a rhabditiform larva. This larva feeds on bacteria and organic debris, and molts twice to form the third-stage filariform larva (L3). This is the infective stage for humans!! The filariform L3 is active and remains in the top one cm of soil. The larvae do not migrate away from their site of development. The L3 does not feed, but exhibits "questing" behavior - it climbs to the top of a blade of grass or soil particle, stands on their tails, and sway. The infective L3 larva is self-reliant in that it gains entry to the body by directly penetrating human skin. L3's are carried in the circulation to the heart, then to the lungs in the pulmonary circulation. |
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Additional Migration pathways of A. duodenale
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From the lungs, they can follow either of two pathways. The classical route - tracheal migration - occurs when the L3 penetrates into an alveolus and is swept in mucus up the airways, then down to the gut. As the third mold occurs en route, it is the L4, with a primordial buccal capsule and developing reproductive system, which attaches to the intestinal villi and starts feeding.
Alternatively, in the somatic migration route, ancylostoma L3's can proceed into the systemic circulation, to be dispersed throughout the tissues and be deposited throughout the tissues and deposited in skeletal muscle fivers as hypobiotic larvae. Here they may remain for many months or longer, until triggered by some unknown mechanism, upon which they recommence their journey and development towards the adult stage in the small intestine. Arrested larvae of A. duodenale can enter the milk of nursing mothers, causing infection in newborns. Adult A. duodenale have short life spans, perhaps only 6-24 months, but an individual infection can persist for years because of intermittent reactivation of hypobiotic larvae. |
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Alternative migration pathways of Necator americanus
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undergoes only tracheal migration in humans, so neither somatic migration nor larval hypobiosis occurs. This spp maintains long infections simply through longevity of the adult worms, on average about 5 years, but up to 18 years.
If ingested, third-stage larvae of N. americanus cannot develop directly in the digestive tract. |
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Pre-patent period of hookworm
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The time from when the infective larva gains entry through the skin until it is a sexually mature, reproducing parasite is about 4-6 weeks, after which egg laying begins.
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Hookworm early, relatively minor pathology
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Early, relatively minor effects: There may be a localized erythema when the larvae enter the skin to initiate hookworm infection. This is often referred to as "ground itch". If a large number of larvae migrate through the lungs at the same time, there may be a bronchitis or pneumonitis "Loeffler's".
When worms first reach the upper small intestine and attach to the mucosa there may be some degree of enteritis w/ associated NV, epigastric discomfort, and diarrhea. There may be gross blood in stool. Some pt's have pica. |
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Hookworm chronic effects
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The pathology d/t hookworm which is important on a global scale is iron deficiency anemia d/t blood loss. Individuals who are most at risk are those whose iron stores are precarious. This includes young children who bear the main burnden of the geohelminths, but unlike Ascaris and Trichuris, intensity of infection does not decrease with age, and adults, in particular pregnant women, are at risk.
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Which of the hookworms causes more severe disease in general?
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A. duodenale both b/c it is a larger parasite and a/w greater blood loss per worm, and because more prolific egg-laying results in more intense infections.
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Hookworm disease in mothers and children
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The overall prevalence and intensity of hookworm infection are higher in males than in females, in part because males have greater exposure to infection. However, women and young children have the lowest iron stores and are therefore most vulnerable to chronic blood loss as the result of hookworm infection.
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Diagnosis of hookworm infection
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Finding eggs in the feces.
Eggs of Necator and Ancylostoma cannot be readily distinguished from one another by eye. Can be seen in fecal smears, but are more easily found in concentrated samples Occasionally, hookworm eggs may hatch in feces samples that have been left standing at room temperature for 24 hours. At that point, one must differentiate from the possibility of infection w/ Strongyloides stercoralis because L1s of hookworms and L1s of S. stercoralis superficially resemble each other. |
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Tx for hookworm
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Albendazole, 400 mg
Mebendazole 100 mg Pyrantel pamoate |
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Prevention of hookworm
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1. Sanitary disposal of human feces; sewage system; privies
2. protection of susceptible individual, e.g. by wearing shoes and good nutrition 3. antihelmintic treatment of infected individual and populations, treatment of anemia |
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True strongyles
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Relatively uncommon parasites of humans, who are incidental hosts
e.g. Oesophagostomum spp, Ternidens spp. They are soil-transmitted |
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Oesophagostomum spp
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e.g. O. bifurcum
"nodular worms". Common parasites of pigs, ruminants and primates, and have a worldwide distribution. Called nodular worms b/c they produce nodule-like abscesses in the host's bowel wall during the course of their maturation. There are endemic foci of human infection in W. Africa, particularly in Togo and Ghana where they may affect 30% of the population |
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Life cycle of Oesophagostomum
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Eggs pass out with feces, deposited in soil, embryonate quickly, hatch, and over several days molt twice to become infective, third stage larvae (L3). Infection is accomplished when (the natural host or) the human eats vegetables contaminated with infective larvae. The larvae burrow into the mucosa of the large intestine forming an inflammatory nodule or sterile abscess in which the parasite undergoes further development. The fourth stage (L4) larva spends about 2 weeks in the nodule. After a final molt in the nodule, the worm re-enters the lumen of the bowel, attaches to the mucosa, and complete its maturation. The pre-patent period is about 5-6 weeks.
In humans, they typically cannot complete their development and they remain in the nodule. However, in some circumstances, the maturation and lifecycle is completed in people - this is the usual situation in the endemic focus in West Africa. |
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Pathology of Oesophagostomum
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Most pts who develop sxs present w/ pain in the RLQ (mimicking appendicitis), and may have one or more palpable abdominal masses. The condition frequently deteriorates, resulting in exploratory surgery. A usual finding is a 4-6 cm mass in or attached to the bowel wall usu in the iliocecal region.
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Diagnoses for Oesophagostomum
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For patent infections, eggs in the feces. For non-patent infections, pathology of nodule w/ larvae
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Tx for Oesophagostomum
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Albendazole 400 mg
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Trichostrongyles
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Bursate nematodes which are responsible for major economic losses in livestock; primarily parasites of herbivores; occasionally and incidentally parasites of humans. Soil-transmitted parasites.
Lack buccal capsule but have a well-developed bursa. |
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Life cycle of trichostrongyles
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Eggs are passed in feces onto the soil. They undergo development there and hatch in the soil, then develop to the infective third stage (L3) larva. L3s crawl up on the blades of grass and accomplish infection of the definitive host when the herbivore or human eats the grass contaminated w/ the L3. The adults develop directly in the intestine of the host w/o a pulmonary migration.
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Prevalence of trichostrongyles
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Human infections are not uncommon in rural areas of the Middle East who live in close association w/ various domesticated herbivores.
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Clinical features of trichostrongyles
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Typically asymptomatic. Adult worms located in the duodenum and jejunum
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Tx of Trichostrongyles
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Albendazole, mebendazole, thiabendazole or pyrantel pamoate
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Metastrongyles
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"Lung worms"
Accidently but frequently infect humans. Economically important parasites of livestock. One of the most conspicuous features of the adult female is the barber-pole-like appearance of the body d/t paired uterine branches that wind around the dark-colored intestine. Most species of metastrongyles live as adults in pulmonary arteries and hence are referred to as lungworms. some inhabit the mesenteric arteries and their branches in rodents. 2 spp that accidentally infect humans: Angiostrongylus cantonensis and Angiostrongylus costaricensis |
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Astiostrongylus cantonensis
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Lungworm of rats
Also found in humans in Asia and the Indo-Pacific region including Hawaii. In the mainland US, it has been reported from rats, primates and occasionally people. |
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Life cycle of Angiostrongylus cantonensis
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Adults live in the pulmonary arteries of rats, where the female discharges eggs, which lodge as emboli in smaller vessels. The eggs develop, larvae hatch from the eggs, and the larvae break into the respiratory tract, migrate up the trachea, are swallowed and pass out with the rat feces. Molluscan intermediate (and paratenic) hosts, snails and slugs of suitable genera, and freshwater prawns either eat the infected feces or larvae, or are penetrated b the larvae.
In the intermediate host, the parasite undergoes two molts from L1 to L3, and remains viable for a long time. The life cycle continues when a rat eats the infected intermediate host. The larvae make an obligatory migration to the CNS. They develop to immature adults in the parenchyma of the brain, and then move to the meninges. After about one month, they leave the CNS and migrate via the venous system to the lungs to complete their development and life cycle. |
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Pathology of Angiostrongylus cantonensis
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Humans become infected by eating snails, slugs, prawns etc infected w/ the L3 or by eating vegetables contaminated w/ larvae in slime trails of snails and slugs. In the human, the larvae migrate to the brain and remain there a long time. Some may move to pulmonary arteries, but they cannot develop to maturity. Invasion of the human brain frequently results in eosinophilic meningitis and meningoencephalitis.
Most larvae die in the brain, where they cause an intense inflammatory reaction, or they may eventually migrate out towards the tlungs. |
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Tx for Angiostrongylus cantonensis
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Antihelmintic therapy is not necessarily recommended; prior reports have not shown benefit and there is the concern that it might trigger a more acute inflammatory response. Corticosteroids can be used to manage sxs.
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Angiostrongylus costarincensis
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This parasite was originally recorded from cotton rats and humans in Costa Rica. In its natural host, A. costaricensis is found from Texas to Argentina, and is common in Central and South America
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Life Cycle of Angiostrongylus constaricensis
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In rats, the adult parasites live in the mesenteric arteries and their branches. The female deposits eggs in the wall of the rat intestine where they embryonate, hatch, and migrate into the lumen of the bowel. The larvae are shed w/ feces. As w/ A. cantonensis, a snail or slug serves as the obligatory intermediate host or the life cycle of A. costaricensis. The L1 molts twice to the infective L3 stage w/i the mollusk, over about 3 weeks. Rodents become infected by eating snails, slugs. L3s migrate via the lymphatics and blood to the mesenteries.
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Angiostrongylus costaricensis in humans
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Humans become infected by eating molluscan or paratenic hosts, or vegetables, carrying or contaminated w/ infective L3s. Larvae migrate to the mesenteric vessels as they do in rodents, and females produce eggs. The eggs do not develop in the human and neither eggs nor L1 larvae are ever seen in human feces
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Pathology of Angiostrongylus costaricensis
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Infections in humans usually are seen in children. Sxs include acute abdominal pain and tenderness localized to RLQ and low-grade fever. Duration of illness usually 2-4 wks, and often a painful tumor-like mass is palpable. Leukocytosis and high eosinophilia are frequent laboratory findings. Histologically the findings are those of a granulomatous, eosinophilic inflammatory reaction w adult worms and effs in tissue.
Serology is available from Mahidol University in Thailand |
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Tx for A. costaricensis
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Surgery may be needed.
Anti-helminthic therapy is unclear |
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A note about Strongyloides stercoralis taxonomy
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S. stercoralis is NOT in the suborder Strongylida, nor the superfamily Strongyloidea, is not a "true strongyle" and is NOT a bursate nematode
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Strongyloides stercoralis
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Geographical distribution: worldwide distribution parallels that of hookworms. Prevalent in warmer areas; its prevalence is much lower than that of hookworms in more temperate zones
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Strongyloides stercoralis epidemiology
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Numbers of people infected - estimated at between 100 and 200 million. Strongyloides stercoralis thrives best in warm, moist climates where sanitation is substandard or lacking. The infection is not uncommon in developed countries w/ generally adequate sanitation practices: there is a higher incidence in mental and other custodial institutions d/t the long-lived nature of this infection combined w/ sub-standard sanitation and/or poor personal hygeine
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Transmission of strongyloides stercoralis
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S. stercoralis is asoil-transmitted parasite. Txn is favored by poor sanitation. The infective stage is the third stage larvae, the L3, which is a filariform larva. This self-reliant L3 larva penetrates the skin directly, in similar fashion to the hookworm larva
Auto-infection is common w/ strongyloidiasis. |
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Strongyloides stercoralis Life Cycle
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The adult parasite is a parthenogenetic female, and that there is not parasitic adult male form of S. stercoralis
Direct cycle: Adult parasitic female lives in human small intestine. The worm lies buried in the mucosa of the intestinal tract, laying eggs. The egg hatches in the mucosa, releasing L1, rhabditiform larva. These larvae pass out with the feces onto soil, where it will develop through the free living L2 stage larva to the infective l3 filariform larva within 1-2 d. Eggs are RARELY found in feces Larvae enter blood vessels and are carried to lungs, where it breaks out of alveolus, coughed up and swallowed. En route, it undergoes third mold in lungs. L4 passes down digestive system to small intestine, where it undergoes a 4th molt to become parasitic adult female. This L5 female penetrates the mucosa of the intestinal villi, where they burrow in serpentine channels in the mucosa, depositing eggs and feeding.The worms are most found frequently in duodenum and jejunum |
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Indirect life cycle of Strongyloides stercoralis
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Parasitic generation is interrupted by a free-living generation
IN the indirect or heterogonic life cycle, the L1 rhabditiform larva shed in human feces develops through free-living L2, L3, L4 and adult stages in the soil. All off these stages are microbial and organic debris feeders, and exhibit a rhaditiform esophagus. this cycle includes both males and females. Copulation occurs in the soil. The female releases eggs that hatch in the soil. Subsequently, the rhabditiform L1 larvae molt twice to become infective, filariform larvae The indirect life cycle can increase the number of infective larvae on the ground by 50x. |
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Auto-infection w/ S. stercoralis
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Occasionally, the L1 develops in the bowel to the infectious L3 filariform larva, which may then re-infect the patient through the bowel wall.
An important consequence with this is that infection w/ S. stercoralis may last a long time and that migration away from endemic locations will not immediately ensure freedom from infection. Direct person-to-person transmission is also possible |
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Larva stage Pathology of S. stercoralis
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d/t low levels of autoinfection, sxs d/t the largal stage can persist and recur over years.
Larva currens = "running larva". This is a CLM-like syndrome caused by infective larvae of S. stercoralis undertaking a dermal migration prior to entering the blood vessels and the normal pulmonary migration. Larvae move quickly. Recurrent pumonary and "allergic" sxs can occur, but since you are continuously exposed to larvae, Loeffler's is not as frequent |
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Pathology d/t adult stage of S. stercoralis
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Adults in intestinal lumen.
Most infections are light and probably go unnoticed. Moderate infections w/ parasitic females embedded primarily in the duodenal region may cause a burning, dull or sharp, non-radiating mid-epigastric pain. NV may occur. Diarrhea and constipation may alternate. Heavy and long-standing infections may result in weight loss and chronic diarrhea accompanied by malabsorption. |
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Hyperinfection syndrom
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On occasion, the percentage of rhabditiform larvae converting to filariform larvae w/i the bowel will increase. This can result in a large increase in the worm load. If only the gastrointestinal tract and the lungs are involved the condition is best describes as hyperinfection syndrome. This can be fatal. Severe and chronic diarrhea, malabdorption and weight loss occur. Pulmonary sxs are likely to be present.
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Disseminated or overwhelming strongyloidiasis
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When the numbers of migrating larvae become so great as to be located in and injure other organs such as the liver, spleen, heart and the CNS, a multiplicity of other sxs may occur. In this situation, various stages of the parasite can be found in ectopic locations. This condition can be fatal even w/ therapy.
Most signigfcant risk factor for dissemination is the administration of exogenous corticosteroids. |
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Dx of strongyloides stercoralis
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Clinical Dx is difficult.
Laboratory dx is accomplished by finding first stage L1, rhabditiform larvae in the feces. Ser-dx by ELISA is useful In dx'in Strongyloides, it is important to be able to distinguis tha largae of strongyloides from those of hookworm. Hookworm larvae can be found in stool that has not been examined promptly, as L1 hookworm larvae may hatch out in just a few hours |
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Tx for strongyloides stercoralis
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Ivermectin 200 microg/kg)
Albendazole 400mg Thiabendazole as alternative. For hyperinfection syndrome: Albendazole or ivermectin |
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Strongyloides fulleborni
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Known from central and East Africa where it infects higher primates and humans. Eggs, rather than the rhabditiform larvae, occur in feces
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Strongyloides fulleborni kellyi
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Occurs on the island of New Guinea. Eggs, rather than rhadbitiform larvae, occur in feces.
It can become common in children, although most infants are asymptomatic. Some exhibit "swollen belly sickness" |
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Zoonotic strongyloidiasis
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"swamp itch" a CLM-type larva currens condition resulting from infection w/ larvae of Strongyloides spp of other animals including raccoons and nutria.
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Cutaneous Larva MIgrans
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Ancylostoma braziliense, a common hookworm of dogs and cats, is the most frequent agent of CLM. Other hookworms of animals also cause CLM: A. caninum, Uncinaria stenocephala, A. tubaeforme, and Bunostomum phebotomun.
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Gnathostomiasis
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Gnathostoma spinigerum and Gnathostoma hispidum, which infect vertebrate animals.
Human gnathostomiasis is d/e migrating immature worms. |
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Geographic distribution of gnasthostoma
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Asia, Thialand and Japan.
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Clinical features of Gnathastoma
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Caused by migration of the immature worms (L3). Migration in the subQ tissue causes intermittent, migratory, painful, pruritic swellings. Migration to other tissues can result in cough, hematuria, and ocular involvement, w/ the most serious manifestiations eosinophilic meningitis w/ myeloencephalitis. High eosinophilia is present.
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Dx of Gnathostoma
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Removal and ID of worm is both diagnostic and therapeutic. Serology is available from Mahidol University in Thailand.
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Benimidazoles
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Mebendaole, albendazole, thiabendazole, etc.
Bind Bbeta-tubulin, preventing its polymerization. Loss of MT function in nematode gut blocks glucose uptake, thus preventing ATP synthesis, effectively staring the worm. Selectivity: don't bind human tubulins well Versatile: active against many intestinal and tissue nematodes; juvenile cestodes Teratogenicity |
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Thiabendazole
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BZ
Effective for intestinal nematodes Best systemic absorption Relatively higher toxicity - now limited use |
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Mebendazole
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BZ
Better tolerated - b/c not well absorbed Rapid 1st pass metabolism |
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Albendazole
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BZ
Variable absorption Low toxicity |
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BZs for intestinal nematodes
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Mebendazole/albendazole good for most intestinal nematodes
Albendazole more effective as a single dose Strongyloides a little harder to treat Trichinella adults Mode of action results in relatively slow clearing - ascaris may wander! |
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BZs for other parasites
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Albendazole used for tissue forms.
Long or repeated tx may be required LM sxs - variable efficacy Trichinella cycsts - maybe Larval cestodes Macrofilaricidal activity Albendazole is included in other control programs for lymphatic filariasis |
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Pyrantel Pamoate
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Imidazothiazole
MoA: ACh agonist and depolarizing NM blocking agent Produces rigid contraction of the muscles. Used for intestinal nematodes - poorly effective for trichuris |
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Piperazine
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Agonist for NT GABA receptor
Flaccid paralysis Effective for ascaris and pinworms |
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Ivermectin
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Active against many nematodes and arthropods
Well absorbed orally Good tissue penetration Long half-life Low side effect profile, but CNS toxicity can occur Mazzotti-type reaction can occur w/ oncho, loa MoA: GABA agonist - flaccid paralysis |
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Ivermectin activity
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Effective against most intestinal nematodes
Not human hookworm Activity against agents of CLM Anti-filarial activity |
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Di-ethyl Carbamazine
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DEC
MoA not well understood. microfilaria - organ damage VERY effective anti-filarial drug Contraindicated in onchocerciasis |
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Praziquantel
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Broad spectrum of acitivity against parasitic flatworms, not so much nematodes.
Interferes w/ calcium ion channels at surface of parasitye. tetany of parasite muscles. Well absorbed orally Drug of choic for all schistosomes Effective for liver, llung and intestinal trematodes Effective for adult human tapeworms. |
