Parasitology nematodes Flashcards

1
Q

Ascaris lumbricoides epidimiiology

A

Ascaris lumbricoides, commonly known as “roundworm” (as a group, all the nematodes are often referred to as ‘roundworms’ although when ‘roundworm’ is used by itself, we generally mean ascaris specifically), is one of the commonest parasitic infections found in the intestine of man. More than 1 billion people harbor this worm! It occurs throughout the world in both tropic and temperate climates. (A. lumbricoides does not have an animal reservoir. A pig ascaris, A. suum, which is almost identical to A. lumbricoides, can infect humans, but this is uncommon and usually found in individuals who raise swine or use pig manure for gardening.)

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2
Q

Ascaris lumbricoides life cycle

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Infection generally occurs when children ingest eggs from contaminated soil. Eggs also may be swallowed when contaminated water or green vegetables are consumed. Infective larvae hatch from the eggs in the small intestine, the larva penetrate the lining of the small intestine, enter the bloodstream, reach the lung, are carried up the trachea to the larynx and are swallowed and develop into adult worms in the small intestine. Live 1-2 years in small intestine.

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3
Q

Ascaris lumbricoides clinical manifestations

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When the tiny larvae migrate through the lungs the patient often develops cough and low-grade fever. Some patients develop a pneumonitis-like condition with transient pulmonary infiltrates, cough, occasional fever and peripheral blood eosinophilia known as Loffler’s Syndrome. (Patients with the parasite Strongyloides stercoralis or the hookworm parasite also may present with Loffler’s Syndrome.) Patients may complain of vague abdominal discomfort or colicky abdominal pain. Often the first clue of the existence of infection with this parasite occurs with the passage, usually from the rectum but occasionally—Gak!—out the mouth or nose, of a disturbingly long (25 cm), flesh colored worm which moves in a most disgustingly “stiff” manner. The victim thinks, “My God! This came out of me?”

Not to worry…humans have harbored large roundworms forever and other than the rare occurrence of intestinal blockage due to massive numbers of worms in small children native to the tropics or the uncommon migration of the worms into the appendix, bile duct, liver, pancreatic duct, diverticuli, or through surgical anastomoses, these critters generally cause no real harm. (High fever from some other illness or certain drugs used in general anesthesia may provoke the worms to undertake aberrant migration.)

It is postulated that the flagellate, Dientamoeba flagilis, and pinworm eggs may be transmitted in Ascaris eggs.

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4
Q

Ascaris lumbricoides Diagnosis

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Diagnosis is made with the observance of passage of one of these large worms from the anus, nose or mouth, or by finding the typical, easily recognized egg by microscopic exam of the stool. (If a mother comes in to your office and says: “My kid passed a fishworm,” think ascaris. Unlike actual fishworms, ascaris worms will have smooth borders, even shapes with tapered ends and are not pigmented.)

Ordering Stool for O and P (ova and parasites) x 3

“Routine detection of intestinal ova and parasites requires examination of at least three stool specimens, preferably collected every other day or on 3 consecutive days.” This rule (a minimum of three specimens) applies for ALL parasitic conditions for which you might possibly encounter the ova or actual parasites in the stool. You won’t find the eggs until 2-3 months after the lung symptoms.

During the migration of larvae through the lungs, examination of a blood sample (CBC with differential) may reveal an increase in blood eosinophils. Chance radiographic examination 5 hours after an opaque meal will often show the worms in the gut. At present, serologic diagnosis is not useful because of cross-reactivity with other helminthic antigens.

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5
Q

Ascaris therapy and prevtion

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Ascaris infection is easily treated using mebendazole for adults and children over two years of age. Albendazole in a single dose is very effective and is probably the drug of choice. Other options include pyrantel pamoate as a single dose or Ivermectin as a single dose.

Intestinal obstruction or migration of a misguided worm into an aberrant location requires surgery

Prevention. Ideally, the use of latrines, hand washing, and the avoidance of leafy vegetables (often contaminated with human excreta) should eliminate the possibility of infection with ascaris. Alas, it’s an imperfect world in which we live; as in the case of Trichuris and many other intestinal parasites, despite one’s best efforts, ascaris infection may turn up as a belated reminder of an otherwise uneventful trip into the tropics.

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6
Q

Visceral larva migrans epidimiology and geographic distribution

A

“…up to 2.8 million African-Americans with toxocariasis…” NY Times, August 18, 2012

Toxocariasis results from infection with the dog ascarid, Toxocara canis or, uncommonly, with the cat ascarid, Toxocara cati or even more uncommonly, with the raccoon ascarid Baylisascaris procyonis. (Baylisascaris in humans is a terrible disease. It can cause an eosinophilic meningoencephalitis and death or permanent neurologic sequelae. To date, there is no effective treatment.)

Infection generally occurs as a result of small children eating dirt contaminated by dog (puppies are a significant source of infection) or cat feces containing the infective eggs. Direct transmission from household pets to children does not occur because Toxocara eggs require approximately one month of extrinsic incubation in the soil. Infection may also occur through ingestion of unwashed raw vegetables contaminated with eggs.

Infection occurs on a worldwide basis. (The frequent reports of infection from the United States and England most likely reflect the degree of current research in those nations and not a greater prevalence of disease.)

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7
Q

Visceral larva migrans Life cycle

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The adult worms live in the small intestine of the dog or cat. In dogs, transmission occurs from mother to puppies via the placenta and milk and virtually all puppies are infected! In the natural cycle in dogs, larvae develop to the adult stage with subsequent egg production. Eggs are passed in the feces, embryonate in the soil for three to four weeks and are ingested by dirt-eating children. The larvae hatch in the small intestine, penetrate the intestine, migrate to the liver, then to the lungs where, after penetration of the pulmonary veins, the larvae are distributed throughout the body to all organs. The larvae do not mature in humans (thus eggs are not produced in humans) and may continue migrating for up to six months.

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8
Q

visceral larva migrans clinical manifestations

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Young children often experience asthma-like attacks, fever, abdominal discomfort, nausea and vomiting. Urticarial rashes are often reported. Enlargement of the liver is fairly common, enlargement of the spleen less so.

Children, usually aged 5 to 10 years, may present with visual loss as a result of larvae entering the eye. In additional to visual changes, retinal lesions resembling a form of cancer known as retinoblastoma may be incorrectly diagnosed leading to unnecessary removal of the eye

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9
Q

visceral larva migrans Diagnosis

A

The diagnosis of toxocara is often first suspected by the finding a marked increase in eosinophils in the blood (20-80% or even up to 90% eosinophilia) as the larvae pass through the lungs—the BIG clue! (In the case of eye toxocariasis, however, the eosinophil count may not be elevated to such a high degree.) In the case of acute infection, presumptive diagnosis may be made on the basis of the ELISA test. (The diagnosis of this parasite is generally made without finding the actual parasite itself. You infer the diagnosis from lab testing.)

Transient pulmonary infiltrates are frequently noted on X-ray.

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10
Q

visceral larva migrans ocular toxocariasis

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Ocular toxocariasis (ocular larva migrans) may be diagnosed using the serum ELISA test. Checking the vitreous humor for ELISA antibody (for T. canis) may help resolve questions regarding ocular toxocariasis versus retinoblastoma. CT has been used to differentiate retinoblastoma from ocular larva migrans.

Note: Demonstration of larvae by liver biopsy or through direct biopsy of granuloma at laparoscopy is a fortuitous event and only rarely is a definitive diagnosis of toxocariasis made on the basis of actual identification of larvae.

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11
Q

visceral larva migrans TX and prevention

A

Treatment. Albendazole or mebendazole also have been shown to be effective in treating Visceral Larva Migrans.

Prevention and Control. Human infection may be reduced by regular worming of puppies and preventing, as much as is possible, defecation by dogs and cats in children’s play areas. Raccoons should be discouraged from visiting homes for food and should not be kept as pets.

Children should be taught to wash their hands before eating and should be discouraged from dirt-eating. (Good luck!)

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12
Q

Whipworm Epidimiology

A

Trichuriasis is caused by the whipworm, Trichuris trichiura. Human infections occur from ingesting eggs in soil contaminated by human feces. After being swallowed, the egg hatches in the small intestine and larvae develop and take up residence in the large intestine where they attach to the intestinal mucosa and develop into the adult stage. This nematode does not have a phase where it passes through the lungs.

It is estimated that eight hundred fifty million people, most of whom live in tropical or subtropical regions of Asia, Africa and the Americas, are infected with whipworm. Trichuris infection is fairly common in West Virginia, if you think to look for it.

Here’s a curious twist: It has been recognized for some time that Inflammatory Bowel Disease (I.B.D) is less common in countries endemic for helminth infections. Recent studies seem to show that patients with I.D.B, such as Crohn’s Disease, often go into complete remission after ingesting 2,500 eggs of pig whipworm (T. suis)! It is postulated that over the course of human existence, helminths have manipulated the immune system (in this instance, in a positive way) and that the de-worming of human populations in North America in the 20th Century has led to the spike in I.B.D. In a study published in Science Translational Medicine (1 December 2010. Vol 2 Issue 60) it was postulated that T. trichiura colonization of the intestine may reduce symptomatic colitis by promoting goblet cell hyperplasia and mucus production.

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13
Q

Whipworm Clinical Manifestations

A

Light infections are usually asymptomatic or may present only with lower abdominal discomfort, nausea, distension, and chronic diarrhea and occasionally there may be blood in the stool in really heavy infection (usually not, though). Occasionally constipation rather than diarrhea occurs. Heavy infections are characterized by epigastric pain, vomiting, abdominal distension, farting, decreased appetite and weight loss. Rectal prolapse (protrusion of the rectum from the anus) may occur in heavy infections in children living in tropical countries. Also, women who have just delivered or are about to deliver may develop rectal prolapse from heavy infections. Some children with heavy worm loads suffer impaired growth. Board exams often have a matching question for “rectal prolapsed”…the answer is Trichuris trichiura.

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14
Q

Whipworm Diagnosis

A

Characteristic barrel shaped eggs are observed under the microscope. In patients with infection heavy enough to produce dysentery, proctoscopy often reveals numerous worms attached to reddened and ulcerated mucosa. Remember, there is usually NO eosinophilia in trichuriasis, however, in severe cases, a slight increase above the normal level of eosinophils in the blood has been reported); there IS eosinophilia in Strongyloides, hookworm, and in ascaris infection (when the larvae are migrating through tissue such as lung).

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15
Q

Whipworm TX and Prevention

A

Treatment. Mebendazole (Vermox) twice daily for three days. Albendazole (Albenza) given in a single dose, is well tolerated and usually very effective. Another option is combining albendazole with ivermectin. Intensive infection may require that treatment be repeated two or three times.

Prevention and Control. Preventive measures include provision of adequate facilities for feces disposal, hand washing after defecation and before food handling. It should be appreciated, however, that long-time residence in a region of high whipworm prevalence virtually guarantees eventual low intensity asymptomatic parasitic infestation despite one’s best efforts in adopting those measures which minimize the chance of infection.

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16
Q

Capillariasis

A

Three types of nematodes of the genus Capillaria produce disease in humans. For the purpose of this parasitology course, the main point is that the eggs of Capillaria could be confused with the eggs of Trichuris under the microscope. However, since Capillaria is only found in certain islands in the northern Philippines (see below), this potential for confusion is rather remote. So, you would only expect to encounter capillariasis in the northern Philippine Islands, or in someone who happened to wind up in America from the northern Philippine Islands.

Intestinal capillariasis, due to C. philippinensis, generally presents as a severe diarrhea (due to autoinfection) with malabsorption and massive protein loss. Unless treated, death from heart failure or intercurrent infection may occur within weeks or months after the onset of symptoms.

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17
Q

ANGIOSTRONGYLIASIS

A

Angiostrongylus cantonensis (rat lungworm), a nematode (roundworm), is the most common cause of human eosinophilic meningitis. It is transmitted to humans from uncooked snails or slugs or from snail slime contaminating food. Outbreaks of Eosinophilic Meningitis due to Angiostrongylus cantonensis have been reported in several countries including Colombia and Ecuador and also has been reported from Hawaii. In several countries, the presence of introduced giant African Land Snails has been associated with human angiostrongylus infection. South Florida has experienced an explosive invasion of introduced giant African Land Snails though, thus far, there has not been an outbreak of Angiostrongylus cantonensis in humans in Florida. Two snail-eating primates in South Florida, however, have died from infection of this parasite. The concern is that it turns out Angiostrongylus cantonensis has been found in several species of snails in Florida, in addition to the dramatic African Land Snail, and the potential exists for some hapless person to consume an infected small-snail in a leafy salad from plants grown in Florida (which are shipped all over the United States) and come down with this illness. (Hey, stranger things have happened!) Patients develop severe headache, neck and back stiffness. There is usually a marked increase in blood eosinophils (up to 80%) and the cerebral spinal fluid will have over 20% eosinophils. Rat lungworm can also cause unilateral blurring of vision without signs of meningitis. There is no proven drug treatment, although many specialists treat patients with pain medicine, corticosteroids and repeated removal of cerebral spinal fluid. Giving antiparasitic medication may actually worsen the condition. Most patients recover completely.

18
Q

ANGIOSTRONGYLIASIS costaricensis

A

Angiostrongyulus costaricensis causes abdominal/intestinal symptoms. The illness is acquired through undercooked snails and snail slime contaminating food. Patients may present with fever and abdominal pain (usually RLQ) and symptoms mimicking acute appendicitis. Sometimes a mass in the RLQ is found on palpation. There is an elevation of blood eosinophils. Medical treatment is controversial. Most patients recover fully after a few weeks or months.

19
Q

Hookworm epidemiology

A

Two forms of human hookworm, Ancylostoma duodenale and Necator americanus, infect between five-hundred million and one billion of the world’s population. The epidemiology of the disease is dependent upon three factors–the suitability of the environment for the eggs or larvae; the mode and extent of fecal pollution of the soil; and the mode and extent of contact between infected soil and skin.

Man is infected when hookworm filariform larvae (the infective larval form) occupying the upper layers of contaminated soil penetrate bare skin, usually of the feet, hands or buttocks. The larvae migrate via the venous system to the right side of the heart and then to the lungs. From the lungs the larvae migrate upwards in the trachea and into the esophagus and eventually to the stomach and small intestine. The worms mature in the small intestine, copulate and the females produce eggs to the tune of 15,000 eggs per day. When these eggs are deposited on warm, moist soil, rhabditiform (noninfective) larvae form which after a passage of time are infective to humans as filariform larvae.

20
Q

Hookworm Clinical manifestations

A

Skin penetration by the larvae may produce an immediate stinging sensation followed by a rash, usually on the feet, hands or buttocks. Patients rarely recall symptoms related to initial infection. During transit through the lungs, hookworm larvae may produce mild bronchitis or pneumonitis with cough and wheezing (Loffler’s syndrome). Discomfort in the pit of the stomach sometimes occurs in heavy infection and may be confused with peptic ulcer disease.

Mental apathy, impaired physical performance, pallor and swelling of the face and feet may occur in heavy infestation with severe chronic blood loss (hypochromic anemia). Patients often develop palpitations of the heart. It is important to keep in mind that the symptoms noted above occur almost exclusively in native populations where shoes are not worn. Infection heavy enough to produce such symptoms would be extremely unlikely in travelers or even expatriates living in hot countries. Heavy hookworm infection can be a major cause of anemia in pregnant and lactating women or women who menstruate heavily.

21
Q

Hookworm Diagnosis

A

The diagnosis is made by finding hookworm eggs by microscopic examination of the stool. (If fresh unpreserved stool specimens are used, they should be examined within an hour or two when looking for hookworm eggs because after several hours the hookworm eggs may hatch and release larvae that can be confused with the larvae of Strongyloides.)

22
Q

Hookworm TX and prevention

A

Treatment. Mebendazole, (the old standard therapy) is very effective. Albendazole is also useful in treating hookworm infection. Ivermectin in a single oral dose is very effective. (Pyrantel pamoate can be used as well.) In severe cases of hypochromic anemia associated with hookworm, oral iron therapy is administered in addition to treatment with mebendazole or albendazole.

Prevention. The key element in the reduction of hookworm prevalence in the poor nations of the world involves the prevention of soil contamination by the installation of latrines or other sanitary disposal systems for human feces and the wearing of shoes. Hookworm disease was largely eliminated from the southern states of the United States long before there was effective medical treatment thanks, in large part, to The Rockefeller Sanitary Commission for the Eradication of Hookworm, founded in 1909 with a $1,000,000 gift from John D. Rockefeller, Sr. The program was successful largely due to: 1) getting people to use toilets and outhouses and not defecate on the ground; 2) the wearing of shoes.

23
Q

Cutaneous larva migrans Epidemiology

A

This condition results from exposure of the skin to the infective larvae of non-human dog or cat hookworm. (Usually Ancylostoma braziliense or Ancylostoma caninum) These animal larvae cannot complete their normal life-cycle in the accidental human host but persist for a time under the skin without developing further.

Creeping eruption is essentially a disease of gardeners, children and sea bathers who come into contact with damp, sandy soil contaminated with dog and cat feces. Creeping eruption is worldwide in distribution.

24
Q

Cutaneous larva migrans Clinical manifestations

A

Symptoms usually start immediately or within a few hours after penetration of the skin. An itchy bump develops at the site of penetration, usually the feet, hands and knees. (Nude sunbathers may develop the rash on the breasts, chest, buttocks and hips.) Itching becomes intense and over a few days’ time a serpiginous—snakelike—slightly elevated, red track develops as the larvae migrate. The advancing border usually moves relatively slowly a few millimeters each day leaving tunnels which become dry and crusted.

The typical form of cutaneous larva migrans is fairly easy to recognize in that the serpentine (“snake-like”) red track is rather distinctive.

Another form of cutaneous larva migrans, however, may not be so easy to diagnose but should be considered in patients who have traveled to endemic areas (tropical tourist beach areas of Thailand, Martinique, Guadeloupe, Mexico, and Brazil) and present with an unexplained severe, widespread, itchy eruption of papulo-pustules, especially on their buttocks and back. In these patients, the pustules are rich in eosinophils. And unlike common variety folliculitis due to bacterial infection, this manifestation of cutaneous larva migrans it VERY itchy whereas frantic itching is not common in bacterial folliculitis. This type of cutaneous larva migrans is called “hookworm folliculitis.” The differential diagnosis includes scabies and bacterial folliculitis.

25
Q

Cutaneous larva migrans diagnosis and therapy

A

Diagnosis. The lab is not much help here. One relies on the classic picture of a slowly advancing serpentine tunnel (in the usual presentation) in the skin associated with intense itching and lesions that persist for months.

To diagnose hookworm folliculitis, you really have to be on your toes and think about this as a possible diagnosis. So, if you see a patient who has a rash all over his or her body, but especially on the buttocks and back, that looks like plain old bacterial folliculitis (but is usually more widespread) you should ask the patient: “Where have you traveled?” If they say they recently returned from a beach vacation in, for example, Thailand, you should begin to think: ‘hmmmmm……..’

Therapy. Albendazole is effective. A single dose of oral ivermectin can be used for treatment. A 10% suspension of thiabendazole applied 4 times daily to the rash and continued for two days after the disappearance of the last track also works.

26
Q

Strongyloidasis epidemiology

A

Strongyloidiasis (“threadworm”), is caused by Strongyloides stercoralis. This parasite is distributed widely in the tropics, subtropics and in many temperate climate areas such as West Virginia. Infection generally occurs as the result of skin contact with infective larvae in the soil. Infection may also be caused by transmission of larvae from contaminated clothing, in fecally contaminated food or water or in feces transmitted by sexual activity involving anal contact. Transmission can occur via breast milk.

Certain individuals are at increased risk for Strongyloidiasis: those who have been on high dose corticosteroids, leukemia or lymphoma patients on immunosuppressive therapy and patients with prior gastric surgery or organ transplant. (Board alert! A question often goes like this: A patient, usually a child, is on steroids for asthma and suddenly goes downhill (crashes). The CBC will show an eosinophil count of 30-70%. Think hyperinfection with Strongyloides!)

27
Q

Strongyloidasis life cycle

A

. This parasite has a very complicated life cycle. For the purpose of this discussion it is enough to know that individuals mainly become infected by entry of the parasite through the skin, usually the feet, with further development within the patient in a cycle similar to that of hookworm. (Passage of larvae via the venous system to the right side of the heart, then the lungs, migration up the trachea, over the glottis and eventual residence in the duodenum and small intestine.) Once infected, patients may re-infect themselves through “autoinfection” (internal autoinfection—from their own intestine—and external autoinfection—from larvae hanging out in stool unwiped/uncleansed from skin around the anus). As the name implies, autoinfection means that larvae from the patient may re-infect that same individual without going through a phase in the soil. Through this process of autoinfection the cycle may continue indefinitely and this capacity to replicate within the host is the basis for both the persistence of infection for as long as forty years after initial contact with the parasite and the potential for “hyper-infection” (overwhelming infection) in the immunocompromised patient.

(Four parasites—3 worms and 1 tapeworm—have the unique capacity for autoinfection: 1) pinworm; 2) Strongyloides; 3) capillaria; 4) Hymenolepsis nana, the dwarf tapeworm.)

28
Q

Strongylodias clinical manifestations

A

The majority of infections are asymptomatic. Passage of larvae through the lungs may produce symptoms of cough and wheezing (Loffler’s Syndrome) and the presence of larvae in the gut may present as pain in the pit of the stomach accompanied by diarrhea.

In the case of chronic disease, patients are often asymptomatic or may present with a history of indigestion, lower abdominal cramping, and intermittent or persistent diarrhea.

Some patients may show an urticarial rash—an itchy rash with hives (not all that common). An interesting rash (even less common than an urticarial rash—but rather diagnostic if you encounter it…and may pop up on a Board question), known as larva currens (racing larva), occurs in some patients with this disease. This rash generally occurs around the buttocks or groin as a poorly defined, rapidly moving serpentine erythemic (red, blush-like) rash that lasts hours to days. Though uncommon, when seen, this rash is pathognomonic for strongyloidiasis. (A Board question may go like this: a child who has been put on steroids or is on chemotherapy for cancer develops a dry cough, nausea, diarrhea, a high eosinophil count and a rash that rapidly moves across the skin at a rate of 1-2 cm per hour. Think Strongyloides.) In contrast, the rash of Cutaneous Larva Migrans (“creeping eruption”) due to accidental penetration of human skin by dog or cat hookworm, presents as an intensely itchy, slowly advancing, serpiginous, well defined, tunnel in with skin with little surrounding redness and persists for months.

Hyper infection with dissemination (“disseminated strongyloidiasis”) occurs in some patients, particularly those who are immunosuppressed either as a result of administration of immunosuppressive drugs, as a result of concomitant disease, or both. In patients with this severe hyper infection syndrome, large numbers of worms migrate and invade organs throughout the body including the liver, spleen, pancreas, thyroid, adrenals, kidney, prostate and central nervous system. The hyper infection syndrome and disseminated strongyloidiasis may be accompanied by a life threatening blood borne bacterial infection and life threatening gram negative sepsis.

29
Q

Strongylodias Diagnosis

A

. A dramatic increase in the blood eosinophil count is often the first clue picked up on routine blood examination in patients who return from an endemic area (or live in an endemic area such as West Virginia) with gastrointestinal complaints often accompanied by cough and wheezing.

It is important for physicians to realize that in life-threatening, overwhelming disease the eosinophil count may plummet to a very low count, or even be absent, just before the patient dies, instead of being markedly elevated as it is in the usual infection.

(On Board questions, the eosinophil count is usually sky high—30 to 70% in a patient with symptoms suggestive of strongyloidiasis. I don’t know the Boards have ever asked the question to reflect the low eosinophil count as a terminal stage, but if they did it would take the form of someone with symptoms of strongyloidiasis who had the usual high eosinophil count, took a dramatic turn for the worse, and just before dying was found to have a very low eosinophil count or a count that bordered on zero. Odds are, any Board test question will take the form of the usual presentation: high eosinophil count.)

When stool is examined under the microscope, larvae (not eggs) are found when this parasite is present. (Stool specimens containing hookworm eggs which are not kept in preservative and are allowed to sit around for several hours may lead to hatching of the hookworm eggs and the appearance of hookworm larvae which can easily be confused with Strongyloides larvae.) Larvae also may be recovered by use of the “string test”. (See discussion of string test under “Giardiasis”.) Strongyloides can be detected on agar plates (the parasites leave visible “tracks” on the surface).

PCR is available. An enzyme immunoassay (EIA) test is available. This test has greater than 90% sensitivity. Unfortunately, the EIA test does not distinguish old infection from newly acquired infection and can give false positive results in patients with filariasis and there can be cross-reactivity with other nematode infections. Still, it is a good place to start…

30
Q

Strongylodias Therapy and prevention

A

Therapy. All infected patients should be treated. Eradication of worms is the goal since any remaining parasites may produce autoinfection which, years later, can lead to life threatening illness in the immunocompromised patient. Ivermectin has been shown to be effective and well tolerated in the treatment of strongyloidiasis. The Medical Letter now lists ivermectin as the drug of choice. Albendazole has been used successfully. Untreated, hyperinfection syndrome has a nearly 100% mortality. And remember, hyperinfection is encountered in WV; several cases have popped up in Huntington over the years and have often been diagnosed by specialist physicians from other countries who are familiar with the hyper-infection manifestations of this parasite!

Prevention. Wear shoes and don’t sit on the ground bare-assed.

31
Q

pinworm epidemiology

A

Pinworm infestation is ubiquitous throughout the world, but especially in temperate climates (e.g. the United States and European countries) and is one of the few parasites that is much more prevalent in temperate climates than in tropical climates. The prevalence in the general childhood population of the United States is estimated at 20%. Some authors put the rate at 100% in institutionalized children.

Humans are the only host. The family dog or cat does not harbor human-pinworm in its intestine. Human pinworm eggs, however, can be transferred on the fur of family pets to humans (fomites). The usual mode of transmission is by fingernail contamination to the mouth of eggs picked up by scratching around the anus. Eggs may be transmitted on soiled bed linen (and other fomites such as clothing, furniture, rugs, toys and pet fur noted above) and it has been shown that contaminated eggs in dust may enter the nose or mouth as a means of airborne transmission. The eggs develop into adult worms and migrate to the anus where the adult female deposits thousands of potentially infective eggs daily. The eggs and resulting larvae are infective within a matter of hours and remain infective for two or three weeks. In addition to the modes of transmission noted above, retroinfection occurs when hatched pinworm larvae crawl from around the anus, back into the rectum where they develop into adult worms and mate.

32
Q

pinworm clinical manifestation

A

Itching around the anus, often intense and especially common at night, is the hallmark of this infection. Adolescent females seem prone to occasionally developing vaginal itch and even urinary tract infections due to wandering worms. Insomnia, restlessness, irritability and bed wetting are common features of pinworm infection. Appendicitis has been reported (rarely) due to obstruction of the appendiceal lumen by pinworms. Some authors, however, feel the presence of a pinworm in the appendiceal lumen of a patient with appendicitis is pure coincidence.

Now, here’s a curious tidbit: Dientamoeba fragilis (long considered an amoeba but now reclassified as an aberrant trichomonad flagellate or, by some authors, an ameba-like flagellate), may be transmitted in pinworm eggs! We’ll discuss this parasite in the winter parasitology course.

33
Q

pinworm diagnosis

A

Checking the stool itself (standard “Stool for O and P x 3”) is a low yield endeavor for finding pinworms or pinworm eggs. You are much more likely to find evidence of pinworm infestation using the “Scotch-tape test”. This test is performed by applying a strip of cellulose, pressure-sensitive tape, such as Scotch Tape, to the skin around the anal opening, then placing the tape sticky side down onto a microscopic slide for examination in the lab. Another equally reliable method used in diagnosis is the digital exam: the gloved little finger—without lubricant—is inserted just inside the anal opening and material from the glove is transferred to a slide and examined under the microscope.

Very often mothers come to my office and ask for medicine to treat pinworm. I ask them why they think their child has pinworm and they seem a little offended and reply, “Well, I saw the worms. Anybody can tell what a pinworm looks like! “When I ask them to describe what they saw they describe small white, moving worms. I perform a digital rectal exam and if no eggs are identified, send the parent and child home with a Scotch Tape test kit. In a significant percentage of patients the lab cannot detect pin worm eggs using this extremely accurate test. After several Scotch Tape tests have been run I am often left with the conclusion that the mother did not see pinworms in the first place.

What is happening here? I have a theory….I think what happens in a significant percentage of cases is that the kid has been scratching his or her rear end, the mother noticed this, she pulled the kid’s pants down and had a good close look. And as she looked she saw little white things moving…alive! But what she really saw were tiny bits of cotton or tissue paper moving from her own breath.

On the other hand, about half the time I actually find the pinworm eggs and the mothers glare at me as if to say, “See, I told you so, you dolt.”

34
Q

pinworm tx

A

The important point to keep in mind is that if one person in the family has pinworm, everyone has it. Therefore, everyone in the household must be treated! Numerous drugs are effective in treating pinworm. Mebendazole may be given in a single oral dose of 100 mg. Albendazole is another excellent drug given as a single oral dose of 400 mg. Repeat the dose of mebendazole or albendazole once more in 2 weeks. Do not use albendazole and mebendazole in pregnancy. Pyrantel pamoate is another favorite drug for treating pinworm. Ivermectin can be used but it is not yet FDA approved for pinworm.

It is often very difficult to eliminate pinworm from a family. Retreatment may be required several times over the course of a year. Also, remember to reassure parents that pinworm infestation has nothing to do with lack of cleanliness in the home or poor parenting.

35
Q

Tricheinellosis epidemiology and geographic distribution

A

Trichinellosis occurs worldwide. The disease is caused by parasites of the genus Trichinella (T.s. spiralis, T.s. nativa and T.s. nelsoni) which humans acquire from eating the undercooked muscles of domestic pigs or wild animals. In many North American and European nations and in Russia, domestic pigs were traditionally the source of infection for humans; today, wild animal meat, particularly bear and wild boar, is an increasingly important source of infection. (Artic walruses and seals have been recognized as a source of infection. Unusual outbreaks have occurred in France and Italy from the human consumption of horsemeat imported from the USA!)

36
Q

Tricheinellosis Life cycle

A

Man acquires the disease by eating raw or inadequately cooked meat, particularly pigs and certain wild animals (principally bear and wild boar) containing larvae encysted in striated skeletal muscle. The larvae are liberated by gastric juices and are transported by peristalsis to the small intestine. After mating the females begin to discharge larvae which then enter the mesenteric lymphatics or the bloodstream and are distributed throughout the body. Larvae that enter tissue other than striated muscle die. Those that enter striated muscle “encyst” and may remain viable for years. Eventually encysted larvae calcify and die.

37
Q

Tricheinellosis Pathology

A

Generally, the degree of illness reflects the number of larvae ingested.

Intestinal Phase: During this phase of worm development to the adult stage, there is mucosal irritation and associated enteritis. During the phase of penetration of the mesenteric lymphatics and capillaries by the larvae there may be an associated bacteremia and patient deaths have been reported.

Muscle Invasion Phase: There is a significant inflammatory response to invasion of larvae into muscle cells, particularly in the masseters, extraocular muscles, the tongue, diaphragm, intercostals, gluteus, biceps and gastrocnemius.

Myocardial Involvement: Acute congestive heart failure may result from myocarditis, generally one to two months after infection.

Neurologic Involvement: Although larvae are unable to successfully encyst in the nervous system, petechial hemorrhages within the brain may occur accompanied by marked meningeal irritation.

38
Q

Tricheinellosis Clinical Manifestations

A

Intestinal Stage: During the first 1 to 7 days after infection, symptoms include diarrhea, abdominal cramping, nausea and vomiting and general malaise. Headache may accompany the intestinal symptoms.

Muscle Invasion Stage: Between 1 to 8 weeks after infection there may be marked muscle pain and tenderness, facial and periorbital edema (often subtle, but when present a significant clue), conjunctivitis, splinter hemorrhages involving the nailbeds (this is another big clue), a diffuse maculopapular rash (in about 10% of patients), rapid heart and respiratory rate, fever and chills. Neurologic and cardiac complications, as noted above in the section on Pathology, may occur.

Chronic Stage: Vague muscle pains and general malaise may persist for months.

39
Q

Tricheinellosis Diagnosis

A

Patients who present with a history of eating poorly cooked pork (often at a family or church picnic), wild pig or bear meat who develop first intestinal and then muscular symptoms, and have laboratory findings of marked eosinophilia, elevated creatinine phosphokinase and aspartate aminotransferase have a strong likelihood of having disease due to Trichinella spiralis. The ELISA test is the lab test most often used for diagnosis.

Muscle biopsy is the definitive test. By the fourth week of infection, one may biopsy the gastrocnemius and pectoralis muscles at sites of swelling or tenderness for fixation and histologic examination. Biopsy material should be compressed between glass slides for microscopic examination to reveal encysted worms. Another standard technique involves digestion in 1% pepsin and 1% hydrochloric acid followed by agitation, concentration by centrifugation and microscopic examination.

40
Q

Tricheinellosis Therapy

A

Therapy

Steroids are recommended for severe infections plus mebendazole.

In many cases, low cost analgesic, antipyretic treatment may be all that is warranted.

Prevention and Control

In European countries each pig is inspected at the time of slaughter. The incidence of swine infection in Germany is approximately 0.00003%. In the United States, pigs are not routinely inspected at the time of slaughter. In one study, when US pigs were inspected, infection for garbage fed hogs was 0.5%.

41
Q

Tricheinellosis prevention and control

A

Prevention of trichinosis includes:

  1. Adequate cooking of pork at 77 degrees C (171 degrees F) until meat changes from pink to gray. Cook until center is gray. Microwave and smoking meat does not always kill the larvae.
  2. Freezing meat less than 15 cm thick at -15 degrees C (5 degrees F) for at least 30 days. Thicker meat may need to be frozen for a longer period of time. Trichinella parasites in meat from arctic animals may be resistant to freezing and must be thoroughly cooked to eliminate the parasite.
  3. Testing carcasses for infection with a digestion technique.
  4. Examination of pigs using ELISA.
  5. Enforce laws requiring cooking of garbage before feeding to swine.
  6. Thorough cooking of wild animals, particularly wild pigs.

This is one of the parasites the folks who write Board questions love to include on exams. Know the clinical manifestations!