ASCARIS LUMBRICOIDES

INTRODUCTION — Ascaris lumbricoides, an intestinal roundworm, is one of the most common helminthic
human infections worldwide. Highest prevalence in tropical and subtropical regions, and areas with
inadequate sanitation. Ascariasis occurs in rural areas of the southeastern United States. In United States,
ascariasis is the third most frequent helminth infection, exceeded only by hookworm and Trichuris
trichiura (whipworm) [1]. A. lumbricoides is the largest intestinal nematode of man. The female worms
are larger than the males and can measure 40 cm in length and 6 mm in diameter. They are white or pink
and are tapered at both ends. The epidemiology, life cycle and clinical features of ascariasis will be
reviewed here.

EPIDEMIOLOGY — It is estimated that more than 1.4 billion people are infected with A. lumbricoides,
representing 25 percent of the world population. A number of features account for its high prevalence
including a ubiquitous distribution, the durability of eggs under a variety of environmental conditions, the
high number of eggs produced per parasite, and poor socioeconomic conditions that facilitate its spread.
Transmission is enhanced by the fact that individuals can be asymptomatically infected and can continue
to shed eggs for years, yet prior infection does not confer protective immunity [2].

Although ascariasis occurs at all ages, it is most common in children 2 to 10 years old, and prevalence
decreases over the age of 15 years. Infections tend to cluster in families, and worm burden correlates with
the number of people living in a home [3]. Infection rates for ascariasis have not been reported to be
higher in patients infected with the human immunodeficiency virus (HIV) [4,5].

The highest prevalence of ascariasis occurs in tropical countries where warm, wet climates provide
environmental conditions that favor year-round transmission of infection. This contrasts to the situation
in dry areas where transmission is seasonal, occurring predominantly during the rainy months [6]. The
prevalence is also greatest in areas where suboptimal sanitation practices lead to increased contamination
of soil and water. The majority of people with ascariasis live in Asia (73 percent), Africa (12 percent) and
South America (8 percent), where some populations have infection rates as high as 95 percent [7,8]. In
the United States the prevalence of infection decreased dramatically after the introduction of modern
sanitation and waste treatment in the early 1900s [9]. It is estimated that the current prevalence of A.
lumbricoides in stool samples is approximately two percent in the United States, but it may be more than
30 percent in children between the ages of one to five years, particularly in rural areas of the South
[10,11]. It is also seen in travelers from endemic areas [7].

Ova can survive in the environment for prolonged periods and prefer warm, shady, moist conditions under
which they can survive for up to 10 years [1]. The eggs are resistant to usual methods of chemical water
purification but are removed by filtration or by boiling. Developing larvae will be destroyed by sunlight
and desiccation. There is no significant animal reservoir, but A. suum, which infects pigs, is
morphologically similar to A. lumbricoides, and the larval forms can occasionally infect humans.
Transmission — Transmission occurs mainly via ingestion of water or food (raw vegetables or fruit in
particular) contaminated with A. lumbricoides eggs and occasionally via inhalation of contaminated dust.
Children playing in contaminated soil may acquire the parasite from their hands. Transplacental migration
of larvae has also occasionally been reported [12]. Coinfection with other parasitic diseases occurs with
some regularity because of similar predisposing factors for transmission [10,13].

LIFE CYCLE — Adult worms inhabit the lumen of the small intestine, usually in the jejunum or ileum. They
have a life span of 10 months to 2 years and then are passed in the stool. When both female and male
worms are present in the intestine, each female worm produces approximately 200,000 fertilized ova per
day. When infections with only female worms occurs, infertile eggs that do not develop into the infectious
stage are produced. With male-only worm infections, no eggs are formed.

The ova are oval, have a thick shell, a mamillated outer coat, and measure 45 to 70 µm by 35 to 50 µm.
The ova are passed out in the feces, and embryos develop into infective second-stage larvae in the
environment in two to four weeks (depending upon environmental conditions). When ingested by
humans, the ova hatch in the small intestine and release larvae, which penetrate the intestinal wall and
migrate hematogenously or via lymphatics to the heart and lungs. Occasionally, larvae migrate to sites
other than the lungs, including to the kidney or brain.

Larvae usually reach the lungs by four days after ingestion of eggs. Within the alveoli of the lungs, the
larvae mature over a period of approximately 10 days, then pass up via bronchi and the trachea, and are
subsequently swallowed. Once back in the intestine, they mature into adult worms. Although the majority
of worms are found in the jejunum, they may be found anywhere from the esophagus to the rectum. After
approximately two to three months, gravid females will begin to produce ova which, when excreted,
complete the cycle.

Adult worms do not multiply in the human host, so the number of adult worms per infected person relates
to the degree of continued exposure to infectious eggs over time. Worm burdens of several hundred per
individual are not uncommon in highly endemic areas, and case reports of more than 2,000 worms in
individual children exist [8]. However the number of eggs produced per female worm tends to decrease
as the worm burden increases. It has been estimated that 9 x 10(14) eggs contaminate the soil per day
worldwide [14].
Life Cycle Figure – Adult worms (1) live in the lumen of the small intestine. A female may produce
approximately 200,000 eggs per day, which are passed with the feces (2). Unfertilized eggs may be
ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several
weeks (3), depending on the environmental conditions (optimum: moist, warm, shaded soil). After
infective eggs are swallowed (4), the larvae hatch (5), invade the intestinal mucosa, and are carried via
the portal, then systemic circulation to the lungs (6). The larvae mature further in the lungs (10 to 14
days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed (7). Upon
reaching the small intestine, they develop into adult worms (1). Between 2 and 3 months are required
from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years.
Source: CDC’s Parasite and Health Page about intestinal ascariasis.

CLINICAL FEATURES — The majority of infections with A. lumbricoides are asymptomatic. However, the
burden of symptomatic disease worldwide is still relatively high because of the high prevalence of disease.
Clinical disease is largely restricted to individuals with a high worm load [1]. When symptoms do occur,
they relate either to the larval migration stage or to the adult worm intestinal stage. Pathophysiologic
mechanisms include

Direct tissue damage

The immunologic response of the host to infection with larvae, eggs or adult worms [2]
Obstruction of an orifice or the lumen of the gastrointestinal tract by an aggregation of worms

Nutritional sequelae of infection [10]

The symptoms and complications of infection can be classified into the following:

1. Pulmonary and hypersensitivity manifestations

2. Intestinal symptoms

3. Intestinal obstruction

4. Hepatobiliary and pancreatic symptoms

1. Pulmonary and hypersensitivity manifestations — Transient respiratory symptoms can occur in

sensitized hosts during the stage of larval migration through the lungs. (See "Pulmonary manifestations
of ascariasis"). Symptoms associated with the pneumonitis, which are known as Loffler's syndrome, tend
to occur one to two weeks after ingestion of the eggs. The severity of symptoms tends to correlate with
larval burden, but pulmonary symptoms are also less common in countries with continuous transmission
of A. lumbricoides.

Urticaria and other symptoms related to hypersensitivity usually occur toward the end of the period of
migration through the lungs.

2. Intestinal symptoms — Heavy infections with Ascaris are frequently believed to result in abdominal
discomfort, anorexia, nausea and diarrhea. However, it has not been confirmed whether or not these non-
specific symptoms can truly be attributed to ascariasis.

With relatively heavy infections, impaired absorption of dietary proteins, lactose and vitamin A has been
noted, and steatorrhea may occur. One review concluded that Ascaris-free or treated children showed
better nutritional status in terms of growth, lactose tolerance, vitamins A and C, and albumin levels than
Ascaris-infected children based upon almost 20 years of published cross-sectional and intervention
studies from Africa, Asia and South America [15]. This review also found significant improvement in weight
or height following therapy for ascariasis. However, other studies have not confirmed these conclusions,
and the true effect of ascariasis on nutrition is still widely debated, especially as additional nutritional
deficiencies commonly co-exist in infected children [16-23]. It has also been proposed that heavy
infections may be associated with impaired cognitive development in school children [24,25].

3. Intestinal obstruction — A mass of worms can obstruct the bowel lumen in heavy Ascaris infection,
leading to acute intestinal obstruction. The obstruction occurs most commonly at the ileocecal valve.
Symptoms include colicky abdominal pain, vomiting and constipation. Vomitus may contain worms.
Approximately 85 percent of obstructions occur in children between the ages of one and five years.
Sometimes an abdominal mass that changes in size and location on serial examinations may be
appreciated [10]. Complications including volvulus, ileocecal intussusception, gangrene, and intestinal
perforation occasionally result.

The overall incidence of obstruction is approximately 1 in 500 children. In endemic areas, it has been
shown that between five and 35 percent of all cases of bowel obstruction are due to ascariasis [1]. One
review estimated the worm burden with intestinal obstruction to be >60 (and ten times higher in fatal
cases) [26]. Ascariasis is said to be the most common cause of acute abdominal surgical emergencies in
certain countries including South Africa and Myanmar [8]. In a recent meta-analysis of morbidity and
mortality related to ascariasis, intestinal obstruction accounted for a mean of 72 percent of complications
of the infection [27].

4. Hepatobiliary and pancreatic symptoms — Symptoms related to the migration of adult worms into the
biliary tree can cause abdominal pain, biliary colic, acalculous cholecystitis, ascending cholangitis,
obstructive jaundice, or bile duct perforation with peritonitis. Strictures of the biliary tree may occur [28].
Hepatic abscesses can also result [29]. Retained worm fragments can serve as a nidus for recurrent
pyogenic cholangitis. The pancreatic duct may also be obstructed, leading to pancreatitis, and the
appendix resulting in appendicitis. Occasionally, migrating adult worms emerge from the mouth, nose,
lacrimal ducts, umbilicus or inguinal canal. High fever, diarrhea, spicy foods, anesthesia and other stresses
have all been associated with an increased likelihood of worm migration [10].

In endemic countries such as India, ascariasis has been found to cause up to one-third of biliary and
pancreatic disease [30,31]. In one study performed in Syria, 300 patients with biliary or pancreatic
ascariasis were diagnosed by endoscopic retrograde cholangiopancreatography (ERCP) over a five-year
period [32]. Of these 300 patients, 98 percent presented with abdominal pain, 16 percent developed
ascending cholangitis, 4 percent developed acute pancreatitis, and 1 percent developed obstructive
jaundice. A previous cholecystectomy or endoscopic sphincterotomy had been performed in 80 percent.
Endoscopic extraction of the worms, successful in all but two cases, led to rapid resolution of symptoms.

Complications associated with A. lumbricoides infections are fatal in up to five percent of cases. It is
estimated that 20,000 deaths from ascariasis occur annually, primarily as a consequence of intestinal
obstruction [33].
Ascaris lumbricoides in small intestine – Intestinal obstruction occurs when large masses of Ascaris
accumulate. Source: Dr. Scott Smith’s lecture on GI Nematodes for “Parasites and Pestilence,” Stanford
University.

DIAGNOSIS — The diagnosis of ascariasis is usually made via stool microscopy. Other forms of diagnosis
are through eosinophilia, imaging, ultrasound, or serology examination.

q Microscopy — Characteristic eggs may be seen on direct examination of feces or following

concentration techniques. However, eggs do not appear in the stool for at least 40 days after infection;
thus, the main drawback of relying upon eggs in feces as the sole diagnostic marker for Ascaris infection
is that an early diagnosis cannot be made, including during the phase of respiratory symptoms. In addition,
no eggs will be present in stool if the infection is due to male worms only. Sometimes an adult worm is
passed, usually per rectum. If an Ascaris worm is found in the feces, a stool specimen can be checked for
eggs to document whether or not additional worms are present prior to instituting therapy [10].
Ascaris lumbricoides in stool – Wet mount of stool (x400) showing the ovum of ascaris lumbricoides.
Source: UpToDate’s Ascariasis Graphics.

q Eosinophilia — Peripheral eosinophilia can be found, particularly during the phase of larval migration
through the lungs but also sometimes at other stages of Ascaris infection [34]. Eosinophil levels are usually
in the range of 5 to 12 percent but can be as high as 30 to 50 percent. Serum levels of IgG and IgE are also
often elevated during early infection.

q Imaging — In heavily infested individuals, particularly children, large collections of worms may be
detectable on plain film of the abdomen. The mass of worms contrasts against the gas in the bowel,
typically producing a "whirlpool" effect [8]. Radiologic detection of adult worms is sometimes made by
detecting elongated filling defects following barium meal examinations of the small bowel. The worms
also sometimes ingest barium, in which case the alimentary canal appears as a white thread bisecting the
length of the worm's body [8]. Radiographs will also show when there is associated intestinal obstruction.
Biliary ascariasis – Cholangiogram obtained during endoscopic retrograde cholangiopancreatography
shows a linear filling defect (arrow) that was later identified as an adult Ascaris lumbricoides worm.
Source: UpToDate’s Ascariasis Graphics page.

q Ultrasound — Ultrasound examinations can help to diagnose hepatobiliary or pancreatic ascariasis.

Single worms, bundles of worms, or a pseudotumor-like appearance may be seen [35]. Individual body
segments of worms may be visible, and on prolonged scanning, the worms will show curling movements
[36]. Computed tomographic (CT) scanning or magnetic resonance imaging (MRI) may also be used to
identify worm(s) in the liver or bile ducts, but this is not usually necessary. Imaging the worm in cross-
section gives a "bull's eye" appearance. When ascariasis involving the biliary tree or pancreatic duct is
suspected, an ERCP will not only establish the diagnosis but also allows for the direct removal of the worm
[32,37].

q Serology — Infected individuals make antibodies to A. lumbricoides which can be detected. However,
serology is generally reserved for epidemiologic studies rather than in the diagnosis in a particular
individual [2]. IgG antibodies are not protective against infection [38]. Antibodies to Ascaris also often
cross react with antigens from other helminths.

TREATMENT — Treatment consists of choosing the right drugs, therapy, follow-up, and supportive
care for each patient.
Choice of Drugs — A number of drugs can be used in the treatment of ascariasis. These include: pyrantel
pamoate, mebendazole, albendazole, ivermectin, piperazine citrate, and levamizole.

Ascaris lumbricoides expelled following effective drug treatment. Source: Courtesy of Dr. Tom Nutman,
NIH.

* Pyrantel pamoate — Pyrantel pamoate (11 mg/kg up to a maximum of 1 g) is administered as a single

dose. Adverse effects include gastrointestinal (GI) disturbances, headaches, rash, and fever. Parasite
immobilization and death occur, although this happens slowly and complete clearance of the worm from
the GI tract may take up to three days. Efficacy varies with worm load, but single dose therapy is
approximately 90 percent effective in eradicating adult worms [6].

* Mebendazole — Mebendazole (100 mg BID for 3 days or 500 mg as a single dose) is an alternative.
Adverse effects include transient GI discomfort, headache, and rarely leukopenia. The three-day regimen
is approximately 95 percent effective, and the single dose seems to have similar results.

* Albendazole — A single dose of albendazole (400 mg) is effective in almost 100 percent of cases,
although reinfection commonly occurs [39]. Albendazole causes the same adverse effects as
mebendazole.

* Ivermectin — Ivermectin causes paralysis of adult worms and is approximately as effective as other
available therapies but is not generally used.
* Piperazine citrate — Piperazine citrate (50 to 75 mg/kg QD up to a maximum of 3.5 g for 2 days) was a
frequent treatment regimen, but it is now being withdrawn from the market in many developed countries
because the other alternatives are less toxic and more efficacious. However, it may still be recommended
when there is suspected intestinal or biliary obstruction since this drug paralyzes worms to aid expulsion.

* Levamisole — Levamisole (150 mg for adults and 5 mg/kg for children) is safe and is effective in 77 to
96 percent of cases of ascariasis.

Choice of therapy — The mainstays of treatment currently are the benzimidazoles, mebendazole and
albendazole. However, they should not be given during pregnancy because of possible teratogenic effects.
Thus, pyrantel pamoate should be used in pregnancy. In a randomized study conducted among 2,294
children aged 6 to 12 years in Zanzibar, single dose mebendazole and albendazole were both found to
have efficacies greater than 97 percent [40]. Similar results with both drugs and good tolerability have
also been observed in other studies [41-43].

Follow-up — All of these therapies act against the adult worm but not the larvae. Following therapy,
patients should be reevaluated at two to three months to ensure that no eggs are detectable, either
because of inadequate elimination of adult worms or because of reinfection. Reinfection occurs
frequently; more than 80 percent of individuals in some endemic areas become reinfected within six
months [1]. Evaluation of other family members should be entertained whenever the diagnosis is made
because of the propensity of the infection to cluster in families [10,12].

Supportive care — In addition to specific anthelminthic therapy, supportive therapy for complications of
ascariasis may be required, including potential surgical intervention for intraabdominal complications. In
biliary infections, conservative therapy with anthelminthics, often combined with antispasmodics, is often
successful. However, surgical or endoscopic interventions may be required.

Since pulmonary ascariasis is a self-limited disease, symptomatic alleviation of wheeze and cough with
inhaled bronchodilators can be instituted. Occasionally, systemic corticosteroids may be required for
symptoms. Following symptomatic therapy, standard therapy for intestinal ascariasis can be given after
the worms have developed to maturity in the small intestine [6]. Anthelminth therapy is not usually given
at the time of pulmonary symptoms because dying larvae may do more harm than migrating ones.
Biliary ascariasis – An adult Ascaris lumbricoides worm protruding from the major papilla is grasped with
forceps during endoscopic retrograde cholangiopancreatography. Source: UpToDate’s Ascariasis Graphics
page.

PREVENTION — Prevention of reinfection poses a substantial problem since Ascaris parasites are
abundant in soil. Good sanitation to prevent fecal contamination of soil is required. An education program
advising against the use of human feces as a fertilizer is also needed in some areas. Soil treatments have
been attempted but are generally not practical.

Mass treatments with single dose mebendazole or albendazole for all school-age children every three to
four months has been used in some communities. This serves the dual function of treating the children
and reducing the overall worm burden in the community. Indeed, mass community therapy has been
shown to reduce Ascaris burden and transmission, although it has a greater effect on the intensity of
infection than on the overall prevalence [44-47]. This approach has been shown to be cost-effective [48].
Because reinfections occur so frequently, shorter intervals between treatments have been found to be
preferable. Targeted treatment helps control the morbidity of infection but does not have a substantial
effect on transmission [44,49,50]. In a large randomized trial of school-based deworming performed in
Zanzibar, for example, single dose mebendazole, given either twice or three times a year, decreased
intensity of A. lumbricoides infection by 63 and 97 percent, respectively, compared to control children
who received no mebendazole [51].
Strongyloides

source: http://www.medstudents.com.br/original/relato/strong/strong1.jpg

INTRODUCTION:

Sometimes known as the threadworm, Strongyloides is an intestinal nematode (roundworm). It has a

unique free-living and parasitic generation. Although it contributes little to morbidity worldwide,
strongyloidiasis is potentially fatal in immunocompromised patients.

Taxonomy:

Class: Secernentasida
Subclass: Rhabditia
Order: Rhabditorida
Suborder: Rhabditina
Family: Strongyloididae
Genus: Strongyloides

Stryongyloides stercoralis is the species that causes the large majority of infections in humans. S.
stercoralis has been found in dogs and cats. Human infection from dogs has been demonstrated, but is
rare. No vector exists for S. stercoralis.

source: http://www2.provlab.ab.ca/bugs/webbug/parasite/artifact/image/89sstercoralis.jpg

History:
In 1867, Louis Normand, a military physician working at the Toulon Naval Hospital in France, observed
small worms in stool samples taken from repatriated soldiers from Vietnam. A colleague of Normand's,
Bavay, first named the worm Anguillula stercoralis (from Latin words for "small eel" and "dung").
Increased interest in the new worm led to the scientist Grassi establishing a new genus
called Strongyloides and he named the nematode from Normand's samples Strongyloides stercoralis.
Scientists Fulleborn (1911), Kreis (1932), and Faust (1933) all worked to elucidate the free-living,
parthenogenesis, and the autoinfection cycles of S. stercoralis. Napier, who carried out extensive clinical
surveys of repatriated British soldiers infected with S. stercoralis, and Galliard, who conducted
experiments in normal and immunosuppressed dogs, both contributed greatly to the understanding of
the clinical importance of strongyloidiasis. (Source: Tropical Infectious Diseases Guerrant, Walker, Weller)

LIFE CYCLE:

Strongyloides stercoralis has a very unique and complex life cycle. It alternates between free-living and
parasitic cycles and has the potential to cause autoinfection and multiply within the host (a characteristic
other nematodes do not possess).

source: http://dpd.cdc.gov/dpdx/HTML/Strongyloidiasis.htm

From the large intestine, rhabditiform larvae are excreted in the stool. The rhabditiform larvae either
develop into free-living adult males and females or they undergo direct development to become infective
filariform larvae.
Free-living adult worms mate and females produce fertilized, embryonated eggs. Rhabditiform larvae
hatch from these eggs, and either develop into filariform larvae or into another generation of free-living
adults.

source: http://www.courses.ahc.umn.edu/medical-school/IDis/Images/Strongyloides_life_cycle.gif
The parasitic cycle begins when the filariform larvae penetrate the human host skin. The circulatory
system allows the larvae to travel to the lungs and penetrate the alveolar spaces. Next, they are
transported to the pharynx, eventually swallowed, and reach the small intestine. In the small intestine,
the larvae molt twice to become adult female worms. These female worms produce eggs that become
deposited in the intestinal mucosa. Once they hatch, the new rhabditiform larvae travel to the lumen.
From there, they are either passed in the stool or cause autoinfection.

source: http://www.bbc.co.uk/gardening/children/images/worms_worms_head.gif

In autoinfection, rhabditiform larvae develop into filariform larvae, which may penetrate the intestinal
mucosa (internal autoinfection), or may penetrate the skin of the perianal area (external autoinfection).
In both cases, after subsequent penetration, the larvae follow the normal life cycle, again heading to the
lungs and eventually the small intestine.

TRANSMISSION:
source: http://barefooters.org/1995_spring/gifs/mtn_pjl_feet.jpg

Most often, transmission occurs through penetration of the human skin by filariform larvae. Because
infective larvae of Strongyloides stercoralis reside in top soil, they most often penetrate bare feet.

source: http://www.quantockonline.co.uk/z_images/kids/gallery_pics/worms.gif

Also, autoinfection is common—rhabditiform larvae in the large intestine mature into filariform larvae,
penetrate the intestinal mucosa, and continue the normal life cycle (See Life Cycle). The process of
autoinfection allows S. stercoralis to remain in the body indefinitely, and is a distinguishing feature of S.
stercoralis.

source: http://www.jorgecruise.com/images1/update2002/flax/stomach.jpg

MORPHOLOGY:

Strongyloides stercoralis is one of the smallest parasites known to infect humans. Female filariform larvae
(males are thought to be non-parasitic) are slender and fast-moving, being approximately 50 µm in
diameter and between 350-600 µm in length. Rhabditiform larvae are shorter and slower, 60 µm in
diameter and between 250-300 µm in length.

source: http://www.jfmed.uniba.sk/epid/atlas/obr74.jpg

They resemble hookworms, but their very short buccal cavity is unique. They can also be distinguished by
their prominent genital primordium (visible in the photo below on the right) and a pointed tail. Also, the
females can be recognized by their cylindrical pharynx with no posterior bulb swelling.

source: http://www2.provlab.ab.ca/bugs/webbug/parasite/artifact/strsterco.htm

Eggs are similar to oval shaped hookworm eggs.

source: http://www.emedicine.com/MED/topic1594.htm

CLINICAL PRESENTATIONS:

source: http://www.fbi.gov/page2/worm.jpg

Initially, the person may present with lesions and dermal itching where S. stercoralis penetrated the skin.
Once the larvae has migrated to the lungs, symptoms similar to moderate, bronchiole pneumonia may be
present along with coughing.

source: http://www.encuentro2000.org/itch.jpg and http://clear.msu.edu/dennie/clipart/cough.gif

In the intestines, S. stercoralis is often asymptomatic and generally goes unnoticed. Moderate infections
may result in a burning pain in the abdomen and diarrhea alternating with constipation. Heavy infections
can cause anemia, weight loss, and chronic diarrhea.
source: http://www.biosci.ohio-state.edu/~parasite/strongyloides.html

DIAGNOSTIC TESTS:

Most frequently, examination of fresh stool will reveal the presence of rhabditiform or filariform larvae in
a person infected with Strongyloides stercoralis. However, in asymptomatic patients, fecal matter may
contain only a small amount of parasite because female S. stercoralis produce a limited number of eggs
at irregular times, making detection difficult (stool sample sensitivity is between 30%-60%). Therefore,
taking many stool samples throughout the day is a way to increase the possibility of detection.

source: http://www.dailyillini.com/nov00/nov07/poop.jpg

The picture below shows rhabditiform larvae of S. stercoralis in feces.

source: http://www.mgh.harvard.edu/depts/aids/fulldemo/demo/strongdx.html

More recently, the enzyme-linked immunosorbent assay (ELISA) has been used to diagnose infection.

source: http://www.genox.com/images/elisa.gif

Also, in the case of disseminated strongyloidiasis, larvae may be present in the patient’s sputum.
source: http://www.nlm.nih.gov/medlineplus/ency/images/ency/fullsize/9945.jpg

TREATMENT:

Dating back to the 1960’s, thiabendazole has been commonly used as the most effective drug to
treat Strongyloides stercoralis. Studies have shown that patients given a dose of 25mg kg taken orally
twice daily for three days will have a greater than 80% chance of being cured, considering it is an
uncomplicated infection.

source: http://www.wholehealthmd.com/refshelf/drugs_view/1,1524,592,00.html and

http://www.hclrss.demon.co.uk/thiabendazole.html

However, treating Strongyloides stercoralis with thiabendazole may result in a number of side effects such
as nausea and neuropsychiatric symptoms.

source: http://www.gut-reaction.freeserve.co.uk/nauseo5.gif

Recently, a single oral dose of 200mg kg of ivermectin has demonstrated a cure rate of greater than 90%,
and treatment with a second dose of ivermectin a few days later will cause complete cure from the
infection.
source: http://www.indimmune.com/ivectin1.jpg

EPIDEMIOLOGY:

Strongyloides stercoralis is most prevalent in tropical and subtropical areas. However, areas of less than
1%-3% endemicity exist in many countries such as northern Italy, Switzerland, Poland, Australia (in
aboriginal populations), and in other temperate areas such as the southern United States and Bangladesh.

Red: hyperendemic; Green: endemic; Yellow: sporadic

source: http://www.reise-tropenmedizin.via.t-online.de/strong.gif

S. stercoralis is most often reported in rural areas and areas of lower socioeconomic status. Also, it
commonly infects adults more than children. Although estimates vary greatly, between 3-100 million
people are believed to be infected with S. stercoralis.
source: http://www.nsf.gov/od/lpa/forum/colwell/rc02_hippocratic/img005.jpg

In people with damaged and weakened immune systems, S. stercoralis can have deathly consequences as
disseminated strongyloidiasis can injur organs such as the liver, heart, pancreas, kidneys or even the
central nervous system. Thus, strongyloidiasis is of special concern in areas suffering from malnutrition,
high rates of HIV/AIDS, and/or human lymphotropic virus type 1 (HTLV-I).

PREVENTION:

source: http://www.cvm.tamu.edu/oncology/faq/faq/05-01.jpg

Studies have demonstrated Strongyloides stercoralis has a low infectivity rate for a population as a whole.
For this reason, mass chemotherapy treatment with drugs such as ivermectin may be effective, but would
not be an appropriate or necessary control to keep S. stercoralis from spreading in a community.
 source: http://www.westsky.com/colorbk3.jpg

Some studies suggest that infection is aggregated within households. This means that selectively targeting
infected households with chemotherapy may be an effective solution to contain the spread of infection.
Furthermore, having a house with a cement floor rather than an earth floor, and using a privately owned
bathroom rather than a public bathroom are household improvements that will reduce the chances of S.
stercoralis infection. On an individual level, wearing shoes in risk-areas is strongly advised and will
significantly lower one's likelihood of becoming infected.
The WHO currently has a program focused generally on intestinal nematodes.

REFERENCES:

https://web.stanford.edu/group/parasites/ParaSites2005/Ascaris/JLora_ParaSite.htm

https://web.stanford.edu/class/humbio103/ParaSites2003/strongyloides/index.html