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Ascariasis

For patient information click here Template:DiseaseDisorder infobox

This page is about clinical aspects of the disease.  For microbiologic aspects of the causative organism(s), see Ascaris lumbricoides.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Ascariasis is a globally occurring helminthic infection of humans.[1] It is the most common human helminth infection.[2] The transmission of infection is usually from hand to mouth, and humans are the only known host.[2] Ascariasis is more common in tropical areas of the world and predominantly affects the pediatric age group.[3]

Historical Perspective

Ascariasis has been around for several years and the scientific study of Ascaris lumbricoides was promoted by Edward Tyson.[4]

Pathophysiology[2][3][1]

The transmission of infection is usually from hand to mouth, and humans are the only known host. Following ingestion of infective eggs, larvae hatch and invade the intestinal mucosa. The larvae are carried via the portal, then systemic circulation to the lungs. The larvae mature further in the lungs, penetrate the alveolar walls, and ascend the bronchial tree to the throat. The larvae are then swallowed. Upon reaching the small intestine, they develop into adult worms. The adult worms can live for 1 to 2 years.

Causes

Ascariasis is a soil helminth infection caused by the nematode Ascaris lumbricoides.[2]

Differentiating Ascariasis from other Diseases

Ascariasis can mimic other worm infections, and also gastrointestinal pathologies like peptic ulcer disease, intussusception in children, bile duct stone, etc.[5][6]

Epidemiology and Demographics

Ascariasis affects at least 1 billion people worldwide and about 4 million people in the United States.[3] It is more common in the pediatric age group (ages 2-10 years).[3] Ascariasis is three times more common in African-Americans compared to Caucasians.[3]

Risk factors

The risk factors for ascariasis are often associated with poor sanitary conditions and environmental fecal contamination.[1]

Natural History, Complications and Prognosis

Ascariasis is often asymptomatic and more than 80% of infected individuals experience minimal or no symptoms of the disease.[7] Complications may arise when adult worms move to certain organs such as the bile duct, pancreas, or appendix.[7] A high worm burden can also result in complications such as intestinal obstruction.[1] The prognosis is good as most cases of ascariasis are asymptomatic, but mortality can sometimes be as high as 60,000 per year.[7] Mortality from ascariasis is usually as a result of complications from the infection, approximately 4.6% of patients hospitalized with complications of ascariasis die from the infection.[8]

History and Symptoms

Ascariasis is often asymptomatic. It can sometimes present with mild pulmonary and abdominal symptoms such as cough, dyspepsia, and nausea. However, severe cases of ascariasis occasionally occur especially following mechanical obstruction of a viscus.[7]

Physical Examination

The physical examination findings in ascariasis vary and it is usually dependent on the worm burden and the involved organ.[1] Abdominal tenderness can occur secondary to intestinal obstruction, appendicitis, biliary colic, acute cholangitis, acute cholecystitis, hepatic abscess, etc.[9]

Laboratory Findings

Ascariasis is frequently diagnosed in the laboratory via microscopic identification of eggs in the feces.[7]

Chest and Abdominal X-ray

A chest x-ray can reveal varying sizes of oval or round infiltrates (Loffler’s syndrome). These infiltrates usually resolve spontaneously.[3] Plain abdominal radiographs and contrast studies can reveal worm masses in bowel loops.[3][7]

CT

CT scan with contrast can reveal foreign bodies such as worms in the gastrointestinal tract.[3][7]

Ultrasound

Ultrasonography can reveal worms in the biliary tree, pancreatic duct and bowel loops.[3][7]

Other Diagnostic Studies

Imaging studies such as endoscopic retrograde cholangiopancreatography (ERCP) can identify worms in the pancreaticobiliary tract.[3]

Medical Therapy

All ascariasis infection (symptomatic and asymptomatic) should be treated with antimicrobial therapy.[7] Due to the high rate of reinfection, it is sometimes necessary to repeat antimicrobial therapy.[1] Antimicrobial therapy with albendazole is usually the treatment of choice for ascariasis, although other antihelminthic medications can effectively eradicate the parasite.[2]

Surgery

Ascariasis is usually managed conservatively with medical therapy but surgery may be indicated when medical management fails or complications arise.[7] Some of the indications for the surgical management of ascariasis include complete intestinal obstruction with inadequate decompression, complications such as volvulus, intussusception or intestinal perforation, acute appendicitis, worms trapped in ducts, etc.[7]

Prevention

The prevention of ascariasis is best achieved through improvements in personal hygiene and environmental sanitation.[10]

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Kliegman, Robert; Stanton, Bonita; St. Geme, Joseph; Schor, Nina (2016). “Chapter 291:Ascariasis (Ascaris lumbricoides)”. Nelson Textbook of Pediatrics Twentieth Edition. Elsevier. pp. 1733–1734. ISBN 978-1-4557-7566-8.
  2. 2.0 2.1 2.2 2.3 2.4 Kim, Kami; Weiss, Louis; Tanowitz, Herbert (2016). “Chapter 39:Parasitic Infections”. Murray and Nadel’s Textbook of Respiratory Medicine Sixth Edition. Elsevier. pp. 682–698. ISBN 978-1-4557-3383-5.
  3. 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 Ferri, Fred (2017). “Chapter:Ascariasis”. Ferri’s Clinical Advisor 2017. Elsevier. pp. 117–117. ISBN 978-0-3232-8048-8.
  4. Crompton DW (1988). “The prevalence of Ascariasis”. Parasitol Today. 4 (6): 162–9. PMID 15463076.
  5. Hamed AD, Akinola O (1990). “Intestinal ascariasis in the differential diagnosis of peptic ulcer disease”. Trop Geogr Med. 42 (1): 37–40. PMID 2260195.
  6. Goel A, Lakshmi CP, Pottakkat B (2012). “Biliary ascariasis: mimicker of retained bile duct stone”. Dig Endosc. 24 (6): 480. doi:10.1111/j.1443-1661.2012.01338.x. PMID 23078449.
  7. 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 Durand, Marlene (2015). “Chapter 288:Intestinal Nematodes (Roundworms)”. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.
  8. de Silva NR, Chan MS, Bundy DA (1997). “Morbidity and mortality due to ascariasis: re-estimation and sensitivity analysis of global numbers at risk”. Trop Med Int Health. 2 (6): 519–28. PMID 9236818.
  9. Das AK (2014). “Hepatic and biliary ascariasis”. J Glob Infect Dis. 6 (2): 65–72. doi:10.4103/0974-777X.132042. PMC 4049042. PMID 24926166.
  10. Centers for Disease Control and Prevention.https://www.cdc.gov/parasites/ascariasis/prevent.html Accessed on the 3rd of March, 2017.

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Ascariasis has been around for several years and the scientific study of Ascaris lumbricoides was promoted by Edward Tyson.[1]

Historical Perspective

Ascariasis is an helminthic infection of man that has been around for so many years. Edward Tyson promoted the scientific study of Ascaris lumbricoides about three centuries ago.[1]

References

  1. 1.0 1.1 Crompton DW (1988). “The prevalence of Ascariasis”. Parasitol Today. 4 (6): 162–9. PMID 15463076.


Template:WikiDoc Sources

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Ascariasis is the most common human helminth infection.[1] The transmission of infection is usually from hand to mouth, and humans are the only known host.[1]

Pathophysiology

Ascariasis is a soil-transmitted helminth infection with the round worm(nematode) called Ascaris lumbricoides, and humans are the only known host.[1] The pathogenesis of ascariasis involves the following processes:[1][2][3]

Transmission

  • The eggs are primarily transmitted from hand to mouth, but they may also be ingested in raw fruits and vegetables grown in soil contaminated with the eggs of ascaris.
  • The eggs may also be ingested in water contaminated with the ova of ascaris or via inhalation of ova in regions with high worm burden. Ascaris infection occurs about 9-12 days after egg ingestion.

Dissemination

  • Following ingestion of the eggs, the fertilized ova hatch in the small intestine and the larvae penetrates the intestinal mucosa.
  • The larvae then proceeds to the lungs via the venous circulation and migrates through the alveoli and the bronchial tree, resulting in pulmonary ascariasis.
  • The larvae ascend the bronchial tree to the throat, and are subsequently swallowed and returned to the intestines where maturation into adult worms occur.

Pathogenesis

  • The adult worms have a life span of 10-24 months within the human host. The adult male worms are 10-30cm long, while the adult female worms are larger and they measure up to 40cm long.
  • Intestinal obstruction associated with intestinal perforation, volvulus and intussusception can occur in patients with large worm burdens. Worms can also migrate into the biliary tree resulting in biliary colic and pancreatitis.
  • Migration of worms to the appendix can result in acute appendicitis.
  • The fecund female worm produces a very high output of eggs (about 200,000 eggs/day), and eggs are passed out of the intestine with the feces where they can survive for years in warm, moist, shaded soil.
  • At temperatures of 5-100C, the eggs of ascaris can remain viable for as long as two years.
The Life Cycle of Ascaris lumbricoides
(1) Adult worms 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. (2) and (3) Fertile eggs embryonate and become infective in 5-10 days depending on the environmental conditions (optimum: moist, warm, shaded soil). (4) Infective eggs are swallowed. (5) The larvae hatch, 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. (7) The larvae are then swallowed. Upon reaching the small intestine, they develop into adult worms. The female ascaris begin depositing eggs in 8-10 weeks. Adult worms can live 1 to 2 years. – Source: https://www.cdc.gov/

References

  1. 1.0 1.1 1.2 1.3 Kim, Kami; Weiss, Louis; Tanowitz, Herbert (2016). “Chapter 39:Parasitic Infections”. Murray and Nadel’s Textbook of Respiratory Medicine Sixth Edition. Elsevier. pp. 682–698. ISBN 978-1-4557-3383-5.
  2. Ferri, Fred (2017). “Chapter:Ascariasis”. Ferri’s Clinical Advisor 2017. Elsevier. pp. 117–117. ISBN 978-0-3232-8048-8.
  3. Kliegman, Robert; Stanton, Bonita; St. Geme, Joseph; Schor, Nina (2016). “Chapter 291:Ascariasis (Ascaris lumbricoides)”. Nelson Textbook of Pediatrics Twentieth Edition. Elsevier. pp. 1733–1734. ISBN 978-1-4557-7566-8.


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Causes
This page is about microbiologic aspects of the organism(s).  For clinical aspects of the disease, see Ascariasis.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]}}; Associate Editor-In-Chief: Imtiaz Ahmed Wani

Overview

Ascaris lumbricoides is the giant roundworm of humans, growing to a length of up to 35 cm (13.779527545 in).[1] It is one of several species of Ascaris. An ascarid nematode of the phylum Nematoda, it is the largest and most common parasitic worm in humans. This organism is responsible for the disease ascariasis, a type of helminthiasis and one of the group of neglected tropical diseases. An estimated one-sixth of the human population is infected by A. lumbricoides or another roundworm.[2] Ascariasis is prevalent worldwide, especially in tropical and subtropical countries.

Lifecycle

File:Ascaris lumbricoides life cycle.tif
Image showing lifecycle inside and outside of the human body of one fairly well described helminth: A. lumbricoides

A. lumbricoides, a roundworm, infects humans when an ingested fertilised egg becomes a larval worm that penetrates the wall of the duodenum and enters the blood stream. From there, it is carried to the liver and heart, and enters pulmonary circulation to break free in the alveoli, where it grows and molts. In three weeks, the larva passes from the respiratory system to be coughed up, swallowed, and thus returned to the small intestine, where it matures to an adult male or female worm. Fertilization can now occur and the female produces as many as 200,000 eggs per day for a year. These fertilized eggs become infectious after two weeks in soil; they can persist in soil for 10 years or more.[3]

The eggs have a lipid layer which makes them resistant to the effects of acids and alkalis, as well as other chemicals. This resilience helps to explain why this nematode is such a ubiquitous parasite.[4]

Morphology

File:Ascaris lumbricoides4.jpg
Fertile egg as can be seen in a microscope
File:Ascaris lumbricoides.jpg
Fertile egg in human faeces (detail)
File:Ascaris lumbricoides non-fertile egg.jpg
Infertile egg

A. lumbricoides is characterized by its great size. The male’s posterior end is curved ventrally and has a bluntly pointed tail. Females are wide and long. The vulva is located in the anterior end and accounts for about one-third of its body length. Uteri may contain up to 27 million eggs at a time, with 200,000 being laid per day. Fertilized eggs are oval to round in shape and are long and wide with a thick outer shell. Unfertilized eggs measure long and wide.[5]

Genus and Species Ascaris lumbricoides
Common Name Giant Intestinal Roundworm
Etiologic Agent of: Ascariasis
Infective stage Embryonated Egg
Definitive Host Man
Portal of Entry Mouth
Mode of Transmission Ingestion of Embryonated egg through contaminated food or water
Habitat Small Intestine
Pathogenic Stage Adult Larva
Mode of Attachment Retention in the mucosal folds using pressure
Mode of Nutrition Feeding of Chyme
Pathogenesis Larva – pneumonitis, Loffler’s syndrome;

Goes through a Blood-Lung Phase (Hookworm and Strongyloides stercoralis also have a blood-lung phase); Adult worm– Obstruction, Liver abscess, Appendicitis.

Laboratory diagnosis Direct Fecal Smear; Concentration methods such as Kato-Katz
Treatment Albendazole, Mebendazole, or Pyrantel Pamoate
Diagnostic Feature – Adult Female – prominent genital girdle
Diagnostic Feature – Egg Coarse mammilated albuminous coating

Epidemiology

More than 2 billion people are affected by this infection.[3] The United States has a reported prevalence of 0.8% of the total population as of 1987. A. lumbricoides eggs are extremely resistant to strong chemicals, desiccation, and low temperatures. The eggs can remain viable in the soil for several months or even years.[5]

Eggs of A. lumbricoides have been identified in archeological coprolites in the Americas, Europe, Africa, the Middle East, and New Zealand, the oldest ones being more than 24,000 years old.[7]

Infections

Infections with these parasites are more common where sanitation is poor,[8] and raw human feces are used as fertilizer.

Symptoms

Often, no symptoms are seen with an A. lumbricoides infection. However, in the case of a particularly bad infection, symptoms may include bloody sputum, cough, fever, abdominal discomfort, intestinal ulcer, passing worms, etc.[9][10] Ascariasis is also the most common cause of Löffler’s syndrome worldwide. Accompanying symptoms include pulmonary infiltration, eosinophilia, and radiographic opacities [11]

Prevention

Preventing any fecal-borne disease requires educated hygienic habits/culture and effective fecal treatment systems. This is particularly important with A. lumbricoides because its eggs are one of the most difficult pathogens to kill (second only to prions), and the eggs commonly survive 1–3 years. A. lumbricoides lives in the intestine where it lays eggs. Infection occurs when the eggs, too small to be seen by the unaided eye, are eaten. The eggs may get onto vegetables when improperly processed human feces of infected people are used as fertilizer for food crops. Infection may occur when food is handled without removing or killing the eggs on the hands, clothes, hair, raw vegetables/fruit, or cooked food that is (re)infected by handlers, containers, etc. Bleach does not readily kill A. lumbricoides eggs, but it will remove their sticky film, to allow the eggs to be rinsed away. A. lumbricoides eggs can be reduced by hot composting methods, but to completely kill them may require rubbing alcohol, iodine, specialized chemicals, cooking heat, or “unusually” hot composting (for example, over 50 °C (122 °F) for 24 hours[12])

Details of infection process

Infections happen when a human swallows water or food contaminated with unhatched eggs, which hatch into juveniles in the duodenum. They then penetrate the mucosa and submucosa and enter venules or lymphatics. Next, they pass through the right heart and into pulmonary circulation. They then break out of the capillaries and enter the air spaces. Acute tissue reaction occurs when several worms get lost during this migration and accumulate in other organs of the body. The juveniles migrate from the lung up the respiratory tract to the pharynx where they are swallowed. They begin producing eggs within 60–65 days of being swallowed. These are produced within the small intestine, where the juveniles mature. It might seem odd that the worms end up in the same place where they began. One hypothesis to account for this behavior is that the migration mimics an intermediate host, which would be required for juveniles of an ancestral form to develop to the third stage. Another possibility is that tissue migration enables faster growth and larger size, which increases reproductive capacity.[13]

Diagnosis and treatment

Most diagnoses are made by identifying the appearance of the worm or eggs in feces. Due to the large quantity of eggs laid, physicians can diagnose using only one or two fecal smears.

Infections can be treated with drugs called ascaricides. The treatment of choice is mebendazole. The drug functions by binding to tubulin in the worms’ intestinal cells and body-wall muscles. Nitazoxanide and ivermectin can also be used.[5]

References

  1. “eMedicine – Ascaris Lumbricoides : Article by Aaron Laskey”. Archived from the original on 27 January 2008. Retrieved 2008-02-03.
  2. Harhay, Michael O; Horton, John; Olliaro, Piero L (2010). “Epidemiology and control of human gastrointestinal parasites in children”. Expert Review of Anti-infective Therapy. 8 (2): 219–34. doi:10.1586/eri.09.119. PMC 2851163. PMID 20109051.
  3. 3.0 3.1 Murray, Patrick R.; Rosenthal, Ken S.; Pfaller, Michael A. Medical Microbiology, Fifth Edition. United States: Elsevier Mosby, 2005Template:Pn
  4. Piper R (2007). Extraordinary Animals: An Encyclopedia of Curious and Unusual Animals, Greenwood Press.Template:Pn
  5. 5.0 5.1 5.2 Roberts, Larry S.; Janovy, John Jr. Foundations of Parasitology, Eighth Edition. United States: McGraw-Hill, 2009Template:Pn
  6. 6.00 6.01 6.02 6.03 6.04 6.05 6.06 6.07 6.08 6.09 6.10 6.11 6.12 6.13 6.14 6.15 “Public Health Image Library (PHIL)”.
  7. Dridelle R. Parasites. Tales of Humanity’s Mostly Unwelcome Guests. Univ. of California, 2010. p. 26. ISBN 978-0-520-25938-6.
  8. “DPDx – Ascariasis”. Archived from the original on 24 February 2008. Retrieved 2008-02-03.
  9. MedlinePlus Encyclopedia Ascariasis
  10. http://www.stanford.edu/group/parasites/ParaSites2005/Ascaris/JLora_ParaSite.htm#Symptoms
  11. Löffler, W (1956). “Transient Lung Infiltrations with Blood Eosinophilia”. International Archives of Allergy and Applied Immunology. 8 (1–2): 54–9. doi:10.1159/000228268. PMID 13331628.
  12. http://weblife.org/humanure/chapter7_18.html
  13. Read, A. F.; Sharping, A. (1995). “The evolution of tissue migration by parasitic nematode larvae”. Parasitology. 111 (3): 359–71. doi:10.1017/S0031182000081919. PMID 7567104.

Template:Helminthiases

Differentiating Ascariasis from other Diseases

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2] Furqan M M. M.B.B.S[3]

Overview

Ascariasis can mimic other worm infections, and also gastrointestinal pathologies like peptic ulcer disease, intussusception in children, bile duct stone, etc.[1][2]

Differential Diagnosis

  • Differential diagnosis of intestinal ascariasis
  1. Peptic ulcer disease[1]
  2. Intestinal obstruction from Ascaris lumbricoides can mimic intussusception[3]
  • Differential diagnosis of biliary ascariasis
  1. Gallbladder cancer[4]
  2. Retained bile duct stone[2]
  • Other worm infections can sometimes have clinical presentations similar to that of Ascaris lumbricoides

The table below summarizes the findings that differentiate from other nematode infections:

Differentiating ascariasis from other Nematode infections[5][6][7]
Infection Nematode Transmission Direct Person-Person Transmission Duration of Infection Pulmonary Manifestation Location of Adult worm(s) Treatment
Ascariasis Ascaris lumbricoides Ingestion of infective ova No 1-2 years Free air in the lumen of the small bowel

(primarily jejunum)

Strongyloidiasis Strongyloides stercoralis Filariform larvae penetrate skin or bowel mucosa Yes
  • Lifetime of the host
Embedded in the mucosa of the duodenum, jejunum
Trichuriasis Trichuris trichiura

(whipworm)

Ingestion of infective ova No 1-3 years
  • No pulmonary migration, therefore, no pulmonary manifestation
Anchored in the superficial mucosa of cecum and colon
Hookworm infection Necator americanus and Ancylostoma duodenale Skin penetration by filariform larvae No Attached to the mucosa of mid-upper portion of the small bowel
Enterobiasis Enterobius vermicularis

(pinworm)

Ingestion of infective ova Yes
  • 1-month
  • Extraintestinal migration is very rare
Free air in the lumen of cecum, appendix, adjacent colon

References

  1. 1.0 1.1 Hamed AD, Akinola O (1990). “Intestinal ascariasis in the differential diagnosis of peptic ulcer disease”. Trop Geogr Med. 42 (1): 37–40. PMID 2260195.
  2. 2.0 2.1 Goel A, Lakshmi CP, Pottakkat B (2012). “Biliary ascariasis: mimicker of retained bile duct stone”. Dig Endosc. 24 (6): 480. doi:10.1111/j.1443-1661.2012.01338.x. PMID 23078449.
  3. Katz Y, Varsano D, Siegal B, Bar-Yochai A (1985). “Intestinal obstruction due to Ascaris lumbricoides mimicking intussusception”. Dis Colon Rectum. 28 (4): 267–9. PMID 3979231.
  4. Kong F, Xi H, Bai Y, Li Z (2015). “Ascaris infestation of biliary tree mimicking gallbladder cancer”. Dig Liver Dis. 47 (2): e3. doi:10.1016/j.dld.2014.09.012. PMID 25308610.
  5. Durand, Marlene (2015). “Chapter 288:Intestinal Nematodes (Roundworms)”. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.
  6. Kim, Kami; Weiss, Louis; Tanowitz, Herbert (2016). “Chapter 39:Parasitic Infections”. Murray and Nadel’s Textbook of Respiratory Medicine Sixth Edition. Elsevier. pp. 682–698. ISBN 978-1-4557-3383-5.
  7. Serpytis M, Seinin D (2012). “Fatal case of ectopic enterobiasis: Enterobius vermicularis in the kidneys”. Scand J Urol Nephrol. 46 (1): 70–2. doi:10.3109/00365599.2011.609834. PMID 21879805.


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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Ascariasis is a globally occurring helminthic infection of humans.[1] It is more common in tropical areas of the world and predominantly affects the pediatric age group.[2]

Epidemiology and Demographics

Prevalence

Ascariasis occur globally and it is the most common helminthic infection of humans.[1] Ascariasis affects at least 1 billion people worldwide and about 4 million people in the United States.[2]

Age

Ascariasis occur in all age groups but it is more common in the pediatric age group (ages 2-10 years).[2]

Sex

Males and females are equally affected.

Race

Ascariasis is three times more common in African-Americans compared to Caucasians.[2]

Geographic Distribution

Ascariasis occurs worldwide although it is more common in tropical regions of the world compared to the temperate regions (the environmental conditions are optimal for the development of the ova in the soil).[1][3] The majority of people at risk for infection (71% of persons) live in Asia and the Western pacific region.[2][3] 22% of persons at risk for infection live in Africa and the Middle East, and 11% of persons at risk for infection live in Latin America.[3] In the US, the majority of the infection occur in the rural southeastern part of the country and it is often associated with poor sanitation.[2]

References

  1. 1.0 1.1 1.2 Kliegman, Robert; Stanton, Bonita; St. Geme, Joseph; Schor, Nina (2016). “Chapter 291:Ascariasis (Ascaris lumbricoides)”. Nelson Textbook of Pediatrics Twentieth Edition. Elsevier. pp. 1733–1734. ISBN 978-1-4557-7566-8.
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Ferri, Fred (2017). “Chapter:Ascariasis”. Ferri’s Clinical Advisor 2017. Elsevier. pp. 117–117. ISBN 978-0-3232-8048-8.
  3. 3.0 3.1 3.2 Durand, Marlene (2015). “Chapter 288:Intestinal Nematodes (Roundworms)”. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.


Template:WikiDoc Sources

Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

The risk factors for ascariasis are often associated with poor sanitary conditions and environmental fecal contamination.[1]

Risk Factors

Risk factors for ascariasis include:[1][2][3]

  • Poor socioeconomic conditions
  • Use of human feces as fertilizer
  • Lack of hand washing
  • Eating unwashed fruits and vegetables
  • Environmental contamination with feces

Risk factors for Biliary ascariasis include:[4]

References

  1. 1.0 1.1 Kliegman, Robert; Stanton, Bonita; St. Geme, Joseph; Schor, Nina (2016). “Chapter 291:Ascariasis (Ascaris lumbricoides)”. Nelson Textbook of Pediatrics Twentieth Edition. Elsevier. pp. 1733–1734. ISBN 978-1-4557-7566-8.
  2. Al-Mekhlafi AM, Abdul-Ghani R, Al-Eryani SM, Saif-Ali R, Mahdy MA (2016). “School-based prevalence of intestinal parasitic infections and associated risk factors in rural communities of Sana’a, Yemen”. Acta Trop. 163: 135–41. doi:10.1016/j.actatropica.2016.08.009. PMID 27515811.
  3. Nwalorzie C, Onyenakazi SC, Ogwu SO, Okafor AN (2015). “PREDICTORS OF INTESTINAL HELMINTHIC INFECTIONS AMONG SCHOOL CHILDREN IN GWAGWALADA, ABUJA, NIGERIA”. Niger J Med. 24 (3): 233–41. PMID 27487594.
  4. Singh D, Yang S, Cappell MS (2016). “Biliary Ascariasis Diagnosed and Extracted by ERCP in the United States”. ACG Case Rep J. 3 (4): e188. doi:10.14309/crj.2016.161. PMC 5226187. PMID 28119939.


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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

Ascariasis is often asymptomatic.[1] Complications may arise when adult worms move to certain organs such as the bile duct, pancreas, or appendix.[1] A high worm burden can also result in complications such as intestinal obstruction.[2]

Natural History

The majority of people infected with Ascaris are asymptomatic although greater than 15% can experience some type of morbidity.[1]

Complications

Complications of ascariasis include the following:[3][2][4]

Prognosis

The prognosis is good and most cases of ascariasis are asymptomatic, but mortality can sometimes be as high as 60,000 per year in symptomatic patients.[1] Mortality from ascariasis is usually as a result of complications from the infection, and approximately 4.6% of patients hospitalized with complications of ascariasis die from the infection.[5]

Case fatality rates in published studies of >100 patients hospitalized due to any complication of ascariasis[5]
Country Period of study Total number of patients Number of deaths (N) % Number of deaths
USA 1940s 202 6 3
South Africa 1958–1962 100 3 3
Brazil 1970s 454 44 9.7
Burma 1981–1983 641 18 2.8
Burma 1984–1986 226 6 2.6
India 1980s 876 38 4.3

References

  1. 1.0 1.1 1.2 1.3 Durand, Marlene (2015). “Chapter 288:Intestinal Nematodes (Roundworms)”. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases Updated Edition, Eighth Edition. Elsevier. pp. 3199–3207. ISBN 978-1-4557-4801-3.
  2. 2.0 2.1 Kliegman, Robert; Stanton, Bonita; St. Geme, Joseph; Schor, Nina (2016). “Chapter 291:Ascariasis (Ascaris lumbricoides)”. Nelson Textbook of Pediatrics Twentieth Edition. Elsevier. pp. 1733–1734. ISBN 978-1-4557-7566-8.
  3. Ferri, Fred (2017). “Chapter:Ascariasis”. Ferri’s Clinical Advisor 2017. Elsevier. pp. 117–117. ISBN 978-0-3232-8048-8.
  4. Kim, Kami; Weiss, Louis; Tanowitz, Herbert (2016). “Chapter 39:Parasitic Infections”. Murray and Nadel’s Textbook of Respiratory Medicine Sixth Edition. Elsevier. pp. 682–698. ISBN 978-1-4557-3383-5.
  5. 5.0 5.1 de Silva NR, Chan MS, Bundy DA (1997). “Morbidity and mortality due to ascariasis: re-estimation and sensitivity analysis of global numbers at risk”. Trop Med Int Health. 2 (6): 519–28. PMID 9236818.


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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | X Ray | CT | MRI | Echocardiography or Ultrasound | Other Imaging Findings | Other Diagnostic Studies

Treatment

Treatment

Medical therapy | Surgery | Prevention | Future or Investigational Therapies

Prevention

Prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Fatimo Biobaku M.B.B.S [2]

Overview

The prevention of ascariasis is best achieved through improvements in personal hygiene and environmental sanitation.

Prevention

The prevention of ascariasis is best achieved by:[1]

  • Avoiding ingesting soil that may be contaminated with human feces, including where human fecal matter (“night soil”) or wastewater is used to fertilize crops.
  • Washing hands with soap and warm water before handling food.
  • Teaching children the importance of washing hands to prevent infection.
  • Washing, peeling, or cooking all raw vegetables and fruits before eating, particularly those that have been grown in soil that has been fertilized with manure.
  • Avoiding defecating outdoors.
  • The use of effective sewage disposal systems.

References

  1. Centers for Disease Control and Prevention.https://www.cdc.gov/parasites/ascariasis/prevent.html Accessed on the 3rd of March, 2017.


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Case Studies

Case Studies

Case #1

See also

See also

External links

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