Helminth infections

Helminths, i.e., parasitic worms, are a group of macroparasites encompassing a variety of species that can infect their hosts in three different ways: ingestion of eggs or larvae (e.g., via contaminated food and water or fecal-oral route), direct penetration of the skin, and via the bite of vectors (e.g., certain species of flies and mosquitoes). Helminths are classified based on their macroscopic appearance as nematodes (i.e, roundworms; genera include Toxocara, Enterobius, Trichuris, Ascaris, Trichinella, Strongyloides, Ancylostoma, Necator), cestodes (i.e.,tapeworms; genera include Taenia, Diphyllobothrium, Echinococcus), or trematodes (i.e., flukes; genera include Schistosoma, Metorchis, Fasciola). Most helminth species colonize the gastrointestinal tract of their hosts, provoking symptoms such as abdominal pain, nausea, and diarrhea. The larvae of certain helminth species, such as those of the Ascaris and Ancylostoma genus, migrate from the intestines via the portal vein to the lungs, potentially causing asthma-like symptoms (e.g., dry cough, wheezing). Other species, such as Taenia solium, are capable of colonizing other human tissue, such as the brain or the liver, which can lead to life-threatening complications (e.g., neurocysticercosis). Diagnosis of helminth infection is made primarily via evidence of eosinophilia in the blood and direct detection of worms, eggs, or larvae in stool samples. Serum IgE levels are often elevated. Treatment consists of anthelmintic agents, such as albendazole or praziquantel. For helminth infection prevention, see “Food and water safety.” Echinococcosis and schistosomiasis are discussed in separate articles.

Nematodes (roundworms) are long, thin, unsegmented, tube-like worms with a longitudinal digestive tract opening at both ends. Adult worms form separate sexes, with the males usually being smaller than the females. Filarial Nematodes are thread-like nematodes. They are transmitted by arthropod vectors.

eating a Toxic TrEAT: Toxocara, Trichiniella, Enterobius, Ascaris, and Trichiuris are transmitted by ingestion.

SANd on your Shins, Ancles, and Neck: Strongyloides, Ancylostoma, and Necator penetrate the skin while walking on sand.

The OWL bites: Onchocera, Loa loa, and Wucheria are transmitted by bites.

• Pathogen
  • Ascaris lumbricoides (giant roundworm)
  • Ascaris are nematodes.
• Epidemiology: most common helminth infection worldwide (mainly affects children in tropical countries with low standards of hygiene)
• Mode of transmission: : fecal-oral (infection occurs in the larval state following the consumption of contaminated food, especially raw vegetables that have been contaminated by human waste used as a fertilizer)
• Life cycle: : Host ingests eggs → Eggs hatch and release larvae → Larvae invade intestinal walls → Larvae migrate to lungs via portal vein → Larvae migrate into alveoli, trachea (“tracheal migration”), and larynx → Larvae are expectorated into the mouth and swallowed back into the intestine → Larvae return to the intestine → Larvae mature into adult worms, which then lay new eggs.
• Clinical features
  • Most patients are asymptomatic.
  • Early symptoms
    • Dry cough, blood-tinged sputum, wheezing
    • Loeffler syndrome: a transient respiratory disorder characterized by accumulation of eosinophils in the lungs due to certain infections (usually parasites) or allergic reactions to drugs. Symptoms are usually mild and resolve spontaneously
  • Late symptoms; : anorexia, abdominal discomfort, nausea, vomiting, and diarrhea
  • Additional symptoms due to blockage by adult worms depend on the location of the obstruction:
    • Bowel obstruction, especially at ileocecal valve (may lead to intestinal perforation)
    • Obstruction of the appendix → features of appendicitis
    • Obstruction of biliary and pancreatic ducts → features of cholestasis, pancreatitis
• Diagnosis
  • CBC shows eosinophilia.
  • Confirmatory test: Stool samples show the presence of worms or visible oval eggs with a knobby appearance under the microscope.
• Treatment
  • Treatment of choice: bendazoles
  • During pregnancy: pyrantel pamoate

• Pathogen
  • Enterobius vermicularis (pinworm)
  • Pinworms are nematodes.
• Epidemiology ^[2]
  • Most common helminthic infection in the U.S.
  • Prevalence in the US: ∼ 12%
  • Primarily affects children 5–10 years of age
• Mode of transmission
  • Initial infection: fecal-oral
  • Reinfection: digital-oral after scratching anal region
• Clinical features
  • Anal pruritus (especially at night)
  • Vulvovaginitis, especially in children
  • Occasionally, symptoms of intestinal infection (i.e., nausea, vomiting, and abdominal pain which may become severe enough to mimic appendicitis)
• Diagnosis
  • Tape test: microscopic detection of oval eggs (ova) and/or pinworms on tape that has been pressed against the perianal region
  • Can be an incidental finding on endoscopy
• Treatment: bendazoles OR pyrantel pamoate ^[3][4]
  • During pregnancy: pyrantel pamoate is the drug of choice
    • Should only be administered if pregnancy is compromised (e.g., weight loss, sleeplessness)
    • Should not be started until the 3^rd trimester, after which the risk to fetus is likely to be low.

Enterobius commonly manifests with perianal pruritus.

• Pathogen
  • Trichuris trichiura (whipworm)
  • Whipworms are nematodes.
• Mode of transmission: fecal-oral
• Life cycle: Host ingests eggs → Eggs hatch and release larvae in the small intestine → Larvae mature into adult worms in colon → Adult worms lay eggs, which are shed in feces.
• Clinical features
  • Mostly asymptomatic
  • In children: severe infection causes diarrhea, iron deficiency anemia, growth retardation, rectal prolapse
• Diagnosis
  • Microscopic examination of stool for eggs
  • Concentration technique can be used for light infections.
• Treatment: mebendazole OR albendazole

• Pathogen
  • Toxocara canis (dog roundworm), Toxocara mystax/Toxocara cati (cat roundworm)
  • Toxocara are nematodes.
• Mode of transmission: : fecal-oral (ingestion of Toxocara eggs from an infected dog or cat feces, e.g., in contaminated playground sand or garden soil) ^[5]
• Incubation period: 2–4 weeks
• Clinical features
  • Visceral toxocariasis (also called visceral larva migrans): caused by larvae migrating through the intestinal wall into the blood and reaching other organs
    • Fever and flu-like symptoms
    • Additional symptoms depend on the affected organs
      • Liver: hepatomegaly and abdominal pain
      • Lungs
        • Dyspnea, wheezing, cough, pneumonia
        • Loeffler syndrome
      • Skin: rash
      • Heart: myocarditis
      • CNS (also called neural larva migrans): seizures, coma
  • Ocular toxocariasis (also called ocular larva migrans): caused by larvae migrating into the eye
    • Unilateral impairment or loss of vision and resulting strabismus
    • Leukocoria
    • Inflammation, scarring, and possible detachment of the retina
• Diagnosis
  • Initial tests
    • Complete blood cell (CBC) count: eosinophilia
    • ↑ Serum total IgE
  • Confirmatory test: ELISA detects IgG antibodies to Toxocara excretory/secretory antigens
• Treatment: : bendazoles

• Pathogen
  • Trichinella spiralis and other Trichinella spp.
  • Trichinella are nematodes.
• Mode of transmission
  • Consumption of undercooked meat (especially pork) containing encysted larvae
  • Fecal-oral (rarely)
• Life cycle: Host ingests meat that contains cysts → Larvae invade the small bowel mucosa → Larvae develop into adult worms → Adult worms release larvae, which then migrate to muscles, where they encyst.
• Incubation period: 7–30 days ^[6]
• Clinical features
  • Intestinal phase : abdominal pain, diarrhea, nausea, and vomiting
  • Muscle phase
    • Myositis: myalgia, muscle swelling, weakness
    • Periorbital edema
    • Other symptoms include: fever, rash, splinter hemorrhages, retinal and conjunctival hemorrhages, chemosis
• Diagnosis
  • CBC shows eosinophilia (and sometimes leukocytosis).
  • Confirmatory test: serological detection of antibodies
  • ↑ Creatine kinase
  • Rarely muscle biopsy
• Treatment: bendazoles
  • In mild cases, the infection is selflimiting and analgetic therapy suffices.
  • Antihelminthics are only indicated in more serious cases with systemic manifestations.
• Complications
  • Cardiac: ECG changes (e.g., arrhythmias)
  • CNS: meningitis, encephalitis
  • Pulmonary: myositis involving respiratory muscles, pneumonia

Consider trichinella infection in patients with myositis, periorbital edema, and eosinophilia.

• Pathogen ^[7]
  • Human hookworms: Ancylostoma duodenale and Necator americanus
  • Zoonotic hookworms, i.e., cat and dog hookworms; (Ancylostoma braziliense and Ancylostoma caninum) can also infect humans.
  • Hookworms are nematodes.
• Mode of transmission: percutaneous penetration of larvae (primarily via the feet,e.g., while walking on a beach)
• Life cycle
  • Human hookworm; : Soil is contaminated with human feces containing hookworm eggs → Eggs hatch and release larvae → Larvae penetrate skin (usually the feet) → Larvae migrate to lungs via blood and lymphatic vessels; → Larvae migrate via bronchi and trachea to the larynx → Larvae are expectorated and swallowed back into the intestine → Larvae mature into adult worms that colonize the intestinal tract → Female hookworms lay eggs in the intestine → Eggs are eliminated with the feces.
  • Zoonotic hookworms are usually unable to break through the basement membrane after entering the human epidermis (humans are accidental intermediate hosts) → Migration through the epidermis for several weeks.
• Clinical features
  • Cutaneous symptoms
    • At entry site: pruritus, erythema, maculopapular rash
    • Cutaneous larva migrans (CLM): serpiginous marks (cutaneous lesion with a progressive, creeping, snake-like border) representing larval tracks
  • In zoonotic hookworm infections, only cutaneous symptoms are present.
  • Respiratory tract; : dry cough, wheezing, Loeffler syndrome
  • Intestine: abdominal pain, weight loss, nausea, vomiting, diarrhea
  • Microcytic anemia (hookworms ingest blood from the intestinal wall)
• Diagnosis
  • Initial test: CBC may show eosinophilia and microcytic anemia.
  • Confirmatory test: stool examination for eggs or worms
• Treatment
  • For human hookworms: bendazoles OR pyrantel pamoate
  • For CLM: bendazoles OR ivermectin

Consider hookworm infection in patients who present with a history of recent travel to a tropical country and microcytic anemia.

• Pathogen
  • Strongyloides stercoralis (threadworm)
  • Threadworms are nematodes.
• Mode of transmission: percutaneous penetration of larvae (primarily via the feet)
• Life cycle ^[8]
  • The Strongyloides eggs hatch in the human intestine and release larvae→ Larvae are excreted with the feces and contaminate the soil→ Larvae penetrate the intact skin of the definitive host upon contact with contaminated soil → Larvae migrate to the lungs via the bloodstream → Larvae migrate to the pharynx via the alveoli and bronchial system → Larvae are swallowed, causing autoinfection → Larvae mature into adult, egg-producing worms in the intestine → Eggs develop into infectious larvae and are excreted in feces.
  • Hyperinfection: Some larvae may penetrate the intestinal wall and enter the bloodstream (rare).
• Incubation period: 1–4 weeks
• Clinical features
  • Cutaneous phase
    • Swelling, erythema, maculopapular rash
    • Serpiginous lesions or urticarial tracts (larva currens is pathognomonic)
    • Pruritus
  • Pulmonary phase: dry cough and wheezing, hemoptysis, rarely pneumonia (Loeffler syndrome)
  • Intestinal phase: inflammation (e.g., duodenitis)
    • Abdominal pain
    • Diarrhea
    • Anorexia, nausea, vomiting
• Complications
  • Hyperinfection syndrome may lead to organ dysfunction and septic shock and occurs especially in immunosuppressed individuals (e.g., steroid therapy, HTLV-1 coinfection, AIDS).
  • Meningitis
• Diagnosis
  • Initial test: CBC may show eosinophilia.
  • Confirmatory test: consecutive stool examination for mobile rhabditiform larvae
• Treatment: ivermectin OR bendazoles

• Pathogen: Loa loa, a filarial nematode ^[9][10]
• Mode of transmission: bite from Chrysops (deer fly), horse fly, mango fly
• Life cycle: Introduction of larvae into bite wound → Larvae mature into adult worms → Adult worms reside in subcutaneous tissue, migrating through the body and causing symptoms → Adult worms produce microfilariae and release them into the bloodstream, where they are ingested by a female fly during a blood meal → Microfilariae mature into larvae, thus completing the cycle.
• Incubation period: 3–5 months
• Clinical features
  • Most infected individuals are asymptomatic.
  • The two cardinal manifestations are:
    • Calabar swelling: transient, localized swellings found commonly on the arms, legs, and around joints, which can cause pruritus and local pain
    • Ocular manifestation (eye worm): Loa loa has a tendency to migrate to the subconjunctival tissue of the eye where it causes self-limiting congestion, pruritus, and pain.
• Diagnosis
  • Initial test: CBC may show eosinophilia.
  • Confirmatory tests
    • Blood smear: detection of microfilariae
    • Visualization of adult worms in subcutaneous tissue or conjunctivae
    • Serology
• Treatment: diethylcarbamazine
• Complications
  • Encephalitis
  • Cardiomyopathy
  • Nephropathy
  • Arthritis
  • Lymphadenitis

• Pathogen: Onchocerca volvulus ^[9][11]
• Mode of transmission: bite of the female blackfly
• Life cycle: Host is bitten by blackfly → Larvae are introduced into bite wound → Larvae mature into adult worms that reside in subcutaneous or intramuscular tissue → Adult worms produce microfilariae → Microfilariae migrate through subcutaneous tissue, causing clinical symptoms → Female fly consumes microfilariae during a blood meal → Microfilariae mature into larvae, thus, completing the cycle.
• Clinical features
  • Ocular onchocerciasis
    • Keratitis
    • Uveitis
    • Optic atrophy
    • Onchochorioretinitis
    • Ocular lesions can progress to blindness (hence the common name river blindness)
  • Onchocercal skin disease
    • Onchocercomata (subcutaneous nodules): deep, nonpalpable nodules containing adult worms that are found over various bony prominences
    • Generalized pruritic lesions
    • Hyperpigmented papules (sowda)
    • Skin atrophy (due to loss of skin elasticity)
    • Hanging groin
    • Depigmentation (leopard-skin appearance)
  • Systemic manifestations
    • Allergic reactions to microfilariae may occur
    • Weight loss
    • Generalized musculoskeletal complaints (e.g., back and joint pain)
    • Inguinal and femoral hernia
• Diagnosis
  • Skin snips (gold standard): superficial skin biopsies are taken from an inflamed area and are incubated in saline, causing microfilariae to leave the skin sample. Microfilarial load can be determined microscopically.
    • At least two specimens are sampled and examined for motile microfilariae.
    • Specimens of subcutaneous nodules can also be sampled and examined for adult worms.
  • Slit-lamp examination: investigation of choice for ocular onchocerciasis
  • Mazzotti test: a provocative test that involves administering diethylcarbamazine (DEC) to induce microfilarial death and exacerbate symptoms. A positive test is highly suggestive of onchocerciasis.
  • Serology: an unreliable means of diagnosis as it cannot distinguish between active and past infection
• Treatment: ivermectin

Everything turns black in onchocerciasis: black flies, black skin nodules, black vision (blindness).

Treat rIVER blindness with IVERmectin.

• Pathogens
  • Wuchereria bancrofti: a nematode; responsible for most cases of lymphatic filariasis worldwide
  • Brugia malayi and Brugia timori: found in Asia
• Mode of transmission: female mosquito bite (Aedes, Mansonia, Anopheles, and Culex)
• Incubation period: 9–12 months
• Life cycle: Mosquito introduces filarial larvae into host via bite wound → Larvae mature into adult worms that reside in the lymphatic system → Adult worms produce microfilariae (the blood circulating stage of filariasis-causing roundworms) → microfilariae move throughout vascular and lymphatic system → microfilariae are consumed by a female mosquito during a blood meal → microfilariae mature into larvae, thus completing the cycle.
• Clinical features
  • Fever
  • Painful lymphadenopathy (due to worms invading lymph nodes, causing inflammation); and retrograde lymphangitis → lymphedema with disfiguration of the lower extremities (elephantiasis)
  • Hydrocele
• Diagnosis
  • Blood smear obtained at night (and staining with Giemsa or hematoxylin and eosin): detection of microfilariae
  • Serology: elevated levels of antifilarial IgG4
• Treatment
  • Diethylcarbamazine (DEC): drug of choice
  • Ivermectin: used in areas where onchocerciasis is prevalent, as DEC can worsen onchocercal eye disease
  • Elevation of the affected extremity, exercise, and wearing therapeutic shoes: recommended for those with lymphedema
  • Surgery for hydrocele

Cestodes (tapeworms) are long, flat, ribbon-like worms composed of numerous segments and a single scolex at the head with which they anchor themselves to the intestine. Since they do not have a digestive tract, all nutrients are absorbed through the tegument. Cestodes are hermaphroditic (they contain both male and female organs).

Cysticercosis can cause brain cysts and seizures.

• Pathogen ^[14]
  • Diphyllobothrium latum (fish tapeworm)
  • Fish tapeworms are cestodes.
• Mode of transmission: consumption of raw or undercooked freshwater fish containing larvae
• Life cycle: Larvae develop into adult tapeworms in the small intestine → Adult worms produce proglottids, which can detach from the tapeworm and are passed in the feces.
• Clinical features
  • Usually asymptomatic
  • Chronic infection leads to vitamin B₁₂ deficiency: fish tapeworms compete with the host for dietary vitamin B12 in the intestine → anemia and/or neurological symptoms
• Diagnosis
  • Initial test: CBC may show eosinophilia and megaloblastic anemia
  • Confirmatory test: stool examination for eggs or proglottids (i.e., segments of adult tapeworms)
• Treatment: praziquantel

Diphyllobothrium causes vitamin B12 deficiency.

• Pathogen: Hymenolepis nana (dwarf tapeworm) ^[15]
• Mode of transmission
  • Ingestion of eggs from contaminated food or water
  • Ingestion of cysticercoids from infected arthropods
• Life cycle: Ingestion of eggs → Develop into cysticercoid larvae in the small intestine villus (alternatively cysticercoids can be consumed from infected arthropods) → Cysticercoids (released upon rupture of the intestinal villus) develop into an adult worm in the intestinal lumen → Eggs are passed through the stool
• Clinical features
  • Mostly asymptomatic
  • Severe infection with Hymenolepis nana presents with:
    • Anorexia, abdominal pain, diarrhea
    • Weakness, headache
• Diagnosis: stool examination for eggs
• Treatment
  • Praziquantel
  • Niclosamide or nitazoxanide

Trematodes (flukes) are small, flat, oval worms with two suckers (one located at the mouth and the other ventrally) and a blind-ending gut. Most species are hermaphroditic, but some also form separate male and female adults.

• Pathogen
  • Clonorchis sinensis (Chinese liver fluke)
  • Clonorchis are trematodes (flukes).
  • Endemic to certain parts of Asia
• Mode of transmission: consumption of raw/undercooked freshwater fish
• Incubation period: 10–26 days ^[16]
• Life cycle: Water is contaminated with human feces containing Clonorchis eggs → Eggs are ingested by freshwater snails and mature into larvae → Larvae are released to water and penetrate fish → Humans eat fish containing larvae → Larvae migrate to biliary tract and mature into adult worms → Eggs of adult worms are released into the bile ducts and carried to the intestinal tract → Eggs are eliminated with the feces, thus completing the cycle.
• Clinical features
  • Most infected individuals are asymptomatic.
  • Acute symptoms
    • Cholangitis
    • Unspecific symptoms (e.g., right upper quadrant pain, diarrhea, fatigue)
  • Chronic symptoms and complications
    • Cholelithiasis with pigmented gallstones
    • Hepatomegaly
    • Malnutrition, weight loss
    • Jaundice
    • Risk factor for cholangiocarcinoma
• Diagnosis
  • Microscopic examination of stool for eggs
  • Serum studies: eosinophilia and ↑ alkaline phosphatase
• Treatment: praziquantel ^[17]

• Pathogen
  • Paragonimus westermani; (responsible for most infections), less commonly P. mexicanus, P. kellicotti, P. heterotremus, P. africanus
  • Paragonimus is a genus of trematodes that commonly infest the lung (lung flukes)
  • Paragonimus species are endemic to Southeast Asia, Latin America, and Africa.
• Mode of transmission
  • Consumption of raw/undercooked crabs, crayfish, and contaminated seaweed
  • Utilization of contaminated cooking utensils
• Incubation period: 2–16 weeks ^[18]
• Life cycle: Larvae in fresh water penetrate crabs, crayfish, and other crustaceans → Larvae encyst to metalarvae → Humans consume infected crustaceans → Metalarvae excyst and penetrate the intestinal wall, then migrate to the lungs → Larvae develop into adults in the lungs and eggs are expectorated with the sputum → Eggs are swallowed and eliminated with the feces, thereby reaching fresh water again.
• Clinical features
  • Rare prodromal signs (e.g., abdominal pain, fever, diarrhea)
  • Possibly asymptomatic
  • Pulmonary form
    • Mild fever
    • Night sweats
    • Productive cough, hemoptysis
    • Pleural effusions
  • Extrapulmonary form
    • Cerebral paragonimiasis
      • Early symptoms resemble meningoencephalitis.
      • Chronic symptoms include headache, vomiting, seizures, and weakness
    • Possibly cyst, abscess, and granuloma formation in the intestine, spleen, peritoneum, and mesenteric lymph nodes
• Diagnosis
  • Microscopic examination: detection of eggs in the sputum, feces, pleural fluid, cerebrospinal fluid, and pus
  • Serological test
    • CBC count: eosinophilia
    • Enzyme-linked immunosorbent assay (ELISA)
  • Chest x-ray showing ring shadows, fibrosis, calcifications, pleural effusions, and/or pleural thickening
• Differential diagnoses: tuberculosis
• Complications
  • Pulmonary complications: secondary infections, bronchiectasis, lung abscess, empyema
  • Cerebral complications: seizures, coma
  • Skin complications: migratory allergic skin lesions
• Treatment
  • Praziquantel ^[19]
  • Triclabendazol
  • Extrapulmonary lesions should be surgically excised
• Prevention: In endemic areas, avoid eating raw or undercooked crustaceans and seaweed.

• Pathogen: Fasciola hepatica, Fasciola gigantica
• Mode of transmission
  • Consumption of contaminated freshwater plants (e.g., watercress)
  • Drinking contaminated freshwater
• Life cycle
  • Metacercariae on freshwater plants are ingested by herbivorous mammals e.g., sheep, cattle (both definitive hosts), or humans (incidental hosts) → Migration of the organism through the intestinal wall, then liver parenchyma, and into the biliary ducts → Adult fluke release eggs into the biliary ducts, which are then passed in the stool of the host.
  • Snails serve as the intermediate hosts.
• Clinical features
  • Acute phase: fever, right upper quadrant pain, and hepatomegaly
  • Chronic biliary phase: abdominal pain, nausea, vomiting, and diarrhea
  • Features of biliary obstruction: biliary colic, cholangitis, cholelithiasis, and obstructive jaundice
• Diagnosis
  • Microscopic examination: detection of eggs in the stool or bile sample
  • CBC count: eosinophilia (marked in the acute phase)
  • Enzyme-linked immunosorbent assay (ELISA)
  • Endoscopy: adult flukes in the biliary tract
• Treatment
  • Triclabendazole
  • ERCP in case of biliary obstruction