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Neurocysticercosis

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Neurocysticercosis
Magnetic resonance image of a patient with neurocysticercosis demonstrating multiple cysticerci within the brain
SpecialtyInfectious diseases Edit this on Wikidata

Neurocysticercosis (NCC) is a parasitic infection of the central nervous system caused by the tapeworm Taenia solium. Neurocysticercosis is often caused by ingesting improperly cooked food or contaminated water. When consumed, cysticerci are released into the small intestine, where they attach to the intestinal wall and grow into a tapeworm. This tapeworm can travel to the brain, muscles, eyes, and skin. Neurocysticercosis presents various signs and symptoms, influenced by the location, number of lesions, and immune response, ranging from asymptomatic to fatal, with common symptoms including seizures, intracranial hypertension, cognitive impairment, and focal deficits.

Neurocysticercosis diagnosis relies on neuroimaging and serology, with diagnostic criteria including the lentil lectin purified glycoprotein (LLGP) enzyme-linked immunoelectrotransfer blot (EITB) assay, CT and MRI. Neurocysticercosis can be categorized as either parenchymal or extraparenchymal. Parenchymal neurocysticercosis is neurocysticercosis lesions within brain parenchyma, while extraparenchymal neurocysticercosis is lesions in ventricles or subarachnoid spaces. Neurocysticercosis can be prevented through improved sanitation, education, awareness, de-worming and vaccines for endemic areas.

Neurocysticercosis requires a tailored treatment approach based on cyst viability, host's immune response, and the location and number of lesions. Symptoms of neurocysticercosis are treated with antiepileptic, antiedema, analgesic, or anti-inflammatory drugs. Surgery, steroids, or other medications are used to treat intracranial hypertension. Antiparasitic medications are used for treating vesicular viable cysts or early colloidal phases and are ineffective against calcified cysts. Steroid administration is used for managing neurocysticercosis-related inflammation in the central nervous system. In severe cases, antiparasitic medication may be ineffective due to mass inflammation risks. Surgical treatments may be necessary for aggressive treatment, such as ventricle-peritoneal shunts and cyst excision. Parenchymal and single lesion neurocysticercosis generally has a favourable prognosis, while extraparenchymal neurocysticercosis can lead to obstructive hydrocephalus, sudden death, or slow death.

Neurocysticercosis is endemic in developing countries, particularly in poorer regions with poor sanitation and clean water, such as Latin America, China, Nepal, Africa, India, and Southeast Asia. Although rare in Europe and the US, immigration has increased its prevalence in these areas. Taenia solium has been described since 1500 BC and has been found in ancient Egyptian mummies. The first recorded cases of neurocysticercosis were likely in 1558. In 1792, a Peruvian physician reported simultaneous taeniasis and cysticercosis in the same individual. In the 19th century, German pathologists found similarities between T. solium and cysticercus scolex, and discovered that consumption of cysticercus from pork caused human intestinal taeniasis.

Signs and symptoms

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Neurocysticercosis has a wide range of signs and symptoms. This range of symptoms is due to the location, amount of lesions, and the immune system's response to the infection.[1] Neurocysticercosis can range from asymptomatic to deadly. Neurocysticercosis has been referred to as the "great imitator" because it can mimic many other neurological disorders.[2] The most common symptoms of neurocysticercosis are seizures, intracranial hypertension, cognitive impairment, and focal deficits.[1][3]

Manifestations of neurocysticercosis[4]
Location Form of the disease Common clinical manifestations
Brain parenchyma Vesicular cysts Seizures; sometimes asymptomatic.
Colloidal cysts Seizures; vomiting; headache; focal signs.
Granulomas/calcifications Seizures, sometimes reoccurring.
Cysticercotic encephalitis Seizures; coma; intracranial hypertension.
Subarachnoid space Giant cysts in CSF cisterns Seizures; focal signs; intracranial hypertension; cognitive impairment.
Diffuse arachnoiditis Focal signs; intracranial hypertension.
Hydrocephalus Intracranial hypertension; cognitive impairment.
Angiitis Acute stroke syndromes.
Ventricular system Ventricular cysts Focal signs; intracranial hypertension
Ependymitis Seizures; intracranial hypertension
Spinal cord Arachnoiditis Root pain; weakness; rarely meningitis
Parenchymal cysts Motor and sensory signs below the level of the lesion
Other Suprasellar cysticercosis Ophthalmologic and endocrinologic disturbances
Ophthalmic cysticercosis Visual loss; extraocular muscle paralysis
Muscle cysticercosis Muscle pseudohypertrophy

Seizures

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The figure summarizes the stages of NCC lesions: living viable cysts (left), degenerating dying lesions with inflammation (center), and dead calcified lesions (right). Markers that are increased in those with active epilepsy compared with NCC-infected subjects without epilepsy are shown: 1) pro-inflammatory cytokines (tumor necrosis factor-α, interferon-γ, and interleukin 1-β) and blood–brain barrier breakdown molecules (MMP-9); 2) lymphocyte adhesion molecules; and 3) mutations in regulators of lymphocyte adhesion (Toll-like receptor 4) associated with pro-inflammatory conditions.

The most common symptom of neurocysticercosis is seizures. In areas where neurocysticercosis is common, neurocysticercosis is the main cause of adult-onset epilepsy.[5] Seizures are more common in parenchymal neurocysticercosis than in other forms of neurocysticercosis.[1] Seizures may occur at any stage of the disease.[3] Partial seizures are the most common presentation.[6] If neurocysticercosis is left untreated seizures will often reoccur and can even persist despite treatment.[7] Seizures are more commonly associated with degenerating cysts.[3] These cysts are often accompanied by edema, inflammation, neuronal damage, and gliosis.[8][9] The seizures are caused by inflammatory responses in the brain and the space-occupying effect of the cysts.[10][11] Seizures are more common with multiple lesions. Active cysts are associated with first time seizures while calcified granulomas are associated with chronic epilepsy.[5]

Focal deficits

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Those with neurocysticercosis can exhibit a variety of specific neurologic symptoms according to the size, number, and location of the parasites. Pyramidal tract indications are the most common; however sensory impairments, parkinsonian rigidity, involuntary movements, language disturbances, and signs of brainstem dysfunction have also been reported. Focal neurologic symptoms are most commonly seen in patients with large subarachnoid cysts compressing the brain parenchyma.[4] Patients with neurocysticercosis and arachnoiditis may present with focal signs and ischaemic strokes caused by small and medium intracranial artery occlusion, cranial nerve entrapment resulting in extraocular muscle paralysis, hearing loss, facial nerve palsy or trigeminal neuralgia, and focal neurological symptoms caused by brainstem compromise. Cysticercosis of the spinal cord often causes radicular pain, weakness, and sensory impairments due to localized mass effects or inflammation in the subarachnoid space.[6]

Intracranial hypertension

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CT scan of the head of a patient with neurocysticercosis showing presence of hydrocephalus and dilation of ventricles

Intracranial hypertension is associated with neurocysticercosis and may be accompanied by other symptoms.[4] It is more common in extraparenchymal neurocysticercosis.[3] The most common cause of intracranial hypertension in neurocysticercosis is hydrocephalus.[4][6] Hydrocephalus can be related to granular ependymitis, compression of the CSF pathways by cysts, cysticercotic arachnoiditis, and inflammation or cysts blocking ventricles.[4][3] In addition, cerebral aqueduct stenosis has been linked to paroxysmal headaches and Parinaud's syndrome. Large subarachnoid cysts as well as cyst clumps, which typically grow in the Sylvian fissure or in the brain's basal cisterns, can also cause a mass effect with intracranial hypertension, with or without hydrocephalus.[12] Intracranial hypertension can present as episodic loss of consciousness when moving the head, known as Bruns syndrome.[4] Other times intracranial hypertension may be subacute or chronic.[6] Intracranial hypertension can also be caused by cysticercotic encephalitis, which is a severe type of neurocysticercosis usually affecting younger women and children.[3] Cysticercotic encephalitis is characterized by seizures, intracranial hypertension, clouding of consciousness, papilledema, headache, reduction of visual acuity, and vomiting.[13][14]

Cognitive and psychiatric disturbances

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Cognitive and psychiatric manifestations of neurocysticercosis can range from mild deficits to severe dementia. Episodes of psychosis which involve, paranoia, confusion, and violent behaviour have been reported to occur with neurocysticercosis. Some of these episodes could be associated with psychomotor epilepsy or postictal psychosis.[13][14] Other psychiatric symptoms of neurocysticercosis include anxiety, delirium, sensory changes, depression, and personality disorders. Those with neurocysticercosis may exhibit depression, cognitive impairments, or a decline in quality of life.[15]

Other symptoms

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Neurocysticercosis can cause a wide range of neurological symptoms, though headaches, strokes, and involuntary movements are the most common symptoms.[14] Spinal arachnoiditis can cause subacute root pain and weakness. Cysts in the spinal cord parenchyma are typically associated with motor and sensory impairments that vary depending on the location of the lesion. Those with cysticerci in the sellar region may have ophthalmologic and endocrinologic symptoms. Intraocular cysticerci are most commonly found in the subretinal space and cause a gradual reduction in visual acuity or visual field abnormalities. The cysts can cause inflammation of the vitreous membrane, uveitis, and endophthalmitis, which is the most serious complication of ocular cysticercosis and can result in phthisis bulbi. Cysticercal infection in striated muscles can cause weakening and hypertrophy over time.[13]

Causes

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Neurocysticercosis is caused by the larvae of a tapeworm called Taenia solium.[16] Many cases of neurocysticercosis result from the consumption of improperly cooked infected pork or other food, or contaminated water.[17][18] Once someone consumes something containing Taenia solium, cysticerci are released into the small intestine.[17] The scolex (head of the tapeworm) then evaginates and attaches to the intestinal wall. Once the scolex attaches, it grows into a tapeworm which penetrates the intestinal wall and gets into the bloodstream where it can travel to various areas of the body such as the brain, muscles, eyes, and skin.[19][20]

Mechanism

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The life cycle of Taenia solium

Taenia solium is a part of the Cestoda class and is a species of genera Taenia.[19] T. solium has two hosts, pigs and humans. Both pigs and humans can act as an intermediate hosts for the larval form, though humans are the only definitive hosts for the adult cestode. T. solium larvae are cystic, fluid-filled membrane vesicles containing a tapeworm head (scolex) with four suckers and a double crown of hooks, a narrow neck, and a huge body composed of several hundred proglottids. Normally, a human host ingests cysts in tainted pork, after which the scolex evaginates and clings to the intestinal wall with its effective suckers and hooks. Once the scolex is connected, the proglottids begin to multiply and mature into a 2–4 m ribbon-like tapeworm about 4 months after infection.[17][20]

When humans consume T. solium eggs, the eggs hatch into larvae that pierce the intestinal mucosa and spread throughout the body, causing cysticercosis. Although cysts can lodge in any tissue, the majority of adult cysts are located in the central nervous system, skeletal muscle, the skin, and the eyes.[21] Cysticerci penetrate the central nervous system as vesicular (viable) parasites with a transparent membrane, clear vesicular fluid, and a usual invaginated scolex. Cysticerci can live for years or, as a result of the host's immune response, degenerate and convert into inactive nodules. The colloidal stage of cysticerci involution is characterized by murky vesicular fluid and hyaline degeneration of the scolex. The cyst wall next thickens and the scolex transforms into mineralized granules; this phase, in which the cysticercus is no further viable, is known as the granular stage. Finally, the parasite remnants become mineralized nodules (calcified stage).[22][19]

Diagnosis

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Neurocysticercosis can be hard to accurately diagnose. The methods used to diagnose neurocysticercosis can be problematic and often hard to implement in areas with fewer resources.[23] Physical examination and laboratory testing are often not helpful in the diagnosis of neurocysticercosis.[24] The diagnosis of neurocysticercosis relies on neuroimaging and serology.[25] Diagnostic criteria have also been created to help with the diagnosis of neurocysticercosis.[26]

Immunodiagnosis

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So far, the lentil lectin purified glycoprotein (LLGP) enzyme-linked immunoelectrotransfer blot (EITB) assay, which employs targeted antigens to identify T. solium antibodies in patient serum, has produced the most consistent findings.[23] Antibodies can be identified in EITB as early as 5 weeks after infection. The LLGP-EITB has a sensitivity of 98% for individuals with multiple brain cysts and a specificity of 100%, while its sensitivity decreases in cases with a single cyst.[24] ELISA detection of anticysticercal antibodies in CSF is 89% sensitive and 93% specific for individuals with live neurocysticercosis infections, and it is still used when EITB is not available.[27]

Different presentation patterns of extraparenchymal neurocysticercosis as revealed by brain MRI

As much as 37% of those with neurocysticercosis had peripheral eosinophilia, the most prevalent hematologic abnormality in this group of individuals. The incidence of positive stool exams for Taenia solium eggs in individuals with neurocysticercosis varies between series and appears to be related to infection severity. Recognizing Taenia eggs is difficult, and many cases may go undetected during testing.[13]

Neuroimaging

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CT and MRI give objective information about the quantity and pattern of lesions, the phase of involution, and the extent of the host's inflammatory response to the parasites.[13] The ability to evaluate views in various spatial planes and the much improved image definition offered by MRI also address problems relating to the visibility of bone structures on CT, which makes it challenging to diagnose small lesions in the posterior fossa or near the skull. But the same robust signal for calcium on CT enables far higher sensitivity to detect calcifications in the brain.[24]

Live vesicular cysts are small, spherical lesions with minimal pericystic edema that do not require contrast enhancement. The tapeworm scolex is typically visible as an interior asymmetric nodule in cysts. Multiple live cysts with scolices corroborate the diagnosis. After the degenerative process has begun (colloid cysts), the cysts have ambiguous borders, are enclosed by edema, and exhibit significant ring or nodular contrast enhancement. Calcified cysticerci are plainly apparent on CT as non-enhancing hyperdense nodules that are usually free of peripheral edema.[14]

Diagnostic criteria

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Neurocysticercosis diagnostic criteria:[28]

(A) Gadolinium-enhanced magnetic resonance imaging (MRI) of the brain showing evidence of a fourth ventricular cystic structure. (B) Histopathology of a surgically removed cyst with i) cuticular layer with microvilli, ii) cellular layer, and iii) reticular layer. (C) Dissected cyst (neurocysticercosis) protruding from fourth ventricle. (D) Cyst post-excision.
  • Absolute criteria:
    • Histological demonstration of the parasite from biopsy of a brain or spinal cord lesion.
    • Visualization of subretinal cysticercus.
    • Conclusive demonstration of a scolex within a cystic lesion[a] on neuroimaging studies.
  • Neuroimaging criteria:
    • Major neuroimaging criteria:
      • Cystic lesions without a discernible scolex.
      • Enhancing lesions.[b]
      • Multilobulated cystic lesions in the subarachnoid space.
      • Typical parenchymal brain calcifications.[c]
    • Confirmative neuroimaging criteria:
      • Resolution of cystic lesions after antiparasitic drug therapy.
      • Spontaneous resolution of single small enhancing lesions.[d]
      • Migration of ventricular cysts[e] documented on sequential neuroimaging studies.
    • Minor neuroimaging criteria:
  • Clinical/exposure criteria:
    • Major clinical/exposure:
    • Minor clinical/exposure:
      • Clinical manifestations suggestive of neurocysticercosis.[h]
      • Individuals coming from or living in an area where cysticercosis is endemic.[i]

Classification

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Neurocysticercosis can be categorized as either parenchymal or extraparenchymal.[29]

  • Parenchymal neurocysticercosis: neurocysticercosis lesions within brain parenchyma.[29]
    • Viable parenchymal cysts: contains the scolex, typically between 0.5 and 2 cm in diameter.[30]
    • Single enhancing lesion (solitary cysticercal granuloma): One or two smaller cysts.[30]
    • Massive infections: hundreds of cysts and a large number of larvae.[30]
  • Extraparenchymal neurocysticercosis: lesions in ventricles or subarachnoid spaces.[29]
    • Ventricular neurocysticercosis: cysts in the brain ventricles.[31]
    • Subarachnoid neurocysticercosis: cysticerci in the subarachnoid space.[32]
  • Other locations
    • Spinal neurocysticercosis: neurocysticercosis in the spine, often the extramedullary subarachnoid spaces.[9]
    • Retinal neurocysticercosis: cysts effecting the retina.[9]

Prevention and treatment

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Neurocysticercosis is preventable.[33] Preventative measures include better sanitation, more education, and raised awareness of the disease.[34] De-worming of pigs in areas where neurocysticercosis is endemic as well as vaccinating pigs with the TSOL18 vaccine are other recommendations for prevention.[33]

A single therapy method is not appropriate for every person with neurocysticercosis. The disease has to be characterized in terms of cyst viability, the degree of the host's immunological response to the parasite, and the location and number of lesions to provide sensible therapy.[35] Symptomatic and antiparasitic medications are typically used in conjunction for treatment. Surgery also plays a part in the care of certain individuals.[36][37]

Brain CT of neurocysticercosis before (A and B) and after (C and D) treatment wirh Albendazole

Neurocysticercosis is a persistent infection, with symptoms appearing months or years later. As a result, removing the parasite is not an emergency, and the first step in treating those with neurocysticercosis is often aimed at minimizing the symptoms. This may be done with the use of antiepileptic, antiedema, analgesic, or anti-inflammatory drugs.[38] Carbamazepine is commonly used to control seizures.[39][40] Surgery, acetazolamide, steroids, or mannitol may be used to help manage intracranial hypertension.[38]

Antiparasitic drugs should not be used in cases where there is a preexisting risk of developing hydrocephalus, such as sub-arachnoid neurocysticercosis or encephalitic neurocysticercosis; in these cases, the inflammation that occurs after treatment may pose a significant risk of rapidly raising intracranial pressure and even death.[41] The two most commonly used antiparasitic medications are albendazole, an imidazole that inhibits glucose absorption and metabolism in the parasite, and praziquantel,[42] an isoquinoline which triggers parasite paralysis by altering calcium pathways and homeostasis. These medications are only appropriate for the treatment of vesicular viable cysts or cysts in the early colloidal phases of development, and they are ineffective against calcified cysts.[35]

Steroid administration is an important step in the modulation of neurocysticercosis-related inflammation in the central nervous system, since it controls the acute inflammatory response that occurs following the destruction of live cysts. Prednisolone and dexamethasone are frequently used as adjuncts to antiparasitic therapy.[35][42][43]

Antiparasitic medication may be ineffective in cases of severe infection due to the hazards associated with mass inflammation, but these forms of neurocysticercosis carry a high risk of consequences if left untreated. In some circumstances, a more aggressive treatment plan, including surgery, may be required.[34] Surgical treatments include ventricle-peritoneal shunts and excision of cysts.[39][36]

Outlook

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Parenchymal and single lesion neurocysticercosis usually has a good prognosis, however the prognosis is not as good for extraparenchymal neurocysticercosis.[33] Extraparenchymal neurocysticercosis can lead to obstructive hydrocephalus, sudden death, or slow death.[44]

Epidemiology

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Geographic maps of Indonesia (upper) showing endemic areas of three human Taenia species ( T. asiatica, endemic in North Sumatra; T. saginata and T. solium, endemic in Bali; and T. solium, endemic in Papua) and Bali (lower)

Neurocysticercosis is endemic in most developing countries, except predominantly Muslim countries.[45][46] It is endemic in Latin America, China, Nepal, Africa, India, and Southeast Asia. It is more common in poorer countries with improper sanitation and a lack of clean water.[19] Neurocysticercosis has been rare in Europe and the US, however immigration has raised the prevalence of neurocysticercosis in the areas.[17]

History

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Descriptions of Taenia solium date back to 1500 BC.[47] Taenia solium cysticerci have even been found in ancient Egyptian mummies.[45] The first recorded cases of neurocysticercosis were most likely described by Rumler in 1558.[47][48] Hipólito Unanue, a Peruvian physician and journalist, most likely first recorded simultaneous taeniasis and cysticercosis in the same individual in 1792, when he reported the case involving a soldier with taeniasis who died following a violent seizure.[47][45][49] During the nineteenth century, German pathologists noticed the morphological parallels between the adult T. solium head and the cysticercus scolex. Friedrich Küchenmeister showed that the consumption of cysticercus from pork caused human intestinal taeniasis by feeding an imprisoned individual sausages and a noodle soup that included cysticerci gathered from a recently killed pig.[45][47] In the second part of the 19th century, research showed that feeding Taenia eggs from infected humans to pigs caused cysticercosis.[45][49]

Society and culture

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Neurocysticercosis was featured in the Pilot episode of House M.D. The episode followed a young woman who contracted neurocysticercosis after eating contaminated ham.[50] Sebastián Ferrat, a Mexican television star died in 2019 at age 41 due to neurocysticercosis.[50][51][52] The New York Times stated that RFK Jr. had contracted neurocysticercosis after travelling to Africa, South America, and Asia.[53] Gaius Julius Cesar is believed to have had epilepsy related to cysticercosis.[47]

See also

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Notes

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  1. ^ Rounded, well-defined lesions with liquid contents and signal similar to that of cerebrospinal fluid on CT /MRI.[28]
  2. ^ Single or numerous ring/ nodular-enhancing lesions, 10-20mm in diameter, with/ without edema, without displacing midline structures.[28]
  3. ^ Single or numerous, solid, and typically less than 10mm in diameter.[28]
  4. ^ The administration of corticosteroids renders this criterion invalid.[28]
  5. ^ Sequential CTs or MRIs reveal a varied location of ventricular cystic lesions.[28]
  6. ^ Antibody identification by enzyme-linked immunoelectrotransfer blot test employing lentil lectin-purified T. solium antigens, and cysticercal antigen detection by monoclonal antibody-based ELISA.[28]
  7. ^ Cysticerci can be identified through a biopsy of subcutaneous lumps, X-ray films or CT scans that reveal cigar-shaped calcifications in soft tissues, or detection of the parasite in the anterior chamber of the eye.[28]
  8. ^ Mostly seizures (typically beginning in persons aged 20-49 years; the diagnosis of seizures in this setting is not disregarded if patients are outside of the normal age range), but other signs include chronic headaches, focal neurologic impairments, intracranial hypertension, and cognitive deterioration.[28]
  9. ^ A location where active transmission is recorded.[28]

References

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Citations

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  1. ^ a b c Del Brutto 2014, p. 1448.
  2. ^ Garcia, Nash & Del Brutto 2014, p. 1204.
  3. ^ a b c d e f Garcia 2018, p. 856.
  4. ^ a b c d e f Del Brutto 2014, p. 1449.
  5. ^ a b Rodríguez‐Leyva et al. 2023, p. 98.
  6. ^ a b c d Garcia, Nash & Del Brutto 2014, p. 1205.
  7. ^ Steyn et al. 2023, p. 106.
  8. ^ Steyn et al. 2023, p. 107.
  9. ^ a b c Bustos et al. 2021, p. 5.
  10. ^ Carpio et al. 2021, p. 124.
  11. ^ Rodríguez‐Leyva et al. 2023, pp. 97–98.
  12. ^ Garcia, Nash & Del Brutto 2014, pp. 1205–1206.
  13. ^ a b c d e Del Brutto 2014, p. 1450.
  14. ^ a b c d Garcia, Nash & Del Brutto 2014, p. 1206.
  15. ^ El-Kady et al. 2021, p. 1604.
  16. ^ Steyn et al. 2023, p. 105.
  17. ^ a b c d Del Brutto 2014, p. 1446.
  18. ^ Garcia 2018, pp. 851–852.
  19. ^ a b c d Gripper & Welburn 2017, p. 219.
  20. ^ a b Garcia, Nash & Del Brutto 2014, p. 1202.
  21. ^ Rodríguez‐Leyva et al. 2023, p. 97.
  22. ^ Del Brutto 2014, p. 1447.
  23. ^ a b Gripper & Welburn 2017, p. 221.
  24. ^ a b c Guzman & Garcia 2021, p. 198.
  25. ^ Garcia 2018, p. 857.
  26. ^ Garcia, Nash & Del Brutto 2014, p. 1208.
  27. ^ Garcia, Nash & Del Brutto 2014, p. 1207.
  28. ^ a b c d e f g h i j Del Brutto et al. 2017, p. 204.
  29. ^ a b c Bustos et al. 2021, p. 1.
  30. ^ a b c Bustos et al. 2021, p. 2.
  31. ^ Bustos et al. 2021, p. 3.
  32. ^ Bustos et al. 2021, p. 4.
  33. ^ a b c Singhi & Suthar 2015, p. 170.
  34. ^ a b Gripper & Welburn 2017, p. 223.
  35. ^ a b c Gripper & Welburn 2017, p. 222.
  36. ^ a b White et al. 2018, p. e53.
  37. ^ Del Brutto 2014, p. 1454.
  38. ^ a b Garcia 2018, p. 859.
  39. ^ a b Bustos et al. 2021, p. 9.
  40. ^ World Health Organization 2021, p. 22.
  41. ^ White et al. 2018, pp. e61–e63.
  42. ^ a b White et al. 2018, p. e51.
  43. ^ World Health Organization 2021, p. 12.
  44. ^ Garcia 2018, p. 858.
  45. ^ a b c d e Del Brutto 2014, p. 1445.
  46. ^ Singhi & Suthar 2015, p. 166.
  47. ^ a b c d e Del Brutto & García 2015, p. 393.
  48. ^ Del Brutto & García 2014, p. 3.
  49. ^ a b Del Brutto & García 2014, p. 4.
  50. ^ a b García & Del Brutto 2020, p. e0008208.
  51. ^ 7NEWS 2019.
  52. ^ DominicanToday 2019.
  53. ^ NBC News 2024.

Sources

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Further reading

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