MEDICINE

Parasitic Diseases Within the Spinal Cord and Nerve Roots

Benjamin Rahmani1 & Shrey Patel1 & Omar Seyam1& Jason Gandhi1,2 & Gunjan Joshi3 &

Inefta Reid1& Noel L. Smith4

& Sardar Ali Khan1,5

Accepted: 20 September 2019# Springer Nature Switzerland AG 2019

AbstractParasitic diseases of the spinal cord and nerve roots are a potentially deadlymatter. They are mainly found in areas where there arepoor sanitary conditions such as Africa, theMiddle East, and theWest Indies. Themost common diseases include schistosomiasisand neurocysticercosis. Furthermore, it is clear that through an understanding of all the various diseases there are, it is imminentthat patients are treated as soon as possible to avoid the deadly outcomes that the diseases can have to the body. This disease canhave several impacts on individuals that include epilepsy, health problems, and implications on various organs.

Keywords Parasitic . Schistosomiasis . Neurocysticercosis . Imaging .Malariasis . Syphilis . Central nervous system . Parasites

Introduction

Parasitic diseases of the central nervous system (CNS),particularly those pertaining to the spinal cord region,are a potentially deadly matter. Parasitic spinal infec-tions are commonly found in areas where there are poorsanitary conditions such as countries that are developingor not as well-equipped in the medical field as countriessuch as the USA [1]. These diseases are generally treat-able, and it is urgent that they are detected and treatedas early as possible to avoid complications [2]. Theresults of leaving these diseases undetected can includeirreversible neurological deficits, as seen in spinal cys-ticercosis [3].

There are a large number of causes for spinal infections.Among the wide range of agents, bacteria, such asBacteroidales and Clostridiales, are the most commonagents, although other organisms also can cause bacterialspinal injuries [4–6]. The bacteria are either single-celledprotozoa or multicellular metazoa [7]. More examples ofbacterial spinal infections include spinal epidural bacterialabscess, Pott’s disease which is also known as tuberculousspondylitis, Lyme disease which is also known asneuroborreliosis, and syphilis which can be classified as ameningovascular disease which is classified by thickened,inflamed meninges, or a parenchymatous disease which isclassified through gummas in the cord [8–12]. Viral spinalinfections can also be found in practice and may have adifferent treatment and course of action compared to bacte-rial diseases [8]. Viral infections can include, but are notlimited to, flaviviruses such as West Nile, varicella zoster,and Epstein-Barr virus [13–15]. This review focuses on par-asitic diseases of the spinal cord and nerve roots, which arewidespread and have the potential to be extremely lethal andinfectious. Such diseases include schistosomiasis, which iscommon in endemic regions, and neurocysticercosis, whichis the most common parasitic disease of the spinal cord[16–18]. Radiologists are very important in this field, as theyare responsible for detecting the disease and working along-side the clinicians to facilitate the appropriate testing neededfor correct treatment and to diagnose it early. Furthermore,radiology has been found to be most effective in diagnosiswhen using detailed structural images, rather than modernmagnetic resonance (MR) techniques [1].

This article is part of the Topical Collection on Medicine

* Sardar Ali Khanskysalik@gmail.com

1 Department of Physiology and Biophysics, Renaissance School ofMedicine at Stony Brook University, Stony Brook, NY, USA

2 Medical Student Research Institute, St. George’s University Schoolof Medicine, West Indies, Grenada

3 Department of Internal Medicine, Stony Brook SouthamptonHospital, Southampton, NY, USA

4 Foley Plaza Medical, New York, NY, USA5 Department of Urology, Health Sciences Center T9-040, Stony

Brook University Renaissance School of Medicine, 101 NicollsRoad, Stony Brook, NY 11794-8093, USA

https://doi.org/10.1007/s42399-019-00156-4SN Comprehensive Clinical Medicine (2019) 1:869–881

/Published online: 28 October 2019

Parasitic diseases, such as those outlined in Table 1, arefound throughout the world. However, they are much morecommon in developing countries with poor sanitary condi-tions such as Africa, the Middle East, and the West Indies[1, 19–23]. Despite this, they are still common in NorthAmerica, as they often transfer when people travel to lessdeveloped territories and carry the disease back to areas thatdid not have it beforehand [1]. Most parasitic diseases humansare of CNS origin [24]. Parasitic conditions in the spinal cordinclude cysticercosis, schistosomiasis, trypanosomiases, andechinococcosis [2]. This review fully examines these commonand rare parasitic diseases of the spinal cord. Using detailedstructural images, histology is a common means for diagnosis[2].We also review the course of action that must be taken, theimplications it has on patients, and the epidemiology of dis-ease development.

Methods

A literature search using theMEDLINE® and Google Scholardatabases was conducted using terms relevant to parasitic spi-nal cord diseases. The search results were restricted to casereports and review articles. There were no language restric-tions. We selected papers that revealed artifacts for pathogen-esis, clinical manifestations, imaging, and treatment of eachparasitic spinal cord disease.

Spinal Cord Disease Manifestations

There are several clinical manifestations to spinal cord dis-eases. In the neurological disorder of the spinal cord calledmyelitis, there are several pertinent clinical manifestations.This includes parasitic or fungal infection symptoms presentas paresthesia from the feet with possible back pain, motordeficits impacting the flexors of legs and extensors of arms,bowel and bladder dysfunctions, temperature dysregulation,

and hypertension [25]. Over 2/3 of patients that have thisdisorder have lasting disabilities despite treatment [25].Another disorder is acute traumatic central cord syndrome.However, this is most commonly caused by cervical spinalcord injury. The clinical manifestations for this include motordeficits that are more severe in the upper extremities than inthe lower extremities. In addition, there is a bilateral loss ofpain and thermal dysfunction, and possible sphincter dysfunc-tion [26, 27]. Another example of a spinal cord disorder isanterior spinal cord syndrome, caused mainly by aortic surgi-cal interventions. The clinical manifestations include possiblequadriparesis and could onset with no previous symptoms[28]. In the following sections, subtypes of parasitic diseasesassociated with the spinal cord will be discussed, and theirspecific clinical manifestations will be mentioned.

Schistosomiasis

Schistosomiasis is one of the most common parasitic diseasesand impacts approximately 200 million people throughout theworld, and ultimately causing symptoms in about 60% of thesecases [8, 16]. This disease is caused by the trematodeSchistosoma [29]. It is often found in sub-Saharan Africa,South America, and Asia but it is also more recently moving toareas that it was not as common previously due to tourism [19,30]. It can occur at any time through parasitic infection [31].

Pathogenesis

The usual causes of this disease can be due to Schistosomamansoni, Schistosoma haematobium, and Schistosomajaponicum. The main way that this disease is transmitted isthrough a transmission of eggs in either the stool or the urinefor the genus Schistosoma [19, 20, 32]. Once this occurs, it canbe transmitted to humans through freshwater snails and penetrat-ing cercariae [20]. Eggs are then shed day-to-day following 6–8 weeks of initial contact, with variable amounts of sheddingthrough each day depending on how much contact with fresh-water therewas and the parasite burden on the affected individual[23, 33–36]. This type of diagnosis is referred to asBparasitological diagnosis^ as there is direct evidence that thereis a pathogen in the body of an individual [19]. There are alsoother types of diagnoses which are through patient serum that aremore sensitive to the extent that low-intensity schistosomiasiscan be detected as well [23, 37–39]. Through this serology, an-tibodies can be detected to note that the disease is in the patient.These antibodies can be directed against any of the four stages ofthe Schistosoma genus which includes penetrating cercariae,schistosomula which is the migration of juvenile worms, thepresence of adult worms, and eggs produced by worms throughmating [23, 32, 35]. For the serological assays that have beentaken, some have been found to be specific for endemic regions

Table 1 List ofimpactful parasiticdiseases of the spinalcord

Schistosomiasis

Neurocysticercosis

Echinococcosis (hydatid disease)

Toxoplasmosis

American trypanosomiasis (Chagas disease)

Malariasis

African trypanosomiasis (sleeping sickness)

Neurotoxocariasis

Baggio-Yoshinari syndrome (BrazilianLyme-like disease)

Paragonimiasis

Syphilis

SN Compr. Clin. Med. (2019) 1:869–881870

of various specificity levels while others are for diagnosis thatrelates to important or travel-related schistosomiasis [30, 38–56].

Clinical Manifestations

This parasitic disease is more commonly reported in childrenand adolescents than older patients [8]. As the disease evolvesand moves to the central nervous system through migration ofpairs of adult worms or embolization of eggs through retro-grade venous means into the Batson venous plexus, caudaequina syndrome has been found to develop [29, 57]. Thissyndrome is a complication that includes back pains due todisc herniation in the spinal cord or spinal tumors [58, 59].When diagnosing schistosomiasis with MRI, it is often diag-nosed as spinal cord neoplasm. This is due to the extremesensitivity associated with MR [60]. There are three forms ofspinal cord schistosomiasis, with a potential progression fromone of the cases that have lower severity to a higher one(Table 2) [59]. Symptoms of acute schistosomiasis includefever, headache, myalgia, diarrhea, and abdominal pain [29].

Imaging

MRI is important in developing a diagnosis for this disease. Inmany cases, this disease is in the medullary form due to ahyperintensity that is patchy in T2-weighted images (T2WIs), anoticeably enlarged spinal cord, and a lower cord and conusmedullaris heterogeneous contrast enhancement on T1WIs [1,24, 31, 59, 62, 63]. Furthermore, this appearance is similar to acord neoplasm [1, 2]. MRI also displays thickening of the spinalcord and allows the eggs and granulomas to be detected throughlinear radicular contrast enhancement [1, 33, 62, 64].

Treatment

For the treatment of schistosomiasis, praziquantel is the mostused immediately following diagnosis after starting corticoste-roid treatment [64, 65]. However, before a patient is officiallydiagnosed but doctors speculate that schistosomiasis is possi-ble, corticosteroids are used as the primary treatment [66].

Neurocysticercosis

Neurocysticercosis (NCC) is another extremely common par-asitic disease of the spinal cord and CNS [67, 68]. This diseaseis caused by pork tapeworm, known as Taenia solium inhumans. Humans are the intermediate host of the pork tape-worm and allow it to survive and induce harmful effects [1].Approximately 50 million people throughout the world havethis specific type of spinal cord disease, and it is much morecommon in endemic areas similar to schistosomiasis, such asAfrica, some regions in Asia, and Eastern Europe and Centraland South America. It affects approximately 3 to 6% of thepopulation in these areas [69]. In addition, due to travel tothese countries, many people become carriers and transferthe disease to non-endemic areas, such as North America[70]. NCC is significant because it has a major onset of epi-lepsy due to intraparenchymal brain cysts [8].

Pathogenesis

NCC occurs following the ingestion of T. solium-infestedeggs. Once these eggs hatch, embryos are ultimately releasedinto the small intestines and invade several different tissuesthroughout the body, including the eyes, skin, and muscles,but the majority of it is implicated in the CNS complications[67, 71]. After the embryos are released and dislodged into thesmall intestines, they then enter neural and subcutaneous tis-sues and then enter skeletal and ocular globes and continuetheir development [1]. When in the CNS, cysticerci can de-velop anytime between 3 weeks and 2 months following theinitial oncosphere formation [1, 17].

There are many types of larval forms for this disease.The most common of these is Cysticercus cellulosae[1]. This type contains a scolex and has implicationson the CNS by causing intraparenchymal lesions inthe brain [1]. Furthermore, Cysticercus racemosus is an-other type, but it is less common and does not have ascolex [1, 2]. Overall, the cysticerci are only 1 cm indiameter and are located in the cerebral cortex or thebasal ganglia [1, 69].

Table 2 Spinal schistosomiasis subtypes [29, 59, 61]

Clinical form Clinical manifestations Imaging

Medullary (most involved in thespinal cord only)

Commonly has high eosinophil CNS levels, symmetric distribution ofsensorimotor abnormalities, spinal cord atrophy in untreated patients.

Hyperintensity in the T2 region with enlargement of thespinal cord is seen. This is associated with mild andheterogeneous enhancement.

Conus-cauda equina syndrome Slower development of symptoms, atrophic leg muscles, asymmetricsensorimotor alterations, high eosinophil CNS levels.

The cauda equina is shown to be thickened; there is agadolinium enhancement of the conus medullaris.

Myeloradiculopathy (involvedwith the spinal cord and rootsof the nerves)

Intermediate form. Necrosis, vacuolization, and further atrophy of thespinal cord tissue occur. Radicular pain in the lower limbs, muscularweakness, sensory disturbances, high eosinophil CNS levels.

Spinal nerve root thickening and leptomeningealenhancement seen.

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Clinical Manifestations

There is a wide range and non-specific clinical manifestationfor cysticercosis that depends on location of the parasite,amount of parasites, and inflammation [1]. In most cases,there is a cyst degeneration in the basal ganglia and edemawhich leads to neurological implications that can often includechronic headaches, focal neurologic deficits, intracranial hy-pertension, and decline in cognition [72]. Most of the spinalcysts are in the lumbosacral regions [73]. Furthermore, inspinal cases of NCC with basal subarachnoid disease, it isimminent that an MRI is done [73].

When cysts occur, it can lead to several different complica-tions including nerve entrapments, hydrocephalus, gait disorders,chronic meningitis, vasculitis, spinal or cerebral stroke, or lym-phocytic meningitis if they rupture [74]. In terms of this diseaseand how it is associated with the spinal cord, it is quite rare and isassociated with other parts of the CNSmore, as it is implicated inthe spinal cord for just 1.2 to 5.8% of reports [1, 75].

Diagnosis

To diagnose patients with this type of disease, serological testingand fundoscopy can be performed to detect the parasite in pa-tients. However, histological review and imaging is the mostcommonmethod to diagnosis, as it allows amore comprehensiveunderstanding of the specific form of neurocysticercosis that thepatient has [76, 77].

Del Brutto et al. have proposed specific diagnostic criteriafor the diagnosis of NCC. This combines clinical history, neu-roimaging, immunological evidence, and epidemiologicalguidelines to ultimately establish defined guidelines that allowthe diagnosis of NCC [67, 78]. For the absolute criteria, theremust be an ability to see the parasite through a spinal cordlesion located in the body. For the neuroimaging of the abso-lute criteria, a scolex must be visible within the cystic lesion.Furthermore, in a fundoscopy, sub-retinal parasites will beseen. For the major criteria of the disease, the lesions willsuggest NCC, EITB assays will detect T. solium antibodies,and cysticidal drug therapy would display a resolution of thelesion following albendazole or praziquantel treatment. Theminor criteria will also show lesions that suggest NCCand there will be symptoms suggesting NCC, and a CSFELISAwould show T. solium antibodies or antigens and cys-ticercosis that is outside the CNS. Pursuing this further, theepidemiological criterion has an origin endemic for the patientcountry and the patient must be living in the endemic area andtravel to endemic areas where there is NCC often.Furthermore, the household that the patient lives in must havehad contact with T. solium in order for it to develop as well[66, 67, 77].

The various diagnoses for NCC can be defined as definitiveor probable. A definitive diagnosis will have 1 absolute

criterion or 2 major criteria and 1 minor and 1 epidemiologicalcriterion. For a probable diagnosis, one must have 1 majorcriterion and 2 minor criteria or could have 1 major and 1minor and 1 epidemiological criterion applicable or 3 minorand 1 epidemiological criterion applicable [66, 67, 77].

Imaging

For this specific type of disease, there are four stages of devel-opment and regression that have been found throughCTandMRimaging. The first stage involves vesicular implications and seescysts and scolex through imaging. The second stage has colloidalinvolvement and has ring enhancement and edema. The thirdstage had nodular-granular involvement and has decreased en-hancement and edema and initiation of calcification. The fourthstage is more calcification and this is seen through a CT or MRI[77]. It is important to note that multiple anatomical sites areinvolved for patients that have this parasitic disease [1, 70, 79,80]. Furthermore, neuroimaging has been shown to be the pre-ferred method for diagnosis in NCC through CT and MRI [66].This is because it allows visualization of the infections and as-sesses the number and location of it [66]. Calcifications, whichoccur in about half of all NCC patients, are seen through the highsensitivity of CT scans of NCC which has a starry sky appear-ance due to several cysts implicated with it [67, 71, 81]. Thereason that MRIs are also effective is that they allow distinctionof the degenerative cysticerci stage and detect parasites in theposterior fossa, basal cisterns, and ventricles that CT scans arenot able to detect [67, 80].

Treatment

Effective methods of treatment for NCC have been developed[8]. In order to control the inflammation that is caused fromthis disease, albendazole with glucocorticoids is administered[82]. Alternatively, praziquantel with corticosteroids or a com-bination of albendazole and praziquantel, if there are morethan 2 active parenchymal cysts, is a recommended drug treat-ment option [65].

A controversial topic for treatment of NCC is cysticidaldrugs. This is because it is believed that it may cause moreharm than benefit to patients as this treatment could increasethe risk for ICP and potentially result in death [67, 83].Therefore, patients should only be treated with regard to theirsymptoms without cysticidal therapy [67, 84].

Due to the fact that neurological issues are a clinical man-ifestation of NCC, anti-epileptic therapies have also been rec-ommended [67, 80]. In these cases, phenobarbitone and car-bamazepine should be used to control seizures, but this is alsonot without controversy, as relapse is quite common followingimprovement while no improvement has also been shown insome cases [17, 67, 68, 84].

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If calcification is present, anti-parasitic treatments shouldnot be administered. The reason for this is because there canbe a potentiation on the excessive inflammatory responses thatare occurring in the brain. For such cases, treatment optionsinclude the aforementioned corticosteroids, osmotic diuretics,and decompressive craniotomy. This will allow control ofbrain edema [85].

Echinococcosis (Hydatid Disease)

Echinococcosis, also known as hydatid disease, is caused bythe larval stage of Echinococcus [1]. The most common hostsof these parasites include carnivores and canines. Unlike theprevious parasites, these are found near the countryside or inhomes that are located in forest areas [1]. When humans havewater or ingest food that are contaminated with eggs of thisparasite, they will then develop the disease as well [1].Furthermore, the most common form of this disease is cysticechinococcosis, which is caused byEchinococcus granulosus,and alveolar echinococcosis, which is due to Echinococcusmultilocularis [1, 86].

Pathogenesis

Asmentioned, it is extremely rare for this disease to be associatedwith the spine, but there are still some cases that have beenreported. In these cases, the segment of the spine that is mostassociated is the thoracic segment as it is 50% of all cases, thenext most frequent is lumbar and sacral which is 20% for each,and the least is cervical segments, which represent only 10% ofall spinal cases [1, 87]. Furthermore, the disease is located inepidural regions in most of the cases [88, 89].

Clinical Manifestations

This disease, when associated with the spinal cord, is mani-fested as isointense cystic lesions without any peripheral ede-ma that is associated with significance [1, 90]. The fibrouscapsules in the body are hypointense on T2WIs and displayperipheral enhancement through inflammations [1, 91].Furthermore, the more common cysts are intradural-extramedullary cysts and present at a young age [87].

Diagnosis

In order to diagnose this disease, serological and imag-ing tests are used. Furthermore, while it is still possibleto have CNS and spinal involvement of this disease, itis only in about 1 to 2% of all cases, as most cases areinvolved with the liver and lungs [1, 77, 86–88, 92].The diagnosis can also be confirmed through surgery byobserving a laminated cyst membrane [88].

For the diagnosis of this disease, the intradural-extramedullaryor intramedullary cysticerci is a copy of echinococcosis [1, 93].Furthermore, a mimic of alveolar echinococcosis and spinalsparganosis can be cestode infections, but this is in more rarecases [1]. This disease can also be classified as spinal arachnoidor spinal aneurysmal bone cysts, confirmed through higher eo-sinophil CNS levels [87].

Treatment

The primary treatment of choice for this specific parasiticdisease is removal through surgical means. However, it isimportant that if the surgery were to occur, there should notbe a perforation of the cyst wall. This can potentially lead todissemination and anaphylactic reactions [88, 94].Furthermore, to avoid this disease from recurring, anti-helminthic therapy and follow-up visits for MRIs after theoperation are imminent [88, 95]. Recurrence and mortalityare quite high for this disease, as they are approximately40% each, showing that diagnosing and treating affected in-dividuals is critical [88, 89, 96]. Albendazole or mebendazoleshould also be taken, regardless of whether there will be sur-gery or not [65].

Toxoplasmosis

Toxoplasmosis can be localized in multiple parts of the spinalcord. It arises from the protozoan Toxoplasma gondii whichcan be found in regions anywhere in the world [1, 97]. It isfrequent in pregnant women and this ultimately results in birthdefects and could lead to a return of weak immunity if indi-viduals had an immune disease previously, leading to enceph-alitis [1, 97, 98]. The pathology of the spinal cord is because ofdeficits in CD4 T cells that are linked to AIDS or T cell leu-kemia or lymphoma [1, 99, 100]. A previous study has shownthat there are only 18 reported cases of spinal cord toxoplas-mosis in AIDS patients [101, 102].

Clinical Manifestations

Several permutations of manifestations occur with thisdisease including pain in the spinal region, a defect inthe motor and sensory system, and complications in theurinary sphincter [1, 98].

Diagnosis

To assist in diagnosing patients with this disease, it is commonthat patients will have a fever, a sensory loss below a specificspinal cord level, urinary retention, and extreme weaknessalso known as paraparesis [103]. In order to definitely diag-nose an individual with spinal toxoplasmosis, a biopsy must

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be done to definitely detect that there is an organism for thisparasitic disease in the body of an individual, but this has beenhighly morbid [103]. Therefore, as an alternative, individualscan be diagnosed if their CD4 lymphocyte cell count is lessthan 100 cells/mm3 [101].

Imaging

In these patients, there are mass effects and edema.Furthermore, cerebral toxoplasma lesions that are also foundin patients assist in diagnosis for spinal toxoplasmosis [1, 2].MRI is also utilized in order to ensure that patients have spinaltoxoplasmosis, rather than bony lesions, epidural abscess, her-pes myelitis, or an HIV vacuolated myelopathy [101, 103].

Treatment

There are multiple methods of treatment for toxoplasmic en-cephalitis. Specifically, in patients with AIDS, pyrimethamine(200 mg dose, 50 mg/day), sulfadiazine (5–6 g/day), andfolinic acid (10–25 mg/day) should be combined and admin-istered daily [101]. Alternative treatments, specific to thespine, include trimethoprim-sulfamethoxazole, which hasbeen found to be most effective, pyrimethamine withatovaquone, pyrimethamine with azithromycin, or sulfadia-zine with atovaquone [101, 104, 105].

American Trypanosomiasis

American trypanosomiasis, or Chagas disease, occurs mainlyin Latin America and some Western countries [1, 77, 106].The parasite responsible for it is Trypanosoma cruzi. Thecause of the disease onto humans is through Triatominae(i.e., conenose or kissing bug), which suck the blood out ofhumans and then can transfer the disease onto them [1, 77].

Clinical Manifestations

The clinical manifestations of this disease can be distin-guished into an acute phase which lasts 6–8 weeks and chron-ic phases [107]. In these acute cases, patients are often foundto have fever, malaise, headache, and hepatosplenomegaly[1]. In chronic cases, some patients develop other complica-tions that include cardiac, gastrointestinal, or both [107–109].The association that this disease has with the spinal cord isthrough acute meningitis or nodular encephalitis, but this is inrarer cases [1, 110]. The direct symptoms that have been foundwhen it is linked to the spinal cord are abnormalities anddeficits in the sensory and motor parts of the body, dementia,and confusions [1, 111]. Furthermore, Chagas disease is oftenconfused as a presentation of AIDS at first, but the other

clinical manifestations allow a final diagnosis of Chagas dis-ease to be confirmed when it is the case [1, 24, 111].

Diagnosis

In order to diagnose Chagas disease, histology, serologic, andCSF tests are often used. Through these methods, abnormal-ities in the CSF are quite common and can confirm the diag-nosis of Chagas disease [1, 24].

Imaging

The way that this disease is seen through MRI and CT imag-ing is expanding hyperintense lesions on T2WIs. When it isfound in the spinal cord, it demonstrated extensive edema andmass effect [1, 24, 110, 112].

Treatment

Due to difficulties with obtaining the drugs that are needed totreat people that have this disease, most cases are left withouttreatment [107, 108, 113, 114].

Malariasis

Malariasis is caused by the agent Plasmodium sp. and is anextremely rare case of a parasitic spinal cord disease. It isimportant to note that it is quite common in endemic areasthat are located in tropical countries [1]. Symptoms are similarto those observed in acute disseminated encephalomyelitis. Inorder to diagnose this disease, imaging is used to detect aspinal cord lesion and potential nerve root enhancement [1].

African Trypanosomiasis

African trypanosomiasis, or sleeping sickness, is also a raredisease of the spinal cord and is caused by the agentTrypanosoma brucei, T. congolense, T. vivax, T. evansi, andT. equiperdum [1, 115]. It is most commonly found in Centraland Western Africa and impacts approximately 70 millionpeople in this region [115, 116]. The manifestation that ithas associated with the spinal cord is meningoencephalitis.Through imaging, meningeal enhancement, lesions of the bas-al ganglia, and white matter diffusions are shown which ulti-mately leads to thickening in the spinal region [1, 117].Because of a lack of vaccines due to variations in hosts, it isdifficult to treat this parasitic disease [115].

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Neurotoxocariasis

Neurotoxocariasis is a rare parasitic disease that arises fromToxocara sp. It can be found in any part of the world. Theclinical manifestations associated with this disease includeassociations with eosinophilic meningitis and optic neuritis.In order to diagnose this disease through imaging, longitudinalextensive myelopathy can be seen in addition to hyperintenseT2WI lesions [1, 118, 119].

Baggio-Yoshinari Syndrome

Baggio-Yoshinari syndrome, previously known as BrazilianLyme-like disease, originates from Brazil [1]. It is transmittedthrough Amblyomma and Rhipicephalus as they release theirticks that will have latent behaviors. The disorders that areassociated with this disease include immune weakness and arecurrence of complications that patients may have had previ-ously [1].

Clinical Manifestations

The symptoms associated with this disease are similar to that ofinfluenza and Lyme disease [1, 120]. Following invasion, there isan infection in the neurological region evident bylymphomonocytary meningitis, cranial neuritis, peripheralradiculopathy, and encephalomyelitis [1, 121, 122]. It is impor-tant to note that similar to the previously discussed disease, thereis a high relapse rate that is associated with it. Furthermore, it iscritical that patients that have this disease are found in the earlyand acute stages; otherwise, there is a much higher chance thatrelapse will occur for these patients [1, 121, 122].

Imaging

Through imaging that has been done in this disease, it is com-monly found that there are multifocal hyperintense lesions onT2WIs, demyelinating lesions, and cranial enhancements onpost-contract T1WIs. When this is seen through MRI exami-nation, it facilitates the diagnosis of this disease [1, 123–126].

Treatment

It is critical that patients are treated for this disease quite in theearly stages to avoid the latent stage, when it becomes irre-versible [127]. Antibiotics has been a common therapy for thedisease, such as ceftriaxone, as well as doxycycline, amoxi-cillin, or penicillin [127].

Syphilis

Syphilis is caused by Treponema pallidum [1]. It is a sexuallytransmitted disease and when it is found in the spine, it in-volves syphilitic gummas, stemmed from leptomeningeal in-flammation and low signal intensity found on T2WIs [8–12].Syphilis peaked during WWII, with a decline due to thefounding of penicillin, yet it is still prevalent as a sexuallytransmitted disease [128, 129].

Although it is extremely rare, this disease could also becaused by tabes dorsalis which is the tertiary form. In thisspecific type, the posterior location of the spinal cord isharmed, evident through imaging that has shown atrophyand hyperintensity on T2WIs [1, 77, 130, 131].

For syphilis in the spinal region, patients are treated withbenzathine penicillin [128, 132]. In addition, it is critical thatpatients are treated rapidly, as complications can arise.

South American Blastomycosis(Paracoccidioidomycosis)

South Amer ican b las tomycos i s , a l so known asparacoccidioidomycosis, is a systemic disease that is causedby Paracoccidioides brasiliensis [1]. It is most commonlyfound in South American regions, hence its name [1, 133].Furthermore, the prevalence of this disease is between 5.6 and17.5% [1, 133, 134].

Pathogenesis

When the fungus of the disease is inhaled, it will thenaffect the CNS as well as other parts of the body in-cluding the kidney, spleen, adrenal gland, and bonesthroughout the body [1].

Diagnosis

Through biopsies, one is able to diagnose an individualwith South American blastomycosis. The correct lesionsfor this biopsy are found in the lungs through CT im-aging [1, 113, 114].

Imaging

For only 4.0% of CNS cases of this disease will there belocalization in the spinal cord [133–135]. The lesions associ-ated with this disease can also be linked to the meningeal formthrough diffuse leptomeningeal enhancement [1, 136].

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Table3

Casestudiesof

parasitic

spinalcord

diseases

Reference

Sym

ptom

sIm

aging

Diagnosis

Treatment

Outcome

Mikulichet

al.[65]

28-year-oldSu

danese

man

with

lower

back

pain,flaccid

paraplegia,sensory

level(T8),

andurinaryretention.

MRIshow

edincreasedsignal/m

asseffectin

spinalcord

from

T6to

conusmedullaris.A

mild

patchy

enhancem

entw

asalso

present

followingIV

contrast.

Differentiald

iagnosisincluded

astrocytom

a,ependymom

a,hemangioblastom

a,schistosom

iasis,andmetastasis.

MRIfindings

suggestspinal

cord

schistosom

iasis.

Dexam

ethasone

at4mg4tim

esperday.3

dosesof

praziquantel25

mg/kg,and

prednisolone

1mg/kg.

Exhibiteddram

aticclinical

improvem

ent.Decreasein

abnorm

alsignalandsw

ellingin

spinalcord.

Zhang

etal.[150]

59-year-oldwom

anwith

paininbilaterallow

erlim

bsandleftlower

limb.Increasing

urinaryfrequency.Hypoesthesiaalong

S2–S

5derm

atom

eson

bilaterallow

erlim

bsanddecreasedperianalsensationon

theleft

side.

Intraduralextram

edullary

lesionsfrom

L1/2to

S1thatwas

hyperintense

atT2and

hypointenseatT1.Thin-walledcystwas

identifiedwith

clearfluidfrom

L2–S1

that

was

8cm

.

Lum

barspinalintradural

neurocysticercosis

Cystic

masswas

removed,fixed

in10%

form

alin

for8hatroom

temperature.

Patient

was

then

treatedwith

albendazoleat15

mg/kg/day

fora

period

of4weeks.

Noadditio

nalcom

plications

andthe

patient

ultim

atelyrecovered.

Abarrategui

etal.[151]

29-year-oldBolivianwom

anwith

headache

for

3days,fever,and

nausea.C

SFglucose

levelsdroppedto

less

than

20%

ofglycem

ia.Inthirdweek,patient

reported

acuteradicularpain

inrightS

1region.L

Pshow

edclearCSF

containing

265WBCs,

73mg/dL

proteins,and

glucoseat

45mg/dL

.

CTscan

displayedscattered

cortical-subcorticalcalcifications

upto

2.5mm.M

RIof

S1territo

ryshow

eda

roundedlesion

atS1

–S2,16

mm

indiam

e-terthatwas

intradural,extramedullary,and

hyperintense

inT2.

Virallymphocyticmeningitis

was

theinitialetiology.

Neurocysticercosiswas

thefinal

diagnosis.

Patient

was

treatedwith

analgesics

toreduce

pain.

Improved

gradually

andfinalL

Pshow

edglycorrhachiaat50%

ofbloodglucoselevels.

Xuet

al.[152]

30-year-oldKazakhstanmalepresentin

gback

andlefthippain,headache,andweaknessin

lower

leftlim

bs.M

inor

epilepsywas

present,musculartension

wasabovenorm

alrange.

MRIandCTresults

displayedlesionsin

head,

lungs,spleen,kidneys,right

scapula,left

second

costalarch,the

leftacetabulum

,the

thirdleftrib,andT5–T8thoracicvertebrae.

Initially

diagnosedas

thoracic

alveolarechinococcus

(AE)due

toback

pain

andthoraciccanal

decompression.T

hepatientwas

ultim

atelydiagnosedas

multiple-organ

AE.

Thoraciclesionsweretreatedwith

canal

posteriordecompression

andfixedwith

hooksandrods.P

atient

was

given

2-yearalbendazoletreatm

ent.

Patient

returned

dueto

progressionof

intracerebralA

Eandwas

given

anotheroperationto

treatit.

Perez-Lazoet

al.[153]

33-year-oldwom

anwith

ahistoryof

10years

ofHIV

andpulm

onarytuberculosis

admitted

dueto

paraparesisin

lower

limbs,

urinaryretention,andsensitive

involvem

ent

atT8level.CSF

studiesdisplayed20

lymphom

ononuclearcells,

hyperproteinorrachia,glucorrachia,and

adenosinedeam

inaseatnorm

allevels.

MRIof

thespinalandspinalcord

show

edintram

edullary

contrastgaugingwith

perilesionaledem

aatT8.

Toxoplasmosis.

Sulfam

ethoxazole/trim

ethoprim

IVwas

givenat5mg/kg

twiceadayfor

4weeks

with

dexamethasone

IV8mg

for7days.T

reatmentthencontinued

with

2weeks

ofsulfam

ethoxazole/trim

ethoprim

taken

orally.P

atient

continued

anti-tuberculosistherapywith

sulfam

ethoxazole/trim

ethoprim

160/800mgsplit

forevery12

h.

Imagingshow

edim

provem

ento

fintram

edullary

lesionswith

adecrease

inthesize

andthelower

contrastenhancem

ent.Muscle

strength

also

improved.

Streitetal.[154]

60-year-oldwom

anwith

fevers,chills,

myalgias,headache,and

2erythematous,

pruriticareas3–4cm

indiam

eter

onher

back

returned

from

Botsw

anaand

Zim

babw

eon

atripwhereshewascanoeing

andcamping.L

abtestsshow

edmild

leu-

kopeniaandmoderatethrombocytopenia.

N/A

African

trypanosom

iasis

Pentam

idineIV

and5dosesof

suramin

through3weeks.

Fatiguedforseveralm

onthsfollowing

treatm

ent.

Uraletal.[155]

44-year-oldmalepatient

with

back

pain

re-adm

itted

with

initialtransverse

myelitis

(TM)diagnosis.W

eaknessandnumbnessin

lower

extrem

ity.C

SFexam

inationshow

edWBCsat20/m

m,protein

at45

mg/dL

,glucoseandchloride

werenorm

allevels.

MRIdiagnosedTM

inlower

segm

ent.

Neurotoxocariasis.

Mebendazolewith

corticosteroid

for

6weeks.

Significant

improvem

entinmyelitis

findings.

Kim

etal.[156]

44-year-oldfemalewith

severeneurogenic

claudicationatL4–L5.Right

side

homonym

oushemianopsiaand

monoparesisin

rightarm

.Paragonimus-specificantibodyinCSF

was

norm

al.

MRIo

flum

berspine

show

edintraduralmasses

hypointenseon

T2andT1show

edmasses

hypointense.There

was

aslight

peripheral

rim

enhancem

ento

nT1.CTshow

edcalcifiednodulesinlumbarintraduralspace.

BrainMRIshowed

nodularorcystic

masses

inleftoccipitaland

parietallobes.

Spinalandcerebralparagonimiasis.

Lum

barfusion

forcoincident

spondylolisthesis,hem

ilaminectomyof

L3,andexcision

ofcysticmasses.

N/A

SN Compr. Clin. Med. (2019) 1:869–881876

Treatment

Antifungal drugs have been shown to be effective in treatingthis disease. This includes azole derivatives such as ketocona-zole, fluconazole, itraconazole, voriconazole, posaconazole,and isavuconazole, sulfonamide derivative, amphotericin B,and terbinafine B [137–145]. In mild cases, itraconazole at200 mg per day is recommended and the duration can rangeanywhere between 9 and 18 months [137].

Prevention and Control of Parasitic SpinalDiseases

In 2011, theWorld Health Organization (WHO) outlined threeessential criteria that are important to preventing and control-ling the parasitic diseases of the CNS [65, 146]. This includeda focus and understanding of the population and the interven-tion that is necessary in general rather than for each specificdisease, innovative tools to detect parasites of the CNS andcontrol them, and a multi-disease, intersectoral, andinterprogrammatic approach [65, 146]. In order for these strat-egies to work, it is important that they are ethical, economi-cally, agriculturally, and environmentally friendly, and havechemoprevention, community sensitization, case and symp-tomatic management, vector control, veterinary public health,and proper sanitary and hygienic conditions [65, 146].

These interventions have been successful since the WHOgave these criteria for prevention and control. For example, ma-laria interventions have reduced malaria by 30% throughout theworld and 34% in Africa [65]. This interventionmethod used theideas that the previous paragraph outlined, and it has been quitesuccessful most notably in Africa, despite a recent increase in theAfrican population that live in areas where malaria transmissionrates are high [65, 147]. There has also been work in other coun-tries in preventing schistosomiasis through means of providingsanitation, constructing dams, and delivering potable water [65,146]. With this said, the outreach throughout the world for theimportance of prevention and control, not just through the workof doctors and medical staff, has been increasing.

Overall, the concept of Bone health^ has risen to increasecollaboration between human health care practitioners, veterinar-ians, and public health and environmental health professional toreduce gaps between prevention and control [65, 148]. Thismethod has also been cost-effective and has been significantlybeneficial in areas that may have not had any collaboration in thepast, such as neglected populations [65, 149]. Through means ofprevention and control, over one billion people in low-incomeendemic areas will have better health and well-being, leading toan abundance of opportunities [65]. Proper control can be threat-ened by difficult or a complex diagnosis, so is important forphysicians to be aware of the case studies (Table 3) as to not befooled by an atypical presentation of a parasitic spinal disease.T

able3

(contin

ued)

Reference

Sym

ptom

sIm

aging

Diagnosis

Treatment

Outcome

Baiet

al.[157]

44-year-oldman

with

lower

back

pain

and

radiatingpain

atthelower

extrem

ities.

Num

bnesswas

presentbelow

thekneesand

theankles

wereweakening.S

pinal

movem

entinthelumbarregionwaslim

ited.

X-ray

oflumbarspineshow

edanarrow

ingof

theintervertebralspacebetweenL4andL5.

Fortheankle,therewas

destructions

atthe

Charcot

joint.Fu

rtherm

ore,aCTscan

displayedan

osteolyticlesionsandnew

bone

form

ationatL4–L5.MRIshow

edbone

destructionandskeletalsofttissue

form

ationatL4.

Neurosyphilis.

Posteriordebridem

ent,andan

allograft

bone

fusion

from

L3toS1

.Treated

with

penicillinGbenzathine

at2.4mUone

timeaweekfor3weeks.

Residualb

ackpain

andleftlower

numbness.After

12months,the

bone

graftswerecompletely

absorbed

andL4moved

forw

ard

progressively.The

patient

ultim

atelydied

ofacutehemorrhage

dueto

aduodenalulcer18

months

followinghisoperation.

SN Compr. Clin. Med. (2019) 1:869–881 877

Conclusion

Though there are several different types of parasitic diseasesof the spinal cord, there is usually a common theme betweenall of them—their immediate need for attention and treatment.Specific criteria have been established for these diseases andhow to properly treat them in order to avoid the significantimplications they can have on individuals. The parasitic dis-eases are most commonly found in endemic areas, althoughthis is not the case for all of them. In addition, traveling tothese endemic areas and returning to locations where the par-asitic diseases are not present may lead to an introduction ofthe disease to a new site if individuals become host to theparasite when in the endemic area. Imaging is often used todetect that the parasitic diseases are present in individuals, dueto several noted discrepancies from the imaging of normalindividuals, as noted throughout the paper. Prevention andcontrol of this disease are extremely important and should beutilizing methods of collaboration and specific guidelinesestablished by the WHO [65, 146].

Acknowledgments The authors are thankful to Drs. Kelly Warren, ToddMiller, and Peter Brink for departmental support, as well as Mrs. WendyIsser and Ms. Grace Garey for literature retrieval.

Compliance with Ethical Standards

Conflict of Interest The authors declare that they have no conflict ofinterest.

Ethical Approval All research conducted including literature reviewthrough PubMed met all ethical standards through the Stony BrookUniversity Renaissance School of Medicine Department of Physiologyand Biophysics.

Informed Consent The study did not contain any human subjects forresearch purposes, and informed consent was thus not applicable.

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