Parasitic Diseases Within the Spinal Cord and Nerve Roots
- 171 Downloads
Parasitic diseases of the spinal cord and nerve roots are a potentially deadly matter. They are mainly found in areas where there are poor sanitary conditions such as Africa, the Middle East, and the West Indies. The most common diseases include schistosomiasis and neurocysticercosis. Furthermore, it is clear that through an understanding of all the various diseases there are, it is imminent that patients are treated as soon as possible to avoid the deadly outcomes that the diseases can have to the body. This disease can have several impacts on individuals that include epilepsy, health problems, and implications on various organs.
KeywordsParasitic Schistosomiasis Neurocysticercosis Imaging Malariasis Syphilis Central nervous system Parasites
Parasitic diseases of the central nervous system (CNS), particularly those pertaining to the spinal cord region, are a potentially deadly matter. Parasitic spinal infections are commonly found in areas where there are poor sanitary conditions such as countries that are developing or not as well-equipped in the medical field as countries such as the USA . These diseases are generally treatable, and it is urgent that they are detected and treated as early as possible to avoid complications . The results of leaving these diseases undetected can include irreversible neurological deficits, as seen in spinal cysticercosis .
There are a large number of causes for spinal infections. Among the wide range of agents, bacteria, such as Bacteroidales and Clostridiales, are the most common agents, although other organisms also can cause bacterial spinal injuries [4, 5, 6]. The bacteria are either single-celled protozoa or multicellular metazoa . More examples of bacterial spinal infections include spinal epidural bacterial abscess, Pott’s disease which is also known as tuberculous spondylitis, Lyme disease which is also known as neuroborreliosis, and syphilis which can be classified as a meningovascular disease which is classified by thickened, inflamed meninges, or a parenchymatous disease which is classified through gummas in the cord [8, 9, 10, 11, 12]. Viral spinal infections can also be found in practice and may have a different treatment and course of action compared to bacterial diseases . Viral infections can include, but are not limited to, flaviviruses such as West Nile, varicella zoster, and Epstein-Barr virus [13, 14, 15]. This review focuses on parasitic diseases of the spinal cord and nerve roots, which are widespread and have the potential to be extremely lethal and infectious. Such diseases include schistosomiasis, which is common in endemic regions, and neurocysticercosis, which is the most common parasitic disease of the spinal cord [16, 17, 18]. Radiologists are very important in this field, as they are responsible for detecting the disease and working alongside the clinicians to facilitate the appropriate testing needed for correct treatment and to diagnose it early. Furthermore, radiology has been found to be most effective in diagnosis when using detailed structural images, rather than modern magnetic resonance (MR) techniques .
List of impactful parasitic diseases of the spinal cord
Echinococcosis (hydatid disease)
American trypanosomiasis (Chagas disease)
African trypanosomiasis (sleeping sickness)
Baggio-Yoshinari syndrome (Brazilian Lyme-like disease)
A literature search using the MEDLINE® and Google Scholar databases was conducted using terms relevant to parasitic spinal cord diseases. The search results were restricted to case reports and review articles. There were no language restrictions. We selected papers that revealed artifacts for pathogenesis, clinical manifestations, imaging, and treatment of each parasitic spinal cord disease.
Spinal Cord Disease Manifestations
There are several clinical manifestations to spinal cord diseases. In the neurological disorder of the spinal cord called myelitis, there are several pertinent clinical manifestations. This includes parasitic or fungal infection symptoms present as paresthesia from the feet with possible back pain, motor deficits impacting the flexors of legs and extensors of arms, bowel and bladder dysfunctions, temperature dysregulation, and hypertension . Over 2/3 of patients that have this disorder have lasting disabilities despite treatment . Another disorder is acute traumatic central cord syndrome. However, this is most commonly caused by cervical spinal cord injury. The clinical manifestations for this include motor deficits that are more severe in the upper extremities than in the lower extremities. In addition, there is a bilateral loss of pain and thermal dysfunction, and possible sphincter dysfunction [26, 27]. Another example of a spinal cord disorder is anterior spinal cord syndrome, caused mainly by aortic surgical interventions. The clinical manifestations include possible quadriparesis and could onset with no previous symptoms . In the following sections, subtypes of parasitic diseases associated with the spinal cord will be discussed, and their specific clinical manifestations will be mentioned.
Schistosomiasis is one of the most common parasitic diseases and impacts approximately 200 million people throughout the world, and ultimately causing symptoms in about 60% of these cases [8, 16]. This disease is caused by the trematode Schistosoma . It is often found in sub-Saharan Africa, South America, and Asia but it is also more recently moving to areas that it was not as common previously due to tourism [19, 30]. It can occur at any time through parasitic infection .
The usual causes of this disease can be due to Schistosoma mansoni, Schistosoma haematobium, and Schistosoma japonicum. The main way that this disease is transmitted is through a transmission of eggs in either the stool or the urine for the genus Schistosoma [19, 20, 32]. Once this occurs, it can be transmitted to humans through freshwater snails and penetrating cercariae . Eggs are then shed day-to-day following 6–8 weeks of initial contact, with variable amounts of shedding through each day depending on how much contact with freshwater there was and the parasite burden on the affected individual [23, 33, 34, 35, 36]. This type of diagnosis is referred to as “parasitological diagnosis” as there is direct evidence that there is a pathogen in the body of an individual . There are also other types of diagnoses which are through patient serum that are more sensitive to the extent that low-intensity schistosomiasis can be detected as well [23, 37, 38, 39]. Through this serology, antibodies can be detected to note that the disease is in the patient. These antibodies can be directed against any of the four stages of the Schistosoma genus which includes penetrating cercariae, schistosomula which is the migration of juvenile worms, the presence of adult worms, and eggs produced by worms through mating [23, 32, 35]. For the serological assays that have been taken, some have been found to be specific for endemic regions of various specificity levels while others are for diagnosis that relates to important or travel-related schistosomiasis [30, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56].
Medullary (most involved in the spinal cord only)
Commonly has high eosinophil CNS levels, symmetric distribution of sensorimotor abnormalities, spinal cord atrophy in untreated patients.
Hyperintensity in the T2 region with enlargement of the spinal cord is seen. This is associated with mild and heterogeneous enhancement.
Conus-cauda equina syndrome
Slower development of symptoms, atrophic leg muscles, asymmetric sensorimotor alterations, high eosinophil CNS levels.
The cauda equina is shown to be thickened; there is a gadolinium enhancement of the conus medullaris.
Myeloradiculopathy (involved with the spinal cord and roots of the nerves)
Intermediate form. Necrosis, vacuolization, and further atrophy of the spinal cord tissue occur. Radicular pain in the lower limbs, muscular weakness, sensory disturbances, high eosinophil CNS levels.
Spinal nerve root thickening and leptomeningeal enhancement seen.
MRI is important in developing a diagnosis for this disease. In many cases, this disease is in the medullary form due to a hyperintensity that is patchy in T2-weighted images (T2WIs), a noticeably enlarged spinal cord, and a lower cord and conus medullaris heterogeneous contrast enhancement on T1WIs [1, 24, 31, 59, 62, 63]. Furthermore, this appearance is similar to a cord neoplasm [1, 2]. MRI also displays thickening of the spinal cord and allows the eggs and granulomas to be detected through linear radicular contrast enhancement [1, 33, 62, 64].
For the treatment of schistosomiasis, praziquantel is the most used immediately following diagnosis after starting corticosteroid treatment [64, 65]. However, before a patient is officially diagnosed but doctors speculate that schistosomiasis is possible, corticosteroids are used as the primary treatment .
Neurocysticercosis (NCC) is another extremely common parasitic disease of the spinal cord and CNS [67, 68]. This disease is caused by pork tapeworm, known as Taenia solium in humans. Humans are the intermediate host of the pork tapeworm and allow it to survive and induce harmful effects . Approximately 50 million people throughout the world have this specific type of spinal cord disease, and it is much more common in endemic areas similar to schistosomiasis, such as Africa, some regions in Asia, and Eastern Europe and Central and South America. It affects approximately 3 to 6% of the population in these areas . In addition, due to travel to these countries, many people become carriers and transfer the disease to non-endemic areas, such as North America . NCC is significant because it has a major onset of epilepsy due to intraparenchymal brain cysts .
NCC occurs following the ingestion of T. solium-infested eggs. Once these eggs hatch, embryos are ultimately released into the small intestines and invade several different tissues throughout 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 the small intestines, they then enter neural and subcutaneous tissues and then enter skeletal and ocular globes and continue their development . When in the CNS, cysticerci can develop anytime between 3 weeks and 2 months following the initial oncosphere formation [1, 17].
There are many types of larval forms for this disease. The most common of these is Cysticercus cellulosae . This type contains a scolex and has implications on the CNS by causing intraparenchymal lesions in the brain . Furthermore, Cysticercus racemosus is another type, but it is less common and does not have a scolex [1, 2]. Overall, the cysticerci are only 1 cm in diameter and are located in the cerebral cortex or the basal ganglia [1, 69].
There is a wide range and non-specific clinical manifestation for cysticercosis that depends on location of the parasite, amount of parasites, and inflammation . In most cases, there is a cyst degeneration in the basal ganglia and edema which leads to neurological implications that can often include chronic headaches, focal neurologic deficits, intracranial hypertension, and decline in cognition . Most of the spinal cysts are in the lumbosacral regions . Furthermore, in spinal cases of NCC with basal subarachnoid disease, it is imminent that an MRI is done .
When cysts occur, it can lead to several different complications including nerve entrapments, hydrocephalus, gait disorders, chronic meningitis, vasculitis, spinal or cerebral stroke, or lymphocytic meningitis if they rupture . In terms of this disease and how it is associated with the spinal cord, it is quite rare and is associated with other parts of the CNS more, as it is implicated in the spinal cord for just 1.2 to 5.8% of reports [1, 75].
To diagnose patients with this type of disease, serological testing and fundoscopy can be performed to detect the parasite in patients. However, histological review and imaging is the most common method to diagnosis, as it allows a more comprehensive understanding of the specific form of neurocysticercosis that the patient has [76, 77].
Del Brutto et al. have proposed specific diagnostic criteria for the diagnosis of NCC. This combines clinical history, neuroimaging, immunological evidence, and epidemiological guidelines to ultimately establish defined guidelines that allow the diagnosis of NCC [67, 78]. For the absolute criteria, there must be an ability to see the parasite through a spinal cord lesion located in the body. For the neuroimaging of the absolute criteria, a scolex must be visible within the cystic lesion. Furthermore, in a fundoscopy, sub-retinal parasites will be seen. For the major criteria of the disease, the lesions will suggest NCC, EITB assays will detect T. solium antibodies, and cysticidal drug therapy would display a resolution of the lesion following albendazole or praziquantel treatment. The minor criteria will also show lesions that suggest NCC and there will be symptoms suggesting NCC, and a CSF ELISA would show T. solium antibodies or antigens and cysticercosis that is outside the CNS. Pursuing this further, the epidemiological criterion has an origin endemic for the patient country and the patient must be living in the endemic area and travel to endemic areas where there is NCC often. Furthermore, the household that the patient lives in must have had contact with T. solium in order for it to develop as well [66, 67, 77].
The various diagnoses for NCC can be defined as definitive or probable. A definitive diagnosis will have 1 absolute criterion or 2 major criteria and 1 minor and 1 epidemiological criterion. For a probable diagnosis, one must have 1 major criterion and 2 minor criteria or could have 1 major and 1 minor and 1 epidemiological criterion applicable or 3 minor and 1 epidemiological criterion applicable [66, 67, 77].
For this specific type of disease, there are four stages of development and regression that have been found through CT and MR imaging. The first stage involves vesicular implications and sees cysts and scolex through imaging. The second stage has colloidal involvement and has ring enhancement and edema. The third stage had nodular-granular involvement and has decreased enhancement and edema and initiation of calcification. The fourth stage is more calcification and this is seen through a CT or MRI . It is important to note that multiple anatomical sites are involved for patients that have this parasitic disease [1, 70, 79, 80]. Furthermore, neuroimaging has been shown to be the preferred method for diagnosis in NCC through CT and MRI . This is because it allows visualization of the infections and assesses the number and location of it . Calcifications, which occur in about half of all NCC patients, are seen through the high sensitivity of CT scans of NCC which has a starry sky appearance due to several cysts implicated with it [67, 71, 81]. The reason that MRIs are also effective is that they allow distinction of the degenerative cysticerci stage and detect parasites in the posterior fossa, basal cisterns, and ventricles that CT scans are not able to detect [67, 80].
Effective methods of treatment for NCC have been developed . In order to control the inflammation that is caused from this disease, albendazole with glucocorticoids is administered . Alternatively, praziquantel with corticosteroids or a combination of albendazole and praziquantel, if there are more than 2 active parenchymal cysts, is a recommended drug treatment option .
A controversial topic for treatment of NCC is cysticidal drugs. This is because it is believed that it may cause more harm than benefit to patients as this treatment could increase the risk for ICP and potentially result in death [67, 83]. Therefore, patients should only be treated with regard to their symptoms without cysticidal therapy [67, 84].
Due to the fact that neurological issues are a clinical manifestation of NCC, anti-epileptic therapies have also been recommended [67, 80]. In these cases, phenobarbitone and carbamazepine should be used to control seizures, but this is also not without controversy, as relapse is quite common following improvement while no improvement has also been shown in some cases [17, 67, 68, 84].
If calcification is present, anti-parasitic treatments should not be administered. The reason for this is because there can be a potentiation on the excessive inflammatory responses that are occurring in the brain. For such cases, treatment options include the aforementioned corticosteroids, osmotic diuretics, and decompressive craniotomy. This will allow control of brain edema .
Echinococcosis (Hydatid Disease)
Echinococcosis, also known as hydatid disease, is caused by the larval stage of Echinococcus . The most common hosts of these parasites include carnivores and canines. Unlike the previous parasites, these are found near the countryside or in homes that are located in forest areas . When humans have water or ingest food that are contaminated with eggs of this parasite, they will then develop the disease as well . Furthermore, the most common form of this disease is cystic echinococcosis, which is caused by Echinococcus granulosus, and alveolar echinococcosis, which is due to Echinococcus multilocularis [1, 86].
As mentioned, it is extremely rare for this disease to be associated with the spine, but there are still some cases that have been reported. In these cases, the segment of the spine that is most associated is the thoracic segment as it is 50% of all cases, the next most frequent is lumbar and sacral which is 20% for each, and the least is cervical segments, which represent only 10% of all spinal cases [1, 87]. Furthermore, the disease is located in epidural regions in most of the cases [88, 89].
This disease, when associated with the spinal cord, is manifested as isointense cystic lesions without any peripheral edema that is associated with significance [1, 90]. The fibrous capsules in the body are hypointense on T2WIs and display peripheral enhancement through inflammations [1, 91]. Furthermore, the more common cysts are intradural-extramedullary cysts and present at a young age .
In order to diagnose this disease, serological and imaging tests are used. Furthermore, while it is still possible to have CNS and spinal involvement of this disease, it is only in about 1 to 2% of all cases, as most cases are involved with the liver and lungs [1, 77, 86, 87, 88, 92]. The diagnosis can also be confirmed through surgery by observing a laminated cyst membrane .
For the diagnosis of this disease, the intradural-extramedullary or intramedullary cysticerci is a copy of echinococcosis [1, 93]. Furthermore, a mimic of alveolar echinococcosis and spinal sparganosis can be cestode infections, but this is in more rare cases . This disease can also be classified as spinal arachnoid or spinal aneurysmal bone cysts, confirmed through higher eosinophil CNS levels .
The primary treatment of choice for this specific parasitic disease is removal through surgical means. However, it is important that if the surgery were to occur, there should not be a perforation of the cyst wall. This can potentially lead to dissemination and anaphylactic reactions [88, 94]. Furthermore, to avoid this disease from recurring, anti-helminthic therapy and follow-up visits for MRIs after the operation are imminent [88, 95]. Recurrence and mortality are quite high for this disease, as they are approximately 40% each, showing that diagnosing and treating affected individuals is critical [88, 89, 96]. Albendazole or mebendazole should also be taken, regardless of whether there will be surgery or not .
Toxoplasmosis can be localized in multiple parts of the spinal cord. It arises from the protozoan Toxoplasma gondii which can be found in regions anywhere in the world [1, 97]. It is frequent in pregnant women and this ultimately results in birth defects and could lead to a return of weak immunity if individuals had an immune disease previously, leading to encephalitis [1, 97, 98]. The pathology of the spinal cord is because of deficits in CD4 T cells that are linked to AIDS or T cell leukemia or lymphoma [1, 99, 100]. A previous study has shown that there are only 18 reported cases of spinal cord toxoplasmosis in AIDS patients [101, 102].
To assist in diagnosing patients with this disease, it is common that patients will have a fever, a sensory loss below a specific spinal cord level, urinary retention, and extreme weakness also known as paraparesis . In order to definitely diagnose an individual with spinal toxoplasmosis, a biopsy must be done to definitely detect that there is an organism for this parasitic disease in the body of an individual, but this has been highly morbid . Therefore, as an alternative, individuals can be diagnosed if their CD4 lymphocyte cell count is less than 100 cells/mm3 .
In these patients, there are mass effects and edema. Furthermore, cerebral toxoplasma lesions that are also found in patients assist in diagnosis for spinal toxoplasmosis [1, 2]. MRI is also utilized in order to ensure that patients have spinal toxoplasmosis, rather than bony lesions, epidural abscess, herpes myelitis, or an HIV vacuolated myelopathy [101, 103].
There are multiple methods of treatment for toxoplasmic encephalitis. Specifically, in patients with AIDS, pyrimethamine (200 mg dose, 50 mg/day), sulfadiazine (5–6 g/day), and folinic acid (10–25 mg/day) should be combined and administered daily . Alternative treatments, specific to the spine, include trimethoprim-sulfamethoxazole, which has been found to be most effective, pyrimethamine with atovaquone, pyrimethamine with azithromycin, or sulfadiazine with atovaquone [101, 104, 105].
American trypanosomiasis, or Chagas disease, occurs mainly in Latin America and some Western countries [1, 77, 106]. The parasite responsible for it is Trypanosoma cruzi. The cause of the disease onto humans is through Triatominae (i.e., conenose or kissing bug), which suck the blood out of humans and then can transfer the disease onto them [1, 77].
The clinical manifestations of this disease can be distinguished into an acute phase which lasts 6–8 weeks and chronic phases . In these acute cases, patients are often found to have fever, malaise, headache, and hepatosplenomegaly . In chronic cases, some patients develop other complications that include cardiac, gastrointestinal, or both [107, 108, 109]. The association that this disease has with the spinal cord is through acute meningitis or nodular encephalitis, but this is in rarer cases [1, 110]. The direct symptoms that have been found when it is linked to the spinal cord are abnormalities and deficits in the sensory and motor parts of the body, dementia, and confusions [1, 111]. Furthermore, Chagas disease is often confused as a presentation of AIDS at first, but the other clinical manifestations allow a final diagnosis of Chagas disease to be confirmed when it is the case [1, 24, 111].
In order to diagnose Chagas disease, histology, serologic, and CSF tests are often used. Through these methods, abnormalities in the CSF are quite common and can confirm the diagnosis of Chagas disease [1, 24].
The way that this disease is seen through MRI and CT imaging is expanding hyperintense lesions on T2WIs. When it is found in the spinal cord, it demonstrated extensive edema and mass effect [1, 24, 110, 112].
Malariasis is caused by the agent Plasmodium sp. and is an extremely rare case of a parasitic spinal cord disease. It is important to note that it is quite common in endemic areas that are located in tropical countries . Symptoms are similar to those observed in acute disseminated encephalomyelitis. In order to diagnose this disease, imaging is used to detect a spinal cord lesion and potential nerve root enhancement .
African trypanosomiasis, or sleeping sickness, is also a rare disease of the spinal cord and is caused by the agent Trypanosoma brucei, T. congolense, T. vivax, T. evansi, and T. equiperdum [1, 115]. It is most commonly found in Central and Western Africa and impacts approximately 70 million people in this region [115, 116]. The manifestation that it has associated with the spinal cord is meningoencephalitis. Through imaging, meningeal enhancement, lesions of the basal ganglia, and white matter diffusions are shown which ultimately leads to thickening in the spinal region [1, 117]. Because of a lack of vaccines due to variations in hosts, it is difficult to treat this parasitic disease .
Neurotoxocariasis is a rare parasitic disease that arises from Toxocara sp. It can be found in any part of the world. The clinical manifestations associated with this disease include associations with eosinophilic meningitis and optic neuritis. In order to diagnose this disease through imaging, longitudinal extensive myelopathy can be seen in addition to hyperintense T2WI lesions [1, 118, 119].
Baggio-Yoshinari syndrome, previously known as Brazilian Lyme-like disease, originates from Brazil . It is transmitted through Amblyomma and Rhipicephalus as they release their ticks that will have latent behaviors. The disorders that are associated with this disease include immune weakness and a recurrence of complications that patients may have had previously .
The symptoms associated with this disease are similar to that of influenza and Lyme disease [1, 120]. Following invasion, there is an infection in the neurological region evident by lymphomonocytary meningitis, cranial neuritis, peripheral radiculopathy, and encephalomyelitis [1, 121, 122]. It is important to note that similar to the previously discussed disease, there is a high relapse rate that is associated with it. Furthermore, it is critical that patients that have this disease are found in the early and acute stages; otherwise, there is a much higher chance that relapse will occur for these patients [1, 121, 122].
Through imaging that has been done in this disease, it is commonly found that there are multifocal hyperintense lesions on T2WIs, demyelinating lesions, and cranial enhancements on post-contract T1WIs. When this is seen through MRI examination, it facilitates the diagnosis of this disease [1, 123, 124, 125, 126].
It is critical that patients are treated for this disease quite in the early stages to avoid the latent stage, when it becomes irreversible . Antibiotics has been a common therapy for the disease, such as ceftriaxone, as well as doxycycline, amoxicillin, or penicillin .
Syphilis is caused by Treponema pallidum . It is a sexually transmitted disease and when it is found in the spine, it involves syphilitic gummas, stemmed from leptomeningeal inflammation and low signal intensity found on T2WIs [8, 9, 10, 11, 12]. Syphilis peaked during WWII, with a decline due to the founding of penicillin, yet it is still prevalent as a sexually transmitted disease [128, 129].
Although it is extremely rare, this disease could also be caused by tabes dorsalis which is the tertiary form. In this specific type, the posterior location of the spinal cord is harmed, evident through imaging that has shown atrophy and hyperintensity on T2WIs [1, 77, 130, 131].
South American Blastomycosis (Paracoccidioidomycosis)
South American blastomycosis, also known as paracoccidioidomycosis, is a systemic disease that is caused by Paracoccidioides brasiliensis . It is most commonly found in South American regions, hence its name [1, 133]. Furthermore, the prevalence of this disease is between 5.6 and 17.5% [1, 133, 134].
When the fungus of the disease is inhaled, it will then affect the CNS as well as other parts of the body including the kidney, spleen, adrenal gland, and bones throughout the body .
For only 4.0% of CNS cases of this disease will there be localization in the spinal cord [133, 134, 135]. The lesions associated with this disease can also be linked to the meningeal form through diffuse leptomeningeal enhancement [1, 136].
Antifungal drugs have been shown to be effective in treating this disease. This includes azole derivatives such as ketoconazole, fluconazole, itraconazole, voriconazole, posaconazole, and isavuconazole, sulfonamide derivative, amphotericin B, and terbinafine B [137, 138, 139, 140, 141, 142, 143, 144, 145]. In mild cases, itraconazole at 200 mg per day is recommended and the duration can range anywhere between 9 and 18 months .
Prevention and Control of Parasitic Spinal Diseases
In 2011, the World Health Organization (WHO) outlined three essential criteria that are important to preventing and controlling the parasitic diseases of the CNS [65, 146]. This included a focus and understanding of the population and the intervention that is necessary in general rather than for each specific disease, innovative tools to detect parasites of the CNS and control them, and a multi-disease, intersectoral, and interprogrammatic approach [65, 146]. In order for these strategies to work, it is important that they are ethical, economically, agriculturally, and environmentally friendly, and have chemoprevention, community sensitization, case and symptomatic management, vector control, veterinary public health, and proper sanitary and hygienic conditions [65, 146].
These interventions have been successful since the WHO gave these criteria for prevention and control. For example, malaria interventions have reduced malaria by 30% throughout the world and 34% in Africa . This intervention method used the ideas that the previous paragraph outlined, and it has been quite successful most notably in Africa, despite a recent increase in the African population that live in areas where malaria transmission rates are high [65, 147]. There has also been work in other countries in preventing schistosomiasis through means of providing sanitation, constructing dams, and delivering potable water [65, 146]. With this said, the outreach throughout the world for the importance of prevention and control, not just through the work of doctors and medical staff, has been increasing.
Case studies of parasitic spinal cord diseases
Mikulich et al. 
28-year-old Sudanese man with lower back pain, flaccid paraplegia, sensory level (T8), and urinary retention.
MRI showed increased signal/mass effect in spinal cord from T6 to conus medullaris. A mild patchy enhancement was also present following IV contrast.
Differential diagnosis included astrocytoma, ependymoma, hemangioblastoma, schistosomiasis, and metastasis. MRI findings suggest spinal cord schistosomiasis.
Dexamethasone at 4 mg 4 times per day. 3 doses of praziquantel 25 mg/kg, and prednisolone 1 mg/kg.
Exhibited dramatic clinical improvement. Decrease in abnormal signal and swelling in spinal cord.
Zhang et al. 
59-year-old woman with pain in bilateral lower limbs and left lower limb. Increasing urinary frequency. Hypoesthesia along S2–S5 dermatomes on bilateral lower limbs and decreased perianal sensation on the left side.
Intradural extramedullary lesions from L1/2 to S1 that was hyperintense at T2 and hypointense at T1. Thin-walled cyst was identified with clear fluid from L2–S1 that was 8 cm.
Lumbar spinal intradural neurocysticercosis
Cystic mass was removed, fixed in 10% formalin for 8 h at room temperature. Patient was then treated with albendazole at 15 mg/kg/day for a period of 4 weeks.
No additional complications and the patient ultimately recovered.
Abarrategui et al. 
29-year-old Bolivian woman with headache for 3 days, fever, and nausea. CSF glucose levels dropped to less than 20% of glycemia. In third week, patient reported acute radicular pain in right S1 region. LP showed clear CSF containing 265 WBCs, 73 mg/dL proteins, and glucose at 45 mg/dL.
CT scan displayed scattered cortical-subcortical calcifications up to 2.5 mm. MRI of S1 territory showed a rounded lesion at S1–S2, 16 mm in diameter that was intradural, extramedullary, and hyperintense in T2.
Viral lymphocytic meningitis was the initial etiology. Neurocysticercosis was the final diagnosis.
Patient was treated with analgesics to reduce pain.
Improved gradually and final LP showed glycorrhachia at 50% of blood glucose levels.
Xu et al. 
30-year-old Kazakhstan male presenting back and left hip pain, headache, and weakness in lower left limbs. Minor epilepsy was present, muscular tension was above normal range.
MRI and CT results displayed lesions in head, lungs, spleen, kidneys, right scapula, left second costal arch, the left acetabulum, the third left rib, and T5–T8 thoracic vertebrae.
Initially diagnosed as thoracic alveolar echinococcus (AE) due to back pain and thoracic canal decompression. The patient was ultimately diagnosed as multiple-organ AE.
Thoracic lesions were treated with canal posterior decompression and fixed with hooks and rods. Patient was given 2-year albendazole treatment.
Patient returned due to progression of intracerebral AE and was given another operation to treat it.
Perez-Lazo et al. 
33-year-old woman with a history of 10 years of HIV and pulmonary tuberculosis admitted due to paraparesis in lower limbs, urinary retention, and sensitive involvement at T8 level. CSF studies displayed 20 lymphomononuclear cells, hyperproteinorrachia, glucorrachia, and adenosine deaminase at normal levels.
MRI of the spinal and spinal cord showed intramedullary contrast gauging with perilesional edema at T8.
Sulfamethoxazole/trimethoprim IV was given at 5 mg/kg twice a day for 4 weeks with dexamethasone IV 8 mg for 7 days. Treatment then continued with 2 weeks of sulfamethoxazole/trimethoprim taken orally. Patient continued anti-tuberculosis therapy with sulfamethoxazole/trimethoprim 160/800 mg split for every 12 h.
Imaging showed improvement of intramedullary lesions with a decrease in the size and the lower contrast enhancement. Muscle strength also improved.
Streit et al. 
60-year-old woman with fevers, chills, myalgias, headache, and 2 erythematous, pruritic areas 3–4 cm in diameter on her back returned from Botswana and Zimbabwe on a trip where she was canoeing and camping. Lab tests showed mild leukopenia and moderate thrombocytopenia.
Pentamidine IV and 5 doses of suramin through 3 weeks.
Fatigued for several months following treatment.
Ural et al. 
44-year-old male patient with back pain re-admitted with initial transverse myelitis (TM) diagnosis. Weakness and numbness in lower extremity. CSF examination showed WBCs at 20/mm, protein at 45 mg/dL, glucose and chloride were normal levels.
MRI diagnosed TM in lower segment.
Mebendazole with corticosteroid for 6 weeks.
Significant improvement in myelitis findings.
Kim et al. 
44-year-old female with severe neurogenic claudication at L4–L5. Right side homonymous hemianopsia and monoparesis in right arm. Paragonimus-specific antibody in CSF was normal.
MRI of lumber spine showed intradural masses hypointense on T2 and T1 showed masses hypointense. There was a slight peripheral rim enhancement on T1. CT showed calcified nodules in lumbar intradural space. Brain MRI showed nodular or cystic masses in left occipital and parietal lobes.
Spinal and cerebral paragonimiasis.
Lumbar fusion for coincident spondylolisthesis, hemilaminectomy of L3, and excision of cystic masses.
Bai et al. 
44-year-old man with lower back pain and radiating pain at the lower extremities. Numbness was present below the knees and the ankles were weakening. Spinal movement in the lumbar region was limited.
X-ray of lumbar spine showed a narrowing of the intervertebral space between L4 and L5. For the ankle, there was destructions at the Charcot joint. Furthermore, a CT scan displayed an osteolytic lesions and new bone formation at L4–L5. MRI showed bone destruction and skeletal soft tissue formation at L4.
Posterior debridement, and an allograft bone fusion from L3 to S1. Treated with penicillin G benzathine at 2.4 mU one time a week for 3 weeks.
Residual back pain and left lower numbness. After 12 months, the bone grafts were completely absorbed and L4 moved forward progressively. The patient ultimately died of acute hemorrhage due to a duodenal ulcer 18 months following his operation.
Though there are several different types of parasitic diseases of the spinal cord, there is usually a common theme between all of them—their immediate need for attention and treatment. Specific criteria have been established for these diseases and how to properly treat them in order to avoid the significant implications they can have on individuals. The parasitic diseases are most commonly found in endemic areas, although this is not the case for all of them. In addition, traveling to these endemic areas and returning to locations where the parasitic diseases are not present may lead to an introduction of the disease to a new site if individuals become host to the parasite when in the endemic area. Imaging is often used to detect that the parasitic diseases are present in individuals, due to several noted discrepancies from the imaging of normal individuals, as noted throughout the paper. Prevention and control of this disease are extremely important and should be utilizing methods of collaboration and specific guidelines established by the WHO [65, 146].
The authors are thankful to Drs. Kelly Warren, Todd Miller, and Peter Brink for departmental support, as well as Mrs. Wendy Isser and Ms. Grace Garey for literature retrieval.
Compliance with Ethical Standards
Conflict of Interest
The authors declare that they have no conflict of interest.
All research conducted including literature review through PubMed met all ethical standards through the Stony Brook University Renaissance School of Medicine Department of Physiology and Biophysics.
The study did not contain any human subjects for research purposes, and informed consent was thus not applicable.
- 9.Berger JR. Infectious myelopathies. Continuum (Minneap Minn). 2011;17(4):761–75.Google Scholar
- 21.Mahmoud AAF. Schistosomiasis. Tropical Medicine: Science and Practice. 2001; 510.Google Scholar
- 95.Singh S, et al. Spinal intradural hydatid cyst causing arachnoiditis: a rare etiology of cauda equina syndrome. J Craniovertebr Junct Spine. 2016;7(4):282–4.Google Scholar
- 109.World Health Organization. Working to overcome the global impact of neglected tropical diseases: first WHO report on neglected tropical diseases. No. WHO/HTM/NTD/2010.1. Geneva: World Health Organization, 2010.Google Scholar
- 117.Kibiki GS, Murphy DK. Transverse myelitis due to trypanosomiasis in a middle aged Tanzanian man. Journal of Neurology, Neurosurgery & Psychiatry. 2006;77(5):684-685.Google Scholar
- 119.Lin J, Arita J, da Rocha AJ, et al. Enlarging the spectrum of inflammatory/post-infectious acute disseminated encephalomyelitis: a further case associated with neurotoxocariasis. J Neuro-Oncol. 2010;1:1–3.Google Scholar
- 122.Shinjo SK, Gauditano G, Marchiori PE, et al. Manifestação neurológica na Síndrome de Baggio-Yoshinari. Rev Bras Reumatol. 2009;49:492–505.Google Scholar
- 146.World Health Organization Accelerating work to overcome the global impact of neglected tropical diseases; a roadmap for implementation (executive summary) [cited 2018 Nov 25;];2012 http://apps.who.int/iris/bitstream/10665/70809/1/WHO_HTM_NTD_2012.1_eng.pdf. Available from.
- 147.World Health Organization World malaria report. [cited 2018 Nov 25;];2014 http://www.who.int/malaria/publications/world_malaria_report_2014/report/en/. Available from.
- 148.The World Bank. People, pathogens, and our planet. Volume 2: the economics of one health. [cited 2018 Nov 25;];2012 https://openknowledge.worldbank.org/bitstream/handle/10986/11892/691450ESW0whit0D0ESW120PPPvol120web.pdf?sequence=1Report no.69145-GLB. Available from.
- 149.World Health Organization investing to overcome the global impact of neglected tropical diseases; third WHO report on neglected tropical diseases. [cited 2018 Nov 25;];2015 http://apps.who.int/iris/bitstream/10665/152781/1/9789241564861_eng.pdf?ua=1. Available from.