Travelers and children (Del Brutto 2013; Del Brutto et al. 2012) and native cases in the Indian subcontinent most frequently present with a single inflamed brain lesion, suggesting an early inflammatory response to a mild challenge (García et al. 2003b; Rajshekhar and Chandy 2000). In this view, a proportion of single lesion cases would correspond to cysticerci that resolved soon after infection, before full establishment and thus not provoking a strong immune response (García et al. 2010). The alternative hypothesis, that these result from existing viable cysts, collides with the very young age and mild antibody reactions which are typical in patients with single enhancing lesions.

Cysts get established soon after infection, likely in less than 3 months (Yoshino 1933). Most cysts in non-immunologically privileged sites are probably destroyed very fast by the host’s immune response (see above under pig cysticercosis). Cysts in the brain and the eye survive preferentially due to the protection of the blood-brain barrier and the hemato-ocular barrier and manifest as symptomatic disease years after (Dixon and Lipscomb 1961).

In a series of detailed clinical descriptions of neurocysticercosis cases published in Germany and England in the early 1900s, several authors noted that subcutaneous parasites resolve years after than brain cysts and that neurological symptoms frequently occur between 3 and 5 years after infection (Dixon and Lipscomb 1961; Henneberg 1912; McArthur 1934). Live brain cysts can survive for many years without initiating the degeneration process. This long asymptomatic or oligosymptomatic stage likely results from active parasite mechanisms of immune evasion. Beyond preferential survival in immunoprotected cysts such as the brain or the eye, cysticercotic cysts may actually utilize molecular mimicry or mimetism mechanisms where the cyst covers itself with host immunoglobulins (Correa et al. 1985; Flisser 1989; Willms 2008), ingest and degrade host immunoglobulins (Damian 1987), inhibit the complement cascade at the C1q and C3b levels (Khan and Sotelo 1989), and secrete chemokines which modulate the immune attack of the host (Evans et al. 1998; Sciutto et al. 2007).

Frequently, symptoms and signs of neurocysticercosis appear or get exacerbated as a result of one or more cysts been attacked by the host immune system. This cellular attack consists of lymphocytes, plasma cells, and macrophages, frequently preceded by a well-defined eosinophil infiltrate, and gradually destroys the cyst (Flisser 1994; Mahanty and García 2010). In pathological specimens this process results in a colloidal stage of early destruction, in which the cysts contents become turbid and jelly, followed by a granular nodular stage in which no discernible liquid content is found anymore, to end as a calcified scar, as classically described by Escobar (Escobar 1983). In general, it is suggested that after an initial pro-inflammatory Th1 period with increased IL-12, TNF-a, and nitric oxide, the parasite establishes in a Th2-type response while asymptomatic, with low IFN-g and IgG2a antibodies and increased IgG1, IgE, IL-4, IL-13, and IL-15 (Alvarez et al. 2002; Bueno et al. 2004; Chavarria et al. 2003; Fleury et al. 2003; Restrepo et al. 2001; Rodriguez-Sosa et al. 2002; Terrazas et al. 1998; Villa and Kuhn 1996), possibly with alternatively activated macrophages as a contributory effector for this modulation (Gundra et al. 2011; Terrazas et al. 2005). It would eventually switch back to a Th1-like profile once the immune equilibrium is lost and the inflammatory response establishes and destroys the parasite, a process which is also triggered by treatment with antiparasitic agents. This inflammatory response causes most of the morbidity associated with neurocysticercosis (White et al. 1997) and responds very well to steroid treatment (Nash et al. 2006).

There is an apparent contrast between the benefit of inflammatory processes in eliminating the parasite and their deleterious effects in terms of clinical manifestations (Sciutto et al. 2007). This is particularly notorious when considering the effects of cyst death, natural of after antiparasitic treatment, in causing brain inflammation. Using steroids to suppress inflammation is required in both cases (Nash et al. 2011). Steroids have a very wide spectrum of action so its use does not contribute that much to deciphered specific inflammation mechanisms in neurocysticercosis. Long-term steroid treatment may lead to complications so judicious use is mandatory. Other generic anti-inflammatory therapies like methotrexate (Mitre et al. 2007) have been used to replace steroids, and immunosuppressive therapy has been used in severe inflammatory cases (Del Brutto and Sotelo 1988). Whether more specific agents such as anti-TNF may be of use in neurocysticercosis remains to be explored.

A large series of specific antigens and epitopes have been identified for Taenia solium (Deckers and Dorny 2010; Rodriguez et al. 2012). Some of them are associated with protection to infection and thus have been used to develop pig vaccines, and most others were identified as potential diagnostic antigens.

Some authors have reported an increased presence of immune diseases with alteration of the immune function in patients with neurocysticercosis (Sanz 1987), and an association between neurocysticercosis and cerebral glioma has been reported both as isolated cases (Agapejev et al. 1992) and in a controlled study (Del Brutto et al. 1997). The underlying hypothesis is that inflammation and suppression of local immune response may result in malignant transformation of glial cells, although the association has not been further studied.

A few cases of neurocysticercosis in transplant recipients have been reported (Barra Valencia et al. 2007; Gordillo-Paniagua et al. 1987; Hoare et al. 2006). Neurocysticercosis is rarely seen in series of patients with HIV infection, most likely as a coincidental association (Moskowitz et al. 1984; Soto Hernandez et al. 1996; Thornton et al. 1992; White et al. 1995). Some authors suggest that extraparenchymal locations including giant cysts would be more common in HIV-infected individuals, but this has not been confirmed in larger series (Soto Hernandez et al. 1996; Walker and Zunt 2005).

Most of the literature is composed of prevalence studies of taeniasis concluding that the population prevalence of intestinal taeniasis in endemic countries locates around 1 %, usually ranging from 0.5 to 2 % (Allan et al. 1996; García et al. 2003a; Sarti et al. 1992, 1994). Most of these surveys determined only the prevalence of adult tapeworms detected by stool microscopy and are likely underestimations of the prevalence because of the suboptimal sensitivity of microscopy and also because they will miss early infections. Parasite antigens can be detected in stools since early in the infection, 3 weeks, and studies using coproantigen detection find between 1.5 and 3 times more tapeworms (Allan et al. 1990; García et al. 2003a). The discordance between coproantigen and microscopy data suggests that either some or many infections establish but resolve before egg excretion, mature tapeworms may have periods where no eggs are excreted, or both of the above.

The tapeworm life span of T. solium was assumed to be of more than 20 years, based on particular cases of long-standing Taenia saginata infection (Faust et al. 1984). However, clinical and epidemiological data including age prevalence curves suggests that the adult tapeworm lives less than 5 years (Allan et al. 1996).

The worm establishes in the small intestine by anchoring its scolex in the mucosa using its four suckers and its double crown of hooks, with a local inflammatory response in the area which is composed by macrophages, plasma cells, lymphocytes, fibroblasts, neutrophils, and eosinophils, with local histamine release (Avila et al. 2002; Willms 2008). The local response may reduce the likelihood of tapeworm establishment and thus it has been explored as a possible vaccine (Leon-Cabrera et al. 2009, 2012). So far partial protection in a rodent model has been obtained. Other vaccines for intestinal cestodes are also being developed, including a dog vaccine for Echinococcus granulosus (Zhang et al. 2006).

Two specific diagnostic antigens specific to the adult tapeworm stage have been identified, namely, T33 and T38 (Levine et al. 2004; Verastegui et al. 2003). These antibodies are present in the sera of 95 % or more tapeworm carriers. However, the antibody response seems to outlast the intestinal tapeworm for a long period, hampering its use as a diagnostic test.

There is little evidence on whether reinfection with a new adult Taenia solium is possible. This is quite difficult to determine since it requires certainty that the patient was cured (meaning an accurate follow-up with negative testing for 3 months or more). From a large series of around 300 patients with T. solium taeniasis and also confirmed cure, only three cases of reinfection were seen by our group in a median of 2 years of follow-up (Cysticercosis Working Group in Peru, 2013, unpublished data).