INTRODUCTION Granulomatous inflammation is a distinctive ...

immunocompetent patients. Symptoms are usually indolent and chronic, such as fever, headache,
and mental status changes. Seizures and focal neurologic deficits can occur. Localized lesions in
the brain occur in one third of patients with CNS involvement (Metwally, 2006-3, Metwally, 2006-
8).
The laboratory diagnosis of fungal disease is general, and histoplasmosis particularly is
challenging because of the nonspecific clinical findings, the difficulty of culturing organisms, and
the confusing array of diagnostic tests available (Metwally, 2006-8).
The typical radiologic manifestations of CNS histoplasmosis include meningitis, encephalitis,
granuloma formation (histoplasmoma), and brain abscess. In a few case reports, a military form
of CNS histoplasmosis as well as vasculitis has been previously reported. The CT scan and MR
imaging characteristics of CNS histoplasmosis are nonspecific relative to other fungal infections,
and diagnosis is typically made from cerebrospinal fluid analysis or from brain biopsy (Stone et
al., 1998; Hadi et al., 1999).
Most acute forms of histoplasmosis in immunocompetent hosts resolve without specific treatment.
Systemic antifungal treatment is indicated for severe cases and any manifestation in an
immunocompromised patient (George and Penn, 1993).
PARASITIC GRANULOMA
Cysticercosis
Before the introduction of modern neuroimaging diagnostic techniques, knowledge of the natural
history of cysticercosis was limited and largely based on cases diagnosed either by the presence of
subcutaneous nodules, plain X-rays showing calcifications in the brain or soft tissues, surgery of
cases with intracranial hypertension, or from necropsy data (Dixon and Lipscomb, 1961). The
image of an aggressive, lethal disease arose from this clearly biased (towards more severe
infestations) group of cases. During the last two decades, the introduction of CT and later MRI
permitted the identification of mild cases with only a few parenchymal cysts (Estanol et al., 1986).
Later, studies in India showed that a vast majority of single enhancing lesions, until then
attributed to TB, were in fact degenerating cysticerci (Chandy et al., 1991; Rajshekhar, 1991).
Pathology
Taenia solium is a two-host zoonotic cestode. The adult stage is a 2 to 4mm long tapeworm that
lives in the small intestine of humans. No other final hosts are known for T. solium tapeworms in
nature. As in all cestodes, the gravid proglottids at the terminal end of the worm are full of eggs
that are the source of infection with the larval stage, or cysticercoids. The natural intermediate
host is the pig, harboring larval cysts anywhere in its body. Humans become infected with cysts by
accidental ingestion of T. solium infective eggs by fecal-oral contamination (Hector et al., 2002) .
After ingestion of Taenia eggs containing infective oncospheres, the parasites become established
in the tissues as larval cysts and reach their mature size in about 3 months. The parasite may
locate almost anywhere in the body. The infection burden varies from a single lesion to several
hundreds, and lesions may range in size from a few millimeters to several centimeters (Garcia and
Del Brutto, 2000). Laboratory studies and information suggest that viable cysts actively modulate
the host's immune system to evade destruction by it (White et al., 1997).
The natural history of cysticercosis has been studied by pathological examination and imaging
studies using CT and MRI. Viable cysts are 10 to 20 mm in diameter, thin-walled sacks filled with
clear cyst fluid. There is little or no evidence of perilesional inflammation, and they do not