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Principles and practice of Clinical parasitology - Gillespie S.

Gillespie S. Principles and practice of Clinical parasitology - Wiley publishing , 2001. - 675 p.
ISBN 0-471-97729-2
Download (direct link): principlesandpracticeofclin2001.pdf
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B. mandrillaris, however, has only been isolated so far from biopsy and autopsy specimens of humans and other animals. It has not been as yet isolated from the environment. Cases of GAE may occur at anytime of the year and therefore have no relation to climatological changes.
Several species of Acanthamoeba, such as
A. castellanii, A. culbertsoni, A. astronyxis,
A. hatchetti, A. lenticulata, A. palestinensis,
A. polyphaga, A. rhysodes and other free-living leptomyxid amebas, such as B. mandrillaris, were considered originally as harmless, inocuous soil microorganisms, incapable of infecting mammals. But it is now known that these amebas can produce encephalitis, keratitis and skin ulcers, primarily in people with defective cellular immune systems without a history of water exposure (John, 1993; Martinez and Visvesvara, 1997; Visvesvara and Stehr-Green, 1990).
Until recently it was thought that N. fowleri infected only humans. However, Lozano-Alarcon et al. (1997) described the first case of N. fowleri infection in an animal (South American tapir) other than a human. Recently, a number of cows died of N. fowleri meningoencephalitis (Kinde, personal communication). Acanthamoeba and Balamuthia are also known to infect animals other than humans and cause GAE (Kinde et al., 1998; Martinez and
Visvesvara, 1997; Rideout et al., 1997; Visvesvara et al., 1990; Visvesvara and Stehr-Green, 1990).
CLINICAL FEATURES Primary Amebic Meningoencephalitis due to Naegleria fowleri
Clinical Signs and Symptoms
PAM is an acute, rapidly progressing illness. It is characterized by bifrontal or bitemporal headaches, fever, nausea, vomiting and stiff neck. The symptoms progress rapidly, leading to lethargy, confusion, coma and, in most cases, to death in a few hours. Seizures, and sometimes abnormalities in taste or smell and ataxia, may be seen. Nuchal rigidity with positive Kernig’s and Brudzinski’s signs may be present. Photophobia may be present late in the clinical course. Palsies involving the third, fourth and sixth cranial nerves may also be present in some patients and indicate brain edema and herniations. Raised intracranial pressure has been reported in the majority of patients. Cardiac rhythm abnormalities detected by ECG have been found in some cases. The peripheral white blood cell count is
generally elevated, with a marked increase in polymorphonuclear leukocytes and with some lymphocytosis. The majority of cases end fatally within 1 week from the beginning of the symptoms; however, a few cases have been reported to have survived without neurological sequelae. The cause of death is usually increased intracranial pressure with brain herniation leading to cardiorespiratory arrest (Butt, 1996; Fowler and Carter, 1965; Seidel et al., 1982).
Pathological Findings
Gross CNS findings. The cerebral hemispheres are usually swollen and edematous. Hemorrhagic necrosis of the cerebral cortex is characteristic (Figure 12.5A). Uncal and cerebellar tonsillar herniations may be seen. The leptomeninges are congested, with scant purulent exudate that may be seen along the sulci and around blood vessels. The olfactory bulbs and the orbitofrontal cortices are usually necrotic and hemorrhagic.
Microscopic findings. Histopathologically,
PAM is characterized by modest amounts of purulent exudate, necrosis and edema, with diffuse hemorrhages of the cortical areas and CNS parenchyma (Figure 12.5B). Amebic trophozoites are present within the perivascular spaces, with minimal or no inflammatory reaction (Figure 12.5B). Cysts are not present within the CNS lesions. Necrotizing angiitis is occasionally seen. The leptomeninges show a fibrinopurulent exudate composed of polymorphonuclear leukocytes and eosinophils with fewer macrophages and lymphocytes. These changes are usually found at the base of the cerebral hemispheres, the brainstem, the cerebellum and the upper portions of the spinal cord. Amebic trophozoites can be seen within the purulent exudate (Butt, 1996; Fowler and Carter, 1965; Martinez and Visvesvara, 1997; Visvesvara and Stehr-Green, 1990).
Granulomatous Amebic Encephalitis (GAE) produced by Acanthamoeba spp. and
B. mandrillaris
Clinical Signs and Symptoms
Granulomatous amebic encephalitis (GAE) is characterized by a protracted, insidious clinical
Fig. 12.5 {A) Primary amebic meningoencephalitis. Coronal section at the level of the optic chiasm showing focal necrosis with
hemorrhage on the orbitofrontal cortices and cingulate gyri. From the Medical College of Virginia, A338-67, with permission. {B) The cerebral cortex contains multiple clusters of N. fowleri trophozoites with negligible acute inflammatory reaction. Hematoxylin and eosin, x250. From the Medical College of Virginia, A338-67, with permission
course {Anzil et al., 1991; Martinez and Visves-vara, 1997). GAE has a clinical picture that mimics a single or multiple space-occupying lesion. Localizing neurologic signs and symptoms, such as hemiparesis and seizures, appear early in the clinical course. Mental status abnormalities, headache and stiff neck may be present. Palsies involving the third and the sixth cranial nerves may be seen. Nausea, vomiting, low-grade fever, lethargy, cerebellar ataxia and diplopia are also part of the clinical features. Chest X-rays of the lungs may demonstrate focal consolidated areas and pneumonitis. The direct cause of death in GAE is usually acute bronchopneumonia, liver or renal failure septicemia {Carter et al., 1981; Martinez and Visvesvara, 1997; Visvesvara and Stehr-Green, 1990).
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