Infections of the Brain Parenchyma

Infections of the Brain
Cerebral Abscess
Localized area of suppurative inflammation in the brain
• The cavity contains thick pus formed from
necrotic, liquefied brain tissue and large numbers
of neutrophils and is surrounded by a fibrogliotic
• Large variety of bacteria;
• Anaerobic bacteria (bacteroides) and anaerobic
streptococci are common.
• Staphylococcus aureus,& gram-negative enteric
• Cerebral abscesses occur as complications of
other diseases
• Grossly, a cerebral abscess appears as a mass
lesion in the brain.
• liquefied center filled with pus and a
fibrogliotic wall whose thickness depends on
the duration of the abscess
• The surrounding brain tissue frequently shows
vasogenic edema
Clinical Features & Diagnosis
• (1) Features of a space-occupying lesion,
including evidence of increased intracranial
pressure (headache, vomiting, papilledema) and
focal neurologic signs,
• (2) Features relating to the source of infection,
such as chronic otitis media, suppurative lung
disease, and endocarditis; and
• (3) General evidence of infection, such as fever,
(elevated ESR), and weight loss in chronic cases.
• In untreated cases, the abscess progressively
enlarges and may cause death from increased
intracranial pressure or rupture into the
ventricular system
• (CT) scan or (MRI).
• Lumbar puncture is dangerous because of the
risk of precipitating tonsillar herniation.
• The CSF may be normal or may show mild
increases in protein, neutrophils, and
• CSF cultures may or may not be positive.
• Surgical evacuation of the abscess
• Antibiotic therapy is effective treatment and
has reduced the previously high mortality rate
of cerebral abscess to about 5–10%.
Viral Encephalitis
• the etiologic virus is identified in only about
30% of cases.
• Worldwide, many cases of acute cerebral
dysfunction in which no attempt is made to
identify a virus probably go unreported.
• The virus usually reaches the brain via the
• It infects brain cells,
• Causing neuronal necrosis and marked
cerebral edema => leads to acute cerebral
dysfunction => increased intracranial
• Perivascular lymphocytic infiltration
• Hemorrhages in severe
Clinical Features
• Acute onset with fever, headache, and signs of
brain dysfunction,
• Convulsions may occur.
• There may be papilledema
• In many cases of viral encephalitis, there is
concomitant meningeal inflammation
• Lumbar puncture with examination and culture
of CSF may provide an etiologic diagnosis.
• Therapy is supportive.
• Control of cerebral edema with high doses of
• The mortality rate from severe viral
encephalitis is high,
• and patients who recover are frequently left
with permanent neurologic deficits due to
irreversible neuronal necrosis
Poliovirus, (enterovirus)
Fecal–oral route.
Through the intestine
Infects the brain and spinal cord via the
• Routine immunization during childhood
The poliovirus selectively infects
• (1) The meninges, producing acute lymphocytic
• (2) The lower motor neurons in the anterior horn
of the spinal cord and medulla oblongata.
• Loss of motor neurons causes acute paralysis of
affected muscles.
• typically asymmetric and flaccid, with muscle
atrophy and loss of deep tendon reflexes.
• With time, the atrophic muscles may undergo
fibrous contracture.
• Rare in humans but occurs in a variety of wild
animals and domestic pets(dogs and cats),
• Fatal illness called hydrophobia characterized by
abnormal behavior, difficulty in swallowing, and
• Humans are infected when bitten by an infected animal.
• The rabies virus enters the cutaneous nerve radicles at the site
of inoculation
• And passes proximally to the central nervous system.
• The incubation period is 1–3 months and is shortest in facial
• Severe necrotizing encephalitis that maximally affects
the basal ganglia, hippocampus, and brain stem.
• Infected neurons show diagnostic eosinophilic
intracytoplasmic inclusion bodies (Negri bodies).
• Electron microscopy and immunoperoxidase
• fever and generalized convulsions that are precipitated
by the slightest of sensory stimulations such as a gust of
wind, a faint noise, or the sight of water.
• Death is inevitable.
Because there is no treatment,
Prevention is essential and
Consists of controlling the disease in wild animals,
Rabies immunization of domestic pets, and
Administration of antirabies vaccine to humans
immediately after viral exposure
Parasitic Infections
• Toxoplasma gondii is a protozoal parasite
• definitive cycle in the intestine of cats.
• Humans become infected through contact with
cat feces containing infective forms of the
• Cerebral toxoplasmosis occurs in two distinct
forms, congenital and acquired.
Congenital Toxoplasmosis
• Fetal infection with T gondii occurs
transplacentally in the third trimester of
• Infects the fetal brain and the retina, leading to
extensive necrosis, calcification, and gliosis.
• Many infants die soon after birth
• those who survive have a variety of defects
such as microcephaly, hydrocephalus, mental
retardation, and visual disturbances.
Acquired Toxoplasmosis
• Rarely causes cerebral lesions in normal
• Opportunistic infection in aids
• Cerebral toxoplasmosis in AIDS is characterized
by the presence of multiple necrotic lesions
ranging in size from 0.5 to 3 cm.
• Toxoplasma pseudocysts and tachyzoites may be
seen in biopsies of lesions.
• Diagnosis in tissues is aided by staining for
Toxoplasma antigens by immunoperoxidase
• (1) Cerebral malaria, due to Plasmodium
• (2) African trypanosomiasis (sleeping
sickness). This is caused by Trypanosoma
rhodesiense in East Africa and Trypanosoma
gambiense in West Africa.
• (3) Cysticercosis, due to the larval form of
Taenia solium, the pork tapeworm.
• (4) Hydatid cyst, due to the larval form of
Echinococcus granulosus.
• (5) Trichinosis, due to Trichinella spiralis.
• (6) Schistosomiasis, due to Schistosoma
haematobium and Schistosoma mansoni (in the
Middle East).
• (7) Amebiasis, due to Entamoeba histolytica,
which causes brain abscesses. Free-living
amebae of the genera Acanthamoeba and
Naegleria are rare causes of

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