Infections of the Brain Parenchyma

1. Infections of the Brain Parenchyma

2. Cerebral AbscessLocalized 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 wall. Etiology • Large variety of bacteria; • Anaerobic bacteria (bacteroides) and anaerobic streptococci are common. • Staphylococcus aureus,& gram-negative enteric bacteria • Cerebral abscesses occur as complications of other diseases

4. Pathology • 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

6. 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

7. (CT) scan or (MRI). • Lumbar puncture is dangerous because of the risk of precipitating tonsillarherniation. • The CSF may be normal or may show mild increases in protein, neutrophils, and lymphocytes • CSF cultures may or may not be positive.

8. Treatment • 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%.

9. 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.

10. Pathology • The virus usually reaches the brain via the bloodstream. • It infects brain cells, • Causing neuronal necrosis and marked cerebral edema => leads to acute cerebral dysfunction => increased intracranial pressure. • Perivascularlymphocytic infiltration characteristic • Hemorrhages in severe

12. 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.

13. Treatment • 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

14. Poliomyelitis • Poliovirus, (enterovirus) • Fecal–oral route. • Through the intestine • Infects the brain and spinal cord via the bloodstream. • Routine immunization during childhood

16. The poliovirus selectively infects • (1) The meninges, producing acute lymphocytic meningitis • (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.

17. Rabies • 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 convulsions. • 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 bites.

18. Severe necrotizing encephalitis that maximally affects the basal ganglia, hippocampus, and brain stem. • Infected neurons show diagnostic eosinophilicintracytoplasmic inclusion bodies (Negri bodies). • Electron microscopy and immunoperoxidase techniques. • 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.

19. 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

20. Parasitic InfectionsToxoplasmosis • Toxoplasmagondii is a protozoal parasite • definitive cycle in the intestine of cats. • Humans become infected through contact with cat feces containing infective forms of the parasite. • Cerebral toxoplasmosis occurs in two distinct forms, congenital and acquired.

21. Congenital Toxoplasmosis • Fetal infection with T gondii occurs transplacentally in the third trimester of pregnancy. • 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.

22. Acquired Toxoplasmosis • Rarely causes cerebral lesions in normal individuals. • 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. • Toxoplasmapseudocysts and tachyzoites may be seen in biopsies of lesions. • Diagnosis in tissues is aided by staining for Toxoplasma antigens by immunoperoxidase techniques

23. (1) Cerebral malaria, due to Plasmodium falciparum. •   (2) African trypanosomiasis (sleeping sickness). This is caused by Trypanosomarhodesiense in East Africa and Trypanosomagambiense in West Africa. •   (3) Cysticercosis, due to the larval form of Taeniasolium, the pork tapeworm. •   (4)  Hydatidcyst, due to the larval form of Echinococcusgranulosus.

24. (5) Trichinosis, due to Trichinellaspiralis. •   (6) Schistosomiasis, due to Schistosomahaematobium and Schistosomamansoni (in the Middle East). •   (7)Amebiasis, due to Entamoebahistolytica, which causes brain abscesses. Free-living amebae of the genera Acanthamoeba and Naegleria are rare causes of meningoencephalitis.