Acute bacterial infections and bacterial abscesses

Published on 19/03/2015 by admin

Last modified 19/03/2015

Print this page

This article have been viewed 2072 times

Acute bacterial infections and bacterial abscesses

The brain is swollen and congested. Hemorrhagic infarcts are common and may be extensive (Fig. 15.1), and a purulent exudate is seen over the cerebral hemispheres or the base of the brain or both (Fig. 15.2). The ventricles may appear compressed by the swollen cerebral hemispheres, or distended if the aqueduct has been obstructed by purulent material. There may be coexistent cerebral abscesses, particularly in association with Citrobacter diversus or Proteus mirabilis meningitis.

15.1 Neonatal meningitis caused by group B streptococcus.
There is focal left temporal infarction (arrow) with thrombosis of the overlying meningeal blood vessels. Elsewhere the meninges are markedly congested and there is blood in the subarachnoid space. (Courtesy of Dr Helen Porter, Bristol Children’s Hospital, UK.)

15.2 Group B streptococcal meningitis.
Purulent exudate over the inferior part of the cerebellum, and patchy discoloration due to hemorrhagic infarction. (Courtesy of Dr Helen Porter, Bristol Children’s Hospital, UK.)

MICROSCOPIC APPEARANCES

The meningeal exudate contains large numbers of neutrophils, scattered macrophages, fibrin, and necrotic cellular debris. The exudate may be particularly prominent over the base of the brain. It extends along perivascular spaces into the brain parenchyma. Bacteria are usually demonstrable within the exudate.

NEONATAL BACTERIAL MENINGITIS

In the UK, USA, and in many other developed countries, group B streptococci and Escherichia coli account for over 65% of cases of neonatal bacterial meningitis. However, the range of bacteria responsible for meningitis in neonates is wide (Table 15.1) and varies in different regions and even at different times in the same region.

Table 15.1

Principal bacterial causes of neonatal meningitis

Gram-positive

Group B streptococcus (Streptococcus agalactiae)

Listeria monocytogenes

Staphylococcus aureus

Gram-negative

Escherichia coli

Citrobacter species (especially C. diversus)

Klebsiella and Enterobacter species

Pseudomonas aeruginosa

Proteus species

Salmonella species

Outbreaks of neonatal meningitis due to group B streptococci or other bacteria may be caused by cross-contamination within hospital wards. Epidemics of listerial meningitis have been traced to contaminated batches of unpasteurized cheese and other uncooked foods.

Infants of low birth weight are at particular risk. Other risk factors include prolonged rupture of the amniotic membranes and postpartum maternal pyrexia.

The absence of alveolar macrophages, a relatively small pool of neutrophils, and low levels of secretory IgA and IgG and a limited capacity for their synthesis, all render neonates particularly susceptible to bacterial infection.

The initial portal of entry is usually oral, from contaminated amniotic fluid, the maternal genital tract, or the hands of the mother or ward staff. The bacteria cross the respiratory or gastrointestinal mucosa, proliferate within the blood, and enter the CNS.

NEONATAL BACTERIAL MENINGITIS

Initial symptoms are usually non-specific (e.g. poor feeding, diarrhea, vomiting, irritability).

Progression to lethargy and coma occurs within a few hours.

Nuchal rigidity, a bulging fontanelle, and septic shock are poor prognostic features.

Mortality rate is 30–60%.

Long-term morbidity (e.g. mental retardation, epilepsy, hydrocephalus, spasticity, deafness, and blindness) affects approximately 35% of survivors.

Inflammatory cells tend to infiltrate the walls of leptomeningeal and cortical arteries and veins (Fig. 15.3). Intimal accumulations of inflammatory cells may be a prominent feature. Venous thrombosis and infarction are often evident (Figs 15.1, 15.3) and may be extensive.

15.3 Neonatal bacterial meningitis.
(a) Intimal infiltration of meningeal artery by neutrophils (arrows). (b) Inflammatory cell infiltration and thrombosis of small cortical veins with acute infarction of the surrounding tissue.

Purulent material is usually seen in the choroid plexus and may also adhere to ventricular walls. An acute, predominantly perivascular, inflammatory infiltrate is present in the adjacent tissue.

COMPLICATIONS

Complications of acute meningitis are:

Obstructive (non-communicating) or communicating hydrocephalus (see Chapter 5).

Cavitation of cerebral gray (Fig. 15.4) and white matter.

15.4 Neonatal bacterial meningitis.
(a) Extensive superficial cavitation of cerebral cortex in a case of neonatal group B streptococcal meningitis. (b) At higher magnification the cortex is seen to consist of cystic spaces containing newly formed blood vessels, foamy macrophages, and scattered lymphocytes.

ACUTE BACTERIAL MENINGITIS IN CHILDREN AND ADULTS

MACROSCOPIC APPEARANCES

The brain is swollen and the leptomeninges are congested. A purulent exudate is seen in the subarachnoid space over the cerebral hemispheres and the base of the brain (Fig. 15.5a), and accumulating in the basal cisterns and cerebral sulci. The exudate associated with pneumococcal infections is often particularly prominent over the cerebral convexities (Fig. 15.5b). There may be little or no macroscopically discernible exudate in patients dying very acutely or those who have been partially treated with antibiotics. Sectioning of the brain may reveal edematous white matter and compressed ventricles or ventricular enlargement due to obstructive hydrocephalus. There is usually purulent fluid within the ventricles. The ventricular exudate may be pronounced in patients with ventricular shunt infection (Fig. 15.6), in whom the leptomeninges appear remarkably clear. Occasionally, the coagulopathy associated with meningococcal septicemia is complicated by ventricular hemorrhage. Small infarcts may result from thrombosis of penetrating arteries (Fig. 15.7). Venous thrombosis and hemorrhagic infarcts are less common than in neonatal meningitis.