Meningitis in Children - I.V. Bohadelnykov 2005

Secondary purulent meningitis in children. General data
Salmonella meningitis

Salmonella meningitis is a secondary Purulent meningitis that most commonly develops as a complication of the septic form of salmonellosis, or less frequently, its intestinal counterpart. It is characterized by an acute or gradual onset, prominent infectious-toxic and/or meningeal syndromes, and a severe, protracted clinical course.

Etiology. The causative agents of the meningitis are salmonellae—small (0.7–1.5 by 2–5 µm), Gram-negative Bacteria that do not form spores or capsules. They exhibit no strict tropism for any specific Organs or Tissues. They are resilient and can survive for prolonged periods (weeks and months) not only in the environment, foodstuffs, vegetables, meat, and eggs, but are also capable of multiplying within them, accumulating toxic metabolites, including endotoxin. Currently, salmonellae are resistant to most antibacterial drugs, yet they are highly susceptible to disinfectants (a clear 0.3% solution of bleaching powder destroys the microbe within 1 hour). Salmonellae possess a complex antigenic Structure; however, for serological Diagnosis, only three major Antigens are taken into account: O, H, and Vi antigens. This principle underlies the Kauffmann-White Classification, which currently includes more than 2,324 serovars, with their number increasing every year. Salmonella meningitis can be caused by various Salmonella serotypes, but most frequently by S. typhimurium, S. enteritidis, S. heidelberg, and S. newport.

Epidemiology. Diseases caused by salmonellae are widespread globally. The primary source of infection for young infants is infected individuals and bacterial carriers, as well as various animals (cows, dogs, cats, pigs), fish, and birds. The Mechanism of salmonellosis transmission is fecal-oral, with Water and food serving as the main routes of transmission. For children, household contact transmission is also significant. Nosocomial infections can occur through fomites and the hands of medical personnel.

Salmonella meningitis predominantly affects infants and children in their first 6 months of life, whereas children of other age groups are rarely affected. This is due to the anatomical and PHYSIOLOGICAL CHARACTERISTICS OF the pediatric body, primarily the immaturity of cellular and humoral Immunity, increased permeability of cellular and vascular membranes, and the immaturity of the Blood-Brain barrier (BBB). Meningitis most frequently develops as a complication of generalized or septic forms of salmonellosis.

Pathogenesis. The gastrointestinal tract serves as the portal of entry for the infection. As with other infections transmitted via the fecal-oral route, The Development of the disease depends on the age and immune status of the child, the size of the infecting dose, and the pathogenicity of the microorganism. When these factors combine unfavorably for the child's body, salmonellae affect the intestinal epithelium, penetrate inside enterocytes across the lamina propria into macrophages, and multiply within them. If the child's body fails to localize the pathological process within the intestine (the local inflammatory stage), a breach of the intestinal and lymphatic barriers occurs, leading to bacteremia (the septic form of salmonellosis). Salmonellae, their endotoxins, and generated endogenous mediators of pathogenesis (elevated concentrations of histamine, kallikrein, proteolytic factors, etc., against a Background of reduced inhibitors) result in systemic microcirculatory and hemodynamic disorders, metabolic disturbances, and damage to Internal Organs, including the Lungs, endocardium, Liver, Kidneys, as well as the Meninges and brain parenchyma.

Clinical Manifestations. The onset of meningitis developing against the background of the intestinal form of salmonellosis is invariably acute. Body Temperature rises to 39°–40 °C, toxicosis intensifies, and a pronounced diarrheal syndrome develops (frequent, loose, foul-smelling stools containing mucus and green discoloration, accompanied by vomiting), alongside escalating symptoms of exicosis (reduced tissue turgor, dry Skin and mucous membranes). Meningeal signs typically emerge from the first days of the illness. With their appearance, the signs of enterocolitis subside and recede into the background, while intoxication symptoms intensify. In this clinical variant of Salmonella meningitis, a CEREBROSPINAL FLUID (CSF) hypotension syndrome frequently develops, manifested by the absence of fullness and tension in the anterior fontanelle, subtle or incomplete meningeal signs, and during lumbar puncture, the CSF fails to flow and instead stalls in the needle.

In patients with the septic form of salmonellosis, meningitis develops more gradually. Septicemia proceeds with pronounced toxicosis, cardiovascular dysfunction—tachycardia, muffled Heart sounds, decreased blood pressure, dyspnea, oliguria, hepatosplenomegaly, and sometimes a hemorrhagic rash. At the peak of septicemia, septicopyemic foci arise, including within the meninges, leading to the clinical picture of meningitis. The clinical course of Salmonella meningitis is severe, protracted, prone to exacerbations despite massive antibiotic therapy, and frequently fatal.

Main diagnostic criteria for Salmonella meningitis:

1. Epidemiological history: the disease invariably arises against the background of a Salmonella infection, predominantly affecting infants and children in their first 6 months of life.

2. The onset of meningitis is acute or gradual.

3. It generally proceeds with pronounced infectious-toxic and meningeal syndromes.

4. The clinical course is severe, protracted, and frequently fatal.

5. Bacteriological isolation of salmonellae from the CSF confirms the diagnosis.

Laboratory Diagnostics. Complete blood count. Peripheral blood findings include leukocytosis, a marked shift of the leukocyte formula to the left, and an elevated ESR.

CSF Examination. The CSF may be clear with a relatively low Cell count, or purulent with high neutrophilic pleocytosis, elevated protein content (up to 3.0 g/L or more), and a decreased glucose concentration.

Bacteriological examination relies on blood, urine, stool, and CSF cultures. For this purpose, enrichment media (Muller, Kauffmann, etc.) and differential diagnostic media (Ploskirev, Endo, Levin, bismuth sulfite Agar) are employed. Blood cultures for salmonellae must be obtained throughout the entire febrile period. To this end, 5–8 mL of blood is inoculated into 10–20% Bile broth or Rappaport medium.

Serological testing is performed by detecting specific Antibodies in blood serum. The presence and titer of antibodies are determined using agglutination reactions (AR) and indirect hemagglutination assays (IHA) with erythrocyte diagnostic Reagents. A diagnostic titer is considered to be 1:100 or a fourfold or greater increase in antibody titer during the course of the disease at 7–10 day intervals. It is also possible to use the IHA with a Cysteine test, which allows for the differential determination of Ig Class antibody titers. The diagnostic titer of cysteine-resistant antibodies in the blood is 1:80 (in infants under one year of age, 1:20).