Meningitis in Children - I.V. Bohadelnikov 2005

Differential diagnosis of purulent meningitis

The etiological Cytology/practical/136.html">Differential Diagnosis OF primary Purulent meningitis, excluding Meningococcal meningitis, often presents major challenges. It is essential to comprehensively evaluate epidemiological data (such as the presence of an infection source, seasonality, contact with an infected person, and the child's age), characteristic clinical manifestations of the disease, and laboratory test results (general clinical, bacteriological, bacterioscopic, and serological). The main differential diagnostic distinctions among primary purulent meningitides are summarized in Table 2.

During the autumn-winter period, the incidence of Influenza and other acute respiratory viral infections (ARVI) accompanied by Central Nervous system (CNS) involvement increases sharply every year. CNS dysfunction manifests in various ways, ranging from lethargy and adynamia to loss of consciousness. Because CNS disorders during influenza and other ARVIs are widespread, physicians' vigilance regarding the potential development of meningitis tends to diminish, which can sometimes lead to diagnostic errors. The differential diagnosis between serous and Purulent meningitis with neurotoxicosis in influenza and other ARVIs is presented in Table 3.

In addition to frequent CNS involvement during widespread outbreaks of influenza and other ARVIs, these conditions are frequently accompanied by hemorrhagic syndrome. Furthermore, improper performance of a lumbar puncture and trauma to the vascular intima can yield Blood-stained CEREBROSPINAL FLUID (CSF). In such cases, CSF analysis not only fails to aid in diagnosis but raises new questions and necessitates a differential diagnosis from intracranial hemorrhages (Table 4).

The diagnosis and differential Diagnosis of Secondary purulent meningitides present significant difficulties. This is because they typically develop against the Background of a severe primary underlying disease accompanied by toxicosis, with simultaneous or sequentially emerging involvement of individual Organs or systems (such as otitis media, enterocolitis, Pneumonia, or Pyelonephritis).

At the initial stage, it is necessary to perform a differential diagnosis between Primary and secondary purulent meningitides. The primary clinical manifestations of primary meningococcal meningitis and secondary purulent meningitides differ substantially, and their differential diagnosis is outlined in Table 5.

The Development of a pathological process in multiple organs simultaneously often masks the manifestations of meningitis, especially in the Early stages of the disease when meningeal and hypertensive syndromes may still be absent. Consequently, the diagnostic value of lumbar puncture increases sharply in secondary purulent meningitides. The indications for this Procedure should be broader the younger the child is, and the longer and more severely they suffer from and unsuccessfully are treated for purulent-septic diseases.

The main differential diagnostic criteria for secondary purulent meningitides are presented in Tables 6 and 7.

In some cases, particularly with the development of purulent meningoencephalitis, it is also necessary to perform a differential diagnosis with conditions such as Brain Tumors and abscesses. The differential diagnosis of meningitis with the aforementioned conditions is presented in Tables 7 and 8.

Table 2

Differential diagnosis of meningococcal meningitis and other primary purulent meningitides

Disease / Signs	Meningococcal meningitis	Pneumococcal meningitis	Haemophilus influenzae meningitis
1	2	3	4
Age	Most commonly in children under 3 years of age; neonates are rarely affected.	From 1 to 5 years, most commonly children under 3 years of age.	Usually children aged 6 months to 4 years; neonates are rarely affected
Premorbid background	Unchanged	Pneumonia, sinusitis, otitis media, recent ARVI	Debilitated children (Rickets, hypotrophy; frequent ARVI, pneumonia)
Seasonality	Winter-spring	Autumn-winter	Autumn-winter
Onset of the disease	Acute	Subacute in younger children, acute in older children	Usually subacute
Fever intensity and duration	High, 39°–40 °C, lasting 3–7 days	High, 39°–40 °C, lasting 7–25 days	Initially high, 38^o–39 °C, then low-grade (subfebrile), lasting up to 4–6 weeks
Meningeal syndrome	Pronounced from the first hours of illness	Pronounced, sometimes incomplete	Moderately pronounced, incomplete, appearing from the 3rd–5th day of illness
Encephalic syndrome	Characteristic of infants in their first year of life	Pronounced, characteristic of 3/4 of patients	May rarely occur in infants in their first year of life
Leading clinical syndrome	Meningeal, infectious-toxic	Infectious-toxic, encephalic	Meningeal, infectious-toxic
Presence of rash	In 70–90% hemorrhagic, stellate, with central necrosis	Not characteristic	Not characteristic
Symptoms of CNS involvement	Impaired consciousness in the first days, seizures. Hearing loss, hemiparesis, ataxia	Impaired consciousness, focal seizures, paralysis, cranial nerve palsies. Hydrocephalus	Occasionally cranial nerve involvement, limb paresis
Course	Acute, rarely protracted	Acute in older children, protracted in younger children	Wavy (relapsing). Tendency toward CSF pathway block
Possible somatic disorders	Arthritis, pneumonia	Pneumonia, otitis media, sinusitis	Tracheitis, Bronchitis, rhinitis
Blood test	Leukocytosis, neutrophilia with a left shift, elevated ESR	Leukocytosis, neutrophilia with a left shift, elevated ESR	Anemia, leukocytosis, neutrophilia, rarely elevated ESR
CSF	Turbid, whitish; pleocytosis ranging from hundreds to thousands per 1 µL, predominantly neutrophilic; elevated protein, decreased glucose	Turbid, greenish; pleocytosis 300–1500 per 1 µL, predominantly neutrophilic; elevated protein level	Turbid, greenish; pleocytosis 300–900 per 1 µL, predominantly neutrophilic; elevated protein level
Source material for pathogen isolation	Blood, CSF, urine, nasopharyngeal mucus	CSF, content from purulent foci	CSF, blood, mucus, sputum, content from purulent foci
Bacterioscopic examination	Intracellularly located Gram-negative diplococci	Intra- and extracellularly located Gram-positive diplococci in pairs	Polymorphic coccobacilli forming short and long threads, occasionally micrococci in pairs

Table 3

Differential diagnosis of serous and purulent meningitides with neurotoxicosis in influenza and other ARVIs

Disease Sign	Viral serous meningitis	Neurotoxicosis in influenza and other ARVI	Meningococcal meningitis
1	2	3	4
Epidemiological history	Contact with an infected person, more often in rural areas	Contact with a patient with ARVI	Contact with a patient or meningococcal carrier
Age	Any	Any	Any, but predominantly children under 3 years of age
Incidence	Sporadic, epidemic	Sporadic, epidemic	Sporadic
Seasonality	Autumn-winter-spring	Autumn-winter	Winter-spring
Transmission routes	Airborne, alimentary, rarely contact	Exclusively airborne	Airborne
Onset of the disease	Acute	Acute	Acute (onset can often be timed to the exact hour)
Fever intensity	38°–39 °C, may be biphasic	Often above 40⁰ °C	39°–40 °C and higher
Catarrhal manifestations	May be present	Pronounced significantly	May be present
Oropharyngeal mucosal changes	Not characteristic	Hyperemia, edema, petechial hemorrhages, granularity of the posterior pharyngeal wall	May resemble changes seen in ARVI
Skin rash	Not characteristic	Fine-spotted hemorrhagic rash on the skin and mucous membranes	Hemorrhagic stellate rash with central necrosis
Vomiting	In the acute period, recurrent	Only at the peak of toxicosis	Recurrent, multiple
Headache	Severe, but not prolonged	Severe, but not prolonged	Pronounced, intense, diffuse or localized in the frontotemporal regions
Consciousness	Agitation or depression of consciousness may occur, up to loss of consciousness	Impaired, ranging from somnolence to complete loss of consciousness	Impaired, ranging from somnolence to complete loss of consciousness
Seizures	At the peak of toxicosis	At the peak of fever, brief tonic-clonic	Generalized tonic-clonic
Predominant syndrome	Intracranial Hypertension	General infectious	General infectious, meningeal, hypertensive
Meningeal syndrome	Moderately pronounced, dissociated	Inconstant and incomplete	Pronounced from the first hours
Encephalic syndrome	Not characteristic	May be present	Clonus of the feet, muscular hypotonia, cranial nerve palsies
Severity of general condition	Mostly moderate, less frequently severe	From mild to extremely severe	Severe or extremely severe
Peripheral blood	Leukopenia, slight neutrophilia with a left shift of the formula, normal ESR	On the first day – leukocytosis; on days 2–3 – leukopenia, eosinophilia, lymphocytosis, normal ESR	Leukocytosis, eosinophilia, band neutrophil shift to the left, elevated ESR
CSF	CSF pressure is elevated; fluid is clear and colorless; pleocytosis initially mixed, then predominantly lymphocytic, ranging from tens to hundreds per 1 µL; protein, glucose, and chloride levels within normal limits	CSF pressure significantly elevated; clear, whitish fluid; slight lymphocytic pleocytosis; moderately elevated protein level; glucose and chloride levels normal	CSF pressure elevated; fluid is turbid, milky or yellowish-green; neutrophilic pleocytosis ranging from hundreds to thousands per 1 µL; protein level elevated to 1–4.5 g/L; glucose and chloride levels decreased

Table 4

Differential diagnosis of viral meningitis and intracranial hemorrhages

Disease/Signs	Viral meningitis	Subarachnoid Hemorrhage	Subdural hemorrhage or effusion	Epidural hemorrhage
1	2	3	4	5
Age	Any	Early childhood and school age	Any	More often older school age
Etiology	Viruses (enteroviruses, influenza virus)	Vascular malformations (angiomas, arteriovenous aneurysms)	Birth trauma, Skull trauma, previous bacterial meningitis	Skull trauma with bone fracture
Onset of the disease	Acute	Sudden, with progressive signs of impaired consciousness	Gradual, slow	Gradual
Temperature reaction	38°–39 °C for 2–5 days	Sometimes subfebrile	Absent	Absent
Meningeal syndrome	Moderate or pronounced in the first days, sometimes dissociated	Pronounced	Clearly pronounced	Not characteristic
Leading CNS syndrome	Intracranial hypertension	Impaired consciousness, meningeal signs	Progressive increase in intracranial pressure	Progressive increase in intracranial pressure
Other symptoms	Catarrhal signs, intestinal disorders, epidemic parotitis signs, etc.	Vascular bruit over skull bones, tense pulse, elevated blood pressure	Refusal to feed	Signs of brain herniation
Headache	Severe, but not prolonged	Sudden, excruciating pain in the occipital region	Severe, recurring, localized in the occipital region	Severe, persistent, diffuse
Vomiting	Recurrent		Recurrent	May be present
Other CNS symptoms	Focal symptoms, transient cranial nerve involvement	Motor disorders (hemiplegia, seizures), cranial nerve involvement	Epileptic seizures (partial, secondary – generalized), progressive hemiparesis, hemianesthesia, gaze palsy, anisocoria.	Hemiparesis on the side opposite to the trauma, clonic seizures on the side opposite to the hematoma, homolateral mydriasis
CSF	No blood admixtures, clear, opalescent, pleocytosis within 0.1–0.2×10⁹/L, lymphocytic in nature	Uniformly bloody, xanthochromic, erythrocytes have a thornapple shape	No blood admixtures, absence of inflammatory signs	No blood admixtures, absence of inflammatory signs
Fundus oculi	Unchanged	Hemorrhages	Papilledema	Papilledema
Other CNS symptoms	Focal symptoms, transient cranial nerve involvement	Motor disorders (hemiplegia, seizures), cranial nerve involvement	Epileptic seizures (partial, secondary – generalized), progressive hemiparesis, hemianesthesia, gaze palsy, anisocoria.	Hemiparesis on the side opposite to the trauma, clonic seizures on the side opposite to the hematoma, homolateral mydriasis
CSF	No blood admixtures, clear, opalescent, pleocytosis within 0.1–0.2×10⁹/L, lymphocytic in nature	Uniformly bloody, xanthochromic, erythrocytes have a thornapple shape	No blood admixtures, absence of inflammatory signs	No blood admixtures, absence of inflammatory signs
Fundus oculi	Unchanged	Hemorrhages	Papilledema	Papilledema

Last update: 08/08/2026

Editorial and Educational Adaptation: This material has been compiled based on the primary/original source text. The project team performed an editorial review, corrected technical inaccuracies, structured sections, and adapted the content for an educational format.

What was processed:

elimination of formatting defects (OCR errors, structural breaks, corrupted characters);
editorial organization of content;
standardization of terminology in accordance with academic sources;
verification of factual statements against the original source text.

All mentions of the author, publication year, and origin of the primary text have been preserved in accordance with the source.