Meningitis in Children - I.V. Bohadelnikov 2005

Differential diagnosis of serous meningitis

The clinical manifestations and pathomorphological Changes in the Meninges of the Central Nervous system caused by various Viral serous meningitis share many similarities. Nevertheless, an analysis of epidemiological data, Clinical Features, lumbar puncture findings, and the results of Blood and CEREBROSPINAL FLUID (CSF) Laboratory tests makes it possible to differentiate between them. The main differential diagnostic criteria for viral serous meningitis are summarized in Table 10.

In some cases, serous viral meningitis can be caused by Viruses that typically target the Brain parenchyma, leading to encephalitis or meningoencephalitis. However, encephalitis is occasionally preceded by a stage of serous meningitis without subsequent involvement of the brain tissue in the pathological process.

Table 10

Cytology/practical/136.html">Differential Diagnosis OF serous Meningitis caused by lymphocytic choriomeningitis virus, enteroviruses, mumps virus, and poliovirus

Disease/Signs	Lymphocytic choriomeningitis	Enteroviral meningitis	Mumps meningitis	Meningeal form of poliomyelitis
1	2	3	4	5
Epidemiological features	Contact with mice or small rodents; rural areas	Contact with an infected person or carrier; sporadic or epidemic incidence	Contact with a mumps patient; onset of meningitis simultaneously with, concurrently with, or immediately following salivary gland involvement	Contact with an infected person or carrier
Contagiosity rate	Low	High	Low	Low
Incidence	Sporadic, group outbreaks	Sporadic or epidemic outbreaks	Sporadic, with an increase in meningitis cases during mumps epidemics	Sporadic, less commonly group outbreaks
Seasonality	More often winter-spring	Summer-autumn	Winter-spring	Summer-autumn
Age	Preschool, early school-age	Preschool, early school-age	Preschool, early school-age	Infancy, children under 3 years of age
Route of transmission	Airborne, alimentary, vector-borne	Airborne, fecal-oral	Airborne, alimentary, waterborne, contact, potentially transplacental	Alimentary, less commonly airborne
Incubation period	1.5 - 3 days	2 - 7 days	2 - 3 weeks	4 - 12 days
Fever height and duration	38.5°-39°C followed by prolonged subfebrile Temperature, sometimes undulating	37.5°-38 ^oС, 2-5 days	37.5°-39.5 ^oС, 3-7 days	38°-39^оС, brief, typically biphasic
Headache	Severe, initially constant, then paroxysmal	Sharp, brief, 2-3 days	Severe, lasting 3-4 days	Inconsistent, moderate for 3-5 days
Vomiting	Repeated for several days, then accompanying headache paroxysms	Initially frequent and repeated, stopping rapidly	Recurrent, lasting 3-4 days	One to two episodes over 1-3 days
Meningeal syndrome	Pronounced, lasting 1-2 weeks	Mild, dissociated, absent in 15-20% of cases	Moderately pronounced, dissociated	Pronounced, persistent
Leading CNS involvement syndrome	Marked meningeal and Hypertension syndrome	Intracranial hypertension	Intracranial hypertension	Meningoradicular syndrome
Focal CNS symptoms	Anisoreflexia, pyramidal signs, coordination impairment	Occasional anisoreflexia, mild cranial nerve involvement (facial, oculomotor)	Occasionally facial and auditory nerve involvement, ataxia, hyperkinesia	Not characteristic, nystagmus occasionally present
Clinical course	Acute	Acute	Acute	Acute
CSF profile, normalization timeframe	Lymphocytic pleocytosis ranging from 100 to 1,300 per 1 µL, moderate protein elevation; normalizes by days 14-21 of illness	Mixed or lymphocytic pleocytosis, ranging from 50 to 500 per 1 µL, normal or decreased protein content; normalizes by days 7-21	Lymphocytic or mixed pleocytosis, ranging from 100 to 1,000 per 1 µL, normal or elevated protein content; normalizes by days 14-21	Mixed pleocytosis, ranging from 50 to 300 per 1 µL, slight protein elevation; normalizes by days 7-14

Table 11

Differential diagnosis of selected arboviral meningitis

Disease Signs	Meningeal form of tick-borne encephalitis	Meningeal form of Japanese encephalitis
1	2	3
Age	School-age	School-age
Incidence	Sporadic or epidemic outbreaks	Sporadic or group outbreaks
Route of transmission	Vector-borne, less commonly alimentary	Vector-borne
Fever height and duration	38°-40^оС, lasting 4-6 days, potentially biphasic	High, 39°-40^оС, lasting 7-10 days
Headache	Severe, distressing	Severe
Vomiting	Repeated in the first days of illness in half of patients	In the first days of illness, repeated
Meningeal syndrome	Pronounced, lasting 2-3 weeks	Pronounced, progressing from the 3rd-4th day of illness
Predominant CNS syndrome	Meningeal syndrome	Meningoencephalitic syndrome
Other CNS symptoms	Lethargy, somnolence, sopor, delirium, impaired consciousness	Impaired consciousness up to coma, oculomotor disturbances, paresis, limb paralysis, psychiatric disorders
CSF	Moderate lymphocytic pleocytosis from 50 to 150 Cells per 1 µL, high protein content — up to 6–10 g/L	Moderate lymphocytic pleocytosis from 30 to 100 cells per 1 µL, protein content 0.15–1.3 g/L

Table 12

Differential diagnosis of serous viral meningitis versus intracranial Hemorrhage

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/Causes	Viruses (enteroviruses, Influenza Viruses)	Vascular malformations (arterial aneurysms, arteriovenous malformations)	Birth trauma, Skull trauma, previous bacterial meningitis	Skull trauma with cranial bone fracture
Onset of illness	Acute	Sudden with progressive signs of altered consciousness	Gradual, slow	Gradual
Temperature reaction	38° - 39°С, 2-5 days	Sometimes subfebrile	None	None
Other symptoms	Catarrhal symptoms, intestinal disorders, manifestations of mumps infection, etc.	Vascular bruit over the cranial bones, tense pulse, elevated BP	Refusal to feed	Signs of brain compression
Headache	Severe, but not prolonged	Sudden, excruciating occipital pain	Severe, recurrent, localized in the occiput	Severe, progressive
Vomiting	Recurrent	Recurrent	Recurrent	May be present
Meningeal syndrome	Moderate or pronounced in the first days, sometimes dissociated	Pronounced	Clearly pronounced	Not characteristic
Leading CNS syndrome	Intracranial hypertension	Impaired consciousness, meningeal	Progressive intracranial hypertension	Progressive increase in intracranial pressure
Other CNS symptoms	Focal symptoms, short-term cranial nerve involvement	Focal motor deficits, hemiplegia, seizures	Hemiparesis, aphasia, visual disturbances, local and secondary generalized seizures	Contralateral hemiparesis, seizures, aphasia, hemianopsia, focal symptoms, homolateral mydriasis
CSF	Blood-free, transparent, opalescent, pleocytosis ranging from 100 to 2,000 cells per 1 µL, lymphocytic in nature	Uniformly bloody, xanthochromic, erythrocytes are thornapple-shaped; erythrocytes appear in the sediment after 12 hours	Blood-free, absence of signs of inflammation	Blood-free, absence of signs of inflammation
Funduscopy	Unchanged	Hemorrhages	Papilledema	Papilledema

These pathogens include tick-borne and Japanese encephalitis viruses, Herpesviruses, and several others. Table 11 presents the differential diagnostic Criteria for the meningeal forms of tick-borne and Japanese encephalitis.

Intracranial hemorrhages in children are, unfortunately, not a rare pathology. They can occur both in the neonatal period and throughout the child's subsequent life. Medical, social, and traumatic factors may underlie the occurrence of intracranial hemorrhages. Therefore, pediatricians frequently encounter them in daily practice. The main differential distinctions between serous viral meningitis and intracranial hemorrhages are presented in Table 12.

In clinical practice, viral serous meningitis must frequently be differentiated from neurotoxicosis in influenza and other acute respiratory viral infections (ARVI), Meningococcal meningitis, and, given an unfavorable epidemiological situation, Tuberculous meningitis. The main differential diagnostic criteria among these diseases are presented in Table 13.

The differential diagnosis of bacterial serous meningitis is presented in Table 14.

Table 13

Differential diagnosis of enteroviral, meningococcal, and tuberculous serous meningitis versus neurotoxicosis in influenza and other ARVI

Disease/Sign	Enteroviral serous meningitis	Neurotoxicosis in influenza and other ARVI	Meningococcal meningitis	Tuberculous meningitis
1	2	3	4	5
Epidemiological history	Contact with an infected person or carrier, swimming in pools	Contact with an ARVI patient	Contact with a meningococcal patient or carrier	Contact with a tuberculosis patient or M. tuberculosis spreader
Age	Most often 3 to 10 years	Any	Any, but most often children in the first 3 years of life	Early, junior, and senior school age
Seasonality	Spring-summer	Autumn-winter	Winter-spring	More often winter-spring
Mechanism of infection	Airborne, fecal-oral	Exclusively airborne	Airborne	Hematogenous-liquorogenic dissemination from a tuberculous focus
Incubation period	2 to 10 days	From several hours to 2 days	2 to 10 days	Several weeks
Onset of illness	Acute	Acute	Acute (exact hour of onset may be noted)	Gradual, acute in infants
Temperature reaction	38°-39°C, potentially biphasic	39°-40°C and higher	39°-40°C and higher	Subfebrile with a gradual rise to 38°-39°C after the prodromal period
Catarrhal manifestations	May be present	Marked	May be present	Not characteristic
Oropharyngeal mucosa changes	Bright hyperemia and lymphoid granularity of the posterior pharyngeal wall	Hyperemia, edema, petechial hemorrhages, granularity of the posterior wall	May resemble ARVI changes	Not characteristic
Skin rash	Transient polymorphic rash	Fine punctate hemorrhagic rash on mucous membranes and skin; herpetic eruptions on the Lips and nasal alae possible	Hemorrhagic stellate rash with central necrosis; herpetic eruptions on the lips, nasal alae, and along the Branches of the trigeminal and facial nerves possible	Pronounced autonomic disorders: sweating, Trousseau spots, persistent red dermographism
Peripheral Lymph Nodes	Cervical lymph nodes may be enlarged	Unremarkable	Unremarkable	Lymphadenopathy is characteristic
Loss of consciousness and seizures	Not characteristic	Impaired consciousness ranging from somnolence to loss of consciousness	Impaired consciousness ranging from somnolence to loss of consciousness	Rapid loss of consciousness is characteristic
Characteristic clinical symptoms	Herpangina, myalgia	Upper Respiratory Tract involvement, fever, myalgia	Arthritis, typically of small joints, myocarditis	Tuberculosis of the Lungs, lymph nodes, or other Organs
Leading syndrome	Intracranial hypertension	General infectious	General infectious, meningeal, hypertensive	Progressive intoxication and meningeal syndrome, cranial nerve involvement
Meningeal syndrome	Moderately pronounced, dissociated, short-term, may be absent	Inconsistent and incomplete	Sharply pronounced from the first hours	Pronounced, gradually intensifying after the prodromal period
Encephalic syndrome	Absent	Absent	FOOT clonus, muscular hypotonia, cranial nerve involvement	Appearance of focal brain lesion symptoms and cranial nerve involvement from the second week of illness; decerebrate rigidity in the terminal stage
Severity of condition	Predominantly moderate, rarely severe	Mild to extremely severe	Severe or very severe	Severe with progressive deterioration in the absence of specific therapy, up to coma
Peripheral blood	Leukopenia, slight neutrophilia and left shift, normal ESR	Leukocytosis on day 1, leukopenia, eosinophilia, lymphocytosis on days 2-3; normal ESR	Leukocytosis, eosinophilia, band neutrophil left shift, elevated ESR	Moderate leukocytosis, neutrophilia with a left shift, lymphopenia, high ESR
CSF	Elevated pressure, clear and colorless CSF, pleocytosis initially mixed, then lymphocytic, 50 to 500 cells per 1 µL, protein elevated to 0.3-0.6 g/L, glucose and chloride levels within normal limits	Significantly elevated pressure, clear, whitish CSF, mild lymphocytic pleocytosis, moderately elevated protein, normal glucose and chloride levels	Elevated CSF pressure, turbid, milky or yellowish-green, neutrophilic pleocytosis ranging from hundreds to thousands of cells per 1 µL, protein increased to 1-4.5 g/L, decreased glucose and chloride levels	Clear, colorless or xanthochromic CSF, lymphocytic or mixed pleocytosis from 100 to 1,000 per 1 µL, protein content 2-3 g/L, glucose level below 2 mmol/L. A delicate fibrinous web forms upon standing for 24 hours, in which M. tuberculosis can be detected

Table 14

Differential diagnosis of bacterial serous meningitis

Disease/Signs	Tuberculous meningitis	Leptospiral meningitis	Syphilitic Meningitis
Age	Early, junior, and senior school-age	Senior school-age	Infants or young children
Route of transmission	Hematogenous-liquorogenic	Waterborne, alimentary, contact	Transplacental, contact
Seasonality	Any time of year	Summer-autumn	Any time of year
Fever height and duration	Initially subfebrile, then 38°-39°C, 1-1.5 weeks	38°-40°C, sometimes undulating, 5-10 days	Subfebrile or febrile
Headache	Constant, severe	Moderate or severe	Moderate or severe
Vomiting	Initially 1-2 times, then frequent, projectile	Recurrent	Recurrent
Other early symptoms	Prior chronic intoxication, pulmonary or extrapulmonary foci of tuberculosis	Fever, chills, myalgia, headache for 3-6 days	"Unexplained" crying, seizures
Meningeal syndrome	Pronounced, gradually intensifying	Pronounced, persisting up to 20-30 days	Moderate or pronounced
Predominant syndromes	Infectious-toxic, meningeal	Infectious-toxic, hemorrhagic, hepatic-renal	Infectious-toxic, meningeal
CNS involvement symptoms	Progressive symptoms of cranial nerve involvement, loss of consciousness, coma	Meningoencephalitis, oculomotor disturbances, facial Muscle paresis, pathological Reflexes	Impairment of cranial motor nerve function
Clinical course	Gradual, acute in infants	Acute	Acute, sometimes asymptomatic
CSF	Lymphocytic or mixed pleocytosis from 100 to 1,000 cells per 1 µL, protein content elevated to 2-3 g/L, glucose level decreased to 2 mmol/L and lower	Lymphocytic pleocytosis from 100 to 500 cells per 1 µL, slightly elevated protein, normal glucose level	Lymphocytic pleocytosis from 100 to 200 cells per 1 µL, protein content elevated to 6-12 g/L, normal glucose level

Table 15

Differential diagnosis of mycotic meningitis

Disease/Signs	Candidal meningitis	Aspergillar meningitis	Histoplasmal meningitis	Blastomycosis meningitis
1	2	3	4	5
Endemic regions	Ubiquitous	Ubiquitous	North America (Ohio R., Missouri R., Mississippi R.), Central America (Panama)	Canada, Latin America, Africa, Israel, North America (Ohio, North Carolina)
Age	No age restrictions
Primary form of disease	Generalized candidiasis	Involvement of the Nasal cavity, nasal sinuses, bronchopulmonary and skeletal systems	Skin, lung, and gastrointestinal tract involvement	Skin and lung involvement
Predisposing factor	Mixed candidal-staphylococcal infection, immunodeficient state	Immunodeficient state	Immunodeficient state	Immunodeficient state
Route of pathogen entry into CNS	Hematogenous dissemination	Hematogenous dissemination	Lymphohematogenous dissemination	Hematogenous dissemination
Onset of meningitis	Gradual	More often acute	Gradual	Gradual
Body temperature	Periodic spikes up to 37.5°-38°C	Subfebrile or normal	Subfebrile or normal	More often normal
Headache	Moderate, sometimes intense	Intense	Intense	Intense
Vomiting	Occasionally	Recurrent	Occasionally	Recurrent
Meningeal syndrome	Often pronounced or absent	Pronounced	Nuchal rigidity; other symptoms dissociated or absent	Nuchal rigidity; other symptoms dissociated or absent
Predominant syndrome	General intoxication, in the late stage of illness — hypertensive	Hypertensive	Hypertensive	Hypertensive
Clinical course	Indolent, undulating	Progressive, chronic	More often acute	Progressive
Prognosis	More often unfavorable	Unfavorable	Unfavorable	Unfavorable
CSF	Opalescent or turbid, normal or elevated pressure, pleocytosis from 100 to 300 cells per 1 µL, neutrophilic or lymphocytic, protein 0.9–3.3 g/L, decreased glucose level	Clear, turbid, or hemorrhagic, elevated pressure, pleocytosis from 10 to 100 cells per 1 µL, neutrophilia (70–90%), protein content greater than 6–10 g/L, decreased glucose level	Clear or turbid, pleocytosis from 10 to 100 cells per 1 µL, lymphocytic or mixed, elevated protein content, decreased glucose level	Clear, less commonly opalescent or xanthochromic; pleocytosis from 10 to 100 cells per 1 µL, lymphocytic or mixed, decreased or normal glucose level

Table 16

Differential diagnosis of mycotic meningitis with brain abscess and brain tumor__________

Disease/Features	Fungal meningitis	Brain abscess	Brain tumor
1	2	3	4
Pathogen	Pathogenic Fungi (Cryptococcus, Coccidioides, etc.)	Bacterial flora	not established
Preceding conditions	Primary pulmonary or cutaneous focus of mycosis	Pneumonia, empyema, sinusitis, meningitis	TBI, frequent ARVI, otitis media, periodic headaches
Temperature	Low-grade, high, or absent	Moderate elevation	Unexplained fever
Headache	Intense, progressive	Progressive, severe	Depending on localization (nocturnal attacks with nausea and vomiting)
Vomiting	Recurrent	Infrequent or absent	Recurrent, progressive
Other CNS symptoms	Manifest upon The Development of meningoencephalitis	Depending on localization	Depending on localization
Meningeal signs	Pronounced	Nuchal rigidity, dissociation	May be dissociated
Seizures	not typical	May occur	Depending on localization: focal or secondary generalized
Fundus oculi	unaffected	Papilledema	Papilledema, secondary optic disc atrophy, hemorrhages
Main diagnostic Methods	Cryptococcal antigen and antibody tests in CSF, blood, and urine. Blood and urine cultures for cryptococci. Serological tests for Coccidioides, Histoplasma	Magnetic Resonance imaging, computed tomography of the brain, blood cultures	Magnetic resonance imaging, computed tomography of the brain
CSF	Pleocytosis 25-500 cells per 1 μL, monocytes, low glucose level, but normal in early stages. Protein level elevated to 0.5–5.0 g/L, normal in early stages.	Pressure is elevated. Pleocytosis 0–200 cells per 1 μL, monocytes or neutrophil leukocytes, normal glucose level, protein level ranging from normal to slightly elevated	Pleocytosis 0–300 cells per 1 μL, sometimes higher, monocytes and/or atypical cells, glucose level unchanged but can be very low. Protein-Cell dissociation

Last update: 08/08/2026

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