primary amebic meningoencephalitis
Introduction
Introduction to primary amoebic meningoencephalitis Primary amoebic meningoencephalitis is a neurological infectious disease caused by the free-living of A. striata. Acute amoebic meningoencephalitis is more common in children and adolescents who have recently swam in polluted ponds or swimming pools. After the insect invades the nasal mucosa, it enters the brain along the olfactory nerve through the sieve plate, causing inflammation and destruction of the olfactory bulb and brain tissue. The onset is rapid, the early symptoms are similar to the upper respiratory tract infection, but the forehead headache is more severe, followed by meningeal irritation such as neck stiffness, and there are taste, smell and even visual impairment, and the disease rapidly develops into a coma and dies. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: sinusitis chronic frontal sinusitis
Cause
Causes of primary amoebic meningoencephalitis
(1) Causes of the disease
The pathogen of this disease is a pathogenic strain of thermophilic genus in the genus Neroli, and it has been found that there are seven strains of the genus Nellis, namely Naegleria fowleri, N.andersoni, N. australiensis, N. gruberi, N. Jadini, N. jamiesoni and N. lovaniensis, currently confirmed to be infected with the central nervous system of the human body caused by the primary amoebic meningoencephalitis only N. fowleri, the protozoa life history has three stages: Trophozoites, flagella and cysts (Fig. 1), trophozoites with a diameter of about 10 to 30 m, characteristic large nucleus with a halo, with a single round or blunt pseudopod at one end and the other end Forming a finger-shaped pseudo-tail, which is fast and non-directional. When the trophozoite is in an uncomfortable environment or placed in distilled water, it can form a temporary flagellate. It usually has one or more flagella, and the diameter is 10-15 m. Round or pear-shaped, swimming fast, non-feeding stage, can change back to trophozoite within 24h, but does not directly form cysts, trophozoites are thermophilic, can grow normally at 40~45°C And rapidly proliferate in a mitotic manner, feeding on bacteria or other organic matter. For the pathogenic stage in his life history, when the trophozoite is in adversity, a highly resistant cyst can be formed, the capsule is round, the diameter is 10m, the capsule wall is smooth with 2 to 3 holes, and the nucleus and nourishment The nucleus is similar.
(two) pathogenesis
The N. falciparum first enters the human nasal cavity, is ingested by phagocytosis through the supporting cells of the olfactory epithelium, and then passes through the unmyelinated olfactory nerve terminal silk mesenteric space, passes through the sieve plate, and reaches the sub-cylinder containing fluid. The arachnoid space proliferates and diffuses to invade the central nervous system, forming histopathological features such as hemorrhagic necrosis and abscess. Protozoa can enter the ventricular system to reach the choroidal plexus causing choroidal neuritis and acute ependymitis. The histopathological features of meningococcal encephalitis are severe edema in the cerebral hemisphere and cerebellum; cerebellar tonsil protrusion and hyperemia; olfactory bulb olfactory necrosis, hemorrhage, moderate amount of purulent exudate; anterior orbital cortex Necrosis, hemorrhage, and abscess are also present; third, fourth, and sixth cranial nerve spasm, trophozoites can be found in the vascular space, the non-myelinated axon plexus of the olfactory nerve, and purulent exudate, but no cysts.
Prevention
Primary amoebic meningoencephalitis prevention
There is no vaccine for this disease, avoid swimming in the non-flowing lake pond water or warm water, try not to sneak into the water, or avoid splashing water into the nasal cavity. Recently, it is considered that the water in the swimming pool and the rotating pool should be completely disinfected with chlorine gas. It is effective. According to the Australian International Health and Medical Research Council's recommendation to use chlorine in the swimming pool, when the water temperature is lower than 26 ° C, the chlorine concentration is 1 mg / L, above 26 ° C, at least 2 mg / L, higher than At 28 ° C, it should reach 3 mg / L.
Complication
Primary amoebic meningoencephalitis complications Complications, sinusitis, chronic frontal sinusitis
Complications of sinusitis and frontal sinusitis.
Symptom
Primary amoebic meningoencephalitis symptoms common symptoms high fever severe headache meningeal irritation symptoms cerebral edema coma
The incubation period is short, generally only 3 to 5 days, up to 7 to 15 days. In the early stage, there will be abnormal taste and smell. This is the reaction of pathogen invasion, often starting with severe headache, high fever, jet vomiting, etc. Sexual or localized seizures, and obvious symptoms of meningeal irritation, such as neck stiffness, Kernigger's sign and Bruzinski's sign positive, most of them transferred into sputum, sputum and coma within a few days, because the disease is A fulminant and fatal meningoencephalitis, which is almost incapable of causing protective cellular and humoral immune responses in patients. Therefore, it often causes death due to severe brain edema, respiratory and circulatory center failure within 1 week. In the case of primary amoebic meningoencephalitis, less than 10 survivors survived hospital rescue.
Examine
Examination of primary amoebic meningoencephalitis
The total number of white blood cells in the blood increased, mainly neutrophils, the left nucleus, cerebrospinal fluid was purulent or bloody, the average number of white blood cells reached 2780 × 106 / L, culture sterile, but can be found in Foster Miba, commonly used methods are:
1. Direct smear method: After the cerebrospinal fluid is naturally precipitated, take a smear microscopy of the sediment, carefully observe the movement of the pseudopod, or judge the morphological characteristics of the nucleus after fixed staining;
2. Culture method: the cerebrospinal fluid is inoculated on a 1.5% non-nutritive agar and cultured in a medium of Enterobacter aerogenes or Escherichia coli, and cultured at 37 ° C for 3 to 5 days to observe the results;
3. Animal inoculation method: The cerebrospinal fluid is inoculated into the brain of the mouse. After the symptoms occur, the brain tissue of the mouse is examined to check for the presence or absence of the present insect. There is no applicable immunodiagnostic technique.
4, CT examination showed a diffuse density increase in the brain, and involved gray matter, cerebral cistern occlusion in the brain and between the feet of the brain, the submicroscopic structure of the upper part of the cerebral hemisphere surrounding the midbrain and arachnoid space disappeared.
Diagnosis
Diagnosis and diagnosis of primary amoebic meningoencephalitis
Diagnostic points
It can be diagnosed from the following aspects.
1. The epidemiological history is mostly in the summer, and it has been swimming in the non-flowing lake or warm water 5 to 7 days before the onset.
2. Have the clinical manifestations of the above central nervous system lesions.
3. CT examination revealed a diffuse density increase in the brain, involving gray matter, occlusion of the cerebral ventricle at the brain and between the feet of the brain, and submicroscopic structures surrounding the midbrain and arachnoid space in the upper part of the cerebral hemisphere disappeared.
4. Lumbar puncture showed a significant increase in intracranial pressure [2.94 ~ 6.37kPa (300 ~ 650mm H2O)], the average number of red blood cells in cerebrospinal fluid was 2.78 × 109 / L, the percentage of polymorphonuclear white blood cells increased, protein increased, sugar content decreased, cerebrospinal fluid Microscopic examination or in vitro culture confirmed to be a trophozoic trophoblast, in order to confirm the diagnosis.
Differential diagnosis
It should be differentiated from purulent meningitis, herpes simplex encephalitis, and epidemic encephalitis.
