Nervous system manifestations of leptospirosis

Introduction to the performance of the leptospirosis nervous system Leptospirosis, referred to as leptospirosis, is a natural epidemic acute infectious disease caused by various serotypes of pathogenic Leptospira. Commonly known as "threshing yellow" or "rice blast", its clinical features are high fever, body aches, fatigue, ball-bound membrane congestion, lymphadenopathy and obvious gastrocnemius pain. In severe cases, pulmonary hemorrhage, jaundice, meningoencephalitis and kidney Functional failure, etc. Due to the vigorous prevention work, various leptospirosis cases with pulmonary hemorrhage and liver and kidney failure have been reduced, but it is not uncommon for cerebral arteritis and multiple radiculitis after infection with leptospirosis. Cerebral edema, cerebral palsy leads to respiratory failure, and the nervous system is more common. Early onset is characterized by mononeuritis, polyneuritis, radiculitis and cranial nerve spasm. see. Clinically, it is mainly characterized by ischemic cerebrovascular disease. Patients often have symptoms such as hemiplegia and aphasia 1 to 5 months after the symptoms disappear in the acute phase. Repeated and variable is one of its clinical features. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of transmission: plague spread Complications: sepsis, renal failure

Leptospirosis neurological manifestation etiology

Infection (30%):

Leptospira is a family of Treponemae. One or both ends of the cell are bent and hooked, and rotate along the central axis. It is difficult to see under ordinary microscope and needs to be observed by dark field microscopy. It can also be examined by silver staining. Dark brown or black, sensitive to heat, acid, dryness and general disinfectants.

Route of infection (20%):

The pathogen enters the human body through the skin, mucous membrane or wound, passes through small blood vessels and lymphatic vessels to the blood circulation, multiplies in the bloodstream, forms sepsis, and releases pathogenic factors such as hemolysin and endotoxin-like substances to cause clinical symptoms, and the hook body invades the internal organs. Such as the lungs, liver, kidney, heart and central nervous system, that is, causing organ damage, and complications of the corresponding organs.

Pathological changes (25%):

The pathological basis of leptospirosis is systemic capillary toxic damage. In addition to the poisoning reaction, there is no obvious visceral damage, and severe cases may have pathological changes of different organs.

Mainly manifested as extensive expansion and congestion of pulmonary capillaries, diffuse patchy hemorrhage, alveolar contains red blood cell fibrin and a small amount of white blood cells, some alveolar contains exuded serous, pulmonary interstitial with varying degrees of congestion, edema, lighter Inflammatory reaction, some cytoplasm has denatured hooks.

The hepatic lobules show hyperemia, edema, hepatocyte degeneration and necrosis, and degenerative hooks in hepatocytes and stellate cells.

Renal tissue is extensively hyperemic, edema, renal tubule degeneration and necrosis, renal interstitial edema, mononuclear and lymphocyte infiltration, see small hemorrhage, and the hallmark can also be seen in the interstitial.

Myocardium showed punctiform hemorrhage, focal necrosis and interstitial inflammation, skeletal muscle, especially gastrocnemius swelling, focal necrosis.

Meningeal and brain parenchymal hyperemia, hemorrhage, neuronal degeneration and inflammatory cell infiltration, cerebrovascular disease mainly involves the end of the internal carotid artery, the anterior and middle cerebral arteries, the arterial lesions are segmental, and the arterial thickness is uneven. Stiff or gray-white rope-like, both sides of the blood vessels can be violated, slightly different in weight and weight, microscopic examination: the intima of the affected artery is significantly proliferated, the lumen is narrowed or occluded, and the disease is shorter, the majority of the tumor is visible in the adventitia. Infiltration of cells and monocytes, mixed with polymorphonuclear cells, adventitial connective tissue hyperplasia, only a small number of lymphocytes and monocytes infiltrated in the adventitia and media of the disease, and the internal elastic membrane showed different degrees. The hyperplasia, part of the division, the mesenteric muscle layer can be gradually destroyed, showing a change in arteritis. The capillaries and venules in the brain parenchyma of the basal ganglia are obviously dilated and congested, and some are clustered. The brain parenchyma can be caused by ischemia. There are edema, hemorrhage and multiple softening spots in different parts and weights (Liu Ximin et al., 1990).

Pathogenesis : Pathogens multiply in the bloodstream, form sepsis, and release hemolysin, cell pathogenic substances, cytotoxic factors and endotoxin-like substances and other pathogenic substances, causing clinical symptoms, severity of the disease and the gland type of the hook. The amount of bacteria and virulence are related. After the leptospira invades the human body, the granulocytes and mononuclear phagocytic cells in the blood increase, showing the phagocytosis of the leptospira. After 1 week of onset, specific IgM antibodies appear in the blood, followed by IgG. Antibodies, with the gradual elimination of leptospirosis, humoral immunity plays an important role in anti-infection, some patients have hypersensitivity reactions to leptin toxin, resulting in symptoms after the first heat retreat or in the recovery period.

Prevention of neurological manifestations of leptospirosis

1. Avoid contact with contaminated animals (especially pigs and rodents) and water contaminated by their urine.

2. Repelling rats and killing rats.

3. It is strictly forbidden to eat sick meat and raw meat and other products of infected animals.

4. Manage pigs, dogs and other livestock, inoculate veterinary hookworm vaccine, avoid using fresh livestock fertilizer, apply lime nitrogen to the farmland before transplanting, and drain the field water 10 days before cutting.

5. The population was inoculated with leptospirosis vaccine one month before the popular season.

Leptospirosis neurological manifestation of complications Complications sepsis renal failure

The hook body invades a large number of internal organs such as the lungs, liver, kidney, heart and central nervous system. The pathological basis is systemic capillary toxic damage, leading to congestion of related organs, punctiform hemorrhage, ischemia and hypoxia damage, and corresponding organs appear. Complications such as dysfunction and/or cell necrosis.

Leptospirosis nervous system symptoms Symptoms Common symptoms Drowsiness coma jaundice fatigue convulsions sepsis respiratory failure muscle pain kidney failure

1. Clinical stage and type

The incubation period is about 10 days, most of the onset is rapid, the clinical manifestations are complex, and the difference in severity is very large.

According to the pathogenesis, the clinical course of the disease can be divided into sepsis and immune response.

According to clinical characteristics, it can be divided into influenza typhoid type, pulmonary hemorrhage type, jaundice hemorrhagic type (also known as Weil disease), meningoencephalitis type, renal failure type and late onset.

(1) sepsis period:

1 acute phase (1 to 10 days after onset) mainly has fever, body aches, conjunctival hyperemia, gastrocnemius pain, lymphadenopathy, etc., with gastrocnemius pain is more prominent, in addition to the above symptoms of toxemia, involving all organs Its special performance, such as flu, pulmonary hemorrhage, jaundice, renal failure and meningoencephalitis symptoms.

2 Recovery period (after 7 to 10 days after onset) Most patients recover after various symptoms of heat retreat. A few patients may have fever after a few days to 6 months or more after heat retreat. Commonly known as iridocyclitis, choroiditis or total uveitis) and neurological complications.

(2) immune response period:

Generally, the symptoms occurring in the early and middle stages of the disease are called sepsis or complications, and the symptoms that are caused by the remission of the symptoms of poisoning are called after-effects, which is caused by an immune reaction.

2. Clinical manifestations of acute nervous system damage

It is manifested as meningoencephalitis. Two to three days after onset, severe headache, frequent vomiting, lethargy, paralysis or coma. Some patients have convulsions, convulsions, neck stiffness, and both Klinefelter and Brine's signs.

In severe cases, cerebral edema can occur, cerebral palsy leads to respiratory failure, and simple meningitis has a good prognosis. Encephalitis or meningoencephalitis is more serious, and the nervous system is more common. Early onset is caused by a single neuritis. Multiple neuritis, radiculitis and cranial nerve spasm are predominant, and late complications are more common in cerebrovascular disease.

Patients with leptospirosis cerebral arteritis are mostly children and young people under the age of 12, with multiple light or recessive infections. The clinical manifestations are ischemic cerebrovascular disease. Patients often have symptoms 1 to 5 months after the acute phase disappears. Symptoms such as hemiplegia and aphasia are one of the clinical features.

Examination of the manifestations of leptospirosis

1. Peripheral blood leukocyte count increased, neutrophils increased, thrombocytopenia, mild anemia.

2. Some patients have bleeding and prolonged clotting time.

3. Urine routine protein and cast, urine protein increased significantly when kidney damage, microscopic examination of red blood cells, urinary bilirubin positive.

4. SGPT increased, blood bilirubin also increased, and urea nitrogen increased significantly.

5. Cerebrospinal fluid (CSF) is generally normal, a small number of patients with CSF white blood cells mildly or moderately increased, mainly lymphocytes, protein slightly increased, normal or slightly lower sugar, normal chloride.

6. Serum immunological examination The agglutination lysis test (MAT) titer is positive at or above 1:400; complement binding assay, indirect agglutination assay for the determination of Leptospira specific antibodies, which facilitate early diagnosis.

In recent years, leptin antibody-sensitized latex has been used for reverse lactation test. Leptospirosis antigen can be detected within 3 days of the disease, which is simple, rapid, sensitive and has early diagnostic value.

The cellulose film staining method (DSA) is a newly developed method, which has practical value for the diagnosis and rapid screening of leptospirosis.

7. Brain CT can find a low-density shadow of cerebral infarction caused by cerebral arteritis.

8. Brain MRI can more accurately find brain infarcts of varying sizes.

9. Cerebral angiography showed arteritis changes, which showed the end of the internal carotid artery, different degrees of stenosis in the anterior and middle cerebral arteries, uneven lumen thickness, unsmooth wall, necrosis, and even complete occlusion. Without development, at the same time, there are abundant collateral circulations, small newborns and vascular networks dominated by the base of the skull, sometimes densely smoky.

Diagnosis and differential diagnosis of leptospirosis

Diagnostic criteria

1. In the epidemic area of this disease, in the summer and autumn, there is a history of contact with infected water or contact with sick animals within 1 to 3 weeks.

2. Clinically, there are three symptoms, such as cold and heat, soreness, general malaise, red eyes, leg pain, and swollen lymph nodes.

3. Clinical manifestations of neurological damage; or manifestations of cerebrovascular disease and peripheral nerve damage from half a month to 9 months after leptospirosis.

4. Combined with serological tests, a diagnosis can be made.

However, the diagnosis of this disease should be based on the pathogen. The blood, cerebrospinal fluid and urine culture of the patient can find the pathogen, but it is difficult to achieve the purpose of early diagnosis. Serum immunological examination, whether in the acute phase or the immune phase, can help It is diagnosed, especially for patients with cerebral arteritis without acute phase manifestations.

The agglutination lysis test (MAT) titer is positive at or above 1:400; it appears at 1 week after the disease, peaks at 15-20 days, and can last for many years. It can also be tested by complement fixation test and indirect agglutination test for leptospira specific antibodies. It can help early diagnosis. In recent years, the lump-body antibody-sensitized latex is used for reverse lactation test. The leptin antigen can be detected within 3 days of the disease, and the result is simple, rapid, sensitive and has early diagnosis value within 3 to 5 minutes.

The cellulose film staining method (DSA) is a newly developed method in which a test strip-like test strip is prepared by impregnating a cellulose sheet with a broad-spectrum reaction substance to detect a hook-specific IgM antibody (Zhang Zhi'an et al., 2000). Studies have confirmed that DSA has practical value for the diagnosis and rapid screening of leptospirosis.

Differential diagnosis

In the acute phase should be identified with influenza, typhoid, bacterial sepsis, tuberculosis, various meningoencephalitis, viral hepatitis, malaria, etc.

Leptospira cerebral arteritis is distinguished from cerebral arteritis caused by various other causes.

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