Appears in the early stage of tuberculous inflammation, or when the body's resistance is reduced, the bacteria are abundant and the virulence is strong. The main manifestation is serous or serous fibrinitis.

There was local infiltration of neutrophils in the early stage of the disease, but this was quickly replaced by macrophages, and combined bacilli could be found in the exudate and macrophages.

The exudate can be completely absorbed without leaving any trace, or it can transform into lesions dominated by proliferation or necrosis.

When the amount of bacteria is small, the virulence is low or the body's immune response is strong. It is mainly hyperplasia. Formation of diagnostic tuberculous nodules, also known as tuberculous granuloma.

Tuberculous nodules are composed of epithelioid cells and Langhans giant cells. Plus peripheral accumulation of lymphocytes and fibroblasts. Typically, there is caseous necrosis in the center of the nodule.

The macrophages that phagocytosed the conjugated bacilli increased in size and gradually transformed into epithelial-like cells, which were spindle-shaped and had abundant cytoplasm and nuclear staining in pale eosin. There is very little chromatin, which can sometimes be vacuolated, and there are one or two nucleoli in the nucleus. Increased activity of epithelial cells is beneficial to phagocytosis and killing of Mycobacterium tuberculosis

Most epithelioid cells fuse with each other into one cell, with mitotic nuclei but no cytoplasmic division, forming Langhans giant cells. The number of nuclei ranges from a dozen to dozens. The nuclei are arranged around the cytoplasm in a rosette shape, horseshoe shape or densely packed at one end of the cell body.

When the number of Mycobacterium tuberculosis bacteria is large and the virulence is strong. Caseous necrosis may occur. Tuberculosis necrosis is light yellow due to its high lipid content, and is uniform, fine and solid in texture, like cheese, and is called caseous necrosis. Under the microscope, it appears as red-stained, structureless granular matter.

Caseous necrosis often contains a certain amount of conjugative bacilli, which may be responsible for the worsening of tuberculosis.

Absorb and dissipate.

Fibrosis, fibrous encapsulation and calcification.

Invasion progression

Dissolve and spread.

Tuberculosis is caused by the first infection with Mycobacterium tuberculosis. It occurs mostly in children and occasionally in teenagers or adults who have not been infected with Mycobacterium tuberculosis.

After Mycobacterium tuberculosis is inhaled into the alveoli, it initially forms a 1-1.5 cm primary lesion in the lower part of the upper lobe of the lung or the upper part of the lower lobe near the pleura where ventilation is better. The lesions are gray-white in color and are characterized by tuberculous granuloma formation along the inflammatory consolidation foci, with caseous necrosis visible in the center of the lesions.

Primary lesions of the lung, lymphangitis and hilar lymph node tuberculosis are called primary syndromes. After the formation of the primary syndrome, although bacteria spread to other organs throughout the body through blood or lymphatic channels in the first few weeks, 95% of cases no longer develop due to the establishment of cellular immunity, and the lesions undergo fibrosis and calcification.

The x-ray shows a dumbbell-shaped shadow.

It is more common in adults and can occur a short time after the primary infection of pulmonary tuberculosis, but most cases occur more than ten years after the initial infection due to relapse due to reduced resistance.

Focal tuberculosis.

Infiltrative pulmonary tuberculosis.

Chronic fibrocavitary tuberculosis.

Caseous pneumonia.

Tuberculosis balls.

Tuberculous pleurisy.

Mycobacterium tuberculosis invades the branches of the pulmonary veins in large numbers once or repeatedly within a short period of time, and spreads through the left heart to the general circulation to various organs throughout the body such as the lungs, liver, spleen, meninges, etc., which can cause acute systemic miliary tuberculosis.

naked eye

under the mirror

X-ray can find scattered distribution in both lungs, uniform density, millimeter size, and fine dot-like shadows. The condition is critical. If treated in time, the prognosis is still good.

The clinical condition is dangerous, with symptoms of poisoning such as high fever, exhaustion, irritability and restlessness.

The acute phase cannot be controlled in time and may last for more than three weeks. Or the conjugated bacilli enter the blood irregularly and repeatedly in small amounts over a long period of time. The formation of chronic miliary tuberculosis.

The nature and size of the lesions are inconsistent, and hyperplasia, necrosis, and exudative lesions can be seen at the same time. More common in adults.

Due to caseous necrosis of the hilar, mediastinal, and parabronchial lymph nodes, they penetrate into adjacent large veins. Or the lymph fluid containing Mycobacterium tuberculosis may flow from the chest to the tube and back into the right heart. Caused by spread along the pulmonary artery to both lungs. It may also be part of acute systemic miliary tuberculosis.

To the naked eye, gray-yellow or gray-white miliary-sized nodules can be seen on the lung surface and section.

More common in adults. The patient's original tumor has recovered due to intermittent entry of conjugated bacilli from tuberculosis lesions in an organ outside the lungs into the blood and caused the disease.

The course of the disease is long, and the lesions are old and new and vary in size, ranging from small ones as small as millet grains to large ones with a diameter of several centimeters or more. The lesions are mainly proliferative.

It is divided into primary and secondary. Primary is rare and often occurs in children. It is usually infected by drinking milk or dairy products that contain Mycobacterium tuberculosis.

The vast majority of intestinal tuberculosis is secondary to active cavitary tuberculosis caused by repeated swallowing of sputum containing Mycobacterium tuberculosis.

Intestinal tuberculosis mostly occurs in the ileocecal region, where lymphoid tissue is the most abundant, and germs can easily invade the intestinal wall through the lymphatic tissue of the intestinal wall, and food stays here for a longer time, giving more opportunities to come into contact with bacteria.

Ulcerative type

Proliferative type

Most common in men aged 20 to 40 years. Most of them are unilateral. Mycobacterium tuberculosis comes from the blood dissemination of pulmonary tuberculosis. The lesions mostly start at the renal corticomedullary junction or the renal pyramidal papilla.

Initially, it is a focal tuberculosis lesion, followed by caseous necrosis, and then the renal papilla is destroyed and penetrates into the renal pelvis to form a tuberculous cavity. Later, as the lesions continue to expand and form multiple cavities, the kidney can be left with only an empty shell and renal function is lost.

Mycobacterium tuberculosis can infect the prostate and seminal vesicles, and can spread to the vas deferens, epididymis, etc. Epididymal tuberculosis is one of the important causes of male infertility.

Tuberculosis of the female reproductive system is mostly spread from the blood or lymphatic channels, and can also spread from tuberculosis in adjacent organs. Fallopian tube tuberculosis is the most common and is one of the causes of female infertility.

Bone tuberculosis often invades the vertebrae, finger bones, and long bone epiphyses. Divided into two types

Caseous necrosis type shows obvious caseous necrosis and sequestrum formation. After the necrosis is liquefied, a tuberculous abscess forms next to the bone, because there is no local redness, heat, or pain. Also known as a cold abscess, the lesions break through the skin and can form sinus tracts that will not heal for a long time.

The hyperplastic type is relatively rare, mainly forming tuberculous granulation tissue, and the trabeculae within the lesion are gradually eroded, absorbed, and disappeared, but there is no obvious caseous necrosis and dead bone formation.

Spinal tuberculosis is the most common form of bone tuberculosis, and is more common in the tenth thoracic vertebra to the second lumbar vertebrae. If the lesion penetrates the bone cortex, cold abscesses can be formed on both sides of the spine, or necrosis can flow down along the fascial space to form cold abscesses in distant locations.

Tuberculosis is more common in joints such as hips, knees, elbows, and ankles, and is often secondary to bone tuberculosis.

When joint tuberculosis heals. The joint cavity is often filled with a large amount of fibrous tissue, causing joint ankylosis and loss of movement function.

In the first week of the disease, the lymphatic tissue in the lower ileum is slightly swollen and bulges on the mucosal surface. It is gray-red in color, soft in texture, and bulges on the surface of the tissue, resembling the sulcus of the brain. Peyer's lymph node lesions are the most prominent.

Occurs in the second week of onset, and local intestinal mucosal necrosis occurs due to various reasons.

Ulcers form after the necrotic intestinal mucosa falls off. The edge of the ulcer is raised and the bottom is uneven. The long axis of the ulcer that occurs in the Peyer's lymph nodes is parallel to the long axis of the intestine.

Ulcers at solitary lymph nodes are small and round. It also penetrates deep into the submucosal layer. In severe cases, the necrosis can reach deep into the muscle layer and serosal layer, and even perforate. Invading small arteries can cause severe bleeding, which usually occurs in the third week of onset.

Equivalent to the fourth week of the onset of the disease, the granulation tissue proliferates and fills the ulcer, and the edge of the ulcer is regenerated and covered with epithelium to heal.

It refers to the proliferation of endothelial cells and fibroblasts in small arteries, thickening the walls of the arteries, and narrowing and occlusion of the blood vessel lumen. The constant appearance of plasma cells is one of the characteristics of this disease. Such lesions can be seen in all stages of syphilis.

Gum-like swelling, also known as syphilioma, is a characteristic lesion of syphilis. The lesions are gray-white and vary in size. Small ones can be seen under the microscope, while large ones can reach several centimeters. They are tough and elastic, like gum, so they are called gummy swellings.

The structure under the microscope is quite similar to a tuberculosis nodule, with coagulative necrosis in the center, similar to caseous necrosis, but the necrosis is not as complete as caseous necrosis, and the elastic fibers are still preserved.

The granulation tissue around the necrotic focus is rich in lymphocytes and plasma cells, with fewer epithelioid cells and Langerhans cells, and obliterative arteriolar endoarteritis and periarteritis must be present.

primary syphilis

secondary syphilis

Tertiary syphilis

Meningitis includes dura meningitis and leptomeningitis. Leptomeningitis is more common and involves infection of the leptomeninges, arachnoid mater and cerebrospinal fluid.

Meningococcal meningitis, also known as meningococcal meningitis. It is an acute suppurative inflammation of the meningeal membrane caused by Neisseria meningitidis infection. Most patients are children and adolescents. Clinically, fever, headache, vomiting, skin petechiae, and meningeal irritation may occur. Severe cases may lead to toxic shock.

Neisseria meningitidis has a capsule that resists phagocytosis by leukocytes in the body. It enters the human body through droplet transmission, but most of them do not become ill and cause disease when immunity is reduced. Pyogenic bacteria can rapidly multiply and spread in the cerebrospinal fluid in the subarachnoid space, so meningeal inflammation is generally diffusely distributed.

Upper respiratory tract infection period.

sepsis stage

Meningeal inflammation stage

Symptoms of meningeal irritation.

Symptoms of increased intracranial pressure.

Cerebrospinal fluid changes.

Hydrocephalus: caused by meningeal adhesion and cerebrospinal fluid circulation disorder.

Cranial nerve damage and paralysis: such as deafness, visual impairment, facial nerve paralysis, etc.

Skull base arteritis causes obstructive lesions and causes cerebral infarction in corresponding parts.

Fulminant meningococcal septicemia.

Fulminant meningoencephalitis.

The cerebral parenchymal blood vessels are highly dilated and congested, and sometimes small focal hemorrhages can be seen. Brain tissue is edematous and the spaces around blood vessels are widened.

The virus proliferates in nerve cells, destroys their metabolism, function and structure, causing swelling of nerve cells, disappearance of Nissl bodies, vacuoles in the envelope, and nuclear deviation.

When the disease is severe, liquefaction necrosis of focal nerve tissue can occur, forming hollow mesh-like lesions with loose texture and light staining, which are called cribriform softening lesions, which have certain characteristic significance for the diagnosis of this disease.

Mainly caused by diffuse or focal proliferation of microglia, the latter are mostly located near necrotic nerve cells or next to small blood vessels, forming microglial nodules.