Acne

Introduction Pox is also called smallpox. Smallpox is a potent infectious disease caused by smallpox virus and the first infectious disease that has been eliminated by humans worldwide. Smallpox is caused by infection with poxvirus. There is no medicine to cure. The patient will have pockmarks on his face after healing. The "smallpox" is named after it. The appearance of smallpox virus is brick-shaped, about 200 nm × 300 nm, strong resistance, can resist dryness and low temperature, and can survive for months to a year and a half in suede, dust and clothing.

Cause

It is a strong infectious disease caused by smallpox virus.

Poxviridae is a large and complex DNA virus. It is brick or elliptical and has a size of (200nm to 90nm) × (100nm ~ 260nm). It is one of the largest viruses and is barely visible under the optical microscope.

The poxvirus replicates in the cytoplasm of the cell to form eosinophilic inclusion bodies. The affected person develops a papule on the skin after the onset of the disease and then converts it into a blisters and pustules. Most of the virus can grow on the chicken chorioallantoic membrane, producing macroscopic acne-like lesions.

Pathogenesis

Inhalation through the respiratory tract is the main route of transmission for smallpox. Smallpox virus is adsorbed on the surface of epithelial cells of the upper respiratory tract of susceptible individuals, and rapidly reaches lymph nodes such as local lymph nodes and tonsils. After a large amount of replication, it enters the bloodstream to form the first transient viremia. Through the bloodstream, systemic mononuclear macrophages are infected and continue to replicate and release into the bloodstream, resulting in a second viremia. Through blood circulation, the virus spreads more widely to the skin, mucous membranes and internal organs of the body. At this time, the patient developed high fever and general malaise. After 2 to 3 days of prodromal symptoms, smallpox pox appears.

Since variola virus is not heat-resistant, viremia is only maintained for a short period of time after the patient has fever. On the next day of fever, it is generally difficult for patients to detect the virus in the blood. The virus mainly exists in tissues with low temperature such as skin. After variola virus invades skin tissue cells, it first proliferates in the dermis layer, causing the dermal layer to dilate with capillaries, vacuoles in the cytoplasm, nuclear condensation and disappearance, and clinical appearance of macules. Subsequently, the virus invades the epidermal cells and proliferates a lot. Swelling, thickening of the cortex, and appearance of papules. Thereafter the cells are denatured and necrotic. There is fluid leakage between cells to form herpes. The destructive cells become separated in herpes, forming many small chambers, and the central part of the herpes is concave into a umbilical shape due to the traction of the deep cell wall. Under the microscope, the corpus cytoplasm of the epithelial cells around the herpes showed a clear inclusion body with a round shape with a diameter of 1 to 4 m. When a large number of inflammatory cells infiltrate into the blister, it becomes a pustular rash. After the liquid in the pustule is absorbed, it forms a hard sputum. Due to rupture and scratching, pustular rash is prone to secondary bacterial infection, which worsens the deep lesions of the local skin and increases the toxic symptoms of the whole body. In the pustular period, the liver and spleen can be swollen.

If the secondary infection occurs in the mouth and nasopharynx, it can cause cervical lymphadenopathy. If the pustule only invades the epidermis, the scar after dislocation is not obvious. If the dermis is involved or there is a secondary infection, a lifelong depressed scar will be formed. Due to the lack of the stratum corneum, the mucosal lesions are broken faster than the skin, and the mucosal lesions are easy to form different depths of ulcers without forming herpes. The virus is easily excreted from the ulcer. Therefore, mucosal lesions play an important role in the early infectiousness of patients. Mucous membranes in the respiratory tract, digestive tract, urinary tract, and vagina can be affected. Significant inflammatory reactions around the ulcer can cause severe symptoms. If it affects the cornea, it can cause corneal opacity, ulceration, or secondary bacterial infection, resulting in blindness.

an examination

Related inspection

Blood routine smear microscopy

According to the characteristics of its rash, distribution and development process, combined with epidemiological conditions, the diagnosis of typical cases is not difficult. The diagnosis of difficult cases depends on the examination of virus and serum immunology.

Blood picture

The total number of white blood cells in the prodromal phase was slightly lower, the lymphocytes were relatively increased, and the total number of white blood cells and neutrophils in the pustule stage increased.

2. Pathogen examination

(1) Direct smear examination of variola virus inclusion body: Take the herpes liquid, or the bottom swab of the herpes ulcer on the slide, dry it and stain with hematoxylin-eosin (HE), observe the cells of epithelial cells under light microscope. Quality, if it is a smallpox patient, you can find the scorpion virus eosinophilic inclusion body, but the negative smear can not exclude smallpox.

(2) Electron microscopy: The material was taken from the lesion and observed by electron microscopy. The variola virus was brick-shaped and could be diagnosed within a few hours.

(3) Chicken embryo inoculation or cell culture: Take herpes liquid, sputum suspension, blood or nasopharynx secretion, inoculate virus into chicken chorioallantoic membrane, or inoculate monkey kidney cells or amniotic cells for culture, 12h After seeing most of the tiny inclusion bodies, the inclusion bodies increased significantly after 48 hours, and sometimes the inclusion bodies in the nucleus were visible.

3. Serological examination

Complement binding assay, erythrocyte agglutination inhibition test, neutralization test to detect the presence of specific antibodies in the patient's serum to help diagnose, smallpox patients can appear variola virus antibodies in serum as early as the fourth day of the disease. On the 7th day after the disease, most patients had a positive complement test, and the titer on the 10th to 11th day was 1:640. However, in non-small patients with a history of acne, the titer rarely exceeded 1:40; If a suspicious patient with a history of acne has a serum antibody titer that is four times higher than the early stage at the end of the course, it is of diagnostic value.

4. Pathological changes: the epidermis has reticular degeneration, balloon-like degeneration or coagulative necrosis. Because of the obvious reticular degeneration, most of them produce multi-atrial vesicles. The Guamieri body can be found in the early affected cytoplasm, which is round or egg. Round, eosinophilic and Feulgen-positive, surrounded by a transparent area that is not colored. In addition, intranuclear eosin inclusion bodies are common in old lesions, except for mild inflammation in the dermis. See bleeding.

Differential diagnosis

Should be differentiated from chickenpox. Chickenpox: Early white blood cell vasculitis occurs in children, without scaly papules, hemorrhagic necrosis and scar formation. The blood vessels around the blood vessels are infiltrated.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.