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1. Hepatitis A: Hepatitis A is caused by Hepatitis A virus (HAV). The HAV particle is spherical, measuring 27–32 nm in diameter, without an envelope, possessing a 20-sided cubic symmetry structure—a small RNA virus containing single-stranded RNA. HAV can be inactivated by heating at 100°C for 5 minutes, exposing to ultraviolet light for 1 hour, or by treating with chlorine at a concentration of 1 mg/L for 130 minutes. Both rhesus monkeys and chimpanzees are susceptible to infection. Clinical samples can isolate HAV, but cell culture does not induce cytopathic effects. HAV has only one serotype and one antigen-antibody system; gM antibodies are present only within 12 weeks after onset, while IgG antibodies persist for a long time. The feces and blood of Hepatitis A patients are infectious, primarily transmitted orally; sporadic cases arise from everyday contact, while water and food contamination often lead to outbreaks. For example, in 1988, Shanghai experienced a major Hepatitis A epidemic due to the consumption of raw wax, infecting approximately 300,000 people. Hepatitis A is most common in children, with no chronic or asymptomatic carriers. Post-infection immunity is generally strong. In addition to hygiene measures, vaccination against Hepatitis A can prevent Hepatitis A.
2. Hepatitis B: Hepatitis B is caused by the Hepatitis B virus (HBV). HBV belongs to the family Hepadnaviridae, with a genome length of about 3.2 kb, consisting of partially double-stranded circular DNA. After HBV enters the human body, it binds to receptors on the surface of hepatocytes, detaches its envelope, and enters the cytoplasm of hepatocytes. Once inside, HBV sheds its capsid, and part of the double-stranded HBV DNA enters the nucleus of hepatocytes. Under the action of host enzymes, the negative-sense DNA serves as a template to extend the positive-sense strand, repairing gaps in the positive-sense strand and forming covalently closed circular DNA (cccDNA). Subsequently, cccDNA acts as a template, and under the influence of host RNA polymerase II, multiple mRNA transcripts are produced. Among these, the 3.5-kb mRNA contains all the genetic information of HBV-DNA, known as the pre-genomic RNA. The latter enters the cytoplasm of hepatocytes as a template, where HBV reverse transcriptase synthesizes negative-sense DNA; then, using negative-sense DNA as a template, HBV DNA polymerase synthesizes positive-sense DNA, forming partial double-stranded DNA copies, which eventually assemble into complete HBV virions and are released outside hepatocytes. The daughter double-stranded DNA copies in the cytoplasm can also enter the nucleus of hepatocytes, where they form cccDNA and continue to replicate. The half-life of cccDNA is long, making it difficult to completely eliminate from the body. Based on differences in the full HBV genome sequence or the S-region gene sequence, HBV can be divided into eight genotypes: A–H8. Each genotype further subdivides into different subgenotypes. Different genotypes respond differently to antiviral therapies. During antiviral treatment, HBV genotypes can easily mutate, leading to drug resistance and complicating treatment. The HBV antigen-antibody system includes HBsAg and anti-HBs, HBcAg and anti-HBc, HBeAg and anti-HBe. HBsAg is present in the blood and various bodily fluids of infected individuals and asymptomatic carriers, serving as an indirect indicator of HBV presence. Anti-HBs are protective antibodies; when these antibodies appear in the blood after infection or vaccination, it signifies that the individual has acquired immune protection. HBcAg is mainly located in the nucleus of hepatocytes, while it is generally not detected in peripheral blood. Antibodies against HBcAg come in two forms: IgM and IgG; the former indicates active infection, while the latter reflects past infection. HBeAg, along with HBV-DNA and DNA-P, are key indicators of HBV replication and infectivity; anti-HBe appears in the blood as HBeAg disappears, indicating reduced HBV replication and decreased infectivity. Monitoring these HBV markers in the blood dynamically can help assess the level of infectivity, changes in disease progression, and prognosis. HBV has strong resistance; it can be inactivated by heating at 65°C for 10 hours, boiling for 10 minutes, or through high-pressure steam sterilization. Chlorine-based agents, ethylene oxide, glutaraldehyde, peracetic acid, and iodophor also demonstrate good inactivation effects. HBV infection is widespread globally, though the prevalence varies significantly across regions. According to the World Health Organization, approximately 2 billion people worldwide have been infected with HBV, with 350 million becoming chronic HBV carriers. Each year, around 1 million people die from liver failure, cirrhosis, and primary hepatic carcinoma (HCC) caused by HBV infection. China is a region with a high prevalence of HBV infection; the HBsAg positivity rate among the general population is about 9%. The HBsAg positivity rates among vaccinated and unvaccinated individuals are 4.51% and 9.51%, respectively. The main HBV serotypes prevalent in China are adrq+ and adw2, with C-type and B-type being the most common genotypes. HBV is primarily transmitted through blood and blood products, mother-to-child transmission, broken skin and mucous membranes, and sexual contact. Mother-to-child transmission is a major mode of transmission in China, with infants often contracting HBV through exposure to the blood and bodily fluids of HBV-positive mothers at birth. Skin and mucous membrane transmission occurs mainly through the use of improperly sterilized medical instruments, syringes, invasive diagnostic and therapeutic procedures, and surgical operations, as well as intravenous drug abuse. Other modes of transmission include foot care, tattooing, ear piercing, accidental exposure during medical procedures, sharing razors and toothbrushes, and other similar practices. Sexual contact with HBV-positive individuals—especially those with multiple sexual partners—increases the risk of HBV infection significantly. Thanks to strict HBsAg screening programs for blood donors, HBV infections caused by blood transfusions or blood products are now rare. Everyday contact, such as handshakes, hugs, living in the same dormitory, dining in the same restaurant, or sharing toilets, generally do not transmit HBV. Transmission via blood-sucking insects like mosquitoes and bedbugs has not been confirmed. Vaccination against HBV is the only effective method for preventing HBV infection, and it has been incorporated into routine immunization programs. When HBV infects a person, if the virus persists for 6 months without being cleared, the individual is considered a chronic HBV carrier. The age at infection is the primary factor influencing the likelihood of chronicity. The vertical transmission rate from mother to child reaches 90%; infants infected in early childhood have a chronicity rate of 25–30%, while adolescents and adults only have a chronicity rate of 5–10%. After HBV infection, the disease typically progresses through three phases: the immune tolerance phase, the immune clearance phase, and the inactive or low-replication phase. Many chronic HBV carriers, after a certain period, experience recurrent episodes of disease activity, continuous progression, and significant liver damage—sometimes even liver failure—and develop cirrhosis or HCC at rates of 23% and 4.4%, respectively.
3. Hepatitis C: Hepatitis C is caused by the Hepatitis C virus (HCV). HCV belongs to the Flaviviridae family, with a size of 50–60 nm, and its outer shell contains lipids. Its genome is a single-stranded positive-sense RNA, prone to mutation; currently, it can be divided into six genotypes and different subtypes. Following international standards, HCV genotypes are represented by Arabic numerals, while gene subtypes are indicated by lowercase English letters (such as 1a, 2b, 3c, etc.). Genotype 1 is globally distributed, accounting for over 70% of all HCV infections. After HCV infection, a certain period allows the virus to form a viral population dominated by a single strain—known as quasispecies—within the infected host. The HCV genome contains an open reading frame (ORF) that encodes more than ten structural and non-structural proteins. The NS3 protein is a multifunctional protein with protease activity at its amino terminus, and 1

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羧基端具有螺旋酶/三磷酸核苷酶活性; NS5B protein is an RNA-dependent RNA polymerase, both essential for HCV replication and critical targets for antiviral therapy. HCV is sensitive to common chemical disinfectants; heating at 100°C for 5 minutes, or at 60°C for 10 hours, as well as high-pressure steam sterilization and formaldehyde fumigation, can all inactivate the virus. Hepatitis C is globally prevalent and is a leading cause of end-stage liver disease in Europe, America, Japan, and other countries. The global HCV infection rate is approximately 3%. Epidemiological surveys in China show that the anti-HCV positivity rate among the general population is 3.2%, with no significant difference between men and women. The predominant HCV genotype is 1b, followed by 2a, while other genotypes are less common. Hepatitis C is primarily transmitted through blood, such as through the transfusion of blood and blood products, or via broken skin and mucous membranes—such as through intravenous drug use, the use of non-disposable syringes and needles, sharing razors, toothbrushes, tattooing, and ear piercing. Sexual transmission is also an important route of HCV spread, and mother-to-child transmission can occur, though the transmission routes of some HCV-infected individuals remain unknown. Kissing, hugging, sneezing, coughing, eating, drinking from shared utensils and cups, and other contact without skin breaks or blood exposure generally do not transmit HCV. Like Hepatitis B, Hepatitis C is prone to chronicity and is a major cause of cirrhosis and liver cancer. The markers of infection in the blood include anti-HCV and HCV-RNA positivity. Vaccines are currently under development. 4. Hepatitis D: Hepatitis D is caused by the Hepatitis D virus (HDV), also known as the Hepatitis Delta virus. HDV is a subviral pathogen associated with HBV, causing both acute and chronic hepatitis. HDV is a member of the Arenaviridae family, specifically the deltavirus genus. Mature HDV is spherical, with a diameter of 35–37 nm, and its viral particles contain ribonucleoproteins composed of viral genomes and antigens, with HBsAg as its envelope. HDV is a defective virus that requires assistance from HBV or other hepatotropic viruses to replicate. The routes of infection and preventive measures are similar to those for Hepatitis B; however, a vaccine has not yet been developed. 5. Hepatitis E: Hepatitis E is caused by the Hepatitis E virus (HEV). HEV is a 32–34 nm RNA virus that spreads via the fecal-oral route, often resulting in large-scale outbreaks due to fecal contamination of drinking water sources. Its clinical and epidemiological characteristics are similar to those of Hepatitis A. From 1986 to 1988, a major Hepatitis E outbreak occurred in southern Xinjiang, China, caused by contaminated water sources, affecting nearly 120,000 people. A Hepatitis E vaccine has not yet been developed. 6. Hepatitis G: Hepatitis G is caused by the Hepatitis G virus (HGV). HGV is also known as GBV-C.

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Input: Under the influence of the normal gut microbiota and intestinal-specific secretory IgA, it is often eliminated. Once it enters the intestine, even a small amount of bacteria (such as those in the Shigella group—only 10 bacteria are needed) can trigger disease. Shigella primarily invades the colonic epithelial cells in the intestine and penetrates into the lamina propria through the basement membrane, causing mucosal inflammatory responses. In typical cases, the main pathological changes include diffuse purulent inflammation and ulcer formation in the colonic mucosa; however, the submucosal layer is rarely affected, and septicemia is rare. The onset of toxic dysentery may be associated with specific genetic predispositions, resulting from acute microcirculatory disorders caused by endotoxins. The primary pathologies include cerebral edema, neuronal degeneration, and, in some cases, damage to the adrenal glands and their cortex, while intestinal lesions are relatively mild.

Acute bacillary dysentery can present in five clinical forms: typical, atypical, mild, severe, and toxic. Atypical cases may lack obvious fever or pus-blood in the stool. Severe cases are more common in elderly patients, those who are frail or malnourished, with diarrhea occurring more than 30 times per day, potentially leading to the discharge of patchy pseudomembranes and causing toxic intestinal paralysis. Toxic dysentery commonly presents as shock-type, cerebral edema (respiratory failure), or mixed types. If acute bacillary dysentery persists for more than two months, it becomes chronic bacillary dysentery, which can manifest in three forms: latent, prolonged, or acute-onset, with frequent involvement of the Fausti group. Laboratory tests reveal white blood cell counts ranging from 10 to 20 × 10⁹/L, with elevated neutrophil counts and left shift in the nuclear morphology. Stool microscopy often shows more than 10 pus cells per high-power field, along with red blood cells and macrophages; stool cultures can yield positive results.

II. Diagnosis

(1) Diagnostic Criteria

1. Epidemiology: A history of contact with patients suffering from bacillary dysentery and poor dietary hygiene (in 2/3 of cases) is significant, and regional, seasonal, and age-related factors also play a role.
2. Clinical Manifestations: Acute onset with chills and fever, abdominal pain, diarrhea, tenesmus, and bloody stools (initially watery), which provide valuable diagnostic clues. Toxic dysentery is characterized by high fever, altered mental status, convulsions, or collapse. Atypical cases may present with mild diarrhea, while acute bacillary dysentery often manifests primarily with symptoms of small intestinal inflammation.
3. Laboratory tests rely mainly on stool examinations and cultures to confirm the diagnosis; when toxic dysentery is suspected, early collection of rectal swabs or fecal samples via saline enemas should be performed. For chronic bacillary dysentery, endoscopic examination can be used to collect mucus and purulent secretions from the intestinal mucosa. In recent years, rapid pathogenetic diagnostics have been employed, including immunofluorescence bacterial agglutination tests, enrichment latex agglutination tests, co-agglutination tests, and immunofluorescent staining techniques, which are reported to achieve a positivity rate of over 90%, aiding in the early diagnosis of acute bacillary dysentery.

(2) Differential Diagnosis

1. Acute Bacillary Dysentery (1) Amoebic Dysentery (Parasitic Dysentery): Often has a gradual onset without fever, abdominal pain, mild tenesmus, and fewer bowel movements; stool volume is large, often dark red (like jam), with a foul odor. Stool microscopy reveals clusters of red blood cells, along with Charcot–Leyden crystals, and amoebic trophozoites can be identified. Ulcerative lesions in the intestinal mucosa are deeply recessed, with minimal bleeding from the ulcer surfaces. (2) Enteric Infection with Helicobacter pylori: Patients often have a history of contact with poultry or livestock, typically presenting with low to moderate fever. Stool is often watery, with mild abdominal pain; in some cases, abdominal pain worsens after diarrhea subsides, but there is no tenesmus. (3) Acute Necrotizing Hemorrhagic Small Intestine Inflammation: Commonly seen in adolescents, this condition is associated with severe toxemia, rapid onset of shock, and often accompanied by generalized abdominal tenderness and severe abdominal distension. Stool microscopy predominantly shows red blood cells, while stool cultures fail to grow any dysenteric bacteria.
2. Chronic Bacillary Dysentery (1) Rectal and Colonic Cancer: This condition is more prevalent in middle-aged individuals, with persistent disease progression, poor response to antibacterial treatments, and generally poor overall health, often worsening over time. Generally speaking, early rectal examination or endoscopic evaluation should be performed for chronic patients. (2) Intestinal Tuberculosis: Patients often experience alternating episodes of diarrhea and constipation, frequently accompanied by low-grade fever in the afternoon, night sweats, weight loss, and other general symptoms of tuberculosis. Abdominal pain is often located in the right lower quadrant, with palpable masses and an increased erythrocyte sedimentation rate. X-ray barium studies, endoscopic examinations, and anti-tuberculosis treatment can aid in diagnosis. (3) Non-Specific Ulcerative Colitis: This condition has a long course, with endoscopic findings showing congestion, edema, and ulcer formation in the intestinal mucosa; the mucosa is fragile and prone to bleeding, and antibacterial treatments are often ineffective. Corticosteroids and immunosuppressants are often required. Serum antibodies against lipopolysaccharides on intestinal epithelial cells are present.
3. Other Conditions Toxic dysentery must be differentiated from type B encephalitis (brain-type) and other forms of toxic shock (shock-type). Patients with chronic bacillary dysentery in southern regions should also be distinguished from schistosomiasis.

III. Traditional Chinese Medicine’s Understanding and Treatment of Bacillary Dysentery