Sexually transmitted diseases (STDs) are diseases transmitted through sexual contact and include syphilis, gonorrhea, inguinal lymphogranuloma, condyloma acuminata, AIDS, chlamydia and mycoplasma infections, and intestinal pear-shaped flagellates. Not only do they have a high prevalence in homosexuals, but they can be transmitted through heterosexual contact. The incidence is highest among gay men with multiple sexual partners. The diversity of sexual contact makes the anorectum a highly susceptible organ. The following is a brief description of several common anorectal STDs. The pathogen of syphilis is syphilis spirochete, also known as pale spirochete, a slim and movable spiral microorganism, which can enter the body from the microscopic skin or mucous membrane, reproduce locally and rapidly enter the human system through lymphatic, after about 3 weeks of latent reproduction, a hard shallow ulcer occurs at the invasion, i.e. hard chancre, which is called stage 1 syphilis. The hard chancre can subside on its own without treatment, but 7 to 10 weeks after infection, i.e. 6 to 8 weeks after the appearance of the hard chancre, the spirochete multiplies in the body and causes a widespread skin rash and invasion of the eyes, bones, joints, etc., which is known as stage II syphilis. The skin rash of stage II syphilis can also subside naturally due to the increase of antibody production in human body, and there are no clinical symptoms, but the presence of cellular and humoral immune antibodies in the serum makes the laboratory test positive for antigenic antibody reaction, which is called occult syphilis or latent syphilis. Within 2 years, skin lesions can reappear, i.e. second stage recurrent syphilis. Syphilis skin lesions that are more than 2 years old show large deep ulcers, i.e. syphilitic dendritic swelling, which is called stage III or advanced syphilis, when syphilis has invaded the cardiovascular system and the central nervous system and different symptoms appear, which is called cardiovascular syphilis or neurosyphilis. Syphilis spirochetes can be transmitted to the fetus through the placenta of the mother, that is, fetal syphilis, to the fetus that is congenital syphilis. The syphilis spirochete can invade the perianal skin and rectal mucosa, appearing as first and second stage syphilis damage. The route of infection: the infected party has syphilis spirochetes in the damage on the body (mainly the body surface), and the infected person has damage to the skin and mucous membranes (this damage is often very subtle and not easily detectable to the naked eye) is a necessary condition for syphilis transmission. The route of infection is determined by this condition. In the process of transmission, the infected person must receive a certain number of pathogens before infection occurs. 1. Sexual contact This is the most important route of infection. It includes not only sexual intercourse, but also other kinds of sexual behavior, such as anal sex, oral sex, mutual masturbation, kissing, etc., causing direct infection. 2. Direct infection other than sexual contact Direct infection can also occur through breastfeeding, hand shaking, direct contact between health care workers and patients, receiving blood from patients (blood transfusion), etc. 3. Indirect infection Contact with clothing, utensils, tableware, medical instruments, etc. contaminated by syphilis spirochetes can cause infection. However, the chance of indirect infection is much smaller than that of direct infection. 4. Fetal transmission During pregnancy, the spirochete passes through the placenta with the blood of a woman with syphilis and enters the fetus, causing the fetus to become infected with syphilis. This infection peaks in the 6th to 8th month of pregnancy. Clinical manifestations Syphilis is mainly transmitted through sexual intercourse, the external genital area is the most affected, other sexual contact areas can also be infected, homosexual anal sex can be transmitted by anal skin or mucous membrane, by indirect contact with everyday objects, bathing utensils, tableware, etc. and the infection is not much, but syphilis patients as blood donors can be directly infected by blood transfusion to the recipient. The clinical manifestations are as follows: 1. Stage I syphilis (hard chancre) The main manifestation, mostly within 2-4 weeks after infection. The hard chancre appears where the syphilis spirochete invades, mostly in the external genital area, including the glans, coronal sulcus, foreskin, and tether in men, and the labia in women, and also in the cervix. In homosexuals, it is on the anal or rectal mucosa. The damage is shallow in ulcers, mostly solitary, 1-2 cm in diameter, round, with clear boundaries, its surface is smooth or erosive, with a small amount of secretion, hard to touch like ointment, and generally painless. Pale spirochetes can be detected on the smear of the secretion. The skin of the chancre is clear or vesicular, with a small amount of discharge, hard to the touch like ointment. The hard chancre appears within 1 week with corresponding local lymph node enlargement. 2. Stage II syphilis rash: It appears 7-10 weeks after infection, i.e. 6-8 weeks after the onset of hard chancre. The rash has various forms, including macules, papules, maculopapular rash, scaly rash, pustular rash and ulcerated rash. The skin is flat and the surface is uneven. The lesions are warty and proliferate like cauliflower, vesicular or covered with mist-like film. 3. Stage III syphilis: more than 2 years of infection. There are mainly: gum swelling, nodular syphilis rash, bone, eye, cardiovascular and neurosyphilis. 4. Latent syphilis: a history of syphilis infection, asymptomatic, syphilis seropositive. The clinical diagnosis of hard chancre and flat warts must be based on medical history (mainly history of unclean sexual intercourse or history of anal intercourse of homosexuals), physical signs and laboratory tests. The anal rash must be differentiated from herpes simplex, soft chancre and squamous carcinoma; the anal rash of stage II syphilis must be differentiated from dermatophytosis, acne, psoriasis and lichen planus; the flat warts must be differentiated from condyloma acuminata and squamous carcinoma; the anal mucosal rash of stage II syphilis must be differentiated from candidiasis and other causes of anorectal ulcers; the syphilitic white spots of perianal skin must be differentiated from vitiligo and sweat spots; Syphilitic proctitis should be distinguished from various non-specific proctitis; rectal syphilis tumor should be distinguished from malignant tumor of rectum and anus. Laboratory examination: Take smear of surface secretion of hard chancre or flat warts and send it immediately for dark-field microscopic examination or immunofluorescence staining and examination under fluorescent microscope. The most important thing is that it is not only the best way to get the best results, but also the best way to get the best results. Penicillin is the drug of choice for the treatment of syphilis, with reliable efficacy. 2. Tetracycline or erythromycin Tetracycline or erythromycin is available for those who are allergic to penicillin. V. Prevention and review 1. Advise syphilis patients to abstain from sexual intercourse. Sexual partners who are known to have had sexual relations should be advised to seek medical examination in time to confirm the diagnosis and give appropriate treatment. The resumption of family sexual life should be 3 months after penicillin treatment, strengthen the publicity of syphilis prevention and control knowledge and strictly prohibit prostitution and prostitution. 2. After treatment, patients with stage I and stage II syphilis should have their serum tests reviewed every 3 months for the first year, and every 6 months for the second to third years, for a total of 8 times, with all tests being negative. If the positive serum test is changed to negative during the review period and then reappears as a serum relapse, the treatment should be repeated, but the amount of medication should be doubled. Section 2: Anal and rectal gonorrhea I. Etiology Gonorrhea is caused by Neisseria gonorrhoeae, a gram-negative diplococcus. Human is the only natural host of Neisseria bacterium, there is susceptibility but no innate immunity, so gonorrhea can be re-infected or repeated infection. The gonococci that invade the human mucosa are attached to the mucosa or embedded in cells by their special structured hairs, and gonococci can be found microscopically in multinucleated leukocytes. The gonococcus invades the mucous membrane of the biological urinary tract and causes inflammation, mostly urethritis in males and endocervicitis in females, sexual disorders or homosexuals have anal intercourse so that the gonococcus directly enters the anus and causes gonorrheal proctitis, gonococcus and gonorrheal secretions stain the perianal skin and cause dermatitis, and can also invade indirectly infected young girls. The main manifestation of gonorrhea in men is urethritis. After the incubation period of 2 to 5 days after infection, there is urethral discomfort, burning sensation in the urethra within 24 to 48 hours, frequent and painful urination, overflow of purulent secretions in the urethra, cloudy urine, and redness and swelling of the urethral orifice. Patients have varying degrees of systemic symptoms, malaise, fever, and loss of appetite. In untreated cases, gonorrhea infects the posterior urethra in 10 to 14 days, causing posterior urethritis, and can be complicated by prostatitis, vesiculitis, and epididymitis. Improperly treated or untreated gonorrhea gradually reduces urethral symptoms after 1 week and turns into chronic gonorrhea, but there is still discomfort in the urethra and mild painful urination, and there is still discharge from the urethra, and there is suspended flocculent material called gonorrhea silk in the urine, and the discharge from the urethra in the morning is pus crust blocked in the urethra. 2. Female gonorrhea manifests mainly as endocervicitis. The vagina can discharge a lot of purulent secretions – purulent leucorrhea, contaminating the vulva, perineum, anus and buttocks, making the local skin flushed, burning and itching, showing dermatitis. Infiltration of secretions or entering the mucous membrane of the anal canal due to the friction of contaminated underwear can cause inflammation of the rectal mucosa. On examination of the cervix, there is cervical congestion with purulent discharge and significant tenderness, but the patient’s conscious symptoms are not obvious. In cases of urethral infection, the urethral orifice is congested with purulent discharge and there is also frequency, urgency, painful urination and burning sensation in the urethra, but it is less severe than in men. If the vestibular gland is infected, there is redness, swelling and painful heat in the vestibular gland, and if an abscess is formed, there are systemic symptoms and an increase in body temperature. 3. gonorrheal proctitis is mainly seen in gay men, while in women it is mostly caused by vaginal self-infection. Most patients have symptoms similar to other rectal inflammatory diseases, anal itching and burning sensation, purulent or bloody mucus during defecation, and in severe cases, shortness of breath, frequent stools, pus and blood stools, and in a few patients, reflex abdominal pain. 4. perianal dermatitis of gonorrhea, i.e., dermatitis of perineum, intergluteal area and perianal area due to contamination by overflow of secretion, with local skin flushing, swelling and tenderness, some epidermis peeling off to form erosion, or inflammatory redness, and also purulent scab formation, most patients complained of itching and burning sensation. Diagnosis and differential diagnosis Gonorrhea diagnosis should be a combination of history, clinical manifestations and laboratory tests, gonorrheal proctitis patients mostly have a history of anal sex or homosexuality, should be cautious and patient inquiries. Laboratory tests: ① smear examination: check the urethra or vaginal or anal secretion smear, send it immediately for Gram staining, and microscopically find Gram-negative diplococci in extracellular or intracellular can be used as a basis for diagnosis; ② culture examination; ③ direct fluorescent antibody staining method; ④ polymerase chain reaction (PCR). The treatment of gonorrhea should be timely, adequate and standardized, taking into account the site of infection, bacterial resistance, the presence of comorbidities and affordability. Prevention The prevention of gonorrhea depends on the continuous improvement of the social environment including economy, culture and morality in order to effectively control the sexually transmitted diseases, and only the preventive measures of individual family life are mentioned here. ①Gonorrhea patients should have enough rest, avoid sexual intercourse during treatment, and sleep in separate beds; ②No stimulating food, including alcoholic beverages and spicy food; ③Improve personal hygiene, wash and disinfect the anus and external genital area as prescribed by the doctor; ④Change the clothes and bedding contaminated by secretions and store them in plastic bags, and iron and disinfect them after washing; ⑤The patient’s toiletries and tableware should be set separately. (6) Avoid sleeping in the same bed with young children, and use effective eye drops if there are infants at home; (7) Sexual partners should seek medical examination as soon as possible; (8) Patients should be examined regularly after being cured to prevent recurrence and reinfection. The pathogenic agent of anal chancre is Haemophilus ducreyi. It is called soft chancre when ulcers are formed in and around the anus due to infection by Haemophilus ducreyi. The infection is often due to unclean clothing or vaginal and urethral secretions, and ulcers may also occur on the penis or labia. It starts as a red spot, gradually becomes a papule, then a pustule, and then an ulcer when it breaks down. The ulcers are round or oval with subtle margins, soft, with gray necrotic tissue at the base, and often covered with purulent secretions. It is often the case that several ulcers occur at the same time and spread outward, and some of them unite with each other. Clinical manifestations The incubation period of soft chancre is short, about 24-72 hours. The pain is severe, often with purulent secretions stimulating the skin and sphincter of the anus, and the pain increases when defecating. Multiple lesions with soft ulcers and Haemophilus ducreyi in the secretions. The diagnosis of anal chancre mainly relies on medical history, clinical manifestations and laboratory tests. The diagnosis can be based on the history, clinical manifestations and laboratory tests. Lymphogranuloma venereum is also known as inguinal lymphogranuloma, fourth venereal disease, and Frei’s disease, and is known as one of the four major venereal diseases along with syphilis, gonorrhea, and soft chancre. The pathogen of venereal lymphogranuloma is Chlamydia trachomatis serotype 1, 2 and 3. The disease is an acute or chronic chlamydial disease transmitted through sexual intercourse. Its main manifestations are ulceration of the external genitalia, anus and other sites of chlamydial invasion, enlargement, granulomatous hyperplasia and inflammation of lymph nodes (mainly inguinal lymph nodes) in the area of lymphatic drainage at the site of pathogenic invasion, septic perforation, and advanced external genital elephantiasis and rectal stricture. The disease is transmitted mainly through sexual intercourse and occasionally by contact with the patient’s secretions. In recent years, foreign literature has reported an increase in rectal lesions caused by this disease due to the increase in male homosexuality, and it has new features. Clinical manifestations The incubation period of the disease is 5 to 21 days, with an average of 7 to 12 days, and also up to 5 weeks. The clinical course can generally be divided into three phases. The primary damage phase (primary sore phase) occurs in the male genitalia, female vulva and cervix, posterior vaginal vault, as well as in the anal canal and rectum of homosexuals, where the pathogen invades, with papules, herpes, pustules and nodular damage. The rash (mucocutaneous rash) is dark red and about 1-10 mm in size, and the lesions quickly break down, resulting in small superficial vesicles and shallow ulcers, 1-4 mm in diameter, with clear margins, no hardness, no obvious inflammatory reaction, no infiltration, and mostly single lesions (herpetic lesions can generally be 2-3). After 10 to 20 days, the vesicles or ulcers heal on their own without leaving a scar. The whole process is often neglected because the patient has no conscious symptoms, or the symptoms are very mild and painless. If it occurs in the anal canal, rectum, posterior vaginal vault, cervix and other hidden areas, it is more likely to be ignored. 2. Lymphatic dissemination phase Lymphadenopathy in the lymphatic drainage area of the primary damage site begins to appear 1 to 6 weeks, on average 3 weeks, after the occurrence of the first stage damage. Most of the lymphadenopathy occurs in the inguinal lymph nodes, but it can also be in the pararectal lymph nodes, internal iliac lymph nodes, sacral lymph nodes, and even abdominal group lymph nodes. Lymphadenopathy other than inguinal lymph nodes is mostly found in female patients and in male homosexual patients. This is because the lymphatic fluid return to the female genitalia is different from that of males, except for the vulva and lower vagina which return to the inguinal lymphatic group, the upper 2/3 of the vagina and the cervix, which have many traffic branches connected to the rectal lymphatic group; in male homosexuals, the primary damage is in the rectum of the anal canal, and their lymphatic fluid return, naturally, has a significant portion of people in the perirectal lymphatic group. Lymphadenopathy occurring in the inguinal lymph node group has the typical manifestations of venereal lymphogranuloma; the lymph nodes are enlarged and painful, mostly on one side and rarely on both sides. The enlarged lymph nodes are initially isolated and scattered, and then fuse with each other and adhere to the surrounding tissue to form a mass. The inguinal ligament may separate the adherent masses, and the so-called groove sign appears. After 1 to 2 weeks, the lymph nodes will soften, rupture, and discharge yellow plasma or bloody pus, forming most fistulas, resembling a spout. After the lymph nodes break down and flow pus, they can heal after several months to years, leaving scarring after healing. In a few patients, the lymph nodes do not become purulent, and the enlargement resolves spontaneously. In female patients and in those whose primary damage is located in the anorectum, perirectal lymph nodes may also develop damage similar to that of the inguinal lymph node group, resulting in proctitis and perirectitis, and even left-sided colitis or even total colitis due to lymphatic reflux. Endoscopy reveals granulomas and erosions of the intestinal mucosa, with reddish-purple nodes that bleed easily, and sometimes inflammatory polyps of the intestinal wall. Clinical symptoms such as diarrhea, urgency, abdominal pain, stools with pus and blood, and constipation, as well as bleeding from the anus and purulent discharge, are sometimes seen. However, the systemic reaction is usually not severe. Granulomatous inflammation of lymph nodes at this time can lead to damage such as perianal abscess, anal fistula, rectovaginal fistula, and rectourethral fistula. After the damage of the second stage has basically disappeared, the chronic lymphangitis continues and the scar tissue produced by the damage repair continues to cause harm. After several years or even more than ten years, chronic lymphangitis and poor lymphatic fluid return caused by scar contraction can lead to elephantiasis in the external genitalia and other areas. After the healing of proctitis and perirectitis, the scarring and contraction of the scar resulting from the repair can lead to stenosis of the colon and rectum. The strictures are often 5-10 cm from the anal verge and are tubular, irregular in shape, uneven, and not clearly demarcated from the normal anal canal and rectum, or they may be circumferential and membranous. There is also connective tissue hyperplasia around the anus and anal canal, and the elasticity of the anal canal decreases, resulting in an open anus that does not close properly. Finger examination of the anus reveals thickening of the anal canal wall, a variable number of solid masses, a curved and uneven anal canal, and a narrowing obstacle when the finger is extended to 5 cm. The disease develops slowly and becomes more serious with time, and eventually even the finger cannot be extended into the stenosis. As the stenosis worsens, the stool becomes thinner and thinner (even pencil-like), and the manifestations of rectal stenosis, such as constipation, unclean bowel movements, shortness of breath, lower abdominal distension, and intra-abdominal discomfort, become more and more serious. In the later stage, there may be symptoms of chronic intestinal obstruction such as increased frequency of fecal discharge and discharge from the anus. In women, the disfiguring ulcers and scars formed by rectovaginal or urethral fistulas are often called “female vaginal erosions”. The diagnosis of venereal lymphogranuloma is mainly based on: (1) a history of unclean sexual intercourse. (2) The presence of superficial erosions or ulcers (primary sores) on the genitals or anus and other sites of sexual contact. ③The group of inguinal lymph nodes is in the form of an adhesive mass with grooved signs, and when the lymph nodes break down, several fistulas are formed in the shape of a spout, with thin pus flowing out. ④When lymphadenitis occurs, there are systemic symptoms such as fever, chills, arthralgia, increased clots in blood sedimentation, increased total leukocyte count and lymphocyte and monocyte ratio, and significant inversion of serum albumin and globulin. ⑤ Slow progression of the disease process. (6) Positive complement binding test and pathogen isolation culture. ⑦Frei test is positive and can be used as a reference condition. ⑧ Differential diagnosis: It must be carefully differentiated from soft chancre, syphilitic transcutaneous flaccid, and purulent lymphadenitis. The pathogen of anal warts is human papillomavirus, the only host of which is human. It is often caused by contact with virus-bearing objects or sexual contact. The incubation period varies from 1 month to several months, and it is a common anal skin disease. The actual fact is that there is no significant gender difference in the incidence of the disease. The incubation period after the infection of condyloma acuminata is about 3 months, mostly in the male and female external genitalia and female vagina. The anal condyloma is more typical, as the skin between the buttocks is more wet. The rash is a light brown superfluous organism if it has been present for a long time, and some have a tip at the root. Due to infiltration and impregnation, the rash is vesicular or covered with oozing blood or pus and blood crusts. Clinical reports are not infrequent of huge warts with damage up to the size of a fist, and their pathological histology is like a low grade malignant process. Intrarectal warts are not easily detected clinically, and the larger ones are only found during anoscopy when the patient complains of pain or frequent bowel movements. The anal condyloma is usually not obvious conscious symptoms, but the secretions are more impregnated anal itch induced. The actual fact is that you can find a lot of people who are not able to get a good deal on a lot of things. They are commonly found on the vulva or perineum of women and outside the coronal sulcus of the penis of men. History of venereal disease, positive syphilis serology test. 2. Proliferative anal tuberculosis The nodules are proliferating in the form of warts or papillary nodules, forming lamellae, surrounded by inflammatory redness, clearly defined, with a papilloma-like central protrusion, with purulent secretions and a filthy appearance, and the culture of the secretions can detect tuberculosis bacteria, and pathological tissue examination, tuberculosis nodules can be found. 3. Genital cancer Cervical cancer and penile cancer are mostly seen after middle age, with single occurrence, obvious infiltration, hard texture, often forming ulcers, easy to bleed, and easy to identify by pathological tissue examination. 4. genital Bowen-like papulosis is a disease that has been recognized only in recent years, which is a multiple small papules, light red or brownish red, about 4mm in diameter. It is a good idea to have a good look at the website. It is easy to misdiagnose, but histologically similar to Bowen’s disease changes, biopsy can be distinguished. 2. cryotherapy with liquid nitrogen CO2 dry ice for genital warts, anal warts, vaginal warts, urethral orifice treatment 1-3 times. 3. Laser therapy CO2 laser can treat all parts of the warts. 4. electrocautery Larger warts can be cauterized in batches. The advantage of this is that the warts can be completely removed and can be examined pathologically, especially if there is a suspicion of cancer, which should be removed for biopsy. The first is the acquired immunodeficiency syndrome (AIDS), a human immunodeficiency virus (HIV) caused by severe immunodeficiency as the underlying pathology, to Pneumocystis carinii pneumonia, Kaposi (Kaposi) sarcoma, chronic lymph node enlargement, non-Hodgkin’s lymphoma, a variety of conditionally tumorigenic pathogenic infections as the main clinical manifestations of sexually transmitted diseases. The incidence of this disease is significantly higher in men than in women. The incidence of the disease is significantly higher in men than in women, but it is more common in young adults. Until now, there is no treatment to improve the immune deficiency significantly, and most patients die within 5 years, therefore, the prevention and treatment of this disease should be given great attention worldwide. Clinical manifestations (a) AIDS is divided into three clinical phases from the appearance of clinical symptoms: HIV infection, AIDS-related syndrome and AIDS. The division of the three phases is distinguished by the degree of damage to the quantity and quality of T4 cells affected by HIV, that is, by the degree of immune function impairment. 1. HIV infection stage Also known as subclinical infection stage, or considered as latent stage. It often exhibits signs and symptoms similar to those of acute infectious mononucleosis. Thereafter, the lesions gradually develop into unexplained generalized chronic lymph node enlargement that lasts for at least 3 months. However, some patients may be completely asymptomatic and appear healthy. 2. AIDS-related syndrome Also known as mild AIDS, patients present with clinical symptoms and persistent lymphadenopathy indicated by certain immune deficiencies, and about 1/4 develop AIDS within a few months to 3 years, and the remainder eventually develop AIDS over a longer period of time. Signs of impaired immune function: ① delayed allergic response; ② non-fatal viral, bacterial and fungal infections causing damage to mucous membranes and skin; ③ enlargement of non-inguinal lymph nodes lasting 5-6 months and numbering more than 2; ④ weight loss of more than 10%; ⑤ fever over 38°C for 3 months; ⑥ fatigue; ⑦ night sweats. 3. AIDS Its clinical manifestations have three main features: (i) conditional infection and (especially) Pneumocystis carinii pneumonia; (ii) malignancy, especially Kaposi’s sarcoma; and (iii) severe cellular immunodeficiency of unknown origin, especially T4 lymphocyte deficiency. AIDS differs from other STDs in that the latter (e.g. syphilis, gonorrhea) usually have symptoms localized at the site of pathogen invasion (mostly genital organs) before developing to other organs, but the localized symptoms of AIDS are not manifested by viral invasion of local skin and mucous membranes, but are often detected by the occurrence of conditional infections and characteristic malignant tumors due to immunodeficiency. Therefore, the clinical manifestations of AIDS are also basically the manifestations of various infections and tumors. (b) AIDS combined with specific anorectal diseases, male homosexuals have a higher risk of certain malignant lesions in the anorectum than the general population, these lesions are: Kaposi’s sarcoma, lymphoma and squamous cell carcinoma. Kaposi sarcoma Kaposi sarcoma can occur in the anorectal area, as a raised plum-like wart, which can cause a lot of bleeding if biopsied. It is often discovered by inadvertent tissue biopsy, such as wart excision or abscess wall biopsy. Although Kaposi’s sarcoma of the rectum can be primary, it is often combined with diffuse disease, so that an oversized resection is not necessary. Kaposi’s sarcoma can present as a rectal ulcer, but it is often an advanced presentation and local radiotherapy is of little help. 2. perianal lymphoma Primary non-Hodgkin’s lymphoma of the anorectal region has been reported, but is uncommon. However, it is thought that this disease will increase. It is occasionally found during biopsy for other diseases, such as anal fistula biopsy in homosexuals with AIDS, and should be treated with appropriate chemotherapy once diagnosed. 3. squamous cell carcinoma of the anal canal Whether homosexual men are susceptible to this malignant disease is currently debated. Careful investigation suggests that male homosexuality is a risk factor for anal canal cancer because squamous anal canal cancer often has a history of genital warts. A large number of homosexual men have been reported to have anal canal cancer in some centers, and there is a growing trend. Ulcers combined with herpes simplex virus (HSV), syphilis and trauma can be seen in homosexual men. The ulcers often have a wide base, oval or round, and can be located at the upper or lower end of the anal canal, where a swab biopsy can reveal HSV. chronic, symptomatic and non-healing ulcers are best treated by excision. Some perianal ulcers can cause severe pain and sometimes require a proximal dysfunctional enterostomy, but long-term results are poor. Diagnosis Any positive HIV isolation test or positive HIV antibody confirmation test can confirm the diagnosis of HIV infection. Diagnosis of AIDS disease pay attention to the following aspects: 1. careful understanding of medical history ① whether there is a history of intravenous drug injection, whether syringes and surgical instruments are strictly sterile or disposable; ② whether there are same-sex or several sexual partners or a history of sexual contact with AIDS patients; ③ whether there is a history of HIV-contaminated blood or blood products transfusion, hemophiliacs applying factor VIII; ④ whether infection through the birth canal or placenta, organ transplantation or medical transmission. (4) whether the infection is through the birth canal or placenta, organ transplantation or medical transmission, etc. Careful physical examination is of great diagnostic value in cases of prolonged high fever, intractable diarrhea, ulcers caused by fungal infections of the mouth, pharynx and anus, swollen lymph nodes, herpes zoster extending along a certain superficial cutaneous nerve, and skin and mucosal lesions of Kaposi’s sarcoma. 3. Clinical diagnosis: ①AIDS can be diagnosed after excluding other causes of cellular immune deficiency and severe decrease in body resistance, and after confirming that the patient has one or several opportunistic infections with severe cellular immune deficiency and severe tumors (Kaposi’s sarcoma) through serological testing and histological examination; ②Diagnosis can be made or proposed based on the main and secondary clinical symptoms. The main symptoms are: ① weight loss of more than 10%; ② unexplained diarrhea for more than 1 month; ③ prolonged fever for more than 1 month. Secondary symptoms: ① persistent cough for more than 1 month; ② generalized skin itching; ③ recurrent herpes zoster; ④ chronic disseminated herpes simplex; ⑤ candida infection of the mouth and pharynx; ⑥ generalized lymph node enlargement; ⑦ memory and mental retardation; ⑧ peripheral nerve damage. The diagnosis of AIDS can be made by excluding known causes of severe immune impairment and by having two major symptoms and one minor symptom as described above, while having systemic Kaposi’s sarcoma or cryptococcal meningitis can help confirm the diagnosis. Treatment There is no effective treatment for AIDS. 1. Anti-HIV drugs mainly act on HIV itself or inactivate the reverse transcriptase of the virus. Among them, azidothymidine (AZT) is recognized as a practical anti-HIV drug, which has a good effect of blocking HIV replication and relatively few toxic side effects, prolonging the patient’s survival and enhancing the patient’s ability to live. 2. Immune-enhancing agents can be tried, but the effect is not great. The main ones are interleukin-2 (IL-2), γ-interferon, which is a mediator of immune response released by T lymphocytes and is useful for treating immune deficiency in AIDS patients. 3. Treatment of conditional infection 4. Anti-cancer treatment For Kapozi sarcoma, radiotherapy or chemotherapy with vincristine, adriamycin and bleomycin can be used; lymphoma and other malignant tumors can be treated with the usual chemotherapy regimen commonly used for this type of tumor. 5. Chinese medicine treatment Adopt the treatment methods of tonifying and fostering, clearing heat and detoxifying, regulating qi and activating blood, benefiting qi and nourishing yin, etc., which have certain efficacy. 6. Risk of surgery in AIDS patients Risk of anorectal surgery in AIDS patients: Most anorectal surgeries in HIV patients are minor surgeries, such as small abscess incision and drainage, transrectal biopsy, hemorrhoidectomy, internal sphincterotomy and anal fistula surgery, etc. Although these are minor surgeries, wound healing is still a big problem. Postoperative mortality, complications, and recurrence rates are often unpredictable, and some authors argue that reduced CD4 counts do not reduce wound healing rates and cannot be relied upon to avoid surgery. However, it has been suggested that reduced CD4 is associated with reduced wound healing rates and poor prognosis. Risk of bowel resection in AIDS patients: Mortality and complications of bowel resection in AIDS patients are related to their pathology. Cytomegalovirus when combined with ileocolitis or rectocolitis resulting in bleeding or perforation is the most common indication for colectomy, while other lesions such as lymphoma and Kaposi’s sarcoma occasionally require colectomy. Acute subtotal colectomy is extremely poor, with a mortality rate of 71% within 30 days, while elective surgery has a better prognosis.