Changes in the organ of vision during HIV infection. Does HIV affect the eyes: main diseases and their features. How HIV enters a healthy human body or routes of transmission of HIV infection

– these are specific changes in the organ of vision caused by the addition of an opportunistic infection in patients with a history of HIV infection. Clinical picture determined by the nature of the lesion. General symptoms for most forms - decreased visual acuity, scotoma, photopsia, color vision disturbances, photophobia, increased lacrimation. Diagnosis is based on the use of PCR, ELISA, instrumental methods diagnostics (visometry, ophthalmoscopy, perimetry, tonometry, biomicroscopy, ultrasound, CT scan of the head). Antiretroviral and symptomatic therapy is used for treatment.

General information

Ocular manifestations occur in 70-80% of patients with HIV infection. Approximately 50% of patients have symmetrical involvement in pathological process both eyeballs. Prevalence of cytomegalovirus retinopathy in humans, infected with the virus immunodeficiency is 30-40%. In 5% of cases, irreversible damage is observed optic nerve. 30-35% of people with this pathology have high risk irreversible vision loss. In 30-50%, intraorbital manifestations are complicated by lesions nervous system. Ocular manifestations occur with equal frequency among males and females. Geographical features no spread has been observed.

Causes of ocular manifestations of HIV

The cause of eye damage is infection with the human immunodeficiency virus, which belongs to the retrovirus family, and the addition of an opportunistic infection. The source of spread is a sick person. The virus is contained in biological media of the body (blood, semen, breast milk, vaginal discharge, cerebrospinal fluid). The infectious dose is 10,000 viral particles. Routes of transmission of infection: sexual, hematogenous and vertical (from mother to child). The eyes are affected when infected blood comes into contact with open mucous membranes (conjunctiva) or the virus penetrates the blood-ophthalmic barrier.

Pathogenesis

The immunodeficiency virus can be identified in the membranes of the eye and aqueous humor, however, pathological changes are caused not by the pathogen itself, but by associations of other microorganisms. Activation of an opportunistic infection causes recurrent inflammatory processes in the intraocular localization. Infection with cytomegalovirus leads to cell lysis and the development of a granulocytic reaction. Due to violation rheological properties blood, ischemic manifestations occur due to occlusive arteritis, periphlebitis. Appendages of the eye (eyelids, tear ducts) are most often affected by the herpes zoster virus, Kaposi's sarcoma, and less commonly by molluscum contagiosum.

Neurological symptoms include photophobia, double vision, small-scale movements of the eyeballs when trying to fixate the gaze. In some cases, blepharospasm occurs due to paralysis cranial nerves. With intrauterine infection of the fetus, there is a high risk of developing visual abnormalities (anophthalmos, corneal coloboma). Kaposi's sarcoma localized to the eyelids or orbital conjunctiva long time characterized by an asymptomatic course. The growth of the tumor complicates the process of closing the eyelids and leads to the development of local inflammatory reactions in the form of hyperemia and swelling of the membranes of the anterior segment of the eyes.

Complications

Hemorrhage in vitreous can reach the degree of total hemophthalmos. Less commonly, hypopyon and hyphema occur. The prolonged course of aspergillosis leads to the formation of cataracts and multiple erosive defects on the surface of the cornea with the risk of perforation. High probability of bacterial and infectious lesions anterior section eye (conjunctivitis, keratitis). The development of secondary dacryocystitis is possible. In rare cases, the pathological process spreads to the bones of the skull and brain tissue. 20% of patients experience retinal detachment due to necrosis individual areas inner shell of the eyes. Complications from the nervous system are represented by cryptococcal meningitis, lymphoma meninges, neurosyphilis.

Diagnostics

To diagnose HIV infection, a polymerase test is performed chain reaction(PCR), which makes it possible to detect fragments of RNA or DNA of the virus. Linked immunosorbent assay(ELISA) allows you to detect specific antibodies to the virus. To assess the severity of immunodeficiency, the content of CD4 lymphocytes is studied. Into a complex of specific ophthalmological examination includes:

• Ophthalmoscopy. When examining the fundus of the eye, the ophthalmologist identifies signs of retinal microangiopathy and vascular aneurysm. On the inner shell of the eye, “cotton-wool-like” spots, areas of hemorrhage, and signs of optic nerve atrophy are detected. The retinal vessels acquire a milky white color. With retinochoroiditis of toxoplasmosis origin, pigmented scars are visualized on the retina.
• Ultrasound of the eye. Ultrasonography indicated for clouding of the optical media of the eye. Pathological changes of the optic nerve are represented by an increase in the depth of its physiological excavation in the presence of areas of edema on the retina.
• CT head. It is used to identify neoplasms of intraorbital localization (Kaposi's sarcoma, lymphoma).
• Retinal angiography. A violation of regional blood flow caused by aggregation of formed elements is determined.
• Biomicroscopy of the eyes. With eye aspergillosis, the affected area on the cornea is white or yellowish in color with a dry surface. The focus is limited by the shaft of infiltration.
• Perimetry. There is a concentric narrowing of the visual field. Multiple scotomas are detected.
• Visometry. The degree of decrease in visual acuity depends on the nature of the retinal lesion and optical nerve fibers, varies from minor dysfunction to complete blindness.
• Non-contact tonometry. Availability volumetric formations intraocular localization provokes an increase in intraocular pressure.

Treatment of ocular manifestations of HIV

Causative therapy for HIV infection has not been developed, but the use of antiretroviral drugs can slow down the progression of the disease. Efficiency symptomatic treatment visual impairment increases with the use of antiviral drugs that inhibit the persistence of the virus in the body. With the development of infectious keratitis, retinitis or vesiculobullous dermatitis caused by herpes zoster, intravenous administration of acyclovir, famciclovir is indicated. Dry keratoconjunctivitis in combination with xerophthalmia requires the use of artificial tears and moisturizing ointments.

Treatment of toxoplasmic retinochoroiditis is based on the use of pyrimethamine, sulfonamides, and clindamycin. Acute course Iridocyclitis in HIV-infected patients requires instillation of glucocorticosteroids in combination with short courses antibacterial therapy. For cytomegalovirus retinitis, cidofovir, foscarnet, and ganciclovir are used. Treatment tactics for patients with Kaposi's sarcoma boil down to chemotherapy or cryotherapy, surgical excision of the tumor, and intratumoral administration of cytostatics. With aspergillus lesions of structures eyeball antifungal therapy is indicated. The feasibility of intravenous use of amphotericin B and itraconazole has been proven.

Prognosis and prevention

The outcome of the disease is determined by the viral load, the characteristics of eye damage and the course of the underlying pathology. According to statistical data collected in ophthalmology, the risk total loss vision is 40%. Nonspecific preventive measures boil down to preventing infection with the immunodeficiency virus (use of contraception, sterilization of medical instruments, combating injection drug addiction). Patients are recommended to give preference to spectacle correction of visual acuity over contact lenses. Specific methods prophylaxis has not been developed, but the use of antiretroviral therapy significantly improves the prognosis.

Despite all preventive measures held in last years, HIV infection is still a widespread disease. Thus, in the United States alone, over 50,000 new cases of the disease are observed annually. HIV infection is caused by retroviruses. After infection, acute retroviral syndrome develops within 1-6 weeks: patients experience fever, rash, myalgia, headache or gastrointestinal symptoms. The number of CD4+ T-lymphocytes decreases and there is often an increase in the level of liver enzymes in the blood.

After the initial infection, the disease itself, which is called AIDS (syndrome) primary immunodeficiency person), arises through enough long period time (about 10 years). AIDS is the most serious manifestation of HIV infection and develops when the immune system is already severely damaged by the virus. With such damage to the immune system, patients develop opportunistic infectious diseases caused by Pneumocystis jiroveci (for example, Pneumocystis pneumonia), Cryptococcus neoformans, cytomegalovirus, Candida fungi ( oral candidiasis) or so rare malignant processes, like Kaposi's sarcoma. Patients also experience encephalopathy due to the direct effect of the virus on the brain.

HIV infection is primarily transmitted through sexual contact intravenous administration medicines(especially when using reusable syringes or when multiple people share the same syringe) and during blood transfusions. Intrauterine transmission of infection from mother to fetus is also possible. Cases of infection have been described during childbirth or during breastfeeding. In addition, healthcare workers are at risk.

The ocular manifestations of HIV infection are quite diverse: the virus can affect all tissues of the eye - from the eyelids to the optic nerve. Most often, patients experience dry eye syndrome, retinal microangiopathy and cytomegalovirus retinitis. Retinal microangiopathy is observed in 25-92% of patients with HIV infection: upon examination, small pinpoint hemorrhages of the retina and damage to the nerve fibers are observed (areas of necrosis, which are visible in the form of “lumps of cotton wool” when examining the fundus). Presumably, this retinopathy develops as a result of the interaction between viral antigens and the body's antibodies, which circulate in the blood and are then deposited in the tissues of the eye. The formation of superficial and deep retinal hemorrhages, retinal pervasculitis and occlusion of retinal vessels is also possible.

Infectious lesions eyes with HIV infection is usually associated with the development of opportunistic infections. Clinical manifestations Diseases and treatment will depend on what infection caused the pathological process. Opportunistic eye infections more often caused by pathogens such as cytomegalovirus, treponema pallidum(syphilis), toxoplasma (toxoplasmosis), mycobacterium tuberculosis (tuberculosis), herpes virus. Besides specific treatment pathogen that caused the opportunistic infection, patients are treated for HIV infection. Treatment is usually individualized based on symptoms, pathogen levels, and CD4+ T cell count. As a rule, a highly effective antiretroviral combination of three drugs (AIDS cocktail) is prescribed.

With the development of cytomegalovirus uveitis and iridocyclitis, the most frequent lesions In case of HIV infection, anticytomegalovirus drugs (ganciclovir, foscarnet) are prescribed together with the AIDS cocktail. As the immune system improves and the level of CD4+ T-lymphocytes increases, anticytomegalovirus drugs can be discontinued.

The well-known AIDS, or acquired immunodeficiency syndrome, is the final terminal stage HIV infections. According to World Organization healthcare since 1981 of this disease More than 50 million people died.

HIV-infected patients are present in all countries of the world.

Historical summary

The disease became known in 1981. Main scientific reports There were 2 articles on AIDS that described strange cases of pneumonia of pneumocystis etiology, as well as Kaposi's sarcoma in homosexual male patients. The term AIDS was only coined in July 1982.

What is HIV infection?

It is a slowly progressive disease that gradually destroys the immune system. As a result, the patient’s body becomes highly susceptible to various opportunistic and even saprophytic flora, which cause fatal pneumonia.

Epidemiology

The source of infection is a sick person and a virus carrier. In a sick person, the virus is present in all tissues and secretions, even in breast milk and saliva, urine and sweat. The role of each secretion is different in the infection process. Broadcast HIV infection carried out by the most common routes – sexual and parenteral.

The virus is an RNA-containing microorganism belonging to the group of lentiviruses, which contribute to the latent and slow course of the disease. There are 4 types of viruses:

1. HIV-1 is the more common form. This virus has caused a worldwide epidemic. Thus, it is very virulent and dangerous;
2. HIV-2 is less common and therefore less virulent. It can most often be found in West Africa;
3. HIV-3 and HIV-4 are rare and do not cause an epidemic.

If we talk about what's going on HIV infection, must mean HIV-1.

Features of the virus

It is not stable in external environment. Its inactivation occurs at 56 degrees Celsius for half an hour, and at 100 degrees for 1 minute. Any disinfectant destroys the virus. The virus can survive in dry semen for 24 hours.

HIV is an immunotropic microorganism, but it also has a neurotropic effect. Damage to the nervous system is one step lower than damage to the immune system.

Damage to the ocular analyzer

Viral eye injuries manifest as diseases of the back and front of the eye. Diseases of the anterior part of the eye include tumors, changes in the microvasculature of the conjunctiva, various infections. Diseases of the back of the eye are retinopathy, which is associated with HIV (cotton wool-shaped lesions, lack of blood movement in the capillaries, telangiectasia), infectious diseases, primary lymphoma.

Exudate occurs in half of patients and is an early sign of infectious retinopathy in AIDS. Exudate inherently represents necrosis nerve structures. It appears due to ischemia of individual areas. Such signs should be separated from exudate and foci of ischemia of cytomegalovirus infection. When exposed to cytomegalovirus, all morphological manifestations are larger and the lesions are larger.

More common are hemorrhages that are located in various layers of the retina. With AIDS in many scientific works and articles describe microaneurysms, telangiectasia, neovascularization of the optic discs, and ischemic zones.

In addition, damage to the optic discs occurs non-infectious are much less common than non-communicable diseases retina. This pathology is manifested by neuropathy, optic nerve atrophy, and swelling of the optic disc.

Among tumors, lymphoma can be distinguished, which is more common. Kaposi's sarcoma causes metastases to the brain.

In patients with AIDS, there are features of the clinical manifestation of uveitis compared to patients without immunodeficiency states. For example, in ordinary patients with normal immune system Uveitis of one eye occurs. Patients with AIDS more often suffer from a bilateral process, the course of which is more severe. Such patients respond less well to therapeutic measures. The effect occurs in the 3rd week of treatment.

CMV infection and AIDS

The occurrence of uveitis in HIV-infected patients mainly occurs due to exposure to several opportunistic infections. Wherein treatment of HIV infection led to a decrease in the incidence of CMV infection.

CMV retinitis was described already in 1982 and was diagnosed in individuals with a critically reduced number of T lymphocytes.

CMV causes the formation of necrosis in the fundus. The infection spreads hematogenously and often manifests itself as vasculitis of the optic discs or retina.

When symptoms are relieved, foci of atrophy form with deposits small quantity pigment.

Treatment of this infection is carried out quite successfully with ganciclovir and foscarnet, however, due to the possibility of recurrence, patients should be observed by an ophthalmologist. For greater effect, drugs are often administered intravitreally, that is, into the vitreous body. The disease can become generalized.

With absence antiviral therapy The life expectancy of patients with retinitis and AIDS is significantly reduced.

Toxoplasmosis and AIDS

Retinitis with necrosis is also caused by toxoplasmosis infection. Characteristic feature retinitis of this etiology is damage to the deep layers of the retina and the release of exudate into the vitreous body in the form of a mushroom cap. This retinitis is treated with perimethamine, clindamycin, azithromycin and clarithromycin.

Eye damage in AIDS can manifest as diseases of both the anterior and posterior segments of the eye. Lesions of the anterior segment of the eye include (1) tumors of the periocular tissues, (2) microvascular changes in the conjunctiva, (3) various infections. Lesions of the posterior segment of the eye are manifested by (1) AIDS-associated retinopathy (non-infectious retinopathy) and (2) infectious diseases, (3) primary lymphoma.

TO AIDS-associated retinopathy include cotton-wool spots, microaneurysms, telangiectasia, lack of capillary perfusion (ischemic zones). These microvascular changes are the most common manifestation of retinal damage in AIDS and occur in approximately 70% of patients.

Soft exudate is present in 50–60% of AIDS patients and is one of the earliest and most persistent manifestations of non-infectious retinopathy in AIDS. Morphologically, soft exudate represents necrosis or necrobiosis of nerve fibers, which occurs due to occlusion of precapillary arterioles. It should be differentiated from cytomegalovirus lesions, which, as a rule, have larger size, confluent in nature, greater depth, tends to progress and does not disappear as quickly as soft exudate. Hemorrhages are less common than soft exudate, and can be located in different layers of the retina, as a result of which their shape is different.

Telangiectasia, microaneurysms, ischemic zones, neovascularization of the optic disc, confirmed by fundus fluorescein angiography, have been described in AIDS. There are reports of the development of central retinal vein thrombosis and occlusion central artery retina.

Non-infectious lesion of the optic nerve head It is much less common than retinal damage and is manifested by papilledema, anterior ischemic optic neuropathy, and optic nerve atrophy. The appearance of congestive optic disc is usually a consequence of increased intracranial pressure for tumors of the central nervous system. Among the most common tumors of the central nervous system is lymphoma. There are reports of Kaposi's sarcoma metastasizing to the brain.

Infectious lesions of the posterior segment of the eye in patients with AIDS have their own characteristics compared to persons in whom uveitis occurs without immunodeficiency. So, if in people without immunodeficiency infections usually lead to disease in one eye, in patients with AIDS both eyes are often affected and the process is much more severe. These patients respond less well to therapy, and the effect of its administration should be expected by the end of the 2nd or even 3rd week from the start of treatment. Often, despite therapy, inflammatory process inflammation continues or relapses occur. It is also possible for combined infections to occur in one eye. Uveitis in patients with AIDS is caused mainly by opportunistic infections, and the leading place among them is occupied by cytomegaloviruses (CMV).

Typically, CMV retinitis occurs in individuals with a CD4+ lymphocyte count of 50/μL or less. However, even with 200/μl CD4+ lymphocytes, CMV retinitis can develop. According to Ai E. (1998), when the level of CD4+ lymphocytes is below 50/μl, CMV retinitis occurs in 42% of patients, at 51–100/μl – in 26% and at 101–250/μl – in 15%. Based on this, it is intended to carry out preventive examinations fundus with a CD4+ lymphocyte level of 50/μl every 2–3 months, 50–250/μl – every 3–4 months. and 250–500/µl – every 5–6 months. CMV infection causes characteristic changes in the fundus due to the fact that the virus has a necrotizing effect. Multiple infiltrates appear in the retina white, resembling soft exudate and merging with each other. The lesions spread along the vessels or nerves and have the shape of a line, arch or triangle. Hemorrhagic activity may be pronounced, but sometimes absent. The spread of infection occurs hematogenously or in the form of “satellites” near old foci. It is possible to develop serous retinal detachment in the macular zone or the entire retina. Along with serous detachments, breaks can form in the area of ​​retinal necrosis, which can be quite difficult to diagnose due to pronounced thinning of the retina. It should also be remembered that exudation may be accompanied by proliferation, which leads to tractional retinal detachments. There are known cases of CMV infection in the form of vasculitis of the retina or optic nerve head. The severity of vitreous exudation depends on the activity of inflammation in the membranes of the eye and ranges from 1+ to 2+. As inflammation in the area subsides former inflammation atrophic foci with slight pigment deposition are formed. Cytomegalovirus infection is treated with ganciclovir 5 mg/kg intravenously every 12 hours for 2–3 weeks, followed by a daily single intravenous administration of the drug or 1.0 g orally 3 times a day. as maintenance therapy. Foscarnet is also prescribed at 60–90 mg/kg 2 or 3 times a day. The duration of treatment with these drugs depends not only on the relief of changes in the fundus, but also on the viral load and the number of CD4+ lymphocytes/μl, and the indicators of the latter, in turn, are directly dependent on the effectiveness of antiretroviral therapy. In order not to miss relapses of CMV retinitis, these patients should be under constant supervision of an ophthalmologist. In case of intolerance to systemic therapy, as well as with unilateral lesions, it is possible to administer the drug intravitreally: 0.2 mg of ganciclovir in 0.1 ml isotonic solution sodium chloride 2-3 times a week (Ussery F.M. 3rd et al., 1988). Young S., et al. (1998) reported successful intravitreal administration of a higher dose of ganciclovir (2 mg/0.1 ml). Foscarnet 1.2–2.4 mg in 0.1 ml of isotonic sodium chloride solution is also administered intravitreally 2–3 times a week (Everett A., 1997). If resistance to ganciclovir and foscarnet occurs, cidofovir (20 mcg/0.1 ml) is prescribed intravitreally once every 5–6 weeks (Rahhal F.M., et al., 1996). To maintain a longer-term effect of therapy (up to 6 months), an implant is inserted into the vitreous body containing gradually released antiviral drug. To the disadvantages this method include the risk associated directly with the intervention, involvement in infectious process the other eye and generalization of CMV infection. Primary prevention carried out with ganciclovir 1.0 g orally 3 times a day. if there are antibodies to CMV in the blood, CMV DNA ( PCR method) and CD4+<50/мкл.

CMV infection accounts for 40% of the decrease in visual function in AIDS. The second common cause of decreased vision is complicated cataracts. It has been noted that the survival of patients with CMV retinitis and AIDS is reduced if they do not receive antiviral therapy or if they develop CMV resistance to antiviral agents. In turn, drug resistance appears more often the longer AIDS patients live.

Toxoplasmosis infection may also cause necrotizing retinitis. In contrast to immunocompetent individuals, with AIDS there are many foci in the fundus, both eyes are affected. Toxoplasmosis retinitis is characterized by the onset of the disease with damage to the inner layers of the retina and the release of exudate into the vitreous body in the form of a “mushroom cap”. This distinguishes it from other forms of necrotizing retinitis. Then the inflammatory process affects the deeper parts of the retina and choroid. When inflammation resolves, atrophic foci with coarse pigment deposits form in this area. Sometimes inflammation can occur in the form of exudative retinal detachment and be complicated by the development of proliferative vitreoretinopathy. Differential diagnosis is carried out with other forms of necrotizing retinitis. Laboratory diagnostics do not always give the necessary results: false negative reactions are possible. If agammaglobulinemia develops during the critical phase of AIDS, anti-toxoplasma antibodies are not detected in patients with toxoplasmosis. In the treatment of toxoplasmosis, pyrimethamine is prescribed at a dose of 50–100 per day in combination with sulfadiazine orally at a dose of 1–1.5 g 4 times a day. Clindamycin (2.4 g/day), clarithromycin (1 g 2 times/day orally), azithromycin 1.2–1.5 g/day) are also prescribed for 3–6 weeks, followed by maintenance therapy with pyrimethamine ( 25–50 mg/day) and sulfadiazine (2–4 g/day) or clindamycin (0.9–1.2 g/day). Prevention of toxoplasmosis is carried out in CD4+<100/мкл и наличии в крови антител к токсоплазме.

Patients with AIDS may develop acute retinal necrosis, which is a rapidly progressing viral disease. Acute retinal necrosis is caused by viruses of the herpetic group, and the most common of them is herpes zoster. It is believed that the virus is the trigger for the development of an autoimmune process directed against rods and cones, which leads to local immune complex disease and retinal vasculitis. Acute necrosis is characterized by the appearance of white lesions on the periphery of the retina, which increase in size and merge with each other. There are clear boundaries between the affected and unaffected retina. As the inflammatory process progresses, narrowing of the arteries occurs, infiltration and exudation along the vessels, “coupling” and occlusion of the retinal arteries. In some cases, paravenous “couplings” and retinal hemorrhages are observed. Swelling of the optic disc is often detected. After resorption of the exudate, retinal atrophic foci are detected, retinal necrosis with the formation of giant breaks and subsequent retinal detachment, which occurs in 50–75% of cases and develops within 1 to 3 months from the onset of the disease. The presence of occlusive retinal vasculitis can lead to the emergence of ischemic zones and the development of neovascularization of the retina and/or optic nerve head. Along with this, anterior uveitis, vitreitis, and scleritis are present. For the treatment of acute retinal necrosis caused by herpes simplex, acyclovir is prescribed IV 5 mg/kg every 8 hours for 5 days, then 200 mg 5 times a day. until clinical symptoms disappear. If the process is caused by herpes zoster, the dose of the drug is increased 3–4 times. It is possible to prescribe valacyclovir orally 1 g 2 times/day, famciclovir orally 250 mg 3 times/day. In order to stop autoimmune reactions, which play a large role in the pathogenesis of acute retinal necrosis, glucocorticoids are prescribed, but their doses depend on the level of CD4+ lymphocytes.

Among other causes that cause inflammatory diseases of the eye in AIDS, one can name candida, mycobacteria, plasmacysts, cryptococci, etc. It should be especially emphasized that in patients with AIDS, systemic manifestations of infection may be leading in the lesion, therefore, in most cases, the doses of prescribed drugs are consistent with infectious disease specialists. It must be remembered that ocular manifestations are often the primary manifestation of AIDS, therefore, when determining the etiology of uveitis, HIV infection must be excluded.

Acquired immunodeficiency syndrome (AIDS) is one of the most dangerous outcomes of HIV infection. Mortality most often develops as a result of a complete decrease in immunity and, as a consequence, the addition of a secondary infection. All systems and tissues are affected to the same extent, but one of the most frequently affected organs in HIV is the eyes.

During the acute period of the disease, the eyes are rarely affected. The peak incidence is observed in the chronic stage of the disease, that is, approximately 4-6 months after infection. How does HIV affect vision?

Causes of eye damage due to HIV

Eye pathology is usually observed as a result of the addition of an infectious process, some neurological or tumor pathologies.

AIDS and HIV in ophthalmology manifest themselves both in the form of “neoplasms” and in the form of decreased or loss of vision. What are the main causes of visual impairment due to HIV?

First of all, with the development of AIDS, the appearance of specific “lumps of cotton wool” is observed, which are determined in the patient’s eyes during ophthalmoscopy. They develop as a result of the progression of the ischemic process and the death of the nerve fibers of the retinal layer. They can disappear on their own, but most often persist throughout the rest of their lives. They are usually caused as a result of decreased blood flow through the vessels of the cornea.

Pain syndrome with HIV

Many patients suffering from this disease often ask the question: do their eyes hurt with HIV infection? As already mentioned, most often with AIDS secondary processes develop that significantly worsen the patient’s life. Pain syndrome often occurs, which may indicate the development of tissue necrosis of the organ of vision or thrombosis of the vessels supplying it. With HIV, the eyes hurt as a result of the spread of an infectious disease such as herpes zoster, or rather its ocular form.

Pain develops due to damage to nerve fibers located in the cornea and sclera. In this case, patients complain of blurred vision and pain in the eyeballs. Loss of vision in HIV is possible as a result of bilateral retinal detachment or its complete destruction by fungal mycelium or soaking in blood.

Changes in eye color with HIV

Visually, there may be a change in the color of the sclera or, which is extremely rare, the iris. Yellow eyes in HIV are usually a symptom of liver damage. Because of this, difficulties arise in diagnosing the disease that provoked the change in color. An immunological study is necessary to more accurately verify the virus. In the later stages of AIDS, both of these diseases can occur. The addition of hepatitis indicates an unfavorable outcome for the patient.

A change in color is also possible with the development of iridocyclitis (most often of an infectious nature). In this case, the iris acquires a reddish tint due to the presence of small hemorrhages in it or is destroyed (typical of mycotic eye damage). On the Internet you can find a fairly large number of photos of the eyes of patients with HIV infection. In some cases, only the initial manifestations of the disease (cotton wool flakes) are visible; in more advanced patients, destruction of the eyeball, as well as the tissues adjacent to it, can be observed.

Timely diagnosis of infection, as well as adequately selected antiretroviral therapy, can delay the development of secondary diseases, including blindness, for a fairly long period. That is why, if patients value their vision, they should not be ashamed of their diagnosis and seek help from a qualified infectious disease specialist or ophthalmologist as soon as possible.

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HIV infection today is widespread throughout the entire Earth. AIDS is called acquired immunodeficiency syndrome, which is the last, terminal stage of HIV - the human immunodeficiency virus. According to the World Health Organization, over the past 35 years, about 50,000,000 people have died from AIDS in the world.

The world community first learned about AIDS in 1981, when two male homosexuals were diagnosed with pneumonia of Pneumocystis etiology and Kaposi's sarcoma. And exactly one year later, scientists gave a “name” to this unfortunate deadly disease of the 20th century, calling it AIDS.

As we have already said, AIDS is caused by HIV infection. HIV infection, when entering the human body, begins to slowly develop and gradually and irrevocably destroy the immune system, making a person highly susceptible to any diseases, opportunistic flora, and even naturally beneficial (saprophytic) microorganisms, which cause death.

How HIV enters a healthy human body or ways HIV transmission?

For a healthy person to become infected with HIV, even a short contact with the biological fluids of a sick person or a carrier of the infection is enough. In people who are both carriers and patients, the virus is present in all body secretions, for example, in saliva if there is tissue damage, and, of course, in blood and sexual secretions. But each biological fluid acts differently, that is, the degree of infectiousness of each individual biological fluid depends on the concentration of the pathogen at a given moment in that fluid.

HIV infection is transmitted parenterally (through blood) and sexually.

HIV is a microorganism containing RNA and belongs to the group of lentiviruses, and they are provocateurs of a latent (slow) ongoing pathogenic process.

Types of HIV:

1. HIV-1. It is the most common form of HIV infection. It was this virus that caused the epidemic throughout the world. It has a high degree of variability and danger.
2. HIV-2. It is not so widespread and has less virulence (variability). Most of all it is found and recorded in West Africa.
3. HIV-3, like HIV-4, is rare and cannot cause epidemics.

So the phrase " HIV infection» should immediately indicate HIV-1 infection.

What are the characteristics of HIV?

One of the main, and one might say, important features of HIV is its instability to the external environment. In the external environment, it begins to deteriorate already at 55 degrees Celsius and after half an hour in such conditions it dies. And if it is placed in a 100-degree temperature, then its decay period will be one minute. Also, any disinfectant has a detrimental effect on HIV infection. But HIV can survive in dry semen for 24 hours.

Another important feature of HIV is its penetration into the nucleus of T-lymphocytes, where it begins to actively multiply (replicate), thereby destroying immune cells. T-lymphocytes are one of the most important parts of the immune system, as they participate in the absorption (phagocytosis) of pathogenic microorganisms. So their destruction leads to a total “revelry” of representatives of atypical flora.

Diseases caused by HIV infection and which are signs of HIV infection can be divided into several groups:

Although HIV infection lives by “eating” immune cells, its diet also includes cells of the nervous system. The immunotropic effect of HIV infection is only an order of magnitude higher than the neurotropic effect.

Damage to the organ of vision due to HIV

Eye disease in HIV is characterized by damage to the front or back of the eye. Diseases of the anterior part of the eye include: changes in the microvasculature of the conjunctiva, tumors and infections. Diseases of the back of the eye include retinopathy, infectious lesions and primary lymphoma.

The appearance of exudate in some patients becomes the first and early sign of AIDS-associated retinopathy. It results from necrosis of nerve tissue and is associated with ischemia of some areas. Differential diagnosis of AIDS-associated retinopathy is carried out with ischemia due to cytomegalovirus infection. Cytomegalovirus is characterized by a more pronounced course with larger morphological signs and lesions. Most often, doctors encounter hemorrhages located in different layers of the retina. AIDS-associated retinopathy is also accompanied by microaneurysms, telangiectasis, optic disc neovascularization, and ischemic areas.

Also, most often in AIDS there are cases of non-infectious lesions of the optic discs, which manifest themselves in the form of optic nerve atrophy, neuropathy and optic disc edema.

Tumors of the organ of vision in AIDS are represented by lymphomas. And metastasis occurs with Kaposi's sarcoma.

As for the disease called uveitis, in HIV-infected people it usually manifests itself in both eyes at the same time, unlike people who do not suffer from immunodeficiency. And the course of uveitis in HIV patients is much more severe, and the response to treatment is weaker, with the effect appearing only after three weeks.

Cytomegalovirus (CMV) and AIDS

HIV-associated uveitis occurs under the influence of certain types of infections (opportunistic), resulting from decreased immunity in HIV, and which almost never occur in healthy people. Treatment of HIV infection led to a decrease in cytomegalovirus infection.

Retinitis caused by cytomegalovirus was first described in 1982, when it began to be diagnosed in people with critically compromised immunity. Cytomegalovirus causes fundus necrosis. The spread of infection occurs through the blood (hematogenous transmission) and often manifests itself as vasculitis of the optic discs and retina.

When the symptoms stop, slightly pigmented deposits form on the atrophic foci.

This disease is treated with foscarnet and ganciclovir and is quite successful. But given the immunological status of patients and the high degree of relapse, observation by an ophthalmologist is extremely necessary for them. The greatest effect of treatment is obtained if medications are injected directly into the vitreous body, that is, intravitreal. It is not uncommon for the disease to progress to a generalized form.

If antiviral therapy is not carried out, the life of patients with retinitis and AIDS is sharply reduced.

Toxoplasmosis in AIDS

Toxoplasma gondii is also a provocateur of retinitis. AIDS-associated toxoplasmosis is characterized by damage to the deep layers of the retina, in which exudate is released into the vitreous body in the form of a mushroom cap. Treatments for AIDS-associated toxoplasmosis include clarithromycin, perimethamine, clindamycin, and azithromycin.

Acute retinal necrosis in AIDS

This is a fairly common disease in AIDS. It is characterized by acute retinal necrosis and the appearance of individual lesions, which subsequently merge into one large lesion with clear boundaries. There are cases when swelling and hemorrhage are noted. Subsequently, acute retinal necrosis develops into occlusive vasculitis, and after this, areas with ischemic changes in the retina appear.

But this is not the only HIV-associated eye disease. Scleritis, vitreitis and uveitis also exist.

Retinal necrosis is caused by the herpes virus and such necrosis is treated with acyclovir.

We must understand and remember that these diseases in HIV-infected people can be the first sign of AIDS. Therefore, every doctor should potentially perceive patients as HIV-infected and warn themselves against the danger of infection.

General practitioner at a city clinic. Eight years ago I graduated from Tver State Medical University with honors. I decided not to stop there and am currently specializing in cosmetology and massage courses. Rate this article:

Good evening. My diagnosis is HIV (made on 10.2012) stage 4b ​​(CD4-109 BN-155000) + hepatitis C. CD 4-220 VN is not detected. Therapy - Kivexa + Kaletra (2 years). When registering, only candidiasis was detected; no other diseases were identified. At the beginning of February 2015, I had a head injury in the left temporal region without loss of consciousness and I did not pay attention to the injury at all. I didn’t see a doctor right away. There has been an increase in headaches and double vision (I have astigmatism). A month later, a difference in my pupils appeared that was not there before (the left one did not dilate, or dilated but weakly compared to the right one). The neurologist prescribed gliatilin based on the results of Doppler and MRI. I drink it for two weeks and the result is that the difference in the pupils is less noticeable in the light, but it still remains; in the dark it is still clearly pronounced. The pain in the superciliary part and directly under the eye itself intensified. And also the area of ​​the forehead and bridge of the nose - it’s like they put an iron on it, sorry for the stupid comparison. The pain is pressing. Periodically, the vision on the left seems to fade, but then everything is fine. I don't know if this is related to the injury or not. There is also a lot of pain in the lower back, which was not there before, and it also radiates into the lower back when walking. It is the center of the lower back. And my left hand sometimes seems to be taken away and hurts a lot. Maybe I’m very suspicious and I need to forget everything about it, or this is how it should be... I don’t know, I’m just worried. Does anyone know if this could be dangerous? Below are brief extracts from the surveys conducted. Thanks if anyone responds and helps.

For quotation: Eye damage due to HIV infection // Breast cancer. 1999. No. 1. P. 10

E. Nurmukhametova

Ye.Nurmukhametova

BY MATERIALS:
Cunningham ET, Margolis TP
Ocular manifestation of HIV infection
N Engl J Med 1998;339:236-44.