Lectures on infectious diseases.
Infectious diseases Lecture 11. Professor K.A. Aitov Lecture topic: "HIV infection"
A bit of history Some 25 years ago, mankind was convinced that infectious diseases no longer pose a serious danger to the civilized world. If anything continues to threaten human health, it is cancer, cardiovascular and degenerative diseases. However, with the advent of AIDS in the early 1980s, this confidence was significantly shaken. The first AIDS patient in the world was identified in 1981. HIV AIDS
HIV. Historical Facts On July 3, 1981, The New York Times published an article announcing that 41 cases of a rare and extremely dangerous form of cancer, Kaposi's sarcoma, had been diagnosed in New York and California. The article noted that all the patients were homosexuals and that the patients were found to have mysterious impairments in their immune defenses. These were the first signs of an approaching catastrophe called "AIDS". As early as 1988, the UN General Assembly declared that the spread of HIV/AIDS had assumed the proportions of a global pandemic. The first case of HIV infection in a citizen of the USSR was identified and described by Acad. IN AND. Pokrovsky (1987). The first case of death from AIDS in the USSR was described by prof. A.G. Rakhmanova et al. (1989).
The threat of AIDS in Russia during the period of socialism was practically zero, the iron curtain, in addition to numerous shortcomings, had a huge advantage - it protected the inhabitants of the USSR from the penetration of alien, including HIV infection. After democratic changes, the country became open to the world and everything poured in here: both good and bad, and HIV infection too. The first cases of HIV infection in Russia were registered in 1987. But the real collapse of the epidemic occurred in 1999-2001, and today the spread of HIV/AIDS continues.
The history of the discovery of HIV In 1980. R. Gallo isolated a human retrovirus called HTLV (from Human T-Cell Leukemia Virus). In 1983 Luc Montagnier isolated a retrovirus from the cells of the lymph node of a homosexual with lymphadenopathy syndrome, which was already considered to be a characteristic manifestation of AIDS, it was called LAV (Lymphadenopathy-associated Virus). (Human Immunodeficiency Virus) or HIV (human immunodeficiency virus) In the study of blood sera of patients who died from an unknown disease in 1959, 1969, 1976. HIV was isolated. Luc Montagnier Pasteur Institute, France Robert Gallo US National Cancer Institute
ETIOLOGY HIV is a family of retroviruses, a subgroup of lentiviruses or "slow" viruses. Dimensions nm (1/10000 mm). Thousands of virions are located per 1 cm. The rate of virus replication is particles per day. HIV protein group - 1 North America, Western Europe, Australia HIV - 2 Africa HIV - 3 Virus envelope proteins gp160, gp120, gp41 gp140, gp105, gp36 Developed by transfusion of imported contaminated blood or contact with an infected person infected in another region Core proteins p55, p24, p17p56, p26, p18 Virus enzymesp66, p51, p31p68
Site of action NNRTI (Block HIV replication by binding to RT and blocking DNA synthesis from viral RNA) HIV RNA core Reverse transcriptase XXXXXXXXXXXXX DNA XXXXXXXXXXX CD4 VVVVVV protease HIV RNA actions of PIs (They block the assembly of viral particles and their release from CD4 cells) HIV REPLICATION © К.А. Aitov, 2007 CD4 cell Provirus
Life cycle of HIV Binding by gp120 I. Fusion by gp41 Ia. Entry into the cell with the formation of structural proteins of new viral particles II. Transcription - in the cytoplasm of the cell, the transformation of viral RNA into DNA III is carried out. Integration The new HIV DNA is transported into the cell nucleus and integrated into the DNA of the IIa host cell. Synthesis of copies of RNA (mRNA) V takes place on the DNA template of the provirus. Budding The virus buds, surrounded by a “patch” of the host cell membrane (gp120), which determines the ability of HIV to infect new cells IV. Replication Long chains of proteins and enzymes are cleaved by protease into smaller ones, forming mature viral particles.
Peculiarities of the HIV/AIDS epidemic in Russia characterized by a high incidence of risk groups and an increase in morbidity among the general population, a real threat to the socio-economic development of the country. Intravenous drug use remains the leading factor in HIV infection, which is primarily due to the development of the drug addiction epidemic in our country Among the infected, 70-80% are young people over the age of years Since 1999, there has been an increase in sexual transmission and the active involvement of women in the HIV epidemic\ AIDS, as a result - an increase in the birth of children from HIV-positive mothers
Stages in the development of the HIV epidemic in the Russian Federation (years) The emergence of primary cases of HIV infection and local outbreaks of nosocomial infection among children in (Elista, Rostov-on-Don, Volgograd). “Pseudo-calm period” (years), when a small number of HIV infections were diagnosed. The period of rising incidence, when in 1996 the rapid spread of HIV infection among people who use drugs intravenously began and continues to this day. The spread of HIV infection among drug users, against the background of promiscuity, leads to the transition of the epidemic to other groups of the population, mainly through heterosexual contacts.
The number of HIV infections per 100,000 people in the Russian Federation
HIV: statistics for the Russian Federation As of February 31, 2005, more than 333.5 thousand HIV-infected people were registered in Russia, of which 12.9 thousand were children. More than 7.5 thousand Russians have died from AIDS. In the Irkutsk Region, 20.5 thousand HIV-infected people were registered, 868 people died, three of them in 2005. More than 1.5 thousand children born from HIV-positive mothers are registered in the region. 221 children were diagnosed with HIV. More than 100 new Russians infected with HIV are detected in Russia every day. More than 100 new Russians infected with HIV are detected daily in Russia.
The epidemic situation of HIV infection in the Irkutsk region in the city Cumulatively registered - HIV cases (780.4 per 100 thousand population) Total number of children born from HIV-infected mothers - 1407, incl. in 2004 - 413 people. Died HIV-infected cumulatively - 822, incl. in 2004 - 185 people. AIDS patients died cumulatively - 26 people, incl. in 2004 - 3 people. Patients in the AIDS stage cumulatively - 30 people, incl. in 2004 - 5 people. The leading places in terms of cumulative incidence are occupied by the territories: Irkutsk - 1352.8 per 100 thousand population, Usolye-Sibirskoe - 792.4 per 100 thousand population, Sayansk - 779.3 per 100 thousand population. GUIN institutions - 1358.5 0 / 0000
Dynamics of the incidence of HIV infection in the Irkutsk region per year (by gender)
Dynamics of HIV transmission routes in the Irkutsk region over the years.
HIV. Routes of transmission SEXUAL: unprotected SEXUAL: unprotected (without a condom) penetrating sexual contact, both homosexual and heterosexual. PARENTERAL: sharing or reusing use use PARENTERAL: sharing or reusing syringes, needles and other injecting equipment; - use of non-sterile instruments for tattoos and piercings; - use of other people's shaving accessories, toothbrushes with blood residues; VERTICAL: transmission of the virus VERTICAL: transmission of the virus from an HIV-positive mother to her child - during pregnancy, childbirth and breastfeeding. In the presence of infections In the presence of sexually transmitted infections, the risk of HIV transmission through sexual contact increases by 2-5 times. The presence of infections is especially dangerous! The presence of sexually transmitted infections (STIs), accompanied by the occurrence of open sores (for example, herpes), is especially dangerous!
HIV is not transmitted: - by shaking hands or hugging; - through sweat or tears; - when coughing and sneezing; - when using shared dishes or bed linen; - when sharing a bath and/or toilet; - when playing sports together; - in public transport; - through animals or insect bites; - with a kiss / through saliva. HIV is not transmitted by kissing, since the concentration of the virus in saliva is not enough for infection.
HIV: Expert Opinion (G. Onishchenko, 2006) In June 2006, on the pages of Rossiyskaya Gazeta, ch. state dignity. Russian doctor Gennady Onishchenko said: “Most HIV-positive Russians do not yet experience serious symptoms of the disease. Many are not even aware of their "status", and in the absence of symptoms do not seek additional information, medical assistance. Nevertheless, according to Gennady Onishchenko, "in the coming decades, the epidemic could become a real threat to national security, economic development and Russia's international relations."
STRUCTURE and phases of the pathogenesis of HIV (Two types of the virus are currently known: HIV-1 and HIV-2 (West Africa) 1st phase. Penetration of HIV into the human body, damage to target cells; 2nd phase. Viremia; Phase 3. Progressive damage to immunocompetent cells; 4th phase: Deepening of immunodeficiency, development of opportunistic infections or oncological diseases; 5th phase. Terminal phase leading to death of the patient. Total immunodeficiency.
HIV: The pathogenesis of HIV selectively affects helper T-lymphocytes, macrophages and monocytes. The normal ratio between them and suppressors, cytotoxic lymphocytes, equal to the norm of 1.5-2.0, becomes less than 1.0. Immunity is broken. There is immunodeficiency. Opportunistic infections are activated: fungi (Cand. albicans, Pneumocysta carinii, etc.), viruses (CMV, herpes virus), bacteria (strepto-, staphylococci, etc.). In addition, there is an active production of autoantibodies, and not only to HIV-affected cells. Also, HIV can be in a dormant state and not activated for a number of months and even years (up to 10 years).
HIV: pathogenesis Free protein gp 120 can bind to the CD4 receptor of uninfected T4 lymphocytes, while both infected and uninfected lymphocytes are recognized by the immune system as foreign and destroyed by T-killers. The reason for the death of CD4 cells can be biologically active substances - cytokines secreted by HIV-infected macrophages: TNF, IL-1. In addition, HIV-infected T-helpers acquire the ability to form massive clusters - SYNTICIA, resulting in a sharp decrease in their number. Other mechanisms for reducing the number and function of T4 lymphocytes are also being studied. HIV-infected T4 cells cannot carry out their immune function, and, consequently, B cells stop synthesizing specific antibodies.
Russian classification of HIV infection (V.I. Pokrovsky, 2001) 1. Stage of incubation 2. Stage of primary manifestations, course options: -2A. Asymptomatic – 2B. Acute HIV infection without secondary disease. -2V. Acute infection with secondary diseases. 3. Latent stage 4. Stage of secondary diseases, course options: -4A. Less than 10% weight loss; recurrent infections. -4B. Weight loss over 10%; organ damage; localized Kaposi's sarcoma. -4V. cachexia; damage to the central nervous system of various etiologies. 5. Terminal stage
Class Sub-class Category Criteria P-O -- Undifferentiated (undetermined) infection P-1 -A-A ---- Asymptomatic infection B- Impaired immune status C- Immune status not studied Classification of HIV infection in children (WHO, 1987) .) P-2 Manifest infection A- Two or more "non-specific" signs of HIV infection B- Progressive diseases of the nervous system C- Lymphoid interstitial pneumonias D- 1 Secondary infections associated with HIV immunodeficiency D2D2 Severe recurrent bacterial infections D3D3 Other infections EE1E1 AIDS indicator tumors (lymphoma, KS, etc.) E2E2 Other tumors possibly associated with HIV F Other disease states, possibly secondary to HIV infection: hepatitis, cardiopathy, nephropathy, anemia, thrombocytopenia, skin diseases
HIV: clinic The incubation period for HIV infection is usually 2-3 weeks, but can be delayed up to 3-8 months, sometimes more. Following it, 30-50% of infected people develop symptoms of acute HIV infection, which is accompanied by: fever (96%), lymphadenopathy (74%), erythematous-maculopapular rash on the face, trunk, sometimes on the extremities (70%), myalgia and arthralgia (54%). Less common are other symptoms such as diarrhea, headache, nausea and vomiting, hepatosplenomegaly. Neurological symptoms occur in about 12% of patients and are characterized by the development of meningoencephalitis or aseptic meningitis, etc. The stage of persistent generalized lymphadenopathy (PGL) lasts quite a long time - 5-8 years. (gradual decrease in CD4 cells - cells of one mm 3 per year. At these stages, patients do not go to doctors, because nothing bothers them.
HIV: clinic Following these stages (2-3 years), the symptomatic chronic phase of HIV infection begins, which is characterized by various infections of a viral, bacterial, fungal nature, which still proceed quite favorably and are stopped by conventional therapeutic agents. There are repeated diseases of the upper respiratory tract - otitis media, sinusitis, tracheobronchitis, etc., superficial skin lesions - the mucocutaneous form of recurrent herpes simplex and herpes zoster, candidiasis of the mucous membranes, dermatomycosis, seborrhea, etc. Then these changes become deeper, do not respond to standard methods of treatment, acquire a stubborn, protracted character. A person begins to lose weight, weight loss is more than 10%, fevers, night sweats, diarrhea appear. Against the background of increasing immunosuppression, severe progressive diseases develop that do not occur in a person with a normal immune system - AIDS-indicator diseases.
FEATURES OF HIV INFECTION IN CHILDREN Faster rates of disease development than in adults Acute onset of the disease more often than in adults High frequency of recurrent severe bacterial infections (otitis media, sinusitis, impetigo, cellulitis, urinary tract infections) Frequent incidence of acute respiratory infections Delayed HIV encephalopathy psychomotor and physical development due to brain damage (50-90% of cases) Lymphadenopathy, hepatolienal syndrome Interstitial lymphoid pneumonia - 14-35% Increase in heart size, arrhythmias, ECG changes - 32% Rare tumors, especially Kaposi's sarcoma Rapid weight loss Itching of the skin , rash, parotitis Hyperplasia of the pulmonary lymph nodes Anemia, thrombocytopenia with hemorrhagic syndrome (can be fatal) Intrauterine infection, the prognosis is unfavorable. Infection at the age of over 1 year is prognostically more favorable than in adults.
Candidiasis of the skin of the hand Often combined with oropharyngeal candidiasis The skin in the area of the folds is affected - "diaper" dermatitis In children 2-6 years old, chronic candidal paronychia occurs Treatment: local, if ineffective - systemic antifungal therapy
Dermatophytosis FORMS: -dermatomycosis of smooth skin (tinea corporis); – inguinal ringworm (tinea cruris); – dermatomycosis of the feet (tinea pedis); – onychomycosis (tinea unguium); – tinea capitis TREATMENT: – topically: miconazole or ketoconazole (cream) – stable forms: ketoconazole 6 mg/kg for 1-2 doses, itraconazole 100 mg, griseofulvin mg/kg orally – onychomycosis: itraconazole 100 mg x 2 times a day / 1 week per month 2-4 months
Varicella zoster virus Shingles - there may be extensive lesions followed by scarring, generalization of infection. Treatment: in non-immunosuppressed children, aciclovir 20 mg/kg orally x 4 times daily If immunosuppressed, trigeminal nerve involvement, or multidermatomal lesions present, aciclovir 10 mg/kg iv x 3 times daily
Drug rash While taking antibacterial drugs, especially sulfonamides, as well as NNRTIs and PIs Often morbilliform, macular, maculopapular rash, accompanied by itching Less common - urticaria, Stevens-Johnson syndrome, toxic epidermolysis bullosa
HIV: diagnosis The fact of infection after contact with the virus can be established after 25 days - 3 months (in some cases up to six months) using a special test - a blood test that detects antibodies to the virus. The period between the entry of the virus into the body and the formation of antibodies to it in the blood is called the “window period”.
PCR Used for rapid diagnosis of the acute period of HIV infection (detection in the blood) ENZYME IMMUNE ASSAY (ELISA) Repeat. ELISA positive. Rep. ELISA - negative. IMMUNOBLOT PositiveNegative HIV (+) HIV (-) © К.А. Aitov, 2007 ELISA is screening
HIV: Diagnosis PCR (HIV RNA) is used to diagnose acute HIV infection. The main method of laboratory diagnosis of HIV infection is the detection of antibodies to HIV using ELISA - it is screening (in the case of a + result, the analysis is performed twice with the same serum. Upon receipt). Antibodies to HIV appear 1-3 months after infection in 90-95% of those infected. In 5-9% - after 6 months. and 0.5 - 1% - at a later date. The diagnosis of HIV infection is established on the basis of epidemiological, clinical, laboratory data, indicating the stage, deciphering secondary diseases.
PRINCIPLES OF TREATMENT of patients with HIV infection I. Etiotropic antiretroviral therapy. II. Prevention of opportunistic diseases, their timely treatment. III. Pathogenetic therapy aimed at restoring the morphofunctional state of the affected organs. IV. Diet, balanced in proteins, fats, carbohydrates, rich in vitamins. V. Favorable psychological regimen VI. The scope of therapy pp. I, II, III is determined by the stage of the disease, the presence of opportunistic diseases, the nature of the damage to individual organs and systems
GLOSSARY: CD4 cells are the cells that HIV infects. The CD4 cell count gives an indication of the state of the immune system: if the number of cells is reduced, then the immune system is damaged. Combination therapy A combination of at least three ARVs that reduces the amount of HIV in the body. PI protease inhibitors. A group of antiretroviral drugs that inhibit the reproduction of HIV. Included in combination therapy. NRTI nucleoside reverse transcriptase inhibitors. A group of antiretroviral drugs. Included in combination therapy. NNRTI non-nucleoside reverse transcriptase inhibitors. A group of antiretroviral drugs. Included in combination therapy.
Antiretroviral treatment What is ART? Medicines used to treat HIV are called antiretroviral drugs (ARVs). They were developed in order to act on the virus and preserve the immune system of patients. HAART is a highly active antiretroviral therapy that involves the simultaneous use of a combination of three or more antiretroviral drugs and is the standard treatment for HIV infection. Does ARV therapy cure HIV infection? No. Today, there are no drugs that cure HIV infection. ARV drugs slow down the replication of the virus in the body. This allows you to save more CD4 cells and avoid further damage to the immune system. 69 When to start treatment? 1. There are no hard and fast rules about when is the best time to start ART. Different countries use different standards. 2.According to WHO recommendations, HAART should be started: Any patient with symptoms of AIDS (the so-called criteria for defining AIDS); Any patient with a CD4 cell count below 200 cells per cubic millimeter of blood (200/mm3); Any patient whose HIV RNA copy/mL blood level is higher than
HIV drugs HIV drug class Generic name (generic or generic) Brand name (brand name) Nucleoside reverse transcriptase inhibitors (NRTIs) AZT, zidovudine ddi, didanosine 3TC, lamivudine d4T, stavudine abacavir Retrovir Videx Elivir , Lamivir Zerit, Stavir Ziagen Non-nucleoside inhibitors arr. transcriptase inhibitors (NNRTIs) efavirenz nevirapine Stokrin, Sustiva Viramune, Nevimun Protease inhibitors (PIs) lopinavir/ritonavir indinavir nelfinavir saquinavir ritonavir Kaletra Crixivan Viracept Invirase Fortovase Norvir
According to World Health Organization guidelines and BHIVA protocols, the best option to start therapy is the following combination of ARVs: 2 NRTIs + 1 NNRTI Zidovudine + lamivudine + efavirenz Zidovudine + lamivudine + nevirapine This combination is generally recommended for people who are taking ARV therapy for the first time . 3 NRTIs Zidovudine + lamivudine + abacavir Highly recommended for people who are not sure they can take many pills a day or who for various reasons cannot use the above regimens 2 NRTIs + 1 PI Zidovudine + lamivudine + lopinavir/ritonavir Zidovudine + lamivudine + indinavir/ritonavir Zidovudine + lamivudine + saquinavir/ritonavir Zidovudine + lamivudine + nelfinavir Regimens that include PIs are the most difficult to take because of the large doses and the large number of pills that must be taken per day. Combinations with ritonavir were designed specifically to reduce the dosage and the number of tablets to be taken per day. These are called "enhanced" PI combinations.
Side effects of antiretroviral drugs During the adaptation period (first 3-4 weeks) - Headache - Nausea, vomiting, weakness, etc. - Abdominal pain - Diarrhea Side effects - Rash - Hepatotoxicity - Pancreatitis - Lactic acidosis - Hyperglycemia - Lipodystrophy, redistribution of body fat – Polyneuropathy – Anemia, neutropenia
Poor efficacy Inconsistency of effect Suboptimal pharmacokinetics Poor tolerance Inconvenience of administration Resistant Virus Drug Patient Non-adherence Side effects or inconvenience of administration Barriers to effective antiretroviral (ARV) therapy High replication rate High mutation rate - resistance Latent HIV reservoirs PHYSICIAN Testing the patient before starting therapy Selection of treatment regimen Support patient during treatment
What blood tests should be done to confirm the effectiveness of ART? viral load. This test shows the amount of virus in your blood. immune status. This test checks your CD4 count and tells you how strong your immune system is.
Regulatory framework 1. Fundamentals of the legislation of the Russian Federation on the protection of the health of citizens, adopted by the Supreme Council of the Russian Federation and signed by the President of the Russian Federation, Order of the Ministry of Health of Russia dated 170 On measures to improve the prevention and treatment of HIV infection in the Russian Federation Ministry of Health and Medical Industry of the Russian Federation (Approved by the Ministry of Justice). 3. Federal Law No. 38-FZ On Preventing the Spread of Disease Caused by the Human Immunodeficiency Virus in the Russian Federation.” 4. Federal Law of the city of 2-FZ "On the sanitary and epidemiological well-being of the population." 5. Order of the Ministry of Health and Social Development of the Russian Federation On approval of the list of medicines dated 601 Moscow. Registered in the Ministry of Justice of the Russian Federation, registration Order of the Federal Service for Supervision in Health and Social Development "On Approval of the List of Trade Names of Medicinal Products" 2578 dated Moscow.
Regulatory framework 1. Fundamentals of the legislation of the Russian Federation on the protection of the health of citizens of July 22, 1993 No. establish that any medical intervention requires informed voluntary consent of the patient. This means, inter alia, that blood sampling cannot be legally enforced. 2. An exception is made for patients whose health condition does not allow them to express their will (in this case, the decision is made by the medical council), and for adolescents under 15 years of age (the decision is made by legal representatives). 3. There are also 4 situations in which the provision of HIV test results is mandatory (but not forced - anyone can simply refuse to participate): 1) donation of blood, other biological fluids and organs; 2) when applying for a job as a medical worker or other specialist in an institution that directly processes or accepts materials known to contain HIV; 3) for foreign citizens - obtaining visas for residence in the territory of Russia for a period of more than 3 months; 4) testing of persons in places of deprivation of liberty if there are clinical indications (and in this case, the examination can be carried out only with the consent of the patient).
Prevention of HIV Specific immunoprophylaxis of HIV infection has not been developed. Preventive measures include: - examination of donors; - Examination of all pregnant women; - control of childbearing in infected women and refusal to breastfeed children.
Internal Diseases: Lecture Notes Alla Konstantinovna Myshkina
LECTURE No. 1. The subject of internal diseases, history and tasks
Internal diseases is a field of clinical medicine that studies the etiology, pathogenesis, semiotics, treatment, prognosis and prevention of diseases of internal organs.
Internal medicine is the most important section of practical medicine, covering most human diseases. The term "internal diseases" came into practice in the 19th century. and supplanted the more general term "therapy".
From the point of view of a clinician, any disease is a change in the normal functioning of the body, characterized by a violation of the functional activity of a particular system, a limitation of the adaptive, compensatory and reserve capabilities of the body as a whole and a decrease in its ability to work.
Disease is a dynamic process in which dynamism is determined by the coexistence of damage and repair reactions. The ratio between these reactions reflects the direction of the disease towards either recovery or progression. Elucidation of this direction makes it possible to assess the outcome of the disease, to predict the fate of the patient.
Diagnosis of the disease (from the Greek. diagnosis- "recognition") - a brief definition of the essence of the pathological process, reflecting the cause of its occurrence, the main mechanisms that led to the development of changes in the body, and the characteristics of these changes. Every diagnosis a physician makes is (ultimately) a differential diagnosis—a weighing of each individual symptom, evaluating and differentiating it.
In the early stages of development, medicine was not a science and was purely empirical knowledge based only on observations. For the first time, a representative of ancient Greek medicine, Hippocrates, when examining a patient, used palpation, listening, and compiled a description of many symptoms and syndromes of diseases. The doctrine of the pulse was created by the representative of the Alexandrian school Herophilus, the description of some signs of pleurisy, stomach ulcers, meningitis was presented by the Tajik scientist Abu-Ali Ibn-Sina (Avicenna).
In the XVIII-XIX centuries. questions of internal medicine were developed in detail by Auenbrugger, Laennec, G. I. Sokolsky, M. Ya. Mudrov, G. A. Zakharyin.
The scientific clinical school of internal medicine was created by S. P. Botkin, subsequently developed by many brilliant clinicians: I. M. Sechenov, V. P. Obraztsov, N. D. Strazhesko, B. E. Votchal, A. M. Myasnikov, N S. Molchanov, E. M. Tareev, V. Kh. Vasilenko, etc.
At the present stage of development of internal medicine, a great contribution was made by domestic scientists E. I. Chazov, P. E. Lukomsky, F. I. Komarov, G. I. Dorofeev, A. G. Chuchalin, A. I. Vorobyov and others.
The final diagnosis of the disease should include information about the etiology (etiological diagnosis), its pathogenesis (pathogenetic diagnosis), morphological changes (morphological diagnosis) and functional state (functional diagnosis) of the affected organ or system. The final diagnostic formula accumulates all types of diagnoses, and reflects the doctor's view of the pathological process by highlighting the underlying disease, complications and concomitant diseases. In the future, the doctor determines the direction of the development of the pathological process, possible outcomes and consequences of the disease. The assessment of all these changes is carried out as a result of observation of the patient, the use of special additional studies, the treatment used.
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Actually morbidity (primary morbidity) - the frequency of new, nowhere previously recorded and for the first time in a given calendar year, diseases detected among the population (according to statistical coupons for updated diagnoses with a “+” sign).
Prevalence (general morbidity or morbidity) - the frequency of all diseases among the population, both first detected in a given calendar year and registered in previous years, for which the patient again sought medical help in a given year (all statistical coupons for updated diagnoses).
Pathological affliction - the frequency of pathology among the population, established during one-time medical examinations (examinations), as a result of which all diseases are taken into account, as well as premorbid forms and conditions.
General morbidity (by negotiability). The unit of observation in the study of general morbidity is the primary appeal of the patient in the current calendar year for this disease.
The indicator of general morbidity is determined by the number of primary applications for medical care to medical institutions in a given year per 1,000 or 10,000 inhabitants. The overall indicator is the ratio of the number of cases per year to the total population.
Primary morbidity is the morbidity detected for the first time in life and registered during the year.
Infectious and non-epidemic morbidity (by negotiability). The incidence of infectious diseases is studied by counting each infectious disease or suspicion of it. The accounting document is an emergency notification of an infectious disease (f. -058 / y). An emergency notification is prepared for each infectious disease or suspected disease and sent to the SSES center. An emergency notice before departure is registered in the journal of infectious diseases (f. -060 / y). Based on the entries in this journal, a report is compiled on the dynamics of infectious diseases for each month, quarter, half year and year.
The incidence of non-epidemic diseases (tuberculosis, venereal diseases, neoplasms, trichophytosis, etc.) registered for the first time in a given year is calculated per 1,000,000 inhabitants (level, structure). The unit of observation in the study of non-epidemic morbidity is each patient with a diagnosis of one of these diseases for the first time in his life. Diseases are registered in dispensaries.
Methods for studying morbidity Main statistical document 1. Morbidity according to the data of appealability Coupon for registration of final (refined) diagnoses (registration form No. 025-2/u-04) Including: incidence of acute infectious diseases, food poisoning, acute occupational poisoning diseases, food poisoning, acute occupational poisoning (educational form No. 058 / y) incidence of the most important non-epidemic diseases (tuberculosis, venous diseases, cancer, etc.) Notification of the most important non-epidemic diseases (accounting forms No. 089 / y-00; s) morbidity with VUT Disability certificate hospitalized morbidity Card of a person who left the hospital (registration form No. 066 / y) /y-04). 3. Incidence by cause of death Medical certificate of death (registration form No. 106/u-84)
Morbidity with temporary disability (by negotiability). The unit of observation in the study of morbidity with VUT is each case of temporary disability due to a disease or injury in a given year. The accounting document is a certificate of incapacity for work, which is not only a medical statistical, but also a legal document certifying temporary release from work, and financial, on the basis of which benefits are paid from social insurance funds.
The assessment of morbidity with VUT is carried out both according to the generally accepted method based on reports of temporary disability (form No. 16-VN), and according to an in-depth method using the police method.
Number of cases of temporary disability per 100 employees: calculated as the ratio of the number of cases of illness (injury) to the average number of employees, multiplied by 100 (on average, about 80-100 cases per 100 employees).
Number of days of MTD per 100 workers: the ratio of days of morbidity (injury) to the number of workers, multiplied by 100 (about 800 - 1200 per 100 workers);
Average duration of one case of MTD: the ratio of the total number of days of incapacity for work to the number of cases of incapacity for work (about 10 days).
Health groups of workers: 1) healthy (who did not have a single case of disability in a year); 2) practically healthy (who had 1-2 cases of disability in a year due to acute forms of diseases); 3) who had 3 or more cases of disability in a year due to acute forms of diseases; 4) having chronic diseases, but not having cases of loss of ability to work; 5) those who have chronic diseases and who had cases of loss of ability to work due to these diseases.
Indicators of hospital morbidity (according to referrals). The incidence of hospitalized patients is a record of persons treated in a hospital during the year.
Materials on the incidence of the population in the practice of a doctor are necessary for: operational management of the work of healthcare institutions; evaluation of the effectiveness of ongoing medical and recreational activities, including medical examinations; assessing the health of the population and identifying risk factors that contribute to the reduction of morbidity; planning the volume of preventive examinations; determination of the contingent for dispensary observation, hospitalization, sanatorium treatment, employment of a certain contingent of patients, etc.; current and long-term planning of personnel, a network of various health services and departments; morbidity forecast.
International Statistical Classification of Diseases and Health Problems The International Classification of Diseases (ICD) is a system of grouping diseases and pathological conditions that reflects the current stage in the development of medical science. The ICD is the main regulatory document in the study of the health status of the population in WHO member countries.
In the ICD, all diseases are divided into classes, classes - into blocks, blocks - into headings (encrypted with three characters), headings - into subheadings (encrypted with four or more characters).
ICD-10 consists of 3 volumes. The first volume (in the Russian edition - in two books) contains a complete list of three-digit headings and four-digit subheadings, a list of headings for which countries submit information on diseases and causes of death to WHO, as well as special lists for the statistical development of mortality and morbidity data. The first volume also contains definitions of the main ICD-10 terms, mainly for child and maternal mortality.
The second volume includes a description of the ICD-10, its purpose, scope, instructions, rules for using the ICD-10 and rules for coding causes of death and disease, as well as basic requirements for statistical reporting. For specialists, the section on the history of the ICD may also be of interest.
The third volume consists of an alphabetical list of diseases and the nature of injuries (injuries), a list of external causes of injuries and tables of medicines and chemicals (about 5.5 thousand items).
What are the main innovations in the ICD tenth revision? Compared to the ninth revision, ICD-10 has increased the number of classes (from 17 to 21). The class of diseases of the nervous system and sensory organs is divided into classes VI "Diseases of the nervous system", VII "Diseases of the eye and its accessory apparatus" and VIII "Diseases of the ear and mastoid process". The auxiliary E-code has been replaced by an independent class XX "External causes of morbidity and mortality", and the V-code has been replaced by class XXI "Factors influencing the state of health of the population and visits to healthcare institutions".
There is no person who would be like an island, in itself, each person is a part of the Mainland, a part of the Land; and if the Wave blows the coastal Cliff into the sea, Europe will become smaller, and also if
wash away the edge of the Cape or destroy your Castle or your Friend; the death of every Man implores me too, for I am one with all mankind, and therefore never ask,
for whom the Bell Tolls; he calls for you.
Fundamentals of infectious pathology | ||
Acute intestinal infections | ||
Physiology of water-electrolyte metabolism. Cholera | ||
Streptococcal angina. Diagnostics. Treatment. Features of modern | ||
diphtheria |
||
Typhoid fever | ||
Flu and SARS | ||
Hemorrhagic fever with renal syndrome (HFRS) | ||
Meningococcal infection | ||
Yersiniosis | ||
Erysipelas (erysipelas infection) | ||
Botulism | ||
Viral hepatitis. Acute viral hepatitis | ||
Acute viral hepatitis (continued) | ||
Chronic viral hepatitis | ||
anthrax | ||
Rickettsioses | ||
Tetanus | ||
Leptospirosis (Vassiliev-Weil disease) | ||
Helminthiases | ||
Brucellosis | ||
SARS |
IX semester
Lecture No. 1 (09/08/2005)
Lecturer - Head of the Department of Infectious Diseases, Doctor of Medical Sciences, Professor Fazylov Vildan Khairullaevich
History of the Department of Infectious Diseases. Fundamentals of Infectious Pathology The department was organized in 1923. Founder - B.A. Walter (1923-1957), A.E. Reznik (1957-1979), Dilyara Shakirovna Yanaleeva (1979-1995), Fazylov Vildan Khairullaevich (since 1995).
Fundamentals of infectious pathology Infectious diseases are a large group of diseases caused by pathogenic and conditionally
pathogenic microorganisms. The essence of infectious diseases is the interaction of two independent biological systems (macro- and microorganism), each of which has its own biological activity.
Infection (from Latin infectio - I pollute, infect; inficio - pollute, infect) is a broad general biological concept that characterizes the penetration of a pathogen into another more highly organized (plant or animal) organism and their subsequent interaction under certain conditions of the external and social environment.
Infectious process - a set of physiological, protective and pathological reactions of a macroorganism, manifested at the molecular, subcellular, cellular, tissue, organ and organism levels in response to the introduction of a pathogen into it and their interaction under certain conditions of the external and social environment (i.e. in response to "infection").
An infectious disease is such a degree (phase) of the development of an infectious process when a macroorganism has certain pathological signs, accompanied by changes (violation) of the pathophysiological, biochemical, immunological, anatomical and other order.
To date, there are more than 1200 nosological forms of infectious diseases.
Classification of infectious diseases according to L.V. Gramashevsky (see textbook)
The classification is based on the mechanism and ways of transmission of the infectious principle. There are groups of intestinal, respiratory, blood contact, wound infections, infectious diseases transmitted by various mechanisms and ways.
Features of infectious diseases in contrast to non-communicable diseases:
1. The presence of a specific pathogen
2. Contagiousness (contagiousness) of many of them
3. The propensity of many of them to spread epidemically (from local epidemic outbreaks to pandemics, such as influenza)
4. The cyclical course of the infectious process, which manifests itself in the clinic of infectious diseases by periods, each of which is characterized by symptoms, syndromes and symptom complexes specific for this period.
5. Formation of a specific immune response
Features of a specific pathogen. Pathogenicity is a species characteristic of a microorganism, fixed genetically and characterizing its ability to cause a disease. There are pathogenic, conditionally pathogenic and non-pathogenic microorganisms (saprophytes).
Factors determining pathogenicity:
1. Virulence is the degree (measure) of pathogenicity individually inherent in a particular strain of a pathogenic agent.
2. Toxigenicity is the ability to produce and release toxins (exo- and endotoxins), which have a tropism for certain tissues of organs and systems at the cellular level.
3. Invasiveness (aggressiveness) - the ability to penetrate into the tissues and organs of the macroorganism and spread in them.
There are highly contagious, contagious, low contagious and non-contagious diseases.
Cyclicity of the infectious process
1. I phase. Penetration of the pathogen into the macroorganism: mobilization of the protective forces of the macroorganism through the activation of nonspecific and specific factors of immune defense ( incubation, latent period: from the moment of infection to the onset of the disease)
3. III phase. Violation of metabolic processes and functions of vital organs and systems (peak period of illness with organic pathology and specific clinical signs).
4. IV phase. Aggravation of the above disorders by products of impaired metabolism (nonspecific intoxication). Denaturation of tissue structures, the formation of autoantigens and autoantibodies with the formation of autoimmune complexes (autoimmune aggression), the addition of secondary microflora. In the clinical picture - the development of complications. With adequate therapy, the phase may not be.
aimed at eliminating "antigenic disturbances" (i.e., restoring the antigenic constancy of the body).
Restoration of impaired functions of vital organs and systems with the release of the body from the pathogen ( recovery period, convalescence)
Partial or complete restoration of impaired functions of vital organs
and systems, but with the preservation of the pathogen in the body (chronic infection) Diagnosis of infectious diseases
2. Clinical picture: identification of leading clinical syndromes specific to a particular infectious disease (based on an objective examination of the patient, taking into account the development of the disease).
3. Specific and non-specific laboratory, instrumental, morphological diagnostics.
Leading clinical syndromes of infectious pathology
General infectious-toxic syndrome (intoxication syndrome)
Catarrhal (respiratory) syndrome
Gastrointestinal lesion syndrome (diarrheal, dyspeptic) its variants: gastritis, gastroenteritis, gastroenterocolitic, colitis
Dehydration syndrome (exicosis)
Meningeal, encephalitic, meningoencephalitic syndromes; encephalopathy syndrome
Jaundice Syndrome (Cholestasis)
Lymphadenopathy syndrome (lymphoproliferative)
Hepatolienal
Tonsillitis syndrome (tonsillitis)
Syndrome of urgent conditions (respiratory distress syndrome, acute vascular insufficiency syndrome - infectious-toxic, hypovolemic, anaphylactic shock, acute renal failure, acute hepatic-renal failure, acute hepatic encephalopathy, etc.)
Specific laboratory methods
Immunological or serological (agglutination reaction, complement fixation reaction, indirect hemagglutination reaction, enzyme immunoassay, immune agglutination reactions, etc. - RA, RSK, RNGA, ELISA, RIA, etc., respectively)
Biological
Molecular biological (polymerase chain reaction - PCR)
Immunological
Express Methods
Bacterioscopy smear
Immunofluorescence methods
Specific skin allergy tests Non-specific laboratory methods
Clinical blood test
Clinical urinalysis, urinalysis according to Zimnitsky, Nechiporenko, Kakovsky Addis
Biochemical blood test (FPP, urea, creatinine, glucose, α-amylase, acid-base state, K+, Na+, Mg2+, Ca2+, Cl–, etc.)
Study of immune and cytokine status: macrophages, lymphocytes and their phenotypes CD3, CD4, CD8, CD16, CD22, HLA-DR, etc. Phagocytic reactions (FAN, FN, FR, NST-test), non-specific humoral factors (fibronectin, β-lysine, etc., as well as IgA, M, G, CEC, Co), cytokines (IL-1, 2, 6, 8, 10, TNF, etc.)
Additional methods of non-specific diagnostics
Endoscopy (sigmoidoscopy, FGDS, etc.)
Fluoroscopy
Ultrasound, CT, MRI
Live biopsy (of the liver, lymph nodes and other organs with morphological and histological examination of the biopsy)
Principles of therapy
1. The principle of etiotropic (specific) therapy is the destruction of an infectious agent, the elimination of it and its toxins
2. The principle of pathogenetic therapy, which is aimed at correcting and restoring impaired functions of vital organs and systems. Ways of implementation:
Detoxification
Dehydration
Rehydration
Desensitization
Immunocorrection
Correction of hemostasis
Lecture No. 2 (09/15/2005)
Lecturer - Candidate of Medical Sciences, Associate Professor Malova Albina Azatovna Acute intestinal infections (AII)
Acute intestinal infections are characterized by:
1. Widespread (2nd place after acute respiratory infections and influenza)
2. Diagnostic difficulties:
Similarity of clinical symptoms
Low percentage of etiological interpretation
High percentage of diagnostic errors (10-15% in modern conditions)
3. The lack of unified approaches to therapy with a huge variety of drugs on the pharmaceutical market.
4. The severity of the course and the frequency of adverse outcomes in individuals with an unfavorable premorbid background. Risk groups: the elderly, young children, cancer patients, asocial persons.
5. The ability to give outbreaks is an epidemic spread.
The WHO defines AII as diarrheal disease. They are characterized by a leading acute diarrheal syndrome. The number of OKIs is 30 nosological units.
Microbiological list of causative agents of AII
bacteria |
||
Family | ||
Escherichia, Shigella, Salmonella, Citrobacter, |
||
Enterobacteriaceae | Klebsiella, Enterobacter, Hafnia, Serratia, Pro- |
|
teus, Yersinia, Edwardsiella, Erwinia |
||
Bacillus (B. cereus), Clostridium |
||
Lactobacillaceae | ||
Pseudomonadaceae | Pseudomonas aeruginosa |
|
Vibrio cholerae asiatica, El Tor, NAG- |
||
vibrios |
||
Rotavirus |
||
Norwalk, Snow Mountain |
||
Enteroviruses Coxsackie and ECHO, calicivi- |
||
Diagnosis of acute intestinal infections is based on clinical and epidemiological data. 2 main leading syndromes:
1. Syndrome of intoxication
2. diarrheal syndrome
OCI is characterized by coexistence and simultaneity of their occurrence. Differential diagnosis with acute surgical pathology, for example, in acute appendicitis, “scissors” are noted: diarrhea regresses, but intoxication increases.
The severity of diarrhea causes dehydration syndrome. Diarrheal syndrome is divided according to the level of damage to the gastrointestinal tract: gastritis, enteritis, colitis and mixed forms.
Clinical classification implies the allocation of the clinical variant of the course of various acute intestinal infections.
Characteristics of the stool in enteritis and colitis.
The volume of stool with enteritis is plentiful, with colitis it is scanty, colitis is characterized by "rectal spitting". Characteristics of the stool: watery, thin, mushy, semi-formed, formed. It is advisable not to use gastronomic terms: sausage-like, pea-like, creamy, raspberry jelly, etc. Epidemiological history. Product characteristics (taste, shelf life, cooking method)
cooking); sanitary and hygienic literacy, living conditions, level of mental development.
Pathogenesis of the development of acute intestinal infections on the example of acute dysentery Mechanism of infection: fecal-oral, 3 main ways: alimentary, water, contact-household.
After swallowing, Shigella enter the stomach, where they partially die (hydrochloric acid is a non-specific defense factor).
Phase I takes place in the small intestine, where the remaining shigella produce cyto- and enterotoxins, when the shigella dies, endotoxins are released, which leads to increased motility, secretion and absorption are disturbed. As a result, a large amount of liquid is formed; absorption of toxins leads to intoxication (Shigella releases up to 30 toxins). Next, the microbes enter the distal colon - the invasive (II) phase begins. Here, bacteria also secrete toxins, actively penetrate into the wall of the colon, as a result of which peristalsis is disturbed, mainly spasm is formed, therefore the stool is scanty, all this leads to inflammation of the large intestine with the development of infiltration, abscesses, ulcerative necrotic changes, intoxication progresses.
All causative agents of AII are divided into 2 pathogenetic groups
Enterotoxigenic (secretory diarrhea) | Enteroinvasive (exudative diarrhea) |
Enterotoxigenic E. coli | |
Rotaviruses | Enteroinvasive E. coli |
Enteroviruses | |
Salmonella can cause both types of diarrhea, this is determined by the number of microbes, the protective properties of the macroorganism, etc.
Characteristics of the stool with secretory diarrhea: watery, profuse, the threat of hypovolemic shock.
Characteristics of the stool in exudative diarrhea: scanty, colitis, mucus, blood. Systemic complications: in severe hypertoxic forms - infectious-toxic shock; local complications: anal fissures, prolapse of the rectum, exacerbation of hemorrhoids, etc.
Laboratory diagnostics There are specific and non-specific diagnostics.
Specific diagnostics reveals the pathogen or traces of its stay (AT, Ag, T-lymphocytes).
1. Bacteriological examination of feces, vomit, gastric lavage to isolate a pure culture of the pathogen (remember the stages of bacteriological culture for the exam). Diagnostics is retrospective, it allows to judge the structure of the causes of AEI without affecting the therapy.
2. Serological diagnosis. Paired sera are taken: the first at the time of admission (negative titer), after 5-7 days in dynamics, you need to take a second serum and check; with an increase in titer by 4 times - decoding of the etiology. RPGA with various diagnosticums. Retrospective diagnosis.
3. Express diagnostics: ELISA, RIF
4. PCR
Non-specific diagnostic methods allow to clarify the degree of severity, the presence of complications, to conduct differential diagnosis.
Complete blood count: moderate leukocytosis, neutrophilia, slight shift of the leukocyte formula to the left, hematocrit (degree of dehydration). General urine analysis. Coprological research method (microscopy of feces). The coprogram reveals the presence of colitis (leukocytes, erythrocytes in large numbers, which is important when the colitis is hidden); enzymatic viability of the gastrointestinal tract in terms of the ratio of digested and undigested muscle fibers (creatorrhea), digested and undigested fiber, starch grains, fats (steatorrhea); worm eggs and protozoa (in this case, analysis is a specific research method).
Sigmoidoscopy is prescribed in severe cases for the differential diagnosis of oncological diseases with local disorders. Colonoscopy is now more commonly performed to differentiate between ulcerative colitis and Crohn's disease.
Treatment Necessary conditions for the correct appointment of adequate therapy for intestinal infections:
1. Determine the infectious nature of the disease (2 syndromes + epidemiological history)
2. Assume a possible etiology and determine the pathogenetic group (invasive or secretory diarrhea)
3. Set the severity of the disease and the leading syndrome
4. Determine the phase of the disease and the nature of the course
5. Assess the age, premorbid background of the patient and risk factors for an unfavorable course of AII
6. Solve questions about the place of therapy (outpatient clinic, hospital)
Indications for hospitalization are divided into 2 groups:
1. Clinical (moderate and severe degrees of the disease); burdened premorbid background; age (children, old people), etc.
2. Epidemiological indications (the patient may be dangerous in terms of the spread of infection). Allocate a decreed group: food workers, bathhouse workers
laundry facilities, persons living in a hostel, employees of preschool institutions.
Principles of rational therapy
1. Complexity
diet therapy
Etiotropic therapy
Pathogenetic therapy
Symptomatic therapy
2. Individual approach
3. Principles of minimum sufficiency for solving the problem:
In the acute phase - the fight against the pathogen, the excretion of its metabolic products, the relief of syndromes
During the period of reparation and convalescence - restoration of the function of the gastrointestinal tract.
4. Avoid polypharmacy!
Prescribing antibiotics or chemotherapy Absolute indications for prescribing antibiotics:
1. Dysentery
2. Amoebiasis
3. Typhoid fever
4. Cholera
Indications for antibiotic therapy
1. In invasive acute intestinal infections in the acute phase of the disease
severe forms
Moderate forms - children under 2 years old, the elderly, patients at risk for shigellosis, hemocolitis.
2. All patients with generalized forms of the disease (septic diseases), with mild forms of the disease - only for children at risk and with hemocolitis.
Contraindications to antibiotic therapy
1. All patients with secretory diarrhea
2. Patients with mild and moderate forms of invasive AII (with the exception of young children from risk groups and with hemocolitis)
3. Everyone with subclinical OKI
4. For post-infectious functional diarrhea
Morphological healing occurs 4-5 weeks after the transferred AII. Intestinal antiseptics
1. Quinoline drugs: intestogen, intetrix (3-5 days), enterosedin, 5-NOC, nitroxoline
2. Preparations of the nitrofuran series: ersefuril, furazalidon, quinoxidine
3. Quinolones:
I generation: nalidixic acid
Fluoroquinolones: ciprofloxacin (250-500 mg 3-5 days 2 times a day), ofloxacin, pefloxacin, norfloxacin, etc.
4. Sorbents: activated carbon, carbogen, carbolong, polyphepan, reban (attakulpit), enterodez, enterosgel
5. Mixed action drugs: Smecta
Pathogenetic therapy: detoxification therapy, rehydration therapy. Vegetable antiseptics, enveloping, astringent substances: oak bark, alder, decoction of bird cherry fruits, pomegranate peels.
Recovery and regeneration period: enzymes are prescribed for 1 week: abomin, orase, somilase, pancreatin, panzinorm, festal, digestal, enzistal, mezim forte, creon, pancitrate. Multivitamins. The appointment of probiotics for 2-3 weeks during the convalescence period: bifidumbacterin multi (3 types of bifidobacteria, Jerusalem artichoke extract, which stimulates the growth of bacteria in the intestine).
The appointment of loperamide (Imodium, Lopedium) is contraindicated in diarrhea with intoxication, because. this can lead to its aggravation, and the absence of diarrhea and the increase in intoxication can lead to diagnostic errors and referral of the patient to the surgical department.
Lecture No. 3 (22.09.2005)
Lecturer - Candidate of Medical Sciences, Associate Professor Malova Albina Azatovna Physiology of water-electrolyte metabolism. Cholera
Water makes up 70% of the adult human body. Of these, 60-70% is intracellular water, 30-40% is extracellular water. Intercellular water is divided into interstitial and intravascular (7%, plasma, lymph, cerebrospinal fluid). The body's need for input is determined by its losses. Diuresis averages 1.5 liters, breathing - 400 ml, sweat, feces - 600 ml. Total daily requirement: 2-2.5 liters. Approximately 600 ml is compensated by internal metabolism, the rest of the water must come exogenously. Water exchange is one of the most intensive exchanges. The flow of water into the cells occurs according to the laws of osmosis and with the help of enzyme systems. 7-8 liters of fluid enter the intestinal cavity daily: with food 2 liters, gastric juice 2.5 liters, saliva 1 liter, intestinal juice 1 liter, bile 0.5 liters. 200-300 ml is lost with feces. The rest of the liquid is absorbed. 70% of the liquid is absorbed in the small intestine. The main cell is the enterocyte. Suction area - 100 m2 (due to folding, length, villi and microvilli). Water is absorbed predominantly passively through osmosis. Stimulation of absorption is achieved by glucose and amino acids. The main cell of the large intestine is a colonocyte, the remaining 30% of the liquid is absorbed there, absorption mainly occurs with the help of active transport.
The causative agent of cholera is Vibrio cholerae (Vibrionaceae family, genus Vibrio). For humans, serogroup O1 (O139 Bengal?) is pathogenic. Biovars: classic (Asian) and El Tor. Serovars: Inaba, Ogawa, Gikoshima. The vibrio is motile, has a flagellum, is comma-shaped, does not form spores, is an obligate aerobe.
The only toxin of cholera vibrio (exotoxin - cholerogen) determines the entire pathogenetic picture.
cholera pathogenesis
1. The penetration of the pathogen through the mouth (transmission mechanism fecal-oral, water way)
2. Its reproduction in the small intestine with the release of cholerogen.
3. Cholerogen, firstly, activates enterocyte adenylate cyclase, accumulation of cAMP occurs, which leads to blockade of absorption; secondly, it activates the secretory cells of the small intestine (secondarily), leading to increased secretion of intestinal juice. There is an abundant secretion of isotonic fluid in the gastrointestinal tract (diarrhea and vomiting) and malabsorption.
4. Develops hypovolemia, hypokalemia, hypochloremia, metabolic acidosis, respiratory alkalosis (secondarily)
With each liter of feces during diarrhea loses 5 g of Na+ , 4 g HCO3 - , 1 g K+ . Water is lost through the interstitial fluid.
Differential diagnostics (clinic – …)
1. Absence of intoxication syndrome (endotoxin is not absorbed)
2. Severe diarrhea(up to 3 liters at a time)
3. The onset of the disease always occurs with diarrhea, and then vomiting joins, because. The “battlefield” is the small intestine, the intensity of secretion is so high that the liquid does not have time to be completely evacuated through the intestine and enters the stomach, vomiting occurs (mechanical vomiting pathogenesis).
4. Vomiting is always a fountain and without nausea (no inflammation, no gastritis).
5. Rapid increase in dehydration.
The degree of dehydration according to V.I. Pokrovsky and their clinical characteristics
1. I degree - compensated, 1-3% of body weight. thirst, dry mouth; BP, pulse normal.
2. II degree - subcompensated, 4-6% of body weight. Dryness of the tongue, dry mucous membranes, blood pressure is reduced (SBP 80-90 mm Hg), in hypotensive patients it is more than 60 mm Hg. Art., tachycardia, there may be cyanosis of the lips, a slight decrease in diuresis (threshold for the kidneys SBP 60 mm Hg. Art.).
3. III degree - decompensated, 7-10% of body weight. Weakness, weak voice, hemodynamic disturbances, SBP< 60 мм рт. ст., тахикардия, акроцианоз, анурия, компенсаторная одышка, складка кожи не расправляется (на животе или спине), снижен тургор кожи, у детей западает родничок, могут западать глаза.
4. IV degree - terminal, more than 10% of body weight.
Water loss of more than 12% is not compatible with life. This state of cholera can be reached in 6 hours.
Laboratory indicators of dehydration: hematocrit, relative plasma density, blood viscosity, plasma osmolarity - indicators of the severity of hemoconcentration. Indicators of electrolyte metabolism: K+, Na+, Cl–. Cholera is characterized by isotonic dehydration. During vomiting, K + is mainly lost (typical for food poisoning). Additional laboratory indicators: the severity of the acid-base disorder - pH (acidity), pCO2 (carbon dioxide tension in the blood), pO2 (oxygen tension in the blood). BE (base excess - excess of bases), BD (base deficit - lack of bases).
Specific diagnosis of cholera Collection of feces on form 30, bacteriological method is carried out - sowing at 1%
peptone water (presumptive positive after 12 hours, finally positive after 24 hours, finally negative after 36 hours). Slide agglutination reaction with O1 cholera diagnosticum: positive result - cholera, negative result - non-agglutinated vibrios (NAG-vibrios). PCR - isolation of the Tox gene from the genome of Vibrio cholerae.
Treatment The goal is to combat dehydration. Rehydration therapy - pathogenetic therapy - ve-
Two heads and six legs; four walk, and two lie still
Self-esteem - what is it: concept, structure, types and levels
Cassandra's Path, or Pasta Adventures War on Earth and Underground