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"description": "Африканский трипаносомоз человека, известный также как сонная болезнь, является трансмиссивной паразитарной болезнью. Она развивается в результате инфицирования простейшими паразитами, принадлежащими к роду Trypanosoma. Они передаются людям при укусах мух цеце (род Glossina), которые приобретают инфекцию от людей или животных, являющихся хозяевами этих патогенных паразитов человека. ",
"etiology": "<p>Существуют три морфологически идентичных подвида возбудителя сонной болезни: T. brucei brucei - возбудитель заболевания у домашних и диких животных, T. brucei gambiense - возбудитель гамбийской, или западноафриканской сонной болезни людей, и T. brucei rhodesiense - возбудитель родезийской, или восточноафриканской сонной болезни людей. Эндемично в ряде регионов Африки южнее пустыни Сахара, охватывающих территории 36 стран с населением 60 млн человек. </p>\r\n<p>Заражение человека происходит при укусе насекомого-переносчика - мухи цеце (р. Glossina). Обычно заражение человека возбудителем западноафриканского трипаносомоза происходит недалеко от водоёмов и вдоль берегов рек, в то время как заражение возбудителем восточноафриканского трипаносомза - в саваннах и на местах недавно вырубленных тропических лесов. Человек является основным хозяином для T.b. gambiense, и случайным хозяином для T.b. rhodesiense, зооноза, преимущественно поражающего домашний скот и диких животных.</p>\r\n<p>Паразиты морфологически идентичны: плоские, продолговато-веретенообразны по форме, от 12 до 35 мкм в длину и 1,5 - 3,5 мкм в ширину. Подвижны, для перемещения используют тянущуюся вдоль тела волнистую полупрозрачную мембрану. Из организма инфицированного человека обычно выделяют трипомастигоит. </p>\r\n<p> </p>",
"pathogenesis": "<p>После укуса инфицированной мухи в месте входных ворот развивается местно-воспалительная реакция в виде болезненного зудящего шанкра и регионарный лимфаденит. Через 1-3 недели, после проникновения трипаносом в кровяную и лимфатическую систему развивается гемолимфатическая стадия сонной болезни. Поздняя (менингоэнцефалитическая) стадия африканского трипаносомоза обусловлена проникновением паразита в ЦНС. В ответ на инвазию иммунная система реагирует выработкой специфических антител класса IgM, позволяющих некоторое время сдерживать паразитемию. Однако высокая антигенная изменчивость трипаносом нарушает формирование специфического иммунитета, обусловливая непрерывное прогрессирование и возвратно-рецидивирующий характер сонной болезни. <br class=\"SCXW199365423\" /> </p>",
"diagnostics": "<p>Предварительная диагностика сонной болезни осуществляется на основании клинико-эпидемиологических данных, важнейшими из которых служат пребывание в эндемичных районах Африки, наличие длительной, рецидивирующей лихорадки, первичного аффекта, шейного лимфаденита, отеков, сонливости и др. </p>\r\n<p>Лабораторная диагностика основана на обнаружении паразита в мазке крови или в жидкости лимфатического узла. Для определения разницы между первой и второй стадией болезни часто требуется люмбальная пункция. </p>",
"treatment": "<p>Чем раньше назначена терапия, тем больше шансов на выздоровление. На успех лечения влияют также возраст и общее состояние пациента, стадия заболевания и чувствительность трипаносомы к препаратам. Для уничтожения возбудителя сонной болезни применяются следующие лекарства: </p>\r\n<ol>\r\n<li>Пентамидин и сурамин. Применяются на гемолимфатической стадии заболевания. Первый препарат эффективен при гамбийской форме болезни, второй – родезийской. </li>\r\n<li>Меларсопрол. Назначается на менингоэнцефалитической стадии заболевания, эффективен при обеих клинических формах. </li>\r\n<li>Эфлорнитин. Применяется при гамбийской форме, необходим для лечения пациентов, болезнь у которых достигла второй стадии. </li>\r\n<li>Нифуртимокс. Применяется совместно с эфлорнитином. Такая схема позволяет уменьшить дозировку и продолжительность применения последнего, снижая тем самым выраженность побочных реакций. </li>\r\n</ol>",
"prevention": "<p>В профилактике сонной болезни главную роль играет истребление мух цеце с помощью инсектицидных препаратов, вырубки кустарниковых зарослей близ населенных пунктов, использование средств индивидуальной защиты от укусов кровососущих насекомых в эндемичных районах Африки. В периоды эпидемических вспышек сонной болезни среди местных жителей и приезжих проводится массовая химиопрофилактика пентамидином. Иммунопрофилактика африканского трипаносомоза не разработана.</p>",
"clinical_picture": "<p>Ранняя стадия африканского трипаносомоза характеризуется как гемолимфатическая и длится около года с момента заражения. Примерно по истечении недели после укуса мухи на коже больного образуется первичное узелковое образование – шанкр. Такого рода эритематозный элемент локализуется в большинстве случаев на голове или конечностях инфицированного. Как правило, шанкр самопроизвольно заживает через несколько недель. </p>\r\n<p>Одновременно с образованием узла на теле и конечностях больного появляются розовые и фиолетовые пятна – трипаниды. Дальнейшее течение заболевания обусловливается попаданием паразитов из подкожного пространства в кровь и лимфу. На поздних стадиях африканская трипаносома проникает сквозь гематоэнцефалический барьер, что приводит к стойким нарушениям мозговой деятельности. Помимо этого, симптомы сонной болезни по мере прогрессирования патологии могут выражаться в следующих типичных состояниях: </p>\r\n<ul>\r\n<li>лихорадке; </li>\r\n<li>болезненных подкожных отеках; </li>\r\n<li>лимфадените; </li>\r\n<li>сильных головных болях; </li>\r\n<li>дневной сонливости; </li>\r\n<li>атаксической походке; </li>\r\n<li>треморе (подергивании) языка, конечностей; </li>\r\n<li>заторможенности; </li>\r\n<li>нарушении восприятия; </li>\r\n<li>судорогах; </li>\r\n<li>эпилептических припадках. </li>\r\n</ul>\r\n<p>Важно отметить, что родезийская форма болезни отличается скоротечным развитием. Интоксикация и лихорадочное состояние выражены сильнее. Намного быстрее развивается истощение. Нередко у пациентов с данной формой африканского трипаносомоза возникают сердечно-сосудистые патологии (миокардит, аритмия). Гибель инфицированного лица наступает задолго до перехода болезни в менингоэнцефалитическую стадию. В большинстве случаев летальный исход наступает по причине интеркуррентных инфекций (пневмония, малярия). </p>",
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},
"code": "B57",
"name": "Болезнь Шагаса",
"icd_name": "Болезнь Шагаса",
"gender": 0,
"age_min": 0,
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"cause": [
2,
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],
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"slug": "b57_bolezn_shagasa",
"lead": "Трансмиссивная протозойная инфекция, возбудителем которой является патогенная Trypanosoma cruzi, а переносчиком триатомовые клопы.",
"description": "Инфекционное заболевание",
"etiology": "<p>Возбудителем болезни Шагаса является жгутиковое простейшее Trypanosoma cruzi, сложный цикл развития которого включает смену хозяев - позвоночных животных и человека, а специфическим переносчиком служат кровососущие клопы подсемейства Triatominae (триатомовые). T. cruzi имеет веретенообразную форму, жгутик и ундулирующую мембрану. Паразит проходит несколько фаз жизненного цикла: амастигота, обитающая в тканевых клетках человека; эпимастигота, растущая в кишечнике переносчиков; и трипомастигота, находящаяся в крови животных и человека. Основным хозяином T. cruzi служит человек, дополнительными - броненосцы, муравьеды, обезьяны и домашние животные (собаки, кошки, свиньи). Инвазионной стадией для переносчиков и хозяев являются трипомастиготные формы.</p>\r\n<full></full>\r\n<p>Заражение клопов происходит в процессе питания кровью человека или животных, содержащей трипомастиготы. В организм человека возбудитель болезни Шагаса заносится вместе с инфицированными фекалиями клопов при расчесывании ранок после их укусов на коже и слизистых губ, носа, конъюнктивы.Наиболее распространенный способ заражения болезнью Шагаса – трансмиссивный, возможна передача алиментарным, половым, трансплацентарным, гемотрансфузионным путем и при трансплантации органов. Для T. cruzi характерна персистенция в организме хозяина в течение всей жизни.</p>",
"pathogenesis": "<p>Характерной особенностью T. cruzi является способность к внутриклеточному паразитизму в макрофагах кожи и слизистых оболочек, в клетках миокарда, эндотелия лимфатических узлов, селезенки, печени, легких, нейроглии. После разрыва пораженных клеток, переполненных размножившимися амастиготами, происходит заражение новых клеток. Паразитирование трипаносом приводит к воспалительно-дистрофическому и дегенеративному поражению внутренних органов.</p>",
"diagnostics": "<p>Диагностика болезни Шагаса включает тщательный сбор анамнеза (с учетом места рождения больного, поездок в эндемичные по заболеванию районы), анализ данных клинической картины и лабораторных исследований (микроскопического и культурального методов, серологических анализов и ПЦР).</p>\r\n<full></full>\r\n<p>В качестве исследуемого материала используется кровь, спинномозговая жидкость, пунктаты из первичных мест поражения, лимфоузлов, селезенки, костного мозга. В острую стадию болезни Шагаса (первые 6-12 недель) паразитов можно обнаружить при микроскопии толстой капли крови или фиксированных окрашенных препаратов. Бактериологический посев крови больного помогает выявить чистую культуру T. cruzi. При болезни Шагаса применяется ксенодиагностика, включающая исследование содержимого кишечника неинвазированного триатомового клопа после насыщения его кровью больного. Возможно проведение биологической пробы с введением крови пациента морским свинкам или белым мышам и последующим изучением образцов тканей.</p>\r\n<p>При хронической болезни Шагаса более эффективна серодиагностика: реакция связывания комплемента, реакция непрямой флюоресценции, реакция непрямой гемагглютинации, ИФА. Наличие специфических IgM говорит об острой стадии болезни Шагаса, при хронической имеются только IgG.</p>",
"treatment": "<p>На сегодняшний день лечение болезни Шагаса малоэффективно; терапия позволяет снизить летальность среди больных, но не дает уверенности в полной эрадикации внутриклеточных форм T. cruzi. В лечении болезни Шагаса применяются два антипаразитарных препарата: нифуртимокс и бензнидазол, прием которых более эффективен в острую стадию заболевания. В хронической стадии инфекции лечение направлено на облегчение симптомов развившихся осложнений болезни Шагаса. При сердечной недостаточности и аритмии, для профилактики тромбоэмболических состояний назначаются ингибиторы АПФ, сердечные гликозиды, антиаритмические средства, антикоагулянты, в тяжелых случаях показаны аортокоронарное шунтирование, имплантация кардиостимулятора, трансплантация сердца. Лечение менингоэнцефалита – симптоматическое; при поражении ЖКТ могут использоваться кортикостероиды; при мегаколоне возможно хирургическое вмешательство: наложение колостомы, резекция толстой кишки.</p>",
"prevention": "<p>Профилактика болезни Шагаса включает инсектицидную обработку жилья человека, птичников, свинарников – основных мест обитания клопов - переносчиков паразитов, благоустройство жилища; отбор и обследование на трипаносомоз потенциальных доноров крови и органов, санитарное просвещение населения. </p>",
"clinical_picture": "<p>Инкубационный период заболевания продолжается 1-3 недели. Затем в месте проникновения трипаносом может развиться местная воспалительная реакция (шагома) в виде эритематозного узла с припухлостью и покраснением либо одностороннего багрового отека века (симптом Роминьи) с конъюнктивитом, сопровождающиеся увеличением регионарных лимфоузлов. Болезнь Шагаса проходит в 2 стадии: острую (первые 2 месяца) с циркуляцией большого количества паразитов в крови и хроническую - с концентрацией трипаносом во внутренних органах.</p>\r\n<p>В острую стадию болезни Шигаса в большинстве случаев симптомы отсутствуют, у части больных проявляются в легкой форме. У детей до 5 лет ра</p>\r\n<full></full>\r\n<p>звивается наиболее тяжелая форма с системными проявлениями и летальностью до 10-14%. Среди общих симптомов болезни Шагаса может отмечаться <a title=\"Перейти на страницу симптома Утомляемость\" href=\"../../../symptom/utomlyaemost/\">недомогание</a>, постоянная или ремитирующая <a title=\"Перейти на страницу симптома Высокая температура 38-42° \" href=\"../../../symptom/vysokaya_temperatura_38-42/\">лихорадка</a> (до 39-40°С), головная и <a title=\"Перейти на страницу симптома Боль в мышцах\" href=\"../../../symptom/bol_v_myshcah/\">мышечная боль</a>, отеки на ногах, одутловатость лица, мелкая макулезная <a title=\"Перейти на страницу симптома Сыпь\" href=\"../../../symptom/syp/\">сыпь</a>. Характерен шейный, паховый и подмышечный лимфаденит, гепатоспленомегалия. Могут возникать вторичные шагомы – плотные узлы в подкожной клетчатке. Отмечается преимущественное поражение сердца, ЦНС и периферических ганглиев, органов ретикулоэндотелиальной системы. Развивается острое <a title=\"Перейти на страницу симптома воспаление\" href=\"../../../symptom/vospalenie/\">воспаление</a> и расширение всех камер сердца (кардиомегалия), диффузный миокардит, нарушение сердечной деятельности. У некоторых больных (особенно, у детей раннего возраста) может возникнуть острый специфический менингоэнцефалит, кровоизлияние в мозговые оболочки. Врожденная болезнь Шагаса может приводить к спонтанному аборту или преждевременным родам; у новорожденных сопровождается тяжелой анемией, гепатоспленомегалией, желтухой, судорогами, нередко - летальным исходом.</p>\r\n<p>При хронической форме болезни Шагаса симптомы могут долго отсутствовать, пока не произойдут необратимые повреждения внутренних органов. Чаще всего развивается кардиомиопатия, выражающаяся сердечной недостаточностью, аритмией, тромбоэмболией. Со стороны ЖКТ характерны патологическое расширение пищевода (мегаэзофагус), проявляющееся дисфагией, болью при глотании, и расширение толстой кишки (мегаколон), сопровождающееся кишечной непроходимостью, скоплением каловых камней. Возникают вегетативные нарушения и периферическая нейропатия. С течением времени болезнь Шагаса может приводить к внезапной смерти вследствие прогрессирующего разрушения сердечной мышцы.</p>",
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},
"code": "B58",
"name": "Токсоплазмоз",
"icd_name": "Токсоплазмоз",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
2,
5,
7,
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],
"periodicity": 1,
"slug": "b58_toksoplazmoz",
"lead": "Паразитарное заболевание, характеризующееся преимущественно латентным или хроническим течением, поражением нервной системы, органов ретикулоэндотелиальной системы, мышц, миокарда и глаз.",
"description": "Инфекционное заболевание.",
"etiology": "<p>Возбудитель - Toxoplasma gondii относится к простейшим.Токсоплазмоз относится к зоонозам с природной очаговостью. Окончательным хозяином являются домашние кошки и некоторые дикие представители семейства кошачьих (рысь, пума, оцелот, бенгальский кот, ягуар и др.). Ооцисты, выделяющиеся с их испражнениями, могут приводить к инфицированию как человека, так и многих других животных (свыше 200 видов), которые служат промежуточными хозяевами. Заражение наступает лишь при употреблении в пищу сырого мяса (мясного фарша) этих животных. Контакт с промежуточными хозяевами (собаками, сельскохозяйственными животными) к инфицированию людей не приводит. Больной человек не выделяет возбудителя во внешнюю среду и никакой опасности для окружающих не представляет.</p>\r\n<full></full>\r\n<p>У человека возможны три пути передачи инфекции: пероральный (заглатывание ооцист или цист), трансплацентарный, а также возможно инфицирование при переливании крови и пересадке органов.</p>\r\n<p>Пероральное инфицирование происходит при употреблении недостаточно термически обработанного мяса (мясного фарша), содержащего цисты. Баранина и свинина, также как и мясо других животных, часто содержат цисты токсоплазм (от 10 до 25%). Заражение может наступить и при проглатывании ооцист (контакт с загрязненными кошачьими испражнениями, землей, песком и др.). Около 1% домашних кошек с испражнениями выделяют ооцисты, однако - только на протяжении 2-3 недель за время жизни, так как после первичного инфицирования у животных развивается иммунитет, предохраняющий их от повторного заражения.</p>\r\n<p>Трансплацентарное заражение плода может происходить при инфицировании матери во время беременности. При заражении матери в I триместре беременности врожденный токсоплазмоз наблюдается в 15-20% и протекает тяжело. При инфицировании в III триместре инфицированными оказываются 65% новорожденных, но у некоторых инфекция может протекать без выраженных клинических проявлений. Если женщина инфицирована до беременности (за 6 мес и более), внутриутробного поражения плода не наступает, а если заражение произошло незадолго до наступления беременности, риск инфицирования плода очень мал.</p>\r\n<p>Инфицированность доноров токсоплазмами такая же, как клинически здоровых лиц, однако достоверных случаев передачи токсоплазмоза реципиентам не наблюдалось. Такая возможность становится реальной при переливании крови лицам с резко ослабленным иммунитетом (больные СПИДом, лейкемией и др.), а также при пересадке органов. В этих случаях доноры не должны быть инфицированными.</p>",
"pathogenesis": "<p>Воротами инфекции чаще служат органы пищеварения, хотя известны случаи внутрилабораторных заражений высоковирулентными штаммами токсоплазм при повреждении кожи (пипеткой или шприцем с культурой токсоплазм). Внедрение возбудителя происходит в нижних отделах тонкой кишки, затем с током лимфы токсоплазмы достигают регионарных (мезентериальных) лимфатических узлов. Здесь развиваются воспалительные изменения с формированием инфекционных гранулем, напоминающих по клеточному составу туберкулезные или бруцеллезные гранулемы. Мезентериальные лимфатические узлы значительно увеличиваются.</p>\r\n<full></full>\r\n<p>Затем токсоплазмы попадают в кровь, разносятся по всему организму и фиксируются в различных органах и тканях (печень, селезенка, лимфатические узлы, нервная система, глаза, миокард, скелетные мышцы). В этих органах образуются скопления паразитов в виде цист, которые могут сохраняться в организме десятки лет и даже пожизненно. В местах фиксации возникают воспалительные очаги, а в некоторых органах (нервная система, скелетные мышцы) - очажки некроза, в которых затем откладываются соли кальция и образуются кальцинаты.</p>\r\n<p>В результате жизнедеятельности паразита и выделения антигенов и аллергенов наступает аллергическая перестройка организма (по типу реакций гиперчувствительности замедленного типа) и вырабатываются антитела, которые выявляются в различных иммунных реакциях (РСК, реакция с красителем Сэбина-Фельдмана, РПГА, ИФА и др.). В развитии иммунитета большое значение имеют как клеточные, так и гуморальные факторы. Наличие антител предохраняет от нового заражения даже высоковирулентными штаммами токсоплазм и обусловливает бессимптомное (латентное) течение токсоплазмоза у большинства инфицированных лиц. При ослаблении защитных сил организма и снижении напряженности иммунитета может наступить обострение заболевания (переход латентной формы в манифестную). Обострение хронического токсоплазмоза, как правило, провоцируется интеркуррентными заболеваниями (грипп, ОРЗ, пневмонии и др.) и может наблюдаться иногда спустя длительное время (до 10-20 лет) после инфицирования. Описаны обострения с развитием тяжелого токсоплазмозного энцефалита после лечения лиц с латентным токсоплазмозом цитостатиками и иммунодепрессантами. В последние годы важное значение приобрела проблема генерализации латентного токсоплазмоза у ВИЧ-инфицированных. В этих случаях токсоплазмоз приобретает острое злокачественное течение с развитием некротического локализованного или диффузного менингоэнцефалита, в процесс вовлекаются глаза и многие органы (сердце, печень, легкие). На фоне развернутой картины СПИДа наслоившееся обострение (генерализация токсоплазмоза) может приводить к гибели больных.</p>",
"diagnostics": "<p>Диагноз ставят по результатам анализа крови, в ходе которого в крови выявляют наличие антител против токсоплазмы. При серьезных нарушениях используется компьютерная томография (КТ) или магнитно-резонансная томография (МРТ) головного мозга.</p>",
"treatment": "<p>При остром токсоплазмозе используются химиотерапевтические препараты. <br /><br />Делагил (по 0,5г 2 раза в сутки) в сочетании с сульфаниламидами (по 0,5г 2 раза в сутки) в течение 10 дней. Фансидар назначается в количестве 5 таблеток на курс: по 1 табл. через 2 дня или в виде внутримышечных инъекций по 1 ампуле в 2,5 мг один раз в 2 дня в количестве 5 инъекций. Проводится один или два курса лечения. <br /><br />Из антибиотиков назначаются: линкомицина гидрохлорид (по 0,5г 2 раза в сутки); метациклина гидрохлорид (по 0,3г 2 раза в сутки) в течение 5-7 дней в сочетании с сульфаниламидами; ровамицин. <br /><br />Лечение хронического токсоплазмоза во много раз труднее, чем острого, так как химиопрепараты не оказывает значительного эффекта. Главное место занимает гипосенсибилизирующая и иммуномодулирующая терапия. В комплекс лечения включают витамины, десенсибилизирующие средства, лидазу, церебролизин и пр. <br /><br />Имеются данные о положительном действии левамизола в терапии хронического токсоплазмоза. Левамизол назначается по 150 мг 3 дня подряд с перерывами 1 нед между циклами, всего 2 - 3 цикла.</p>",
"prevention": "<p>Профилактика инфицирования токсоплазмами заключается в употреблении в пищу только хорошо термически обработанного мяса и мясопродуктов, чисто вымытых овощей, фруктов и ягод. В процессе приготовления пищи запрещается пробовать на вкус сырой мясной фарш. Необходимо тщательно мыть руки после обработки сырых мясопродуктов, работе в саду, огороде, детям после игры на детской площадке и, особенно, в песочнице. Следует тщательно соблюдать санитарно-гигиенические правила содержания в квартире домашних животных, не забывая мыть руки после контактов с ними. <br /><br />При наступлении беременности каждая женщина должна быть обследована на токсоплазмоз в женской консультации. При выявлении у беременной клинических проявлений токсоплазмоза, а также обнаружение антител к токсоплазмам класса IgM, следует решить вопрос о необходимости лечения или прерывания беременности.</p>",
"clinical_picture": "<p>Симптомы легкого лимфатического токсоплазмоза сходны с проявлением инфекционного мононуклеоза. Происходит <a title=\"Перейти на страницу симптома Увеличение лимфатических узлов\" href=\"../../../symptom/uvelichenie_limfaticheskih_uzlov/\">увеличение лимфатических узлов</a> шеи и подмышечных областей, наблюдается чувство общего недомогания, боль в мышцах, периодическое <a title=\"Перейти на страницу симптома Высокая температура 38-42° \" href=\"../../../symptom/vysokaya_temperatura_38-42/\">повышение температуры</a>. Возможны легкая анемия, снижение артериального давления, увеличение числа лимфоцитов и снижение уровня лейкоцитов в крови.</p>\r\n<p>При хроническом токсоплазмозе наблюдается <a title=\"Перейти на страницу симптома воспаление\" href=\"../../../symptom/vospalenie/\">воспаление</a> внутренних структур глаза.</p>\r\n<full></full>\r\n<p>Острый диссеминированный токсоплазмоз проявляется в виде сыпи, повышенной температуры и выраженного истощения. Чаще всего эта форма токсоплазмоза встречается у людей со сниженным иммунитетом. В худшем варианте эта форма проявляется у больных СПИДом, у которых токсоплазмы могут распространиться по всему организму. При этом развивается <a title=\"Перейти на страницу симптома воспаление\" href=\"../../../symptom/vospalenie/\">воспаление</a> мозга (энцефалит), что приводит к параличу, судорогам, головным болям и коме.</p>",
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