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},
"code": "B60.1",
"name": "Акантамебиаз",
"icd_name": "Акантамебиаз",
"gender": 0,
"age_min": 1,
"age_max": 100,
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"slug": "b60.1_akantamebiaz",
"lead": "инфекционное заболевание, вызванное паразитическими простейшими",
"description": "<p> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Акантамебиаз - это протозойное поражение глаз, кожных покровов и центральной нервной системы, которое вызывается свободноживущими амебами</span></p>",
"etiology": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Акантамебы – это аэробные микроорганизмы, которые живут в почве, стоячей пресной воде природных и искусственных водоемов, особенно тех, которые загрязнены сточными водами. Такие простейшие также могут обитать в водопроводной воде, канализации и воде циркулирующей в отопительной системе. Значительному увеличению численности популяции акантамеб способствует повышение температура воды более 28°С и содержанием в ней различных органических веществ. При понижении температуры либо высыхании водоема акантамебы инцистируются. При нахождении в состоянии цисты паразитам нестрашны температурные изменения, некорректная кислотность и влияние антисептических и дезинфицирующих веществ.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">После проникновения микроба в организм человека паразит переходит в вегетативное состояние.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">У здоровых лиц акантамебы могут выявляться в носоглоточной слизи и фекалиях, однако акантамебиазное поражение центральной нервной системы подвержены больные страдающие иммунодефицитом.</span></p>",
"pathogenesis": "",
"diagnostics": "<p> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Диагноз акантамебного поражения глаз, кожи, головного мозга подтверждается путем обнаружения вегетативных и цистных форм акантамеб в исследуемом материале. При акантамебном кератите - это слезная жидкость, смывы и соскобы роговицы; при акантамебном дерматите - отделяемое инфильтратов, биоптаты кожи; при гранулематозном энцефалите - спинномозговая жидкость. Кроме микроскопического исследования препаратов, для верификации диагноза акантамебиаза применяется культуральный метод, серологические тесты, биологическая проба. При подозрении на акантамебиаз следует исключить у пациента кератиты, энцефалиты и дерматозы иной этиологии.</span></p>",
"treatment": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Лечение акантамебного кератита требует отказа от ношения контактных линз. Местная терапия включает ежечасную инстилляцию в конъюнктивальную полость антибактериальных препаратов (гентамицина, неомицина, полимиксина В и др.), кортикостероидов; применения противогрибковых средств (амфотерицина В, кетоконазола). В комбинации с глазными каплями используются мазевые аппликации за веко этих же средств. При прогрессирующих изменениях роговицы может быть показано проведение кератопластики.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">При акантамебиазе кожи проводится системная антибиотикотерапия препаратами из группы аминогликозидов, местное нанесение мазей с неомицином, полимиксином и др. Наиболее сложную задачу представляет терапия акантамебного энцефалита. При данной клинической форме акантамебиаза показано внутривенное введение амфотерицина В, назначение комбинации триметоприма и сульфаметоксазола, аминогликозидов. Лечение акантамебиаза ЦНС оказывается эффективным лишь в единичных случаях.</span></p>",
"prevention": "<p> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Для профилактики данного патологического процесса следует избегать купания в грязных водоемах, соблюдать правила хранения и использования контактных линз, а также следить за качеством используемой для питья воды.</span></p>",
"clinical_picture": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Наиболее частая клиническая форма акантамёбиаза - акантамёбный кератит. Первоначальные симптомы:</span></p>\r\n<ul>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">краснота глаз,</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">режущая боль в глазах,</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">светобоязнь, слёзотечение,</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">затуманенность, размытость взора,</span></li>\r\n<li><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">ощущение наличия в глазу инородного тела.</span></li>\r\n</ul>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Позже образуется кольцевидной или дисковидной формы помутнение роговицы. Протекает в виде чередования обострений и ремиссий, что нередко становится причиной увеита, склерита, иридоциклита, гипопиона. Без лечения болезнь быстро прогрессирует, приводя к перфорации роговицы.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Акантамёбиазное поражение кожного покрова может быть первичным и вторичным. Первичное развивается в результате попадания загрязнённой цистами воды на травмированную кожу. Возникают одиночные или же многочисленные узелки, папулы, пятна серого, чёрного цвета, до 0,5 - 3 см в диаметре. Позднее в этих местах образуются язвы, покрытые коркой. Вторичное поражение обусловлено распространением акантамёб из первичного очага.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"> </p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 6.999999999999999pt; font-family: Verdana; color: #000000; background-color: transparent; font-weight: 400; font-style: normal; font-variant: normal; text-decoration: none; vertical-align: baseline; white-space: pre-wrap;\">Акантамёбное поражение ЦНС протекает в форме гранулематозного воспаления головного мозга. Встречается редко и развивается в результате гематогенного заноса акантамёб в головной мозг. Может поражаться собственно ткань головного мозга или оболочки. При сниженной резистентности организма может образоваться абсцесс. В начальном периоде имеется непостоянный субфебрилитет, сонливость, головные боли. Возможны судороги, нарушение конвергенции. При прогрессировании возможно развитие комы и смерти. </span></p>",
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},
{
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"code": "B59",
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"description": "Инфекционное заразное заболевание.",
"etiology": "<p>Возбудитель - Pneumocystis carinii относится к типу простейших, подтип Sporozoa, класс Haplospora. Местом естественного обитания в нормальных условиях являются легкие. Жизненный цикл построен таким образом, что в альвеолярной ткани можно обнаружить 2 основные формы этого микроорганизма: мелкие одноядерные трофозоиты (1-5 мкм) и размножающиеся бинарным делением цисты (10 мкм), имеющие толстую стенку и содержащие от 2 до 8 клеток (1-2 мкм), называющихся спорозоитами. Когда зрелая циста разрывается, спорозоиты либо продолжают цикл развития в альвеолах, превращаясь в трофозоит, либо выходят во внешнюю среду (с капельками слизи при кашле) и, в случае обретения нового хозяина, также включаются в свой цикл развития.Пневмоцисты широко распространены у людей и животных. Передаются воздушно-капельным путем. Известно, что от 1 до 10% здоровых людей являются носителями пневмоцист. </p>",
"pathogenesis": "<p>Заболевания развиваются только у лиц с первичными или приобретенными нарушениями иммунитета. Ведущую роль играют нарушения механизмов клеточного иммунитета. У больных пневмоцистозом отмечается местная и системная продукция антител, не обладающих, однако, протективным действием. Не встречая противодействия со стороны клеточных элементов защиты (в первую очередь альвеолярных макрофагов), пневмоцисты постепенно заполняют всю полость альвеол. При гистологическом исследовании обнаруживают типичный пенистый вакуолизированный альвеолярный <a title=\"Перейти на страницу симптома Выпот\" href=\"../../../symptom/vypot/\">экссудат</a>, содержащий микроорганизмы, белки сыворотки крови и остатки органических веществ. Отмечается выраженная дистрофия альвеолоцитов I типа, репаративная гипертрофия альвеолоцитов II типа. Указанные изменения постепенно приводят к нарушению газообменной функции альвеолярного эпителия и, соответственно, тяжелой (при отсутствии лечения фатальной) дыхательной недостаточности.</p>\r\n<full></full>\r\n<p>Отягощающим моментом является образование участков ателектаза, что усугубляет нарушения вентиляции и газообмена. У ослабленных детей можно обнаружить интенсивный инфильтрат из плазматичеких клеток, что и легло в основу прежнего названия болезни - интерстициальная плазмоклеточная пневмония. Вне ткани легких пневмоцисты практически не обнаруживаются.</p>",
"diagnostics": "<p align=\"justify\">Клинические, физикальные и рентгенологические данные при пневмоцистозе не являются патогномоничными, что затрудняет своевременную диагностику заболевания. Между тем, пневмоцистную пневмонию всегда следует исключать у иммунокомпрометированных пациентов. С целью верификации пневмоцистоза проводится комплекс лабораторных и инструментальных исследований.</p>\r\n<full></full>\r\n<p align=\"justify\">На рентгенограммах и КТ легких в типичных случаях определяется облаковидное понижение прозрачности легочных полей, получившее название «хлопьев снега» или «ватного легкого». Иногда рентгенологические изменения отсутствуют или имеют атипичную картину. С помощью ФВД обнаруживаются признаки дыхательной недостаточности по рестриктивному типу; исследование газового состава крови свидетельствует о гипоксемии.</p>\r\n<p align=\"justify\">Для подтверждения диагноза пневмоцистоза выполняется бронхоскопия с забором бронхиального секрета, трансбронхиальная биопсия легкого, сцинтиграфия легких с галлием-67. Для лабораторной детекции P.carinii микроскопически исследуются окрашенные мазки мокроты, бронхиальный и трахеальный аспират; выполняется гистологическое исследование биоптатов, исследование мокроты методом ПЦР. Проводится иммунологическая диагностика: определение титра противопневмоцистных IgG и IgM в сыворотке крови с помощью РИФ и ИФА.</p>",
"treatment": "<p>Лечение пневмоцистоза проводится в стационаре. Лица с иммунодефицитом и недоношенные дети должны быть помещены в отдельные стерильные палаты с ламинарным воздушным потоком. В большинстве случаев для проведения специфической фармакотерапии пневмоцистоза используется ко-тримоксазол (триметоприм, септрин, бактрим), пентамидин, триметрексат, триметоприм+дапсон, эфлорнитин, атоваквон в течение 2-3 недель. Для устранения побочных эффектов терапии назначают фолиевую кислоту, глюкокортикоиды. Проводится инфузионная терапия (введение гамма-глобулина, гемодеза, глюкозы, плазмы крови, альбумина и др.), кислородотерапия. У больных ВИЧ-инфекцией этиотропная терапия пневмоцистной пневмонии сочетается с высокоактивной антиретровирусной терапией.</p>",
"prevention": "",
"clinical_picture": "<p>Пневмоцистоз у детей развивается обычно на 4-6-м месяце жизни (недоношенные, больные рахитом, гипотрофией, поражениями ЦНС) и в более старших возрастных группах (при гемобластозе, злокачественных новообразованиях, СПИДе). Заболевание начинается постепенно - у ребенка снижается аппетит, прекращается нарастание массы тела, появляются бледность и <a title=\"Перейти на страницу симптома Цианоз\" href=\"../../../symptom/cianoz/\">цианоз</a> носогубного треугольника, легкое покашливание. Нормальная в начале заболевания температура сменяется субфебрильной с подъемами до фебрильной. В легких появляются непостоянные мелко- и среднепузырчатые <a title=\"Перейти на страницу симптома Хрипы\" href=\"../../../symptom/hripy/\">хрипы</a>. Появляются <a title=\"Перейти на страницу симптома Одышка\" href=\"../../../symptom/odyshka/\">одышка</a> (до 50-70 в 1 мин), <a title=\"Перейти на страницу симптома Цианоз\" href=\"../../../symptom/cianoz/\">цианоз</a>, <a title=\"Перейти на страницу симптома Кашель\" href=\"../../../symptom/kashel/\">кашель</a> коклюшеобразного характера. Нередко <a title=\"Перейти на страницу симптома Кашель\" href=\"../../../symptom/kashel/\">кашель</a> сопровождается выделением пенистой мокроты, в которой могут обнаруживаться пневмоцисты. Рентгенологически регистрируются очаговые тени разной величины и плотности, дающие картину \"облаковидного\" легкого. В крови обнаруживается лейкоцитоз, умеренная эозинофилия и увеличение СОЭ.</p>\r\n<full></full>\r\n<p>Иногда пневмоцистоз у детей протекает под маской острого ларингита, обструктивного бронхита или бронхиолита. В ряде случаев наступает летальный исход при клинической картине отека легких.</p>\r\n<p>У взрослых пневмоцистоз развивается у лиц, получающих иммуносупрессивную терапию (обычно - кортикостероиды), и у больных СПИДом. При медикаментозной иммуносупрессии заболевание часто манифестируется на фоне снижения дозы кортикостероидов. Продромальный период длится обычно 1-2 нед, а у больных СПИДом он достигает 10 нед. Постепенно появляется субфебрилитет, умеренная <a title=\"Перейти на страницу симптома Одышка\" href=\"../../../symptom/odyshka/\">одышка</a> при физической нагрузке, сухой <a title=\"Перейти на страницу симптома Кашель\" href=\"../../../symptom/kashel/\">кашель</a>, боли в грудной клетке. Через 1-2 нед могут появиться <a title=\"Перейти на страницу симптома Высокая температура 38-42° \" href=\"../../../symptom/vysokaya_temperatura_38-42/\">лихорадка</a>, <a title=\"Перейти на страницу симптома Одышка\" href=\"../../../symptom/odyshka/\">одышка</a> в покое, усиливается сухой <a title=\"Перейти на страницу симптома Кашель\" href=\"../../../symptom/kashel/\">кашель</a> (продуктивный <a title=\"Перейти на страницу симптома Кашель\" href=\"../../../symptom/kashel/\">кашель</a> отмечается редко). При осмотре обнаруживается тахипноэ, <a title=\"Перейти на страницу симптома Тахикардия\" href=\"../../../symptom/tahikardiya/\">тахикардия</a>, <a title=\"Перейти на страницу симптома Цианоз\" href=\"../../../symptom/cianoz/\">цианоз</a>. В легких часто выслушиваются сухие, реже - влажные <a title=\"Перейти на страницу симптома Хрипы\" href=\"../../../symptom/hripy/\">хрипы</a>. Количество лейкоцитов обычно зависит от фонового заболевания. При газовом анализе крови обнаруживают прогрессирующую гипоксемию, повышение альвеолярно-артериального кислородного градиента и респираторный алкалоз.</p>\r\n<p>Пневмоцистная пневмония при СПИДе обычно характеризуется вялым хроническим течением. Первоначально аускультативная симптоматика не выявляется, рентгенологическая картина тоже может оставаться без патологических изменений. По мере прогрессирования заболевания появляются двухсторонние прикорневые инфильтраты, трансформирующиеся затем либо в фокусные, либо интерстициальные изменения. Изредка обнаруживаются солитарные узелки, которые могут кавернизироваться с образованием обширной центральной полости. Причиной абсцедирования, вероятно, является присоединение бактериальных и микозных инфекций.</p>",
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{
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{
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"name": "мышечная боль"
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{
"name": "боль в мышцах"
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{
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},
{
"name": "Миалгия"
},
{
"name": "ломота"
},
{
"name": "боль в мышцах рук"
},
{
"name": "боль в мышцах ног"
},
{
"name": "боль в мышцах после тренировки"
},
{
"name": "боль в мышцах спины"
},
{
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"lead": "Мышечная боль, которая периодически возникает у людей при нагрузке или в покое, называется миалгией. Она может вызываться различными причинами и сопровождаться другими симптомами",
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{
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},
"code": "B58",
"name": "Токсоплазмоз",
"icd_name": "Токсоплазмоз",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
2,
5,
7,
9
],
"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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"icd_name": "Болезнь Шагаса",
"gender": 0,
"age_min": 0,
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"cause": [
2,
5,
6,
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10
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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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