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"code": "B53",
"name": "Другие виды паразитологически подтвержденной малярии",
"icd_name": "Другие виды паразитологически подтвержденной малярии",
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"lead": "Нарушение здоровья, относящееся к группе протозойные болезни",
"description": "Малярия - группа трансмиссивных инфекционных заболеваний, передаваемых человеку при укусах самками комаров рода Anopheles («малярийных комаров») и сопровождающихся лихорадкой, ознобами, спленомегалией (увеличением размеров селезёнки), гепатомегалией (увеличением размеров печени), анемией. Характеризуется хроническим рецидивирующим течением. Вызывается паразитическими протистами рода Plasmodium ",
"etiology": "<p>Возбудители малярии — простейшие рода Plasmodium ovale. </p>\r\n<p>Источником болезни являются люди, в крови которых циркулируют зрелые гаметоциты. При кровососании вместе с кровью в желудок комара проникают гаметоциты, и комар становится резервуаром инфекции. Ведущий механизм заражения человека — трансмиссивный, реализующийся самками комаров рода Anopheles при кровососании. </p>\r\n<p>Возможен парентеральный путь заражения при гемотрансфузиях, использовании плохо обработанного или не подлежащего повторном у использованию инструментария, а также передача плазмодиев от матери к плоду (при тропической малярии) — так называемая шизонтная малярия. </p>",
"pathogenesis": "<p>Человек заражается плазмодиями в момент инокуляции (впрыскивания) самкой малярийного комара одной из стадий жизненного цикла возбудителя (так называемых спорозоитов) в кровь или лимфатическую систему, которое происходит при кровососании. </p>\r\n<p>После кратковременного пребывания в крови спорозоиты малярийного плазмодия проникают в гепатоциты печени, давая тем самым начало доклинической печёночной (экзоэритроцитарной) стадии заболевания. В процессе бесполого размножения, называемого шизогонией, из одного бывшего спорозоита, который в клетке печени превращается в шизонта, в итоге образуется от 2000 до 40 000 печёночных мерозоитов. В большинстве случаев эти дочерние мерозоиты через 1—6 недель снова попадают в кровь. </p>\r\n<p> </p>",
"diagnostics": "<p>Диагноз устанавливается на основе выявления паразитов в мазках крови. Традиционно используют два типа мазков — тонкий и толстый (или так называемую «толстую каплю»). Тонкий мазок позволяет с большей надёжностью определить разновидность малярийного плазмодия, поскольку внешний вид паразита (форма его клеток) при данном типе исследования лучше сохраняется. Толстый мазок позволяет микроскописту просмотреть больший объём крови, поэтому этот метод чувствительнее, но внешний вид плазмодия при этом изменяется, что не позволяет легко различать разновидности плазмодия. Поставить диагноз на основе микроскопического исследования зачастую бывает затруднительно, так как незрелые трофозоиты разных видов малярийного плазмодия плохо различимы, и обычно необходимо несколько плазмодиев, находящихся на разных стадиях созревания, для надёжной дифференциальной диагностики. </p>\r\n<p>В настоящее время используются также быстрые диагностические тесты с использованием иммунохимических наборов и ПЦР диагностика (определения генома паразита в крови). </p>",
"treatment": "<p>Режим: </p>\r\n<ul>\r\n<li>полупостельный (малярия без осложнений);</li>\r\n<li>постельный (при развитии осложнений).</li>\r\n</ul>\r\n<p> Диета (легкоусвояемая); </p>\r\n<ul>\r\n<li>диета №5</li>\r\n<li>диета №7 (при развитии нефротического синдрома).</li>\r\n</ul>\r\n<p> Обильное питье до 2,5-3,0 л жидкости. </p>\r\n<p>Медикаментозное лечение </p>\r\n<p>Лечение проводится препаратом хлорохином. Лечение хлорохином не гарантирует полного, радикального излечения трехдневной малярии, так как гематошизотропные препараты не действуют на гипнозоиты в печени, поэтому курс купирующего лечения должен дополняться назначением радикального лечения гистошизотропным препаратом Примахин. </p>\r\n<p>Лечение неосложненной малярии, устойчивой к хлорохину проводится хинином. При устойчивости к хинину применяют артемизинин (экстракт полыни) и его производные. </p>\r\n<p>Лечение осложненной малярии (церебральная малярия, малярийный алгид) проводят в отделении интенсивной терапии. </p>",
"prevention": "<p>Методы, которые используются для предотвращения распространения болезни или для защиты в областях, эндемичных для малярии, включают профилактические лекарственные средства, уничтожение комаров и средства для предотвращения укусов комаров. </p>\r\n<p>Современные лекарственные средства для профилактики включают мефлохин (Лариам), доксициклин и атовакуон-прогуанил гидрохлорид. </p>",
"clinical_picture": "<p>Инкубационный период, составляет 11-16 дней.</p>\r\n<p>Заболевание характеризуется невысокой паразитемией, рецидивирующим течением, интермиттирующей (чередование периодов нормальной и высокой температуры) лихорадкой с трехдневной или ежедневной периодичностью, вечерним временем наступления пароксизмов, умеренно выраженным увеличением печени и селезенки, анемией, обычно мягким доброкачественным течением с частым спонтанным выздоровлением после небольшого числа приступов.</p>\r\n<p>Клинические проявления заболевания очень сходны с таковыми при трехдневной малярии, но все же имеют свои особенности.</p>\r\n<p>Селезенка, как и печень, увеличивается крайне медленно и может быть доступна пальпации только через несколько недель от момента первичного приступа. Выраженных ознобов, нарушения общего состояния при этой форме малярии практически не наблюдается. Можно также отметить спонтанность прекращения приступов при сохраняющейся на низком уровне паразитемии.</p>\r\n<p>Прогноз при овале-малярии благоприятный, заболевание заканчивается полным выздоровлением.</p>",
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"code": "B54",
"name": "Малярия неуточненная",
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"lead": "Нарушение здоровья, относящееся к группе протозойные болезни",
"description": "<p>Малярия - группа трансмиссивных инфекционных заболеваний, передаваемых человеку при укусах самками комаров рода Anopheles («малярийных комаров») и сопровождающихся лихорадкой, ознобами, спленомегалией (увеличением размеров селезёнки), гепатомегалией (увеличением размеров печени), анемией. Характеризуется хроническим рецидивирующим течением. Вызывается паразитическими протистами рода Plasmodium .</p>",
"etiology": "<p>Возбудители малярии — простейшие рода Plasmodium. </p>\r\n<p>Источником болезни являются люди, в крови которых циркулируют зрелые гаметоциты. При кровососании вместе с кровью в желудок комара проникают гаметоциты, и комар становится резервуаром инфекции. Ведущий механизм заражения человека — трансмиссивный, реализующийся самками комаров рода Anopheles при кровососании. </p>\r\n<p>Возможен парентеральный путь заражения при гемотрансфузиях, использовании плохо обработанного или не подлежащего повторном у использованию инструментария, а также передача плазмодиев от матери к плоду (при тропической малярии) — так называемая шизонтная малярия. </p>",
"pathogenesis": "<p>Человек заражается плазмодиями в момент инокуляции (впрыскивания) самкой малярийного комара одной из стадий жизненного цикла возбудителя (так называемых спорозоитов) в кровь или лимфатическую систему, которое происходит при кровососании. </p>\r\n<p>После кратковременного пребывания в крови спорозоиты малярийного плазмодия проникают в гепатоциты печени, давая тем самым начало доклинической печёночной (экзоэритроцитарной) стадии заболевания. В процессе бесполого размножения, называемого шизогонией, из одного бывшего спорозоита, который в клетке печени превращается в шизонта, в итоге образуется от 2000 до 40 000 печёночных мерозоитов. В большинстве случаев эти дочерние мерозоиты через 1—6 недель снова попадают в кровь. </p>\r\n<p> </p>",
"diagnostics": "<p>Диагноз устанавливается на основе выявления паразитов в мазках крови. Традиционно используют два типа мазков — тонкий и толстый (или так называемую «толстую каплю»). Тонкий мазок позволяет с большей надёжностью определить разновидность малярийного плазмодия, поскольку внешний вид паразита (форма его клеток) при данном типе исследования лучше сохраняется. Толстый мазок позволяет микроскописту просмотреть больший объём крови, поэтому этот метод чувствительнее, но внешний вид плазмодия при этом изменяется, что не позволяет легко различать разновидности плазмодия. Поставить диагноз на основе микроскопического исследования зачастую бывает затруднительно, так как незрелые трофозоиты разных видов малярийного плазмодия плохо различимы, и обычно необходимо несколько плазмодиев, находящихся на разных стадиях созревания, для надёжной дифференциальной диагностики. </p>\r\n<p>В настоящее время используются также быстрые диагностические тесты с использованием иммунохимических наборов и ПЦР диагностика (определения генома паразита в крови). </p>",
"treatment": "<p>Режим: </p>\r\n<ul>\r\n<li>полупостельный (малярия без осложнений);</li>\r\n<li>постельный (при развитии осложнений).</li>\r\n</ul>\r\n<p> Диета (легкоусвояемая); </p>\r\n<ul>\r\n<li>диета №5</li>\r\n<li>диета №7 (при развитии нефротического синдрома).</li>\r\n</ul>\r\n<p> Обильное питье до 2,5-3,0 л жидкости. </p>\r\n<p>Медикаментозное лечение </p>\r\n<p>Лечение проводится препаратом хлорохином. Лечение хлорохином не гарантирует полного, радикального излечения трехдневной малярии, так как гематошизотропные препараты не действуют на гипнозоиты в печени, поэтому курс купирующего лечения должен дополняться назначением радикального лечения гистошизотропным препаратом Примахин. </p>\r\n<p>Лечение неосложненной тропической малярии, устойчивой к хлорохину проводится хинином. При устойчивости к хинину применяют артемизинин (экстракт полыни) и его производные. </p>\r\n<p>Лечение осложненной тропической малярии (церебральная малярия, малярийный алгид) проводят в отделении интенсивной терапии. </p>",
"prevention": "<p>Методы, которые используются для предотвращения распространения болезни или для защиты в областях, эндемичных для малярии, включают профилактические лекарственные средства, уничтожение комаров и средства для предотвращения укусов комаров. </p>\r\n<p>Современные лекарственные средства для профилактики включают мефлохин (Лариам), доксициклин и атовакуон-прогуанил гидрохлорид</p>",
"clinical_picture": "<p>От заражения до начала заболевания проходит от 8 до 25 суток. При трехдневной малярии (P. falciparum) инкубационный период может достигать 8–14 месяцев.</p>\r\n<p>Симптомы малярии: боль в суставах (артралгия), лихорадка, озноб, рвота, анемия и выделение гемоглобина в моче (гемоглобинурия). Также наблюдается увеличение размеров селезенки (спленомегалия) и печени (гепатомегалия), сильная головная боль. Наиболее тяжело, как правило, протекает тропическая малярия с развитием комы, менингитов, менингоэнцефалитов.</p>\r\n<p>Лихорадка приходится на момент выхода паразитов из разрушенных эритроцитов. Интервал между приступами лихорадки зависят от биологического цикла паразита.</p>\r\n<p>Характерно острое начало, температура тела может достигать 40–41,7°С, через несколько часов падает до 35–36°С. Анемия возникает вследствие массивного разрушения эритроцитов. Подъем температуры тела обуславливает нарушения кровообращения (артериальная гипотензия, брадикардия). Последующие спазм сосудов, закупорка капилляров разрушенными эритроцитами, повышение вязкости крови приводят к ишемии тканей и органов. Возможно поражение почек (характерно для тропической лихорадки) с развитием острой почечной недостаточности.</p>\r\n<p> </p>",
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"code": "B55",
"name": "Лейшманиоз",
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"lead": "кожное заболевание Leishmania tropica, которое вызывается простейшими паразитами – лейшманиями. Распространено в регионах с жаркими и теплыми климатическими условиями",
"description": "<p><span id=\"docs-internal-guid-8065f457-7fff-33ff-6f6b-bd4e6b7ad323\"><span style=\"font-size: 7pt; font-family: Verdana; background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; vertical-align: baseline; white-space: pre-wrap;\">Лейшманиоз - это инфекционная болезнь, вызываемая простейшими и сопровождающаяся поражением кожных покровов, реже слизистых оболочек.</span></span></p>",
"etiology": "<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 7pt; font-family: Verdana; background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; vertical-align: baseline; white-space: pre-wrap;\">Возбудитель инфекции – паразит Leishmania, относящийся к простейшим. Резервуарами паразитов в природе служат москиты, енотовидные собаки, ленивцы, грызуны, лисы и дикобразы. Основным способом заражения является трансмиссивный путь, реализуемый с помощью переносчиков – москитов, реже песчаных мух.</span></p>\r\n<p style=\"line-height: 1.38; margin-top: 0pt; margin-bottom: 0pt;\" dir=\"ltr\"><span style=\"font-size: 7pt; font-family: Verdana; background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; vertical-align: baseline; white-space: pre-wrap;\">Микроорганизм нуждается в смене двух хозяев для размножения, при этом безжгутиковая фаза развития проходит в организме людей либо животных, а жгутиковая – в пищеварительном тракте самки москита. При укусе переносчик срыгивает в ранку лейшманий, которые внедряются в толщу кожи. </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: 7pt; font-family: Verdana; background-color: transparent; font-variant-numeric: normal; font-variant-east-asian: normal; vertical-align: baseline; white-space: pre-wrap;\">Другие пути инфицирования (вертикальный, при гемотрансфузиях и оперативных вмешательствах) встречаются редко. Группами риска по кожному лейшманиозу являются дети, сельские жители, путешественники, ВИЧ-инфицированные люди и онкологические больные. Чаще всего заболевают молодые мужчины и пожилые женщины.</span></p>",
"pathogenesis": "<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;\">Возбудитель проникает в толщу кожи человека при укусе москита, формируя в области входных ворот лейшманиозную гранулему. Впоследствии, при висцеральной форме инфекции гранулема рассасывается, а при кожной - прогрессирует в язву. Лейшмании разносятся по организму с током лимфы, поражая регионарные лимфатические узлы. Вдоль лимфатического сосуда паразиты могут формировать лейшманиомы – ряд последовательно располагающихся специфических язв.</span></p>",
"diagnostics": "<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 подозрении на лейшманиоз для подтверждения диагноза могут быть использованы следующие методы диагностики:</span></p>\r\n<p> </p>\r\n<ul style=\"margin-top: 0; margin-bottom: 0; padding-inline-start: 48px;\">\r\n<li style=\"list-style-type: disc; font-size: 7.5pt; 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;\" dir=\"ltr\">\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;\">Микроскопия и ПЦР-исследование пунктатов органов и тканей, соскоба с пораженной области кожи</span></p>\r\n</li>\r\n<li style=\"list-style-type: disc; font-size: 7.5pt; 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;\" dir=\"ltr\">\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;\">ПЦР-исследование крови может быть информативным при лейшманиозе у пациентов с ВИЧ-инфекцией</span></p>\r\n</li>\r\n<li style=\"list-style-type: disc; font-size: 7.5pt; 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;\" dir=\"ltr\">\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;\">Серологическое исследование (ИФА IgG) применяется при подозрении на висцеральный лейшманиоз, но стоит помнить, что возможно получение как ложноотрицательных результатов (например, при ВИЧ-инфекции, при раннем и пожилом возрастах), так и ложноположительных (СКФ, лейкоз, сифилис, и др.). При этом серологические исследования не проводятся для определения эффективности проводимого лечения - это связано с длительным обнаружением IgG в крови после излечения. </span></p>\r\n</li>\r\n<li style=\"list-style-type: disc; font-size: 7.5pt; 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;\" dir=\"ltr\">\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;\">Также может быть информативным культуральное исследование пунктатов - посев на специальные среды.</span></p>\r\n</li>\r\n</ul>",
"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;\">Пациенты с кожными формами болезни не нуждаются в стационарном лечении. Постельный режим показан при выраженной лихорадке, болевом синдроме и гнойных осложнениях. Специальная диета не разработана, из-за возможных лекарственных побочных эффектов рекомендуется отказаться от приема алкоголя, наркотических средств и никотина, исключить на время лечения трудноперевариваемую пищу (жирное, жареное, маринады). Показана местная антисептическая обработка язв, полоскание рта и промывание носовых ходов при расположении очагов на слизистых, применение стерильных повязок с ежедневной сменой.</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;\">Специфическое антипротозойное лечение осуществляется с учетом вида возбудителя преимущественно препаратами пятивалентной сурьмы (натрия стибоглюконата). Возможно использование милтефозина, пентакарината, липосомального амфотерицина В. Системное применение этих средств сопряжено с риском развития побочных эффектов, поэтому в настоящее время ведется изучение местных медикаментов (кремы, мази) в качестве дополнения к основной терапии. Симптоматическое лечение подразумевает прием жаропонижающих, обезболивающих, дезинтоксикационных и других препаратов. При резистентности лейшманиоза проводится спленэктомия.</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;\">Местное лечение лейшманиозных кожных язв неразрывно связано с тепловым воздействием, поскольку возбудители крайне чувствительны к высоким температурам. Среди подобных методов терапии распространена радиочастотная, преимущество которой заключается в отсутствии повреждения здоровой кожи в процессе применения. Используется фотодинамическая и прямая электрическая терапия, инфракрасная стимуляция, лазеролечение. </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;\">Профилактика лейшманиоза включает меры по благоустройству населенных пунктов, ликвидацию мест расселения москитов (свалок и пустырей, затопленных подвальных помещений), дезинсекцию жилых помещений. Индивидуальная профилактика заключается в использовании репеллентов, других средств защиты от укусов москитов. При обнаружении больного производят химиопрофилактику пириметамином в коллективе. Специфическая иммунная профилактика (вакцинация) производится лицам, планирующим посещение эпидемически опасных районов, а также неимунному населению очагов инфекции.</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;\">Инкубационный период городской формы патологии длится от 10 суток до года, чаще – 3-5 месяцев; для сельского варианта время инкубации может сокращаться до 1-8 недель. Начало болезни постепенное, с лихорадкой до 38°C. Острый дебют характерен для маленьких детей и ВИЧ-позитивных пациентов, часто приводит к кожно-висцеральному поражению и гибели. На месте укуса москита появляется бурого цвета бугорок, который постепенно вырастает до 2-х и более сантиметров, покрывается мелкими чешуйками (лейшманиома). Затем образование продолжает свой рост и через полгода изъязвляется с появлением характерного слизисто-гнойного отделяемого. Заживление язвы завершается образованием рубца.</span></p>\r\n<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;\">Сельская форма болезни протекает гораздо быстрее и агрессивнее: лейшманиомы практически сразу переходят в язвенную стадию с формированием дочерних бугорков, через 2-4 месяца дно язвы начинает напоминать рыбью икру и центробежно заживать с появлением рубцового дефекта. Лимфатические сосуды воспаляются, пальпируются в виде твердых узлов-бусин, часть из которых вскрывается. После перенесенного городского кожного варианта в редких случаях отмечается хроническое течение процесса с образованием небольших бугорков около рубца, которые не изъязвляются и могут персистировать всю жизнь человека.</span></p>",
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"code": "B56",
"name": "Африканский трипаносомоз",
"icd_name": "Африканский трипаносомоз",
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"lead": "Нарушение здоровья, относящееся к группе протозойные болезни",
"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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{
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