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"etiology": "<p>Этот патологический синдром обусловлен гиперфункцией коры надпочечников, которая может быть вызвана:<br /><br />1) генетически обусловленной недостаточностью ферментной системы 21-гидроксилазы в коре надпочечников (врожденный адреногенитальный синдром);<br /><br />2) гиперплазией или опухолью коры надпочечников (приобретенный адреногенитальный синдром).</p>",
"pathogenesis": "<p>Сущность патологии состоит в том, что вследствие дефекта в энзимной системе коры надпочечников (врожденного или приобретенного) нарушается способность последней синтезировать гидрокортизон и кортизон из 17-λ-гидроксипрогестерона. Недостаточное образование гидрокортизона корой надпочечников обусловливает увеличение секреции АКТГ гипофизом, что вызывает еще большее образование 17-λ-гидрокортизона. Избыток последнего ведет к усиленному образованию различных андрогенов (мужских половых гормонов). Большое количество андрогенов угнетает гонадотропную функцию гипофиза, что ведет к снижению функции яичников.</p>",
"diagnostics": "<p>Диагностирование основано на наличии характерных клинических симптомов, исследовании экскреции 17-кетостероидов с мочой – при адреногенитальном синдроме она увеличивается в 2–3 раза и составляет 25–40 мг/сут., при опухолях надпочечников она увеличивается до 200 мг/сут.</p>",
"treatment": "<p>При опухолях коры надпочечников проводят удаление опухоли, после операции проявления вирильного синдрома исчезают. При врожденном адреногенитальном синдроме огромную роль играет возраст, в котором начато лечение. Чем раньше начата терапия, тем она эффективнее.<br /><br />Лечение заключается в применении кортизона или преднизолона, они тормозят темп роста и процесс окостенения. Тело приобретает черты женского организма, формируются молочные железы, появляются вторичные половые признаки, присущие женскому организму. Необходимо оперативное вмешательство – коррекция наружных половых органов (удаление пенисообразного клитора и формирование входа во влагалище).<br /><br />Прогноз<br /><br />При своевременно начатой адекватной терапии и успешной операции благоприятный, однако такие девочки остаются бесплодными.</p>",
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"clinical_picture": "<p>При врожденном адреногенитальном синдроме сразу же после рождения обращает на себя внимание нарушение строения наружных половых органов. Нарушения выражаются в увеличении клитора различной степени (от гипертрофии до пенисообразного), наличии урогенитального синуса, углублении преддверья влагалища, высокой промежности, недоразвитии малых и больших половых губ. Если вирилизация значительно выражена, то нередко возникают затруднения в определении пола ребенка. Соматическое развитие детей с адреногенитальным синдромом характеризуется резко выраженным ускорением темпа роста в первое десятилетие жизни (в 2–3 раза по сравнению со здоровыми девочками). К 12 годам рост прекращается, окостенение почти завершено. Телосложение в связи с этим носит диспластический характер: рост ниже среднего, широкие плечи, узкий таз, короткие конечности, массивные трубчатые кости. Период полового созревания происходит рано, в 6–7 лет, и протекает по гетеросексуальному типу. Молочные железы и менструальная функция отсутствуют. У половозрелых женщин (с приобретенным адреногенитальным синдромом) наблюдается вирилизация различной степени. Она проявляется чрезмерным гирсутизмом (оволосением), олигоменореей или аменореей, уменьшением размеров матки и яичников, бесплодием, атрофией молочных желез. Голос становится низким, кожа становится пористой, начинают расти волосы на подбородке и щеках.</p>",
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"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>",
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"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>",
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"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;\">Единственным достоверно установленным возбудителем заболевания является боррелия, передающаяся человеку при укусе клеща Ixodes ricinus. Некоторые дерматологи считают, что хронический атрофический акродерматит может развиться на фоне сбоев нейроэндокринной системы, хотя, вероятнее всего, эти системные нарушения являются такими же проявлениями третьей стадии болезни Лайма, как и сам хронический атрофический акродерматит.</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;\">Другие авторы относят заболевание к аутоиммунной патологии, возникшей при инфицировании организма возбудителями сифилиса, туберкулёза, малярии. В качестве триггеров патологического процесса иногда рассматривают травмы или температурно-холодовой фактор. Однако современные представления о механизме возникновения хронического атрофического акродерматита всё-таки связаны с боррелиозом.</span></p>",
"pathogenesis": "<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;\">Кожные проявления третьей стадии болезни Лайма являются следствием повреждающего действия циркулирующих иммунных комплексов (ЦИК). Развитие хронического атрофического акродерматита в течение двух первых стадий боррелиоза носит латентный характер, заключается в формировании и накоплении этих комплексов. После укуса клеща спирохета попадает в кровь и лимфу, разносится во все органы и ткани, оккупирует лимфатические узлы. В них спирохета способна жить и размножаться годами.</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;\">Часть боррелий, циркулирующих в крови, погибает, выбрасывая в кровоток эндотоксин, стимулирующий иммунную систему. Возникают иммунные реакции антиген-антитело, результатом которых становится формирование циркулирующих иммунных комплексов, образующихся после каждой встречи антигена с антителом.</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;\">ЦИК начинают оказывать негативное влияние на дерму, нарушая её морфологию, изменяя проницаемость сосудов и формируя воспалительные инфильтраты. В область образовавшегося инфильтрата из крови мигрируют нейтрофилы. Живые боррелии, циркулирующие в крови, стимулируют синтез интерлейкинов, что усугубляет воспаление, способствующее более интенсивному разрушению структуры дермы.</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;\">Одна стадия боррелиоза сменяет другую, в кровь в это время постоянно выбрасываются новые «порции» спирохет из лимфатических узлов. Они снова выделяют эндотоксин, который стимулирует образование циркулирующих иммунных комплексов. Так происходит до тех пор, пока количество ЦИК в крови не станет достаточным для гиперстимуляции воспаления в дерме, дополнительного изменения проницаемости стенки капилляров кожи с визуальными кожными проявлениями. Это происходит одновременно с переходом боррелиоза в третью стадию и свидетельствует о хронизации процесса.</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;\">Клинический диагноз выставляют дерматолог и инфекционист. Основаниями для постановки диагноза являются анамнез, клиническая картина и серологические тесты. Гистологию подключают для дифференциации патологического процесса. Консультации узких специалистов необходимы для исключения системной патологии.</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;\">РНИФ (реакцию непрямой иммунофлуоресценции) используют для определения титра боррелиозных антител. ИФА (иммуноферментный анализ) позволяет установить наличие боррелий в крови пациента. ПЦР и иммуноблоттинг дают возможность подсчитать точное количество боррелий в единице объёма крови.</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;\">Эффективность терапии зависит от стадии патологического процесса и своевременности начатого лечения. Терапия хронического атрофического акродерматита патогенетическая, проводится курсами антибиотиков, суммарная доза которых рассчитывается с учетом результатов серологического тестирования и веса пациентов. Одновременно применяют витаминотерапию и препараты железа. Если выявлена соматическая патология, осуществляют её коррекцию.</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 хроническом атрофическом акродерматите эффективны физиопроцедуры: УФО, дарсонваль, гальванизация, УВЧ, диатермия, сероводородные тёплые минеральные ванны, грязевые обёртывания, аппликации с озокеритом, парафином, массаж. Наружно показаны мази, содержащие витамины и вазоактивные препараты. После консультации с хирургом возможно хирургическое удаление подкожных узлов.</span></p>",
"prevention": "<p><span id=\"docs-internal-guid-91c1bc22-7fff-0b92-2c37-1932b9203040\"><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;\">Профилактика сводится к внимательному отношению к своему здоровью, регулярному наблюдению у дерматолога и ведению здорового образа жизни.</span></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;\">Отличительной особенностью хронического атрофического акродерматита является его стадийность. В клинической картине патологического процесса выделяют несколько периодов.</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;\">Первый, эритематозно-инфильтративный (предатрофический) характеризуется возникновением яркой спонтанной эритемы с синюшным оттенком на фоне отёчной кожи, которая со временем диффузно инфильтрируется, создавая основу будущей атрофии. Локализуются кожные проявления преимущественно на конечностях. Высыпания сопровождаются продромальными ощущениями, снижением кожной чувствительности, артралгиями, уменьшением сократительной способности мышц.</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;\">Второй, переходный (прогрессивно-атрофический) период протекает с нарастанием экссудативно-воспалительных явлений, которые в последующем постепенно стихают. Кожа теряет влагу, шелушится, снижается её эластичность. Она легко собирается в складки, становится настолько тонкой, что сквозь неё начинают просвечивать сосуды.</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;\">Третий период (стационарно-атрофический) характеризуется развитием не только атрофии кожи, но и дерматосклероза. Кожа приобретает коричневый оттенок, в очагах хронического атрофического акродерматита возникает дисхромия – гипопигментация и апигментация чередуется с гиперпигментацией.</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;\">В процесс вовлекаются придатки кожи, нарушается секреция сальных и потовых желёз, выпадают пушковые волосы, деформируются ногти. Отличительной особенностью кожной патологии при хроническом атрофическом акродерматите являются не только высыпания, но и нарушение тактильной чувствительности кожи с сохранением температурной и болевой составляющей.</span></p>\r\n<p><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;\"> </span></p>",
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"description": "",
"etiology": "<p>Возбудители — различные виды актиномицетов, или лучистых грибов. Основными из них являются следующие: Actinomyces israelu, Actinomyces bovis, Actinomyces albus, Ac. violaceus. Актиномицеты хорошо растут на питательных средах, образуя колонии неправильной формы, нередко с лучистыми краями. Патогенны для многих видов сельскохозяйственных и лабораторных животных. В патологическом материале встречаются в виде друз, которые представляют собой желтоватые комочки диаметром 1—2 мм. При микроскопии в центре друз обнаруживается скопление нитей мицелия, а по периферии — колбовидные вздутия. При окраске гематоксилин-эозином центральная часть друзы окрашивается в синий цвет, а колбы в розовый. Встречаются друзы, у которых кайма из колбообразных клеток отсутствует. Актиномицеты чувствительны к бензилпенициллину (20 ЕД/мл), стрептомицину (20 мкг/мл), тетрациклину (20 мкг/мл), левомицетину (10 мкг/мл) и эритромицину (1,25 мкг/мл).</p>\r\n<p>Эпидемиология. Актиномикоз распространен во всех странах. Им заболевают люди и сельскохозяйственные животные. Однако случаев заражения человека от больных людей или животных не описано. Возбудители актиномикоза широко распространены в природе (сено, солома, почва и др.). Актиномицеты часто обнаруживают у здоровых людей в ротовой полости, зубном налете, лакунах миндалин, на слизистой оболочке желудочно-кишечного тракта. Имеет значение как экзогенный, так и эндогенный способы заражения.</p>",
"pathogenesis": "<p>Наиболее частым является эндогенный путь инфекции. Актиномицеты широко распространены в природе, в частности на растениях, могут попадать с растениями в организм и находиться на слизистых оболочках в качестве сапрофита. Переходу актиномицетов из сапрофитического в паразитическое состояние способствуют воспалительные заболевания слизистых оболочек полости рта, респираторного и желудочно-кишечного тракта. На месте внедрения актиномицетов образуется инфекционная гранулема, которая прорастает в окружающие ткани. В грануляциях возникают абсцессы, которые, прорываясь, образуют свищи. Поражение кожи имеет вторичный характер.</p>\r\n<p>В образовании нагноений играет роль и вторичная, преимущественно стафилококковая инфекция. Антигены лучистых грибов приводят к специфической сенсибилизации и аллергической перестройке организма (гиперсенсибилизация замедленного или туберкулинового типа), а также к образованию антител(комплементсвязывающие, агглютинины, преципитины и др.).</p>",
"diagnostics": "<p>Диагноз основан на серологических реакциях, выделении грибка из крови.</p>",
"treatment": "<p><br />Эффективно применение поливалентной актиномицетной сыворотки, актинолизата, при осложнениях используются антибиотики широкого спектра действия, в тяжелых случаях – переливание крови, плазмы, внутривенное введение дыхательных аналептиков, кардиотонических средств, биостимуляторов, удаление каверны хирургическим методом.</p>",
"prevention": "",
"clinical_picture": "<p>Длительность инкубационного периода не известна.Он может колебаться в широких пределах и доходить до нескольких лет (от времени инфицирования до развития манифестных форм актиномикоза). Основные клинические формы актиномикоза: 1) актиномикоз головы, языка и шеи;2) торокальный актиномикоз; 3) абдоминальный; 4) актиномикоз мочеполовых органов; 5) актиномикоз кожи; 6) мицетома (мадурская стопа); 7) актиномикоз центральной нервной системы. Актиномикоз относится к первично-хроническим инфекциям с длительным прогрессирующим течением. При разрастании инфильтрата в процесс вовлекается кожа. Вначале определяется очень плотный и почти безболезненный инфильтрат, кожа становится цианотично-багровой, появляется флюктуация, а затем развиваются длительно незаживающие свищи. В гное обнаруживают беловато-желтоватые мелкие комочки (друзы).</p>\r\n<p>Шейно-челюстно-лицевая форма встречается наиболее часто. По выраженности процесса можно выделить глубокую (мышечную) форму, когда процесс локализуется в межмышечной клетчатке, подкожную и кожную формы актиномикоза. При мышечной форме процесс локализуется преимущественно в жевательных мышцах, под покрывающей их фасцией, образуя плотный, хрящевой консистенции инфильтрат в области угла нижней челюсти. Лицо становится асимметричным, развивается <a href=\"/symptom/trizm/\" title=\"Перейти на страницу симптома Тризм\">тризм</a> различной интенсивности. Затем в инфильтрате появляются очаги размягчения, которые самопроизвольно вскрываются, образуя свищи, отделяющие гнойную или кровянисто-гнойную жидкость, иногда с примесью желтых крупинок (друз). Синюшная окраска кожи вокруг свищей длительно сохраняется и является характерным проявлением актиномикоза. На шее образуются своеобразные изменения кожи в виде поперечно расположенных валиков. При кожной форме актиномикоза инфильтраты шаровидные или полушаровидные, локализующиеся в подкожной клетчатке. Тризма и нарушений процессов жевания не наблюдается. Кожная форма встречается редко. Актиномикозный процесс может захватывать щеки, губы, язык, миндалины, трахею, глазницы, гортань. Течение относительно благоприятное (по сравнению с другими формами).</p>\r\n<p>Торакальный актиномикоз (актиномикоз органов грудной полости и грудной стенки), или актиномикоз легких. Начало постепенное. Появляются <a href=\"/symptom/slabost/\" title=\"Перейти на страницу симптома Слабость\">слабость</a>, <a href=\"/symptom/povyshennaya_temperatura_37-38/\" title=\"Перейти на страницу симптома Повышенная температура 37-38°\">субфебрильная температура</a>, <a href=\"/symptom/kashel/\" title=\"Перейти на страницу симптома Кашель\">кашель</a>, вначале сухой, затем со слизисто-гнойной мокротой, нередко с примесью крови (<a href=\"/symptom/vlazhnyy_kashel/\" title=\"Перейти на страницу симптома Влажный кашель\">мокрота</a> имеет запах земли и вкус меди). Затем развивается картина перибронхита. Инфильтрат распространяется от центра к периферии, захватывает плевру, грудную стенку, кожу. Возникает <a href=\"/symptom/otek_tkaney/\" title=\"Перейти на страницу симптома Отек тканей\">припухлость</a> с чрезвычайно выраженной жгучей болезненностью при пальпации, кожа становится багрово-синюшной. Развиваются свищи, в гное обнаруживаются друзы актиномицетов. Свищи сообщаются с бронхами. Они располагаются не только на грудной клетке, но могут появиться на пояснице и даже на бедре. Течение тяжелое. Без лечения больные умирают. По частоте торокальный актиномикоз занимает второе место.</p>\r\n<p>Абдоминальный актиномикоз также встречается довольно часто (занимает третье место). Первичные очаги чаще локализуются в илеоцекальной области и в области аппендикса (свыше 60%), затем идут другие отделы толстой кишки и очень редко поражается первично желудок или тонкий кишечник, пищевод.</p>\r\n<p>Брюшная стенка поражается вторично. Первичный инфильтрат чаще всего локализуется в илеоцекальной области, нередко имитирует хирургические заболевания (аппендицит, <a href=\"/symptom/invaginaciya/\" title=\"Перейти на страницу симптома Инвагинация\">непроходимость кишечника</a> и др.). Распространяясь, инфильтрат захватывает и другие органы: печень, почки, позвоночник, может достигнуть брюшной стенки. В последнем случае возникают характерные изменения кожи, свищи, сообщающиеся с кишечником. Расположены обычно в пахо-вой области. При актиномикозе прямой кишки инфильтраты обусловливают возникновение специфических парапроктитов, свищи вскрываются в перианальной области. Без этиотропного лечения летальность достигает 50%.</p>\r\n<p>Актиномикоз половых и мочевых органов встречается редко. Как правило, это вторичные поражения при распространении инфильтрата при абдоминальном актиномикозе. Первичные актиномикозные поражения половых органов встречаются очень редко.</p>\r\n<p>Актиномикоз костей и суставов встречается редко. Эта форма возникает или в результате перехода актиномикозного инфильтрата с соседних органов, или является следствием гематогенного заноса гриба. Описаны остеомиелиты костей голени, таза, позвоночника, а также поражения коленного и других суставов. Нередко процессу предшествует травма. Остеомиелиты протекают с деструкцией костей, образованием секвестров. Обращает на себя внимание, что несмотря на выраженные костные изменения, больные сохраняют способность передвигаться, при поражениях суставов функция серьезно не нарушается. При образовании свищей возникают характерные изменения кожи.</p>\r\n<p>Актиномикоз кожи возникает, как правило, вторично при первичной локализации в других органах. Изменения кожи становятся заметными, когда актиномикозные инфильтраты достигают подкожной клетчатки и особенно характерны при образовании свищей.</p>\r\n<p>Мицетома (мадуроматоз, мадурская стопа) — своеобразный вариант актиномикоза. Эта форма была известна давно, довольно часто встречалась в тропических странах. Заболевание начинается с появления на стопе, преимущественно на подошве, одного или нескольких плотных отграниченных узлов величиной от горошины и более, покрытых сначала неизмененной кожей, в дальнейшем над уплотнениями кожа становится красно-фиолетовой или буроватой. По соседству с первоначальными узлами появляются новые, кожа отекает, стопа увеличивается в объеме, меняет свою форму. Затем узлы размягчаются и вскрываются с образованием глубоко идущих свищей, выделяющих гнойную или серозно-гнойную, иногда кровянистую жидкость, нередко с дурным запахом. В отделяемом заметны мелкие крупинки обычно желтоватого цвета (друзы). Узлы почти безболезненны. Процесс медленно прогрессирует, вся подошва пронизывается узлами, пальцы ноги поворачиваются кверху. Затем узлы и свищевые ходы появляются и на тыле стопы. Вся стопа превращается в деформированную и пигментированную массу, пронизанную свищами и полостями. Процесс может переходить на мышцы, сухожилия и кости. Иногда наблюдается атрофия мышц голени. Обычно процесс захватывает только одну стопу. Заболевание продолжается очень долго (10—20 лет).Осложнения. Наслоение вторичной бактериальной инфекции.</p>",
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