STEP 1
STEP 2
· Anak laki 8 th :
o Gatal2 di anus trutama malam hari
o Sejak 2 inggu sering terbangun pd malam hari
o Rewel pada siang hari
o Nafsu makan turun
o BB turun
o Adiknya mengalami keluhan yg sama
Pf : kurus, mengantuk
Pemeriksaan local : bekas garukan di anus, warna kulit kemerahan, nyeri bila dipegang
Ø Mengapa gatal pada malam hari
Ø Mengapa gatalnya di anus?
Ø Apakah penyakitnya bisa menular apa tidak?
Ø Kenapa nafsu makan menurun?
Ø Hubungan penyakit dengan nnilai pelajaran yang turun?
Ø Mengapa Nampak kurus dan mengantuk?
Ø Mengapa warna kulit sekitar kmerahan dan nyeri bila dipegang?
· DD : OXYURIASIS à CACING OXYURIS VERMICULARIS
ASCARIASIS
STEP 3
Ø Mengapa gatal pada malam hari?
Disebabkan oleh parasit, sifat parasitnya mencari makan pada malam hari.
- Bertelur pada malam hari.
- Cacing betina hamil pda malam hari bergerak ke anus untuk meletakkan telurnya di perineumà gatal
Ø Apakah penyakitnya bisa menular apa tidak?
Bisa, melalui: sprei, baju, fekal-oral, udara,
garukanàmakanà tertelan lagi
Ø Kenapa nafsu makan menurun?
- Sifat parasitnya mngeluarkan toksin yg menyebabkan pnurunan nafsu makan
- Cacaingà usus halusà colon descendenànaruh di perineum untuk melindungi telurnya karena berlipat2à mempengaruhi motilitas ususà cepat kenyang
- Cacing à obstruksià distensi abdomen à cepat kenyang
-
Ø Hubungan penyakit dengan nilai pelajaran yang turun?
Waktu tidur malam terganggu à siang mengantuk à konsentrasi kurang à belajar kurang à nilai turun
Ø Mengapa Nampak kurus dan mengantuk?
Nafsu makan turunà bb turun à kurus
Tidur malam terganggu à siang mengantuk
Ø Mengapa warna kulit sekitar kmerahan dan nyeri bila dipegang?
Karena ada bekas garukanà iritasi à kemerahan à nyeri
DD : SOIL TRANSMINT HELMINT & NON SOIL TRANSMIT HELMINTH
· OXYURIASIS à CACING OXYURIS VERMICULARIS
§ DEFINISI
Infeksi cacing kremi adalah suatu infeksi parasit yang terutama menyerang anak2 dimana cacing enterobiasis vermicularis tumbuh dan berkembang biak di dalam usus
§ ETIOLOGI
Cacing enterobiasis vermicularis
§ EPIDEMIOLOGI
Bias terjadi pada semua umur tapi biasanya menyerang pada anak2, pada daerah yang panas.
o Anak yang terkena umumnya umur 5-14 th
§ PATOGENESIS
Cacing dewasa bertelurà malam hari migrasi ke anusàmeletakan telur di daerah sekitar anusàgatalà digaruk2à telurnya masuk ke jari à saat makan masuk ke mulut ( oral-fekal )
Dari orang ke orang : bergantian baju, tempat tidur,
Telur yang udah di buahi tertelan à di duonenum à tumbuh à dewasa tinggal di duodenum dan ileum à apabila sudah membuahi betina à jantan matià dikeluarkan lewar feses.
Cacing betina dapat bermigrasi ke vagina à radangà vaginitis
§ PATOFISIOLOGI
LI
§ MK
· Gatal hebat di sekitar anus
· Rewel karena rasa gatal dan tidur malam hari terganggu
· Gatal malam hari à kurang tidur
· Nafsu makan berkurang
· Bb turun
· Kulit sekitar anus lecet akibat garukan
§ DIAGNOSIS
Anamnesis
Pemeriksaan lbih lanjut ditemukan cacing dewasa dan telurnya pada pemeriksaan tinja.
Anal swab à dijumpai telur cacing
Anus anak malam harià ditemukan cacing dewasa kurang lebih 1-2 jam setelah anak tidur
Ditemukan telur pada usapan kuku
§ PENATALAKSANAAN
Mebendazol dosis tunggal 100 mg
Cara kerja :
a. Di cacing à merusak struktur sel2 cacing
b. Larva
Eksresi lewat urin
Garam piperazin
Pyrantel pamoat
Bikin spasmeà kontraksi àspasmeà obstruksià konstipasi.
Eksresi lewat tinja
Trabendazol
§ PENCEGAHAN
o Cuci tangan sebelum makan dan setelah BAB
o Memotong kuku
o Mencuci sprei min. 2x seminggu
o Membersihkan jamban tiap minggu
o Menghindari penggarukan daerah anus karena dapat mencemari jari tangan dan tiap benda yang dipegang
o Menjauhkan tangan dan jari tangan dari hidung dan mulut
o Pemberian obat tiap 3-4 bulan pada lingkungan yang mudah terpapar
§ KOMPLIKASI
· Ileus obstruksi
· Salpingitis : peradangan saluran indung telur
· Vaginitis : peradangan vagina
· Prolaps recti
§ PROGNOSIS
· Kalo diobatin baik
· ASCARIASIS
§ DEFINISI
Infeksi yang dibabkan oleh ascaris lumbricoides yang merupakan nematode usus terbesar
§ ETIOLOGI
ascaris lumbricoides
§ EPIDEMIOLOGI
LI
§ PATOGENESIS
Telur ascaris yang infektif tertelanà mencapai duodenumà berubah menjadi larvaà menembus dinding usus à melalui sal. Limfe bermigrasi ke hepar dan paru. Paru à loeffler syndrome.
Larva mencapai epiglottis à kembali ke usus kecil àtumbuh menjadi cacing dewasa àbertelur lagi.
§ PATOFISIOLOGI
LI
§ MK
o Biasanya tanpa gejala
o Mual, muntah,sakit perut,nafsu makan menurun, kurus, sukar tidur, sedikit panas
o Sesak napas
o Obstruksi usus
§ DIAGNOSIS
§ PENATALAKSANAAN
§ PENCEGAHAN
§ KOMPLIKASI
§ PROGNOSIS
Cari semua kecacingan ^__^
STEP 4
STEP 5
STEP 6
Ø Mengapa gatal pada malam hari?
Disebabkan oleh parasit, sifat parasitnya mencari makan pada malam hari.
- Bertelur pada malam hari.
- Cacing betina hamil pda malam hari bergerak ke anus untuk meletakkan telurnya di perineumà gatal
Ø Apakah penyakitnya bisa menular apa tidak?
Bisa, melalui: sprei, baju, fekal-oral, udara,
garukanàmakanà tertelan lagi
Ø Kenapa nafsu makan menurun?
- Sifat parasitnya mngeluarkan toksin yg menyebabkan pnurunan nafsu makan
- Cacaingà usus halusà colon descendenànaruh di perineum untuk melindungi telurnya karena berlipat2à mempengaruhi motilitas ususà cepat kenyang
- Cacing à obstruksià distensi abdomen à cepat kenyang
-
Ø Hubungan penyakit dengan nilai pelajaran yang turun?
Waktu tidur malam terganggu à siang mengantuk à konsentrasi kurang à belajar kurang à nilai turun
Ø Mengapa Nampak kurus dan mengantuk?
Nafsu makan turunà bb turun à kurus
Tidur malam terganggu à siang mengantuk
Ø Mengapa warna kulit sekitar kmerahan dan nyeri bila dipegang?
Karena ada bekas garukanà iritasi à kemerahan à nyeri
DD : SOIL TRANSMINT HELMINT & NON SOIL TRANSMIT HELMINTH
· OXYURIASIS à CACING OXYURIS VERMICULARIS
§ DEFINISI
Infeksi Cacing Kremi (Oksiuriasis, Enterobiasis) adalah suatu infeksi parasit yang terutama menyerang anak-anak, dimana cacing Enterobius vermicularis tumbuh dan berkembangbiak di dalam usus.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ ETIOLOGI
Cacing enterobiasis vermicularis
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ EPIDEMIOLOGI
Bias terjadi pada semua umur tapi biasanya menyerang pada anak2, pada daerah yang panas.
o Anak yang terkena umumnya umur 5-14 th
§ PATOGENESIS
· Infeksi biasanya terjadi melalui 2 tahap. Pertama, telur cacing pindah dari daerah sekitar anus penderita ke pakaian, seprei atau mainan. Kemudian melalui jari-jari tangan, telur cacing pindah ke mulut anak yang lainnya dan akhirnya tertelan.
Telur cacing juga dapat terhirup dari udara kemudian tertelan.
Setelah telur cacing tertelan, lalu larvanya menetas di dalam usus kecil dan tumbuh menjadi cacing dewasa di dalam usus besar (proses pematangan ini memakan waktu 2-6 minggu).
Cacing dewasa betina bergerak ke daerah di sekitar anus (biasanya pada malam hari) untuk menyimpan telurnya di dalam lipatan kulit anus penderita.
Telur tersimpan dalam suatu bahan yang lengket. Bahan ini dan gerakan dari cacing betina inilah yang menyebabkan gatal-gatal.
Telur dapat bertahan hidup diluar tubuh manusia selama 3 minggu pada suhu ruangan yang normal. Tetapi telur bisa menetas lebih cepat dan cacing muda dapat masuk kembali ke dalam rektum dan usus bagian bawah.
Telur cacing juga dapat terhirup dari udara kemudian tertelan.
Setelah telur cacing tertelan, lalu larvanya menetas di dalam usus kecil dan tumbuh menjadi cacing dewasa di dalam usus besar (proses pematangan ini memakan waktu 2-6 minggu).
Cacing dewasa betina bergerak ke daerah di sekitar anus (biasanya pada malam hari) untuk menyimpan telurnya di dalam lipatan kulit anus penderita.
Telur tersimpan dalam suatu bahan yang lengket. Bahan ini dan gerakan dari cacing betina inilah yang menyebabkan gatal-gatal.
Telur dapat bertahan hidup diluar tubuh manusia selama 3 minggu pada suhu ruangan yang normal. Tetapi telur bisa menetas lebih cepat dan cacing muda dapat masuk kembali ke dalam rektum dan usus bagian bawah.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html danhttp://forum.um.ac.id/index.php?topic=8715.0)
§ PATOFISIOLOGI
LI
§ MK
· Gejalanya berupa:
- rasa gatal hebat di sekitar anus
- rewel (karena rasa gatal dan tidurnya pada malam hari terganggu)
- kurang tidur (biasanya karena rasa gatal yang timbul pada malam hari ketika cacing betina dewasa bergerak ke daerah anus dan menyimpan telurnya disana)
- nafsu makan berkurang, berat badan menurun (jarang terjadi, tetapi bisa terjadi pada infeksi yang berat)
- rasa gatal atau iritasi vagina (pada anak perempuan, jika cacing dewasa masuk ke dalam vagina)
- kulit di sekitar anus menjadi lecet atau kasar atau terjadi infeksi (akibat penggarukan).
- rasa gatal hebat di sekitar anus
- rewel (karena rasa gatal dan tidurnya pada malam hari terganggu)
- kurang tidur (biasanya karena rasa gatal yang timbul pada malam hari ketika cacing betina dewasa bergerak ke daerah anus dan menyimpan telurnya disana)
- nafsu makan berkurang, berat badan menurun (jarang terjadi, tetapi bisa terjadi pada infeksi yang berat)
- rasa gatal atau iritasi vagina (pada anak perempuan, jika cacing dewasa masuk ke dalam vagina)
- kulit di sekitar anus menjadi lecet atau kasar atau terjadi infeksi (akibat penggarukan).
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ DIAGNOSIS
Cacing kremi dapat dilihat dengan mata telanjang pada anus penderita, terutama dalam waktu 1-2 jam setelah anak tertidu pada malam hari.
Cacing kremi berwarna putih dan setipis rambut, mereka aktif bergerak.
Telur maupun cacingnya bisa didapat dengan cara menempelkan selotip di lipatan kulit di sekitar anus, pada pagi hari sebelum anak terbangun.
Kemudian selotip tersebut ditempelkan pada kaca objek dan diperiksa dengan mikroskop.
Cacing kremi berwarna putih dan setipis rambut, mereka aktif bergerak.
Telur maupun cacingnya bisa didapat dengan cara menempelkan selotip di lipatan kulit di sekitar anus, pada pagi hari sebelum anak terbangun.
Kemudian selotip tersebut ditempelkan pada kaca objek dan diperiksa dengan mikroskop.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ PENATALAKSANAAN
Infeksi cacing kremi dapat disembuhkan melalui pemberian dosis tunggal obat anti-parasit mebendazole, albendazole atau pirantel pamoat.
Seluruh anggota keluarga dalam satu rumah harus meminum obat tersebut karena infeksi ulang bisa menyebar dari satu orang kepada yang lainnya.
Untuk mengurangi rasa gatal, bisa dioleskan krim atau salep anti gatal ke daerah sekitar anus sebanyak 2-3 kali/hari.
Meskipun telah diobati, sering terjadi infeksi ulang karena telur yang masih hidup terus dibuang ke dalam tinja selama seminggu setelah pengobatan.
Pakaian, seprei dan mainan anak sebaiknya sering dicuci untuk memusnahkan telur cacing yang tersisa.
Langkah-langkah umum yang dapat dilakukan untuk mengendalikan infeksi cacing kremi adalah: # Mencuci tangan sebelum makan dan setelah buang air besar
# Memotong kuku dan menjaga kebersihan kuku
# Mencuci seprei minimal 2 kali/minggu
# Mencuci jamban setiap hari
# Menghindari penggarukan daerah anus karena bisa mencemari jari-jari tangan dan setiap benda yang dipegang/disentuhnya
# Menjauhkan tangan dan jari tangan dari hidung dan mulut.
Seluruh anggota keluarga dalam satu rumah harus meminum obat tersebut karena infeksi ulang bisa menyebar dari satu orang kepada yang lainnya.
Untuk mengurangi rasa gatal, bisa dioleskan krim atau salep anti gatal ke daerah sekitar anus sebanyak 2-3 kali/hari.
Meskipun telah diobati, sering terjadi infeksi ulang karena telur yang masih hidup terus dibuang ke dalam tinja selama seminggu setelah pengobatan.
Pakaian, seprei dan mainan anak sebaiknya sering dicuci untuk memusnahkan telur cacing yang tersisa.
Langkah-langkah umum yang dapat dilakukan untuk mengendalikan infeksi cacing kremi adalah: # Mencuci tangan sebelum makan dan setelah buang air besar
# Memotong kuku dan menjaga kebersihan kuku
# Mencuci seprei minimal 2 kali/minggu
# Mencuci jamban setiap hari
# Menghindari penggarukan daerah anus karena bisa mencemari jari-jari tangan dan setiap benda yang dipegang/disentuhnya
# Menjauhkan tangan dan jari tangan dari hidung dan mulut.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ PENCEGAHAN
Sangat penting untuk menjaga kebersihan pribadi, dengan menitikberatkan kepada mencuci tangan setelah buang air besar dan sebelum menyiapkan makanan.
Pakaian dalam dan seprei penderita sebaiknya dicuci sesering mungkin.
Pakaian dalam dan seprei penderita sebaiknya dicuci sesering mungkin.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ KOMPLIKASI
# Salpingitis (peradangan saluran indung telur)
# Vaginitis (peradangan vagina)
# Infeksi ulang.
# Vaginitis (peradangan vagina)
# Infeksi ulang.
(http://kliksehat.blogspot.com/2010/09/infeksi-cacing-kremi.html dan http://forum.um.ac.id/index.php?topic=8715.0)
§ PROGNOSIS
· Kalo diobatin baik
· ASCARIASIS
§ DEFINISI
Infeksi yang dibabkan oleh ascaris lumbricoides yang merupakan nematode usus terbesar
§ ETIOLOGI
ascaris lumbricoides
§ EPIDEMIOLOGI
LI
§ PATOGENESIS
Telur ascaris yang infektif tertelanà mencapai duodenumà berubah menjadi larvaà menembus dinding usus à melalui sal. Limfe bermigrasi ke hepar dan paru. Paru à loeffler syndrome.
Larva mencapai epiglottis à kembali ke usus kecil àtumbuh menjadi cacing dewasa àbertelur lagi.
§ PATOFISIOLOGI
LI
§ MK
o Biasanya tanpa gejala
o Mual, muntah,sakit perut,nafsu makan menurun, kurus, sukar tidur, sedikit panas
o Sesak napas
o Obstruksi usus
§ DIAGNOSIS
§ PENATALAKSANAAN
§ PENCEGAHAN
§ KOMPLIKASI
§ PROGNOSIS
Cari semua kecacingan ^__^
Necatoriasis atau Ancylostomiasis merupakan infeksi yang disebabkan oleh cacing tambang (Necator americanus dan Ancylostoma duodenale). Penyebaran cacing terutama di daerah perdesaan. Diagnosa klinik penyakit cacing ini tidak dapat diketahui dengan tepat sebab cacing tambang tidak memberikan gambaran klinik yang jelas dengan demikian untuk membantu menegakkan diagnosa perlu dilakukan pemeriksaan laboratorium. Pada infeksi yang berat dengan pemeriksaan langsung mudah dilakukan, sedangkan infeksi yang ringan dapat dilakukan pemeriksaan dengan pengendapan atau biakan. Tehnik pengapungan ZnSO4, memberikan hasil yang baik untuk mencari telur maupun larva cacing tambang tetapi memerlukan alat pemusing, dan tehnik biakan memerlukan waktu yang lama, sedang dengan tehnik sediaan tinja tebal menurut Kato meskipun kurang peka dibanding tehnik sentrifugasi seng sulfat tetapi alat yang digunakan lebih sederhana. Untuk pemeriksaan cacing tambang sebaiknya dilakukan kombinasi pemeriksaan langsung dengan cara Kato.
Cacingan merupakan masalah kesehatan yang perlu penanganan serius terutama di daerah tropis karena cukup banyak penduduk menderita kecacingan. Penyakit ini dapat mengakibatkan menurunnya daya tahan tubuh terhadap penyakit dan terhambatnya tumbuh kembang anak, karena cacing mengambil sari makanan yang penting bagi tubuh, misalnya protein, karbohidrat dan zat besi yang dapat menyebabkan anemia.
Cacing penyebab panyakit pada manusia terdiri dari :
- Cacing gelang (Ascaris lumbricoides)
- Cacing cambuk (Trichuris trichiura).
- Cacing kremi (Enterobius vermicularis atau Oxyuris vermicularis)
- Cacing tambang (Necator americanus dan Ancylostoma duodenale)
- Tremadota
1. Cacing Gelang
Cara penularan penyakit cacing gelang adalah melalui telur matang yang tertelan. Dalam usus halus telur akan menetes, dan keluar larva yang dapat menembus usus, mengikuti aliran darah menuju jantung kanan lalu ke paru. Larva merangsang laring sehingga terjadi batuk dan dapat masuk ke dalam saluran cerna melalui kerongkongan. Larva menjadi cacing dewasa di dalam usus halus.
Cara penularan penyakit cacing gelang adalah melalui telur matang yang tertelan. Dalam usus halus telur akan menetes, dan keluar larva yang dapat menembus usus, mengikuti aliran darah menuju jantung kanan lalu ke paru. Larva merangsang laring sehingga terjadi batuk dan dapat masuk ke dalam saluran cerna melalui kerongkongan. Larva menjadi cacing dewasa di dalam usus halus.
Gejala Penyakit Cacing Gelang ( Askasiasis )
- Rasa tidak enak pada perut (gangguan lambung)
- Kejang perut, diselingi dengan diare
- Kehilangan berat badan.
- Demam
2. Cacing Cambuk
Daur hidup cacing cambuk mirip dengan daur hidup cacing gelang, hanya pada cacing cambuk tidak ada siklus paru.
Gejala Penyakit cacing cambuk (trikuriasis)
Daur hidup cacing cambuk mirip dengan daur hidup cacing gelang, hanya pada cacing cambuk tidak ada siklus paru.
Gejala Penyakit cacing cambuk (trikuriasis)
- Nyeri di ulu hati
- Kehilangan napsu makan
- Diane
- Anemia
3. Cacing Kremi
Cara penularan penyakit cacing kremi adalah melalui telur yang tertelan. Larva menetas dalam usus, yang kemudian menembus dan tumbuh dalam mukosa usus menjadi dewasa. Cacing dewasa akan mengembara ke sekitar dubur dan bertelur.
Gejala Penyakit cacing kremi (enterobiasis atau oksiuriasis)
Cara penularan penyakit cacing kremi adalah melalui telur yang tertelan. Larva menetas dalam usus, yang kemudian menembus dan tumbuh dalam mukosa usus menjadi dewasa. Cacing dewasa akan mengembara ke sekitar dubur dan bertelur.
Gejala Penyakit cacing kremi (enterobiasis atau oksiuriasis)
- Gatal disekitar dubur terutama pada malam hari pada saat cacing betina meletakkan telurnya
- Gelisah dan sukar tidur.
4. Cacing Tambang
Cara penularan penyakit cacing tambang adalah melalui larva cacing yang terdapat di tanah yang menembus kulit (biasanya diantara jari-jari kaki), cacing ini akan berpindah ke paru kemudian ke tenggorokan dan akan tertelan masuk saluran cerna.
Gejala Penyakif cacing tambang (ankilostomiasis dan nekatoriasis)
Cara penularan penyakit cacing tambang adalah melalui larva cacing yang terdapat di tanah yang menembus kulit (biasanya diantara jari-jari kaki), cacing ini akan berpindah ke paru kemudian ke tenggorokan dan akan tertelan masuk saluran cerna.
Gejala Penyakif cacing tambang (ankilostomiasis dan nekatoriasis)
- Gangguan pencernaan berupa mual, muntah, diare dan nyeri di ulu hati.
- Pusing, nyeri kepala.
- Lemas dan lelah.
- Anemia.
- Gatal didaerah masuknya cacing.
Cacing masuk tubuh manusia dengan berbagai cara. Bisa dari telur, larva atau karena makan daging.
GEJALA
GEJALA
- Kadang-kadang tanpa ada gejala
- Keluhan tidak spesifik, kelelahan dan berat badan menurun
- Jarang terjadi: sakit perut, kembung dan sumbatan usus.
YANG DAPAT ANDA LAKUKAN
- Hati-hati bila maka makanan mentah atau setengah matang terutama pada tempat-tempat dimana sanitasi masih kurang
- Masak bahan makanan sampai matang
- Selalu mencuci tangan setelah dari kamar mandi/WC atau sebelum memegang makanan
- Infeksi cacing tambang bisa dihindari dengan selalu mengenakan alas kaki.
- Gunakan desinfektan setiap hari di tempat mandi dan tempat buang air besar.
Introduction
Ascariasis is a disease caused by a parasite, which is an organism that
depends on another organism for its survival. The specific parasite involved in
Ascariasis is known as Ascaris lumbricoides. A. lumbricoides is a type of
nematode or roundworm. It has also been referred to more commonly as the giant,
intestinal roundworm. A. lumbricoides is actually the largest intestinal roundworm
found in humans. It is also one of the most common parasites found in humans.
It currently affects more than 1-1.5 billion people worldwide.
Most people harboring A. lumbricoides show no signs of infection with
the roundworm. Some people may show early pulmonary symptoms and
eosinophilia during the larval migration of the parasite. Later on, some patients may
also have abdominal symptoms. Occasionally, A. lumbricoides can cause life-
threatening disease from the worm bolus or ectopic migration of the worms. The worm
lives in the upper part of the small intestine, and there are no reservoirs for the parasite.
Some effective drugs exist to treat the Ascaris.
A picture of a female A. lumbricoides.
This roundworm was passed by a young girl living in Florida.
Image taken from DPDx (Identification and diagnosis of Parasites
Of Public Health Concern. http://www.cdc.gov/ncidod/dpd/parasites/ascaris
***************************************************
Agent
The disease known as ascariasis is caused specifically by the parasitic agent
Ascaris lumbricoides. Occasionally, the swine ascarid, Ascaris suum, can infect
humans as well. It is still debated whether or not A. lumbricoides and A. suum are
different species.
A. lumbricoides is a type of organism grouped with other helminthes or
worms. Three different phyla comprise the group known as Helminths. There are
Cestodes, which include blood parasites or flukes, Trematodes, which consist of
segmented worms like tape worms, and Nematodes, which are roundworms like
Ascaris. Nematodes or roundworms are a type of invertebrate, animals without
backbones. Specifically, nematodes are characterized by their long, round bodies.
Common parasitic roundworms apart from A. lumbricoides include: the pinworm,
the hookworm, and the whipworm.
A. lumbricoides gets its name from the earthworm Lumbricus terrestrias.
When it was first discovered, this roundworm was called Lumbricus teres.
Here is the specific classification of Ascaris lumbricoides:
Domain Eukarya
Phylum Nematoda
Order Asaridida
Family Ascaridoidea
Genus Ascaris
Species lumbricoides
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Synonyms
Ascaris is also known as a large, intestinal roundworm.
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History of Discovery
The anatomy of A. lumbricoides was first described by Edward Tyson in
1683. However, at that time it was known as Lumbricus teres not A. lumbricoides.
It was actually Linnaeus, who renamed Ascaris and gave it its current name.
Linnaeus named the roundworm Ascaris lumbricoides because it showed very
similar morphology as that of the earthworm, Lumbricus terrestrias.
Then in 1917, Brayton Ransom and Winthrop Foster were able to document
the actual life cycle of Ascaris. Afterwards in 1922, Shimesu Koino experimented
on himself and his younger brother in order to describe the clinical disease produced
by Ascaris. Koino worked with both A. lumbricoides and A. suum. He swallowed
2000 A. lumbricoides eggs, and he made his younger brother swallow 500 A. suum
larvae. Koino became very ill for the experiment but luckily no lasting damage
occurred, and his brother did not suffer from as severe a disease. Specifically, in
this daring self-experiment, Koino showed that a pneumonia-like syndrome can
develop during early infection with Ascaris. He also discovered that this syndrome
was caused by migration of larvae through the lungs to the stomach.
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Clinical Presentation in Humans
Clinical Case Study
Taken from an article by C. Randall Clinch and LCDR March B. Stephens.
“Case description of Ascaris,” Arch Fam Med. 2000, 9; 1193-1194.
A 37-year-old man comes to your office after passing something in his stool
that he thought was a rubberband. He became worried when he saw the object
moving in the toilet. Apart from this occurrence, he is a healthy man and is not
taking any medications. He has had no recent change in bowel habits or stool
appearance. He has not had fever, abdominal pain, cough or rash. He does not
smoke, drink alcohol, or use recreational drugs. He has been physically active
and recently completed a weeklong backcountry hiking expedition in the
Southeastern U.S. Other than this expedition, he has not been traveling recently.
With the clinical history and presentation in mind the following are some
possible diagnoses: 1) Ascaris lumbricoides (round worm) infection 2) Toxocara
(visceral larva migrans) infection 3) Trichuris (whipworm) infection 4) rubberband
ingestion. It turned out that this patient had Ascaris lumbricoides.
Clinical Correlation (Signs and Symptoms)
Ascariasis is the disease caused by the parasite Ascaris lumbricoides.
Typically, Ascaris infection does not cause visible disease. Most cases of Ascaris
infection tend to be asymptomatic. Clinically inapparent disease occurs with low
infection of Ascaris, meaning that not many eggs are ingested. However, if hundreds
of eggs are ingested, as seen in the early experiments by Shimesu Koino, the patient
can develop pneumonitis. Pneumonitis occurs when the larvae migrate to the lungs.
This pneumonitis also known as Loeffler’s syndrome, can appear four days to two
weeks after infection occurs.
Some patients may also develop asthma, and the asthma attacks can persist
until worms are removed. Often times the development of asthma in a nonsasthmatic
person can be a clue of ascariasis. In addition, liver enlargement and general toxicity
can also occur during this period and persist for up to two weeks. Other health
problems include fever, urticaria, malaise, nausea, vomiting, diarrhea, central nervous
system disorders, and colic. Nutritional problems that may develop can then lead to
abnormal development in children.
While the worms are in the intestine, they can sometimes cause a life-
threatening disease. If many worms are present, they can become entangled and
form a bolus, which blocks the lumen. Each year two cases out of one thousand
have been reported noting this severe intestinal obstruction. Another fatal condition
has been reported where the worms have penetrated the small intestine leading to
acute peritonitis.
In addition, adult worms can migrate ectopically to the appendix, common
bile duct, and pancreatic duct. This is another life-threatening condition that is most
often seen in small children with high parasite loads. As a result of the worm in the
biliary duct, cholecystitis, cholangitis, hepatic abscess, and pancreatitis can occur.
Suppuration can follow from deterioration of the trapped worm and secondary
bacterial infection.
General Summary of Symptom Timeline
Early phase (The early phase coincides with larval tissue-migration. Typically,
4-16 days after egg ingestion.) The main symptoms include the following:
-fever
-cough
-wheeze
Late Phase (The late phase coincides with the mechanical effects of the worms.
These include GI symptoms from mechanical irritation. Typically, 6-8 weeks
after egg ingestion) The main symptoms include the following:
-vague abdominal complaints (cramping, nausea, vomiting)
-small bowel obstruction (mainly in children)
-pancreatitis (2ndary to worm migration)
-cholecystitis (2ndary to worm migration)
-appendicitis (less common, 2ndary to worm migration)
Multiple Nematode infections. Four year old Puerto Rican patient
with multiple parasites including Strongyloides stercoralis,, hookworm,
Ascaris lumbricoides and Trichuris trichiura. He was small of stature
(equivalent to 1 3/4 year old) and his weight was that of a 2 year old.
Ascaris in the small intestine. A. lumbricoides penetrating the
http://parasitepics.biosci.uga.edu small intestine causing an acute
condition known as peritonitis.
Dr. Scott Smith’s lecture on ascariasis
Child passing A. lumbricoides.
Bolus of A. lumbricoides passed from intestinal tract.
From Dr. Scott Smith’s The large mass was about 1.5 inches in length.
Lecture on Ascariasis.
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Transmission
A. lumbricoides is transmitted primarily through fecal-oral contamination.
The transmission can occur by ingesting contaminated soil, water, or food. Usually,
ascariasis is caused by directly or indirectly eating soil contaminated with feces
carrying these eggs. These eggs mature in the body, and adult female worms can
then lay eggs that come out in the feces. Note, however, that in order for the eggs
to be infective or embryonated, the feces must have been infected 2-4 weeks before it
is ingested. Infection with Ascaris eggs is so common because the eggs are frequently
found in the environment due to poor sanitation practices and the use of night fertilizer.
In addition to fecal-oral transmission of A. lumbricoides, it is also believed
that ascariasis can occur by way of trasnplacental transmission, since many
neonatal cases have been documented.
It should be noted that Ascaris eggs are some of the most resistant
existing microorganisms. Their hearty egg shells consist of four layers: ascaroside,
chitinous, vitelline and uterine. The eggs are not responsive to chlorine, high pH, low
pH, and UV irradiation. They are resistant to high and low temperatures. Alcohol,
ether, and surfactants can inactivate the eggs. In fact, Ascaris eggs can survive for
many years in the soil.
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Life Cycle
Adult worms reside in the upper part of the small intestine, where they
survive on predigested food. The worms make themselves into an S-shape
and press against the epithelium of the intestine while moving against the peristalsis
to keep themselves in the small intestine. The female worm lays eggs, and she can
produce up to 200,000 eggs per day. These eggs are fertilized but
nonembryonated, and the eggs are passed out with feces.
The fertilized eggs develop through embryonation in feces deposited
in the soil. The process of embryonation takes 2-4 weeks. The eggs can survive
many months before embryonation starts, but they need a moist aerobic
environment to develop. The eggs are only infective once they are embryonated
and have larvae in them.
Once embryonated, the infective egg must be swallowed to complete
the life cycle of A. lumbricoides. Bile salts and alkaline enteric juice of the small
intestine stimulate the release of the larvae from the eggs. These second-stage larvae
then travel from the small intestine to the liver. Then the larvae migrate to the heart
via pulmonary circulation. The larvae are now third-stage larvae in the alveolar
capillaries, and they enter the alveolar spaces. Afterwards they migrate to the bronchi
into the tranchea and then to the epiglottis.
The larvae are then swallowed, and they pass once again to the small
intestine. There they molt twice and mature into adult worms. The adult worms
can live up to one year, and the females can lay eggs in the small intestine. However,
A. lumbricoides cannot reproduce in the intestine, and it can only lay eggs that are
not yet infective.
Found in Feachem et al, 1983
From webpage by Kara Nelson.
to 240,000 eggs per day, which are passed with the feces . Fertile eggs
embryonate and become infective after 18 days to several weeks , depending
on the environmental conditions (optimum: moist, warm, shaded soil). After
infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa,
and are carried via the portal, then systemic circulation to the lungs . The
larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls,
ascend the bronchial tree to the throat, and are swallowed . Upon reaching the
small intestine, they develop into adult worms . Between 2 and 3 months are
required from ingestion of the infective eggs to oviposition by the adult female.
Adult worms can live 1 to 2 years.
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Reservoir
No reservoir for this type of Ascaris exists outside of humans. Pigs
have their own type of Ascaris, which was mentioned previously.
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Vector
No vector exists for Ascaris.
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Incubation Period
The appearance of early symptoms of clinical disease can occur
anywhere between 4-16 days after ingestion of the eggs. Loeffler’s syndrome
and other symptoms. Such as fever, coughing, and wheezing take this long to
develop. However, GI symptoms take 6-8 weeks after ingestion of the eggs to
develop.
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Morphology
Ascaris is a large intestinal roundworm. It superficially resembles the
common earthworms found in the soil. Female worms can be as long as 20-35
cms, and males tend to be smaller, no larger than 30 cms. They can be anywhere
from 2-6 mm wide. Mature worms are cylindrical, creamy white or light brown.
They tend to have tapered ends.
The worms have a thick cuticle, 3 lips at its head, small teeth, and its own
digestive tract. The fertilized eggs are oval shaped, and they are about 65 to 40
um in size. The eggs are brown or yellow brown, and they have a thick shell.
An adult male (coiled posterior end) and a female A. lumbricoides.
Note that the anterior ends are more slender than the posterior ends.
image taken from “A pictorial Presentation of Parasites”
This picture shows the male and female worms. The female shown is approximately
16 inches long.
Taken from P. Darben.
A scanning electron micrograph picture taken of the
anterior end of Ascaris. The three lips of the worm are shown.
Taken from “Wormland” site.
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Diagnostic Test
Diagnosis is usually not made clinically based on signs and symptoms.
Sometimes it can be diagnosed using ultrasonography and endoscopic
retrograde cholangiopancreatography (ERCP).
Instead, diagnosis is made primarily by examining a stool specimen.
Infection with A. lumbricoides is determined by microscopic identification of
eggs in the stool. Typically, the procedure used involves the following:
1) collecting stool specimen 2) fixing specimen in 10% formalin
3) concentrate using formalin-ethyl acetate sedimentation technique
4) examine wet mount of sediment
Occasionally, emergence of a worm in the stool or coughed up can be used
to diagnosis the patient.
Comparative egg morphology for different Nematodes and Cestodes using in diagnostics.
A picture of a fertilized egg.
Note the rounded shape, Another picture of a fertilized egg.
the thick shape, external mammilated Taken from “Atlas of Medical Parasitology.”
layer. (brown from bile).
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Management and Therapy
Image taken from Brian E. Keas
webpage on Ascaris lumbricoides.
People with Ascaris should be treated regardless of the presence of
high worm load, for ectopic migration of worms can cause life-threatening health
problems. The choice drugs for the treatment of Ascaris infection are albendazole,
mebendazole, and pyrantel pamoate. These drugs are effective with few side-effects.
Mebendazole (Vermox) and Albedazole are one class of drugs used to treat
Ascaris infection. Mebendazole has often times been considered the choice drug to
treat intestinal roundworm infections. The adult dose is 100 mg PO BID on 3
consecutive days or 500 mg once. A second course is administered if the patient is
not cured in 3-4 weeks. Side-effects are mild, but migratory activity has been reported
in response to the drug. The dosage for Albendazole is 400 mg once.
Pyrantel pamoate is also effective in treating Ascaris. It can treat
other nematodes, and it works by paralyzing the worms. The dosage is 11mg/kg once
(max. 1 gram).
Apart from the 3 drugs listed above, a few other treatments exist. Yet, these are
choice drug treatments listed by the CDC. Levamisole hydrochloride is another type
of drug used to treat Ascaris. This drug has more side-effects than Mebendazole and
Pyrantel, and it works by paralyzing the worm. In addition, piperazine salts can also be
used to treat Ascaris. Not many side-effects have been noted, but they tend to be more
common than other drugs available. They are often times used because they are
cheap and effective.
Courtesy Dr. Tom Nutman at the NIH
From Dr. Scott Smith’s lecture.
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Epidemiology
Ascariasis plagues more people in the world than any other parasitic
infection. Some estimate that as many as 1-1.5 billion people or approximately 1
out of 4 people are infected with Ascaris. In some tropical areas, 100% of the
population have Ascaris.
Ascariasis tends to occur more commonly in places where sanitation is
minimal and human feces is used to fertilize crops. As a result, the majority of
Ascaris infections are concentrated in the developing world.
Approximately, 59 million people are at risk of morbidity or clinical illness from
Ascaris. Children are more likely to be infected and have higher levels of worms.
1.5 million children with Ascaris infections will suffer from irreversible growth
retardation. While death from Ascaris is rare, approximately 10,000 people die from
Ascaris each year.
Males tend to be more infected then females, due to behavioral habits that
make it more likely for them to ingest soil. Some evidence of genetic predisposition
has also been noted in a study of families in Nepal.
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Country Information Image taken from Brian E. Keas webpage
on A. lumbricoides.
Ascaris is found all over the world. However, it is most prevalent in warm,
tropical climates, where eggs can survive the longest in the soil. It is less common
in places that are arid and seasonal. Concentration of Ascaris seems to fall most
heavily in South-EastAsia with less cases in Africa and Latin America. In South-East
Asia approximately 73% of the people are infected. India, Bangladesh, Burma,
Indonesia, Malaysia, Philippines, Vietnam, China, Kenya, Tanzania, West Africa,
Turkey, Iran, Afghanistan, Brazil, Columbia, Mexico, and Peru have all reported areas
where Ascaris occurs in more than 50% of the local population living in these places.
Even in the U.S., many cases of Ascaris occur. Approximately 4 million
people in the U.S. are infected with Ascaris, and the majority of these cases are
concentrated in the rural southeast part of the country.
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Public Health and Prevention Strategies (Vaccines)
Prevention and control of Ascaris can occur on two fronts: drug treatment
and sanitation improvement. Mass chemotherapy programs given every 6 months
can help break the cycle of constant Ascaris infection. It is also important to educate
people about adopting healthier living habits. For instance, people can avoid eating
noncooked vegetables and fruits in places lacking proper sanitation and areas that
use human fertilizer. No vaccines are currently in use to prevent the spread of this
parasite.
Listed below are some of the World Health Organization’s listed combined
strategies to control soil-transmitted helminthes such as A. lumbricoides:
1) ensuring the wide availability of single dose antihelminthic drugs
in all health services in endemic areas
2) ensuring good passive and active case management
3) regularly treating at least 75% of all school-age children at
risk of morbidity by 2010
4)regularly treating children at risk of morbidity through the IMCI strategy
5)improving access to safe water and sanitation through intersectoral
collaboration
6) improving hygiene behavior by scaling up sanitation education, targeted at
high-risk groups such as school-age children, women, and special
occupation groups
Trichinosis
(Trichinella spp.)
Introduction
Trichinosis is a food-borne parasitic disease caused by the consumption of raw or undercooked meat, especially pork, or wild game infected with the tissue nematode Trichinella larvae. Infection is commonly seen in animals with cannibalistic and scavenging behavior [1]. While there are eight species in the genus Trichinella, the species most important and pathogenic towards humans is T. spiralis. Trichinosis infection was previously common worldwide, but its prevalence has decreased due to the establishment of new legislation regarding food preparation [2]. Today, trichinosis is mostly found in Europe and North America [2].
Synonyms
Trichinellosis, Trichina
Agent and taxonomy
Taxonomy:
Kingdom: Animalia
Phylum: Nematoda
Class: Adenophorea
Order: Trichurida
Family: Trichinellidae
Genus: Trichinella
Phylum: Nematoda
Class: Adenophorea
Order: Trichurida
Family: Trichinellidae
Genus: Trichinella
Figure 1. Trichinella spiralis larvae freed from cyst. (CDC) [2]
Agent
The disease-causing agent includes the eight species of Trichinella, but T. spiralis is the most important to humans due to its worldwide distribution and high pathogenicity. The other seven (T. nativa, T. nelsoni, T. britovi, T. pseudospiralis, T. murrelli, T. zimbabwensis, and T. papuae) have different ranges in host and geographic distribution [3]. Five species are encapsulated, meaning they encyst in muscle tissue, while three are nonencapsulated (T. pseudospiralis, T. zimbabwensis, T. papuae) [4].
T. spiralis - most adapted to swine and pathogenic to humans; distributed worldwide and is also present in wild game and horse meat
T. britovi – second most common species to infect humans as it can also affect domestic pig populations; distributed throughout Europe, Asia, and Northern and Western Africa.
T. nativa – distributed in Arctic and subarctic regions with the polar bear as an important reservoir; hosts include the arctic fox, walrus, and other wild game, and it has a high resistance to freezing.
T. pseudospiralis – infects both mammals, including humans, and birds; nonencapsulated, doesn’t coil; found worldwide
T. papuae – infects both mammals and reptiles, including crocodiles, pigs, and humans; found in Papua New Guinea and Thailand; nonencapsulated
T. nelsoni – found in Eastern Africa; intermediate in pathogenicity; few human cases have been documented
T. murrelli – spread among wild carnivores in North America; does not develop in swine; infects humans, especially from black bear meat
T. zimbabwensis – detected in reptiles of Africa; can infect mammals and possibly humans [5]; nonencapsulated.
History of discovery
Discovery of the parasite
Due to the lack of medical records, the circumstances surrounding the first observation and identification of Trichinella spiralis are controversial. In 1835, James Paget, a first-year medical student, first observed the larval form of Trichinella spiralis during an autopsy at St. Bartholomew’s Hospital in London. Paget took special interest in the presentation of muscle with white flecks, described as a “sandy diaphragm.” He later remarked ‘All the men in the dissecting rooms, teachers included, ‘‘saw’’ the little white specks in the muscles: but I believe that I alone ‘‘looked at’’ them and ‘‘observed’’ them.’ [6].
While Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor, Richard Owen, who is now credited for the discovery of the Trichinella spiralis larval form [10].
Life cycle discovery
From 1850 to 1870, a series of experiments conducted by the German researchers Rudolph Virchow, Rudolph Leukart, and Friedrich Zenker, discovered the life cycle of Trichinella by feeding infected meat to a dog and performing the subsequent autopsy. Through these experiments, Virchow was able to describe the development and infectivity of T. spiralis [7].
Species discovery
The invention of new biotechnologies in the 1900s and experimental studies lead to the finding of seven more species in addition to Trichinella spiralis [8].
Morphology
Larvae
Microscopy shows that infective larvae curl up as they encyst in striated muscle tissue, newborn larvae measuring 0.08 mm long by 7µm in diameter. Free T. spiralis larvae move in a coiling and uncoiling manner [9].
Adult worms
The adult male nematodes have claspers at their posterior end and measure 1.4mm to 1.6 mm long while adult females are twice as long, with the uterus at the posterior end and hatching eggs at the anterior end. Both worms are more slender at the anterior than posterior end [9].
a)
b)
Figure 2. a) Male adult Trichinella spiralis worm with claspers on its posterior end. b) Female adult T. spiralis (www.trichinella.org) [10]
Transmission
The transmission of trichinosis occurs through the ingestion of cysts in infected undercooked or raw meat or wild game. This is especially concerning to hunters of wild game and in cultures where raw meat is prepared as food. Humans cannot infect other humans or animals unless the infected muscle is ingested. In normal circumstances humans present an end to transmission [3].
There are two cycles in which transmission of trichinosis occurs: sylvatic and domestic. The sylvatic cycle includes all Trichinella species and centers around wildlife transmission through the ingestion of infected prey or carrion. The ability of Trichinella species to remain infectious even in decaying tissue promotes effective wildlife transmission through carcasses and carrion [9].
The domestic cycle involves the feeding of garbage containing raw pork scraps and carrion to swine. Rats may also become infected through contact with swine and ingestion of the same swinefeed, and therefore spread the infection to other animals [8].
Life cycle
Ingested infectious larvae break free from their cysts due to the acidity of the stomach, allowing the larvae to enter the small intestine. There they mature into adults and mate, depositing newborn larvae into the intestinal mucosa in as little as three days. The larvae then enter the lymphatic vessels and travel around the body via the bloodstream, entering various organs such as the retina, myocardium, or lymph nodes. However, only larvae that penetrate skeletal muscle cells survive and reach their full size within a month.
Encystation involves three major stages: 1. the formation of the host cell into a nurse cell, 2. encapsulation of the larvae (excluding T. pseudospiralis and T. zimbabwensis), and 3. development of a capillary network around the nurse cell. These infected cells can remain infectious for months to years, whether or not calcification occurs [3][11][12].
Figure 3. Life cycle of Trichinella spp. (CDC) [10]
Reservoirs
The different species of Trichinella encompass a wide range of reservoirs:
T. spiralis: mammals, domestic swine, rats, bears
T. britovi: foxes, raccoons, dogs, cats
T. nativa: polar bears, walruses, sled dogs
T. pseudospiralis: bird, mammals
T. papuae: wild and domestic pigs, reptiles
T. nelsoni: hyenas, large cats
T. murrelli: wild carnivore, humans
T. zimbabwensis: crocodiles, mammals [13]
Vectors
There are no known vectors for Trichinella spp. [3]
Clinical Symptoms and Pathogenesis
Incubation period
The incubation period is the time from exposure to the pathogen to the onset of symptoms. Once the ingested larvae enter the intestine, they mature into adults in 3 days. Symptoms during the intestinal stage may be minor and go undetected. However if symptoms do appear, they do so suddenly in 2-7 days and are similar to gastroenteritis (stomach flu). While the length of the incubation period depends on the amount of larvae ingested and varies by species, it has been averaged to be 10-14 days [14].
Clinical manifestations
Symptoms for a Trichinella infection range widely according to the amount and species of larvae ingested. They can be separated by the two phases of pathogenesis: the enteral phase of adult worms at the intestinal level, and the parenteral phase, or invasion of muscle by migrating larvae [8].
Enteral phase
The symptoms during this adult phase may be minor and unnoticeable, and consist of a general gastroenteritis. Diarrhea, nausea, vomiting, and abdominal pain may present with a larger worm burden, while symptoms may be unnoticeable if the number of larvae ingested is low. These nonspecific gastroenteritis symptoms may present anywhere from 2-7 days after ingestion of Trichinella larvae. Eosinophilia, an increase in white blood cells, also presents early and increases rapidly [8].
Parenteral phase
The severity of symptoms caused by the migration of larvae into muscle tissue is dependent on the number of larvae produced by the adult worms. A moderately severe infection may present with about 50-100 larvae per gram of muscle. The body’s inflammatory response is provoked by the invading larvae and edema, muscle pain and swelling, fever, and fatigue may occur. Severe muscle pain, weakness, and hardening, as well as facial edema are common. The classic sign of trichinosis is circumorbital edema, or swelling around the eyes, and may be connected to the inflammation of blood vessels that is caused by larval migration. This vasculitis also leads to the presentation of splinter hemorrhages in the nails [3].
Fatal infections of trichinosis often involve effects on the heart, lungs, and central nervous system, giving rise to serious complications including myocarditis, pneumonia, and encephalopathy, respectively [15].
a)
b)
Figure 4. Classic signs of trichinosis. a) Splinter hemorrhages, b) circumorbital edema [25].
Pathogenesis
Trichinella’s pathogenic effects arise mostly from the destruction of muscle tissue during larval migration. These effects are characterized by eosinophilia, elevated creatine phosphokinase (CPK), and parasite-specific IgG. Pathogenesis varies by species, although the differences have not been thoroughly researched. A report comparing two Italian outbreaks of T. spiralis and T. britovi describe a few differences in pathogenesis: T. spiralis presents with more severe enteral phase symptoms, and a longer duration of CPK and IgG elevation [16].
Diagnosis
History of exposure
The determination of trichinosis infection depends heavily on a history of exposure to, most commonly, raw or undercooked pork or bear meat. Often, the meat in question is home-prepared and thus provides a good source for microscopy. Besides direct consumption of confirmed infected meat, other exposure includes consumption of products from a confirmed infected animal, or sharing exposure to a common source as a confirmed infected human [12].
Clinical diagnosis
The typical clinical symptoms of circumorbital edema, splinter hemorrhages, muscle pain, and gastroenteritis may also suggest trichinosis infection. The European Center for Disease Control states as its case definition for trichinosis “At least three of the following six: fever, muscle soreness and pain, gastrointestinal symptoms, facial edema, eosinophilia, and subconjunctival, subungual, and retinal hemorrhages.” [12].
Laboratory testing
Serology
Useful laboratory indicators of infection are eosinophilia, increased levels of creatine phosphokinase (CPK), parasite-specific immunoglobulin G, and antibodies against newborn larvae [16]. Serum tests can detect eosinophilia or the presence of muscle enzymes such as CPK. Immunoassays such as ELISA, indirect immunofluorescence, or Western blot can be performed for anti-Trichinella antibodies [12].
Microscopy
The finding of Trichinella larvae in a muscle biopsy confirms a trichinosis infection. After the first week of infection, tissue biopsies of skeletal muscle, most commonly of calf muscle, or aspirate samples of cysts will show encysted larvae [12].
a)
b)
Figure 5. a) Encysted Trichinella larvae b) Encysted Trichinella larvae in striated muscle tissue. (CDC) [2]
Treatment
Early treatment is desirable as the later an infection progresses without treatment, the greater the chance of larval encystations in the patient’s muscle. These cysts may then remain infectious for years, despite treatment [12].
Primary treatment
Anthelmintics such as albendazole and mebendazole can be prescribed to prevent newborn larvae from growing. If this treatment is given in the early stages of infection, especially in the first three days, larvae may be prevented from encysting, therefore preventing disease and pain. It is important to note that anthelmintics may be useless against long-term infections as larvae have already encysted -- therefore, treatment should be given as early as possible. Unfortunately, most cases of trichinosis are diagnosed too late and larvae have already been established [3][12].
Mebendazole is the preferred treatment, with a dosage of 200 to 400 mg three times daily for three days, followed by 400 to 500 mg three times daily for 10 days.
Alternatively, the dosage for the albendazole is 400 mg twice a day for 8 to 14 days.
These drugs should not be taken by pregnant women and are not recommended for children under two years of age [12].
New research
Extension of the effectiveness of anthelmintics to allow for later treatment of helminthic infections has been demonstrated in a mouse model by using 2-hydroxypropyl-β-cyclodextrin. Similar results were obtained using cymetidine for human cystic echinococcosis (hydatid disease), but studies in human trichinosis have not been conducted [17].
Secondary treatment
Steroids such as prednisone may be used as secondary treatment after infection to relieve muscle pain due to larval migration. Pyrantel is safe for pregnant women and children, but only effects adult worms in the intestines [12].
Vaccine research
While there are currently no vaccines for Trichinosis, experimental mice studies have suggested a potential vaccine may be produced. In one such study, microwaved larvae of T. spiralis were used to immunize mice and results ranged from a decreased larval count to complete protection depending on dosage. This technology may be used to create an effective barrier to human or animal transmission [18].
A candidate vaccine for use in domestic swine herds has been developed and may help in management of the disease. However, the production of the vaccine may be too costly [19].
Epidemiology
The worldwide prevalence of trichinosis infection has declined largely due to legislation requiring proper preparation of garbage used as hog food, storage of pork products, public awareness, and possibly a decline in the consumption of pork [3]. Reported cases of trichinosis today occur mainly in developed countries, including Europe, Asia, and North America [12].
Cultural factors such as the traditional preparation of dishes based on raw or undercooked meat is often the source of occasional outbreaks. These eating habits range from raw horse meat delicacy in France [26], dog meat in China and the Slovak Republic, and the consumption of improperly cooked wild game by hunters worldwide. Interestingly, in Muslim populations where the consumption of pork is forbidden, trichinosis infection has only been found in Europeans [12].
Resurgence
In the 1990s, trichinosis was labeled as a “reemerging zoonosis” despite the previous veterinary efforts to control it in the past century. This may be due to the relaxation of veterinary public health systems, the changing climate, increasing sylvatic transmission, and expanding food marketing systems, among other factors [19].
It is suggested that the success of trichinosis control in the 1960s led to inspectors and food workers letting down their guard and relaxing inspection protocol. Other reasons for the reemergence of trichinosis include the mass marketing of meat products in transferring the disease to non-endemic areas as well as a shift in human behavior towards consuming more game meat [12].
Increased outbreaks in recent years by the sylvatic Trichinella species indicates an increase in transmission to the domestic cycle and therefore to humans. These outbreaks were seen with T. pseudospiralis in Thailand [20], T. nativa in indigenous Arctic populations [21], and potentially T. zimbabwensis in Taiwan [5]. This may be a result of “risky behaviour” that subjects wildlife to exposure of the parasite, such as the habit of hunters in leaving carcasses in the wild. These outbreaks not only provide more information about the different Trichinella species, but also indicate that the Trichinella epidemiology is changing [19].
Changing political arenas may also lead to the reemergence of Trichinosis, as indicated by Serbia. An outbreak in 2001 was determined to have resulted from a weak veterinary public health system and economy affected by the breakup of the former Federation of Yugoslavia [22].
Prevention and Public Health Strategies
Legislation
Outbreaks can be prevented by legislation requiring standards and control for food packaging companies. To improve food safety for consumers, the European Commission established rules for the control of Trichinella in meat, including required inspections, rodent control, and hygiene standards. [12]. In the United States, the United States Department of Agriculture (USDA) guidelines for establishment responsibilities in the inspection of meat and poultry include procedures to follow in identifying cysts in pork products [23]. These rules targeting food –packaging companies may aid in the prevention of a trichinosis outbreak.
Legislation that sets standards for pig farming may also help in preventing transmission through the establishment of hygienic conditions, certified feedstuff, and veterinary control [12].
Education and training
Public and consumer education about the risks of consuming raw or undercooked meat products of both domestic animals and wild game may reduce infection rates [12]. As hunters are part of the at-risk population, some states such as New York require the completion of an education course which includes food preparation in order to apply for a hunting license [24].
Food preparation
Trichinella larvae can be inactivated by heating, freezing, and irradiation of meat.
Heating: at 71°C for at least one minute until “the meat must change the color from pink to gray, and muscle fibers are easily separated from each other” [12]
Freezing: Cuts of meat up to 15 cm thick must be frozen at a minimum of -15°C for at least 3 weeks. This only applies to T. spiralis infections, as other species, particularly the freeze-resistant T. nativa, may survive cold temperatures.
Irradiation: In countries where irradiation of food is permitted, irradiation at 0.3 kGy inactivates Trichinella and is only recommended for seals packaged food [12].
Unsafe methods of preparation include cooking by microwave ovens, curing, drying, and smoking of meat, as those methods vary and are difficult to control [12].
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