TYPHUS ABDOMINALIS

a. Pengertian

Typhus abdominalis merupakan infeksi sistemik yang disebabkan oleh kuman SalmonellaTyphosa, Salmonella Paratyphi A, B da C. yang menyerang usus halus khususnya daerah illeum. Penyakit ini termasuk penyakit tropik yang sangat berhubungan erat dengan kebersihan perseorangan dan lingkungan. Dapat dengan mudah berpindah ke orang lain melalui Fecal Oral, artinya kuman Salmonella yang ada pada pada feses penderita atau karier mengkontaminasi makanan atau minuman orang sehat.

b.  Etiologi

Penyakit ini disebabkan oleh kuman :

a. Salmonella Typhosa

b. Salmonella Paratyphi A, B dan C

Kuman Salmonella termasuk golongan bakteri berbentuk batang, gram negatif mempunyai flagel yang memungkinkan kuman ini dapat bergerak, tidak berspora serta mempunyai tiga antigen ,yaitu :

a. Antigen O (HgO) : antigen pada bagian Soma

b. Antigen H (AgH) : antigen pada bagian flagel

c. antigen Vi (AgVi) : antigen pada bagian kapsul.

c. Gejala Klinik

Gejala klinik thyphus abdominalis pada pasien dewasa biasanya lebih Berat dibandingkan anak. Masa tunas rata-rata 10-20 hari. Yang tersingkat 4 hari jika infeksi melalui makanan sedangkan yang terlama sampai 30 hari jika infeksi melalui minuman. Selama masa inkubasi diketemukan gejala prodromal yaitu perasaan tidak enak badan, lesu, nyeri kepala, pusing-pusing dan tidak bersemangat.

Kemudian menyusul gejala klinik yang biasa ditemukan yaitu 1) demam, 2) Gangguan pada saluran pencernaan, 3) Gangguan Kesadaran.

1. Demam. Pada kasus – kasus yang khas demam berlangsung 3 minggu. Bersifat febris remitens dan suhu tidak berapa tinggi. Selama minggu pertama, suhu badan berangsur-angsur meningkat pada sore hari meningkat dan biasanya menurun pada pagi atau malam hari. Dalam minggu ke dua penderita terus berada dalam keadaan demam. Dalam minggu ke tiga suhu badan berangsur-angsur turun dan normal kembali pada minggu ke empat.

2. Gangguan pada saluran pencernaan. Pada mulut terdapat bau nafas tidak sedap. Bibir kering dan pecah-pecah (rhagaden). Lidah ditutupi selaput putih kotor (coated tongue), ujung dan tepi lidah kemerahan, jarang dosertai tremor. Pada abdomen ditemukan keadaan perut kembung (meteorismus). Hati dan limpa membesar diserta nyeri pada perabaan. Defekasi biasanya konstipasi, mungkin normal dan kadang-kadang diare.

3. Gangguan kesadaran. Umumnya kesadaran penderita menurun walaupun tidak berapa mendalam, yaitu apatis sampai somnolen, jarang terjadi sopor, koma atau gelisah. Disamping gejala diatas kadang-kadang ditemukan pada punggung atau anggota yaitu roseola berupa bintik-bintik kemerahan karena embolus basil dalam kapiler kulit terutama diketemukan pada minggu pertama demam. Kadang-kadang ditemukan bradikardia dan mungkin didapatkan epistaksis.

d.      Patofisiologi

     Makanan atau minuman yang telah terkontaminasi oleh kuman Salmonella Typhosa masuk kedalam lambung, selanjutnya lolos dari sistem pertahanan lambung, kemudian masuk ke usus halus, melalui folikel limpa masuk kesaluran limpatik dan sirkulasi darah sistemik, sehingga terjadi bakterimia. Bakterimia pertama-tama menyerang Sistem Retikulo Endoteleal (RES) yaitu : hati, lien dan tulang, kemudian selanjutnya mengenai seluruh organ di dalam tubuh antara lain sistem syaraf pusat, ginjal dan jaringan limpa.Cairan empedu yang dihasilkan oleh hati masuk ke kandung empedu sehingga terjadi Kolesistitis. Cairan empedu akan masuk ke Duodenum dan dengan virulensi kuman yang tinggi akan menginfeksi intestin kembali khususnya bagian illeum dimana akan terbentuk ulkus yang lonjong dan dalam. Masuknya kuman ke dalam intestin terjadi pada minggu pertama dengan tanda dan gejala suhu tubuh naik turun khususnya suhu akan naik pada malam hari dan akan menurun menjelang pagi hari. Demam yang terjadi pada masa ini disebut demam intermiten (suhu yang tinggi, naik turun dan turunnya dapat mencapai normal) Disamping peningkatan suhu tubuh juga akan terjadi obstipasi sebagai akibat penurunan motilitas suhu, namun ini tidak selalu terjadi dapat pula terjadi sebaliknya. Setelah kuman melewati fase awal intestinal, kemudian masuk ke sirkulasi sistemik dengan tanda peningkatan suhu tubuh yang sangat tnggi dan tanda-tanda infeksi pada RES seperti nyeri perut kanan atas, splenomegali dan hepatomegali. Pada minggu selanjutnya dimana infeksi Focal Intestinal terjadi dengan tanda-tanda suhu tubuh masih tetap tinggi, tetapi nilainya lebih rendah dari fase bakterimia dan berlangsung terus menerus ( demam kontinue ), lidah kotor, tepi lidah hiperemis, penurunan peristaltik, gangguan digesti dan absorbsi sehingga akan terjadi distensi, diare dan pasien merasa tidak nyaman, pada masa ini dapat terjadi perdarahan usus, perforasi dan peritonitis dengan tanda distensi abdomen berat, peristaltik menurun bahkan hilang, melena, syock dan penurunan kesadaran.

e.       Diagnosis

Untuk membuat diagnosa pasti perlu dilakukan pemeriksaan laboratorium

1. Pemeriksaan darah tepi untuk mendapatkan gambaran mengenai :

a. leukopenia

b. limfositosis relatif

c. eosinopilia

d. Trombositopenia

2. Pemeriksaan sumsum tulang untuk mengetahui RES hiperaktif ditandai dengan adanya sel makrofag, sel hemopoetik, granulopoetik,eritropoetik dan trombopoetik berkurang

3. Biakan empedu

Untuk mengetahui Salmonella typhosa dalam darah penderita terutama pada minggu pertama. Selanjutnya diketemukan dalam faeces / urine dan mungkin tetap positif dalam waktu lama.

4. Pemeriksaan widal

Dasar pemeriksaan adalah reaksi aglutinasi yang terjadi bila serum penderita dicampur dengan suspensi antigen salmonella typhosa. Pemeriksaan dinyatakan positif bila terjadi reaksi aglutinasi

Untuk membuat diagnosis yang diperlukan ialah titer zat anti terhadap antigen O yang bernilai 1/200 atau lebih dan atau menunjukan kenaikan yang progresif. Titer O dipakai untuk menentukan diagnosis karena mencapai puncaknya bersamaan dengan penyembuhan penderita. Sedangkan titer H tidak diperlukan untuk diagnosis karena dapat tetap tinggi setelah penderita lama sembuh.

f.        Penatalaksanaan Medik

1. Isolasi penderita

2. Perawatan untuk mencegah terjadinya komplikasi.

3. Istirahat selama demam sampai 6 hari bebas panas.

4. Diet.

5. Obat. Pilihan terbaik Chloramphenicol dengan dosis tinggi 100 mg/kg BB/hari (maksimum 2 gram perhari) diberikan 4 x sehari peroral atau intravena, kecuali penderita tidak cocok dapat diberikan obat lain.

6. Bila terjadi komplikasi diberikan terapi yang sesuai. Misalnya Intravena fluid drip (IVFD).

g.       Komplikasi

Komplikasi yang terjadi yaiut a) pada usus dan b) diluar usus.

a. Pada Usus yaitu (1) perdarahan usus, (2) Perforasi usus (3) Peritonitis.

b. Diluar usus yaitu (1) Meningitis (2) Bronchopneumonia (3) dll.

h.      Pengobatan

Kloramfenicol  250mg (4x1) dan 500 mg ( 3x1)

i.         Pencegahan

-      Penyediaan makanan sehat

-      Kebersihan perseorngan yang baik

-      Kebersihan lingkungan tetap terjaga.

Cegah perkembangbiakan vektor.( tumpukan sampah, lantai kotor,WC. Terbuka dan kotor ) Bersihkan lingkungan dalam dan sekitar rumah setiap hari.

Cegah aliran air kotor yang tersumbat.

article about environmental health and summary

Name              : Putri Kilaswari Winarto

Class                : XI.2 perawat

Article I

Air pollution increases risk of autism by 50 percent in newborns

(NaturalNews) A recent study by the California Department of Health Services indicates that industrial air pollutants may increase the risk of autism by 50 percent in young children and unborn babies. The report was published online in the journal Environmental Health Perspectives.

Researchers compared 959 children from six San Francisco Bay area counties who were born in 1994. Out of these, 284 were diagnosed with autism-spectrum disorders. The study showed that children with autism were more likely to be born in areas with high levels of mercury, cadmium, nickel, trichloroethylene and vinyl chloride. Elemental mercury -- which is released into the air from coal-burning power plants, chlorine factories and gold mines -- appears to be particularly hazardous.

In their report, the study authors said their research suggests "living in areas with higher ambient levels of hazardous air pollutants -- particularly metals and chlorinated solvents -- during pregnancy or early childhood, may be associated with a moderately increased risk of autism. These findings illuminate the need for further scientific investigation, as they are biologically plausible but preliminary and require confirmation."

Mercury levels are increasing in many parts of the world, and over the past 10 years the number of children diagnosed with autism has increased as well. This leads many scientists to suspect there may be a connection between pollutants and the neurological disorder. However, the study's lead author Gayle Windham cautions that more definitive evidence is needed before scientists will have a clear understanding of the effect of environmental pollutants on autism.

Summary

Paragraph 1    : industrial air pollutants can increase the risk of autism by 50 percent in children and unborn babies.

Paragraph 2    : children with autism are more likely to be born in areas with high levels of mercury, cadmium, nickel, vinyl chloride, and trichloroethylene.

Paragraph 3    :  live in areas with higher ambient levels of hazardous air pollutants during pregnancy or early childhood, may be associated with risk of autism is increasing.

Paragraph 4    : more definitive evidence is needed before scientists will have a clear understanding of the environmental effect of pollutants on autism.

Article II

Exposure To Environmental Tobacco Smoke Causes Respiratory Symptoms In Healthy Adults

Over time, inhaling environmental tobacco smoke (ETS)--a process often called "passive smoking"--can cause otherwise healthy adults to develop chronic respiratory symptoms. 

The findings appear in the second issue for November 2006 of the American Journal of Respiratory and Critical Care Medicine, published by the American Thoracic Society. 

Margaret W. Gerbase, Ph.D., of the Division of Pulmonary Medicine at the University Hospitals of Geneva in Switzerland, and 11 associates assessed the respiratory symptoms in 1,661 never-smokers over an 11-year period. All individuals in the study cohort participated in the Swiss Study on Air Pollution and Lung Diseases in Adults in 1991 and again in 2002. The two-part study was the first large-scale investigation of the long-term health effects of moderate ambient air pollution in Switzerland. 

"The results of our longitudinal assessment of ETS effects in asymptomatic never-smokers showed that exposure to ETS was associated with the development of respiratory symptoms," said Dr. Gerbase. "A particularly strong effect of continued exposure to ETS was observed among previously asymptomatic individuals with bronchial hyper-reactivity." 

The researchers found ETS exposure to be strongly associated with the development of cough. In subjects with bronchial hyper-reactivity, they observed a link between ETS and symptoms like wheeze, cough, dyspnea (shortness of breath) and chronic bronchitis. However, only the association between dyspnea and ETS reached statistical significance. 

According to the authors, individuals with bronchial hyper-reactivity who are persistently exposed to ETS are at particular risk of developing early-onset chronic respiratory disease. "Symptom development in our subjects was accompanied by decrements in spirometric indices reflecting peripheral airway narrowing, notably in subjects with bronchial hyper-responsiveness," said Dr. Gerbase. 

Of the 1,661 participants, 1,202 individuals (72.4 percent) reported never being exposed to ETS, 309 persons (18.6 percent) reported exposure only during the 1991 survey, and 150 subjects (9 percent) reported exposure both in 1991 and 2002. 

"Indirect evidence derived from smokers shows that airway responsiveness increases the risk to develop cough, phlegm, dyspnea and chronic bronchitis," said Dr. Gerbase. "Cessation of smoking leads to remission of symptoms and improvement in airway hyper-reactivity." 

Excluded from participation in the study at baseline (1991) were all potential participants who reported such symptoms as wheeze, cough, phlegm, dyspnea and chronic bronchitis, or who were taking a medication for asthma at the time. 

The researchers concluded that their findings support the need for policies protecting all nonsmokers from the "detrimental effects" of ETS.a

Summary

1.      secondhand smoke can cause healthy adults to develop chronic respiratory symptoms.

2.      The results of our longitudinal assessment of ETS effects in asymptomatic never-smokersshowed that exposure to 

3.      was associated with the development of respiratory symptoms

4.      the association between dyspnea and ETS reached statistical significance. 

5.      individuals with bronchial hyper-reactivity who are persistently exposed to ETS are at particular risk of developing early-onset chronic respiratory disease.

6.      smokers shows that airway responsiveness increases the risk to develop cough, phlegm, dyspnea and chronic bronchitis

7.      Cessation of smoking leads to remission of symptoms and improvement in airway hyper-reactivity.

Article III

Higher Heart Attack Risk Associated With Increased Pollution Levels

Research published on bmj.com today revealed that high levels of pollution could increase the risk of having a heart attack for up to six hours after exposure, however, the risk diminishes after a six hour time frame. 

Researchers speculate that the heart attack would have happened regardless and was merely pulled forward by a few hours. They base their assumption on the transient nature of the increased risk known as a short-term displacement (or "harvesting") effect of pollution. 

Although research has proven that high pollution levels are linked to premature death from heart disease, according to the authors, the association with an increased risk of heart attack is less clear. 

Krishnan Bhaskaran, an epidemiologist from the London School of Hygiene and Tropical Medicine, and his team conducted a study in which they evaluated 79,288 heart attack cases from 2003 to 2006 and hourly exposure to pollution levels. 

By using the UK National Air Quality Archive they investigated the levels of specific pollutants in the atmosphere, including pollutant particles (PM10), carbon monoxide (CO), nitrogen dioxide (NO2), sulphur dioxide (SO2) and ozone. 

Bhaskaran stated that higher levels of PM10 and NO2 are well-known markers of traffic related pollution. 

 

Seeing that there was no net increase in heart attack risk over a broader timescale, the authors argue that there may be: 

"limited potential for reducing the overall burden of myocardial infarction through reductions in pollution alone, but that should not undermine calls for action on air pollution, which has well established associations with broader health outcomes including overall, respiratory and cardiovascular mortality."

Professor Richard Edwards and Dr Simon Hales from the University of Otago in New Zealand say in an accompanying editorial that: 

"despite the strengths of the study, it is possible that a true effect was missed because of imprecise measurements and inadequate statistical power. Given other evidence that exposure to air pollution increases overall mortality and morbidity, the case for stringent controls on pollutant levels remains strong."



Summary

1.      high levels of pollution could increase the risk of having a heart attack for up to six hours after exposure

2.      the heart attack would have happened regardless and was merely pulled forward by a few hours.

3.      the association with an increased risk of heart attack is less clear

4.      higher levels of PM10 and NO2 are well-known markers of traffic related pollution. 

 

5.      limited potential for reducing the overall burden of myocardial infarction through reductions in pollution alone

6.      possible that a true effect was missed because of imprecise measurements and inadequate statistical power