Monday, September 12, 2016

Leptospirosis ေရာဂါ

Leptospirosis
လက္ပတိုစပိုင္႐ိုးစစ္ ေရာဂါ

ႂကြက္မွတဆင့္ကူးစက္သည္၊
စပိုင္႐ိုခိ ပိုးသည္ ႂကြက္ေသးမွ
တဆင့္ညစ္ပတ္ေသာေျမႀကီးထဲ
တြင္ေရာက္ရိွသြားၿပီး
လူတို႔အသက္႐ွဴ လမ္းေၾကာင္းမွတဆင့္လည္းေကာင္း၊အစာလမ္းေၾကာင္းမွလည္းေကာင္း၊ပြန္႔ပဲ့ေနေသာအေရျပားမွတဆင့္လည္းေကာင္လူ႔ခႏၶာကိုယ္ထဲသို႔ဝင္ေရာက္ပါသည္။
..လယ္သမားမ်ား၊ျမဴ နီစပယ္လုပ္သားမ်ား၊တံငါမ်ား၊
စစ္သားမ်ား၊ေက်ာက္မီးေသြးမိုင္းတြင္းလုပ္သား
မ်ား၊ အားအဓိကကူးစက္တတ္သည္။
ေရာဂါလကၡဏာမ်ား
၁။႐ုတ္တရက္ျဖစ္သည္၊
၂။ေမာပန္းသည္၊
၃။ကိုယ္ပူခ်ိန္ျမင့္မားသည္၊
(၃၉.၅ ံစင္တီဂရိတ္မွ ၄၀.၅ ံစင္တီဂရိတ္ထိျမင့္မားၿပီး
၃ရက္မွ၁၀ရက္အတြင္း
အဖ်ားက်လာသည္)
၄။ဝမ္းဗိုက္နာမည္၊
၅။ပ်ိ ဳ ့မည္၊အန္မည္၊
၆။ႂကြက္သားမ်ားအထူးသျဖင့္
ေက်ာဘက္ႂကြက္သားမ်ားအရမ္းနာမည္၊
အာ႐ုံေၾကာစနစ္ကိုထိခိုက္ပါက
၁။ျပင္းထန္စြာေခါင္းကိုက္မည္၊
၂။စိတ္ကေယာင္ေခ်ာက္ျခားျဖစ္
မည္၊
၃။ဦးေဏွာက္အေျမႇးေရာင္သကဲ့
သို့ဇက္ေတာင့္မည္၊
၄။မ်က္ေစ့ဝါျခင္း၊အသားဝါျခင္းျဖစ္မည္၊
၅။ႏွားေခါင္း၊အစာလမ္းေၾကာင္း၊
  အဆုတ္၊တိုတြင္ေသြးယိုျခင္းျဖစ္မည္၊
အေရျပားတြင္ေသြးယိုမႈေၾကာင့္အေရျပားေပၚတြင္အနီစက္မ်ား
ျဖစ္ေပၚမည္၊
၆။ေခ်ာင္းဆိုးျခင္း၊လည္ေခ်ာင္းနာျခင္း အသက္႐ွဴ
ၾကပ္ျခင္းႏွင့္အတူအဆုတ္ေရာင္မည္၊
၇။အသားဝါျခင္းသည္၈၀ရာခိုင္နဴန္း
ေသာလူနာမ်ားတြင္ေတြ႔ရသည္၊
ျဖစ္ပြားရက္၄ရက္ေျမာက္ေန႔မွ
၇ရက္ေျမာက္ေန႔ၾကားတြင္စတင္ျဖစ္ပြားသည္၊
၈။အသဲ၊ေဘလံုးႀကီးမည္၊
၉။ေသြးထဲတြင္ယူရီးယားUrea
Levelတက္မည္၊
၁ဝ။ဆီးမသြားႏိုင္ျဖစ္မည္၊
၁၁။ေက်ာက္ကပ္အလုပ္မလုပ္ႏိုင္
၍ေသဆံုးႏိုင္ပါသည္။
ကုသမႈအေနျဖင့္
Inj..Benzyl penicillin
600mg......1200mg 6 hourly
for 7 day
BHSအမ်ားစုသည္ေတာရြာမ်ားတြင္အေနမ်ားသည္ျဖစ္၍
သိေစခ်င္ေသာေစတနာျဖင့္တင္ေပးလိုက္ပါသည္။
လထဆရာဝန္မ်ားခြင့္ယူထား
လို႔အလုပ္မအားေပမဲ့တင္ေပးလိုက္ပါသည္။
အသားဝါjaundiceေတြ႔ပါကမေပါ့ဆရန္

copy from စိုင္းေဗဒါ facebook


Leptospirosis is an infection caused by corkscrew-shaped bacteria called Leptospira. Signs and symptoms can range from none to mild such as headaches, muscle pains, and fevers; to severe with bleeding from the lungs or meningitis.[4][5] If the infection causes the person to turn yellow, have kidney failure and bleeding, it is then known as Weil's disease.[5] If it causes lots of bleeding from the lungs it is known as severe pulmonary hemorrhage syndrome.[5]
Quick facts: Classification and external resources, Specialty, ...

Up to 13 different genetic types of Leptospira may cause disease in humans.[6] It is transmitted by both wild and domestic animals.[5] The most common animals that spread the disease are rodents.[7] It is often transmitted by animal urine or by water or soil containing animal urine coming into contact with breaks in the skin, eyes, mouth, or nose.[4][8] In the developing world the disease most commonly occurs in farmers and poor people who live in cities.[5] In the developed world it most commonly occurs in those involved in outdoor activities in warm and wet areas of the world.[4] Diagnosis is typically by looking for antibodies against the bacterium or finding its DNA in the blood.[9]

Efforts to prevent the disease include protective equipment to prevent contact when working with potentially infected animals, washing after this contact, and reducing rodents in areas people live and work.[4] The antibiotic doxycycline, when used in an effort to prevent infection among travellers, is of unclear benefit.[4] Vaccines for animals exist for certain type of Leptospira which may decrease the risk of spread to humans.[4] Treatment if infected is with antibiotics such as: doxycycline, penicillin, or ceftriaxone.[4] Weil's disease and severe pulmonary haemorrhage syndrome result in death rates greater than 10% and 50%, respectively, even with treatment.[5]

It is estimated that seven to ten million people are infected by leptospirosis a year.[10] The number of deaths this causes is not clear.[10] The disease is most common in tropical areas of the world but may occur anywhere.[4] Outbreaks may occur in slums of the developing world.[5] The disease was first described by physician Adolf Weil in 1886 in Germany.[4] Animals which are infected may have no symptoms, mild symptoms, or severe symptoms.[6] Symptoms may vary by the type of animal.[6] In some animals Leptospira live in the reproductive tract, leading to transmission during mating.[11]

Signs and symptoms
Leptospiral infection in humans causes a range of symptoms, and some infected persons may have no symptoms at all. Leptospirosis is a biphasic disease that begins suddenly with fever accompanied by chills, intense headache, severe myalgia (muscle ache), abdominal pain, conjunctival suffusion (red eye), and occasionally a skin rash.[12] The symptoms appear after an incubation period of 7–12 days. The first phase (acute or septic phase) ends after 3–7 days of illness.[13] The disappearance of symptoms coincides with the appearance of antibodies against Leptospira and the disappearance of all the bacteria from the bloodstream. The patient is asymptomatic for 3–4 days until the second phase begins with another episode of fever.[12] The hallmark of the second phase is meningitis (inflammation of the membranes covering the brain).[14]

90 percent of cases of the disease are mild leptospirosis. The rest experience severe disease, which develops during the second stage or occurs as a single progressive illness.[15] The classic form of severe leptospirosis is known as Weil's disease, which is characterized by liver damage (causing jaundice), kidney failure, and bleeding.[16] Additionally, the heart and brain can be affected, meningitis of the outer layer of the brain, encephalitis of brain tissue with same signs and symptoms; and lung affected as the most serious and life-threatening of all leptospirosis complications. The infection is often incorrectly diagnosed due to the nonspecific symptoms.

Other severe manifestations include extreme fatigue, hearing loss, respiratory distress, and azotemia.

Cause

Scanning electron micrograph of a number of Leptospira sp. bacteria atop a 0.1 µm polycarbonate filter
Leptospirosis is caused by spirochaete bacteria belonging to the genus Leptospira. 21 species of Leptospira have been identified.[6] 13 species cause disease or have been detected in human cases.[6][17]

Leptospira are also classified based on their serovar. About 250 pathogenic serovars of Leptospira are recognized. The diverse sugar composition of the lipopolysaccharide on the surface of the spirochete is responsible for the antigenic difference between serovars. Antigenically related serovars are grouped into 24 serogroups, which are identified using the microscopic agglutination test (MAT). A given serogroup is often found in more than one species, suggesting that the LPS genes that determine the serovar are exchanged between species.[17]

The traditional serologic system currently seems more useful from a diagnostic and epidemiologic standpoint—but this may change with further development and spread of technologies like polymerase chain reaction (PCR).

Transmission
Leptospirosis is transmitted by the urine of an infected animal and is contagious as long as the urine is still moist. Although Leptospira has been detected in reptiles and birds, only mammals are able to transmit the bacterium to humans and other animals.[18] Rats, mice, and moles are important primary hosts—but a wide range of other mammals including dogs, deer, rabbits, hedgehogs, cows, sheep, raccoons, opossums, skunks, and certain marine mammals carry and transmit the disease as secondary hosts. In Africa, the banded mongoose has been identified as a carrier of the pathogen, likely in addition to other African wildlife hosts.[19] Dogs may lick the urine of an infected animal off the grass or soil, or drink from an infected puddle.

House-bound domestic dogs have contracted leptospirosis, apparently from licking the urine of infected mice in the house. The type of habitats most likely to carry infective bacteria includes muddy riverbanks, ditches, gullies, and muddy livestock rearing areas where there is a regular passage of wild or farm mammals. The incidence of leptospirosis correlates directly with the amount of rainfall, making it seasonal in temperate climates and year-round in tropical climates. Leptospirosis also transmits via the semen of infected animals.[20]

Humans become infected through contact with water, food, or soil that contains urine from these infected animals. This may happen by swallowing contaminated food or water or through skin contact. The disease is not known to spread between humans, and bacterial dissemination in convalescence is extremely rare in humans. Leptospirosis is common among water-sport enthusiasts in specific areas, as prolonged immersion in water promotes the entry of this bacterium. Surfers and whitewater paddlers[21] are at especially high risk in areas that have been shown to contain these bacteria, and can contract the disease by swallowing contaminated water, splashing contaminated water into their eyes or nose, or exposing open wounds to infected water.[22]

At risk occupations
Occupations at risk include veterinarians, slaughterhouse workers, farmers, sewer maintenance workers, waste disposal facility workers, and people who work on derelict buildings.[23] Slaughterhouse workers can contract the disease through contact with infected blood or body fluids. Rowers, kayakers and canoeists also sometimes contract the disease.[24] It was once mostly work related but is now often also related to adventure tourism and recreational activities.[5]

Diagnosis

Kidney tissue, using a silver staining technique, revealing the presence of Leptospira bacteria
On infection the microorganism can be found in blood and cerebrospinal fluid (CSF) for the first 7 to 10 days (invoking serologically identifiable reactions) and then moving to the kidneys. After 7 to 10 days the microorganism can be found in fresh urine. Hence, early diagnostic efforts include testing a serum or blood sample serologically with a panel of different strains.

Kidney function tests (blood urea nitrogen and creatinine) as well as blood tests for liver functions are performed. The latter reveal a moderate elevation of transaminases. Brief elevations of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and gamma-glutamyltransferase (GGT) levels are relatively mild. These levels may be normal, even in children with jaundice.

Diagnosis of leptospirosis is confirmed with tests such as enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR). The MAT (microscopic agglutination test), a serological test, is considered the gold standard in diagnosing leptospirosis. As a large panel of different leptospira must be subcultured frequently, which is both laborious and expensive, it is underused, especially in developing countries.

Differential diagnosis list for leptospirosis is very large due to diverse symptoms. For forms with middle to high severity, the list includes dengue fever and other hemorrhagic fevers, hepatitis of various etiologies, viral meningitis, malaria, and typhoid fever. Light forms should be distinguished from influenza and other related viral diseases. Specific tests are a must for proper diagnosis of leptospirosis.

Under circumstances of limited access (e.g., developing countries) to specific diagnostic means, close attention must be paid to the medical history of the patient. Factors such as certain dwelling areas, seasonality, contact with stagnant contaminated water (bathing, swimming, working on flooded meadows, etc.) or rodents in the medical history support the leptospirosis hypothesis and serve as indications for specific tests (if available).

Leptospira can be cultured in Ellinghausen-McCullough-Johnson-Harris medium (EMJH), which is incubated at 28 to 30 °C.[25] The median time to positivity is three weeks with a maximum of three months. This makes culture techniques useless for diagnostic purposes but is commonly used in research.

Prevention
Doxycycline has been provided once a week as a prophylaxis to minimize infections during outbreaks in endemic regions.[26] However, there is no evidence that chemoprophylaxis is effective in containing outbreaks of leptospirosis.[27] Pre-exposure prophylaxis may be beneficial for individuals traveling to high-risk areas for a short stay.[28]

Effective rat control and avoidance of urine contaminated water sources are essential preventive measures. Human vaccines are available only in a few countries, such as Cuba and China.[5] Animal vaccines only cover a few strains of the bacteria. Dog vaccines are effective for at least one year.[29]

Treatment
Effective antibiotics include penicillin G, ampicillin, amoxicillin and doxycycline. In more severe cases cefotaxime or ceftriaxone should be preferred.

Glucose and salt solution infusions may be administered; dialysis is used in serious cases. Elevations of serum potassium are common and if the potassium level gets too high special measures must be taken. Serum phosphorus levels may likewise increase to unacceptable levels due to kidney failure.

Treatment for hyperphosphatemia consists of treating the underlying disease, dialysis where appropriate, or oral administration of calcium carbonate, but not without first checking the serum calcium levels (these two levels are related). Administration of corticosteroids in gradually reduced doses (e.g., prednisolone) for 7–10 days is recommended by some specialists in cases of severe hemorrhagic effects.[citation needed] Organ-specific care and treatment are essential in cases of kidney, liver, or heart involvement.

Epidemiology
It is estimated that seven to ten million people are infected by leptospirosis annually.[10] One million cases of severe leptospirosis occur annually, with 58,900 deaths.[30] Annual rates of infection vary from 0.02 per 100,000 in temperate climates to 10 to 100 per 100,000 in tropical climates.[26] This leads to a lower number of registered cases than likely exists.

History
The disease was first described by Adolf Weil in 1886 when he reported an "acute infectious disease with enlargement of spleen, jaundice, and nephritis." Leptospira was first observed in 1907 from a post mortem renal tissue slice.[31] In 1908, Inada and Ito first identified it as the causative organism[32] and in 1916 noted its presence in rats.[33]

Leptospirosis was postulated as the cause of an epidemic among Native Americans along the coast of present-day Massachusetts that occurred immediately before the arrival of the Pilgrims in 1620 and killed most of the native population.[34] Earlier proposals included plague, yellow fever, smallpox, influenza, chickenpox, typhus, typhoid fever, trichinellosis, meningitis, and syndemic infection of hepatitis B with hepatitis D.[35][36][37][38] The disease may have been brought to the New World by Europeans and spread by the high-risk daily activities of the Native Americans.[34]

Before Weil's characterization in 1886, the disease known as infectious jaundice was very likely the same as Weil's disease or severe icteric leptospirosis. During the Egyptian campaign, Napoleon's army suffered from what was probably infectious jaundice.[39] Infectious jaundice occurred among troops during the American Civil War.[40]

It was also reported among troops at Gallipoli and other battles of World War I, where the sodden conditions of trench warfare favored infection. Terms used in early 20th century descriptions of leptospirosis include the pseudo-dengue of Java, seven-day fever, autumn fever, Akiyama disease, and marsh or swamp fever. L icterohaemorrhagiae was identified as the causative agent in pre-World War II outbreaks in Japan, which were characterized by jaundice and a high mortality rate.

In October 2010 British rower Andy Holmes died after contracting Weil's Disease.[41] His death has raised awareness of the disease among the public and medical professionals.[42]

Names
Leptospirosis has many different names including: "7-day fever",[1] "harvest fever",[1] "field fever",[1] "canefield fever",[1] "mild fever",[1] "rat catcher's yellows",[2] "Fort Bragg fever",[3] and "pretibial fever".[3]

It has historically been known as "black jaundice"[43] and in Japan it is called "nanukayami fever".[44] Weil's disease or Weil's syndrome is also known as spirochaetosis icterohaemorrhagica.[45]

Other animals
Incubation (time of exposure to first symptoms) in animals is anywhere from 2 to 20 days. In dogs, leptospirosis most often damages the liver and kidney. In addition, recent reports describe a pulmonary form of canine leptospirosis associated with severe hemorrhage in the lungs—similar to human pulmonary hemorrhagic syndrome.[46][47] Vasculitis may occur, causing edema and potentially disseminated intravascular coagulation (DIC). Myocarditis, pericarditis, meningitis, and uveitis are also possible sequelae.[24]

At least five important serovars exist in the United States and Canada, all of which cause disease in dogs:[24][46][48]

Icterohaemorrhagiae
Canicola
Pomona
Grippotyphosa
Bratislava
In dogs when leptospirosis is caused by L. interrogans it may be referred to as "canicola fever".[44] Leptospirosis should be strongly suspected and included as part of a differential diagnosis if the sclerae of a dog's eyes appear jaundiced (even slightly yellow). The absence of jaundice does not eliminate the possibility of leptospirosis, and its presence could indicate hepatitis or other liver pathology rather than leptospirosis. Vomiting, fever, failure to eat, reduced urine output, unusually dark or brown urine, and lethargy are also indications of the disease.

In dogs, penicillin is most commonly used to end the leptospiremic phase (infection of the blood), and doxycycline is used to eliminate the carrier state.

References
Tap to expand
External links
U.S. Disease Control and Prevention Center page on Leptospirosis
"Leptospira". NCBI Taxonomy Browser. 171.

ေခြးရူးျပန္ေရာဂါ

ေခြး ရူး ျပန္ေရာဂါ
~~~~~~~~
ေခြး ရူးျပန္ေရာဂါ သည္ virus ပိုး Rabies virus , Lyssavirus genus of the Rhabdoviridae family ေၾကာင့္ျဖစ္ သည္။
အလြန္ေၾကာက္စရာေကာင္း ေသာ ေရာဂါ ျဖစ္သည္။ ေခြးရူးေရာဂါပိုးသည္ ေခြး၏ သြားရည္ မွတဆင့္ လူ၏ကိုယ္ ထဲသို.၀င္သြား ျပီး ၊ ဥိးေနွာက္ နွင့္ အာရံု ေၾကာ ထဲ ေရာက္သြား ျပီး အ သက္ ဆံုးရွုံး နိုင္သည္။ ေခြး ကိုက္ခံရ ျခင္း အျပင္ ၊ ေခြး ကလ်ွာ ျဖင့္ရက္ ျခင္း၊ လူ ၏အေရျပား အပြန္း အ ပဲ့သို . ေခြးသြားရည္ ထိျခင္း တို.ေၾကာင့္လည္း ကူးစက္ႏုိင္သည္။

ေခြး ရူးျပန္ေရာဂါ လကၡဏာမ်ား

အကိုက္ခံရျပီး ၉ ရက္ မွ လ အေတာ္ၾကာထိ ေရာဂါ မျပဘဲ ရွိနိုင္ သည္။ အကိုက္ခံရ ေသာ အ နာ ၾကီး ျခင္ း၊ မ်ားျခင္း၊ ဦးေခါင္း နွင့္ လည္ ပင္း တ ၀ိုက္တြင္ ကိုက္ခံရ ပါ က ေ၇ာဂါ လကၡဏာ ျမန္ျမန္ ျပတတ္သည္။
ေခြး ရူးျပန္ေရာဂါ စ ျဖစ္လာပါ က ၊ ဖ်ားျခင္း၊ ေခြးကိုက္ခံရေသာ ေနရာတ၀ိုက္တြင္ နာ ျပီး ထံုက်င္ျခင္း ၊ စတင္ခံစားရမည္။ ထို.ေနာက္ စိတ္လႈပ္ရွား ဂဏာ မျငိမ္ ျဖစ္ လာမည္။ ထင္ရွားေသာ လကၡဏာမွာ ေရဆာေသာ္လည္း ေရလံုး၀ မေသာက္နိုင္ဘဲ ေရကိုအလြန္ေၾကာက္ေနျခင္းျဖစ္သည္။
စိတ္ ဂေရာက္ကယက္ျဖစ္ျခင္း၊ တကယ္မရွိေသာ အရာမ်ား ကို ျမင္ေယာင္လာျခင္း ၊ အရူး လိုေအာ္ဟစ္ေနျခင္း၊ ပံုမွန္ လူစိတ္မရွိေတာ့ျခင္း ၊ သတိမရွိေတာ့ျခင္း။ အသိစိတ္ ၀င္လိုက္ေျပာက္လိုက္ ျဖစ္ျခင္း၊ စေသာေ၀ဒနာ မ်ားခံစားရျပီး ၊ ၁ ပတ္ - ၁၀ ရက္အၾကာ တြင္ ေသဆံုးရေပမည္။
ေခြး ရူးျပန္ေရာဂါ စျဖစ္လွ်င္ ကုသေဆး မရွိပါ။
ေခြး ရူးျပန္ေရာဂါ စျဖစ္ပါက အသက္မေသေသာလူ အလြန္ ရွားပါးပါသည္။

ေခြး ရူးျပန္ေရာဂါ ကာကြယ္ျခင္း

( ၁) ေခြး ကိုက္မခံရ ခင္ ကာကြယ္ျခင္း
ေခြးကိုက္မခံရေအာင္ေနျခင္း၊ ေခြးကို လက္ပြန္းတတီး မေနျခင္း ၊ အိမ္ေမြးေခြးကို ကာကြယ္ေဆး ထိုးထား ျခင္း ၊ မိမိတြင္ေခြး ကိုက္ခံရ နိုင္ေသာ အေျခေနရွိပါက ၾကိဳ တင္ ကာကြယ္ေဆးထိုးထာျခင္း ( အေရျပားေအာက္ သို.မဟုတ္ အသားေဆး ၄ ပတ္ျခား ၂ ၾကိမ္ )

(၂) ေခြးကိုက္ခံရျပီး မွ ေခြးရူးျပန္ေရာဂါ မျဖစ္ရန္ ကာကြယ္ျခင္း
ဆရာ၀န္ အျမန္ျပရန္ လိုသည္။ ဆရာ၀န္ မွ အနာကို လိုအပ္ သလိုေဆးေၾကာ ေပးမည္။ antirabies antiserum ျဖင့္ လူအေလးခ်ိန္ ေပၚ မူတည္ ျပီးေဆးပမာဏ တြက္ခ်က္ကာ တ၀က္ကို အနာတ၀ိုက္ စိမ့္၀င္ေအာင္ လုပ္ေပးျပီး ၊ က်န္တ၀က္ကို အသားေဆး ထိုးေပးမည္။
Human diploid cell strain vaccine ေခြး ရူးျပန္ေရာဂါ ကာကြယ္ေဆးကို Day 0 ,3 ,7 ,14 , 30 ,90 တို.တြင္ အသားေဆးထိုးရမည္။ ( ခ်က္ မွာမထိုးပါ) ။ လက္ေမာင္း၊ တင္ပါးမွာထိုးနိုင္သည္။

မွတ္ခ်က္ ။ ။ ေခြးကိုက္ခံရျပီးမွ ထိုးေသာကာကြယ္ေဆးသည္ အျမန္ဆံုးထိုးနိုင္ေလ ေဆးအာနိသင္ အျပည့္အ၀ ရေလျဖစ္သည္။ ေနွာင့္ေႏွးျခင္း ၊ ေခြးရူး မရူး ေစာင့္ၾကည့္ေနျခင္း ျဖင့္ေဆးထိုးေနာက္က် ပါက ၊ေဆး၏ကာကြယ္မႈ စြမ္းအင္ေလ်ာ့ နဲ ပါသည္။

ကိုက္ေသာေခြး ကိုသတ္ပစ္ျခင္းသည္လည္း လြဲမွားေသာ အယူ အဆျဖစ္သည္။ ေခြးေသ သြားလ်င္ လူမွာေခြးရူး မျပန္ေတာ့မွာ မဟုတ္ပါ
Negri Bodies ေခၚ including bodies တမ်ိဳးကို ေခြးရူး၏ ဦးေနွာက္ထဲတြင္ ေတြ.နိုင္ေသာ္လည္း ၊ စမ္းသပ္အေျဖေစာင့္ေနျခင္းျဖင့္ ၊ အခ်ိန္ေနွာင့္ေနွးနိုင္သျဖင့္ ကာကြယ္ေဆး အျမန္ ထိုးတာ အေကာင္းဆံူျဖစ္ သည္။

ကိုက္ေသာေခြး က ေခြးရူးမဟုတ္ ဆိုကာ ေဆးမထိုးဘဲ မေနသင့္ပါ။ ယဥ္ယဥ္ေလးရူးေန တတ္ပါသည္။ ေခြးရူူး မဟုတ္ေလာက္ပါဘူး ဟု ၊တခ်က္ေပါ့ဆ ပါက အသက္နွင့္ ရင္း ရတတ္ပါသည္။

ေဒါက္တာဆု ေဆးပညာဌာန

Saturday, September 10, 2016

အတတ္ေရာဂါ


Category
ဂ်ာနယ္မ်ား၊ မဂၢဇင္းမ်ားႏွင့္ သတင္းမ်ား
        ဦးေႏွာက္ႏွင့္အာ႐ံုေၾကာေရာဂါတစ္မ်ိဳးျဖစ္သည့္ အတက္ေရာဂါသည္ လူဦးေရ 10 ဦးလွ်င္ 1 ဦးႏႈန္း ျဖစ္ပြားလွ်က္ရွိေနၿပီး အသက္အႏၲရာယ္လည္းရွိေသာ ဂ႐ုျပဳရမည့္ေရာဂါတစ္မ်ိဳးျဖစ္ပါသည္။ လက္ရွိတြင္လည္း ႏိုင္ငံေတာ္အစိုးရမွ အတက္ေရာဂါပေပ်ာက္ေရးစီမံကိန္းကို 2014 ခုႏွစ္မွစတင္၍ အေကာင္အထည္ေဖာ္လုပ္ေဆာင္ေနကာ ထပ္မံ၍လည္းတိုးခ်ဲ႕ေဆာင္ရြက္မည္ကိုသိရ၍ ရန္ကုန္ျပည္သူ႕ေဆး႐ံုႀကီး ဦးေႏွာက္ႏွင့္အာ႐ုံေၾကာေဆးကုသဌာန အထူးကုဆရာဝန္ႀကီး တြဲဖက္ပါေမာကၡ ေဒါက္တာဦးစမ္းဦးႏွင့္ေတြ႕ဆုံေမးျမန္းျဖစ္ခဲ့ပါသည္။

ေမး ။    ။ အတက္ေရာဂါစီမံခ်က္ကို စတင္ျဖစ္ခဲ့ျခင္းႏွင့္ လက္ရွိမွာ မည္ကဲ့သို႔ေဆာင္ရြက္မႈရွိေနသလဲ သိပါရေစရွင့္။

ေျဖ ။    ။ အတက္ေရာဂါစီမံခ်က္ကို 2014 ခုႏွစ္ထဲက စတင္ခဲ့တာျဖစ္ၿပီး ၿမိဳ႕နယ္ေပါင္း 9 ခုမွာ စီမံခ်က္အရ ေရာဂါရွိသူေတြရွာေဖြၿပီးကုသမႈနဲ႔ အသိပညာေပးမႈေတြေဆာင္ရြက္ခဲ့ပါတယ္။ ေနာက္ထပ္လည္း တိုးခ်ဲ႕ၿပီးေဆာင္ရြက္တဲ့အေနနဲ႔ စစ္ကိုင္းတိုင္းဘက္တြင္ အတက္ေရာဂါရွိသူမ်ားကိုရွာေဖြကုသမႈႏွင့္ အသိပညာေပးမႈမ်ား ျပဳလုပ္သြားဖို႔ရွိပါတယ္။

ေမး ။    ။ အတက္ေရာဂါကဘာေၾကာင့္ျဖစ္တာပါလဲ။ ေရာဂါလကၡဏာေတြကေရာ ဘယ္လိုမ်ိဳးရွိတတ္ပါသလဲ။

ေျဖ ။    ။ အတက္ေရာဂါဟာ ေရရွည္ေဆးကုသမႈခံယူေနေသာ ဦးေႏွာက္ႏွင့္အာ႐ုံေၾကာေရာဂါတစ္မ်ိဳးျဖစ္ၿပီး အသက္အရြယ္မေရြး၊ လူမ်ိဳး၊ ဘာသာမေရြးျဖစ္နိုင္ပါတယ္။ 24 နာရီျခား၍ အေၾကာင္းအရင္းခံမရွိဘဲ အနည္းဆုံး 2 ႀကိမ္ႏွင့္အထက္တက္လွ်င္ အတက္ေရာဂါျဖစ္ပြားေနတယ္လို႔ သတ္မွတ္ႏိုင္ပါတယ္။ အဓိကေရာဂါလကၡဏာေတြအေနနဲ႔က သတိလုံးဝလစ္သြားမယ္။ ကေလးေတြဆိုရင္ တက္ေနတဲ့အခ်ိန္ခႏၶာကိုယ္ေတာင့္တင္းျခင္း၊ ေပ်ာ့ေခြျခင္းေတြျဖစ္ၿပီး လူႀကီးေတြအေနနဲ႔ဆို တစ္ကိုယ္လုံးဆက္ကနဲ အေၾကာလိုက္သလိုျဖစ္တာ၊ ေကာက္ေကြးသြားတာေတြက တက္တဲ့အခ်ိန္မွာျဖစ္ႀကပါတယ္။

ေမး ။    ။ အတက္ေရာဂါကို ဘယ္လိုကုသမႈမ်ိဳးေပးႏိုင္ပါသလဲ။

ေျဖ ။    ။ အတက္ေရာဂါအေၾကာင္းႏွင့္ အတက္ေရာဂါရွိသူမ်ားအတြက္ ျပဳစုကုသနည္းမ်ားကို အသိပညာေပးျခင္းအားျဖင့္ ျပည္သူလူထုမွ အတက္ေရာဂါအေၾကာင္းကိုသိရွိနားလည္၍ သတိျပဳမိေစ႐ံုသာမက အတက္ေရာဂါအေပၚထားရွိေသာ မွားယြင္းသည့္သေဘာထားအယူအဆမ်ား ေျပာင္းလဲလာၿပီး အတက္ေရာဂါရွိသူမ်ားကို စာနာနားလည္ႏိုင္ရန္လိုအပ္ပါတယ္။ အတက္ေရာဂါရွိသူမ်ားမွလည္း သင့္ေလ်ာ္ေသာေဆးကုသမႈခံယူနိုင္ၿပီး ပုံမွန္လူေနမႈဘဝကိုအခက္ခဲမရွိ ျဖတ္သန္းႏိုင္မွာျဖစ္ပါတယ္။ က်န္းမာေရးဝန္ႀကီးဌာနအေနနဲ႔လည္း အတက္ေရာဂါေဝဒနာရွင္မ်ားကို အခမဲ့ေဆးဝါးပံ့ပိုးမႈမ်ားရွိေနကာ နီးစပ္ရာက်န္းမာေရးဝန္ထမ္းမ်ားထံ ေဝဒနာရွင္မ်ားက အခမဲ့ေဆးဝါးရယူႏိုင္ရန္ ေဆာင္ရြက္ထား တာေတြရွိပါတယ္။

ေမး ။    ။ အတက္ေရာဂါကမ်ိဳး႐ိုးေၾကာင့္ျဖစ္ပြားတာပါလား။

ေျဖ ။    ။ အတက္ေရာဂါရွိသူအားလုံးသည္ မ်ိဳး႐ိုးလိုက္ျခင္းေၾကာင့္တက္ျခင္းမဟုတ္ပါဘူး။ အခ်ိဳ႕သည္ မိခင္ဝမ္းတြင္း သေႏၶသားဦးေႏွာက္ေကာင္းမြန္စြာမဖြံ႕ၿဖိဳးျခင္းေၾကာင့္ ေမြးရာပါ ဦးေႏွာက္ခ်ိဳ႕ယြင္းျခင္း၊ ေမြးဖြားခ်ိန္တြင္ ညႇပ္ဆြဲျခင္း၊ ေမြး ခ်ိန္ၾကာျခင္းတို႔ေၾကာင့္ ဦးေႏွာက္ဒဏ္ရာရျခင္းႏွင့္ ဦးေႏွာက္ထိခိုက္ေစေသာေရာဂါမ်ားေၾကာင့္ ျဖစ္ပြားရတာျဖစ္ပါတယ္။ အတက္ေရာဂါက စိတ္ေရာဂါလည္းမဟုတ္ပါဘူး။

ေမး ။    ။ အတက္ေရာဂါက ဦးေႏွာက္အာ႐ံုေၾကာဆိုင္ရာေရာဂါျဖစ္လို႔ စာေပသင္ၾကားမႈေတြျပဳလုပ္ႏိုင္ပါသလားဆရာ။

ေျဖ ။    ။ ေရာဂါရွိတဲ႔သူေတြအေနနဲ႔က စာသင္လို႔ေတာ႔ရႏိုင္တယ္ဆိုေပမယ္႔ ခဏခဏတက္ေနတာေတြက အခက္အခဲေတာ့ျဖစ္ႏိုင္ပါတယ္။ ဥပမာ- မိန္းကေလးေတြဆိုလည္း ဓမၼတာလာစဥ္ခဏခဏတက္မယ္။ အဲ႔လိုရက္မ်ိဳးက ေဟာ္မုန္းအေျပာင္းအလဲေၾကာင့္ျဖစ္တတ္တယ္ဆိုရင္ အဲ႔ဒီ့ရက္မ်ိဳးဆို ေဆးေတြ ဘာေတြေသာက္ဖို႔ မွတ္မွတ္ရရထည့္ထားတာ ဂ႐ုတစိုက္ေဆးေသာက္တာေလးေတြ လုပ္ထားသင္႔ပါတယ္။

ေမး ။    ။ အတက္ေရာဂါက ေပ်ာက္ကင္းသြားႏိုင္ပါသလားဆရာ။

ေျဖ ။    ။ အခ်ိဳ႕လည္းေဆးပုံမွန္ေသာက္ၿပီး လုံး၀မတက္ေတာ့တာေတြရွိသလို၊ အခ်ိဳ႕က်ေတာ႔ေဆးကိုေသခ်ာမေသာက္ဖူး ေပ်ာက္သြားၿပီမတက္ေတာ႔ဘူးဆိုတာနဲ႔ ခဏေလးနဲ႔ ေဆးျဖတ္လိုက္တယ္။ ေရာဂါကျပန္ျဖစ္ၿပီး ေဆးျပန္ေသာက္ေနရတာေတြရွိပါတယ္။ တစ္ဦးနဲ႔တစ္ဦးေတာ႔မတူဘူး။ ကြားျခားမႈေတြရွိပါတယ္။

ေမး ။    ။ အတက္ေရာဂါကေသဆုံးႏိုင္ပါလား။ ကုသမႈမျပဳပဲထားပါက မည္သို႔ျဖစ္ပြားႏိုင္ပါသလဲ။

ေျဖ ။    ။ အတက္ေရာဂါက 3 မိနစ္ထက္ပိုၿပီးတက္ေနပါက အသက္အႏၲရာယ္ရွိႏိုင္ပါတယ္။ တက္ေနတဲ့အခ်ိန္မွာ ဦးေႏွာက္က ေအာက္စီဂ်င္ျပတ္သြားတဲ့အတြက္ အခ်ိန္ၾကာၾကာတက္တာနဲ႔ ခဏခဏတက္တာေတြက မကုသပဲေနပါက အသက္ေသဆုံးမႈရွိႏိုင္သလို ဦးေႏွာက္ကိုထိခိုက္ၿပီး မွတ္ဉာဏ္မ်ားဆုံး႐ႈံးမႈရွိႏိုင္ပါတယ္။ အတက္ေရာဂါရွိသူေတြအေနနဲ႔ ေရာဂါေၾကာင့္မဟုတ္ရင္ေတာင္ တက္တဲ့အခ်ိန္မွာ ေလွကားဆင္းေနရင္ ေလွကားကျပဳတ္က်ၿပီး ခႏၶာကိုယ္ထိခိုက္တာ အသက္အႏၲရာယ္ရွိတာေတြျဖစ္ေစႏိုင္ၿပီး တက္တဲ့အခ်ိန္မွာ ခၽြန္ထက္တဲ့အရာရွိပါကထိခိုက္မိျခင္း စသျဖင့္အႏၲရာယ္ရွိေစႏိုင္တာေတြနဲ႔လည္း ႀကဳံေတြ႕ႏိုင္ပါတယ္။

ေမး ။    ။ အတက္ေရာဂါလူနာကို မည္သို႔ေဆးဝါးကုသ၍ အသိပညာေပးဖို႔ ဘယ္လိုအခ်က္ေတြ လိုအပ္ပါသလဲ။

ေျဖ ။    ။ ေဆးကုသမႈခံယူေနေသာ အတက္ေရာဂါလူနာေတြအေနနဲ႔ ေဆးမွန္မွန္ေသာက္ရန္ အလြန္အေရးႀကီးၿပီး လူနာအပါအဝင္မိသားစုမ်ား လိုက္နာရမယ့္အခ်က္ေတြက ေဆးကိုပ်က္ကြက္မႈမရွိပဲ မွန္မွန္ေသာက္ဖို႔သတိျပဳရန္၊ ဆရာဝန္၏ၫႊန္ၾကားခ်က္မရွိဘဲ မိမိသေဘာျဖင့္ေဆးတိုးျခင္း၊ ေဆးေလ်ာ့ျခင္း၊ ေဆးရပ္ျခင္းမ်ားမျပဳလုပ္ရန္၊ ဆရာဝန္ကလူနာအားၾကည့္႐ႈမည့္ရက္ခ်ိန္းအတိုင္း မွန္မွန္ျပရန္လိုအပ္ပါတယ္။ ဒါမွသာ ေဆးအၫႊန္းကိုစိစစ္ႏိုင္ၿပီး ေဘးထြက္ဆိုးက်ိဳးရွိ/မရွိကိုလည္း သိႏိုင္မွာပါ။

ေမး ။    ။ အတက္ေရာဂါစီမံကိန္းရဲ႕ရည္မွန္းခ်က္နဲ႔ ဦးတည္ခ်က္ေလးကို ျဖည့္စြက္ေျပာၾကားေပး ပါဦးရွင့္။

ေျဖ ။    ။ အတက္ေရာဂါအေၾကာင္းသိရွိနားလည္ၿပီး အတက္ေရာဂါရွိသူမ်ားအား ေရွးဦးသူနာျပဳစု တတ္ေစရန္ႏွင့္ အတက္ေရာဂါအေၾကာင္း ျပည္သူလူထုအား က်န္းမာေရးပညာေပးတတ္ေစရန္ရည္ရြယ္ၿပီး အတက္ေရာဂါရွိသူ၏ စိတ္ပိုင္းဆိုင္ရာခံစားမႈမ်ားႏွင့္ လူေနမႈဘဝအခက္အခဲမ်ားအား ေဖးမကူညီေပးႏိုင္ရန္ ဦးတည္ထားပါတယ္။

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Zika Virus


Zika virus (ZIKV) is a member of the virus family Flaviviridae and the genus Flavivirus.[3] It is spread by daytime-active Aedes mosquitoes, such as A. aegypti and A. albopictus.[3] Its name comes from the Zika Forest of Uganda, where the virus was first isolated in 1947.[4] Zika virus is related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses.[4] Since the 1950s, it has been known to occur within a narrow equatorial belt from Africa to Asia. From 2007 to 2016, the virus spread eastward, across the Pacific Ocean to the Americas, leading to the 2015–16 Zika virus epidemic.
Quick facts: Virus classification, ...

The infection, known as Zika fever or Zika virus disease, often causes no or only mild symptoms, similar to a very mild form of dengue fever.[3] While there is no specific treatment, paracetamol (acetaminophen) and rest may help with the symptoms.[5] As of 2016, the illness cannot be prevented by medications or vaccines.[5] Zika can also spread from a pregnant woman to her fetus. This can result in microcephaly, severe brain malformations, and other birth defects.[6][7] Zika infections in adults may result rarely in Guillain–Barré syndrome.[8]

In January 2016, the United States Centers for Disease Control and Prevention (CDC) issued travel guidance on affected countries, including the use of enhanced precautions, and guidelines for pregnant women including considering postponing travel.[9][10] Other governments or health agencies also issued similar travel warnings,[11][12][13] while Colombia, the Dominican Republic, Puerto Rico, Ecuador, El Salvador, and Jamaica advised women to postpone getting pregnant until more is known about the risks.[12][14] Zika is pronounced  or .[15][16]

Virology
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A video explanation of the Zika virus and of Zika fever
The Zika virus belongs to the Flaviviridae family and the Flavivirus genus, and is thus related to the dengue, yellow fever, Japanese encephalitis, and West Nile viruses. Like other flaviviruses, Zika virus is enveloped and icosahedral and has a nonsegmented, single-stranded, 10 kilobase positive-sense RNA genome. It is most closely related to the Spondweni virus and is one of the two known viruses in the Spondweni virus clade.[17][18][19][20][21]

Cross-section of Zika virus, with capsid layer (pink), membrane layer (purple), and RNA genome (yellow)[22]
A positive-sense RNA genome can be directly translated into viral proteins. As in other flaviviruses, such as the similarly sized West Nile virus, the RNA genome encodes seven nonstructural proteins and three structural proteins.[23] One of the structural proteins encapsulates the virus. The RNA genome forms a nucleocapsid along with copies of the 12-kDa capsid protein. The nucleocapsid, in turn, is enveloped within a host-derived membrane modified with two viral glycoproteins. Viral genome replication depends on the synthesis of double sided RNA from the single stranded positive sense RNA (ssRNA(+)) genome followed by transcription and replication to provide viral mRNAs and new ssRNA(+) genomes.[24][25]

There are two Zika lineages: the African lineage and the Asian lineage.[26] Phylogenetic studies indicate that the virus spreading in the Americas is 89% identical to African genotypes, but is most closely related to the Asian strain that circulated in French Polynesia during the 2013–2014 outbreak.[26][27][28]

Transmission
The vertebrate hosts of the virus were primarily monkeys in a so-called enzootic mosquito-monkey-mosquito cycle, with only occasional transmission to humans. Before the current pandemic began in 2007, Zika "rarely caused recognized 'spillover' infections in humans, even in highly enzootic areas". Infrequently, however, other arboviruses have become established as a human disease and spread in a mosquito–human–mosquito cycle, like the yellow fever virus and the dengue fever virus (both flaviviruses), and the chikungunya virus (a togavirus).[29] Though the reason for the pandemic is unknown, dengue, a related arbovirus that infects the same species of mosquito vectors, is known in particular to be intensified by urbanization and globalization.[30] Zika is primarily spread by Aedes aegypti mosquitoes,[31] and can also be transmitted through sexual contact[32] or blood transfusions.[33] The basic reproduction number (R0, a measure of transmissibility) of Zika virus has been estimated to be between 1.4 to 6.6.[34]

In 2015, news reports drew attention to the rapid spread of Zika in Latin America and the Caribbean.[35] At that time, the Pan American Health Organisation published a list of countries and territories that experienced "local Zika virus transmission" comprising Barbados, Bolivia, Brazil, Colombia, the Dominican Republic, Ecuador, El Salvador, French Guiana, Guadeloupe, Guatemala, Guyana, Haiti, Honduras, Martinique, Mexico, Panama, Paraguay, Puerto Rico, Saint Martin, Suriname, and Venezuela.[36][37][38] By August 2016, more than 50 countries (list and map) had experienced active (local) transmission of Zika virus.[39]

Mosquito

Global Aedes aegypti predicted distribution. The map depicts the probability of occurrence (blue=none, red=highest occurrence).
Zika is primarily spread by the female Aedes aegypti mosquito, which is active mostly in the daytime, although researchers have found the virus in common Culex house mosquitoes as well.[31] The mosquitos must feed on blood in order to lay eggs.[40]:2 The virus has also been isolated from a number of arboreal mosquito species in the Aedes genus, such as A. africanus, A. apicoargenteus, A. furcifer, A. hensilli, A. luteocephalus and A. vittatus, with an extrinsic incubation period in mosquitoes of about 10 days.[20]

The true extent of the vectors is still unknown. Zika has been detected in many more species of Aedes, along with Anopheles coustani, Mansonia uniformis, and Culex perfuscus, although this alone does not incriminate them as a vector.[41]

Transmission by A. albopictus, the tiger mosquito, was reported from a 2007 urban outbreak in Gabon where it had newly invaded the country and become the primary vector for the concomitant chikungunya and dengue virus outbreaks.[42] There is concern for autochthonous infections in urban areas of European countries infested by A. albopictus because the first two cases of laboratory-confirmed Zika infections imported into Italy were reported from viremic travelers returning from French Polynesia.[43]

The potential societal risk of Zika can be delimited by the distribution of the mosquito species that transmit it. The global distribution of the most cited carrier of Zika, A. aegypti, is expanding due to global trade and travel.[44] A. aegypti distribution is now the most extensive ever recorded – across all continents including North America and even the European periphery (Madeira, the Netherlands, and the northeastern Black Sea coast).[45] A mosquito population capable of carrying Zika has been found in a Capitol Hill neighborhood of Washington, D. C., and genetic evidence suggests they survived at least four consecutive winters in the region. The study authors conclude that mosquitos are adapting for persistence in a northern climate.[46] The Zika virus appears to be contagious via mosquitoes for around a week after infection. The virus is thought to be infectious for a longer period of time after infection (at least 2 weeks) when transmitted via semen.[47][48]

Research into its ecological niche suggests that Zika may be influenced to a greater degree by changes in precipitation and temperature than Dengue, making it more likely to be confined to tropical areas. However, rising global temperatures would allow for the disease vector to expand their range further north, allowing Zika to follow.[49]

Sexual
Zika can be transmitted from men and women to their sexual partners.[32][50] As of April 2016 sexual transmission of Zika has been documented in six countries – Argentina, Chile, France, Italy, New Zealand and the United States – during the 2015 outbreak.[8]

In 2014, Zika capable of growth in lab culture was found in the semen of a man at least two weeks (and possibly up to 10 weeks) after he fell ill with Zika fever.[51][52] In 2011 a study found that a US biologist who had been bitten many times while studying mosquitoes in Senegal developed symptoms six days after returning home in August 2008, but not before having unprotected intercourse with his wife, who had not been outside the US since 2008. Both husband and wife were confirmed to have Zika antibodies, raising awareness of the possibility of sexual transmission.[51][53] In early February 2016, the Dallas County Health and Human Services department reported that a man from Texas who had not travelled abroad had been infected after his male monogamous sexual partner had anal penetrative sex with him one day before and one day after onset of symptoms.[51][54][55] As of February 2016, fourteen additional cases of possible sexual transmission have been under investigation, but it remained unknown whether women can transmit Zika to their sexual partners.[56] At that time, the understanding of the "incidence and duration of shedding in the male genitourinary tract [was] limited to one case report." Therefore, the CDC interim guideline recommended against testing men for purposes of assessing the risk of sexual transmission.[51]

In March 2016, the CDC updated its recommendations about length of precautions for couples, and advised that heterosexual couples with men who have confirmed Zika fever or symptoms of Zika should consider using condoms or not having penetrative sex (i.e., vaginal intercourse, anal intercourse, or fellatio) for at least 6 months after symptoms begin. This includes men who live in—and men who traveled to—areas with Zika. Couples with men who traveled to an area with Zika, but did not develop symptoms of Zika, should consider using condoms or not having sex for at least 8 weeks after their return in order to minimize risk. Couples with men who live in an area with Zika, but have not developed symptoms, might consider using condoms or not having sex while there is active Zika transmission in the area.[57]

Pregnancy
The Zika virus can spread from an infected mother to her fetus during pregnancy or at delivery.[58]

Blood transfusion
As of April 2016, two cases of Zika transmission through blood transfusions have been reported globally, both from Brazil,[33] after which the US Food and Drug Administration (FDA) recommended screening blood donors and deferring high-risk donors for 4 weeks.[59][60] A potential risk had been suspected based on a blood-donor screening study during the French Polynesian Zika outbreak, in which 2.8% (42) of donors from November 2013 and February 2014 tested positive for Zika RNA and were all asymptomatic at the time of blood donation. Eleven of the positive donors reported symptoms of Zika fever after their donation, but only three of 34 samples grew in culture.[61]

Pathogenesis
Zika virus replicates in the mosquito's midgut epithelial cells and then its salivary gland cells. After 5–10 days, the virus can be found in the mosquito’s saliva, which can then infect humans. If the mosquito’s saliva is inoculated into human skin, the virus can infect epidermal keratinocytes, skin fibroblasts in the skin and the Langerhans cells. The pathogenesis of the virus is hypothesized to continue with a spread to lymph nodes and the bloodstream.[17][62] Flaviviruses generally replicate in the cytoplasm, but Zika antigens have been found in infected cell nuclei.[63]

Zika fever
Main article: Zika fever

Rash on an arm due to Zika
Zika fever (also known as Zika virus disease) is an illness caused by the Zika virus.[64] Most cases have no symptoms, but when present they are usually mild and can resemble dengue fever.[64][65] Symptoms may include fever, red eyes, joint pain, headache, and a maculopapular rash.[64][66][67] Symptoms generally last less than seven days.[66] It has not caused any reported deaths during the initial infection.[65] Infection during pregnancy causes microcephaly and other brain malformations in some babies.[6][7] Infection in adults has been linked to Guillain–Barré syndrome (GBS).[65]

Diagnosis is by testing the blood, urine, or saliva for the presence of Zika virus RNA when the person is sick.[64][66]

Prevention involves decreasing mosquito bites in areas where the disease occurs, and proper use of condoms.[66][68] Efforts to prevent bites include the use of insect repellent, covering much of the body with clothing, mosquito nets, and getting rid of standing water where mosquitoes reproduce.[64] There is no effective vaccine.[66] Health officials recommended that women in areas affected by the 2015–16 Zika outbreak consider putting off pregnancy and that pregnant women not travel to these areas.[66][69] While there is no specific treatment, paracetamol (acetaminophen) and rest may help with the symptoms.[5][66] Admission to hospital is rarely necessary.[65]

Vaccine development
Effective vaccines have existed for several viruses of the flaviviridae family, namely yellow fever vaccine, Japanese encephalitis vaccine, and tick-borne encephalitis vaccine, since the 1930s, and dengue fever vaccine since the mid-2010s.[70][71][72] World Health Organization (WHO) experts have suggested that the priority should be to develop inactivated vaccines and other non-live vaccines, which are safe to use in pregnant women and those of childbearing age.[73]

The US NIH Vaccine Research Center began work towards developing a vaccine for Zika per a January 2016 report.[74] Bharat Biotech International (India) reported in early February 2016, that it was working on vaccines for Zika[75] using two approaches: "recombinant", involving genetic engineering, and "inactivated", where the virus is incapable of reproducing itself but can still trigger an immune response with animal trials of the inactivated version to commence in late February.[76] As of March 2016, 18 companies and institutions internationally were developing vaccines against Zika, but none had yet reached clinical trials.[73] The first human trial for Zika vaccine, a synthetic DNA vaccine (GLS-5700) developed by Inovio Pharmaceuticals, is approved by FDA in June 2016. Interim results of the Phase 1 study is expected in later 2016.[77] Nikos Vasilakis of the University of Texas Medical Branch (UTMB) predicted that it may take two years to develop a vaccine, but ten to twelve years may be needed before an effective Zika vaccine is approved by regulators for public use.[78]

A single dose of two distinct vaccine candidates (DNA-based and inactivated virus vaccines) protected mice against the Zika virus.[79]

History
See also: Zika fever § Epidemiology, and Zika virus outbreak timeline

Countries that have past or current evidence of Zika transmission (as of January 2016)[80]

Spread of Zika[28][81][82]

Spread of Zika in Africa and Asia, based on molecular sequence data
Virus isolation in monkeys and mosquitoes, 1947
The virus was first isolated in April 1947 from a rhesus macaque monkey that had been placed in a cage in the Zika Forest of Uganda, near Lake Victoria, by the scientists of the Yellow Fever Research Institute.[83] A second isolation from the mosquito A. africanus followed at the same site in January 1948.[84] When the monkey developed a fever, researchers isolated from its serum a "filterable transmissible agent" that was named Zika in 1948.[20][85]

First evidence of human infection, 1952
Zika had been known to infect humans from the results of serological surveys in Uganda and Nigeria, published in 1952: Among 84 people of all ages, 50 individuals had antibodies to Zika, and all above 40 years of age were immune.[86] A 1952 research study conducted in India had shown a "significant number" of Indians tested for Zika had exhibited an immune response to the virus, suggesting it had long been widespread within human populations.[87]

It was not until 1954 that the isolation of Zika from a human was published. This came as part of a 1952 outbreak investigation of jaundice suspected to be yellow fever. It was found in the blood of a 10-year-old Nigerian female with low-grade fever, headache, and evidence of malaria, but no jaundice, who recovered within three days. Blood was injected into the brain of laboratory mice, followed by up to 15 mice passages. The virus from mouse brains was then tested in neutralization tests using rhesus monkey sera specifically immune to Zika. In contrast, no virus was isolated from the blood of two infected adults with fever, jaundice, cough, diffuse joint pains in one and fever, headache, pain behind the eyes and in the joints. Infection was proven by a rise in Zika-specific serum antibodies.[86]

Spread in equatorial Africa and to Asia, 1951–1983
From 1951 through 1983, evidence of human infection with Zika was reported from other African countries, such as the Central African Republic, Egypt, Gabon, Sierra Leone, Tanzania, and Uganda, as well as in parts of Asia including India, Indonesia, Malaysia, the Philippines, Thailand, Vietnam and Pakistan.[20][88] From its discovery until 2007, there were only 14 confirmed human cases of Zika infection from Africa and Southeast Asia.[89]

Micronesia, 2007
Main article: 2007 Yap Islands Zika virus outbreak
In April 2007, the first outbreak outside of Africa and Asia occurred on the island of Yap in the Federated States of Micronesia, characterized by rash, conjunctivitis, and arthralgia, which was initially thought to be dengue, chikungunya, or Ross River disease.[90] Serum samples from patients in the acute phase of illness contained RNA of Zika. There were 49 confirmed cases, 59 unconfirmed cases, no hospitalizations, and no deaths.[91]

2013–2014
Oceania
Main article: 2013–2014 Zika virus outbreaks in Oceania
Between 2013 and 2014, further epidemics occurred in French Polynesia, Easter Island, the Cook Islands, and New Caledonia.[16]

Other cases
On 22 March 2016 Reuters reported that Zika was isolated from a 2014 blood sample of an elderly man in Chittagong in Bangladesh as part of a retrospective study.[92]

Americas, 2015–present
Main article: 2015–16 Zika virus epidemic
As of early 2016, a widespread outbreak of Zika was ongoing, primarily in the Americas. The outbreak began in April 2015 in Brazil, and has spread to other countries in South America, Central America, Mexico, and the Caribbean. The Zika virus reached Singapore and Malaysia in Aug 2016.[93] In January 2016, the WHO said the virus was likely to spread throughout most of the Americas by the end of the year;[94] and in February 2016, the WHO declared the cluster of microcephaly and Guillain–Barré syndrome cases reported in Brazil – strongly suspected to be associated with the Zika outbreak – a Public Health Emergency of International Concern.[4][95][96][97] It is estimated that 1.5 million people have been infected by Zika in Brazil,[98] with over 3,500 cases of microcephaly reported between October 2015 and January 2016.[99]

A number of countries have issued travel warnings, and the outbreak is expected to significantly impact the tourism industry.[4][100] Several countries have taken the unusual step of advising their citizens to delay pregnancy until more is known about the virus and its impact on fetal development.[14] With the 2016 Summer Olympic Games hosted in Rio de Janeiro, health officials worldwide have voiced concerns over a potential crisis, both in Brazil and when international athletes and tourists, who may be unknowingly infected, return home and possibly spread the virus. Some researchers speculate that only one or two tourists may be infected during the three week period, or approximately 3.2 infections per 100,000 tourists.[101]

References
Tap to expand
This article incorporates public domain material from websites or documents of the Centers for Disease Control and Prevention.

External links
Zika virus – Centers for Disease Control and Prevention
World Health Organization Zika virus Fact Sheet
Zika virus illustrations, 3D model, and animation
ViralZone: Zika virus (strain Mr 766)
Zika virus at NCBI Taxonomy Browser
Schmaljohn, Alan L.; McClain, David (1996). "54. Alphaviruses (Togaviridae) and Flaviviruses (Flaviviridae)". In Baron, Samuel. Medical Microbiology (4th ed.). ISBN 0-9631172-1-1. NBK7633.
Animation on Zika from Scientific Animations Without Borders and the World Health Organization (WHO)

intestinal TB

Intestinal Tuberculosis အူ (တီဘီ)

၁။ က်မက အသက္ ၃၉ နွစ္ရိွၿပီး အိမ္ေထာင္က်တာ ၃ နွစ္ေက်ာ္ပါၿပီ။ ႕႕႕႕႕ မွာေနတာ ၆ နွစ္ေက်ာ္ပါၿပီ။ ဓမၼတာလည္း ပံုမွန္လာပါတယ္။ သားသမီးမရိွေသးပါ။ ၿပီးခဲ့တဲ့သံုးပတ္ေက်ာ္က ဝမ္းသြားရာ သြားမရ၊တခါသြားလ်င္ နာရီဝက္ေက်ာ္ ထိုင္ၿပီး ႀကိဳးစားရပါတယ္။ၿပီးလ်င္ ဝမ္းက်န္သလိုခံစားရၿပီး ဗိုက္မွာလည္း မအီမလည္ဆိုး႐ြားစြာခံစားရပါတယ္။ အူတြင္း မွန္ေျပာင္းၾကည့္ရပါတယ္ရွင္။ အူမႀကီးမွာ ၁ စင္တီမီတာနဲ႔ ၅ မီလီမီတာ အနာ၂ ခု ေတြ႔ရပါတယ္။ အခုအသားစ အေျဖရေတာ့ အူတီဘီလို႔ေျပာပါတယ္ရွင္။ က်မရဲ႕ ေဆးရီပို႔စ္ေတြ ဆရာ့ဆီကို တြဲေပးလိုက္ပါတယ္။ အူတီဘီက ဘာေၾကာင့္ျဖစ္တာပါလဲဆရာ။ က်မ ဘယ္မွခရီးမထြက္တာ တနွစ္ေလာက္ရိွပါၿပီဆရာ။ ေဆးရံုကေတာ့ မနက္ျဖန္ စေနေန႔မွ တီဘီဆရာဝန္နဲ႔ေတြ႔ဖို႔ ရိွပါတယ္ဆရာ။ အဲ့ဒါ အူတီဘီက တျခားသူေတြကို ကူးတတ္ပါသလားရွင္။ အစားအစာ က်မခ်က္ျပဳတ္ျပင္ဆင္ေပးလို႔ ရမရလည္းသိခ်င္ပါတယ္ရွင္။ ေရွာင္ရန္ေဆာင္ရန္ေတြလည္း သိခ်င္ပါတယ္ရွင္။ အိမ္ေထာင္သည္ျဖစ္တဲ့အတြက္ ေရွာင္စရာေတြရိွရင္လည္း ေျပာျပေပးပါရွင္။ က်မက ေခ်ာင္းမဆိုးပါ။ ကိုယ္အေလးခ်ိန္လည္းမက်ပါ။ ၅ဝ kg ရိွပါတယ္။

၂။ လြန္ခဲ့တဲ့ ၂ ပတ္ေလာက္က၊ ေခ်ာင္းဟန္႔လုိက္တာေသြးစေလးေတြပါလာတယ္။ ဆရာဝန္ျပေတာ့ ဓာတ္မွန္ ရုိက္ရတယ္။ အဆုတ္မွာေတာ့ ဘာမွမျဖစ္ဘူးတဲ့၊ သလိပ္စစ္ရေအာင္လဲ၊ သလိပ္ကမထြက္ေတာ့ဘူး။ ကိုယ္အေလးခ်ိန္ေတာ့ က်တယ္ဆရာ။ အူတီဘီဆိုတာ ဘယ္လိုသိႏုိင္လဲဆရာ။ က်ေနာ္က ဝမ္းခဏခဏ ပ်က္တတ္တာနဲ႔ ဆုိင္ပါသလား။ နည္းနည္းေလာက္အစာမွားတာနဲ႔ ပ်က္တတ္တာ၊ ေက်းဇူးျပဳၿပီးေျဖေပးပါဆရာ။

၃။ ကၽြန္ေတာ္ အေမက အသက္ ၆၂ ရွိပါၿပီ။ ညာဖက္မွာ ဗိုက္မွာနာနာေနလို႔ ေဆးစစ္တာ ဗိုက္ထဲမွာ အက်ိတ္ေတြ႔တယ္ ေျပာပါတယ္။ ကင္ဆာေတာ့ မဟုတ္ဘူးတဲ့။ ေဆးေတာ့ေပးလာတာ ေသာက္ၿပီးပါၿပီ။ ေတာင္ႀကီးေရာက္မွ ေဆးစစ္ခ်က္ကို ေမးလ္ပို႔ ေပးလာတယ္။ အူတီဘီရွိတယ္လို႔ ေျပာပါတယ္။ အဲဒါ တီဘီေဆး ေျခာက္လေသာက္ၿပီးပါၿပီ။ တီဘီ ဆရာဝန္ႀကီးက ေနာက္ထပ္ သံုးလေဆးဆက္ေသာက္ခိုင္းပါတယ္။ ဗိုက္နာတာေတာ့ ေကာင္းေကာင္း မေပ်ာက္ေသးပါဘူးဗ်။ အဲဒါ အူတီဘီအေၾကာင္း သိခ်င္လို႔ပါခင္ဗ်ာ။

၄။ Causes of intestinal TB က ဘာေတြပါလဲ ဆရာ။ Due to drinking of impure milk?

အူ (တီဘီ) ကိုလည္း အဆုပ္မွာျဖစ္ေစတဲ့ Mycobacterium tuberculosis ဗက္တီးရီယားကေနျဖစ္ေစတယ္။ အဆုပ္နဲ႔မတူတာက ဒီမွာျဖစ္ရင္ မသိမသာေလးပဲျဖစ္လာတယ္။ (တီဘီ) ဟာဦးေႏွာက္၊ ႏွလံုး၊ ေက်ာက္ကပ္ နဲ႔ အရိုးေတြမွာလဲ (တီဘီ) ျဖစ္ႏိုင္တယ္။

အူသိမ္၊ အစာအိမ္၊ ေဘလံုး၊ ဝမ္းတြင္းဖံုးအလႊာ၊ ဝမ္းတြင္းတက္ေစ့၊ သရက္ရြက္ေတြမွာလည္း ျဖစ္ႏိုင္တယ္။ HIV အျဖစ္မ်ားရာကေတ တီဘီေရာဂါလည္း ေခါင္းေထာင္လာတယ္။

တျခားအစာလမ္းေရာဂါေတြနဲ႔ မွားတတ္တယ္။ ေရာဂါဟုတ္-မဟုတ္ လုပ္ရတာ ပိုခက္တယ္။ အမ်ားအားျဖင့္ အာဖရိကနဲ႔ အာရွမွာ ျဖစ္တယ္။ ခုေနာက္ပိုင္းမွာ HIV/AIDS ေတြေၾကာင့္ ခ်မ္းသာတိုးတက္တဲ့ ႏိုင္ငံေတြမွာလဲ ပိုတိုးလာေနတယ္။ အဆုပ္မွာ ျဖစ္ေနရာကေန ေသြးနဲ႔ (လင့္ဖ္) ကတဆင့္ အူကိုေရာက္လာတာလည္းရွိတယ္။ အူမွာတိုက္ရိုက္လာျဖစ္တာက Bovine strain of mycobacterium tuberculosis ေခၚတဲ့ပိုးေၾကာင့္ျဖစ္လာတယ္။ တီဘီပိုးပါေနတာကို စားမိရာကေနလည္း ကူးစက္လာႏိုင္တယ္။ ႏြားနို႔ကို မက်ိဳခ်က္ဘဲ ေသာက္ရာကေန ျဖစ္တာအမ်ားဆံုးဘဲ။ ေသြးကလည္း ကူးလာႏိုင္တယ္။

အူတီဘီ ေရာဂါလကၡဏာေတြကို တခ်ိဳ႕ ဘာမွမခံစားရဘူး၊ တခ်ိဳ႕က ကိုယ္ပူ၊ ဝမ္းမမွန္၊ ဗိုက္ေအာင့္၊ ညေခြ်းထြက္၊ အစားအေသာက္ပ်က္၊ အားယုတ္၊ ပ်ိဳ႕ခ်င္၊ ေလထ-ေလတက္၊ အစာတခ်ိဳ႕ကို လက္သင့္မခံႏိုင္၊ စားျပီးရင္ ဗိုက္တင္း၊ ကိုယ္အေလးခ်ိန္က်ဆင္း။ ဒီေရာဂါလကၡဏာမ်ိဳးေတြက အူကင္ဆာနဲ႔ Malabsorption syndromes အစာကို မစုပ္ယူႏိုင္တဲ့ ေရာဂါေတြမွာလည္းရွိတယ္။

ဝမ္းသြားတာ အရင္လိုမဟုတ္တာကေန စသိႏိုင္တယ္။ ဝမ္းပ်က္တာ။ ဝမ္းခ်ဳပ္တာျဖစ္လို႔ေပးရမဲ့ ရိုးရိုးေဆးေတြနဲ႔ မသက္သာရင္ ဒါကိုသံသယရွိရတယ္။ နာတာရွည္ျဖစ္တယ္။ ျပန္ျဖစ္တာလဲရွိႏိုင္တယ္။ ဗိုက္ေအာင့္သလို နာေနမယ္။ ျဖစ္တဲ့ေနရာအေပၚမူတည္ျပီး ဗိုက္ေနရာအမ်ိဳးမ်ိဳးမွာနာမယ္။ စားျပီးရင္ အစာမေက်သလိုေနမယ္။ စားရက္နဲ႔ ဝမလာဘူး။
ညေခြ်းထြက္တာ၊ ညေနခင္း ကိုယ္နဲနဲပူတာေတြ အူ (တီဘီ) မွာမေတြ႔ရတတ္ဘူး။ အားယုတ္ျပီး အာဟာရခ်ိဳ႕တဲ့လို႔ ေဆးလာကုမွ သိရတာလဲရွိတယ္။

Biopsy အသားစျဖတ္ယူစစ္ေဆးတာလုပ္မွသာေရာဂါမွန္းသိတယ္။ အႏုၾကည့္မွန္ဘီလူးနဲ႔ ၾကည့္တာသာမက ပိုးေမြးျမဴနည္းနဲ႔လဲ စမ္းႏိုင္တယ္။ အဆုပ္ (တီဘီ) လိုမ်ိဳး ပိုးကို တိုက္ရိုက္ၾကည့္တာနဲ႔ မတြ႔တတ္လို႔ လုပ္ရတာ ျဖစ္တယ္။ Complete blood count, ESR, X-ray, Tuberculosis antibody, Sputum for AFB, Ultrasound, Barium meal, MRI စစ္ေဆးနည္းေတြလဲ လုပ္ႏိုင္တယ္။

ေရာဂါေဗဒအရ (၃) စားခြဲထားတယ္။
၁။ Ulcerative form အူမွာအနာျဖစ္ေနသူ ၆ဝ% ရွိတယ္။ အနာအလ်ားကအူရဲ႕ အလ်ားကိုေဒါင့္မွန္က်ေနတဲ့ အနာဟာ Epithelial surface မွာျဖစ္ေနတယ္။
၂။ Hypertrophic form ထူထဲေနတဲ့အနာမ်ိဳးကို ၁ဝ% မွာေတြ႔ရတယ္။ အူနံရံထူေနမယ္။ အမာရြတ္လိုျဖစ္ေနမယ္။ မာေနမယ္။ ကင္ဆာနဲ႔ မွားတတ္တယ္။
၃။ Ulcerohypertrophic form အမ်ိဳးအစား (၁) နဲ႔ (၂) တြဲျဖစ္ေနတာမ်ိဳးကို ၃ဝ% မွာေတြ႔ရတယ္။

အမ်ားဆံုးသံုးတဲ့ေဆးေတြကေတာ့ Isoniazid, Rifampin, Ethambutol နဲ႔ Pyrazinamide ေတြျဖစ္တယ္။ ေဆးေပးတာကို ၆ လအထိေပးတတ္တယ္။ ေပ်ာက္တယ္။ တခ်ိဳ႕ကိုေတာ့ ၁၂-၁၈ လအထိေပးရတယ္။

ေဆးေတြရဲ႕ ေဘးထြက္ဆိုးက်ိဳးေတြလဲ ခံစားလာရႏိုင္တယ္။ ဥပမာေျခေထာက္ေတြ ပူေလာင္သလိုခံစားရရင္ Isoniazid ေၾကာင့္ျဖစ္လာတာမို႔ ဗီတာမင္ ဘီ-၆ လိုေနျပီ။ မစားခ်င္မေသာက္ခ်င္ျဖစ္တာ၊ အသားဝါတာ၊ မ်က္စိၾကည့္မေကာင္းတာ ျဖစ္ႏိုင္တယ္။ ဒါေပမဲ့ ေဆးကို မျဖတ္လိုက္ပါနဲ႔။ ေဆးဝါးေတြကိုသာမက အစာအာဟာရ မွ်တလံုေလာက္ေအာင္ စားဘို႔လဲ လိုတယ္။ ကိုယ္လက္ေလ့က်င့္ခန္း လုပ္ေပးပါ။ ေဆးလိပ္ျဖတ္ပါ။ သူမ်ားကို လြယ္လြယ္နဲ႔မကူးစက္ပါ။ တကိုယ္ေရ သန္႔ရွင္းေရးလုပ္ရင္ မိသားစုအတြင္း မကူးစက္ႏိုင္ပါ။ ေခ်ာင္းဆိုးလို႔လည္း သူမ်ားကိုမကူးစက္ပါ။

ေနာက္ဆက္တြဲျဖစ္ႏိုင္တာေတြက ေသြးယိုမယ္။ အူေပါက္သြားမယ္။ ေရဖ်င္းစြဲလာႏိုင္တယ္။ အစာလမ္းပိတ္တာ ျဖစ္လာႏိုင္တယ္။ အန္တာမ်ားရင္ ဓါတ္ဆားအခ်ိဳးအဆ မမွ်တာျဖစ္လာမယ္။ အူေပါက္တာ၊ အစာလမ္းပိတ္တာ ျဖစ္ရင္ေတာ့ ခြဲစိတ္ေပးရတယ္။

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