In addition to the obvious risks (e.g., known exposure to a patient with MDR-TB), risk factors for MDR-TB include male sex, HIV infection, previous incarceration, failed TB treatment, failure to respond to standard TB treatment, and relapse following standard TB treatment. A large proportion of people with MDR-TB are unable to access treatment due to what Paul Farmer describes as an "Outcome Gap". The majority of people struck with MDR-TB live in "resource-poor settings" and are denied treatment because international organizations have refused to make technologies available to countries who cannot afford to pay for treatment, the reason being that second line drugs are to expensive therefore treatment methods for MDR-TB are not sustainable in impoverished nations. Farmer argues that this is social injustice and we cannot allow people to die simply because they are faced with circumstances where they cannot afford "effective therapy".Treatment of MDR-TB must be done on the basis of sensitivity testing: it is impossible to treat such patients without this information. If treating a patient with suspected MDR-TB, the patient should be started on SHREZ+MXF+cycloserine pending the result of laboratory sensitivity testing. A gene probe for rpoB is available in some countries and this serves as a useful marker for MDR-TB, because isolated RMP resistance is rare (except when patients have a history of being treated with rifampicin alone). If the results of a gene probe (rpoB) are known to be positive, then it is reasonable to omit RMP and to use SHEZ+MXF+cycloserine.
Has 82% incidence in diagnosis cases)However, in actuality, only a small percentage of patients experience all three symptoms, and the full triad occurs more frequently among those who have overused alcohol. Also a much more diverse range of symptoms has been found in patients with this condition, including:

pupillary changes, retinal hemorrhage, papilledema, impaired vision and hearing, vision loss
hearing loss,
fatigability, apathy, irritability, drowsiness, psycho and/or motor slowing
dysphagia, blush, sleep apnea, epilepsy and stupor
lactic acidosis
memory impairment, amnesia, depression, psychosis
hypothermia, polyneuropathy, hyperhidrosis.Although hypothermia is usually diagnosed with a body temperature of 35 °C / 95° Fahrenheit, or less, incipient cooling caused by deregulation in the central nervous system (CNS) needs to be monitored because it can promote the development of an infection. The patient may report feeling cold, followed by mild chills, cold skin, moderate pallor, tachycardia, hypertension, tremor or piloerection. External warming techniques are advised to prevent hypothermia.Among the frequently altered functions are the cardio circulatory. There may be tachycardia, dyspnea, chest pain, orthostatic hypotension, changes in heart rate and blood pressure. The lack of thiamine sometimes affects other major energy consumers, the myocardium, and also patients may have developed cardiomegaly. Heart failure with lactic acidosis syndrome has been observed. Cardiac abnormalities are an aspect of the WE, which was not included in the traditional approach, and are not classified as a separate disease. Infections have been pointed out as one of the most frequent triggers of death in WE.