Where all your ID needs are met! Sort of.
Originally described as a pathogen in 1923, Corynebacterium equi was isolated from the lungs of ten foals (aka a young horse) who had pneumonia (1). Its name was later changed to rhodococcus (aka red coccus), and can be mistaken for mycobacterium spp due to its sometimes acid-fast appearance (2). It is known to infect horses,
What is this? I am writing about a topic related to transplant infectious diseases? Something has to be going on! I had originally intended to write about CMV serostatus and risk of organ rejection in SOT patients, but that was a more difficult topic to tackle (just like that HTLV-1 post; yeah that one is
Primary infection with T. cruzi, also known as American trypanosomiasis, is generally asymptomatic with a small percentage having non-specific symptoms such as fever, malaise, lymphadenopathy, and in certain cases, a Chagoma. The vast majority of people go on to develop an “intermediate” form of the disease, where serology is positive but there is no sign
Consider this post a continuation of the prior one on prophylaxis. I mention a bit on the pathophysiology, where adaptive immunity seems to play a key role in the way the body deals with the fungus, with mice with SCID infected with pneumocystis not being able to mount an inflammatory response. As a result of
Hyperammonemia is the accumulation of ammonia within the blood that leads to cerebral edema, herniation, and death in patients with inborn errors of metabolism and hepatic failure. These are the types of patients where we would commonly see such accumulation of ammonia. In absence of liver failure, inborn errors of metabolism, urea cycle disorders, or
Dr. Germophile 