In addition, a third subspecies of the parasite known as Trypanosoma brucei brucei is responsible for affecting animals but not humans.Humans are the main reservoir for T. b. gambiense but this species can also be found in pigs and other animals. Wild game animals and cattle are the main reservoir of T. b. rhodesiense. These parasites primarily infect individuals in sub-Saharan Africa because that is where the vector (tsetse fly) is located. The two human forms of the disease also vary greatly in intensity. T. b. gambiense causes a chronic condition that can remain in a passive phase for months or years before symptoms emerge and the infection can last about three years before death occurs.T. b. rhodesiense is the acute form of the disease, and death can occur within months since the symptoms emerge within weeks and it is more virulent and faster developing than T. b. gambiense. Furthermore, trypanosomes are surrounded by a coat that is composed of variant surface glycoproteins (VSG). These proteins act to protect the parasite from any lytic factors that are present in human plasma. The hosts immune system recognizes the glycoproteins present on the coat of the parasite leading to the production of different antibodies (IgM and IgG).These antibodies will then act to destroy the parasites that circulate around the blood. However, from the several parasites present in the plasma, a small number of them will experience changes in their surface coats resulting in the formation of new VSGs.
Potter analyzed approximately 5000 autopsy cases performed on fetuses and newborn infants over a period of ten years and found that 20 of these infants presented with BRA, all of which had distinctive facial characteristics which did not appear to them to have any specific embryologic correlation with the renal anomaly. It was only much later when she and others attributed the multiple congenital deformities, including the features of Potters facies and also pulmonary hypoplasia, to have been caused by the prolonged severe lack of amniotic fluid. These facial characteristics have subsequently been termed as being known as Potter facies. From her analysis, she was able to deduce the sequence of events that leads to what is now known as Potter sequence.Potter went on to become a pioneer in the field of human renal development and her contributions are still employed and appreciated by clinicians and researchers to this day. Terminology
Potter syndrome is not technically a syndrome as it does not collectively present with the same telltale characteristics and symptoms in each and every case. It is more accurately described as a "sequence" or chain of events  that may have different beginnings (absent kidneys, cystic kidneys, obstructed ureters or other causes), but which all end with the same conclusion (absent or reduced volume of amniotic fluid). This is why Potter syndrome is often called Potter sequence or oligohydramnios sequence by some clinicians and researchers.