I believe the historians use the sources that described his illness, like William of Tyre who watched it as a witness, but it was so long and the medicine has changed so much. So, could it be another illness?
I answered a previous question about Baldwin’s leprosy:
There was some discussion with u/lcnielsen and u/LuxArdens about what kind of leprosy it was, but I can expand further on that point here.
It’s certainly possible that when “leprosy” is mentioned in medieval texts, it's just a catch-all term for any sort of skin disease. But in this case we have enough evidence to determine that Baldwin really did have leprosy (in the modern sense), and even the specific kinds of leprosy that he had.
Leprosy is caused by a bacteria Mycobacterium leprae. It takes sustained contact (months or even years) with an infected person to spread, so it tends to spread among family members, and could take even more years to incubate before symptoms develop. The bacteria is relatively harmless, but it causes various symptoms as the body tries to kill it, which is the real problem. Sometimes it develops into tuberculoid leprosy, where white blood cells attack and destroy the bacteria but also damage tissue and cause inflammation, muscle weakness, and skin numbness. If numb areas of the skin are injured and the person can’t feel it, they can develop ulcers, which lead to infections, and then bone and tissue damage and limb deformations. Most modern leprosy is tuberculoid, but it often heals on its own.
The other likely possibility is lepromatous leprosy, where antibodies try to attack the bacteria cells; but since the bacteria usually ends up inside of a normal cell, antibodies can’t reach it. The bacteria cells grow to form disfiguring skin nodules (especially on the nose). But unlike tuberculoid leprosy, numbness and nerve damage (and therefore ulcers and infection) comes much later after the other more obvious symptoms occur. It’s rather rare now, but since it doesn’t heal on its own and causes massive skin deformations, it’s the most visible kind of leprosy and the kind we’re probably picturing when we think of a “typical” person with leprosy.
There are also other types of leprosy with symptoms in between these two types; one is polyneuritic leprosy, which has symptoms of numbness nerve damage but without the disfiguration and ulcers. The different kinds of leprosy can develop into other forms as well, due to age or stress. Lepromatous leprosy doesn’t turn into any other kind of leprosy, but polyneuritic leprosy, with the initial symptoms of numbness and nerve damage, can later turn into the lepromatous or tuberculoid forms.
So this modern medical understanding of leprosy can be applied to Baldwin to see what kind(s) of leprosy he probably had. As you mentioned, the main eyewitness is Baldwin’s tutor, the historian William of Tyre, who left a pretty detailed description:
“It happened that, as he was playing with some boys of noble birth who were with him and they were pinching each other on the arms and hands with their nails, as children often do when playing together, the others cried out when they were hurt, whereas he bore it all with great patience, like one who is used to pain, although his friends did not spare him in any way…finally I came to realise that half of his right arm and hand was dead, so that he could not feel the pinchings at all, or even feel if he was bitten…His father was told, and after the doctors had been consulted, careful attempts were made to help him with poultices, ointments and even charms, but all in vain…It grieves me greatly to say this, but when he became an adolescent he was seen to be suffering from leprosy to a dangerous degree.” (William of Tyre, quoted in Hamilton, pp. 27-28)
We have no idea who he got it from - maybe a family member, a nurse, one of the other kids he was playing with. It was probably the polyneuritic form of leprosy at first, which explains the numbness and the lack of disfiguration and ulcers.
They tried various treatments, but nothing worked:
“The general approach to the treatment of those with leprosy complex disease in the crusader period was by modification of diet, bathing in hot springs, the use of drugs, bloodletting, avoidance of sexual activity and segregation in leprosaria.” (Mitchell, in Hamilton, pg. 254)
He was able to succeed his father as king when he was 16 so he probably didn’t “look” like he had leprosy yet - otherwise there probably would have been a lot of opposition, since there was such an enormous social stigma against people with obvious signs of leprosy. They probably still hoped it was some other disease. But then he developed the symptoms of lepromatous leprosy when he got older. He could no longer feel or use his hands and feet, and had skin ulcers and disfiguring growths, especially on his nose and face. Eventually he went blind as well, and he died in 1185 at age 23. Lepromatous leprosy itself wouldn’t have killed him, but due to his overall weakness, and the skin ulcers, he could have easily developed something deadly:
“Possibilities include infectious diseases such as malaria, typhoid, a chest infection or perhaps septicaemia from an infected foot wound, common in untreated leprosy patients.” (Mitchell, in Hamilton, pg. 253)
So, in brief, he probably had polyneuritic leprosy as a child, which developed into lepromatous leprosy (rather than tuberculoid) as a teenager/adult, and he eventually died of an unknown disease, which he contracted through his infected ulcers.
Sources:
The medievalist and medical historian Piers Mitchell is the best source here:
Piers D. Mitchell, “An evaluation of the leprosy of King Baldwin IV of Jerusalem in the context of the medieval world”, in Bernard Hamilton, The Leper King and His Heirs (Cambridge University Press, 2000)
Piers D. Mitchell, Medicine in the Crusades: Warfare, Wounds and the Medieval Surgeon (Cambridge University Press, 2004)
Piers D. Mitchell, “Leprosy and the case of King Baldwin IV of Jerusalem: mycobacterial disease in the crusader states of the 12th and 13th centuries”, in International Journal of Leprosy and Other Mycobacterial Diseases 61 (2) (1993), pp. 283-291.