Thrombocytopenia is sometimes extreme, with alteration in prothrombin time (PT) and partial thromboplastin time (PTT) suggestive of disseminated intravascular coagulation (DIC). Acidosis and acute kidney failure can be seen as in any severe sepsis. Meningococci can be readily cultured from blood or cerebrospinal fluid, and can sometimes be seen in smears of cutaneous lesions. Difficulty swallowing, atrophy of the tongue, and cracks at the corners of the mouth are also characteristic features. Causes
Multiple species of bacteria can be associated with the condition:

Meningococcus is another term for the bacterial species Neisseria meningitidis; blood infection with said species usually underlies WFS. While many infectious agents can infect the adrenals, an acute, selective infection is usually meningococcus. Pseudomonas aeruginosa can also cause WFS. WFS can also be caused by Streptococcus pneumoniae infections, a common bacterial pathogen typically associated with meningitis in the adult and elderly population. Mycobacterium tuberculosis could also cause WFS. Tubercular invasion of the adrenal glands could cause hemorrhagic destruction of the glands and cause mineralocorticoid deficiency. Staphylococcus aureus has recently also been implicated in pediatric WFS. It can also be associated with Haemophilus influenzae.Viruses may also be implicated in adrenal problems:

Cytomegalovirus can cause adrenal insufficiency, especially in the immunocompromised. Ebola virus infection may also cause similar acute adrenal failure. Diagnosis
Diagnostic criteria are based on clinical features of adrenal insufficiency as well as identifying the causal agent. If the causal agent is suspected to be meningitis a lumbar puncture is performed.
Death, which is often from pneumonia, usually occurs 1 to 3 years after the start of the disorder.About twenty-five percent of patients with PBP eventually develop the widespread symptoms common to ALS. Cause
The cause of PBP is unknown. One form of PBP is found to occur within patients that have a CuZn-superoxide dismutase (SOD1) mutation. Progressive bulbar palsy patients that have this mutation are classified with FALS patients, Familial ALS (FALS) accounts for about 5%-10% of all ALS cases and is caused by genetic factors. Within these, about 20–25% are linked to the SOD1 mutation. It is not currently known if and how the decreased SOD1 activity contributes to Progressive Bulbar Palsy or FALS, and studies are being done in patients and transgenic mice to help further understand the impact of this gene on the disease.A case study was done on a 42-year-old woman who complained of muscle weakness 10 months prior to admission in the hospital. Upon neurological examination, the patient showed muscle atrophy, fasciculation in all limbs and decreased deep tendon reflexes. The patient’s older brother, father, and paternal uncle had previously all died of ALS or an ALS type syndrome. The patient developed progressive bulbar palsy, became dependent on a respirator, and had two episodes of cardiac arrest. The patient died from pneumonia two years after the onset of the disease. After studying the patient, it was found that the patient had a two base pair deletion in the 126th codon in exon 5 of the SOD1 gene.