Prepatellar bursitis is an inflammation of the prepatellar bursa at the front of the knee. It is marked by swelling at the knee, which can be tender to the touch and which generally does not restrict the knees range of motion. It can be extremely painful and disabling as long as the underlying condition persists. Prepatellar bursitis is most commonly caused by trauma to the knee, either by a single acute instance or by chronic trauma over time. As such, the condition commonly occurs among individuals whose professions require frequent kneeling. A definitive diagnosis can usually be made once a clinical history and physical examination have been obtained, though determining whether or not the inflammation is septic is not as straightforward. Treatment depends on the severity of the symptoms, with mild cases possibly only requiring rest and localized icing. Options for presentations with severe sepsis include intravenous antibiotics, surgical irrigation of the bursa, and bursectomy. Signs and symptoms
The primary symptom of prepatellar bursitis is swelling of the area around the kneecap. It generally does not produce a significant amount of pain unless pressure is applied directly. The area may be red (erythema), warm to the touch, or surrounded by cellulitis, particularly if infection is present, often accompanied by fever.: p. 608  Unlike arthritis, except in severe cases  prepatellar bursitis generally does not affect the range of motion of the knee, though it may cause some discomfort in complete flexion of the joint.: p.
Neutrophil-specific granule deficiency ( previously known as lactoferrin deficiency) is a rare congenital immunodeficiency characterized  by an increased risk for pyogenic infections due to defective production of specific granules and gelatinase granules in patient neutrophils. Symptoms and signs
Atypical infections are the key clinical manifestation of SGD. Within the first few years of life, patients will experience repeated pyogenic infections by species such as Staphylococcus aureus, Pseudomonas aeruginosa or other Enterobacteriaceae, and Candida albicans. Cutaneous ulcers or abscesses and pneumonia and chronic lung disease are common. Patients may also develop sepsis, mastoiditis, otitis media, and lymphadenopathy. Infants may present with vomiting, diarrhea, and failure to thrive.Diagnosis can be made based upon CEBPE gene mutation or a pathognomonic finding of a blood smear showing lack of specific granules. Neutrophils and eosinophils will contain hyposegmented nuclei (a pseudo-Pelger–Huet anomaly). Genetics
A majority of patients with SGD have been found to have mutations in the CEBPE (CCAAT/enhancer-binding protein epsilon) gene, a transcription factor primarily active in myeloid cells. Almost all patients have been found to be homozygous for the mutation, suggesting the disease is autosomal recessive. One patient, heterozygous for the mutation, was found to be deficient in GFI1, a related gene. Pathophysiology
The defect in CEBPE appears to block the ability of neutrophils to mature past the promyelocyte stage in bone marrow. Since specific (secondary) and gelatinase (tertiary) granules are only produced past the promyelocyte stage of development, these are deficient in SGD.