AssessmentsSeronegative and septic arthritis: Pathology review
USMLE® Step 1 style questions USMLE
A 35-year-old man presents to his primary care physician’s office for evaluation of right knee and ankle pain for the past 2 days. He had similar pain over the left wrist and shoulder joints in the past year that self resolved. The patient has a painless rash on his hands which appeared around the same time. Past medical history is significant for a urinary tract infection 2 months ago which was treated with antibiotics. He has had 7 sexual partners over the past year and is currently sexually active. He uses condoms inconsistently. He denies any recent travel. His temperature is 38.2 °C (100.8°F), pulse is 80/minute, respirations are 16/minute, and blood pressure is 130/80 mmHg. Physical examination shows multiple nontender papulovesicular lesions on his hands. Passive flexion of wrists elicits a sharp pain. Which best describes the route of transmission regarding the causative organism resulting in this patient’s clinical condition?
Content Reviewers:Yifan Xiao, MD
Maurice is a 28 year old male who presents with a 2 year history of gradually progressive low back pain and stiffness. He mentions that the pain wakes him up several times at night, and that the stiffness tends to be worse when he wakes up and improves as he moves. Examination shows mild deformity of the spine and hip, as well as tenderness over the buttock. Then you see Clint, a 63 year old male shows up with a red, warm and swollen left knee, which hurts so much he can barely walk. Clint tells you that symptoms started a few days ago, after he tripped and cut his knee. His body temperature is 38 celsius degrees or 100.4 degrees Fahrenheit. X-rays are ordered in both cases, showing, in Maurice’s case, erosion of the sacroiliac joint. On the other hand, in Clint’s case, X-rays look pretty normal, so an arthrocentesis is performed, revealing that synovial fluid is purulent.
Based on the initial presentation, both cases seem to have some form of arthritis. But first, a bit of physiology real quick. There are many types of joints, including fibrous, cartilaginous, and synovial joints. synovial joints, like those of the wrist, elbow, knees, shoulders, and hips, are mobile joints that connect two bones via a fibrous capsule that is continuous with the periosteum, which is the outer layer of bones. The fibrous capsule is lined with a synovial membrane, which has cells that remove debris and produce synovial fluid. This is a viscous fluid found inside the joint capsule which lubricates joint. Together, the synovial membrane and articular cartilage form the inner lining of the joint space.
Now, arthritis refers to a group of diseases that cause destruction of one or more joints. First, we have seronegative arthritis, which is called seronegative because there’s an absence of both rheumatoid factor or RF, and anti-cyclic citrullinated peptide antibody or anti-CCP, which are commonly found in rheumatoid arthritis. Something specific to note is that seronegative spondyloarthropathies have a strong association with the gene HLA-B27, which encodes for a specific type of MHC class I molecule.
Now there are several subtypes of seronegative spondyloarthropathies and you can remember them by a mnemonic PAIR, where P stands for Psoriatic arthritis; A for Ankylosing spondylitis; I for Inflammatory bowel disease-associated arthritis; and R for Reactive arthritis.
Let’s start with psoriatic arthritis, which occurs in some individuals with psoriasis or with a family history of psoriasis. It is an autoimmune disease characterized by joint inflammation. Exactly what causes the immune system to go haywire and attack the joints is unclear. Although the HLA-B27 gene is linked to the disease, it’s not enough to trigger psoriatic arthritis on its own, and environmental factors like physical trauma or an infection seem to play a role as well. Now, it all starts with psoriasis, which is an autoimmune condition where skin self antigens are seen as foreign. When that happens, T cells start releasing cytokines that recruit and activate other immune cells to release TNF, IL-12, and IL-23. This triggers keratinocytes and fibroblasts to proliferate, which leads to the formation of psoriatic plaques. These are red, raised patches with silvery scales made up of dead skin cells. In some individuals with psoriasis, T cells also go to the joints and trigger the activation of osteoblasts and osteoclasts, leading to joint erosion and ossification, which can ultimately cause arthritis and severe deformities. Now, arthritis usually occurs after the psoriatic plaques have appeared, but it can sometimes precede them, which makes diagnosis that much harder. For your exam, it’s important to note that less than 30% of individuals with psoriasis develop psoriatic arthritis.
Symptoms of psoriatic arthritis typically include pain, swelling, and stiffness of the affected joints. There are several types of psoriatic arthritis, depending on which joint is affected. The most common one is the distal interphalangeal predominant type, which generally affects the joints nearest to the ends of the fingers and toes, leading to dactylitis, which is the inflammation of the fingers, also known as sausage fingers and nail abnormalities like ridging or pitting. Over time, some individuals with distal interphalangeal predominant type can also develop severe bone erosions and