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Joint Session

April wedding brings May hospitalization

JEFFERY JOHNSTON PHOTOGRAPH

My right ankle was huge. It happened all of a sudden. I didn’t realize it was swollen until I took off my boot,” says Christopher Oster, a 30-year-old industrial painter and Holy Cross High School graduate. “It didn’t bother me that much at first, but later that evening it was hurting so much I could hardly get off the sofa.”

His wife Wendy drove him to the emergency room at Ochsner Baptist Medical Center on a Friday night last May. As Oster hobbled into the emergency room, the physician on duty took one look and called for a syringe to drain the hot, swollen joint. In went the needle and out came a syringe of pus, a ticket for admission and an orthopedic consult.

Normal joint fluid is the WD-40 of the skeletal system. It is clear and slightly viscous. Infections and certain inflammatory conditions cause white blood cells, the foot soldiers of the immune system, to stream into the joint. The abnormal accumulation of these cells causes pain, swelling and a change in the cloudy joint fluid. Sticking a needle into a swollen joint can reduce abnormal pressure and pain. It also gives the physician a specimen to send to the laboratory to culture for bacteria. But just like a high white blood cell count doesn’t always indicate infection, pus in a joint doesn’t always equate to an infection.

Day 2

“For a week or so before my ankle started hurting, my eyes turned bloodshot and were glued shut with crusts each morning. My doctor prescribed a Z-Pak. Wendy and I thought I just had the flu until my ankle started hurting,” said Oster the morning after admission when a physician was asking about other recent infections. 
 
“It looked like Chris had a septic ankle. Overnight his swelling returned in spite of the intravenous antibiotics. His swollen ankle was hot, red and very painful,” says Dr. Kevin Watson, an orthopedist. Watson, like Oster, was a Holly Cross graduate before he zigzagged from undergraduate studies at Vanderbilt, Tulane for medical school, University of Alabama in Birmingham for an orthopedic residency and then back to New Orleans to practice in 2007.

“We see a lot of hot, swollen joints. The common culprits are gout, pseudogout and frank infections. I took him to surgery,” says Dr. Watson, who made a 1-inch-plus incision and inserted an arthroscope for a look-see. “There wasn’t that much pus left, but he had some inflamed synovial tissue. The cartilage surfaces looked undamaged.”

Day 3

The lab reported “no growth” from a culture of the pus collected in the emergency room. The etiology of his ankle inflammation was turning into a medical mystery, until his wife gave the clue that cracked the case.

“You know it may not be important but we both came down with food poisoning from a wedding reception about a month ago. It got my aunt, too,” said Wendy. “The reception was on a Friday night, about 50 people at a St. Bernard reception hall. I started feeling queasy on Sunday, but Monday I started with non-stop diarrhea. It lasted a couple of days. It didn’t seem that big of a deal,” added Christopher.

The diagnosis

So how did a wedding reception in April bring a swollen ankle in May? Chris had reactive arthritis, a post-infectious reaction to an earlier bacterial infection in another part of the body. The classic clinical presentation for reactive arthritis is sudden onset of arthritis one to four weeks after an intestinal or urinary tract infection. Usually only one knee, ankle or foot becomes swollen and painful, but up to five joints can be involved, including the fingers. Low-grade fever and malaise often pre-date the joint symptoms. Concurrent eye irritation or conjunctivitis is commonly reported and sometimes wrongly diagnosed as pink eye.

Chlamydia, Clostridium difficile, Salmonella, Shigella and Campylobacter are some of the more common bacterial triggers for reactive arthritis. Chlamydia causes urethritis, a sexually transmitted disease usually much milder than gonorrhea. The enteritis caused by Clostridium difficile is a complication of antibiotic use. But most other bacterial species linked to reactive arthritis are those that cause foodborne infections.  

Reactive arthritis is uncommon but not rare. It is like winning a full jackpot from a video poker machine in reverse rather than wining the power ball. For every 100,000 persons with acute bacterial intestinal infections, maybe two or three develop reactive arthritis symptoms. The percentage of reactive arthritis after Chlamydia infections is higher.  

White males between 20 and 40 years old are most at risk for reactive arthritis. The disease seems milder in women. There is an increased prevalence in Scandinavian countries. This epidemiology and other data point to a genetic predisposition as post-infectious inflammation occurs in only a small percent of persons following any foodborne outbreak.

The trigger infection

The foodborne bacteria associated with reactive arthritis must first survive a stomach acid wash and a dousing by digestive juices before finding the right intestinal niche to attach and begin multiplication. The various incubation periods, calculated as the time interval between ingestion of tainted food and the first onset of symptoms, is measured in days not hours. By the time reactive arthritis develops, the foodborne bacteria that caused the initial symptoms are long gone.

First line treatment for reactive arthritis is the same as for osteoarthritis: non-steroidal antiinflammatory drugs such as Motrin, Aleve and Naprosyn for several weeks to months as needed for symptom control. If symptoms persist, additional therapy can be steroids or other disease-modifying drugs pulled from a rheumatologist’s quiver.

If you have to have arthritis, reactive arthritis might be the one you want. The acute swelling usually resolves within a few weeks and all signs and symptoms of inflammation resolve within four to six months. Occasionally persistent musculoskeletal symptoms transition into chronic reactive arthritis. In additions, persons who test positive for the genetic marker HLA B27 are prone to other immune and rheumatologic problems including ankylosing spondlitis and inflammatory bowel disease.


From Reiter’s Syndrome to Reactive Arthritis

German physician Dr. Hans Reiter published a case report about a World War I soldier with urethritis, conjunctivitis and arthritis. This triad of “can’t see, can’t pee and can’t climb a tree” became known as Reiter’s Syndrome.

But Reiter was an enthusiastic Nazi. “Anti-tobacco research flourished in the Third Reich” according to the Anti-Defamation League in 1996. With an orchestra playing Mozart in the background, Reiter keynoted the opening of a Hitler-inspired anti-tobacco institute in ’41. Citing tobacco use was an “epidemic, a plague, dry drunkenness and lung masturbation.”
 
After World War II, Reiter’s old Nazi days led to a Nuremberg conviction for war crimes. Having one’s name associated with a disease is an honor in medicine not worthy of a Nazi guilty of war crimes. Hence, the more descriptive name of “reactive arthritis” now describes what was once known as Reiter’s Syndrome.

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