Anthrax is caused by Bacillus anthracis, a spore-forming gram-positive rod. Naturally acquired infection results from contact with contaminated animals. No human-to-human transmission of the disease has ever been confirmed.

The virulence of B. anthracis is dependent on its capsule and the two toxins it produces. The poly-D-glutamic acid capsule is antiphagocytic and prevents bacterial lysis of the organism by host proteins. The anthrax toxins have been shown to be composed of three entities that act synergistically to produce the clinical effects of anthrax:

- Protective antigen (so named because it is the main protective constituent of the anthrax vaccine) binds to target cell receptors and then cleaves off a portion of its protein, which allows attachment by either edema or lethal factor.

- Edema factor can bind to the exposed region on protective factor and form edema toxin, which can disrupt cellular water balance, causing intracellular edema.

- Lethal factor, a metalloprotease, can bind to the exposed domain on protective antigen and form lethal toxin, which at sufficient concentrations inhibits neutrophil function and can destroy cellular tissues. Lethal toxin also stimulates macrophages to release tumor necrosis factor and interleukin-1, which contribute to sudden death in cases of systemic anthrax.

Clinical disease can occur when endospores of B. anthracis are introduced into the body by abrasion, inhalation, or ingestion. These spores are ingested by local macrophages and transported to regional lymph nodes, where germination to form vegetative bacilli may occur up to 60 days later. These bacteria release themselves from macrophages and multiply within the lymphatic system, elaborating toxins that overwhelm the clearance ability of regional lymph nodes. Bacteremia and the systemic production of toxins can then ensue.

*206/348/5*

You can do a behavioral experiment alone or with your therapist or a friend: It can be an advantage to take someone with you, because you can get someone else’s input as to whether the hypothesis was confirmed or not. It’s best, at least initially, to do experiments with your therapist, but whether this is feasible will depend on factors such as where your therapist’s office is located and whether there’s enough time during your session.

Do lots of experiments: It takes lots of experiments and lots of practice to get the full benefit of behavioral experiments. It isn’t realistic to think that just a few experiments will get rid of your BDD.

You can combine your behavioral experiments with cognitive restructuring: It can help to try to anticipate the negative thoughts you’ll have about your appearance during the experiment and to do some cognitive restructuring on a thought record form to help you prepare for the behavioral experiment. For example, Lorenzo could have filled out a thought record form for the thought “People will look at me with disgust because I look so bad” before he did his experiment.

*314\204\8*

Unfortunately, we don’t know whether it’s better to augment an inadequately effective SRI, or discontinue the SRI and switch to another SRI, because this question hasn’t been well studied. However, in my clinical practice, I found that among patients who hadn’t responded well to an adequate SRI trial, augmenting the first SRI was successful in 33% of cases, whereas switching to another SRI was successful in 44% of cases. This difference wasn’t significantly different statistically.

However, I found something interesting when I considered whether the patient had had no response, versus a partial response, to the first SRI. Of those people who hadn’t responded to the first SRI (i.e., were not “much improved” or “very much improved”), only 18% responded when I added an augmenting medicine to the SRI. But among people who’d had a partial response to the SRI (i.e., were “much improved” or “very much improved”), 41% responded when I added an augmenting medicine. This difference was statistically significant. This finding suggests that you may be better off augmenting an SRI if you’ve partially responded to it, but it may be better to switch to another SRI if you haven’t responded to the first SRI. However, because this study was relatively small and not very scientifically rigorous (because it was based on my clinical practice), it’s best not to draw firm conclusions about which approach is more effective.

There are other things you might want to consider when deciding whether to augment or switch. If you haven’t responded to numerous SRIs (for example, 3 of them) without any attempt at augmentation, it would make sense to try augmentation. Conversely, if you haven’t responded to several augmentation strategies with one SRI, it’s probably best to switch to another SRI.

Another consideration is that the better you’ve responded to an SRI, the less appealing it is to discontinue it and try another one. For example, if you no longer feel suicidal, and your BDD and depression are a lot better (even if not completely better) on an SRI, it may be too risky to discontinue that SRI and try a new one. It’s possible that the second one won’t work or won’t work as well as the first one, and your symptoms could get worse again (although it’s possible that another SRI could work better). Continuing the SRI and adding another medicine allows you to maintain your partial response to the SRI, whereas if you stop the SRI you risk losing whatever response you had.

So when deciding whether to augment or switch, there are several things to consider, including your individual situation and your and your doctor’s preference. The approach you take needs to be tailored to you. If the approach you choose doesn’t work, you can always try the other one.

*264\204\8*