CANDIDA OSTEOMYELITIS
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Hematogenous dissemination of candida can result in Candida osteomyelitis. Gathe et al reviewed infections in 32 adults reported in the literature and reported on five patients with Candida osteomyelitis. They concluded that Candida osteomyelitis frequently occurred with hematogenously disseminated candidiasis or as a late sequela. Infrequently Candida osteomyelitis also has presented secondary to postoperative wound infections. Therapy with amphotericin B usually controls local infection but rarely eradicates concurrent osseous focus. The diagnosis of Candida osteomyelitis usually is delayed for several months or years because infection is insidious, with local pain being the most prominent feature. Complicating and further delaying the diagnoses are the nonspecific natures of laboratory and radiographic findings. Definitive diagnosis is usually made by culturing the organism from samples obtained using closed-needle or open-needle aspiration. Combination therapy including surgical debridement and antifungal therapy, usually with amphotericin B, is often successful at eradicating infection.
CANDIDA AND ANTIBIOTIC ASSOCIATED DIARRHEA
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Nosocomial diarrhea is a well-recognized problem in several hospitals across the United States, with Clostridium difficile being one of the most common etiologic agents. Candida species also are being associated with diarrhea. Danna et al evaluated the role of candida in antibiotic-associated diarrhea in elderly patients. The 24 patients with antibiotic-associated diarrhea were matched by age and sex with two selected controls who were either on antibiotics and had no diarrhea or were not on antibiotics and had no diarrhea. They concluded that 7 of 24 patients with stools negative for Clostridium difficile and other intestinal pathogens had intestinal overgrowth caused by Candida species (104 cfu/mL). None of the 24 matched, antibiotic-treated control patients without diarrhea had candida overgrowth. The five patients with diarrhea and candida overgrowth had resolution of their diarrhea and lowering of fecal counts to less than 104 cfu/mL within 7 days of antifungal therapy with nystatin despite continuation of the antibiotics. Two other patients who had overgrowth of candida were not treated with antifungal therapy, and the diarrhea resolved with lowering of fecal candida counts to less than 104 cfu/mL at the time antibacterial agents were withdrawn. In patients without candida overgrowth, diarrhea persisted until antibiotics were withdrawn, at a mean of 16 days after study entry. Several questions remain unanswered after reviewing this study. Why did patients recover despite overgrowth of candida in the stool in the absence of antifungal therapy? Were stool samples from patients without diarrhea accurately reflecting the true bioburden of candida (none of these stools had candida counts 105 cfu/mL)? Finally, can these samples be compared with watery stools obtained from patients with diarrhea?
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Weese-Mayer et al looked at factors important in the development of candidemia in 20 case patients less than 4 months of age who were matched with control infants by birth weight and date of admission to the neonatal intensive care unit. Univariate analysis identified duration of hyperalimentation, administration of fat emulsion, endotracheal intubation or tracheostomies or both ( p = 0.01), and antibiotic therapy ( p = 0.0002) as risks significantly associated with the development of candidemia. Antibiotic therapy had the greatest association with candidemia when discriminate function analysis was used to evaluate risk factors independently. No predictive discriminate function distinguishing infants at risk for candidemia was possible from the study. Fifteen of twenty-two episodes of candidemia were cured after two episodes, and death followed infection in five. Removal of catheters only resulted in clearance of infection in 9 of 22 patients (41%). Therapy with combination of amphotericin B and 5-fluorocytosine (5-FC) was successful in 4 of 5 patients (80%). Five of 20 infected patients (25%), compared with 1 of 20 (5%) control patients, died in this series.
NEW SIGNS AND SYMPTOMS
Differentiating infection from colonization is difficult and is a major handicap in the prevention and therapy of candidiasis in hospitalized patients. Helpful clinical findings that may be suggestive of infection caused by candida species include endophthalmitis, macronodular skin lesions, suppurative peripheral thrombophlebitis, hepatitis, purpura fulminans, bullous dermatitis, epiglottitis, and candida osteomyelitis. It usually is not possible to differentiate bacterial infections from local or systemic candidiasis by these clinical signs and symptoms. Neutropenia or the presence of nonalbicans species are factors associated with a reduced likelihood of candida endophthalmitis developing or becoming clinically recognizable infections.
HEPATIC CANDIDIASIS
Although not rare, hepatosplenic candidiasis is rarely recognized ante mortem. Immunocompromised patients are especially at risk for liver and spleen abscess caused by Candida species. This has been demonstrated by the increased number of the infections in these patients in the last 10 to 15 years. Thaler et al, using information from literature review and their own experience at the National Cancer Institute, concluded that the signs and symptoms of hepatosplenic candidiasis are reasonably characteristic. Useful findings in a cancer patient recently recovered from an episode of neutropenia include persistent fever, abdominal symptoms, and elevated alkaline phosphatase concentrations. Canadian viagra online
Ultrasonography is more specific than the more sensitive noninvasive technique of CT at detecting candida hepatosplenic abscesses; however, both techniques are subject to false-negative results. It is important to establish the diagnosis with certainty because the therapy required to ensure cure for hepatic candidiasis is a long course of amphotericin B (up to one year and 9 g). Liposomal amphotericin B or amphotericin B and 5-FC are options for therapy. Cure is documented by absence of symptoms, normalization of laboratory results, and disappearance of lesions by invasive and noninvasive techniques.
IMPACT OF CANDIDA
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Opportunistic infections caused by Candida species have increased substantially over the past 10 to 15 years. National data from the Centers for Disease Control and Prevention (CDC) indicate that Candida species caused 7.7% of bloodstream infections nationwide from 1985 through 1988.
RISK FACTORS FOR ACQUISITION, DISEASE, AND DEATH
Seriously ill, immunocompetent patients and severely immunocompromised patients are at particular risk for nosocomial candidal infections. Included in these groups are neonates, patients with various forms of cancer who are leukopenic, and patients who have had major surgery (especially gastrointestinal and pancreatic), severe burns, or bone marrow transplants.
Given the presence of high-risk diagnoses (especially gastrointestinal and pancreatic), some identified risk factors for acquisition of candidemia include exposure to multiple antibiotics and steroids, presence of Swan-Ganz catheters, length of stay in the intensive care unit, artificial respiratory assistance, use of steroids, candida colonization, and repeated transfusions. In the study by Wey et al, four independent risk factors were identified by multivariate analysis: (1) number of antibiotics received, (2) isolation of Candida species from a site other than blood, (3) prior hemodialysis, and (4) prior use of Hickman catheter.
I want to say something about the hallucinogens. We are seeing LSD nowadays. It’s in lower concentrations than when we were teenagers and so people aren’t flying out the window thinking they can fly like Art Linkletter’s daughter did which is one of the things that turned people off to LSD. But acid is back in a lower concentration and kids are using it at parties and it is producing problems acutely. Tolerance showing it has a serotonergic effect. It can also produce an adrenergic state. PCP, while developed as an anesthetic, has a very interesting dose response and this is one line I would circle just so it stays in your head. At low dose, it acts like alcohol or the benzodiazepines with ataxia. At the middle dose you get illusions and a propensity to violent outbursts with paranoia. At a high dose, 70 mg or greater, you see coma so it’s a particularly bad therapeutic window assuming you think intoxication is therapeutic. So even there it’s bad.
Management. I still find the urine is the key issue and there are several ways to do this. 10% of mental health patients are abusing anticholinergics, particularly Cogentin and just review why because that’s a likely thing to show up on the test.
The final thing is anabolic steroids. One out of 10 high school kids is using them. Mark McGwire didn’t help because androstenedione, while not excluded from baseball, does increase testosterone levels and the withdrawal is the problem. The stimulus to mania is a problem. Rageful behavioral and aggression on withdrawal.
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You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s a weak one. It’s a serotonergic agent and in preliminary animal studies it seems to reduce self administration for opiates and stimulants. So that’s kind of interesting.
You might hear about ibogaine. Ibogaine is a hallucinogen actually, though it’s a weak one. It’s a serotonergic agent and in preliminary animal studies it seems to reduce self administration for opiates and stimulants. So that’s kind of interesting.
I’m going to skip over concomitant substance abuse except to point out that alcoholism is present in 50% of heroin addicts even treated ones in methadone programs so if you see that question, 50% is huge so it’s called a majority. I would also point out that what if somebody is dependent upon both opiates and benzodiazepines or opiates and alcohol? Well you want to maintain methadone during the alcohol or benzo detox and do the methadone detox later. So that sequence is important.
Now I’m going to cover a couple of other substances. Just nicotine. We’re on the bottom of page 289 and I point out that there has been, in the past five years, a 25% increase in college smoking. Now who wanted that? Well, the advertising industry and the tobacco manufacturers want that and that’s what they got. It’s crossing all the lines of society and it’s very strange.
There are physiologic effects from smoking. Decreasing muscle tone. Decreasing GI motility. This is the reason that Virginia slims. If I don’t feel like eating because my GI tract ain’t doing much when I smoke I’m going to lose weight and retain my youthful figure. So that’s the story behind that. Heart rate goes up so it’s a mild stimulant but it’s important in depression in kids, depression in adults which enhances the relapse rate particularly in women. Cheap levitra at family pharmacy.
So what do we do? Well, we used to think that it was a counseling challenge but the point I want to make and this is on page 290 under letter C, the longitudinal approaches, take a look at item 4. Pharmacotherapy is now the first line approach. Counseling is an important primary issue and can be done in primary care. You don’t have to go to specialized groups but all pharmacotherapies work and they all work about equally well. Viagra professional information - news, articles.
Bupropion is showing nice hard numbers – about 30% are abstinent in a year and that means, well, if the patient relapses try them again. Maybe you’ll get a 60% likelihood of success the second time and it’s just a contraindication in a seizure patient. It can be a problem with anorectic or bulimia patients. We can’t use it if the patient is already on MAOIs. The patch adds some, perhaps another 5 or more percent, and there’s no harm in combining the patch. Think about the patch as a tribute taper not just stopped at the full dose because that leaves the patient experiencing a withdrawal from the patch believe it or not.
A couple of other areas. Cannabinols, page 291, there’s some description of what’s going on there. The key thing to know is that this is now the primary leading illicit substance of abuse in America. More than half of high school seniors are trying marijuana. There are many agents, there are at least many dozens of agents active. Delta-9-THC is probably the highest concentration agent. The therapeutic use. There’s still some data although glaucoma is a little bit less supported now but the antiemetic effect of chemotherapy is still supported.
The main problem in overdose is brainstem respiratory CO2 sensitivity falls and the patient stops breathing. The purity of heroin on the streets is strong enough now that we’re seeing this even with inhaled and smoked heroin sometimes. Now, tolerance occurs rapidly particularly to the nausea and that kind of discomfort and it becomes purely pleasurable at that point but only one in ten people who try heroin tend to become addicted to it. So we have to be realistic about this and reasonable, not that heroin could ever be thought of as a legalized substance, but not everybody who walks in who says, you know, “I used heroin at a party” is a heroin addict and we have to do some work to tease out “Do we have a criteria of dysfunction being met?”
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What’s the withdrawal amount? Well, the locus caeruleus is suppressed by chronic heroin use and when that suppression is released we have up-regulation of noradrenerigic receptors and suddenly the adrenergic arousal goes wild. There isn’t up-regulation of the opioid receptors themselves but there is up-regulation in terms of dopamine activity and the two sides are the ventral tegmental area – VTM – and nucleus accumbens which we talked about before but both of these are involved. Heroin is not a one site reinforcer. It seems to involve this system.
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I’m not going to talk about the long term treatment, for instance methadone. Harm reduction is an important goal nowadays because it reduces HIV transmission. So needle exchange works. Even in areas with lots of severe heroin addicts, we see reduction in HIV transmission thanks to needle exchange regardless of what the government’s policy is. Generic viagra 100 mg online at cheap pharmacy mall. Rapid detox can be done in less than five days with a combination of either these two – clonidine or naltrexone – plus or minus buprenorphine which I think actually improves the experience and retention for the patients and the L Group published on this. I think it’s definitely better combined.
Anesthesia detox. You actually can get a full blown heroin addict onto full dose naltrexone totally blockaded at the mu-receptor – they can’t become high now – in five hours using anesthesia. The problem is you don’t know if the therapeutic change has happened so that the patient doesn’t go out and then try and overcome naltrexone and dose themselves so badly that they overshoot and go into coma which has happened now a few times.
LAM – levo acetyl methadone. LAM is now FDA approved. It’s just a long acting type of methadone. So you can dose 100 mg Monday, 100 mg Wednesday, 150 mg on Friday and the patient is covered in the intervening days. They have more freedom. They can return to a more normal life. The patients like it. They retain better on it. Not available in all states. Call for details.
Buprenorphine. I hope it’s going to come out this year from the FDA. I keep saying that. The slowdown has been that the FDA is being pushed to allow dispensing in physicians’ offices. Buprenorphine is another long acting opioid like LAM, like methadone, safer and we may get to use it in office practice.
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