Chancroid is a sexually transmitted disease caused by the short gram negative bacillus Haemophilus ducreyi. The incubation period ranges from three to five days. At the location of inoculation, a vesicopustule develops that breaks down to form a painful, soft ulcer with a necrotic base, surrounding erythema, and undermined edges. There may be multiple lesions due to autoinoculation. The adenitis is usually unilateral and is composed of tender, matted nodules of moderate size with overlying erythema. The patient may also present with lymph node involvement, chills, malaise, and fever. While women typically have no external signs of infection, balanitis and phimosis are frequent complications in men. The diagnosis is established by culturing a swab of the lesion onto a special medium. To treat the disease, a single dose of azithromycin (1g orally) or ceftriaxone (250 mg intramuscularly) is effective as is erythromycin (500 mg orally four times a day for seven days) or ciprofloxacin (500 mg orally twice a day for three days).

Yaws is a contagious disease that is limited to tropical regions and is caused by the T pallidum subspecies pertenue. The malady is characterized by granulomatous skin lesions, mucous membranes, and bone. While Yaws is rarely fatal, it can lead to chronic disfigurement and disability if left untreated. Yaws is acquired by direct non-sexual contact (usually in childhood) although it can occur at any age. The first papule (which later ulcerates) appears three to four weeks after exposure. There is usually associated regional lymphadenopathy. Six to twelve weeks later, secondary lesions that are raised papillomas and papules that seep highly infectious material appear and last for several months or years. Late gummatous lesions may occur with associated tissue destruction involving large areas of skin and subcutaneous tissues.

Botulism is a paralytic disease caused by botulism toxin, which is produced by C botulinum, an anaerobic spore-forming bacillus found in soil. Four toxin types – F, E, B, and A cause disease in humans. Naturally occurring botulism comes in three forms: wound botulism, infant botulism, and food borne botulism. Food borne botulism is caused by ingestion of preformed toxin present in vacuum packed, canned, or smoked foods. Infant and wound botulism are both caused by the presence of organisms in the gut or wound that secrete toxins. Symptoms include diplopia and loss of accommodation, fixed dilated pupils, cranial never palsies with extraocular muscle impairment, dry mouth, dysphonia, dysphagia, and ptosis. Paralysis that develops into respiratory failure and death may occur unless assistance is provided. To test for the disease, the practitioner should use mouse inoculation and specific antiserum. If the practitioner suspects that her patient is suffering from botulism, she should contact State health authorities or the |Centers for Disease Control for assistance in procuring the equine serum heptavalent botulism antitoxin and the assays for toxin in serum, stool, or food. Skin testing is also recommended to remove hypersensitivity to the antitoxin preparation. Antitoxin should be administered within twenty-four hours of the onset of symptoms and parenteral fluids should be provided while the patient has difficulty swallowing.

Human herpes virus 8 (HHV-8) or Kaposi sarcoma associated herpes virus is the cause of all forms of Kaposi sarcoma. Kaposi sarcoma occurs primarily in homosexual men with HIV infection as an AIDS defining illness and can complicate immunosuppressive therapy. Improvement is often seen after the immunosuppression is stopped. The patient will typically present with red or purple plaques or nodules on cutaneous or mucosal surfaces. Marked edema can occur with few or no skin lesions. Kaposi sarcoma commonly involves the GI tract and can be screened with fecal occult blood testing. In asymptomatic patients, these lesions are not sought or treated. Pulmonary Kaposi sarcoma, which can be asymptomatic and appear only on chest radiography, can present with shortness of breath, cough, hemoptysis, or chest pain. Chronic Kaposi sarcoma can develop in patients with HIV infection, high CD4 counts, and low viral loads. Here, the Kaposi sarcoma is in its endemic form and is indolent as well as localized. The sarcoma can be clinically aggressive, though. The presence of Kaposi sarcoma at the time of antiretroviral initiation is associated with Kaposi sarcoma-immune reconstitution inflammatory syndrome which has an especially aggressive course in patients with visceral disease. As far as treatment is concerned, in more seasoned patients, palliative local therapy with intralesional chemotherapy or radiation is usually all that is required. If the patient has iatrogenic immunosuppression, treatment consists of reduced doses of immunosuppressive medications. On the other hand, if the patient has AIDS associated Kaposi sarcoma, she or he should be given ART. Other therapeutic options include cryotherapy or intralesional vinblastine (0.1-0.5 mg/mL) for cosmetically objectionable lesions; radiation therapy for accessible and space occupying lesions; and laser surgery for certain intraoral and pharyngeal lesions. Systemic therapy is indicated in patients with rapidly progressive skin disease, edema or pain, and symptomatic visceral disease or pulmonary disease. Liposomal doxorubicin is highly effective in severe cases and may be used alone or in combination with bleomycin and vincristine. Paclitaxel and other taxanes can be effective even in patients who do not respond to anthracycline treatment.

Patients with anorexia nervosa may present with severe emaciation and complain of cold intolerance or constipation. Amenorrhea is almost always present and may be accompanied by bradycardia, hypotension, and hypothermia. An examination will reveal loss of body fat, dry and scaly skin, and increased lanugo body hair. Parotid enlargement and edema may also occur. Patients may have elevated serum cholesterol levels, depressed levels of luteinizing and follicle stimulating hormones, and an impaired response of luteinizing hormone to luteinizing hormone-releasing hormone. In a few instances, medications such as tricyclic antidepressants, selected serotonin reuptake inhibitors (SSRIs), and lithium carbonate are effective. All cases should be co-managed with a psychiatrist and, a patient should be admitted if she presents with hypovolemia or major electrolyte disorders.

Bulimia nervosa is the episodic uncontrolled ingestion of large quantities of food followed by recurrent inappropriate compensatory behavior to prevent weight gain such as self-induced vomiting, diuretic or cathartic use, or a regime that calls for strict dieting or overly vigorous exercise. Gastric dilatation and pancreatitis have been reported after binges. Moreover, vomiting can result in poor dentition, pharyngitis, esophagitis, aspiration, and electrolyte abnormalities. Treatment requires supportive care and psychotherapy. Individual, group, family, and behavioral therapy have all been used. On occasion, prescription of fluoxetine hydrochloride and other SSRIs may be helpful. All cases should be co-managed with a psychiatrist.

Patients with very high levels of serum triglycerides (greater than 1000 mg/dL) are at risk for pancreatitis. Most patients with congenital abnormalities in triglyceride metabolism present in childhood. By way of contrast, hypertriglyceridemia-induced pancreatitis in adults is often due to an acquired lipid metabolism problem. Although, there are no clear triglyceride levels that predict pancreatitis, most clinicians treat fasting levels above 500 mg/dL. The risk of pancreatitis here may be more related to the triglyceride level following consumption of a fatty meal. Thus, because postprandial increases in triglyceride are inevitable if fat-containing foods are eaten, fasting triglyceride levels in persons prone to pancreatitis should be kept below that level. The primary treatment for high triglyceride levels is dietary and calls for reduced consumption of alcohol, simple sugars, and refined starches as well as saturated and trans fatty acids. In patients with fasting triglycerides greater than or equal to 500 mg/dL despite adequate dietary compliance, a triglyceride lowering drug such as niacin, a fibric acid derivative, an omega-3-acid ethyl ester, or an HMG-CoA reductase inhibitor may be helpful.

Most patients with high cholesterol levels have no specific symptoms or signs. Indeed, the vast majority of patients with lipid abnormalities are detected with a lab test either as part of a preventative screening program or patient workup. Extremely high levels of chylomicrons or VLDL particles (triglyceride levels above 1000 mg/dL or 10 mmol/L) result in the formation of eruptive xanthomas (red-yellow papules typically on the rear end). High LDL concentrations result in tendinous xanthomas on certain tendons (usually the back of the hand and the patella). Finally, a patient presenting with lipemia retinalis (cream-colored blood vessels in the fundus) may have extremely high triglyceride levels.

Riboflavin deficiency almost always occurs in connection with other vitamin deficiencies. The most common causes are alcoholism, interactions with a variety of medications, dietary inadequacy, and the other causes of protein-calorie undernutrition. Symptoms include anemia, corneal vascularization, weakness, seborrheic dermatitis, glossitis, angular stomatitis, and cheilosis. A riboflavin deficiency diagnosis can be confirmed by measurement of the riboflavin-dependent enzyme erythrocyte glutathione reductase. Readers should note that activity coefficients greater than 1.2-1.3 are suggestive of riboflavin deficiency. Patients can be treated by consuming the vitamin itself (5-515 mg/day) or foods such as fish or dairy products. While riboflavin can be provided parenterally, practitioners should note that the vitamin does not dissolve well in aqueous solutions.

Vitamin A deficiency is one of the most common vitamin deficiency syndromes and is most prevalent in developing States. The malady is a leading cause of blindness. In the United States, vitamin A deficiency is usually due to fat malabsorption syndromes or mineral oil laxative abuse and is typically exhibited by older adults and individuals living in urban areas. The earliest symptom here is night blindness, which is followed by xerosis, and the development of Bitot spots on the conjunctiva. Ulceration and necrosis of the cornea, endophthalmitis, perforation, and blindness are late manifestations. Hyperkeratinization of the skin may also occur. Dark adaptation abnormalities are strongly suggestive of vitamin A deficiency as are serum levels below the normal range of 30-65 mg/dL. The most common treatment, of course, is vitamin A (30,000 international units daily for one week orally). Advanced deficiency with corneal damage calls for 20,000 international units/kg for at least five days. The potential antioxidant effects of beta-carotene can be achieved with supplements of 25,000-50,000 international units of beta-carotene. Excess intake of beta-carotene, however, can result in a staining of the skin in a yellowish-orange color. The change should be most apparent on the patient’s palms and soles. Practitioners, on the other hand, should also note that vitamin A can be quite toxic. Chronic toxicity often occurs after ingestion of daily doses of over 50,000 international units per day for more than three months. Symptoms here include vomiting, anorexia, mouth sores, hair loss, dry skin, lethargy, headache, and painful hyperostosis. Excessive vitamin A intake can also predispose patients for a hip fracture.