Predisposing factors to infection

Uncontrolled diabetes alters host immune response and has been implicated in disorders of immune function by alteration of polymorphonuclear leukocyte (PML) chemotaxis, phagocytosis, and decreased intracellular bactericidal activities. The effect of hyperglycemia on phagocytic activity is associated with an increase in cytosolic calcium and is reversible with the improvement of blood glucose level. There are other metabolic imbalances, which impair the immune system, such as presence of acidemia. In addition, presence of chronic inflammatory changes may contribute to the metabolic imbalances. Tumor necrosis factor-α, interleukin-1β, interleukin-6, and interleukin-18, are known to activate the stress hormones, creating hyperglycemia and insulin resistance.

Hyperglycemia was reported to impair complement receptor-3- and Fcy receptor-mediated phagocytosis. Defective cellular immunity includes decreased opsonization, decreased response to phytohemagglutinins, and poor skin test reactivity. Diabetics also have poor granuloma formation. All these changes are aggravated by microcirculatory failure, which alters the diffusion of both cellular and humoral factors to the affected site. The risk of infection also is enhanced by presence of peripheral and autonomic neuropathy and presence of peripheral arterial disease (PAD). Obesity is also a risk factor for moderate or severe infection-related morbidity.

Respiratory infections

Respiratory infections in the diabetic population are associated with increased mortality. Diabetic patients are four times more likely to die from pneumonia or influenza compared to nondiabetics. The risk of developing staphylococcal pneumonia is increased since 30% of diabetics are nasal carriers of Staphylococcus aureus. Patients with diabetes have a higher risk of developing pneumonitis and pneumonia (Klebsiella, Legionella) following influenza, and for this reason immunization against pneumococcus and influenza is recommended. The incidence of acute bronchitis, pneumonia, or exacerbation of chronic pulmonary obstructive disease (COPD) is similar in type 1 and type 2 diabetics. Diabetic patients are also prone to aspiration pneumonia, especially in the presence of gastroparesis (occurs in 40% to 60% of patients with diabetes). The risk of aspiration also increases with impairment of consciousness (i.e., hypoglycemia, hyperosmolar state).

The incidence of tuberculosis is 16 times higher in the diabetic population than in the nondiabetic population, and atypical locations are common. For this reason, the presence of a positive purified protein derivative (PPD) skin test, even with a normal chest radiograph, requires isoniazid (INH) prophylaxis for a minimum of 6 months, regardless of age. Diabetes also predisposes to cavitary lung disease with coccidioidomycosis considered to be a more severe form of infection. Pulmonary mucormycosis is complicated with fungal vascular invasion and high mortality. These infections require cultures, serology, and biopsy for positive diagnosis. Antifungal agents (i.e., itraconazole, voriconazole, posaconazole, or amphotericin B) should be initiated early pending the laboratory results.

Mucormycosis

More than three-fourths of cases of rhinocerebral mucormycosis occur in diabetics, particularly in the presence of diabetic ketoacidosis. Mucormycosis is caused by a group of fungi known as Mucorales, the most common genera being Rhizopus, Absidia, and Rhizomucor. These fungi invade nasal and paranasal membranes, as well as blood vessels, resulting in thrombosis and tissue infarction. Local spread of infection results in ophthalmoplegia, blindness, cavernous sinus thrombosis, meningoencephalitis, and brain abscesses, leading to rapid death in untreated cases. Patients with mucormycosis may present with facial or ocular pain, nasal stuffiness, generalized malaise, and fever. Periorbital edema, chemosis, and nasal black eschars or necrotic turbinates are common presentations. Diagnosis is made by biopsy of the necrotic eschars and demonstration of nonseptate thick-walled hyphae with special staining. Computed tomography (CT) scan or magnetic resonance imaging (MRI) can be helpful in assessing the extent of disease and can aid the surgeon in debridement. Treatment with intravenous amphotericin B, 1 mg/kg/day, or liposomal amphotericin B, 5 mg/kg/day, should be started as soon as possible. Posaconazole (800 mg in divided doses) is the only oral agent that is useful in zygomycosis and can be effective in 60% to 70% of patients. Hyperbaric oxygen therapy was reported to be also beneficial, since it inhibits fungus growth and improves wound healing. Those who survive may require reconstructive surgery and long-term psychological counseling due to facial disfiguration. Even with early diagnosis and treatment, mortality with mucormycosis can be as high 50%, but is 100% if untreated.

Invasive otitis externa

Invasive otitis externa is an aggressive infection usually caused by Pseudomonas aeruginosa. Rarely, the etiologic agent is Aspergillus, Klebsiella pneumoniae, or other organisms. More than 90% of patients have diabetes, often with poor metabolic control. Characteristically, the disease begins with periauricular cellulitis and granulation tissue at the junction of the cartilaginous and osseous portions of the external auditory canal. When infection spreads it may result in parotitis, mastoiditis, septic thrombophlebitis, cranial nerve palsy, and meningitis. Osteomyelitis of the temporomandibular joint, skull base, and cervical vertebrae can also occur. Facial nerve VII palsy occurs in 30% to 40% of cases and does not necessarily carry a poor prognosis. However, development of palsies of cranial nerves IX and XII implies deep infection. This can be complicated by sinus thrombosis and central nervous system (CNS) infection, which results in death in 30% of patients. The use of MRI or CT scan can help to assess the extent of infection and needed debridement.

Four weeks of parenteral antipseudomonal antibiotic therapy is generally recommended. Combination therapy of β-lactam agents (piperacillin, ceftazidime, cefipime, imipenem, or aztreonam) with an aminoglycoside can be used. If oral quinolones are used, longer therapy (3 months) is recommended by some authorities. If aspergillus is the causative organism, liposomal amphotericin B needs to be used for at least 12 weeks. Hyperbaric oxygen therapy may have an adjuvant effect.

Gastrointestinal infections

Since 1993, periodontal infections are considered the sixth most common complication of diabetes; these affect 17.3% of the diabetic population and 9% of the general public. The risk factors for periodontal disease are: increased salivary glucose, decreased salivary pH, small vessel disease, changes in collagen metabolism, and immune changes (i.e., inflammatory cytokines). Porphyromonas gingivalis is the most common pathogen. Professional cleaning and local treatment of periodontal infections may be adequate. However, antibiotic treatment is needed if patients develop fever or lymphadenopathy.

Candida esophagitis has been reported to occur with increased frequency in diabetic patients and more often in those who receive broad-spectrum antibiotics. The most common presentation is retrosternal pain or dysphagia after the ingestion of cold or hot drinks. Oral thrush can be absent. Endoscopic examination and biopsy are the preferred diagnostic procedures. Treatment with oral fluconazole (400 mg initial dose, followed by 200 mg/day) is necessary for a minimum of 3 weeks or at least for 2 weeks after resolution of symptoms. An alternative therapy is itraconazole, 100 mg swished in the mouth daily for 3 weeks. Oropharyngeal infection can be treated with itraconazole, 200 mg swished in the mouth daily for 1 to 2 weeks. Infections with Candida

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