Infections in the elderly
St Lukes Roosevelt Hospital Center, New York. NSS32@Columbia.edu
As people age they experience more illness and this applies in particular to skin infections. Pathogenic states that provide the milieu for infection are more common in the elderly. Infections that occur more common in the elderly include Gram-positive bacterial infections of the skin, intertriginous infections, herpes zoster/shingles and onychomycosis. These will be reviewed in the article. Newer treatments such as valacyclovir, famcyclovir, terbinafine and linezolid exist to treat these infections. Recognizing the varying presentations enhances the health and treatment of disease of elderly patients.
As people age they experience more illness and this applies in particular to skin infections. Some have estimated that the age matches the percentage of population of elderly people with skin disease, in particular, infection. For the purposes of this article elderly is defined as over age 65.
The integrity of the skin declines with age. The reasons for this are complex. The elderly are paradoxically more prone to both malnutrition and obesity, factors that facilitate the entry of pathogens into the skin. The immune system functions less vigorously in the elderly. With age the function of sweat glands decreases, the skin thins, and the ambient moisture content of the skin declines. Complicating the diagnosis of infection is that the response is often less florid with fewer symptoms than the response in younger persons. Presentation can initially be non-specific with acute disorientation, anorexia and weakness, and simple erythema of the skin. Fever in some cases does not occur in the elderly and the white blood cell count does not rise while an infection rages.
Pathogenic states that provide the milieu for infection are more common in the elderly. In particular diabetes and neoplasms undermine the function of the immune system. Diseases such as hyperlipidemia and hypertension decrease blood flow to the skin decreasing the ability of the elderly body to fight off infection. Decreased blood flow slows healing, increases xerosis and allows pathogens the opportunity to enter broken skin, such as cuts, sores, abrasions, erosions, ulcers, and fissures. It bears emphasis and repetition that the skin of the elderly is more xerotic; this helps to provide portals for the entry for infections as xerosis and skin break down undermines the integrity of the integument.
General principles for the therapy of the elderly exist. In most cases treatment should be initiated as soon as an infection is suspected. At the same time, apposite diagnostic tests should occur. When possible, antibiotic treatment should be tailored to killing the pathogen causing disease. Culturing pus, fluids, blood, and scale can be useful in this regard. When assessing the results of laboratory tests, the results must be interpreted with rigor because some positive culture results represent colonization rather than infection of the skin. Inflammatory skin diseases and systemic diseases that mimic skin infection should be excluded with the aid of apposite analysis, such as blood and urine chemistry tests and skin biopsy.
Excellent reviews have been written on these subjects in the last decade [1, 2, 3, 4, 5, 14]. Infections that occur more commonly in the elderly include Gram-positive bacterial infections of the skin [8, 9,10, 11,12,14, 16, 17, 23, 24, 25] intertriginous infections, herpes zoster (shingles) [6, 19, 21], and onychomycosis [13, 15, 18, 22]. These will be reviewed in the article. Other problems, such as scabies, will not be considered here .
A variety of Gram-positive bacterial infections are more common in the elderly than in younger persons. These include cellulitis (in particular of the lower legs), erysipelas, necrotizing fasciitis, folliculitis, impetigo, folliculitis, and furunculosis [8, 9, 10, 11, 12, 14, 16, 17, 23, 24, 25].
Cellulitis and Erysipelas
Cellulitis and erysipelas are common infections in the elderly [1, 2, 3, 4, 5, 14]. Cellulitis should be clinically distinguished from erysipelas . Erysipelas involves the dermis, most commonly involves the legs and tends to be sharply demarcated in contrast to cellulitis, which also most commonly occurs on the lower leg, involves the subcutaneous fat, and is less well demarcated. A classic sign is the orange-peel (peau d'orange) appearance of the infected skin. Vesicles and bullae may be present in the advancing margin of either one. Cellulitis and erysipelas are both usually cased by Gram-positive organisms. Potential complications of cellulitis and erysipelas include spread of the infection and include septicemia, thrombophlebitis, septic arthritis, osteomyelitis, and endocarditis.
Cellulitis and erysipelas require antibiotic treatment. In most cases, they should be treated if at all complicated, of significant extent or if present with coincident disease with intravenous antibiotics. The most common antibiotics used to treat cellulitis and erysipelas are penicillins and cephalosporins. Other therapeutic options include clindamycin, quinolones, and macrolides. The typical duration of therapy is 10-14 days. Cellulitis associated with leg ulcers or pressure sores usually requires longer courses of treatment that can last up to 3-4 weeks.
The differential diagnosis of cellulitis in the legs includes allergic contact dermatitis, deep venous thrombosis, and stasis dermatitis. The elderly suffer from stasis dermatitis associated with diminished blood flow; breakdown of skin may result in impetigo or cellulitis.
If there is any doubt about the diagnosis of cellulitis when a leg is red and painful, a doppler ultrasound or related imaging tests should be carried out to rule out thrombophlebitis. Allergic contact dermatitis and stasis eczema tend to be bilateral in comparison to cellulitis, which is unilateral. However all the four processes can manifest atypically, so cultures and imaging can be helpful at establishing a definitive diagnosis.
Necrotizing fasciitis involves a particularly destructive infection causing rapidly advancing deep tissue necrosis . Necrotizing fasciitis is a polymicrobial infection including Gram-positive and Gram-negative bacteria and anaerobes such as E. coli, Klebsiella pneumonia and P. aeruginosa. About 10 percent of cases are caused by streptococci, mostly group A. In the past infection caused by such pathogens were referred to as streptococcal gangrene. A variety of underlying conditions that include prior injury, surgery, irradiation, cancer, diabetes mellitus, alcoholism, and malnutrition facilitate necrotizing fasciitis. Minor skin infections such as furuncles were found to be present in about 20 percent of patients before developing necrotizing fasciitis.
Treatment for necrotizing fasciitis necessitates therapy involving several antibiotics such as gentamicin and clindamycin. Consideration should be given to cover both aerobes and anaerobes. Among the most pivotal therapies is the swift and vigorous debridement of all necrotic tissue. Supportive care includes proper nutrition, hydration, and close monitoring.
Impetigo, folliculitis, and furunculosis
Staphylococcus aureus and β-hemolytic streptococci are the most common organisms that cause cutaneous infections. They are associated with cellulitis, erysipelas, impetigo, folliculitis and furunculosis.
Impetigo manifests with honey-colored crusted erosions. Although the diagnosis of impetigo can be made clinically, the clinician should obtain a sample of fluid or pus for gram stain and culture to define the causative organism. The need for pathogen identification is especially important if other household members are also infected so that therapy is curative and re-infection by a family member does not occur. A nasal culture of the patient and other family members is often helpful in assessing if nasal carriage of Staphylococcus aureus is the source of the infection (up to 20-25 % of persons carry Staphylococcus aureus in their noses).
Bacterial infection of the pilosebaceous follicles is termed folliculitis. Folliculitis usually occurs on body surfaces with short, coarse hair such as the scalp, neck, beard area, axillae, buttocks, and limbs. A fungal folliculitis (Majocci granuloma) can occur if a superficial fungal infection is treated with topical steroids. A furuncle or boil is the manifestation of a deeper infection of the hair follicle generally with Staphylococcus aureus. It results in a red, hot, tender inflammatory nodule (a boil) from which pus can be expressed. Carbuncles are multiloculated, or multiple furuncles. The differential diagnosis for a furuncle is an inflamed epidermal or pilar cyst. Although antibiotics may help treat an inflammed cyst because it is secondarily infected or because antibiotics may have anti-inflammatory effects, the definitive treatment of an epidermal cyst is surgical.
A variety of conditions may increase the liklihood of infections of the superficial skin and hair follicle. These factors include bacterial carriage in the nostrils, scabies, vigorous scratching of the skin, diabetes mellitus, obesity, lymphoproliferative neoplasms, malnutrition, and the administration of glucocorticosteroids and other immunosuppressive drugs.
The optimal treatment begins with culture of eruptions that are suspected of having infectious etiologies. Empiric treatment should be started if an infection is suspected. While resistance and atypical organisms can be the cause of a skin infection, treatment should be directed towards gram positive organisms with the expectation that some response will be seen in 2-3 days. If the patient has systemic symptoms (fever, malaise, nausea, vomiting) or the infection occurs on a sensitive area (e.g., genital or ocular sites), the patient should be admitted to the hospital and treated with intravenous antibiotics. If the culture of fluid of a folliculitis or furunculosis reveals that the infection is resistant to the initial therapy, treatment should be altered. Alternatives for organisms resistant to penicillins include intravenous vancomycin and oral linezolid. Typical courses of therapy are 7-10 days.
Rashes of the intertriginous areas
Infections can occur in areas of the body folds that include erythrasma and candidiasis . Erythrasma, presenting with reddish-light brown slightly scaly patches typically in the groins and axillae, is associated with Corynebacterium minutissimum. This infection has a predilection for the body folds, especially the axillae and groin, and topical therapy is usually sufficient. Intertrigo, inverse psoriasis and other inflammatory diseases and systemic diseases (e.g., histocytosis) should be excluded when a diagnosis of erythrasma is considered; appropriate investigations include blood tests and skin biopsy. Topical antifungal agents as well as erythromycin or clindamycin are effective treatments for erythrasma; severe cases can be treated with oral erythromycin.
Candidiasis is a yeast infection most commonly associated with Candida albicans that commonly occurs in body folds . Use of antibiotics, corticosteroids, and other immunosuppressive drugs as well as local factors such as prolonged occlusion with moisture and warmth in skin flexures predispose patients to candidiasis. Cutaneous candidiasis usually develops in body folds such as groins, inframammary areas, axillae, and perineal area. It manifests as well-defined erythema with slight scaling, and often with satellite papules and pustules. It can be treated with topical antifungal agents and, when severe, oral fluconazole.
Herpes zoster (also known as shingles) is caused by reactivation of latent varicella zoster virus (VZV). Varicella zoster virus infection is the pathogenic etiology of chickenpox also referred to as varicella, an infection that usually happens in prepubescent children. After a chickenpox infection, VZV remains latent in an individual's dorsal root and cranial nerve ganglia even for decades. Reactivation often happens for no apparent reason. Outbreaks of zoster have been associated with stress and immune suppression [1, 2, 3, 4, 5, 6,14, 19, 21].
A patient with zoster usually first notices unilateral dysesthesia and pain on one side of the body almost in line (dermatomal) before any rash occurs [1, 2, 3, 4, 5, 14]. Within 1-3 days after the initial pain, clusters of grouped vesicles on an erythematous base or urticarial-like plaques develop. The urticaria can vesiculate and the vesicles can transform into pustules that break down leaving behind crusts. Zoster remains infectious until all the vesicles and pustules evolve into crusted plaques. The plaques of zoster usually evolve and resolve over the course of 2-3 weeks. In a minority of cases, scattered vesicles occur outside one or two dermatomes. These scattered vesicles are termed satellite lesions. In an even smaller minority of cases patients may experience dysesthesia without urticarial plaques or vesicles; a state that is referred to as zoster sine herpeticum. Acyclovir, valacyclovir, and famcyclovir can be used to treat zoster and are used for 7 days. Antiviral treatment also appears to reduce the prevalence, severity, and duration of postherpetic neuralgia, a chronic pain condition that occurs in areas affected by zoster. Postherpetic neuralgia, which leads to chronic pain in a dermatome, is particularly frequent and severe in the elderly, occurring in 25-40 percent of patients over age 60 with herpes zoster [6, 19, 21].
There are subtypes of zoster that must be understood by clinician for effective treatment and diagnosis because they require intravenous antiviral therapy . Ophthalmic herpes zoster involves the first division of the fifth cranial nerve. Ophthalmic herpes zoster may result in scarring of the cornea and secondary panophthalmitis with subsequent loss of vision. Lesions on the tip of the nose and an ocular foreign body sensation are characteristic signs. Ramsay-Hunt syndrome is herpes zoster infection of the geniculate ganglion, which lies at the genu of the seventh nerve. It results in ipsilateral facial palsy similar to Bell's palsy and vesicles develop in the external auditory meatus, on the pinna and sometimes in the soft palate, and can result in deafness. Disseminated herpes zoster is zoster that involves more than three dermatomes or has more than 20 lesions occurring outside a dermatome and can occur in particular in the setting of non-Hodgkin lymphoma or human immunodeficiency virus. Disseminated zoster can involve internal organs and present as hepatitis, pneumonitis, meningoencephalitis, myelitis, or motor radiculopathy. Ophthalmic zoster, Ramsay-Hunt Syndrome and disseminated zoster should be treated with intravenous acyclovir .
Onychomyocosis must be understood as a skin disease of the elderly [13, 15, 18, 22]. Dermatophytes, most commonly Trichophyton rubrum, are the most common cause of onychomycosis or tinea unguium. Onychomycosis or tinea unguium can also be caused by Candida and nondermatophyte molds. Onychomycosis is found more frequently in the elderly and more often in males than females. The prevalence of fungal nail infections was about 18 percent in the 60-79 years age group compared to 0.7 percent in patients younger than age 19. Increasing age, male gender, diabetes mellitus, family history of onychomycosis, psoriasis, concurrent intake of immunosuppressive drugs, and peripheral vascular disease are associated with a greater prevalence of onchomycosis [13, 15, 18, 22].
There are four types of onychomycosis: distal subungual onychomycosis, proximal subungual onychomycosis, white superficial onychomycosis, and candidal onychomycosis. Distal subungual onychomycosis, which manifests with thickened and friable nails with associated discoloration and subungual hyperkeratosis, is the most prevalent type and accounts for 75-85 percent of cases [1, 2, 3, 4, 5, 14]. Some patients experience pain or limited mobility resulting in impaired quality of life. The most sensitive and specific way to diagnosis onychomycosis is by a PAS stain performed on a nail clipping. A definitive diagnosis is useful because nail dystrophy from psoriasis, lichen planus, and eczema may result in onychodystrophy that resembles onychomycosis. Onchymycosis can provide a portal of entry for other pathogens and can be related to secondary bacterial infections in diabetic patients leading to foot ulcers and gangrene, recurrent cellulitis, and erysipelas [13, 15, 18, 22].
Useful treatments exist for onychomycosis. Onychomycosis can be treated with oral terbinafine (250 mg daily for 3 months), itraconazole (400 mg daily for 1 week in every 4 weeks for either 12 or 16 weeks), or fluconazole, or topical amorolfine nail lacquer or ciclopirox nail lacquer [13, 15, 18, 22]. Terbinafine is probably the most effective agent with few drug interactions but it is only effective against dermatophytes while other agents are also effective against nondermatophytes. Topical application of urea 40 percent gel or cream, which breaks down keratin and softens the nail plate, may enhance penetration of topical antifungal drugs. After therapy is initiated it can take up to 6 months to see the effect of these therapies on toe nail onychomycosis. Combinations of treatments (e.g., oral and topical or oral/topical and surgical) appear to be associated with resulted enhanced cure rates It can be useful to disinfect or discard old footwear (some recommend using moth balls to do this) and to keep feet dry and clean and continue to use topical antifungal agents.
Infections in the elderly are more common than in younger individuals. They are more complicated by the multiple medications used to control the diseases that accompany normal aging. There are however effective treatments that have arrived on the scene that include terbinafine and linezolid. Understanding the diseases an elderly patient might suffer enhances their health and well being.
The most important developments that pertain to infections in the elderly pertain to the development of antibiotics for antibiotic resistant bacteria for example tigecycline, a derivative of minocycline. Also it is possible that combination regimens of topical and oral agents for onychyomycosis will be defined to enhance cure rates.
References1. Weinberg JM, Vafaie J, Scheinfeld NS. Skin infections in the elderly. Dermatol Clin 2004 ;22:51-61.
2. Laube S, Farrell AM. Bacterial skin infections in the elderly: diagnosis and treatment. Drugs Aging 2002;19:331-42.
3. Nagami P. Management of common infections in the elderly outpatient. Geriatrics1986;41:67-9, 74-7, 80.
4. Laube S. Skin infections and ageing. Ageing Res Rev 2004;3:69-89.
5. Weinberg JM, Scheinfeld NS. Cutaneous infections in the elderly: diagnosis and management. Dermatol Ther 2003;16:195-205.
6. Alper BS and Lewis PR. Treatment of postherpetic neuralgia: a systemic review of the literature. J Pham Pract 2002;51:121-128.
7. Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996;334:240-245.
8. Brandt MM, Corpron CA, Wahl WL, Necrotizing soft tissue infections: a surgical disease. Am. Surg. 2000;66:967-970.
9. Cox NH, Colver GB and Paterson WD, Management and morbidity of cellulitis of the leg. J. R. Soc. Med. 1998;91:634-637.
10. Cummings DM and Uttech KM. Antibiotics for common infections in the elderly. Prim. Care 1990;17:883-903.
11. Dahl PR, Perniciaro C,Holmkvist, KA, O'Connor MI and Gibson LE. Fulminant group A streptococcal narcotising fasciitis: clinical and pathological findings in 7 patients. J Am Acad Dermatol 2002;47:489-492.
12. Dupuy A, Benchikh H, Roujeau JC, Bernard P, Vaillant L, Chosidow O, Sassolas B, Guillaume JC, Gorb JJ, Bastuji-Garin S. Risk factors for erysipelas of the leg (cellulitis): case-control study. Br Med J 1999;318:1591-1594.
13. Evans EG. Causative pathogens in onychomycosis and the possibility of treatment resistance review. J. Am. Acad. Dermatol. 1998;38:S32-36.
14. G. Gavazzi and K.-H. Krause, Ageing and infection. Lancet Infect Dis 2002;2:659-666.
15. Gupta AK, Jain HC, Lynde CW, MacDonald P, Cooper EA, Summerbell RC. Prevalence and epidemiology of onychomycosis in patients visiting physicians' offices a multicenter Canadian survey of 15,000 patients. J Am Acad Dermatol 2000;43:244-248.
16. B.H. Lertzman and A.A. Gaspari. Drug treatment of skin and soft tissue infections in elderly long-term care residents. Drugs Aging 1996;9:109-121.
17. Morris A. Cellulitis and erysipelas. Clin Evid 2003;9:1804-1809.
18. Mukherjee PK, Leidich SD, Isham N, Leitner I, Ryder NS, Ghannoum MA. Clinical Trichophyton rubrum strain exhibiting primary resistance to terbinafine. Antimicrob. Agents Chemother 2003;74:82-86.
19. Naesens L, De Clercq E. Recent developments in herpesvirus therapy. Herpes 2001;8:12-16.
20. R.S. Purvis and S.K. Tyring, An outbreak of lindane-resistant scabies treated successfully with permethrin 5% cream. J Am Acad Dermatol 1991;25:1015-1016.
21. Raeder CK, Hayney HS. Immunology of varicella immunization in the elderly. Ann. Pharmacother 2000;34:228-234.
22. Scher RK. Onychomycosis is more than a cosmetic problem. Br J Dermatol 130 Suppl. 1994;43:15.
23. Stone HH. Soft tissue infections. Am Surg 2000;66:162-165.
24. Sule O, Brown N, Brow DFJ, Burrows N. Judicious use is advisable. Br Med J 2002;324:1394.
25. Veien NK, The clinician's choice of antibiotics in the treatment of bacterial skin infection. Br Dermatol 1998;139:30-36.
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