Oral infections in HIV disease
Oral infections in HIV disease |
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Key words: infections, HIV, mouth
Introduction
During the course of HIV infection and AIDS a spectrum of oral infection due to opportunistic organism can be found. Some of these are particular to the oral cavity such as oral hairy leukoplakia and necrotising ulcerative gingivitis but others may infect the entire gastrointestinal system. Fungal, bacterial, viral and occasionally parasitic infections may affect oral cavities during the course of HIV infection.
Fungal infections
Oro-pharyngeal candidiasis is the disease of the diseased and is the most frequent oral infection during HIV disease (figure1). Prevalence ranges from 11% to 90% (1) and is associated with the progression of HIV disease and the state of immune competency. Oral candida is a surrogate predictor for the development of AIDS and subsequent opportunistic infections. Oral candidiasis may take 2 forms:
· Pseudomembranous candidiasis, which appears as white velvet plaques, or spots on the oral mucosa, which can be wiped 'clean' usually revealing an erythematous base. The adjacent mucosa is often normal in colour and texture. With immunocompromise, the pseudomembranous candidiasis is often more extensive and appears thicker than candidiasis in the immunocompetent.
· Erythematous candidiasis was formally known as atrophic candidiasis and appears as red lesions, most commonly affecting the dorsum of the tongue and the palate. Erythematous candidiasis may mimic denture stomatitis and is characterised by a pin point erythematous patches or confluent areas of erythema.
Both pseudomembranous and erythematous candidiasis may occur simultaneously and there has been discussion whether pseudomembranous candidiasis is a pre-cursor of erythematous candidiasis or vice versa. The diagnosis of oral candidiasis is made on clinical appearance and the use of microscopy and culture from swabs to determine the species of candidia and antifungal sensitivities, although most are sensitive to fluconazole. Oral candida may also manifest as angular cheilitis or exfoliative cheilitis and both these lesions are commonly observed in up to 70% of HIV positive patients.
Deep mycosis: cryptococosis and histoplasmosis
Deep mycoses may cause orofacial lesions and appear as ulceration, although the number of publications of both these infections have been relatively small. Oral cryptococcosis may present as non-healing extraction wounds or chronic ulceration of the palate or maxillary gingiva or tongue. Cases of Penicillinosis have been reported but mainly from North Thailand (2) and clinically these lesions appear as multiple ulceration, often involving the palate. Aspergillosis involving the orofacial region, mainly affecting the maxillary sinus, has been described (3). The recommended treatment for deep-seated mycosis is similar to systemic mycosis using Amphotericin or Itraconazole.
Bacterial infections mainly involve the gingival and peri-orodontal structures and 3 main conditions are recognised, linear gingival erythema, necrotising ulcerative gingivitis and necrotising ulcerative periodontitis.
Linear gingival erythema appears as band shaped or punctate erythema and is characterised by distinctive erythema of the free and attached gingivae and alveolar mucosa, which may bleed spontaneously. Plaque accumulation is minimal. Lineal gingival erythema is resistant to local treatment measures.
Necrotising ulcerative gingivitis appears as red and swollen gingivae with marginal areas of necrosis and loss of interdental papillae. Rapid progression is common and has been reported as having a prevalence of 5 to 11% (4) and correlates with depleted CD4 counts. Borellia and other spirochetes, gram-positive cocci, haemolytic streptococci and candida albicans may be found on bacteriological swabbing.
Necrotising ulcerative periodontitis in patients with HIV presents with progressive, rapidly developing periodontitis with soft tissue loss and bone destruction and has a prevalence of approximately 5% or less. Patients are more likely to have a CD4 count of below 200 and it may progress to necrotising stomatitis or even noma. Usual oral organisms are found and occasionally atypical organisms such as pseudomonas, enteric rods and non-oral bacteria have been isolated.
Occasionally other bacteria may present as oral ulceration such as mycobacterium avium intracellularae, mycobacterium tuberculosis, E.coli, actinomyces, Klebsiella and pseudomonas. Oral bacillary angiomatosis caused by a Rochalimaea henselae has been described in a small number of cases.
Viral infections
Viral infections of the oral cavity are common in HIV disease and infections with human herpes virus and human papilloma virus are most common. Herpes simplex virus (HSV) 1 and 2, Varicella-zoster virus (VZV), Epstein Barr virus (EBV), cytomegalovirus (CMV) and Kaposi's sarcoma human herpes virus (KSV8/HHV8) infections are reasonably frequent.
Herpes Simplex Virus 1 in 2
The phenomenon of viral shedding into the oral cavity is common in immunocompromised individuals and most of the oral and peri-oral lesions in HIV are caused by herpes simplex virus-1 although some may be herpes simplex virus-2. Co-infections with CMV and EBV has been described but HSV alone is mainly responsible for primary and recurrent oral ulceration. Primary herpetic gingivostomatitis is uncommon and most disease is due to HSV reactivation.
Varicella-Zoster Virus infection results in varicella as primary infection, or herpes zoster as reactivation. Recurrent herpes zoster usually indicates a poor prognosis in HIV infection and involvement of the cranial nerves; particularly the trigeminal nerve is reasonably common. Oral and facial lesions present unilaterally with vesicles or ulcers in the oral mucosa or skin in the corresponding branches of the trigeminal nerve. Lesions are extremely painful and have involvement of the alveolar bone and osteonecrosis may occur.
Epstein Barr Virus (oral hairy leukoplakia)
Oral hairy leukoplakia is an oral mucosal lesion occurring in immunocompromised individuals and occurs in about 25% of patients with HIV and marked immunocompromise (figure 2). Oral hairy leukoplakia is most frequently seen in the lateral border of the tongue and appears as vertical white striations, corrugations, flat or raised plaques with hair-like keratin projections. Most frequently it is bilateral and asymptomatic. Oral hairy leukoplakia is not pre-cancerous.
Cytomegalovirus Virus reactivation commonly found in HIV sero-positive patients and up to 90% of patients with AIDS develop CMV pathology during the course of their disease. Oral ulceration appears as punched out lesions, which are very painful.
The appearance of oral ulceration is non-specific and the diagnosis in most cases can only be truly established histologically, finding cytomegalovirus inclusion bodies.
Kaposi's Sarcoma Virus 8
Human herpes virus 8 has been observed in 12 to 20% of patients with AIDS and is most frequently encountered in homosexual AIDS patients. Oral Kaposi’s sarcoma lesions appear as erythematous, slightly bluish to brownish macules or nodules on the palate, gingivae or tongue. Single or multiple lesions may occur with symmetrical distribution of lesions.
Human Papilloma Virus
Patients with HIV infection can develop multiple papillomatous lesions in the oral mucosa of 3 types; verruca vulgaris, condyloma acuminatum and focal epithelial hyperplasia. Oral lesions secondary to human papilloma virus occur in up to 10% of patients with HIV. Therapy consists of surgical excision or laser surgery but recurrences are common.
Molluscum Contagiosum
Molluscum contagiosum also affect perioral, or rarely, soft tissue oral tissues.
Oral infections since the introduction of highly active anti-retroviral therapy (HAART)
Since the introduction of highly active antiretroviral therapy (HAART) the prevalence of HIV oral disease has declined and oral candidiasis, herpes simplex, Kaposi’s sarcoma and periodontal disease is less commonly seen. However, parotid enlargement has been reported to have increased from zero to up to 5% (5,6) and there has also has been an increase in the prevalence of oral warts and human papilloma virus lesions. There has also been an increase in salivary gland disease. The reason for this is not clear and although some have interpreted these results as a possible complication of HAART the truer reason may be more complicated than this.
FIGURES
Figure 1: Oral candidiasis with angular cheilitis
Figure2: Oral hairy leukoplakia
References:
Samaranayake (1992) Oral mycoses in HIV infection. Oral Surg Oral Med Pathol 73:171-180.
Nittayananta W (1995) Penicilliosis marneffei: another AIDS defining illness in South East Asia. Oral Dis 5:286-293.
Scully C, de Almedida OP, Sposto MR (1997) The deep mycoses in HIV infection. Oral Dis 3 (suppl I): S200-207
Ceballos-Salobrena A, Gaitan-Cepeda LA,Ceballos-Garcia L, Lezma-Del Valle D (2000)Oral lesions in HIV/AIDS patients undergoing highly active anti-retroviral treatment including protease inhibitors: a new face of oral AIDS? AIDS Patient Care and STDs 14: 627-635.
Patton LL, McKaig R, Strauss R, et al (2000) Changing prevalence of oral manifestations of human immunodeficiency virus in the era of protease inhibitor therapy. Oral Surg Oral Med Oral Pathol Oral Radio Endod 89: 299-304.
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