[STDs] Atlas of Human Immunodeficiency Virus Infection

These are the images, diagnosis and treatment of cases the disease caused by Human Immunodeficiency Virus Infection. This is a Viral Sexually Transmitted Diseases.

Human Immunodeficiency Virus Infection

The acquired immunodeficiency syndrome (AIDS) is by far the most important STD of all time, responsible for substantially more morbidity and loss of life than syphilis in its heyday. The causative agents, human immunodeficiency virus (HIV) types 1 and 2, are transmitted by intimate exposure to blood as well as to sexual and certain other body secretions, and sexual activity is the main transmission route worldwide. HIV-1 is the predominant virus type worldwide and is responsible for almost all infections diagnosed in the United States and most industrialized countries. To date HIV-2 infections are limited to endemic areas and a few cases imported from those areas.

Particular sexual practices have variable HIV transmission efficiencies. Vaginal intercourse is the dominant route of transmission globally, but not the most efficient mode. Sexual transmission efficiency is highest by anal intercourse, largely explaining the high rates of HIV/AIDS in men who have sex with men (MSM). Transmission by blood exchange through illicit drug use, with shared injection equipment, contributes variably to HIV transmission in different populations. Mother-to-child transmission of HIV during labor and delivery and postnatally through nursing explains most infections in young children. Nosocomial transmission to health workers, primarily though injury with contaminated sharp instruments, is inefficient and infrequent. Transmission by transfusion and organ transplantation now is rare worldwide, owing to routine, universal testing of donors. Universal testing of pregnant women, combined with antiretroviral (ARV) therapy of infants born to infected mothers, has greatly curtailed perinatal transmission in industrialized countries and is beginning to have substantial impact in many developing countries.

All inflammatory STDs are associated with enhanced efficiency of HIV acquisition in exposed persons, increased transmission of HIV by dually infected individuals, or both. Noninflammatory STDs like bacterial vaginosis and human papillomavirus infection also may increase HIV transmission risk. Owing to the high prevalence of infection with herpes simplex virus type 2 (HSV-2) in most populations, HSV-2 has the greatest population-level influence of all STDs on HIV transmission, and in some populations up to half of 157 Human Immunodeficiency Virus Infection 11

all HIV transmission events may be attributable to HSV-2. HSV-1 infection, whether oral or genital, apparently has little if any influence on HIV risk. These associations imply that treatment of STDs might blunt the spread of HIV, but that concept has been difficult to prove. In large randomized controlled trials, suppressive treatment of HSV-2 infected persons with acyclovir did not reduce the incidence of HIV and, with one exception, several trials of treatment for bacterial STDs had no demonstrable effect on HIV transmission. Nonetheless, HIV shedding and susceptibility clearly are enhanced by many STDs, and HIV viral load in genital secretions falls dramatically following treatment of gonorrhea, genital herpes, and other STDs. Notwithstanding the clinical trial results, it remains likely that treatment of STD does indeed reduce individual patients’ risk of acquiring or transmitting HIV, and successful prevention of STDs probably helps limit the spread of HIV.

Male circumcision also is an important factor in heterosexual transmission of HIV, and three large randomized controlled trials in southern Africa documented about a 50% reduction in incident HIV infections following circumcision of sexually active adult men. However, the fraction of HIV infections attributable to circumcision status is highly variable in different populations, and the importance of either adult or routine infant circumcision for HIV prevention in industrialized countries is unknown. Behavioral factors that operate at both individual and population levels, such as number of sex partners and especially rates of concurrency (overlapping partnerships) in sex partner networks, are among the most important determinants of HIV spread (see Chap. 1). Wide variations in these factors, combined with differences in STD rates and the frequency of routine male circumcision, are the primary reasons for the widely divergent rates of heterosexually transmitted HIV infection between countries, regions, and populations.

Clinicians who provide STD care should be prepared to recognize the common signs and symptoms of HIV infection and AIDS, and should provide serological screening and diagnostic testing for HIV infection. Routine HIV screening, with opt-out consent and without required pre-test risk assessment or counseling, is recommended in the United States by the Centers for Disease Control and Prevention (CDC) for all 13- to 64-year-old persons obtaining health care for any reason, and similar strategies likely would bring enhanced prevention benefits in most countries. All clinicians providing STD services should be prepared to provide postexposure prophylaxis with antiretroviral drugs when patients present following exposures with high risk of HIV transmission, and to either provide comprehensive management for HIV infected persons or to have an established referral plan for their infected patients. It is beyond the scope of this book to review all aspects of HIV infection or to address the increasingly complex therapeutic aspects of HIV/AIDS and opportunistic diseases. Rather, the focus is on the epidemiology of HIV infection, prevention, and the recognition of HIV infection and AIDS. The emphasis is on the United States, but the information is applicable to most industrialized countries. 

11–1. Clinical manifestations in a patient with AIDS. a. Facial seborrheic dermatitis; there is also a
lesion of molluscum contagiosum below the right eye. b. Oral candidiasis of soft palate. c. Hairy leukoplakia of tongue.  

CASE 1

Patient Profile Age 33, gay male roofer

History Intermittent fever for 6 months, 15-lb weight loss; skin rash of face for 2 months; sore throat for 2 weeks; occasional unprotected sex with anonymous partners; repeatedly declined HIV testing over preceding decade (“I just didn’t want to know”) 

Examination Erythematous facial rash with fine scale, involving forehead, nasolabial areas, and cheeks; umbilicated papular lesion below right eye; patchy white exudate on soft palate; hypertrophic striae of lateral aspects of tongue 

Laboratory HIV antibody positive by EIA, confirmed by Western blot; VDRL negative; rectal tests for N. gonorrhoeae and C. trachomatis negative; hematocrit 34%, WBC 4,600 per mm3 with reduced lymphocytes; CD4 lymphocyte count 122 per mm3; plasma HIV-1 viral load 188,000 per mm3; oral swab showed yeasts and pseudohyphae microscopically

Diagnosis HIV infection, stage 3 (AIDS) with oral candidiasis, oral hairy leukoplakia, seborrheic dermatitis, and facial molluscum contagiosum

Treatment ARV therapy initiated with indinavir, zidovudine, and didanosine; oral fluconazole; topical ketoconazole; molluscum contagiosum lesions treated with liquid nitrogen cryotherapy; trimethoprim/sulfamethoxazole prophylaxis against Pneumocystis jiroveci pneumonia; pneumococcal and influenza immunizations

Comment After 4 months, the patient was asymptomatic, had regained his lost weight, and the seborrheic dermatitis and thrush had resolved. The CD4 lymphocyte count was 290 cells per mm3 and the plasma HIV viral load was 5,000 per mm3. Trimethoprim/suflamethoxazole was discontinued. 

11–2. Primary HIV infection, with poorly demarcated erythematous macules and
papules of the neck and upper trunk  

CASE 2

Patient Profile Age 24, unemployed gay man

History Sore throat, fever, and skin rash for 5 days; onset 10 days after unprotected receptive anal sex with unknown partner in a bath house

Examination Oral temperature 38.3°C; pharyngeal erythema, prominent tonsils with white exudate in crypts; cervical and axillary lymphadenopathy with 1–2 cm, slightly tender nodes; nonblanching maculopapular rash of upper trunk, neck, shoulders

Laboratory HIV antibody test negative; plasma p24 antigen and NAAT positive for HIV-1 RNA, 62,000 copies per mm3; hematocrit 36%, leukocyte count 7,600 per mm3 with 48% lymphocytes, platelet count 84,000 per mm3; CD4 lymphocyte count 322 per mm3; VDRL (negative); rectal NAAT for N. gonorrhoeae (positive) and C. trachomatis (negative); throat culture negative for Streptococcus pyogenes and N. gonorrhoeae

Diagnosis Primary HIV infection (CDC stage 1), subsequently stabilizing at stage 1; rectal gonorrhea

Treatment Patient declined antiretroviral therapy; ceftriaxone 250 mg IM, azithromycin 1.0 g PO 

Comment Typical primary HIV infection syndrome, mimicking infectious mononucleosis with thrombocytopenia; HIV antibody test was positive 2 weeks later; fever, rash, and pharyngitis resolved

over 2 weeks; clinical status stabilized to CDC stage 2 over 3 months: lymphadenopathy resolved, differential leukocyte count returned to normal, thrombocytopenia resolved, CD4 lymphocyte count was 665 per mm3, and plasma HIV-1 viral load 5,500 copies per mm3

11–3. Generalized maculopapular rash in primary HIV infection. 

11–4. Chronic herpes due to HSV-2 in HIV-infected patients. a. Extensive perianal ulceration
due to HSV-2; such lesions can be very debilitating due to pain. (Courtesy of Steven J. Medwell, M.D.) b. Chronic facial ulcers, atypically due to HSV-1.  

11–5. Macular Kaposi sarcoma lesion of the forearm in a patient with AIDS. Kaposi sarcoma
lesions usually are nodular (see Fig. 11–6), with violaceous or brown color due to vascular proliferation and hemosiderin deposition, but the appearance is highly variable. Kaposi sarcoma is
caused by human herpesvirus type 8 (HHV-8)  

11–6. Nodular Kaposi sarcoma skin lesions of the foot in a man with AIDS. Similar lesions
were widely distributed, especially on the trunk, and were the first recognized manifestation of
the patient’s HIV infection. The lesions regressed with ART  

11–7. Kaposi sarcoma of the palate in AIDS. Kaposi sarcoma often presents with
oral lesions.  

11–8. Gingivitis in AIDS. Gum retraction and gingivitis are common oral findings
in HIV infection.  

11–9. Oral candidiasis in AIDS; not all cases present with white patchy exudate typical of thrush (see Fig. 11–1b). a. Erythematous candidiasis of tongue. b. Erythematous and pseudomembranous candidiasis of tongue. c. Angular cheilitis due to Candida albicans.  

11–10.  ; early lesions mimic premalignant leukoplakia and may lack the prominent linear pattern seen in advanced cases (compare with Fig. 11–1c). Hairy leukoplakia is a manifestation of Epstein-Barr virus infection and often responds to therapy with high-dose valacyclovir or famciclovir  

11–11. AIDS-related ichthyosis. HIV-infected persons with advanced immunodeficiency often
complain of dry skin and generalized pruritus, with evidence of dyshidrosis. Advanced cases present with overt ichthyosis, with dry, raspy skin, fine scale, and hyperpigmentation.  

11–12. Molluscum contagiosum of the cheek in a patient with AIDS. Facial molluscum or warts
may result from recrudescence of latent infection, perhaps dating to childhood, due to cellular
immunodeficiency

11–13. Herpes zoster (shingles) in a patient with CDC stage 2 HIV infection 

(CD4+ lymphocyte count 320 cells per mm3).  

  

11–14. Advanced seborrheic dermatitis in a patient with AIDS. Seborrheic dermatitis occasionally is sufficiently severe to suggest herpes zoster. This case resolved promptly with topical ketoconazole therapy.

REFERENCES

H. Hunter Handsfield, MD, Color Atlas & Synopsis of Sexually Transmitted Diseases, Third Edition.