Prospective Monitoring

The CD4⁺ T-cell count is a valuable marker to determine when patients are at increased risk for development of a specific opportunistic infection.^26–32 For example, P. jirovecii pneumonia (PCP) occurs rarely in patients who have CD4⁺ T-cell counts greater than 200 to 250 cells/mm^{3 8,26–28} and disseminated MAC occurs rarely in patients with counts greater than 50 cells/mm³.^8,32,33 This information is helpful for focusing a diagnostic evaluation. If a patient with a CD4⁺ T-cell count of 700 cells/mm³ develops cough, fever, and diffuse interstitial pulmonary infiltrates, for instance, the likelihood that this syndrome is caused by PCP is extremely low (but not zero). Therefore, sputum examination for Pneumocystis is not initially indicated, and most attention, when processing respiratory secretions and choosing empirical therapy, should be directed at common bacterial and viral pathogens. In contrast, if the CD4⁺ T-cell count were 25 cells/mm³ in the same patient, the search for Pneumocystis in sputum or bronchoalveolar lavage would be an important focus because PCP is so common in this patient population.^26,27 If a patient with HIV develops chronic fever and weight loss without focal findings, disseminated Mycobacterium avium complex becomes a more important consideration if the CD4⁺ T-cell count is less than 50 cells/mm³ than if the CD4⁺ T-cell count is more than 300 cells/mm³, in which case tuberculosis, endemic mycoses, or an HIV-related malignant neoplasm would be more appropriate considerations.

Although CD4⁺ T-cell counts provide a useful estimate of susceptibility to infections, they are not perfect predictive tools. For example, although more than 90% of cases of PCP occur in patients with CD4⁺ T-cell counts less than 200 cells/mm³, some cases occur in patients with counts in the range of 200 to 300 cells/mm³ and a few occur in those with counts greater than 300 cells/mm³.^26–34 When the most recent CD4⁺ T-cell count was obtained many months before the patient’s presentation, it may be difficult to judge the patient’s current immune status.

A frequent concern has been that CD4⁺ T-cell counts in patients receiving ART may not accurately reflect the clinical susceptibility to opportunistic infections. Evaluation of several large databases demonstrated that ART does not alter the relationship between CD4⁺ T-cell counts and the occurrence of opportunistic infections in any substantial manner, regardless of how low the nadir CD4⁺ T-cell count was before initiation of ART.³⁵

CD4⁺ T-cell counts are not the only laboratory predictors of opportunistic infection. HIV viral load in the peripheral blood is an independent predictor: with each log increase in titer, the likelihood of occurrence of an opportunistic infection increases.^35,36–38 Furthermore, at a given CD4⁺ T-cell count, patients with viral loads that are below the level of assay detection (e.g., <50 copies/µL) are at far less risk for developing an opportunistic infection than patients with detectable viral loads.³⁶

Cytomegalovirus (CMV) viral load is also an independent predictor of the occurrence of AIDS-defining events, although CMV viral loads are currently used only for diagnosis of acute CMV disease in this patient population.^39,40

Specific skin, blood, or urine tests for individual pathogens are also useful predictors for the occurrence (or relapse) of opportunistic infections. Such tests include the purified protein derivative (PPD) skin test, the interferon-γ release assay (IGRA) for tuberculosis (TB), and antibody tests for varicella-zoster virus (VZV), CMV, herpes simplex virus (HSV), Toxoplasma, HBV and HCV, Treponema pallidum, or Coccidioides. These tests indicate whether patients have been previously infected with specific organisms, and might, therefore, reactivate latent infection. Specific antigen tests or nucleic acid amplification tests such as cryptococcal antigen test, Histoplasma antigen, HCV polymerase chain reaction (PCR) assay, HBV PCR assay, or CMV PCR assay are used to assess the presence of active disease.^41–44

Clinical findings can be useful predictors of opportunistic infection susceptibility to supplement the information derived from CD4⁺ T-cell counts and HIV viral loads. For example, the development of otherwise unexplained oropharyngeal candidiasis or oral hairy leukoplakia, wasting, or any type of pneumonia is an indicator of current susceptibility to PCP or other opportunistic infections.⁸ Such findings indicate a need to consider prophylaxis, independent of the CD4⁺ T-cell count and the HIV viral load.⁸

Spectrum of Opportunistic Pathogens

Many of the opportunistic diseases that characterize HIV-induced immunosuppression occur in patients with HIV infection much more frequently than in almost any other patient group. For example, without prophylaxis or effective ART, PCP ultimately develops in at least 80% of HIV-infected patients in North America.^8,27 The annual attack rate for patients with CD4⁺ T-cell counts less than 100 cells/mm³ is about twice that for patients with severe combined immunodeficiency syndrome and more than 10 times the rate for patients with organ transplantations, solid tumors, or most hematologic malignant neoplasms.⁴⁵ Disseminated MAC was rarely recognized in humans before the advent of HIV infection, yet it occurred in 30% to 50% of patients with advanced HIV infection in North America before ART and specific chemoprophylaxis became standard of care.^32,33,46

Cerebral toxoplasmosis, chronic cryptosporidiosis, microsporidiosis, and Kaposi sarcoma are examples of other processes that only rarely occur in patients other than those with HIV infection. Indeed, their presence should strongly suggest that HIV testing be performed.

Environmental exposure is an important determinant of the complications of HIV infection. Some pathogens are ubiquitous, so that many patients have colonization or latent infection before they develop HIV infection, such as Candida, HSV type 1 (HSV-1), or CMV. Other pathogens occur only because of specific, geographically related exposure. These exposures may be respiratory (e.g., TB, endemic mycoses, and Pneumocystis), enteric (e.g., Salmonella, Cryptosporidium, and Microsporidium), vector borne (e.g., Leishmania, Bartonella, trypanosomes), contact mediated (e.g., methicillin-resistant Staphylococcus aureus [MRSA]), or sexual (e.g., HSV type 2 [HSV-2], human herpesvirus 8 [HHV-8], Treponema pallidum).^8,47–56

Traditionally, most HIV-associated opportunistic infections were thought to be caused by reactivation of latent infection, but this conclusion was based primarily on speculation rather than data. Some episodes of opportunistic infection in adults clearly represent primary infection rather than reactivation. For some patients, second episodes of disease, such as TB and PCP, have been caused by different strains than the initial episode, suggesting that acquisition of a new strain rather than reactivation of the initial disease-causing strain can produce acute infection. Cases of Pneumocystis and TB reinfection have been well documented.^{57–60,61–63}

Management of Antiretroviral Therapy for Patients with Acute Opportunistic Infection

If a patient who has not been on ART develops acute PCP, cryptococcal meningitis, TB, severe microsporidial diarrhea, or some other acute or severe opportunistic infection, the question often arises whether to initiate ART. Unquestionably, the immune augmentation that ART produces will ultimately be beneficial in preventing HIV-related opportunistic complications and prolonging survival.⁶⁴ However, there are complications associated with initiation of ART, which must factor into the decision about when to initiate ART. For ART-naïve patients, the initiation of ART may produce an enhanced inflammatory response (immune reactivation inflammatory syndrome [IRIS]) that can cause considerable morbidity.^{8,13–15,64–67,68} For example, a patient with cryptococcal or tuberculous meningitis may develop dangerously increased intracranial pressure if ART is initiated and the inflammatory response to meningeal organisms or antigen is enhanced.^13–15 IRIS may also unmask a site that had latent infection due to the pathogen being treated or another pathogen.^65–68 For instance, when ART is started, a patient who is being treated for PCP may develop exacerbation of the pneumonitis related to Pneumocystis organisms or could develop chorioretinitis in response to latent CMV.

Other challenges to successful initiation of ART are also prominent problems in some patients. When patients with acute opportunistic infections initiate ART, their drug pharmacokinetics may be unpredictable owing to severe diarrhea, malabsorption, or altered renal or hepatic function. Drug interactions between ART and opportunistic infection therapies may enhance serum levels of either, therefore likely enhancing toxicity. Because almost no clinical facilities have the resources to do real-time drug level monitoring for most of the agents in question, a preferable strategy may be to withhold ART until predictable drug kinetics are likely to be achieved.

Managing drug toxicities is also especially difficult when patients initiate ART at the time they have an acute opportunistic infection. For example, if rash, liver function test abnormalities, or renal dysfunction occur after ART is initiated, it can be difficult to know whether the abnormality is due to the opportunistic pathogen, the specific therapy for the opportunistic infection, or ART.

Thus, as a general principle, for patients not already receiving ART, ART should be initiated within the first 2 weeks of treatment of the opportunistic infection.^8,64 However, considerable clinical judgment is needed to determine whether the severity of the illness, the specific opportunistic infection, potential drug absorption or interaction issues, or patient readiness to take ART regularly should merit a different strategic approach.

For patients receiving ART when the opportunistic infection is diagnosed, ART should generally be continued if possible. However, as discussed earlier, drug absorption issues or potential drug interaction complexities may be sufficiently compelling that temporary ART interruption may be the best management strategy.

For some opportunistic infections, ART is the only intervention available that has the potential to ameliorate the clinical syndrome. Cryptosporidiosis, JC virus encephalitis, and certain forms of microsporidiosis have no specific therapy that is effective, and thus starting ART is the only intervention likely to resolve the infectious complication.^69–73 For patients with severe diarrhea due to cryptosporidiosis or microsporidiosis, however, drug absorption can be a major limitation to therapeutic efficacy.

Infections Due to Pathogens That are Not Opportunistic

Patients with HIV infection develop nonopportunistic as well as opportunistic infections. HIV-infected patients are as likely to acquire common, community-acquired, or hospital-acquired pathogens as HIV-uninfected patients. Therefore, if a patient with HIV infection develops a respiratory syndrome, diagnostic considerations should include influenza virus, Mycoplasma pneumoniae, and Legionella infections, although these processes may not occur with increased frequency or severity in patients with HIV infection. Similarly, patients with HIV infection can develop ventilator-associated pneumonia, intravascular access–associated bacteremia, or bacterial urinary tract infections, and such processes should not be overlooked when assessing fever or new-onset organ dysfunction.

MRSA infections, including soft tissue infections, primary bacteremia, and necrotizing pneumonia, have become frequent occurrences among HIV-infected patients.^47,48 There is no clear evidence that MRSA is an opportunistic pathogen in this population. Skin and pulmonary infections due to MRSA are not consistently documented to be more severe or more frequent than in HIV-uninfected patients with the same behavioral risk factors. However, MRSA infections are common among homosexual men and are related to sexual contact, intravenous substance use, and contact with health care facilities, all factors that are overrepresented among HIV-infected individuals.

Similarly, when HIV-infected patients develop diarrhea that persists for more than a few days, clinicians reflexively consider Salmonella, Cryptosporidium, microsporidia, and Cystoisospora (Isospora). However, Clostridium difficile, which is not clearly opportunistic, is one of the most common identified causes of bacterial diarrhea among patients with HIV infection in the United States.^74,75 Some data suggest that the severity of C. difficile disease increases with declining CD4⁺ T-cell counts, which could indicate that this is an opportunistic infection. Thus, although patients with HIV infection and low CD4⁺ T-cell counts need to be assessed for HIV-associated pathogens such as Cryptosporidium and microsporidia, nonopportunistic processes such as C. difficile or norovirus or food-borne toxins need to be considered as well.

Drug Interactions

Some drugs used for treatment or prevention of opportunistic infections can interact with each other or with other drugs such as anti­retroviral agents.⁸ Such interactions can alter the efficacy and toxicity of prescribed drugs. This most often occurs with drugs that share the same hepatic cytochrome metabolic pathway. Protease inhibitors and non-nucleoside reverse transcriptase inhibitors (NNRTIs), as well as rifampin, rifabutin, azoles, atovaquone-proguanil, and quinolones, need special attention because they are all metabolized by hepatic enzymes. For example, darunavir, ritonavir, and lopinavir-ritonavir can each increase the rifabutin area-under-the-concentration-time curve (AUC) substantially. Ritonavir decreases the AUC of voriconazole, but co-administration of voriconazole and efavirenz leads to decreased voriconazole AUC and increased efavirenz AUC.⁸

Useful tables are available in the U.S. Department of Health and Human Services Guidelines for Antiretroviral Therapy in Adolescents and Adults, as well as websites, package inserts, and published investigations of specific drug-drug interactions.⁸

General Principles of Management

The optimal approach to prevention of opportunistic infections is to initiate effective ART. As noted earlier, ART can probably never restore immune function completely to normal, and some pathogens such as Mycobacterium tuberculosis, herpes zoster, and probably Streptococcus pneumoniae will still cause more disease than in HIV-uninfected patients, even with comparable CD4⁺ T-cell counts. Although ART is now the most important method for minimizing the impact of opportunistic infections in patients with HIV infection, other strategies are effective for improving patient quality and duration of life. This is especially pertinent for patients who for some reason cannot or will not take ART, or perhaps for patients whose CD4⁺ T-cell counts have not yet risen substantially despite apparently optimal viral suppression. For the latter group, admittedly, the value of primary or secondary prophylaxis is controversial if their viral load is effectively suppressed with ART. The successful pathogen-directed management of opportunistic infections that are treatable depends on (1) primary prevention, (2) prompt diagnosis, (3) initiation of therapy early, before the clinical syndrome is severe, (4) recognition that a poor response to therapy requires reassessment of the diagnosis and treatment of the identified pathogen, and (5) lifelong suppression with secondary prophylaxis to prevent relapses or recurrences unless ART is able to substantially increase the CD4⁺ T-cell count and also suppress HIV.

Some opportunistic infections are so likely to occur in patients with AIDS that primary prevention is appropriate when the patient’s CD4⁺ T-cell count falls to a certain, pathogen-specific threshold. Thus, primary PCP chemoprophylaxis is appropriate when the CD4⁺ T-cell count decreases to 200 cells/mm³; and in North America, MAC chemoprophylaxis is appropriate when the CD4⁺ T-cell count decreases below 50 cells/mm³. Similarly, immunization with pneumococcal vaccine is appropriate regardless of CD4⁺ T-cell count, as is HBV vaccine. However, such pathogen-specific prophylaxis is only feasible for certain pathogens in terms of having a regimen that is effective, well tolerated, convenient to take, and economically feasible.

Some opportunistic infections are so likely to recur that secondary prophylaxis is appropriate to prevent a relapse or recurrence. Such infections include PCP, toxoplasmosis, cryptococcosis, infection with MAC, and cytomegalovirus (CMV) infection.

The manifestations and natural history of specific processes such as PCP, toxoplasmosis, cryptococcosis, or CMV infection are different in patients with HIV compared with other causes of immunosuppression.^8,76–80 For instance, PCP is characteristically more subacute in patients with HIV infection than in organ transplant recipients.⁷⁶ CMV infection in patients with HIV infection characteristically causes retinitis or colitis, whereas CMV infection in cancer patients or transplant recipients more characteristically causes pneumonia or colitis. Toxoplasmosis is more likely to cause encephalitis in patients with HIV infection, whereas it more often manifests as disseminated disease in other immunosuppressed populations.⁷⁹ Each of these infections is much more likely to relapse in patients with untreated HIV infection than in other immunocompromised populations, perhaps because the immunosuppression is more prolonged and progressive.

Establishing a diagnosis of AIDS-related opportunistic infections is also associated with some important differences from other immunosuppressed populations. The detection of CMV in the oral secretions, bronchoalveolar lavage, or blood has little positive predictive value in patients with HIV infection, even at low CD4⁺ T-cell counts. In contrast, the detection of CMV by culture or PCR assay in the serum or bronchoalveolar lavage from a recent stem cell transplant recipient, particularly at high copy number, has important prognostic implications. Similarly, evaluating a prolonged fever in a patient with HIV infection and low CD4⁺ T-cell counts warrants blood cultures for Mycobacterium and perhaps Bartonella, and a serum cryptococcal antigen test, but such tests would have very low yield in other patient populations.

When choosing chemotherapeutic agents for opportunistic infection treatment or prevention, drug intolerances are special considerations. Trimethoprim-sulfamethoxazole (TMP-SMX) is associated with considerably more adverse reactions in patients with HIV infection than in any other patient population.^8,76,78 The reasons for this are not clear. Multiple drugs may have overlapping toxicities, such as bone marrow suppression (valganciclovir, TMP-SMX, pyrimethamine, zidovudine), renal dysfunction (amphotericin B, tenofovir, pentamidine, cidofovir), or liver dysfunction (protease inhibitors, NNRTIs, azoles, TMP-SMX, isoniazid, rifampin). As noted earlier, drug inter­actions are a special concern given the multiplicity of prescription and nonprescription drugs directed against opportunistic infections, HIV infection, and other disorders associated with aging or metabolic abnormalities. Such interactions can reduce drug efficacy or augment drug toxicity.

An issue that frequently arises is whether to use immediate empirical antimicrobial regimens or to withhold therapy until a specific diagnosis is established by invasive techniques. There are clearly urgent situations in which empirical therapy is prudent while diagnostic tests are organized and performed, with the plan to alter the empirical regimen when more specific information becomes available. In addition, there may be situations in which the diagnosis is so predictable (e.g., retinitis with hemorrhage and exudates in patient with a CD4⁺ T-cell counts <50 cells/mm³ or a cerebral mass lesion in a patient who is Toxoplasma IgG positive and has a CD4⁺ T-cell count <50 cells/mm³ or a patient with dysphagia, oral candidiasis, and a CD4⁺ T-cell count <50 cells/mm³) that expensive or invasive diagnostic tests are not mandatory if the patient responds as expected to empirical therapy.

Most AIDS-related opportunistic infections will relapse within weeks or months after acute therapy is stopped if effective ART cannot be initiated and maintained.⁸ Experience during the first decade of AIDS clearly documented that, for example, PCP, toxoplasmosis, cryptococcosis, disseminated MAC infection, and CMV retinitis would relapse if chronic suppressive pathogen-specific therapy were not maintained lifelong. For a few opportunistic infections, such as mucosal candidiasis, herpes simplex infections, and herpes zoster infections, such secondary prophylaxis was not believed to be indicated because the disease was not life threatening, recurrences could be easily treated, and pill burden, cost, drug toxicity, and potential drug interactions appeared to outweigh the small potential benefit.

Patients who respond to ART, as manifested by sustained increases in CD4⁺ T-cell counts, are very unlikely to experience opportunistic infection relapse, and thus do not need to receive prolonged secondary prophyalaxis.^{81–86,87,88} There are sufficient data to recommend that for patients who have raised CD4⁺ T-cell counts above the thresholds suggested in well-established, evidence-based guidelines,⁸ primary prophylaxis (preventing a first episode of disease) or secondary prophylaxis (preventing relapse or recurrence) can be discontinued. Prophylaxis should be restarted if the CD4⁺ T-cell count subsequently falls below the threshold indicated in the guidelines.⁸

If patients have an appropriate virologic response to ART, but their CD4⁺ T-cell count fails to rise substantially, they are probably at low risk for opportunistic infection.³⁶ However, the cautious approach would be to provide primary and secondary prophylaxis until their CD4⁺ T-cell count rises above indicated threshold levels, realizing those rises may never occur in some patients.

If a patient develops an opportunistic infection at an uncharacteristically high CD4⁺ T-cell count (e.g., if PCP occurs at CD4⁺ T-cell counts above 200 cells/mm³, or disseminated MAC occurs at CD4⁺ T-cell counts above 100 cells/mm³), it is probably prudent to manage primary and secondary prophylactic regimens as if the CD4⁺ T-cell count were low.³⁵ Tables 131-1 through 131-3 summarize current recommendations from the National Institutes of Health, Centers for Disease Control and Prevention, and Infectious Diseases Society of America for prophylaxis to prevent first episodes (Table 131-1); to treat acute opportunistic infections (Table 131-2); and to start, discontinue, and restart prophylaxis (Table 131-3).

TABLE 131-1

Prophylaxis to Prevent First Episode of Opportunistic Disease

OPPORTUNISTIC INFECTIONS	INDICATION	PREFERRED	ALTERNATIVE
Pneumocystis pneumonia (PCP)	CD4 count <200 cells/mm3, or oropharyngeal candidiasis, or CD4 <14%, or history of AIDS-defining illness, or CD4 count >200 but <250 cells/mm3 if monitoring CD4 cell count every 3 mo is not possible Note: Patients who are receiving pyrimethamine-sulfadiazine for treatment or suppression of toxoplasmosis do not require additional PCP prophylaxis.	TMP-SMX 1 DS tablet PO daily, or TMP-SMX 1 SS tablet PO daily	TMP-SMX 1 DS tablet PO three times a week, or Dapsone 100 mg PO daily or 50 mg PO bid, or Dapsone 50 mg PO daily + pyrimethamine 50 mg + leucovorin 25 mg PO weekly, or Dapsone 200 mg + pyrimethamine 75 mg + leucovorin 25 mg PO weekly; or Aerosolized pentamidine 300 mg via Respirgard II nebulizer every month, or Atovaquone 1500 mg PO daily, or Atovaquone 1500 mg + pyrimethamine 25 mg + leucovorin 10 mg PO daily
Toxoplasma gondii encephalitis	Toxoplasma IgG-positive patients with CD4 count <100 cells/mm3 Seronegative patients receiving PCP prophylaxis not active against toxoplasmosis should have Toxoplasma serology retested if CD4 count declines to <100 cells/mm3. Prophylaxis should be initiated if seroconversion occurred. Note: All regimens recommended for primary prophylaxis against toxoplasmosis are also effective as PCP prophylaxis.	TMP-SMX 1 DS tablet PO daily	TMP-SMX 1 DS tablet PO three times a week, or TMP-SMX 1 SS tablet PO daily, or Dapsone 50 mg PO daily + pyrimethamine 50 mg + leucovorin 25 mg PO weekly, or Dapsone 200 mg + pyrimethamine 75 mg + leucovorin 25 mg PO weekly; or Atovaquone 1500 mg PO daily; or Atovaquone 1500 mg + pyrimethamine 25 mg + leucovorin 10 mg PO daily
Mycobacterium tuberculosis infection (i.e., treatment of LTBI)	Positive screening test for LTBI, with no evidence of active TB, and no prior treatment for active TB or LTBI, or Close contact with a person with infectious TB, with no evidence of active TB, regardless of screening test results.	INH 300 mg + pyridoxine 25 mg PO daily × 9 mo, or INH 900 mg PO twice weekly (by DOT) + pyridoxine 25 mg PO daily × 9 mo.	Rifampin 600 mg PO daily × 4 mo, or Rifabutin (dose adjusted based on concomitant ART) × 4 mo. For persons exposed to drug-resistant TB, select anti-TB drugs after consultation with experts or public health authorities.
Disseminated Mycobacterium avium complex (MAC) disease	CD4 count <50 cells/mm3 after ruling out active disseminated MAC disease based on clinical assessment.	Azithromycin 1200 mg PO once weekly, or Clarithromycin 500 mg PO bid, or Azithromycin 600 mg PO twice weekly	Rifabutin (dose adjusted based on concomitant ART); rule out active TB before starting rifabutin.
Streptococcus pneumoniae infection	For individuals who have not received any pneumococcal vaccine, regardless of CD4 count, followed by: if CD4 count ≥200 cells/mm3 if CD4 count <200 cells/mm3	PCV13 0.5 mL IM × 1. PPV23 0.5 mL IM at least 8 wk after the PCV13 vaccine. PPV23 can be offered at least 8 wk after receiving PCV13 or can wait until CD4 count increased to >200 cells/mm3.	PPV23 0.5 mL IM × 1
	For individuals who have previously received PPV23	One dose of PCV13 should be given at least 1 yr after the last receipt of PPV23.
	Revaccination: If age 19-64 yr and ≥5 yr since the first PPV23 dose If age ≥65 yr, and if ≥5 yr since the previous PPV23 dose	PPV23 0.5 mL IM × 1 PPV23 0.5 mL IM × 1
	All HIV-infected patients	Inactivated influenza vaccine annually (per recommendation for the season) Live-attenuated influenza vaccine is contraindicated in HIV-infected patients.
Histoplasma capsulatum infection	CD4 count ≤150 cells/mm3and at high risk because of occupational exposure or live in a community with a hyperendemic rate of histoplasmosis (>10 cases/100 patient-years)	Itraconazole 200 mg PO daily
Coccidioidomycosis	A new positive IgM or IgG serologic test in patients who live in a disease-endemic area and with CD4 count <250 cells/mm3	Fluconazole 400 mg PO daily
Varicella-zoster virus	Preexposure prevention: Patients with CD4 counts ≥200 cells/mm3 who have not been vaccinated, have no history of varicella or herpes zoster, or who are seronegative for VZV Note: Routine VZV serologic testing in HIV-infected adults and adolescents is not recommended.	Preexposure prevention: Primary varicella vaccination (Varivax), two doses (0.5 mL SQ each) administered 3 mo apart. If vaccination results in disease because of vaccine virus, treatment with acyclovir is recommended.	Preexposure prevention: VZV-susceptible household contacts of susceptible HIV-infected persons should be vaccinated to prevent potential transmission of VZV to their HIV-infected contacts.
	Postexposure prevention: Close contact with a person with chickenpox or herpes zoster and is susceptible (i.e., no history of vaccination or of either condition, or known to be VZV seronegative)	Postexposure prevention: Varicella-zoster immune globulin (VariZIG) 125 IU/10 kg (maximum 625 IU) IM, administered as soon as possible and within 10 days after exposure. Note: VariZIG is available through Cangene, Canada. Individuals receiving monthly high-dose IVIG (>400 mg/kg) are likely to be protected if the last dose of IVIG was administered <3 wk before exposure.	Alternative postexposure prevention: Acyclovir 800 mg PO five times a day for 5-7 days, or Valacyclovir 1 g PO tid for 5-7 days These alternatives have not been studied in the HIV population. If antiviral therapy is used, varicella vaccines should not be given until at least 72 hr after the last dose of the antiviral drug.
Hepatitis A virus (HAV) infection	HAV-susceptible patients with chronic liver disease or who are injection drug users or MSM.	Hepatitis A vaccine 1 mL IM × two doses at 0 and 6-12 mo. IgG antibody response should be assessed 1 mo after vaccination; nonresponders should be revaccinated when CD4 count >200 cells/mm3.	For patients susceptible to both HAV and hepatitis B virus (HBV) infection (see below): Combined HAV and HBV vaccine (Twinrix), 1 mL IM as a three-dose (0, 1, and 6 mo) or four-dose series (days 0, 7, 21 to 30 and at 12 mo)
Hepatitis B virus (HBV) infection	Vaccine nonresponders: Anti-HBs <10 IU/mL 1 mo after vaccination series For patients with low CD4 counts at time of first vaccine series, some specialists might delay revaccination until after sustained increase in CD4 count with ART.	Revaccinate with a second vaccine series	Some experts recommend revaccinating with 40-µg doses of either HBV vaccine.

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