We are dealing with a patient with HIV infection in a situation of severe immunosuppression (<50 CD4+) and a very high viral load, who has followed the expected evolution from the immunovirological point of view after the start of treatment (after 12 weeks, the viral load has ostensibly decreased - answer 2 would not be correct, remember that it is desirable that it becomes negative 24 weeks after the start of treatment, although in patients with higher CV like ours, it could take longer - and the CD4+ count has begun to rise). A negative Mantoux test does not rule out tuberculosis (incorrect answer 4), since in patients with severe immunosuppression it can give false negatives. The diagnosis of lymph node tuberculosis is immediate when detecting "isolated acid-fast bacilli and epithelioid granulomas" in the puncture of one of the lymph nodes, however: considering the patient profile, this process will have been clinically unmasked during the immunological reconstitution and the infection is not the consequence of an incomplete immunological recovery (correct answer number 3).

We are dealing with a patient with HIV infection in a situation of severe immunosuppression (<50 CD4+) and a very high viral load, who has followed the expected evolution from the immunovirological point of view after the start of treatment (after 12 weeks, the viral load has ostensibly decreased - [HIDDEN], remember that it is desirable that it becomes negative 24 weeks after the start of treatment, although in patients with higher CV like ours, it could take longer - and the CD4+ count has begun to rise). A negative Mantoux test does not rule out tuberculosis ([HIDDEN]), since in patients with severe immunosuppression it can give false negatives. The diagnosis of lymph node tuberculosis is immediate when detecting "isolated acid-fast bacilli and epithelioid granulomas" in the puncture of one of the lymph nodes, however: considering the patient profile, this process will have been clinically unmasked during the immunological reconstitution and [HIDDEN].

A 45-year-old patient was diagnosed with HIV infection three months ago, presenting at that time with CD4 45 lymphocytes/µl and an HIV-1 viral load of 500,000 copies/ml. At that time he had a negative Mantoux test. He started treatment with an integrase inhibitor and two reverse transcriptase inhibitors, and at one month he had 25,000 copies and CD4 had risen to 80/µL. She consulted for presenting a picture of cervical lymphadenopathy and fever of two weeks of evolution. The puncture of one of the lymph nodes showed isolated acid-fast bacilli and epithelioid granulomas:

It is a lymph node tuberculosis related to an incomplete immunologic recovery.

Treatment failure and it is an opportunistic infection.

This is an opportunistic infection unmasked within a picture of immune reconstitution.

A negative Mantoux test rules out tuberculosis.

Mycobacterium avium complex and Cryptococcus neoformans co-infection in a patient with acquired immunodeficiency syndrome: a case report.

Opportunistic infections (OI) are common in patients with acquired immunodeficiency syndrome (AIDS). Cryptococcus neoformans and Mycobacterium avium complex (MAC) are frequently responsible of such infections. However, concurrent infection with these two pathogens is uncommon and underreported in the literature. We describe the case of a 28-year-old Caucasian Belgian patient with no travel history, who presented with low-grade fever, headache and wasting syndrome. He was diagnosed with human immunodeficiency virus (HIV) infection at AIDS stage, with a HIV viral load of 506,000 viral copies/mL and a CD4 + T-cells count of 10 cells/µL. Diagnosis of disseminated Cryptococcus neoformans infection was made by positive serum cryptococcal antigen and positive culture for Cryptococcus neoformans in blood and in cerebrospinal fluid. Diagnosis of disseminated Mycobacterium avium complex infection was made by positive culture on a biopsy of a mediastinal lymph node. With adequate anti-retroviral therapy (ART) and treatment of these OIs, the patient recovered well and had a good clinical evolution. To our knowledge, this is the second case of coexistence of these two dangerous OIs reported in the post ART era. Clinicians should be aware that such co-infections still happen in high-income countries, in patients with severe immunodeficiency. Early detection and treatment of HIV is of paramount importance to prevent AIDS and its complications. We highlight the importance of thoroughly excluding all opportunistic infections in patients with newly diagnosed AIDS.<bAbbreviations:</b ABC: abacavir; AIDS: acquired immunodeficiency syndrome; AFB: acid-fast bacilli; ART: antiretroviral therapy; CM: cryptococcal meningitis; CrAg: cryptococcal antigen; CSF: cerebrospinal fluid; CT: computed tomography; EACS: European AIDS Clinical Society; FTC: emtricitabine; HIC: high-income countries; HIV: human immunodeficiency virus; HIV-VL: HIV-viral load; ICP: intracranial pressure; IRIS: immune reconstitution inflammatory syndrome; MAC: Mycobacterium avium complex; MRI: magnetic resonance imaging; MSM: man who has sex with men; NR: normal range; OD: omne in die = once daily; OI: opportunistic infection; RAL: raltegravir; TAF: tenofovir alafenamide fumarate.

[Skin manifestations of immune restoration syndrome in treated tuberculosis].

Immune restoration syndrome was first described in 1998 and involved mycobacterium avium complex. We report the case of a patient with acquired immunodeficiency syndrome who had disseminated cutaneous lesions due to Mycobacterium tuberculosis, following initiation of highly active antiretroviral therapy. A 42 year-old HIV-infected man, was admitted for fever, cough, nocturnal sweat and impaired of general condition. He had a viral load of 127,200 copies/ml and 199/ml CD4 T-cells. He was treated with triple tuberculosis combination therapy according to tuberculous contagium, positivity of the tuberculin intradermoreaction (15 mm) and right upper lung nodule on thoracic scan. M. tuberculosis was not found. Fever improved at day 3. Highly active antiretroviral therapy with zidovudine, lamivudine, indinavir, was started at day 11 and 33 days after, fever and dermohypodermal nodules with necrotising evolution appeared. Skin biopsy specimen showed tuberculoid granuloma. The levels of viral load and CD4 T-cells were less than 200 copies/ml and 497/ml respectively. Fever and cutaneous lesions spontaneously resolved without changing therapy. Immune restoration syndrome appears after initiation of antiretroviral therapy, in patients with advanced HIV infection and without prophylactic treatment versus MAC. This case report probably involves mycobacterium tuberculosis. Bacterial lysis and immune restoration take part in cutaneous pathogenesis. Subclinical mycobacterial infection should be monitored during initiation of antiretroviral therapy in patients with advanced HIV infection.

Development of opportunistic infections after diagnosis of active tuberculosis in HIV-infected patients.

Despite advances in highly active antiretroviral therapy (HAART), its use during tuberculosis (TB) treatment is fraught with challenges, often leading to delayed therapy. This report describes the course of HIV infection and outcomes of 26 consecutive TB/HIV coinfected patients who received TB treatment in Rhode Island. HIV infection was diagnosed in 26 (4%) of 598 TB cases in during a 10-year period. Of these patients, TB was the first indication of HIV infection in 15 patients (58%). Of the 21 patients who were not on antiretrovirals at the time of TB diagnosis, 17 (81%) met criteria for immediate initiation of HAART. The median CD4 cell counts and HIV-1 plasma viral load were 80 cells per microliter (range, 2-800 cells per microliter) and 255,631 copies per milliliter (range, 50,000 to > 500,000 copies per milliliter), respectively, for the patients whose baseline measurements were available. CD4 lymphocyte count was less than 200 cells per microliter in 13 (76%) of the 17 patients whose measurements were available. Three (30%) of the 10 patients whose CD4 cell count was less than 100 cells per microliter developed subsequent AIDS-defining illness prior to the initiation of HAART and a fourth patient, within 30 days of starting HAART. None of the patients who had CD4 cell counts 100 cells per microliter or greater developed subsequent AIDS-defining illness during TB treatment. The median time to starting HAART after starting TB treatment was 12 weeks (range, 3-36 weeks). From our limited experience based on this case series, we recommend early initiation of HAART in coinfected patients with CD4 cell counts less than 100 cells per microliter.

[Clinical course of HIV-infected tuberculosis patients who admitted to the tuberculosis isolation ward: current problems of medical care].

To clarify the problems of medical care of HIV-infected tuberculosis patients, we investigated clinical course of six cases admitted to our tuberculosis isolation ward. All cases were sputum smear positive for tubercle bacilli at the time of diagnosis of tuberculosis. HIV-positive was confirmed at the same time or soon after the diagnosis of tuberculosis in four cases. CD4+ cell count was on the average 21/mm3 on admission, and all cases were defined as acquired immunodeficiency syndrome (AIDS) by the criteria of AIDS surveillance committee in Japan. Two patients presented with miliary tuberculosis and five documented evidence for intrathoracic and/or cervical lymph node involvement. All cases but one responded well to antituberculosis drugs, and sputum smears and cultures became negative soon after the initiation of therapy. However, the patients were still needed to be hospitalized for the treatment and control of complications other than tuberculosis after sputum negative conversion, and they stayed in the isolation rooms of our tuberculosis ward for 110 +/- 49 days. During the treatment for tuberculosis, each patient developed 3 to 8 complications of HIV infection such as pneumocystis carinii pneumonia (PCP) (four cases), bacterial infection (four cases), neuropathy (four cases), and HIV encephalopathy (three cases). The last two complication worsened active daily life. White blood cell count was more likely to fall when sulfamethoxazole/trimethoprim mixture for the prevention of PCP and antituberculosis drugs were administered together. In three cases, ST mixture could not be continued, then two patients developed PCP after changing to an alternative pentamidine inhalation. Although three patients discharged from our tuberculosis ward, four died of AIDS related complications other than tuberculosis, one died of tuberculosis (multidrug-resistant M. tuberculosis strain was not documented initially but was detected five months later), one died of tuberculosis meningitis after the discharge, and one was lost because he returned to his own country. The survival time between the start of treatment and death ranged from 90 to 244 days in five cases. Integrated medical care system both for HIV and tuberculosis is warranted for the management of HIV-infected tuberculosis patients since they suffer many complication in addition to tuberculosis. A guideline of methods and duration of isolation for tuberculosis is needed for the most effective care of HIV-infected tuberculosis patients in Japan.

Unmasking tuberculosis-associated immune reconstitution inflammatory syndrome in HIV-1 infection after antiretroviral therapy.

The exaggerated immune response to the subclinical opportunistic microorganisms or their antigens can be found in HIV-1 infected patients after receiving antiretroviral (ARV) therapy. We report a case of unmasking tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) in the HIV-1 infected patient who had no previous history of mycobacterial infection. She had tuberculosis of intestines, peritoneum and mesenteric glands within 2 months of ARV. However, her sputum acid-fast bacilli stain, sputum, blood and cervical lymph node aspiration cultures for mycobacterium were negative. Her CD4 cell count increased of from 46 cells/microL at baseline before receiving ARV to 155 cells/microL at month 6 of ARV. In addition, her plasma pro-inflammatory (IFN-gamma and TNF-alpha) and anti-inflammatory (IL-10) cytokine measurement was supported the occurrence of immune restoration reaction. Therefore, the changing in these cytokine profiles may be an important marker of developing unmasking TB-IRIS.

Clinical presentation and outcome of patients with HIV infection and tuberculosis caused by multiple-drug-resistant bacilli.

To determine the clinical manifestations of patients with human immunodeficiency virus (HIV) infection and tuberculosis caused by multiple-drug-resistant bacilli compared with those with single-drug-resistant or susceptible bacilli. Descriptive, case-control, and cohort studies. A large urban teaching hospital. Sixty-two patients with tuberculosis caused by multiple-drug-resistant bacilli (cases) and 55 patients with tuberculosis caused by single-drug-resistant or susceptible bacilli (controls). Characteristics of clinical presentation, radiographs, pathologic abnormalities, antituberculosis treatment, and clinical course. Twenty cases (32%) had concomitant pulmonary and extrapulmonary disease at presentation compared with 9 controls (16%; odds ratio, 2.4; 95% CI, 1.0 to 5.9). More cases had alveolar infiltrates (76%; odds ratio, 3.6; CI, 1.2 to 11.4), interstitial infiltrates with a reticular pattern (67%; odds ratio, 7.8; CI, 1.0 to 83.5), and cavitations (18%; odds ratio, 6.6; CI, 0.8 to 315.3) on initial chest radiographs compared with controls (49%, 19%, and 3%, respectively). Pathologic specimens from cases showed extensive necrosis, poor granuloma formation, marked inflammatory changes with a predominance of neutrophils, and abundant acid-fast bacilli. Twenty-five cases received two or more effective antituberculosis drugs for more than 2 months. Only 2 cases had three consecutive negative cultures for Mycobacterium tuberculosis; one patient died within 1 day of the last negative culture, and the other had positive cultures 496 days later. The remaining 23 cases had persistently or intermittently positive cultures despite therapy. The clinical course of these cases suggested overwhelming miliary tuberculosis with involvement of the lungs (77%), pleura (15%), stool (34%), meninges (13%), bone marrow (16%), blood (10%), lymph nodes (10%), and skin (8%). The median survival time was 2.1 months for cases compared with 14.6 months for controls (P = 0.001, log-rank test). Tuberculosis caused by multiple-drug-resistant bacilli in patients with HIV infection is associated with widely disseminated disease, poor treatment response with an inability to eradicate the organism, and substantial mortality.

Medium-term survival, morbidity and immunovirological evolution in HIV-infected adults receiving antiretroviral therapy, Abidjan, Côte d'Ivoire.

To evaluate survival, morbidity, and CD4 and viral load (VL) evolution in HIV-infected adults receiving antiretroviral therapy (ART) in Côte d'Ivoire. Since 1996, 723 HIV-infected adults have been followed up in the ANRS 1203 cohort study in Abidjan. For those patients who received ART, we describe data between ART initiation and August 2002. One-hundred-and-one adults (61% women) were followed up under ART for a median of 17 months. At ART initiation, median age, CD4 count and VL were 36 years, 135/mm3 and 5.3 log10 copies/ml, respectively. Initial ART regimens were two nucleoside reverse transcriptase inhibitors (NRTIs) plus one protease inhibitor in 74 patients, two NRTIs plus one non-nucleoside reverse transcriptase inhibitor in 16, and two NRTIs in 11. No patient was lost to follow-up. The most frequent causes of severe morbidity were bacterial infections [11.6/100 person-years (PY), 95% CI: 7.2-18.7], drug-related events (6.5/100 PY, 3.5-12.0), tuberculosis (3.1/100 PY, 1.3-7.4) and malaria (3.1/100 PY, 1.3-7.4). The incidence of death was 3.0/100 PY (1.1-8.0) in patients with baseline CD4 > or = 50/mm3 and 16.1/100 PY (7.2-35.9) in patients with CD4 < 50/mm3. Fifty percent of causes of death were active infections pre-existing ART initiation, mainly atypical mycobacteriosis. After 1 year, 51% of patients had undetectable VL, 28% had detectable VL reduced by more than 0.5 log10 copies/ml since ART initiation, and the median gain in CD4 was +115/mm3. Medium-term survival under ART may be as good in Africa as in industrialized countries, provided that patients benefit from access to care for opportunistic infections, including bacterial diseases, tuberculosis and malaria.

Clinical and laboratory profile of patients with TB/HIV coinfection: A case series of 50 patients.

Tuberculosis (TB) is said to be one of the commonest opportunistic infection in patients with HIV/AIDS. To study the clinical and laboratory profile of patients with HIV/TB coinfection. Fifty adult TB patients having confirmed HIV seropositivity were included in randomized manner. A detailed history and thorough physical examination was done. Laboratory and radiological investigations were carried out as appropriately warranted. Most of the patients were farm workers (30%) followed by manual laborers (22%) and transport drivers (16%). Heterosexual route was found in 86% of patients. Cough was present in 94% while fever and weight loss in 86% and 78% of patients, respectively. Out of 50 patients, 40% had only pulmonary TB (PTB), 46% had pulmonary and extra-pulmonary TB (EPTB), 10% had only EPTB and 4% had multisystemic EPTB. Mediastinal lymphadenopathy was present in 34% while pleural effusion and extra-thoracic lymph nodes was present in 20% and 18% of patients, respectively. Positive smear for acid-fast bacilli (AFB) was found in 25.58% while positive Mantoux test was found in 32.14% of patients. HIV/TB coinfection is more common in sexually active age group and commonest mode of HIV infection is heterosexual transfer. Sputum smear AFB and Mantoux test positivity is low in TB patients having HIV. Disseminated TB is common in HIV. Mediastinal lymphadenopathy is common site among extra-pulmonary tuberculosis.

HIV/AIDS

The World Health Organization first proposed a definition for AIDS in 1986. Since then, the WHO classification has been updated and expanded several times, with the most recent version being published in 2007. The WHO system uses the following categories: Primary HIV infection: May be either asymptomatic or associated with acute retroviral syndrome Stage I: HIV infection is asymptomatic with a CD4+ T cell count (also known as CD4 count) greater than 500 per microlitre (µl or cubic mm) of blood. May include generalized lymph node enlargement. Stage II: Mild symptoms, which may include minor mucocutaneous manifestations and recurrent upper respiratory tract infections. A CD4 count of less than 500/µl Stage III: Advanced symptoms, which may include unexplained chronic diarrhea for longer than a month, severe bacterial infections including tuberculosis of the lung, and a CD4 count of less than 350/µl

A 34-Year-Old Man With a Neck Mass.

A 34-year-old man presented to Queen Elizabeth Central Hospital in Blantyre, Malawi with multiple enlarged right cervical lymph nodes. He had no associated constitutional symptoms. Fine-needle aspirate (FNA) of one of the lymph nodes was negative for acid-fast bacilli (AFB) by smear microscopy. The FNA specimen was not sent for histological examination. Mycobacterial culture and Xpert MTB/RIF were not available at the time. He tested positive for HIV but CD4 T-cell count was not requested at the time of HIV diagnosis, and he did not start antiretroviral therapy (ART) pending confirmation of the cause of lymphadenopathy. Excision biopsy of the lymph nodes was planned; however, the patient was lost to follow-up before the procedure was performed.

Indinavir

ACTG 320 This study took a look at clinical efficiency of the different treatments. Patients had to have CD4 cell counts less than 200 and at least 3 months of AZT therapy before the trials. 1156 patients with a mean of 87 CD4 cell counts and mean viral load of 100,000 copies/ml were randomized to one of the two groups: AZT plus lamivudine or AZT plus lamivudine plus indinavir. Just like Study 035, patients couldn't be in the study if they had prior protease inhibitor treatment or lamivudine for more than one week. The end point of the study was death or development of opportunistic infections. After 38 weeks, 6% of the people in the three-drug group died while 11% of the people died in the two-drug group. There were higher CD4 cell counts and less viral load in patients assigned to the three-drug group, proving that a three-drug treatment is more efficient than a two-drug one. Controversy

[HIV infection and tuberculosis].

The number of people infected with human immunodeficiency virus (HIV) is gradually increasing in Japan, and the morbidity rate from tuberculosis in the Japanese people is high. Accordingly, the number of cases with both infections is considered to increase in the future. Our hospital has already encountered 31 cases of HIV associated tuberculosis. HIV infects mainly CD4-positive cells. The extreme decrease in the cell count results in serious cellular immunological disorder. CD4-positive cell disorder induces disorders of B lymphocytes, cytotoxic T cells, natural killer cells, and macrophage functions. These destructive conditions show the state of immunodeficiency including macrophage that are most important for defense of acid-fast bacterial infection. Migration and activation of macrophages with cytokines derived from T cells are impaired to induce the following phenomena: hypoplasia of granuloma, failure of tubercule bacillus suppression, the spread to regional lymph nodes (hilar or mediastinal lymph nodes), and hematogenous dissemination. On this occasion, caseous necrosis and cavitation are unlikely to occur, and false-negative tuberculin reaction is often observed. The incidence of severe cases, which include miliary tuberculosis, tuberculous meningitis, etc., and extrapulmonary tuberculosis, are high among acquired immunodeficiency syndrome (AIDS)-associated tuberculosis cases. HIV-infected tuberculosis cases are generally regarded as endogenous exacerbation, but they include primary infection and reinfection as well. Even during the treatment for drug-sensitive strains particularly, some cases may have reinfection with multidrug-resistant bacteria, suggesting that caution should be taken against this point. Conversely, the association of tuberculosis is a factor for the poor prognosis of HIV infection, since it facilitates the development of HIV infection. If the bacteria belong to a drug-sensitive strain, the infection with them responds well to antituberculous drugs, the same as in tuberculosis cases without HIV infection, showing a favorable prognosis. However, the mortality rate of infection with multi-drug-resistant tuberculosis is extremely high. The combined use of a protease inhibitor, i.e., anti-HIV drug, with rifampicin is regarded as contraindication for the treatment because rifampicin strongly induces hepatic cytochrome P-450 and increases the metabolism of protease inhibitors and nonnucleoside reverse transcriptases to markedly decrease the blood concentrations. Accordingly, the treatment for tuberculosis should take priority over that for HIV infection in HIV-infected tuberculosis, and highly active antiretroviral therapy (HAART) may be administered after the treatment of tuberculosis. When HAART is necessary for the treatment during the tuberculosis treatment, rifampicin had better be exchanged to rifabutin because the effect of rifabutin to induce cytochrome P-450 is less potent than that of rifampicin. A report has recently shown that the exacerbation of pyrexia and chest X-ray findings was transiently observed approximately 2 weeks after potent anti-HIV therapy for HIV-infected tuberculosis, which included a protease inhibitor. The reason for the exacerbation has been believed to be that the impaired function of CD4-positive cells is improved by the administration of anti-HIV drugs to raise temporarily the reaction of the vital part to M. tuberculosis. A tuberculin skin test (TST) reaction size of > or = 5 mm of induration is considered positive (i.e., indicative of M. tuberculosis infection) in persons who are infected with HIV. Persons with a TST reaction size > or = 5 mm who have not previously received treatment for M. tuberculosis infection should receive tuberculosis preventive treatment. Prevention by BCG vaccination is regarded as contraindications for HIV-infected patients, because disseminated M. bovis infection may be associated with them. Many HIV-positive patients infected with tuberculosis show uneventful healing, when M. tuberculosis is the sensitive strain. However, since some patients show the rapid course of tuberculosis, clinical physicians keep the early detection of tuberculosis for HIV-infected patients and the association of HIV infection for tuberculosis patients in their mind, respectively.

Françoise Barré-Sinoussi

transcriptase activity. If reverse transcriptase activity is present, it confirms that the virus is a retrovirus. In December 1982, heavy research began and clinical observations suggested that the disease attacked immune cells because of the significant CD4 cell depletion. However, the depletion of the CD4 lymphocytes made it very difficult to isolate the virus in patients with the disease later known as, AIDS. Because of the difficulty isolating an infected cell from a patient with late disease progression, Barré-Sinoussi and her colleagues decided to use a lymph node biopsy from a patient with generalized lymphadenopathy. Generalized lymphadenopathy was a common symptom of patients in the early stages of disease progression. In the second week of checking the biopsied cell cultures for reverse transcriptase activity, enzymatic activity was detected and increased for a short time until the reverse transcriptase activity decreased dramatically after the T-lymphocytes in the culture

Immune reconstitution inflammatory syndrome

Infections most commonly associated with IRIS include Mycobacterium tuberculosis and cryptococcal meningitis. Persons living with AIDS are more at risk for IRIS if they are starting for the first time, or if they have recently been treated for an opportunistic infection (OI). It is generally advised that when patients have low initial CD4 T cell count and opportunistic infection at the time of their HIV diagnosis, they receive treatment to control the opportunistic infections before HAART is initiated approximately two weeks later. This is true for most OIs, except for OIs involving the central nervous system. In cryptococcal meningitis IRIS is particularly problematic in cryptococcal meningitis as IRIS is fairly common and can be fatal.

HIV set point

The asymptomatic or clinical latency phase is marked by slow replication of the HIV virus, followed by steady depletion of CD4 T cells with little to no symptoms. For individuals that are rapid progressors, this phase can be short lived, with an average of 2-3 years. Long-term progressors (LTNPS) can remain stable in this stage for over a decade. An uninfected person has 500-1500 CD4 T cells/µL of blood. When this count lowers to less than 500 CD4 T cells/µL, opportunistic infections can occur where the immune system is no longer able to fight pathogens it would have easily cleared in an unimpaired state. The infection progresses to AIDS when the count falls below 200 CD4 T cells/µL, at which point opportunistic infections can be lethal. At this stage, an infected person has 2-3 years of life expectancy. The use of antiretroviral therapy (ART) can greatly slow the progression of the virus to AIDS.

The Emergence of Resistance Under Firstline INSTI Regimens.

We reported an HIV-naïve patient from a resource-limited area who was detected with multiple resistance sites associated with nucleoside reverse transcriptase inhibitors (NRTIs) and integrase strand transfer inhibitors (INSTIs) after the failure of the initial antiviral regimen dolutegravir/lamivudine (DTG/3TC) and subsequent Bictegravir/emtricitabine/tenofovir alafenamide (BIC/FTC/TAF). On May 8, 2021, a 53-year-old man was diagnosed with AIDS, Marneffei talaromycosis and fungal esophagitis, and was suspected of having tuberculosis (TB) in Guangxi, China. His baseline HIV RNA was 559,000 copies/mL and the CD4 count was 12 cells/µL, but resistance genotype testing was not performed. The patient remained immunosuppressed (CD4 count 3 cells/µL) after 12 weeks of initial antiviral treatment (ART) with DTG/3TC. After he was switched to BIC/FTC/TAF and started anti-TB treatment, the viral load (HIV RNA 163,200 copies/mL) was not effectively controlled, and there were multiple NRTIs drug-resistant mutations (D67N, K70R, M184V, T215V, K219Q) and INSTIs mutations (E138K, G140A, S147SG, Q148R). This suggested that in resource-limited areas, for HIV-naïve patients in advanced stages with active opportunistic infections, HIV RNA>500,000 copies/mL, and low CD4 count, baseline resistance testing and increased HIV RNA testing frequency should be recommended, DTG/3TC was not recommended as initiation, and opportunistic infections should be treated promptly. In addition, switching to other INSTIs was not recommended in the absence of resistance testing and ineffective use of DTG.

[Problems in the diagnosis and therapy of lymph node tuberculosis in HIV-negative patients].

Tuberculosis is the world's foremost cause of death from a single infectious agent in adults. During the past decade the nature and magnitude of the problem of tuberculosis have dramatically changed. Much of what physicians have learned about this disease is no longer true and tuberculosis has become a new entity. Migration from developing areas with a high prevalence of tuberculosis to industrialized countries, and the problem of HIV infection, have introduced new components to the epidemiology. We report three cases of young immigrants with lymph node tuberculosis. One patient was successfully treated with the usual 9-month-regimen. The other 2 patients, however, developed new lymph nodes or enlargement of existing nodes during treatment. They underwent further examinations, including surgical biopsies, because of diagnostic uncertainty (tuberculosis, superinfection or lymphoma). Finally the 2 patients were successfully treated with antituberculous agents for 12 and 15 months. These cases prompted a review of the literature and a reevaluation of the management of lymph node tuberculosis, including the value of surgical biopsy in the diagnosis of tuberculous lymphadenitis. We conclude that selective surgical biopsies should be recommended for differential diagnosis of tuberculous lymphadenitis. Histological examination (caseating epitheloid cell granulomas and giant cell formation) and microbiological examination (Ziehl-Neelsen staining and culture of native material) should be performed. Newer methods, such as amplification and detection of mycobacterial DNA, are rapid and sensitive tests helpful for diagnosis. Lymph nodes may increase in size and new nodes may appear both during and after chemotherapy, without indicating a failure of treatment or relapse. The usual treatment is a 9-month-regimen with rifamipicin, isoniazid, pyrazinamid and ethambutol. Prolonged or modified regimens are, however, necessary in some individuals.

Characteristics of residual lymph nodes after six months of antituberculous therapy in HIV-negative individuals with cervical tuberculous lymphadenitis.

The therapeutic response of cervical tuberculous lymphadenitis (CTBL) may be delayed or paradoxical, with the frequent development of residual lymph nodes (LNs) during and after antituberculous treatment. We investigated the incidence of residual LNs and the clinical, radiological, microbiological, and pathologic responses of patients with CTBL after 6 months of antituberculous therapy. The medical records of HIV-negative adult patients with CTBL diagnosed between July 2009 and December 2017 were analyzed. After 6 months of first-line antituberculous treatment, computed tomography (CT) scans were conducted to evaluate for residual LNs. Fine-needle aspiration biopsy (FNAB) was carried out if a patient presented with residual LNs > 10 mm in diameter with central necrosis, peripheral rim enhancement, or perinodal inflammation on CT scan. Residual LNs were detected in 35 of 157 patients who underwent follow-up CT scans and were more commonly observed in younger patients who completed the treatment (mean years ± standard deviation [SD]: 33 ± 13 vs. 44 ± 16, p < 0.001). The recurrence rate was approximately 5%, which was not significantly different in both groups. Among the 15 patients who underwent FNAB, 3 (30%) presented with granuloma, and 2 of 15 and 10 of 14 patients had positive AFB and TB PCR results, respectively. The TB culture results of 15 patients were negative. Residual LNs may still be observed after 6 months of antituberculous treatment. Although the radiologic and pathologic findings after treatment are still indicative of TB, not all residual LNs indicate recurrence or treatment failure. A six-month therapy may be sufficient for cervical tuberculous lymphadenitis.

[Focal mycobacterial lymphadenitis after starting highly active antiretroviral therapy].

A 30-year-old man with a known HIV infection for 7 years presented for treatment with antiretroviral drugs. He was known to have had herpes zoster, oral hairy leukoplakia and recurrent Candida stomatitis, but was otherwise without symptoms. The CD4 lymphocyte count was 19 cells/mm3 and there were 41,000 HIV-RNA copies/ml. The HIV infection was in CDC stage B3, indicating the need for combined antiretroviral treatment. A week after starting stavudine, saquinavir and ritonavir he had to be admitted because of nausea and vomiting, colicky abdominal pain, diarrhea, fever up to 39 degrees C and a rise of C-reactive protein to 207 mg/dl. Bacteriological examination of feces and biopsy of an enlarged retroperitoneal lymph node revealed atypical mycobacteria. Antituberculosis treatment was started. The CD4 cell count rose to 56/mm3 and the viral count fell to 11,000/ml. Each time after initiating a different antiviral regimen the symptoms recurred. This case illustrates an atypical manifestation of on opportunistic infection: during combined antiviral treatment the CD4 cell count rose and thus precipitated an heretofore subclinical mycobacterial infection with focal lymphadenitis. If, on starting antiretroviral treatment at a late HIV stage, new symptoms develop within 1-3 weeks, one should consider drug-induced side effects or the onset of an opportunistic infection that has become manifest as the result of an improved immunological state.

[Relapse of pulmonary tuberculosis in the context of tuberculosis-HIV co-infection in Abidjan (Côte d'Ivoire). Short note].

A cohort study was carried out from October 2001 to March 2002, in order to analyze the main characteristics of 53 adults patients (38 HIV-positive and 15 HIV-negative), who had a relapse of pulmonary tuberculosis. The observance in the first period of the treatment of tuberculosis was regular in 79% of tuberculous patients infected by the HIV (30/38) and in 87% of tuberculous patients who where HIV-negative (13/15) (p = 0.7). The relapse occurred before one year after recovery in 74% among the HIV-positive (28/38) and in 33% among the HIV-negative patients (5/15) (p = 0.00). Most of the HIV-positive patients (74%) had CD4 counts under 200/mm3 and 80% of the HIV-negative patients had more than 500 CD4 counts/mm3 (p = 0.00). After two months of retreatment following the relapse diagnosis, the rate of improvement in patients was about 16% in HIV infected (6/38) and about 67% in HIV-negative patients (10/15) (p = 0.00).

InternalMed_Harrison

HIV-Associated TB (See also Chap. 226) TB is one of the most common diseases among HIV-infected persons worldwide and a major cause of death in this population; more specifically, it is responsible for an estimated 24% of all HIV-related mortality. In certain urban settings in some African countries, the rate of HIV infection among TB patients reaches 70–80%. A person with a positive TST who acquires HIV infection has a 3–13% annual risk of developing active TB. A new TB infection acquired by an HIV-infected individual may evolve to active disease in a matter of weeks rather than months or years. TB can appear at any stage of HIV infection, and its presentation varies with the stage. When CMI is only partially compromised, pulmonary TB presents in a typical manner (Figs. 202-6 and 202-7), with upper-lobe infiltrates and cavitation and without significant lymphadenopathy or pleural effusion. In late stages of HIV infection, when the CD4+ T cell count is <200/μL, a primary TB–like

Immune reconstitution inflammatory syndrome associated with secondary syphilis.

Immune reconstitution inflammatory syndrome (IRIS) is a condition associated with paradoxical worsening and/or new onset of an opportunistic infection in HIV patients following the initiation of anti-retroviral therapy or switching to more potent antiretroviral therapy (ART) regimen. Although IRIS associated with many opportunistic infections (OIs) has been well reported, syphilis has very rarely been mentioned in this regard. A 52-year-old male, diagnosed with AIDS six weeks ago, presented with the disseminated non-pruritic painless skin rash. He denied any fever, cough, shortness of breath, and joint pain or swelling. The patient had no similar symptoms, genital ulcers, or any medical illness in the past. CD4 cell count and viral load were 40 cells/mm<sup3</sup and 280,000 copies/ml, respectively, while screening tests for OIs including rapid plasma reagin test, quantiferon, cryptococcal antigen, and toxoplasma tests were negative at the time of HIV diagnosis. After three days of initiation of anti-retroviral therapy, he developed the above-mentioned skin rash. Repeat rapid plasma regain (RPR) test at this time was also negative. Punch biopsy of the skin lesion demonstrated findings suggestive of secondary syphilitic lesions, which was confirmed by immunostain. The repeat RPR, CD4 cell count, and viral load showed a titer of 1:256, 257 cells/mm<sup3</sup, and 5000 copies/ml, respectively. His skin rashes faded away, and RPR titer trended down on treatment with benzathine penicillin without discontinuation of ART. The presence of an IRIS response does not predict overall HIV or OI treatment responses, and discontinuation of ART is not generally recommended as the benefits of treating HIV infection outweighs the risk associated with IRIS.

Human immunodeficiency virus and the outcome of treatment for new and recurrent pulmonary tuberculosis in African patients.

The purpose of this study was to evaluate the impact of human immunodeficiency virus (HIV) infection on treatment for tuberculosis (TB). The study population comprised 28,522 black Southern African gold miners. Patients with sputum culture-positive new or recurrent pulmonary TB diagnosed in 1995 were prospectively enrolled in the cohort. Directly observed therapy (DOT) was practiced and outcomes were assessed at 6 mo after treatment was begun. There were 376 cases of TB (incidence 1,318 per 100,000), of which 190 (50%) were HIV positive and 82 (22%) had recurrent TB. There was no association between HIV status and history of previous TB or drug resistance. Neither the treatment interruption rate (2%) nor the rate at which patients transferred out of the treatment program (1.6%) were associated with HIV status. Excluding deaths, cure rates were similar for HIV-positive and HIV-negative patients (89% versus 88%), but significantly lower in those with recurrent than in those with new TB (77% versus 92%). Mortality was 0.5% in HIV-negative patients versus 13.7% in HIV-positive patients, and in the latter group was associated with CD4(+) lymphocyte depletion. Autopsy examination showed that in HIV-positive patients, early mortality was due to TB whereas late deaths were most commonly due to cryptococcal pneumonia. The study showed that a well-run TB control program can result in acceptable cure rates even in a population with a very high incidence of TB and HIV infection. Particular vigilance is needed for concurrent infections, which may contribute significantly to mortality during treatment of TB in HIV-positive patients.

Clinical course of human immunodeficiency virus type 1 associated pulmonary tuberculosis during short-course antituberculosis therapy.

To describe the clinical response to antituberculosis therapy in HIV-1 disease, 49 HIV-1 positive Ugandan adults (mean age 29.4 years; 68% men) with active pulmonary tuberculosis (PTB) were studied in a trial of rifampicin containing short-course antituberculosisis regimens. At presentation, 18 patients were PPD non-reactors (PPD skin test induration < 2mm), ten patients (20%) had non-cavitary lung disease. The mean CD4 lymphocyte count at presentation was 339/microliters (+/- SD 275). Among patients with abnormal baseline clinical values, the median time to resolution of fever, weight gain of 10%, increase of haemoglobin to 10g/dl and of Karnofsky performance score (KPS) to 80 occurred before sputum smear and culture conversion. Short-term survival was associated with: baseline lymphocytes < 1200/microliters, (Odds ratio (OR) 17.5), CD4+ lymphocytes < 200/microliters (OR 9.8), cavitary lung disease, (OR 0.6), atypical chest radiograph, (OR 6.7), and PPD non-reactivity, (OR 13.5), PPD non-reactivity and non-cavitary disease were associated with significantly lower CD4 lymphocyte counts. Affordable serial measurements parallel the response to therapy and predict survival in HIV-associated PTB.

Tuberculous pyelonephritis in children: three case reports.

Tuberculous pyelonephritis is rare in children; three case reports are presented. Case 1 was an 11-year-old girl with a previous history of pulmonary tuberculosis who presented with flank pain and fever for 10 days. An ultrasound suggested focal pyelonephritis, and a contrast-enhanced computed tomography (CECT) scan demonstrated acute focal pyelonephritis and a perinephric collection. Mycobacterium tuberculosis was cultured in the urine. She responded well to anti-tuberculous treatment (ATT). Case 2 was a 13-year-old boy who presented with fever, haematuria, burning micturition, proteinuria (3+) and cervical lymphadenopathy. The Mantoux test was strongly positive. Chest radiograph demonstrated right hilar lymphadenopathy and ultrasonography showed evidence of acute pyelonephritis. Tuberculous lymphadenitis was diagnosed by fine-needle aspiration cytology (FNAC) from cervical lymph nodes and he responded to ATT. Follow-up urinalysis and ultrasound were normal. Case 3 was a 6-year-old boy, a known case of pulmonary tuberculosis (from 2 years of age) and a previous defaulter from ATT. He presented with symptoms of lumbar pain and dysuria. Chest radiograph demonstrated mediastinal lymphadenopathy and a CECT of the head showed a tuberculous granuloma. CECT of the abdomen showed an enlarged left kidney with focal pyelonephritis, an abscess in the upper pole and parenchymal calcification. FNAC of the cervical lymph nodes supported a diagnosis of disseminated tuberculosis with tuberculous pyelonephritis. He was given 8 months of ATT. Fifteen months later he presented again with clinical and urinary findings of urinary tract infection. CECT now demonstrated gross hydronephrosis of the left kidney, and it was confirmed to be non-functioning by a DMSA scan and magnetic resonance urogram. Diethylenetriaminepentaacetic acid showed a GFR of 44.3 ml/min/1.73 m<sup2</sup. Nephrectomy was undertaken and the histology confirmed tuberculous pyelonephritis. Six months later he was well with an eGFR of 87.2 ml/min/m<sup2</sup. In patients with symptoms of urinary tract infection but sterile urine who do not respond to antibiotics or have evidence of tuberculous elsewhere in the body, careful consideration should be given to the possibility of tuberculous pyelonephritis.

[Clinical features of 23 cases of AIDS complicated by tuberculosis].

To discuss the clinical features, treatment and prognosis of patients with AIDS complicated by tuberculosis(TB). The clinical features of 23 patients with AIDS complicated by tuberculosis admitted from 1997 to July 2004 were retrospectively analyzed. Of the 23 patients, most (94.3%) were young or middle-aged, and 11 (47.8%) died within half a year. The main HIV transmission was via sexual contact in 15 (65.2%) patients. Loss of body weight by 5 - 15 kg was present in all patients, cough for over 1 month in 15 (65.2%), and multiple opportunistic infections were complicated in most cases. Out of the 23 cases, 14 (60.9%) showed only pulmonary TB, and 8 (34.8%) showed lymph node TB. In 12 cases with infiltrated pulmonary TB, X-ray showed bilateral infiltration and no cavity formation was found. Slightly positive PPD test was found in 2 (8.7%) cases, and positive acid-fast bacilli was detected in sputum in 1 case (4.4%). The pre-treatment CD(4)(+) cell number in 23 patients was much lower than that in AIDS patients without complicated TB (P < 0.05). The pre-treatment CD(4)(+) cell number in patients died shortly after diagnosis was much lower than that in survived patients (P < 0.05). The HIV RNA level in the 23 patients was much higher than that in patients without complication of TB (P < 0.05). The mortality in patients treated with therapy against both TB and HIV was much lower than that in patients untreated or treated only with anti-TB therapy (P < 0.05). For patients with AIDS complicated by TB, the high negative rate in PPD test and the atypical chest X-ray manifestations are common. However, lymph node TB is quite common with high mortality. The pre-treatment CD(4)(+) level decreases significantly, and is associated with mortality. The TB bacilli may accelerate HIV virus duplication. It is suggested that the patients be treated with a combination of anti-TB and anti-HIV therapies.

[Severe oral mucositis in a patient with HIV infection].

A 50-year-old man with HIV infection (first diagnosed > 20 years ago) presented at our hospital with fulminant oral mucositis. Antiretroviral therapy (tenofovir, emtricitabine, raltegravir) had been started 2 months ago. Previously he had no opportunistic infections and no other pre-existing illnesses. He had not travelled outside Europe but stayed in Spain for several weeks during summer. Physical examination revealed swelling of the lips and severe ulcerative mucositis of the gums and pharynx. The patient complained of painful swallowing. The blood-chemistry showed no abnormalities. The microscopical analysis of a smear and a biopsy of the buccal mucosa revealed amastigotes of leishmania. By means of PCR technique, Leishmania donovani complex was specified. The patient was treated with liposomal amphotericin B (1 mg/kg) for 21 days. Because of the immunosuppression he was put on maintenance therapy afterwards (liposomal amphotericin B every 3 weeks). However, 4 months later there was a clinical relapse of the mucositis and a new cultural and PCR detection of leishmania in a buccal biopsy. After another course of 21 days with liposomal amphotericin B (3 mg/kg) and miltefosine (150 mg/d), the mucositis subsided. Therapy with liposomal amphotericin B (3 mg/kg single dose every 3 weeks) has since been maintained. The antiretroviral therapy was changed meanwhile to lamivudin, abacavir and raltegravir because of kidney failure with elevated urea and creatinine. The patient has been clinically stable ever since without any other HIV-related problems. The latest CD4 count was 456/µl and the HIV load 340 copies/ml. Leishmaniasis is a severe infection in HIV-positive patients. Clinical manifestations can be atypical in immunosuppressed patients and the treatment is complicated with HIV coinfection. This is also due to a lifelong persistence of the parasite with potential reactivation especially in patients with suppressed CD4 cells. Therefore maintenance therapy after standard therapy of leishmaniasis is mandatory at least for a CD4 count below 350/µl. Especially in HIV patients with a leishmaniasis relapse lifelong maintenance therapy should be considered.

Clinical and biological evolution of HIV-1 seroconverters in Abidjan, Côte d'Ivoire, 1997-2000.

To describe the clinical and biologic evolution of HIV-1 infection in Africa. One hundred four HIV-1-infected individuals were identified prospectively from regular blood donors in Abidjan, Côte d'Ivoire. The date of seroconversion was estimated from results of sequential serologic tests. Biologic and clinical follow-up was performed every 6 months, starting as early as possible after seroconversion. Case management followed national guidelines. The median interval between estimated seroconversion and study inclusion was 9.7 months, and the median window of seroconversion was 2.8 months. At baseline, all but two patients were asymptomatic; the median CD4 + cell count was 527/mm 3 (interquartile range [IR], 395-684), and the median plasma HIV RNA level was 4.6 log 10 copies/ml (IR, 3.8-4.9). The median follow-up was 23.9 months, and 95% of the patients received primary prophylaxis with co-trimoxazole for opportunistic infections. Of the patients, 1 presented with wasting syndrome, 3 developed tuberculosis, and 17 had a Centers for Disease Control and Prevention category B-defining event. The 3-year AIDS-free and symptom-free probabilities were 96.7% (95% confidence interval [CI], 87.0-99.2] and 79.3% (95% CI, 67.5-87.2), respectively. During the first 3 years of follow-up, we observed that the median plasma viral load stabilized at >4 log 10 copies/ml and that the median CD4 + cell count declined by 20 to 25/mm 3 per year. These African seroconverters were moderately immunosuppressed. The median HIV RNA level was high and varied very little during the first 3 years, and there were few clinical events.

[A pediatric case of HIV who diagnosed by virtue of disseminated cryptococcus infection].

Cryptococcus neoformans is an important opportunistic pathogen that causes serious mortality and morbidity in AIDS patients. Although its incidence has decreased with proper antiretroviral treatment (ART), it is still a major concern in areas with low socioeconomic HIV endemic countries with poor sources of therapy. In our country, pediatric HIV infection and so, HIV-related opportunistic infections are very rare. In order to pay attention to this unusual collaboration; herein, we presented a pediatric case who was diagnosed with HIV and disseminated cryptococcus infection concomitantly. A 6.5-year-old previously healthy girl has admitted to our hospital with the complaints of prolonged fever, cough and hemoptysis. On her physical examination she had oral candidiasis, generalized lymphadenopathy and hepatosplenomegaly. Laboratory findings were as follows; white blood cell count: 3170 µL (neutrophil: 2720 µL, lymphocyte: 366 µL), hemoglobin level: 7.8 gr/dl, hematocrit: 25.5% platelets: 170.000 µL, CRP: 15.2 mg/L and serum IgG level: 1865 mg/dl. Her anti-HIV test yielde,d positive result and confirmed by Western blot assay, together with a high viral load (HIV-RNA: 3.442.000 copies/ml). She was started ART (lamivudine, zidovudine and lopinavir/ritonavir combination) with the diagnosis of stage 3 HIV infection (AIDS). Posteroanterior chest radiograph showed mediastinal extension and nodular parenchyma. Since the patient was suspected to have pulmonary tuberculosis based on the clinical and radiological findings, empirical antituberculosis therapy was started. Because of the insistance of fever, three different blood specimens, bone marrow and gastric aspirates were collected for culture, in which all of them yielded C.neoformans growth. She was then diagnosed as disseminated cryptococcosis and treated with liposomal amphotericin B and fluconazole successfully. Although pediatric HIV infection is usually diagnosed secondary to maternal disease, it can rarely be presented later in life with opportunistic infections. In the case of unusual infectious diseases, in addition to primary immune deficiency syndromes, HIV infection should also be kept in mind. Herein, we discussed a pediatric case with two rare infectious agents reported in our country and wanted to focus on secondary immune deficiency related with pediatric HIV infection.

[Paradoxical aggravation of tuberculosis after antiretroviral therapy in HIV-infected patients].

Restoration of immunocompetence in HIV-infected patients after antiretroviral treatment can have unexpected effects. An unusual course of treated tuberculosis was observed in four HIV-infected patients soon after initiation of antiretroviral therapy. These patients developed fever and enlarged necrotic adenopathies despite an efficacious antituberculous therapy. They were in the initial stage of their antituberculous therapy that had been initiated a mean 12 days prior to initiation of antiretroviral therapy. The antiretroviral therapy led to an undetectable HIV load within 2 months. These unusual features, which also occurred with an increase in CD4 cell counts, could be related to the immunological restoration and to the reappearance of delayed type hypersensitivity. The onset of antiretroviral therapy could thus be delayed by several weeks in HIV-infected patients treated for active tuberculosis and who have never received antiretroviral therapy.

Disseminated lupus vulgaris.

A 28-year-old woman presented with reddish raised, shiny lesions over the face and ears present for the past 3 years. Four years ago, she developed in her left axilla a nodule that became fluctuant and tender, which ruptured to discharge seropurulent material. It subsided after the patient had received antibiotics for 6 months, leaving puckered scarring. There was no history of antituberculous treatment. After 1 year, she developed papulonodular lesions on her face, nose, and ears. There was now a history of malaise, fever, dry cough, and anorexia and weight loss for the past 2 months. The patient was fully vaccinated in childhood, including against varicella infection. The general physical examination revealed lymphadenopathy involving cervical, axillary, and inguinal lymph nodes 0.5 x 0.5 cm to 1 x 1.5 cm, firm in consistency, and nontender. They were discrete except in the left axilla where multiple matted lymph nodes were present with overlying scarring and a papule. Her systemic examination was normal. Cutaneous examination showed a shiny erythematous plaque 3x2 cm with central atrophy and scarring on the face (Figure). It was comprised of multiple shiny nontender soft papules arranged in annular configuration. Similar discrete papules and nodules with adherent fine scaling were seen bilaterally on the alar prominence of the nose, lower lip, and post-auricular area. On diascopy, apple jelly nodules were seen. The hemogram, liver function tests, and renal function tests were normal, except for an elevated erythrocyte sedimentation rate. The Mantoux test showed erythema and an induration of 20 x 20 cm. A posteroanterior view on the chest x-ray showed fibrotic changes suggestive of pulmonary tuberculosis. Ultrasonography of the abdomen and pelvis showed no tubercular foci. Human immunodeficiency virus serology by enzyme-linked immunosorbent assay with 3 different kits was nonreactive. Histopathology from a nodule showed a focally thinned-out epidermis with follicular plugging and multiple epithelioid cell granulomas, rimmed by lymphocytes in the deeper portion of the dermis, mainly peri-appendageal. Stain for acid-fast bacteria was negative. Cultures from the skin lesions were negative. The patient was diagnosed as having lupus vulgaris with multiple lesions of varying morphology at different sites with pulmonary tuberculosis and healed lymph node involvement.

[Recurrence of tuberculosis in patients infected with the human immunodeficiency virus].

To determine the clinical manifestations of the relapse of the tuberculosis (TB) in the patients infected by the human immunodeficiency virus (HIV) and the degree of immunodeficiency shown. They are analyzed retrospectively 121 cases, all they HIV+, diagnosed of TB from November of 1985 until December of 1999. All they fulfilled correctly the specific treatment of the tuberculosis. Of 121 studied cases, a total of 13 (10.7%) presented relapse of tuberculosis finally of a mean of 31.8 months (range 1-95). In 7 cases the affectation was pulmonary (2 typical, 5 non typical), in 3 mixed (pulmonary and extrapulmonary) and in 3 extrapulmonary. The clinical sintomatology were present in 92% of the cases and, predominantly, was: fever (92%), cough (69%), sweating, weight loss (61%). Hepatomegaly results be the exploratory finding quite frequent (54%). The mean of CD4+ lymphocytes was 141.7 (range 3-406), in 8 (61%) the lymphocyte counts was inferior to 100 cells/mm3. PPD was positive in 1 case (14%) and with respect to delayed-type hypersensitivity reaction test, it was observed not normoergia in all the cases (100%). Relapse of the tuberculosis in patient infected by the VIH is presented with a manifested clinical expresivity in the course of a severe degree of immunodeficiency. In certain groups of risk as the intravenous drugs users, it must of be had a high level of suspicion of the relapse of the disease, above all in those patients that show low CD4+ lymphocyte counts.