I am highlighting this fact due to having watched, helpless and astonished, a family losing one of their most loved ones. So, maybe my fault, which I'm trying to minimize now, speaking openly of…
… Pneumocystosis By Pneumocystosis Karinee
Pneumocystosis was something that I, Claudio, saw in a sad parade of people who, somehow, died suffocated in their own secretions! I will not give names. Even because it costs me to remember them; their faces are enough for me. In times without ART this was a reality with a great possibility of “materialization” and, with it, the result was rarely "survival".
And this survival ...
Over the past 30 years, major advances have been made in our understanding of HIV /AIDS and from Pneumocystis pneumonia (Pneumocystosis), but there are still significant gaps. Pneumocystis it is classified as a fungus and is specific to the host species, but an understanding of its reservoir, mode of transmission and pathogenesis is incomplete.
Pneumocystosis remains a frequent AIDS-defining diagnosis and is a frequent opportunistic pneumonia in the United States and Europe, but comparable epidemiological data from other areas of the world that are burdened with HIV / AIDS are limited.
The HIV Pneumonia Agent, the Pneumocystis Cannot be grown
Pneumocystis cannot be cultured, and bronchoscopy with bronchoalveolar lavage is the gold standard procedure for diagnosing Pneumocystosis, but noninvasive diagnostic tests and biomarkers are promising.must be validated.
Trimethoprim-sulfamethoxazole is the recommended first-line treatment and prophylaxis regimen, but putative resistance to the drug sulfamethoxazole-trimethoprim is an emerging concern. The International HIV-Associated Opportunistic Pneumonia (IHOP) study was established to address these knowledge gaps.
This review describes recent advances in the pathogenesis, epidemiology, diagnosis and management of pneumocystosis associated with HIV and ongoing areas of clinical and translational research that are part of the IHOP study and the Longitudinal Studies of HIV-Associated Lung Infections and Complications (Lung HIV).
The prominence of Pneumocystis Pneumocystosis pneumonia as a herald of the HIV / AIDS epidemic and as a major cause of HIV-related morbidity and mortality has attention and resources on this previously unusual opportunistic pneumonia.
In the past 30 years, great strides have been made in our understanding of HIV / AIDS and Pneumocystosis, but there are still significant gaps. This review describes recent advances in the pathogenesis, epidemiology, diagnosis and management of HIV-associated Pneumocystosis and ongoing areas of clinical and translational research that are part of the International Study of HIV-Associated Opportunistic Pneumonies (IHOP) and Longitudinal Studies of HIV-Infections pulmonary and associated complications (Lung HIV).
Pneumocystis it is an opportunistic eukaryote that is classified as a fungus (1). The gender Pneumocystis it infects mammal species and is specific to the host species. Infection in humans is caused by Pneumocystis jirovecii; Pneumocystis carinii currently refers to one of the Pneumocystis species that infect mice.
BACKGROUND AND PATHOGENESIS
Human beings are a reservoir of P. jirovecii, although the exact relationship is not fully understood and environmental reservoirs have also been suggested. Primary infection occurs early in childhood, probably manifesting itself as a self-limited disease of the upper respiratory tract (2, 3), and most children worldwide have detectable antibodies between 2 and 4 years of age (4-6).
Animal studies demonstrate that the Pneumocystis is transmitted from animal to animal by air. Animal studies also show that animals with Pneumocystis develop Pneumocystosis after immunosuppression (reactivation of latent infection) and that immunocompromised animals free of Pneumocystis develop Pneumocystosis after exposure to immunocompromised animals infected with Pneumocystis (new exogenous infection) and immunocompetent animals that are colonized by Pneumocystis.
Numerous reports of pneumocystis cluster outbreaks among different immunocompromised populations support the transmission from person to person and the recent acquisition of infection in the pathogenesis of Pneumocystosis in humans.
In addition, molecular typing P. jirovecii genetic loci of people with Pneumocystosis demonstrated the diversity of P. jirovecii infecting humans and provided molecular evidence to support interhuman transmission and recent infection (7-9).
Before the HIV / AIDS epidemic, Pneumocystosis was uncommon.
From November 1967 to December 1970, a total of 194 patients were diagnosed with Pneumocystosis and reported to the Centers for Disease Control, which was the only provider of pentamidine isethionate, the only treatment for Pneumocystosis at the time (10).
In 1981, two reports of Pneumocystosis in 15 previously healthy men who had sex with other men and / or who were injecting drug users announced the start of the HIV / AIDS pandemic (11, 12) which currently affects about 33,4 million people worldwide and caused an estimated 25 million deaths (13).
Pneumocystosis is a frequent diagnosis of AIDS in the United States and Europe. At its peak in the United States, Pneumocystosis was the main defining diagnosis of AIDS and it was responsible for more than 20.000 new AIDS cases per year, from 1990 to 1993 (14-17).
At this time, the disaster was more than cruel to me, taking a thousand to my right and ten thousand to my left, so many times and in so many ways that this stretch of psalms seemed more sadistic than anything. A thousand times in a thousand for the right and ten thousand times for me, for the squid… Yes, on those dis, I would be better off, but it just happens that way. One funeral a day. Sometimes two. This is cruelty even to me .;
Here comes a fool, says he doesn't have “these references” and apologizes!
The only friend forever, it seems to me that Braga was right, is death.
She does, she promises, she comes, she takes, and she stays with you, forever!
In Europe, Pneumocystosis was the main AIDS-defining disease in the World Health Organization's HIV / AIDS Surveillance Report 2008, accounting for 16,4% of AIDS cases diagnosed in adults and adolescents that year (18).
Pneumocystosis remains a major cause of AIDS in North American and European HIV cohorts.
In the Antiretroviral Therapy Cohort Collaboration, a network composed of 15 North American and European cohorts established in 2000, Pneumocystosis was the second most frequent event for the definition of AIDS after esophageal candidiasis (19).
Pneumocystosis remains a major cause of HIV-associated pneumonia, but rates of Pneumocystosis have decreased.
San Francisco and Pneumocystosis
At the General Hospital of São Francisco, almost 1.000 cases of pneumocystosis associated with HIV were diagnosed microscopically from 1990 to 1993 (average of 250 cases per year).
This number has dropped to 20 to 30 cases per year. Most of these cases occurred in people who were not receiving antiretroviral therapy or Pneumocystosis prophylaxis, and many were unaware of their HIV infection at the time of presentation (21, 22). This experience is similar in other institutions, where 23 to 31% of Pneumocystosis cases reported occurred in patients who were recently diagnosed with HIV infection at the time of Pneumocystosis (21, 23, 24).
Annual number of microscopically confirmed cases of Pneumocystis Pneumonia (Pneumocystosis) diagnosed at San Francisco General Hospital, 1990–2009. ART = antiretroviral therapy.
Pneumocystosis associated with HIV is reported at variable rates worldwide (25, 26). Clinical studies in Africa that performed bronchoscopy with bronchoalveolar lavage (BAL) in HIV-infected patients with pneumonia report that Pneumocystosis was responsible for 0,8 to 38,6% of cases (26-28). At Mulago Hospital in Kampala, Uganda, the frequency of Pneumocystosis among HIV-infected patients hospitalized with suspected pneumonia who had acid-resistant negative smear microscopy and underwent bronchoscopy decreased from almost 40% of bronchoscopy to less than 10% (28, 29 ). However, the mortality associated with Pneumocystosis remains high. Although its current incidence is low in Uganda, Pneumocystosis patients had a higher mortality (75%, 3/4) than those with positive culture pulmonary tuberculosis (31%, 59/190) or cryptococcal pneumonia (10%, 1/10) (30).
PRESENTATION AND DIAGNOSIS
Classically, pneumocystosis associated with HIV presents with fever, non-productive cough and dyspnoea. Symptoms may be subtle at first, but progress gradually and may be present for several weeks before diagnosis. This presentation differs from that typically seen in immunocompromised patients without HIV with Pneumocystosis in which the duration of symptoms is often much shorter (31). Lung examination is usually normal, but, when abnormal, inspiratory rales are the most common finding.
Chest X-ray Essential for Diagnosis
Chest radiography is the basis for diagnostic evaluation and demonstrates bilateral, symmetrical, reticular (interstitial) or granular opacities (Figure 2) (32, 33). Pneumocystosis may also present with pneumothorax or bilateral pneumothorax. Although relatively uncommon, pneumothorax presents a difficult problem, often requiring prolonged management of the chest tube. Pneumocystosis occasionally presents with a normal chest X-ray.
In these cases, high-resolution computed tomography (HRCT) can be useful. HRCT scan of the chest shows irregular areas of ground-glass opacity (Figure 3) (34).
We must try to avoid pneumocystosis! And the best way is to treat yourself, after testing yourself!
Psychosomatic it's a science
Although the presence of ground-glass opacities is nonspecific for Pneumocystosis, its absence argues strongly against the diagnosis of Pneumocystosis, and no other diagnostic test for Pneumocystosis or treatment with Pneumocystosis is generally guaranteed in these cases (34).
There is no universal approach to managing suspected Pneumocystosis. Some institutions treat these individuals empirically, while others seek a definitive diagnosis.
Regardless of the selected approach, strict monitoring is recommended, as the presentation of Pneumocystosis may overlap with other pneumonia associated with HIV, and HIV-infected patients may have more than one concomitant pneumonia.
High-resolution computed tomography of the chest demonstrating the ground-glass opacities characteristic of an HIV-infected patient with Pneumocystis pneumonia because he had a normal chest X-ray (courtesy of L. Huang, used with permission).
Cannot be cultivated
Pneumocystis cannot be cultured, and the diagnosis of Pneumocystosis depends on microscopic visualization of characteristic cystic or trophic forms in respiratory specimens obtained with a higher frequency of sputum induction or bronchoscopy.
Bronchoscopy with BAL is considered the gold standard procedure for diagnosing Pneumocystosis in HIV-infected patients and has a reported sensitivity of 98% or more (20). However, bronchoscopy requires specialized personnel, rooms and equipment, in addition to being expensive and having an associated risk of complications.
Thus, bronchoscopy is limited in its availability in many areas of the world that are burdened with HIV / AIDS, and an accurate non-invasive procedure to diagnose Pneumocystosis would be a significant clinical advance.
The Limitation of Bronchioscopy and Even Violence in the Process Generated a Need
The development of specific PCR assays has revolutionized the diagnosis of many infectious diseases and PCR assays for P. jirovecii were developed. P. jirovecii
Os PCR assays combined with BAL samples have been shown to be sensitive for the diagnosis of Pneumocystosis.
The availability of sensitive PCR-based assays has led to studies that examined whether these assays could be combined with a non-invasive lung procedure (those who have had a bronchoscopy know ...) to effectively diagnose Pneumocystosis.
Two studies at the San Francisco General Hospital examined oropharyngeal lavage samples (OPW; gargle) and tested three different PCR-based trials, comparing the results with sputum samples or induced BAL and the microscopic examination after Diff-Quik staining as standard- gold.
Gold Standard OPW-PCR
These studies found that OPW-PCR had a diagnostic sensitivity of up to 88% and a specificity of up to 90% for Pneumocystosis (35, 36). Procedural factors, such as collecting the OPW sample before starting Pneumocystosis treatment or within 1 day after starting and with the patient coughing vigorously before sample collection, increased the sensitivity of the test.
Although the OPW-PCR sensitivity for Pneumocystosis approaches BAL microscopy and may exceed that of induced sputum microscopy, OPW-PCR can detect P. jirovecii DNA in the absence of Pneumocystosis, resulting in false positive PCR results. The imperfect specificity of PCR for Pneumocystosis is probably related to the highly sensitive nature of these assays and the fact that HIV-infected patients and other patients can be colonized with Pneumocystis (that is, the Pneumocystis DNA is detected by PCR in the absence of Pneumocystosis) (37, 38).
Many Studies Still Needed
Further studies are needed to determine whether applying a cut-off in quantitative PCR assays can be used to distinguish between Pneumocystosis and Pneumocystis colonization of.
The plasma and serum assays were studied for the diagnosis of Pneumocystosis. One trial examined plasma S-adenosylmethionine (SAM or AdoMet) as a potential biomarker for Pneumocystosis. SAM is an important biochemical intermediary involved in methylation and polyamine synthesis reactions (39, 40). The original reasoning for developing a SAM trial was that the Pneumocystis does not have a SAM synthetase and is therefore unable to synthesize its own SAM and must collect this intermediate from the host (a subsequent study has shown that the Pneumocystis has a functional SAM synthetase) (41).
Thus, patients with Pneumocystosis may have low levels of MAS.
A series of New York studies found that plasma levels of AdoMet could be used to distinguish between HIV-infected patients with Pneumocystosis and those with non-Pneumocystosis pneumonia and healthy control subjects (39, 40).
In one study, patients with Pneumocystosis had significantly lower plasma AdoMet levels compared to patients with non-Pneumocystosis pneumonia (bacterial pneumonia or TB), and there was no overlap in AdoMet levels between these two groups of patients (40). A subsequent study that measured serum SAM found overlapping levels between HIV-infected patients with Pneumocystosis and those with non-Pneumocystosis pneumonia (42).
Whether the divergent results of these studies are related to differences between plasma and serum SAM levels, as hypothesized, or to other factors, is unclear, and further studies are needed.
serum (1-3) -β-D-glucan biomarker for Pneumocystosis
More recently, serum (1-3) -β-D-glucan, a component of the cell wall of all fungi, including Pneumocystis, has been investigated as a biomarker for Pneumocystosis because patients with Pneumocystosis may have high levels (43, 44).
One report found that patients with Pneumocystosis with and without underlying HIV infection had significantly higher serum levels of (1-3) -β-D-glucan compared to patients without Pneumocystosis (43). Using a cutoff point of 100 pg / ml, another study reported a diagnostic sensitivity of 100% and a specificity of 96,4% (44). (1-3) -β-D-glucan is elevated in several fungal pneumonias, and this test cannot distinguish between fungal etiologies (eg, Pneumocystosis and Aspergillus species of). Thus, although the results of these diagnostic tests or non-invasive biomarkers are promising, additional validation is necessary, and bronchoscopy with BAL remains the gold standard diagnostic test for Pneumocystosis.
TREATMENT OF CFP
Trimethoprim-sulfamethoxazole is the recommended first-line treatment for Pneumocystosis in HIV-infected patients with mild, moderate, and severe Pneumocystosis, with intravenous therapy generally recommended for patients with moderate to severe illness and oral therapy used for outpatients with milder illness (45).
Alternative regimens include intravenous pentamidine, clindamycin plus primaquine, trimethoprim plus dapsone and atovaquone suspension.
Adjuvant corticosteroids are recommended for patients with moderate to severe pneumocystosis, as demonstrated by PaO2 less than 70 mmHg or alveolar-arterial oxygen gradient greater than 35 mmHg (45). Patients should start adjunctive corticosteroids at the same time that Pneumocystosis therapy is started.
The recommended duration of treatment is 21 days (45).
However, a substantial proportion of individuals cannot complete a full trimethoprim-sulfamethoxazole cycle due to treatment-limiting toxicity or are switched to an alternative treatment regimen due to perceived treatment failure (46).
Although there are only limited data from prospective randomized controlled trials comparing second-line treatments with Pneumocystosis, a tri-central observational study and a systematic review suggest that the combination of clindamycin with primaquine is an effective alternative to intravenous pentamidine as second-line pneumocystosis treatment.
Chemo Prophylaxis by sulfamethoxazole-trimethoprim
This is also the first-line regimen recommended for primary and secondary prophylaxis against Pneumocystosis. Alternative regimens include dapsone with or without pyrimethamine and leucovorin, suspension of atovaquone and pentamidine in aerosol.
HIV-infected adolescents and adults, including pregnant women, should receive Pneumocystosis prophylaxis if the cell count CD4 + is less than 200 cells / μl or if you have a history of oral candidiasis (primary prophylaxis) and after an episode of Pneumocystosis (secondary prophylaxis) 45).
People with a CD4 + cell count below 14% and those with a history of AIDS-defining disease should also be considered candidates for Pneumocystosis prophylaxis (45).
Once initiated, prophylaxis with Pneumocystosis is recommended throughout the life, but it can be discontinued in HIV-infected adolescents and adults who are receiving combination antiretroviral therapy and have responded with an increase in CD4 + cell counts below 200 / µl to above 200 / µl for at least 3 months (45).
A potential exception is patients who developed Pneumocystosis when the CD4 + cell count was above 200 cells / μl; these individuals are likely to remain on Pneumocystosis prophylaxis, regardless of CD4 + cell count (45).
Following discontinuation of Pneumocystosis prophylaxis, the risk of subsequent Pneumocystosis in antiretroviral therapy combined with a sustained CD4 + cell count above 200 cells / μl (and usually accompanied by a sustained suppression of plasma RNA below detection limits) demonstrated extremely low, but rare cases have been described (49).
Prophylaxis should be resumed if the CD4 + cell count falls below 200 cells / μl (45). Recent data from a collaboration of 12 cohorts suggest that the incidence of Pneumocystosis is low in HIV-infected people with a CD4 + cell count of 100 to 200 cells / µl and RNA levels below 400 copies / ml, regardless of the use of prophylaxis. Pneumocystosis, suggesting that it may be safe to stop prophylaxis earlier, although additional data are needed (50).
PUTATIVES-trimethoprim sulfamethoxazole RESISTANCE TO DRUGS IN P. carinii
The widespread use of trimethoprim-sulfamethoxazole for the prophylaxis of Pneumocystosis has been associated with increases in resistant trimethoprim-sulfamethoxazole bacteria (51) and has raised concerns about the potential resistance to trimethoprim-sulfamethoxazole drugs P. jirovecii (52).
Similar concerns have been raised about the use of atovaquone and potential resistance to atovaquone drugs (53). Resistance to trimethoprim-sulfamethoxazole drugs may also result in resistance to trimethoprim plus dapsone (a sulfone), further limiting the therapeutic options available to treat (and prevent) Pneumocystosis. The inability to cultivate P. jirovecii has hampered efforts to document drug resistance in Pneumocystis, but the researchers explored this important issue by examining genetic mutations in the dihydrofolate reductase (DHFR) and dihydropteroate synthase (DHPS) genes, the enzyme targets for trimethoprim and sulfa (sulfamethoxazole and dapsone), respectively.
And correlating the observed genetic mutations with clinical outcomes (52).
This approach was chosen because the genetic mutations of DHFR and DHPS have been shown to cause drug resistance, as demonstrated in other microorganisms, such as Plasmodium falciparum (54).
Six studies examined P. jirovecii DHFR mutations in patients with Pneumocystosis with and without underlying HIV infection in the United States, Japan, Europe, South Africa and Thailand (55-60). The first two studies reported that DHFR mutations were uncommon and unrelated to the use of trimethoprim as part of Pneumocystosis prophylaxis (ie, trimethoprim-sulfamethoxazole) (55, 56).
In these studies, non-synonymous DHFR mutations were found, resulting in substitution of amino acid (s), in 0% (0/37) and 7% (2/27) of the Pneumocystosis samples.
Trimethropine Not Associated with Pneumocystic Mutations Kanrinee
A similar proportion (4%, 5/128 samples) was found in the largest study to date, which also found no association between the use of trimethoprim and the presence of non-synonymous DHFR mutations (59).
In contrast, a European study reported non-synonymous DHFR mutations in 33% (11/33) of Pneumocystosis samples (57). This study found that the use of DHFR inhibitors (trimethoprim or pyrimethamine) for Pneumocystosis prophylaxis was associated with the presence of DHFR mutations (P = 0,008) and that the majority of patients with DHFR mutations were receiving pyrimethamine (n = 7) instead of trimethoprim (n = 2) as part of their prophylaxis regimen.
This study raises the possibility that different DHFR inhibitors may select for different DHFR mutations or may select non-synonymous DHFR mutations at different frequencies.
Since no outcomes were reported in this study, it is not known whether the presence of mutations in the DHFR gene is associated with increased morbidity, mortality, or failure to treat Pneumocystosis in people receiving trimethoprim-sulfamethoxazole or trimethoprim plus dapsone.
Compared to six DHFR studies, more than 20 studies examined P. jirovecii DHP mutations among Pneumocystosis patients with and without underlying HIV infection in North America, Europe, Asia, Africa, South America and Australia.
The preponderance of studies on DHPS compared to DHFR refers to the fact that sulfamethoxazole is more active against Pneumocystis compared to trimethoprim in animal models of Pneumocystosis, and therefore DHPS mutations would be expected to be more important than DHFR mutations for the development of trimethoprim potential.
Resistance to sulfamethoxazole drugs.
These studies report a wide range in the frequency of DHPS mutations (from 3,7 to 81%) (58, 61, 62).
In general, these studies also reveal a geographical variation in the proportions of DHPS mutations observed, with the highest proportions reported in the United States (San Francisco) and the lowest reported proportions in Spain and South Africa.
In addition, some studies report an increase in the proportion of DHPS mutations over time (63). Specifically, two non-synonymous mutations that result in amino acid substitutions at amino acid position 55 (Thr → Ala) and / or at position 57 (Pro → Ser) are almost exclusively reported (64, 65).
In general, these studies generally demonstrated a significant association between the use of sulfa (sulfamethoxazole or dapsone) as part of Pneumocystosis prophylaxis and the presence of nonsynonymous DHON mutations (52).
A Noteworthy Find
This finding is noteworthy because the DHPS locus is well maintained in Pneumocystis obtained from other mammals and because DHPS mutations are rarely found in non-human primates (66), suggesting that the use of sulfa drugs by humans selected P. jirovecii DHPS mutations of.
In several studies, the presence of DHPS mutations has been linked to poor results in people infected with HIV with Pneumocystosis.
One study reported that the presence of DHPS mutations was an independent predictor associated with a 3-month increase in mortality (adjusted risk ratio, 3,10; 95% confidence interval, 1,19-8,06; P = 0,01) (67).
Another study noted that the presence of DHPS mutations was associated with an increased risk of treatment failure with Pneumocystosis with trimethoprim-sulfamethoxazole or trimethoprim plus dapsone (RR = 2,1; P = 0,01) (68).
There was a failure in treatments with trimethoprim-sulfamethoxazole
Finally, a small study reported that all four patients with DHPS mutations who were treated with trimethoprim-sulfamethoxazole failed therapy with Pneumocystosis (69).
In contrast, other studies have failed to demonstrate these associations and, instead, reported that risk factors such as low serum albumin and early ICU admission were stronger predictors of pneumocystosis mortality than the presence of DHPS mutations (62).
Thus, there is an apparent paradox regarding the clinical significance of DHPS mutations and inferences related to putative resistance to the drug sulfamethoxazole-trimethoprim.
Studies consistently report that the majority of patients with Pneumocystosis and DHPS mutations treated with trimethoprim-sulfamethoxazole respond to this treatment (62, 67, 68, 70). However, patients with DHP mutations who are treated with trimethoprim-sulfamethoxazole tend to have worse results compared to those with wild-type DHPS, who are treated with trimethoprim-sulfamethoxazole and compared to those with DHP mutations who are treated with a base non-sulfa-regime (62).
The precise explanation for these observations is not clear, but concomitant DHFR mutations, low serum levels of trimethoprim-sulfamethoxazole and host factors have been postulated as potential co-factors for failure of treatment with trimethoprim-sulfamethoxazole in patients with Pneumocystosis mutations and DHPS.
No study has examined all of these factors postulated at the same time in patients with Pneumocystosis. Until the clinical significance of DHPS and possibly DHFR mutations can be better defined, clinicians treating patients with Pneumocystosis should use trimethoprim-sulfamethoxazole as first-line therapy in all patients, unless contraindicated by allergic reaction or adverse effects .
the longitudinal studies of infections and pulmonary complications associated with HIV (Lung HIV) Study is a novel, collaborative, multi-R01 consortium of research projects established by the National Heart, Lung, and Blood Institute (NHLBI) to examine a wide range of diseases infectious and non-infectious lung diseases that affect people living with HIV / AIDS. The specific objectives of the lung HIV study, the study design and study protocols are described in this edition's online supplement. Within the Lung HIV Study, eight clinical centers conduct their own separate research studies, but also participate under the administration of the NHLBI and a data coordination center to conduct collaborative studies at multiple locations and at the group level.
Each clinical site has its own research focus. The IHOP study focuses on opportunistic pneumonias, especially pneumocystosis, but includes the establishment of a clinical and specimen database that enables research on tuberculosis, bacterial pneumonia and other opportunistic pneumonias. For example, studies on tuberculosis, the dominant opportunistic pneumonia in sub-Saharan Africa, are incorporated into the IHOP infrastructure.
The specific objectives of the IHOP Study include:
(1) determine the frequency and mortality of HIV-associated opportunistic pneumonia in an international longitudinal cohort and test the hypothesis that pneumocystosis is associated with increased mortality.
(2) estimate the sensitivity and specificity of molecular tools for the diagnosis of Pneumocystosis and TB and test the hypotheses that OPW samples combined with PCR assays are sensitive tests for diagnosing Pneumocystosis and TB; and
(3) test the hypothesis that DHPS gene mutations are associated with increased morbidity and mortality and explore potential mechanisms for these outcomes. IHOP and Lung HIV have established specimen banks linked to clinical data, and researchers interested in studying HIV-associated opportunistic pneumonia are encouraged to contact the authors of this review.
The HIV / AIDS pandemic has witnessed significant advances in our understanding of HIV / AIDS and Pneumocystosis, one of the prominent diseases associated with the pandemic. This review describes recent advances in the pathogenesis, epidemiology, diagnosis and management of pneumocystosis associated with HIV and ongoing areas of clinical and translational research that are part of the IHOP and Lung HIV Studies. IHOP and Lung HIV studies have established a bank of clinical samples, accompanied by clinical data for future studies. Given the decline in the incidence of Pneumocystosis, but its lasting importance as a cause of morbidity and mortality in HIV-infected and other immunosuppressed patients, this specimen bank can accelerate and deepen our understanding of P. jirovecii and Pneumocystosis.
Getting to know AIDS better can give you a better view on why it’s better to test! In this case, better late than never, the old man lying there is there, about to die ”
Translated by Claudio Souza, the original HIV-Associated Pneumocystis Pneumonia
Supported by the National Heart Lung and Blood Institute grants HL087713, HL090335 and HL090335-02S1.
Author Disclosure: A LH received financial support from the Foundation for New Innovative Diagnostics (FIND). AC and JLD received financial support from WHO and FIND.
SdB and JK have no financial relationship with a commercial entity that has an interest in the subject of this manuscript. SM received financial support from Abbott and the Gates Foundation.
RFM received fees for lectures from Gilead and Merck. PDW, WW and HM have no financial relationship with a commercial entity that is interested in the subject of this manuscript.