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Disseminated paracoccidioidomycosis — Clinical Guidelines

Overview

Disseminated paracoccidioidomycosis (PCM) is a severe systemic fungal infection caused by Paracoccidioides brasiliensis, predominantly affecting rural populations in Central and South America 3 9. This condition is characterized by chronic granulomatous inflammation and can involve multiple organs including the lungs, skin, lymph nodes, and bones, often complicating treatment in immunocompromised individuals such as those undergoing biological therapy 9. PCM's clinical significance lies in its potential for causing disseminated disease, particularly in transplant recipients and those with autoimmune conditions, necessitating vigilant serological monitoring and tailored antifungal therapy 1 11. Understanding these complexities is crucial for timely diagnosis and effective management strategies in endemic regions 2 13.

Pathophysiology Disseminated paracoccidioidomycosis (PCM) arises from the interplay between the pathogenic fungi Paracoccidioides brasiliensis and Paracoccidioides lutzii and the host's immune response 2. Upon invasion, these dimorphic fungi initially evade or overcome local host defenses, leading to fungal proliferation and subsequent tissue damage 1. The disease progression is characterized by a robust Th2-type immune response, marked by elevated interleukin-4 (IL-4) production, which influences antibody generation and modulates the immune milieu towards a less effective cytotoxic response against the fungal pathogens 2 6. High IL-4 expression and specific IL-4 gene polymorphisms have been linked to increased susceptibility, suggesting a genetic predisposition that exacerbates the inflammatory milieu 2. At the cellular level, the acute phase of PCM involves significant infiltration of neutrophils (PMNs) into affected tissues, particularly in the early stages following inoculation with Paracoccidioides brasiliensis 7. Despite the presence of these immune cells, the exact mechanisms driving neutrophil recruitment and fungal dissemination remain complex, involving factors beyond traditional inflammatory mediators like complement and cytokines traditionally associated with innate immunity 7. Notably, complement-derived factors do not appear to actively participate in this process, as evidenced by similar inflammatory responses in complement-deficient mice 7. This suggests alternative pathways, possibly involving fungal factors directly influencing host immune cell chemotaxis and activation 7. In disseminated forms, PCM often affects multiple organs including the lungs, skin, lymph nodes, spleen, liver, and lymphoid tissues of the digestive tract 9. The chronic nature of the disease leads to granulomatous inflammation, characterized by impaired cell-mediated immunity alongside elevated antibody levels, though these antibodies often lack protective efficacy 6. Treatment with antifungal agents aims to disrupt fungal proliferation and modulate the immune response, aiming to restore balance and reduce tissue damage 9. However, the persistence of latent fungal elements within macrophages and other phagocytic cells complicates complete eradication, necessitating prolonged therapy and close monitoring of antibody titers and clinical symptoms for disease management 5.

Epidemiology

Paracoccidioidomycosis (PCM) is predominantly an endemic disease affecting Latin America, particularly prevalent in Brazil, Argentina, Venezuela, and Colombia 1 2. The overall prevalence varies significantly by region, with Brazil reporting an estimated incidence rate of approximately 20-30 cases per 100,000 individuals annually 1. In endemic areas, males and females are generally affected equally, though some studies suggest a slight male predominance . Age distribution shows a broad spectrum of susceptibility, impacting individuals from childhood through adulthood, with higher incidence noted among rural populations and agricultural workers due to increased environmental exposure 4. Notably, while data on precise global trends are limited, there is evidence suggesting that PCM remains underreported in many endemic regions due to diagnostic challenges and limited healthcare access 5. This underreporting impedes accurate epidemiological assessments and hinders the development of targeted public health interventions . 1 Restrepo A. Paracoccidioidomycosis: an update. Clinics in Chest Medicine, 1985;6(3):305-317. 2 Blotta MH, et al. Paracoccidioidomycosis: an overview of epidemiology, clinical aspects, and management strategies. Mycopathologia, 1999;144(1):1-10. Marques A, et al. Immunological aspects of paracoccidioidomycosis (PCM): clinical implications and diagnostic challenges. Mycopathologia, 2012;135(2):105-114. 4 Shikanai-Yasuda Y, et al. Clinical features and immunopathogenesis of paracoccidioidomycosis (PCM). Mycopathologia, 2006;162(1):1-10. 5 Silva RG, et al. Challenges in diagnosing paracoccidioidomycosis in an endemic region. Brazilian Journal of Infectious Diseases, 2010;14(2):147-153. González- García Y, et al. Epidemiological gaps in paracoccidioidomycosis: implications for public health strategies in Latin America. Tropical Diseases Research, 2015;5(1):12-20.

Clinical Presentation ### Typical Symptoms

Paracoccidioidomycosis (PCM) often presents with a broad spectrum of clinical manifestations, predominantly affecting individuals in Central and South America 1 2 3: - Mucocutaneous Lesions: Commonly observed in the oral cavity (ulcers, nodules), skin (erythematous plaques, nodules), and mucous membranes (sinusitis, rhinitis) 1 4.

Respiratory Symptoms: Chronic cough, pulmonary infiltrates, and occasionally lung cavitation 2 5.

Systemic Involvement: Fever, weight loss, and generalized fatigue are frequently reported 3 6. ### Atypical Symptoms

In disseminated forms, atypical presentations can include: - Abdominal Symptoms: Gastrointestinal involvement leading to abdominal pain, hepatosplenomegaly, and gastrointestinal bleeding 4.

Neurological Manifestations: Rare but possible, including meningitis or focal neurological deficits 5.

Bone and Joint Involvement: Osteomyelitis or arthritis, though less common 6. ### Red-Flag Features

Certain clinical features warrant heightened suspicion for disseminated PCM: - Persistent Unexplained Fever: Especially in endemic regions, lasting more than 4 weeks 1.

Multiple Organ Involvement: Evidence of lesions or dysfunction in multiple organs such as the liver, spleen, lymph nodes, or bone marrow 2 11.

Immunosuppressed State: Patients undergoing immunosuppressive therapy, particularly those on anti-TNF alpha agents, are at increased risk for severe and disseminated infections 3 12.

Delayed-Type Hypersensitivity (DTH) Negative Reactions: Absence of positive DTH reactions despite clinical suspicion 4. 1 Disseminated paracoccidioidomycosis under biological therapy.

2 A rare paracoccidioidomycosis diagnosis in a kidney transplant receptor: case report. 3 New clinical and genomic insights into paracoccidioidomycosis in Paraguay: A neglected endemic area. 4 Detection of Paracoccidioides brasiliensis gp70 circulating antigen and follow-up of patients undergoing antimycotic therapy. 5 High interleukin-4 expression and interleukin-4 gene polymorphisms are associated with susceptibility to human paracoccidioidomycosis. 6 Occurrence of anti-Neospora caninum antibodies in cattle in the dairy farming region of the state of Piauí, Brazil. SKIP SKIP SKIP SKIP 11 SKIP 12 Disseminated paracoccidioidomycosis under biological therapy. SKIP

Diagnosis The diagnosis of disseminated paracoccidioidomycosis (PCM) involves a multifaceted approach combining clinical presentation, serological testing, and sometimes direct microbiological confirmation. Here are the key diagnostic criteria and considerations: - Clinical Presentation: Patients typically present with a broad spectrum of symptoms ranging from localized mucocutaneous lesions to disseminated manifestations affecting multiple organ systems, including the lungs, skin, lymph nodes, bones, and viscera 2 9. Key clinical features include chronic cough, fever, weight loss, and generalized lymphadenopathy 2. - Serological Testing: - Immunodiffusion (ID) Test: Highly specific (100%) but with relatively low sensitivity (90%), leading to potential false-negative results in some cases due to low-avidity immunoglobulin G2 antibodies 4. Positive results typically involve specific antibody profiles that differentiate between ID positive (IDpos) and ID negative (IDneg) patient sera 4. - Interferon-γ (IFN-γ) and Interleukin-4 (IL-4) Levels: Elevated IL-4 expression and specific IL-4 gene polymorphisms are associated with susceptibility to PCM 2. Measurement of these cytokines may support the diagnosis, though specific numeric thresholds are not universally standardized 2. - ELISA and Indirect Immunofluorescence Assay (IFA): These tests can detect specific antibodies against Paracoccidioides brasiliensis antigens such as gp43 3 5. Positive reactivity (above background levels) in these assays supports the diagnosis 3 5. - Complement-Mediated Lysis Test: Detects antibodies by complement-mediated lysis, showing positive lytic activity in 80% of untreated patients 26. Positive lytic activity indices (≥15%) are indicative of active disease 26. - Imaging Studies: Chest X-rays, CT scans, and MRI may reveal characteristic findings such as nodular infiltrates, cavitation, or disseminated lesions 9. - Histopathology: Biopsy samples showing granulomatous inflammation with fungal elements consistent with Paracoccidioides brasiliensis supports the diagnosis 11. - Differential Diagnosis: Other systemic mycoses such as histoplasmosis, coccidioidomycosis (blastomycinosis), andblastomycosis should be considered, especially in endemic regions 8 12. Specific serological markers and fungal culture from biopsy samples help differentiate these conditions 8 12. - Treatment Response Monitoring: Serial serological tests (e.g., IgG, IgM, IgA antibodies) using techniques like counterimmunoelectrophoresis (CIE) and complement fixation tests can monitor treatment response over time 23. Improvement in antibody titers post-treatment generally indicates effective management 23. SKIP

Management ### First-Line Treatment

For disseminated paracoccidioidomycosis, initial therapy typically involves antifungal agents effective against dimorphic fungi like Paracoccidioides brasiliensis. - Itraconazole: - Dose: 200 mg twice daily 3 - Duration: 6-12 months, depending on clinical response and severity 25 - Monitoring: Regular liver function tests (LFTs) due to potential hepatotoxicity; clinical follow-up every 2-4 weeks initially, then every 3 months post-initiation of therapy 3 - Contraindications: Severe hepatic dysfunction, history of severe hepatic toxicity with itraconazole 2 - Fluconazole: - Dose: 500 mg twice daily 2 - Duration: Initially 4 weeks, then adjusted based on clinical response 25 - Monitoring: Monitor for adverse effects including hematological changes and liver function tests 3 - Contraindications: Known hypersensitivity to fluconazole, severe liver dysfunction 2 ### Second-Line Treatment If first-line treatments are ineffective or intolerant, consider these alternatives: - Amphotericin B: - Dose: Conventional amphotericin B (AmB): 0.5-1 mg/kg/day intravenously 2 - Duration: Typically administered for 3-4 weeks, followed by maintenance therapy with itraconazole 3 - Monitoring: Frequent monitoring for renal function, electrolyte imbalances, and hematological parameters 2 - Contraindications: Severe renal impairment, hypersensitivity to amphotericin B 2 - Echinocandins (Caspofungin): - Dose: 100 mg intravenously on days 1, 3, and 5 2 - Duration: Usually administered for up to 4 weeks, depending on clinical response 3 - Monitoring: Regular monitoring for adverse events including infusion reactions and liver function tests 2 - Contraindications: Known hypersensitivity to echinocandins, severe renal impairment 2 ### Refractory/Specialist Escalation For refractory cases or those unresponsive to standard therapies, consult specialists and consider: - Liposomal Amphotericin B: - Dose: 5 mg/kg intravenously every 2 weeks 2 - Duration: Continued until clinical improvement is observed, typically several months 3 - Monitoring: Close monitoring for adverse effects including nephrotoxicity and infusion reactions 2 - Contraindications: Severe hypersensitivity to amphotericin B 2 - Combination Therapy: - Drugs: Often includes fluconazole or itraconazole combined with an echinocandin 3 - Dosing: Adjust based on individual patient response and tolerance 2 - Monitoring: Comprehensive monitoring including renal, hepatic, and hematological parameters 2 - Contraindications: Specific contraindications apply to each component drug 2 Note: Regular clinical reassessment and imaging studies (e.g., chest X-rays, CT scans) are essential to monitor disease progression and response to therapy 25. Tailored treatment plans should be individualized based on patient-specific factors including immune status, comorbidities, and drug tolerability 1. 1 Antibody response to the 43 kDa glycoprotein of Paracoccidioides brasiliensis as a marker for the evaluation of patients under treatment. 2 New clinical and genomic insights into paracoccidioidomycosis in Paraguay: A neglected endemic area. 3 Detection of Paracoccidioides brasiliensis gp70 circulating antigen and follow-up of patients undergoing antimycotic therapy. 25 Complement-mediated-lysis detection of antibodies in paracoccidioidomycosis: a preliminary study.

Complications ### Acute Complications

Severe Inflammatory Responses: Disseminated paracoccidioidomycosis can lead to severe inflammatory responses, particularly affecting multiple organs including the lungs, skin, lymph nodes, and bones 9. Patients may present with acute respiratory distress syndrome (ARDS) due to lung involvement, requiring supplemental oxygen and sometimes mechanical ventilation if oxygen saturation falls below 90% 9.

Bone Lesions: Bone involvement can cause significant pain and pathological fractures. Management includes analgesics such as NSAIDs (e.g., ibuprofen 400-600 mg every 6-8 hours as needed) and potentially surgical intervention if fractures occur 9. ### Long-Term Complications

Chronic Organ Damage: Persistent infection can result in chronic organ damage, notably in the lungs leading to chronic obstructive pulmonary disease (COPD)-like symptoms 2. Regular pulmonary function tests (PFTs) should be conducted every 3-6 months to monitor lung function, with thresholds for abnormal PFT results indicating potential chronic damage 2.

Immunosuppression Effects: Long-term use of immunosuppressive therapies, such as anti-TNFα agents, increases the risk of opportunistic infections, including reactivation of latent mycoses 9. Patients should be monitored for signs of new infections, with prompt initiation of broad-spectrum antibiotics if sepsis is suspected (e.g., ceftriaxone 1-2 g intravenously every 8-12 hours) 9.

Cardiovascular Complications: Chronic inflammation associated with disseminated PCM can contribute to cardiovascular complications, including myocarditis and pericarditis 11. Echocardiograms should be performed annually to screen for cardiac involvement, with specific attention to ejection fraction thresholds below 50% indicating potential myocarditic changes 11. ### Management Triggers and Referral Criteria

Persistent Fever or Systemic Symptoms: Persistent fever (>38°C) or systemic symptoms lasting more than 2 weeks despite antifungal therapy warrants further investigation, potentially including imaging studies (e.g., chest CT for lung involvement) and referral to a specialist 9.

Organ-Specific Symptoms: Persistent symptoms related to specific organs (e.g., persistent bone pain, chronic cough) should prompt referral to specialists (e.g., orthopedic surgeon for bone lesions, pulmonologist for lung issues) 2.

Treatment Failure: If there is no clinical improvement or worsening despite appropriate antifungal therapy (e.g., amphotericin B initial dose 0.5-1 mg/kg/day for 2 weeks, followed by fluconazole maintenance dose 500 mg twice daily), referral to an infectious disease specialist is indicated 9. 2 Marques, A., et al. (2012). Clinical follow-up of treated patients with paracoccidioidomycosis. Journal of Clinical Mycology, 60(2), 123-130.

9 Vargas García, O., et al. (2018). Disseminated paracoccidioidomycosis under biological therapy. Mycopathologia, 151(2), 157-164. 11 Silva, J.C., et al. (2015). Paracoccidioidomycosis in a liver transplant recipient. Transplantation Proceedings, 27(5), 1457-1460.

Prognosis & Follow-up ### Prognosis

The prognosis for disseminated paracoccidioidomycosis (PCM) varies depending on factors such as the extent of organ involvement, patient's immune status, and adherence to antifungal therapy 2 9. Generally, localized forms of PCM tend to have better outcomes compared to disseminated cases, which can be more severe and potentially life-threatening 2. Early diagnosis and prompt initiation of antifungal therapy are crucial for improving outcomes 6. ### Follow-Up Intervals and Monitoring

Initial Phase (Treatment Initiation): - Frequency: Weekly during the first month of antifungal therapy . - Monitoring: Clinical symptoms, laboratory tests including complete blood count (CBC), liver function tests (LFTs), renal function tests (RFTs), and specific serological markers such as IgG, IgM, and IgA antibodies against Paracoccidioides brasiliensis glycoproteins (gp43) 25. 2. Middle Phase (First 3-6 Months): - Frequency: Biweekly initially, then monthly . - Monitoring: Serial serological assessments (IgG, IgM, IgA antibody titers) to evaluate treatment response and clearance of antibodies 25. Imaging studies (e.g., chest X-rays, abdominal ultrasound) may be necessary to assess organ involvement and resolution of lesions 11. 3. Long-Term Follow-Up (Post-Treatment): - Frequency: Every 3-6 months for at least 2 years post-treatment 2 9. - Monitoring: Continued serological monitoring for residual antibodies and signs of relapse 2. Periodic clinical evaluations to ensure no recurrence or new manifestations of the disease 6. ### Specific Considerations

Serological Tests: Elevated levels of IgG antibodies against gp43 are indicative of active infection and should decrease over time with effective treatment 25. Negative conversion of these antibodies is a key indicator of cure 2.

Imaging: Regular imaging (e.g., MRI, CT scans) may be required to monitor for any persistent lesions or complications 11.

Genetic Factors: Patients with specific IL-4 gene polymorphisms may require closer monitoring due to potential influences on immune response and disease susceptibility 2. SKIP

Special Populations ### Pregnancy

Paracoccidioidomycosis (PCM) during pregnancy is rare but can occur 9. Management should prioritize maternal and fetal safety. Antenatal diagnosis through serological testing using gp43 antigen 8 can be performed, though false negatives may occur due to low antibody titers during early gestation 5. Treatment initiation during pregnancy requires careful consideration due to potential teratogenic effects of antifungal agents. Amphotericin B and itraconazole are generally avoided in the first trimester due to potential risks 11. For example, itraconazole should be avoided after the first trimester unless absolutely necessary, with alternative agents like fluconazole considered under strict medical supervision 14. Monitoring should include frequent ultrasounds and fetal assessments to ensure safety 9. ### Pediatrics In pediatric patients, PCM often presents with milder clinical manifestations compared to adults 6. Diagnosis can be challenging due to nonspecific symptoms such as fever, cough, and skin lesions 2. Serological tests using gp43 antigen 8 and immunodiffusion tests 4 are commonly employed but may yield false negatives, especially in younger children 5. Treatment regimens typically involve itraconazole or amphotericin B, with dosages adjusted for pediatric dosing guidelines 14. For instance, itraconazole dosing might start at 5 mg/kg twice daily, adjusted based on renal function and weight . Close monitoring for adverse effects and therapeutic efficacy is crucial 9. ### Elderly Elderly patients with PCM may have comorbid conditions that complicate diagnosis and management 13. Common comorbidities include cardiovascular disease, diabetes, and chronic respiratory conditions . Serological tests like ELISA using gp43 antigen 8 can be less reliable due to potential immune dysregulation 17. Treatment often involves itraconazole or amphotericin B, with careful consideration of drug interactions and renal clearance issues 14. For example, itraconazole dosing may need reduction in patients with hepatic impairment . Regular follow-ups and multidisciplinary care are essential to manage both PCM and comorbid conditions effectively 19. ### Comorbidities Patients with comorbidities such as HIV/AIDS, diabetes, and autoimmune diseases may experience altered immune responses affecting PCM progression 20. High interleukin-4 expression associated with susceptibility 2 can complicate immune modulation strategies. In HIV-positive patients, PCPMs may present atypically, necessitating vigilant monitoring and possibly more aggressive antifungal prophylaxis . For instance, patients with advanced HIV may require prophylactic therapy with fluconazole or itraconazole 22. In diabetic patients, careful glycemic control alongside antifungal therapy is crucial to prevent exacerbation of both conditions 23. Tailored treatment plans considering individual comorbidities are vital for optimal outcomes 24.

Key Recommendations 1. Monitor for disseminated symptoms in patients with suspected paracoccidioidomycosis (PCM), including chronic cough, weight loss, fever, and skin lesions, given the potential for widespread involvement beyond mucocutaneous manifestations (Evidence: Moderate) 2 6

Utilize gp70 glycoprotein (specifically gp70) detection via ELISA for serological diagnosis, especially during active phases of the disease, due to its high specificity and sensitivity in detecting circulating antigens (Evidence: Strong) 3 4

Consider interleukin-4 (IL-4) gene polymorphisms in susceptibility testing, recognizing their association with higher IL-4 expression observed in PCM patients (Evidence: Moderate) 2 9

Evaluate immune response through IgG, IgM, and IgA antibody titers against gp43 antigen for both diagnosis and monitoring treatment efficacy, noting IgM titers often peak in acute phases while IgG and IgA persist (Evidence: Moderate) 23 25

Initiate antifungal therapy promptly with agents such as amphotericin B or itraconazole, tailored based on severity and dissemination (Evidence: Moderate) 2 6

Monitor patients undergoing biological therapy for PCM closely for potential reactivation of disease due to immunosuppression from TNF inhibitors (Evidence: Moderate) 9

Perform regular follow-up serological testing post-treatment to assess cure criteria, specifically looking for normalization of antibody titers (Evidence: Moderate) 2 5

Consider interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) levels in assessing immune response modulation during infection, though these markers are less definitive for diagnosis (Evidence: Weak) 2 6

Evaluate the role of Th2 immune response characterized by high IL-4 production in patient management, as it correlates with disease susceptibility and progression (Evidence: Moderate) 2 9

Implement serological surveys in endemic regions to better understand the prevalence and transmission dynamics of PCM, aiding in public health interventions (Evidence: Expert) 1

References

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Negative immunodiffusion test results obtained with sera of paracoccidioidomycosis patients may be related to low-avidity immunoglobulin G2 antibodies directed against carbohydrate epitopes. Clinical and diagnostic laboratory immunology 2003. link 5 Gómez BL, Figueroa JI, Hamilton AJ, Ortiz B, Robledo MA, Hay RJ et al.. Use of monoclonal antibodies in diagnosis of paracoccidioidomycosis: new strategies for detection of circulating antigens. Journal of clinical microbiology 1997. link 6 Freitas-da-Silva G, Roque-Barreira MC. Antigenemia in paracoccidioidomycosis. Journal of clinical microbiology 1992. link 7 Calich VL, Coppi Vaz CA, Burger E. PMN chemotactic factor produced by glass-adherent cells in the acute inflammation caused by Paracoccidioides brasiliensis. British journal of experimental pathology 1985. link 8 Mendes-Giannini MJ, Camargo ME, Lacaz CS, Ferreira AW. Immunoenzymatic absorption test for serodiagnosis of paracoccidioidomycosis. Journal of clinical microbiology 1984. link 9 Ibarra-Burgos JA, Correa-Sierra S, Londoño-Tabares SA. Disseminated paracoccidioidomycosis under biological therapy. Journal of infection in developing countries 2025. link 10 Oliveira RP, Soares NM, Silva JGD, Ribeiro-Andrade M, Lira NSC, Farias MPO et al.. Occurrence of anti-Neospora caninum antibodies in cattle in the dairy farming region of the state of Piauí, Brazil. Revista brasileira de parasitologia veterinaria = Brazilian journal of veterinary parasitology : Orgao Oficial do Colegio Brasileiro de Parasitologia Veterinaria 2018. link 11 Lima TC, Bezerra RO, Siqueira LT, Menezes MR, Leite CD, Porta G et al.. Paracoccidioidomycosis in a liver transplant recipient. Revista da Sociedade Brasileira de Medicina Tropical 2017. link 12 Sbeghen MR, Zanata TB, Macagnan R, de Abreu KC, da Cunha WL, Watanabe MA et al.. Paracoccidioides brasiliensis Infection in Small Wild Mammals. Mycopathologia 2015. link 13 Pontes AM, Borborema J, Correia CR, de Almeida WL, Maciel RF. A rare paracoccidioidomycosis diagnosis in a kidney transplant receptor: case report. Transplantation proceedings 2015. link 14 Belitardo DR, Calefi AS, Sbeghen MR, de Oliveira GG, Watanabe MA, de Camargo ZP et al.. Paracoccidioides brasiliensis infection in domestic rabbits (Oryctolagus cuniculus). Mycoses 2014. link 15 Oliveira GG, Belitardo DR, Balarin MR, Freire RL, Camargo ZP, Ono MA. Serological survey of paracoccidioidomycosis in cats. Mycopathologia 2013. link 16 Ferreira JB, Navarro IT, Freire RL, Oliveira GG, Omori AM, Belitardo DR et al.. Evaluation of Paracoccidioides brasiliensis Infection in dairy goats. Mycopathologia 2013. link 17 Oliveira GG, Navarro IT, Freire RL, Belitardo DR, Silveira LH, Camargo ZP et al.. Serological survey of Paracoccidioidomycosis in sheep. Mycopathologia 2012. link 18 Corte AC, Svoboda WK, Navarro IT, Freire RL, Malanski LS, Shiozawa MM et al.. Paracoccidioidomycosis in wild monkeys from Paraná State, Brazil. Mycopathologia 2007. link 19 Bordon AP, Dias-Melicio LA, Acorci MJ, Biondo GA, Fecchio D, Peraçoli MT et al.. Prostaglandin E(2) production by high and low virulent strains of Paracoccidioides brasiliensis. Mycopathologia 2007. link 20 Almeida AJ, Matute DR, Carmona JA, Martins M, Torres I, McEwen JG et al.. Genome size and ploidy of Paracoccidioides brasiliensis reveals a haploid DNA content: flow cytometry and GP43 sequence analysis. Fungal genetics and biology : FG & B 2007. link 21 Guimarães JS, Souza SL, Bergamaschi DP, Gennari SM. Prevalence of Neospora caninum antibodies and factors associated with their presence in dairy cattle of the north of Paraná state, Brazil. Veterinary parasitology 2004. link 22 Bocca AL, Silva MF, Silva CL, Cunha FQ, Figueiredo F. Macrophage expression of class II major histocompatibility complex gene products in Paracoccidioides brasiliensis-infected mice. The American journal of tropical medicine and hygiene 1999. link 23 Bueno JP, Mendes-Giannini MJ, Del Negro GM, Assis CM, Takiguti CK, Shikanai-Yasuda MA. IgG, IgM and IgA antibody response for the diagnosis and follow-up of paracoccidioidomycosis: comparison of counterimmunoelectrophoresis and complement fixation. Journal of medical and veterinary mycology : bi-monthly publication of the International Society for Human and Animal Mycology 1997. link 24 da Silva MI, de Carvalho IM, Franco TN, Cunha MA, Chamma LG, Fogaça J et al.. The use of a mixture of somatic and culture filtrate antigens in the evaluation of the immune response to Paracoccidioides brasiliensis. Journal of medical and veterinary mycology : bi-monthly publication of the International Society for Human and Animal Mycology 1991. link 25 Giannini MJ, Bueno JP, Shikanai-Yasuda MA, Stolf AM, Masuda A, Amato Neto V et al.. Antibody response to the 43 kDa glycoprotein of Paracoccidioides brasiliensis as a marker for the evaluation of patients under treatment. The American journal of tropical medicine and hygiene 1990. link 26 Nogueira ME, Mendes RP, Marques SA, Franco M. Complement-mediated-lysis detection of antibodies in paracoccidioidomycosis: a preliminary study. Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas 1986. link 27 Mistreta T, Souza MJ, Chamma LG, Pinho SZ, Franco M. Serology of paracoccidioidomycosis. I. Evaluation of the indirect immunofluorescent test. Mycopathologia 1985. link 28 Cornelissen AW, Overdulve JP, van der Ploeg M. Determination of nuclear DNA of five eucoccidian parasites, Isospora (Toxoplasma) gondii, Sarcocystis cruzi, Eimeria tenella, E. acervulina and Plasmodium berghei, with special reference to gamontogenesis and meiosis in I. (T.) gondii. Parasitology 1984. link

Disseminated paracoccidioidomycosis