Diagnosis relies on identifying Talaromyces marneffei in cultures from clinical specimens such as sputum, blood, skin scrapings, lymph node, and bone marrow, by which time the disease is in the late-stage. Fungi in blood are found in half of case.Non-specific laboratory findings may show evidence of the fungus invading tissue, such as low platelets due to bone marrow infiltration, and elevated transaminases due to liver involvement.Biopsies of skin lesions, lymph nodes, and bone marrow demonstrate the presence of organisms on histopathology. Intracellular and extracellular forms are oval and have a characteristic transverse septum. In culture, colonies are powdery green and produce red pigment; however, cultures are negative in a significant number of cases.Medical imaging may reveal shadows in the lungs. Differential diagnosis
The disease can look similar to tuberculosis and histoplasmosis

Treatment
Talaromycosis may be prevented in people at high risk, using the antifungal medication itraconazole, and is treatable with amphotericin B followed by itraconazole or voriconazole. Outcomes
With treatment, less than 25% of those affected die. Without treatment, more than 75% will die. Epidemiology
The exact number of people in the world affected is not known. Once considered rare, its occurrence increased due to HIV/AIDS to become the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.
Buspirone also has lower affinities for the serotonin 5-HT2A, 5-HT2B, 5-HT2C, 5-HT6, and 5-HT7 receptors.In addition to binding to serotonin receptors, buspirone is an antagonist of the dopamine D2 receptor with weak affinity. It preferentially blocks inhibitory presynaptic D2 autoreceptors, and antagonizes postsynaptic D2 receptors only at higher doses. In accordance, buspirone has been found to increase dopaminergic neurotransmission in the nigrostriatal pathway at low doses, whereas at higher doses, postsynaptic D2 receptors are blocked and antidopaminergic effects such as hypoactivity and reduced stereotypy, though notably not catalepsy, are observed in animals. Buspirone has also been found to bind with much higher affinity to the dopamine D3 and D4 receptors, where it is similarly an antagonist.A major metabolite of buspirone, 1-(2-pyrimidinyl)piperazine (1-PP), occurs at higher circulating levels than buspirone itself and is known to act as a potent α2-adrenergic receptor antagonist. This metabolite may be responsible for the increased noradrenergic and dopaminergic activity observed with buspirone in animals. In addition, 1-PP may play an important role in the antidepressant effects of buspirone. Buspirone also has very weak and probably clinically unimportant affinity for the α1-adrenergic receptor. However, buspirone has been reported to have shown "significant and selective intrinsic efficacy" at the α1-adrenergic receptor expressed in a "tissue- and species-dependent manner".Unlike benzodiazepines, buspirone does not interact with the GABAA receptor complex. Pharmacokinetics
Buspirone has a low oral bioavailability of 3.9% relative to intravenous injection due to extensive first-pass metabolism. The time to peak plasma levels following ingestion is 0.9 to 1.5 hours.