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Immunomodulating and immunosuppressive therapies are being used more and more frequently. Depending on the mechanism of action and the underlying disease, there is an increased risk of infection with these therapies. In everyday clinical practice, the individual risk of infection depends on a large number of patients, and environmental as well as pathogenspecific factors. Elderly and multimorbid patients are at particular risk of infection. Classical bacterial infections with possible atypical manifestation, hepatitis B virus, herpes viruses, mycobacteria and other granulomatous infections are prevalent. Typical clinical signs of infections may be missing and laboratory chemical parameters may fail as diagnostic tools. Systematic screening for latent or chronic infections prior to initiation and close monitoring of patients during immunomodulatory or immunosuppressive therapy are necessary to reduce morbidity and mortality. [ABSTRACT FROM AUTHOR]

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Primary HIV-infection (PHI) encompasses the first 6 months after HIV infection. Phylogenetic analysis demonstrates that PHI accounts for approximately half of onward transmissions. Between 25 and 90 % of patients with PHI present with an acute retroviral syndrome, but asymptomatic or atypical manifestations of PHI are substantially underestimated and occur in up to one third. Signs and symptoms include fever, fatigue, sore throat, exanthema, lymphadenopathy and diarrhea. The unspecific nature of these signs and symptoms preclude a reliable clinical diagnosis. Therefore, an HIV test should be performed routinely amongst persons at risk. The 4th generation Combo test detects PHI in most cases within two to three weeks after infection and should be used for screening. A routine use of the HIV-specific PCR for screening purposes is discouraged. During the last decade early antiretroviral therapy has been recognized as beneficial for patients with PHI and therefore is recommended.

A 52 year old Swiss presented with a sore throat and progressive hoarseness. The histology showed a granulomatous inflammation of the epiglottis. Microbiology revealed dimorphic fungi in the sputum which were identified as Histoplasma sp. The histoplasma antigen was positive in urine and serum. Antimycotic therapy with itraconazol p.o. was started and switched to Amphotericin B i. v. due to clinical deterioration. Adrenal insufficiency should be considered in any patient with disseminated histoplasmosis since both the infection as well as the antimycotic treatment may cause Morbus Addison. An alternative therapy for the disseminated histoplasmosis is voriconazol. The investigation of the travel history is an important point.