The ddx for cutaneous manifestations in HIV patients is broad: bacterial (typical and unusual like bacillary angiomatosis), seborrheic dermatitis, viral (HSV, VZV, CMV, molluscum contagiosum), HIV exanthem, STI (syphilis), endemic fungi, drug reaction, neoplasm, TB/NTM, scabies…
Here is a great article about cutaneous manifestations in HIV
This patient’s Histo urine Ag was >20, and pathology of the neck lesion showed yeast with narrow based budding in the dermis consistent with histoplasmosis.
His right thigh skin lesion path was consistent with molluscum contagiosum.
Cutaneous presentations of disseminated endemic mycoses
Some of the disseminated fungal infections that can cause skin manifestations in people with HIV include: Cryptococcus, histoplasmosis, coccidioidomycosis, and blastomycosis among others.
Geographic Distribution of Histoplasmosis
Histoplasmosis has a geographic distribution that includes a large portion of the eastern and southern united states (Not just the Ohio River Valley). It is also widely seen in portions of South America where disseminated histoplasmosis is a common AIDS-defining illness.
See CDC guide for maps and information about these fungi geographically:
Spectrum of Disease
Histoplasmosis can range from mild pulmonary disease that self resolves in people with intact immune systems to life-threatening disseminated disease in immunocompromised people such as those with AIDS.
Cough and dyspnea are common along with systemic symptoms. Pancytopenia along with elevated LFTs, ferritin, and LDH is frequently seen. (Alkaline phosphatase elevation is particularly common in those with disseminated histoplasmosis).
Since most patients with AIDS present with disseminated disease, the most sensitive and specific test is detection of Histo antigen. Note that Histo antigen testing can crossreact with other endemic mycoses (blastomycosis and coccidioidomycosis), so history and exposure history are important considerations.
The sensitivity of antigen in disseminated disease is higher in immunocompromised patients and with more severe illness.
Antigen detection is most commonly sent on urine and serum; can also send from cerebrospinal and BAL fluid.
Antigen levels decline in response to treatment.
Culture remains the gold standard but can take weeks, and often lacks sensitivity to rule out infection if it is suspected.
Multiple OIs can occur together.
Since patients with HIV and histoplasmosis often are very immunocompromised, they may be concurrently infected with another OI. Always have a high index of suspicion for this!
Rapid treatment is indicated due to high mortality with disseminated disease.
This case illustrates the dulling of Ockham’s razor and serves as a reminder that sometimes Hickam’s Dictum (“Patients can have as many diseases as they damn well please”) prevails.
Severe immunosuppression, disseminated disease, clinical instability- are considered to have severe disease. Treatment of severe disease requires amphotericin B induction phase.
Patients with mild symptoms and a single focus of disease (other than CNS) are considered mild to moderate. Treatment is itraconazole, as early studies showed increased MICs after several weeks of treatment with fluconazole, and more recent studies have shown better outcomes with itraconazole than with voriconazole.
Itraconazole was also found to be superior for histoplasmosis (less mortality) compared to fluconazole.
To prevent relapse, suppressive therapy is often indicated in patients who are immunosuppressed.
Case reviewed by @BradCutrellMD