Every Nook and Cranny

Several noninfectious and inflammatory conditions can explain his symptoms. Eosinophilic granulomatosis with polyangiitis is considerably less likely in the absence of asthma, and vasculitic processes, in general, are less likely given the nongravity dependent nature of the rash. SLE and sarcoidosis are possible causes of a systemic inflammatory illness presenting acutely with fever, rash, and pulmonary symptoms.

The patient’s expanded history makes several infections less likely. Although much of the presentation is consistent with measles, the initial appearance of the truncal rash is atypical, and there is no mention of coryza or conjunctivitis. Likewise, the description of the exanthem is not suggestive of varicella, and dengue and chikungunya are much less likely in the absence of a headache and arthralgias. Other infections including leptospirosis and scrub typhus are possible, and both might be contracted in greater Delhi. Typhoid is another infectious syndrome endemic to the Indian subcontinent that should be considered. The presence of rash involving the face and extremities would be highly atypical, however; and the presence of dyspnea and the absence of a headache argue against typhoid. Acute HIV infection and Mycoplasma pneumonia remain possible diagnoses. Toxic shock syndrome is possible, but a faster and fulminant course would be expected.

On physical examination, the temperature was 103° Fahrenheit, heart rate was 120 beats per minute and regular, respiratory rate was 24 breaths per minute, blood pressure was 100/60 mm Hg, and resting oxygen saturation was 93% while breathing ambient air. He appeared uncomfortable. Jugular venous pulse was elevated at 10 cm H₂O. Mild icterus was present, but there was neither conjunctival congestion nor subconjunctival hemorrhage. S1 and S2 heart sounds were loud, but there were no murmurs. Chest auscultation revealed bilateral basal coarse crackles. The abdominal right upper quadrant was mildly tender to palpation, and the liver edge was palpable 2 cm below the subcostal margin. There was neither splenomegaly nor peripheral lymphadenopathy. Kernig and Brudzinski signs were negative, and there were no focal neurological deficits. A generalized, nonpalpable, maculopapular and petechial rash was present on the face, extremities, and trunk.

The patient’s presentation must now incorporate the additional findings of bibasilar chest crackles, maculopapular/petechial rash, icterus, modest hypoxia, and hepatomegaly. Some of the noninfectious entities already mentioned (SLE and sarcoidosis) remain possible explanations. Hemophagocytic lymphohistiocytosis (HLH) may also explain most of the patient’s presenting signs and symptoms, and several other infectious diseases account for his presentation. Scrub typhus (or a more uncommon rickettsia disease, Indian tick typhus), leptospirosis, and perhaps infective endocarditis seem most likely to provide a unifying diagnosis for the symptoms mentioned above. Leptospirosis presents in a minority of instances as a severe illness known as Weil disease, characterized by several of this patient’s findings including icterus, kidney injury, and pulmonary symptoms. However, the rash is relatively uncommon in leptospirosis and when present, is usually more localized. The patient’s rash as described is not typically expected in infective endocarditis, although high-grade Staphylococcus aureus bacteremia will occasionally present with a diffuse rash that may be confused with that of meningococcemia. The etiology of the patient’s elevated jugular venous pressure is not readily apparent, with the cardiac examination making acute valvular insufficiency much less likely. Myocarditis, however, is possible in the setting of several of the diseases listed above, including leptospirosis, scrub typhus, SLE, and dengue.