RheumaRiddles
Infection in the immunosuppressed , Primary immunodeficiency , Infectious mimics, Vaccination , Prophylaxis
Dr Akshay Raju
Senior Resident (final year)
Christian Medical College Vellore
Each one is a suspect. You are the detective. Who or What Am I?
I gave your patient a seronegative migratory arthritis for eight years. Two rheumatologists tried methotrexate, a third tried a TNF blocker and I got dramatically worse. My party trick is a jaw that chews in time with the eyes. Only when I create weight loss and diarrhoea do they think of me, or even then not. Who am I, and what is my treatment duration?
I am a master of serological illusions. I will hand you a positive RF, a glowing ANA, and even an ANCA. I can drop a wrist or inflame a joint, but my true diagnosis is always hiding in plain sight, waiting for a pinprick to prove the silence. Who am I?
I am a something that hides in the soil but dreams of living inside macrophages. Birds and bats help scatter my invitations, but my favourite guests are those whose T-cell immunity has been turned down. I give you pulmonary nodules. I give you haematuria. I give you constitutional symptoms. ANCA may even be positive. Look for me hiding when you get fever, hepatosplenomegaly, cytopenias and very high ferritin. Who am I?
I have lived quietly in your patient’s duodenum since a barefoot childhood in a paddy field. Give steroids and I abandon my quiet life – I multiply, burrow through gut wall, and drag Klebsiella into the bloodstream with me. Who am I?
I am a virus almost everyone carries and almost no one notices. Strip the B cells or block the integrin and I play with the white matter – no fever, no headache, just a hemiparesis and a personality that isn’t theirs any more. There is no drug for me. Who am I?
I am a symmetrical, sterile, non-deforming polyarthritis in a patient with florid active tuberculosis. Aspirate my joint and you will find nothing acid-fast, nothing on culture. I have no sacroiliitis, no uveitis, no HLA-B27. Treat the lung and I vanish. Who am I?
I am the septic arthritis that behaves badly. Instead of one hot knee, I give migratory polyarthralgia, tenosynovitis of the wrist and ankle, and a scatter of pustules on acral skin. My joint fluid is often culture-negative – swab the throat, urethra, cervix and rectum instead. Recurrent me should trigger a CH50. Who am I?
I am a thymoma with a secret. After my resection the patient still has no B cells and no immunoglobulin, and starts collecting CMV colitis, PJP and chronic diarrhoea. Who am I?
I am the diabetic’s tropical assassin. I make abscesses anywhere – psoas, prostate, spleen, joint – with a pneumonia that mimics TB. I am a safety-pin bacillus, endemic to paddy fields, and I demand two weeks of intravenous therapy followed by months of oral eradication or I will come back. Who am I?
My patients get recurrent sinopulmonary infection and bronchiectasis, but also ITP, granulomatous lung disease that gets misdiagnosed as sarcoidosis, and a sterile inflammatory arthritis. Their IgG is low, their vaccine responses are poor, and no live vaccine may ever be given. Who am I?
I bring fever, splinter haemorrhages, glomerulonephritis, a positive RF, low complement, and – to complete the deception – a positive PR3-ANCA. Give cyclophosphamide and you will kill the patient. Who am I?
The child at home had a slapped cheek. The mother now has a symmetric small-joint polyarthritis, a transiently positive RF and ANA, and would meet ACR/EULAR criteria if you were careless. Wait six weeks and I am gone. Who am I?
I arrive with the monsoon. My acute phase is a fever with a rash and a patient bent double with joint pain. My real crime is the sequel – a symmetrical polyarthritis that outstays its welcome by two years and gets mislabelled as seronegative RA across half of South India. Who am I?
I steal the fever, I mute the CRP, and I flatten the ESR. Your patient’s perforated diverticulum will introduce itself only by a whisper of abdominal discomfort. Trust the abdomen, not the acute-phase reactants. Who am I?
I am the Sjogren imposter. I give bilateral parotid swelling and sicca, but my infiltrate is CD8, not CD4, my anti-Ro and anti-La are negative. Who am I?
I hide in the liver. I precipitate in the cold, sludge in small vessels, and present as palpable purpura, neuropathy and MPGN. My RF is positive, my C4 is on the floor, and my definitive treatment is not a steroid but a twelve-week course of direct-acting antivirals. Who am I?
Unpasteurised milk, an abattoir, or a village goat in history. I give an undulant fever, drenching sweats, orchitis, and backpain with a unilateral sacroiliitis. My blood cultures need patience. Who am I?
I am the earliest brick in the classical pathway. Lose me and you get lupus with near-total penetrance – florid skin, early onset, and, to confuse everyone, an ANA that may be negative and a CH50 that is unmeasurable. Who am I?
I am the mortar in the granuloma wall. Block me and old walls crumble – the bug that was walled up in 1998 walks free in 2026, often without a single lung cavity to announce itself. Who am I, and which of my blockers is the safest bet in a TB-endemic region clinic?
I refuse to Gram stain, I refuse to grow on any culture plate. I was renamed after a Czech parasitologist, but everyone still uses my old surname. I love the ANCA crowd on cyclophosphamide and high-dose steroid. A cheap tablet three times a week evicts me. Who am I, and at what steroid dose and duration should the tablet start?
I am an oxidative burst that never happens. My male patients get Serratia, Burkholderia and Aspergillus, plus a granulomatous colitis that gets called Crohn’s. My female carriers get photosensitive discoid lesions and aphthous ulcers and land in the lupus clinic. My test is a flow-based dye. Who am I, and what two lifelong prophylactic drugs do I need?
To the neurologist, I am a cascade of pediatric ischemic and hemorrhagic strokes. To the immunologist, I am a mimic of CVID with empty immunoglobulin stores, and to the hematologist, I am pure red cell aplasia. I am a genetic typo that causes a vasculopathy so brittle, giving anticoagulation for my strokes invites a fatal bleed. Steroids merely delay me, and cytopenias often betray my underlying immunodeficiency. I answer only to TNF inhibitors. Who am I ?
I am the vaccine that finally became safe for the immunosuppressed because I abandoned the live virus for a glycoprotein and an adjuvant. Two doses, 2 – 6 months apart. Name me, and name my banned predecessor.
I am the marker that stays low in a lupus flare and climbs in bacterial sepsis, unlike the reactant everyone actually orders. I am imperfect, but I am the best tiebreaker you have at 2 a.m. Who am I?
I am frequently missed by the most common in my class. Most of my patients don’t even know I’m there, except for perhaps some mild sinus issues or associated celiac disease. But give them a blood transfusion containing my missing protein, and I’ll throw a deadly anaphylactic tantrum. Who am I?
I am the great imitator. In my second act, I mimic psoriasis with a scaly rash on the palms and soles. In my final act, I destroy the posterior columns of the spinal cord, leaving the knees entirely numb to trauma until they collapse into a painless bag of loose bones. Who am I?
CLICK TO VIEW ANSWERS
Tropheryma whipplei (Whipple disease), oculomasticatory myorhythmia, IV ceftriaxone 2 weeks followed by TMP-SMX for 12 months.
Leprosy with type 2 reaction (erythema nodosum leprosum) – treated with thalidomide (or steroids/clofazimine).
Histoplasma capsulatum
Strongyloides stercoralis hyperinfection – empiric ivermectin 200 µg/kg × 2 days before immunosuppression in endemic regions.
TNF-α, etanercept (soluble receptor) carries the lowest TB reactivation risk versus infliximab/adalimumab. Reactivation is disproportionately extrapulmonary and disseminated.
Pneumocystis jirovecii, TMP-SMX prophylaxis for prednisolone ≥15 – 20 mg/day for ≥4 weeks
