SummaryEnteric fever is a major cause of morbidity and mortality in tropical areas worldwide. The Indian subcontinent bears the brunt of the disease, both in terms of absolute case numbers and drugresistant strains. Recent phylogenetic studies suggest that the multidrug-resistant clade H58 originated in India and subsequently expanded through Asia and Africa. In Africa, it caused unrecognised outbreaks in areas previously considered free of the disease. In this study, we discuss the current status of enteric fever in India, the factors preventing its control and its future directions in this rapidly developing nation.

Rabies, a zoonotic viral encephalitis, continues to be a serious public health problem in India and several other countries in Asia and Africa. Survival is rarely reported in rabies, which is considered to be almost universally fatal. We report the clinical and radiological findings of eight patients with laboratory-confirmed rabies who survived the illness. With the exception of one patient who recovered with mild sequelae, all survivors had poor functional outcomes. The reported survival from rabies in recent years may reflect an increased awareness of the disease and greater access to better critical care facilities in rabies-endemic countries. Nonetheless, there is an urgent need to focus on preventive strategies to reduce the burden of this dreadful disease in rabies-endemic countries.

BackgroundRabies is nearly universally fatal with about 60,000 annual deaths globally; <0.1% cases survive. Reports of therapeutic coma leading to survival are outnumbered by reports of failure. On the basis of personal discussions with a leading rabies expert (Dr Rodney Willoughby), we hypothesized that limiting CNS immune response based on CSF antibody titre (ABT) might prove useful. We report on successful use of immunosuppression in 1 patient.MethodsA 26-year-old male was admitted with 2-day history of flu-like syndrome. He had category III dog bite on face 17 days prior. RIG was not given due to nonavailability; he had received ARV day 0, 3, 7, and 14 on time. On 4th day of admission (day 0), neurological features started—difficulty in walking and diplopia; hydrophobia was noted. Working diagnosis of rabies was made. MRI brain on day 1 showed subtle abnormal T2 and flair hyper intensities in pons, medulla, and left hippocampus. CSF (day 1) showed 105 cells; all lymphocytes. The RFFIT serum and CSF ABTs and rabies PCRs are tabulated below. Since ADEM was a possibility, he was begun on IVIg. Work up for other viral encephalitis was negative. Repeat CSF ABT on day 6 confirmed rabies. Postulating risk of death due to cerebral edema due to CNS immune response, dexamethasone (dexa) 6 mg/kg/day in 4 divided doses was begun on day 8. Serial MRI and CSF were done. Dexa taper was done based on MRI and CSF ABT. Intensive supportive care was given.ResultsMRI on day 9 and day 12 showed no cerebral edema. Dexa taper was started from day 13 by half every alternate day; it was given till day 28. By day 17, there was intermittent eye opening, withdrawal to pain and some orofacial and limb movements. Further recovery had waxing and waning course. Now he is nearly 1 year post rabies encephalitis. He is unable to talk or comprehend, but can sit independently and is able to walk with support.ConclusionImmunosuppressive therapy with dexa to improve outcomes in rabies seems an exciting option. Optimal dose, time of start, and taper schedule need further studies. CSF ABT-based tapering appears promising. Larger studies with this approach are needed.Table 1Day13613172055Serum ABT2048X81923276816384163848192CSF ABT64X10248192X40964096Saliva PCRNegative (Neg)XNegXXXXCSF PCRNegXNegXXXXNuchal biospyxNegxXXXX Disclosures All authors: No reported disclosures.

Poster session 2, September 22, 2022, 12:30 PM - 1:30 PM Introduction: Cryptococcal infections are commonly seen in immunocompromised hosts, especially HIV-infected patients and patients on immunosuppressive therapy. Cryptococcus shows a strong tropism for the central nervous system however cutaneous tropism is not uncommon. Here we describe an HIV-negative immunocompromised patient who developed disseminated cryptococcosis with the predominant presentation being painful thigh lesions. Case Details: A 56-year-old lady presented with skin lesions and burning pain over both thighs for 1 month and a high-grade fever for 15 days. Her thigh lesions were initially treated elsewhere as tinea corporis. Her previous medical history was significant for poorly controlled diabetes, and chronic liver disease (secondary to autoimmune hepatitis or AIH). Her ongoing medications included prednisolone, anti-diabetics, and tenofovir. At presentation, the only significant physical findings were large irregular areas of central hypo-pigmentation with peripheral hyper-pigmentation and superficial small blisters over both thighs. These areas showed signs of inflammation. The empiric antimicrobial therapy included piperacillin-tazobactam and fluconazole (in view of prior urine culture growing Candida species). Over the next 48 h, fever continued, thigh pain worsened and the lesions on thighs blistered with violaceous discoloration. Her blood cultures sent at admission grew Candida kruzei, resistant to fluconazole, sensitive to voriconazole, amphotericin and echinocandins. Beta-D Glucan was also elevated. Fluconazole was discontinued, and anidulafungin was initiated. A repeat culture (prior to the start of anidulafungin) was still positive for C. krusei, but a subsequent blood culture (after the start of anidulafungin) was negative. Echocardiography did not show features of endocarditis. After a transient improvement, she worsened again with breakthrough fever, hypotension, and worsening of thigh lesions with eschar formation. Wound debridement was done, and antibiotics were escalated to carbapenem and polymyxins. Tissue cultures (sent during wound debridement) grew carbapenem-resistant klebsiella pneumonia. With these, the fever and her wounds were better; but the fever still persisted and she described a persisting severe burning pain over both the thigh wounds which did not respond to several analgesics. A few days later, the fever worsened, and she had hypotension and disorientation. Blood and urine cultures were repeated. Repeat Serum beta D glucan levels were elevated. CSF examination was not possible in view of severe coagulopathy. The blood and wound cultures both grew C. neoformans (confirmed on MaldiTOFF). Antibiotics and anidulafungin were discontinued; liposomal amphotericin and flucytosine were started. Patient had significant improvement in sensorium, fever, and thigh pains within the next 72 h. Later, liposomal amphotericin was switched to conventional amphotericin because of financial constraints. This was followed by acute kidney injury and a flare of AIH. Amphotericin and flucytosine were withheld for a few days; a pulse of methylprednisolone was needed for AIH. Following resolution of acute kidney injury and AIH flare, conventional amphotericin B and flucytosine were restarted (and given for cumulative 3 weeks). This was followed by fluconazole consolidation. At hospital discharge, although there were raw areas over the thighs, these were healthy and she was otherwise well. A total of 3 months later, skin grafting was successfully performed. Conclusions: Cryptococcus can be a great masquerader, and can mimic a variety of conditions. A high index of suspicion is required to clinch the diagnosis.

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