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Infectious Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Susanna J. Dunachie, Hanif Esmail, Ruth Corrigan, Maria Dudareva
Symptoms occur within 3–14 days of transmission and include: Rash: typically, sudden onset maculopapular rash which is itchy and may start on the head and move to the trunk, arms and legs, as well as affecting the palms and solesLow-grade fever (<38.5 °C)Non-purulent conjunctivitis, arthralgia and joint swelling as well as other non-specific symptoms such as headache, myalgia, nausea and vomiting
Neuroinfectious Diseases
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Jeremy D. Young, Jesica A. Herrick, Scott Borgetti
The illness is often biphasic. After a 5- to 10-day incubation period, LCMV causes fevers and headache, with laboratory studies frequently showing leukopenia and thrombocytopenia. A maculopapular rash may also be observed. A patient then typically improves for 2–4 days, followed by the sudden onset of frank meningitis. Several organ systems can be involved, and patients with LCMV occasionally develop myocarditis, arthritis, and orchitis 1–3 weeks after onset.
Infectious Disease and Foreign Travel Emergencies
Published in Anthony FT Brown, Michael D Cadogan, Emergency Medicine, 2020
Anthony FT Brown, Michael D Cadogan
There are abrupt fever, chills, retro-orbital or frontal headache, myalgia, back pain, lymphadenopathy and rash. The initial rash is a transient, generalized, blanching macular rash in the first 1–2 days.A secondary maculopapular rash with areas of sparing occurs lasting 1–5 days.A later haemorrhagic rash may be associated with thrombocytopenia.
Spotted fever diagnosis: Experience from a South Indian center
Published in Pathogens and Global Health, 2021
Elangovan D, Perumalla S, Gunasekaran K, Rose W, Verghese V p, Abhilash K Pp, Prakash Jaj, Dumler Js
Among these 48 spotted fever (SF) cases, 41 (84%) were children. Male (n = 28) to female (n = 21) ratio among these was 4:3. Rash appeared by the fifth day after fever onset in 45 (92%) of the 48 cases. Maculopapular rash was observed in 34 (70.8%) patients; while six (12.5%) had macular rash, purpuric or petechial rash (severe rash) was seen in 8 patients (16.7%). Rash on palms and soles was observed in 35 (71.4%), pedal edema in 19 (39.6%) and hepatomegaly in one (2.1%) case. Among the 48 patients, 43 received doxycycline and 5 received azithromycin, and all demonstrated defervescence of fever within 72 hours of initiation of therapy. Rickettsia-specific therapy (doxycycline or azithromycin) was initiated in 44 (90%) of the 48 patients before samples were sent for spotted fever diagnostic assays. None of our spotted fever cases had eschar and there were no fatalities.
Myelopathy in West Nile virus encephalitis: Report of a case and review of literature
Published in The Journal of Spinal Cord Medicine, 2020
Jayantee Kalita, Amar Vibhute, Mritunjai Kumar, Usha K. Misra
Our patient had encephalomyelitis due to WNV infection and remained wheelchair bound due to necrotizing transverse myelopathy. Encephalitis was consistent with fever, headache, seizure, altered sensorium, CSF pleocytosis and cranial MRI showing brainstem involvement. The complete transection of spinal cord involvement was consistent with persistent flaccid paraplegia, electromyography showing evidence of anterior horn cell involvement (fibrillations and sharp waves), unrecordable tibial somatosensory findings and MRI revealing both horizontal and vertical extensive signal changes. About 80% of WNV infected individuals remain asymptomatic. Symptomatic illness develops 2–14 days following mosquito bite. About 20% of patients develop self-limited flu-like illness characterized by fever, myalgia, headache, gastrointestinal disturbance (20–30%) with a maculopapular rash in 25–50%. The CNS invasion of WNV is considered to be a part of hematological dissemination and WNV gains entry after disruption of blood-brain barrier by proinflammatory cytokines, tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and macrophage migration inhibitory factor (MIF). In the brain, WNV can infect and replicate in various types of cells, including neurons, astrocytes, microglial cells and anterior horn cells.
Squamous cell carcinoma of the lung: improving the detection and management of immune-related adverse events
Published in Expert Review of Anticancer Therapy, 2022
Lara Kujtan, Rama Krishna Kancha, Beth Gustafson, Lindsey Douglass, Christopher RH Ward, Blake Buzard, Janakiraman Subramanian
Dermatologic toxicity is the most common IRAE associated with checkpoint inhibitors. Rashes are more common (5% ≥G3) with combination anti-CTLA4 and anti-PD-1 therapies compared to single agent anti-PD1 therapy (10%, <1% G3) with an average onset of 3–4 weeks [38,41,42]. Patients typically present with a pruritic maculopapular rash on the trunk or extremities. For mild rashes covering <10% of the body surface area (BSA), continuation of the ICI and treatment with moderate potency topical steroids and oral antihistamines is appropriate. These patients need to be counseled to avoid skin irritants and sun exposure [37]. GABA agonists may also be considered for pruritus, which may present in conjunction with rash or without obvious skin lesions [38,43]. ICIs should be held for grade 2 moderate to severe rash covering 10–30% of the BSA or when rash significantly affects quality of life. Initiate class one high-potency topical corticosteroids (such as clobetasol or betamethasone) and consult dermatology for possible skin biopsy to rule out bullous pemphigoid, Stevens-Johnson syndrome, or toxic epidermal necrolysis. Systemic steroids may be considered for grade 2 dermatologic toxicities, and initiated for grade 3 toxicities [38]. For grade 3 or 4 skin toxicity with skin sloughing, blisters, or severe rash unmanageable with prior interventions consult dermatology and consider high dose intravenous corticosteroids with consideration for permanent ICI discontinuation [37]. Grade ≥2 dermatologic toxicities may recur after a steroid taper. Dermatologist consultation and or steroid-sparing agents, such as dupilumab for eczema and rituximab for pemphigus, may be considered for these patients [44,45].