Acquired syphilis in a 3-year-old boy: a case report

RAT BITE FEVER is a rare systemic febrile illness caused by Streptobacillus moniliformis that can be transmitted by the bite of a rat or a small rodent or ingestion of food or water contaminated with rat feces [1]. The diagnosis can often be missed if health care providers fail to obtain a careful and extensive patient history. We report an unusual case of rat bite fever in a 19-year-old college student who presented with a fever and a rash. Case report A 19-year-old female college student presented to the emergency department in July because of fever, rash, and bilateral ankle and shoulder pain of approximately 6 days' duration. Her medical history was unremarkable. She was living alone in an apartment in Syracuse, New York, and denied any recent travel outside the area over the previous several months. She was not sexually active and denied using drugs. She was taking no medications. Her immunizations were up to date. At the time of physical examination her temperature was 103°F. Examination of the head, eyes, ears, and throat revealed nothing remarkable. The neck was supple. There were no enlarged lymph nodes palpable. The lungs were clear and there was no heart murmur. Examination of the extremities revealed symmetrical swelling of her hands, shoulders, and ankles. The skin revealed a petechial rash over the hands, palms, ankles, and soles of her feet (Figs. 1, 2). A few of the lesions on her hands and feet were papulopustular. Pelvic examination findings were normal.FIGURE 1.: Petechial lesions located on the palms of the hands.FIGURE 2.: Petechial lesions located on the ankles and feet.Laboratory studies revealed a normal complete blood cell count, platelet count, and differential, and findings of chest radiography and serum chemistry were normal. A throat culture was negative. Vaginal culture for gonorrhea was negative, and a GenProbe assay (GenProbe, San Diego, CA) of an endocervical specimen was negative for chlamydia. Urinalysis was negative. Antinuclear antibody, rapid plasma reagin, and rheumatoid factor testing were negative, and the erythrocyte sedimentation rate was normal. Two sets of blood cultures were performed, and ampicillin–sulbactam (3 g intravenously every 6 hours) was administered. Over the next 2 days her fever resolved. A skin biopsy was performed, which revealed leukocytoclastic vasculitis with focal epidermal necrosis (Fig. 3). Immunofluorescent staining revealed C3 deposition along papillary dermal vessels and along the dermal–epidermal junction (Fig. 4). There was no immunoglobulin deposition. Five days after admission the blood cultures yielded a gram-negative rod that was later identified as Streptobacillus moniliformis.FIGURE 3.: Hematoxylin–eosin staining of skin biopsy specimen showing leukocytoclastic vasculitis with focal epidermal necrosis.FIGURE 4.: Immunofluorescence staining of skin biopsy specimen showing C3 deposition along papillary dermal vessels and along the dermal-epidermal junction, without evidence of immunoglobulin deposition.Further questioning of the patient's mother revealed she lived with 2 cats, 2 hissing cockroaches, 3 African frogs, 2 lizards, 1 mouse, and 10 rats. One of the rats bit her approximately 1 week prior to the onset of her symptoms. The rash improved, and after 7 days of intravenous antibiotic therapy the patient was discharged to her mother's care with oral amoxicillin, to complete a 14-day course. A health department referral was initiated. She was seen for follow-up 2 weeks after discharge and was well. Discussion Rat bite fever is rare in the United States, and accurate data about incidence rates are unavailable because the disease is not reportable in any state [1]. Most cases in the United States are caused by S. moniliformis acquired through rat bites or scratches [2]. The rate of nasopharyngeal carriage in healthy laboratory rats ranges from 10% to 100%, and that among wild rats is 50% to 100% [1,2]. Bites from mice, squirrels, and gerbils and exposure to animals that prey on these rodents (e.g., cats and dogs) have been associated with cases of rat bite fever [2]. There have also been cases reported in which indirect contact, such as living in dwellings that are rat-infested or ingestion of water or food contaminated with rat feces, resulted in S. moniliformis bacteremia [3]. Contamination of drinking water and raw milk has been linked to other cases [4]. In 1996 two cases were linked to common exposures to the same dog and to consumption of surface water that could have been contaminated with rat feces [5]. The incubation period of rat bite fever caused by S. moniliformis can range from 1 to 22 days. Onset usually occurs 2 to 10 days after the rat bite. Clinical presentation is characterized by relapsing fever and asymmetric polyarthritis, followed by a maculopapular rash within 2 to 4 days on the extremities, palms, and soles. Other manifestations reported include headache, nausea, vomiting, myalgias, lymphadenopathy, endocarditis, meningitis, pneumonia, and focal abscess [5]. Thirteen percent of untreated cases are fatal, but most cases resolve spontaneously within 2 weeks [5]. Rat bite fever due to Spirillum minus occurs most commonly in Asia and has a longer incubation period, of about 1 to 3 weeks [5]. Diagnosis is made by blood culture only. The organism has strict growth requirements. It is slow-growing, and unless the laboratory is notified that Streptobacillus moniliformis is suspected, it is difficult for most laboratories to culture it [6]. Serologic testing is no longer available. Recommended treatment is with intravenous penicillin for 5 to 7 days, followed by treatment with oral penicillin for an additional 7 days. Tetracycline is an alternative agent that can be used when there is a history of penicillin allergy. There is limited experience with erythromycin, clindamycin, and ceftriaxone. The pet history was not obtained until late in the course of this patient's hospital stay. Initially, the patient denied having any pets at home because she was fearful they would be confiscated. The importance of obtaining a thorough history for a patient who presents with a fever and rash cannot be overemphasized.

Index of Suspicion

False positive reactive plasmin reagin (RPR) reactivity following a COVID-19 vaccine has been reported, and it is therefore conceivable that individuals who receive frequent coronavirus disease 2019 (COVID-19) vaccinations may exhibit durable RPR responses. Here, we sought to investigate the extent to which repeated mRNA COVID-19 vaccines can elicit chronic false RPR reactivity in a longitudinal cohort. Participants (n = 119) in an IRB-approved (#20201026), longitudinal SARS-CoV-2 cohort study were screened for RPR reactivity via manual RPR card assays. Samples with reactive results underwent additional testing, including follow-on RPR screening at additional timepoints, confirmatory fluorescent treponemal antibody (FTA-ABS) testing and anti-nuclear antibody (ANA) testing. Medical histories were collected. We observed (n = 2) screen-positive RPR results (1.7% [2/119]) following booster vaccination, for which two individuals exhibited chronic, vaccine-induced RPR reactivity for up to 9 months following booster vaccination. Both participants were ANA-negative. It is imperative for clinicians to be mindful of the potential immunologic interference of COVID-19 vaccines with standard infectious disease assays, including RPR testing. Detailed medical histories and clinical contexts, including recent vaccination, should be reviewed prior to proceeding with distressing and invasive workups.

Hearing loss, uveomeningitis, and stroke in a 55‐year‐old man

Sir, we report a rare autopsy case of microscopic polyangiitis (MPA) with myocardial infarction (MI) and pulmonary hemorrhage. A 41-year-old black woman presented with recent onset of severe headache, arthralgia, myalgia, and chest pain. Physical examination revealed macular facial rash. No oral ulcers, photosensitivity, alopecia, weight loss, fever, or Raynaud’s phenomenon were present. Past medical history was unremarkable. The white blood count, hemoglobin, hematocrit, platelets, sodium, potassium, chloride, carbon dioxide, blood urea nitrogen, creatinine, glucose, and liver enzyme studies were normal. The erythrocyte sedimentation rate (ESR) was 27 mm/h. The antinuclear antibody (ANA) titer was 1:2560 with a speckled pattern. Rheumatoid factor was negative. Creatine phosphokinase (CK) was 99 mU/ml. Her electrocardiogram (EKG) showed normal sinus rhythm. The patient was given 400 mg ibuprofen twice a day. One month later, her symptoms were not relieved and prednisone 15 mg/day was initiated by her primary care physician. There was no improvement. Prednisone was discontinued at the patient’s request. Three months later the patient was hospitalized due to dyspnea and chest pain of 5-day duration. Physical examination revealed bilateral basilar crepitations in the lungs. Cardiovascular and neurological examinations were insignificant. EKG and chest roentgenogram (CXR) were normal. There were no skin lesions or joint tenderness. Further immunological studies showed: ANA titer 1:1280; negative anti-double strand DNA, anti-ribonucleoprotein, anti-Smith, antineutrophil cytoplasmic antiantibody (ANCA), anti-SSA, anti-SSB, and anti-glomerular basement membrane (GBM) antibodies. Rapid plasma reagin was non-reactive. C3 and C4 were 103 mg/dl and 14.4 mg/dl, respectively. Prothrombin (PT) was 13.3 s and partial thromboplastin time (PTT) was 53.5 s. ESR was 27 mm/h. Urinalysis showed protein 100 mg/dl, red blood cells, and

Colorectal Spirochetosis in a Child with Rectal Bleeding: Case Report and Literature Review

SIMI 2015 A 59-year-old woman presented with a 2-month history of headache, difficulty in finding words, and slow speech. Those symptoms were associated with intermittent bilateral jerky movements of the upper extremities. The patient had noted a memory decline over the prior 2 months. Her past medical history was significant for hypothyroidism, and her medications included levothyroxine. Her father was diagnosed with Alzheimer’s disease at the age of 85. Physical examination did not reveal myoclonus, motor, or sensory deficits, hyper- or hyporeflexia, cerebellar signs, or ataxic gait. The patient had intermittent dysphonia, but her speech comprehension was intact. Results of laboratory studies, including a complete blood count, comprehensive metabolic profile, thyroid function tests, anti-thyroglobulin level, vitamin B12 level, homocysteine level, erythrocyte sedimentation rate, antinuclear antibody, anti-double stranded antibody, anti-endomysial antibody, rapid plasma reagin test, Lyme antibody test, HIV-1/2 immunoassay, serum cryptococcal antigen, paraneoplastic panel, heavy metal screening, and drug toxicological tests, were normal. The electroencephalography (EEG) study was normal. Magnetic resonance imaging (MRI) brain with and without intravenous gadolinium, including diffusion-weighted imaging (DWI), fluid-attenuated inversion recovery (FLAIR), and apparent diffusion coefficient (ADC) sequences, was performed. Cerebral MRI DWI demonstrated a ribbon-like signal hyperintensity of cerebral cortical gyri (cortical ribboning) of the right frontal, parietal, and occipital regions, known as the cortical ribbon sign

The Shrinking Lungs Syndrome in Systemic Lupus Erythematosus

Posttreatment lesional hyperpigmentation

62-Year-Old Man With Back Pain and Lower Extremity Weakness

Adult-onset Still's disease (AOSD) is an uncommon idiopathic disorder with various clinical manifestations. The absence of specific serological and pathological findings often makes the disease difficult to diagnose. The presence of skin lesions is important to the correct diagnosis of the disease. Various atypical skin lesions have been reported in association with Adult-onset Still's disease. We present a 52-year-old male who had atypical cutaneous manifestations of Adult-onset Still's disease. The rash manifested as persistent, pruritic, dark reddish, confluent, erythematous maculopapules and plaques on his chest, abdomen, upper back and proximal extremities. He suffered high, spiking fevers and had marked elevations of ferritin, C-reactive protein, and the erythrocyte sedimentation rate, which are characteristic of Adult-onset Still's disease. The fever and systemic symptoms improved after the administration of intravenous pulse methylprednisolone therapy. The skin lesions improved after prednisolone and methotrexate combination therapy. Therefore, to make the correct diagnosis, it is important to understand that patients with Adult-onset Still's disease may present with various types of skin lesions.

A 16-year-old female honor student presented for evaluation of vertigo, headache, mild aphasia, and blurred vision. Her symptoms started approximately 2 months earlier when she experienced 3–4 days of intense vertigo and ear pain that waxed and waned and then gradually subsided. Her bifrontal headache initially was intermittent, but over the next several months, increased in severity and duration and by the time of presentation had become persistent. Her family indicated that she understood language normally but was having increasing difficulty with word finding. Visual symptoms were vaguely characterized as blurriness with intermittent diplopia. She occasionally stumbled while walking, which she attributed to difficulty seeing. She had no significant medical history. The patient was assessed at another hospital where brain MRI was abnormal. Lumbar puncture revealed a protein of 53 mg/dL (normal, 14–45 mg/dL), glucose of 36 mmol/L (normal, 50–80 mmol/L), 1 leukocyte, and 1 erythrocyte. The opening pressure was not recorded, and cytological examination was not performed. IgG index was normal, and oligoclonal bands were absent. Other unremarkable CSF studies included polymerase chain reaction (PCR) for herpes simplex viruses 1 and 2, cytomegalovirus, and JC virus, assay for myelin basic protein, and staining for acidfast bacillus. Serologic and blood studies were negative or normal, including white blood cell count, hemoglobin, hematocrit, platelet count, ferritin level, angiotensin-converting enzyme, anti-nuclear antibody, single-stranded DNA, double-stranded DNA antibody, PCR for human immunodeficiency virus, rapid plasma reagin, rheumatoid factor, very long-chain fatty acids, Lyme disease, and aquaporin-4 channel antibodies. When evaluated at our institution, the patient’s visual acuity was 20/20 in each eye with no relative afferent pupillary defect. Extraocular motility showed slight limitation of abduction of the left eye. External examination, anterior segment examination, and intraocular pressure were normal in both eyes. Dilated fundus examination revealed moderate bilateral optic disc swelling (Fig. 1). There was no evidence of vitritis or other posterior segment abnormalities. Automated perimetry revealed a right homonymous hemianopia and a left inferior homonymous quadrantanopia (Fig. 2). The patient had normal vital signs and was afebrile. No abnormalities were found on general physical examination. Neurologic examination revealed normal sensation and strength in the face and extremities. Cerebellar function, deep-tendon reflexes, and gait were normal. The patient’s speech was moderately fluid with poor naming of lowfrequency objects. Comprehension was moderate with slowing during 3-step commands. Reading was poor, and she was able to write only simple sentences. Brain MRI was obtained.

Scabies is a contagious parasitic dermatitis that is a significant cause of morbidity, especially outside of the United States. Scabies is diagnosed most often by correlating clinical suspicion with the identification of a burrow. Although scabies should be on the differential for any patient who presents with a pruritic dermatosis, clinicians must consider a wide range of diagnostic possibilities. This approach will help make scabies simultaneously less over- and underdiagnosed by clinicians in the community. Atypical or otherwise complex presentations may necessitate the use of more definitive diagnostic modalities, such as microscopic examination of KOH prepared skin scrapings, high-resolution digital photography, dermoscopy, or biopsy. Scabies therapy involves making the correct diagnosis, recognizing the correct clinical context to guide treatment of contacts and fomites, choosing the most effective medication, understanding how to use the agent properly, and following a rational basis for when to use and reuse that agent. Although the development of new therapeutic agents is always welcome, tried and true treatments are still effective today. Permethrin is the gold standard therapy, with malathion being an excellent topical alternative. Ivermectin is an effective oral alternative that is especially useful in crusted scabies, patients who are bed ridden, and in institutional outbreaks. Despite the availability of effective therapeutics, treatment failures still occur, mostly secondary to application error (ie, failure to treat the face and scalp or close contacts, failure to reapply medication) or failure to decontaminate fomites. Because increasing resistance to scabies treatments may be on the horizon, we propose that standard of care for scabies treatment should involve routine treatment of the scalp and face and re-treating patients at day 4 on the basis of the scabies life cycle to ensure more efficient mite eradication. Practitioners should attempt to treat all close contacts simultaneously with the source patient. To eradicate mites, all fomites should be placed in a dryer for 10 minutes on a high setting, furniture and carpets vacuumed, and nonlaunderables isolated for a minimum of 2 days, or, for those who wish to be rigorous, 3 weeks.

A 32‐year‐old nursing student with hoarseness and dysphagia to solids

A severe paraneoplastic form of acute encephalitis associated with antibodies against the N-methyl D-aspartate (NMDA) receptor typically occurs in young individuals and is associated, but not always, with an underlying tumor. If diagnosed early, initiation of immunotherapy and tumor removal (if present) may result in recovery. We report a case in a 25-year-old young woman who presented to our medical center with postpartum psychosis. Treatment with rituximab (a chimeric monoclonal antibody against the protein CD20) resulted in gradual improvement in mental status and resolution of seizure activity episodes. A year after diagnosis and treatment, the patient was doing well without recurrences, and no tumors appeared. This is the first described case of anti–NMDA-receptor antibodies encephalitis that presented initially as a postpartum psychosis disorder and was successfully treated with rituximab.