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13 year old male with history of pre B cell ALL, currently in relapse and on chemotherapy, admitted with acute onset fever, vomiting and headache. 5 days prior to admission, he had a scheduled neurosurgical procedure of removal of a nonfunctioning VP shunt that was in place for congenital hydrocephalus. • • • • Patient presented to the ER with a history of fever to 102.9F that began about 4 hours prior to arrival, associated with 6-7 episodes of nonbloody, non-bilious emesis. He also complained of headache and neck pain. A CBC done in the ER showed neutropenia and thrombocytopenia. He was given a dose of vancomycin and ceftazidime. Although meningitis was suspected, an LP was deferred due to the recent neurosurgical procedure and thrombocytopenia. Patient was admitted to the oncology floor for further management. 1) Pre B cell ALL diagnosed in December 2005cancer was in remission after chemotherapy 2) Bone marrow relapse diagnosed in September 2008- started on chemotherapy. Most recent BM biopsy showed persistence of blasts. Chemotherapy was continued to attain remission in preparation for HSCT. 3) History of E. coli sepsis following induction chemotherapy in September 2008. An evaluation at that time showed pulmonary nodules. Due to neutropenic state, he was started on empiric antifungal therapy with voriconazole for suspicion of fungal etiology for the nodules. 4) Congenital hydrocephalus-VP shunt placement at 6 months of age. Most recent evaluation showed a disconnection in the shunt with stable ventricle size. Since the presence of the shunt was a concern for infection following the planned HSCT, shunt was removed 5 days prior to admission. Shunt removal was complicated by adherence to the subdural area that caused a small portion to be broken off. The shunt removal from ventricle also was difficult. However, post op, patient did well and was discharged 3 days prior to admission. 5) Herpes simplex virus gingivostomatitis 6) Port-a-catheter in place since 2005 6-mercaptopurine Voriconazole Inhaled Pentamidine monthly ALLERGIES: Sulfa drugs Vancomycin-red man syndrome Patient had persistent fevers of greater than 400C. Around 12 hours into admission, patient had a generalized tonic clonic seizure. The ID team was consulted for possible herpes simplex virus meningoencephalitis. No history of illness in other family members. Pet dog at home. No history of travel. No history of consumption of unpasteurized dairy or undercooked meats. Immunizations are up to date. Father unsure of PPD placement. • • • • • • T-40.80C, HR-160, Saturation-97% in RA Mildly responsive to touch, obtunded. No obvious respiratory distress. Cracked lips; no obvious oral lesions; surgical scalp wounds are well healed. Port-a-catheter in place; heart and lung exam normal Abdomen soft with no hepatosplenomegaly Skin-No rashes, no petechiae or purpura • • • • • • WBC-500 cells/mm3, Hemoglobin-9.1 g/dl, Platelets-25,000 cells/mm3 Na-124, K-4.3, Cl-87, CO2-25 mmol/L, BUN-8, Cr-0.8 mg/dl Urinalysis-normal Chest radiograph-normal CT head-Stable intra-ventricular hemorrhage (noted immediately post op). No infarction. LP done one day into admission-CSF WBC-27, RBC-6625 cells/mm3, N-36%, L-58%, glucose47, protein-383 mg/dl Gram stain-pending • Gram positive bacteria-Streptococcus pneumoniae, Staphylococcus aureus, coagulase negative staphyloccus, • Enterococcus sp, Listeria monocytogenes Gram negative bacteria-Pseudomonas sp., Enterobacter sp., Klebsiella sp., Escherichia coli • Herpes simplex virus • • Cryptococcus neoformans Toxoplasma gondii Gram stain-gram positive rods (many were intra-cellular). Culture-Listeria sp 13 y/o with AML CSF, Gram stain 1000X Intracytoplasmic gram positive rods Courtesy by Niaz Banaei, MD Figure 1 13 y/o with AML Broth culture, Gram stain 1000X Gram positive rods Courtesy by Niaz Banaei, MD Figure 2 Patient , at the time of consult , was empirically started on broad coveragevancomycin, meropenem, acyclovir, voriconazole. Patient had persistent uncontrolled seizures. Developed cardio-respiratory compromise. Patient noted to have anisocoria. He had a burr hole in an attempt to decompress. Eventually support was withdrawn. • • • Listeriosis is caused by infection by Listeria monocytogenes, a motile, nonsporulating, facultative anaerobic gram positive bacillus. Out of the 6 species of Listeria, L. monocytogenes is the only human pathogen. Infection most often begins after ingestion of the organism in a foodborne source. L. monocytogenes can grow in high salt and cold environments, particularly suiting it to survive and grow in processed and refrigerated foods. Although bacteremia is a common presentation of listeria infection, the bacterium has tropism for the central nervous system, resulting in meningoencephalitis or cerebritis. • • • The overall disease prevalence in the US is 0.7 in 100,000, however in infants is 10 in 100,000 and elderly 1.4 in 100,000. Patients with abnormalities of T-cell mediated immunity are at particular risk. Hence, listeriosis is an important opportunistic infection in individuals on chronic steroid treatment, hematological malignancy, solid organ transplant and bone marrow transplant recipients, neonates, pregnant women and patients with AIDS. The prognosis for cancer patients with listeria bacteremia seems to be better than that for patients with meningoencephalitis. • • • Listeria is the fourth most common cause of bacterial meningitis after S. pneumoniae, N. meningitidis and Group B streptococcus. It is one of the 3 major causes of neonatal meningitis and is the most common cause of bacterial meningitis in patients with lymphoma, patients with organ transplants, or those receiving corticosteroid immunosuppressive therapy. Trimethoprim-Sulfamethoxazole used primarily for Pneumocystis prophylaxis is also protective against Listeria. However, breakthrough infections are known to occur. The preferred agent for treatment of Listeria infection is Ampicillin with Gentamicin added for synergy. Other agents such as Vancomycin and Carbapenems have in vitro activity against Listeria sp.. 11 yo F presented to the ER with a 2 day history of abdominal pain and vomiting Pain began at left lower quadrant and progressed to become generalized. History of nausea and over 20 episodes of nonbloody, nonbilious emesis. Denies diarrhea, fever, or urinary symptoms. No medications given at home except Chamomile tea for upset stomach. PMH: Previously well. No history of surgeries. Menarche 1 year back. Last menstrual period was 1 month back. Meds: None; Allergies: None SH: Immigrated to the US 2 years back from Mexico. No history of animal exposure. Denies sexual activity. Wt: 44.8Kg/ 70th percentile T- 36.4; HR-100; RR-18; BP-110/64; O2 sat99% Non-toxic appearing Abdominal exam: Tenderness at right lower quadrant. Positive obturator and psoas signs. Remainder of the exam was normal CBC: WBC-19.1 (90%N, 5%L), Hemoglobin8.9, Platelets-340 Electrolytes-Normal; Liver enzymes-Normal Urinalysis: Sp gr >1.070, 1+ protein, negative LE and nitrites, 0-2 WBC CT abdomen: Enlarged appendix with hyperemic mucosa with surrounding periappendiceal inflammatory stranding consistent with acute appendicitis. A calcified mesenteric lymph node was also noted. No lymphedenopathy. Patient taken to OR for laparoscopic appendectomy Intra-operative findings: acute appendicitis PLUS bilaterally enlarged fallopian tubes left greater than right, chronic adhesions from the omentum to the anterior abdominal wall, adhesions from the anterior surface of the liver to the anterior abdominal wall and some yellow plaques on the liver surface. Gynecology consultation to perform intraoperative examination. Findings and management: dilated, hyperemic appearance of the fallopian tubes, with the fluid within the tubes appearing to be less purulent than would be the appearance of a typical pyosalpinx. A pelvic examination revealed copious yellow vaginal discharge, a nulliparous cervix, and fimbriated hymen with no evidence of trauma. Cervical specimens were sent for Gonorrhea and Chlamydia nucleic acid amplification tests (NAAT) and cultures. 1. Fitz-Hugh-Curtis and pelvic inflammatory disease due to sexually transmitted agent 2. Abdominal/pelvic Mycobacterium disease 3. Peritonitis from ruptured appendicitis 4. Acute Yersinia sp. infection 5. Inflammatory bowel disease 6. Celiac disease PPD placed and positive at >25mm at 40 hours. Quantiferon-Gold positive. Gonorrhea and Chlamydia NAAT negative. Chest x-ray negative for active or past evidence of tuberculosis. On review of history again, family has a history of consumption of unpasteurized cheese. Endometrial biopsy was eventually obtained for microbiologic diagnosis. Pathology- proliferative endometrium with granulomatous inflammation and rare acidfast-bacilli Microbiology- Cultures confirmed Mycobacterium bovis. Susceptibility testing showed sensitivity to INH, Rifampin and Ethambutol and resistance to Pyrazinamide. Pathology slide of the endometrial tissue biopsy Proliferative phase endometrium with granulomatous inflammation, H&E stain, at 600X (Courtesy of Lisa Pate, MD) Pathology slide of the endometrial tissue biopsy Proliferative phase endometrium with rare acid-fast bacilli (arrow), AFB stain, at 1000X (Courtesy of Lisa Pate, MD) Treated with INH and Rifampin for 1 year. +Ethambutol for first 2 months Patient did very well throughout therapy. Follow up laparoscopy after 2 months of end of therapy showed normal fallopian tubes and ovaries with minimal adhesions of cul-de-sac and a few plaques on the liver. One of the species of the Mycobacterium tuberculosis complex Tuberculosis due to M. bovis is a zoonosis M. bovis primarily infects cattle and the pathogen is transmitted to humans by consumption of unpasteurized dairy products. Rare in developed countries due to pasteurization of dairy and testing and culling of infected cattle. Higher burden in developing world but due to inadequate resources for diagnosis, number of affected humans is unknown. Accurate diagnosis is important for appropriate choice of anti-tuberculosis medications and length of therapy since M. bovis is intrinsically resistant to pyrazinamide. Manifests as primary infection and reactivation. Can cause pulmonary, extrapulmonary and disseminated disease. Extrapulmonary infection (Gastrointestinal tract, peritoneum, genito-urinary tract) is more common as the infection is usually acquired by ingestion of the bacilli. Direct microscopy to visualize granulomatous inflammation and acid-fast bacilli Isolation in cultures which can take 3-6 weeks and identification of species of the Mycobacterium tuberculosis complex by PCR. M. bovis is intrinsically resistant to Pyrazinamide. Therapy for M. bovis is usually longer since pyrazinamide cannot be used (9-12 month regimen) GR is a 11 month IM with h/o ‘noisy breathing’ worse when lying supine and difficulty feeding for 3-4 months. 3-4 days PTA had worsening stridor. CXR showed possible mass at trachea. Exposure history significant for visit to India at 3 months of age and a grandmother with chronic cough. Underwent laryngoscopy, bronchoscopy and esophagoscopy. Failed extubation following procedure and remained intubated for about 10 days. Underwent Chest/Abdomen CT scan that showed multiple hilar and mediastinal LNs and hypodense lesions in spleen. Differentials included oncological process (such as lymphoma/neuroblastoma) and infectious process. ID team consulted. PPD placed as TB was high on the differential PPD positive at 15mm Patient underwent hilar LN biopsy and cultures grew Mycobacterium tuberculosis. CSF studies normal. CT head-normal INH/Rif/Pyr/Etm was started Completed 9 months of treatment for disseminated Mycobacterium tuberculosis infection. An 8 year-old girl developed fever ten days after family camping trip ◦ Five days of fever to 102-104 ◦ Diffuse headache, nausea, and two episodes of non-bloody, non-bilious emesis ◦ History of three small “insect bites” on abdomen, which quickly resolved ◦ No photophobia, phonophobia, or neck stiffness ◦ No sore throat, cough, conjunctivitis, diarrhea, arthralgias, or myalgias ◦ Fevers resolved on the fifth day of illness ◦ Afebrile for 5 days ◦ Recurrent fever prompted outpatient evaluation. Past Medical History: ◦ Seasonal allergic rhinosinusitis ◦ History of obstructive sleep apnea, status-post tonsillectomy and adenoidectomy Medications: ◦ Fexofenadine ◦ Montelukast Allergies: ◦ NKDA Social History: ◦ Lives in Menlo Park, CA Parents and a healthy 6 year-old brother No pets ◦ Recently returned from a trip to national parks throughout southern Utah and Northern Arizona Stayed in hotels with the exception of an “upscale” lodge at Bryce Canyon National Park Did not recall any indoor or outdoor animal exposures ◦ No sick contacts Physical Examination: Labs: ◦ T 100.4 F (38 C), pulse 104 bpm, BP 110/58 mm Hg, R 20 breaths per minute ◦ Complete physical examination unremarkable ◦ Chemistries, liver function tests, and creatinine normal ◦ White blood cell count 12,400/uL (range 4,50013,500/uL) 67% neutrophils (>20% bands), 12% lymphocytes, and 20% monocytes. ◦ Hemoglobin was 11.7g/dL (11.5-15.5g/dL) ◦ Platelets were normal ◦ Erythrocyte sedimentation rate was 90 mm/hr (range 0-10mm/hr) ◦ C-reactive protein was 6.9 mg/dL (range 0-0.9 mg/dL) ◦ Heterophile antibody positive 1. Lyme disease (Borrelia burgdorferi) 2. Leptospirosis (e.g. Leptospira interrogans) 3. Epstein-Barr virus 4. Colorado tick fever 5. Tick-borne relapsing fever (e.g. Borrelia hermsii) 6. Rat-bite fever (e.g. Streptobacillus moniliformis) Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.) 1. 2. 3. 4. Lyme disease (Borrelia burgdorferi) Leptospirosis (e.g. Leptospira interrogans) Tick-borne relapsing fever (e.g. Borrelia hermsii) Syphilis (Treponema pallidum) Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.) Clinical Course Prior to Diagnosis: Treatment/Follow-up: ◦ Admitted to Lucile Packard Children’s Hospital for observation ◦ A presumptive diagnosis of TBRF was made ◦ After first dose of doxycycline T 39.5 deg C, pulse 156 bpm, SBP 90 mmHg Emesis, rigors, and myalgias ◦ Received acetaminophen and a 20ml/kg normal saline bolus, with subsequent resolution of symptoms and normalization of vital signs ◦ Discharged home, completed a 10 day course of doxycycline without complications ◦ Borrelia hermsii serologies subsequently became available: IgM 1:64 (range <1:16) IgG 1:64 (range <1:64) 25 documented cases per year in the United States Spring/summertime predominance Associated with sleeping in rustic cabins Clusters of cases of B. hermsii described at the north rim of the Grand Canyon, Big Bear Lake in southern California, and Lake Tahoe near the California-Nevada border. Centers for Disease Control and Prevention: National Center for Zoonotic, Vector-borne and Enteric Diseases (NCZVED) Division of Vector-Borne Infectious Diseases (DVBID) United States - tick-borne relapsing fever is caused by: ◦ Borrelia hermsii (mountainous western states) ◦ B. turicatae (Texas) ◦ B. parkeri Rodents are natural hosts Transmitted by the soft-bodied tick Ornithodoros (e.g. O. hermsii) Nocturnal feeder Drawn to exhaled breath Painless bite Remains attached for 5-30 minutes. History of tick bite is often not elicited 3mm Red Book Online Visual Library, 2009. Image 018_07. Available at: ttp://aapredbook.aappublications.org/visual. Fever, headache, myalgias, arthralgias, nausea Hepatomegaly (17%), splenomegaly (41%), and rash (28%) Initial febrile episode lasts 2-7 days Afebrile period lasts days to weeks During initial febrile episode, organisms can exceed 100,000/mm3 Alteration of surface proteins allows escape from recognition by antibodies, causing recurrent spirochetemia Febrile episodes shorter, less frequent over time Giemsa- or Wright-stained thin and thick peripheral blood smears ◦ Thicker than other spirochetes ◦ Higher avidity for routine stains ◦ Present in higher number Sensitivity ~70% during the febrile phase Higher sensitivity with acridine orange/fluorescence microscopy Specific for relapsing fever B. hermsii Peripheral blood, Giemsa stain, 1000x (Courtesy of Niaz Banaei, M.D.) L. interrogans T. pallidum Red Book Online Visual Library, 2009. Image 128_43. Available at: http://aapredbook.aappublications.org/visual . Serology ◦ cross reaction occurs with Borrelia burgdorferi, Leptospira spp, and Treponema pallidum. Blood culture ◦ Barbour-Stoenner-Kelly medium Mouse inoculation Children > 8 years: Children < 8 years and pregnant women: ◦ Doxycycline x 5-10 days ◦ Penicillin or erythromycin can be used. Therapy can cause Jarisch-Herxheimer reaction: ◦ Close monitoring, especially during the first 4 hours ◦ Acute febrile response, headache, myalgia ◦ Occasional hypotension ◦ Resolves in hours with supportive care 5 y/o boy from northern California presented with a 6 weeks of fevers and a 3 week history of progressive frontal headache waking him from sleep and emesis following a 5-day flulike illness. Developed diplopia and decreased hearing from left ear, then brought to ER for acute slurring of speech. • • • PMHx: born at term via vaginal delivery SHx: two pet dogs. No other pets or contact with other animals. No pica. Yearly travel to Phoenix, AZ for 7 days – returned 2 months prior to current illness. No exposure to known or suspected tuberculosis. No dietary risk factors. Meds: had received amoxicillin/clavulanate (two courses), azithromycin, cefdinir over 6 weeks preceding admission Physical Examination: ◦ T 38.6 deg C, P 82, BP 104/56, R 22, SpO2 97% on room air ◦ Alert, awake, interactive. No alterations in mentation. ◦ Neuro: L-sided esotropia; decreased hearing L ear by finger rub. No other focal deficits. ◦ Remainder of exam normal • • Studies: White blood cell count 18,700/μL (normal 5,00010,000/μL) – 81% neutrophils, 16% lymphocytes, 2% monocytes, and no eosinophils. • • • • • The hemoglobin and platelet counts normal C-reactive protein was 19.4mg/dL (normal <0.2mg/dL). Sodium 129mmol/L (normal 135-145mmol/L); other routine chemistries were unremarkable. Liver function tests normal. CSF white blood cell count was 195 cells/μL (normal <10/ μL ) – 1% neutrophils, 61% lymphocytes, 12% monocytes, and 26% eosinophils • CSF protein 49 mg/dL, CSF glucose of 39mg/dL. CSF with abundant eosinophils Permission obtained from Lezlee Pasche, M.D., Dept. of Pathology, Stanford University Studies: ◦ ◦ ◦ ◦ PPD neg Gastric aspirates neg for AFB x3 Blood cultures and CSF bacterial cultures negative HIV ELISA negative Imaging: ◦ Chest film: left lower lobe nodule with hilar adenopathy ◦ Brain MRI: left-sided subependymal leukomalacia Left lower lobe pulmonary nodule with L hilar prominence Coccidioides spp. Baylisascaris procyonis Mycobacterium tuberculosis Angiostrongylus cantonensis Balamuthia mandrillaris Serum Coccidioides immunodiffusion (IgM) positive Serum Coccidioides quantitative immunodiffusion (IgG) 1:16 (nl negative) CSF Coccidioides quantitative immunodiffusion positive 1:1 (nl negative) Fungal cultures from CSF were negative Had been started on fluconazole 12mg/kg empirically, which was continued. Had been started on dexamethasone, which was continued Completed a course of albendazole Had complete resolution of neurologic deficits and was discharged home Re-admitted one week later with L-sided weakness and aphasia Despite aggressive antifungal therapy, eventually became quadraparatic Later, developed hydrocephalus Diffusion-restricted lesions in bilateral basal ganglia (not seen – lesions in bilateral frontal lobes), consistent with vasculitic infarctions Dimorphic fungus Two species ◦ Coccidioides immitis (CA, AZ) ◦ Coccidioides posadasii (AZ, TX, Mexico, S. America) Described in 2002 ◦ No clinical difference between species Acute pneumonia Chronic or progressive pneumonia Pulmonary nodules/cavities Extrapulmonary, non-meningeal disease CNS disease Cutaneous disease ◦ Found in 50% of patients with dissemination ◦ Occurs weeks to months after initial infection ◦ Symptoms: fever variable; HA, altered mental status, personality changes, nausea, vomiting, neurologic deficits ◦ Signs: meningismus (50%), gait abnormalities, focal neuro findings ◦ Hydrocephalus can occur early or late (30-50%) ◦ Vascultic infarcts can occur early or late (15-20%) Diagnosis: ◦ Cerebrospinal fluid wbcs low double-digits to >10000 Lymphocytic predominance most common Neutrophil predominance can occur Eosinophils uncommon, but highly suggestive Protein usually >150mg Glucose usually low Histopathology: not directly applicable ◦ identification in other body sites useful Fungal culture: rarely positive ◦ More likely positive with VP shunt in place ◦ Mycelial forms occasionally seen CSF serology ◦ Low sensitivity, high specificity ◦ High-titer IgG diagnostic (complement fixation) “spill-over” can cause low-titer positivity ◦ CSF IgG is followed Therapy: ◦ Winn, 1946: intrathecal amphotericin-B deoxycholate ◦ Einstein, 1961: IT ampho-B became gold standard Direct cisternal injection, via Ommaya, or lumbar injection Therapy 2-8 years Complications common (bacterial infection, arachnoiditis – back pain, paraplegia, quadriplegia, urinary retention, sexual dysfxn) ◦ Classen, 1988: fluconazole for meningitis described ◦ Galgiani, 1993: fluconazole new gold standard (400mg) Higher-dose fluconazole now preferred Therapy is lifelong ◦ Case reports for voriconazole, caspofungin, posaconazole Long-term management ◦ Periodic LPs to follow IgG ◦ Monitoring for hydrocephalus, shunt if needed ◦ Monitor for drug toxicity Prognosis ◦ Mortality 100% prior to antifungals ◦ Mortality ~30% with intrathecal ampho-B ◦ Mortality ~30% with fluconazole CNS vasculitis ◦ No consensus on management 6yo female in USOGH until 17 PTA when she developed Sx of N/V x 24 hours and fever (103oF) which were persistent, nightly and associated w/ chills and sweats. She had fatigue/wt. loss (~6 lbs.) and decreased appetite Sibling w/ GAS-pt. placed on amox. w/o improvement See on multiple occasions WBC 9600; 45 segs 15 bands ESR 60 then 77 GSP including LFTs nl CXR nl SXR nl U/A and Cx: NG PPD: neg Bone scan: uptake in R mandible AUS: multiple small lesions throughout the liver and spleen Lives on a farm in Half Moon Bay 2 yr. old cat, several dogs, chickens, rabbits, horses. Farm worker recently PPD converter H/O tick bites Well appearing VSS w/ 38.7oC 1 cm L axillary node No HSM Otherwise nl WBC 8300; 59S 28L AST 26: ALT 18 CXR: Interstitial infiltrate R lung: viral pneumonia ACT: Multiple tiny low attenuation foci in parenchyma of liver and spleen: DDX: fungal vs. bacterial abscess vs. lymphoproliferative dis. Echo. Nl PPD: neg Naficillin, gentamycin, flagyl initiated Pt. febrile for first 5 days By day 5 she became asymptomatic and was eating well D/C to home on antibiotics Repeat ACT at day 10 showed foci smaller in size Cat scratch serology: 1:512 PT changed to po rifampin and completed 3 week course AUS after 2 months nl