All Posts Tagged With: "myalgias"

Case Report – A 52-year-old Man with Increasing Fatigue and a Syncopal Episode

Full article: http://www.amc.edu/amr/archives/200606/case1.html

Excerpt:

A 52-year-old male marathon runner with a past medical history significant for glaucoma presented to the emergency department with a two-week history of increasing fatigue after an episode of syncope.

He initially presented to his primary care doctor’s office complaining of flu like symptoms one week after running a marathon and three weeks prior to admission. He described fever, chills, night sweats, increasing fatigue and body aches. He was noted to be an avid runner who had finished within the top five to ten athletes in prior marathons. He stated that despite training intensely, he only finished in 50th place. During this visit, a chest x-ray was obtained which showed no evidence of pneumonia or other abnormalities. He was diagnosed with a minor viral upper respiratory tract infection and over the following week began to notice improvement of his symptoms.

He returned to the office two weeks after the initial visit with worsening fatigue and decreased exercise tolerance. He had become increasingly short of breath after running more than 2 milles. A serologic test for Lyme disease was performed to rule out Lyme carditis after an EKG showed first-degree heart block.

Human granulocytic anaplasmosis affecting the myocardium.

Full article: http://ukpmc.ac.uk/articles/PMC1490240;jsessionid=7D7D2D45FB70B5A24793992EDD921DFB.jvm4

Excerpt:

Abstract

A case of 65-year-old male is reported who presented with myalgias, headache, and fever. He subsequently developed myocarditis and was diagnosed to have anaplasmosis on peripheral blood smear. He was treated with doxycycline for 30 days. A coronary angiogram done after recovery showed normal epicardial arteries. The case illustrates the importance of a careful examination of the peripheral smear, with a high index of clinical suspicion, which led to prompt treatment and complete recovery of the patient

Ehrlichiosis, first discovered before 1910, has been recognized to cause human infection since 1986.1 It belongs to Rickettsiaceae family. Ehrlichiae are small, obligate intracellular bacteria that grow in cytoplasmic vacuoles to form clusters called morulae. Three distinct species cause human ehrlichiosis. E. chaffeensis predominantly affects the monocytes and is hence termed human monocytic ehrlichiosis (HME) while E. phagocytophilium, and E. ewingii cause human granulocytic ehrlichiosis.2E. phagocytophiliumE. equi are now recognized as the same organism and has been renamed Anaplasma phagocytophilum; the disease is now known as Human Granulocytic Anaplasmosis (HGA). Both HME and HGA share similar clinical and laboratory features and are treated with the same antimicrobials.

Bartonella spp. Infections, Thailand

Volume 16, Number 4–April 2010

Excerpt:

We conducted a prospective study to determine causes of acute febrile illness in 4 community hospitals, 2 in Chiang Rai (northern Thailand) and 2 in Khon Kaen (northeastern Thailand). We enrolled patients >7 years of age with a temperature >38°C who were brought to study hospitals for treatment from February 4, 2002, through March 28, 2003. Patients were excluded if they had a history of fever for >2 weeks or an infection that could be diagnosed clinically. Acute-phase serum samples were collected at the time of enrollment and convalescent-phase serum samples 3–5 weeks later. We enrolled nonfebrile control patients >14 years of age who had noninfectious conditions; acute-phase serum samples were collected. Clinical information was abstracted from patient charts. Nurses conducted physical examinations and personal interviews to collect information on patients’ demographic characteristics, exposures to animals, and outdoor activities.

Serum samples were tested for immunoglobulin (Ig) G antibodies to Bartonella spp. by immunofluorescent antibody assay at the Bartonella Laboratory of the Centers for Disease Control and Prevention, Fort Collins, CO, USA. Strains used for antigen production were: B. elizabethae (F9251), B. henselae (Houston-1), B. quintana (Fuller), and B. vinsonii subsp. vinsonii (Baker). Homologous hyperimmune serum specimens were produced in BALB/c mice as previously described (8). Bartonella infection was considered confirmed in febrile patients who had a >4-fold rise in IgG antibody titers and a convalescent-phase titer >64. Probable infection was defined as 1) a 4-fold antibody titer rise but convalescent-phase titers of 64, or 2) high and stable titers (>512 in acute-phase and convalescent-phase serum samples), or 3) acute-phase titer >512 with a >4-fold titer fall. Paired serum samples from febrile patients were also tested for serologic evidence of other common causes of febrile illness in Southeast Asia.

Febrile patients with acute-phase and convalescent-phase IgG antibody titers <128 were considered not to have Bartonella infection; we compared demographic and clinical characteristics of these patients to Bartonella-infected patients. To evaluate potential risk factors, we compared Bartonella-infected case-patients >14 years of age without serologic evidence of other infections (n = 20) to nonfebrile controls with IgG to Bartonella <128 (n = 70). Age adjusted odds ratios (AORs) with 95% confidence intervals (CIs) were calculated.

Lyme Encephalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists. First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued

Lyme Encepalopathy

Encephalopathy is like fine art: Most people know it when they see it, but there is very little agreement on how to define it. At the 14th International Lyme Disease Conference, Brian A. Fallon, MD,[1] of Columbia University and the New York State Psychiatric Institute, New York, NY, tried to do just that. More importantly, he described the different ways one can define encephalopathy, the strengths and limitations of each approach, and significantly, what other aspects of life can give the impression of encephalopathy where none exists.
First, one must evaluate patients with persistent Lyme encephalopathy by asking the following questions:

Is the diagnosis correct?
Are there comorbid psychiatric disorders that could be treated better? Does the patient have a psychogenic medical illness? What was the patient’s response to prior antibiotics?
Was previous treatment adequate? How long was the course, and what was the route of administration? Was there a subsequent relapse Continued