Recent Viral Illness Research Articles

Virus-induced chalazion

To investigate a viral etiology in certain chalazia. A prospective study over 7.5 years of all newly presenting chalazia associated with diffuse follicular conjunctivitis but without any other aetiological factors. Patients were investigated for ocular or systemic infections by history, physical exam, slit-lamp exam, and/or histology of conjunctival biopsy (including transmission electron microscopy). A total of 27 patients developed follicular conjunctivitis without meibomian gland dysfunction, blepharitis, or sexually transmitted diseases. Evidence for a viral aetiology included: recent systemic viral illness (15/27), recent contact with subjects with chalazia or follicular conjunctivitis (5/27), preauricular lymphadenopathy (4/27), viral corneal disease (4/27), or viral particles by ultrastructure (4/4). Chalazia may be associated with viral conjunctivitis. Intralesional corticosteroids should be considered with great caution for viral-induced chalazia.

LEFT ARM PAIN AND SWELLING IN A COLLEGE FOOTBALL PLAYER

HISTORY An 18 year old African American male presented with left arm swelling after starting summer football camp. He had been weightlifting the day prior to developing swelling, stiffness and arm pain confined to his left forearm and mid-biceps. He noted that the intensity of the weightlifting, which was primarily bicep and shoulder work, was greater than normal for him. He denied any previous episodes of arm pain and had been working out alone during the summer. He denied any dizziness, numbness or tingling or recent viral illness. He denied chest pain, SOB, nausea or vomiting, fever, chills or rash. He denied any hematuria but his urine may have been a bit darker than normal. He denied using any supplements, illegal drugs or alcohol. PMHX: exertional heat cramps in the past; NKDA, MEDS: none, FHX: significant for sickle cell trait in his father and mother. His review of systems was negative. PHYSICAL EXAMINATION general: WDWN African American male in NAD, height 68 inches, weight 167 lbs. vitals: stable, BP 110/60, afebrile. HEENT: unremarkable. neck: FROM, no nodules or LAN chest: CTA. heart: RRR, normal S1 and S2, no MRG. abdomen: benign. extremities: Left arm; ecchymosis or erythema, mid bicep circumference was 36 cm, right mid bicep circumference was 34 cm, tenderness to palpation over left biceps and brachialis muscles. Limited left elbow extension to 150 degrees, flexion WNL neuro: Left bicep strength 4+/5 limited by pain, otherwise was 5/5 in all major muscles of upper and lower extremities; no sensory deficit was noted; 2+ radial and brachial pulses bilaterally, no cyanosis, cap refill < 2 seconds. DIFFERENTIAL DIAGNOSIS Musculoskeletal: delayed-onset muscle soreness (DOMS), compartment syndrome, exertional rhabdomyolysis. Infection: cellulitis. Vascular: venous or arterial thrombosis. Bone: fracture, tumor. TEST AND RESULTS WBC 12.8, Hgb 39.1, MCV 79.9, CPK 63,880 U/L, BUN 15.0, creatinine 1.5, Urinalysis: negative, no blood or RBCs. Hgb A 59%, Hgb F 0%, Hgb S 38%, HgC 0%, HgA2 3%, postive for sickle cell trait; repeat testing 1 week later confirmed sickle cell trait and CPK had decreased to 2001 U/L. FINAL/WORKING DIAGNOSIS Exertional in the presence of sickle cell trait. TREATMENT AND OUTCOMES Pain and swelling subsided with rest and aggressive hydration. He was placed on relative rest and restricted to activities of daily living. Two weeks after presentation, he had no swelling, pain or stiffness in his left arm. His CPK returned to normal. He was permitted to return to football but limited to sprints less than 400 yards. He was advised to modify his exercise regimen to avoid excessive muscle injury. The genetics and potential complications of sickle cell trait were discussed with him.

A Virological Investigation of Transient Synovitis. 354

It is believed that Transient Synovitis may be caused or preceded by a viral infection. OBJECTIVE: This study's objective is to evaluate children with Transient Synovitis (TS) for serological evidence of Parvovirus B-19(PVB) and Human Herpesvirus 6 (HHV6) infection. DESIGN/SETTING: Prospective patient series in an urban children's hospital emergency department. PATIENTS: 20 children ages 15 months to 6 years (12 boys) diagnosed with TS. INTERVENTIONS: Clinical data were collected and acute PVB and HHV6 IgG and IgM titers were performed on all patients. Ten patients returned 4-6 weeks later for convalescent titers. RESULTS: Mean age was 4.1 years. Prodromal symptoms within a week of presentation were noted in 50% of patients, most commonly fever (25%) and upper respiratory infection (20%). Mean sedimentation rate was 11 mm/hr (range 2-22), and mean white blood count was 11,000/ul (range 5-22). Parvovirus results: no patients had an elevation of acute or convalescent IgM titers, and none of the 10 returning for convalescent titers had a significant rise of IgG. For HHV6: no patients had elevated acute or convalescent IgM titers. A majority (80%) had elevated acute HHV6 IgG reflecting immunity from previous infection. No patients demonstrated a significant rise in convalescent IgG titers. CONCLUSION: Although many patients with Transient Synovitis have a history suggestive of a recent viral illness, there is no serological evidence in this series for recent Parvovirus B-19 or Human Herpesvirus-6 infection.

Blue Jeans Thighs

To the Editor.— We wish to report an interesting phenomenon that is probably more widely prevalent than is recognized. An 18-month-old girl was brought to our Emergency Department by her parents for the sudden onset of a bluish rash on the toddler's thighs and abdomen. There was no history of recent viral illness, fever, change in appetite or activity, recent drug or toxin ingestion, or trauma. The mother thought the thighs appeared swollen, but the child was walking normally without any apparent pain or discomfort.

Idiopathic thrombocytopenic purpura: predictors of chronic disease.

We studied the extent to which patient characteristics influenced outcome in childhood idiopathic thrombocytopenic purpura in a historical cohort of 289 children over a 20 year period (1968-87). Outcome was classified as acute or chronic depending on whether the platelet count had returned to normal (150 X 10(9)/l) by six months after diagnosis. Fifty three cases (18%) had chronic idiopathic thrombocytopenic purpura. The likelihood of chronic disease was determined by logistic regression analysis of five patient variables: age, sex, season of onset of symptoms, history of recent viral illness, and duration of symptoms at presentation. A history of symptoms of greater than 14 days at presentation, adjusted for the other variables, was strongly predictive of chronic idiopathic thrombocytopenic purpura; the other variables did not significantly affect outcome. At 28 days after diagnosis 138 (47%) of the study cohort had normal platelet counts. Children whose platelet counts were less than 150 X 10(9)/l had a threefold risk of progressing to chronic idiopathic thrombocytopenic purpura, which increased to fivefold if counts were less than 50 X 10(9)/l. Two thirds of patients in the chronic group, irrespective of treatment, remained thrombocytopenic two years after diagnosis. We conclude that a history of symptoms for greater than two weeks at presentation is strongly predictive of chronic idiopathic thrombocytopenic purpura. If platelet counts are subnormal 28 days after diagnosis the risk of chronic idiopathic thrombocytopenic purpura is increased with prolonged thrombocytopenia being very likely if platelet counts remain low three months after diagnosis.

Analysis of chromosomal aberrations in workers exposed to low level benzene.

Metaphase chromosome preparations were analysed as part of a larger study from a population occupationally exposed to benzene and compared with a control group. Forty eight of the 66 exposed individuals and 29 of the 33 controls had samples in which metaphase spreads could be evaluated. The incidence of chromosomal aberrations (particularly chromatid deletions and gaps) in the exposed group were slightly increased compared with the control group. This increase was of borderline significance in parametric statistical tests but was significant using Fisher's exact test. No lifestyle factors had any consistent effect on the incidence of chromosome aberrations, although there was a small reduction in gaps with increasing cigarette smoking. Older individuals had a higher incidence of chromosome exchanges and "other" aberrations. Individuals who reported a recent viral illness had a higher incidence of aberrations particularly gaps. There was no evidence of any correlation in the incidence of chromosome aberrations with any of the other biological parameters previously reported. The increased incidence of aberrations seen in the group exposed to benzene may result from a history of exposure to benzene. Nevertheless, other explanations such as sampling, interindividual variability, and unintentional bias in the selection of two groups cannot be excluded.

Delayed diagnosis in pediatric appendicitis.

Delay in appendectomy occurs from failure to contact a physician, or from a physician's failure to make a proper diagnosis. In our study delay was due to physician error in 32 of 422 children who had appendectomy. Symptoms consistent with appendicitis were documented on the initial visit in each case, but 22 patients had a history of previous similar pain or recent viral illness to confuse the diagnosis. Misdiagnosis was responsible for the delay in 14 cases (gastroenteritis in ten and urinary tract infection in four). Antibiotics given before proper diagnosis in 22 instances increased diagnostic difficulty in 20. Late referral is increasing, perhaps because of a perceived innocuous nature of appendicitis. Complicated appendicitis was found in 26 children (81%), compared with 38% of the total experience. Their hospital stay averaged nine days, as opposed to 6.6 days in the nondelayed group. Failure of resolution of symptoms after therapy begins mandates reassessment to avoid progression of this common surgical disease.

Splenic pathology in immune thrombocytopenia.

Splenic pathology was analysed in 73 patients with immune thrombocytopenic purpura who underwent splenectomy for bleeding that had been resistant to adrenocorticosteroids. The mean splenic weight was 100 g. The only notable macroscopic feature was the prominence of Malpighian corpuscles in 15 cases. Microscopic examination showed formation of germinal centres in the lymphoid tissue of the white pulp in 40 cases, prominence of the histiocytes in the red pulp in 18 cases, and infiltration with neutrophils in the same area in 49 cases. Myeloid metaplasia throughout the splenic tissue was minimal in 58 cases, moderate in 15, and extreme in two. No distinguishing features were found in the spleen from patients who had not received previous immunosuppressive treatment (n = 3), those treated with prednisone (1 mg/kg/day) for a median of 14 days (n = 62), or those who had received the same dose of prednisone and additional azathioprine or cyclophosphamide (2 mg/kg/day) for a median of four weeks (n = 8). No correlation could be shown between histological features and the age of the patient or titre of antiplatelet antibodies. Similarly, no distinguishing features were found in patients with associated systemic lupus erythematosus (n = 8), hyperthyroidism (n = 6), immune haemolysis (n = 3), or recent viral illness (n = 3).

Reyeʼs syndrome

Reye's syndrome, encephalopathy and fatty change in the liver and other viscera, typically occurs suddenly in infants and children recovering from a viral illness, particularly influenza or varicella. Its rapid clinical course may suggest a drug-related insult and the differential diagnosis includes a variety of toxins. There are grounds for suspicion that exogenous substances--including aspirin--may be cofactors with recent viral illness in the syndrome's pathogenesis. For these reasons, medical examiners may be called upon to rule the diagnosis in or out, to assess the possibility of direct toxic injury, or to document presence or absence of possible cofactors. With these tasks in mind, this review summarizes the diagnostic, pathologic, and laboratory findings of Reye's syndrome and considers the roles of viral infection, heritable predispositions, and exogenous toxins in its causation. It singles out salicylate treatment for special considerations as a possible cofactor, and concludes with a suggested approach to the forensic medical investigation of possible cases of Reye's syndrome.

THE POSSIBLE ADJUVANT ROLE OF BORDETELLA PERTUSSIS AND PERTUSSIS VACCINE IN CAUSING SEVERE ENCEPHALOPATHIC ILLNESS: A PRESENTATION OF THREE CASE HISTORIES

The clinical and some laboratory details of three children who had severe neurological sequelae after either infection with Bordetella pertussis or immunisation with diphtheria, tetanus and pertussis vaccine and oral polio vaccine are reported. Each of these patients had had a recent or concurrent viral illness. The severity of their encephalopathic illness may have been due to an adjuvant role of B. pertussis or a component of the vaccines they received.

An "outbreak" of juvenile diabetes mellitus: consideration of a viral etiology.

Huff. J. C., J. C. Hierholzer (Respiratory Virology Section, Center for Disease Control. Atlanta, Ga. 30333) and W. A. Farris. An “outbreak” of juvenile diabetes mellitus: consideration of a viral etiology. Am J Epidemiol 100:277–287. 1974.—Nine of twelve cases of juvenile diabetes mellitus, representing an unusual geographic and temporal cluster, were investigated for evidence that a specific viral infection might be etiologically related to their occurrence. Eight diabetics had experienced recent “viral-like” illnesses, predominantly repiratory, but these illnesses bore no uniform temporal relation to their onsets of diabetes. Diabetics demonstrated no serologic evidence of a recent viral illness common to all. Elevated titers to only one virus, coxsackie B-3, were more prevalent in diabetics than in controls (33% vs. 6%), but geometric mean titers of diabetics to a panel of 26 common viral antigens were similar to those of controls. These data neither support nor negate the hypothesis that infection with a specific virus precipitates juvenile diabetes mellitus.

Platelet defect of infectious mononucleosis.

Platelet function has been studied in 16 patients with uncomplicated infectious mononucleosis. Some abnormality of platelet aggregation and/or release of platelet factor III or platelet factor IV was found in all patients. Six patients with platelet defects were retested after three to four months and were found to have normal platelet function and appreciably higher platelet counts. Abnormal platelet function may reflect a platelet defect which predisposes to premature platelet destruction. Recent viral illness should be excluded before attributing abnormal platelet function to other factors or to a congenital disorder.