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Acute hemolytic anemia secondary to infectious mononucleosis R.L. PERKIN,* MD, CCFP, FCFP; A.D. Fox,t MB, FRCP[C]; W.L. RTCHARDS,4 MD, FRCP[C]; M.H. KING,. MD, FRCP[C] Acute hemolytic anemia is a rare complication of infectious mononucleosis. The degree of hemolysis ranges from mild to severe. We describe the case of a man who presented with severe hemolysis in association with high serum levels of cold agglutinins. Case report A 31-year-old white businessman was admitted to hospital on a Friday evening in October 1978 with an illness that had started 3 weeks earlier and had become acute in the 3 days prior to admission. The initial symptom had been a sore throat. Ten days prior to admission malaise, myalgia, headache, general weakness and some dyspnea with jogging had developed, and 3 days later fever and chills had appeared. Three days before admission dyspnea and palpitations occurred with slight exertion and he became weak to the point of almost fainting on one occasion. He was anorexic and nauseated, and noted low back pain that was partly relieved by lying down. He observed that his urine was dark and his eyes were slightly yellow. His wife recorded his temperature to be as high as 41 0C. The only drugs he had taken during the illness were acetylsalicylic acid and 222® tablets, and he had not been exposed to other chemicals. His previous health had been excellent. His wife and two small children were not ill, and the man From the departments of *family practice, tpathology and $medicine, Mississauga Hospital, Mississauga, Ont. Reprint requests to: Dr. R.L. Perkin, 2200 Dixie Rd., Toronto, Ont. L4Y 1Z4

had not, to his knowledge, been ex- below the left costal margin and was tender to palpation. There was posed to infection. At the time of initial physical bilateral costovertebral angle tenexamination the slim young man derness. The remainder of the was acutely ill. He was pale and examination yielded normal results. The hemoglobin concentration sweating. His oral temperature was 390C. The sclerae were mildly was 5.8 g/dl and the hematocrit icteric. His pharynx was normal was 14.6%. The leukocyte count and there was no cervical lympha- was 22 x l0./l, with 35% neutrodenopathy. He was dyspneic with phils and 65% lymphocytes; most slight exertion but not orthopneic; of the lymphocytes were atypical, there was no cough and the lungs being medium to large and having were clear. The cardiac rate was 84 deep blue cytoplasm (with Wright's beats/mm and the rhythm was reg- stain); a small proportion were imular. The blood pressure was mature. The platelet count was 120/65 mm Hg. No murmurs or normal. Many agglutinated erythrosigns of congestive heart failure cytes were noted in the blood smear were noted. The liver was not en- together with irregularly contracted larged but the edge was tender. erythrocytes and polychromasia The spleen was enlarged to 4 cm (Fig. 1). The initial reticulocyte

FIG. 1-Agglutinated and irregularly contracted erythrocytes and polychromasia in blood smear from patient with acute hemolytic anemia secondary to infectious mononucleosis.

CMA JOURNAL/OCTOBER 20, 1979/VOL. 121 1095 .-For prescribing information see page 1108

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ly. His major symptoms resolved has a temperature higher than the within 12 hours and his fever within thermal range of the antibodies.9 2 days, and his hemoglobin concen- The temptation to transfuse or to tration spontaneously rose 2 g/dl in administer corticosteroids should be 1 week. After 2 weeks the cold ag- resisted at least until this simple glutinins of high thermal amplitude measure has been tried. were no longer detectable and the room temperature was returned to References 1. JENKINS WJ, KOSTER HG, MARSH normal; the clinical improvement WL, et al: Infectious mononucleosis: was maintained. The cold aggluan unsuspected source of anti-i. Br tinins titre decreased toward normal J Haematol 11: 480, 1965 while the heterophile antibodies 2. WOODRUFF RK, MCPHERSON AJ: Severe haemolytic anaemia compliwere still present. cating infectious mononucleosis. As blood flows through the skin Aust NZ J Med 6: 569, 1976 and subcutaneous tissues, especially 3. ROSENFIELD RE, SCHMIDT PJ, CALVO in the extremities, its temperature RC, et al: Anti-i, a frequent cold agglutinin in infectious mononuclefalls to as low as 280C if the amosis. Vox Sang 10: 631, 1965 bient temperature is low.10 Our case 4. CAPRA JD, DOWLING P, COOK 5, reinforces the point that a patient et al: An incomplete cold-reactive with cold agglutinins of high ther"G antibody with i specificity in mal amplitude should be treated by infectious mononucleosis. Vox Sang 16: 10, 1969 being placed in an environment that

5. Hoss.mu AA: Anti-i in infectious mononucleosis. Am J Clin Pathol

53: 198, 1970 6. GREEN N, GOLDENBERG H: Acute hemolytic anemia and hemoglobinuna complicating infectious mono-

nucleosis. Arch Intern Med 105: 108, 1960 7. TONKIN AM, MOND HG, ALFORD FP, et al: Severe acute haemolytic anaemia complicating infectious mononucleosis. Med J Aust 2: 1048,

1973 8. WINTROBE MM: Clinical Hematology, 7th ed, Lea & Febiger, Philadeiphia, 1974, pp 914, 925 9. PRUZANSKI W, SHUMAK KH: Biologic activity of cold-reacting autoantibodies [two parts]. N Engi J

Med 297: 538, 583; 1977 10. BARCROFT H, EDHOLM OG:

Tem-

perature and blood flow in the human forearm. J Physiol (Lond) 104:

366, 1946

Human tularemia at an urban zoo J.K. PREIKSAITIS, MD; G.J. CRAWSHAW, MS, MRCVS; G.S.P. NAYAR, DVM; H.G. STIVER, MD

Tularemia is a disease of animals that is transmissible to humans. It is caused by a gram-negative, nonfermentative coccobacillus - Francisella tularensis. infection in humans is most commonly caused by the handling of infected lagomorphs and rodents, or by a tick or deerfly bite.1 However, transmission of disease to humans by inhalation of the organism,2.' contact with contaminated water4'5 and ingestion of infected meat0 has also been described. Tularemia is most often contracted in a rural setting. We describe an outbreak of tularemia in a monkey colony of an urban zoo and a case of ulceroglandular tularemia in a human resulting from a monkey bite. A serologic From the departments of medicine and medical microbiology, University of Manitoba, and the Manitoba Veterinary Laboratory, Winnipeg Reprint requests to: Dr. H.G. Stiver, Section of infectious diseases, Department of medicine, St. Boniface General Hospital, 409 Tache Ave., Winnipeg, Man. R2H 2A6

survey of zoo personnel was undertaken to determine the risk the outbreak presented to the employees and the public. Epizootic Between June 29 and July 19, 1978 four monkeys (three tamarin and one talapoin) collapsed and subsequently died at the Assiniboine Park Zoo in Winnipeg. These animals belonged to a group of seveii monkeys (five tamarin and two talapoin) in two adjacent cages. The surviving male tamarin monkey was asymptomatic, but the female had depressed activity and clinical evidence of glomerulitis. The surviving talapoin monkey had both a submandibular and a tongue abscess. The surviving monkeys were isolated. Monkeys in a cage adjacent to the two cages of the infected animals were not affected. The agoutis (South American rodents) on the bottom of the cages containing the infected monkeys remained well.

In all the monkeys F. tularensis was isolated from specimens of the liver or spleen taken post mortem. In one monkey with pneumonia the organism was also isolated from lung tissue. An aspirate of the tongue abscess of the surviving talapoin monkey also yielded F. tularensis, and the monkey's serum contained F. tularensis agglutinins in a titre of 1:640. Ground squirrels were often found around the monkey cages, but the mesh of the cages was too small to allow entry. Two Franklin ground squirrels from the area were captured Aug. 1, and post-mortem cultures yielded F. tularensis. Fleas removed from the squirrels were ground and cultured, and they also yielded F. tularensis. Cultures and serologic tests done on a Richardson ground squirrel captured Sept. 29 were negative for F. tularensis. Case report On July 19 the zoo veterinarian was bitten on the right index finger

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Acute hemolytic anemia secondary to infectious mononucleosis.

BRIEF COMMUNICATIONS! Acute hemolytic anemia secondary to infectious mononucleosis R.L. PERKIN,* MD, CCFP, FCFP; A.D. Fox,t MB, FRCP[C]; W.L. RTCHARD...
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