Yersinia pseudotuberculosis
Yersinia pseudotuberculosis Bacteremia and Splenic Abscess in a Patient With Non-Insulin-Dependent Diabetes Mellitus
Report of a Case
The patient, a 56-year-old woman with a long history of diet-controlled non-insulin-dependent diabetes mellitus, had a two-week history of fevers, chills, malaise, and loose stools but no abdominal pain. On admission to the hospital, her temperature was 38.5°C. Her abdomen was nontender without hepatosplenomegaly. Her aspartate aminotransferase (AST) level was 103 U per liter; alanine aminotransferase (ALT), 34 U per liter; alkaline phosphatase, 132 U per liter; lactate dehydrogenase (LDH), 1,032 U per liter; leukocyte count, 10.1 X10^9 per liter; platelets, 83X10^9 per liter; and an international normalized ratio, 1.6. A urinalysis showed 4 to 10 leukocytes and many bacteria. A week before her hospital admission, her laboratory values were as follows: AST, 30 U per liter; ALT, 25 U per liter; alkaline phosphatase, 89 U per liter; and LDH, 214 U per liter.
She was admitted to the hospital for probable pyelonephritis and treated empirically with a regimen of intravenous gentamicin sulfate and generic ampicillin. A chest roentgenogram demonstrated elevation of the left hemidi-aphragm, which suggested a possible subdiaphragmatic abscess. An abdominal ultrasonogram showed an enlarged, inhomogeneous spleen. An abdominal computed tomographic scan (Figure 1A) demonstrated an enlarged spleen with multiple 1-cm areas of decreased attenuation, suggestive of splenic abscesses. The urine culture grew more than 10^6 colonies of lactobacilli, thought to be a contaminant, and two of four blood cultures grew Yersinia pseudotuberculosis on days 4 and 7, which was sensitive to canadian ampicillin, trimethoprim-sulfamethoxazole (Septra), cefazolin, cefote-tan, ceftazidime, gentamicin, and tetracycline. Antibody titers were negative for the human immunodeficiency virus, hepatitis В surface antigen, and hepatitis C.
Figure 1 .—Abdominal computed tomographic (CT) scans were taken of the spleen. A, A CT scan with contrast medium taken on hospital day 2 reveals multiple sharply demarcated, 1- to 2-cm areas of low attenuation filling the enlarged spleen. B, A CT scan with contrast medium taken after 10 days of treatment demonstrates a slightly smaller spleen with persistent 1 – to 2-cm areas of low attenuation, with some coalescence.
The patient defervesced on hospital day 3 and on hospital day 4 again became febrile. Her platelet count decreased to 35X10^9 per liter on hospital day 3, with a normal panel for disseminated intravascular coagulation, suggesting that she probably had isolated thrombocytopenia associated with her bacteremia. Her platelet count then increased steadily to 164X10^9 per liter by day 10. By hospital day 8, her laboratory values were as follows: AST, 46 U per liter; ALT, 32 U per liter; alkaline phosphatase, 231 U per liter; LDH, 384 U per liter; and leukocyte count, 8.3 X10^9 per liter. An abdominal computed tomographic scan after ten days of antibiotic therapy showed persistent multiple 1-cm lesions with some coalescence (Figure IB). She also continued to be febrile and then had a splenectomy with a partial gastrectomy on day 13 (gastrectomy done to repair gastroduodenal fistula). Cultures of the spleen were negative for pathogens, and the histopathologic examination noted multiple 1-cm nodules containing necrotic tissue and masses of macrophages (Figure 2). After the operation, she received ten more days of cheap ampicillin and gentamicin therapy. At the time of discharge, her laboratory values were as follows: AST, 24 U per liter; ALT, 12 U per liter; alkaline phosphatase, 254 U per liter; and LDH, 303 U per liter.
Figure 2.—This pathologic specimen of spleen reveals multiple 1-cm nodules filled with necrotic tissue and organizing macro¬phages, replacing most of the splenic parenchyma.
Discussion
Yersinia species are small gram-negative coccobacilli that grow optimally at cooler temperatures, between 25°C and 32°C. Because these are relatively uncommon pathogens, automated microbiologic identification systems should not be relied on, and speciation is usually determined with manual batteries of biochemical tests. If there is a strong suggestion of infection with a Yersinia species, the microbiology laboratory needs to be alerted so that a special culture medium, cefsulodin irgason novobiocin (CIN) plate, can be used. The culture also needs to be grown at room temperature because Yersinia species grow better in a cooler environment. Four key reactions differentiate Y pseudotuberculosis from Yersinia pestis, the causative agent of plague. The former reliably demonstrates motility at room temperature, hydrolyses urea, and ferments both rhamnose and meli-biose, whereas Y pestis may rarely have a positive reaction to one of these tests.
Yersinia pseudotuberculosis is a rare human pathogen. It is a zoonotic organism carried primarily by rodents, although domesticated farm animals also serve as a reservoir. Most commonly, the infection manifests as a mesenteric lymphadenitis with abdominal pain, fever, and diarrhea; in infants and small children, it presents mostly as a nonbloody gastroenteritis. Bacteremia resulting from Y pseudotuberculosis infection is rare and usually occurs in patients with underlying disorders such as diabetes mel-litus, hepatic cirrhosis, or iron overload. Overall mortality, even with appropriate antimicrobial therapy, has been estimated to be as high as 75%. Only a few patients with diabetes as their sole underlying risk factor have been described. Furthermore, although reports of cases involving liver, pulmonary, and suprarenal abscesses have been published, there have been no reports of Y pseudotuberculosis as a cause of splenic abscess in a patient with diabetes mellitus.
Splenic abscess itself is another uncommon phenomenon. Autopsy studies suggest that the incidence of splenic abscess is between 0.2% and 0.7%. It is, however, a diagnosis increasingly made due to the improved therapies for immunocompromised patients and advancements in diagnostic imaging techniques, particularly computed tomography. Underlying illnesses, like diabetes and endocarditis, and various immunodeficiency states are predisposing conditions to the development of splenic abscess. Causes of splenic abscess include Staphylococcus aureus, fungi, and aerobic and anaerobic enteric gram-negative rods. The clinical outcome without antibiotic treatment is universally fatal, and even with aggressive treatment, mortality remains around 50%. The treatment of bacterial splenic abscess requires drainage, regardless of the inciting organism. In cases of a single abscess, percutaneous drainage has been successful in 68% of patients. In a patient with multiple abscesses, splenectomy is recommended.
This patient was an otherwise healthy woman with diet-controlled non-insulin-dependent diabetes mellitus as her only risk factor for the infection with Y pseudotuberculosis and the formation of splenic abscess. She presented with nonspecific symptoms of a generalized illness without abdominal pain or splenomegaly on clinical examination. The only clues on admission that led to an evaluation of her spleen were the abnormal findings on chest roentgenogram and elevated aminotransferase levels. Both of these findings are sensitive for splenic abscess but are nonspecific. Because the organism grows best at lower temperatures, the blood cultures were negative until almost a week into her hospital stay.
An extensive review of the literature suggests that this is the first reported case of Y pseudotuberculosis bacteremia, and splenic abscess in a diabetic patient. Diabetes is a commonly encountered condition that predisposes to both infection with unusual organisms like Y pseudotuberculosis and the development of abscesses. This case emphasizes the potential for occult abscess in diabetic patients and the unusual spectrum of infectious agents to which they are susceptible.