Clin J Gastroenterol (2014) 7:41–47 DOI 10.1007/s12328-013-0452-4

CASE REPORT

Mesenteric lymph node abscess due to Yersinia enterocolitica: case report and review of the literature Ken Watanabe • Noboru Watanabe • Mario Jin • Tamotsu Matsuhashi • Shigeto Koizumi • Kengo Onochi • Masayuki Sawaguchi • Shin Tawaraya • Hideaki Miyazawa • Hiroshi Uchinami Yuzo Yamamoto • Hiroshi Nanjo • Hirohide Ohnishi • Hirosato Mashima



Received: 22 November 2013 / Accepted: 24 December 2013 / Published online: 9 January 2014 Ó Springer Japan 2014

Abstract We describe the case of a 74-year-old female with a mesenteric lymph node abscess caused by a Yersinia enterocolitica infection. She had been administered an immunosuppressive drug and was admitted to the hospital due to a high fever, right lower abdominal pain and advanced leukocytosis. We initially diagnosed her with lymphadenitis based on the symptoms and the imaging studies. However, conservative treatment with antibiotics did not yield any improvement, and abscess formation was suspected. Surgical treatment was performed, and the culture from the drainage fluid grew Y. enterocolitica. The histological findings suggested that an ulcerative lesion of the terminal ileum was the entry port of Y. enterocolitica. The pathogen infected the mesenteric lymph nodes and spread along the ileocecal lymphatic vessels, resulting in the formation of an abscess. We also provide a review of the previously published literature on lymph node abscesses due to Y. enterocolitica infections.

K. Watanabe and N. Watanabe have contributed equally to this article. The contents of this article were presented in the 195th Tohoku branch meeting of the Japanese Society of Gastroenterology in 2013. K. Watanabe  N. Watanabe  M. Jin  T. Matsuhashi  S. Koizumi  K. Onochi  M. Sawaguchi  S. Tawaraya  H. Ohnishi  H. Mashima (&) Department of Gastroenterology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan e-mail: [email protected] H. Miyazawa  H. Uchinami  Y. Yamamoto Department of Gastroenterological Surgery, Akita University Graduate School of Medicine, Akita 010-8543, Japan H. Nanjo Division of Clinical Pathology, Akita University Faculty of Medicine, Akita 010-8543, Japan

Keywords Yersinia enterocolitica  Abscess  Mesenteric lymph node Abbreviations CT Y. enterocolitica

Computed tomography Yersinia enterocolitica

Introduction Of the 11 species within the genus Yersinia, Yersinia enterocolitica, Y. tuberculosis and Y. pestis are regarded to be pathogenic for humans [1]. Among the three pathogenic Yersinia species, Y. enterocolitica and Y. pseudotuberculosis can cause a clinical syndrome dominated by fever, abdominal pain and diarrhea [1]. Y. Enterocolitica, a Gramnegative bacillus that is endemic worldwide [2, 3], can be isolated from soil, water and a wide variety of foodstuffs (usually raw or inadequately cooked pork) [2]. The majority of foodborne infections caused by Y. enterocolitica are sporadic, and the infection sources are unknown, but large outbreaks have sometimes been reported [1]. Most intestinal illnesses are self-limiting, and generally do not require antimicrobial treatment. Acute mesenteric lymphadenitis and terminal ileitis are the most characteristic forms of Y. enterocolitica infection in humans. Therapy should be considered in patients with septicemia, focal extra-intestinal infection or who are in an immunocompromised state with enterocolitis [3, 4]. We present a case of an adult mesenteric lymph node abscess caused by Y. enterocolitica infection where the patient was under the administration of an immunosuppressive drug, and review previously published literature on lymph node abscesses due to this organism.

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Case report A 74-year-old Japanese female complained of abdominal fullness for 3 days and then developed right lower abdominal pain in July 2012. The pain worsened and she visited a hospital the next day. She suffered from a high fever, but no diarrhea, and the laboratory tests showed advanced leukocytosis and a highly elevated C-reactive protein (CRP) level. Acute appendicitis was suspected, and she was admitted to our hospital. She had been diagnosed with rheumatoid arthritis 18 years earlier, which was controlled with methotrexate (4 mg/week) and prednisolone (2.5 mg/day). In addition, she had been diagnosed with Basedow’s disease when she was 69 years old, which was well-controlled. She had no past history of gastrointestinal diseases. A physical examination on admission revealed that her body temperature was elevated to 38.7 °C. She showed tenderness and rebound tenderness in the right lower quadrant, but no muscular defense. Liver, kidneys, spleen, superficial lymph nodes, and any masses were not palpable. Laboratory tests on admission disclosed advanced leukocytosis, a high CRP level, hypoproteinemia and hyponatremia (Table 1). The hyponatremia was probably due to the compensation for respiratory alkalosis, although a blood gas analysis was not performed. A computed tomography (CT) scan of the abdomen showed wall thickening of the ileocecal intestine and an increased intensity of the surrounding adipose tissue (Fig. 1, arrowhead). Some low-density masses of several millimeters diameter were observed in the right anterior region of the abdominal aorta (Fig. 1, arrows). The appendix vermiformis remained intact. A fecal sample was processed for bacterial culture. We diagnosed the patient with mesenteric lymphadenitis and treated her conservatively with flomoxef sodium; however, her clinical symptoms and CRP level did not show any improvement up to the fifth hospital day (white blood cells 12,500/lL, CRP 21.1 mg/dL). A stool culture was negative. Abdominal ultrasonography showed irregular low-echoic masses in the right side of the abdomen (Fig. 2). We speculated that there was an abscess, and another CT scan was performed. The thickening of the wall of the ileocecal intestine had not improved, and the lowdensity masses had increased in size and fused together, as indicated by ultrasonography (Fig. 3). The encapsulating walls and partitioning walls of the masses were enhanced, but the inside was not. The intensity of the surrounding adipose tissue was increased. We therefore diagnosed a mesenteric lymph node abscess, and the patient underwent surgery the next day. At laparotomy, the main abscess was found in the mesentery of the ileocecal region. The abscess extended

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Clin J Gastroenterol (2014) 7:41–47 Table 1 Laboratory findings on admission Peripheral blood WBC

22,600 4

/lL

(4,000–9,000)

RBC

311 9 10

/lL

(380–480 9 104)

Hb

10.4

g/dL

(12.0–15.2)

Ht

30.9

%

(34.0–42.0)

MCV

99.3

fL

(78.0–110.0)

MCH

33.6

pg

(28.0–35.0)

MCHC

33.8

%

(21.0–36.0)

Plt

19.1 9 104

/lL

(11.7–32.9 9 104)

AST

31

IU/L

(13–33)

ALT

26

IU/L

(6–27)

LDH

215

IU/L

(119–229)

ALP

381

IU/L

(115–359)

T-Bil BUN

0.8 6.5

mg/dL mg/dL

(0.2–1.2) (8.0–22.0)

Blood chemistry

CRE

0.65

mg/dL

(0.40–0.80)

Na

128

mmol/L

(138–146)

K

3.5

mmol/L

(3.6–4.9)

Cl

96

mmol/L

(99–109)

TP

5.8

g/dL

(6.7–8.3)

Alb

3.1

g/dL

(4.0–5.0)

CRP

16

mg/dL

(0.00–0.19)

Glucose

113

mg/dL

(70–109)

CEA

1.3

ng/mL

(0.0–4.9)

CA19-9

4.7

U/mL

(0.0–37.0)

Tumor markers

cranially along the ileocecal vessels. A small incision was made over the abscess, and thick purulent material was aspirated. The appendix vermiformis looked normal, but the ileocecal region felt hard and abscess formation in the intestinal wall was also strongly suspected. Therefore, an ileocecal resection was added. The resected specimen showed ulcerative lesions in the terminal ileum (Fig. 4a, b, arrowheads) and abscess formation in the mesentery just near the ileocecal valve (Fig. 4b, arrow). A pathological examination revealed ulceration (UL-III) in the terminal ileum (arrowheads), with marked inflammatory cell infiltration, edema, granulation and fibrosis. There was an abscess in the mesenteric lymph node (Fig. 4c, d). There was no caseation necrosis. Perforation or penetration of the intestinal wall was not found anywhere in the resected specimen. Cultures from the drainage fluid grew only Y. enterocolitica. There was no growth of resident flora like Escherichia coli. On further interview, the patient denied recent travel or exposure to animals. She had no history of ingestion of contaminated food, water or milk. She had not eaten inadequately cooked meat for several weeks before the

Clin J Gastroenterol (2014) 7:41–47

43

Fig. 1 Abdominal CT scan taken on admission shows thickening of the wall of the ileocecal intestine (arrowhead) and several low-density mesenteric masses (arrows)

Fig. 2 Abdominal ultrasonography shows irregular low-echoic masses on the right side of the abdomen (on the fifth hospital day)

onset of abdominal pain. Therefore, the source of infection was unknown in this case. The postoperative course was uneventful, and she was discharged from hospital on day 25.

Discussion Y. enterocolitica is primarily a gastrointestinal tract pathogen, and is known to cause gastroenteritis. It causes sporadic illness and occasional foodborne outbreaks. Many domestic animals harbor this organism, and the pig is a major reservoir of pathogenic Y. enterocolitica [1–4]. Transmission may occur zoonotically or through the consumption of contaminated foods, usually inadequately cooked pork [1–4]. It may also occur through the

consumption of unpasteurized milk or water not treated with chlorine [1, 3]. Person-to-person transmission is considered to be rare [1]. Symptoms (fever, diarrhea and abdominal pain) develop about a week after exposure to the source of contagion, and typically last for 1–3 weeks, but can last longer [5, 6]. In infants and young children, enterocolitis with inflammatory diarrhea occurs. In older children and adults, acute terminal ileitis and mesenteric lymphadenitis mimicking appendicitis are common clinical syndromes [4]. After ingestion, Y. enterocolitica has a predilection for the terminal ileum, where the bacteria are able to penetrate M cells within Peyer’s patches [1, 7]. It is within these specialized phagocytic cells that they replicate and infect adjacent tissues [1]; this process may result in microabscess formation and ulceration. Most intestinal illnesses caused by Y. enterocolitica are self-limiting, and extra-intestinal manifestations of Y. enterocolitica infection are rare in healthy adults. Occasionally, Y. enterocolitica becomes blood-borne and spreads to other organs, including the liver, spleen, lungs and even brain. This has been proven to be especially common in patients with diabetes mellitus, liver cirrhosis, leukemia, patients taking immunosuppressive drugs and patients with iron overload [4]. This is considered to be because iron is an essential growth factor for virtually all bacteria [8]. When an abscess is detected, surgical drainage and/or appropriate antibiotic therapy is necessary. Y. enterocolitica is typically resistant to aminopenicillins and narrowspectrum cephalosporins due to the production of penicillinase and/or cephalosporinase [9]. Therefore, empirical therapy with broad-spectrum cephalosporins or fluoroquinolones is recommended for serious conditions [4, 9, 10]. Aminoglycosides and tetracycline are also effective [4,

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Clin J Gastroenterol (2014) 7:41–47

Fig. 3 Abdominal CT scan taken on the fifth hospital day. The thickening of the wall of the ileocecal intestine had not improved (arrowhead). The low-density masses had increased in size and fused together, forming a large, complex, mesenteric mass (arrows). The

encapsulating walls and partitioning walls were enhanced, but the inside was not. The intensity of the surrounding adipose tissue was increased

9, 11, 12]. Amoxicillin/clavulanate is not effective, when prescribed alone [9]. We searched the medical literatures using PubMed with the key words ‘Y. enterocolitica’, ‘abscess’, ‘suppurative’, ‘lymph node’ and/or ‘lymphadenitis’ and identified six other cases presenting with a lymph node abscess (Table 2) [8, 10, 13–15]. They were all adult patients (five males and one female), ranging in age from 21-74 years, with a mean age of 47 years. Most of the patients were suffering from underlying diseases such as diabetes, thalassemia major, chronic hepatitis C, alcoholism and rheumatoid arthritis, except for one case whose occupation was a meat (pork) cutter (Case 5). The present case had been administered an immunosuppressive drug and prednisolone (Case 7). Only one patient suffered from diarrhea before the abscess was detected (Case 4). In two patients with a right axillar lymph node abscess, the cause of infection was attributed to cuts on fingers (Cases 5 and 6). In the patient with a left inguinal lymph node abscess, the source may have been attributable to her cat, which had died of diarrhea (Case 2). The cause of infection was unknown in the other four cases (Cases 1, 3, 4 and 7). The diagnosis can be determined by testing for Y. enterocolitica in the blood, feces or in other biological materials (ascites, pus, lymph node or samples taken from the ileal and cecal mucosa) [1–4]. The organism was cultured in all cases using drainage, aspiration or biopsy specimens. However, blood and stool cultures were negative in three cases examined (blood, Case 5; stool, Cases 2 and 7). The detection rate in stool cultures is low [3] but that of blood cultures in cases of Y. enterocolitica liver abscess was reported to be 63 % [11]. An indirect

diagnosis may be determined through Y. enterocolitica antibody titration, specifically against human pathogen serotypes [1–4]. Antibodies reach a maximum concentration after 8–10 days, and they remain high for about 18 months after the infection [6]. When there is a diagnosis of Y. enterocolitica infection in patients presenting with septicemia or extra-intestinal manifestations, proper antibiotic therapy should be selected according to drug sensitivity testing. In the present case, the pathogen was sensitive to most of the antibiotics tested, other than cefazolin sodium. However, the clinical findings did not show any improvement with the conservative treatment using flomoxef sodium and fosfomycin calcium. Considering the patient’s clinical course and CT scan images, the formation of the lymph node abscess had already proceeded prior to admission, and it is likely that the antibiotics did not reach inside the abscess, explaining the lack of a response to treatment. All of the cases in the literature resulted in a full recovery; however, before 1987, 52.4 % (11/21) of patients suffering from liver abscesses due to Y. enterocolitica infection died [11]. The mortality of patients with Y. enterocolitica septicemia treated between 1985 and 1991 according to the French national registry was reported to be 7.5 % (4/53) [9]. The improvement in the survival rate is likely due to the availability of more effective antibiotics, such as thirdgeneration cephalosporins and fluoroquinolones, and the ability to more rapidly identify and better delineate the susceptibility profile of Y. enterocolitica [9]. The histological findings in the present case showed that there were no signs of intestinal perforation or penetration. Notably, the ulcerative lesions in the terminal ileum and

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Clin J Gastroenterol (2014) 7:41–47

45

Fig. 4 Macroscopic and microscopic findings. The resected ileocecal specimen showed ulcerative lesions in the terminal ileum (a). The specimen was cut along the line in (a), and the section showed abscess formation (arrow) in the mesentery near the ulceration (arrowheads) of the terminal ileum (b). Microscopic examination revealed

ulceration (UL-III, arrowheads) in the terminal ileum, with marked inflammatory cell infiltration, edema, granulation and fibrosis. There was abscess formation in the mesenteric lymph node [c, d (boxed area in c)]. Intestinal perforation or penetration was not found. A ascending colon, V ileocecal valve, I ileum

the abscess in the mesenteric lymph nodes were very closely located (Fig. 4). These findings strongly suggest that the primary site of infection was the mesenteric lymph node, and the ulceration was the entry port of the pathogen. The fact that no resident flora were cultured from the abscess other than Y. enterocolitica also supports the fact that the abscess formation in this patient was not due to the usual breakdown of the intestinal wall, like a penetration from diverticulitis. In patients presenting with right-sided abdominal pain with underlying diseases such as diabetes, chronic hepatitis, an iron overloaded state or the administration of an immunosuppressive drug, Y. enterocolitica infection should be considered in the differential diagnosis, even when blood and stool cultures are negative. When lowdensity masses are detected, they may be due to the spread of the pathogen to mesenteric lymph nodes, causing lymphadenitis with central necrosis or an abscess. In

particular, increasing the size and fusion of low-density masses, increasing the enhancement of encapsulating and partitioning walls and failing to improve the patient’s clinical symptoms and laboratory data despite the administration of antibiotic treatment, all which were noted in the present case, strongly suggest the formation of an abscess. Abdominal lymphadenopathy, predominantly in the mesenteric and peri-pancreatic areas, is also a common manifestation of abdominal tuberculosis. Low-density centers with enlarged nodes are a characteristic feature of tuberculosis, although there are no pathognomonic CT findings of this disease [16, 17]. However, the clinical course of abdominal mycobacterial infection is rarely fulminant or associated with septicemia [18]. Hence, monitoring the patient’s clinical course may aid diagnosis. When abscess formation is suspected, it is necessary to consider interventional drainage for the diagnosis and treatment.

123

123

Sanford [14]

Pallister et al. [8]

Kelesidis et al. [13]

Menzies [10]

Watanabe et al. (2013) (present case)

2

3

4

5

6

F, 74

M, 54

M, 55

M, 21

Rheumatoid arthritis, Basedow’s disease

Chronic hepatitis C

None

Thalassemia major, splenectomy

Type 1 diabetes

Type 2 diabetes

F, 61

M, 27

Alcoholism

Underlying condition

M, 40

Sex, age (years)

Coalescent mesenteric lymph nodes

Right axilla

No

No

Right axilla

Coalescent mesenteric lymph nodes

Transverse colon, mesocolon

Left groin

Mediastinum extending to the neck

location

7 cm

NP

NP

Negative

[10 cm

8 cm

NM

NM

NM

NM

Blood culture

9 cm

8 cm

6 cm

10 cm

Size (max)

Lymph node abscess

No

Yes, 1W

No

No

No

Diarrhea

max maximum, NM not mentioned, ND not performed, M male, F female, W week

Toshniwal et al. [15]

1

References

Negative

NP

NM

NM

NM

Negative

NM

Stool culture

Table 2 Cases with a lymph node abscess due to Yersinia enterocolitica: a summary of the literature

Laparotomy to drain the abscess and ileocecal resection

Aspiration

Incision and drainage

Laparotomy to drain the abscess

Transverse colectomy with primary anastomosis

Emergency surgery (not described precisely)

Incisional biopsy

Interventional procedure

Culture of the abscess

Culture of the aspirated specimen

Culture of the abscess

Culture of the abscess

Culture of the abscess

Culture of the abscess

Culture of the biopsy specimen

Diagnosis

Flomoxef sodium ? (additional) fosfomycin calcium ? cefmetazole sodium

Trimethoprim– sulfamethoxazole

Unknown

Splinter trauma on his right finger during a visit to landfill

Occupation: meat (pork) cutter

NM

Cefotetan ? trimethoprim– sulfamethoxazole

Amoxicillin– clavulanate ? ciprofloxacin

NM

Her cat had died of diarrhea.

Cefazolin ? tobramycin

Cefoxitin

NM

Suspected cause

Cefoxitin

Antibiotics

46 Clin J Gastroenterol (2014) 7:41–47

Clin J Gastroenterol (2014) 7:41–47

We reported here a typical and interesting case of a mesenteric lymph node abscess in an immunosuppressed patient caused by Y. enterocolitica infection, in which the histological and radiological findings clearly demonstrated the entry port of the pathogen, the primary site of infection and its spread along the ileocecal lymphatic vessels. Disclosures Conflict of Interest:

All of the authors have no conflict of interest.

Human/Animal Rights: This study is a case report and does not contain any data about the subjects that need to be approved by the ethics committee. Informed Consent: Informed consent was obtained from the patient for being included in the study.

References 1. Sabina Y, Rahman A, Ray RC, et al. Yersinia enterocolitica: Mode of transmission, molecular insights of virulence, and pathogenesis of infection. J Pathog. 2011. doi:10.4061/2011/ 429069. 2. Bottone EJ. Yersinia enterocolitica: overview and epidemiologic correlates. Microbes Infect. 1999;1:323–33. 3. Cover TL, Aber RC. Yersinia enterocolitica. N Engl J Med. 1989;321:16–24. 4. Bottone EJ. Yersinia enterocolitica: the charisma continues. Clin Microbiol Rev. 1997;10:257–76. 5. Cook GC. Gastroenterological emergencies in the tropics. Baillieres Clin Gastroenterol. 1991;5:861–86.

47 6. De Berardis B, Torresini G, Brucchi M, et al. Yersinia enterocolitica intestinal infection with ileum perforation: report of a clinical observation. Acta Biomed. 2004;75:77–81. 7. Autenrieth IB, Firsching R. Penetration of M cells and destruction of Peyer’s patches by Yersinia enterocolitica: an ultrastructural and histological study. J Med Microbiol. 1996;44:285–94. 8. Pallister C, Rotstein OD. Yersinia enterocolitica as a cause of intra-abdominal abscess: the role of iron. Can J Surg. 2001;44:135–6. 9. Gayraud M, Scavizzi MR, Mollaret HH, et al. Antibiotic treatment of Yersinia enterocolitica septicemia: a retrospective review of 43 cases. Clin Infect Dis. 1993;17:405–10. 10. Menzies BE. Axillary abscess due to Yersinia enterocolitica. J Clin Microbiol. 2010;48:3438–9. 11. Khanna R, Levendoglu H. Liver abscess due to Yersinia enterocolitica: case report and review of the literature. Dig Dis Sci. 1989;34:636–9. 12. Nemoto H, Murabayashi K, Kawamura Y, et al. Multiple liver abscesses secondary to Yersinia enterocolitica. Intern Med. 1992;31:1125–7. 13. Kelesidis T, Balba G, Worthington M. Axillary abscess in a patient with Yersinia enterocolitica infection as a result of exposure to pork. Am J Med. 2008;121:e1. 14. Sanford AH. Yersinia enterocolitica abscess of the transverse colon. Report of a case. Dis Colon Rectum. 1990;33:985–6. 15. Toshniwal R, Kocka FE, Kallick CA. Suppurative lymphadenitis with Yersinia enterocolitica. Eur J Clin Microbiol. 1985;4:587–8. 16. Hulnick DH, Megibow AJ, Naidich DP, et al. Abdominal tuberculosis: CT evaluation. Radiology. 1985;157:199–204. 17. Suri S, Gupta S, Suri R. Computed tomography in abdominal tuberculosis. Br J Radiol. 1999;72:92–8. 18. Klempner MS, Talbot EA, Lee SI, et al. Case 25-2010. N Engl J Med. 2010;363:766–77.

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Mesenteric lymph node abscess due to Yersinia enterocolitica: case report and review of the literature.

We describe the case of a 74-year-old female with a mesenteric lymph node abscess caused by a Yersinia enterocolitica infection. She had been administ...
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