Scand J Infect Dis 31: 324–325, 1999 CASE REPORT

Visceral Larva Migrans Syndrome ComplicatedBy Liver Abscess

ABDUNNABI RAYES1, DANIELA TEIXEIRA1, VANDACK NOBRE1, JOSE C. SERUFO1,RONAN GONCALVES2, LAIS VALADARES2 and JOSE R. LAMBERTUCCI1

From the 1Department of Internal Medicine, Infectious Disease Branch, School of Medicine, Federal Uni6ersity of MinasGerais, and 2Department of Pediatrics, Santa Casa Hospital, Belo Horizonte, Brazil

We describe a case of visceral larva migrans syndrome complicated by liver abscess, pericardial effusion and ascites. To ourknowledge, these findings have not been reported previously. The structural and immunological alterations caused by viscerallarva migrans are thought to lead to the development of visceral abscesses.

J. R. Lambertucci, MD, Departamento de Clınica Medica, Faculdade de Medicina da UFMG, A7. Alfredo Balena 190, CEP30130-100, Belo Horizonte-MG, Brazil

INTRODUCTION

Visceral larva migrans syndrome (VLM) consists of fever,hepatosplenomegaly, pallor, respiratory symptoms andchronic eosinophilia. It is common among children and isusually caused by the larvae of Toxocara canis (1).

We treated a child who had an initial clinical presenta-tion of VLM complicated by the development of pyogenicliver abscess (PLA) and pericardial effusion.

CASE REPORT

A 2-y-old boy was admitted with a 3-month history of weight loss,abdominal distension and malaise. Three days before admission hehad been observed to have fever, dry cough and diarrhoea. Therewas a history of contact with dogs.

At admission he was febrile, weighing less than expected for hisage, with generalized painless lymphadenopathy and non-tenderhepatosplenomegaly. There were bilateral expiratory ronchi on chestexamination.

His laboratory make up was significant for 6.6 g/dl haemoglobin,white cell count (WBC) of 14.8×109/l, 6.808×109/l neutrophils,0.296×109/l band cells and 1.332×109/l eosinophils. The serumalbumin was 3.4 g/dl and globulin 4.0 g/dl. Chest x-ray showedcardiomegaly suggestive of pericardial effusion and bilateral mildinterstitial pulmonary infiltrates.

Because of the persistent high fever and a tender hepatomegaly,an abdominal ultrasound was carried out on the seventh hospitalday, and showed hepatosplenomegaly with a hypoechoic areasuggestive of an abscess measuring 37×35×36 mm in the left lobeof the liver and a pericardial effusion. A leukogram carried out atthis point revealed a WBC of 19.0×109/l with 0.19×109/leosinophils. A CT scan revealed hepatosplenomegaly with left lobeliver abscess (Fig. 1), mediastinal and axillary lymphadenopathy,pericardial and pleural effusions and left lower lobe lung consolida-tion. A transthoracic echocardiography confirmed the pericardialeffusion but was otherwise normal. A myelogram revealed increasednumbers of eosinophils and a stool examination showed eggs ofAscaris lumbricoides, which was treated with piperazine.

He was treated with ceftriaxone and clindamycin and showedclinical improvement. Because of the bronchospasm, he was treatedwith micronebulization using bronchodilators. In the 23rd day oftreatment his WBC was 15.4×109/l and the eosinophil countincreased to 4.0×109/l when a suspicion of VLM was made that was

confirmed by ELISA test (1 : 1,218) and treated with a 7-d courseof thiabendazole, resulting in normalization of these alterations.

DISCUSSION

Infection with T. canis can result in a variety of non-spe-cific clinical features (2, 3). Other clinical presentations areocular toxocariasis (2), pneumonia with or without respira-tory failure, generalized lymphadenopathy, anaemia andgeneralized arthritis (3), granulomatous hepatitis (4), my-ocarditis (5) and pleural effusion (6).

Anaemia, leukocytosis, eosinophilia and hypergamaglob-ulinaemia are common laboratory features of VLM (2).

In our patient, the initial symptoms were suggestive ofVLM. The laboratory and radiographic findings confirmedthis hypothesis.

To our knowledge pericardial effusion, as seen in thiscase, has never been described in the literature in associa-tion with VLM. Its presence could be caused by hypoalbu-minaemia, but this was not the case in our patient, or itcould be associated with myocarditis, though this could not

Fig. 1. A left lobe liver abscess in a boy with visceral larva migranssyndrome.

© 1999 Scandinavian University Press. ISSN 0036-5548

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Scand J Infect Dis 31 Visceral lar6a migrans syndrome with li6er abscess 325

be confirmed in our case, in which the echocardiographywas normal.

In the liver the larvae of T. canis induce formation ofgranuloma that contain collagen, laminin and fibronectinand are targets for adherence of bacteria, especially of S.aureus, the commonest agent of PLA in children, throughits receptors for these structures (7, 8) and it seems that inthe case described here the presumed liver abscess devel-oped in the later stages of the patient’s VLM.

VLM systematically induces the production of IL-4 andIL-5 by TH2 cells, which indirectly inhibit the TH1 cellswhich normally produce IL-2 and g-IFN necessary for theactivation of the macrophages and IgG production. Thisresults in increased IgE and histamine levels andeosinophilia, leading to impaired neutrophil function simi-lar to Job’s syndrome (9, 10).

In a clinical study of 17 patients with PLA, ELISA forVLM using the Toxocara secretory-excretory antigen (TSE)(11) was positive in 10 of 16 patients (63%) against 1 of 16controls (6%) (p=0.003). These results were confirmed byan experimental study in which mice infected with thelarvae of T. canis and with S. aureus developed morehepatic abscesses than mice infected with the bacteria only(unpublished results).

REFERENCES

1. Beaver PC, Snyder CH, Carrera GM, Dent JH, Lafferty JW.Chronic eosinophilia due to visceral larva migrans: report of

three cases. J Pediatr 1952; 9: 7–19.2. Taylor MRH, Keane CT, O’Connor P, Mulvihill E, Holland C.

The expanded spectrum of toxocaral disease. Lancet 1988:692–4.

3. Jacob CMA, Pastorino AC, Peres BA, Mello EO, Okay Y,Oselka GW. Clinical and laboratorial features of visceraltoxocariasis in infancy. Rev Inst Med Trop Sao Paulo 1994; 36:19–26.

4. Kaushik SP, Hurwitz M, McDonald C. Toxocara canis infectionand granulomatous hepatitis. Am J Gastroenterol 1997; 92:1223–5.

5. Vargo TA, Singer DB, Gillette PC, Fernbach DJ. Myocarditisdue to visceral larva migrans. J Pediatrics 1977; 90: 322–3.

6. Jeanfaivre T, Cimon B, Tolstuchow N, Gentile L, Chabasse D,Tuchais E. Pleural effusion and toxocariasis. Respiratory Med1996; 51: 107–8.

7. Kayes SG, Oaks JA. Development of the granulomatous re-sponse in murine toxocariasis. Initial events. Am J Pathol 1978;93: 277–85.

8. Vercellotti GM, McCarthy JB, Lindholm P, Peterson PK, JacobHS, Furcht LT. Extracellular matrix proteins (fibronectin,laminin, and type IV collagen) bind and aggregate bacteria. AmJ Pathol 1985; 120: 13–21.

9. Davis SD, Schaller J, Wedgwood RJ. Job’s syndrome. Recurrent‘‘cold’’, staphylococcal abscesses. Lancet 1966; 1013–5.

10. Caldwell K, Lobell M, Coccia PF. Mitogenic response toToxocara antigen and chemotactic defect in visceral larvamigrans. Am J Dis Child 1980; 134: 845–7.

11. Glickman L, Schantz PM, Dombroske R, Cypess R. Evaluationof serodiagnostic tests for visceral larva migrans. Am J TropMed Hyg 1978; 27: 492–8.

Submitted March 26, 1999; accepted April 20, 1999

Scand J Infect Dis 31: 325–326, 1999 CASE REPORT

Pyogenic Infection of the Pubic Symphysis in aDiabetic Patient

MASAAKI TAKAHASHI1,2, HIDEO MIYAKE3, MASANORI IWASE3 andYOICHI KOIDE2

From the 1Department of Orthopedic Surgery, Hamamatsu Uni6ersity School of Medicine, Hamamatsu, Japan2Department of Orthopedic Surgery and the 3Department of Surgery, Iwata Municipal General Hospital, Iwata, Japan

A 51-year-old woman with diabetes mellitus had swelling in the inguinal area leading to discharge. Insulin, irrigation of thewound and intravenous antibiotics had no effect. Fistulography and a fistula-CT showed a fistula connecting to the pubissymphysis. After curettage of the pubic symphysis, the wound was closed.

M. Takahashi, MD, Department of Orthopedic Surgery, Hamamatsu Uni7ersity School of Medicine, 3600 Handa,Hamamatsu 431-3192, Japan

INTRODUCTION

Osteomyelitis of the pubis is pyogenic infection of the pubicbone and marrow. It sometimes occurs after various typesof urological procedures (1). Osteitis pubis was previouslycommon in athletes. Although pyogenic infection was be-lieved to be the primary factor of osteitis pubis in athletesyears ago, it plays a very small or no role in athletes today(2). Osteitis pubis in athletes is now believed to be a chronic

inflammatory condition of the pubic symphysis; thus pyo-genic osteomyelitis of the pubis is rarely seen in healthyathletes. In contrast to the above, pyogenic infection of thepubic symphysis is unusual. Pyogenic infections of thepubic symphysis have been reported to occur in intravenousdrug users (3, 4). We report here a case in which the subjectwith diabetes experienced Pseudomonas aeruginosa infec-tion of the pubic symphysis..

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