key: cord-0006414-vla4tovu
authors: Caldeira, L.; Dutschmann, L.; Carmo, G.; Abreu, J.; Sousa, Gabriela
title: FatalPasteurella multocida infection in a systemic lupus erythematosus patient
date: 1993
journal: Infection
DOI: 10.1007/bf01728904
sha: 74c040f8ca42a669df8e80ce4dff68e66c1c890b
doc_id: 6414
cord_uid: vla4tovu

nan

We report the case of a 21-year-old white woman who was admitted to the Hospital Santa Maria in Lisbon with the diagnosis of septic shock. The patient had a previous diagnosis of systemic lupus erythematosus (SLE) made 6 years ago upon the appearance of fever lasting more than a month, migrating arthralgia of the hips and knees and rash, which developed after prolonged sunlight exposure on the face and hands. A thorough blood evaluation was performed which revealed the presence of a positive LE test, anti-nuclear antibodies, anti-dsDNA antibodies, lupus anticoagulant and VDRL with a negative TPHA. Steroid therapy was then initiated, but she was admitted to this hospital 5 years later due to repeated episodes of thrombosis of the lower limbs, at which time she refused to continue with any form of specific drug therapy for SLE. After having been treated for the acute thrombotic episode, the patient was discharged and kept on oral anticoagulation. Two weeks before the present admission, she suffered a cat scratch injury in the left hand. Two days later she complained of a haemorrhagic wound at the site of the injury and painful swelling in her left axilla. She went to a local hospital, where the wound was surgically cleaned and oral erythromycin was prescribed. Three days later she returned to the same hospital with the same complaints and physical signs. At that time blood samples were collected for biochemical and bacteriologic evaluation and antibiotic therapy was changed to cefradin. Despite the medication, she developed a picture of fever, prostration and confusion over the following days. As the results of the bacteriologic tests were not yet available, she was brought to the Hospital Santa Maria and admitted to an ICU, At the time of admission, the patient was conscious but deeply prostrated and confused. Her skin was sun-tanned and she presented an evident "butterfly-shaped" erythema on her face. Her extremities were cold. Peripheral arterial pulses and arterial blood pressure could not be detected or measured. Respiratory rate was 32/min and axillar temperature was 37.8°C. Cardiac auscultation revealed tachycardia and pulmonary auscultation was normal. The abdomen was diffusely painful on palpation, and although there was no muscular resistance the evaluation of any possible organ enlargement could not be made. There was a wound scar in the left hand, a painful lymphadenopathy in the left axilla and a small haemorrhage on her left heel, which was related to a fall that had occurred some days ago. There wei'e no signs of meningeal inflammation. The haemoglobin was 6.6 g/dl, the haematocrit was 17.7%, the white blood cell count was 66,000 cells/mm 3 with 91% neuta'ophils, the platelet count was 80,000 mm 3. Erythrocyte sedimentation rate was 55 mm in the first hour. Prothrombin time was 45.5(13)s and APTT was 100(30)s. Search for fibrin degradation products was negative. Blood urea was 104 mg/dl, the glucose was 148 mg/dl (not fasting), the creatinine was 4.9 mg/dl, the sodium was 134 mmol/1, the potassium was 5.7 mmol/t and the chloride was 8t mmol/1. The SGOT was 140 U, SGPT was 72 U, total bilirubin was 3.75 mg/dl and direct bilirubin was 2.46 mg/dl. Total protein and albumin were 49 g/l and 23 g/l, respectively. The ECG showed only a sinus tachycardia. The patient's vital parameters were monitored and, after collecting blood and urine specimens for bacteriological examination, therapy was begun including fluid replacement and blood transfusion (washed red blood cells), dopamine infusion, intravenous methylprednisolone administration, oxygen by nasal prong and intravenous antibiotic therapy with dicloxacillin (lg q3h), piperacillin (4g q6h) and amikacin (500 mg q24h with blood level monitoring). With this therapy we observed a slight improvement in the patient's overall state that lasted for more than 12 h, with a systolic blood pressure of 90 mm Hg and a diuresis averaging 50 cc/h, but less than 24 h after admission her state rapidly worsened as she went in a progressive coma with persistent hypotension, anuria and respiratory distress, and she died 24 h after admission. Pathological examination showed a large abscess at the left axilla, enlargement of the abdominal lymph nodes with signs of haemorrhage and necrosis, multiple punctiform haemorrhages in the epicardium, endocardium, pleurae, renal parenchyma and ovaries, small verrucous formations in the endocardium near the valvular insertion, left ventricular hypertrophy, numerous erosions of the gastric mucosa with blood filling the stomach and small bowel, hepatomegaly, splenomegaly, haemorrhagic filling of the bronchi and trachea, congestion of the lower lobes of both lungs, serous effusions in all serous cavities and cystic ovaries. Blood cultures collected at the time of admittance have grown colonies of Pasteurella multocida which was sensitive to penicillin. Serious infections are a frequent cause of morbidity and mortality in SLE patients and have been related to the immune system compromise derived both from the disease itself and from the drugs which are currently used in its treatment [ 1 ] . P. multocida infections, although quite rare and seldom fatal, can be very serious in this particular pathological context, and should be suspected whenever a cat or a dog wound is reported [2] [3] [4] . This patient had a history of recurrent deep venous thrombosis of inferior limbs, a positive lupus anti-coagulant and a positive VDRL with negative TPHA. These findings were consistent with the presence of an anti-phospholipid syndrome associated with her SLE [5] . The clinical presentation, along with the finding of multiple haemorrhages in the pathological examination are consistent with disseminated intra-vascular coagulation (DIC) which often complicates bacterial sepsis and has already been described in fatal P. muItocida infections [6] . Although the antiphospholipid syndrome could have contributed to the development of DIC, the temporal association with the documented septic state along with the clinical evolution have led the authors to think that it occurred as a consequence of the P. multocida infection. Verrucous formations found in the endocardium at pathological examination were probably a manifestation of Liebmann-Sachs endocarditis and may not have contributed in a significant way to the fatal evolution of the patient's condition. The authors think that this case dramatically illustrates the need for an early and correct diagnostic and therapeutic approach of infectious complications in these patients. Adenovirus-specific primers with particular respect to type 40 and type 41 are recommended for routine diagnosis in gastroenteritis of younger children. The detection of other adenovirus subgenera by nested primers is cited. " The section "Disease Causing RNA Viruses" deals with the detection of enterovirus in meningitis or myocarditis with respect to the heterogenicity of the genotypes. Other chapters give information on PCR techniques in the diagnosis of infections by rotavirus, flavivirus, hantavirus, and rabies virus. These reports are of special value since for some of these viruses a practicable method for virus detection does not exist. This book should be successful in giving an up-to-date overview of this rapidly developing subject and especially the beginner in the employment of I~R techniques will find much valuable information.

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